2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .5'-Tetrachlorobiphenyl (PCB 44) 2.4.4.4.2'.3-Tetramethylbutyl] phenol) Triclosan (2.2'.1-Dichloroethene (Vinylidene chloride) cis-1.What’s New in this Report What’s New in this Report In this Fourth Report.4-Dichlorobenzene (p-Dichlorobenzene.4.1.2-Dichlorobenzene (o-Dichlorobenzene) 1.3-Dichlorobenzene (m-Dichlorobenzene) 1.2'.4-Tribromodiphenyl ether (BDE 17) 2.2-Dichloropropane 2.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.3'.3.2'.6-Pentabromodiphenyl ether (BDE 100) 2.3’.3. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.html.4.4'-Tetrabromodiphenyl ether (BDE 66) 2.2.cdc.6'-Hexabromodiphenyl ether (BDE 154) 2.2'4.4'.1-Dichloroethane 1.4'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1. Table 1.6-Heptabromodiphenyl ether (BDE 183) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6.5’.2'.4.3.5'-Hexabromodiphenyl ether (BDE 153) 2.2’. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4’.2-Dichloroethene trans-1.1-Trichloroethane (Methyl chloroform) 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4’.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.5.4'.4.3.4.4'-Tribromodiphenyl ether (BDE 28) 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 (2.4'-Tetrabromodiphenyl ether (BDE 47) 2.4'.2'.2-Trichloroethane Trichloroethene (Trichloroethylene) m.1.2'.5.4. Paradichlorobenzene) 1.4.5'.2'. The process for selection is described at http://www.4'-Pentabromodiphenyl ether (BDE 85) 2.1.4.5.5-Pentabromodiphenyl ether (BDE 99) 2.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2-Dichloroethane (Ethylene dichloride) 1.gov/exposurereport/chemical_selection.2'.5.1.5'-Tetrachlorobiphenyl (PCB 49) 2.2'3.4'.

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

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

gov/nchs/nhanes/ nhanes2003-2004/analytical_guidelines. gender..htm. furans. and verification of traceable calibration materials. Urinary levels are expressed both ways in the literature and used for different purposes. In each table. For example. and organochlorine pesticides. Serum levels reported per gram of total lipid reflect the amount of these compounds that are stored in body fat. Table 2.0. Other racial/ethnic groups are included in estimates that are based on the entire population sample. probability-cluster design.S. Sample weights also are used to adjust for possible bias resulting from nonresponse and are post-stratified to U.S. and race/ethnicity as defined in NHANES. Serum levels per whole weight of serum are also included to facilitate comparison with studies investigating exposure to these chemicals and reported levels in these units. Useful unit conversions are shown in Table 2. This design does not permit straightforward analysis of exposure levels by non-targeted strata such as locality.Data Sources and Data Analysis metabolites in blood. seasons of the year. or urine levels for each environmental chemical. Data Analysis Because the NHANES is a complex. if one person has consumed more fluids than another person. serum. levels are presented two ways: per volume of urine and per gram of creatinine. multistage. but the proportion of the total population represented by other racial/ethnic groups is not large enough to produce valid estimates. and urine were based on isotope dilution mass spectrometry. Levels per gram of creatinine (i. Other racial/ethnic groups are sampled. results are given for the total population as well as by age group. 2002) and the statistical software package SUDAAN (SUDAAN Release 8. Age groups are as described for each chemical in each data table. Units of measurement are important. This type of distribution is common in the measurement of environmental chemicals in blood or urine. and nonHispanic white. For dioxins. or region. or graphite furnace atomic absorption spectrometry. including the lipid in serum. creatinine corrected) adjust for urine dilution. the measurement of quality control samples in each analytical run to detect unacceptable performance in accuracy or precision. micrograms per liter). 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. Units: For chemicals measured in urine. proximity to sources of exposure. population. These compounds are lipophilic and concentrate in the body’s lipid stores. Ninety-five percent confidence intervals around this Fourth National Report on Human Exposure to Environmental Chemicals 5 . Other mostly non-lipophilic chemicals measured in serum are expressed per liter of serum (e. 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. generally conforming to those most commonly used in biomonitoring measurements. References for the analytical methods used to measure the different chemicals are provided in Appendix C. stratified. Results are reported here using standard units. his or her urine output is likely higher and the urine more dilute than that of the other person. serum levels are presented per gram of total lipid and per whole weight of serum. including tolerance limits for operational parameters. 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.cdc. serum. non-Hispanic black. The Report presents descriptive statistics on the blood.. 2001). Laboratory measurements underwent extensive quality control and quality assurance review. PCBs. sample weights must be used to adjust for the unequal probability of selection into the survey. Statistics include unadjusted geometric means and percentiles with confidence intervals. race/ethnicity is categorized based on the sample design as Mexican American.g. state. Gender is coded as male or female. For these analyses.e. Guidelines for the analysis of NHANES data are provided by NCHS at http://www. The geometric mean is influenced less by high values than is the arithmetic mean. or by use of particular products. SUDAAN uses sample weights and calculates variance estimates that account for the complex survey design. Data were analyzed using the statistical software package Statistical Analysis System (SAS) (SAS Institute Inc.. Acrylamide and glycidamide adducts are expressed as the picomoles per gram of blood hemoglobin to which the adduct is bound. Census Bureau estimates of the U. inductively coupled plasma mass spectrometry.

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

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

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

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

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

6) 73. drinking water. 1994).2 (58. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. and cosmetics (NTP-CERHR.Acrylamide Acrylamide CAS No.5 (52.0.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.7-64.5) 66.1-64. Fourth National Report on Human Exposure to Environmental Chemicals 11 .4 (54.4-60.1 (88.2) 57. 2005).4-83. mineral processing.6 (81.0 (57. Elimination occurs mainly in the urine as mercapturic acid conjugates.S.7) 75th 79.8 (81. EPA. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. acrylamide has produced upper airway irritation following inhalation of high levels. Since acrylamide has limited volatility and high water solubility. 217 million pounds of acrylamide were produced commercially in the U. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.8 (91.7) 73.9-52.9) 58. 2005).0 (53.3-2. Estimated intakes in children are about twice that of adults (DiNovi and Howard.3-71.8 (57.0-108) 152 (139-175) 126 (111-142) 108 (86.0-66.6-65.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. and from dermal contact with products that contain residual acrylamide.4-76.1 (73. it was discovered that acrylamide is formed when starch-rich foods.4) 57.2-67. Acrylamide is not thought to accumulate in the body at environmental doses..S. People may be exposed to acrylamide from foods. 2004.5 (74. Recently.1-57.2-91. but can covalently bind to form adducts with proteins.7 (55.8-55.5-80. such as potatoes and some grains. Commercially.4 (51. widely distributed in tissues.2 (75. (NTP-CERHR.6) 71. ocular and dermal irritation from direct contact with acrylamide containing materials. 2004).1 (52. the main source of exposure is from the diet.9 (69. as an absorbent in disposable diapers. Fennell et al.9 (60. FDA. are heated at temperatures used for frying and baking.9-61.0 (67.0-49.9) 75.5-85.0) 57.6-104) 82. 2005). and an average daily intake is estimated as 0. EPA.3 (55.7 (58. Natural substances in the food are converted to acrylamide.6) 90. soil conditioners.2 μg/kg/day (U.8-57.6-108) 61.7) 58.2 (62. acrylamide is synthesized and used in the production of polyacrylamide polymer. 1990. 2005). population from the National Health and Nutrition Examination Survey.1) 53.6-75..0-58.4 (59.7-64.7 (65.S. EPA reference dose of 0.S. or to glutathione conjugates (Calleman et al.4) 57. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.1) 62. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.9) 63. 2006.5) 58.1 (83.2) 57.1-64.1) 55.1 (47.5 (79. 2002). glycidamide. in permanent press fabrics.3) 63. In 1997.S.2-118) 98.6-66.4) 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. Polyacrylamides are useful water-compatible polymers used in water treatment.8 (52.3) 70. and well below doses known to cause nerve damage or carcinogenicity in animals.2-114) 163 (147-191) 96. and in the synthesis or compounding of dye materials.1-61. pulp and paper production. in some sealing grouts.6) 50.1) 101 (95.7 (63.7) 54.2-93.7) 96.2-77.4 (54. Animal studies indicate that acrylamide is well absorbed. In the general population.4-60.0 μg/kg for adults (FAO/ WHO. 2005). but are generally above the U.6-61. 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. FAO/WHO. gels.9) 57. Survey Geometric mean (95% conf.2-59. In humans. smoking.1) 46.0) 85.3) 86. and in some cosmetics.5 (44. 2006).0 (69. These estimated intakes are hundreds of times lower than occupational exposures..4) 100 (89.6 (51. interval) 61.6 (56.9-105) 86.4 (53. and binding agents.3 (53.0-104) 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. Tareke et al. and is either metabolized to the reactive epoxide.7-60. 2005.4-89.2-70.9 (54. see Data Analysis section) for Survey year 03-04 is 3.

and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.2) 55.3) 59. 2006)..S.0 (75. male germinal cell injury. 1997..6-64.1-70.7 (57.3) 85. 2005..9-62.2 (56.2-68.9) 65.epa. 2005) and sperm DNA adducts (Xie et al. Maniere et al. 1997.2) 87..7 (61.8) 45.4 (56. 2005). Additional information is available from U.0-93..5) 87.5) 75th 85. Rice.7-64.4 (51.7) 74.2-90.9-76.5 (42.6 (66.4) 46..0 (70.4-103) 79..9) 59. and other sites) (FAO/WHO.5-94.1 (82. 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. 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. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al..4 (57.1 (66.. 2003. 2002. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2004). 2005).8 (44.1) 60.2 (63.4 (81. 2005).2 (72. 2005.. 2005.1-60.1 (70.. U.1 (56.5) 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. probably through its epoxide metabolite.4-59.. scrotal.5 (83. Vesper et al. most non-smokers had levels less than about 100 pmol/gram hemoglobin. After exposure ceases. Vesper 2005) and smoking (Bergmark. 2005.8) 60.8 (51.who.. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).5-66.4) 83. interval) 59..7-62. adrenal. 2006) have been demonstrated after acrylamide dosing.. 2005). gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. see Data Analysis section) for Survey year 03-04 is 4.0 (80. EPA at: http://www. although different analytic methods can affect results. Klaunig et al.1) 56. population from the National Health and Nutrition Examination Survey. and cancer (mammary. uterine.9) 75. EPA. 2006.1 (57. In addition.1-62.4-98. Acrylamide is clastogenic and can produce dominant lethal mutations. 2009). 2005. U. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.1-56. altered gene expression in testicular tissues (Yang et al. respectively) are markers of integrated acrylamide exposure over the preceding few months.pdf.5 (59.9) 87..0) 94.4 (90.S. dominant lethality). fetal death. Schettgen et al.7) 61.int/ ipcs/food/jecfa/summaries/summary_report_64_final. Puppel et al. Mucci et al.4) 53.0-103) 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 64.5-64.5-92. and neuronal DNA reactivity (Doerge et al. 2005.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.4-65. 2001). Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. Schettgen et al. 2005..6-90.7 (87..7) 60. 2006).5) 71.8-61.0 (52. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. Glycidamide has been shown to react with DNA (Doerge et al. AHA levels have been shown to increase with dietary intake (Hagmar et al.9-78.7-86. 2002.S.4 (61.8-48. 2008).0) 118 (103-126) 121 (112-134) 113 (94. Puppel et al.9-138) 143 (130-159) 96. Axonal degeneration.9 (57. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.. 2005. 2005) have been demonstrated in animals.7) 90. presynaptic nerve terminal binding (LoPachin.Acrylamide occupational exposures.3-78.3-101) 95. 2005. 2005.S. thyroid. EPA.8-49. 12 Fourth National Report on Human Exposure to Environmental Chemicals . Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.1) 62.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.9 (58.0-62. IARC classifies acrylamide as probably carcinogenic to humans.2) 65.3) 59.6 (90.. NTP-CERHR. reproductive effects (reduced litter size.6-62.5 (56.3 (56. Hagmar et al.9 (81. 2004. 2005.2-91. Survey Geometric mean (95% conf.0.7 (84.3) 59. glycidamide (NTP-CERHR.9-64. 2008).9-77.

. Malmberg B. Paulsson B. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Wu Y. Adv Exp Med Biol 2005. Costa LG.56. Churchwell MI.int/ipcs/ food/jecfa/summaries/summary_report_64_final. et al. Calleman CJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Tornqvist M.120(1):45-54. Godard T. Yang JS.pdf. 64th Meeting: Summary and Conclusions (FAO/WHO). Tian G. Food and Drug Administration (FDA). morphological and molecular endpoints in animal models. Granath F. Available at URL: http://www.cfsan. Alexander J. Guffroy M. Mutat Res 2005.fda. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 2006. February.gov/chemicals/ acrylamide/Acrylamide_Monograph. Burgess J. 2/3/09 Perez HL. Metabolism and hemoglobin adduct formation of acrylamide in humans. LoPachin RM. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Survey data on acrylamide in food: individual food products. Bridson WE. Duale N. Farmer PB. NIH Publication No.3:406-412.580(1-2):131-141. 2004. J Agric Food Chem 2008.27(4):219-226. Nordander C. 2009 Jan 8. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Andersen M. April 13-15. Kamendulis LM. DiNovi M and Howard D. 054472. Beland FA. Doerge DR. 2/3/09 Klaunig JE. 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. 1999). Available at URL: http://cerhr. Hagmar L. He F. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.561:21-37. Zhang S.580(1-2):119-129. 2001. Snyder RW. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.who. 2/3/09 Hagmar L.. Calleman CJ. 6013-6019.html#u1004. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide.. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Food Chem. Mutat Res 2005. Acrylamide neurotoxicity: neurological. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Aprea P. Perez et al. et al.561:49-62. and Research Strategies. Rosen I.Toxicol Appl Pharmacol 1994. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Axmon A. Becher G. Toxicol Appl Pharmacol 1993. Wilson KM. et al. Osterman-Golkar S. CFSAN/Office of Plant and Dairy Foods.Acrylamide In occupational settings. Paulsen JE. Rome. Bruze M. Wirfalt E. Adv Exp Med Biol 2005. Finding a measurable amount of acrylamide or glycidamide hemoglobin adducts in blood does not mean that these levels of acrylamide or glycidamide hemoglobin adducts cause adverse health effects. gov/~dms/acrydata. Spicer R. 1993. Cheong HK.niehs. Toxicol Sci 2005. Toxicol 2005. Doerge DR. Scand J Work Environ Health 2001. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. He F. Maniere I. Summer SCJ. 2005. Uncertainties. July. Italy. [Epub ahead of print] Dybing E.pdf. Chicago.nih. et al.. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. National Toxicology Program. Available at URL: http://www. Calleman CJ. The Updated Exposure Assessment for Acrylamide.10(1):78-84. smoking habits and gender. Bergmark E. In another study. et al.43:365–410. Costa LG. Hagmar et al. Mucci LA. smokers and nonsmokers. Magnusson AL. Twaddle NC. References Bergmark E. 2004 Acrylamide in Food Workshop: Update Scientific Issues.. da Costa GG. 2001). Tornqvist M. Joint FAO/WHO Expert Committee on Food Additives.126(2):361-371. Chem Res Toxicol 1997 Jan. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Fennell TR. 8-17 February 2005. Mechanisms of acrylamide induced rodent carcinogenesis. Bergmark E. Laurentie M. 1994). Chem Res Toxicol 1990.580(1-2):157-165. McDaniel LP. Bjellaas T. Human exposure and internal dose assessments of acrylamide in food. Kautiainen A. Acrylamide intake through diet and human cancer risk. Fennell TR.85:447-459. 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. Mutat Res 2005. Bergmark E. Churchwell MI. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Haugen M. Toxicol Sci. Illinois.

Xie Q. J Agric Food Chem 2008. Broding HC. Choi JH. 2/3/09 Vesper HW. Toxicological effects of acrylamide on rat testicular gene expression profile.S. Benetou V. Angerer J. Tjønneland A. Schettgen T. Lee SH. Ingham L. et al. Liu K. Slimani N. Chemical Summary for Acrylamide. Office of Pollution Prevention and Toxics. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Acrylamide. The carcinogenicity of acrylamide. Liu Y. a carcinogen formed in heated foodstuffs. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Available at URL: http://www.134(1-3):65-70. Drexler H.163(2):101-8.S. EPA).207(6):531-9. Environmental Protection Agency (U. Kutting B. Gray JG. Fueller F. Mutat Res 2005. J Agric Food Chem 2002.580(1-2):71-80. Lee MH. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. revised 1/3/06. Hemoglobin adducts of ethylene oxide. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Vesper HW. Tjaden Z. Vesper HW. Tornqvist M. 1994. Rydberg P. Mutat Res 2005 Feb 7. Toxicol Lett 2006.580(1-2):3-20.htm. Agudo A. Yang HJ. Anal Biochem 1999. U.19(4):527-34. Schettgen T.epa. Rice JM. propylene oxide. Toxicol Lett 2002.gov/chemfact/s_acryla. EPA). Angerer J. Letzel S. Hallmans G. Eriksson S.561:89-96. Rapid Commun Mass Spectrom 2006.txt. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.20(6):959-64. Myers GL. Drexler H. Rossbach B. Ospina M. Meyers T. Han CH. Licea-Perez H.Acrylamide glycidamide by gas chromatography-mass spectrometry. Marko D. Analysis of acrylamide. Int J Hyg Environ Health 2003. Fu D. Available at URL: http://www. Ding X. Jin Y. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Sun H. et al. Environmental Protection Agency (U. Ospina M. Han DU. Smith A. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. 2/3/09. Adv Exp Med Biol 2005.274(1):59-68. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Karlsson P.gov/iris/subst/0286. Puppel N. Chae C.S. Drexler H. Angerer J. Weiss T. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions.206(1):9-14.S. Schettgen T.50(17):4998-5006. Reprod Toxicol 2005. U. September. Washington (DC).epa.56(15):6046-53. Int J Hyg Environ Health 2004. Tareke E. Integrated Risk Information System (IRIS). Meyers T.

02) 1.148-.197) . Fourth National Report on Human Exposure to Environmental Chemicals 15 . < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.S.073) < LOD .060-.990) .111-.32-2.47-3. Cigarettes contain about 1.540-.500 (. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.20) .S.070-.040-.060 (<LOD-. 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.120-.120 (.220-.87-3.17 (.047-.35 (2.506 (.110-.05) 1.740-1.120 (.39) 3. ear problems.09-3.193) .75) 1.77 (1.12) 1.190-.213) .32) 1.540 (.198) * .104-.02) 1.860 (.23-2.050 (.77 (2.120-.108) * .625) .78) 2.234) .44 (2.580-1.110-.950 (. and 0.110 (.930 (.216 (.430-1. emphysema. 83% of measurements had an LOD of 0.071 (.260) 1.14) .50-1.14-1.087) < LOD < LOD .190-.180 (.120 (.140 (.110 (.077) .54 (1.580) .280 (.110-.70) 2.230 (.180) .85 (1.160 (.533-.190-.800 (.00) 1.30) * .054 (.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 .066-.126) .22) 2. DHHS.620 (.140-.160 (. see Data Analysis section) for Survey years 99-00.20) 1.180) .080-.360) .057-.505 (.060-.12-4.050 (<LOD-.920 (.726) .150) .068) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .50-4.043-.040 (.39 (1.310) .55 (1.090-.059-.12 (2.68) 2.480-1.21-1.220) .210 (.050 (<LOD-.660) .12 (1.570-1.68 (1.080-.160) .050 (<LOD-.57) 2.050) .167 (.061) < LOD .220) .20 (.850 (.410) .54) 1.030-.670) .050-.160 (.310) 90th 1.11) .18-3.400-.23 (2.060 (.070) .26-1.110) .95) 1.080 (.059-.071) .130 (..120 (.260-1.53-4.17 (1.54 (1.080-.28-1.350-.23 (1.120 (.15 (2.053 (<LOD-.00) .230) .110 (.080-.047-.302) .350-.5% nicotine by weight (Kozlowski et al.20-2.180 (.28) .05.88 (.040-.710 (.89) 1.094) .310-1.S. DHHS. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 1998).49) 1.040 (.630 (.44) 2.730 (.187) .88 (1.42 (1.090-.770) .450-.690 (.070) 75th . cardiovascular disease.53 (1.087 (.38-2.131 (.201) . acute respiratory infections.154-. acute respiratory illness.084) .60-2.139) * .470-.910-1.99) 2.01) 3.21-1. and various other disorders (U.020-.030-.015.077) .740-1.089) Age group 3-11 years 99-00 01-02** 03-04 .066) .990 (.45) 1.063) .300) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer. population from the National Health and Nutrition Examination Survey.180) .23 (.62 (2.110 (. 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.320) .70-2.76 (1.15) 2.630 (.43 (1. maternal exposure during pregnancy can result in lower birth weight.350 (.16) .62) 2.164 (.520 (.050 (<LOD-.310-1.770) .052 (<LOD-.050) .65 (1.308 (.088-. 2004).77 (1.93) .164 (.84-3.19-2.100-. respectively. and exacerbated asthma (U.630 (.200) 1.240 (.050-.160) .090-.790) .81-2.63 (2.142-.510 (.370-.48-2.49) 1. and 17% had an LOD of 0.312) .620-1.150) . producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.19) 1.480-.070) . stroke.900-1.080) < LOD .30) 2. Survey Geometric mean (95% conf.66 (1.34 (1.66) 1.570 (.32-2.30) 2.060) .087-.09-2.840) 3. and 03-04 are 0.163 (.96-4.950-1.075 (. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.68) .180) .55-2.145) .153-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .44) 2.060 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.060-.83-2.50 (1.140 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.144 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.33-2.820) .02 (.770-1.058 (.99) 2.621-1.110) .070 (<LOD-.163) .997-3.Cotinine Cotinine CAS No.44 (1.96) 2.137-.01 (1.015 ng/mL.05 ng/mL.080 (.42-4.04 (1.79) 3.21 (. ** In the 2001-2002 survey period.48-3.960-1.124 (.160-.052 (<LOD-.140-.062 (.600-1.17) .92 (1.086 (.580 (.137 (.060 (.96 (1.14) .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.106-.09-3.120) .030-.19) .63-2.130) . 2004).110 (.040 (.175 (.180) .066 (.076-.50) 3.115-.188) . 2006).080) < LOD < LOD .428-.068) .94) 1.40) .030 (.20 (1.66-3.

3 to 30 µg/m3. salivation. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. 2005).. and hair. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005.. 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. Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. and peppers. 2004). Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . 2006).. urine. Symptoms of 16 nicotine withdrawal include irritability. 1998). Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al. In homes with one or more smokers. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. Hukkanen et al. saliva. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. Cotinine. 1975.. 1999. 2005). 1998). The IARC and the NTP consider tobacco smoke to be a human carcinogen... 2005. Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system.. diaphoresis.. contains nicotine in larger amounts than other nicotine-containing plants. Children are primarily exposed to ETS by parents and caregivers who smoke. Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al. Workers who harvest tobacco can be exposed to nicotine and become intoxicated as a result of the transdermal absorption of nicotine contained in the plant. craving. 2004). Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff.. eggplants. 2006). non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans.. 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. or skin patches that contain nicotine. chewing tobacco. cognitive and sleep disturbances. 1994). 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. Once absorbed. (CDC. 1991). html. 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. 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. During each previous NHANES survey.. variable changes in blood pressure and heart rate. NCI. Wilson et al. More information about the effects of smoking and nicotine can be found at: http://www.. the adjusted geometric mean serum cotinine was higher in children (aged 4–11 years) than in adults among both non-Hispanic blacks and non-Hispanic whites (Pirkle et al. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. Over the previous decade. Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al. diarrhea. Hukkanen et al. Soliman et al.nida. a process involved in the development of addiction. with higher levels measured in restaurants and bars.. Serum cotinine has been measured in many studies of nonsmoking populations.nih. with heavy exposure to ETS producing levels in the 1–10 ng/mL range. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. seizures. However. which include potatoes. 1996). mean air concentrations typically range from 2 to 14 µg/m3 (NTP. The tobacco plant. 1999). Nicotiana tabacum. 1999. Pirkle et al. Acute tobacco or nicotine intoxication can produce dizziness. 2006. nausea. Iwase et al. 2005). nicotine has a half-life in blood plasma of several hours (Benowitz. 1996). vomiting. 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. or chewing gum. tomatoes...gov/researchreports/nicotine/nicotine. For an adult. Perez-Stable et al. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration.Cotinine 1994. and increased appetite. the primary metabolite of nicotine. nasal sprays. 2005. and death. Cotinine can be measured in serum.

Tobacco Smoke and Involuntary Smoking.niehs. Pirkle JL. Smoking and Tobacco Control Monograph 10 [online]. George CF. U. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. IARC Monogr Eval Carcinog Risks Hum.S. Vol 83.114(6):853-858.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Department of Heath and Human Services. Coordinating Center for Health Promotion. June. J Pharmacol Exp Ther 1999.S.S Department of Health and Human Services (U. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Clin Pharmacol Ther 1994.php. Sweeney CT. Office on Smoking and Health [online] 2006.56:483-493. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.15:302-307.niosh. Atlanta (GA): 2005. Mehta NY. Hukkanen J. Caraballo R. U.275:1233-1240. Strauss WJ. and the United States.S. JAMA 1996.gov/tcrb/monographs/10/. Summary of Data Reported and Evaluation [online] 2004. Vol 38. Available at URL: http://monographs. et al.4:313-316.nih. Dollery CT. 4/13/09 International Agency for Research on Cancer. 1999-2002. Tobacco related exposures. 11th ed. Pirkle JL. 4/13/09 U. Herrera B. Racial/ethnic differences in serum cotinine levels among adult U. 1988-1991. Available at URL: http://www. Absorption and metabolism of nicotine from cigarettes. 4/13/09 Iwase A. Available at URL: http://ntp. Cotinine as a biomarker of environmental tobacco smoke exposure. Metabolism and disposition kinetics of nicotine. available at URL: http://mtn. Pharmacol Rev 2005. et al. Ethnic differences in N-glucuronidation of nicotine and cotinine.iarc. 1991.php. Centers for Disease Control. Benowitz NL. Bernert JT. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Available at URL: http://monographs.fr/ENG/Monographs/ allmonos90. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.cancer.S. Bernert JT. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Modin G. 4/13/09 Centers for Disease Control and Prevention (CDC). References Armitage AK. Brody DJ. Centers for Disease Control and Prevention. Available at URL: http:// cancercontrol. Third National Report on Human Exposure to Environmental Chemicals. population to secondhand smoke: 1988-2002.pdf.7:369-375. the United Kingdom. Exposure of the U. 4/13/09 Perez-Stable EJ. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. U. Aiba M. Environ Health Perspect 2006. Maurer KR. iarc. Benowitz NL. Fong I. Tob Control 2006. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. National Institute for Occupational Safety and Hygiene (NIOSH). Giovino G. National Toxicology Program (NTP).57(1):79115. Jacob P. Nicotine metabolism and intake in black and white smokers.fr/ENG/Monographs/allmonos90. Turner DM. Kira S. Sosnoff CS. In Report on Carcinogens. Mowery PD.280:135-140. 2004. Kozlowski LT. Jarvis MJ. Jacob III P. Respiratory nicotine absorption in non-smoking females during passive smoking. DHHS). Centers for Disease Control and Prevention. Pechacek TF. IARC Monogr Eval Carcinog Risks Hum. Etzel RA. Pickett MA. Caudill SP. DHHS).S. Richter PA.gov/library/ secondhandsmoke/. Benowitz NL. Perez-Stable EJ. 4/13/09 National Cancer Institute (NCI). Lewis PJ. 1988-1991.63:139-43.cdc. National Center for Chronic Disease Prevention and Health Promotion. Epidemiol Rev 1996. Brody DJ. Houseman TH.280:152-156. Jacob P III. Giovino GA. Trends in the exposure of nonsmokers in the U. Department of Heath and Human Services. Tob Control 1998. Jacob P III. Pollack HA. Schober SE. Am J Public Health 2004. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.94(2):314-320.S Department of Health and Human Services (U. Soliman S. Flegal KM. Coordinating Center for Health Promotion.gov/eid/rmca/critdocs/ criteriadoc/33. BMJ 1975.S. cigarette smokers: the Third National Health and Nutrition Examination Survey. International Agency for Research on Cancer.291(3):1196-1203. Vogler GP. [online]. Summary of Data Reported and Evaluation [online] 1986.pdf.gov/ntp/roc/eleventh/profiles/ s176toba. JAMA 1998. Warner K. Benowitz NL. Curtin LR. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.18:188-204.S. Tobacco Smoke. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Benowitz NL. Herrera B. Pechacek TF. 1999. JAMA 1998. Int Arch Occup Environ Health 1991.surgeongeneral. Schwartz SS.

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

epa.S.140 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.170 (.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .1.190) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 . 134-62-3 General Information N.180 (.100-. 2003).250) < LOD . DEET is not a developmental or reproductive toxicant in animals (U. population from the National Health and Nutrition Examination Survey.S.180) < LOD .100-.120-.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110 (<LOD-.110 (.560) < LOD . 1998).110 (.210 (. Urinary N. Neurological effects in humans.240) < LOD . One survey detected DEET in 74% of sampled streams in the U.110 (<LOD-. 1998). DEET is also used in combination with dermal sun screens (U.S.150) < LOD .170 (. have been reported as result of self-poisoning by ingestion or excessive dermal application.110 (.270) 688 678 518 700 598 956 Limit of detection (LOD.140-. and they range in concentration from 4% to 100%. 2002). Survey Geometric mean (95% conf.110 (.130-.EPA.140) < LOD .EPA. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. including seizures and encephalopathy.100-. Its use is recommended for prevention of several vector-borne diseases. Sudakin and Trevathan.N-Diethyl-meta-toluamide (DEET) CAS No. 2005). (U. < LOD means less than the limit of detection.EPA at: http://www.180 (.100 (<LOD-.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.140) < LOD . DEET is not registered for use on agricultural commodities. 2002).140) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.130 (.N.130) < LOD . About 3-8% of dermally applied DEET is absorbed.S.N-Diethyl-meta-toluamide (DEET) N..110-.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.449 and 0. After absorption.100-.gov/pesticides/.130-.. DEET can be applied to clothing and the skin to repel biting insects..130) < LOD .S.160) < LOD .120-. EPA.180 (.100-. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. Additional information is available from U. 1995.520) < LOD . DEET is not genotoxic.130 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . DEET has low acute toxicity.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. (Kolpin et al. 2003).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 .220 (. There are over 225 insect repellents brands containing DEET. which may vary for some chemicals by year and by individual sample.110-.130 (.100-.130-. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.130-.

representative subsamples from NHANES 2001-2002.480 (.250-.410-.250 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U. 20 Fourth National Report on Human Exposure to Environmental Chemicals .490) < LOD .370) < LOD .130 (<LOD-.170-.280-1.390-. 2007).630) < LOD .270 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < 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.230) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.. population from the National Health and Nutrition Examination Survey.240-.270-.350) < LOD .330 (.320 (.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.330 (. 2005).370-.500 (.230-.270 (<LOD-.190 (. 1992).190 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.640 (.240) < LOD .150-.190 (<LOD-.410 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.190-.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 .500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.N.230-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.290-.410 (.140-.440) < LOD .280 (. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.. Urinary N.270) < LOD .S.300 (. In this survey period.S.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.350) < LOD .200 (.350-.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 .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 .150) < LOD .93) < LOD . Urinary DEET levels as high as 5.320) < LOD .250) < LOD .

gov/teach/chem_summ/ DEET_summary. N.N-Diethyl-meta-toluamide (DEET) References Arcury TA. pdf. Trevathan WR.41(6):831-839. hormones. Environ Sci Technol 2002. Lowry LK.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Schoenig GP. Centers for Disease Control and Prevention (CDC). Available at URL: http://www. pp. J Anal Toxicol 1992. Barr DB. Diethyltoluamide (DEET). Tapia J.S. Furlong ET. September 1998. et al. Quandt SA.S. Hartnagel RE Jr. Third National Report on Human Exposure to Environmental Chemicals.N-diethyl-mtoluamide following dermal application to human volunteers.S.gov/oppsrrd1/REDs/0002red. 1-118. streams. 2005. Osimitz TG. Washington (DC): U.S.N.S. Meyer MT. Sudakin DL. Page BC.2:341352. 1993-1997. Chen H. Int J Toxicol 2002. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Absorption.epa.epa.25:95-100. Thurman EM. Fundam Appl Toxicol 1995. 1999-2000: a national reconnaissance. Grzywacz JG.pdf. Selim S.115(8):1254-1260.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Environ Health Perspect 2007.36(6):1202-1211. Environmental Protection Agency (U. 4/9/09 U. Bell JW. Smallwood AW. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Atlanta (GA). Zaugg SD. EPA 738-R98-010.S. Pharmaceuticals. and excretion of N. 2005 Kolpin DW. DEET: a review and update of safety and risk in the general population. Environmental Protection Agency (U. Available at URL: http://www. Barber LB. J Toxicol Clin Toxicol 2003. U.EPA). Veltri JC.EPA. Reregistration Eligibility Decision (RED): DEET.16(1):10-13.EPA). DeBord KE. Toxicity and Exposure Assessment in Children’s Health. U.S. EPA. Chemical Summary. metabolism. Human exposures to N. and other organic wastewater contaminants in U. Gabriel KL.

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

pdf . 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). et al. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Hara K.36(6):1202-1211. Leranth. niehs. Ye X. Endocrinology 2008. Italy. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. U. Imai H. Exposure of the U. Kawamura N. Available at URL: http://ecb. hormones. Ema M. Watanabe C. Reidy JA. K. Rat two-generation reproductive toxicity study of bisphenol A. Munro IC. Ekong J. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). 2007.59(9):625-628. May 22. Han SY. and Hardy MP. Biochem Biophys Res Commun 2003. Arakawa C. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.nih. Furlong ET.pdf. N. Bisphenol A. Ispra.europa.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Doull J. Keimowitz AR. Caudill SP. Barr JR.S.gov/chemicals/bisphenol/bisphenol. and other organic wastewater contaminants in U. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. vom Saal FS. Cha SW. Marr MC. 2/4/09 Fujimaki K. In vitro and in vivo interactions of bisphenol A and its metabolite.pdf . bisphenol A glucuronide. Hanaoka T. Thomas BF. Howdeshell KL. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Timms BG. Calafat AM. 2/4/09 European Commission. 2008. Belgium. et al. Tsugane S.nih.J. Brussels. Zaugg SD. Myers CB. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Reidy JA.nih. 1999-2000: a national reconnaissance. Toxicol Sci 2002. Environ Sci Technol 2002. T. Barber LB.S. Gender differences in the levels of bisphenol A metabolites in urine.10:875-921. Reprod Toxicol 2001. Park S. Kim CS. Kroes R. Environ Health Perspect 2008. Thurman EM. 2003. Cohen JT. Pharmaceuticals. Han SS.14(2):149-157.niehs.145:592-603. European Commission. Bradley S. Needham LL.pdf. Watanabe S. 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.35(2 Pt 1):238-254. Kim YH. et al.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Hughes C. Rhomberg et al. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Needham LL. NC. Occup Environ Med 2002. Yoshinaga J. Serizawa S. Nippon Eiseigaku Zasshi 2004. Shin HC. Human Health.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. McConnell EE. DirectorateGeneral Health and Consumer Protection. Barr DB. Lynch BS.gov/chemicals/bisphenol/BPAFinalEPVF112607. Twomey K. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.102(19):7014-7019.312(2):441-448. National Toxicology Program. Regul Toxicol Pharmacol 2002. and Hajszan.59(4):403-408.113(4):391-395. Hlywka JJ. Szigeti-Buck. National Institutes of Health. 4. Klinefelter GR.. Chung MK. Richter CA.780(2):365-370.. Proc Natl Acad Sci USA 2005. Available at URL: http://cerhr.149:988-994. 2002. Needham LL. C. Cunha G. Matthews JB. 2/4/09 Ouchi K. Department of Health and Human Services. Chem Res Toxicol 2001. Koulova AI. Barton L.eu/ health/ph_risk/committees/sct/documents/out156_en. 5: 505-523. Calafat AM. Available at URL: http://ntp. Wong LY.jrc. with estrogen receptors alpha and beta. Sottas CM.S. niehs. Life Sci 2001. Rubin C. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Available at URL: http://cerhr. Haighton LA. An evaluation of the possible carcinogenicity of bisphenol A to humans. Available at URL: http://ec. Zacharewski TR. Research Triangle Park.137(3):353-362. Kolpin DW. Furukawa M. Fujii S. Gray GM. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. streams.. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Ikka T. Brine DR. Harazono A. November 26.pdf. Hum Ecol Risk Assess 2004.Environmental Phenols References Akingbemi BT. Kiguchi M. Kuklenyik Z.Scientific Committee on Toxicity. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Environ Health Perspect 2005.69(22):2611-2625. Endocrinology 2004. Tyl RW.116(1):39-44. 32 Fourth National Report on Human Exposure to Environmental Chemicals . J Am Dent Assoc 2006. Yang M. Calafat AM. National Institute of Environmental Health Sciences. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. September. Ecotoxicity and the Environment (CSTEE). Koh WS. Pyo MY.68(1):121-146. Kim JC. August 2001. Meyer MT. Joint Research Centre Institute of Health and Consumer Protection. MacLusky. Joskow R.

Csanady GA. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chuang JC. Large effects from small exposures. Chang SS.103(1):9-20. Jang JY. Wilson NK. et al. Nagel SC. and nonylphenol at home and daycare. Biological monitoring of bisphenol a in a Korean population. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Endocrinology 2006.44(4):546-51. Kim SY. bisphenol-A. Morgan MK. Kawamoto T. Vom Saal FS. vom Saal FS. Arch Environ Contam Toxicol 2003. Food Chem Toxicol 2002. Chem Res Toxicol 2002.40(7):905-12. III. Filser JG.113(8):926-33.Environmental Phenols Volkel W. Environ Health Perspect 2005. Lordo RA. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Sheldon LS. Witorsch RJ. Dekant W. Lee SM. Hughes C. Environ Res 2007. An observational study of the potential exposures of preschool children to pentachlorophenol.15:12811287. Yang M. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Colnot T. Welshons WV.147(6 Suppl):S56-69.

30) 90th 1.268-. 140-66-9 General Information 4-tert-Octyphenol.5% of 139 U. industrial cleaners. which may vary for some chemicals by year and by individual sample.70 (1. see Data Analysis section) for Survey year 03-04 is 0. 1996).. and impaired spermatogenesis (e.50-2.90) 2.900 (. During the 1980s and 1990s.50) 1.. The alkylphenol ethoxylates enter the environment through human use of products containing them..60) 613 652 1092 Limit of detection (LOD.600) . Several alkylphenols.. In rats.507) * < LOD . the various alkylphenols have also been used as emulsifiers and modifiers in paints.00 (.60-3.40) 2. orally administered 4-tert-octylphenol was well absorbed.700-1.10) 2.60-3.500 (.70 (1. and to alkylphenoxycarboxylates.3.50-3.40) 1. 2002).30) 2.600) 1. textiles. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. including 4-tert-octylphenol.900 (.20-2.900 (. In 1999-2000.40) * 03-04 03-04 03-04 .3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.600) .. through sewage. 1995.60-3.389 (.50) .20-2.20-2. fish) and drinking water.S.497) * . Saito et al.50) .30 (1. to shorter chain alkylphenol ethoxylates.200-. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.477) . several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.60-3.300 (<LOD-. and through manufacturing waste streams (Warhurst. 2004).40) 2.300 (<LOD-. have demonstrated estrogenic effects particularly when injected at high doses in animals. 2000. < LOD means less than the limit of detection.50 (1. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. 4-octylphenol monoethoxylate was detected in 43.20) 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 . and the polyethoxy chain may consist of up to 50 ethoxy units. Disposition in humans has not been studied sufficiently. and some personal care products.500) .70 (1. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.300 (<LOD-. Ying et al. 2003.200-. an alkylphenol. which are anionic surfactants used in detergents. altered estrus cycles and reproductive outcomes. population from the National Health and Nutrition Examination Survey.00) 1229 1288 03-04 03-04 03-04 * .20-2. is used to manufacture alkylphenol ethoxylates. In the 1990s. Less frequently.20) 314 715 1488 03-04 03-04 * * . leading to inhalation as another potential exposure route (Rudel et al.300-.30 (1.500) 75th . The alkylphenols can bioaccumulate in some fish. 2002).80 (1.300 (<LOD-. pesticides. Laws et al.Environmental Phenols 4-tert-Octylphenol CAS No..80) 2.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..80 (1.299-.300-.50) 1.369 (. 1997.500) .20 (1.10 (1.500) .900 (.600-1.500-1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. Survey Geometric mean (95% conf.90) 2. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.20-2. 34 Fourth National Report on Human Exposure to Environmental Chemicals .357 (.274-.g. streams in 30 states (Kolpin et al.600-1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.20) 1.70 (1. and was quickly eliminated from the blood (Certa et al.30-2.30 (.900 (.20) 2.600-1. and some of their degradation products are toxic to aquatic life.10) 1.80 (1.800-1.60-3.30 (1. Bian et al. over 500.600-1. 2000.60-3.300 (<LOD-.10-2.400 (. Blake and Boockfor.40 (1.. and emulsifiers.600-1.1. Urinary 4-tert-Octylphenol (4-[1. Indoor and to a lesser extent.600) .600-1.30 (1.000 tons of alkylphenol ethoxylates were produced annually worldwide.00 (.400) 1. did not bioaccumulate.60) .400 (.30) 1. impaired steroidogenesis.2.. Katsuda et al.50) 1. 2006.500-1. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.400 (.g.S.10 (. testicular atrophy. altered neonatal sexual development. and from contact with some personal care products and detergents.40) 1.10 (.20-2. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.60) 1. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).00 (1.

06 (2.620) .05-2. Fourth National Report on Human Exposure to Environmental Chemicals 35 . 2001.03 (1.73) 2.500-1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.460 (. Nagao et al.740 (.280-.03-6.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78) 3.64 (. 2004.59) 1.22) .199-.00) 1.11) 1.410 (.640-1.450) 1. or their corresponding ethoxylates with respect to human carcinogenicity.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 .910 (. 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.29) 2.349) * < LOD .76 (2.3.40 (1..54) * 03-04 03-04 03-04 .33 (2.43-3.43) 1..730-1.470-1. In a small number of adult Japanese volunteers.270-.11) 2..260 (<LOD-.S.36-3. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure..62 (1.50 (2.530) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.860 (.00) 2.620-1. 2001).00) 2.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.170-.53-3.470) 75th .550-1.78 (1.435 (.610) .25-2.11-2.10-2.270 (. representative subsample of NHANES 2003-2004.384) * ..207-.33) 3.770 (. Sweeney et al.540-1. IARC and NTP have not rated octylphenol.740 (.41) .20 (1.68-2.25) 90th 1.62 (1.Environmental Phenols Myllymaki et al. Calafat et al.00 (.420) ..08) 1.570) . 4-tert-Octylphenol is not considered directly genotoxic.560) . (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.31-2. Kawaguchi et al.S.03 (1.270 (.85 (1. Survey Geometric mean (95% conf.14) 314 713 1487 03-04 03-04 * * . 2004). at lower or environmentally relevant doses (Blake et al.81 (1. 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.269 (.60 (1.15) 1.160-.00 (.320 (<LOD-.300 (<LOD-.59 (1. It is unclear if estrogenic or other effects occur in animals through oral dosing.400) .31 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. Urinary 4-tert-Octylphenol (4-[1. Tyl et al.370 (<LOD-. nonylphenol.17 (.65-3.25) 2. 2000.276 (.1.02-4. 2003.40-4.18-4. Yoshida et al.62) .68) 2.380 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.67-2.470-1.337-.850 (. population from the National Health and Nutrition Examination Survey.71) 2. 1999).890-2.96-4. 2005.630-1.43) 1.78) 1228 1286 03-04 03-04 03-04 * .450) .

15(6):683-692. Watanabe G.54(1):154-167. Haavisto TE.Environmental Phenols References Bian Q. Cooper RL. Bolt HM. Environ Sci Technol 2002. Ferrell JM. Calafat AM. alkylphenols. Endocrinology 2000. polybrominated diphenyl ethers.57(2):255-266. Environ Health Perspect 2008. Camann DE.121(1):21-33. Carey SA. Taya K.36(6):1202-1211.18(1):43-51. Korn LR. Certa H. Sweeney T. hormones. Roche JF. Bodman GJ. Nagao T. Brody JG. Taya K. Izumi S. Onuki A.14(5):325-332. Sakui N. Maekawa A. Saito Y. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Barber LB. Takai N. Nair-Menon JU. and testosterone. Kawaguchi M. J Chromatogr B Analyt Technol Biomed Life Sci 2004. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. and sertoli cell number. Song L. Toxicol Appl Pharmacol 2005. bisphenol A and methoxychlor in rats. Indoor Air 2004. Phthalates. Yoshimura S. McCoy GL. Ye X. et al. Tyl RW. Toxicol Lett 2001. Reprod Toxicol 2004. 1999-2000: a national reconnaissance. Katsuda S. Nakagomi M. Environ Int 2002. Arch Toxicol 1996. Reidy JA. Boockfor FR. Indoor air pollution by alkylphenols in Tokyo. nonylphenol. Biol Reprod 1997. Blake CA. testis size. Yoshida M. Anal Chim Acta 486:41-50. Qian J. Xu L. 2/4/09 Ying GG. et al. Maekawa A.165(3):217-226. Needham LL. Marr MC.folliclestimulating hormone.foe. Wong LY. Zaugg SD. Muller AM. Inoue K.co. Wang X. et al. Available at URL: http:// www. Ito R. Usumi K. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Environ Sci Technol 2003. pesticides. Wiegand HJ.37(20):4543-53. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Spengler JD. Inoue K. Estrogenic activity of octylphenol. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Kawaguchi M. Myers CB. Okada F.71(1-2):112-122. 2003. Raychoudhury SS.116(1):39-44. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Millette CF. et al.44(8):1355-1361. Takenaka A. and other endocrine-disrupting compounds in indoor air and dust. Rudel RA.799(1):119-125. Regul Toxicol Pharmacol 1999. and other organic wastewater contaminants in U. Warhurst AM. Boockfor FR. Yoshida M. streams. Two-generation reproduction study with para-tert-octylphenol in rats.30(2 Pt 1):81-95. Kookana R. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Myllymaki SA. 1995. Brooks AN. Karjalainen M. Food Chem Toxicol 2006. Ono H. Laws SC. 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. Katsuda S. Yoshimura Y. Williams B. Meyer MT. Fedtke N.uk/resource/reports/ethoxylates_alkylphenols.141(7):2667-2673.28(3):215-226. Fail PA. Seely JC. Thurman EM. Seto H. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Saito I. Pharmaceuticals. Watanabe G. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Exposure of the U. Toxicol Sci 2000. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Nicol L. Paranko J. Furlong ET. Kolpin DW. Horie M. Toxicol Appl Pharmacol 2000.207(1):59-68. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Brine DR. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. prolactin. Chen J.pdf.S. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Reprod Toxicol 2001. Toppari J. Blake CA.S. Makino T.

.S. Triclosan enters the aquatic environment mainly through residential wastewaters. and has also been impregnated into some kitchen utensils. 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. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent.. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. and wound disinfection solutions. Fourth National Report on Human Exposure to Environmental Chemicals 37 . Triclosan is not considered teratogenic at maternally toxic doses. It can be photochemically and biologically degraded. IARC and NTP do not have ratings with respect to human carcinogenicity. In a U. deodorants. 2007. 2002). In animal studies. 1996.Environmental Phenols Triclosan CAS No. and medical devices. Triclosan formulations may rarely cause skin irritation. 2008 has shown higher levels during the third decade of life and among people with the highest household income. representative subsample of NHANES 2003-2004. toys. young girls. acne medications. triclosan was found in 57. Calafat et al. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al.S.. General population exposure results from dermal and oral use of products containing triclosan.8-dichlorodibenzo-p-dioxin (Aranami et al. 2004). toothpastes. Triclosan has a low bioaccumulation potential in fish. 1988. 2007).. it has low acute toxicity.. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. Moss et al. 1987). 2000)... Lyman and Furia.. 2007). In 1999-2000. streams sampled in 30 states (Kolpin et al.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. 2005.2 µg/L was comparable to the median level (8. In animal and human studies. In a study of 90 U. It acts by inhibiting bacterial fatty acid synthesis.. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1969). 2000. Triclosan has been added to soaps. Triclosan can be absorbed across skin into the blood stream. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al.. Some reports show endocrine effects are observed in amphibians and fish (Foran et al.6% of 139 U. Calafat et al. 2006). Biomonitoring Information Urinary triclosan levels reflect recent exposure. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al.... 2008). Mezcua et al.. In the body it is conjugated to glucuronides and sulfates (Bodey et al. but not by race/ethnicity and sex. 1976. (Sandborgh-Englund et al. mouthwashes. Veldhoen et al.S. the median urinary triclosan level of 7. a process that can result in the formation of small amounts of 2. Matsumura et al. 2007..

86-12.7 (39.93 (7.3) 47.4 (38.1-39.6) 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 9.20 (7.0-73.3-35.16 (6.0) 65.6) 39.7) 292 (151-432) 132 (78. Survey Geometric mean (95% conf.3-67. Urinary Triclosan (2.94 (7.20 (7.50) 10.1 (15.10-9.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.1) 50.5) 13.2 (11. population from the National Health and Nutrition Examination Survey.0-19.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.3 (26.90-10.4.22-10.8) 9.29-12.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.0-15.2-46.1 (8.9 (11.1) 14.6-15.6-37.55 (4.0 (34.S.7) 123 (36.21 (6.4-19.40-17.6 (9.1) 9.4) 25.3 (8.8-63.0-213) 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 .6-111) 33.20-13.3-31.2 (25.4) 51.60 (8.00-8. interval) 12.45 (5.40-11.Environmental Phenols Urinary Triclosan (2.9 (33.48 (8.0 (26.6) 10.6-20.89-11.2) 9.10) 84.5) 66.4) 90th 249 (188-304) 03-04 03-04 03-04 8.7 (11.2) 12.2 (27.74 (5.11-11.2-58.20-11.9-61. population from the National Health and Nutrition Examination Survey.7 (28.9) 75th 47.2) 13.38-18.9-236) 193 (90.2-14.7 (14.32-14.6-65.3 (11.48-10.0 (11.6) 31.8 (21.1) 7.0 (8.2-58.0) 49.6 (30.1 (45.S.6 (12.45-10.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50-10.0-15.4) 75th 43.8) 14.7 (9.3-15.82 (8.4) 7.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.18 (5.0) 9.8-60.9 (50.5 (11.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.8) 7.1) 9.3) 6.72-13.6-14.00 (4. Survey Geometric mean (95% conf.6-14.30-14.92-12.8-85.8) 116 (39.4 (32.9) 7. interval) 13.4) 317 (231-433) 144 (96.4) 357 (225-456) 203 (87.1) 9.2 (13.4) 73.7) 10.1) 9.43-13.0 (36.4-18.1) 13.60 (6.6) 12.5-86.9) 32.9 (8.5) 11.2 (10.6) 90th 212 (172-241) 03-04 03-04 03-04 9.8-112) 30.5-14.1) 11.6 (10.54 (8.3 (9.4 (11.3.4.80 (5.2 (37.9) 8.20-10.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.3) 10. see Data Analysis section) for Survey year 03-04 is 2.4 (12.5) 20.8-127) 37.45-13.70-16.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.

Gunderson MP. Hernando MD.66:1052-1056. et al. Hong HC. Percutaneous penetration and dermal metabolism of triclosan (2. and other organic wastewater contaminants in U.23(5):579-583. Toxicology of 2. Pilot study of urinary biomarkers of phytoestrogens. et al. Williams FM.38(4):361370. Okui T. Ebersole R. Britton JA. Osachoff H. Evidence of 2. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development.7/2. Teitelbaum SL. Readman JW. Wolff MS. Furia T. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Ekstrand J. Bhargava HN.116(3):303-307. Lyman FL. Fernandez-Alba AR. J Invest Dermatol 1976. Skirrow RC. Aranami K. Windham G. Erratum in: Aquat Toxicol 2007.24(3):209-218. Shiratsuchi H. Benson WH. Ishibashi H. Watanabe N.69(20):1861-1873. Br J Clin Pharmacol 1987. Developmental evaluation of a potential non-steroidal estrogen: triclosan.Environmental Phenols References Aiello AE.45 Suppl 2:S137-S147. Calafat AM. hormones. Clapson DJ. Barber LB. Chelimo C. The oral retention and antiplaque efficacy of triclosan in human volunteers. Biol Pharm Bull 2005.36(6):1202-1211. Wong LY. Needham LL. Howes D. Urinary concentrations of triclosan in the U. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Nagao Y. Bodey GP.83(1):84. Aguera A.28(9):1748-1751. Hirano M. and phenols in girls. Zaugg SD. Williams PE. Moss T. Am J Infect Control 1996. streams. Kolpin DW. Bennett ER. Environ Health Perspect 2007.80(3):217-227. Reidy JA. Triclosan: applications and safety. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Meyer MT. Chemosphere 2007. Kanetoshi A.4. Environ Sci Technol 2002. Veldhoen N. Leonard PA. Anal Chim Acta 1004. 4’-trichloro-2’-hydroxydiphenyl ether. Larson EL. Foran CM.115:116-121. Ferrer I. Mezcua M. Pharmacokinetics of triclosan following oral ingestion in humans. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Pharmaceuticals.38(2):64-71.S. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. J Toxicol Environ Health A 2006. phthalates. Gomez MJ. Ogawa H. Furlong ET. Matsumura N.50(1-5):153-156. Ye X. Photolytic degradation of triclosan in freshwater and seawater.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.S.17(5):637-644. Sandborgh-Englund G.. Thurman EM. Aquat Toxicol 2006. Levy SB. Katsura E. Food Chem Toxicol 2000. population: 2003-2004. Adolfsson-Erici M. Kaneshima H. Pinney SM. Arch Environ Contam Toxicol 1988.524:241-247. et al. et al.4’-trichloro-2’hydroxydiphenyl ether). Odham G. Gilbert RJ. Environ Health Perspect 2008.67(4):532-537. Mar Environ Res 2000. 4. 1999-2000: a national reconnaissance. Wigmore H. IMS Ind Med Surg 1969.

350 (.76) .350) .650 (.10) 1.73 (1.350) < LOD .390 (.350) < LOD . air.650) 1.47-5.890 (. PCP is absorbed rapidly and well by all exposure routes.350 (.30) .350 (.350) 90th .62 (.350 (.30) 1.90 (1..350) < LOD .990-2. along with small amounts of tetrachlorohydroquinone and conjugates.350-.350-.70) 2. Since 1984.350-1. < LOD means less than the limit of detection. are eliminated in the urine.350-1. the elimination half-life may be a week or more (Uhl et al. mollusicide. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.00) 2.00) 1.70) . PCP is distributed to most tissues and is not extensively metabolized.23 (. with repeated or chronic exposure. and animals. After a single dose.00 (.83 (2.58-2.350) < LOD .530) 1.48 (. plants.32 (.680-1. PCP is eliminated over a few days (Braun et al.350-1.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-.60) 1.350-.350-.94 (1.30 (.350 (.350 (.350-. Human exposure to PCP has become less common.350-.960) 1.30 (1.350 (.25 and 0.350-. In the environment.770 (.350-.350 (. ingestion of contaminated food or water.10 (1.350-2.350) < LOD .850-2.350 (. PCP is degraded by sunlight and metabolized rapidly by microorganisms.390 (.58-2.350 (. PCP use in the U.350-1.350 (.37) .10 (.54-2.S. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (<LOD-1.47-3.890-1. General population exposure to PCP may occur by inhalation of contaminated air.33) . has been restricted.350-.350-2.660 (.42) 696 680 521 696 603 951 Limit of detection (LOD. water and sediments because of the large amounts that were produced and used historically. hypertension.350) < LOD . and metabolic acidosis were observed in CAS No.10) 1.350 (.350 (. Kohli et al. and it is used primarily as a preservative for wood to be used outdoors (e.S.990 (<LOD-2.480-2.76) 1.48-2.50) 1. 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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.590-1. and possibly of lindane (IPCS.350-.350-.350) < LOD .350-. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene. herbicide.350) < LOD .67) 1.98 (1.350-2.350 (.350-. bactericide..510-5.37 (.350 (.91 (1.350-.350-2. algaecide and insecticide.350-. After absorption.350 (.350) < LOD .350) < LOD .350) < LOD < LOD 75th .g..350) < LOD .08-3. and dermal contact with PCP-treated products. 1976.00) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. which may vary for some chemicals by year and by individual sample.350-.350 (.860-2.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .980 (.64) 1. The parent compound and conjugates.90) 1.350 (. Acute. 1997). other polychlorinated benzenes.350) < LOD .5. PCP has been detected in soils.350-..33-2. population from the National Health and Nutrition Examination Survey..350-.80) . Effects including hyperthermia.51) 1.30 (.09) .04) 1.45-2.94 (1. 1986).42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .75) 2.350-. 1979).630 (.78) 1.65 (.350) < LOD . PCP cannot be used on wood in residential or agricultural buildings.90) 2.350 (.500-2.350) < LOD .350 (.350-2.510-3. utility poles and fence posts). To-Figueras et al.65 (.01 (<LOD-1. 2002.350) < LOD .350-.30) 1. so it is relatively non-persistent.40 (. 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.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 . Survey Geometric mean (95% conf. 40 Fourth National Report on Human Exposure to Environmental Chemicals .18 (<LOD-1.350 (.350-.60) 1.

Pentachlorophenol is not mutagenic or teratogenic.25-1.500-1.950-1.250 (.25-2.560) < LOD .. Survey Geometric mean (95% conf.84 (1.710-1.67 (1. 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 (4.650 (.650 (.430-. More information about external exposure (i.52 (<LOD-1.490) < LOD .48-2.650) 90th 1.82 (1.320) < LOD < LOD 75th . Among adults in the NHANES 1999-2000 subsample.380-. 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.350) < LOD .35-2.630 (.40) 1.300 (.500 (.30 (.9 mg/L.850 (.16 (.Fungicides adults and children severely exposed to PCP through ingestion.11) 2.34 (.320) < LOD .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 .590) < LOD . carcinogenic.51) 1.82) 1.78) 1.16-1.560) < LOD .26 (1.06 (.290-.21-2.67-3.94 (1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . In NHANES 2001-2002 subsamples.25) 1. The U.. and adversely affected thyroid function (U.19 (1.0 mg/L.25 (1.67 (1.30) 1. 1995).36) .55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .84-4. respectively) (Becker et al.21 (.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.310-.610 (.19) 2.950-1.55) 1. OSHA has established an occupational standard.08 and 5. 2003).360 (.250 (.57 (. 1989).260 (.52 (1.57 (1.19) 2. respectively) (Seifert et al.52) 1.26 (1.06) 1. In a small sample of U.gov/ pesticides/ and from ATSDR at: http://www.760 (.920 (.35-2.00-1.570 (.35) 1. Urinary Pentachlorophenol (creatinine corrected) Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.430) < LOD . IARC has determined that pentachlorophenol is possibly carcinogenic to humans.510-.30-2. In animals. or skin absorption.25-2.67 (1.92) 1.67-3.420) < LOD .S.56) 1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .910-1.510-. 1991).52 (<LOD-1.830) < LOD . chronically administered high doses of PCP were hepatotoxic. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.75 (<LOD-2.69 (1. 2004. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.310) < LOD .. van Raaij et al.280) < LOD .S.94 (1. Death can result from seizures and cardiovascular collapse.html.440 (.220-.400 (.18) . and the FDA has established a standard for bottled water.990 (.300 (.270-.40) 1.470 (.67 (1.67 (1.S. EPA at: http://www.500-. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.13 (.30) 1.10 (1.360-.83 (1.09-1.EPA.78) 1.40) 1.40) 1. 2003).580-.590-1.25 (1.epa. EPA has developed standards for PCP in drinking water and the environment.84) 1.800) < LOD 1.atsdr.90) 1.900-1.340-..40-2.270-. 1989). 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.73 (1..6 and 14.780) < LOD .95) 3.00-1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .S. environmental levels) and health effects is available from the U. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.300 (..780-1.18 (1.S.800-1. population from the National Health and Nutrition Examination Survey.700-2.290-. children in the 1980’s.730) < LOD . 2000).75) 1.e.560-.950-1.220-.320 (.gov/ toxpro2.35) 1.10-2.79) 1.09 (<LOD-2.67-2. inhalation.240-.330-..94-3.40) 1.06-3.370 (.00) 1.290) < LOD .29-3.320) < LOD .19) 2..cdc.

Hill RH Jr. Environmental Protection Agency (U. References Becker K.4:289296. Barrot C. Sala M. 11/30/2004. r e g u l a t i o n s . Fast DM. 206:15-24. Uhl S. 2002. Seifert B. Safe A. Helm D. Phillips DL. Seiwert M. Becker K.54(3):203-208. 4/21/09 Kohli J. Needham LL. Baker S. Seifert B. Engel R. Hill RH. Hill RH Jr. 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. Dev Toxicol Environ Sci 1979. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.inchem. International Programme on Chemical Safety (IPCS). et al. Santiago-Silva M. Head SL. Schlatter C. Available at URL: h t t p : / / w w w. Otero R. drinking water and indoor air. van den Berg KJ. Environ Health Perspect 1997. Shealy DB.18:475-481. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Bailey SL. Gregg M. 4/21/09 van Raaij JA. Cline RE. Pesticide residues in urine of adults living in the United States: reference range concentrations. Holler JS. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Seiwert M. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Pharmacokinetics of pentachlorophenol in man. Kaus S.org/documents/jmpr/jmpmono/2002pr08. EPA). available at URL: http://www. Notten WR.71:99108. Krause C. Chenoweth MB. Schmid P. To T.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Schulz C. Int J Hyg Environ Health 2003. et al. Blau GE.105(1):78-83. Toxicology 1991: 67(1):107-16. htm. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Arch Environ Contam Toxicol 1989. Smith SJ. house dust. et al.18(4):469-474. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.S. Needham LL. To-Figueras J. Schulz C. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.S. hair.10:552-65. Jones D. Arch Toxicol 1986.58:182-186. J Expo Anal Environ Epidemiol 2000. 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. Environ Res 1995. Arch Environ Contam Toxicol 1989. PCP: Human Risk Characterization [online]. U. Bragt PC. Rodamilans M. Braun WH. urine. The metabolism of higher chlorinated benzene isomers. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Lindane. Can J Biochem 1976.

EPA.00 (1.552 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. interval) .40-5.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .S.420 (<LOD-.770 (.60 (1.S.3.10) 1.50) < LOD .19 (.509 (.670) 2. Survey Geometric mean (95% conf. SOPP is applied topically to the crop and then rinsed off.34) 1. General population exposure can occur via dermal.33 (. Estimated human intakes have been below recommended intake limits (U. whereas SOPP is not volatile and is more water soluble.570-2.EPA.880-2.20) < LOD 2.570 (. 2006). sodium ortho-phenylphenate (SOPP). or apply these chemicals may be more highly exposed than the general population.50) .40-5..600-1.349-.00 (1. Both have been used in agriculture to control fungal and bacterial growth on stored crops.466 (.28-3.570-1.20) 2.690) < LOD . 2006).850 (. Workers who manufacture. OPP is volatile. in paints.80 (2.560-8. 1998).480-1.76) 1.80-3.22) 2.S.20) < LOD 1.60 (1.493 (.540-2.92 (.696) * .386-.30) < LOD .610 (. leaving the chemical residue OPP. but OPP and SOPP are still used on pears and citrus (U.30 (1.690-1.750-2.50-4.50) 1. on ornamental plants and turfs.10) 1. population from the National Health and Nutrition Examination Survey.760-2.80) 1.09) 2.30) < LOD 1.60-3.433-.20-2.770 (. and sanitizers. OPP is considered to be moderately toxic after acute oral doses in animal studies. inhalational.636) * .50 (1.600) < LOD 75th .00 (1.10 (1.03) 1. and it has limited water solubility.40-2. Both chemicals degrade within hours to weeks in the environment (U.389-.17 (. Timchalk et al. such as fruits and vegetables.3 and 0. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.630) < LOD .790) 2.580-1.07 (.820 (. 2002. 2006). In the past.60 (1.800-3.780) < LOD .890) 1.389-.20-3. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. however.00) < LOD .61) 2.450 (<LOD-.10-2.50) < LOD . OPP is still used as a disinfectant fungicide for industrial applications.00-2.496 (.30-7.640) < LOD .710-2.40-7.80) 1.830 (.890 (.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 .10) .370-. and as a wood preservative. Most agricultural food applications have been revoked. Cnubben et al.50) < LOD ..490 (<LOD-.410-.10) 2.Fungicides ortho-Phenylphenol CAS No.570-.30) 1.364-.450 (<LOD-.50 (1.836) * .350-1.28 (.00) .570 (. 90-43-7 General Information Ortho-phenylphenol (OPP.30) < LOD 90th 1.30-2.40 (.497 (.50-2.00 (1.02) 1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.10) .23) 695 680 520 695 603 953 Limit of detection (LOD.890 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) 1.50-3.600-1.S. Chronic dosing in animals resulted in such systemic effects as weight loss and Urinary ortho-Phenylphenol Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.860 (. or 2-phenylphenol) and its water-soluble salt.90 (1.490 (<LOD-.490 (<LOD-.90) 2. Fourth National Report on Human Exposure to Environmental Chemicals 43 .370-. which may vary for some chemicals by year and by individual sample.600) < LOD .20 (.490 (<LOD-. are antimicrobial agents used as bacteriostats.85) 2.740 (.498 (. 1989).645) * .710) 3.88) 1.624) * .520 (.90 (1.10-1.370-. it was used in home sanitizers for surfaces.EPA.600) < LOD 1. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.600-1.450 (<LOD-.840-1.621) * . 1998.508 (. 2006).600) < LOD . OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.402-.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .90) .490 (<LOD-.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .50 (1.10) .610-1. Available evidence suggests that OPP does not accumulate in the body.390-.500-2. < LOD means less than the limit of detection.00) .10 (1.550-1.950) < LOD .. formulate.20 (1.14 (<LOD-3.470 (<LOD-.27 (.20 (1. fungicides.742) * .90) .638) * .970 (.567 (.60-2.930 (.590-2.22 (.

970) 1.88-4.620-1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect..S.810-1.980 (<LOD-1. but no neurologic.74 (1.91 (1. 1999.750 (.09-3.43-2.580) < LOD .29) 1.43-2. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1992.78 (2.32) 3..33) .21-2.910 (<LOD-1.26) 1.484) * .910-1.33) 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 .27) < LOD .00 (.93) .550 (.S.361-. Bomhard et al. reproductive.860 (. Smith et al. CDC.444 (.385 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Survey Geometric mean (95% conf. 2002). OPP was not found to be mutagenic.580-1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. or.810) < LOD .61 (1.880-1.4 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.666) * .311-.gov/pesticides/.44 (1.93) 1.04-4.690 (.06-5. Brusick.96 (1.62) .620-1.770-2.47) .17 (. Additional information is available from U.09-6.11-1.S.453 (.940-2.500) < LOD .93 (1.33-2. 2002.. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.24-2.11) 4.860 (..470) < LOD .570) < LOD 1...09 (1.780 (.17) 2. interval) .508) * .32) 1.11 (. 2005.S.13) 1. Zhao et al.53) 1.61 (. 1986).20) < LOD 3.81) 1..96-4.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .Fungicides anemia.69 (1.43) 3.910 (. 2000.58) 2.21) 1. and it has classified OPP as not classifiable with respect to human carcinogenicity.06 (1.75 (1.96 (1.670 (.780-14.38-3. Kwok et al.420 (<LOD-.01) 1.640-1.12-2.382 (.02 (.84 (1.93) .410 (<LOD-.950) < LOD .11) < LOD 90th 1.08-1.08-2.510 (<LOD-.670 (.840 (.0) 1.420 (<LOD-.380 (.51-3. Nakagawa et al.52 (. U.64 (2.990) < LOD .40-13.320 (<LOD-. Murata et al.4) 3.28 (<LOD-4.18) 2.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.97 (2.750-2. 1984.600-1. 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.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .270-. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. 1998.329-.00 (1.96) 1.epa.24-2.610) < LOD 1.EPA 2006).590) * .08) 1.28 (2.410 (<LOD-.480-.514 (.05-2. 2005).470 (<LOD-.. less likely.900) < LOD .510-.61 (2.59) .560-2.06-4. Ito et al. leading to production of two metabolites.455-.29) 1.343 (. population from the National Health and Nutrition Examination Survey. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.360 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.21 (. 2002.07) 2.473) * .750 (. IARC has classified SOPP as a possible human carcinogen. 2005).25-6.568) * .403-. Volunteers exposed to 0.980 (. Biomonitoring Information Urinary OPP levels reflect recent exposure..EPA 2006)..301-.17 (. 1999.43 (1. 44 Fourth National Report on Human Exposure to Environmental Chemicals .791) * .496 (. 1997.38) 1. Pathak and Roy. U.550) < LOD .30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .550-.31) < LOD . or developmental toxicity was observed (Bomhard et al.89 (1.12) < LOD 1.656) * .353-.86 (1.460-. by possible genotoxic mechanisms (Hagiwara et al.46) < LOD 1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.248-.EPA at: http:// www.800-1.560) < LOD 75th . In high dose animal studies. Detectable levels were seen in over half the U.75 (1. 1984.11 (.38) 2.291-.59) 1.900-1.440 (. 1993.650-1.670) < LOD .

Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.S. Kwok ES. Eadon G. Brzak KA.50(11):3351-3358.54(16):5731-5735. 4/9/09. Timchalk C. Hagiwara A. Zhao S.150(2):402-413. Bartels MJ. Food Chem Toxicol 1984. Turteltaub KW. Mutat Res 1993.74(2):61-71. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Available at URL: http://ntp. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Freyberger A. St John MK. 2005. Stanley JS. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats.22(10):809-814. Timchalk C. Ito N. Buchholz BA. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.286(2):309-319. Regul Toxicol Pharmacol 2002.S. U.pdf. J Chromatogr B Biomed Sci Appl 1997. Hum Exp Toxicol 1998. March 1986. Smith RA.45(5):460-481. Bartels MJ. Bartels MJ. Herbold BA. Toxicol Appl Pharmacol 1998. Narang A. Roy D. Carcinogenesis 1999. Shirai T. Kawanishi S. J Agric Food Chem 2006. Arch Toxicol 2000. van de Sandt JJ.159(1):18-24. Roberts AL. Imaida K. 4/13/09 Onstot JD. National Toxicology Program (NTP). Hirose M. Murata M. et al. Arnold LL. rat and man. 2006. Sangha G. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Coelhan M. Bomhard EM.niehs. Hakkert BC. Mendrala AL. Centers for Disease Control and Prevention (CDC). Xenobiotica 1998. Environmental Protection Agency (U. Richter M.Fungicides References Appel KE.S. Meuling WJ. Toxicol Appl Pharmacol 1999. Biochem Pharmacol 1992..EPA). Nakagawa Y.pdf. et al. 90-43-7) in Swiss CD-1 mice (dermal studies). Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Moldeus P. Shibata M. Office of Toxic Substances.S. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats.20(5):851-857. The carcinogenicity of the biocide ortho-phenylphenol.nih.17(8):411-417. Cnubben NH. EPA). Identification of SARA compounds in adipose tissue. Leser KH. Environ Mol Mutagen 2005. J Agric Food Chem 2002. Atlanta (GA). The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers.gov/ntp/htdocs/LT_ rpts/tr301. Cano M.(56):399-407. EPA-560/5-89-003. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Fukushima S. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Brusick D. Inoue S. U. Elliott GR. McNett DA. Crit Rev Toxicol 2002. Ito N. Glas K. Comparative metabolism of orthophenylphenol in mouse. Hagiwara A.32(6):551-625. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Bromig KH. Tayama S. Pathak DN. Brendler-Schwaab SY. Christenson WR. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry.43(7):14311437. Vogel JS. Fukushima S. Third National Report on Human Exposure to Environmental Chemicals. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Moriya K. 1989. EPA 739 R-06004. Environmental Protection Agency (U. Eastmond DA.28(6):579594.35(2 Pt 1):198-208. Bartels MJ. IARC Sci Publ 1984. Selim S. Sangha GK. Gierthy J.gov/oppsrrd1/REDs/ phenylphenol_red. Bormett GA. Available at URL: http://www. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. July 28. Moore GA. Drugs. Christenson WR.703(12):97-104.epa. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No.

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

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

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

Hsiao JJ. Ward EM. March 2006. 1998. J Expo Anal Environ Epidemiol 2005. EPA). Burkhardt MR.S. Sci Total Environ 2000. Feng PCC. reservoirs and ground water in the Midwestern United States. Curwin BD. Andrews HF. Comparative metabolism and elimination of acetanilide compounds by rat. Volume 65. Heederik D. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.15(6):500-508. U.11(4):353359. Quistad GB. Sci Total Environ 2000. Hum Exp Toxicol 1996.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Battaglin WA. Kinney PL. Reynolds SJ. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.17(6):559-566. Larsen GL.Herbicides References Ashby J. Davison KL. Available at URL: http://www.248(2-3):123-133. 5/30/06 U. Federal Register: January 24.S. Hines CJ. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Hladik ML. Whyatt RM. Thurman EM. Linderman R. et al.248(2-3):115-122. J Agri Food Chem 1989. Wratten SJ. Environmental Protection Agency (U. Chem Res Toxicol 1998. and metolachlor herbicides in rats. Furlong ET. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Barr DB. Number 15. Occurrence of sulfonylurea. Linhart SM. Kolpin DW. and other herbicides in rivers. imidazolinone. Green T.S. Wilson AG. et al. 5/30/06. Acetochlor (Harness) Pesticide Petition Filing 1/00. Bravo R. Atlanta (GA).EPA): http://pmep. J Expo Sci Environ Epidemiol 2007. Environ Health Perspect 2000. Striley CA.pdf. Barr DB. epa. Barr DB. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Kier L. Casida JE. Camann DE. Deddens JA. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Lefevre PA. Alavanja MC. pages 3682-3690.24(10):1003-1012. sulfonamide.108(12):1151-1157. EPA 738-R-00-009. 2005. Jefferies PR.111(5):749-756.39(17):6561-6574. Tinwell H. acetochlor. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Sanderson WT.37(4):10881093. 2000. Rose RL. et al. Third National Report on Human Exposure to Environmental Chemicals. Peter CJ.S. Barr JR. Xenobiotica 1994. Dialkylquinonimines validated as in vivo metabolites of alachlor. Olsson AO. EPA).cce. Environ Sci Technol 2005. Environ Health Perspect 2003.S. Coleman S. Hodgson E.html. Centers for Disease Control and Prevention (CDC).cornell. Hein MJ. Available at URL(non U. Environmental Protection Agency (U.gov/oppsrrd1/reregistration/REDs/acetochlor_tred.15(9):702-735. Feil VJ. Roberts AL.

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

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

2007. Geological Survey (USGS). Comparative metabolism and elimination of acetanilide compounds by rat. Background document for development of WHO Guidelines for Drinking-water Quality. 1999.39(17):6561-6574.S. Casida JE. Quistad GB. Brown MA. Brown KK. Shealy DB. An evaluation of the carcinogenic potential of the herbicide alachlor to man.43(25):2087-94. 1999. Burkhardt MR. Alachlor in Drinking-water.56(6):853-859. Deddens JA. Hines CJ. Hsiao JJ. Biagini RE. 2/27/09 U. MacKenzie B.11(4):353359. Tessier DM. Larsen GL. Barr DB.S. Sanderson WT. Biagini R. revised February 15. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Lau H. Hladik ML.56(9):883-889. EPA). Centers for Disease Control and Prevention (CDC). Wratten SJ. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.18(6):363-391. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . California. Thelin GP.pdf. acetochlor. 2005. 86. Jefferies PR. Casida JE. 98-4245 (by Barbash JE. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Geneva. Sci Total Environ 2000.47(6):503-517. Feil VJ.S. Barr JR. Mutat Res. Heydens WF. Sci Total Environ 2000. Thake DC. Shoemaker DA. Henningsen G. Wilson AG. DNA adduct formation by alachlor metabolites. Geological Survey (USGS). Environmental Protection Agency (U. who. Available at URL: http:// www.epa.htm. Linhart SM. Reregistration Eligibility Decision (RED) Alachlor.inchem. Supplemental Technical Information (available on-line only). Circular 1291. Kier LD.43(9):2504-2512.Herbicides References Battaglin WA. International Programme on Chemical Safety (IPCS). Sacramento. Kolpin DW. Feng PCC. Kimmel EC.24(10):1003-1012. Xenobiotica 1994. 4/2/09 U.248(2-3):123-133. Hines CJ.int/water_sanitation_health/dwq/chemicals/en/alachlor.php. U. ALACHLOR. 1992-2001. Roberts AL. December 1998. World Health Organization (WHO). Furlong ET. Hill RH Jr. March 2006. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Bull Environ Contam Toxicol 1996. Hill AB. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Andrews HF. Environ Health Perspect 2003. 2003. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Available at URL: http://www. 2/27/09 Jefferies PR. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Quistad GB.395(2-3):159-171. Clark JM. imidazolinone. Camann DE.37(4):10881093.S. Available at URL: http://www. Thurman EM. Davison KL.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. J Agri Food Chem 1989. Dialkylquinonimines validated as in vivo metabolites of alachlor. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Peter CJ. Chem Res Toxicol 1998. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.gov/oppsrrd1/ REDs/0063.pdf. Hull RD. No. et al. Occurrence of sulfonylurea. Life Sci 1988. 1998. Kolpin DW. sulfonamide.org/documents/pds/pds/pest86_e. EPA 738R-98-020.248(2-3):115-122.44(18):1325. 1997. Casida JE. Third National Report on Human Exposure to Environmental Chemicals. Whyatt RM. and metolachlor herbicides in rats. Striley CA. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Ann Occup Hyg 2003. 1996. Am Ind Hyg Assoc J 1995. Kinney PL.usgs. reservoirs and ground water in the Midwestern United States. J Ag Food Chem 1995. Driskell WJ. et al. Atlanta (GA). Tolos W. Erratum in: Life Sci 1989. Environ Sci Technol 2005. Hum Exp Toxicol. World Health Organization.111(5):749-756. Gilliom RJ). Martens MA. Available at URL: http://water. WHO/ FAO Data Sheets on Pesticides. and other herbicides in rivers.

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

myocardial muscle degeneration. altered estrus cycles. 2000. 2003b). 2003. 1997).. Sanderson et al..atsdr.Herbicides particularly diaminochloroatrazine (the main dealkylated product). 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... the dealkylated atrazine metabolites and hydroxyatrazine can occur in the environment from the breakdown of the parent chemical. liver toxicity.. and U. Survey Geometric mean (95% conf. EPA at: http://www.gov/pesticides/ and from ATSDR at: http://www. 2005.. propazine. including simazine. 2005. Eldridge et al. IARC considers atrazine not classifiable with respect to human carcinogenicity.S. may mediate some effects of atrazine (Laws et al. Additional information is available from U. Some human ecologic and epidemiologic studies of reproductive and cancer outcomes have shown either positive or no associations. U. Sathiakumar and Delzell.html. and testosterone (Gillis et al. Stoker et al. 2002. increased pituitary weight. 2000 and 2002. Dealkylated metabolites from atrazine can also result from metabolism of other chlorotriazine pesticides. In mammalian studies. Stevens et al. 1999).S. Estimated human exposures are thousands of times lower than doses that caused effects in animals (Gammon et al. developmental ossification defects. and cyanazine. 54 Fourth National Report on Human Exposure to Environmental Chemicals . 2003). Atrazine is not considered genotoxic. Atrazine product formulations can be mild skin sensitizers and irritants.S. Gammon et al..EPA.. Gammon et al. and reduced levels of luteinizing hormone.epa.. delayed onset of puberty. Chronic high dose toxicity observed in animals includes decreased body weight. atrazine is rated as having low acute toxicity.S.gov/toxpro2. Thus. 2004. 1994 and 1999. Rayner et al. detection of these dealkylated metabolites in a person’s urine may also reflect exposure to these degradates in the environment. prolactin. Atrazine and the dealkylated chlorinated metabolites did not have estrogen receptor activity. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 808 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1314 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 683 550 918 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey.cdc.EPA considers atrazine unlikely to be a human carcinogen. 2000 and 2003.. impaired fertility. Human health effects of atrazine at environmental doses or at biomonitored levels from environmental exposure are unknown... but the effects are difficult to attribute due to lack of exposure markers or due to mixed chemical or pesticide exposures (ATSDR. Laws et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In addition to being human metabolites of atrazine. Urinary Atrazine mercapturate (creatinine corrected) Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005). 1994.

J Toxicol Environ Health 1994. 1993). Stoker TE. Goodrow MH. Cooper RL. Toxicological profile for atrazine. Agency for Toxic Substances and Disease Registry (ATSDR). Deddens JA.. Shoemaker DA. World Health Organization.30(2):244-247. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.99(8):5476-5480. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Pfeifer KF. Biomonitoring studies on levels of atrazine mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of atrazine than are found in the general population. In a small number of field workers. Vonk A. Cooper RL.58(2):366-376.atsdr. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.115(8):1254-1260. 2001). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Stuart AA. Tapia J. ATRAZINE. Ferrell JM.61(4):331-355. Tyrey L. Barr DB. Centers for Disease Control and Prevention (CDC). Jones AD. Carr WC Jr. Collins A. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . et al. levels of atrazine mercapturate were generally not detectable (CDC. In small studies of Maryland residents in 19951996 (MacIntosh et al. Eldridge JC. Pest Manag Sci 2005. Noriega N. 82. Reynolds SJ. Cooper RL.64(9):672-678. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Wetzel LT. Sanborn JR..109(6):583-590. Ferioli A. Stoker TE.html. WHO/ FAO Data Sheets on Pesticides. Eldridge JC. Toxicol Sci 2003. et al. Geneva. Goldman JM.43(2):155-167. et al. Moseman RF.cdc. Lioy PJ. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Ann Occup Hyg 2003. atrazine was detected in only four children (Arcury et al. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Environ Health Perspect 2007.inchem. 1996. Grzywacz JG.69(2):217-222. 2000). Atlanta (GA). 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Ferrell JM. 2005). In the NHANES 2001-2002 subsample. Blewett C.gov/toxprofiles/tp153. J Toxicol Environ Health 1994. Laws SC. Biagini RE. 2005. Brown KK. Cottica D. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Schmid J. Catenacci G. 2005). Hayes TB. Gammon DW. No.. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.. Toxicol Sci 2000. Curwin BD. Striley CA. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. et al. The geometric mean of urinary atrazine mercapturate was 1.76(1):190-200. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.. Barbieri F. Bradway DE. Proc Natl Acad Sci USA 2002. Hines CJ.53(2):297-307. et al. Available at URL: http:// www. Aldous CN. Freeman NC.15(6):500-508. Toxicol Sci 2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sanderson WT. 3/11/09 Laws SC. J Agric Food Chem 1982. Clayton CA. References Adgate JL. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.. Maroni M. Wetzel LT. Bersani M. Available at URL: http://www. Perry et al. 2001 [online]. J Expo Anal Environ Epidemiol 2005. Chen H. Third National Report on Human Exposure to Environmental Chemicals. Heederik D. Toxicol Lett 1993. Fleenor-Heyser DG. Simpkins JW. Lucas AD. Biological monitoring of human exposure to atrazine. Gillis JH. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Hein MJ.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. 2007). Stevens JT. et al. International Programme on Chemical Safety (IPCS). Breckenridge CB.htm.. Quandt SA.org/documents/pds/pds/pest82_e. 2003. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Eberly LE. In a study of 60 farm worker children. Extrom PC. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Hermaphroditic. Lee M.43(2):155-167. Gillis JH. A risk assessment of atrazine use in California: human health and ecological aspects. Stoker TE. 3/11/09 Arcury TA. Barr DB. Steroids 1999. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. McElroy WK. Seiber JN. Environ Health Perspect 2001. Mendoza M. diamino-S-chlorotriazine and hydroxyatrazine.47(6):503-517. Saiz SG. Barr DB. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.

S. Dagenhart D. Available at URL: http://www.epa.9(5):494-501. Boerma J. Hammerstrom KA.epa. 0062. A risk characterization for atrazine: oncogenicity profile. Lansbergen GW.usgs. Singzoni B.S. MacIntosh DL. Environmental Protection Agency (U. Langvardt PW.61(1):27-40. Stoker TE. 6/1/09 U. March 2006. Toxicol Sci 2002. White paper on potential developmental effects of atrazine on amphibians. Stevens JT. May 2003a. Tortorelli J. Ryan PB.gov/oppsrrd1/REDs/ atrazine_ired. EPA Office of Pesticide Programs. 2007. Perry M. Laws SC. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. 3/11/09 U.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.pdf. Pesticides and Toxic Substances. Toxicol Appl Pharmacol 2004. Toxicology 1990. Timchalk C. 2003b. Sathiakumar N. Supplemental Technical Information (available on-line only). Ann Epidemiol 2000. Delzell E. Sanderson JT. Available at URL: http://www. Dryzga MD.php. Cooper RL.27(6):599612. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .195(1):23-34. Cooper RL.S. Christiani D.S. EPA). Office of Prevention. Toxicol Sci 2000.182(1):44-54. Guidici DL. J Expo Anal Environ Epidemiol 1999. Case No. EPA). Geological Survey (USGS).S. Wood C.10(7):479. Rayner JL. Toxicol Appl Pharmacol 2002.67(2):198-206.pdf. Washington (DC). Circular 1291. Crit Rev Toxicol 1997. Interim Reregistration Eligibility Decision For Atrazine.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. revised February 15. Breckenridge CB. Guidici DL. Available at URL: http://water. Laws SC. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. J Toxicol Environ Health A 1999. A longitudinal investigation of selected pesticide metabolites in urine.58(1):50-59. Wetzel L. Fenton SE. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. U. van den Berg M. Needham LL. Osborne DW. Urinary biomarkers of atrazine exposure among farm pesticide applicators. A review of epidemiologic studies of triazine herbicides and cancer.56(2):69-109.Herbicides development of a biomarker of exposure. 1992-2001. The Quality of Our Nation’s Waters. Environmental Fate and Effects Division. Kastl PE.6(1):107-116. Chem Res Toxicol 1993. Pesticides in the Nation’s Streams and Ground Water. Stoker TE. Environmental Protection Agency (U.

43) 1. Sauerhoff et al. MCPA. It is not well absorbed through the skin.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .810-1.260 (<LOD-. Once absorbed. it acts as a plant growth hormone.4-D can be applied either as an aqueous salt or as oil-soluble esters. It is rarely detected in ground waters (USGS. < LOD means less than the limit of detection. 94-75-7 General Information Widely used throughout the United States. 4-D.320) 90th . It was first registered with U. 2005).560-.420-.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . As much as 62 million pounds of 2. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. 2.48) < LOD 1.. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 2. with a half-life of several days to several weeks.4-D have been below recommended intake limits (U.02-1.4-D or exposed for prolonged periods.400) < LOD .490) < LOD < LOD < LOD .24 (. the chlorophenoxy herbicide 2.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. abdominal pain. 2. 1977). agricultural. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.310 (.03) 695 659 520 668 589 892 Limit of detection (LOD. 1989.730 (.51 (1. Kohli et al.760 (.410) < LOD . hypotension.930-1. 2007).230 (<LOD-. At low levels.250 (<LOD-. and aquatic environments.60) 1.210-.20 (.930 (.21) 1. 2004).22) < LOD .4-D were used in the U.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .910) 1.S.00-2.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.890) < LOD .670-1.30 (<LOD-2. in 2001 (U.27-2.690 (.S.07 (.250 (<LOD-.370-.. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. General population exposure to 2. 1974.40) 1.440-1.S.4-D has low acute toxicity.4-D is rapidly absorbed via oral and inhalation routes.350) < LOD < LOD < LOD .13) < LOD . these herbicides can enhance plant growth. population from the National Health and Nutrition Examination Survey.680-1.550-1.690-1.27 (.55 (1.690 (.EPA in 1948. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660) 1. dizziness.10 (<LOD-1. Similar to other chlorophenoxy herbicides. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.610-.310) < LOD .952 and 0. 2.560-1. nausea. Fourth National Report on Human Exposure to Environmental Chemicals 57 .20 (<LOD-1.230-.70) 1. It is poorly bound in soils. which may vary for some chemicals by year and by individual sample.10 (<LOD-1.80) 1.210 (<LOD-. and delayed Urinary 2.4-D may occur during residential applications.4-Dichlorophenoxyacetic Acid CAS No.540-. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.960-1. Recent estimates of chronic intakes of 2.910) < LOD . renal and hepatic injury.27 (1.420) < LOD .08) < LOD . by direct contact with agricultural and residential areas after applications.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 .610 (.4-dichlorophenoxyacetic acid (2.S.330 (. and by consuming food or drinking water contaminated with 2.490 (.690 (.05-2.2.S.16) < LOD .32 (1.10) < LOD 1.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.66) < LOD 1.EPA. myotonia.4-D) controls broadleaf weeds in residential. and mecoprop). Human health effects from 2.Herbicides 2. headache..890 (.740 (. but at higher levels they are herbicidal.EPA.

58 Fourth National Report on Human Exposure to Environmental Chemicals . CDC. 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. 1995. 2.S.56) .490 (.920) < LOD 1. population from the National Health and Nutrition Examination Survey. 2.13 (. Kutz et al..gov/pesticides/.7.380) < LOD .790) 1. Frank et al.4-D reflect recent exposure.Herbicides neuropathy (Bradberry et al. or teratogenic effects in chronic rodent studies (Charles et al.670 (. Knopp et al.EPA.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. 2002.4-D production plant workers and a few forestry workers spraying 2.27-1..440 (.520-. in small samples of children (Hill et al.990-1.epa.560-.380 (<LOD-.590 (<LOD-1. myotonia..620-.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 .680) < LOD .790) < LOD . adrenals and gonads (NTP. 2005. 2005. 1994).S. 1996. IPCS. 2006.14 (.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 1995).660) < LOD . IOM.810-1.S.780-1.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .550-. Post-application levels in farmers and home gardeners were dependent on Urinary 2.780) .270-.350 (<LOD-. It is unclear whether these associations are related to the chlorophenoxy herbicides.640 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Additional information is available from U.3.470) < LOD .08 (.16) 1.340 (.930-1.720 (.700 (. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.19) .270 (<LOD-.. 2005). 2000). IPCS. thyroid.EPA at: http://www. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. 2002.890-1. U. Hill et al.340-.73) ..670 (<LOD-1.410) < LOD < LOD < LOD .330-. 2005).390) < 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 . population (Hill et al. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides..S.570) < LOD . urinary 2..810-1.24) 1.850) < LOD . liver. 2005.39) < LOD 1.17 (..8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 2003. Kolmodin-Hedman and Erne. other exposures.S. 1989).380 (<LOD-.EPA.. In previous samples of the U. Pearce and McLean. 2005).610-.EPA 2005).4-D are eye irritants. eyes.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.980) < LOD 1. and of adults and children (Baker et al. 2. Acute high doses administered to laboratory animals produced ataxia. 1985.4-D does not have significant reproductive.35) < LOD .670 (. Survey Geometric mean (95% conf. Epidemiological studies have reported associations of several types of cancer.590 (<LOD-1.EPA.05) . 1996. 1980. U.S. 1992).740 (.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 1996.610-. and evidence of histological injury to the kidneys. 2001.480 (.820-1. 2005).4-D levels were detectable in less than a quarter of the individuals studied.890) < LOD 1. developmental. 2005.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.41 (1.08 (. The acid and salt forms of 2. IPCS. 2004). Average post-application urinary levels of 2. Biomonitoring Information Urinary levels of 2.410) < LOD 1. or to contaminants in the herbicide formulations (specifically 2.13 (. U.380-.410) 90th .08 (.560-.S. U.32 (<LOD-2.410 (<LOD-.580-.780 (..660 (.

van Ravenzwaay B.4:318-321.4-D): exposure and urinary excretion. Smith SJ. Chapman P. Biomonitoring studies of 2. 1992).4-Dichlorophenoxyacetic Acid). Frank R. Hanley TR Jr. Harris SA. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Murphy RS. Developmental toxicity studies in rats and rabbits on 2..php?record_id=10603. Baker BA. Khanna RN. Finding a measurable amount of 2. Absorption and excretion of 2. J Environ Sci Health B 1992. Atlanta (GA).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. the number of acres to which it was applied (Curwin et al.4-D will result in an adverse health effect. Exposure of homeowners and bystanders to 2.4-D were highest in the farmers who applied the 2. Driskell WJ. Cook BT. International Programme on Chemical Safety-INCHEM (IPCS).htm. Solomon KR.5-T). Sirons G J.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.4-D. Biomonitoring of herbicides in Ontario farm applicators. References Arbuckle TE. Dhar MM. Barr DB. Bailey SL.51(3):152-159.4-D and 2. Updated March 7.4-D) epidemiology and toxicology.edu/catalog. Hein MJ. Sircar KP.inchem. et al. geometric mean urinary levels of 2. Tandon JS. Bus JS. Shealy DB. Brody D. Estimation of occupational exposure to phenoxy acids (2.4-D than levels found in the general population.org/documents/jmpr/jmpmono/v96pr04. et al. and the use of protective clothing or equipment (Arbuckle et al.37(2):277-291.niehs. Wilson RD. Fast DM. Barr DB.31 Suppl 1:98-104. Ripley BD. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Holler JS.4-. Pesticide residues in urine of adults living in the United States: reference range concentrations. Biomonitoring for farm families in the farm family exposure study. Mandel JS. Scand J Work Environ Health 2005. Assessment of exposure to 2. 914. Philbert MA. 2. Review of 2. general population. Carter-Pokras OD. Available at URL: http:// www. Available at URL: http:// www.71(2):99-108. Arch Environ Contam Toxicol 1985.4-D in urine does not mean that the level of the 2. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Occup Environ Med 1994. Hill RH Jr. Forestry workers involved in aerial application of 2.4 dichlorophenoxyacetic acid (2. 2005).31 Suppl 1:90-97. Survival and Growth Curves from NTP Toxicity Studies. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005. Baker S. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4:97-100. Baker SE. Arch Environ Contam Toxicol 1989. TOX-63: TOXICITY REPORT CURVES. Scand J Work Environ Health 2005. Beasley VR. Reynolds SJ.gov/index. To T. Washington (DC): National Academies Press. Needham LL. Kutz FW.4-dichlorophenoxyacetic acid (2.18(4):469-474. Hill RH Jr. Head SL. In farm families. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4-dichlorophenoxyacetic acid in man. Cole DC. Sanderson WT. Erne K. Arch Toxicol Suppl 1980. J Toxicol Environ Health 1992. J Expo Anal Environ Epidemiol 2005 Nov.32(4):233-257. Curwin BD. Dichlorophenoxyacetic acid.15(6):500-508. Acquavella JF. Kohli JD. Heederik D.. Ritter L.. 2005. Gregg M. Alexander BH. 2006. Beeson MD.60(1):121-131. J Expo Anal Environ Epidemiol 2000. 3/17/09 Knopp D. Veterans and Agent Orange: update 2002.4-dichlorophenoxyacetic acid (2. Selected pesticide residues and metabolites in urine from a survey of the U. Tables. Arnold EK.. TOX-63 Peroxisone Project (2.4. National Toxicology Program (NTP). Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Third National Report on Human Exposure to Environmental Chemicals. Harris et al. 2003. Toxicol Sci 2001. the amount of pesticide applied. Stephenson GR. Available at URL: http://ntp. 3/17/09 Institute of Medicine (IOM). Vet Hum Toxicol 1989.nap. et al.Herbicides the time since application.4-dichlorophenoxyacetic acid and its forms.31(2):121-125. Campbell RA.nih. Environ Res 1995. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.S. Xenobiotica 1974.4:427-435. Centers for Disease Control and Prevention (CDC).27(1):23-38. Honeycutt R. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4-D). Kolmodin-Hedman B. Gupta BN. Garabrant DH. 2005).10(6 Pt 2):789-798. Pesticides residues in food: 1996 evaluations Part II Toxicology. Board on Health Promotion and Disease Prevention. Needham LL. Mandel et al. Crit Rev Toxicol 2002. 2005 Charles JM.

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

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

200 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .2.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.670 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.440 (<LOD-.200 (<LOD-. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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.S. 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 . * 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 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 . which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.

html. Biagini RE. Centers for Disease Control and Prevention (CDC). Shoemaker DA. Hsiao JJ. Ward EM. Background document for development of WHO Guidelines for Drinking-water Quality. World Health Organization (WHO). Environ Health Perspect 2003.Herbicides References Battaglin WA. U. reservoirs and ground water in the Midwestern United States. Linhart SM.11(4):353359. Sacramento.248(2-3):115-122. Linderman R. Comparative metabolism and elimination of acetanilide compounds by rat. and metolachlor herbicides in rats.pdf.37(4):10881093. Geological Survey (USGS). Dialkylquinonimines validated as in vivo metabolites of alachlor. 2005. EPA 738R-95-006.39(17):6561-6574. Deddens JA. Camann DE. Feil VJ.S. Environ Sci Technol 2005. Available at URL: http://water. usgs. Coleman S. Gilliom RJ). Thurman EM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.int/water_sanitation_health/dwq/chemicals/ metolachlor. Sanderson WT. 4/2/09 U. 2003.111(5):749-756. Environmental Protection Agency (U. et al.epa. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Thelin GP. Available at URL: http://water.15(6):500-508. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Casida JE. Geological Survey (USGS). Andrews HF. Jefferies PR. Hein MJ. Wratten SJ. et al. Available at URL: http://water. Metolachlor in Drinkingwater.gov/nawqa/pnsp/pubs/files/051507.who. revised February 15. Pesticides in U.pdf. Hodgson E. Brown KK. 6/1/09 Whyatt RM. Gillion. imidazolinone. Rose RL. Hladik ML. 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. Kolpin DW. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Curwin BD.24(10):1003-1012.pdf 3/30/09 Hines CJ. 1998. sulfonamide. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.S. Occurrence of sulfonylurea.S. Peter CJ. Larsen GL. Available at URL: http://www. Davison KL. Kolpin DW. Environ Health Perspect 2000. Quistad GB. April 1995. 1999. Barr DB. March 2006. Sci Total Environ 2000. Ann Occup Hyg 2003. Kinney PL. Heederik D.S. Xenobiotica 1994.gov/oppsrrd1/ REDs/0001. Third National Report on Human Exposure to Environmental Chemicals. 2007. Roberts AL. J Expo Anal Environ Epidemiol 2005. Alavanja MC.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.ESTfeature_gilliom. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Striley CA. Sci Total Environ 2000. Barr JR. acetochlor.S. Atlanta (GA).47(6):503-517. California. Available at URL: http://www. R. 1992-2001. streams and groundwater. and other herbicides in rivers.248(2-3):123-133. Environ Sci Technol 2007.41:3409-3414. Barr DB.usgs. EPA). 3/26/09 U.usgs.php.108(12):1151-1157. Reregistration Eligibility Decision (RED) Metolachlor. Supplemental Technical Information (available on-line only). 98-4245 (by Barbash JE. Feng PCC. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Furlong ET. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.gov/nawqa/ pnsp/pubs/wrir984245/text. Circular 1291. Burkhardt MR. J Agri Food Chem 1989. Reynolds SJ. Chem Res Toxicol 1998.

4. 1989. Chlorophenoxy herbicides act as plant growth hormones.4. abdominal pain. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.5-Trichlorophenoxyacetic acid (2.5-T has been rarely detected in ground waters (USGS. Survey Geometric mean (95% conf. Although 2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 2.5-T (Holson et al. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 1992.7. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. population from the National Health and Nutrition Examination Survey.4-D were used as defoliants in the Vietnam War (e. 2. renal and hepatic injury. Omer. and concern about contamination with 2.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. 2007). Given the commercial unavailability of 2.5-T and 2.3.g.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. Epidemiological studies have reported associations of several types of cancer.4. Ester forms of 2.Herbicides 2.5T is rapidly absorbed via oral and inhalation routes. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. ranging from several weeks to many months. dizziness. and delayed neuropathy (Bradberry et al.4. 93-76-5 General Information 2. 2.1. 64 Fourth National Report on Human Exposure to Environmental Chemicals . Kohli et al.5-T in soil varies with conditions. with an elimination half-life of approximately 19 hours (Arnold et al..4.4.4.4.4.5-T use as a herbicide in 1985. nausea.4. myotonia.. 2004). At low levels.5-T degrades to 2.4.4. Human health effects from 2. 1974)..4. hypotension. Mohammad and St.. but higher levels are herbicidal.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Agent Orange). < LOD means less than the limit of detection.5-trichlorophenol and other degradates.4. headache.4.. 1992).8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. 1986.5-Trichlorophenoxyacetic Acid CAS No. the general population is unlikely to be exposed to it.S.. Once absorbed into the body.4.2 and 0.5-T is eliminated mostly unchanged in the urine. The half-life of 2. Nelson et al. these herbicides can enhance plant growth. 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. it is not well absorbed through the skin.5-T. 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.

S.3.5-T also were below the limit of detection (Kutz et al.4.EPA at: http://www.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. Pearce and McLean. Survey Geometric mean (95% conf. urinary levels of 2. Biomonitoring studies on 2. Additional information is available from U.5-T than levels found in the general population. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. other exposures.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. 2002.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. It is unclear whether these associations are related to the chlorophenoxy herbicides.4. 2003. 1996. 1992).4. similar to results of NHANES II (19761980). 2004). IOM. population from the National Health and Nutrition Examination Survey..Herbicides or contaminated herbicides. Mean urinary levels of 2.4. Fourth National Report on Human Exposure to Environmental Chemicals 65 .gov/pesticides/.EPA.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-T does not mean that the level will result in an adverse health effect. 2005). 2005.epa.7.5-T reflect recent exposure. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Urinary 2. 1980). IPCS.4. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.5-T were generally below the limit of detection.4. Biomonitoring Information Urinary levels of 2.4. U.S.5-T itself is not mutagenic. or to contaminants in the herbicide formulations (specifically 2.4. in which urinary levels of 2. 2. Finding a measurable amount 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.

Toxicol Rev 2004. International Programme on Chemical Safety-INCHEM (IPCS). Gupta BN.5-T).19(2):286-297.4:318-21.htm.5-T). Developmental toxicity of 2. et al. S.4. Gaines TB. discussion 5-7. Erne K. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. McCallum WF.2000 and 2001 market estimates. Developmental toxicity of 2. Multireplicated dose-response studies with technical and analytical grades of 2.edu/catalog. Poisoning due to chlorophenoxy herbicides. Behavioral and developmental effects in rats following in utero exposure to 2. Kutz FW.5-T).31(2):121-125. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .5-T in four-way outcross mice. 2003.pdf.nap. Wolff GL. Pesticide industry sales and usage . 3/17/09 Kohli JD. Brody D. St Omer VE. Khanna RN.31 Suppl 1:1825. Vale JA.5-trichlorophenoxy acetic acid in man.Herbicides References Arnold EK.4. Available at URL: http://www. Office of Prevention Pesticides and Toxic Substances. McLean D.4. Arch Int Pharmacodyn Ther 1974. Environmental Protection Agency (U. Kolmodin-Hedman B. LaBorde JB. Washington (DC): National Academies Press. Sircar KP.4-dichlorophenoxyacetic acid (2. I. Nelson CJ. Mohammad FK.5-trichlorophenoxyacetic acid (2. Nelson CJ. May.EPA. Third National Report on Human Exposure to Environmental Chemicals. Scand J Work Environ Health 2005. Agricultural exposures and non-Hodgkin’s lymphoma. et al. Atlanta (GA). Neurobehav Toxicol Teratol 1986. gov/oppbead1/pestsales/01pestsales/market_estimates2001.4. 2004. Holson JF. Arch Toxicol Suppl 1980.37(2):277-91. Available at URL: http:// www. Veterans and Agent Orange: update 2002. II. general population.32(4):233-257. 2. Pearce N.19(2):298-306. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Tandon JS.inchem. Available at URL: http:// www. Pesticides residues in food: 1996 evaluations Part II Toxicology. Holson JF.23(2):65-73. Crit Rev Toxicol 2002.EPA).8(5):551-60. U.4.php?record_id=10603.4. Estimation of occupational exposure to phenoxy acids (2. Absorption and excretion of 2. Beasley VR.5-trichlorophenoxyacetic acid (2. Philbert MA. Gaylor DW.4-D and 2. 914. Dichlorophenoxyacetic acid.4-D) epidemiology and toxicology.4-.S. Carter-Pokras OD.epa. Washington (DC): U. Fundam Appl Toxicol 1992. Gaines TB. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Cook BT.org/documents/jmpr/jmpmono/v96pr04. Garabrant DH.S. Selected pesticide residues and metabolites in urine from a survey of the U.4.S. LaBorde JB. 2005. Proudfoot AT. 210:250-255.4.5-t mixture. Centers for Disease Control and Prevention (CDC). Sheehan DM. Bradberry SM.4-D/2. Review of 2. Vet Hum Toxicol 1989. Murphy RS. Dhar MM. J Toxicol Environ Health 1992. Board on Health Promotion and Disease Prevention. 3/17/09 Institute of Medicine (IOM). Fundam Appl Toxicol 1992.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

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

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

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

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

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

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

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

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

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

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

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

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

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Organochlorine Pesticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

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

Dieldrin

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

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

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

Fourth National Report on Human Exposure to Environmental Chemicals

77

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

149) . see Data Analysis section) for survey years 01-02 and 03-04 are 10. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD 9.112) 95th .130-.093) .053 (<LOD-.8) < LOD 8.7 (<LOD-15.062 (.160 (.7-19.4 (12.4 (12.150 (.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .9 (13.110 (.7 (14.090 (<LOD-.054-.3 (14.113 (.8-25.070-.110 (.090 (.147 (.9-22.4) 19.8 (18.190) .110 (.110) .4) 21.120) .117) < LOD .5 and 7.100-.6 (15.103 (.5 (<LOD-11.10 (<LOD-16.6) 16.120-.7-22.70 (7.130-.100-.0) 19.089 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-24.083-.40-10.1) 20.50 (8.6) 19.0 (15.2) 15.8) 14.1 (18.058) < LOD .6-33.130) .9 (12.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.063-.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.3 (13.30 (8.8) 15.088-.3 (18.1-16.190) .100 (.0 (10.S.80 (<LOD-10.60-10.5-15.1) 13.056-.8-17.130) .1-19.3 (18.8-17.112-.048 (<LOD-.6-24.055 (.6) 9.077 (.130 (.5) 21.120 (.073-.062-.2-15. 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 .054-. which may vary for some chemicals by year and by individual sample.2) 11.6 (14. Survey years 01-02 03-04 Geometric mean (95% conf.180) .086-.069) < LOD < LOD .109 (.160 (.090-.242) .4-17.0-25.120 (.109-.049-.1) 15.90) 90th 15.30 (8.1-18.062 (.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 8.100) .5-17.108-.9 (14.098 (.054-.8 (11.40-9.0) < LOD 9.7) 15.4) 95th 20.140 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .4) 539 456 484 487 980 885 Limits of detection (LOD.075) < LOD . 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.50) 15.064) 90th .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 .9 (13.110) .084-.4) 14.070 (<LOD-.180) .100) .140-.064 (.0) 21.138) .5) 15.1) 15.4) < LOD < LOD 16.139 (.0-21.0 (11.80-9.8-19.138 (.1-24.4-18.4) 20.102 (.110-.1) 14.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.080-.3-21.150 (.100-.090-.1 (13.096-.158) .090-.139 (.8-24.3 (19.2) 12.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.130) .070) .9-38.00 (8. population from the National Health and Nutrition Examination Survey.S.103 (.2) 14.9-23.077-.6 (15.059 (.80-10. < LOD means less than the limit of detection.140) .9 (12.1) < LOD 9.080 (.116) .124) .130-.5 (16. population from the National Health and Nutrition Examination Survey. Survey years 01-02 03-04 Geometric mean (95% conf.7 (15.160) . which may vary for some chemicals by year and by individual sample.0 (10.00-14.1) 10.060) .5) 19.170) .8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-17.109-.8 (9.101) .080) .182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .120 (.

New York. 15. International Programme on Chemical Safety (IPCS).47:1059-1087. plasma dieldrin. 731-915. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Cox. Kanthasamy A. et al. Chung KL.org/documents/ehc/ ehc/ehc91. Available at URL: http://pubs. Neurotoxicol 2005. David VL. Exp Neurol 1998. 4/21/09 Bates MN. Jr. Olea N. Ginsburg KS. et al. PA. No:429-436. United States Geological Survey (USGS). and epidemiology in the United States. Narahashi T. Needham LL. Priestly BG. Anantharam V. and lymphocyte sister chromatid exchange. Reprod Toxicol 2000. J Occup Environ Med 2005. Chemosphere 2004. Roy ML.109(Supp1):113-139. Patterson DG Jr. Sonnenschein C. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. are nonestrogenic in transfected HeLa cells. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Turner W. Academic Press. Soto AM. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Aldrin and Dieldrin [online]. Smith AG.gov/toxprofiles/ tp1. 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. Kitzazwa M.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Jorgensen T. Mumtaz MM.9:1357-1367. 2 Classes of Pesticides. Frey JM.59:229-234. Mann D. Serrano FO. August 2008.atsdr. Buckland SJ.66(4):229-234.gov/~dms/ pesrpts. 1992-2001. Chlorinated Hydrocarbon Insecticides. Handbook of Pesticide Toxicology. Li AA. 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. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. toxicology. Patterson DG Jr.352:1816-1820. Eds. J Toxicol Environ Health. Kanthasamy AG.26:701-719. Vol. Int Arch Occup Environ Health 1994. Finley B.html. 1991. Inc. Toxicological profile for aldrin/dieldrin [online]. Carlson JN. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Daniel SE. Ellis H. Revised Feb.usgs. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Lancet 1998.gov/ circ/2005/1291/. Schulte P. Brock JW. Food and Drug Administration (FDA). J Toxicol Environ Health 1989. Corrigan FM. Available at URL: http://www. VT. 1989. Teta MJ. Edwards JW. bioaccumulation. Facca A. 4/21/09 Jorgenson JL. Toxicol Lett 1992. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Pesticides in the Nation’s Stream and Ground Water. Wienburg CL. Part A 2000. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Psychopharmacology (Berl) 1987. Six high-priority organochlorine pesticides.64-65 Spec. Tully DB. References Agency for Toxic Substances and Disease Registry (ATSDR). Fernandez MG. McIntosh LJ. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Basit A. Sanchez-Ramos J. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Andersen A.inchem. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. September 2002. Grajewski B. Rosellini RA. Stehr-Green. Environ Health Perspect 2001. Cancer Epidemiol Biomarkers Prev 2000. Shore RF.cdc.27:405-421.91(1):122-126. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Grandjean P. Environmental Health Criteria 91. Garrett N. Demographic and seasonal influences on human serum pesticide residue levels.fda.html.14:95-102. either singly or in combination.150:263-271. In Hayes WJ. Available at URL: http://www.103(Suppl 7):113-122. 2007 [online].cfsan. Mink PJ.54:1431-1443. Organochlorine exposure and risk of breast cancer. Song S. Chapin RE. Jr and Laws ER. Available at URL: http://www. 4/21/09 Hoyer AP. Hartvig HB.htm. pp. 6/1/09 Ward EM. Environ Health Perspect 1995.

3-43.9 (15.7 (<LOD-13.8) 52. buildings.8 (10.7) 42.0-12.5 (31.7) 35.5-41.3) 18. respectively. population from the National Health and Nutrition Examination Survey.2) 37.4) 12. 57-74-9 Heptachlor CAS No.4 (22.4-45.1) 16.4) 29.8-33.7-12. Chlordane is not currently produced or used in the U. Until 1988.3-24.6 (9.9-21.5-32.0-25. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.5) 21.3 (28. and 03-04 are 14. 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.9) 47.7 (34.5-42.1 (15.1 (16.2 (28.5-40.2) 34.1-19.0) 41.9 (31.70 (<LOD-10. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.S.6-45.3) 37.0) 31.6 (43.4) < LOD 11.1 (25. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.4) 37.9) 23.6 (16. heptachlor use has been limited to treatment of fire ants near power transformers.2 (41. 2007).4) 39.5 (34.9) 31.6-18.6-24.0) 20. fish.9) 39.20-11.8-20.0-13.S.8-31.1 (11.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.2-49.7 (17.4) 22.5) 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 * * * * 11.1 (20.0 (20.0 (<LOD-12.7 (43.9) 17. 1994). Since 1992.9 (26. in addition to trace amounts of numerous other related compounds (ATSDR.4-14.9 (36.6) < LOD 11.1) * 11. chlordane was used to kill termites and other insects on agricultural crops.4 (30.1-50.90 (8. lawns. foods high in fat such as meat.1 (40.8-42. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.7 (<LOD-32.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. and dairy products are the usual sources of exposure to these chemicals in the general population.37 (8.0) 27.1 (<LOD-12.6) 48.7-56.7) 28.6-12.10 (8.5) 56.9 (11.2) 46. 10.10-18.3-45.6) 39.S.8) 44.2 (39.6-24.1 (<LOD-12.1-15.1) 30.1) * 11.8 (17.8 (10.9 (11.82-11.0) 21.36-11.3) 10. Technical grade chlordane had contained 7% trans-nonachlor.1-65. see Data Analysis section) for Survey years 99-00.0-61.6) 8.5) 37.5-44.8-33.2 (21.2) * 12.0) 37.6-53.7) 31.3 (<LOD-19.2) 33.9-40.5 (41.5.8.1 (27.7) 19.8) 53.5) < LOD < LOD < LOD < LOD 13.9) 11.6 (9.8-73.2) 36.4 (<LOD-12.1) 90th 34.3 (21.9) 13. As a result of the manufacturing process. Survey Geometric mean (95% conf.20-10.8-43.7 (34.89-10. Fourth National Report on Human Exposure to Environmental Chemicals 81 . 01-02.5) < LOD < LOD 9.5 (33.7 (32.9 (18.4 (10.3 (25.6 (25.7-14.4-51.10-11.9-42.9 (26.5) 10.1) 30.9) 11.7-25.1) 22.6) 20. Consequently.7 (10.6) 23.5-47.5 (<LOD-12.3-45.3) 10.3) 18.9) 36.5-65.7) 9.8 (42.3-49.0-33. 1994.2-28.9-38.9 (21. and in soil.2 (10.69-10.4 (30.1 (44.74 (<LOD-10.6) 9.0 (32.30-11.9) 10.2-56.9 (15.5.6) 48.5-38.4 (31.4-40.8-61.5) 9.8-23. and 7.7 (42.2-49.8) 27.7) 19.2) 22.3 (27.7 (19.0) 75th 20.0-67.Organochlorine Pesticides Chlordane CAS No.5-43.9) 37.9) 23.2) < LOD 11.2 (9.7-39.2-21. the technical grade product of each chemical contains 10%-20% of the other chemical.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.8-32.4-21.7-70. < LOD means less than the limit of detection.0 (37.4) < LOD < LOD < LOD 23.8) 18.1-25.8) 52. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (40.6) 9.1 (17.3) 41.9-21.5) 44.0 (26.4 (35. which may vary for some chemicals by year and by individual sample.6) 11.0-18. 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.3 (26.5) 38.4) 18.8 (17.3 (9.9 (17.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) 36.0 (16.8 (18. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.3-32.2 (36..1 (<LOD-12.3 (11.9 (29.5 (8.63 (8.1-51.3 (20.5-13.2) < LOD 11.1) < LOD < LOD < LOD < LOD < LOD 8.1-25.20 (<LOD-11. from the early 1950’s until the mid-1980’s.2-26. 2007).6) 49.2 (37.

058-.S.189 (.160) .079) < LOD < LOD < LOD .058-.070) < LOD < LOD < LOD < LOD < LOD .104-.070-.048-.240 (.120 (.110-.230 (.180) . which may vary for some chemicals by year and by individual sample.058 (. In laboratory animal studies.080 (.250 (.140) .077) .200-.146) < LOD < LOD . 2007.128 (.063-.510) .070 (<LOD-. 1986).430) .130-.063 (. 2006).291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD . 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.204 (.220-.115-.170-.063) * . 2001.080 (. Takahashi et al.061-.240-.047 (<LOD-.271 (.310-.300) . FDA established allowable residues of chlordane.315 (. and the U.160) .130) .260 (.270 (.083) .370 (..286 (.090) .069 (<LOD-.150 (. 1981).300-.104) .225 (.240-.126) .070 (<LOD-. Acute. characterized by seizures and paralysis.050 (<LOD-.440) .S.199-.077) .290 (. Survey Geometric mean (95% conf.056 (. and inhalation exposure. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.063) .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 * * * * . 82 Fourth National Report on Human Exposure to Environmental Chemicals . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.280-.068) 75th .290-.130 (.260 (. The U.170) .083 (.130) .130-. IARC.100-.350) .290) .280 (.320 (. dermal.Organochlorine Pesticides (Dallaire et al.231) .120-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.180-.076) < LOD .068) .090) .170) .200-.450) .216-.120-.140 (.168-.230-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.070) .150-.310) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. chronic doses of heptachlor have produced liver enlargement and injury.280) .300) . and breast milk is a major excretion route in lactating women.320 (.302) .200 (.310 (. Elimination of all these chemicals from the body occurs over months to years. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.230-.080) .280-.077) .130 (.100-.120-.227) < LOD .310) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .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.230) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.066-.190-.253-.150 (.077) .400) .290-.250 (.189-. which is also persistent in the body (ATSDR.370 (.450) .108-.258-.090-.258 (.230-. 1991. Rogan.223) .066 (<LOD-.049 (<LOD-.203-.050-.087-.063 (.160 (.057-. Chlordane and heptachlor are absorbed after oral.S. Shindell and Ulrich.070 (<LOD-. 1977a.140 (..160) .300 (.100 (<LOD-.119 (.170) .320) .074-.136) .220 (. 1977b.290-.110 (<LOD-.180-.148) . 2002.057 (.150) .140-.242-.100 (.060 (<LOD-.075 (..053-.106-.140 (. OSHA has established occupational exposure criteria..150 (.220-.210 (. The major metabolite of heptachlor is heptachlor epoxide.400) .130 (.290) .057) * .148-.246-.066-.130-.064) < LOD .260 (.066 (.130-. to heptachlor.070-.091) . and alterations in immune function of offspring.280-.065-.146) . 1991). EPA has established environmental criteria for chlordane and heptachlor.320 (.070 (<LOD-.126 (.073) < LOD < LOD < LOD < LOD .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .280 (.170) .350 (. and heptachlor epoxide in foods and bottled water.082 (.380) .270 (.207) . heptachlor.320 (.063 (.430) .373) .055-.260-.250-. Smith.245-.170) .115 (.350 (.149 (.112 (.070-.165-.190-.073 (.320) .240) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.269 (.080) .360) .068-.062) < LOD .230 (.330 (.287) .080) .210 (. population from the National Health and Nutrition Examination Survey.070 (.071 (. neonatal mortality.092) .063 (.410) .190-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent. 2007).213) * . 1996.208 (.133) 90th .370 (.340) .079) .300) .053-.300) .310) . 1986).067 (.340) .286 (.140 (.130-.348) .140-.270 (.180) .200-.207 (.210-. Le Marchand et al.560) .

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

4 (<LOD-54.8) 13. 84 Fourth National Report on Human Exposure to Environmental Chemicals .8) 16.7 (10.3) 18.0) 13.1 (19. respectively.2 (18.5 (10.5 (11.8) 13.8 (13.3) 27.6-17.4 (11.0-19.3) 18.8) 19.8) 15.3-18.9) 15.3) 22.3 (13.5.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.6 (<LOD-27.1) 23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-46.50) < LOD < LOD < LOD 17.5) 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 7.3) 18.8-24.5 (18. and 7.8 (<LOD-23. 01-02.1-29. see Data Analysis section) for Survey years 99-00.5) 19.5 (<LOD-21.1) 13.8-24.6) 22.6-21.9-23.8 (15.6 (8.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.2) 26.7-19.3) 16.8) 19.0 (11.1-38. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.0-17.3 (<LOD-25.6 (14.9 (12.6) < LOD < LOD < LOD 27.8 (18.8) 14.6 (16.4) 18.S.2-16.7-18.9 (15.0-16.3) 23.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.8-23.5) < LOD 14.4 (11.20 (<LOD-9.2-17.0 (15. population from the National Health and Nutrition Examination Survey.8.8) 14.4) 21.2-27.9-25. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.8 (13.2 (<LOD-25.40) 15.6) 14.90 (<LOD-9.1-16.10-13.8) 21. 10.2 (<LOD-62.0-54.9-29. and 03-04 are 14.2 (<LOD-16.9-16.4 (15.7-25.6 (11.9-29.4 (<LOD-19.2) 15.6 (16.1) 20.5 (<LOD-32.2) 20. Survey Geometric mean (95% conf.5 (11.8) 20.7 (13.6 (13.6.8 (18.8-24.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2-27.1 (16.7 (16.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.6) 13.6 (12.2) 13.1-15.3) 10.0-17.

173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130 (<LOD-.120 (<LOD-.107-.070-.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.200) .135 (.113-. Survey Geometric mean (95% conf.170 (.120 (.140) .111-.190) .108-.090-.130) .157) .130-.120) .090 (.180) .101 (.101 (.150 (<LOD-. which may vary for some chemicals by year and by individual sample.170) .130 (.100 (.150 (.170) .097) < LOD .076-.310) .110 (.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.090-.053-.087 (.077-.110 (. Fourth National Report on Human Exposure to Environmental Chemicals 85 .200 (.094 (.100-.180 (.140) .111) .135 (.100 (.180) .067-.117) .104) .130-.380) .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .110-.077-.190) .090-.071-.140-.130) .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 .149) .096 (.110 (<LOD-.090-.130-.100 (<LOD-.108) .170) .190 (.090 (<LOD-.082-.110 (<LOD-.120-.190) .094 (.116) < LOD < LOD < LOD .170 (.063) < LOD < LOD < LOD .120) .270) .S.120 (<LOD-.100-.180 (<LOD-. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .128 (.100 (.100 (.110-.126 (.110) .133 (.220) .090-.113) .240) .098 (.090-.150 (.063) .180) .130-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.055 (<LOD-.069 (.200) .173) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .170 (<LOD-.057 (<LOD-.310) .110) .180) .106-.170 (.074-.

7) 73.1-51.5) 35.5) 14.4) 19.1-18.6 (56.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.3 (58.4) 59.0-93.5) 19.3-21.2 (19.4 (30.1 (41.8-67.7 (11.7-20.7-29.3) 16.9 (36.2 (64.0 (13.6-20.0 (14.1) 78.1) 16.7) 52.8 (26.4 (67.7-17. population from the National Health and Nutrition Examination Survey.7 (74.5) 78.8-19.5-87.1 (47.5) 20.6) 34. and 7.7-23.9 (28.5 (25.2-18.0 (62.8 (28.2 (27.0) 19.0-113) 68. 01-02.1 (65.3) 30. 10.7-38.0 (15.5-111) 68.8 (42.0) 13.3-74.7) 15.4) 48.3 (14.4-52.4) 55.8-129) 74.2 (26.9-35.3 (49.4 (16.3 (17.1-16.8) 47.2-18.7-21.7) 59.4-22.2) 59.6) 56.2 (14.7-18. interval) 18.9-89.7-34.0 (42.8-41.7-32.9) < LOD < LOD < LOD 20.1-34.9-64.1) 78.6-22.6) 60.1) 18.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.9) 51.0-22.9 (51.2) 19.7) 78.8 (11.4) 16.0 (13.1-20.1 (10. 86 Fourth National Report on Human Exposure to Environmental Chemicals .1) 62.0 (15.6 (12.1-28.2-37.6 (15.8 (13.3 (16.3 (14.7-113) 68.6) 82.3 (56.8.1) 14.1) 30. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-95.7 (28.1-34.7 (13.6 (32.5) 36.0 (16.8 (71.0-59.7 (59.9) 14.6 (52.8 (16.0-93.4 (45.1) 17.4-23.8 (26.10 (<LOD-11.9 (15.6-88.0-23.8 (13.1 (22.9 (19.8) 19.5) 30.9 (66.0 (60.5) 48.5) 90th 55.3) 18.9-20.8 (30.3) 18.0 (19.4-67.7 (59.0 (29.5 (15.9 (<LOD-14.2) 17.2) 30.7-160) 86.8-79.3) 32.7-22.3-39.1-22.3) 15.7 (30.5-19.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.6) 84.2-23.8) 51.3-32.8 (19.4) 107 (84.0) 33.1) 32.9-65.7) 17.8-90.3) 19.4) 20. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.5) 14.0-38.8 (<LOD-20.6 (<LOD-14.9 (15. which may vary for some chemicals by year and by individual sample.7) 56.5-69.6-66.9-36.2 (60.7 (35.2) 39.1) 18.9 (51.2) 20.8-19.6 (56.2-88.3-30.5) 22.6) 56.7 (18.5 (13.6) 13.7) 35. and 03-04 are 14.2 (25.7) 28.3) 25.1) 17.6-54.9 (47.5 (15.5) 9.0-23.7-35.4 (11.8-16.3-86.2-21.0) 75th 31.8 (17.1) 31.8-77.0 (48.0-68.6 (57.8-110) 59.1 (17.5 (44.1 (48.7) 14.3-57.2) 34.0) 49.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.8 (45.2 (36.3) 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.5) 77.1) 17.0) 40.3-58.8 (12.6 (16.6-82.0-37.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.3) 36.0) < LOD < LOD 8.0-123) 74.9-45.9 (29.0-24.2) < LOD 10.1-55.9 (16.8 (28.9-58.6) 25.8 (49.6) 54.0-20.4-62.5-36.8) 80.3) 32.5-17.3-50.9-40.4-36.2 (14.1) 17.2 (7.0 (16.2 (15.8 (15.2-16.8-21.4 (28.6-19. respectively.5 (45.8 (28.9-69.5-20.0-143) 112 (68.7) 78.1) 17.1-126) 67.5.70 (<LOD-12.6) 10.8-90.S.3 (45.1) 17.9-22.9-65. Survey Geometric mean (95% conf.8 (26.5) 26.2 (59.3) 30.4-18.9) 51.0 (42.1-16.1) 17.9) 14.6 (50.8-16.2-17.4-35.0) 18.4 (12.7 (16.86-13.7-77.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.5.

458 (.240 (.220 (.171-.130) .490 (.120 (.054-.450) .177-.330-.410-.340-.134) .093-.310-.085-.220 (.400-.060-.087 (.580 (.510-.190-.120) .250) .084-.220 (.210 (.630) .590) .380 (.420) .096) .095-.410-1.260) .125 (.190-.130) .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.117) .106 (.110) .540) .430-.310-.310-.145-.091) .400 (.120 (.085-.110 (.170 (.099-.180-.250) .061-.390 (.232) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .680) .240-.310-.800) .211) 90th .062 (.310 (.096-.126) .480) .104-.590 (.090-.270-.400) .840) .573 (.090-.285-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .106 (.400-.131) .055 (<LOD-.092 (.651) .110 (.680 (.397-.113) .100 (.220 (.150) .430-.108) .390-.186 (.327 (.440-.240) .093-.202 (.594) .114) .080-.324 (.112 (.190-.350 (.080) .220 (.390 (.122) .069-.690) .116-.160 (.520) .078 (.098 (.098-.110-.367) .286-.460) .300-.096-.301-.081-.240) .461 (.161-.080 (.069) .079-.640 (.340-.093) .250) .440) .122) .960) .430-.109 (.470 (.116) .20) .098 (.091-.090-.390 (.109 (.279-.405) .110 (.600 (.082) .120-.460) .160-.559) .497-.390 (.120 (.098) .080-.103 (.510 (.100-.210) .395) .090 (<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 .760 (.590 (.094 (.150) .090 (.210) .130 (.490) .414 (.120) .230 (.280) .130) .520 (.180-.100 (.930) .191 (.S.210 (.119) Selected percentiles ( 95% confidence interval) Sample 95th .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.290-.120-.580 (.085-.111-. Survey Geometric mean (95% conf.360-.580 (.090-.210 (.141) .395-.060) .490 (.161) .260) .460-.099-. interval) .340) .078-.112 (.100-.420 (.272-.080-.080-.210) .128 (.125) .520 (.071 (<LOD-.470-.070 (. which may vary for some chemicals by year and by individual sample.106 (.105 (.119) < LOD < LOD < LOD .110 (.500) .409-.300) .124) .129) .090-.111 (.089 (.470-.180-.079-.060 (<LOD-.240) .288-.108) 75th .183 (.120) .130) .237) .600) .110 (.630) .190-.343 (.242) .220 (.120-.330 (.390) .237) .127) < LOD < LOD .355 (.130) .330-.565) .490-.470 (.100-.108 (.220) .234) .130 (.103 (.140) .097) .210-.220 (.173-.830) .190-.120) .141) .690) .093-.090) .830) .360-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .190-.320-.684) .550 (.205 (.110 (. population from the National Health and Nutrition Examination Survey.113) < LOD .390) .370 (.288 (.100-.047-.370 (.320-.090-.130) .210-.350-.630) .186-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .417 (.158-.116 (.135 (.130) .041 (<LOD-.081 (.470 (.400 (.104 (.317 (.371) .068-.092 (.220 (.310) .

Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Jr and Laws ER. Keller JA. 1994-1997 organochlorine compounds. National Toxicology Program (NTP). Arch Environ Health. Bleiweiss IJ. 1963-1967. gov/toxprofiles/tp12. Environ Health Perspect 2002. August 2007. Ayotte P. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.heptachlor. International Agency for Research on Cancer (IARC) .50(3):108-118. Hansen JC. Wong L. Available at URL: http://www.gov/ntp/ htdocs/LT_rpts/tr009. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Bjerselius R. 6/1/09 National Toxicology Program (NTP). Aune M. Royce W. Saidein D. Chlordane and heptachlor [online]. Available at URL: http://www. Siegel BZ.84:151-161.41:145–148.niehs. 731-915. et al. Granath F. Takahashi W. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2003. Voorspoels S.pdf. Laliberte C. Senie R. Distribution of polychlorinated biphenyls. Academic Press. Wohlleb JC. Available at URL: http://ntp. JAMA 1988.259(3):374-377. Environ Res 2000. Willman E. Hertz-Picciotto I. 1991 pp. Stehr-Green P. Kolonel LN.atsdr. Sci Total Environ 2004. Circumpolar maternal blood contaminant survey. Available at URL: http://ntp. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. 4/21/09 Dallaire F. KalubaSkotarczak A. Handbook of Pesticide Toxicology. Jr. Lulek J.cdc. Canada). Bioassay of heptachlor for possible carcinogenicity. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Baker DB.330:55-70. Bull Environ Contam Toxicol 1981:27:506-511.html.inchem. May 1994. Pollutants in breast milk. Available at URL: http://www.nih. Glynn AW. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. 79. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Poland. Covaci A.372:20-31. New York.org/ documents/cicads/cicads/cicad70.110(8):835-838. Muckle G. 6/1/09 Rogan WJ.28:497501.inchem. 4/21/09 James RA. Organochlorines in Swedish women: determinants of serum concentrations. Hawaii Med J 1991. 2001.htm. et al.cdc. et al. 1979-1980.gov/toxprofiles/tp31. Organochloride pesticide residues in human milk in Hawaii. J Occup Med 1986. Dewailly E. A Report to the Hawaii Heptachlor Research and Education Foundation.9:1-109. Charles MJ. et al. Toxicological profile for chlordane [online]. Gilman A.html. Chlorinated Hydrocarbon Insecticides. 1986.8:1-123.110:617-624.gov/ntp/ htdocs/LT_rpts/tr008. Dewailly E.pdf. Drews K. Tartter P. In Hayes WJ. 1993. Toxicological profile for heptachlor and heptachlor epoxide [online]. Chashchin V. Atuma S. Environ Health Perspect 2002. 2006. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR).org/documents/iarc/ vol79/79-12. Bioassay of chlordane for possible carcinogenicity. Darnerud PO. Takei G.org/site/foundation/ research/projects2. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Arch Pediatr Adolesc Med 1996. maternal serum and milk from Wielkopolska region. Sci Tot Environ 2006. International Agency for Research on Cancer (IARC). 9/25/07 International Programme in Chemical Safety (IPCS). Shindell S and Ulrich S. Available at URL: http://www.niehs. Head SL. Mortality of workers employed in the manufacture of chlordane: an update. Eds.htm. Brower S. Dendle WH. Jaraczewska K.nih. Van Oostdam JC.Summaries & Evaluations. 2 Classes of Pesticides. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort.150:981-990. Wolff MS. Berkowitz GS.atsdr.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Concise International Chemical Assessment Document 70 Heptachlor [online]. Vol. Barker J. Available at URL: http://www.html. Organochlorine exposures and breast cancer risk in New York City women. Smith AG. Loo S. Odland JO. Vol. Inc. Lawrence River (Quebec.111:349355. 4/21/09 Baker DB. LeMarchand L.

9 (21. 1991).2-65.0-155) 83.1 (<LOD-39.7. and 03-04 are 20. when virtually all use of it was banned.6 (22. In the general U.p’-DDT (15%-21%). population.5) 25.9-34.0 (18.0) 26. fish. o.8-26.5 (23. 01-02.1’-dichloro-(2.0-37.1) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 21.1 (33. and 7.10-13. population from the National Health and Nutrition Examination Survey.7 (15.2) < LOD < LOD 9.9 (10.5 (23.1) 31.8) 30.3-590) 293 (104-541) 48. 17.7) 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 imported from countries that still use DDT may contain the chemical or its residues. DDT is converted to DDE and several other metabolites. 2008. particularly meat.p’-DDT (65%-80%).6 (31. sediments.8-17.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.8) 36.9) < LOD < LOD 9. Survey Geometric mean (95% conf.50-11.1-71. DDT was used at one time as a treatment for head and body lice. or dermal exposure.1’-(2.5) 23.3 (<LOD-31.0 (21. and trace amounts of several related compounds. inhalation.0 (18. although DDT and DDE intakes have decreased over time (FDA.7 (19.0) 19. DDT can be absorbed after ingestion.5) < LOD < LOD 9.3-236) 24. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.S. air.0-35.4) < LOD 17. respectively. Only a small proportion of DDT is metabolized and excreted (Smith.6 (<LOD-25. It is still used in some countries.8-23.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.9 (10.2) 155 (59.1-27. particularly for endemic vector and malaria control. Both Serum p.90 (<LOD-12.9) 17. food.2 (11.6 (9. depending on conditions.5 (15. continues to be the primary source of DDT exposure. 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.2 (<LOD-40.9-28.1 (23.3 (<LOD-21.0 (10. 2002.9 (10.9) 14.7) < LOD 18.4 (23.6 (25.0-53. as well as in plant and animal tissues. It was produced and used in the U.3) 21.8) 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. DDT usually refers to the technical product.5 (14.9) 29. see Data Analysis section) for Survey years 99-00.8.0) 20. DDT is converted in the environment to other more stable chemical forms.2) 30.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 89 . The biodegradation half-life of DDT in soil varies from 2 to 15 years.3 (27.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.10 (<LOD-12. p.00 (<LOD-10. which is a mixture containing p. < LOD means less than the limit of detection.3) 28.70 (8.3-16. DDT and DDE can cross the placenta. These chemicals are highly persistent in soil.6-33. 1991).3) 22.0) 40. Gunderson.5-36.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. resulting in fetal exposure. 1988). In the body.7-16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.5-54. and dairy products.8-39.9 (<LOD-20. Smith. after World War II until 1972.0-15. including 1.2-95.p’-DDD (4% or less).7) 12.8) 15.4) < LOD < LOD < LOD 61.S.2-bis(p-chlorophenyl) ethane (DDD).0-27.S. and water.4.

106) .079) < LOD < LOD .150 (<LOD-.00) . Longnecker et al.S. and altered behavior after neonatal exposure (Eriksson and Talts.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 . Studies of DDT exposure and pancreatic cancer.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 .048 (<LOD-.230) . 1995..150 (<LOD-. DDT may bind to estrogen receptors (Chen et al.00 (. polychlorinated biphenyls. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.26) 1.107) 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.160-. 2006.170 (.313 (.220) .150) .078-.p’-DDE can produce anti-androgenic effects (Gray et al.240) .170) .064 (. accidental exposures.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * ..142 (. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.098-. 2001)..112 (.203) . 2001).400) .106-. and leukemia have also been inconclusive (ADSDR.01) . Gladen and Rogan.343) < LOD .170-.. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .087 (.150-. 2006).180 (.Organochlorine Pesticides chemicals are excreted in breast milk. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.114-.180-. Mariussen and Fonnum. Gray et al.190-1.075) 1. 2002. 2002..054-.140-. 2006.084 (.290) .106) < LOD < LOD . 2000. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. 1998).200 (.074-. resulting in exposure to nursing infants (Rogan.095) < LOD .180) . Jusko et al. Animal studies reported reduced fertility.086 (.108 (. Survey Geometric mean (95% conf.130 (<LOD-.120 (<LOD-. 1997).330-4. A workplace standard for DDT has been established by Serum p.132-. Jusko et al.240 (.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 .. 90 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.063 (<LOD-..570-4.180 (.130-..130 (<LOD-. 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. 2006). 2001).530 (.530) .250 (. 1956).105-.143) < LOD < LOD .220) .068-. 2001).62 (.400 (. In laboratory animals. overt signs of acute human toxicity include vomiting.. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 2002.250-1. tremor. reproductive organ abnormalities.140) .p’-DDD and p. other organochlorines. lung cancer.189-. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. and seizures. Calle et al.230) .078 (.g. and duration of lactation. 1996).34) . 2006).150-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004.146 (. dioxins and furans). Hayes et al.260) . fertility.071-..071 (.128 (.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.051 (<LOD-.420) . and o.059-. premature delivery.627) .146 (.190 (.180) . 2006..065-. have not been consistently demonstrated (Beard.069) . In high dose.130 (<LOD-. Reproductive effects in humans affecting birth weight.080-..190 (. Beard.120-.061) < LOD < LOD < LOD .201 (. 2002. Snedeker.

. 2003). Link et al.6. respectively. Heudorf et al. In general.S. 1998. 1991).p’-DDT) as a possible human carcinogen... In a population-based sample of men and women from eastern Slovakia. and 03-04 are 18. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. NTP considers DDT as being reasonably anticipated to be a human carcinogen. mean serum levels of DDT and DDE in the U. see Data Analysis section) for Survey years 99-00. Biomonitoring Information DDE persists in the body longer than DDT. IARC classifies DDT (p. More information about external exposure (i..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. 2002.S. 2002.gov/ toxpro2.0-114) 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..Organochlorine Pesticides OSHA and a guidance established by ACGIH. population declined by about fivefold to tenfold.3. population from the National Health and Nutrition Examination Survey. environmental levels) and health effects is available from the U. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.S..7-119) 113 (100-140) 93.6 (81.8.. Declining DDE levels over time have also been observed in the German population. 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. Since the 1970’s.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. 2005).epa. Median DDE levels among a population-based sample of Swedish women in 19961997 were similar to females in the NHANES 1999-2000 subsample (Glynn et al. respectively. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. EPA at: http://www. 1989). compared to levels observed in this Report (Anderson et al. Survey Geometric mean (95% conf.e. 8. Compared to females in the NHANES 1999-2000 subsample. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Smith. Stehr-Green. for males and females in the NHANES 19992000 subsample (Pavuk et al. 2004).. Fourth National Report on Human Exposure to Environmental Chemicals 91 . 2004).gov/ pestcides/ and from ATSDR at: http://www. 01-02. 2003.cdc.html. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. 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.atsdr. and 7.

34) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.32 (1.26-2.6) 11.43-4.7 (8.623 (.63 (1. 309 versus 268 ng/g lipid.87 (5.0) 2.3 (8.81 (7.02) 1..3) 16.29 (1.32) 1.12 (.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 .38 (1.18-1.36-2.34-11.58) 1.870 (.57-2.25) 8.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.456 (.66) 3.97 (3.37-10.6) 12.76) 1.385-.680-1.63 (6.76 (2.06) 3.36-11.44) 1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.14) 2.57-3.24) 1. o. or p.40-4.33-1.79) 4.26 (1.76) 1.39 (3..35) 1.994-2.8 (9.32-1.75) 6.10-5. 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.50-17. In the NHANES 1999-2000.91-3.58) 75th 3.p’-DDT (Stehr-Green.4 (8.76-3.6) 8.5) 10.01-1.48 (6.57) 2.890-1.25-14.18) 1.03-1.34-3.37 (1.65 (1.6 (9.2 (9.500-.68 (2.66) 1.6 (17.4-19.43-8. interval) 1.36) 3.6 (8.430-.3-43.13 (1.7) 16.75 (4.58) 1.64-2.05) 1.53) 7. 1991).47 (1.2) 26.17-3.600) .52 (3.46 (1.36-1.21) 90th 7.43-4.92 (3.646) . less than one percent had detectable serum levels of o.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.25-16.51 (1.7-19.65) 1.00-1.6) 13.59 (1.31-2.16 (2.66) 4.01) 1. 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 1.2 (19.19) 4.69 (1.7-48.59) 6.3) 10.59) 3.6) 9.51-49.01-15.68-4.820-1.9 (15.49) 8.32-1.96) 1.18-1.1) 7.36 (3. Finding a measurable amount of p.30 (1.2 (6.60-13.61-2.S.07) 1.22) .99) 1.85-10.12-1.52-6.91-2. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.96) .57 (3.9) 7.13) 4.13-2.39-2.561 (.37-4.32 (1.81) 11.80) 3.16-1.81-18.80) 1.82) 1.53-15.82 (1. 1989).40-4.84 (3.37-1.p’-DDT were below the limits of detection.90) 22.71) 32.49 (1.77 (1.40-8.57-13.0 (9.41-12.01-1.39-1.24-17.19-14.8 (14.02-8.7-20.69 (2.46-2. population from the National Health and Nutrition Examination Survey. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.56-3.91) 3.26-10.5) 16.63-15.611-1.25 (1.66-2.726) ..18-4.80 (2.3 (9.6) 9.54) 8.516 (.590 (.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. 2004).72) 1.83 (1.59 (1.25 (.34 (7.75) 2.31-12.10) 2.88 (2.14 (1. serum levels of o.9 (26.30-1.90-8.80) 1. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.61 (1.8 (13.07 (5.27) 3.15-4.8) 15.52 (1.18 (6.2-32.1) 40.Organochlorine Pesticides nearby agriculture (Botella et al.66) 1.70-3..12 (6. considerably higher than levels in this Report (Smith.04-1.8 (13.97-4.10-1.34) 6.32-9.557) 1.14-9.7) 9.47) 3.18-3.45 (1.51-8.70) 1.09-1.72) 1.520 (.37-16.8-90.75 (8.p’-DDT.5) 5.03-4.796 (.6) 9.5) 22.9) 5.07) 1.31 (1.54 (1.30-1.3) 13.84-3.43 (5. 2005).69) 4.30 (1.00 (.91 (6.53) 1.54-7.78 (4.39) 1.860 ng/L) and DDE (about 14.10) .93 (7.4 (12.51) 1.48-4.40 (3. Serum p.2 (9.01-11.965-1.71 (5.22 (7.46 (1.2) 19.4) 13.77 (1.00 (6.00) 7.488-.963-1.49 (1.92) 1.87-16.57 (1.41 (1. Survey Geometric mean (95% conf.23 (7.11 (2.51-15.0 (12.p’-DDT.14-1.4) 9.06) 1.57 (1.27-1.53 (2.24 (1.01-5.5) 7.28) 1.59 (4.4) 14.55 (2.51) 3.1 (8. 2004).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.75) 1.17 (3.1) 12.71) 12.26) 3.85 (1.66-4.6) 9.56) 2.62-6.64) 3.04 (6.63 (1.7) 13.56-2.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .05 (3.6 (7.1 (9.534-.56-6.69) 8.11-1.88-35.635) 1. High mean levels of whole blood DDT (about 3.69 (.20 (.25) 1.14) 2.01) 1. In a subsample of NHANES II (19761980) participants.81 (1.66-17.9-17.730) .38 (1.01-11.9-38.50 (2.21) 3.68) 2. 1971).p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.419-.22-1.02 (2.49 (6.45 (1. 2001-2002 and 2003-2004 subsamples.55-9.92 (3.71 (6.85-4.81-5.

Survey Geometric mean (95% conf. 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8. and 7. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.Organochlorine Pesticides Serum o.4. see Data Analysis section) for Survey years 99-00. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 03-04 are 20.7.S. respectively. Fourth National Report on Human Exposure to Environmental Chemicals 93 . population from the National Health and Nutrition Examination Survey.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 01-02.

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. 94 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < 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.

et al.21(1-2)37-48. et al. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Available at URL: http://www. Bull Environ Contam Toxicol 2004. Hediger ML. Ostby J. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.7(3):248-264. Lepom P. Levels of DDT. HCH. Sci Tot Environ 2006. DDT and human health. Darnerud PO. Rogan WJ.fda. hexachlorobenzene. Am J Public Health 1995. Arnold SF. Zhou H. Neurotoxicol 2000. Herrman T. Botella B. Burse VW. Calle EE. Greenfield TA.cfsan. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Available at URL: http://www. lindane (g-HCH). Vorojeikina DP. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Food and Drug Administration (FDA). et al. Zhou H. Crespo J. Gladen BC. Ellis H. Paepke O.205:297-308. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Jusko TA. et al. Zoellner I. Biochem Pharmacol 1997.85:504508. Schulz C. Bhatnagar VK. Jr. Int J Hyg Environ Health 2003.355:7889.358:110-114. Rivas A. Parks L. Kulkarni PK. Longnecker MP. Savitz DA. selected elements. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. DDE and shortened duration of lactation in a northern Mexican town. Wolf CJ. Notides AC. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Environ Health Perspect 2003. Longnecker MP. Lambright C. Gabrio T. Frumkin H. Olea-Serrano MF.html. Chemosphere 2005. dietary intakes of pesticides.gov/ toxprofiles/tp35. Olson JR. Gray LE Jr. Patterson DG Jr. hypospadias.106(5):279-289.111:349355. Lancet 2001. Cerrillo I.52:301-309. Falk C. Biomonitoring of persistent organochlorine pesticides. Bloom MS. Klebanoff MA. Heudorf U. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.gov/~dms/ pesrpts. Bates MN. Toxicological profile for DDT.155(4):313-322. et al. Gray KA. Baker RJ. Environ Res 2005.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Chemosphere 2004. et al.. Barr DB. Davis MD. Thun MJ. and other chemicals.206:485-491. Willman EJ. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP).1-dichloro2. Epidemiology 2006. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Piechotowski I. Buckland SJ. Moysich KB. Beard J. Talts U. April 1982 to 1984. Zaidi SS. Katz SH. Angerer J.cdc. Drexler H.53(8):1161-1172. Am J Epidemiol 2002. Int J Hyg Environ Health 2002. The Great Lakes Consortium.97(2):178192. Hurd C.72:261265. and HCB residues in human blood in Ahmedabad. Durham WF. Needham LL. Bjerselius R.58:1185-1201.atsdr. Atuma S. Hayes WJ. 4/21/09 Gladen BC. and polythelia among male offspring. Needham LL. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Garrett N. Olson J. dichlorodiphenyldichloroethylene. Hum Reprod Updat 2001. India. Profiles of ortho-polychlorinated biphenyl congeners. FDA total diet study. Environ Health Perspect 2004. Furr J. Eriksson P.162:890-897. Aune M. and dichloro(diphenyl)ethylene (DDE). Maternal DDT exposures in relation to fetal and 5-year growth. Kashyap R. Environ Health Perspect 1998. Swanson MK. Koepsell TD. et al. Chen CW. CA Cancer J Clin 2002. Krause C.54:1431-1443. September 2002. Gunderson EL. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. DDE. Charles MJ. Vena JE. Kaus S. Klebanoff MA. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Needham LL. Becker K. et al. Jr. Effects of environmental antiandrogens on reproductive development in experimental animals. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.112(17):1761-1767. Exposure of women to organochlorine pesticides in Southern Spain. Seiwert M.html. Hanrahan L. Olea N. August 2008. 4/21/09 Anderson HA. Brock JW. and DDD [online]. Saiyed HN. Organochlorines in Swedish women: determinants of serum concentrations. Maternal serum level of 1.96:34-40. J Assoc Off Anal Chem 1988. et al.71(6):1200-1209.17(6):692-700.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Cueto C. Henley SJ. Link B. Granath F. Organochlorines and breast cancer risk. Glynn AW. Klebanoff MA. Environ Res 2004. Brock JW. JAMA 1956.

Inc.109:35-47. Chemosphere 2004. Rey AA. J Toxicol Environ Health Part A 1998. Fonnum F. 731-915. New York.20(2):186-193. Cerhan JR. Fox S. Academic Press.53:455-477. Pesticides and breast cancer risk: a review of DDT. et al. Toxicol Appl Pharmacol 1971. Vol. Chovancova J. children and newborn infants. Reddy AB. Pollutants in breast milk.27:405-421. Demographic and seasonal influences on human serum pesticide residue levels. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. 1991 pp. Jones CR. Radomski JL. Snedeker SM. Stehr-Green. Lynch CF.54:1509-520.150:981-990. Lubet R. Astolfi E. Arch Pediatr Adolesc Med 1996. 2 Classes of Pesticides. Jr and Laws ER. Petrik J. Neurochemical targets and behavioral effects of organohalogen compounds: an update.Organochlorine Pesticides Mariussen E. DDE. Thomas PE. Crit Rev Toxicol 2006. Rogan WJ. Environ Health Perspect 2001. Chlorinated Hydrocarbon Insecticides. Nims R. PA. DDE. et al. Environmental exposure to PCBs and cancer incidence in eastern Slovakia.36:253-589. In Hayes WJ. and dieldrin. Schecter A. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Deichmann WB. and DDD in male rat liver and cultured rat hepatocytes. Pavuk M. Eds. Jr. Handbook of Pesticide Toxicology. Comparative pharmacodynamics of CYP2B induction by DDT. Smith AG. J Toxicol Environ Health 1989.

1992). Endrin is absorbed rapidly after ingestion.50) < LOD 5. Depending on soil conditions. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. 1979. At high doses.40-5. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. Endrin was not widely used as a termiticide. 2008).S. Endrin was used as an insecticide. Hepatic effects of endrin exposure have included necrosis. < LOD means less than the limit of detection. or discarded. 72-20-8 General Information Endrin. and occasionally at low levels in sediment and surface waters. Smith. unless the dose is high and the exposure is very recent. endrin usually is not detected in serum of exposed individuals..50) < LOD < LOD < LOD 5. Because it is metabolized so rapidly. Ketoendrin is a major photodegradation product (IPCS. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. population from the National Health and Nutrition Examination Survey.30 (<LOD-6.40) < 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 5.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. manufactured. rodenticide and avicide. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.S. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. unlike aldrin and dieldrin. Survey Geometric mean (95% conf. inhalation or dermal exposure routes. 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. Fourth National Report on Human Exposure to Environmental Chemicals 97 .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. 1996.30) < LOD 5. 1991).09 and 7. Endrin does not accumulate in body tissues (IPCS.20 (<LOD-5. endrin can persist for years. 1992). or from contact with contaminated soils and sediments in areas where endrin was applied.10 (<LOD-5.. Endrin has been detected in soils. anti-12hydroxyendrin. fatty infiltration. 1992). 1987). endrin has been detected with declining frequency in U. endrin is converted rapidly to its major metabolite. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5.10 (<LOD-5. In the body.Organochlorine Pesticides Endrin CAS No. IPCS. All uses of the pesticide in the U. 1981). 1992. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.S. which may vary for some chemicals by year and by individual sample.S.S.8. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. Kavlock et al. is no longer manufactured in the U.. EPA..60 (5. total diet surveys (FDA. 1991).20 (<LOD-5. have been cancelled by the U. a stereoisomer of dieldrin. An epidemic of acute endrin poisoning. and inflammation (Smith. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Over time.40 (<LOD-6. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

Fourth National Report on Human Exposure to Environmental Chemicals 99 . Garrett N. In Hayes WJ. Inc. Grajewski B. Available at URL: http://www. Narahashi T.cfsan.html. Convulsions caused by endrin poisoning in Pakistan. Liddle J. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.gov/toxprofiles/tp89. Frey JM. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Jr and Laws ER. Gray JA. 2 Classes of Pesticides. Chemosphere 2004.cdc. Toxicological profile for endrin [online]. Olea N. Botella B. Cerrillo I. I. Saleem M.html.13:155-165.9:1357-136. Rivas A. 1991.atsdr. Smith AG. 731-915. Chlorinated Hydrocarbon Insecticides. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. et al. Hardjotanojo W. et al. Toxicology 1981. Whitehouse DA. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Chernoff H. Handbook of Pesticide Toxicology. Perinatal toxicity of endrin in rodents. Olea-Serrano MF. Available at URL: http://www. New York. Patterson DG Jr. II. Sokal D. Burse VW. Roy ML. Ward EM.org/documents/ehc/ehc/ ehc130.54:1431-1443. 1992. Fetotoxic effects of prenatal exposure in hamsters.96:34-40. Environ Res 2004. Ginsburg KS. Ellis H. Endrin [online]. Food and Drug Administration (FDA). Vol. 4/21/09 Kavlock RJ. Turner W. Exposure of women to organochlorine pesticides in Southern Spain.inchem. 4/21/09 Bates MN. Rowley DL.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Schulte P.htm. 4/21/09 International Programme on Chemical Safety (IPCS). Environmental Health Criteria 130. Academic Press. Available at URL: http://www. Hanisch RC.64-65 Spec. Eds. Fetotoxic effects of prenatal exposure in rats and mice. Cancer Epidemiol Biomarkers Prev 2000. Chernoff N. Gray LE. Gray J. August 2008. Andersen A. Pediatrics 1987. Toxicology 1979. et al. Toxicol Lett 1992. Rogers E. Kavlock RJ. Hanisch RC. Rab MA. Crespo J.79(6):928-934. August 1996. Needham LL. No:429-436. Jr. Gray LE. Perinatal toxicity of endrin in rodents. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. et al.21:141-150. Buckland SJ.fda. pp.gov/~dms/ pesrpts. Patterson DG Jr.

4.S.0-16.6) < LOD < LOD 26.4) < LOD < LOD 23.3-26.0-19. 2002).3) < LOD < LOD 20.9) < LOD < LOD 20. 01-02. Therefore.9-17.S.4) < LOD < LOD 33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3-20. population from the National Health and Nutrition Examination Survey.9-32. distributes widely throughout the body. Survey Geometric mean (95% conf.6 (24.7-26. HCB is slowly metabolized.7 (15.3 (12. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.9 (25.9 (23. and foods with a high fat content.9) 19.7-22.3 (22.1 (14.1 (14.5 (14.4.7 (27.9 (14.8 (26. HCB has been detected in fewer foods since the 1980s (FDA.5 (13.2-31.7) < LOD < LOD 24. 1976).0-25. 100 Fourth National Report on Human Exposure to Environmental Chemicals .7-16.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.6) < LOD < LOD 14.4.6-trichlorophenol (2.7-15.4-15..1) < LOD < LOD 15.3 (16.5-14.2-15. 31.8 (15.7 (15. < LOD means less than the limit of detection.1-20. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.7 (19. or game taken from areas with HCB contamination.4 (22.1 (17.6) < LOD < LOD 25.4 (18.5) < LOD < LOD 18.7-21. wildfowl. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.7-16.6 (21.3) < LOD < LOD 29.7-30. and elimination occurs by renal and fecal routes. 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. Although it is not manufactured as an end-product in the U.2) < LOD < LOD 13.4) < LOD < LOD 22.5 (13.7-29.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. EPA cancelled its use in 1984.5-TCP) and 2.6) < LOD < LOD 24.S.9-24.3 (20.0 (18.0.9-30.5-33.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) < LOD < LOD 29.9) < LOD < LOD 28. Gunderson. 2008.6-26. Urinary metabolites include pentachlorophenol (PCP). particularly by consuming fish.4) < LOD < LOD 18.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. see Data Analysis section) for Survey years 99-00.1 (13.6 (23. and has been detected in soil..4 (18. and accumulates in fatty tissues where it persists for years. primarily as a fungicide and seed treatment until the U. HCB is well absorbed after oral administration. 1997).9) < LOD < LOD 16.7) 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. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.2 (24. The FDA dietary surveys have shown that over time. and sediment (Barber et al. and 03-04 are 118.3-22.5-18.9) < LOD < LOD 19.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.1-16.0) * * 15.9) < LOD < LOD 20.0 (14.0) < LOD < LOD 24..0 (25.0 (18.9-15.2 (14. air.6-TCP) (To-Figueras et al.1) * * 15.5-15. breast milk is an additional route of elimination in nursing women. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.2 (14. water.6-44.8) < LOD < LOD 27.4-16.4 (11. The general population may be exposed to HCB through diet. which may vary for some chemicals by year and by individual sample.5-14. respectively. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.5-15.6-33.9) < LOD < LOD 15. 2005).4) < LOD < LOD 14..9 (25.6) < LOD < LOD 26.3 (22.6-19.0) < LOD < LOD 15.9-20. and 7.0) < LOD < LOD 15.0-28.2 (17. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.8 (22.S. 2.2-15.4) < LOD < LOD 19.6-32.4.2 (13.7) * * 14.8-15.5-trichlorophenol (2.Organochlorine Pesticides Hexachlorobenzene CAS No.3) 24.3) * * 15.3 (14. 1988).4.8.

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

Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. April 1982 to 1984... but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Int J Hyg Environ Health 2002. respectively. Kohli J. FDA total diet study. Paepke O.39(12):744-749.77:173182.html. Atuma S. Lackman. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. levels. Dogramaci I. 4/21/09 Glynn AW. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. IARC Sci Publ 1986. Bertram HP. Organochlorines in Swedish women: determinants of serum concentrations.44 mg/L. Toxicological profile for hexachlorobenzene update [online]. dietary intakes of pesticides. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Sci Tot Environ 2005. August 2008. As a result of the lower limit of detection in NHANES 2003-2004. The metabolism of higher chlorinated benzene isomers. Bjerselius R. et al.gov/~dms/ pesrpts. van Wijk D. J Exp Sci Environ Epidemiol 2007. Reference values updated. Peters HA. September 2002. HCB levels were directly related to age. Santiago-Silva M. only 4. Glynn et al. the more recent values in these studies were similar to the lipid adjusted limit of detection in NHANES 1999-2000 and 2001-2002 (Dallaire et al. 2002) and among children (Link et al. Arch Neurol 1982. J Assoc Off Anal Chem 1988. selected elements. Schwartz JM. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Link B. Biol Neonate 2002. Muckle G..17:388–399. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. 2002. Gocmen A. Environ Health Perspect 2002.205:297-308. Bradman A. Eskenazi B. Bradman et al. Chemosphere 2005.. Fenster L. more HCB levels were quantified. Krause C. In Spain. Gunderson EL. 2005. Lawrence River (Quebec. Dewailly E. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. and the geometric mean concentration of HCB in whole blood was 0.111:349355. Link et al. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. however. Bryan GT. Otero R.html. 2005). Aune M. Kaus S. Becker K.. 1986. Canada). Available at URL: http://www. Lecha M. trends and processes. HCB detection in serum also was proportional to age. Piechotowski I..71(6):1200-1209.atsdr. Food and Drug Administration (FDA). Schulz C. et al.58:1185-1201. Dallaire F. Lepom P. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Can J Biochem 1976. Seiwert M.135(4):400404. In the 1976-1980 NHANES subsample. Lackmann GM. Holland NT. Muller C. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Arch Dermatol 1999. In a representative sample of the 1998 German adult population. distribution. 2002). Ayotte P. Hexachlorobenzene in the global environment: emissions. Gabrio T. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Zoellner I. et al. Biomonitoring of persistent organochlorine pesticides.cdc. 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. 4/21/09 Barber JL.110(8):835-838. but overall. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Sala M.. Jones KC. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. and other chemicals. Herrero C. 1989). Sweetman AJ.. Laliberte C.. Safe A.54(3):203-208. Herrman T. Jones D.9% of participants had quantifiable levels (Stehr-Green.349:144. 2002. Ozalla D. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Cripps DJ.gov/ toxprofiles/tp90. Lackmann. Darnerud PO. 2002. Over the past two decades. 2002.cfsan. 1999).. Available at URL: http://www. 2003).81(2):82-85..Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Kemper FH. References Agency for Toxic Substances and Disease Registry (ATSDR). German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 2006). than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Bertram et al. Barr DB. Environ Health Perspect 2003. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.fda. Granath F. 2005).

Fourth National Report on Human Exposure to Environmental Chemicals 103 . Santiago-Silva M. et al.263:397-398.27:405-421. PA.Organochlorine Pesticides Schmid R. Rodamilans M. Otero R. Stehr-Green. Barrot C. Demographic and seasonal influences on human serum pesticide residue levels. To-Figueras J. Cutaneous porphyria in Turkey.105(1):78-83. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Sala M. J Toxicol Environ Health 1989. N Engl J Med 1960. Environ Health Perspect 1997.

1-15.2 (34.7) 27.3) 14.9-21.2-87.1 (30.9 (9. 2005). containing about 64% alpha and 10%-15% gamma isomers.43 (<LOD-9.8 (17.7 (13.6) 18.3) 37.1-36.9 (40.1) 12.90) 7. 319-85-7 gamma-Hexachlorocyclohexane CAS No. including alpha.2 (18.5 (24.1 (9.0) 7.9) 17.0) 17. 6.2-17.4) 44.1 (21.4) < LOD < LOD < LOD 46.8.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.7-96. 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. EPA cancelled agricultural uses of lindane (ATSDR.2-46. and 7.70 (6.6-20.9-14.30-11.9) 45.0 (35.2 (31.04-10. formerly referred to as benzene hexachloride. and delta.70-19.6-37.S.7 (30. It is no longer produced or sold in the U.5-123) 49.7) 73. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. water.7) 23.7) 56.7-69.80 (<LOD-14.1 (11.1 (27.0 (19.5) 29.7 (53.0 (33.3-56. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.5) 11.8-54.8) 12.89 (<LOD-9.1-32.4) 51.2 (29.9-56.6) 50.8-68.9-24.6 (22.5 (16. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.87 (9.7 (<LOD-16.6-42.1 (16.4) 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 21.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. population from the National Health and Nutrition Examination Survey.0) 41.9-81.0) 8.0) 35. the U. 01-02.2-22.76.66-12.4) 21. The other isomers can be formed during the synthesis of lindane. **In survey period 2001-2002.7-96. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.9-178) 48.0 (8.5 (43.3-85.68 (<LOD-10.4 (52.1 (18.2) 9.3-38.2-67.4-45.9 (32.3 (42.0-34.7) 10.4) < LOD 9. see Data Analysis section) for survey years 99-00.5) 14.8 (64.1-27.0-111) 70.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.5) 22.5) 90th 42.8) < LOD 10.0-23. See the section “What’s New” at the beginning of this Report for details.9-51.8 (23. Lindane has a half-life of about two weeks in soils and water.6) 47. which may vary for some chemicals by year and by individual sample.5528.6 (10.0-21.S.1) 31.7) 97.1-37.46-11.4-111) 84.0-20.9 (50.2) 36.7) 10.7) 32.5 (8. < LOD means less than the limit of detection. 608-73-1 beta-Hexachlorocyclohexane CAS No.6 (17.6-62.9) 15.3) 25.70-12.9 (62.2-20.2-52.7 (25.6 (40. particularly alpha and gamma have been detected widely in air. and 03-04 are 9.1) 71.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.7-166) 70.9 (26.2-42.2) 13.0-70.5) 40.7-69.2 (48.0-70. and have been used either as fungicides or to synthesize other chemicals.8) 27. 58-89-9 General Information Hexachlorocyclohexane (HCH).8 (21. The gamma isomer.4 (11.8-16.6) 36.4 (12.2 (9. 104 Fourth National Report on Human Exposure to Environmental Chemicals . In 2006.3 (62. HCH isomers are lipophilic.8 (33. soil.3) 34.5) 16.Organochlorine Pesticides Hexachlorocyclohexane CAS No.3) 51.8-87.6) 653 758 589 1240 1533 1370 20 years and older 10. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.5) 67.4) 901 1067 952 992 1224 1007 Females 11.0 (<LOD-12.0) 71.70 (8.7 (29.60-13.4-73.1) 12.56-12.8) * * * * * * 15.6-89.2) 62. commonly known as lindane.6-18.20-16.61-12.6) 35.8-19.6-14.4-50.8 (32.6 (33.7) 18.5-29.3 (13.5 (37.1-49.7 (62.2-55.90-8.5 (11. Technical grade HCH is a mixture of all four isomers. environmental levels declined.2) 142 (99.36. However. interval) 9. 2005). exists in several isomeric forms.2 (50.7-26. As pesticide applications of HCH were increasingly restricted or eliminated.3 (42.5 (14.4 (16.8-199) 134 (85.8) 7.1 (12.1-16.4) 11.1 (9.8 (10.4 (8.7-20. each result has been multiplied by 1.80 (6.0 (14.1) 13.1-32.2-98. so they can accumulate in fatty tissues of animals.8 (9.9 (11.6-135) 69.6-47.90-8. gamma. respectively.8) 39.6) 16.8) 52.50) 8.0 (37.4) 27. beta. and sediment as a result of historic production and use.9 (30.3 (26.6 (16.S.8) 95th 68.9) 81.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.7 (35. HCH isomers.4 (50.4) 10.

072 (.080-.32) .340-.050-. which may vary for some chemicals by year and by individual sample.078 (.100) .587) 653 758 589 1240 1533 1370 20 years and older .620) .310) .083 (. respectively.070-. Saxena et al.059-.221-.372 (. OSHA and ACGIH have established workplace standards and guidelines.220-.240-. paresthesias. After dermal application of lindane 1% lotion.150-.460 (. EPA has established a drinking water standard.110-.140) .056-.050 (.S.220) .254) 95th .140) .S. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.410 (.090 (.319) .680) .160-.100 (.120 (.051-.089) .120) .340) . 1981).191-. 1983).390-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .056-.410) .067) . 1986).250-.281 (.065 (. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.290 (.220 (.270 (. probably by blocking inhibitory neurotransmitters in the central nervous system.190-1. each result has been multiplied by 1.Organochlorine Pesticides exposure to HCH is through the diet.092 (.216 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.300-.090 (.120) .234 (.910 (.360 (.580 (.250-.510) .297-.110) .130-.057 (<LOD-.390 (..070) .01 (.174) .144 (.360-. enlarged livers.065 (.064) .190) . **In survey period 2001-2002.210-.086) < LOD < LOD < LOD < LOD < LOD < LOD .620-1.050-. 2008. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans. ataxia. U.290) .120 (.330 (.120-..070-.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.450 (. ingestion.081-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .450-.840) . Workers who directly handled HCH have complained of headache.470 (.080 (.570 (.05) .051 (<LOD-.090 (.120-. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.501) .480 (. 2002).410) .140 (.400) . hepatic enzyme induction.140) .404) .310 (.150) .064 (.073-.048 (<LOD-.294-.067 (.700) .050) .130 (.290 (. or dermal exposure. and memory loss (Nigam et al.103-.280-.167 (.560) .260-.110) .350) .062 (.096) .103 (.690) .400) .220-. When animals were chronically fed lindane at high doses.600) .080) * * * * * * .050-.382-.814) .222 (.200-.050 (<LOD-.230-. and FDA has established a bottled water standard and food residue tolerances for lindane. HCH crosses the placenta and is also excreted in breast milk (Radomski et al. 1996.450) . See the section “What’s New” at the beginning of this Report for details.580-1. Gunderson 1988).250 (. 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.100-.139 (.250) .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 .180-.050 (<LOD-.37) 1. Rogan..118 (.250 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.062 (.100-.080 (. population from the National Health and Nutrition Examination Survey.170-.100 (.120 (.125) < LOD < LOD < LOD .173-.360) .320 (.077) < LOD . interval) .260) . and seizures.160) .170-. from 6% of samples in 1982-1984 to 2% in 1994 (FDA. 1971.098 (.244-.100) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .060) .250 (.442 (.710) .050 (..521 (.080-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .070-.103) 90th .370-. and nephropathy developed (IPCS.190-.661) 901 1067 952 992 1224 1007 Females .160 (.119) .210 (.150) ..057-.131-.210) . HCH isomers are absorbed after inhalation.290) .460) .S. 1977).057-.070 (.050-.083) .070 (. for lindane.480 (. the serum half-life was about 20 hours among children (Ginsburg et al.305) .470) .047-. resulting in a half-life of about seven years.200-.191-.146-.380 (.420-.5528.290 (.210 (. tremors.287 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240 (.118-.130) .331 (.040-.560 (.077) < LOD . The U.200 (.280-.308-.350 (.080-.310) .124-.480) . Distribution is mainly to fatty tissues.069) .214) .089-.068-.190) .110) .410-.120-.100-.175 (.412 (.091) .260) .330-.080) .150 (.058 (<LOD-. The beta isomer accumulates in fatty tissues and is metabolized more slowly. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.090-.

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

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. 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. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. In a small study of adults who consumed sport fish from the Great Lakes. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.S. Fourth National Report on Human Exposure to Environmental Chemicals 107 .. population from the National Health and Nutrition Examination Survey.Organochlorine Pesticides 2001-2002 survey period (Link et al. 2003). 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. in this Report (Nigam et al. 1986. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2005). 1971). 1998)... 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).. A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al. respectively. Radomski et al.. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al.

Placental transfer of pesticides in humans. Ellis H. Int J Hyg Environ Health 2002. Environ Health Perspect 2003. selected elements. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Astolfi E.cfsan. Majumder SK. Int Arch Occup Environ Health 1986. August 2008.150:981-990. Rothman N. Bhargava AK.91:998-1000. FDA total diet study.57(4):315-320. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Angerer J. Becker K.58:1185-1201. Toxicol Appl Pharmacol 1971. Maass R.48:127-134. et al. Deichmann WB. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Arch Toxicol 1981.96:34-4Food and Drug Administration (FDA). Seiwert M. Karnik AB. Krishna Murti CR. Buckland SJ. Paepke O. Patterson DG Jr. Kashyap R. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. PA. et al. gov/toxprofiles/tp43. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. 4/21/09 Ginsburg CM. 2002. Rogan WJ. dietary intakes of pesticides. Aune M. Needham LL. Olea-Serrano MF. Olson J. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Bhatnagar VK. Lepom P. J Toxicol Environ Health 1989. Atuma S. Bjerselius R.71(6):1200-1209. Metabolism of gammahexachlorocyclohexane in man. Visweswariah K. Gunderson EL. Kaus S.html. Levels of DDT.inchem. Heinrich R. org/documents/jmpr/jmpmono/2002pr08. 4/21/09 Kutz FW. Bottimore DP. Garrett N. Schulz C. Absorption of lindane (g benzene hexachloride) in infants and children. and HCB residues in human blood in Ahmedabad. Demographic and seasonal influences on human serum pesticide residue levels. Kutty D. Occupational exposure to hexachlorocyclohexane. Link B. The Great Lakes Consortium.72:261265. et al. available at URL: http://www. et al. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. J Pediatr 1977.gov/~dms/pesrpts. Chemosphere 2004.111:349355.20(2):186-193. Krause C.106(5):279-289. Stehr-Green. Zaidi SS. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Cancer Causes and Control 1998. Needham LL. Burse VW. Radomski JL. Kulkarni PK. Falk C. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. August 2005. et al. Darnerud PO.54:1431-1443. Olea N. Saiyed HN. Wood PH. Available at URL: http://www. VI. Crespo J. and other chemicals.fda. Available at URL: http://www. April 1982 to 1984. Brinton LA. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Reisch JS. Toxicological profile for hexachlorocyclohexanes update [online]. Glynn AW. Exposure of women to organochlorine pesticides in Southern Spain.cdc. et al. Brock JW. Arch Pediatr Adolesc Med 1996.html. Zoellner I. Biomonitoring of persistent organochlorine pesticides. Organochlorines in Swedish women: determinants of serum concentrations. Environ Res 2004. Bai KM. children and newborn infants. Piechotowski I. Bull Environ Contam Toxicol 2004.27:405-421. India. et al. HCH. Potischman N. Sturgeon SR. Gabrio T.120:1-82. Lowry W. Cerrillo I. Rey AA. Pollutants in breast milk. Bates MN.htm. Nigam SK. Chemosphere 2005.205:297-308. Lindane.9(4):417-424. Rivas A.52(1):59-67. Siddiqui MKJ. Int Arch Occup Environ Health 1983. Granath F. Environ Health Perspect 1998. Rev Environ Contam Toxicol 1991.atsdr.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Hanrahan L. Herrman T. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Botella B. 4/21/09 Anderson HA. Raju GS. Saxena MC. Needham LL. International Programme on Chemical Safety (IPCS). J Assoc Off Anal Chem 1988.

8 (12.8.6. (Kutz et al.3 (15.5 (9. Formerly. respectively.5 (<LOD-42. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.4) < LOD 63. Mirex can cross the placenta and be excreted in breast milk.S.4) < LOD 15. Fourth National Report on Human Exposure to Environmental Chemicals 109 .5-425) 40. 1995). and 03-04 are 14.5-291) 11. 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. 1991). Survey Geometric mean (95% conf. disposal. Mirex is absorbed through the skin and from the gastrointestinal tract.7 (<LOD-47.3 (15.6) < LOD < LOD < LOD < LOD 71.10 (<LOD-15.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. 2385-85-5 General Information Mirex has not been produced or used in the U. or pesticide application.6 (<LOD-23. 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. soil. Occupational exposure is limited to workers at sites where mirex contamination is present.70 (<LOD-15. after which it is widely distributed in the body and stored in fat..4 (8. In studies conducted in the 1970’s and 1980’s.S. which may vary for some chemicals by year and by individual sample. where it has a half-life of 12 years.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7 (12. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. Mirex is not metabolized in the body.8) < LOD 15. < LOD means less than the limit of detection. Mirex has been detected in air.Organochlorine Pesticides Mirex CAS No.S. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.1 (8. where it was applied directly to soil and by aerial spraying.6-305) 15.2) 51. and foods.0 (<LOD-108) < LOD < LOD 50. aquatic organisms.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. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.5.7) 8. it is a highly persistent chemical in the environment.90-29.6 (<LOD-31. sediments. mirex was detected in human adipose samples.2-230) 13. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. animals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (<LOD-73. Some states and the U. water..3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. population from the National Health and Nutrition Examination Survey.70-40.10-37. resulting in exposure to newborns and nursing infants.7) < LOD 66.0) * * * 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 19.5 (<LOD-115) 153 (30. see Data Analysis section) for Survey years 99-00.S.70-24.4-230) 18.1 (13.40 (<LOD-13.0 (12.1 (<LOD-65.6 (<LOD-108) 9. Mirex binds strongly to soil.5-82.6) 9.0 (14. 1985.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. and 7. 01-02.2 (7.3-225) 15.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16.S. 10.0-374) 11. especially those from persons living in the southeastern U. since 1977.

1995..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.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 .cdc.510) < LOD < LOD . and NTP classifies mirex as reasonably anticipated to be a human carcinogen.090-1.450) 1.077 (<LOD-. and 2003-2004 subsamples. 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.610) < LOD < LOD < LOD < LOD .220) . reproductive toxicity included decreased fertility and testicular damage.080-1.73) . The geometric mean mirex levels of the Inuit mothers were 8.atsdr. as well as in a subsample of NHANES II (1976-1980) participants.090-1.635) < LOD . 110 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides exposures are unknown.37) . and 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions.070-1.8.112 (.370 (.S.470 (. The U.79) .92) . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.090 (<LOD-. In samples obtained between 1994 and 1997.41) .220 (<LOD-.html. 7.310 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.079 (<LOD-..e. environmental levels) and health effects is available from the ATSDR at: http://www.053-.090-1.02) . Biomonitoring Information In the NHANES 1999-2000. More information about external exposure (i.268) < LOD .062-.064 (<LOD-.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . IARC classifies mirex as possibly carcinogenic to humans. 2004).080-1.450 (.093 (.090 (<LOD-. 2005). serum mirex levels were generally below the limits of detection (Stehr-Green. 1989).108 (.110 (<LOD-.102) < LOD < LOD < LOD < LOD .256 (.410 (. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.170-3.100 (<LOD-.059 (<LOD-. Smith.089-. In addition..106) < LOD .140 (<LOD-.08 (.055-. Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . EPA has established environmental standards for mirex.470) .215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Laboratory animals fed high doses developed liver enlargement and liver tumors. which may vary for some chemicals by year and by individual sample.054 (<LOD-.100 (<LOD-. population from the National Health and Nutrition Examination Survey.690) .052-.106 (.430 (.79) .S.090 (<LOD-.gov/toxpro2. Survey Geometric mean (95% conf.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 .170) < LOD . 2001-2002.7 ng/g of lipid.470) . 1991).

Circumpolar maternal blood contaminant survey. Toxicological profile for mirex and chlordecone [online]. Chlorinated Hydrocarbon Insecticides. Rev Environ Contam Toxicol 1991. Strassman SC. Vena JE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Stehr-Green. Sci Total Environ 2004. Swanson MK. Van Oostdam JC. J Toxicol Environ Health 1989. Demographic and seasonal influences on human serum pesticide residue levels. 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. 731-915. Jr. Hansen JC. 4/21/09 Bloom MS. Leininger CC.Organochlorine Pesticides effect. et al. dichlorodiphenyldichloroethylene.97(2):178192. et al.gov/toxprofiles/ tp66. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Olson JR. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. The human body burden of mirex in the southeastern United States. Wood PH.15:385-394. 1994-1997 organochlorine compounds. Watts DL. Kutz FW. Chashchin V. Kutz FW. Inc. Academic Press. hexachlorobenzene.atsdr. Dewailly E. PA.cdc. Odland JO. Profiles of ortho-polychlorinated biphenyl congeners. New York. Vol. Stroup CR. Moysich KB. J Toxicol Environ Health 1985. Eds. Handbook of Pesticide Toxicology. Environ Res 2005. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. 2 Classes of Pesticides. Gilman A. August 1995.330:55-70. References Agency for Toxic Substances and Disease Registry (ATSDR).27:405-421. Carra JS. Smith AG. In Hayes WJ.html. Bottimore DP.120:1-82. Jr and Laws ER. Available at URL: http://www. 1991 pp.

Trichlorophenols are no longer manufactured commercially.90-33.4.20) < LOD 90th 5.4.0) < LOD 5. 2006). 2.60 (4. Exposure to trichlorophenols also may result from metabolism of lindane.00-8..71 (<LOD-8.9.0 (4.20) < LOD 5.80) < LOD 1. and polychlorinated benzenes (Kohil et al.40-11. are metabolites of several organochlorine chemicals. may occur by inhalation or dermal routes.5-TCP) and 2.0 (3. 2.950 (<LOD-1.40 (2.30-27.Organochlorine Pesticides 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.03) 9. < LOD means less than the limit of detection.50 (1.0 (5.4. surface water.80 (2. 1976). Occupational exposures.31 (<LOD-9. 1999).57 (<LOD-15.40) < LOD 1. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. other organochlorines.60 (2.60-8.30-27.6-TCP in any of the samples (U.4. Formation of 2. however.0) 2.5-trichlorophenol.0 (3.50-25.40 (1. 95-95-4 2.40 (.4.63) 18. 112 Fourth National Report on Human Exposure to Environmental Chemicals .60) < LOD 8.0) < LOD 5.40) < LOD 4.42 (<LOD-8.71 (<LOD-8.30-40. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40 (2.72) < LOD 1.900-2. including hexachlorobenzene and hexachlorocyclohexanes.50 (2.940-3.0) 2.6-TCP were used as intermediates in the production of certain pesticides.6-TCP).30) < LOD 4.7. usually at herbicide production or waste incineration facilities. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.4.50-16. Both chemicals have been detected in air.4.0) < LOD 21.10-3.00-3.50 (.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR. Such workers would probably Urinary 2.30) < LOD < LOD < LOD < LOD < LOD 1.5-Trichlorophenol CAS No.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.9 and 0. hexachlorobenzene. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.42 (<LOD-12.40 (1.0) < LOD 5.S.20-36.0 (4.20) < LOD 1. 2.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.30-44.80-41. and sediments.27) 696 661 521 696 603 939 Limit of detection (LOD.40) < LOD 6.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.9 (<LOD-121) 9.980-3. which may vary for some chemicals by year and by individual sample. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.6-trichlorophenol (2.0) 2.27) 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 1.19 (<LOD-6.5TCP and 2.0) < LOD 11.40 (2.4. EPA.30 (.920-3.4.4.S. Survey Geometric mean (95% conf.0 (4.30-27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.7) 24.40-18.50) < LOD 1.50-63.30-11.8) 21.60-18. public drinking water systems did not detect 2.00 (2.40 (.6-Trichlorophenol CAS No.00-3. Historically.0) < LOD 11. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.0) 14.00 (3.20-71.60 (.980-3.3.40 (2. population from the National Health and Nutrition Examination Survey.20 (4. recent sampling of U. soils.0) 2.0) 2.0) 2.30-3.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.5-trichlorophenol (2.4.0 (8.4. 1999).80 (1.0) 5.

. 7.81 (<LOD-9.cdc..4.4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.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 2.2) 2.00-29.6) 4.15) < LOD 2.5) 11. the 95th percentile urinary 2.19-12.90 (4.5) < LOD 12.37) 16.4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).27-17. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11..69-18.37-11.4.4) < LOD 3. However. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.78) < LOD 1.55 (4.24) < LOD 6.4. Fourth National Report on Human Exposure to Environmental Chemicals 113 .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.75 (3.20-6.64 (4. Neither 2.67 (1..2) < LOD 5.02-3.4.78-19.5-TCP nor 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.16) < LOD 90th 5.0 mg/L.50) < LOD 2. urinary 2.4.46 (1. Among 6-11 year old children in NHANES 1999-2000.3 (5.47-8. in addition to dioxins.33) < LOD < LOD < LOD < LOD < LOD 2. Human health effects from 2. 1995) were similar.67 (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. 2003). 2004).82 (<LOD-32.05-17.29 (1.6-TCP levels at the 95th percentile were up to eight times higher than 3.88-16.5-TCP or 2.0) 7. The 95th percentiles for 2.36 (1.4.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. population from the National Health and Nutrition Examination Survey. IARC classifies combined exposures to polychlorophenols.4 (6..83-12. Radon et al.8 (5.1 (<LOD-58.3 mg/L reported in German adults aged 18-69 years (Becker et al..11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.60-3.. Survey Geometric mean (95% conf.43 (2.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1989). as being possibly carcinogenic to humans.5-TCP and limited for 2.78 (3.7 (4.24-11.4) 5. 2003). Urinary 2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.820-2.Organochlorine Pesticides be exposed to mixtures of chlorophenols.13-13.6) 4.00) < LOD 4.4.75 (<LOD-6.73 (<LOD-8.93-11. Laboratory animals chronically fed high doses of 2.31) < LOD 2.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.69 (2.4.5-TCP. environmental levels) and health effects is available from ATSDR at: http://www.28-25.8) 4.9 (5.6) 4.00-19.74) 11.32) < LOD 4.e. the 95th percentile urinary 2.17) 9.S.79-4.24) < LOD 1.53-3.4) < LOD 3.49 (1. leukemias.57 (<LOD-7. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.19-4.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.html.02) < LOD 7. More information about external exposure (i.1) 2.86 (3. and other chlorinated compounds.57 (<LOD-7. In the same 2-6 year old children.43) < LOD 12. 1995) and up to 19 times higher than the 95th percentile value of 1.16 (. NTP classifies 2.24 (3.4. and lymphomas. furans.gov/toxpro2.68-4.980 (<LOD-1.44 (1..68 (<LOD-8.53-3.24) < LOD 5.atsdr.2 (2. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.9) 12.57 (3. 2003.05-8.95 (3. animals showed hepatocellular abnormalities.4.4. which includes trichlorophenols.44 (. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2..8) < LOD 9. At lower doses.62-20.920-2.80 (1. 1989).6-TCP had increased rates of hepatic tumors.6-TCP.6-TCP as reasonably anticipated to be a human carcinogen.

Urinary 2.10-3. < LOD means less than the limit of detection.26 (2.60-3.12) 2.68 (<LOD-2.10-2.0 (12.4.85) * 3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U..3-26.5-TCP or 2.08 (2. 114 Fourth National Report on Human Exposure to Environmental Chemicals .0) 7.7 (13.84) 2.6-19.4. respectively.4.09) 15.32-4.4.67-12.1 (8.4 (10.30-33.4.70-6.0 (6.0) 12.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002. In harbor workers exposed to chlorophenol-contaminated river silt.32) 3.3) 37.3.4.4 (8. Survey Geometric mean (95% conf.46-3.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.4.70) 5.40-14.70) 3.7) 33.44) 75th 4.0) 7.0-54.40-2.6-TCP level.70) 1.95-6.0 (14.80) 1.54) 6.4.20-23.0 (8.6-TCP exposure and health effects.0-50.04) 2.10) 2.95) 3.5 mg/g creatinine) were similar to the limit of detection for 2.49 (6.58-3.70) 5.50 (2.20 (3.6-TCP in urine does not mean that the level of 2.40-4.3 (11.45 (5.9) 694 677 519 696 602 931 Limit of detection (LOD.60-21.4.28) * 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.60-37.28) 24.67) 4.5-TCP or 2.40 (2.7) 21.40) 3.80 (2.01-6.6) 21.5-TCP and to the median 2.8) 32.4.2) 25.2) 12.90 (3. for males in NHANES 19992002 (Agramunt et al.6 (11.0) 17.95 (4.60 (3.3) 23.4.40-2.57 (<LOD-2.20-3.60) < LOD 5.36 (1.40) 4.32) * 3.79 (5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.85 (2.02) 2.20 (3.23) 3.8 (9. 1991).4.74 (2.80-25.90) 2.0-38.1 (10.8) 18.40) 2.23-2.0-41.7-16.65 (5.90 (4.24 (2.0) 13. 2003).80-20.0) 19.0 (13.0) 9.4.5-TCP and 2.70-6.9) 13.4.80 (2.0) 13.00-21.9 (13.8-13.30) 4.9 (11.4-17.30-2. Finding a measurable amount of 2.59-6.40-32.73-9.6-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..2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.07 (<LOD-3.40 (2.0 (6.3 (11.70-3.10 (5.6-17.7-3.0 (15.53) 4.0 (9.66 (8.18-3.51-12.00 (1.0) 11.65) 15.06) * 2.0 and 1.9) 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 2.0) 10.87-14.4.0 (14.2 (14.91-4.0-44.5-46.0 (8.52-3.40) 2. population from the National Health and Nutrition Examination Survey.70 (2. Urinary 2.8-24.4.0 (20.78 (2.0 (7.74-3.30-11.80-7.0 (4.20) 4.5-TCP or 2.0) 11.50-5.6 (12.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.5-TCP level of 0.70 (2.5-TCP and 2.63) 90th 15.89 (3.6 mg/g creatinine) and 2.0 (14.S.23) 2.80 (3.0 (15.09-7.0) 9.48-26.60) 6.6TCP values.58 (1.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.89-6.4 (17.2-0.90-8.4.59) 4.0) 6.0 (6.98-7.69 (3.6) 26.5-TCP (0.1) 16.6-TCP (0.75 (8.52 (2.4.6-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.56 (3.0) 14.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.98-11.35-3.45) < LOD 11. was about six times lower than the median urinary levels for males in this Report (Radon et al. 2004). which may vary for some chemicals by year and by individual sample.8-15.33-4.36 mg/g creatinine.55-3.53) 2.78 (2.31) * 2.6TCP causes an adverse health effect. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. 0.99) 6.60 (3.45 (2.0 (16.0) 17.0 (20.4. similar to the limit of detection for this Report (Anderson et al.0 (11.0) 15.45-9.25-11. 1998).6-22.00 (4. Mean values of 2.0) 13.31 (3.0-38.4 (9. interval) 2.0) 19.20-6.5-TCP or 2.1-25..80-6.00 (2.3) 20.0) 13.0) 10.10-3.72-10.0) 14.6-TCP than are found in the general population.00-4.60 (2.0-18.30-2.47 (3..10) 6.7 mg/L.0-37.92 (2.3-17.40-7.7 (9. the median urinary 2.14 (2.36-5.0-43. Biomonitoring data will also help scientists plan and conduct research about 2.4.0-68.76) 3. Biomonitoring studies on levels of 2.

17) 2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13-6.82-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.29-4.53) * 2.2 (13.7) 25.72) 32.98) 10.9) 7.5) 8.38 (4.05 (6.88 (2.17) 13.79-17.59 (2.50 (2.76) 4.9-34.8) 19.6 (5.15 (1.40 (7.49-3.51) 18.6 (9.24 (1.4) 9.68) 2.06-2.83-5.65-21.22 (1.96) < LOD 4.1 (8.6) 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 2.52) 2.82 (3.78) 90th 12.41 (3.56-5.8) 11.87-6.8) 12.5 (10.7 (14.9 (9.88) * 2.6) 12.2 (8.73) 5.15 (6.7-36.76) 1.00) 4.8) 21.88) 5.54 (2.22-9.42) 2.22-2.1) 11.41-6.25-15.63) * 4.52 (3.71 (3.49) 4.3-23.29 (6.6 (22.00 (3.4 (11.0) 8.40 (2.5) 11.51-21.9) 19.67-17.00) 4.88) 4.53-11.26 (6.42 (2.52 (5.2 (7.5 (7. interval) 2.18-4.1) 14.62-15.9) 8.65) 2.66-4.4) 8.6 (6.22 (<LOD-2.1-32.70-9.43-7.5) 11.53) 4.60 (4.3) 8.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.5-28.89-2.20-2.9-29.56) < LOD 11.73-22.25 (3.02) 3.06) 11.3-37.11) 10.83 (3.05 (3.29-4.14-13.95-2.06) 4.1-21.01 (3.88-7.22 (3.92) 4.55-2.63 (<LOD-2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .63) 4.91 (3.Organochlorine Pesticides Urinary 2.6-31.13 (1.17-4.10) 4.43 (<LOD-2.00 (2.6 (12.19-5.0) 10.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.38 (2.9) 8.48-2.02 (1.4) 4.91-2. Survey Geometric mean (95% conf.77-4.87) 2.5 (8.89) 10.1 (13.25-17.7) 6.30-2.90) 2.04-2.99-2.94-13.53 (3.63 (2.33-2.43 (2.08-2.90 (1.65) 18.26-13.6 (10.46-14.09-3.0 (6.0 (11.56 (7.2) 19.9-64.14-2.63-13.68) 2.5) 9.32 (2.76) 2.35 (3. population from the National Health and Nutrition Examination Survey.51 (2.0 (9.76-8.47-5.83-6.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78) 2.38) 22.27-9.25 (3.10 (6.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.2 (12.63-15.33 (7.50-8.87-7.8 (7.4.87 (3.32-19.82) 2.21-11.8 (8.6) 13.91 (7.10-9.82 (8.23 (1.58 (4.9 (9.52) 2.38-5.25-2.33) * 2.S.33 (1.6) 8.65-2.81-9.88) 4.87) * 2.18-2.9-32.78 (2.81) 2.04-16.16-10.88) 1.72-16.83-6.77) 2.60-2.3 (9.23) 4.5) 12.6 (9.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.98 (1.28-4.4 (12.44 (3.75) 75th 4.

Domingo JL. Environ Res 1995. Holler JS.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.63:57-62. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Jarvisalo J. Needham LL. Wegner R. Safe A. The Great Lakes Consortium. Seifert B. 4/21/09 Agramunt MC. Can J Biochem 1976. Baker S. S.146:83-91. Kohli J.epa. Arch Environ Contam Toxicol 1989.18(4):469-474. Luotamo M.atsdr.45:440-445. Hill RH Jr. July 1999. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 206:15-24. Jones D. Environ Health Perspect 1998. Available at URL: http://www. Aitio A. Int Arch Occup Environ Health 1991. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Am J Ind Med 2004. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . html. et al.S. Toxicol Lett 2003. Int J Hyg Environ Health 2003. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. To T. et al.gov/toxprofiles/tp107.54(3):203-208.pdf. Urinary excretion of chlorinated phenols in saw-mill workers. Anderson HA. Pesticide residues in urine of adults living in the United States: reference range concentrations. 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]. U. Hill RH Jr. Heinrich-Ramm R.cdc. Radon K. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Baur X.71:99108. Fast DM. Poschadel B. Becker K.106(5):279-289. Seiwert M.EPA). Corbella J. Head SL. Burse VW. December 2006 Draft. Falk C. Pekari K. Domingo A. Bailey SL.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Kaus S. et al. The metabolism of higher chlorinated benzene isomers. Lindroos L. Hanrahan L. Olson J. Needham LL. Available at URL: http://www. Szadkowski D. Shealy DB. Gregg M. Schulz C. Toxicological profile for chlorophenols [online]. Smith SJ. Environmental Protection Agency (U.

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

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

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

10 (2.5) 15.56 (4.5 (11.97) 8.80) 2.70-11.1-17.780) < LOD 3.810-1.81) 1.63) 1.80-22.9) 14. respectively.51) 2.00 (1.20 (.12-19.10) < LOD < LOD 4.50 (.37 (3.70-14.60-25.58 (3.56-13.97) 90th 7.08-2.02) 4.9 (8.0) 6.98-5.50 (4.3) 14.10) < LOD .50 (2.60-11.93-24.40-11.4 (9.79-7.33-18.47) * * 1.50-36.80) 3.55-6.7 (12.6) 18.89) 9.74 (8.70 (4.30 (2.60) < LOD < LOD 4.1.82) 10.0) 6.22 (.80) .13 (2.0) 15. 01-02.16 (2.4 (9.90 (1.8) 19.2 (11.0 (7.2) 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 1.79 (5.52-11.954 (.0) 6.2) 16.2) 16.4) 20.40-19.3-15.2 (14.8) 11.40-5.23-5.07-10.26 (5.61 (3.35-11.56 (6.2 (9.93 (4.1) 10.0) 10.12) 4.840-1.670-1.0) 5.4) 17.0) 12.00-12.1 (10.0) 10.98-12.82-12.740-2.00 (5.0 (7.56 (1.0) 10.74 (8.15-12.0) 11.0 (6.30 (2.60 (5.20 (2.8-32.27-15.1 (9.757-2.72) 5.28) 1.1) 95th 13.2-20.9) 8.66) * * 1.01) * * 1.46) 10.27-3.3) 17.60) . 120 Fourth National Report on Human Exposure to Environmental Chemicals .10 (.80) 2.0) 10.0) 11.73) * * .39 (3.0 (9.20 (.71-9.71 (2.34-7.39 (8.95) 5.0-27.86-15.0) 9.2 (14.00-27.54 (3.0 (7.5-16.02-5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and 0.10 (2.32) 1.830 (<LOD-3.21) 9.2 (7.0 (12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.45 (2.0) 5.67) 3.750-1.0) 11.53) 4.8 (14.34-3.890 (<LOD-2.60 (1.00-27.579-1.0) 5.599-1.00-19.13 (2.70) < LOD < LOD 1.42-3.80) 2.5) 20.758-1.4 (7.19) 9.17-3.00-12.57-7.0 (8. interval) 1.0) 7.40 (.620-1.9-18.08-15.00 (4.35-12.55-8.81) 11.26-8.32 (. < LOD means less than the limit of detection.80) .290 (<LOD-.61) 4.0 (8.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40-1.80-4.20-7.33 (5.16) 4. and 03-04 are 0.530 (<LOD-2.91) 4.955 (.94) * * .58 (2.94) 3.70 (2.1) 13.30-6.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.40-16.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.2) 14.20-4.623-1.600 (<LOD-1.0 (7.43-12.0) 10.20 (.8 (8.90-4.0 (4.0 (8.60-18.0) 11.0 (6.85 (3.40-14.2 (7.44-3.860-2.4) 18.981 (. 0.47) 5.44 (2.44-38.83 (5.7 (14.80-24.3) 16.717-1.1-23.90-5.11 (.5-17.21 (.04) < LOD 1.35-16.290 (<LOD-1.70) . population from the National Health and Nutrition Examination Survey.S.20 (.52) * * 1.90) 2.20-30.4 (7.0 (5. which may vary for some chemicals by year and by individual sample.38-5.26-6.8 (9.58 (5.42) .96-3.52) 6.5 (8.7) 11.50-5.86 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80 (2.80) 4.8) 7.490-2.10-7.2.03 (.6) 7.15) 14.8 (12.80) 11.70) < LOD < LOD 75th 3.13-2.0 (9.00) 3.00) 3.2 (7.2.05-7.76 (2.00-7.0) 20.70-23. see Data Analysis section) for Survey years 99-00.700-1.80 (4.2 (9.30-4.29) * * 1.08 (<LOD-2.48-7.70-19.9) 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 1.30 (4.970-2.0-28.14) * * .36-4.68-7.50) 2.10 (.8) 7.81) 11.90) 3.99 (5.

68) < LOD < LOD 3.4 (9.41-12.57 (4.40) 4.21-23.8) 8.55-20.5-16.8 (10.8) 16.66-34.04-6.47) * * .67-19.780 (<LOD-1.41) Selected percentiles ( 95% confidence interval) Total * * 50th .87 (3.960 (.4) 4.66 (2.820 (.90-5.41) .560-1.09) 2.47 (1.29) * * .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 1.1 (10.82-14.40-28.81 (1.56) .40) < LOD < LOD 75th 2.00-13.06-2.773-1.98) 9.09 (.69) 4.37-5.30 (1.19 (4.7 (9.32-12.40-5.7) 5.3) 16.9) 11.6 (9.94-10.54-15.61 (1.54-4.924 (.710 (<LOD-1.15-10.88) 2.98) .440 (<LOD-2.5) 7.34) < LOD < LOD .04 (1.79-9.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.37 (4.94 (4.94 (2.66 (1.1 (9.42) 12.56) 4.35 (1.6) 11.57) 4.74) 90th 7.67) 1.34 (6.5) 12.5) 11.95) 2.2) 7.25) < LOD .78 (2.13) 4.40 (3.6) 13. interval) .92-2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .03) 2.45-11.93-5. population from the National Health and Nutrition Examination Survey.5 (4.69-10.98) .27) < LOD 2.860 (.2) 5.00) 8.29 (2.8) 12.10-13.53-11.24-3.76) < LOD .54-2.9 (9.94-23.28-9.00 (4.4) 13.430-1.43) 2.44 (2.2 (8.23) 4.60-9.37) 9.6 (10.26) * * .540-1.43 (.0) 6.09-11.02 (7.31-14.5) 7.3) 12.94-9.47) 2.93-9.28) 10.S.2) 8.53 (6.05 (1.46-5.2) 5.0 (8.47 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.98 (3.36) * * 1.2 (6.1) 4.02-2.7 (10.54-11.43 (3.87 (1.6) 9.84 (5.75 (3.620-1.28 (4.98-5.608-1.82-6.5-13.46) 2.62-5.1 (8.03-6.1 (6.4) 4.69 (4.76-4.56) 7.510-1.42 (3.05 (.93) 9.3) 5.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.82-14.2) 9.855 (.95 (3.75 (7.28 (5.4 (4.88 (5.03 (7.6) 8.11-6.8) 7.81-5.890 (<LOD-1.01-2.66-15.75) 2.90-8.574-1.60) 2.72) 11.67) 4.23 (4.9 (5.7) 18.05) .57 (6.69) 2.38 (1.818 (.890 (<LOD-1.53) 9.2) 13.56-13.80 (6.88-15.25) 6.54) .533-1.0) 7.61-29.30) 2.34 (6.31 (3.52) 4.37 (5.75) 14.64-5.920 (.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 .71-2.5-20.7 (8.03) 2.83) 8.37-3.5) 8.77 (6.75-7.1) 4.79-3.88-10.80 (2.57-10.89) * * 1.500-1.51-5.45-5.3) 15.07 (.50) 7.1 (7.45-5.39 (2.35) < LOD < LOD 3.28 (2.870-2.750 (<LOD-1.8) 6.996 (.830-1.85) 2.61-13.549-1.932 (.14 (3.02-14.9-28.47 (3.633-1.40-3.7) 12.18 (.1 (11.900 (.92-5.1) 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 1.2 (10.94-22.2) 95th 12.83 (7.61 (1.80) 9.40-14.34) * * .02 (2.5-32.60) * * .73 (1.66 (5.84) 7.00-17.9) 12.40-12.00-19.10 (3.03 (2.9 (9.566-1.38) .20-8.650-1.80 (7.71) 10.62) .570-1.68-4.00 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.790 (.85 (6.89-3.98-22.9) 16.74) 4.1-15.82-26.883 (.58) * * 1.87-5.960 (<LOD-2.

60 (2.18 (3. which may vary for some chemicals by year and by individual sample.95-9. population from the National Health and Nutrition Examination Survey.0) 6.650-1.8-20.90 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.670 (<LOD-1.0 (10.5.740 (<LOD-1.1) 11.27 (7.9) 95th 14.15-6.00) 7. 122 Fourth National Report on Human Exposure to Environmental Chemicals .00) 8. < LOD means less than the limit of detection.90 (5.77-3.41-5.7 (11.00-18.90 (6.0) 13.10 (<LOD-1.8 (12.90 (1.39 (5.62-17.35) 4.7) 16.90 (6.5.35 (6.35-3.73) 7.3 (9.0 (10.00 (.6-19.95 (5.29) < LOD < LOD < LOD < LOD 3.670 (<LOD-1.16-1.3 (6.0) 19.90) 4.3) 10.67) 3.10-15.10-10.17 (7.00-18.3) 8.9-17.24 (2. see Data Analysis section) for Survey years 99-00.7-21.31-12.9) 10.88) 10.42 (1.58 (1.80 (2.0 (14.64) 10.00-16.7) 10.0) 14.90-31.0) 18.0) 14.20) 3.40) < LOD < LOD 75th 2.75 (3.8 (12.3 (12.22-12.30) < LOD < LOD .58.99 (3.80-14.20-18.5) 21.0-24.910 (<LOD-2.80 (2.30) < LOD < LOD 4.50) 5.70 (1.2) 14.95 (2.670 (<LOD-1.70-5.2 (9.31) 1.10) 6.50-5.53 (3.80) 5.22 (6.0) 9.61-32.3 (9.22 (6.92) 9.29-4.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.70-9.0) 12.80) .5 (8.8) 9.680 (<LOD-1.0 (7. respectively.8-21.9 (12.66) 4.80-3.78) 5.3 (7.67) 4.80 (5.00-4.37 (3.31-7.46-4.97-4.3) 14. 0.72) 2.39-13.45 (3.1 (10.7) 14.6) 14.27) 4.34 (6.00-9.86-10.7) 22.0 (5.00) < LOD .27 (3.9 (7.8) 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80-21.14 (6.47-6.90-9.8) 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 1.04 (3.96) 3.92-17.67-10.4) 11.40 (2.7) 15.0 (13.3) 20.6) 18.25 (2.0-19.34-10.49-4.20 (<LOD-2.00) 3.790 (<LOD-1.20-8.34-5.37) 2.12 (4.S.50-4.30) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 12. and 03-04 are 0.50) .9-15.0) 9.1-23.4 (10.82) 8.7-19.98-9.88) 3.80-8.2 (7.30) 3.90) 8. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .84-4.0-33.8-17.33-11.0) 11.6) 14.4) 7.580-2.6-41.60 (6.80-4.90-15.27) .8-20.90-15.89 (2.5 (8.70-9.3) 22.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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 * * * * * * .80-6.9-14.75 (2.0) 11.20) .7 (10.90 (6.89) 2.20-4.9) 16.4-17.63-14.6 (10.4 (14.70) 2.96) 90th 7.60 (5.60) < LOD < LOD 2.5-26.10 (.10-4.74) * * * * * 1.51) < LOD 1.77-14. and 0.50) 3.0 (8.11-6.970 (<LOD-2.06 (2. 01-02.670 (<LOD-1.0-29.34-3.5 (9.15-2.24-5.66-13.61 (3.6 (10.3 (11.0) 23.00) 3.90 (2.52 (6.0) 13.0 (9.6) 11.40 (2.46-28.30) 3.0) 7.1 (10.9) 9.0 (15.0-24.90 (2.41) 3.80-12.90 (6.0) 12.00-4.81-6.59-3.22) 8.70 (8.4 (10.28 (7.80) .0 (9.18) * * * * * * * * 1.01 (2.70-8.27) 9.20) 3.

1 (8.29 (5.30) 8.2) 8.54 (7.S.5-17.45) 6.1) 10.33) 3.29) 3.8 (8.74-19.9-17.55) 16.910 (<LOD-1.4) 7.04) 9.6) 13.50-17.6 (11.87 (3.34-18.5 (11.3 (7.4-16.2) 15.32-8.3-17.85-8.00) 8.00) 2.950) .07 (5.92) 3.93 (6.39-17.28 (1.71) < LOD < LOD 2.96-10.63 (2.52-3.8) 14.3-34.29 (2.82-11.50 (6.27) * * * * * * * * 1.21-21.42-19.18) 2.2) 12.12 (7.91) 3.44-6.79-6.3-17.81 (7.68-19.27) 1.77 (2.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .12) < LOD < LOD 4.54) 9.5 (15.32) 2.69-11.4-18.47-9.02-4.11-3.4) 7.89-3. population from the National Health and Nutrition Examination Survey.54-5.89-3.83 (6.38 (1.9) 19.38 (2.28) 6.20-3.15 (1.00 (2.4) 7.03 (2.28-12.09-11.5) 8.75-3.6-19. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.73 (5.0-19.93-10.0 (11.94-14.21) * * * * * 1.25 (4.4) 15.4-16.09-11.88-7.59-3.2) 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.03 (6.92 (5.89 (2.51-7.810 (<LOD-1.850 (<LOD-1.3) 12.5) 10.30) 2.6) 95th 16.3-15.38 (.78 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.64-11.94 (5.6) 7.61 (2.780-1.6 (13.77) 3.30-5.00 (3.0) 14.6 (13.42) 8.85-17.2) 10.2) 16.6) 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 * * * * * * .89-10.68) .97-4.0 (8.9 (9.6 (12.45) 3.4-15.6) 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 1.70-2.11 (5.67 (7.5 (10.6 (11.00 (5.7-23.890-2.7-19.55 (2.7 (10.29-2.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.7 (10.06 (<LOD-1.7) 15.37-5.75-3.6) 12.00 (<LOD-1.14 (2.96-11.79-9.940) < LOD < LOD 1.8) 11.91-9.00 (7.95 (2.4) 9.530-1.30) 7.78-10.36 (2.8) 16.1 (19.2 (9.760 (<LOD-1.0 (10.7) 12.86 (3.25-9.620 (<LOD-.5) 13.78) 4.99) 2.2) 19.16-14.86) 9.2-30.9 (9.42) 7.89) 5.03) 3.88 (1.3) 6.68-10.9-25.7) 14.51-10. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .33-10.55) .27-13.690 (.3) 8.2) 12.63 (6.77 (2.93 (2.6 (10.2 (9.27) 5.38-13.74-4.19) 3.920 (<LOD-1.1) 20.48 (2.5 (9.78 (4.16 (3.590 (<LOD-.34) < LOD < LOD < LOD < LOD 3.97) < LOD .5) 22.95) 90th 8.07) 2.00 (<LOD-1.7) 9.4) 6.8 (10.67 (1.0-21.4) 16.41 (7.99 (4.27) < LOD .0 (13.68-4.71 (1.89-13.01-5.89 (3.83 (7.95) 3.86-3.72) 4.07) 2.2-15.07-3.93 (<LOD-2.23-3.70-35.43 (2.80) 3.05-3.7 (11.9) 16.15) < LOD < LOD 75th 2.4 (11.1) 13.3) 9.1 (13.5 (8.6) 6.06) .7) 14.6) 14.37) 3.82-8.53-8.3-21.973 (.58 (4.9 (9.2) 12.38) 1.72-4.7 (8. Fourth National Report on Human Exposure to Environmental Chemicals 123 .

910 (.22-3.580-1.13) .59-2.587) * * .600 (<LOD-.740-1.380) . 01-02.48 (2. see Data Analysis section) for Survey years 99-00.39) 2.390-.592-.20-2.22 (1.98 (2.960) .09 (.457 (. 124 Fourth National Report on Human Exposure to Environmental Chemicals .390-.32 (1.740-.160 (<LOD-.960 (.50 (1.80) 5.20 (1.30 (.30-1.880 (.08 (2.10) 1.10) 3.800 (.79) .54 (2.83) 2.780) .350-.96-3.36-4.850) < LOD .620-1.20 (1.64 (1.455 (.657) * * .780 (.16) 2.840 (.580-.86) 3.210 (<LOD-.720 (.720-1.47) 2.54-2.20-2.46-3.380-.73 (2.80 (1.21) 3.505 (.98-3.340-.460-.700) .35) 1.45 (1.70 (1.690-. respectively.31) 95th 2.730) .50 (1.80 (2.710 (.20) 3.50 (1.2. and 03-04 are 0.350-.80) 3.450 (<LOD-.240 (<LOD-.500 (<LOD-.560-.30-3.46) 1.570 (<LOD-.05-3.17) 1.00) 2.760 (.510 (<LOD-.10) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.960) .336-.425 (.80) 2.33-2.70 (1.01-1.60) 3.49) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.720-1.592) * .74-5.27 (2.540 (.11-3.76 (1.20) 2.14 (1.590-.549 (.930) < LOD .16) 1.550 (.89) 1.600-.79) .970) .618) * .13) 2.459 (.1.930 (.31-3.680-1.91) 2.78) .29-2.570) * .26 (2.750) 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.353-. and 0.96-5.63 (1.94) .20) 1.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .690 (.47 (1.880) < LOD 75th .30 (1.01-3.690) .58 (1.31-3.04) .930) 1.32) 3.73-5.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.41 (2. population from the National Health and Nutrition Examination Survey.31) 2. 0.78) 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 * .15) 2.34) 2.50 (1.77 (1.95 (2.50-2.83 (2.14-1.87-3.30) 2.88) 1.00) 1.54) .510 (.41-5.89) .00 (1.65 (2.570 (.467 (.600-1.820 (.60) 2.09.90) 2.970) 1.949) .597) * .70-2.05-2.01) .570-1.90 (1.22-3.57 (1.90-4.750-1.585) * * .388-.77-2.20) 3.880) < LOD .280-.45 (2.910) 1.80) 2.10) 1.584) .59-6.17) 1.780 (.690-1.37-2.76-6.04) 1.343 (.08 (2.359-.680-1.700) .990-1.19-1.20) 2.38) 1.400) .60-4.46 (2.25-1.89-6.94 (2.80) 3.70 (1.83 (2.90) 2.592) * 50th .95) 2.20 (2.50 (1.74) 3.69-4.930-1.382-.960-1.749 (.820 (.15) 2.45 (1. < LOD means less than the limit of detection.48 (1.57 (2.45-4.20-1.940) < LOD .00-4.S.22-8.490 (<LOD-.260 (<LOD-.18 (.03) 1.30-3.61 (1.26) .17-4.20) 1.55 (3.00-2.30 (.46 (1.34) 2.759) * .650-.95-5.740 (.40 (1.75 (2.27 (3.570 (.453 (.10-1.97 (2.73 (1.670) . which may vary for some chemicals by year and by individual sample.830 (.550 (.810) .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 * .980) 1.23-3.30) 4.10-1.22-2.30) 1.16-3.32-1.20 (1.710) .60 (2.20-3.860) < LOD < LOD .303-.80) 3.49) 2.94 (3.75-2.30 (.30) 4.398-.380-.910-1. interval) Selected percentiles ( 95% confidence interval) Total * .29) 1.201-.50-2.449 (.440-.50) 1.960) 1.42-2.40 (1.83) 1.98) .950) 90th 1.710 (.70-7.570 (<LOD-.68-5.11-3.86 (1.18 (1.90) 3.790 (.83) .740 (.

597) * .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 * .61 (3.32-1.33 (1.739) * .91 (1.390) .22) 4.84 (2.460-1.930-1.88) .10) 2.00-3.75-3.57 (1.08-3.530 (.520 (.870) .550-.460) . interval) Selected percentiles ( 95% confidence interval) Total * .535 (.32) 2.22-3.90) 2.61-3.71) 2.900) 1.448 (.630) * .05-2.75) 6.73-3.02-3.36) 3.990-1.08-2.08-3.45 (2.02-3.590 (.560-.350) .75 (1.66) .688) * .318-.08-3.17) 2.63 (1.490 (.39) 2.71 (1.20-2.550-1.69 (3.24) 4.04) 95th 2.750 (.470 (<LOD-.42-8.136-.47 (1.03-2.22 (2.310-.23) 1.49-4.280 (<LOD-.00-1.44-2.89-3.77-3.453 (.552 (.850) 1.23 (.64 (2.14 (2.500-.97) 2.07) 1.71) .390-1.16-2.20) 1.560 (.820) 1.62 (1.377-.700 (.92) 3.88 (1.99) 1.61-3.310 (<LOD-.07) 5.04-1.690) < LOD < LOD .510-.300-.03-1.06-2.520-.72 (2.380-1.08 (.43) 1.750 (.45 (1.29-4.98) 1.980-1.92-8.73 (2.07) 1.16) 1.42-6.22-3.25-3.790 (.09) .77 (3.08-2.13 (1.34 (1.580 (.06) 4.370-.840) 1.412-.50 (1.800) < LOD .97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.53) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.23) 2.590-1.471-.720 (.270 (<LOD-.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 * .840) .700 (.270-.11) 1.250 (<LOD-.58 (1.305 (.55 (1.510 (.08-2.28 (1.700 (.300 (<LOD-.560-.440-1.550-.720-1.80) 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 * .480-1.230 (<LOD-.32) 5.08) 1.920) .69 (1.41 (.04-5.57-4.645) .820) .07-3.64 (2.800-1.89 (1.30) 3.680 (.60) 1.00 (3.08 (2.60 (2.444-.52 (1.742) * * .47-4.49 (1.400) .640 (.55-3.32) 1.640 (.20-7.08-3.42) .60 (1.480) .253-.97) 1.72 (1.43) 2.30-2.17) 2.368) * .540-.67) 1.42 (.23) 3.590) * 50th .250 (<LOD-.730) .285-.78) 3.447 (.591 (.910) < LOD .550) .515) * * .38-3.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.S.65) 2.16-1.72-4.43) 2.660-.61) 2.67) .79 (1.08) 2.710 (.335-.270-.62 (2.470) .02-6.580-.22) 1.38 (1.320-.97 (1.92 (1.870 (.460 (.60) .11-2.87 (2.640 (.50) 1.234 (.38 (2.47 (1. population from the National Health and Nutrition Examination Survey.33) .05) 1.18-2.509 (.580) .320-.70 (2.82 (2.310 (<LOD-.330-.66 (2.82) 2.70 (3.81) 2.05) < LOD .52) 3.39 (1.11 (.740) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.670 (.880) 1.19 (1.80) 2.510 (.180 (<LOD-.380) .22) . Fourth National Report on Human Exposure to Environmental Chemicals 125 .830 (.740) < LOD 1.372 (.67 (1.760) .75 (2.94) .05-4.710 (.393 (.57 (3.76) 1.330 (<LOD-.07 (.58) 3.07) 1.17-2.97 (1.77-4.710 (.348-.95) 1.07-2.22-2.99) 2.32 (.790) .67-3.380-.840) 1.84-6.43 (1.950-2.31-1.44) 2.05 (1.940-1.57-2.403) .830) 90th 1.760) < LOD 75th .79) 1.400-1.58-6.72) 1.67 (1.485) * * .23) 2.

8) 39.0) 28. 126 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.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.8 (22.4 (10.70) 5.0) 33.48) 5.0) 15.0-41.0-53.50-2.10 (1.0) 16.0-41.05) 1.6-27.0) 42.10 (7.40-16.83 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 4.9) 18.27-6. interval) 1. 0.60) < LOD 1.16) 2.04) 3.61 (1.43-7.5-20.0-69.1) 38.06) * 2.0 (38. see Data Analysis section) for Survey years 99-00.25-3.90 (1.80-2. and 03-04 are 0.95 (5.70 (7.86 (1.1 (11.7) 20.88) 3.9 (27.11) 2.78) 9.2-47.0) 19.6-54.0 (6.21 (3.1 (22.0 (17.13) 12.71) 5.9) 48.0-58.0) 5.6-45.6 (15.70) 1.0-47.5-40.0-92.0) 3.29) 2.0) 20.87-7.10) .88) 1.44) 2.40) < LOD 1.10 (1.98) * 2.0 (11.0) 16.0 (32.0 (20.14) 5.1-20.9 (19.57-2.2-26.7 (12.2-39.54 (1.63-6.92) * 2.31-6.30-14.79-2.44-7.83 (3.0 (7.10-4.53) * 2.8) 62.0-31.67 (1.36-2.9 (23. which may vary for some chemicals by year and by individual sample.69) 2.65 (4.09 (4.0-230) 35.5) 30.53) 40.7-22. 01-02.10) 39.76 (2.77 (1.0 (25.0 (38.5-74.21 (4.72 (1.57-2.0-49.0-39.0-110) 42.21 (1.8-21.0 (20.97) 6.8-24.86-3.53) 1.0) 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 2.470 (<LOD-1.60 (2.19-2.50-20.20 (2.0-58.0 (37.20) 1.9 (10.8 (26.64-3.46-2.0 (33. and 0.0 (38.5-45.1 (26.9) 17.3) 38.23-2.49-2.0-53.0 (26.690-3.0-41.00 (.90-8.3 (10.1-40.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 3.6 (11.0 (24.0-62.18) 14.96) 5.0 (8.9-51.0) 18.90 (1.05-3.1-25. < LOD means less than the limit of detection.59 (1.13 (1.2-33.78 (1.26 (.1 (25.0 (38.80) 90th 38.54 (3.33 (5.00 (.83-2.76 (2.0 (19.04-8.26) 75th 11.41) 1.41) 1.2 (19.07-5.18) 6.3) 26.0) 6.0) 3.7 (28.5) 69.4 (15.30 (.4) 38.44) 3.58-2.0) 15.90) 11.06 (1.0 (40.30) 11.9) 38.6-22.530-4.3) 28.71-2.40) < LOD 2.0 (8.16) * 1.0-29.70-6.50-7.41) 5.610 (<LOD-1.70) 1.3 (12.1) 38.4) 19.23) 9.29-4.3) 33.85 (1.0) 17.05) * 2.70 (1.77) 38.0-52.13 (1.52 (4.0 (38.64-8.70 (.1 (10.0-50.00-24.0) 30.46 (.80-18.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.98 (1.0-39.93-3.6) 52.0) 28.1) 18.45) 2.2-80.02 (2. respectively.8 (12.74-2.3 (14.53 (1.0-62.0 (38.7-41.2-62.9-21.2-27.32 (2.91 (4.3 (12.79 (2.1-19.6 (26.59 (1.0 (38.66-5.50-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-43.04 (<LOD-2.0) 4.4-76.0 (21.58) 16.70 (1.10-13.0) 3.29-9.1 (25.12) 1.19) 2.94 (1.6 (9.7) 47.82 (1.18.48-2.81-3.92-5.46-6.41-4.9 (19.35-6.1) 140 (46.40-4.17-2.S.2-27.42) 1.5 (24.0) 45.80) < LOD 1.44) Selected percentiles ( 95% confidence interval) Total * 2.4-22.99 (2.8) 32.81-2.4.20-4.0) 13.11 (4.41 (1.3 (24.10 (1.7 (12.0) 8.50-17.2) 31.83-2.12 (3.8) 41.0-110) 34.600-2.830-4.0) 17.1) 95th 48.70-17.0-260) 34.71 (4.50 (2.8 (12.2 (12.18) 20.5-27.1-47.48-2.4 (19.0 (13.61-2.23-2.80) 1.0) 20.3) 31.0) 32.45) 2.1-46.5.85) * 2.10 (1.80) .3 (23.0) 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 2.2) 16.0) 31.830-3.40) 50th 2.0) 4.30) 4.0 (8.75-14.79 (1.660-2.

899-2.19) 5.19 (1.9) 24.40 (5.3 (9.29-5.18-1.51) .2-28.2) 13.84-13.9) 3.88 (1.66) 8.71 (1.0) 13.38) 5.1) 25.88 (1.36 (4.8-26.2 (22.83) .93) 5.1 (39. population from the National Health and Nutrition Examination Survey.4 (5.3 (8.22-2.4 (21.7 (24.1-63.7) 26.930 (<LOD-1.63-5.7) 15.8) 3.7 (18.0-70.47 (1.0 (32.16 (1.96) 2.11-2.7-20. Fourth National Report on Human Exposure to Environmental Chemicals 127 .55 (2.06) 1.19-14.7-19.5-97.6-49.08 (1.82) 1.60 (.1) 15.97 (1.46-6.61-2.0) 25.00) 6.30) 28.01 (.46) 1.1) 13.94-20.2-47.37 (1.03) 1.38-1.2) 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 2.3 (10.91-2.45 (1.5 (6.2) 36.0) 3.7) 95th 51.5 (17.00-16.8-45.0 (23.79 (2.70-4.69-5.7) 34.6 (11.58-2.33) 2.0-40.2 (16.67-16.91 (6.9-41. interval) 1.32 (3.6) 3.3 (20.1) 52.07) 9.23) 37.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.2) 4.4) 14.68 (1.4 (12.20) Selected percentiles ( 95% confidence interval) Total * 1.94) 1.16-2.9) 12.8) 15.43-2.25-3.4 (19.27-3.4-71.50 (2.4 (9.9 (19.7-109) 22.66 (1.7-38.0-71.86) * 3.870-3.35 (2.870-3.75-6.7) 61.4-34.83 (.2) 13.03-2.9-36.82 (2.57) 4.11) < LOD 1.4 (25.2-38.2 (9.33) < LOD 1.06) 75th 9.61 (1.34) * 1.61-22.80 (1.1 (12.76-2.750 (<LOD-1.95) 90th 32.2) 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 1.09 (5.38 (3.0) 47.51) < LOD 1.7) 30.02) 1.5 (8.3-19.9 (26.0-118) 29.9 (10.1) 13.27 (6.4 (25.1 (34.90 (.37-2.0) 30.5) 70.4) 12.54-15.48 (4.69-18.08) 1.66 (1.18) * 2.68) 47.6 (7.7) 23.7) 66.24 (1.39 (1.8-37.62) 4.27) 10.5 (15.94) 19.2) 41.15 (.45-1.870-3.33-5.23) < LOD 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-37.36-13.17) 2.95 (2.5 (13.53) 1.9-18.6) 23.47 (3.6-51.70 (1.58-17.7-43.80-8.3) 28.6-32.890-4.2-70.4 (11.8) 11.8-43.670-1.72) 2.59-15.47-17.16 (1.56) 1.50-5.888-1.1 (50.0 (23.1-60.75 (1.35) .4) 3.31) 2.6) 7.33) 1.8) 32.1-22.9) 54.12) 3.6 (24.22-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7-37.71) 8.48) 1.3-22.12 (1.9 (13.54-2.7 (18.88 (4.59-2.5-36.18) 3.5 (41.36) 10.7 (10.75 (1.0 (17.4) 12.0 (19.62 (2.26-4.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 48.14-8.0 (6.43) * 2.0 (39.2 (15.5-190) 30.6) 112 (40.06-1.23-1.22 (.860 (<LOD-1.4-39.2 (8.32-3.1 (33.1) 36.5 (34.9-95.27) 50th 2.17-3.5) 27.67 (1.02 (.8) 31.71-2.46-5.4-67.35) 1.67-3.88 (4.46-22.60) 4.7 (11.8 (7.6) 3.95-16.6) 11.2 (21.19) 5.57 (6.2) 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.40-4.40 (2.96-16.5 (15.99-4.52-4.9-52.8) 23.2) 33.6 (27.86) * 2.14 (.26-2.06) 1.2-34.21 (4.28) 1.95-16.79-17.4-21.07-2.38-5.9) 24.41 (2.3) 13.02) * 1.3 (10.67 (1.00 (4.8-34.07-2.1) 17.00) 1.9 (39.9 (7.52 (1.44) 9.0 (14.1) 27.40-7.S.1) 25.3-27.7-47.0 (25.3-42.680-4.16 (1.1) 27.64 (1.59-2.75) * 1.6) 19.56 (2.20-5.28 (1.19-6.9) 3.5-43.1 (25.43-12.0) 10.6-38.22 (2.

900 (.680 (.850 (.840) .760) < LOD .730-.60) 1.180) .160-.117 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .220 (.460 (.990) .550) .430 (.310) < LOD < LOD < LOD < LOD .140-.10) .410-.130-.420-.650) .300-.150) .850 (.930 (.680-1.650-1.120 (<LOD-.540 (<LOD-.360-.780) < LOD 1.440-1.640) .390) < LOD < LOD . respectively.050-.830 (.140-.310 (.350) < LOD < LOD < LOD < LOD .210 (.560 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .58) .410-1.640 (. and 0.130-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .230-.450 (.700-1.400-.860) .130 (.310-.10 (.610-1.740) < LOD .150 (<LOD-.700-1.210 (.870 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 01-02. and 03-04 are 0.300-1.650-1.240 (<LOD-.15) .380-.640-1.630 (.090 (<LOD-.140-.080 (<LOD-.40) .140) .450 (.320-.162) * * * * * .00) .510-1.090 (<LOD-.30) .990) .680) .320 (.840) .380-.190 (.660 (.410) < LOD < LOD < LOD < LOD .870 (.720-1.S.290) < LOD < LOD < LOD < LOD .120-.30) .10) .620 (.450 (.410-.310) < LOD < LOD < LOD < LOD .110-.430-.12 (.700-1.470 (.720) .370-.130-.090 (<LOD-.10) .290) < LOD < LOD < LOD < LOD 90th .160) .530-.360-.230) . 0.171) * * .170-.870 (.190 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.770 (. which may vary for some chemicals by year and by individual sample.05.080 (<LOD-.700-1.130) .870 (.490 (.160) .680-1.860-1.090 (<LOD-.650 (.270 (.290 (<LOD-.20) .1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120-. < LOD means less than the limit of detection.32) .830 (.720 (.13) .830) .42) .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 * * * * * * * * * .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.610 (.650) .370-.990 (.850) < 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 .390 (.200) < LOD < LOD .560 (.610 (.870 (.460-.099-.770) < LOD 95th .090 (<LOD-. see Data Analysis section) for Survey years 99-00.580) 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 * * * * * * .1.42) .870) < LOD .830) < LOD .820 (.36) .730) .540) .310 (.380-.630 (.03) .30) .100 (.090 (<LOD-. population from the National Health and Nutrition Examination Survey.190 (.084-.690-1.610-.130) .280) < LOD < LOD < LOD < LOD .470-1.640) .260 (.940 (.820 (.220 (<LOD-.600 (.350) .330-.570) .540) .

410 (.340-.640-1.110) .410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.14) 1.12) < LOD .057-.140-.140-.450) .940) .760) .230) < LOD < LOD < LOD < LOD .78) .700 (.230-.730) .140-.450 (.330-.580 (.380-.080) .150-.400 (<LOD-.390-.700 (.500 (<LOD-.720 (.330-.970) .070 (<LOD-.490-1.050 (<LOD-.03 (.02-1.990) .570-1.060-.410-.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 * * * * * * * * * .520-.190 (.100 (<LOD-.090 (.300 (.580) < LOD .990) .670-1.410) .290) < LOD < LOD < LOD < LOD 90th .084-.730 (.58) 1.180-. Fourth National Report on Human Exposure to Environmental Chemicals 129 .540 (.720 (.380 (.24 (.20) 1.360-.710-1.600-1.00) < LOD .03 (.550 (.410) < LOD < LOD .110) .410-.270 (.670 (.440-1.390-.110) .116 (.161) * * .780) < LOD 1.60) .870) .170 (.510-.540) .540 (.62) 1.19 (.880-1.01 (.080 (<LOD-.330 (.440 (.860-2.470 (<LOD-.03) .111) * * * * * .500-1.940) .730) .200 (.320 (<LOD-.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 * * * * * * .550 (.190 (.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 .700-1.360-.66) 1.670 (.300-.580) .300-.580 (.660-1.860 (.170) < LOD < LOD .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .170 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.650-1.500) .43) .120) .29 (.330 (.100-.110-.67) .S.380-.730) .260-.190-.460 (.210 (.890 (.750) < LOD 95th .24) .230 (<LOD-.580-1.600) .960) .070 (<LOD-.200 (.400) .360 (.070 (<LOD-.370 (<LOD-.140-.36 (1.270) < LOD < LOD < LOD < LOD .140) .220) < LOD < LOD < LOD < LOD .86) .700) .780 (.38) 1.110) .740 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.380-1.310) < LOD < LOD < LOD < LOD .330-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .260) .850 (.560 (.740) < LOD 1.570 (.810 (.380-.09) .220 (.360) < LOD < LOD < LOD < LOD .02) .86) .080 (.880 (. population from the National Health and Nutrition Examination Survey.280) < LOD < LOD < LOD < LOD .090 (<LOD-.650) < LOD .070 (<LOD-.120) .610-1.250-.570-.860 (.800-1.03 (.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.240-.140-.

6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10-9.190-1.97) 20.62) 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 * * * * * * .86) 4.360-1.74 (3.07 (3.88-3.83) 2.18) 1.05 (3.425-1.170-1.62-8.30) .0-38.600 (.800) 90th 13.40-20.510-.30 (1.850) 16.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.28) .90 (1.50) 2.07 (3. 0.30) 95th 19.83-3.68) 2.890 (.52 (1.0 (5.63 (3.0-39.640 (.690 (.00) .0 (5.12) * * * * * * * * .00-17.29-10.40-8.99 (1.83-3.23-6.S.37) .20 (1.67 (1.20-4.0) 7.33 (4.00) 1.0) 2.0) 3.0 (3.82-4.480-.94-8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.87) 5.720) 2. 01-02.20-4.370-.0 (13. population from the National Health and Nutrition Examination Survey.11) .6) 5.0) 4.61 (1.30-7.350-.21) 3.250 (<LOD-.46 (1.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.51 (2.0) 2.42) .67 (2.94-3.49 (1.31) .08.14) .76 (1.0) 4.01) 5.30-6.00) .49) 17.0 (17.40-4.900 (.610) < LOD < LOD < LOD < LOD < LOD 2.0) 2.51-8.15) 14.10 (3.0 (17.1.59-5.30 (1.96 (1.48 (2.05 (2.99) 19. and 0.0 (16.10 (3.740 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.66) 4.07-3. respectively.52) 5.42) 2.55-8.0-40.15) 19.10 (.870) < LOD < LOD .99) 11.840 (<LOD-1.960 (.14) 2.0) 5.94 (1.24-7.110 (<LOD-.750-1.31-10.90-37.80 (4.750-2.0 (4.40) 1.960 (<LOD-1.0 (17.90) .48) 13.00-17. which may vary for some chemicals by year and by individual sample.1.0) 2.65) 1.03 (.00 (1.400-1.380-.350-.74) 5.90) .52 (1.28) 1.07 (1.49 (1.30-3.260-.90-28.0) 2.53-7.770 (<LOD-1.580 (.97) 20.0 (7.800) 17.20 (1.13 (3.840 (.0) 2.610 (.12-1.0-40.90) .85-3.0 (4.00 (.47 (3.70) 2.0 (6. and 03-04 are 0.0 (17.910) 2.40) 2.70-3.0 (5.60) .45 (2.080-1.30 (. < LOD means less than the limit of detection.60) 1.20) < LOD < LOD < LOD < LOD < LOD 1.40-7.0 (5.55-4.36-3.770) 2.39) .63) 32.11) 13.70-7.67) .90-20.691 (.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 .0) 5.70-30. see Data Analysis section) for Survey years 99-00.50) .40 (1.70-17.3) 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 * * * * * * * * * .840-3.21-3.0 (17.30 (1.330 (<LOD-1.0-38. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0 (5.590 (.43-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.14-5.90 (2.26 (2.40 (1.640 (.11 (1.0) 5.35-10.800-4.36-3.90-9.53 (2.730 (.70-50.35) 11.0-44.32 (1.10-3.07) 1.620-1.28-9.07-3.38-3.0-38.05-3.53) 20.20-17.880) 5.830 (.0) 5.210-1.35) 5.30 (2.39 (2.0) 2.32-9.87) 12.0) 4.10-3.0) 4.

710 (<LOD-1.09-3.64-4.02) .730-3.45 (1.25 (1.56) .370 (.540 (.82-11.790) 11.0 (4.5 (8.53) .50 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840-3.39) 20.1) 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 * * * * * * .31) .620-3.10-3.80 (.90-6.830 (.97) .860-2.14 (1.49-2.5 (11.04-16.370) < LOD < LOD < LOD < LOD < LOD 1.89 (2.38 (2.7 (12.700) 6.84) 9.55) 21.5 (9.04 (1.8) 7.08) .32) 9.320-1.29 (4.24) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (2.71 (.940-4.650 (.4-34.81-17.8) 2.7) 6.48 (4.8-33.02 (1.41 (4.47-10.67-6.8 (20.12-4.73 (4.18) 95th 21.270-.0) 4.340 (.01 (1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.580) 16.85 (1.560 (.670 (.3) 3.67 (2.450 (.2-38.33-5.92 (2.88-3.500 (.79 (.00) .17) 5.630-1.57-40.11) .88 (.9) 6.650) 90th 10. population from the National Health and Nutrition Examination Survey.11-5.970-3.96-8.7 (6.7) 5.67) 1.340-.56 (1.07 (2.14-6.62 (1.5) 2.37) 4.23-7.57) 8.17 (1.18) * * * * * * * * .330-1.07-21.800-2.03) 16.57) 1.2 (8.35 (.430) 1.21-3.540-1.96-25.50 (2.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.56) 2.31-18.69) 2.748 (.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 .9) 5.33 (1.31) .91) 2.74 (2.960 (.57 (.370-1.28-6. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.5-40.7) 4.51-44.40-2.820) .190-1.71 (2.8) 4.40) 1.55) 21.31-7.02 (.32-6.790 (.0 (9.06 (.91-4.50) 11.36 (.12 (4.1) 2.86) .44) .13 (2.270 (<LOD-.9 (11.580) 1.43) .47) 5.44-11.8) 2.4) 2.40 (.474-1.47-10.820 (.80) 3.22-27.77 (.65 (2.60 (1.48-7.62-17.48-42.18) 1.740-1.7) 3.88) 17.50) .83-11.580-1.690-5.53) 27.390-.30 (4.150 (<LOD-.310-.59 (1.360 (.430 (<LOD-.55 (3.29-4.1 (7.33-4.240-.770) .250 (<LOD-.590) 2.600 (<LOD-1.85-3.98 (4.64) 30. Fourth National Report on Human Exposure to Environmental Chemicals 131 .15) 9.96) 2.25-38.27 (2.830-3.260-.51-4.340-.5) 7.47) .260-.930) .83 (4.1 (5.850-3.66-47.580 (.22) 2.40-12.33-3.86 (3.33 (3.340-.5) 2.88 (2.S.700) < LOD < LOD < LOD < LOD < LOD 1.8) 1.470 (.52 (.890 (.3) 2.02-4.00-19.6) 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 * * * * * * * * * .67) 2.4 (4.10) 2.25-9.03) 2.660) < LOD < LOD .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.8) 7.780-4.05) .69-7.41) 18.75) 5.

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Claypoole K. Lambert WE. et al. Thompson ML. Weisskopf C. Hore P. National Research Council (NRC). 4/7/09 Young JG. Stephens R. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Phillips J. vibration sense and tremor among South African farm workers. Steenland K. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Occup Environ Med 2001.332(1-3):71-80. Frasca G. et al. Gladstone EA. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Pesticides in the Diets of Infants and Children.43(1):38-45. Burcar PJ.84(5):731-736.26(2):199-209. U.338(8761):223-227. Arch Environ Health 1988. Lasarev M. Smit LA. Arch Environ Contam Toxicol 2000. Caltabiano LM.24(1):18-29. Gillham R. Neurotoxicology 2005. Washington (DC). Jenkins B. Johnson C. Environ Health Perspect 2006. low-level organophosphate exposure on delayed recall. Am J Ind Med 1987.S. Tumino R. Savage EP.52(10):648-653. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Lancet. Buccafusco JJ. Robson MG. Rosenstock L. Seiber J. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Mounce LM. et al. Bull Environ Contam Toxicol 1994. discrimination. Stokes L. Washington (DC): U. and spatial learning in monkeys and rats. Rothlein J. Bradman A. Pesticide industry sales and usage . Nell V.20(2):115-22. Petchuay C. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Muniz J. Irish RM.edu/ openbook. Ames RG. Scherer J. Marshall E. 1/12/09 Peiris-John RJ. Daniell WE. Stark A. Lancet 1995. Vitayavirasak B. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Calvert IA. Visuthismajarn P. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Heaton RK. J Occup Environ Med 2002.epa. McConnell R. EPA). EPA. McCauley L. Rodnitzky RL. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Buchanan D. Am J Public Health 1994. Pilkington A. Hansen S. Environmental Protection Agency (U. Ruberu DK. May. Beach J.12(2):153-172. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Muniz J. van der Hoek W. Levy LS. Kidd M. Eskenazi B. Jamal GA. Masala G. Pedersen L. Aprea C. Keefe TJ. Schenker M. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Available at URL: http://www.345(8958):11351139. Salvini S.114(5):691-696. Rohlman D. Lasarev M. Russo J. Chrislip D.52(2):190-195. Barr DB.S. Dinoff TM. Berry H. Santana J.68(3):209-227 Maizlish N. Wickremasinghe AR. metabolite clearance. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Lu C. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.php?record_id=2126&page=1. J Toxicol Environ Health A 2005. Weerasekera G. 2004. Chronic neurological sequelae to organophosphate pesticide poisoning. Neurotoxicity among pesticide applicators exposed to organophosphates.38(4):546-563.pdf. Takamiya K. Prendergast MA. Lewis JA. Occup Environ Med 1995. 1993 [online]. et al. Keifer M. Neurotoxicol Teratol 1998. Environ Health Perspect 2005.44(4):352-357. Terry AV Jr. Bravo R. Spurgeon A. Saieva C. Available at URL: http://books. Malathion deposition. and cholinesterase status of date dusters and harvesters in California. Effects of chronic. S. The Pesticide Health Effects Study Group. Scand J Work Environ Health 1998. et al.113(4):504-508. 1991. Sci Total Environ 2004. Rothlein J.12(2):134-141. National Academy of Sciences. Samuels S. Effects of long-term organophosphate exposures on neurological symptoms. A behavioral evaluation of pest control workers with short-term. Arch Environ Health 1975. Int J Occup Environ Health 2006.30(2):98-103. low-level exposure to the organophosphate diazinon. Office of Prevention Pesticides and Toxic Substances.58(11):702710. Narang A.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. 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.2000 and 2001 market estimates. O’Malley M.nap. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Myers JE. London L.

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

00) 3.9 (9.80 (7.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. After 2001.68 (7.70-16.27 (7.50 (1.25) 3.90 (2.50-2.20-14.0) 10. Approximately 80.00-24.71 (2.10 (5.00-8.26) 7.09 (3.67 (2.97) 2.80-10.90 (1.4 and 0.1-16.6) 7.7-23.91) 16.30-11.30-9.10) 2.05-5.00) 1.83) 1.70 (1.36 (4.4-15.52-12.5. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.51) 1.84) 1.30-2.88 (1.55-5.81-2.35) 2.43-2.7) 8. in 142 urban homes and preschools in North Carolina.51 (1.28-3. staying bound to soil particles.3 (8.76 (1.97) 7. Estimated intakes from diet and water have not exceeded recommended intake limits.61-7.20 (4.00) 2.59-2.80) 12.47-11. 2005).79-2.9-18.59) 2.29-1. interval) 1. dermal.0) 9.40 (5.13-3.04-10.40) 9.53 (1.50 (2.90) 3.8) 10.5-24.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.17 (1.0) 8.68-2.20-3.66-4.60-4.20) 2. USGS.4 (10. and inhalation routes.10) 6. 2002).77-15.0) 6.0 (7.91 (1.35) 1.90-8.000 pounds are used per year.0) 12. Survey Geometric mean (95% conf.50-5.60 (2.70-11.10 (4.0) 12.31-2.0 (9.09 (2.21) 3. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 10. Approximately 21-24 million pounds per year were used domestically from 1987-1998.24-3.32-1.0 (7.50-14. population from the National Health and Nutrition Examination Survey.20 (2.57 (2.97) 2. but can be detected in streams receiving runoff from application sites.95 (4.3 (10.67 (1.4 (9. 2921-88-2 Chlorpyrifos-methyl CAS No.90-4.47-9. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.70) 1.64) 3.0 (7.98-15.74-9..20) 10.20-16.25) 1.90 (6.7) 13.90 (3.9) 11.71 (1.70-15.EPA.9 (10.67 (2.44-5.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04-10.22) 2. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.30 (4. Chlorpyrifos is Urinary 3.80-8.10 (3.99-4.60-2.60 (4.94 (4.52-2.90-2.9) 697 660 521 701 602 947 Limit of detection (LOD.87-6.2 (10.77 (1.15 (1.63 (8.80) 4.9 (7.20) 2.40 (5.96) 3.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.31-2.44 (3.0) 18.S.0) 12.61 (1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No. and sprayed to kill mosquitoes.43-2. 2007).50-2.0) 12. The general population may be exposed to chlorpyrifos via oral.60 (5.02) 1.0) 10.77-6.47) 1.8-15. For instance.and post-construction structural applications for termite control were to be phased out by 2005 (U.02 (7. 5598-13-0 General Information The chemical 3.62-2.30-12.50 (2.3 (11.51-2.89 (2.10 (1.50 (1.20-2.90-7.3) 8. and dust. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.70-17.13 (1.0) 14.0) 15. 1999.90 (1.0-28. It also has been applied directly on animals to kill mites.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 1.63 (1.45 (1.0) 8.30) 4. applied to structures to kill termites.5) 7.66-15.50-4.30) 5.60-3.39) 4.38 (3.92 (1.72) 2.0) 12.0 (7. It has low leachability.70-5.20) 4.10-17.30 (2.16) 2.19-3.50 (2.50-8.20-4.44-2.97) 4. and is infrequently detected in ground water (IPCS.34) 1. Exposure can also result from contact with contaminated surfaces.40-26.30 (2. chlorpyrifos was no longer registered for indoor residential uses in the United States.5 (8.97-7.40-10.40-13.47-13.37 (1.28) 2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.90) 7. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.60) 5. and on plants for days to several weeks.47 (4.46-2.0) 11.74 (1.80 (1.0) 7.5.37) 5.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.80) 2.4 (8.24-1.30) 4. air.29) 90th 7.71 (6.30-5.80) 1. Fourth National Report on Human Exposure to Environmental Chemicals 135 .4.32) 2.40-2.03) 1.19 (1.02 (1.0 (13.40) 2. pre.39-2.01) 1.EPA. 2002). Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.89-2.86) 4.50-4.76 (1.20-11.1) 5.S.61) 75th 3.40 (6.37 (4.70 (1.63 (2. 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.78 (7.S.05) 1.95) 7.8) 9.30-1.77) 1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.72-4.7) 9.0 (10.60-3.0 (7.22 (1.

21-1.83) 1.70-4.09-2. weakness.82) 8. and other metabolites.11 (2.11 (2.940-1.48 (1. Survey Geometric mean (95% conf.27-7.55 (1.22) 1. 2005.49-2.31) 1.33 (1.15 (4.75) 6.82 (2.30-1. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.12-1.25-1.73 (1.20 (2.12-3. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.91) 10.58-5.1-38.33 (5.97-3.80-11. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).09-1. 2006b)..44-6.08) 6.19-2.43 (4. paralysis. Based on animal data and human cholinesterase monitoring during occupational exposure.58) 5. 2000).30-4.88-9.31-1.0) 6.28) 2.98 (7.38) 3.29 (3.5.84-6.98 (6.57) 9.25-11.46 (2.95 (3.34-1.85-4. 2006.92 (1.65-15.41 (1.22 (6.06 (1.37 (1.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.94-14.80-6.22 (4.75 (1.14) 1.5) 5.27-1.47-2.91 (3.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .53 (2.72-2.57-2.64-2.71 (1.62) 90th 5. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.91) 2.2 (7..86 (3. Urinary 3.02 (5. Once absorbed.24) 5. TCPy is more persistent in the environment than chlorpyrifos itself (U.0) 10.97) 3.36) 1. resulting in excess acetylcholine at nerve terminals.86 (1.1-21.76 (2.42 (6.59) 3. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.93 (2. Thus.22-6.47 (5.33-7. Roy et al.92) 3.02) 7.91 (4.49-2. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.6) 9. 2006.03) 1.01) 3.85) 4.58) 1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.90-9.53-5.51 (1.21-6.47 (1. population from the National Health and Nutrition Examination Survey.56) 5.92-2.85) 1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.24-5.7) 7.66 (1.17-4.1 (7.35-1.47 (1.9 (12.35) 1.0) 12.81) 2.88) 6.00 (7. and producing acute symptoms such as nausea.4) 4.63-2. Ricceri et al.74) 1..17-4.43-10.14-8. vomiting.93 (4.23-1.20-1.71) 3.55 (4.07) 5.05-3.07) 1.44 (5.05-1.19) 3.91) 1.62-7.64 (1..49 (1.97 (3.87-3.88-8. and seizures.65-11.24-24.58 (1. 1984).01) 99-00 01-02 99-00 01-02 99-00 01-02 3.99) 1.00) 1. neurotransmission.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.91) 1.6) 10.24) 75th 2.60-3.59-2.. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.8) 9.06-4.86 (1.97) 3.28) 2.44 (1.EPA.39) 6.0) 16.94-12.26-14.56) 2.24-4.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.80-4.2) 6.99-8.3) 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 1.05-8.40) 1. 2006a.66) 1.01) 3. Metabolic hydrolysis leads to the formation of TCPy.05-4.83-2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1. 2005.93) 2.42 (5.3) 8. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.39 (4.39 (2. cholinergic effects.24-1.54) 5.42-2.77) 1.58 (4.11-9.93) 5. Slotkin et al.57-2. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Howard et al.82-4.68) 6.S.89) 4.S.56 (4.3) 9.16 (4.79-13.1 (10.50 (4..62) 1.93 (1..32) 1.45 (1.. interval) 1.78 (1.09 (1.88-10.00-8.64-7.44 (6.54 (2.88 (1.63 (4.56-2.31-4.09-3.85 (3.80) 3.19-1.33 (. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.52 (5.46 (1.95 (1.56 (1.33) 2.85 (2. Betancourt et al.72) 2.16) 6.81 (3. In pesticide applicators.60 (1.24 (1.48 (2.66-11. TCPy can also occur in the environment from the breakdown of the parent compounds. 2005.58 (1.11) 7.44 (5.19) 6.35) 2.00-13.44 (1.25-12..57) 2.72) 1.96) 3.63 (5.68) 1.06 (5. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.97 (2.05) 3.3) 8.49-2.23) 14. 2002).3 (7.76 (3.39-1.12) 1.82 (3.01) 1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.88 (1.88-8.91-13.91-4.83-11.5 (6.45-1.55) 1.69 (1.

2000).. 1992. Lioy PJ. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Slotkin TA. 2005). environmental levels) and health effects is available from ATSDR at: http://www. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U.e. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos.atsdr.S. Garabrant D. 2005).EPA. Freeman NC..Organophosphorus Insecticides: Specific Metabolites 2004.Reference values of urinary 3. 2005). but not chlorpyrifos. Clayton CA. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC..63(3):218220. Levels of TCPy in the U. Environ Health Perspect 2005. et al. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Meyer A.S. population (CDC. Eberly LE.5. 2001). 2002). urinary TCPy levels in children were reported not to have increased (Hore et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Whyatt et al. Perera et al.. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. Additional information about external exposure (i. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Betancourt AM.cdc. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Lotti A. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. but levels were roughly four to six times higher than the geometric means in the U.gov/pesticides/. References Adgate JL. representative subsample of NHANES 19992000 (CDC. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.. 2005. In a probability-based sample of 102 Minnesota children aged 3-13 years.109(6):583-590.html and from U.. J AOAC Int 1999. Aprea C. Berent S. 2005.S. U. Haidar S. 2001) and Italy (Aprea et al. et al. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.. 1999). 2005).. Barisano A. Catenacci G. Curwin et al. In Iowa farm families using several different pesticides. Betta A. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Following crack-and-crevice application of chlorpyrifos in their homes. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.. Occup Environ Med 2006. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 2005). Of 482 pregnant women living in an agricultural community. Barr DB. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Environ Health Perspect 2001.. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Albers JW.. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.113(8):1027-1031.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Koch et al. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. EPA at: http://www. 2005). 2005. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al..S...gov/toxpro2. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Burns CJ.epa. Carr RL. Chlorpyrifos exposure and biological monitoring among manufacturing workers. CDC. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. 2004).. Seidler FJ. 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. 2003. Aldridge JE. In Minnesota and South Carolina farmers who used chlorpyrifos. 2004).S. Giordani B. et al. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Magnaghi S.82(2):305-312. 2006).92(2):500-506. the geometric mean urinary TCPy levels were similar in parents and children. MacIntosh et al. 2007). Toxicol Sci 2006. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Burgess SC.

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Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. MacIntosh DL.htm. 1992. Ricceri L. Ryan PB. Morgan MK.S. Hore P. Environmental Protection Agency (U. Freeman N. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Bucelli R.114(2):260-263.15(4):297-309.114(5):746-751. Shealy DB. Bennett DH. International Programme on Chemical Safety-INCHEM (IPCS). Tate CA. Available at URL: http://www.93(1):105-113. Howell RJ. J Expo Anal Environ Epidemiol 1999. 4/7/09 Koch HM. 2921-882. Environ Health Perspect 2004. Bailey SL. Slotkin TA.15(3):271-281.71:99108. Lu C. Toxicol Appl Pharmacol 1984. 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. Slotkin TA. Exposures of preschool children to chlorpyrifos and its degradation product 3. Ozkaynak H. Wartenberg D.

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

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

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

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

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.45 (<LOD-3.49 (<LOD-2.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. but is rapidly absorbed orally (IPCS. in the past. diazinon cannot be sold for residential use. 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. seed and foliar applications are planned to be phased out (U. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. USGS. Survey Geometric mean (95% conf. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. but these uses have been phased out.EPA. 2004). < LOD means less than the limit of detection. Estimated intakes from diet and water do not exceed recommended intake limits (U. Before these restrictions. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. and other metabolites. Prior to 2000. 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). 2007). since 2004. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). in some pest strips. 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. Once absorbed. and forage crops.2 and 0.EPA. and particularly when it was ingested in granular form. diazinon was widely used in residential and garden application. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity.S. Most granular formulations. aerial.7. Inhalational and dermal routes of exposure can be significant for pesticide applicators. population from the National Health and Nutrition Examination Survey.S.S. It is toxic to birds. an organophosphorus insecticide that is used to control insects on nuts. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. which may vary for some chemicals by year and by individual sample. Diazinon is not well-absorbed through the skin. It is also used for cattle ear tag applications to control flies and ticks and. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. diazinon produced wild bird kills before use restrictions were in place. fruits. 1998). Fourth National Report on Human Exposure to Environmental Chemicals 143 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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. 1998. vegetable.

diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection.. or reproductive toxicant (IPCS. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. Olsson et al.e. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.S. 1986 Rajendra et al.72 (<LOD-4.. and seizures. respectively. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. Survey Geometric mean (95% conf.cdc.html and from U. subsamples of NHANES 1999-2000 and 20012002. Thus. 1992).gov/toxpro2. environmental levels) and health effects is available from ATSDR at: http://www.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 144 Fourth National Report on Human Exposure to Environmental Chemicals .. In two nonrandom samples of United States adults and children.76 (<LOD-3. and producing acute symptoms such as nausea. weakness. animal carcinogen. Seifert and Pewnim.epa. EPA at: http://www. 2003).S. resulting in excess acetylcholine at nerve terminals. Diazinon is not considered to be a mutagen. 1986. agricultural. In addition to being a human metabolite of diazinon. diazinon does not accumulate in tissues (IPCS. paralysis.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. At high doses.S. 1998). 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.EPA considers diazinon unlikely to be carcinogenic in humans. The U.49 μg/L.atsdr.. teratogen. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. cholinergic effects.S. 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 animals. Intoxications in humans from intentional overdose. and indoor applications have been documented.. population from the National Health and Nutrition Examination Survey.gov/pesticides/. 2000.. Additional information about external exposure (i. Diazinon has moderate acute toxicity in animal studies. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2002). respectively (Baker et al. 1998).45) < LOD < LOD < LOD < LOD 454 580 632 828 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. in the 2001-2002 subsample (CDC. vomiting. In the U.45 and 1.

Organophosphorus Insecticides: Specific Metabolites 2005). urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Diazinon. Barr DB.usgs. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry..44(11):2243-2250. Anal Bioanal Chem 2003. In 23 children. Environ Health Perspect 2003. Driskell WJ. Drobnis EZ. International Programme on Chemical Safety-INCHEM (IPCS). Rajendra W. et al. 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.inchem. References Anthony J. Biomonitoring studies of 2-isopropyl-4-methyl-6-hydroxypyrimidine provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of diazinon than are found in the general population. EPA 738-R-04-006. 2005.50(5):505-515.114(2):260-263. Oloffs PC.10(6 Pt 2):789-798. Jones K. Carrier G. Irish R. Needham LL. Interim reregistration eligibility decision (IRED. revised February 15. Brunet RC. In a small number of men visiting fertility clinics in Missouri and Minnesota. Nguyen JV. EPA). Baker SE. Dumas P. 2007 [online]. Garfitt SJ. Oloffs PC. Available at URL: http://pubs. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Geological Survey (USGS). Pewnim T. Noisel N. Drug Chem Toxicol 1986.gov/circ/2005/1291/. Bull Environ Contam Toxicol 1986.pdf. Available at URL: http://www. Semen quality in relation to biomarkers of pesticide exposure. Swan SH. 2006). Toepel K.S. Third National Report on Human Exposure to Environmental Chemicals.htm. Olsson AO. Banister E.37(4):501-507. Bouchard M. Redmon JB. Mason HJ. March 2006. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. 1/14/09 U. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al.gov/ oppsrrd1/REDs/diazinon_ired. Study for Future Families Research Group. May 2004. U.134(1-3):105-113.org/documents/ehc/ehc/ehc198. Ann Occup Hyg 2006. Barr DB. Atlanta (GA). Kruse RL. 4/7/09 Lu C. In 54 Canadian greenhouse workers. Effect of sublethal levels of diazinon: histopathology of liver. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.S. Beeson MD. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 1992-2001. Toxicol Lett 2002. Biochem Pharmacol 1992. Environ Health Perspect 2006.epa. Banister EW. 1998. Liu F. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Cocker J. The Quality of Our Nation’s Waters. Fenske RA.111(12):1478-1484.S. Centers for Disease Control and Prevention (CDC). Bravo R.. Environmental Health Criteria 198.376(6):808-815.9(2):117-131. Environmental Protection Agency (U. Swan et al. Available at URL: http://www. Barr DB. Sadowski MA. 2006). Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Seifert J. Barr DB. J Expo Anal Environ Epidemiol 2000. Diazinon. Pesticides in the Nation’s Streams and Ground Water. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids.

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

gov/pesticides/.74 (<LOD-5. 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. 2001. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. 1999). Malathion itself has not been considered genotoxic (U. Giri et al. and it is not considered an animal teratogen or a reproductive toxicant. 1993.S. 2006).e. Toxicity from unprotected bystander exposure during applications is rare (U. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. CDC. Survey Geometric mean (95% conf. 2005). 1996. 2005. 2004). Pluth et al. but isomalathion..S.. 2003). 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. 2005). but cholinesterase activity was not affected.S.atsdr. 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. 2000). Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 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. 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...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. environmental levels) and health effects is available from ATSDR at: http://www.. 2006). EPA at: http://www.cdc.S. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al.. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al.S. 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al. population from the National Health and Nutrition Examination Survey..5 and 5.0 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. Of 382 pregnant women living in an agricultural community. Fourth National Report on Human Exposure to Environmental Chemicals 147 . Flessel et al. Additional information about external exposure (i. IARC considers malathion not classifiable as a human carcinogen. 1999. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human studies of single oral doses between 0..gov/toxpro2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Thomas et al. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure.EPA. 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.. Lu et al.EPA.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions.epa. 1990).. representative subsample from NHANES 19992000 (Adgate. 1987. 2006). some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 2002.html and from U.

S. Kedan G. Flessel P. Eberly LE. Hammerstrom KA. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. O’Neill JP.112(10):1116-1124.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Third National Report on Human Exposure to Environmental Chemicals. 2007 [online]. et al. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Carrier G.74(2):following table of contents. Sharma GD. revised February 15. et al. Brunet RC.usgs. Thomas D. Griffith W. Jaloszynski P. Clayton CA. Centers for Disease Control and Prevention (CDC).S. March 2006. Petitti D. Barr DB. Environ Health Perspect 2001. Lu C. Mutat Res 2002. Freeman NC. Lu C. htm. Harley K. Genetic toxicity of malathion: a review. EPA). Available at URL: http://www. Am J Public Health 1987.77:1009-1010. J Expo Anal Environ Epidemiol 1999. Available at URL: http://pubs. Swan SH. Barr DB. Goldhaber M. Am J Epidemiol 1990.9(5):494-501. Lioy PJ. Samuel O. Grether JK. 6/1/09 U. Ryan PB. Dinoff TM. 2005. Gosselin NH. and cholinesterase status of date dusters and harvesters in California. Curl CL. Needham LL. Albertini RJ. Available at URL: http://www. Irish R. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Bouchard M.56(10):2393-2399. Hooper K. metabolite clearance.114(2):260-263. Nicklas JA. Trzeciak A. Environ Health Perspect 2006.gov/circ/2005/1291/. Environ Health Perspect 2004.org/documents/jmpr/jmpmono/v2003pr06.epa. Giri A. Mutat Res 1999. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Environ Mol Mutagen 1993. Blasiak J. MacIntosh DL. Atlanta (GA). Erratum in: Toxicol Sci 2003 Aug. The Quality of Our Nation’s Waters. Eskenazi B. Pluth JM. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Geological Survey (USGS). Toxicol Sci 2003 May. 1992-2001.15(2):164-171. Rappaport E. Malathion deposition. Quintana PJ. Barr DB.pdf. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers.38(4):546-553.109(6):583-590. U. Toepel K. July 2006.132(4):794-795. Giri S.445(2):275-283. A longitudinal investigation of selected pesticide metabolites in urine. Reproductive outcome in women exposed to malathion. Cancer Res 1996. J Expo Anal Environ Epidemiol 2005. Dumoulin MJ. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Neutra R. Krieger RI. Bradman A.73(1):182-94. Bravo R. Szyfter K. Pesticides in the Nation’s Streams and Ground Water. Jewell NP. Weltzien E. International Programme on Chemical Safety-INCHEM (IPCS).22(1):7-17. Harris JA. Environmental Protection Agency (U. 4/7/09 Kissel JC. Barr DB. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Prasad SB. Reregistration eligibility decision (RED) Malathion. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.gov/oppsrrd1/REDs/ malathion_red.S. Fenske RA. Hertz-Picciotto I. et al. Malathion (addendum). Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.514(1-2):223231. Arch Environ Contam Toxicol 2000. EPA 738-R06-030.inchem.

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. Once absorbed. 2007).47) 2.70-6.37-4.10 (3.0) 2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.50 (1.70) 2.89 (2..32 (1.71 (2.44) 2.10) 22. < LOD means less than the limit of detection.EPA.0) 3.50 (1.70 (2. It had been applied to cotton.28 (1.40 (1.26 (1. methyl parathion was rapidly absorbed after ingestion. 1977).S. with limited applications in agriculture. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.S.37-2.66 (2.37) 2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.70 (<LOD-3. on cereal grains.33) 2. first registered in 1948.8 and 0. more slowly absorbed through the skin.13-1.910) < LOD . but by 2003.70) 2.18-3.74) 5. In animal studies.10 (3.46 (3.0) 4.02-6.70 (3. binds tightly to soils resulting in low leachability. population from the National Health and Nutrition Examination Survey.730 (<LOD-.41-4.79) 4.30 (1. Ethyl parathion.30-5.940 (<LOD-2.15-3.990-1. was once a restricted-use insecticide with limited applications on certain agricultural crops.40-4.80 (2.20 (2. In the 1990s.01) 695 660 518 679 603 941 Limit of detection (LOD. Both are toxic to birds.19 (.80) 2.62 (1. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.45) 5.770 (.0) 3.85 (2. Estimated intakes from diet and drinking water have been below recommended limits.50 (1.92-2.49 (1.0) 3.50) 2.34 (3.12) < LOD < LOD 1.80 (1.60-36.32-3.37-4. which may vary for some chemicals by year and by individual sample.60 (4. 2006).02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .00) 3.50-14.58) 3.50) 3.00 (2.70 (2.40-4.20-5. and of the chemical nitrobenzene. and aquatic invertebrates. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Many previous registered agricultural uses of methyl parathion have been cancelled (U. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.09-1.32-1.50 (2.57-4.21-1.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .60-5.70) 2. and has a short half-life in soils and on plants.71 (3. Methyl parathion has low water solubility. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .67 (1.860 (<LOD-1. and oral routes can occur in pesticide and agricultural workers (Muttray et al.05) 4.28-4.21 (2. Methyl parathion use is highly restricted. Morgan et al.40) 1.90-11.28 (1.30 (2.27) 2.33 (1.30-16.00 (2. 2002.790 (<LOD-. Survey Geometric mean (95% conf.300-.10-11.90 (1.30-3.22-3. ethyl parathion. 2000). 2003).50 (1.70-3.850) < LOD .298-00-0 Ethyl Parathion CAS No.60-24.01-4.50 (2.700 (<LOD-.92) 5.36-1.0 (3.S.72 (3.40-3.20 (<LOD-2..70-6.60-19.69 (2. pulmonary.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. Increased risk of exposure via dermal.60) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. fish.90-9. and eliminated rapidly from the body after absorption (Kramer et al.11-4. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.80 (2.EPA.48) 90th 2. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.50) 1.10-1.11) 2.910) < LOD < LOD .32-1. Given its limited use.50) 3.45 (1.01) 4.20) 5. and to a lesser extent.910) < LOD < LOD < LOD 1.0) 3.70-6.10) 4.40) 2.91-3. Fourth National Report on Human Exposure to Environmental Chemicals 149 .61) < LOD 1.70-3.57) 1.1.0) 3.16) < LOD 1. Methyl parathion is not registered for residential use in the United States.40) 4.61) < LOD 1. peak domestic use was as high as 5-6 million pounds per year. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. all registered uses were voluntarily cancelled (U.69) 4.67) < LOD 1.50-9..10 (<LOD-6. Methyl Parathion.70 (2.

43) 4.78-2.00) 2.89 (2.930 (.95) 1. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.05) 4.970 (. paralysis.07) 2. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.33-3.S.2) 2.690-1. does not inhibit acetylcholinesterase enzymes.23) 1.08-3.70) 3.78-2.10) 90th 2.2) 2.950) < LOD . and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.92 (2.55) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.21) 1.9) 1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .08 (1. and seizures. 2004).17-4.57-2.21-21..25) 1...16-4. but lists ethyl parathion as a possible human carcinogen. ethyl parathion.. EPA at: http://www.880 (. Methyl parathion is not considered genotoxic.80 (1.97-10.31) < LOD .830-1.30-1. 2006.3) 2.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th .97 (2.940 (<LOD-1. 2005.44-3.59 (1.30) 3.57-7.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .html and from U.cdc.87 (1.720 (<LOD-.720-1. accidental exposure.970 (. Survey Geometric mean (95% conf.atsdr.26 (1. and other metabolites.01 (.530) < LOD < LOD < LOD .71 (1.640) < LOD < LOD 1.73 (1. and unintentional acute or chronic high-level occupational exposure (Hill et al.33-6.04) 1.25 (2.20 (3. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.EPA considers methyl parathion unlikely to be carcinogenic to humans.. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. 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.96 (1. paranitrophenol.S. Additional information about external exposure (i.07 (1. Methyl Parathion.90 (1. and producing acute symptoms such as nausea.870) < LOD . environmental levels) and health effects is available from ATSDR at: http://www.77-7. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Zurich et al.71) 1. Parathion and methyl parathion have high acute toxicity in animal testing.61) 4.60-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.84) 3.370 (<LOD-.930 (. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion. 1995. 1978.56-2. WHO.26) 17. U.48-4.44-3.S.7) 3.epa. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.15-10. methyl parathion.76-14.20) 3.35-3. 150 Fourth National Report on Human Exposure to Environmental Chemicals .1) 2.93 (2.840 (.91 (1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. gov/pesticides/.38-3.60 (1.55 (<LOD-3. resulting in excess acetylcholine at nerve terminals.13) 4.39 (1. Jaga and Dharmani.67 (3.13-12.08) < LOD .440 (<LOD-. 2006.800-1. In addition to being a metabolite of methyl and ethyl parathion.79) 1.00 (1.79 (1.400 (<LOD-.88 (1.67-2.88) 1. Orsorio et al.91) 1. The metabolite.11) 1. 2003.14-3. Thus. Karanth and Pope et al.29) 2.39) 1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .850-1.790-1.e.94-47. 1990. Lores et al.97 (<LOD-4.430 (.790-.60) 2..33-3. vomiting.500) < LOD < LOD .09) 2.57) 6. At high animal doses of methyl parathion.980 (.94-4. gov/toxpro2.31-3.20) .80 (1. cholinergic effects.00 (1.35-3. weakness.540) < LOD .86 (2.96 (1.89 (2.04 (2. population from the National Health and Nutrition Examination Survey.730-1.29) 1.310-. 1991).78) 2. Slotkin et al.82) < LOD .01-3.15) 3.29 (2.82 (2.10 (1. In large doses.01 (2.37-1.Organophosphorus Insecticides: Specific Metabolites Metabolites”)..680 (<LOD-1. 2004).17) .41-2.78 (2.72-2.98-7.83 (1. 1995).4 (3.11-4. teratogenic..

33(5):270-276. oral or dermal administration. 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. A study of 13 children from an agricultural region of Washington State reported median levels that were more than threefold higher than median levels in the NHANES 1999-2000 subsample (Kissel et al.25(5):599-606. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. J Biomed Sci 2002. Arch Environ Health 1978. 2005.6(2-3):159-173. Hill et al. Occup Environ Med 1999..71:99108. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. CDC. ACGIH recommends a BEI of 0. et al. 2005). Kissel JC. 2005. Karanth S. et al. J Anal Toxicol 1990. 1999). Harley K. Giordano G. 2002. Hryhorczuk DO. Laboratory investigation of a poisoning epidemic in Sierra Leone. Shealy DB. Hill RH Jr. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Environ Health Perspect 2004. Cline RE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..15(2):164-171. Rubin et al. Eskenazi B. Wellman SE.14(4):213-216. Baker RC. Jewell NP. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Turner WE. Lin LI. Role of individual susceptibility in risk assessment of pesticides. general population (CDC.5 mg (500 µg)/g creatinine for workers at the end of shift.110 Suppl 6:1085-1091. Atlanta (GA). Barr DB. Clark JM. Available at URL: http:// www. and levels were similar or slightly lower that those in a small convenience sample of the U. Needham LL. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 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. 2002). Moomey CM. Griffith W.112(10):1116-1124. Alley CC.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. and many residents were symptomatic (Barr et al.110 Suppl 6:1075-1078. Centers for Disease Control and Prevention (CDC). McCann et al. et al.. Morgan DP. J Expo Anal Environ Epidemiol 2005. et al. Chicago area methyl parathion response.inchem.. a range of values several hundred times higher than levels found in the U.htm. Lewalter J. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Parathion-Methyl (addendum). Guizzetti M.org/documents/jmpr/jmpmono/v95pr14. Neurotoxicol Teratol 2003. Costa LG.56(7):449553..S. Arch Environ Contam Toxicol 1977.S. 1995).215(3):182-190.9:311-320. Bradman A. Environ Health Perspect 2002. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Barr DB. 2005. population (Olsson et al. 2005). Dharmani C. 2004). Moseman RF. Methyl parathion: an organophosphate insecticide not quite forgotten... Bailey SL. Pesticide residues in urine of adults living in the United States: reference range concentrations. Ashley DL. Environ Health Perspect 2002. 1995. Baker SE. Lores EM. Slach EF. Rockhold RW. Rev Environ Health 2006. Pope C. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Pathak S. 4/7/09 Jaga K. Baker S. Barr DB. Head SL. Barr JR. Lu C. Head SL. Kramer RE. Runkle KD. et al. Toxicology 2005. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Weltzien E. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Kedan G. Hill RH Jr. Third National Report on Human Exposure to Environmental Chemicals. 2002. Gregg M. International Programme on Chemical Safety-INCHEM (IPCS). McClure PC. Environ Res 1995. References Barr DB. Curl CL. DiPietro E. McCann KG. Hetzler HL. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Bradway DE. Pesticide workers may have much higher levels following pesticide applications. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. In a study of workers who handle parathion. Leng G.21(1):5767. Biomonitoring studies of para-nitrophenol can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of parathion than are found in the general population.

R. Sadowski MA. Environmental Protection Agency (U. Facts. Hill RH Jr.gov/circ/2005/1291/. Olsson AO. Rosenberg J. EPA). Available at URL: http://www. Honegger P. WHO/SDE/WSH/03. Ethyl parathion.S. 0153. Pesticides in the Nation’s Streams and Ground Water. Yacovac R.201(2):97-104. Investigation of a fatality among parathion applicators in California. 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.int/water_sanitation_health/dwq/chemicals/ methylparathion. Schilter B.114(10):1542-1546.376(6):808-815.S. Tate CA. Ohio.110 Suppl 6:1047-1051. Toxicol Lett 2006.S. Am J Ind Med 1991. Mengle DC. External and internal exposure of wine growers spraying methyl parathion. Esteban E. September 2000.pdf. Toxicol Appl Pharmacol 2004.S.D.pdf. Seidler FJ.epa. Letzel S. Backer G. Ames RG.epa. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. 6/1/09 World Health Organization (WHO). Case No. 1/14/09 U. Available at URL: http://www.04/106. The Quality of Our Nation’s Waters.E. et al. Costa LG. Nguyen JV. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Monnet-Tschudi F. Kieszak S. 1/12/07 U.20(4):533-546. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Methyl parathion in drinking water. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Environ Health Perspect 2002. Geological Survey (USGS). 2004. May 2003. Available at URL: http://pubs. Environ Health Perspect 2006. Jung D.S.162(2-3):219-224. revised February 15. Available at URL: http://www. Levin ED. U. Anal Bioanal Chem 2003. pdf.gov/oppsrrd1/REDs/factsheets/0155fct.who. Rubin C. gov/oppsrrd1/REDs/methylparathion_ired. Dunlop B.Organophosphorus Insecticides: Specific Metabolites Muttray A. 5/19/09 Zurich MG. EPA). EPA-738-FOO-009. Slotkin TA. Environmental Protection Agency (U. Barr DB. Ryde IT.usgs. 1995-1996. Osorio AM. 2007 [online]. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. March 2006. 1992-2001. Hill G.

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

500 (.470 (.680 (<LOD-.700-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .210-1.780 (.610 (<LOD-1.700-.31) . which may vary for some chemicals by year and by individual sample.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2. see Data Analysis section) for Survey year 01-02 is 0.740-1.780 (<LOD-1.64) .780 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .17 (.27) .950) < LOD < LOD 1.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .410 (<LOD-1.780 (<LOD-1.430 (<LOD-.850 (.820) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (<LOD-. population from the National Health and Nutrition Examination Survey. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th . population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. 154 Fourth National Report on Human Exposure to Environmental Chemicals .250 (<LOD-.840) 669 687 929 Limit of detection (LOD.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.21) < LOD .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 (<LOD-1.300-1.55) .210-.840 (.S.740 (.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.580-1.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.94) .760 (<LOD-.15) < LOD .200-.07) .

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

1992).. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. EPA. organophosphorus. Woollen et al. The table shows the urinary pyrethroid metabolites measured in this Report. warehouses. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al.2-Dichlorovinyl)-2. but pyrethroids are highly toxic to fish and some aquatic invertebrates. 2007).2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. WHO.EPA. and then eliminated over several days in urine and bile (Kuhn et al.. 2002. 2006a. and are rarely detected in ground waters (USGS. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. cypermethrin. pyrethroid pesticides have less acute toxicity in animals and people. and sumithrin) are also registered for use in mosquito-control programs in the United States.. Woollen et al. and deltamethrin have been used frequently on cotton. They are ranked as having moderate acute oral toxicity. Generally. Estimated intakes from diet and drinking water are below recommended limits. After absorption from inhalation or ingestion.. Possible other additional actions on neuroreceptors Pyrethroid Insecticides Metabolites in this Report Pyrethroid (CAS number) Cyfluthrin (68359-37-5) Cypermethrin (52315-07-8) Cyfluthrin (68359-37-5) and Permethrin (52645-53-1) Deltamethrin (52918-63-5) Cyhalothrin (68359-37-5) Cypermethrin (52315-07-8) Deltamethrin (52918-63-5) Fenpropathrin (39515-41-8) Permethrin (52645-53-1) Tralomethrin (66841-25-6) Urinary metabolite (CAS number) 4-Fluoro-3-phenoxybenzoic acid (77279-89-1) cis-3-(2.2-Dichlorovinyl)-2. or carbamate pesticides.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins.. cyfluthrin. This class of pesticides has low toxicity in birds and mammals. There are about 30 different pyrethroid pesticides in use. followed by conjugation. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. Certain pyrethroid insecticides (such as permethrin. In agriculture. resmethrin. solvent oils. Unmetabolized pyrethroids have been measured in breast milk. Soderlund et al. but may be poorly transferred across the placenta (ATSDR. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. 2006b).2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. 1997. 2003.2-Dibromovinyl)-2. They are also applied on livestock to control insects.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. Outside the U. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. 1999.S. pyrethroids are rapidly metabolized. animal facilities.. Pyrethroid pesticides have low volatility. such as piperonyl butoxide. and synergists. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. 2002). which are natural chemicals found in chrysanthemum flowers. Pyrethroids are not well absorbed through the skin (ATSDR. they are not persistent in the environment due to their rapid degradation within days to several months. bind to soils. in some situations replacing the use of DDT. and greenhouses. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. 2005). Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. Compared with other classes of insecticides such as organochlorines. agricultural fields.S. by either ester hydrolysis or hydroxylation. so usage is restricted near water (U. Soderlund et al. 1992). 2005. 2003. 2002). Leng et al..S. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown.

hypersensitivity. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Lewalter J. et al.cdc. Kamita Y. Chen JH. Sugiri D. Hu et al. Neurotoxicol Teratol 2005.8(1):18-21. Guillot TS. References Agency for Toxic Substances and Disease Registry (ATSDR). Wieseler B. Miller GW. Kim HS. motor activity. 2003. Adhami VM. Pauluhn J.50(2):245-255. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line... Eriksson P. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Spinosa HS. Go V. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. epa. Berger-Preiss E. Neurotoxic effects of two different pyrethroids. Idel H. salivation. 2002). Shukla Y.. dopaminergic. Florio JC. Lee SJ. Wang SL. Bull Environ Contam Toxicol 1999.1/15/09 Aziz MH. J Reprod Dev 2004..35(2 Pt 1):227-237. Richardson JR.62:101-108. Lazarini CA. Salzgeber SA.. Leng G. Elwan et al.107(3):173-177. Moniz et al. In California.html. Seth PK. Lazarini et al. et al. et al. Idel H.8(1):197-202. Ray et al. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Regul Toxicol Pharmacol 2002. 1991. 1998. Thomson BM. Leng A. Kuhn KH. Bernardi MM. Kuhn K. Kim TS. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Kunimatsu T. Go et al. Toxicological profile for pyrethrins and pyrethroids. Environ Health Perspect 1999.S. 2003.gov/toxpro2. Additional information about pesticides is available from U. EPA at: http://www. Pogo BG. Varoli FM.300(3):161-165. Cruz-Casallas PE. neurochemical changes in cholinergic. WHO. 2005). Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Neurosci Lett 2001. Ranft U.108(1):78-85. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Garey and Wolff. Caudle WM. Toxicol Appl Pharmacol 1991. 2005). Kunimatsu et al.27(12):1273-1283. Elwan MA. choreoathetosis. 2004. Okuno Y. Wolff MS. Wolff MS. tremor..atsdr. Neurotoxicol Teratol 2001. Moniz AC. 2006). The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Shaw IC. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Generally. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation..23(6):665-673. September 2003. Kang IH. cdc. bioallethrin and deltamethrin.. Garey J. 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. 2000. Agrawal AK.. In developing rodents. 2001. 2005). and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. 2005). Pyrethroid pesticide-induced alterations in dopamine transporter function. Shafer. 2002. Fredriksson A. Kim IY. Levsen K. 2006. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Hu JY. Int J Hyg Environ Health 2002. 2003. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.gov/toxprofiles/ tp155. McCarthy AR. Soderlund et al. Sunami O..gov/pesticides/ and from ATSDR at: http://www. 1999. McCarthy et al. Biochem Biophys Res Commun 1998. Leng G.. J Environ Monit 2006. 2003. and seizures (ATSDR. Abell AD.. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.205(6):459-472.251(3):855-859. and striatal dopamine levels in male and female rats. et al. Shin JH.27(4):609-614.211(3):188-197. Lemonica IP. on immature and adult mice: changes in behavioral and muscarinic receptor variables.. Yang J. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Eriksson and Fredriksson.atsdr. Toxicol Appl Pharmacol 2006. Bernardi MM. 2001. and permethrin) in the Hershberger and uterotrophic assays. Ose K. 2006.html. Garey J. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. fenvalerate. 2002). Available from URL: http://www.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Zhao RC. Estrogenicity of pyrethroid insecticide metabolites. Leng G. Kim et al. Xenobiotica 1997. Song L.

Environmental Protection Agency (U. Revised February 25. Safety of pyrethroids for public health use. 2007.S.usgs.htm. Sargent D. Clark JM.pdf. June 2006a. U. Geological Survey (USGS). Mullin LS. Piccirillo VJ. Reregistration Eligibility Decision for Cypermethrin.10. sumithrin synthetic pyrethroids for mosquito control. Laird WJ. 5/26/09 Woollen BH. and therapy. 5/26/09 U.gov/ circ/2005/1291/. Pesticide and Evaluation Scheme. Meyer DA. 1992–2001.22(8):983-991. Crofton KM. J Toxicol Clin Toxicol 2000. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). synergies.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Available at URL: http://pubs.gov/oppsrrd1/REDs/cypermethrin_red.S. World Health Organization (WHO). Pesticides in the Nation’s Streams and Ground Water.S. March 2006. Rev Environ Contam Toxicol 2006.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. 19962002. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .S.epa. Available at URL: http://www. EPA).S.htm. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.who. pdf. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.S. Forshaw PJ. Spencer J. Available at URL: http://www. Lesser JE. Environ Health Perspect 2005. Permethrin.Pyrethroid Pesticides Ray DE. O’Malley M.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. April 2002. 5/26/09 U. 2005. Toxicology 2002. Environmental Protection Agency (U. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. et al.epa. Soderlund DM.171:3-59. Environmental Protection Agency (U. EPA). Available at URL: http://whqlibdoc. 5/26/09 U. Sheets LP.epa. Pyrethroid illnesses in California. Available at URL: http://www. Xenobiotica 1992. Pyrethroid insecticides: poisoning syndromes. June 2006b. Marsh JR.113(2):123-136.38:95-101.186:57-72. EPA).S. Shafer TJ. resmethrin.

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

S.2 and 0.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < 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. 160 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf. 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. which may vary for some chemicals by year and by individual sample.2. population from the National Health and Nutrition Examination Survey.

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

Environ Health Perspect 2001. Int Arch Occup Environ Health 2004. Krieger RI. Kolossa-Gehring M. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Rev Environ Contam Toxicol 2006. Angerer J.206(2):85-92. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Atlanta (GA). J Expo Anal Environ Epidemiol 2003. Pyrethroid illnesses in California.209(3):293-299. Schulz C.77(1):67-72. Olsson AO.209(3):221-233. Williams RL. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.13(2):112-119. Centers for Disease Control and Prevention (CDC). Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.Pyrethroid Pesticides References Baker SE. Leng G. Int J Hyg Environ Health 2006. Bernard CE. Heudorf U. Butte W. O’Malley M. Barr DB. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Spencer J. Angerer J.109(3):213-217.46(3):281-288. Ball M. Heudorf U. Heudorf U. Int J Hyg Environ Health 2003. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Seiwert M. Hoppe HW. Becker K. Angerer J. Berger-Preiss E. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Drexler H. 19962002. Hadnagy W. Ranft U.186:57-72. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2006. Idel H. Sugiri D. 2005. Arch Environ Contam Toxicol 2004. et al. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.

250 (..670-1.44 (.270 (.270 (.890 (.2-dichlorovinyl)2.420-.470 (.68) .710-1. ciscypermethrin and cis-cyfluthrin.300-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.330 (.510 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.870) 1. Biomonitoring Information Urinary levels of cis.780) .500 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.920) 1.180) .680-3.230) . transcypermethrin and trans-cyfluthrin.710) .1. 1985.380) .680 (.220) .310) .340-.155-.150 (.850 (.600-1. 1999).410) .950-2.890 (.960 (.510 (.570-.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .21) .260 (.630-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.24) 1.370-.2-dichlorovinyl)-2.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.220-.250-.1 and 0.50) .200 (.670-2.790) .13 (.490-1.200) . cis-permethrin.110-..2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.740-1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.610) .470-1.220-.270-.820 (.43) .790-1.240) . Fourth National Report on Human Exposure to Environmental Chemicals 163 . Cyfluthrin.630 (.53) .220-.440 (.670 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . 1985.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .740) 1.140 (<LOD-.or trans-3-(2.300 (.790-1.600) .740-2.110-. trans-cypermethrin. and ciscyfluthrin.2dichlorovinyl)-2.340) .280 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George. In the body.510 (. more of the trans-metabolite than Urinary cis-3-(2. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. cis-cypermethrin. and trans-cyfluthrin.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.380-. Survey Geometric mean (95% conf. the presence of trans-3-(2.600 (.610) . 52315-07-8 CAS No.580) 1. which may vary for some chemicals by year and by individual sample.700) .410) .28) 671 680 518 701 591 957 Limit of detection (LOD.380-.2dichlorovinyl)-2.120-. cis-3-(2. Kuhn et al.160 (.340) .160 (<LOD-.550) .210-.350) .380 (.and trans-isomers.640 (.210) . trans-permethrin.15) .300-.140 (.240) .77 (.07 (.690) .180 (.200) < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.730 (.300 (.460-.490-.520) .900 (.170 (.68359-37-5 Cypermethrin Permethrin CAS No.500 (. but can also reflect exposure to trans-3(2.110 (<LOD-.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 . Similarly.80) . The chemical trans-3(2.S.730 (.120-.32) .430-.200-.370 (.460 (.160 (.2-dichlorovinyl)-2.530 (. Kuhn et al.740 (.880 (.120-. Generally.490-.54) .220-.790 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.200) .210) 90th .2-dichlorovinyl)- CAS No.2-dichlorovinyl)-2. The presence of cis-3-(2.200-.35) 1.330) .12 (. < LOD means less than the limit of detection.270 (.380-.490-1.2-Dichlorovinyl)-2.110-.68) . but it can also reflect exposure to cis-3-(2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11) .570 (.630) .910-5.68 (. 1999).Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.202 (.460-1.200-.262) * * * < LOD < LOD .120-.47 (.08) .280-.670-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400-.630) .35) .770-1.770) .580-1.650-1.730 (.

representative NHANES 2001-2002 subsample (CDC.200) .840 (.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.270) . In a study of volunteers.710-3.138 (.300) .680-1. urinary trans-3-(2.900 (. Lu et al.67 (.270) .350 (.340) . In these volunteers.200 (.and trans-3-(2.190) . 2005).370-. urinary levels of cis-3-(2..350) . In a study of urban residents in Germany (Berger-Preiss et al.810 (.880) .29 (.260-.280 (.190) .67) .440 (.750 (.800 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.320) .430-1. 2002). 2005).540 (.640-1. 164 Fourth National Report on Human Exposure to Environmental Chemicals .240 (<LOD-. 2006.11) 1..2-dichlorovinyl)-2. 2003).400 (. 2006).590) .59) .210-.360-1.750-1.640-.300-.260 (.49) .300 (.2-dichlorovinyl)-2.450-. 2003)..2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .700-2. 2001) showed urinary levels of cis.690-1.560) 1..560) .290) ..11) .59 (1.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al..37) .440-.250) .33 (.24) .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.700) .600 (.540) .220 (.250) .250-.. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.290 (.220 (.170 (.390-.830) .530 (. the median and 95th percentile of urinary levels of cis-3-(2. In the same residents.410) .180 (.550) . 2005) In a small group of indoor pest-control operators.260 (.570) .03) 1.500 (.550-1.03) size 1951 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th . 2005).2dichlorovinyl)-2.S.12-2. median urinary levels of trans-3-(2.Pyrethroid Pesticides 2.700) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-dichlorovinyl)-2.190 (.510-1.380) ..170) < LOD < LOD < LOD .580) .120 (.780 (.290-.430-.140-.920 (.530 (.420 (.12 (.780) 1.180-.640) 1.and trans-3(2.580-1.170 (.680 (.370-.230-.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.300 (.59) .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.300) .470-1.380 (.550-1. 2002). the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.230-.33) .270-. Cyfluthrin. Survey Geometric mean (95% conf.290) .550 (..14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.540 (.640 (.430 (.250-.220) .280-.S.104-.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.200-..890) .150-. Studies in Germany of 396 children and adolescents (Becker et al.130-.400-1.2-dimethylcyclopropane carboxylic acid did not increase. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. 2006.440-. post- Urinary cis-3-(2.260) .80) .340-.11 (.890 (.250-. 2005).640-1.21) . 2006) and 1177 urban adults and children (Heudorf et al.2-Dichlorovinyl)-2.150-.260 (.710 (. 2004).11) .340) . 2004.370-.270 (.550) .390-.31) .2dichlorovinyl)-2.. population from the National Health and Nutrition Examination Survey.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .182) * * * < LOD < LOD .440 (. 2006).590 (.840 (.250) 90th .380-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.450 (.230-.200-.390 (. Schettgen et al.2-dichlorovinyl)-2.320-.080-.230 (. Other studies have provided evidence that urinary levels of cis. 2001.160 (<LOD-.250 (<LOD-.150-.680-1.450-1.

12-6.4 and 0. Urinary trans-3-(2.700) .620) < LOD 2.08-4.and trans-3-(2.910-1.16) 1.63) 1.680-1.40 (1.90) 1.60) 1.20 (.910-1.580 (.49-3.97-11.56) 2.Pyrethroid Pesticides application median urinary levels of summed cis. 2005).2-dichlorovinyl)-2.08-6.09 (.39-5.17 (. Survey Geometric mean (95% conf.54 (1.800-1.60-4.59 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.37 (1.08) 1.68-2.970 (.43) 2.84 (1.780 (.14-6. trans-Cypermethrin.7) 2.500) .560 (.85) 4.490 (<LOD-.11-1.440 (<LOD-.95) 3.420 (<LOD-. 2005).81) 2. population from the National Health and Nutrition Examination Survey.480-.470 (<LOD-.660) 1.730) .940 (.76-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.850-1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .64-4.810-1.07 (1.920-1.69 (1.410 (<LOD-.63) 1.55-4.03-1.or trans-3-(2.13) .2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect. which may vary for some chemicals by year and by individual sample.26 (.27 (1.460-.55-3.35) 1.460-.62 (1. Finding a measurable amount of cis.68) 1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . however. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.23 (.670) .28 (1. < LOD means less than the limit of detection.76-4.4.14) 1.400-.670) . The maximum post-application urinary levels.400 (<LOD-.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 .19 (3.42 (2.68) 1.49-3.66) 691 680 518 690 595 954 Limit of detection (LOD.28 (2.830-1.56) 2.01) 4. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.42) 1.55-5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.520-.39 (1.14-2.410-.60) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.01 (1.610) 1. Fourth National Report on Human Exposure to Environmental Chemicals 165 .700-1.56 (1.410-.20 (.410 (<LOD-.520) .22 (1.860) .11-2.750) .41 (1.17-1.490-1.560 (.710 (.470 (.41-14.19) 1.820) .570) 90th 1.S.68) 2.03-1.68-3.87 (1.07-3.2dichlorovinyl)-2.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.77) 1.56 (1.89 (2.77 (1.25 (1.48) 4.20 (.25-3.17 (.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .95) 2.2-Dichlorovinyl)-2.5) 2.10) 2.94 (1.91 (1.550 (.500 (.560 (.840-1.23) 2.49-5. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (1.66) .19 (2.530) .760) .77) 2.500-.69) 1. Biomonitoring studies on urinary levels of cisor trans-3-(2.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.54) 4.

640) .27-2.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.Pyrethroid Pesticides Urinary trans-3-(2.08 (.S.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .780) .55 (2.780 (<LOD-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.31) 1.07-2.42) 1.610-.00) 1.2-Dichlorovinyl)-2.67 (2.530 (<LOD-.970 (.22-1.07) 2.720-1.12 (.87 (1.900 (<LOD-1.730) .22-2.410-.880 (.26 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.81 (2.27-2.87) 1.720-1.56-5.33-2.45-2.87-8. trans-Cypermethrin. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.44) 2.30-6.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .64 (1.660) .00 (1.48 (1.480-.40-2.580) .36) 2.470 (.580 (.700 (.68) 3.89) 2.55 (2.00-5.70 (.86 (2.3) 2.13) .02-1.57) 3.48-2.770) < LOD 2.22) 1.39) 1.16 (1.440-.850) 1.87-3.42 (.36 (1.15 (1.00) 5.800-1.98 (1.540) .800-1.670) .520 (<LOD-.15-3.47-2.80) 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 .65 (2.700-.470-.57 (1.60) 2.880 (<LOD-1.750) .30-3.850) .75 (1.35) 1.500-.11) .35 (1.530 (. Survey Geometric mean (95% conf.65) 1.33-1.570 (.74) .39 (1.33 (1.880-1.20 (1.29) 1.820-2.34-3.28) 2.930-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.56-2.00) 1.15) 3.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.08 (.47 (1.15) 2.15-3.60 (1.07) 2.41) 1.34-4.56 (1.850-3.560 (.720 (<LOD-.55 (2.47-2.61) 1.91) 1.60) 2.740) .570 (<LOD-.91 (1.91-11.07-3.780) 90th 1.19) .31 (.37 (1.31 (2.15-3.13) 1.19 (1.20-2.570-.87) 1.12-1. population from the National Health and Nutrition Examination Survey.74) 2.07-1.700 (.45 (1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .760 (.

Barr DB. Schulz C.209(3):221-233. Butte W. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Sugiri D. Ranft U. Int J Hyg Environ Health 2002. Wieseler B. Int Arch Occup Environ Health 2003. Kuhn K. Hoppe HW. Seiwert M. Idel H. Int J Hyg Environ Health 2006. Lu C. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Pearson M. Int J Hyg Environ Health 2006. Angerer J. Levsen K. Ball M.209(3):293-299. Drexler H.Pyrethroid Pesticides References Becker K. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Heudorf U. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.134(1-3):141-145. Leng G. Leng G. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.77(1):67-72. Angerer J.62:101-108. Kolossa-Gehring M. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides.205(6):459-472. 2005. Angerer J. Drexler H. Heudorf U. Schettgen T. Environ Health Perspect 2006. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Biological monitoring of workers after the application of insecticidal pyrethroids. Ranft U. Leng G. Berger-Preiss E. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Permethrin and its two metabolite residues in seven agricultural crops. et al. George DA. Bravo R. Angerer J. Centers for Disease Control and Prevention (CDC). Heudorf U. Environ Health Perspect 2001.114(9):14191423.206(2):85-92. Sugiri D. Idel H. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Int Arch Occup Environ Health 2004. Heudorf U. Idel H. Hadnagy W.68(6):1160-1163.76(7):492-498. Int J Hyg Environ Health 2003. Bull Environ Contam Toxicol 1999.109(3):213-217. J AOAC 1985. Bartell S. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Hardt J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Angerer J. Berger-Preiss E.

2-dibromovinyl)-2. mean peak urinary levels of cis-3-(2.2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. Thus. in some situations replacing the use of DDT.. deltamethrin has been used against mosquitoes that carry malaria. urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. 168 Fourth National Report on Human Exposure to Environmental Chemicals . Following residential spraying with deltamethrin for malaria protection in Mexico.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 2005).S. Biomonitoring Information Urinary levels of cis-3-(2. 2005).2-dibromovinyl)-2. Outside the U.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dibromovinyl)2. in detection of cis-3-(2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.1 μg/L) for the NHANES 2001-2002 subsample (CDC. 2004).39 µg/L. 2001..2-dimethylcyclopropane carboxylic acid of 0. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount 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.2dimethylcyclopropane carboxylic acid formed in the environment.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. 1990).2-dibromovinyl)-2. 2006) and 1177 urban adults and children (Heudorf et al. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2001) showed that urinary levels of cis-3-(2.5 μg/L) than the detection limit (0.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dibromovinyl)-2.. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. (2004) reported a geometric mean concentration of cis-3(2.Pyrethroid Pesticides Deltamethrin CAS No... 2005). Baker et al. Deltamethrin can degrade to cis-3(2..2-dibromovinyl)-2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.3-0.2-dibromovinyl)-2. Studies in Germany of 396 children and adolescents (Becker et al.

which may vary for some chemicals by year and by individual sample.Pyrethroid Pesticides Urinary cis-3-(2. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 169 .2-Dibromovinyl)-2. population from the National Health and Nutrition Examination Survey.1.1 and 0. < LOD means less than the limit of detection. 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.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

2-Dibromovinyl)-2.S. 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 . Survey 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.Pyrethroid Pesticides Urinary cis-3-(2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

Centers for Disease Control and Prevention (CDC). Seiwert M. Heudorf U. Grimaldo M. Torres-Dosal A. et al. Carranza C. Butte W.113(6):782-786. Angerer J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Int Arch Occup Environ Health 2004. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.htm.77(1):67-72. Kolossa-Gehring M. Angerer J. Third National Report on Human Exposure to Environmental Chemicals.209(3):293-299. Lopez-Guzman OD. Environmental Health Criteria 97.Pyrethroid Pesticides References Becker K.inchem. Int J Hyg Environ Health 2006. Hoppe HW. 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. Ball M.209(3):221-233. Available at URL: http://www. International Programme On Chemical Safety (IPCS). 2005. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Heudorf U. Drexler H. Angerer J. Heudorf U.org/documents/ehc/ehc/ ehc97. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Int J Hyg Environ Health 2006. Deltamethrin. Environ Health Perspect 2001.109(3):213-217. and genotoxicity in exposed children. [online] 1990. Schulz C. et al. Batres LE. 5/26/09 Ortiz-Perez MD. toxicokinetics. Angerer J. Atlanta (GA).

. Saieva et al. 2005). Fenpropathrin Permethrin CAS No. 2003. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. 2003. 2006). 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 . The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. 2006) 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. Becker et al.. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2006. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.Pyrethroid Pesticides Cyhalothrin CAS No. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. In one study of 145 urban residents in 80 private homes in Germany. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 2005). Baker et al.. CDC. Thus. 52645-53-1 Tralomethrin CAS No. CDC. representative NHANES 2001-2002 subsample (CDC. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above... Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 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. 52918-63-5 use and house dust levels (Lu et al. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC.. A study of 396 German children (Becker et al.52315-07-8 CAS No. 2005). 2002. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2003).. 39515-41-8 CAS No. 2005). urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al. In a small group of indoor pest-control operators. In the New York City study. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al. CDC. 2005). Hardt and Angerer. 2005). 2005. 2005. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 2004).S. 2005). Following residential spraying with deltamethrin for malaria protection in Mexico. 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. 68359-37-5 Cypermethrin Deltamethrin CAS No.

292 (.450 (.233-.230-.46) .640 (.328 (.25-1.810) 1.76 (1.250 (.750) .16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .38 (2.590-.406) .340) 75th .267 (.1) 3.32 (1.560-1.03 (3.570-.710 (.570-1.18 (2.336 (.320) .34) 8.45 (2.33) .26) 2.850) .260 (.220-.200-.53-3.13 (.190-.295) .1) 3.29-1.300) .780) 4.430-.507 (.160-.90) 1.13) .800 (.25-4.12) 4.49-2.12) .27-2.250-.72 (1.387) .321 (.8) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.370) .271-. Deltamethrin.373) .49-2.21 (2.79) 3.65-2.05) 1.990) .26-2.750-1.314 (.250 (.288-. interval) .69) 3.190-.280 (.470-.590 (.730 (.353 (.820) .45-5.292-.30 (.314) .276-.71 (1.600 (.427) .300 (.73) 1.18 (1.417 (.390) .260 (.430-.510-.490-.23 (2.490) .83-11.04) .830-2.364) .35) 2.610) .12 (.320) .530-.320) .26) 2.60) .78) 1.49 (1.940) 1.374) 99-00 01-02 99-00 01-02 99-00 01-02 .800) 1.75 (1.34 (2.315 (.440) .64) 697 680 524 701 603 957 Limit of detection (LOD.41) 3.740 (.32 (2.39) 2.35 (1.260-.56-5.311 (.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 .434) .620-1.48-2.230 (.25 (2.320 (.250 (.27-11.33 (1.200-.870 (.51-3.62-6.01 (1.960 (.30) 3.247-.92-3.46) 2.230-.670 (.630) .35) 1.226-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04-5.428-.05) .246-.48-2.190-.1.53) 1.740 (.510-.41 (1.30 (1.300 (.530-.330) .230 (.35) 2.62) 5.253-.277-.560-.700-1. Fourth National Report on Human Exposure to Environmental Chemicals 173 .266-.454 (.93 (1.560-.25-7.350-.270 (.230-.41-2.86 (1.63-3.44) 5.298 (.16) 1.297 (.362) .52-4.62-8.16-1.288 (.240 (.160-.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.750) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.38 (2.190-.180-.355) .290 (.1) 3.34-6.550-.55 (1.680 (.265-.200-.830) 90th 1.50 (2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 . population from the National Health and Nutrition Examination Survey.63 (3.300 (.227-.520 (.78 (1.595) .32-21.420) .340) 1.700 (.850) .33 (2.52-5. Survey Geometric mean (95% conf.760 (.340) .65 (1.69 (1.330) .S.270) .210-.820) .28) 1.273 (.369) .325 (.260 (.27-2.43) 3.210-.320) .42-2.78) 6.41-3.1 and 0.360) .81 (1.54) 1.51-6.586) .384) .238-.840-1.89-71.14-6.352-.36) 1.601) .02-6.650 (.78) 1.49 (1.35 (2.25 (2.240 (.710 (.

35-3.480 (.309 (.36 (1.88-5.75-8.250 (. interval) .09) 3.299-.640 (.310) .39) 1.720) 90th 1.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .49) 1.590) .500) .43 (1.280-.91) 9. Survey Geometric mean (95% conf.290) .630) .16-4.590-1.270 (.261 (.420-.860-1.0) 3.930) .760) .48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .240 (.229-.52) 2.25-5.230) .238-.730-1.41) 1.173-.700-1.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.240-.960-1.64-5.S.07-5.19 (2.330) 75th .230-.00) 1.440-.44) 2.02-1.311 (.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 .49) 3.860-1.17 (.335-.19) 2.300-.309) .55) 3.423 (.550 (.52 (1.13-1.03-1.740) .40 (1.17-1.62) 1.323 (.43) 1.357) .05-3.02 (2.530-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.390-.320) .210-.440-.240-.200-. population from the National Health and Nutrition Examination Survey.226-.67) 1.410-.90) 3.316 (.83) 1.36-6.730) .60-4.590) .300-.224-.48 (1.202-.330) .63) 1.91 (2.640 (.330) 1.387) .227 (.510 (.490 (.35) .250 (.09-2.930) 1.234 (.84 (1.44 (1.04 (.35) 1.720 (.329) .00) 5.362 (.63-3.62) .94 (1.49-2.225-.09-2.550 (.670) 3.272 (.40) 2.35 (1.280 (.677) .80) 4.22 (1.330 (.190-.216-.446) .54 (1.540 (.178-.330) .13-1.270) .480-.380-.81 (1.272) .580) .560 (.730) .440-.329) .290-.378 (.264 (.72 (1.37) 1.21 (1.240 (.37 (1.230-.350 (.490 (.43 (2.67 (1.32 (2.510 (.312 (.220-.271-.860 (.200-.10 (2.437) .00) 1.07) 2.370-.60) 1.83 (1.220 (.460-.400-.274-.06-3.73-4.400) .380 (.21-4.372) .61-2.270) .401) .95) 1.650) .534) .253) .13 (.250) .200-. Deltamethrin.74) 3.278) .280) .19-6.86 (1.150-.96 (1.280 (.190 (.67 (1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.350) .450 (.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .570) .25) 2.240-.261-.49 (1.160-.240 (.09 (.43-64.41-4.270-.321-.91) .290) .15-2.200-.610 (.550 (.04 (3.27) 1.510 (.03 (.365) 99-00 01-02 99-00 01-02 99-00 01-02 .370 (.11 (.25-2.270 (.240-.490-.210 (.530-.460-.51-7.750-1.810) 1.246 (.11 (.590) .91-4.240 (.210 (.274 (.840-1.410) .280) .580 (.280 (.670) .400-.328) .55 (1.275 (.190-.53 (1.73) 1.

205(6):459-472.111(1):79-84.76(7):492-498. Obel J. et al.113(6):782-786.Pyrethroid Pesticides References Baker SE.209(3):221-233. Deych E. Berkowitz GS. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Biological monitoring of workers after the application of insecticidal pyrethroids. Bravo R. et al. Environ Health Perspect 2006. Barr DB. Torres-Dosal A. Environ Health Perspect 2003. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Idel H. Ortiz-Perez MD. Carranza C. Ranft U. Lapinski R. Levsen K. Kolossa-Gehring M. Third National Report on Human Exposure to Environmental Chemicals. Becker K. Olsson AO. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Centers for Disease Control and Prevention (CDC). Leng G. Berger-Preiss E. toxicokinetics. Pearson M. Grimaldo M. Sugiri D. Ball M. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Hadnagy W. urban cohort. Hoppe HW. Sugiri D. Ranft U. et al. 2005. Environ Health Perspect 2005. Hardt J. Int J Hyg Environ Health 2006. Berger-Preiss E. Angerer J. Bartell S. Lopez-Guzman OD. Liu Z. Atlanta (GA). Int J Hyg Environ Health 2002. Leng G. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Godbold J. Barr DB. Batres LE. Idel H. Int J Hyg Environ Health 2003. Exposure to indoor pesticides during pregnancy in a multiethnic. Arch Environ Contam Toxicol 2004. and genotoxicity in exposed children.114(9):14191423. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Lu C. Seiwert M.46(3):281-288.206(2):85-92. Int Arch Occup Environ Health 2003.

070 (<LOD-.095 (. and excretion of antimony vary depending on its oxidation state.250 (.07.112-.180-.320) . coal-fired plants.400) .117-.390-. population from the National Health and Nutrition Examination Survey.130 (.350 (.300-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.130) < LOD .130 (. 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.280 (.120 (.280) .350 (.134-.180-.310) .360 (.140) .190 (.210 (.270-.310 (. which may vary for some chemicals by year and by individual sample.140 (.120-.170-. castings.240 (.280) .154-.310 (.150 (.093 (. People are exposed to antimony primarily through food and.170-.130-.160) .070-.400) .080 (<LOD-.300-.120-.200-.470 (.120 (.350) .260) .250 (. Antimony enters the environment from natural sources and from its use in industry. and pewter.190) .108-.350) .130-.220-.200 (.180 (.510) .160) .260 (.180) . 01-02.250-.350-.200) .150-.120 (.144) .210) .135) * .170) .170 (.120-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220 (.190 (.350) .117-.087-.280-.119-.178) .120-.128 (.330) .130) .150) .310 (.134 (.210) .200) .240-.090 (.460 (.120-. ammunition.390-.100-.340) .250-.090-.280-.Metals Antimony CAS No.200) . water.160-.122 (.110 (. and 03-04 are 0.133) * .176 (.110-.200 (.410) .120-.250-.140) .190) .207) .220-.370-.119) .160 (.230 (.230-.260) .110-. solder.132 (.400 (.080) .090 (<LOD-.170-. distribution.200 (.04.500) .150 (. Stibine is a metal hydride form of antimony used in the semiconductor industry.310 (.160-.390 (.120-.190 (. Workplace exposures can occur at smelters.170-.460 (.160 (. interval) .300) .080) .440 (.250-.160) .330 (.04.280-.230) .157) .200-.160-.150-.300 (.160 (.430 (. 0. 0. fireworks.320) Total .260-.280-. enamels.175 (.220-.150-. see Data Analysis section) for Survey years 99-00.130-.160) .350-.280) .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 .350 (.136) * .126 (. metal bearings.270 (.250) .137) .710) .100 (.160) .150-.200) .300) .300 (.360-.190-.390) .320-.170 (.430 (.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 .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.161) .410-.390-.180-.400-.310-.080-.099 (.340 (.120) .180-.141-.130-. < LOD means less than the limit of detection.S.100 (.090) 75th .260) .330) . The absorption.140-.140) .500) .340 (.220-.360) .120 (.098-.360) .110-.130 (.390) .570) .470) .190 (.250 (.146 (.100-.490) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.130 (.103) .150) .108 (.430 (.105 (.310-.320 (.260-.140 (.140) .200 (.240) .210-.210-.230 (.184) .160) .100) . +3.190-.350-.095-. It is also used in paints.136-.090-.220) .600) .128 (.420) .130-.154) .200 (.120) .140) .180 (.154) .240 (. and refuse incinerators that process or release antimony.440) .300) .220-.210) .150) .170-.290-.270 (. to a lesser extent. from air and drinking water.145 (.220) .079-.110-.240 (.220 (.400 (. or other substances containing antimony is another means of exposure.330 (.169 (.130) .190-. It is used in metal alloys.180 (. and +5. storage batteries.140 (. and 0.142 (.560) .130 (.300-.400) .220-.230-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.143 (.156-.360 (.131-.164-.137) .350 (.230) .220) .330) .120 (.130-.280) .125 (.180 (.197) .109-.330-.126-.120-.330 (.230-. sheet and pipe metal.330-.114) .230) .290-.230-.320 (.180 (.140 (.230-. respectively.190 (.130) .140) . and glass.370) .310) . Dermal contact with soil.320-.150) 90th .088-.070 (<LOD-.123 (.158 (.440) .390) .180) .330) .190-.148-.130 (.270) .260 (.132 (.320-. and as a fire-retardant in textiles and plastics. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.150 (.200-. 7440-36-0 General Information Antimony is found in ores or other minerals.270 (.190) .190) .530) .460 (.460) .200 (.260 (.240-.350) .150-.210 (.280 (.120-.200-.130 (.145) Selected percentiles ( 95% confidence interval) 50th .120) .210) .115-.210) .180-.130-.290 (. ceramics.110) .240 (.220) 95th .120) .190) .470) .320-.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 .190-.270 (.270) .400 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .115) .130 (.350 (.240 (.410) .490 (.390) .230 (.180 (.280-.

391) .119 (. interval) .136) .338 (.147-.253 (.417) .163 (.238) .100 (.364 (.176 (.121 (.200) .205-.338 (.112-.271-.357) .156 (.278) . species.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 .148-.098-. liver.149) .268) . 1986).159-.181) .229-.164 (.106-.200-.154-.373) .265-.131 (. population from the National Health and Nutrition Examination Survey.235-.102-.117-.178-.143) 90th . 1986).203) .333 (.253-. Inorganic antimony salts irritate the mucous membranes.108-.138 (.124-.255-. skin.421) .209-.082 (<LOD-.191 (.167 (.159-.129) .471 (.193 (.280-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.225) .238 (.277 (.318-.121 (. 1954).175 (.097-.089) .098-.092-.320) .213 (.118 (.185-.267 (.135) .139 (.241-.116-.196 (.125 (.099-.228-.236 (.085) .076-.152) .194-.244-.S.167 (.227-. and kidney have been demonstrated in high dose animal studies depending on the dose.288 (.143) Selected percentiles ( 95% confidence interval) 50th .Metals than for trivalent compounds (Elinder and Friberg.317) .181) .207) .357-.128-.444) .084) .405) . abdominal pain.148) * .333 (.095-.242-.195 (.250-.123 (.074 (.081 (<LOD-.352) .121) .170 (.098) .111-. and eyes.130 (.185 (.187) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .247) .245) .109 (.082) . 1944).133) .134) .127) .135 (.115) .109-. and ulcers (Werrin.132) .226 (.160 (.199-..113-. 1962)..082) .176 (.115-.120 (.272) . myocardium.208-.109 (.102-.238) .117-.104-.162-.300 (.087) .179-.259 (. 1988.152) .129 (.294) Total .068 (.741) .429 (.107-.429) .209 (.075 (.480) .108-.061-.444) .125-.112 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.108-.222 (.320 (.113-.310) .115 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.333) .139 (.161) .250 (.230) 95th .114 (.233 (.164-.146-.118 (.145) .189 (.310) .143) .137 (.107-.385 (.130) .239-.333 (.119-.127) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.080 (<LOD-.134) * Sample size 2276 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .069-.076-.250-.068-. Histopathologic inflammatory and degenerative changes in the lung. diarrhea.313-.186) .075 (.203) .116 (.318-. 1973).138-. Ming-Hsin et al.124 (.146-.256 (.079 (<LOD-.257) .198) .209) .183) .173) .267) .233) .250-.321) .096-. Acute antimony poisoning may cause a metallic taste.228 (.230-.120 (.135) .192 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.414) .192) .138) * .214) . and route of exposure (Elinder and Friberg.30) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.161) .248) .310 (.122 (.095-.120 (..250-.320-.104-.135 (.263 (.071-.278 (.081) .127) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .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.127 (.308-.115-. and gastrointestinal symptoms such as vomiting.143) .343 (.300) .192-..217 (.127) .425) .263-.149-.298 (.132 (.119-.122 (.135) .224 (.120 (.471) .430) .447 (.176-.130) .267-.371 (.159-.126 (.167 (.173 (.255) .228 (.315) .206-.286 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.364 (.320-.115 (.438) .129) * .173 (.069-. 1958) and occupational exposures (Briegner et al.333-.250) .143 (. 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.114 (.352 (.164) .171) .209) .188-. 1995).741 (.727) ..185 (.295 (.107-.266 (.250 (.172-.276 (.333-.115 (.188) .112 (.103-.333-1.193) .220) .195-.265 (.163 (.167-.338) .151) .153 (.156-.333-.126) .108 (.500) .200-.195-.181) .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 .131) .138-.173-.308) .281-.146-.485) .113) . 1953).233-.182 (.130) .147) .400 (.178 (.225 (.280 (.106-.153-.208 (.140) < LOD .124) .146) .211) .391) .150-.320 (.124-.111 (.417) .114 (.144-.086) 75th .131-.080 (.103-.126-.078 (.148-.317) .200-.204-.077) .380 (.086 (.150-.105-.092) .140) .248-.317) .099-.129 (.261) .123) .117-.269 (.241-.

46:931-936. External and internal antimony exposure in starter battery production. Biological monitoring of exposures to aluminum. Kiberd B. Petrucci F. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Liao Y-H et al.51:238-240.. Review of elements in blood. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Ju-Sun P. 1991.S. Delves HT. Mayne P. Liao Y-H. Pilgrim L. 2002.59:469-474.76(2):103-115. 1986. 2004. Schacke G. Piatnek DA. arsenic. Third National Report on Human Exposure to Environmental Chemicals.. Urinary antimony in infancy. Handbook on the toxicology of metals.158:165-190. Nau CA. Costeloe K.16: 33-39. Weltle D.atsdr.13:361-362. 20012002.. In: Friberg L. Dunkelberg. Sabbioni E. Minoia C. Friberg L. Pietra R. Schaller KH. Stone FD. and 2003-2004. Stocks J. Fuchs A. Bailly R. Antimony trioxide is rated by IARC as a possible human carcinogen. Matthews T. Sci Total Environ 1994. Shao-Chi C.. Dezateux C. Wade A. Cheng-Wei L. Skulsukai G. et al. Lenert G. 1995.e. Apostoli P. Kuo-Juie Y. indium. Hamilton EI. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Atlanta (GA). Element reference values in tissues from inhabitants of the European community. Industrial Medicine 1944. and hydrogen sulfide. Carelli G. O’Regan M. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Arsine. Suchenwirth R. Yang C-Y. Iavicoli et al.. Stead FM. Ming-Hsin H. Antimony. pp. clinical efficacy. Vouk VB. J Clin Pathol 1998. Ho C-K. Chia-Yu H. VI. 1990. Buchet JP. Roland H. Iavicoli I. eds.521-523. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. 2nd ed. Kentner M. even when exposure levels were below workplace air standards (Bailly et al. respectively. Industrial Medicine and Surgery (Dec.html. Stasney J. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Ludersdorf et al. Kentner et al. Nordberg GF. and future strategies. Biomonitoring of a worker population exposed to low antimony trioxide levels. New York: Elsevier. Yu H-S. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Chemotherapy for leishmaniasis: Biochemical mechanisms. Wu M-T. 1998) or compiled reference ranges (Hamilton et al. Mahieu P. et al. Dernehl CU. EPA. Pozzoli L.64(2):182-185. Leinemann M. Sabbioni E.48:93-97. gov/toxpro2... stibine. Luedersdorf R. Chest 1973. Centers for Disease Control and Prevention (CDC). Van der Venne MT. Elinder CG. 1998. Mayer P. J Trace Elem Med Biol 2002. Arch Dis Child 1997. Gallorini M. and a drinking water standard has been established by the U. which may be due to methodologic. Chin Med J 1958. 1994) have reported values slightly higher than those in this Report. 1997).. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Alimonti A. Earlier measurements in general populations (Minoia et al. 2005. Caroli S.67:119-123. Chen J-R. Pulmonary edema of environmental origin. Int Arch Occup Environ Health 1995. Rev Infect Dis 1988.. HH. Bolten C. gallium. 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.106:33-39. Briegner H.. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Gebel TW. Br J Ind Med 1991. Int Arch Occup Environ Health 1987.cdc. 1987).76:432436. Lauwerys R. Environ Health Perspect 1998. environmental levels) and health effects is available from ATSDR at: http://www. et al. References Berman JD. Cullen A. Information about external exposure (i. Trace element reference values in tissues from inhabitants of the European community I. Konings J. or exposure differences. plasma and urine and a critical evaluation of reference values for the United Kingdom population..Metals to antimony have been established by OSHA and ACGIH. Industrial antimony poisoning. Biological assessment of exposure to antimony and lead in the glass-producing industry. Paschal et al. Antimony in blood and urine of infants. Dezateux et al.)1954.10(3):560-586. Cordasco EM. and antimony in optoelectronic industry workers.. 26-42. Delves HT. population. J Occup Environ Med 2004. 1998). Semisch CW.

Ting BG.Metals in urine. Morrow JC.95:89-105. Renes LE. blood. Werrin M. 27:38-45. Trace metals in urine of United States residents: reference range concentrations. Environ Res 1998. Industrial Hygiene and Occupational Medicine 1953. Paschal DC. Fourth National Report on Human Exposure to Environmental Chemicals 179 .99-108.76(1):53-59. Sampson EJ. Chemical food poisoning. Sci Total Environ 1990. et al. Antimony poisoning in industry. Pirkle JL. and serum of Italian subjects. Jackson RJ. Quarterly Bulletin of the Association of Food and Drug Officials 1962.

to a lesser extent.00 (6. it is found in over 200 crystalline or mineral forms.84) 8.50-14.77) 6.9) 21.4 (26. mental disorders.5) 95th 65.2 (41. Although it is still widely used in the United States. the smelting of copper. population from the National Health and Nutrition Examination Survey. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.30 (6.57) Selected percentiles ( 95% confidence interval) 50th 7. 180 Fourth National Report on Human Exposure to Environmental Chemicals .5 (34. Also. cancers.02-8. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90 (5.90-7. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.90-11. though in some locations arsenite may be prevalent (WHO.0 (14.90) 16.8 (48. and gray forms).10 (6. Arsenic and its compounds have had many uses in the past and present as medicines.41 (7.29 (8.3-111) 78.9-62.2-17.34-10.0 (22.1 (38.10) 10.4 (31. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.80-9.7-95. and.8) 17.90-8.6-35. ocean and fresh waters.5) 66.5-41. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. gaseous hydride manufactured in small quantities for use in the semiconductor industry.7) 24.74. and in lead-acid storage battery grids. Various arsenic compounds were used in paint pigments and for tanning animal hides.4 (7.90 (7.40) 7.4) 40. In the last century. 2005).0-19.12 (6.4 (48.3-19. Survey years 03-04 Geometric mean (95% conf. Since the 1940s.9-46. 2001).8-61.6-43. and foods.2) 46. to a lesser extent.30 (7.97) 8.19-9.5 (23.80 (5. lead.6) 11. from coal burning.9 (8.6 (13.10-7. Arsenic trioxide (As2O3.3) 10.4 (24. black.70 (6.2 (12. trimethylarsine oxide.6 (32.3) 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 7.0 (43. and play sets. and as homicidal poisons.2-61.5) 41. solders. The United States no longer produces arsenic from mining but imports about 22.84) 8.00-9. arsenic as elemental metalloids may be used in some ammunition. and indium arsenides are used in the semiconductor industry. Arsenic is measurable in most soils. and as a cosmetic to lighten complexion. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.2-93. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. aluminum. particularly arsenic trioxide.5 (36.2 (13. such as arsenopyrite (FeAsS) and realgar (As4S4). meats.0 (11.4-65.50 (8.3-15. cacodylic acid.5-52.30) 17. Before the 20th century.0 (15.8) 33.8) 30.8) 34.1) 7.6 (9. sodium arsenite.5-19. see Data Analysis section) for Survey year 03-04 is 0. referred to as inorganic arsenic compounds. and produce.12-10. lead hydrogen arsenate. pesticides. In nature.34-9.9 (17. as alloy in metal bearings.20 (8.6 (15.9-34.9) 68. arsenocholine.4) 60.8-77. interval) 8.80) 6.1) 15.27) 9. arsenites. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.90-14.4) 13.6) 618 722 1074 Limit of detection (LOD.25-9.8) 7. and arsenates (oxidation states of -3. grain.1) 1281 1276 03-04 03-04 03-04 9.7-83. semiconductors. mostly for use in wood preservation (ATSDR.1 (32.08 (5.2 (51.5-178) 46. or rarely as elemental metalloids (yellow. Arsenic trioxide is approved to treat acute promyelocytic leukemia.1-18.2) 15.Metals Arsenic CAS No.5 (40. General population exposure to inorganic arsenic can occur through consumption of drinking water and.13-8.70) 8. Water sources contain mostly inorganic arsenate.55 (7.90) 75th 16.70-9.90 (7.1-40.5) 43. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. Gallium. copper arsenates. were used as treatments for syphilis.6-141) 53.1) 290 725 1542 03-04 03-04 9.90-8.0-60.8) 29.7) 65. arsenic compounds.8) 7. psoriasis.7) 90th 37.000 metric tons annually.7 (11. and arsenosugars. Arsine (AsH3) is a reactive. alloys. +3 and +5).10-10. retaining walls. and other metals.66-8.S.2-20.5 (14.

88) 7.7) 28. 2001). 2001). 2001).5-120) 40.0-69.3 (24.S.S.1) 6. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.4 (12.64 (7.93-9. 2001). gallium arsenide and indium arsenide. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. but is poorly absorbed dermally (WHO.93-8. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.0) 33.7) 95th 50. 2001. 2006. have caused clinical arsenic poisoning.4 (40. age. selenium.0-18.07-9. Extremely high groundwater arsenic levels.38-10. mine tailings).8 (27. cacodylic acid and monosodium methyl arsenate.3) 6.32 (5.2) 15.8 (11.75 (5.4) 54. Fish.9 (45..0) 26. In aquatic organisms.25 (6. EPA. Survey years 03-04 Geometric mean (95% conf. organic arsenic can be converted back to methylated and inorganic arsenic.41) 6.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . WHO.7-188) 27. as observed in Bangladesh where millions of people have been exposed.30-9..88 (5. Gamble et al.3-64. interval) 8.0-38.0) 42.06 (4.8) 27.00 (6.6 (35. and some other seafood can contain organic forms of arsenic including arsenobetaine.3) 9.0) 14.44-11.2-15.96) 12. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.4 (42.66-8. trimethylarsine oxide (TMAO).2-46.45) 5..7 (11.4-64.44) 6.9) 53.8 (20.8 (21.1) 8.04 (5. 2007.3-62.4 (11.3-53. are used in enclosed ultraclean operations within the semiconductor industry.2) 40.11 (5.0-26.04) 7. 2006. Direct exposure to DMA and MMA may result from use of the two pesticides. Tseng. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. 2007. 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. though some reduction may occur in the gut prior to absorption. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. and folate status (Chen et al.12-10. 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. shellfish.81-9.0) 12.23-7. Smoking tobacco is also a source of inorganic arsenic.7-35.6 (17. 2001).35) 7.S. Children may have additional exposures from ingestion of contaminated soils (e. The semiconductor dopants. 2001.2 (12.4 (24.66 (7. kelp. inorganic arsenic is widely distributed within the body. arsenic does not show biomagnification in the food chain (WHO.5 (9.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.2) 90th 30. dose level.10-8..47 (6.8) 22.58-10.5) 17.24 (7.5) 290 725 1542 03-04 03-04 8. WHO.33-10. population from the National Health and Nutrition Examination Survey. Inorganic forms of arsenic demonstrate high acute toxicity.0 (17.1-36. 2001).7-34. In aquatic sediments.8-32.0 (31.20-9. Though modest bioconcentration occurs in some aquatic life.4) 32.1 (11. NRC. U.75) 13. 2003.51) 75th 14.76 (6.31 (6.01) 7.66-8.10-16.4 (26.18 (5. 2001). 2007.8 (12. 2001).7 (25. After absorption.9-56.7-18.g.59) Selected percentiles ( 95% confidence interval) 50th 7. and arsenosugars.6) 45.9) 13..8-62. dust.33 (6. arsenocholine.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. EPA’s maximum contaminant level (Hughes.6 (10.28-7.47 (7.8-75. Chowdhury et al. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.1) 58.1) 7.61 (7.25-9..6-17.40) 8.1 (14. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. 1988).47-6. Steinmaus et al. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.7 (9. so exposure to the general population is extremely limited.3-41.01) 11.86-17. Arsenate is reduced in the body to arsenite (oxidation state +3).3 (27.0) 1281 1276 03-04 03-04 03-04 8.13) 8.5-17.99-9.50 (6. and contact with CCA-preserved wood structures.7-17.1) 24.

30) 1. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. WHO. hematocytopenias. < LOD means less than the limit of detection.80) 1. hyperkeratosis. cell transformations. see Data Analysis section) for Survey year 03-04 is 1. 2004). and by uncoupling oxidative phosphorylation (NRC..0.20 (<LOD-1. Laboratory studies using inorganic arsenic have shown chromosomal aberrations..EPA has established drinking water. NRC. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.60) 1. Cellular glucose uptake.. 2001. and altered gene expression.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.. Chronic elevated arsenic intakes have been associated with diabetes. and DNA repair inhibition (Cohen et al.. 2004). substitution in phosphate metabolism. renal failure. including inhibition of numerous enzymes. Bangladesh. lung. Chronic arsenic exposure in humans is considered to be a cause of skin.20 (<LOD-1. 2007. including drinking water sources with elevated arsenic levels (e.. WHO. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Cohen et al.20 (<LOD-1. 2001). population from the National Health and Nutrition Examination Survey. 2000. 1998. and diarrhea. respectively. and childhood neurodevelopmental effects in observational human studies. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. Chronic human intake of arsenic at less than acutely toxic doses. 2006. fatty acid oxidation. Chile). hepatotoxicity.g. noncirrhotic portal hypertension. 2001..10 (<LOD-1. 2007).S.. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. Survey years 03-04 Geometric mean (95% conf.50) 1.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and hyperpigmentation of the skin (NRC. gluconeogenesis.10 (<LOD-1. which may vary for some chemicals by year and by individual sample. Studies of arsenic at levels typical of U. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. drinking water have not been associated with increased cancer rates (Schoen et al. 2006) or when exposure occurs in smokers (Chen et al. U. The U. 2001). Such actions may lead to decreased energy production.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways.S.S. WHO. Bredfeldt et al. With chronic exposure.20 (<LOD-1. and endothelial injury (Kumagai and Sumi. some of these effects may take years to develop. and it also will inhibit succinate dehydrogenase. Raml et al. vomiting.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. can cause peripheral sensorimotor neuropathies. 2001).g.50) 621 725 1078 Limit of detection (LOD... The organic forms of arsenic occurring in seafood have little known toxicity. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. and bladder cancer (IARC. WHO.60) 1.. 182 Fourth National Report on Human Exposure to Environmental Chemicals . cytotoxicity. hypertension. Cardiac arrhythmias.10 (<LOD-1. Taiwan. 2001). 2004. 2001). 2007. but additional or confirmatory research is needed (Kapaj et al. 2006. leading to a decrease in adenosine triphosphate energy production. arsenic trioxide) includes hemorrhagic gastritis with nausea.10 (<LOD-1. 2006.S. which can lead to dehydration and shock. Acutely. interference in signal transduction pathways. Arsenic has many actions demonstrated in cellular studies. Although arsenate is reduced in the body to arsenite. NRC. peripheral vascular disease.EPA.10 (<LOD-1. and production of glutathione may be affected as well. 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. increased oxidative stress. food residue.. 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. 2001). apoptosis.

Compared with this Report..Metals compounds.S. population from the National Health and Nutrition Examination Survey... 2008..75 (<LOD-2. 2007. median urinary total arsenic levels in 4052 adults varied with seafood intake.69 (<LOD-3. Caldwell et al.41) 3. 1998.. 2006). gov/toxpro2. In the German Environmental Survey III of 1998. DMA produced bladder cancer in some chronic rat studies (Cohen et al. 2006.. population in NHANES 2003–2004 (Schulz et al... 1999).. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.18 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 2001).19) 3. 2004. Meza et al. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.S.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.50) 1.S. Pellizzari and Clayton 2006). 2003. In animal studies. 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. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Josyula et al. 2006. 2007. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. Caldwell et al.atsdr.33 (<LOD-3. Shalat et al. 2006). Pellizzari and Clayton.04 (<LOD-3. population (Rubin et al. 1999. 1999. Valenzuela et al... Vahter et al. Calderon et al..S. environmental levels) and health effects is available from ATSDR at: http://www. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al.html.. Levels of total urinary arsenic in the U. 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. 2006).. Offergelt et al. 2000.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2001).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006). and the FDA has established a bottled drinking water standard.e. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. Consequently. Additional information about external exposure (i. 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 3.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. In a Nevada town where groundwater levels were naturally elevated. WHO..18) 3.00) 1. arsenic has been fetotoxic and teratogenic.cdc. Shalat et al.... 1986). but generally only at maternally toxic doses (WHO..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.80 (<LOD-4.. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 2000). Survey years 03-04 Geometric mean (95% conf.33 (<LOD-3.61 (<LOD-3. 2008). although urinary arsenic levels were not associated with CCA contact (Shalat et al. 2004. 2001). had decreased since the prior 1990– 1992 survey. 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. Pellizzari and Clayton. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1992.75 (<LOD-2... 2008). and were about two-fold lower than those for the U. 2006. 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.

2008). which may vary for some chemicals by year and by individual sample. For residents of Inner Mongolia. Individually measurable species resulting from inorganic arsenic exposure are arsenate.48-2. 2003).6 (25.2 (6.600 (.7) 15. Some noncancer effects of arsenic (e.40-7.80 (.4-35. 1. arsenite. arsenite. Blom et al.. 2001.1-51. Arsenate.6 (13. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine..45 (1.20-190) 31..30) 10. Survey years 03-04 Geometric mean (95% conf. China..5) 621 725 1078 Limit of detection (LOD. Valenzuela et al.6. 2005. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3) 95th 35.3 (9. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.50) 90th 16. 2008).70-21.30 (1.43-1.400-.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 * * 1.800) 1. methylation capacity.8 (17. In most human studies.20-3.7-22...g. When seafood intake is avoided. Caldwell et al.4. arsenocholine..6. 2006).00 (.S.40) 75th 5. 2001).70) 6. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. Caldwell et al.0-23.800 (.500-1. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. interval) 1.0 (26. 2000. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.19 (.871-1. 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. when seafood organic arsenic is subtracted). Caldwell et al.20 (2.17-1.1-25. population in the NHANES 2003–2004 subsample..Metals other areas of the world (Ahsan et al.20) 7.2-35. Pellizzari and Clayton. 4.80 (4.7 (13. geometric mean levels were about 70-fold higher than for the U.11-1. Caceres et al.70 (5.20 (.80 (3. 1996...60) 1.700-1.S. and duration of exposure are also considered important.900 (.29 (1. arsenobetaine.00-12..40) 5. 2005.800-4. population (Sun et al.20-25.3% of a representative sample of the U.50-6.20) 3.1) 45. 1985. and TMAO were detected in only 7.8-40.S..800 (.4) 23. and two methylated metabolic products.00) 3. see Data Analysis section) for Survey year 03-04 is 0.5) 29.31-1. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.6-44.60-3. After recent seafood ingestion.9 (7.3-39.S.1-94.700-1.28) 1. Sun et al. Measurable organic arsenic species in this Report are three biologically generated environmental forms.5 (26.30) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..70-21. 2000. 2008.0 (27. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.9 (6.00 (1.2-38.9) 13.00-4..e.6 (11.55 (1. with DMA. Tseng et al.40-6..10 (4. WHO.10) 8.900-1. 2008). 2005.800-1.7) 13.62) 2. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. 2000.3) 35.37 (1.5) 292 728 1548 03-04 03-04 1. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. These associations are stronger at higher urinary levels.. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.90-29. in NHEXAS 1995–1996.83) Selected percentiles ( 95% confidence interval) 50th 1.30 (2.. 2007) with higher levels of arsenic in the drinking water. 184 Fourth National Report on Human Exposure to Environmental Chemicals . and 0.0) 29. 2008.20 (4.20 (1. population from the National Health and Nutrition Examination Survey.7 (21. arsenocholine.8) 35.05) < LOD . dermal keratosis. In the residents of a Chilean town who consumed water with high levels of arsenic.50) .90-7. respectively.1) 18. and TMAO.00-6. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. Chowdhury et al. population showed a higher contribution of arsenobetaine (Caldwell et al. MMA.5 (14. 1990. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. 2007).8 (12.50) .9-23.66 (1. 2008). population (Ahsan et al.74 (1.80) 1.5) 32.. and other factors such as nutrition.. vasospasm.00-1.8.10) 4. Aposhian et al.0) 4.3 (21.93) 1.S. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.8-50.3) 1284 1284 03-04 03-04 03-04 1. Also..4) 31. The higher percentiles of total urinary arsenic levels in the U. In the late 1980s. < LOD means less than the limit of detection.80-5.4 (16.68) .20) 18.70 (3. DMA and MMA.

7) 9.37-2. 1986.0-36.7) 17.1-36.4) 13.4 (24.12) < LOD .64-29. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998.9-18.61-6. 2001).0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.83) 8.6-46. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.50-15..10 (.28) 1. 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. not to imply a safety level for general population exposure.Metals as with DMA.6) 19.43) 14.54 (1.30-1.2 (12.S.53 (.3 (10.55) 1.531 (.938-1.47 (2.78 (3. 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.82) Selected percentiles ( 95% confidence interval) 50th 1.80-153) 17.19-2.11 (.36) 2.3-24.43) 75th 5.47 (1. 2007).13-39.9) 32.877 (. Survey years 03-04 Geometric mean (95% conf.45) 1.8) 29. which is below the ACGIH BEI (Caldwell et al.32-7.51) 5. population from the National Health and Nutrition Examination Survey. Information about the biological exposure indices is provided here for comparison. 1992.2 (12.9) 14.638) 1.4) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1.833-1.4-28.6-29. 2008)..80) . Timber treatment workers had median urinary DMA levels that were about 15-fold higher than the general adult median levels reported in NHANES 2003–2004 (Morton et al.05 (.2 (4.79 (1.30) 1.83) 2.16 (. interval) 1.612-1.4 (11. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9 (25. WHO.. 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.58 (3.29-14.93 (1.51-2.5-20. 2001). Caldwell et al.18-1.6 (6.40) 1. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.29 (4.73-6.15-4.05) 1.67) 4..9 μg/L.. 2006.65 (1.2 (13.3) 95th 29. 2008).1-18.1 (26.0 (9.7) 30.39-3.5 (18.50-7. Offergelt et al.14 (1..4) 32.6 (9. population for the sum of inorganic related species was 18.4-82.82) 4.15-1.4-21.67) 1.5) 26. 2003.15-1.72) 12. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH.70) 5.88) 2.88 (5.909-1.91 (4. Sun et al.68 (1.00 (1.78-5.25-7.00 (3.25 (.901-2.81 (4.786-1. Vahter et al.40 (1. Fourth National Report on Human Exposure to Environmental Chemicals 185 .91) 90th 16.6-32.5) 17.400-.9 (13.21) 5.5 (18.3 (10.76-27. In recent years.44 (1.4) 292 728 1548 03-04 03-04 1.S.62-6. The 95th percentile of the U.3) 1284 1284 03-04 03-04 03-04 1..1) 26.959-1.

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

Survey years 03-04 Geometric mean (95% conf.20 (<LOD-1. which may vary for some chemicals by year and by individual sample.00 (<LOD-2. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.95 (<LOD-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.44) 2.S. Fourth National Report on Human Exposure to Environmental Chemicals 187 . population from the National Health and Nutrition Examination Survey.00) 1.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 1.00 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 3.80) < LOD 621 725 1078 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.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 1.2.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.08 (<LOD-4.40 (<LOD-1.

60-3.08 (2.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .95 (4.88 (4.92-12.00 (5.00-5.4 (7.00-15. interval) 3.25 (4.9) 5.16 (2.0) 14.00-4.17-4.60-6.24-4.0 (8.73 (3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4. interval) 3.0 (9.0-17.1 (8.84-8.0 (13.57-5.78 (4.0) 11.50 (4.00-13.00) 9.65-6.71 (3.81 (5.22) 4.00-9.20-12.00-11.00) 5.31-4.70-12.00 (3.45) 8.55 (2.S.15) 4.0 (12.00) 6.12 (3.00-8.06) 5.74 (2.9 (7.11) 4.5) 95th 13.0-16.0) 16.86 (2.95-6.0-16.05) 10.29-4.80) 7.34-4.00-4.6-18.0-19.69 (3.03-6.0) 9.00-7.00-10.39-3.70-4.19) Selected percentiles ( 95% confidence interval) 50th 3.86-7.0 (10.7) 12.85 (3.00) 75th 6.18 (6.10) 6.16-11.7) 13.05) 3.14) Selected percentiles ( 95% confidence interval) 50th 3.95-3.00 (5.50-15.00 (5.60-4.0-12.00 (4.0) 9.00) 4.90 (3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.3 (8.34) 3.1-22.52) 3.42) 3.0 (9.00-4.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) 90th 11.80) 2.00 (7.71-4.10) 3.1-18.03 (3.28) 2.84-18.00-12.00 (5.6 (9.38 (3.80-6.0) 17.69-6.69 (3.17 (2.48 (3.78) 4.45 (8.50-5.1-15.0) 16.00) 3.0) 13.67) 9.34 (3.65-8.49) 10.34-4.14) 3.71 (4.16 (4.00) 6.9 (11.90) 5.00-7.0 (9.80 (4.00 (6.69-3.37 (2.46 (4.11 (3.45) 3.0 (8.00) 7.33-4.95-4.91) 75th 5. see Data Analysis section) for Survey year 03-04 is 1.00 (6.0) 11.70 (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.32 (8.49-4.74) 90th 9.0) 12.70) 5.0 (14.0) 621 725 1078 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf.00) 12.0) 13.00-15.00 (7.8) 7. population from the National Health and Nutrition Examination Survey.0-18.80-5.S.00-22.31) 4.17-6.7 (10.0 (12.37 (3.0) 95th 16.00-4.2) 10.3 (7.00 (3.0-25.30 (7.00-7.27 (2.67) 8. population from the National Health and Nutrition Examination Survey.00) 6.0-17.59 (6.44 (2.8) 7.32-10.61-11.80-3.9) 12.00-7.12-4.7-16.97-3.82-9.00) 3.09 (7.7.0 (10.60-7.34 (3.71) 3.00-11.00-15.72 (4.90) 2.9) 13.27 (3.3 (8.30) 3.00 (3.82-5.5) 12.5 (11.05) 5.77 (3.32 (4.33) 3.57 (3.24) 3.62) 4.73) 6.13-4.94-3.0) 9.9) 11.89 (3.0 (13.98) 4.00-12.48 (2.0 (11.20-4.94) 3.00-3.0 (10.61-16.27-2.00 (6.82) 3.0 (10.6) 292 728 1548 03-04 03-04 3.92) 3.20) 11.27-5.00) 4.00) 6.86-21.7) 1284 1284 03-04 03-04 03-04 4.00 (5.6) 1284 1284 03-04 03-04 03-04 4.00 (3.0) 17.00-3.00 (3.79 (3.0) 10.00-4.0) 292 728 1548 03-04 03-04 4.70-3.44) 5.00-11.00 (3. Survey years 03-04 Geometric mean (95% conf.

05-1.22 (1.00-2.35-3.30) 1.16 (2.985) 1.20 (1.60 (1.20 (1.53 (1.70-2.90 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.40 (2.52 (2.90) 1.81) 1.40) 2.88-2.17) 2.18-1.30) 1. population from the National Health and Nutrition Examination Survey.36 (1.00 (2.S.77) 1.10) 95th 2.60) 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 1.70-2. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.57) 95th 2.60) 1.33 (1.30-1.46 (1.00 (<LOD-1.79) 2. Survey years 03-04 Geometric mean (95% conf.20 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.34) 2.50-2.22) 3.80) 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.46-2.80-2.80 (1.10 (<LOD-1.86 (2.00 (1.73-2.10-1.50 (2.9.80 (1.80-2.07) 2.86) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (<LOD-1.88 (1.853-1.10 (.86 (2.62) 2.80 (2.20 (1.10 (1.20 (1.43-3.50) 1.30) 90th 1.816 (<LOD-.90 (2. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.70-3.31 (1.28 (1.10-3.30-2.18-1.61) 2.40-3.30 (2.88 (1.40-2.00 (2.20-1.00-2.28 (1.37 (1.58) 2.61-3.10) 2.50) 621 725 1077 Limit of detection (LOD.10 (1.40 (1.71-2.00) 2.900-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15-1.90) 2.50 (1.90) 2.36) 1.40-3.10 (.20 (1.82-2.30) 2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00 (<LOD-1.82-2.07 (1.07-3.00) 2.40-2.45) 3.00-4.53-2.20-3. which may vary for some chemicals by year and by individual sample.33 (1.84-3.10-1.40) 1. see Data Analysis section) for Survey year 03-04 is 0.40) 1.80 (1.00-1.70) 2.54) 90th 2.30 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.85) 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .80 (1.00) 1.30 (1.23) 1. Survey years 03-04 Geometric mean (95% conf.60-2.20) 2.96-2.60 (2.S.00) 1.85) 1.30-1.63 (<LOD-1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.00-1.86) 2.70-2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.93) .70-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.31-3.11-1.30 (1.00) 1.80) 1.50 (1.14-1.60) 2.

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

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50 (1.69 (1.70) 1. glass.25-1.40 (5.50 (4.49) 4. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.37-8.73) 3.51 (1.30-2.80 (2.24-1. Barium salts have also been available as rodenticides.05% of the earth’s crust.94-6.70-8.78) 1.40 (5.54) 2.85 (2.35 (1. In single dose animal studies.30) 5.80 (2.90) 1.40 (1.70) 7.21-2. Barium compounds are also used commercially in paint.30) 4.35-1.42 (1.45 (1.35 (2.41) 1.46-1.07 (2. such as brazil nuts.4) 6.99-5.50-6.20-8.56 (2.39) 1.73 (6.43 (1.91 (2.12 (2.S.04-2.14 (6.71) 1.35-4.27 (1.60-2.95-6.72) 4.43) 2.11 (3.20 (1.78-2.60) 1.50-6.41-3.26-7.50 (1.82) 1.12) 6.63 (8.45) 7. Workers employed by industries that make or use barium compounds can be exposed to barium dust.18 (6.21-8.57 (5. 0.75) 2.44-5.52 (1.46) 1. 2001).35-1.10 (2.56 (6.80-3.31-2. such as barium chloride.49-1.81-2.00) 4.10-5.43 (1. it combines with other chemicals such as sulfur or carbon and oxygen.68 (1.61 (2.85) 1.59-11.35 (3. tiles.50-1.56) 1.36-1.80-2.50) 2.90-2.10) 3.93-8.70) 3.20-1.86 (4.48-4.65-5.54 (2.20-8.16) 5. and 03-04 are 0.70-3.52 (4.00-76.70) 4.12-1.29-1.62 (1.15-11.14-1.76-2.11 (2.20-5.63 (2. Barium compounds are used by the oil and gas industries to make drilling muds.60-3.73 (5.40) 7.82-6.60 (1.59) 3. bricks.60-10.88) 4. population from the National Health and Nutrition Examination Survey.53) 1.Metals Barium CAS No.60) 4.65-1. Some barium salts are freely soluble in water.50 (4.56) 4.72) 75th 3.64-3.39-1. depilatories.50 (4.70 (1.49) 11.80 (1.00) 1.30-2.15 (1. 7440-39-3 Medically. whereas others are practically insoluble (e.50 (1.10 (4.38) 8.30 (1.90-13.00 (2.12.90 (1.43 (5.47) 4.50) 2.70 (5.82) 2.33 (1.54) 1.88) 1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .73) 1.38) 2.39) 4.61 (1.75-3.61 (1.60) 1.86-4.18-1.32-7.57-7.47-1. fireworks.00) 6.21 (1.26-1.32) 8.73-5.80-7.46) 1.76) 1.51) 7.61 (5.09 (1.37-1.34 (2.40 (4.38 (1.62) 1.4) 9. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.29) 5.71 (2.40) 3.05-2.14-6.49) 2.35) 5.60-6.49-9.93 (4.06-1.50 (1.91) 2. are high in barium (Genter.50) 4. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).50-1.20 (4.88 (5.10 (3.19-1.48 (6.20 (3.2) 6.28) 90th 5.40 (5.20-1.37) 1.48) 1.30-1.1) 9.96-2.8) 9.49 (1.97 (1.43) 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 1.00-8.44-2.87 (6.81-2.86 (4.63) 1.76-7.99 (4.63 (5.60 (2.30 (5.77-3.81-3.36) 5.30-5.30-1.64 (1.20-6.10) 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 1.71) 95th 6.78) 1.12) 7.00 (1.74-3.36 (4.80-5. barium sulfate and barium carbonate).54-1.62 (1.29-5.19) 2.24 (4.53-5.41-1.26) 5.50 (5.49) 8.90 (6.66) Selected percentiles ( 95% confidence interval) 50th 1.03 (1.02 (7. rubber.12 (2.36-1.86) 6.31 (2.39 (1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.77) 1.16 (1..20-1.11 (3.34) 2.76 (3. In nature.70-5.50 (6.54-1.20-1.22) 6.85) 1.34 (1.86-5.40 (1.01-7.65) 1.24-1.84) 5.04-6.47-1.50 (3.62) 1.31.15-1.40 (1.28-1.91) 6.01 (4.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.32-1.22-1.44 (1.98) 1.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.50) 1.11-1.71) 2.34 (1.22-1.72) 1.66 (4.77 (3.56 (1.87 (5.8 (6.30 (5.57) 3.48) 1.20) 2.8) 5. soluble forms of barium.63 (1.g.95 (4.70) 5.27 (1.87-7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 7.40-13.4) 7.00-3.27) 2.51) 2.80 (1.65-8.10) 5. and 0.61-8.87-14.55-7.48-4.36 (1.53) 2.90-9.30 (3.80) 7.30) 3.55-3.18) 3.61 (3.9) 5. 01-02. see Data Analysis section) for Survey years 99-00.90) 2.54) 1.65) 3.74) 3.26) 2.30-3.17-1.15) 5.30) 8.65) 1.78-3.90) 2.90 (4.88) 7.67) 6.63) 1.93-2.70-2.30) 5. and food.56 (1.63) Total 1.20-8.38 (1.37 (4.50 (2.92) 2.30) 2.60-6.51) 1.08-8.09 (2.80 (5. The general population can be exposed to low amounts of barium in air.06-2.37) 5.74-2. Small amounts of barium can be released into the air during mining and other industrial processes.39 (1.65 (5.12.70) 1.50 (1.80) 1. and ceramics.80 (1. Certain foods.08 (6.87-3. interval) 1.25-11.10-4.43) 6.71-9.21 (1.70-2.54-8.15 (6.15-1.15 (2.80) 6. water.30) 5.87-9.25 (1.70-6.87) 7.90) 4.76-3.00) 1.60) 3.54 (6. respectively.30 (2.

Barium is not rated for human carcinogenicity.30 (1.44-2.37-2.37-1.2) 6.29 (1.3 (6.36 (3.54 (1.24-1.99 (4.97 (5.45) 1.29-4.28-7.29) 1.27) 7.96) 7.40-1.24 (5.963 (.20-1.91-2.45-6.921 (.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 1.51) 4.22-1.49 (1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.56-3.24-1.52) 2.32 (2.48-1.54) 2.38 (1.880-1.57-7.38-5.24-11. Symptoms following acute high dose include perioral paresthesias.22-2.46) 1.03) 2.75-22.50) 2.72) 4.10-1.63-4.33 (5.26-1.39) 4.24 (3.68-3. Chronic high doses in animals resulted in kidney damage (McCauley et al.86-7.89 (2. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.58) 4.3) 6.02-5.23-1.13-2.02 (3.62 (2.01) 1. The health effects of exposure to barium compounds depend on the dose.97) 1. are not absorbed when administered.31) 5.96) 4.23-2.38) 1.48-5.25) 4.75) 2.710-1.46) 3.33-4.55 (1.77) Total 1.46-22.00-1.00) 6.22-4.49-1.51 (1.08-2.38 (4.53 (2.83) 3.52-4.58) 75th 2. 1989).77) 1.42 (4.43-6.19-1.02) .39 (3.59) 1.24-6. interval) 1.47 (5.76) 2.06) .39-1. such as those used in medical radiographic procedures.41 (1.60 (1.47) 1.55-6.47-8. 1984.11) .38) 4.54) 1.75) 1.26-1.96 (4.90-2.20) 4.53-21.45-1.777-1.38-7. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.19-1. paralysis.43) 1.00 (2.20-8.80) 3.49-1.12) 2.70) 1.30) 2.39 (2.36 (1.84) 2.33 (1.78 (2.915 (.48) 2.14-2.832-1.25-11.38) 1.53) .10 (6.57-5.64 (1. vomiting.60 (5.42) 1.24-6. hypertension.62) 2.72 (2.75) 2.60) 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 2.74) 1.39-1.92) 2.91) 2.63) 1.47 (2.36-1.29-4.64) 7.28-6.55) .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 1.40 (1.03-1.77) 1.44 (1.45) 95th 6.98 (2. Wones et al.55 (1.28-11.41) 5.09) 6.39-10.44-2. weakness.58) 1.21 (1.96-6. 1986).36-2.62 (4.29 (3.40 (1.80) 4.27-1.51 (3.2 (3. 1990).45 (3.31 (1.58-6.0) 7.81-6.27-3.31-1.28-1.46 (2.25 (1.32 (1.60 (2.48 (1. Insoluble barium salts. 1985.891 (.88 (2.11) .04 (2.16-1.20 (1.703-1.13-3.99) 1.88 (6.19-2. Following intravenous injection in animals.86 (2.51) 6.67-6.4 (5.71 (5.54 (2. water solubility.39 (2.38-1.51) 4.35-1.56) 4.75-3.76 (2.48 (1.91 (3. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.76) 2.50) 1.56 (1.84 (3.881 (.0) 5.34-5.62 (1. 2001).34 (1.60 (2.68 (3.00-7.34-1.36 (1.50 (4.82) 1.31 (4.03-1.57-10.47) 1.00) 4.68 (3.58 (2.81-7. chemical form.19-1.38 (4.69 (5.31-1.49 (1.68) 3.73-4.30 (1.01 (5.24) 3.87) 1. population from the National Health and Nutrition Examination Survey.70) 4.27 (2.20-2.84-2.61 (4.60 (1.68 (2.73) 2.48 (1.35-3.55-5.97-4.85-5.32) 2.55 (5.77) 5.10-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.51 (1.02) 4..31-1.33) 1. Toxicity from soluble barium salts is rare.37 (1.03) 1.40 (1.Metals was eliminated primarily in feces and to a lesser extent.79) 1.50) 1.96 (4. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.41 (1. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.59) 2.32 (1. Perry et al.66 (1.00 (3.00) 1.64) 7.36 (3.29-7.46) 2.96) 4.00) 4.33-1.77) 1.34-3.80-6.33 (1.55 (4.01 (4. NTP.99 (2.57 (6.64 (1.61) 2.29-3.52-10. 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.10) 3.64 (1.26-1.58 (4.2) 5..75) 1. 1994.04) 1.754-1.37 (1.26-4.16) 11.84-5.41 (2.22-1.39-5. diarrhea.33) 6..06) 2.39 (2.82) 1.56) Selected percentiles ( 95% confidence interval) 50th 1.76 (4.24-3.74) 1.04) 5.47) 4.28) 5.34) 1.45-8. and cardiac dysrhythmias.91 (3.70) 10.38 (1.92 (4.42) 1.52 (3.28 (1.15-4.56 (1.16 (1.48-3.4) 5. in urine.59) 1.47) 10.65 (2.52) 1.45-1.05-1.18 (1.32) 2.52) 7.8) 4.72) 6.86) 5.76-3. and route of exposure.81-6.41) 4.905 (.35-1.65 (5.03) 3.0) 6.68) 1.83) 2.89) 90th 4.00 (3.79-5.64 (1.59-7.37) 2.97 (4.18 (1.00 (5.76 (3.97-3.11-2.26-1.45 (1.51-3.96) 4.77-5.36 (5.57) 2.59 (1.68-3.49-1.59 (1.08-1.36-1.26) 4. a benign condition that may occur among barite ore miners.10) 6.76) 1.29-1.69-9.S.73-2.27) 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 .23-5.74 (5.

EPA. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. 2001-2002. Trace metals in urine of United States residents: reference range concentrations. p. Howerton K. Paschal et al. Perry EF.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). ed. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Nordberg GF. 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.niehs.S.. Advances in modern toxicology. pp. Atlanta (GA).html?charset=iso-88591&url=http%3A//ntp. 4/8/09 Paschal DC.atsdr.html. 1998). Pietra R. Laurie RD. PS.95:89-105. New York: John Wiley & Sons. blood.. Levy. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Handbook on the Toxicology of Metals. Exposure to soluble barium compounds: an interventional study in arc welders. 1994.. Sci Total Environ 1990. the welders had no obvious adverse clinical effects (Zschiesche et al.nih.niehs. et al. In: Inorganics in drinking water and cardiovascular disease. et al. Minoia C.gov/toxpro2. New York: Elsevier. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.76(1):53-59. patient population and literature reference intervals for urinary trace elements. Powell C. LA. strontium. Third National Report on Human Exposure to Environmental Chemicals. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Clin Chim Acta 2000. and serum of Italian subjects. 2005.. Douglas BH. barium. Magnesium. Pirkle JL. 1990. Wones RG. Vol 2: Specific Metals. Frohman.nih. Sampson EJ. Investigations into the effect of drinking water barium on rats. Available at URL: http://ntp. [online].28(3):373-388.e. 2nd Ed. Zschiesche W. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report.. Princeton NJ: Princeton Scientific Publications.. Reeves AL. 2005.. Centers for Disease Control and Prevention (CDC). et al.S. Apostoli P. Perry HM. ed. et al. References Brenniman GR. 84-94. Environ Health Perspect 1990. calcium. Gallorini M. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Schaller KH. Jr.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Comparison of representative ranges based on U.cdc. A study of 46 elements in urine.197210. Environ Res 1998. Minoia et al.gov:8080/cs. Lack of effect of drinking water barium on cardiovascular risk factor. Patty’s toxicology. Morrow JC. NTP. Cohressen B.64(1):13-23. 5th ed. Barium. 221-252 Komaromy-Hiller G. 1989. 2001. Int Arch Occup Environ Health 1992. Trace element reference values in tissues from inhabitants of the European community I. Fourth National Report on Human Exposure to Environmental Chemicals 195 . 2000) to levels in NHANES 1999-2000 and 2001-2002. Information about external exposure (i. Sabbioni E. In Friberg L. Ting BG. Stadler BL. and 2003-2004 (CDC. Jackson RJ. J Toxicol Environ Health. Biomonitoring Information Levels of urinary barium reflect recent exposure. Genter MB. eds. In: Calabrese EJ. 231-249. Pozzoli L.. 1986.296(1-2):71-90. Epidemiological study of barium in Illinois drinking water supplies. Costa R. eds. p. Vouk VB. 1984. Ash KO.gov/ntp/htdocs/LT_rpts/tr432. and a drinking water standard has been established by U. Inc. Princeton (NJ): Princeton Scientific Publications.. p.85:355-359. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Weltle D. and radium In: Bingham A. environmental levels) and health effects is available from ATSDR at: http://www. National Toxicology Program (NTP). 1992). Calabrese EJ. McCauley PT. Kopp SJ. 1985.

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 . soil. bertrandite and beryl. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.Metals Beryllium CAS No. or drinking water containing the metal.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. Low-level beryllium exposure in the general population can occur through breathing air. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. which may vary for some chemicals by year and by individual sample. 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 . are mined for commercial recovery of beryllium. and from breathing tobacco smoke. nuclear. and machine-parts industries.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 . population from the National Health and Nutrition Examination Survey. and volcanic dust. and dental bridges. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. coal. respectively.13. computer. In medicine. the lightest of all metals. see Data Analysis section) for Survey years 99-00.13. and 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. near some hazardous waste sites.13. electrical. beryllium is used in instruments. x-ray machines. and 03-04 are 0. 0. Beryllium compounds are commercially mined. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.140 (<LOD-. and refined beryllium is used in mirrors and special metal alloys for the automobile. aircraft. < LOD means less than the limit of detection. Exposure to beryllium occurs mostly in the workplace. In studies of laboratory animals.130 (<LOD-. 196 Fourth National Report on Human Exposure to Environmental Chemicals . Two types of minerals. eating food. and can be found in mineral rocks.S. 01-02. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 7440-41-7 General Information Pure beryllium is a hard gray metal.130 (<LOD-.

Maier.391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 1990). Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. which produces pneumonitis.231 (<LOD-.273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Chronic beryllium disease. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. or berylliosis. EPA. IARC has classified beryllium as a human carcinogen. based upon excess lung and central nervous system cancers in studies of workers. 2002). Fourth National Report on Human Exposure to Environmental Chemicals 197 . population from the National Health and Nutrition Examination Survey. 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. S.346 (<LOD-. NTP considers beryllium to be a known human carcinogen. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. including contact dermatitis and subcutaneous nodules. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. and drinking water and environmental standards have been established by U. 2003. Skin exposure can result in delayed hypersensitivity reactions.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 . 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.

Trace element reference values in tissues from inhabitants of the European community I. environmental levels) and health effects is available from ATSDR at: http://www. Paschal DC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 1998).S. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. 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. 20012002.atsdr. and the 95th percentile for males in NHANES 2001-2002. Hamilton et al. Review of elements in blood.Metals (i. Van der Venne MT. Howerton K. Given these results. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Ting BG. Element reference values in tissues from inhabitants of the European community. Environmental Health Criteria.13 μg/L. 2000.cdc. Clin Chest Med 2002. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect.org/documents/ehc/ehc/ ehc106.. Comparison of representative ranges based on U. Pietra R. Minoia C. 0. 1990. Sci Total Environ 1990. 1990.76(1):53-59. et al. Morrow JC. A study of 46 elements in urine.htm. Centers for Disease Control and Prevention (CDC). Available at URL: http://www. Hamilton EI. 2001).S. Ash KO. Am J Epidemiol 2003.e. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. blood. 198 Fourth National Report on Human Exposure to Environmental Chemicals . References Apostoli P. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Schaller KH. et al. less than 0. Andrew M. Environ Res 1998. McCanlies EC. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures.296(1-2):71-90.23:827-839.158:165-190. In other studies. Beryllium [online].. They reported urinary beryllium levels ranging from 0. Atlanta (GA) 2005. 106. Minoia et al. Costa R. Trace metals in urine of United States residents: reference range concentrations. Sabbioni E.95:89-105. Int Arch Occup Environ Health 2001.1 μg/L).gov/toxpro2.. Apostoli P. Pirkle JL. Maier L. Pozzoli L.12 to 0. Sci Total Environ 1994. Sampson EJ. and the fact that most NHANES participant levels were undetectable. population were generally undetectable in NHANES 1999-2000. International Programme on Chemical Safety (IPCS). Genetic and exposure risks for chronic beryllium disease. Kriess K.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.74:162-166. and serum of Italian subjects. Clin Chim Acta 2000. Third National Report on Human Exposure to Environmental Chemicals. Jackson RJ. Weston A. population are lower than levels in workers. it is likely that urinary beryllium levels in the U. and 2003-2004. HLA-DPB1 and chronic beryllium disease: a HuGE review..inchem.157:388-398. Levels of beryllium in urine for the U.html.S. which approximate this Report’s limit of detection. 3/27/08 Komaromy-Hiller G. Sabbioni E. patient population and literature reference intervals for urinary trace elements. Gallorini M. Paschal et al. VI.e.

500 (.449) Selected percentiles ( 95% confidence interval) 50th .400) .300 (.500-.600-.500) .30-1.313 (.20 (1.20) 1.500-.300) .300-.80) 1.700) . 01-02.600) .600 (.200) . coatings and plating.500) .10 (1.400 (.600) .400) .60 (1.500-.300-.3.300-.20) 1.00 (.30 (1.400-.300-.00) .376-.289-.300 (.300 (.80 (1.400) .400-.600 (.300-.200 (.10) 1.600) .3.400 (.20) .300 (.427) * .600 (.500) .200 (.300) .500 (.50) 1.00 (.424) * .309-.400-.333 (.10 (1.40-1.300-. Since 2001.00-1.400 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .00-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300) .600-.425 (.S.400 (.300-.400) < LOD < LOD < LOD .367-.30) .900-1. and incineration of municipal waste materials.400) < LOD .10) 1.10) 1.10 (1. and 03-04 are 0. U.441) * .60 (1. and nonferrous alloys.300) .600) .200 (.00-1.900-1.10 (.900 (.337) .500 (.300) .600 (.90) 1.300-.400-.00 (.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 * * * * * * .00-1.40 (1.300 (<LOD-.10 (1.386-.600 (.30-1.300 (.30-1.900-1.300 (.10) 1.500 (.400-.200-.400 (.296-.900 (. 0.500-.500) .400 (.800) .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 .382 (.10 (1.368-.40-1.300 (.400 (.50-1.500 (.400 (.S.304 (.00 (1.468 (.300 (. lead.00 (.40 (1.300-.500-.10) 1.400) .200-.500-.275-.800 (.14.500 (.600) .40) 1.20) 1.600-1.600 (.600 (.300 (.300) .30-1.20-1.513) . plastic stabilizers.470) * .500-.600 (.900-1. malleable.usgs.300) .300 (<LOD-.500-.900-1.266-.800-1.700) .00) .20) 1. EPA.20-1.50 (1.500-.10 (1.00 (.300-.00-1.500 (.600) .40 (1.40 (1.300 (.700) .400-.700-1.344) .500 (.70) 1.460) .70) 1.200-.50-1.359-.400 (.50 (1.60) 1.300-.S.400-. interval) .300-.50) 1.80) 1.700) .300-.300-.300) .60 (1.300 (.400) .300 (<LOD-.400) .600 (.452) .500-.403 (.20) 1.362-.420 (. or copper smelters (U.400) .00-1.500-.400) .283 (.50 (1.20-1.304 (. Cadmium also may be emitted into the air from zinc.20-1.700) . cadmium use has declined in response to environmental concerns (http:// minerals. as zinc sulfide) and to a lesser extent.60) 1.500) .200 (<LOD-.900-1.600 (.500-.378 (.800) 1.412 (.421 (.400 (.300) .20) 1. which may vary for some chemicals by year and by individual sample.300-.300) .800-1. see Data Analysis section) for Survey years 99-00. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.800) .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400 (.600) 1.300 (.20 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.70) 1.20) 1.800 (.500-.10) 1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.400 (.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .300-.200-.10) 1.00-1.20) 95th 1.10) 1.500) .50 (1.20) 1.400) .600) .400 (.30) 1.400-.700) .500-.326 (.20) .Metals Cadmium CAS No. The predominant commercial use of cadmium is in battery manufacturing.60 (1.400) .200 (<LOD-.300) .500-.20-1.300-.366) * * .60-1.400) .426-.400 (.50) 1.400) < LOD .900-1.900-1.600 (.900-1.600 (.50-1.300 (.700) .400 (.200) .10 (1.235 (.400) .300 (.331) .600) .00 (.40) 1.400-.300-.400-.255) .600 (.00 (. and 0. respectively.00 (.900-1.398) < LOD < LOD < LOD < LOD < LOD < LOD .500-.30-1.400 (.393 (.300) .40 (1.600) .361-.600) 90th 1.700 (.300-.500-. during refining of lead and copper from sulfide ore.400) .403) . < LOD means less than the limit of detection.300) 1.304-.300-.500) .60) Total * .400) < LOD . Other uses include pigment production.400-. population from the National Health and Nutrition Examination Survey.40 (1.60) 1.00 (.378-.216-.300 (<LOD-.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.300) .300) 75th .600-.500 (.20-1.300-. 7440-43-9 General Information Cadmium is a soft.395 (.600 (.700) .30) 1.400) .40 (1.00-1.60 (1.70) 1.700) 1.700-1.700-1.gov/minerals/pubs/commodity/cadmium).00 (.00-1.400 (.00 (1.30) 1.50-1.20-1.500-.

818 (.870) .191-.260 (.191-.200 (. rice.481) . see Data Analysis section) for Survey years 99-00.329 (. Kikuchi et al.238-.810-1.17 (. 01-02.607) .092 (.17 (. 2004a. including many food crops such as cereal grains.222) .322 (. copper) and protein.128 (.48 (1.366-.201 (.279 (.886) .22 (1.47) 1.13) .498-.151-.281 (.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 .680 (.892 (.362) .178-.551 (.12 (.452 (.20 (1.262) . 2001).183-.233) .550 (.17 (.110-. drinking water is a source for cadmium intake.09-1.500) .257-.640) .195-.02-1.919) .848 (.72) 1.25) 1.519) .223 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.316 (.01 (.210 (.193 (. calcium.390-.230 (.078 (.490) .990) .249) .087-.447 (.284) .235) .112-.717-.476-.289-.387) .308) .210 (.713) .482) .265) .918-1. zinc.480) .36) 1. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.394-..240-.886-1.153-.530 (.207-.700-.940-1.06) .090) .839 (.790 (.354) .980-1. Horiguchi et al.766 (.336) .430) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.285-.04 (.545 (.184-.705-.610) .426 (.192-.232 (. and 03-04 are 0.081) .206 (.13 (.714-1.580) .800 (.372) .260-.30-1.290-.559 (.208-.214-.189) .790 (.330-.32 (1.890 (.433-.980 (. Cadmium is absorbed via inhalation and ingestion.38) . Cadmium in soil is absorbed by plants. ingestion through food is the largest source of exposure.445 (.255) .. To a lesser extent.302 (.733) .210) .193-.229) .170-.199 (.160) .490) 1.230) .892-1.115-. Cadmium absorption may be increased with iron deficiency (Berglund et al..270 (.450 (.19) 1.15 (. and various seeds.880) .15) .261-.231) .270 (.191 (. With chronic exposure.239 (.243-.135 (.157) .519) .04 (.080 (. however.28 (1.238) .388-.06.060-.836-1.170 (.686-.273 (. 2003.206) .20-1.194-.077 (.219 (.210 (.17) . 2003).972 (.246) .173) .S.216 (.507) .800-.265 (. Renal tubular and glomerular damage.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .109 (.061 (<LOD-.510-.067-.393-.20 (1.400-.24) 1.211-.06.Metals 2000). whose body burdens of cadmium can be approximately twice that of nonsmokers.530) .** Survey Geometric mean (95% conf.170-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.41 (.077 (.03) .171-.730-.858 (.. The kidney is a critical target and shows the earliest sign of cadmium toxicity.310) .34) 1. respectively.350 (.360) .06.38) 1.255) .306 (.280 (.13-1.229) .241) .257) .977) .623) .963-1.300) .107-.551) .220-.28) 1.196-.220 (.479) .141 (.980-1. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.10 (1. 2003).175 (.381-.20) 1.165-.090) .43) 1.134) .28-1.299) .806) .227 (.436-. Diamond et al. 1994).233) .412) .440 (.101) . interval) .470-.820) 1.140 (.596) .255) .38) .263) .221 (. 0.339) .211 (.741-1.310 (.820-1. For nonsmokers who are not exposed to cadmium in the workplace.326) .219 (.192-. and 0.210 (.12-1.38) 1. 2003).440 (.135-.200-.114-.210) .150) . an inducible metal binding protein.733-.121 (.450 (.190-.221) .160-.065-.466 (.180 (.813 (.327 (.52 (1.226) .295) .202-.169-..220) .875 (.136) . potatoes.458 (.209 (.539) .980) .237-.283 (.230) 75th .493-.187 (.589 (.500) 90th .22 (.960) 1.219 (.400-.817 (.277 (.100-.07-1.26) 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.092) .130 (.960 (.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 .366-.423-.06-1.249-.148-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.247) .820 (.061-.234 (.763-.510) .202 (.700-.74) 1.240) .875) .150-.980) .475 (.440-.203 (.390-.160) .200-.175 (.51 (1.189-. 1999.320) .260-.01) .855-1.109-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.989-1.57) 1.204 (.126) .01-1.203) .456-. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.282 (.181 (.179-.251) .229-.272-.220-. Inhalation of cigarette smoke is a predominant source of exposure in smokers.890-1.200 (.190-.748-1.313) .700-.06-1.198) .232) .633-1.633 (.540) .445 (.253-.157-.366) .167-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .190-. population from the National Health and Nutrition Examination Survey.430-.390 (. wheat.189-..492 (.351-.753-.15) 1.843-1.210 (.82) 1.817 (.455 (.148) . The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.261-.160 (.83) 1.462 (.177-.520-.860) 1.067-.25 (1. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (1.120 (.300 (.

690-.085-.296 (..666-.143-.097) .184-.490 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.432 (.806-1.241) .221-.645-.491-.281) . interval) .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.719 (.917) .201-.289) .551) .979 (.210 (.537-. 1996. Jarup et al.140-. Horiguchi et al.783) .559-.267 (.647-.917 (.826-1.338 (.225) .199 (.300-.126 (.686 (.05) 1.700 (.391-.335 (.202 (.077-.700) .08) .071 (.147 (.07) .170 (.168-.225) .078-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.100 (. 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.884) .414-.516-.311) .229) .147-.562-.38) .336-.235) .212 (. 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. Olsson et al.617 (.163) .381-.754) .136-.148 (.321) .253) .303) .146-.382) .518) .232) .650-..187-.218) .268 (.545) .156 (.950) .433-.784) .940 (.191-.387 (.226) 75th .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 .208 (.423-.219 (.769 (..476) .13) .607) .415) .10) 1.247-.278) .131-.388-.850) .783 (.472) .185 (.208-. 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.929) .560-.329 (.085 (.674-1.234-.423 (. 2002.865 (. 2004b).02 (.210 (.104) .191 (.176 (.140-.175 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .159 (.182) .101) .242) ..536 (.161-.818) ..325 (. Staessen et al.198) .182) .16) ..487 (.206-.826-1.690 (.418-.261-.06 (.067-.074-.962) .181 (.159 (.178) .194-.757 (.716-.364) .484 (.143) .** Survey Geometric mean (95% conf.716) .304) .261 (.622 (.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.209) Selected percentiles ( 95% confidence interval) Sample 95th .111-.653) .687-.479 (.839) .856) .16) 1.377-.318 (.190 (. 2002.712 (.191) .440) .228-.729 (.767) .541) .187) .941 (.107) .173 (.232) .211 (. 1999).414 (.223) .316 (.856 (.830-1.227-. 2004).297) .175-.288) .274) 1.718 (.531 (.725-1.827) .678 (.688-.470) . 1999).255-..075 (<LOD-.182) .919 (.247-.412 (.631) .316) .727-.184-.123-.222-.245 (.174-.084 (.289) .667) .740 (.083-.293-.792 (..449) .238-.382-. During the 1950’s and 1960’s.426-.873 (.250) .181 (. However.687 (.147-.00 (.094) . can result from high dose chronic exposure.802 (. 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.282 (.267 (.308) .340) .779 (.387-.418) . 2000.931 (.470) .185) .12) 1.14) 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 .196 (.693 (.874-1.813-1.220 (.630-.183 (.136-.614) .501 (.239-.308 (.170-.215 (.818) .137 (.176 (.234) .481 (.199-.224 (.238) .168-.909-1. 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.216-.789 (.156) .204-.352) .288 (.07 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.343-.233 (.106) .533) .150-.757) .240) .207) . population from the National Health and Nutrition Examination Survey.175 (.168 (.261) .500-.084-.833-1.708-1. most often a result of occupational exposure (Roels et al.927-1.123-.446) .156-.350) .281) .207-.421 (.273 (.247-.270 (.162 (.431) .998) .304-.331 (.209) . At lower environmental exposures.143-.441-.828) . 2002.210) .876-1.135) .197-.157-. 2003.830) .236-.219 (.S.078 (.438) 90th .795) 1.266-.440) .538) .122 (.173-.200 (.404) .183) .144-.154 (.256-.091) .678-.767 (.253 (.075-.221 (. 1999).137-.096) .850) .266) .090 (.668-.112) .940-1.063-.171-.906) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th . Fourth National Report on Human Exposure to Environmental Chemicals 201 .434 (.09 (.00 (.691-.104) .177) .240) .444-.205 (.17) .234 (.280 (.184) .190 (.192) .086 (.181-.696-.178-.154-.985 (.166 (.130-.113-.051-. Noonan et al.091 (.663 (.093 (.288-.098) .591 (.292) .252 (.091 (.690-.189-.158-.404 (.398-.438-.813-..163 (.157-.722-.507-.473 (.263 (..263-.283 (.181) .

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

Environ Health Perspect 1994. Lundh T. Serra J. Choudhury H. Uemura T. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Miyamoto K. patient population and literature reference intervals for urinary trace elements. Toxicol Lett 2004. Ash KO. Bregante G. Fourth National Report on Human Exposure to Environmental Chemicals 203 . diabetes mellitus. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Toxicol Appl Pharmacol 2004a.57:668-672. Environ Res 2004b. ShkiryakNizhnyk AZ. Kaus S. Becker K.gov/toxprofiles/tp5. possibly better than b2microglobulin. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Sasaki S. Machida M. Anthropometric.110:699-702. Bellerup P. Comprehensive study of the effects of age. Costa R. Bernard A. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Kumagai N. Environ Res 2006. J Toxicol Environ Health 2003. Seifert B. Thayer WC. Friedman LS.13(11):1627-1631. Fayers PM. Int J Hyg Environ Health 2002. et al.45:43-52. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Machida M. Elinder CG.59:497]. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. References Akesson A. Centers for Disease Control and Prevention (CDC). Taylor AJ. 196:114-123. Ukai H. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Komaromy-Hiller G. Venables KM. Ikeda Y.46:372-374. et al.96:353-359. Int Arch Occup Environ Health 2003. Horiguchi H. 102:10581066. Fukui Y. Hellstrom L. Chislovska NV. Cadmium fume inhalation and emphysema. Ye T.24:717-724. Ezaki T. Okamoto S. Schulz C. Lukyanova EM.atsdr. et al.html. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Berglund M. Davison AG. Moriguchi J. Fatal chemical pneumonitis due to cadmium fumes. Ikeda Y. Ezaki T. Pickering CA.S. et al. Lancet 1999.59:194-8. Miyamoto K. Vahter M.66(Pt A):2141-2164. Wang H. Dekio F. Akesson A. et al. Jin T. Tsukahara T.000 women in the Japanese general population: a nationwide large-scale survey.296(1-2):71-90. Agency for Toxic Substances and Disease Registry (ATSDR). environmental. Mascagni P. Vahter M. Lepom P. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Jarup L. 1999 [online].Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population. Hotz P. Olfactory function in workers exposed to moderate airborne cadmium levels. et al. Neurotoxicology 2003.95:20–31.354:1508– 1513. iron deficiency. Horiguchi H. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Seiwert M. Fernandez MA. Greves HM. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Nerbrand C. Tsukahara T. 206:15-24. Kaus S. Schulz C. 4/8/09 Alfven T. Kikuchi Y. Environ Health Perspect 2002. Occup Med 1996. Carlsson MD. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Bo M. Oguma E. et al. Nordberg G.76:186-196. Furuki K. Lidfeldt J. Howerton K. Lison D. Grubb A. Thorax 2004. Comparison of representative ranges based on U. Environ Health Perspect 2005. Mucha A.148(1-2):11-20. 2005. J Occup Health 2003. Jarup L. Chiappino G. population. Lauwerys R. Clin Chim Acta 2000. Stock AL. Oguma E. Sanz P. Persson B.102:83-89. et al. Diamond GL. Consonni D. et al. Third National Report on Human Exposure to Environmental Chemicals. Environ Res 2004. Alfven T. Toxicological profile for cadmium update. Available at URL: http://www. Savage-Brown A. Jones RL. Sasaki S.cdc. Nermell B. Holguin F. Nomiyama T. Darbyshire J. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Occup Environ Med 2000. Buchet JP. Zhu G.205:297-308. et al. Moriguchi J.1(8587):663-667. Int J Hyg Environ Health 2003. Krause C. Gadea E. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Mannino DM. Fukui Y. et al. Seiwert M. Becker K. Toffoletto F. Palomar M. Takebayashi T. Kundiev YT. Lancet 1988. Furuki K. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Atlanta (GA).

Lundh T. Tawara K. Ginucchio G. and mercury in the population of northern Sweden. age. 4/8/09 Waalkes MP. Olsson IM. and risk of fractures: prospective population study. Zhao YC. Kathman SJ. dietary intake. In: Clarkson TW. Mutat Res 2003. Revised 2000 [online].epa. Salpietro CD. Gangemi S.110:151-155. Ottosson H. Friberg L.30(5):395-399. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Toyama. Suwazono Y. pp. eds. Sager PR.21(3-4):251-262. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Lijnen P. Lundh T. Roels HA. Bruiglia S. Nordberg GF. cadmium. Nakagawa H. Honda R.gov/ttn/atw/ hlthef/cadmium. Environ Health Perspect 2002.59(1):22-25. Lison D. Thijs L. Environ Res 2000. Vangronsveld J. Usefulness of biomarkers of exposure to inorganic mercury. Okubo Y. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Zhang YL. Nordberg GF.353:1140-1144. Honda R. Wilhelm M. Gallmans G. Zhu HD. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium.S. Bergdahl IA. Stelitano A.39:2507-2515. created 1992. 2000. 151-168. Hoet P. Emelianov D.84 (Section A):4455. Time trends in burdens of cadmium. forearm bone density. et al. Japan. Hazard Summary. Revised and new reference values for arsenic. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Saito S. Int J Hyg Environ Health 2006. iron status.59:394-397. Liu QF.209:301305. Nakagawa H. Campagna D. lead. Cadmium compounds. Roels HA.110:1185-1190. Kuznetsova T. lead. Lauwerys R. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. et al. Environ Res 2006. Arch Environ Health. Skerfving S. Ren Fail 1999. Tanebe K. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Wang JX. Mueller PW. Biological monitoring of toxic metals. J Environ Sci Health B 2004. Lybarger JA. Sarasua SM. et al. Environmental exposure to cadmium. Nakagawa H. J Cardiovasc Risk 1996. Oskarsson A. Schwenk M. lead. 2004. Jansson J-H. Environ Health Perspect 2002. Fan YG. and former smoking – association of renal effects. New York: Plenum Press. Bensryd I. 2001. Kobayashi E.html. Tanebe K. Noonan CW. Stegmayr B. et al. Lancet 1999. et al. Nogawa K. Biological monitoring of cadmium. Roels H. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan.Metals Nishijo M. Relationship between newborn size and mother’s blood cadmium levels. United States Environmental Protection Agency (U. Cadmium carcinogenesis. Available at URL: www. Nordberg M. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Staessen JA. Staessen J. Nishijo M. et al. Schultz C. Occup Environ Med 2002.3:26-41. Wennberg M. Buchet JP. Minciullo PL. Kido T. Merlino MV. Cadmium in blood and urine – impact of sex. J Perinat Med 2002.100:330-338.533(12):107-120. EPA).

and 03-04 are 0.99-6.10-7. infrared lamps.40-5.37) 7.6 (9.9) 12.80 (8.6 (9.8) 11.7 (10.05-5.22-4.94) 4.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.91-8.42) 7.16-6.47-4.5-14.9 (11.20) 5. respectively.81) 4.80-11.94 (4.13-8.01-8.9 (11.77 (4.13 (5.60-6.55-11.68 (7.2) 11. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9 (10.04 (4.72) 4.6) 10. population from the National Health and Nutrition Examination Survey.3 (8.00) 4.8) 12.00-8.6 (11.50 (7.1) 9.84) 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 4.46) 7.9 (11. see Data Analysis section) for Survey years 99-00.5-16.01) 7.26-11.62) 4.7 (10.35-5.5-13.34 (4.45-5.20-8.9) 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 4.29 (4.7) 10.8 (11. 2004).98 (7.98 (7.70 (8.21 (4.4) 12.03-4.60-7.36 (3.97-7.67 (4.80-10.62 (5.05) 5.14.7 (10.17-6.33 (5.99) 9.30) 5.3) 10.0 (9.64-5.87-7.60 (8.95) 5.07-11.90) 5.4) 9.74-5.56-11.45-8.7 (9.27 (7.27-5.21) 90th 9.60-7.32-5.00-10.36 (6. interval) 4.1 (9. Most human exposure to cesium occurs through the diet.09-5.82) 5.59) 7. although cesium was generally of low toxicity when given to animals.42) 6.01-6.25-5.36) 3.70 (5.70) 7.09) 5.40-5.00 (7.90-10.82-4.8) 12.13 (8.3) 10. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.84-9.12) 5.96 (6.00) 7.2.64-10. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.90-12.73-5.2-12.52) 7.40) 5.97 (7.37) 5.81-14.30) 7.35 (4.80) 7.2-13. Little is known about the health effects of this metal.92-13.99-11.27) 4.14 (4.6) 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 4.4 (9.26 (3. and high-power gas-ion devices.20) 7.5) 12.08-5.40-5.02 (4.20) 8.70) 5.86-11.50) 5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .84 (4.23) 9.4) 95th 11.9 (11.40-11.1) 11.08-5.20-4.70-8.89-5.Metals Cesium CAS No.3-13.3) 9. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.79 (4. cesium hydroxide is corrosive and irritating at high concentrations.71-5. Radioactive 137Cs has been used medically to treat cancer.54-11.08 (6.9) 8.71) 4.42-7.8) 11.49 (4.05-5. 01-02. and as polymerization catalysts.64 (4.2-13.99) 7.89) 4.4-13.50 (4.9 (10.90) 7.7) 11.04) 7.90-10.80 (8.12-5.14.70 (6.77-8.47-8.03 (4.56 (4. However.3 (8.8-13.61-6.70-5.17 (6.17) 4.20-7.8) 9.71-9.97) 4.30-5.53-11.2) 12.4) 11.95-4.10-9.87) 5.31-8.0) 11.24) 4.84) 8.00-9.30 (6.63 (4.2 (9.7 (11.0-13.3) 12.9) 11.70 (4.08) 7.87 (4.4) 10.4 (9.1-13.00-8.81) 4.10 (8.90 (6.59-5.60-6.49) 75th 7.57-5.26) 7.62 (5.10 (6.80-6. scintillation counters.40) 7.00-4.50 (4.30-10. soil.5) 10.90-12.40-11. nausea.80 (8.87 (4. Whether cesium compounds are carcinogenic is unknown. 0.8) 9.71 (4.12-11.44 (8.50 (4.60 (7.40 (4.50-7.40-7.74) Selected percentiles ( 95% confidence interval) 50th 4.03 (4.10 (8.2 (9.4 (10.3-13.3) 10. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.80-10.76-6.8) 12. the body half-life is estimated to be 70-109 days based on 137Cs exposures.22 (4.61) 7.2-13.0-15.64) 5.39-4.71-8.12 (4.90 (4.59-5.4) 12.70 (6.43 (5.9) Total 4.60) 7.10-8.84-5.7-14. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.08 (7.0) 12.87 (4.88 (8.43-8.7 (8.1-12.0) 9.94 (4.90) 9.93 (4.6 (11.35 (4.20-5.90-10.72-7.1) 11.64) 5.00) 6.38) 5.95 (3.74 (4.S.20) 4.63) 6.3-15.7 (9.77 (9.60-5.80 (4.30 (6.1) 10.63-4.13 (7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.26) 4.29) 4.99-11.10-5.55 (7.3) 10.59-5. and clay.05) 5.77 (9.81) 9.39) 7.23-4.33-5.20 (4. diarrhea.6) 11.8 (10.56 (4.70 (9.07) 4. photographic emulsions.6 (9.90) 5.49) 4.32 (3.1 (10.86 (7.16-6.25 (3.80-10.90-8.59 (5.73-11.34) 9.66 (7.5-14.68) 9.6 (9.90) 4. and cardiac arrhythmia (ATSDR.1) 9.50) 9. semiconductors.33 (6.50 (6.94-4.70) 5.2-14.54) 4.81 (4.1-12.71 (8.56) 5.10 (6.60) 5.32) 4.4) 10.69-6.40-5.80-13.5 (10.80 (4.25) 4.83-4.64) 4.40) 5.53 (6.49 (5.15-8.1 (11. For absorbed cesium salts.52-9.89) 5.86-12.0 (10.7) 11.83) 6.60) 7.7 (9.60-12.5) 9.5 (8.70 (8.0) 12.55 (4.0) 12.8 (10.91 (7.7) 10.20 (6.80 (4.0) 10.0) 11. and 0.

95-12.08) 4.43) 8.48) 90th 7.58-5.46) 6.77 (6.10-4.98) 5.46 (7.0) 7.S.83-7.2 (8.63 (7.50 (5.66 (5.88-4.23 (7.3 (9.53 (6.04-11.00-10.10 (3.82-4.68) 4.14-4.96) 4.63) 6.79 (5.59-8.02-4.41 (4.62-8.66 (5.27-4.3) 11.30-4.06) 4.7) 10.38 (3.19-3.S.21-3.17) 9.83) 8.60 (5.03) 5.95) 10.04) 5.36-6. population from the National Health and Nutrition Examination Survey.97-4.00 (8.06) 5.07 (5.06 (3.27) 4.0 (7.29) 5.56) 3.40) 7.47) 6..50) 4.56-10. population.63-6.33 (5.41) 9.75 (6.07-4.75 (7.00-4.80) 6.43 (3.64) 4.05) 6.65-3.41-7.40) 6.72-5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.52-5.41 (5.33-8.02 (5.08 (5.18 (7.15) 95th 8.84-7.14) 4.14 (6.82) 7.39) 5.87 (5.09 (4.47) 6.2 (8.55-5.38-12.70 (7.58) 8.96) 4.97) 8.91 (5.95 (3.91-6.1) 11.14-7.65 (6.84-7.09) 4.91-9.17) 4.13 (3.42-4.79-5.91) 4.50) 4.60) 3.53) 3.39) 8.56) 4.14-6.37-3.5) 9.08 (6.68) 6.4) 10.87) 5.9 (10.99-4.5 (9.87-4.58 (4.05-4.20-4.24 (3.46-4.56) 4.50 (7.71) 6. Using clinically submitted specimens.43-11.74) 75th 5.65-4.6 (9.09) 8.00-5.35 (4.86 (4.26 (3.54 (5.12-6.17 (6.11 (5.38-7.63-6.24-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 3.21-5.84-9.47 (4.27 (6.50 (6.76-9.49) 3.7) 10.96 (4.22-11.70) 6.18-6.26-6.25) 4.91) 5. interval) 4.73 (3.2) 11.51 (4.93-7.41) 4.79) 4.37) 4.20) 5.05 (4.54 (4.95) 8.45 (4.68 (4.54 (4.6) 6.S.34 (5.03-5.77 (7.67 (6.29) 4.43 (4.71 (7.72) 4.30 (3.58 (6.13) 7.90 (7. 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.42 (4.42 (5.91 (5.78) 4.79) 9.60-20.3-15.98) 5.53 (4.55 (3.8 (9.78) 4.46-8.08-3.67) 5.56 (4.55) 4.10 (3.07) 8.90-3.85-4.75-11.51 (7.30-4.43-6.64) 9.28 (5.16) 5.99-9.66 (6.22 (3.68) 3.20-4.95-6.79) 6.50) 4.88-10.44) 3.00-5.36-10.39 (5.78 (3.8) 5.0) Total 4.64) 5.61 (7.44 (8.03-6.92) 3.51 (3.08 (3.41 (8.74 (4.03) 6.84-11.74) 3.50-5.27 (6.25) Selected percentiles ( 95% confidence interval) 50th 4.00-8.29-3.15-4.5) 7.18) 8.24-10.35 (3.57) 3.10) 7.31-4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.95) 4.30) 10.72 (4.29) 4.05-3.3 (8.14) 4.96-4.28 (4.99) 4.89-4.31 (4.94) 7.28) 7.22) 6.68-11.27-6.70) 7.81 (4.63 (4.35) 3.67 (5.50) 8.42-4.31-6.42-6.44-5.08-7.16-5.16-8..64 (8.51) 4.44-9.11 (5.73-4.62) 5.30) 10.00-9.21-4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.21 (2.38) 10. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.98 (6.54 (3.38 (3. 2004).3) 9.85) 5.30 (7..46 (8.74 (5.07) 8.47) 4.20-8.58) 3.41-4.9) 10.40-5.90-8.64-6.81 (4.18-7.00) 6.26 (4.94 (5.84-9.7-12.51 (4.90-8.93-9.15-11.05-3.15 (7. 1990).43 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.13-9.04) 6.6 (9.9 (9.61-3.96-4.45-6.35-11.30 (4. and were also roughly similar to those in this Report.53) 6.99-9.3) 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 3.74-11.12) 3.04-5. Komaromy-Hiller et al.5) 9.51 (3. Minoia et al.44 (4.64 (4.66-6.87) 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 5.8) 10.63 (6. 2005.01-8.29-3.05) 3.17-4. population results shown in this Report (Alimonti et al.28) 8.08) 3.48-6.33 (5.36-3.0) 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 .95 (5.13-9.48) 7.27 (8.98 (7.85) 4.60 (3.8) 6.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure. Two small studies of European populations reported urinary cesium levels similar to U.12 (3.83-6.06 (5.77) 4.16-8.92 (5.19-6.76-6.91) 5.59) 4.77-5.47) 7.08) 4.43 (8.91-7.60-10.31 (4.10 (5.47 (7.20-4.3 (10.33-3.77 (4.99 (3.35-7.78 (3.97-5.

95:89-105.296(1-2):71-90. Wood CM. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Comparison of representative ranges based on U.2004 [online]. antimony and tungsten. Komaromy-Hiller G. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Apostoli P.19:3131-3138. et al. Pozzoli L. 4/8/09 Alimonti A. Forte G. et al. et al. A study of 46 elements in urine. Costa R.14:120-128. Trace element reference values in tissues from inhabitants of the European community I. Mott JA. and serum of Italian subjects. blood. Paschal D. Voorhees RE.atsdr. Sci Total Environ 1990. 2000. J Expo Anal Environ Epidemiol 2004. Assessment of urinary metals following exposure to a large vegetative fire.S. New Mexico. Spezia S. Available at URL: http://www. Sewell CM.cdc. Sabbioni E. Ash KO. Wolfe MI. Mincione G. Howerton K. Ronchi P. patient population and literature reference intervals for urinary trace elements. Atlanta (GA) 2005.html. cesium. Gatti A. Toxicological profile for cesium. Minoia C. Clin Chim Acta 2000.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Gallorini M. Pietra R. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals.gov/toxprofiles/tp157. Rapid Commun Mass Spectrom 2005.

520 (.340-. hard metal (alloys of cobalt and tungsten carbide).490-.450-.259-.28 (1. Cobalt is used as a drying agent in paints.620-.520-. 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.04) 1.380 (.940-1.03 (.550) 90th .410 (.431) .630 (.65) 1.15 (1.67) 1.398) .47) 1.520 (.320 (.07 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.850) .270-. 01-02.42) 1.16) 1.399) .430 (.740 (.520) .410 (.810-.920-1.68 (1.04-1.530) .650 (. interval) .430 (.28 (1.900-1.940 (.600 (.630-.394) .910-1.16) 1.610 (.680 (.03) 1.369 (.24 (1. and 03-04 are 0.550 (.305-.Metals Cobalt CAS No.371 (.590-.393-.890-1. It is also a component of porcelain enamel applied to steel bathroom fixtures.740-. population from the National Health and Nutrition Examination Survey.410 (.330-.17 (1.370-.92) 1. and in synthesizing polyester and other materials.480-.418 (.600-.S.850-1. and soil.496) .334) .950-1.410-.540-.670 (.350-.386) .430-.740-. Cobalt compounds are used as catalysts in producing oil and gas.950 (.570-.580 (.710 (. Cobalt occurs naturally in airborne dust.564) .410) .367 (.410) .430 (.22) 1.480 (.420) .32-2. and 0.47) 1.410-.540) 1. industry is imported or obtained by recycling scrap metal that contains cobalt. see Data Analysis section) for Survey years 99-00.770) .461 (.540-.760) .327-.670 (.17-1.36) 1.03 (.01 (.319) .710) 1.660) .09 (.316-.800-.04-1.375 (.870-1.73) 1.310-.00) . shiny.640) .680) .370 (. blue-colored pigments.670-.47 (1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.460-.890-1.52 (1.14) .580 (.390 (.350) 75th .39) 1.340) .581) .380 (.32) 1.05 (.300 (.570-.290-.22-1.570 (.900) .26-2.930-1.660-.880 (.980-1.17 (.730) 1.700) .830-1.02-1.499 (.510) 1.660) .28 (1.333-.820 (.16-1.07. 208 Fourth National Report on Human Exposure to Environmental Chemicals .690 (.24 (.374 (.810) .640) .470) .64) 1.15-1.750 (.340-.17 (1.590) .19) .13) 1.06-1.23) .430) .348-.339 (.26) 1.370-.340 (.450) .01 (.48) 1.405-.630 (.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 .890) . respectively. automobile airbags.590-.519 (.380-.850-1.380 (.515 (.410 (. and inks.430) .06 (.500 (.650-.350 (.03) 1.37-1.750 (.400-.330 (.390) .46 (1.48) 1.404) .850) 1.460) .364-.59 (1. and fertilizers.53) 1.21) 1.331-.900) .01-1.340) .05) 1.860 (.930) .870 (.294 (. hard metal or in combination with other elements.610) .370-.790-.313) .940-1.07.373-.490-.56) 1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.450) .338-.417) .610) .790 (.09 (.23-2.690-.700) .450) .377-.520-.32) 1.33-1.520) .450-.424) .05 (.487) . Cobalt compounds are also used in manufacturing battery electrodes.16 (1.32 (1.04-1.352 (.930 (.50) 1.26) Total .47 (1.32 (1.301 (.81) 1.980) .33 (1.750 (. It is emitted into the environment from burning coal and oil and car and truck exhaust.310 (.880-1.670-.640) .620-.650 (.410-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.583) .359 (.336-.530 (.04 (.950 (.820 (.25-1.870 (.435 (.800-.414) .900) .16 (.460) .410 (.330) .440-.12) 1.890-1.308-.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 .45 (1.900-1.469-.26-1.03-1.570) .300-.450) .16 (1.390 (.44) 1.343 (. and magnetic recording media. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.434 (.03) .502) .360-.280-.480 (.800) .350-.285 (.452 (.670 (.680) .07-1.460) .520 (.520 (.60 (1.560 (.460 (.50 (1.710) .428-.420 (.470 (.520-.416) .22 (1.373) .14-1.20 (1.540-.360-.390-.270-.370) .460 (.07-1.316 (.06 (.08) .350-.810) .610-.08-1.81) 1.543) .570) .580 (.333-.379 (.29 (1. 0.454 (.530-. seawater.620-.520-.16-1.379 (.465) . varnishes.620) . large appliances. and kitchenware.680 (.523) .08.420) .291-.960-1.390 (.99) 1.590 (.360-.690-.427-.760 (.431) .890) 95th 1.380-.820 (.388-.S.750-.348-.920) 1. The cobalt used in U.840) .01-2.75 (1. Usual human exposure is from food sources.372) .355-.500) . steel-belted radial tires.419) Selected percentiles ( 95% confidence interval) 50th .09) .463-.950-1.540-.398 (.270-.28-2.12) 1.950) .790) .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 .550-. diamond-polishing wheels.600) .

404-.461) .963) .328 (.36) 1.634-.409) .06 (.49) 1.826-1.895-1.694) .362) .728 (.955) .280-.781-1.274-.248-.251-.290 (.683-.508-. and to a lesser extent.495 (.774 (.337 (.00 (.316 (.462) .271 (.861-1.352 (.10-1.468) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.243-.488) .630-.740-1.435-.728) .342-.12 (.455 (.844 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.647) .16 (.594) . population from the National Health and Nutrition Examination Survey.275-.29 (1.963-1.247 (.615) .10 (.273 (.361-.259) .237-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.750) .513 (.708) .449) .616-.04 (.606 (.500-.00 (.781) 95th 1.03 (. refining or processing alloys.30 (1.15) 1.369 (.277-.821-3.990) .417 (.275-. an essential human nutrient.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 .609) .552 (. interval) .593) .667-1.328) .975 (.964 (.963) .929) .365) .239-.703-.329 (.361 (. Exposure in the workplace may come from electroplating.327-.861 (.282 (.372) .09) 1.600-.700 (.960 (.50) 1.983-1.500 (.438) .393 (.27) 1.298 (.469-.257 (.638-1.352) .463-.452-.319-.704-.12-1.983) . 1994.393-.673-.290 (.679-.382-.542 (.439) .54) 1.324-.408 (.16 (.17) .19) .976 (.750-.738 (.234 (.286) .938-1.329-.278 (.57) 1. respectively.434-.842) .562) .304-.598 (.16 (1..334) .348) .591 (. cobalt is excreted predominantly in the urine.60) 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 . in the feces.296) .00 (.00-1.368) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al. 1979).55) .757-1.937 (.562) . 1972).700 (.00) .561) .753-.503-.391 (.361 (.23 (1. using hard metal cutting tools. Smith et al.429) 1..333-.630-.289) .955) .290 (.426 (.821 (.29) 1.626-.16) .838 (.378 (.476-.301-.667-1.505) .259-..33) .481) 90th .256-.582-.513-.425-.349) .279 (.14 (.830 (.358 (.326-.574-.738 (.938) .331-.386 (.327 (.10) .523 (.829-1.457 (.851 (.391) Selected percentiles ( 95% confidence interval) 50th .25 (.581) .362-.932-1..368) .281) .467-.644 (.895-1.29 (1.337) .550-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.753) 1.537 (.756 (.10) Total .248-.365-.333 (.777-.554 (.296-.309) .11-1.857-1.733-1.428-.303-.554 (.635 (.306 (.73) 1.833-1.302-. 1994).872 (.381) . Cobalt is absorbed by oral and pulmonary routes.792-1.343-.736-.339-.727 (.479-.215-.378-.313-.387) .297) .392 (. or using diamond-polishing wheels that contain cobalt metal.599) .534-.533 (.02 (.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 .293 (.388 (.442-.257-.306) 75th .346 (.786-.396) .952 (.707) .353 (.24) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.792 (.301) .310) .879-1.343 (.848 (.529 (.407 (.444 (.313-.388 (.487-.471-.662) . Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..368 (.632-.608 (.963-1.689 (.850-1.475 (.297-.S. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).949) .355) .500-.317 (.50 (1. 1972).00 (.313-.513) .50) 1.417) .737 (.11-1.294-.35) 1.378-.282-.362 (.00) . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.314 (.29 (1.785) .396) .595) .36) 1.990-1.640) .384) .328 (.419) .313 (.04-1.44 (.380-.. with pulmonary clearance half-lives of from one to two years (Hedge et al.333-.660-.523 (.471-.449-.760-1.669) .360) .376 (.611) .333-.691 (.804) 1.268 (.829) .911-1.378-.471 (.563-. 2003).361-.457) . Once absorbed and distributed in the body.29) .850 (.304) .611) .522) .435 (.27) 1.547 (.515 (.400 (.363) .433) .905) .352 (.259 (.487-.407) .900-1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.15 (.394) .847) .03-1.824 (.548 (.425) .324) .291 (. A portion of cobalt retained for long periods is concentrated in the liver.Metals fabricated from cobalt alloys (Lhotka et al.25 (.585) .560-.313-.479) .344-.898 (.917) .83) 1.279) .534 (.250) .313-.300) .272-.402 (.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 .278-.35) .457-.335 (.323) .421) .33) 1.353-.60) 1.723 (.28) 1.543) .744) 1.

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

Occup Environ Med 1994. Zweymuller K. Sabbioni E.” Contact Dermatitis 2001. Swennen B. Daniel J.533:135-152. Jarvis JQ. Lhotka C. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Goto S. Weyher I. Kusaka Y. Ichikawa Y. et al. Hoher T.44:124-132. Stanescu D. Respiratory health of cobalt production workers. Smith T.204:147-160. Lisi P. Cleland D. Laippala P. Heki S.48:172-173. Weber A. Roto P. Pisati G. Occupationallyinduced “isolated cobalt sensitization. Kiilunen M. Schaller KH. Oksa P. Zhuber K. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Sanghrajka AP. McCalden RW. Thakker DM. Sci Total Environ 1998. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. salt. White MA. Science 1988. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Cobalt and antimony: genotoxicity and carcinogenicity.148:241-248. Sci Total Environ 1994. Meier R. Diepgen TL. cobalt salts.36:732-734. Blunn G. Goto S. et al. Lung cancer risk in hard-metal workers. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Goldberg MA. Molders J. Carnes WH. Outcome of occupational asthma due to cobalt hypersensitivity. Gross RT. J Bone Joint Surg Br 2006. Bourne RB. et al. Ghat IS.55(4):269-276. Bunn HF. and hard metal dust.(1-3):133-139. Kuska Y. Linna A. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Bacis M.88(4):443448. Peltier A. Ziaee H.51(7):447450. Schank M. Int Arch Occup Environ Health 1997. and cobalt metals. Shirakawa T. Leghissa P. Mosconi G. 2001. Occup Environ Med 2001. Kato M. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Christensen JM. DeSantis V.157:117121. Sabbioni E. Edmonds CJ. Falcone G. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Iversen BS. J Trace Elem Med Biol 2006. Dunning SP. HoffmannB.Metals effects of cobalt. Thomassen H. Pradhan C. Epidemiological survey of workers exposed to cobalt oxides. et al. Palmroos P.34:620-626.150(1-3):167-171. Trace element reference values in tissues from inhabitants of the European Union. Cresti R. Dunstan E. A report of two cases from mineral assay laboratories and a review of the literature. Clin Orthop Relat Res 2003. et al.20(1):25-31. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Barnaby CF. Radulescu M. Iavicoli I. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Health Phys 1972.28(5):1121-1128. Steffan I. Moulin JJ. Kristiansen J. oxides. et al. Int Arch Occup Environ Health. Szekeres T.58(10):631-634. Meyer zum Buschenfelde K-H. Lasfargues G. Co-sensitivity between cobalt and other transition metals. Linnainmaa M. Bozec C. Fujimura N. Long-term clearance of inhaled 60Co. De Boeck M. J Rheumatol 2001. Health Phys 1979. Lauwerys R. Lauwerys R. Zedda S. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Zobelein P. Mutat Res 2003. Kriss JP. Lauwerys RB. J Bone Joint Surg Br 2005. Am J Ind Med 2003. Chest 1989. Contact Dermatitis 2003. Sabbioni E. Lison D. Arch Intern Med 1990. Kraus T. Tilley S. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Sci Total Environ 1997. Rorabeck CH. Biological monitoring of workers exposed to cobalt metal. Br J Ind Med 1993. Hedge AG. Cannon SR.50(9):835-842.406:282-296.21(2):189-195. a study of 13 elements in blood and urine of a United Kingdom population. Dickel H. Sci Total Environ 1994.87(5):628-631. Uitti J.150. Wild P. Buchet JP. X. Lison D.22:359367. MacDonald SJ. J Orthop Res 2003. Chess DG. 1985. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors.150:177-183. Romazini S. Robinson C. The release of metals from metal-onmetal surface arthroplasty of the hip. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Absorption and retention of cobalt in man by whole-body counting. Alessandrelli M. Buchet JP. Angerer J. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Cobalt cardiomyopathy. Unwin P. Swennen B. Hammon E. Thabe H. Boca Raton (FL): Lewis Publishers. 3rd ed. Am J Epidemiol 1998. Hoet P. Schramel P. Vitali MT. J Occup Med 1992. Lison D. Salvatori S.95:29-37.45:246-247.216:253-270. Salama A.69(3):193-200.242:1412-1415. Kirsch-Volders M. McMinn DJ.

900-1.70) 4.80 (1.90) 2.70) 1.90 (1. plastics.50 (4.30-4.70) 1.87 (1.80) 1.70-3.40) 2.20 (3.70 (2.70-6.00-2.39-1.90) 5.60) 1.60 (3.68-1.60 (2.90) 1.40) 2.60) 2.62 (1.62-1.70) 2.80 (3.30-6. respectively.90 (4.00) 1.90-4.60-2.30 (1.20) 90th 3.20) 2.30-1.20 (3.10-2.20) 3.19 (1. and 0.30-1.01 (1.32-1.70 (5.31) 1.70 (2.878-1.40-6.36-1.50-4.80 (1.40-3.70-1.75-2.70 (2.20-3.70-1.60 (1.30) 2.89) 1.40 (1.00 (1.50 (1.40 (1.80) 2.90) 3.60) 2.10-2.30 (1.00 (4.66) 1.10-1.30 (2.60 (1. population from the National Health and Nutrition Examination Survey.60-1.80-3. malleable. 7439-92-1 General Information Elemental lead is a soft. brass.80) 1.14-1.43) 1.93-2.50) 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 2.00) 3.90-4.50 (1.40 (3.25 (1.60 (2.50-2. dense.40-1.10-2.10 (1.20) 4.96-2.70) 1.90-4.60-4.25) 1.30 (2.60 (1.78 (1.50) 2.50 (1.40 (1.50 (2.60-1.90-6.30-1.S.80) 2.20 (1.56 (1.40-1.20) .70-2.50-3.80 (4.80 (1.50-2.60) 2.10-6.50 (2.80-4.00) 2.50-2.10) 1.40 (2.20-2.50) 5.50 (1.60) 1.30-5.00) 6.23 (1.37-1.10-4.10-2.30 (4.40-3.45-1.20) 3. In the past.60-4.80-5.40-1.30 (3.30 (4. leaded glass.40) 3.900 (.50) 4.10 (2.30 (2.90) 2.52-1.10-2.00 (3. see Data Analysis section) for Survey years 99-00.10-1.30) 2.75 (1.60) 3.40-1.53) 1.36) 1.50 (3.30) 5. bronze).40 (2.00) 2.60 (1.70) 4.90-2.Metals Lead CAS No.80-2. Lead was used in plumbing for centuries and may still be present.60) 5.70) 3.40 (1.10 (1.00) 1.50-3.32-1. 0.20-3.00-6.90) 2.00-1.75) 1.14-1.60) 3.60 (2.70-4.20 (1.20) 3.20 (3.86) 1.10) 2.60 (3.69) 1.00 (1.00 (4.80) 3.90) 3.00) 2.40 (4.90-2.00-4.90 (3.60) 1.70) 4.50-5.10) 1.90-4.20 (3.50-1.90) 1.20 (1. such as lead phosphate and tetraethyl lead.50 (2.10) 1.10-3.20 (3.30) 95th 5.70-1.30 (2.65 (1.60 (4.04-1.83 (1.50 (2.20-1.90-2.20) 5.800-1.50) 5.60-3.70) 3. Lead has a variety of uses in manufacturing: storage batteries.40-2.60 (3.20 (4.30-2.00-1.49-1.50 (2.30-2.00) 4. Before the 1980’s.40-3.10 (2.50 (3.60-6.900 (.60) 5.00) 1.70) 1.10) 3.10-6.50) 7.60 (1.20-6.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.986) .90 (3.40) 4.20) 3.51 (1. Elemental lead can be combined with other elements to form inorganic and organic compounds.30-1.50) 1.40-6.90-3.50) 4.20 (3.50) 2. antique-molded or cast ornaments.00-4.55 (1.60 (1.40) 2.37 (1.10) 2.69 (1.43) 1.30-1.g.70 (3.3.50-4.10 (3. solders.00) 3.69 (1.30-1.3.60-1.90 (3.30 (2. Lead is most often mined from ores or recycled from scrap metal or batteries. blue-gray metal that occurs naturally in soils and rocks.10-3.30) 1.20-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) Total 1.80 (5.10-3.30-2.14-1.40-5.90 (2.30 (1.50) 1.09) 1.22 (1. and for radiation shielding.70 (1.90) 2.20 (1.10 (1.95) 1.00) 5.60) 4.80 (2.10-1.80-3.55-1.90-2.10) 4.70-2.50-1.60) 4.10-8.52 (1.10-4.36-1.30-2.S.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.80 (2.20) 1.40) 1.60 (1.30 (2.60) 1.00 (2. and 03-04 are 0.66 (1.34-1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.81) 1.90 (3.50) 1.90 (1.30 (4.37 (1.80) 1.70 (1.10-3.10 (2.80) 2.77 (1.60-2.60) 4.90) 1.00 (5.60 (2.70-5.60 (3.40) 5.71-1.39) 1.80-3.20 (2.946 (.43 (1.25 (1.55-1.80-4. metal alloys (e.46 (1.60) 1.20 (1.50 (4.70 (3.40-1.40) 1. interval) 1.40-1.50-2.00) 1.43 (1.60) 2.80 (5. ceramic glazes.80) 1.60) 2.30 (1.20-1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.942 (.80 (2.52-1. 01-02.80 (4.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.90 (3.90) 2.10) 5.00) .00) 1.40 (5.50-5.20) 4.87) 1.12-1.40) 1.50) 75th 2.43-1.60 (2. ammunition.60) 3.20-3.62) 1.80) 2.80 (1.40-2.02) 1.28.50-6.91) 1.10-2.40-4.00) 2. Since lead has been eliminated from gasoline.70) 3.60) 3.60 (2.50-1.00 (6.20-2.10 (4.50) 3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.30) 2.70 (1.80 (1.48) 1.40) 2.00) 4.20-4.80-4.899-. 212 Fourth National Report on Human Exposure to Environmental Chemicals .90 (2.69) 1.50-1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50) 1.75-1. the main source of lead exposure for the general U.60-1.30 (2.10) 3.17) .72) Selected percentiles ( 95% confidence interval) 50th 1.00-4.20 (2.10) 3.70) 1.20 (3.70) 4.70-2.70 (1.80-3.50-1.51) 1.80 (1.60) 4.40-2.00-5.45 (1.80) 1.

older plumbing systems with leaded pipes or lead soldered connections. and 0.00) .40-1.738) .23) .35 (.20 (1.80 (1.700 (.60 (1.745-.30-2.03-2.50) 1.59) 1.90 (1.613) .60 (2.80) 1.90-3.800 (.33-2.30 (2.10 (.44-2.52 (1.80) 1.40) 1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.90 (2.710-1.526-.616) .923 (.680-.30) 2.700) .30) 1.828) Selected percentiles ( 95% confidence interval) 50th .Metals occupational (e.20-1.80) 2.591 (.620 (.833-1.90-2.900 (.20) .40) 2.90 (1.70 (2.560-.580-.660) .600-.90) 2.00) .642 (.10 (.900) .822-1.20-1.00) .14 (1.625-.31 (1.10-1.690) 75th 1.24-1.40-3.800) . However.90) 2. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.S.40-1.78-2.572-.600 (. or after soluble lead compounds are ingested..600) .630 (.900) .78-2.640 (. see Data Analysis section) for Survey years 99-00.60-1.00) 1. bullet fragments retained in human tissue.795 (.900-1.900 (. population from the National Health and Nutrition Examination Survey.80) 3.628) 1.40) 2.70) 1.04 (.50) 1.40 (2.40-2.60-3.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00 (1. 1991).940 (.90-3.11 (1.80) 1.50-2.960 (. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.31-3.766 (.920 (.10-1.573 (.800-1.700 (.20) .90-2.40) 1.27) 1.30-1.590 (.641-.50) 2.773) .07 (.66 (2.862) .960-1.86) 95th 2.990) 2.540 (.857) .50 (2.00 (1.80-2.30) 1.40 (1.600) .30) 2.40 (1. In the blood. and 03-04 are 0.60 (1. lead-contaminated dust in indoor firing ranges.671-.80) 2.900 (.850 (.11) 2.75) 3.900-1.21 (2.659 (.40) 1.900) .40) 1.610 (.30-1.10) .757-.70-3.579-.500-.80) 3.600-.20 (1.800 (.800 (.40 (2.800) .650) 1.651) .00-1.00 (.540-.00) .g.595-.50) 3.808 (.30) 1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .90 (1.674) 1. lead-containing folk remedies and cosmetics.800) .13-3.20 (2.60-2.708-.848 (.00-1.10 (1.749) .62-4.30-1.701) .80) 2.910-.70) 1.70) 1.50-2.558 (.564 (.10-5. battery and radiator manufacturing) and recreational sources.600-.636 (.10) 1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .680-.66 (2.640-.10-3.50) 2.04) 2.40 (2.30) 1.730 (.30 (3.70) 3.86) 1.986) . pewter utensils and drinking vessels.960-1.18-1.00) 2.90-4.710-.800 (.73 (1.800) .12) 90th 2.691-.90) 1.10-3.70-2.78-2.30) .97) 4.30) 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 1.04) .10-1.680) 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 1.30-1.00-2.700 (.30-5. stained glass framing.20) .52-1.75) 4.70 (2.800-.89) 2.700) 1.70) 2.02 (.600 (.64) 2.00 (1.40-1.90-2.13) .752 (. 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.553-. CDC.40 (1.90 (2.40-5.80-2. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.480-.661-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700-.17 (1. dust.604 (.04-2.50-1.688 (.70 (2.800-1. 2007.10 (1.00 (2.50) 1.800-.920 (.91) 2.72) 1.677 (.82 (2.600-.700 (. or water contaminated by mining or smelting operations.52-1.20) 1.570-.40 (1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.33.785) .535-.10-1.00-1.731 (.62) Total .00 (1.90) 2.10) .700-.1.20 (1.718) .60-2.990) 1.14 (1.20 (1.700-.09) 1..20-2.40 (2.700-.30) 1.10) 2.00-2.695 (.22) 1.941) .700 (.900-1.70 (1.20) .41) 2.700-.605) .810-1.556-.790 (.90 (2.620) 1.20-2.40) 1.40 (1.59-2.10 (1.30-3.50 (1.900) .40) 2.30) 2.70 (2. lead-based painted surfaces undergoing renovation or demolition.02) 1.82 (1. interval) .20 (1.753 (.20) 1.70) 3.700-1.20 (2.931) .680) .60) 2.06) .20) 1.10) 2.40) 2.80) 2.815 (. imported children’s trinkets and toys.80) 2.86-2. 2000).20 (3.970-1.50 (2.1.10-3.00-2.07-1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (2.700 (.20 (2.90-2.40) 3.800) . Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.32 (1.60 (1.840 (.10-1.19 (1.23-4.900) .50-3.915-1.50 (1.10 (.49 (1.80-3.50 (2.03 (1.14-1.80 (1.935) 1. Approximately half of the absorbed lead may be incorporated into bone.506-.625 (.60-3.40-1.20 (1.29) 2.30 (1.29 (2.33 (2.60 (1.900-1.50-2.27 (1.04 (.955-1.729-.820-1. respectively.900) .20-1.00) 2.10 (1.637-.579-.86 (1.600-.818) . 01-02. and contact with soil.589-. 0.833 (.

18) 1.55 (1.47) 1.677-. Nash et al.85) 1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.88) 2.718) .56-3.33) 2.28-1.22-1.702-.17 (.707 (. 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.615 (.19-5.04-3.592-.74 (1.89-5. 2007).85-2.644 (.00 (1. In 1991.62-3.428) .44) 1.793-1.380-.722 (.492-. Approximately 70% of lead excretion occurs via the urine.37-1.64) 95th 2.65-2.01) .03) .18) 2.11 (.400) .588-.677 (.679-.645-.693 (.571-.11 (1. scant amounts are lost through sweat.841-1.35) 2.657) 1.79 (1.03 (.688) .712 (.37-1.56-2.529-.686) .698) .914-1.94-2.22) 1.43-1.04) 2.75-2.607-.22) 1.51 (1.11 (.648 (.53) 1.88) 2.50-2.10) 1.33-1. with lesser amounts eliminated via the feces..649 (.838) .61) 1.612-.61) 1.15) 1.635 (. BLLs and associated toxic effects differ in children and adults.720 (.S. 1993).742) Selected percentiles ( 95% confidence interval) 50th .917-1.508) .45 (1.601-.34-1.03) 2. 2004.938-1. O’Flaherty.33) 1.828) .605-.62-2.58) 1.702) .722 (.56 (1.914 (.992-1.623 (.603 (.920-1.708 (.28) 2.63) 4.50 (1.49 (1.594-.50-2. and nails (Leggett.66 (1. abdominal pain. Schwartz.27 (1.28) .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 .92) 2.677) .31) 1.18) 1.85-2.36-2.07) .979 (.40-1.679) 1.594-.38 (2.03) 2.63) 1..43 (2.00 (1.654) .638 (.702) .26) Total .72-2.05-1.52) 1.33 (1.720 (.09-1.862-.22) .579-.41-1. 1991.992-1.88) 1.51) 1.61) 1.43) 1.06) . CDC.97-18.79) 1.47 (1.24 (1.03-2.432 (. through the inhibition of certain enzymes.03 (.933-1.14) 1.742) .655-.08-2.78-4.701) .71-2.460-.64 (1. based on prospective population studies.639 (.659-.Metals 90% of the body lead burden in most adults.97) 1.01 (.18 (1.763) .946-1.721 (.07 (.73) 2.893) .50-1.05-1.658 (.00 (.918 (.753) .608-.25-1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.68 (1.09) 1.603-.06 (1.43 (1.975-1.03 (.19) 1.08) .94 (1.796-1.734) . Staessen et al.988-1.676) .65 (1.593 (.623 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.667-.53-1.586-.639 (.639) .44 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09-1.44 (1. encephalopathy.52 (1.641 (.436) .71 (1. 2003. seizures. The toxic effects of lead result from its interference with the physiologic actions of calcium.79) 2.05 (.571-.20) .31 (1.988 (. 1993.681-.853-1.342-.00 (1.78 (2. zinc.69 (1.622 (.671 (.55 (1.82) 1.20-3.670) 1. 1995).86 (1.23 (1.20) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .83 (2.10 (.604-.98 (1.682) .75 (2.977) 1. and iron.461) . kidney injury.31 (2.559-.41) .22-2.17-1.535) .870 (.09-1.618 (.98) 2. population from the National Health and Nutrition Examination Survey.918-1.709 (.404 (.698) . interval) .625 (.725) . and paralysis.997-1.11) .765) .667) .404 (.77) 2.05 (1.48 (1.62) 2.882-1.50-2.88 (1.72) .70 (1.731-.668-.08) .639 (.00) .876-1. Large amounts of lead in the body can cause anemia.59-3..98-2.11-1. with a half-life of years to decades.03) .26) 2.96 (1.66) 2.67-4.603-.755 (. 1995.541-.746) .683-.633 (.621 (.10 (1.06 (.587-.851) .12-1.383-.64) 2.41 (1.20) .962 (.31 (1.510-.914 (.701 (.43) 2.632 (.46 (1.38 (2.810 (.85 (1.887 (.981-1.38 (2.696 (.569 (.652 (. Lead can cross the placenta and enter the developing fetal brain.667-.703) .83) 1.700-.730) 1.583-.926 (.900 (.14 (1.645-.781-1.0) 3.606-.774 (.64-2.66 (1.87) 1.56) 3. The skeleton acts as a storage depot.739) .615 (.02-1.644) .608 (.03 (1.11 (1.73-2.62-1.39-1.469 (.496 (.07-1.828-1.681-.97) 1.03) 1.408-. For instance.47 (2.50) 1.61) 1.11) 1.963-1.15-2.89-2.25-1.758) .655) 75th 1.88-2.404-.933) .718) 1.551-.790) .03) 90th 1. and through binding to ion channels and regulatory proteins.938 (.15) 1.812-1.990 (.97 (1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.617-.898) .561-.800-.375 (.18) .971 (.03) 1.31) 1.15-2.588-.940 (.710) .06) 1.673) .46 (2.725) .61) 3.15-3. hair.72-2.29 (1.12) 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 .609 (. 1996).957-1.02) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.655) .

and decrease fertility (Alexander et al.. High dose occupational lead exposure.html. Telisman et al. 1999)....75 µg/dL in U. Data submitted through state public health programs from 2006 showed that 1. 1999). Fourth National Report on Human Exposure to Environmental Chemicals 215 . 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.4% in NHANES 1999-2004.e. which is an 84% decline.6%) were lower than those from NHANES 1991-1994. For example. the geometric mean BLL was 3. Lanphear et al. and organic lead compounds not classifiable with respect to human carcinogenicity. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. 1995. approximately 11.7 µg/dL and 4. premature delivery. Bellinger 2005. Payton et al. reduce sperm count. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. may alter sperm morphology. 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. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. 2005a).21% of approximately 3. 2003.S. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 2001).3 million children tested had BLLs of 10 mg/dL or higher (http://www. and low family income (CDC. Urine levels may reflect recently absorbed lead.. Both drinking water and ambient air standards for lead have been established by the U. 2005b. almost double the geometric mean of 1. At low environmental exposures. Pirkle et al..Metals µg/dL or higher as the level of concern in children... 1994).6% in NHANES 1988-1991 to 1.5 per 100.S.g. Surveillance data reported by U. The U. 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.xls). More recently. adults in the 19992000 NHANES sample (Apostoli et al. However.S. 2002. 1991. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. Jones et al. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. the prevalence rate has declined annually since 1994 (CDC.07 µg/dL (Becker et al. 2007). 2009).. Schwartz et al. respectively. lead in women may be associated with hypertension during pregnancy. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.. IARC considers inorganic lead compounds probable human carcinogens.gov/toxpro2. residing in housing built before the 1950’s. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. In NHANES 1999-2002 in children 1-5 years old. 2005b). environmental levels) and health effects is available from ATSDR at: http://www. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR..atsdr. state childhood lead programs also show a decline in the percentage of children younger than 6 years of age who had BLLs of 10 mg/dL or higher. EPA. and peripheral neuropathy generally occurring at much higher levels (e. both the geometric mean (1. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.. usually with BLLs greater than 40 mg/dL. 2003.. Muntner et al. 2000). adults in the 1999-2000 NHANES sample. particularly in the skeleton.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.. Borja-Aburto et al. Korrick et al.2 µg/dL in males and 3.. when the geometric mean BLL was 2. Information about external exposure (i. higher than 100-200 µg/dL). adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. 1987.. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 2000). seizures. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 2006).S..cdc.S. 2002a). urban residence. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.4% of children had BLLs of 10µg/dL or higher (CDC. 2003.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1.. 1998). including minority race or ethnicity. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8...000 adults.0 µg/dL in females (Soldin et al. Overall. In occupationally exposed adults. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. CDC. 2003). 2002).. 2006).cdc.. adult residents. Schwartz.. and spontaneous abortion (Baghurst et al. 1996.S. BLLs reflect both recent intake and equilibration with stored lead in other tissues. 1984. with overt encephalopathy. 1996.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample. Staessen et al. 1996.

Kim R.gov/toxprofiles/tp13. gov/mmwr/preview/mmwrhtml/mm5420a5. Environ Res 2000. Centers for Disease Control and Prevention (CDC). Pirkle JL. Hu H. MMWR Morb Mortal Wkly Rep 2005a.150(6):590-597. Lead and hypertension in a sample of middle-aged women. Dietrich K.htm. IARC Monogr Eval Carcinog Risks Hum 2006. Reese YR. MMWR Morb Mortal Wkly Rep 2006. 4/14/09 Centers for Disease Control and Prevention (CDC).53:411-416. Int J Hyg Environ Health 2002. 1999-2002. Ga.115:521-529. Toxicological profile for lead.87:1-471. Blood lead reference values: the results of an Italian polycentric study. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Occup Environ Med 1996.gov/mmwr/preview/mmwrhtml/ mm5532a2. Bellinger D. Available from URL: http://www. et al. Borja-Aburto VH. Lepom P. 4/14/09 Centers for Disease Control and Prevention (CDC). Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Korrick SA. doi:10. Speizer FE. Vimpani FB. Available at URL: http://www. 1988-2004. Blanco J. et al. Hänninen H. CDC. Coresh J.101(7):598-616. Age-specific kinetic model of lead metal in humans.htm. 4/14/09 Centers for Disease Control and Prevention (CDC).cdc. Farias P. Neurodevelopmental effects of postnatal lead exposure at very low levels. Checkoway H. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Bellinger D.8(3):395-401. Hernberg S. Apostoli P. Payton M. Rotnitzky A.atsdr. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Aug 2007 [online].55(32):876-879. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Jacobson SW. 2005.26:359-371. Managing Elevated Blood Lead Levels Among Young Children. Blood lead levels measured prospectively and risk of spontaneous abortion. Luukkonen R. Bavazzano P. Third National Report on Human Exposure to Environmental Chemicals. Angle CR. Atlanta. Teratogen update: lead and pregnancy. Ganzi A.205:297-308. Batuman V. Baj A. Sparrow D. Rotnitzky A. Available at URL: http://www. Henderson CR. Kuehnemann TJ. Seiwert M. Pediatrics 2009. Cox C. Roberts RR. Preventing Lead Poisoning in Young Children.1542/peds:2007-3608. Am J Epidemiol 1999. Muntner P. Becker K.89:330-335. Korrick S. Hu H. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. 1991 [online].10:43-50. Weiss ST. Inorganic and Organic Lead Compounds. Robertson EF. Lanphear BP. 2005b. Public Health Rep 2000. Rios C. Chiodo LM. Neurotoxicol Teratol 2004. Scand J Work Environ Health 1984. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.82:60-80. McMichael AJ. Leggett RW. et al.113(4):1016-1022. 2002 [online].htm.html.htm. Semen quality of men employed at a lead smelter. Sparrow D. Kaufman JD. Rojas LM. Caldwell KL. van Netten C. Mantere P. Jusko TA. Available at URL: http://www. JAMA 1996.73:409-420.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. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Hunter DJ. Am J Public Health 1999.cdc. Hu H. Sci Total Environ 2002. Cory-Slechta DA. JAMA 1996. Environ Health Perspect 1993. 2003-2004. Homa DM.cdc. Ewers TG. 4/14/09 Alexander BH. Brody DJ. Jones RL. et al. Krause C.cdc. Stanek KL. Available at URL: http://www.54(20):513-516. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Canfield RL. Blood lead levels—United States. et al. Atlanta (GA). Cox C. Atlanta (GA). Neri A. Ronchi L.cdc. Manton WI. Hertz-Picciotto I. Aro A. Wager C. Birth Defects Research (Part A).gov/nceh/lead/publications/ books/plpyc/contents. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study.348:15171526. Meyer PA. Auinger P. References Agency for Toxic Substances and Disease Registry (ATSDR). Wigg NR. 4/14/09 Centers for Disease Control and Prevention (CDC).287:1-11. Kaus S. Pediatrics 2004. Weiss ST.123:e376-e385. The relationship of bone and blood lead to hypertension. N Engl J Med 2003. Vupputyuri S. Schulz C. Acquisition and retention of lead by young children. Adult blood lead epidemiology and surveillance—United States. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Lanphear BP.275(15):1171-1176. Muller CH. Baghurst PA.275:1177-1181. Neurotoxicol 1987.gov/nceh/lead/ CaseManagement/caseManage_main. Lead. Jacobson JL.

Schwartz J. Schwartz BS.140:821-829. stable lead isotopes to determine release of lead from the skeleton. O’Flaherty EJ. zinc.S. cadmium. Stewar WF. Weiss ST. 50:31-37. Rocic B. Magder L.118:16-29. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Arch Environ Health 1995. Toxicol Appl Pharmacol 1993. Int J Hyg Environ Health 2006. Low-level lead exposure and renal function in the Normative Aging Study. Pirkle JL.108(1):45-53. Nash D. Smith DR. Lee SS. and tibia lead with neurobehavioral test scores in South Korean lead workers. Sherwin R. Kaufmann R. Hwang KY. Flegal AR. Hu H. Hanak B.104(1):60-66. Telisman S. Kinetics of lead disposition in humans. Schulz D. Soldin SJ. Lauwerys RR. and copper in men.289(12):1523-1531. Low-level lead exposure and blood pressure. blood pressure. Exposure of the U. Gunter EW. Hickman T. Pizent A. Use of endogenous.327:109-113. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Blood lead concentrations in children: new ranges.106:745-750. Rubin R. Brody DJ.209:301305. Environ Health Perspect 2000. Lee BK. Environ Health Perspect 1996. Staessen JA. Kidney Int 2003. Paschal DC. Kaufmann RB. Association of blood lead. Schwenk M. Lee GS. Environ Health Perspect 1998. blood pressure and cardiovascular disease in men. Am J Epidemiol 1994. Roels H. Cvitkovic P. and hypertension in perimenopausal and postmenopausal women. Revised and new reference values for arsenic. Gavella M. et al. Amery A. JAMA 2003. Soldin OP. cadmium. Physiologically based models for bone-seeking elements. Lead. Lustberg M. Clin Chim Acta 2003.9:303-327.153(5):453464. lead. Wilhelm M.63:1044-1050. Payton M. Jurasovic J. Sparrow D. dimercaptosuccinic acidchelatable lead. Am J Epidemiol 2001. J Hum Hypertens 1995. IV. population to lead: 1991-1994. Osterloh JD. Semen quality and reproductive endocrine function in relation to biomarkers of lead.Metals results from NHANES III. et al. Blood lead.

00 (1. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).70 (1.500-.80 (1..60-5. thermometers. mercuric chloride).800-1.30-6.g.2. The kinetics of the different forms of mercury vary considerably. which create an episodic potential for volatization and inhalation of mercury vapor.80 (3.900) .714-.10) .30 (2.90 (1. to form inorganic mercury compounds or salts.900) 75th 1.30-4.800 (. and mining and smelting.490 (. 1993).20-3. 2002).80 (1. The ingestion of methyl mercury.500 (.50-2. Some cosmetic skin creams from countries other than the U.363-.703-. elemental mercury is absorbed mainly by inhaling volatilized vapor. In addition.00) 1. Apart from methyl mercury.30) 3.500) .419 (.418-. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.80) 1. 1999 .903) Selected percentiles ( 95% confidence interval) 50th .800 (.50) 1.00 (.655-.00-1.40 (3.20-4.886) .30 (1. Also.70 (1.700) .40-3.50) 5.g. constitutes the main source of dietary mercury exposure in the general population.860-1.50-1.60-6.472-.80) 4.00) 1. Woods et al.. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.90) 95th 4.300) .400 (. IARC.700-.20) 2.753-1..30) 1.700-. population from the National Health and Nutrition Examination Survey.40-1.30) 4132 4241 03-04 03-04 03-04 .800-1. an organic form of mercury. such as chlorine (e. After elemental mercury is absorbed.60 (1. thermostats and switches). interval) .500 (. and dental amalgam. Kingman et al.30) 1.60-6. sulfur.800-1.574) . water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.50) 4. see Data Analysis section) for Survey year 03-04 is 0. phenylmercuric acetate) or topical antiseptics (e. merbromin). 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).70) 911 856 2081 4525 03-04 03-04 . predominantly from fish and other seafood.300-.285-.g. and organic forms.700-.776 (.877 (.00-5. 1980.40 (3.60 (1.02) .563 (.40 (4.40-2.00) 4.40) 1. with the highest concentrations occurring in the kidneys (Barregard et al.60 (2.700 (. synthetic organomercury compounds were once used in pharmaceutical applications. electrical lamps.500-.80) 3. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.40-1.90 (1. Poorly absorbed from the gastrointestinal tract.800-1.30) 5. solid-waste incineration. inorganic.40 (4.600) 1..60-3.900) 1. Elemental mercury is a shiny.689-. Survey years 03-04 Geometric mean (95% conf. have often required public health intervention (Zeitz et al. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. sphygmomanometers and barometers.S.781 (.90 (4.60) 1. 1994.900 (.326 (.50-3.50) 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 ...900) 1.00) . it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.60) 2085 2293 3478 Limit of detection (LOD.672) .00 (2. 218 Fourth National Report on Human Exposure to Environmental Chemicals . Hursh et al.70-2.919) .800 (.30-2.00 (.814 (.20 (2. 1998. Atmospheric elemental mercury can be deposited on land and water.60-2. may contain inorganic mercury.90) 90th 3.400-.900) 1.12) .372) .00) 3.00 (2.40-2.700-.90) 3.80 (1.Metals Mercury CAS No.00 (. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. 2007).00 (.. thimerosal.S.797 (.70 (3.30-5. or oxygen.400-.60) 1.600 (.00 (2.30) 3.700-.. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. and is distributed to most tissues. which can bioaccumulate in aquatic and terrestrial food chains.50) 2.800 (.90-3. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.70 (4.800-1. Accidental spills of elemental mercury.40) 3.484) ..10-3.20-4.300 (.700) .927) .g. and mercury compounds are still used as preservatives (e.979 (. Other major uses include electrical equipment (e.

10-1.30 (1. 1999).01) .. a measure of accumulated dose (Cernichiari et al.60) 3.269-.475) .70) 4.90) 5. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.80-3.200-..800 (. Smith et al. 1993).60 (3. 2004. 2005).50) 1.600) . 1971). Sandborgh-Englund et al. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.0) 4.30-3.664-1.30-4.50) 2.20-11. 1992.00) 7.00) 1..377) .70) 1.30 (. After exposure to elemental mercury.90 (4.300) .14.700 (. 1994) and then undergoes slow dealkylation to inorganic mercury.395) .50) 1.30 (1..29) . 1996.900-1.726-1.697-.200 (.00) 2.300 (. Geometric mean Survey years (95% conf.10 (1.00-1.00 (3.200 (.50 (1.20-3.738-.800-1. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.70-5..20 (2.200-. interval) Selected percentiles (95% confidence interval) 50th ..800) 1.30-11.14 and 0.10 (1..00) 4. 1973). 1995.700-.800 (.200-.70 (1.30-6.10 (.40) 2.500 (. Vahter et al. 1993). National Health and Nutrition Examination Survey. 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.30) 3.00) 6.369) 1.40 (1.80 (1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al..297-.700 (.300) .10) . Miettinen et al.300) . Methyl mercury enters the brain and other tissues (Vahter et al. Vimy et al.30) 1.00 (2. 2003). 1994.300) .700) 2.3) 4.377 (.90 (1. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.500-.300 (.60) 1.70-3.40-1.70-3.256-. 1992).30-5. 2003).40 (1.300 (..265-.30-4.70) 4..10 (3.90) 2.60) 1.70-6.10-3. Jonsson et al.800-1.30-6.900 (.407) .919) .800) 1.00 (2.667 (. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith..500 (.23) ..60 (1.10 (1..60 (1.700 (. 1998).500-1.40) 1.90 (1.10) 1.00-6.10 (. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.300 (.70-5. Smith and Farris.700 (.80) 1.02 (. thereafter. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.00-2. Methyl mercury is incorporated into growing hair.940) Race/ethnicity (females.50 (2.06-1.90 (4.500-.600 (.800) 75th .329 (.343 (.40-2. 1969.800) ..60 (3.541-..500-.20 (.20-3.200-.500-.268-.317 (. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.00) . 1984.800) .70 (1. McDowell et al. Myers et al. Suzuki et al.80) 579 527 370 436 588 806 Limit of detection (LOD.20) .90) 2. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . 1975.30-6. 1996).00 (2.500-.50) 3.900 (. Fourth National Report on Human Exposure to Environmental Chemicals 219 .00-2.20-2.00 (1.374) .50-2.7) 4... 1999-2002.600) .06 (..824) 1.200-.700-.20) . and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.20-3.60) 2.300) .Metals the tissues to mercurous and mercuric inorganic forms.200-.70 (1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.. Excretion occurs by renal and fecal routes.318 (. and a useful marker of exposure in epidemiologic studies (Grandjean et al.S.400-.. population.00) 1. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.825-1.700-1.871-1.90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .299-.00-3.90) 3.900-1.944 (.800 (.700-1.800-1. 1991. 1998). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80 (3.50-12. 1994).40) 5..90) 90th 1.73) 1. for both acute and chronic exposures.50) 95th 2.307 (..820 (.10 (5.30 (1. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.900 (.60 (1.40-2.30-2. 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.300) .00-2.10) .35 (1.30) 1. 1990).833 (.50-3.20) 1.27) .60 (2. with most elimination occurring through in the feces (Sherlock et al. 1992 and 1999.90 (3.

700-.. hypertension.600 (. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.. 2002.700 (.500-. Oskarsson et al. the existence of a causal relation is unresolved (Chan and Egeland. Rice.700 (.. irritability. gingivitis. which may vary for some chemicals by year and by individual sample. 220 Fourth National Report on Human Exposure to Environmental Chemicals .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 . and progressive constriction of the visual fields. Sakamoto et al.700 (.600 (. 2006. Salonen et al.700-. < LOD means less than the limit of detection.. pain in the extremities. and sleep disturbance (Bidstrup et al. 1951. 1998..500 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.. ataxia.600 (. Drexler and Schaller..700) 2007 2240 3406 Limit of detection (LOD. 1993).42. hearing impairment. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.600 (.800) . At levels below those that cause acute lung injury. anorexia. Inorganic mercury exposure usually occurs by ingestion.600) .500-. fatigue. cerebellar ataxia. 1995.500-. dysarthria. 2003).700 (. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.. Vupputuri et al. Sakamoto et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. 2004. typically after a latent period of weeks to months.600) . Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. limb deformities.600) . High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.600-. 2004. short-term memory loss. In recent epidemiologic studies. dysarthria. population from the National Health and Nutrition Examination Survey. 1996). 1983). 1987). 1970..600 (.500-.600-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .500) .500-. 1995. causing parasthesias. 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. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.600) .800) .Metals may be more efficient for inorganic mercury (Grandjean et al. Smith et al. Survey Geometric mean (95% conf..500-. Stern 2005. DeRouen et al. 2000.S. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. sensory impairments. Factor-Litvak et al.700 (. and cerebral palsy (NRC.700-.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500-. maculopapular rash.. 2000)..600 (.. 2004).500 (<LOD-.600) .600-. The constellation of findings may include anorexia.. overt signs and symptoms of chronic inhalation may include tremor.600) . Overt poisoning from methyl mercury primarily affects the central nervous system. Rissanen et al.600 (. 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. 1963).500 (<LOD-. altered physical growth. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Once absorbed.600 (.. insomnia.500-.600-. and neurocognitive and behavioral disturbances. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U... 2005). particularly irritability.700) . 2004).500 (. Smith et al.600) . Bellinger et al.700 (. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. 2006. and pinkish discoloration of the hands and feet (Tunnessen et al.600) .800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600) . Acute. 2005..500-. depression. 2000. see Data Analysis section) for Survey year 03-04 is 0.

2009).gov/toxprofiles.26 (1. range 40 years to 78 years) had an average total blood mercury concentration of 2.88 (1.250) .89) 3.770-1.09 (2.413-.63-2.420 (. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.350-.24) 1..442-.370) .96 (1.870-1. interval) .14) 90th 2. population from the National Health and Nutrition Examination Survey.55 µg/L.447 (.570) . see Data Analysis section) for Survey year 03-04 is 0.870-1.930-1..58 µg/L for 4645 adults..01 (..213-.67-3.555) .330-.90) 2. Mahaffey et al.509) . total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.14.. 2000). 2004. 1998).940 (.480 (.700 (.S. 2006).97) 2.382-.08 (1.530) .60) 619 713 1066 Limit of detection (LOD. 2003). Among the three racial/ethnic groups.. 2009). 2001.60-2.23) .509) .34-3. Survey years 03-04 Geometric mean (95% conf.410-.840) 1.88-3.66) 3.495 (. total blood mercury increased with age. Fourth National Report on Human Exposure to Environmental Chemicals 221 .77-2. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.65) 1. A cohort of 1127 U. Benes et al.54 (2.03-4.400 (. 2001. 1998).S. particularly methyl mercury.330-. Total blood mercury levels increase with greater fish consumption (Dewailly et al.. 1995.530-.epa.46 µg/L for children.433 (.8 years.60 (1. These distinctions can help interpret mercury blood levels in people.534) .460) .S.480) 75th 1.07 (.492) Selected percentiles ( 95% confidence interval) 50th .330-. Over the NHANES 1999-2006 survey periods.05) 1.12 (. From 1996 through 1998.68 (2. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.358 (.cdc. Kingman et al. 2002). 2003).e.610-1. and increased slightly in non-Hispanic white children (Caldwell. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.520) .76-4.42) 95th 3.549) . These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.360 (..9 years). In NHANES 19992002. However.406-.396-.76-3.S.441 (. Sanzo et al. 758 children. who participated in a 1998 representative population survey (Becker et al. Biomonitoring Information In the general population.29) 1.960 (. adult women in several ethnic subgroups (Hightower et al.39-3.00) 1.88) 287 722 1529 03-04 03-04 .416 (.840-1.463) ..405-. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.31) 2. the total blood mercury concentration is due mostly to the dietary intake of organic forms.61) 1.340-..18) 2.890 (.19 (2.313-..290-.23) 2.200 (. 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.16 (1. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.700-1.31) 1266 1272 03-04 03-04 03-04 .78 µg/L for adults and 0. slightly higher total blood mercury levels were found in U.gov/mercury and from ATSDR at: http:// www. environmental levels) and health effects is available from the U. and the age-related changes differed across the groups (Caldwell et al.20 (1.160-.28) 1.360-.430 (.. et al.530) .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 .430) .33 (2.460 (. average age 33 years.24 (2.430 (.67-2. Information about external exposure (i.46) 3.atsdr.93 (1. 1997. the median concentration of blood mercury was 0.280-.19 (1. Schober et al.. military veterans (mean age 52.05) 3.304) .580) .S. EPA at: http://www.360-.440 (. aged 18 to 69 years.99-6.476 (.78-2.76-3.13-2.96 (1.52) 2. Grandjean et al.254 (.08 (1.420 (.330 (. total blood mercury geometric mean levels in females aged 16-49 years did not change.14-2. During the same survey periods. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.00 (.840-1.30) 3.408) . EPA.85-2.16 (. In Germany the geometric mean for blood mercury was 0. average age 9..Metals standard for inorganic mercury has been established by U.

619-.11-2.04-3. et al.535) 1.88 (1.07) 1.S.687) . 2009). 2006). The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. 1998). and Italian (Apostoli et al...508 (.46-2.480) .616) .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 . 2002).333-.301-.365 (.61) 1.417) .404-.40 (1.455-.32 (1.31 (1.875-1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.969-1. et al.67 (1.463 (.566) .522-. 1992).362 (. Department of Health and Human Services noted that several studies have observed a modest.18-1.265-. the urine mercury increased by approximately 0.21) 1.485 (. An expert-panel report recently prepared for the U. reversible increase in urinary N-acetyl-glucosaminidase.964-1.297 (. Survey years 03-04 Geometric mean (95% conf.79 (1.599) .39) 1.384 (. mean urinary mercury was 3..785-1.87 (1.03) 2.225-. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.00) 286 722 1529 03-04 03-04 .472-.368) .498) 75th .365 (.12-3.476 (.306 (.41-2. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.455) .343 (. and on average.40-1.545 (.970 (.. interval) .358) .09) 1.392-. 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. Urinary mercury levels in recent German (Becker et al.86) 95th 2..79) 1.11) 1.62 (1.30) 2.00 (.S.88-2.16) 1.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .63) 1. Levels in U.309-.88-2.S. 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.990) . a biomarker of perturbation in renal tubular function.23-2.307-.11) 2. women of childbearing age have generally been much lower than these levels (CDC. 2005)..620-.32-2.391-.400-. Information about the biological exposure indices is provided here for comparison.25 (. In the study of U.77 (2.464 (.280-.630) .400) . Langworth et al.S.255 (.67 (1.276 (.443 (.246-.64-2.00) 90th 1.714-1. not to imply a safety level for general population exposure. 2003).347) .78-4.65 (1.525 (.44) 1.1 µg/L for each surface with a dental amalgam (Kingman et al.532 (.06 (.447 (.06 (.S. DeRouen et al.385-.35 (1.54 (2.537) . Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. Urine mercury and the number of dental amalgams were correlated. population from the National Health and Nutrition Examination Survey.1 µg/L.768 (.Metals 2000).87) 2.800-1.455-. 2006.667-1..208-.217 (.196-.13 (1.376-.587 (. 2009). 1988.28 (. military veterans with dental amalgams.01) 2.30) 1.652) .447-. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.76 (1.13-2. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.696 (.. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L..784) 1.289) .588) .275) .. Czech (Benes et al.391) .486) Selected percentiles ( 95% confidence interval) 50th .56) 1266 1271 03-04 03-04 03-04 .909 (.51-2. 2002) adult population surveys were similar to those in a U.

909-1. 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.45-2.686) .84 (2.45) 2.21-3.14) 3.650 (.16-5.50 (2.520-.92) 4.35 (1.719 (.709) 75th 1.09-1.84 (2.69-3.605-.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.59-5.06 (.00 (3.72) 1.92) 3.18) 3.43-1.475-.56) 3.45) 95th 3.99) 1.600 (.410-.87-4.55-3.658 (. National Health and Nutrition Examination Survey.79) 1.16) 5.45-3.760 (. Geometric mean Survey years (95% conf.620 (.27-1.21 (1.98 (5.31 (1.91 (2.520-.580 (.580-.721 (. population.00) 2.42) 2.52) 3.56 (1.540 (.650 (.38) 4.664) .77) 1.592 (.37 (1.426-.833) . National Health and Nutrition Examination Survey.772 (.502-.420-.68-3.582-.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .99-2.557-.94) 1.631-.831) .664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .27 (2.81-6.24) 6.83-3.809) .553-.47) 1.51 (3.92) 2.91-7.740 (.53-3.32-3.70 (2.89 (2.07-2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .606 (.710 (.54) 595 531 381 442 594 826 Limit of detection (LOD.657 (.95 (2.48 (2.699) 1.45 (1.81 (3.65-4.723 (.85-3.07-5.S.709) .46-4.68 (3. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.69 (1.76) 2.76 (1.05 (2.824) .15-1.624-.07) 1.97) 2.04-10.S.639 (.710) 1. 1999-2002.650) 1.500-.39-3.665) . interval) Selected percentiles (95% confidence interval) Survey years 50th .32) 2.37) 1.27 (1.832-1.50-4.28 (1.615 (.508-.560 (.46 (1.637) .09-1.05 (3.25) 2.62 (4. population.22-3. 1999-2002.870) .655 (.450-.30 (2.97 (1.15 (2.50 (1.55) 90th 3.14.03 (.57-4.13 (2.17) 95th 5.41 (1.632 (.387-.526-.30 (1. 16-49 years) 99-00 01-02 .892) .61) 1.501-.51) .670) 75th 1.579-. interval) Selected percentiles (95% confidence interval) 50th .97) 2.41 (2.685 (.540-.77) 2.742-1.46) 3. Geometric mean (95% conf.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.18 (3.930) .45) 2.616-.65) 1.31-1.744) 1.966) .831) .61-6.21 (2.610-.22 (.790) .14 and 0.35) .710 (.3) 5.850-1.41-6.799) .41 (1.774) .62 (3.516 (.13-4.44) 3.32 (1.30-2.23-1.565 (.68) 3.724 (.30 (2.622-.596 (.99 (2.810) .62 (1.560-.691) .10-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.706 (.03) 1.14-1.99 (3.42-3.03 (. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old. 16-49 years) 99-00 01-02 .79) 3.14-2.Metals Urinary Mercury−Females Aged 16-49 Years Old.97) 2.56) 4.10-4.806) .522 (.00 (2.569-.910) .42) 90th 2.578-.846) .47) 1.636-.656-.24-1.23-1.76-5.04-1.85) 4.03-2.

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Arch Environ Health 1993. Leitao JG. Jones RL. Effects of occupational exposure to elemental mercury on short term memory.79:786789. Whittle K. Smith PJ. Am J Physiol 1990. Patil LS. Environ Health Perspect 2003. Smith AE. The hair-organ relationship in mercury concentration in contemporary Japanese. Br J Ind Med 1983. Schober SE. Acrodynia: exposure to mercury from fluorescent light bulbs.98(1):133-142. Vorwald AJ. Friberg L. Baser M.115(10):1527-1531. et al.48(4):221229. Stern AH. Tunnessen WW. Amiano P. Orr MF. Hislop D. Smith RG. Sherlock J. Environ Health Perspect 2007. Woods JS. Dorronsoro M. JAMA 2003. Methyl mercury pharmacokinetics in man: a reevaluation.97(2):195-200. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. The contribution of dental amalgam to urinary mercury excretion in children. Toxicol Appl Pharmacol 1994. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Zeitz P. Amurrio A. Farris FF.128(2):25125-25126. Goldberg J. Sinks TH. Leroux BG. McDowell M. Shen DD. Environ Res 2005. Blood mercury levels in US children and women of childbearing age. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Environ Res 2005.37:245-252. Langolf GD.Metals Sanzo JM.258(4 Pt 2):R939-945. Azpiri MA.110:129-132. Bolger PM. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Hall LL. Sandler DP. Smith JC. Vimy MJ. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Am Ind Hyg Assoc J 1970. Kaye WE.111(12):1465-1470.40:413-419. Vahter M.289(13):1667-1674. Daniels JL. et al. Toxicol Appl Pharmacol 1994.31:687-700. Longnecker MP. Most B. Imai H. Public Health Nutr 2001. Mooney TF. Turner MD. Vupputuri S. Lorscheider FL. Environ Health Perspect 2002. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Smith JC. Burbacher T. Osterloh J. Matsuo N. et al. Nakazawa M. 1993-1998. Bernardo MF. Aguinagalde FX. Hongo T. McMahon KJ. Guo S. DeRouen TA. Takahashi Y. Effects of exposure to mercury in the manufacture of chlorine. Yoshinaga J. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.2:117-131. Topping G.4(5):981-988. Toxicol Appl Pharmacol 1996. Allen PV. Pediatrics 1987. Hum Toxicol 1984. Stern AH. Martin MD. Mottet NK. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Fisher HL. Suzuki T. 1999-2000.124:221-229. The kinetics of intravenously administered methyl mercury in man. Newton G. Lind B.

Excretion occurs predominantly via the kidneys.2) 79.1) 46.0 (42.2-53.3-47.6) 71.8-49.8) 44.6) 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 (99.6-46.6 (40.1) 35.4) 41.4) 76.1 (91.0-85.2-42.8 (82.9 (33.0) 55. At a daily oral molybdenum dose of 24 µg.0-53. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (43.0-101) 82.7 (71.7) 86.7-84.1) 126 (106-147) 109 (94.9 (37.6) 51. More recently.1-88. and in pigments for ceramics.5-91.0-100) 63.8) 48.7 (37.5-41.7-41.0-71. 2001).8-106) 88.1-44.9-55.6-42.3) 65.6) 93.6) 53.7) 51.3) 41.3 (55.4-82.4) 56.7-51.0 (81.4) 42.9 (52.5-46.9) 67.4 (79.4 (34.9 (73.3) 83.7-91.3-75.5) 44.9 (40. 0.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.5) 60.0-77.7) 78.9 (78.1-52.3 (53.2) 37.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.2 (61.3-115) 152 (120-217) 177 (142-207) 152 (141-169) 206 (150-274) 166 (147-170) 156 (135-175) 187 (146-223) 152 (134-180) 130 (119-142) 780 683 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. population from the National Health and Nutrition Examination survey. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.0 (76. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.6 (43.3) 37.7-60.7-105) 69. which exert homeostatic regulation over molybdenum balance. 2001.5-52.7-73.6) Selected percentiles ( 95% confidence interval) 50th 50.9-82.7 (73.5) 85.5-66. urinary excretion over six days CAS No.7) 78.5) 80.9 (34.7 (44.1-59.8-46.2) 40.2-79.7-92.6-58.9-55.4) 52. 01-02.4 (80.0) 54.1-52.3 (55.8-90.3 (47.2 (56.6-62.1-51. Fourth National Report on Human Exposure to Environmental Chemicals 227 .6 (55. and 03-04 are 0.7) 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 78.3) 85.3 (71.2 (63.1 (34.5 (48.0) 97.5 (37.2-70.1 (71.3 (64. hydrogenation catalysts.9) 62.0) 39.5) 47.4) 49.2) 41.5 (74. and 1.8) 40.7) 75th 84.0 (43.0 (46.5. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.3-44.9 (44.2-37.4 (72.5) 80.1) 59.1) 57.8) 39.8) 75.9-85. 1996).5-65.6 (73.4) 45.7) 45.8 (67.9 (32.3-108) 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 47.4 (48..0) 62.0-56.5-52.7-96.1) 60.9-109) 97.6-72. aldehyde dehydrogenase.4-52. interval) 45. semiconductor and battery industries have begun to use molybdenum.7-39.7) 57.2 (69. chemical reagents in hospital laboratories. 7439-98-7 General Information Elemental molybdenum is a silver-white.0-65.7 (45.3 (38.5 (81.6-111) 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. respectively.4-61.7-50.6) 71.3) 47.4 (48.2 (83.7-47.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.0-62.2 (40.0-38.7 (51.1-55.5 (49. lubricants.7-68. inks.3 (46.6-82.1-48.2-91.9) 34.6 (55.0 (41.2 (55.7 (58.0) 45. In humans.9-83.5 (41.5 (41.3 (84.0-110) 90.3 (79.1) 82.2 (49.8 (85.9-56.2 (49.7-122) 93.3 (37.8.2) 52.5 (67.3 (73.6 (52.6-55. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2-59. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.8-94.5-124) 108 (92.0) 84. WHO.3-91.1-63. Compounds of molybdenum are also used as corrosion inhibitors.5-68.8. 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.S.3) 54.7 (36.8) 46.0 (48. 1997).7 (50. see Data Analysis section) for survey years 99-00. and xanthine oxidase (Kisker et al.4-75.0) 60.8 (42.1 (38.2-59.6 (40.8-108) 87. and paints.2 (38.7) 77.Metals Molybdenum or ore deposits.6-96.2) 48.7) 46.0 (42.2) 53.

5 (38.5-62.5) 63.9-117) 57.4) 58.2) 42. and clinical or epidemiologic evidence of adverse effects is limited.9-118) 91.2 (57.1 (82.1-109) 89.9 (35.5 (37. and urinary levels reflect intake from all sources.9-41.7-43. U.2-47.1 (38.2) 39.03 mg/kg/day in humans (IOM.7-44.4-106) 85.5 (78.0-120) 85.4) 116 (101-126) 104 (88.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.9) 44.3) 43.5 (35.7) 112 (95.6 (36.2 (40.1-41.8 (36.4 (56.6-88.1-34.7-52.7-40.5 (40.2-40.0 (74.4-39.5 (40.5 (41.2 (52.8) 71.0) 62.3) 57. 1993).4) 61.5 (54.3) 37.8) 39.8-67. 1995).5) 90th 108 (97.6-45.0 (80.9-68.3 (55.5 (37.1) 43.6-63.7-137) 129 (109-155) 112 (97.8) 38.3-43.1-43.6-63.1 (38. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.9-45.0-46.5 (41.2-41.0 (35.1 (30.5 (83.7-93.9 (64.5 (65.1-100) 86.3-68. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-92.5-35. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.2-65. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.3) 40.5) 72.9-40.4) 48.8-84.3 (71.2-80. but available epidemiologic data are scant.0 (58.1-43.7 (75. respectively.1 (39.4 (67.3) 56..4 (59.5 (50.9 (36.4) 122 (107-133) 109 (99.2-96.6-41.2-121) 107 (92.8) 37.4-107) 85.1 (44.8-52.5-50.1 (49.6 (59.1) 56.8-66.2) 43.8-47.2-49.7 (66. In industry.6) 39.3-46.1 (33.9) 31.0) 39.7) 45. Biomonitoring Information Molybdenum is an essential element for health.4) 60.6 (38.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.7-38.5 (34.7) 57.5-45.5-97.3-141) 109 (81.0) 33.5-69.4) 44.4-76.5 (39.9 (39.3) 44.1) 40.6 (36.1-112) 78.9 (64.2) 39.1 (42.8 (75.3 (83.8-46.2 (69.4-120) 101 (84.3) 41.8 (56..6 (57.8 (57.8-118) 81.0) 36.3 (51.7) 62.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.6-76..1 (37.4 (44.3 (36.3 (37.5-99.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.3-45. 2001).8) 61.7 (30.6) 43.3-56.3 (58.4) 40.5 (59.1) 65.0) 72.2) 42.2) 55.3 (36.3-52.0) 38.9) 92.5-60.7 (77.1-81.0) 44.6 (42.7) 41.9 (73.9 (39.5) 71.9-71.3-59.6 (71.8) 79.6) 48.7) 75th 63.9-87.5 (80.5) 73.2 (40.6-61.9-96.5 (65.8-65.9-61.1 (54.3-102) 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. Molybdenum is generally considered to be of low human toxicity.4) 47.5-48.9 (40.6-61. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.9 (79.6) 39. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.8 (90.9 (49. at daily oral doses of 95 µg and 428 µg.1-67.1-38. of the ingested dose (Turnlund et al.3 (53.0-38.7-120) 87.8 (37.6) 36.4-185) 106 (94.7) 42.0-46.7) 115 (93.9) 40.9-42.1-79.4 (53.1-39.2 (37.1-127) 90.0) 88.1) 37.Metals was 18% of the ingested dose.5 (79.4) 77.1-39.1) 101 (83.4 (37.7) 53.5-44.4 (78.9) 79.0-56.3) 64.9 mg/kg/day and established a tolerable upper intake level of 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 .2) 37. 1997).2 (40.2-103) 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 42.2 (33. Based on studies finding adverse reproductive effects in rats and mice.7-62.4) 89.0-133) 119 (88. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.4 (40.0-103) 103 (90. 1999).1-45.4-42.6) Selected percentiles ( 95% confidence interval) 50th 41.S.4-41.3-44.5-70. population from the National Health and Nutrition Examination survey.3-115) 98.0-41.0) 39. urinary excretion over six days rose to 50% and 67%.9) 41.6-78.0) 53. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1) 37.5-119) 90.S.4-66.5 (35.3) 61.2) 37.2) 58.8) 45.4 (55.1 (40. interval) 43.8) 38.2) 38.3 (37.9-45.2-46.1-40.8-47.5-46.7-100) 77.3 (71.2-96.2 (36.2 (50. EPA.5 (36.5 (39.5) 60.8) 62.2 (43.8-42. 1961.2 (73.

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

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

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

org/documents/ehc/ehc/ehc125. Schierl R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations.htm. Huber R.35:313-321. Seifert B. Iavicoli I. Wilhelm et al. Senofonte O. van de Weyer C. Schulz C. Environ Health Perspect 1975b. Ewers U. 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. 2000. Platinum concentrations in urban road dust and soil.. International Journal of Hygiene and Environmental Health 2003. Analyst 1998. Arch Environ Health:1969. Levels of platinum in urine for the U.htm.61(7):636-9. Kazantzis G.19:685-691.9:152-158. Herr et al. Kulka U. Czerczak S. Occup Environ Med 1998.. Schulz C. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Part 1: monitoring of urinary concentrations.55(2):138-140. 289-380. 3/31/08 Moore W Jr. pp. Cohrssen B. and gold excretion of patients after insertion of noble-metal dental alloys.04 µg/L) in this Report. 2003. Hauff K.. Rommelt H. osmium. Urinary excretion of platinum from platinum-industry workers.123(3):451-454. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Pethran et al. Pethran A.10:63-71. 2003. 1998). Angerer J. population were below the limit of detection (0. Farago ME. et al. Turfeld M. Seiwert M. 2004).. International Programme on Chemical Safety (IPCS). In: Bingham E. and in blood and urine in the United Kingdom. Saindelle A.S.org/documents/ehc/ehc/ ehc125. Biomarkers 1999.005 µg/L (Iavicoli et al. Biomonitoring Information Urinary platinum levels reflect recent exposure. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Platinum. 2003). Hysell D. Biomonitoring of traffic police officers exposed to airborne platinum. Neuendorf J. Ruff F: Histamine release by sodium cholorplatinate. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Kuster W. Gromiec JP. 1998). 1991 [online]. Crocker W. Int Arch Occup Environ Health 2003.01 µg/L (Becker et al. 2004. Begerow J. Alimonti A. Stilianakis NI. Raab W. Schierl et al. Ruff F: Platinum and platinosis.inchem. Powell CH.. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.. Kaus S. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine.76(1):5-10. Int J Hyg Environ Health 2004. 2004) or less than 0... Hall L. and platinum. Moore W Jr. Arch Environ Health 2001. 206:15-24. Parrot JL. palladium. J Expo Anal Environ Epidemiol 2003. Bocca B. Influences on human internal exposure to environmental platinum. Available at URL: http://www. Ensslin AS. Pethran A. Herr CE. et al. 2003. Campbell K. Fries HG. Duneman L:Long-term urinary platinum. Jankofsky M. Schierl R.. Grimm CH. Nickel. Herr et al. Occup Environ Med 2004. et al. Schierl. et al. Wilhelm M. Thornton I. ruthenium.. Saindelle A. Urinary platinum levels associated with dental gold alloys. Environ Res 1975a. Br J Pharmacol 1969. Petrucci F. palladium.inchem. Blanks R. References Becker K.13(1):24-30. Schierl R.56(3):283-286. Carelli G. Gieler U. Hysell D. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Nowak D. Hebert R. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Kelly J. Schierl R.207(1):69-73. Uptake of antineoplastic agents in pharmacy and hospital personnel. Several studies have shown that background concentrations in general populations were usually less than 0. 5th ed. Environmental Health Criteria 125. Fruhmann G.70(3):205-208. Kavanagh P.Metals the International Programme on Chemical Safety at http:// www. eds. rhodium. Biomonitoring studies on levels of platinum provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of platinum than are found in the general population. Allergy and histamine release due to some platinum salts. 1997. which elevate urinary platinum by five to twelve-fold (Begerow et al. 1999.. Int Arch Occup Environ Health 1997. Patty’s Toxicology. 2001). Boos KS.4(1):27-36. New York: John Wiley & Sons.

280 (.400-.260 (.450 (.270) .202) .172) .250-.260) .480) .310 (.430 (.185-.330-.440) .450 (.181-.270-.270 (.440 (.370 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.280 (.290) .196) .410 (.02.210) .440 (.230) .290 (.470) .310 (.210 (.180 (.165 (. see Data Analysis section) for Survey years 99-00.02.390) .200) .200-.140-.170) .450 (.149 (.170 (.154-.400 (.270) .160-.133-.220 (.250-.350 (.220-.320 (.230) .390-.183) .370) .180-.390-. interval) .170-.380-. respectively.171 (.201 (.218) .147-. 2005).420 (.390) .218) .190 (.180) 75th .135-.150-.S.470) .210 (.173) .410 (.200-.200) .400) .450) .340) .250-.134-.250 (.180-.167 (.159 (.420) .370 (.520) .290) .360-.180) .450 (.156) .370 (.240-.510) .490) .210-.280) .340-.370 (.360 (.178) .220 (.145-.260 (.250-.200) .400-.183) .230) .330-.370-.360 (.220) .380 (.350) .300) .220) .170-.410 (.150-. and 03-04 are 0.460) 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 .370-.400-. 01-02.440) .200 (.290 (.470 (.170) .220 (.270-.390-.176 (.320) .290) .196) .167-. the latter being the current major industrial consumer of thallium in this country.410 (.410-.430) .310-.400 (. 0.200 (.410-.270 (.500) .200) .630) .145 (.148-.420) .217 (.280 (.163) .360 (.400) .220) .340) .160-.370 (.200 (.360-.137-.400 (.270-.184 (.360-.330) .400-.410-.02.170-.410-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.330-.420-.156-.320) .430-.190 (.590) .250-.250-.250) .170 (. thallium was obtained as a by-product of smelting other metals.450 (.380-.173-.230-.159 (.197 (.450 (.470 (.147-.215) .280) .170 (.310) .200 (.440 (. 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 (.410 (.160 (.202 (.146 (.500 (.410) .153-.300 (.260-.250 (.147-.167-.420) .180-.640) .240-.158) .220) .243) .160 (.310 (.690) . and 0.260 (.350-.400-.410-.240) .270 (.217) .170) .239) .270 (. however.390) .430-.400) .320) .370 (.220) .490 (.240) .230-.410 (.470) .220 (.179-.590) .430-.157-.330-.170-.260-.460-.390 (.280-.172 (.160-.180-.162-.400 (.172 (.250-.520) .360-.490) .160 (.440-.500) .156) .188) .200-.160-.187-.180 (.201 (.173) .300 (.290-.175) .290 (.290) .430 (.190-.155 (.170-.420) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.300-.410-.300) .330-.450 (.190 (.330) .159 (.150-. it has not been specifically mined or refined in the United States since 1984.420) .370-.150-.520 (.300) .290 (.350-.197-.430 (. population from the National Health and Nutrition Examination Survey.490) .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 .270 (.192) Selected percentiles ( 95% confidence interval) 50th .225) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.290-. representing distribution into other tissues.430 (.190 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.180 (.350-.290) 90th . In the past.450 (.177) . In addition.240) .490) Total .170-.Metals Thallium depilatory cosmetics.220 (.380) .440) .340-.450 (.200) . In the United States.500) .350-.350) .320-.240-.420-.185 (.230) .390 (.160-.400 (.480) . Thallium disappears from the blood with a half-life of several days.290 (.460 (.202 (.200 (.340-.260-.190 (. From these and other sources.350 (.250-.340 (.430) .420) .330-.460) .390-.165) Sample size 2413 2653 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .360) .200) .280) .360-.206) .160 (.370) .191 (.200-.330) .280-.350-.480) .480) .340-.400) .520) .260-.170-.190 (.300) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .230-.300 (.510 (.182-.160 (.350-. Human health effects from thallium at low environmental CAS No.220) .480) .330-.440 (.560) .330) .370-.370 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.200 (.230 (.145-.420) .400) 95th .390) .260-. thallium readily crosses the placenta and also distributes into breast milk.290 (.360 (..550 (.420-.144 (.150-.150-.420-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.

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

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

810) .084 (.260-.097-.250) .140 (.360-.390 (. see Data Analysis section) for Survey years 99-00.071 (.190) .170) .520) .530 (. mainly as scheelite (CaWO4).180-.107 (.100-.340-.210 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.180 (.100) .250) .400 (.100) Selected percentiles ( 95% confidence interval) 50th .650) .310-.220) .470-.300 (.080 (.060-.100-.490 (.070 (.450 (.370 (.090-.090-.210 (.101-.082) . Evidence is lacking for the carcinogenicity of tungsten.070) .260-.690) .110 (.200-.082 (.096 (.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-.210) .092 (.084-.460) .130-.950) .S.100 (.095-.140 (.080-.260 (.066-. Little information is available on the toxicity of tungsten.060-.340) .520) .135) .240 (.430-.110) . 01-02.390) .170 (.110) .080) .320-.150 (.082 (.220-.250) .090-.360) .060 (.160 (.150 (.140-.530 (.53) .120-.180-.260) .080-.080 (.210 (.470 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.070-. interval) .500 (.800) .093) .170) .100-.180) .120-.140 (.320) .290) .550) .770 (.350) .250-. bronzes in pigments.340-.360-.180-.410 (.130) .050-.290 (.290-.160 (.450-.380) .230) .120-.210 (.410-.140 (.160-.330) .120-.560 (.620) .510-.120) .116) .460 (.077-.170) .300 (.160 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .260 (.310-.370-.230-.130 (.111-.090) .350) . respectively.080 (.110 (.790) .280 (.640 (.160) .100 (.300 (.158 (.070-.090-.370 (.190-. which are used in rock drills and metal-cutting tools.470 (.056-.380-.560) .290-.04.190-.078-.076 (.071-.630) .04.069) .220) .270 (.081 (.090-.190 (.130-.380-. and for producing ferrotungsten.400 (.190-.070) .560) .060 (.050-.510-1.080) 75th .830) .073-.137 (.230-.04.350 (.100) .070-.096-.060-.160 (.130) .270-.100 (.160 (.120) .270 (.160-.290) .510 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.180) .090-.200 (.126) .130 (.350-1.310-.087) .550 (.340-.151) .060-.170-. and 03-04 are 0.230 (.380-.070 (.Metals Tungsten CAS No.260-.093-.056-.091) .132) .070-.100) . and 0.480) Total .420-.060 (.190-.360 (.350) .110-.095-.080) .300-.130-.122) .064-.180-.150) .090 (.500 (.062 (.620) .113 (.380 (.560) .380 (.210 (.090-.120-.430 (.090 (.109) .092) .065-.470) .120) .190 (.280 (.500) .180) .110 (.140) 90th .580) .530 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.250) .120) .160-.088 (.420-.120) .074-.330-.230-.270 (.230-.080 (.087-.470) .380-.090) .090-.200) .270-.076 (.400) .073 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.440) .250-.073-.320-. filaments for incandescent lamps.120-.370) .093 (.050-.062 (.550) .330 (.130) .670) .550) .100) .105 (. 0.590) .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 .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 .370-.220) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.140-.092 (.250) .130) .058-.204) .110-.400 (.100 (.060 (.310-.060-.170 (.270-.080) .070) .060 (.310) .570 (.090) .070 (.120 (.180) .400 (.060 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.113 (.460) . Tungsten is used mainly for producing hard metals.520) .430 (.280-.133) .104) .310 (.460 (.220 (.150-.560) .240-.101 (.130) .090) .270-.230) .430) .069-.100) .080 (.320 (.300) .430-.310-.360 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.330-.330) .086 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.110 (.110-.180 (.065 (.073) .110 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).113 (.084) .082-. population from the National Health and Nutrition Examination Survey.105) .068) .460 (.400-.150 (.120) .060-.088) . Tungsten compounds are used as lubricating agents.070-.620 (.430 (.250) .113 (.070) .160) .00) .490) .160-.370 (.320 (.800) .170) .290-.050-.123-. and as catalysts in the petroleum industry.090 (.360 (. which is used in the steel industry.570 (.300) 95th .130-.210-.

Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.071-.064-.083 (.071 (.067-.482 (.167-.302-.062 (.412 (.190) .078 (.098-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.057-.081 (.139-.426) .070 (.197) .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 .067 (.286-.083 (.073 (.080-.301) .083) .116-.333 (.161) .272-.(Kraus et al.086) .072 (.436) .217-.155-.339 (.077-.414) .077) .287) .063-.133) .308) .255 (.054-.237-.119 (.465) .231 (.090-.081) .880) .075-.098) .205-.359 (.136-.064-.091 (.199 (.071) .144-.095-.364 (.091) .200-.265 (.085-.253 (.258-.136-.270 (.410-.066 (.222-.184 (.379 (.146 (.087 (.293 (.439 (.462) .224) .152-.060-.667 (.333-.200-.074-.084 (.125) .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 .216-.484 (.198-. Patients with medically-inserted tungsten found at increased levels in drinking water.216-. 2001).353 (.074) .109-.188-.059 (.139) .082) .133) 90th .278-.073 (.075) .117) .174) ..214-.339 (.126-.098-.104-.181 (.139 (.078) .165) .116) .439 (.146 (.069 (.107-.206-.218 (.094-.117 (.267-.222) .727) .383 (. and 2003-2004 (Paschal et al.285) .300) .078) .28) .237) .306) .079 (.055-.136-.059-.094) .300-.308) .124 (.170-.500) .080 (.197) .179-.060-.077) . or exposure that a control group of non-metal workers had mean levels differences.158) .075) . population (CDC.360 (.329 (.121 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.168 (.333-.158 (.245-.331-.150-.279 (.081-.341 (.059-.080-.167-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.065-.103-.071) .261-.146) .199 (.431) .179-.120) .086) .093-.299 (.169 (.089 (.231-.554) .084 (.063 (.453) .385 (.301) .538) . 2001-2002.061-.255 (.S.167) .240-.078-.426) .250 (.108) .344-.186 (.095) Selected percentiles ( 95% confidence interval) 50th .061-.154) .283) .452-.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 .136 (.070 (..121-.108-.072-.267) .120) .150-.167) .381) .060 (.158) .326) .201) .333 (.081 (. measure urinary tungsten.148) .208-.053-.209-.211 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.258 (.634 (.176-. population from the National Health and Nutrition Examination Survey.153-.233-.354) .217-.086) . population.094) .255-.174 (.079) .122 (.353 (.084) .215 (.122-.088) .392) . Nicolaou et al.497 (. 1998).098 (.214) .465) .079 (.099-.150 (. 2005).144 (.131-.085 (.090-.105 (.197 (.130-.082 (.091) .153) .302-.122-.105 (. 2003.138) .100 (.125 (.431) .063 (.133) .116 (.068 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.079) .S.093) .216-.301) .059-.100) .605) .300 (.250 (.136-.049-.436-1.075-.054-.061-.197-.317) .157) .180-.187) .215) .284) .203-.216 (.086-.069-.065) .143 (.074-.176-.130 (.092) .082) .151 (.253-. similar to those in this Report (Schramel et al.100) .315-.111 (.079) .083) .098-.329-.439) Total .079) .201 (.084) .300-.359 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.056-.065 (.667) .074 (.317-.088) .484) .294 (. Using neutron activation analysis to 2000. (1987) found possibly due to methodologic.375) .091) .333) .073 (.138 (.431) .067 (.279 (.347 (.075 (.148 (.109 (. interval) .275 (.582) .069 (.198) .071 (. 1997)..143-.065-.077-.063-.074) 75th .459) .058-.071 (.169) .091 (.083-.056-.065-.154) .145 (.354-.089) .358) .253) 95th .087) .250-. 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.279 (.333 (.072-.073 (.075 (.237) .065 (.555 (.340 (.124-.091) .071) .106 (.S.057-.063-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.158) .386) .063-.078 (.333) .317 (.164 (.066 (.739) .333 (.119-.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 .080 (.068-.085) .096) .797) .138 (.823) .216 (.

platinum. National Center for Environmental Health. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Schramel P. Sabioni E. 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. Angerer J. tellurium. Seghizzi P. Paschal DC. lead. urine. Pietra R. Centers for Disease Control and Prevention. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Occup Environ Med 2001.cdc. References Bachthaler M.69(3):219-223. et al. thallium. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. cadmium. Cancer Clusters. J Trace Elem Electrolytes Health Dis 1987. Sampson EJ. Churchill County (Fallon).58(10):631-634. 4/15/09 Centers for Disease Control and Prevention. Available at URL: http://www. Third National Report on Human Exposure to Environmental Chemicals. Jackson RJ. Mosconi G. Cassina G. 2004). Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Morrow JC. 2005.gov/nceh/clusters/Fallon/study.. Paetzel C. Pirkle JL. Angerer J. Link J. Catheter Cardiovasc Interv 2004. Kraus T. Lenhart M. Schramel P.htm. bismuth. Nicolaou G. Trace metals in urine of United States residents: reference range concentrations.76(1):53-59. Ting BG.Metals blood. Feuerbach S. The determination of metals (antimony. Manke C. Int Arch Occup Environ Health 1997. Environ Res 1998. Atlanta (GA). Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. mercury. Wendler I. [online] 2003. Nevada Exposure Asssessment.(2):73-77.62:380-384. palladium. Schaller KH. and hair (Bachthaler et al. Weber A. Zobelein P. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry.

and 03-04 are 0.027 (.008 (.045) .015-.004.046) .011-.009 (. 01-02.019 (.016-.010) .006-.047 (.007-.051) .007-.023) .063) .007 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.004.009-. including nuclear weapons.011-.037) .007-. Uranium has many commercial uses.006-.026-.012 (.027) .020-.038 (.024-.007 (.010-.011) .031 (.017 (.007-.030 (.021-.026) .006-.023-.010) .S.012-.023) .007 (.008-.009) .007-.009-.040 (.010 (.060 (.013 (.029-.016 (.040) .022) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).007-.008 (.007 (.020) .065) .009-.006-.010) * .027 (. Variable concentrations of uranium occur naturally in drinking water sources.072) .021 (. respectively.017-.008 (.050) .027) .028 (.023) .006 (.021 (.041 (.006-.009) .013 (.040 (.010-.013 (.127) .013 (.028 (.040-.015) .009 (.037) .007) 75th .007-.008-.007-.009) Selected percentiles ( 95% confidence interval) 50th .011) .007 (.012) .021) .006-.006-.017-.008 (.020-.011) .067) .024-.008-.007 (.011) .005-.005-.012) .017-.009) * .008-.009 (.034) .035-.022-.048 (.006-.009) .007-.008 (.021) .034-. population from the National Health and Nutrition Examination Survey.015 (.007-.008-.027-.053) .012 (.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 (.010 (.056) .009 (.031 (. interval) .023 (.020-.012-. and as an aid in electron microscopy and photography. Since the 1990’s.72%).019-.008 (.027 (.011-.027-.016) .011) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .054) .019-.016) .026 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.039-.018) .007-.014 (.158) .018) .037) .031 (.037-.016) .031 (.016) .036 (.008-.046 (.027) .033 (.037) Total .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.007) . 235U (about 0.023-.009 (.009) .054-.011 (.009) .007) .014 (.008) .007 (.008) .013 (.045) .007) .009-.006-. or processing.007 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.017-.009) .017-.028-.009-.008) .007-.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.007-.008) .022 (.033) .017) .017) . and 234U.042 (.065) .030 (.013-.015 (.005-.012) .010-.009 (.009) .028-.009-.016) .009 (.012 (.008 (.007 (.027) . see Data Analysis section) for Survey years 99-00.010 (.033-.016-.008 (.014 (.006-.026-.009-.020-.008 (.017) .018 (.006 (.023-.005.022-. human exposure occurs primarily by inhaling dust and other small particles.014 (.043 (.015) .014 (.008 (.006-.011-.011-.013-.005-.016-.010) .007-.022-.114 (.020 (.008 (.013) 90th .012) .036-.054) .028 (.049) .007 (.017) .011) .012 (.015 (.009 (.073) .041 (.012-.008 (.056) .046 (.064 (.036 (.017-.013 (.011 (.026 (.006-.040-. in some ceramics.006 (.007-.010) * .Metals Uranium CAS No.019-.006-.011-.033 (.046 (.040) .026) .012-.030) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.014 (.007) .010-.026 (.010-.024-.006 (.007 (.008 (.021) .009) .016) .009-.023 (.036-. and 0.013 (.067) . 0.009) .010) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.026) 95th .050) .012-.048) . Thus.038) .018-.037 (.043) .009-.023 (.053 (.025-.009-.039) .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 .027-.009) .010) .035) .008 (.029 (.020-.021-.042) . In workplaces that involve uranium mining.010-.088) . 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.046-.007-.012 (.005-.046 (.031-.044 (.020) .035) .066) .018 (.011-.062) .010) .010 (.010) .027 (.036) .007-.009) .034-.018) .021 (.010) .019-.008-.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .017 (.015 (.031 (.013) .007-.007) .011) .029-. nuclear fuel.279) .049) .018) .030-.008) .055 (.010 (.052 (.032 (.012 (.039) .008-.013-.024 (.030 (.017) . milling.036) .009) .009 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.009 (.069) .008 (.012-.023-.009) .

008-.021 (.024) .015-.005-.077) .027-.053) .020-.006-.006-.006 (.007 (.010-.007 (.009-.007 (.050) .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 .014 (.270) .008) .009 (.007 (.009-.022-.007-.026 (.013-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.034 (.014) .012 (.044) .014-.011-.009) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.051) .015 (.037 (.009) .006) .015) .006 (.008) .010-.015-.007) .008) .010-.021 (.006-.010-.016) .019-.006-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.025-.030 (.011-.006) . which can occur occasionally from high occupational exposure.014-.008-.008) 75th .067) .008 (.011) * .005-.025 (.015) . Inhaled uranium-containing particles are retained in the lungs.006) .013 (.007-.012 (.010-.006-.010) .011) .005-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.018 (.039) .008-.021-. Studies of persons with chronic exposure to soluble uranium salts in drinking water have not shown kidney Urinary Uranium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.030-.009-.020-.007 (. 2003).017-.007 (.008-.009 (.011) .048) ..007 (.011 (.035 (.009 (.032) .026 (.020-.008 (. After exposure to soluble uranium salts.018-.010-.006-. Health effects from uranium exposure result from chemical toxicity to the kidney.022 (..034-.016-.017-.007 (.009) .041) . In cases of retained DU shrapnel.012 (.028) .024-.005 (.061) .010 (.028) .007 (.022 (.022-.058) .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.007-.013 (.033) .007-.011-.006-.039) Total .008-.030) .017 (.010 (.027-.016) .008) . 0.013 (.042) .014-.009 (.009) .011-.025-.016-.026) .016) .005 (.014 (.011-.024) .018-.025-.047) .042) .032) .029) .028 (.012 (.007 (.024-.021 (.008 (.016) .023-.009) Selected percentiles ( 95% confidence interval) 50th .015 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .017-.006 (.028-.025) 95th .051) .012-.027) .015-.007-.021) .028) .007 (.005-.018) .013 (.008-.024) .051) .008) .009-.006-.010 (.009) * .007 (. population from the National Health and Nutrition Examination Survey.019) .006-.063) .013) .146) .006 (.020 (.024 (.S.018-.010-.009-.005-.006) .030 (.006 (.013 (.015 (.027) .012 (.080) .031-.009) .006-.011-.027 (.010-.016) .010) .008 (.012-.007-.020) .005 (.024) .006-.056) .017) .010) .006-.012) .039) .010) .100 (.Metals impact.015) .017) . interval) .007 (.008 (.030 (.007 (.012) .029) .022 (.021 (.008 (.006-.013 (.016) .011 (.006-.007-.029 (. with much slower elimination from bone.050) .027 (.010 (.011-.009) .015) .006) . the shrapnel acts as a source of chronic.009) .048) .007-.006-.015-.016) ..007-.010-.053) .042-. liver.024 (. After inhalation.009) .020 (.035 (.026-. which represents distribution and excretion.013 (.022-.031 (.007 (.025 (.027-. 2005).007 (.011-.029 (.019 (.017 (.013 (.007) .017-.040 (.009) .013) .059 (.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 .018-.043 (.008) .007) .014) .026 (.019 (.008 (.034-.010-. 1992).012 (.008) .004-.020 (.013 (.019-.006-.028) .022) . After long term or repeated exposure. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.034 (.012 (.006-.016) .039) .027 (. Radiation risks from exposure to natural uranium are very low.007 (.030) .029) .024-.025-. Uranium is eliminated in feces and urine.034 (.004-.045 (.019-.011-.008 (.008) .006 (.010) * .013) .034 (.005 (.018-.033 (.007 (.006-.006-.016-.006-.014) 90th .005-.006-.074) .015-.010 (.008 (.007 (.007 (.034 (.010-.033 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.008) .016-.013 (.006-.007 (.011) .006-.017) . Depending upon the specific compound and solubility.008) .020-.029 (.012) .007-.033 (. kidneys.034) .016 (.058) .015 (.014) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.009 (.019 (.1%-6% of an ingested dose may be absorbed.019-.005-.028 (.051 (.010) . where limited absorption occurs (less than 5%).029) .024 (.009) .024) .027-.054) .006-.019) .008) .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 .050 (.019-.033 (. low level exposure.010) .009) .030-.008 (.009-.

soldiers who had been injured and had embedded DU shrapnel for as long as eight years.cdc. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.066 μg/g creatinine (Gwiazda 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. Thomas RG. the median urinary concentration was 0.S. although slightly increased during and after deployment.168(8):600-605.110 to 45 μg/L (Ejnik et al. Information about external exposure (i. In: Gerber GB. environmental levels) and health effects is available from ATSDR at: http://www. Drinking water and other environmental standards have been established by U.. Stradling GN.S.162 μg/L) (Orloff et al. respectively.61 μg/g creatinine. 2004). NRC. Six workers in a depleted uranium program showed concentrations of 0. soldiers evaluated before.. the median urinary uranium concentration was 2. References Bhattacharyya MH..atsdr. Kent (England): Nuclear Technology Publishing.S. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.65 μg/L).. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. 2001-2002. Durakovic A. Radiation protection dosimetry. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Komaromy-Hiller et al. Hamilton et al. Sci Total Environ 1991. Byrne AR. 2002... Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. 2004).107:143-157. Centers for Disease Control and Prevention (CDC). Health Phys 2000.. but in whom no shrapnel was embedded. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. (May et al. EPA. Metivier H. In the same study. Uranium content of blood. 2003. 41 (1). 1991. The U. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. 1994..S.011 μg/L (McDiarmid et al.S. 2005. Breitenstein BD. 2006. Karpas et al. Pullat VR. 2002). Ejnik JW. Fourth National Report on Human Exposure to Environmental Chemicals 241 . et al..62:562-566. 2006). Squibb K.. 2006). A cohort of 46 U. and 2003-2004 (Dang et al. Dang HS. IARC and NTP have no ratings for uranium human carcinogenicity. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. with emphasis on quality control.Metals injury associated with elevated urinary uranium levels (Kurttio et al. 2004). Atlanta (GA). Guidebook for the treatment of accidental internal radionuclide contamination of workers. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Vol. Volf V.078 μg/L (ranging up to 5.. Horan P. Hamilton MM.. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Health Phys 1992. In a study of 105 persons exposed to natural uranium in well water. Galletti. Boyd P. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 2000). 2006).78:143-146.. Benedik L. 1978). in that the levels were below their respective detection limits (Byrne et al. during. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Estimate of the time zero lung burden of depleted uranium in Persian Gulf War veterans by the 24-hour urinary excretion and exponential decay analysis. Third National Report on Human Exposure to Environmental Chemicals.. Pillai KC. 28 soldiers who may have been exposed to DU by inhalation.gov/ toxpro2. 2004). 2000).e. urinary levels of uranium were as high as 9.. 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. Muggenburg BA. McDiarmid M.. Tolmachev et al. Mil Med 2003. 1992. In 17 U. eds. (Kurttio et al. McDiarmid et al. Dietz LA. or wound contamination... 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. 2006). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. the geometric mean urinary uranium concentration was 0. had a mean urinary uranium concentration of 0.S. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.1992. pp. and no consistent effects on multiple endpoints of kidney function were found. Carmichael AJ.55 μg/L (median 0. ingestion.1996. Zimmerman I.html. population. 1-49.

Biokinetic modeling of uranium in man after injection and ingestion. Nuclear Regulatory Commission (NRC) Guide 8. Halicz L. Charp P. Lorber A. Howerton K. Smith D. Pinto V. Andrews WS.296(1-2):71-90.158:165-190. et al. Englehardt SA. Paschal DC. Squibb K. Makelainen I. Squibb K. Inductively coupled plasma mass spectrometry as a simple. McDiarmid MA. Saha H. Bennett LG.44:29-40. Roth P. U. July 1978. Health Phys 2006. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Wilson PD. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Health Phys 2004. Health Phys 2004.87:51-56. et al. concentration and daily excretion of uranium in urine of Japanese. J Toxicol Environ Health A 2004. Kidney toxicity of ingested uranium from drinking water. D’Annibale L. Human exposure to uranium in groundwater. Uranium and thorium in urine of United States residents: reference range concentrations. et al.Metals Galletti M. Scott K. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Clin Chim Acta 2000. Ash KO. Komulainen H.79(1):11-21. Am J Kidney Dis 2006.110(4):337-342.71(6):879-85. et al. Sci Total Environ 1994. Washington (DC): NRC.82(4): 527-532. NRC). Metcalf S. Health Phys 2003. Tolmachev S.81:45-51. Karpas Z. Van der Venne MT. Biologic monitoring for urinary uranium in Gulf War I veterans. Salonen L. Hamilton EI. Heller J. Saha H. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Cordero S. Shelly T. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Salonen L. Ting BG.47(6):972-982. Cremisini C. Int Arch Occup Environ Health 2006. Environ Res 2004. Hancock RG. Environ Health Perspect 2002. Oliver M. rapid. Kane R. Auvinen A. Ejnik J. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Costa R. Lewis BM. Oeh U. Jarrett JM.S. VI. Noguchi H. McDiarmid M. Nuclear Regulatory Commission (U. McDiarmid MA. Wahl W. Hollriegl V. Marko R.85:228-235. Mistry K. Review of elements in blood. Uranium daily intake and urinary excretion: a preliminary study in Italy. Pirkle JL.94:319-326. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Karpas Z.86:12-18. Radiat Environ Biophys 2005. Kurttio P. Kuwabara J.S. Paretzke HG. Auvinen A. Jackson RJ. U. Engelhardt SM.S. Orloff KG. Health Phys 2002. Sabbioni E. et al.S. Sampson EJ. Oberbroekling KJ. Renal effects of uranium in drinking water. Harmionen A. patient population and literature reference intervals for urinary trace elements. Element reference values in tissues from inhabitants of the European community. Li WB. Pekkanen J. Marino R. Gucer P. May LM.22–Bioassay at uranium mills.67(8-10):697-714. Health Phys 1996. Katorza E. et al. Kurttio P. Ough EA. Komaromy-Hiller G.91(2):144-153. Kalinsky V. Gwiazda RH. Roiz J. Environ Res 1999. Comparison of representative ranges based on U.

07-4.00) 5.31) 2.93 (4.90-6.70 (3.0 (12.29-3.20 (6.90 (5.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.90-9.20) 7. and certain plants with high water content (e.20 (2.00) 3.70 (3. milk.0 (9.75-3.10 (7.38) 5.70) 3.30 (5.76) 4.70-11.0 (8.90-12.45-4.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.67-5.30-17.40) 2.0) 13.40 (5.0) 8.0 (12. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0 (11.30 (2. interval) 3.19 (3.0) 13.40 (8.90-11.20) 3.40 (3.0 (12. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 95th 14.50) 5. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0 (9.40-7.80 (6.60 (4.0) 11.30-7.0) 708 617 681 652 1228 1092 Limit of detection (LOD.40-5.50) 11.0) 10.20 (4.0) 11.76 (3.40 (4.90-10.60 (4. laboratory analysis.50 (3.44-4.40) 4.0) 9.0) 10.80 (3.0) 13.0) 9. leather tanning.10-11.40 (5. 2005).10-7.00) 3.90-9.0) 14. It is normally found and produced as the anion of a sodium.80) 12.56) 3.62 (3.40-11.70-7.09) 3.10 (5.0) 14.0) 10.51 (3.90 (4.0-19.S.30) 6.0-29.0 (9.20-4.S.47-4.90 (2.40-4.12) 3.20 (8. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.0-17. Perchlorate is stable under most environmental and physiological conditions.40 (3.EPA.60) 8.0 (11. Survey years 01-02 03-04 Geometric mean (95% conf.0-14.02 (3.60) 5.11) 4.81-16. 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 (2.80) 3.30-7.05 and 0. fabric dyeing.16) 3.30-6.0) 13. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.20 (2.05. and limited applications in pharmaceutics.79 (2. matches.0 (11.70-12.40) 3.96 (3. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.10) 3. certain catalytic metals.0-17.10 (6. Perchlorate was added to the U.39-4.0-20.00-6. 1998).0) 9.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.89-3.30-19.0 (13.50-4.0 (8.0 (11.0-18. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0) 13.10-4. or ammonium salt.40-6.0) 14. 2002).80-6.26 (2..70-3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .93-4.03) 3.90 (5.20 (5.00) 7. Other manufactured uses include fireworks.20 (7.0 (8.0) 15.0-15.0-15.50) 6.40) 90th 10.93-3.51 (3.0-17.00) 4.10 (6.0 (10.0 (12.10-12.0) 19.90 (3.50-11.90-3.90) 5. potassium.10-11. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.5 hours and has a small estimated volume of distribution (Crump and Gibbs.80-15.32 (3.10 (2.0) 9.0 (11.0 (11.70-3.50-3.68) 4. lettuce) can be the main sources of intake for humans (FDA.Perchlorate Perchlorate (Urbansky.60-7.20-11.80-12.40) 6.20 (4.0 (9.0 (8. and reducing agents..00-6. and electroplating.0) 13.90) 6.g.90-11.90-3.65) 3.0 (9.60-6.80 (7.0) 15.40-4.0) 8.01 (2.0-17.0-23.80) 75th 6.75 (3.08-3.0 (11.0) 11.80-4.0-17.50-7.81) Selected percentiles ( 95% confidence interval) 50th 3.30) 6.70-5.00-5.30 (2.0 (8.0) 9.10) 5.11) 3.40-13.0) 12. In addition.70-6.40 (5.10) 5.46) 3.0-18.50 (8.0-18.10) 3.80 (3.S.80) 7. but has strong oxidant properties in the presence of concentrated acids.70 (3.74-3.66) 3.49-3.50 (5. population from the National Health and Nutrition Examination Survey. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.20) 4.0) 16.19-4.40) 3.20-4. 2005).20-3.87-3.50) 5.18-3.0 (9.20-12.88) 3.80-4.30 (5.50-4.35 (3.70-9.10) 12.22 (2.40) 3.22-5.90 (5.0 (11. 2007).50) 3.54 (3.0-17.0 (11.0) 9. Drinking water.60) 3.60 (7.0 (9. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.84) 14.40 (4.0) 13.80-8.21 (2.0) 13.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0 (11.

02-4.70) 10..0) 12.19-6.12-2.40 (4. 2006.0) 12.90 (2.87) 2.02) 3.25) 5.90-2.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .3) 8.10) 3.0) 13. U.90-20.72 (3.29-6.10 (6.91) 4.70-5. Greer et al. Lamm and Doemland.54 (2.10 (4.64-3.86) 4.56-3. NAS.39) 2.90-11. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.0) 14. Li et al.66) 3.4 (11.03 (2.60-11.10) 6. population from the National Health and Nutrition Examination Survey.40 (7.30) 75th 5.20-3.26) 4.61-5. gender.80) Selected percentiles ( 95% confidence interval) 50th 3.4-16.10) 4.42 (3.60-8.73) 3. in a representative sample of U.0) 6.1-16.S.04-3.10-3. perchlorate is negative in most genotoxic assays (U..30 (6. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.00) 9.1-14.83 (5.30) 5..30-5.90) 5.98) 3.S.46-4.70 (4.35 (4.60-6.90 (7.74) 7.45-2.80 (7. interval) 3.4 (10.0 (9. 1999.5 (13.3-14. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.93) 3. 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.60-11.0 (11. Steinmaus et al.21 (2.80-3.33-6.61 (5.20-4. 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. 2005.80 (4.89-3.00) 4.40) 5.2) 8. 2002. 2005).12 (6.51-4.10 (1. 2005).05 (4.08 (3.16-3.00-11. chronicity of exposure. Lawrence et al. 2000)..25) 5.39 (3.Perchlorate inhibition (RUI).77 (3.52-9. levels and sufficient in most participants (Tellez et al. up to 68% RUI has been demonstrated.10) 13.50) 6.50) 9. 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.93-7.99 (5.87-3.87 (7.50-5. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.14 (2.S.93-8. Survey years 01-02 03-04 Geometric mean (95% conf.0) 9.0) 11. medications).15-12.60-5. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.2) 8.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.80 (7. dietary iodine intake.0) 10.7 (11.20 (6.93-5.24 (4.0 (9. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.08) 3.18-3.0-44.61-10.22-4.39-4.64) 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.25) 5..32) 5.10-7..90 (4.5) 8.00 (4.0) 4.0 (11.30 (3.95 (2.90-3.30-5. 2005.30) 90th 9.60-8.99-3.45) 3.40 (3.75) 3.40-10.0) 13.0 (9.89 (2.90-15. 2005). 2002.41-9.60-3.00 (2.20 (4.51 (3.82 (5.1) 8.20 (7.22-6.0) 12.47) 2.3) 11. menopausal status.20-3. However.0 (8.30 (5.3) 12.24-2.76 (3.30) 3.50-9..20) 8.6) 20.54 (3.1-22.0 (10.97-5.04-3.40 (3.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.EPA.96) 2.19-10.46-13.4 (8.35 (2.0-14.44-6.50 (3.0) 7.22 (2.52 (8.25 (3.29) 2.34-3.70-15.67) 5.50) 95th 12.50) 5. 2007).0 (11.S.6-17.87) 7.40) 17.S..50) 2.71 (5.37 (4.87 (5.44) 3. and the presence of other substances known to affect thyroid function (e.09 (7.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.3 (10.60) 10.70 (2.22-4.20-9.70) 2.07 (2. thiocyanate.50-3.60) 8.26 (3.33-12.20-10.6) 12.33 (7.43) 6.53 (2.S.59) 3.4) 8.S.46 (3. although iodine intake was higher than U.60-5. During gestation and infancy.10 (2.58) 2.0-14.0-19.20 (3.35) 3.56 (3.84) 2.60) 3.60 (3..0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.4 (11. 2001.8 (11.40) 3.4) 13.70 (2. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.50 (6.09) 3.90 (2.36 (8.80-3. age.50) 2.EPA.00-2. women with urinary levels of iodine less than 100 micrograms per day.0) 9. 2003. Many factors may be important in consideration of perchlorate action on the thyroid: dose. Also..81-3.g.1 (11. nitrate.90-9.60-15.70-3.00 (6.00-3.1 (8.00) 3.30-10.0) 12.10 (4.1-13.0 (8.76-3.37-13.0-17.93-5. In the U. levels. 2002).20) 3.20 (2.70-4.

Washington (DC): National Academy Press. Valentin-Blasini L.S. Erratum in: J Occup Environ Med 2004. J Occup Environ Med 2000. Li Z. Health Implications of Perchlorate Ingestion. epa. Doemland M. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.html and from ATSDR at: http://www. et al. Magnani B. Tellez RT.113(8):10011008.. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Pino S. EPA reference dose (Blount et al. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.. Sesser DE. Greer SE. thiocyanate. population. Additional information about exposure and health effects is available from the U. J Expo Sci Environ Epidemiol 2007. Braverman LE. Low dose perchlorate (3 mg daily) and thyroid function. 2007). 6/2/09 Greer MA. Daaboul JJ. Pino S. (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.10(8):659-663.113(11):A732. Dasgupta PK. Available at URL: http://www.cdc.11(3):295. Blount BC. Jackson WA. Blount BC. Environ Health Perspect 2002.S. 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.atsdr. Benchmark calculations for perchlorate from three human cohorts. Miller MD.45(10):1116-1127. Li FX. Byrd D. The effect of perchlorate. Kirk AB. Dyke JV. Skeels MR. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Deyhle GM. Lawrence J. 2001-2002. Buffler PA. Environ Health Perspect 2005. 2005. and environmental perchlorate exposure among residents of a Southern California community. Also. Goodman G. He X. Lamm S. Valentin-Blasini L. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. 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. Perchlorate Exposure of the US Population. Food and Drug Administration (FDA). Crump KS. Blount et al. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Perchlorate in the United States. 2005). newborn thyroid function. Howd R. May 2007. Osterloh JD. most of the population is considered to be below the U. National Research Council of the National Academies. Thyroid 2000.114(12):1865-1871. Thyroid 2001.gov/safewater/ccl/perchlorate/perchlorate. Caldwell KL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Occup Environ Med 2003.S. Analysis of relative source contributions to the food chain. Braverman LE. Landingham CB. Abarca CR.42(2):200-205.115(9):1333-1338. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Pirkle JL. Barnard JC. Erratum in: Environ Health Perspect 2005. Environ Health Perspect 2007. et al. National Academy of Sciences (NAS). et al. Chacon PM. Lau EC. Steinmaus C. 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.EPA at: http://www.htm.17(4):400-407.. Mauldin JP. Environ Sci Technol 2006.90(2):700-706. Primary congenital hypothyroidism.46(5):509. CFSAN/Office of Plant & Dairy Foods. Environ Health Perspect 2006. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 .41(5):409-411. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Page Last Updated: 05/28/2009. Lamm SH. Neonatal thyroxine level and perchlorate in drinking water.40(21):6608-6614.110(9):927-937. Crump KS. Richman K.fda. and nitrate on thyroid function in workers exposed to perchlorate long-term.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect.html. Cross M. Pleus RC. Lamm SH. References Blount BC. Osterloh JD. Kelsh MA. 2005). Pirkle JL. Gibbs JP. J Clin Endocrinol Metab 2005. Lamm SH. Rutherford GW. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Biomonitoring Information Urinary perchlorate levels reflect recent exposure.gov/toxpro2. Lawrence JE. Braverman LE. et al.

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

Other perfluoroalkyl carboxylates of various chain lengths were also formed in the process used prior to 2002... and their oxidation products.. current manufacturing Perfluorinated Chemicals in this Report practices reduce the formation of these by exclusively using fluorotelomers (Prevedouros et al. such as perfluorochemical telomers. building/construction. Worldwide annual production of PFOA was estimated to be 260 metric tons in 1999 (Prevedouros et al. Other PFCs (including small amounts of PFOA) can also form as side-reaction by-products in the synthesis of POSF (e. Perfluorooctanoic acid (PFOA) has been manufactured since the 1950s. low volatility (as salts or ionized) and can remain in the environment and bioconcentrate in animals (e. finalized perfluorochemical polymer products. manufacture of POSF-based products began ending in about 2000. perfluorooctane sulfonate. 2003). and also as constituents of floor polish. MeFOSE and EtFOSE have been used in food packaging and textile treatments. semiconductor. automotive. and insulation of electrical wire. and fire protection. Global production that year for POSF materials was 3700 metric tons (Prevedouros et al. perfluorooctane sulfonamide.g. In addition. or form in the final product (e. PFOSA). Discussed here are perfluoroalkyl acids. Perfluorononanoic acid (PFNA) was an impurity in the process that produces PFOS... amides. Olsen et al. adhesives. N-methylperfluorooctanesulfonamidoacetic acid (Me-PFOSA-AcOH) and N-ethylperfluorooctanesulfonamidoacetic acid (EtPFOSA-AcOH). Fluoropolymers have applications in waterproofing and protective coatings of clothes. 2006). Perfluorooctanesulfonyl fluoride (POSF) was synthesized as a polymerization starting material. Production rates and emission rates have fallen since 2002 after conversion to a new synthesis process. EPA. A major application of one important fluoropolymer. fluoropolymer products are used in a wide range of industries including aerospace. and textiles.. PFOS) (Hekster et al. and other products. U.g. Perfluorohexane sulfonate (PFHxS) has also been used to synthesize the fluoropolymers used in firefighting foams and some carpet treatments. PFOA is usually not a residual contaminant in non-stick surfaces made of polytetrafluoroethylene. and alcohols which are by-products. textiles.. Because of their properties. The PFCs have limited water solubility. several pathways (during manufacturing) can lead to formation of PFOS or other sulfonyl-containing PFCs as residual contaminants in the final polymer products. respectively. U. 2006). primarily as its ammonium salt. 2006).S. as a solubilization aid in the synthesis of polytetrafluoroethylene. has been the heat-resistant non-stick coatings used on cooking ware and other protected surfaces. chlorofluorocarbons and investigational blood substitutes. electrical and electronics. or form as degradation products during its reaction to create the intermediate reacting monomers. N-methylperfluorooctanesulfonamidoethanol (MeFOSE) and N-ethylperfluorooctanesulfonamidoethanol (EtFOSE).. or processing aids used in the synthesis of fluoropolymers. chemical processing. fire retardant foam. There are many other fluorocarbon type chemicals which are not addressed here.g.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. furniture. some fish bioconcentrate Perfluorinated Compounds Serum Perfluorobutane Sulfonic Acid Serum Perfluorodecanoic Acid Serum Perfluorododecanoic Acid Serum Perfluoroheptanoic Acid Serum Perfluorohexane Sulfonic Acid Serum Perfluorononanoic Acid Serum Perfluorooctanoic Acid Serum Perfluorooctane Sulfonic Acid Serum Perfluorooctane Sulfonamide Serum 2-(N -Ethyl-Perfluorooctane sulfonamido) Acetic Acid Serum 2-(N -Methyl-perfluorooctane sulfonamido) Acetic Acid Serum Perfluoroundecanoic Acid CAS number 335-76-2 307-55-1 375-85-9 355-46-4 375-95-1 335-67-1 1763-23-1 754-91-6 2058-94-8 Abbreviation PFBuS PFDeA PFDoA PFHpA PFHxS PFNA PFOA PFOS PFOSA Et-PFOSA-AcOH Me-PFOSA-AcOH PFUA Fourth National Report on Human Exposure to Environmental Chemicals 247 . 2003.S. end products. POSF-based polymers have been used in a wide variety of products such as waterproofing. 2005. polytetrafluoroethylene. may be markers of food or consumer exposures. However.

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

reproductive. population from the National Health and Nutrition Examination Survey..00) .. PFOA..00 (.00) . 2003a.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 2003). Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality..50) . thyroidal).600 (. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.400-1.400-1. EPA.S. 2003). 2004).S. and changes in thyroid hormone concentrations (Grasty et al. monkeys.. 2003). Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. the potential to estimate risks to humans from animal doses is uncertain. Kennedy et al. PFOS.300 (<LOD-. At doses causing maternal toxicity. 2003. 2003a.800 (. Harada et al. 2003a).800) 1..500 (. which may vary for some chemicals by year and by individual sample.S.400-1. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.600-2. elderly and children. Lau et al.. population.800 (. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.500-1. PFOS.300 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0. and there was no clear evidence of excess all-cause or diseasespecific mortality. Thibodeaux et al.10) . In comparing three separate reports on adults. and humans. 2004a. or increased cancer rates (Alexander et al. Cook et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003a. 2003a). PFOA. 2003.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .500-1. Fei et al. developmental and teratogenic effects were demonstrated in offspring.10 (. EPA. At high but non-toxic maternal doses of PFOS.. 2004). hepatotoxicity.400) .500-1. 1999. Survey Geometric mean (95% conf.40) .300 (<LOD-.. 2004.500 (<LOD-1. Analysis of the NHANES 20032004 subsample demonstrated higher levels of PFOA and PFOS in males and a slight increase in levels of PFOS with age (Calafat et al. Olsen et al. In such studies.400-.20) .800 (. development in offspring was stunted and hypothyroxinemia was observed.500) .800 (.10) * 03-04 03-04 * * < LOD < LOD < LOD . Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al... and no substantial age trends were seen within adults ages 20-69 (Olsen et al. 2001.10) . 2004b). 1992. Fourth National Report on Human Exposure to Environmental Chemicals 249 . Olsen et al. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. However.400-1..300-1.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 2004..500-..500) . 2003.500) 90th .400-. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 2007a..3. Animal studies of PFOS have demonstrated weight loss. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (<LOD-...400 (<LOD-.900 (. 2007). 2005).500-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .900 (. U. 2007b.800) 1. perfluorohexanesulfonate (PFHxS). 2007.500 (.600 (. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. 2007a.700) .S. 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.108 times higher than background serum levels in humans (Butenoff et al.500-3. possibly related to lung immaturity (Lau et al.900 (.500) . 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.00) .80) 640 1454 03-04 03-04 * * < LOD < LOD . U. 2007b). 2005). < LOD means less than the limit of detection.400-1..600 (.500) ..80) 485 538 962 Limit of detection (LOD. Olsen et al.400 (<LOD-.700 (..

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

600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th . < LOD means less than the limit of detection.600) < LOD .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .0.S.S. population from the National Health and Nutrition Examination Survey.300-.400 (. Survey Geometric mean (95% conf.300 (<LOD-.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.400 (<LOD-.900) < LOD . population from the National Health and Nutrition Examination Survey.400 (<LOD-. Survey Geometric mean (95% conf.600 (.300 (<LOD-.500) 485 538 962 Limit of detection (LOD.3. Fourth National Report on Human Exposure to Environmental Chemicals 251 . see Data Analysis section) for Survey year 03-04 is 0.500-.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400) .500 (<LOD-.

700 (.20) 1.984 (.20 (1.86 (1.50-10.40-1.10 (4.20) 2.20-1.60-2.80-4.26) 2.50 (1.14 (.70) 2.30-2.40) 1.60) 3.30) .861 (.16) .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 1.80) 4.00 (2.70) 2.80-7. see Data Analysis section) for Survey year 03-04 is 0.00-1.50 (2.963 (.90) 1.30 (3.30) 3.05-2.50 (6.30 (2.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.93 (1.721-1.00) 2.20-1.30 (7.40) .90) 1.70-2. population from the National Health and Nutrition Examination Survey.70 (1.20-3.40 (1.67-2.30 (1.00 (1.30 (1.80 (1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60 (1.80) 3.00 (1.00) 3. interval) 1.42 (1.50-6.800 (.30) 3.80) 1.10 (.80-3.10 (1.51) 1.73-2.80 (1.04) .77-2.1) 485 538 962 Limit of detection (LOD.17 (1.S.10-9.20 (6.00) 1.80-4.20-1.50-6.689 (.0) 8.70-5.586-.60 (1.40 (1.90-10.900-1.5) 8.900-1.816-1.60) 1.44 (2.40) 640 1454 03-04 03-04 2.20) 1.70) 3.10 (4.72) 1.900) 1.3 (9.50 (1.S.70-10.40 (1.10) 75th 3.50 (4.80-8.87-2.80-2.92 (1.852 (.09 (.900-1.20 (1.50-3.50 (1.60-3.70) 1.90) 3.90 (1.80-6.30) 03-04 03-04 .10-5.60-2.12) . population from the National Health and Nutrition Examination Survey.60 (6.50 (6.00 (5.800-1.912-1.80-4.10) 6.56-1.60-4.50 (4.90) 90th 5.900-1.10 (.00 (1.40) 1.90 (1.00-8.835-1.70) 1.70-2.90-2.900-1.40-1.80) 90th 2.70-6. interval) .30-12.60-2.60-4.700-1.40 (1.20 (6.10) 4.91) 2.20 (1.70-7.80) 5.900 (.20) 03-04 03-04 2.20) .90 (4.966 (.30 (1.17-1.60 (1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .72 (1.6) 7.10) 1.40 (2.60) 9. see Data Analysis section) for Survey year 03-04 is 0.40-3.90 (2.80-8.10) 4.30 (6.70 (2.00 (.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.50) 6.697-1.10) 6.60-8.826-1.40) 4.3.50) 2.90) 1.30 (1.10) 8.80-3.40) 640 1454 03-04 03-04 1.30-6.54) .16) Selected percentiles ( 95% confidence interval) Sample 95th 8.00 (1.80-12.03) 1.40) 2. Survey Geometric mean (95% conf.08) 2.5) 5.80 (4.809) 1.00-6.00) 1.90 (1.30-9.600-.00-7.00 (.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.10) 75th 1.0) 1053 1041 03-04 03-04 03-04 1.10) 5.20) 485 538 962 Limit of detection (LOD.50) 2.70) 13.01 (1.1.60-7.50 (1.900 (.60-3.20-2.20 (1.10-9.20-1.27) 1.10) 1.80-7. Survey Geometric mean (95% conf.90 (4.90-19.10) 1053 1041 03-04 03-04 03-04 .62-2.900-1.90) 8.00-1.30) 3.60) 2.834-1.90 (1.10 (.30 (2.

8-22.1-36.4) 56.7-53.7 (43.50 (4.90 (7.9 (13.30-8.60 (5.91) 3.3 (28.21-3.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.2) 30.9-38. see Data Analysis section) for Survey year 03-04 is 0.3) 41.9) 9. Survey Geometric mean (95% conf.40-17.20-5.1.7-69.60 (4.90 (7.5) 8.95 (3.4) 75th 30.5) 32.5) 18.70) 3.10 (3.4-42.20-4.30-6.20) 5.0) 43.3) 485 538 962 Limit of detection (LOD.4) 21.53) 3.5) 57.8) 32.40) 90th 7.30 (5.00) 3.2-22. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.85-4.80-4.7 (43.50-13.70) 6.7-23.0 (20.84-3.0-20.70-5.0) 36.20 (4.4 (28.00 (5.2-57.60-13.0-70.8-30.2 (18.5) 19.90 (7.40) 75th 5.50) 4.10 (6.9) 22.5) 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. interval) 3.8) 27.50 (3.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.4 (19.60) 03-04 03-04 3.7-49.60 (3.3-61.35) 3. Fourth National Report on Human Exposure to Environmental Chemicals 253 .60-14.0) 21.5) 7. interval) 20.1 (23.0) 485 538 962 Limit of detection (LOD.6) 35.2 (16.90 (5.6 (42.0) 90th 41.8 (45.1 (24.37 (2.65-4.70-7.2 (28.7-30.6 (35.80) 8.30 (3.30) 7.90-12.10-3.5 (28.6 (44.7 (35.7-33.7 (35.6) 1053 1041 03-04 03-04 03-04 3.9-19.20) 10.2 (19.20) 7.9 (22.70 (5.5) 9.40) 5.1) 15.30-5.7 (13.70 (3. population from the National Health and Nutrition Examination Survey.8-35.80 (7.6) 62.80-9.00 (3.50-6.2) 45.30-11.1) 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 4.60 (6.18 (3.00 (5.40-6.1-52.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.3-22.90-4.0) 21.2 (27.5-62.20 (4. population from the National Health and Nutrition Examination Survey.1 (19.90) 6.2) 640 1454 03-04 03-04 4.11 (2.8 (37.6) 9.3 (17.8 (34.60-6.79) 4.6-50.82) 4.40 (4.90-4.4-17.20) 4.40-10.89 (3.1) 57.8-22. see Data Analysis section) for Survey year 03-04 is 0.7) 39.5) 1053 1041 03-04 03-04 03-04 14.4 (17.80 (5.S.0 (27.1-24.47-4.4-25.4 (19.40-14.07-4. Survey Geometric mean (95% conf.9-23.4 (23.8-81.10 (3.50-4.80 (6.6) 21.47 (4.80 (6.70-10.8-22.5-33.40-6.70 (5.20-9.6 (19.7 (19.20) 7.4) 20.6) 18.9 (19.60 (7.70) 4.20) 5.0-16.3) 42.1-25.27) 4.3 (35.60-9.10) 5.96 (3.6-45.5-23.5-21.70-7.3 (44.2) 30.1-33.7 (7.6) 7.0-66.0) 03-04 03-04 19.5 (28.9) 22.30-3.50) 7.99-3.1-35.6-24.80-12.2 (21.3) 28.30) 6.60 (6.70-9.S.60) 8.30 (3.4.9) 27.3 (35.8) 46.6) 42.40) 3.9 (17.4) 640 1454 03-04 03-04 23.67-4.0) 23.8-78.40 (6.

< LOD means less than the limit of detection.300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300-.200-.300 (.2.300 (.200-.300) .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-.300 (. see Data Analysis section) for Survey year 03-04 is 0. 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 .200-.300) .300 (.S.300 (.200-.300 (.300) .300-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . Survey Geometric mean (95% conf.S.200-.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD . Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.400 (<LOD-. Survey Geometric mean (95% conf.500) 485 538 962 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.200-.500) .300 (.300) .200-.300 (. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.500) .300) .500) < LOD 485 538 962 Limit of detection (LOD.300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .4.300) . population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.300-.500) .200-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300-.300) . < LOD means less than the limit of detection.200-.

10) .900-1.3.30) 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 .6.30 (1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900-1.10 (.20-1.00-1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) < LOD .800 (<LOD-.30) 1.10 (. Survey Geometric mean (95% conf.00 (.10-1.900-1. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.900 (<LOD-1.900) 485 538 962 Limit of detection (LOD.300 (<LOD-.40) 1.30 (1. population from the National Health and Nutrition Examination Survey.60) 485 538 962 Limit of detection (LOD.700) 1.20 (1. < LOD means less than the limit of detection.900-1.700 (<LOD-.900-1.20) 1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .900) .400 (<LOD-.70) 1.00 (. which may vary for some chemicals by year and by individual sample.300 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. < LOD means less than the limit of detection.900-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .30) .30) 1.700 (<LOD-.00 (. see Data Analysis section) for Survey year 03-04 is 0.600 (<LOD-1.S.50 (1.700 (<LOD-.800) .10-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .400 (<LOD-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .40) < LOD < LOD .10) .700 (<LOD-.10) 1.300-2.10-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .90) .60) 640 1454 03-04 03-04 * * < LOD < LOD . which may vary for some chemicals by year and by individual sample.00 (.800) .80) 1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10 (1.10) 1.10 (.S.600 (<LOD-1.10-1.50 (1. see Data Analysis section) for Survey year 03-04 is 0.700) .700 (<LOD-2.900-1.900 (.10) * 03-04 03-04 * * < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (<LOD-.600) .900) 1.500 (<LOD-.700) 90th 1.600 (<LOD-1.80) 1.600 (<LOD-.10-1.700) 1.30 (1.700 (<LOD-.

et al. Day RD. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility.134(1):18-25.46(2):141-147. Fillmann G. et al. Needham LL. Fei C. Biegel LB.99(2):253-261.S. Environ Sci Technol 2005. brominated.179:99-121. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Yamashita N. Reidy JA. Gaylor DW.104(2):322-333. Reidy JA. Kuklenyik Z. Aguilar-Villalobos M. Hurtt ME. Loganathan BG. Cook JC.115(11):1677-1682. Kannan K. Laane RW. Environ Sci Technol 2005. Environ Sci Technol 2004. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Crit Rev Toxicol 2004. Burris JM. Jarnberg U.68(6):465-471. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.124(2):119-132. 256 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Arendt MD. et al.7(4):371-377. Kuklenyik Z. Watanabe T. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Bookstaff RC. Mandel JH. Olsen GW. Environ Health Perspect 2007. and ex vivo studies. Environmental and toxicity effects of perfluoroalkylated substances. Chemosphere 2006b. Characterization of risk for general population exposure to perfluorooctanoate. Perfluorinated chemicals in selected residents of the American continent. Harada K. Frame SR. Perkins RG. Moore JA.39(3):363-380. Koizumi A.1968--2003. Wong LY. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. et al. Holmstrom KE. Halden RU. Guruge KS. Rev Environ Contam Toxicol 2003. 2007b. Hurtt ME. The influence of time. Witter FR. Murray SM. Taniyasu S. Toxicol Appl Pharmacol 1995. Tully JS. Chem Biol Interact 2000. Yoshinaga T. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Butenhoff JL. Mandel JH. Inoue K. Reidy JA. Taniyasu S. Inoue K. Bignert A. Mohotti KM. Grey BE. et al. Saito N. Kuklenyik Z. Androgenic deficiency in male rats treated with perfluorodecanoic acid. in vivo. Corsolini S. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Olsen GW. Morikawa A.Koizumi A. Kumar KS.Perfluorochemicals References Alexander BH. Moore RW.115(11):1670-1676. Needham LL. Yun SH. Environ Sci Technol 2005. Calafat AM. O’Connor JC. The toxicology of perfluorooctanoate. and perfluorinated contaminants in livers of polar bears from Alaska. Keller JM. Kuklenyik Z. Seacat AM. Herbstman JB. Toxicol Appl Pharmacol 1990. Toxicol Appl Pharmacol 1992. Suzuki E. Yamashita N. Apelberg BJ. Polyfluoroalkyl chemicals in the U. Fluorotelomer alcohol biodegradation yields poly. Liu RC. Caudill SP. Kudo N. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Hekster FM. de Voogt P. Edwards EA. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Wijeratna S. Birth Defects Res B Dev Reprod Toxicol 2003. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000.115(11):1596-1602. Hurtt ME.39(1):80-84. Needham LL. Kawashima Y. Sasaki S. Katakura M. Olsen GW.39(23):9101-9108. Frame SR. Calafat AM. Needham LL. Chlorinated. Mabury SA.39(23):9057-9063. Saito N. Calafat AM. Kannan K. Rodricks J.38(17):4489-4495. Cook JC. Calafat AM. Caudill SP. Environ Sci Technol 2006a. McLaughlin JK. Environ Health Perspect. Seneviratne HR. Bandai N. Tully JS.60(10):722729. Biegel LB. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Environ Sci Technol 2007a.63:490496. Occup Environ Med 2003. Harada K.41:2237-2242. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Regul Toxicol Pharmacol 2004.113(2):209-217. Lau CS. Tarone RE.38(10):2857-2864. Reidy JA. Butenhoff JL. Calafat AM. Kennedy GL Jr. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years.and perfluorinated acids. Dinglasan MJ.S. Cook JC. Rogers JM. Environ Health Perspect 2007. Evans TJ. Environ Sci Technol 2004. Grasty RC. Ingall GB.60(1):44-55. Olsen J. Ye Y. Peterson RE. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Mandel JS. Yoshinaga T. Kannan K. Environ Res 2005. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. et al. Kamiyama S.34(4):351-384. Falandysz J. Toxicol Sci 2001. J Occup Health 2004. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. J Environ Monit 2005. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. O’Connor JC.40:21282134.

Huang HY. J Occup Environ Med 1999. Coordinate induction of acyl-CoA binding protein. Toxicol Sci 2002. J Ag Food Chem 2007. et al. Mandel JH. (Erratum in: Toxicol Sci 2004. Butenhoff JL. Yamashita N.S. Prevedouros K. Mandel JH. 2003a. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Mandel JH. Horii Y.. Sterchele PF. Toxicol Appl Pharmacol 2004. Burris JM. Washington. Hanson RG. Horii Y. Stanton ME. Taniyasu S. Taniyasu S. et al. Rogers JM. Hansen KJ. Olsen GW. Environ Sci Technol 2003. Bronson R.198(2):231-241.45(3):260-270. EPA). Available from URL: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors.S. et al.1177(2):183-190. Environmental Protection Agency (U. Grey BE. Moisey J. Petrick G. Olsen GW. Kannan K. Olsen GW. Half-life of serum elimination of perfluoroo ctanesulfonate.gov/opptintr/pfoa/pfoara. Environ Sci Technol 2006.epa. Olsen GW. Cousins IT.111(16):1900) Olsen GW. Olsen GW. Mair DC. Seacat AM. 2007a. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Butenhoff JL. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Lau C.Perfluorochemicals Kudo N. Rogers JM. Mandel JH. Buck RC. Kawashima Y. Environ Health Perspect 2005. Church TR. Environ Health Perspect 2003a. fate and transport of perfluorocarboxylates.68(1):249-264. 2003. Church TR. Lau C. fish. Nesbit DJ. and perfluorooctanoate in retired fluorochemical production workers. Hanson RG. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. I: maternal and prenatal evaluations. Burris JM. Seacat AM. Environ Health Perspect. Barbee BD. Toxicol Sci 2003. The developmental toxicity of perfluoroalkyl acids and their derivatives. Ehresman DJ. Biol Pharm Bull 2003. II: postnatal evaluation. perfluorooctanoate andother fluorochemicals in human blood. Yamashita N. Thibodeaux JR. Thibodeaux JR. Richards JH. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation.68:105–111.54(11):1599-1611.40(1):32-44. fish. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Hansen KJ. Cao XL et al. J Occup Environ Med 2003b. Hansen KJ. Reagen WK. fast foods. Butenhoff JL. Olsen GW. Burris JM. Mar Pollut Bull 2005. Burris JM. Hansen KJ. Froehlich JW. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. 1/15/06 Vanden Heuvel JP. Miller JP. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Rogers JM. Historical comparison of perfluorooctanesulfonate.74(2):369-381.) Tittlemier SA. Pepper K. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. and food items prepared in their packaging. Case MT.113(5):539-545. et al. Chemosphere 2004a. Lundberg JK. Olsen GW.51(8-12):658-668. Seymour C. Hansen KJ. Ehresman DJ. Lundberg JK. birds. Ellefson ME.74(2):382-392. Burris JM. et al. van Belle G. Biochim Biophys Acta 1993. Butenhoff JL. Helzlsouer KJ. Kannan K. Zobel LR. htm.55:3203-3210. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees.115(9):1298-1305. Butenhoff JL. A global survey of perfluorinated acids in oceans. Olsen GW. et al.111(16):1892-1901.37(12):2634-2639. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Gamo T.perfluorohexanesulfonate. Burlew MM. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Chemosphere 2007b. J Children’s Health 2004b. Grey BE.26(1):47-51.82(1):359. Toxicol Sci 2003. Larson EB. (Erratum in: Environ Health Perspect. Korzeniowski SH.2(1):53-76. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators.41(9):799-806. Hanari N. Sources. Peterson RE. Butenhoff JL. and humans from Japan. Thomford PJ. Church TR. U.

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

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

Singh NP. Toxicol Appl Pharmacol 2004. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Wang P. Hauser R. Jacobsen H.niehs.html. Environ Health Perspect 1997. 6/2/09 NTP-CERHR. Rylander L. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Milligan SR. NTP-CERHR.210:21-33.105:802-811.gov/chemicals/dehp/dehp-eval. 2000c [online]. 6/2/09 Okubo T. Sumpter JP. David RM.html. Koch HM. Meeker JD. Silva MJ. Yoshimura M. Kessler W. Suzuki T. Calafat AM. Park MG. Environ Health Perspect 2003. 2006 [online]. Kalita JC. Numtip W. Sumpter JP. Environ Health Perspect 2004. Gans G. Reproducibility of urinary phthalate metabolites in first morning urine samples. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. et al. Silva MJ. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.niehs. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. 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 . Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Reprod Toxicol 2004. Baird DD. Jobling S.gov/chemicals/ phthalates/dbp/dbp-eval. Research Triangle Park (NC). Csanády G. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Dalgaard M. Kano I. Giwercman A. 2000a [online]. Borch J. Jonsson BAG. Am Ind Hyg Assoc J 1985. Fromme H. 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Available at URL: http://cerhr.11(5):381-387. Determination of phthalate monoesters in human milk.gov/ chemicals/phthalates/bb-phthalate/bbp-eval.26(8):1219-24. Available at URL: http://cerhr. Environ Health Perspect 2002. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Research Triangle Park (NC). Hanaoka T. Lovekamp-Swan T. Research Triangle Park (NC). Hartle RW. 2000b [online].110(5):515-518. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Scand J Work Environ Health 1985. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).18(1):122.html. Albro PW. Henttu P. Kano K.382:10841092. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Biol Pharm Bull 2003. Hagmar L. Meeker JD.112(17):1734-1740. Bolte G. Epidemiol 2005. Yokoyama Y. 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112(3):331-338.114(11):1643-1648.65:299-308. Crit Rev Toxicol 2006. Barr DB. Abbott BD. Malek NA. Toxicol Sci 2000. Silva MJ. 112(5):A270]. Meek MD. Albro PW. Urinary levels of seven phthalate metabolites in the U. Zacharewski TR. Rusyn I.58:339349. Lambright CR. Pratt IA. Ostby JS. Fielden MR. Environ Health Perspect 2006. Environ Health Perspect 1982. Orton TC. Environ Health Perspect 2004. Parks LG. Reidy JA. Rhodes C. Batten PL. et al. Toxicol Sci 1998. Clemons JH. Klinefelter GR. Jackson SJ. Barlow NJ. Bratt H. et al. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters.Phthalates phthalate (DEHP): a cross-sectional study in China. Hodge CC. Environ Health Perspect 1986. Wu ZF.45:11-17. Peters JM. Matthews JB. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Cunningham ML.36:459-479.46:282-293.S. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Peck CC. et al. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Caudill SP.

respectively.2) 15.1.8 (14.1) 67.5-35.0 (20.6) 35. NTPCERHR.7-35.3-43.2) 13.1-15.9-30.2-116) 122 (102-143) 101 (84.3-125) Total 15.4 (53.0 (15.0 (30.3-130) 122 (88.8 (38.1 (14.6 (13.0) 90th 67.4 (27.5) 55.4) 81.7) 38.8-13.2-20.0) 33.9) 14.4-15.6-79. residents (Blount et al.5) 23.9-14.8-18.8-16.3-27.3 (44.8-17.5-84. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 39.9) 43.7-17.4) 129 (98.6) 35.1-43.5 (26.7-16.3) 13.5 (27.4) 80.7 (11.2) 33.6-39.6) 95th 103 (94.4) 71.8 (71.4 (10.1) 76. and to a lesser extent.2-155) 91.4-92.8 (53. vinyl tile.5 (47.7 (13.4-127) 80.1-16.4) 98.1) Selected percentiles ( 95% confidence interval) 50th 17.9 (16.2) 32.1) 32. 2001-2002.0) 20.3 (12.6) 16.3-91.8-14.1-116) 122 (93.8-72.6 (21.6) 14.1 (14.7-170) 169 (134-198) 152 (99.8 (71.3) 54.6 (41.3) 13.2) 78.8 (30. see Data Analysis section) for Survey years 99-00.1-38.9-49. 01-02.2) 12.0 (55.S.6) 13.9-28. and 0.3) 37.6-38.8 (10.2) 14.6-18.9 (22.8 (86.5 (76.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) 35.7-172) 103 (74.9 (12.3-34.5 (67.4 (68.0-26.4 (10.2-40.5) 15. 2004.2) 17.9-27.0-55.3-75.3-18.6) 67.4 (53.3) 63. it can be released into the ambient air during use or disposal of the products.5-145) 138 (106-241) 143 (127-179) 120 (99.1-15.0 (14.0) 23.0-106) 58.7-14. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.1 (58.7-58.8 (12.6 (53.1) 13.8-41.2-39.8 (50. can produce developmental and reproductive toxicity in rodents.1) 68.8 (80.2 (14.6-132) 103 (84.1-16.4) 65.9-62.7 (51.3) 23. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.5-97.0 (11.3-74.6) 50.5-36.6-29.4 (29.1-18.6) 25.6) 14.8) 24.8-14.3-12.2-38.8 (28.8) 63.9) 13.7 (80. and 03-04 are 0.9) 49.3 (54.8) 33.9) 18.2) 14. interval) 15..2) 69.1) 14.9 (70.6) 37.0 (26.2-17.7-119) 99.8) 14.9-47.1-214) 166 (116-191) 145 (110-213) 88.5 (57. 2000).7-15.0 (15. car care products.9-87.2-33.7 (12. sealants.8-64.0 (43.5-14.4-24.0 (34.4) 35.1-35. because it is not bound to products in which it is incorporated.9) 14.6-43.4 (59.7) 40.2 (43.8-76.S.3 (12. BzBP can be released into the environment during its production and.3 (12.7-16.2 (10.4-16.6 (13.3 (13. and 2003-2004 were generally similar those reported in U.7-82.9) 12.0) 24.0) 34.6-92.2) 66.3) 15.7 (53.4) 108 (96.2 (19.5) 30.9-190) 86.7 (15.8) 28.4) 51.3 (30.6-150) 94.0 (12.1 (20.2-16.9 (28.4-120) 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 13.6) 29.3.1-61.4 (63.5) 82.Phthalates Benzylbutyl Phthalate CAS No.8-16.8-133) 89.3-161) 99.6-72.5-41.9) 15.6) 63.5-25. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.8-17.2-115) 113 (91.6-17.6) 24.0) 70.8-48.2-183) 101 (78.0 (30.1 (19.3 (33.7-13.3-21.6) 13.2 (25.2) 22.4 (32.4) 12.1 (13. including MBzP.5 (66..5-40.5 (61.4) 49.6) 15.4) 14.5 (13.2-19.4-62.5-36.5 (55.4) 33. and diet is the major source for general population exposure.6-92.5) 15.9 (13.9 (11.4-25.1 (10.2 (47.0 (23.9 (21.8 (21.1) 31.8. particularly male animals (McKee et al. population from the National Health and Nutrition Examination Survey. Food crops take up BzBP.0) 16.6 (32. IARC considers BzBP not classifiable with respect to human carcinogenicity.9) 11.5) 27. 262 Fourth National Report on Human Exposure to Environmental Chemicals .1 (32.1-120) 52.5-62.8-35.6 (13.6-116) 122 (102-142) 101 (85.9-16.2-31.1) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 23. 2000).4) 75th 35.2 (19.1-39.8-98.5-94.3) 94.4 (13.0-85.3-88.7-16.6 (13.5-33.5-18.8-121) 79. 0.3 (29.4 (32.1-90.3 (29.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.1) 29.4 (31.0 (33. High dose BzBP and its monoester metabolites.9 (39.2 (11.4 (48.3-18.5) 65. some personal care products.6 (66.7 (82.9 (12.7 (70.0) 32.0-130) 101 (86.8) 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 16.6 (12.5) 16.2-16.3 (22.7-25.1 (55.1 (13.4) 38.0 (27.3-82.

1-29.6) 73.7-31. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. Hoppin et al.8 (30.8-14.5-58.8) 33.4-15.5-13.7) 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. 2004).2-13. 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.2-117) 95.5 (48.6-26.9-13.0 (38.7) 11.4 (13.5) 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 .8-15.0 (11.0 (49.9 (55. 2007).6) 12.8) 24.7) 25.9 (39.8) 68.1 (18.3) 13.0 (33.2-21.4-90. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al.7) 56.4) 15.8 (12.6) 38.9 (10.4 (63.8 (46.4 (11. in men attending a Boston infertility clinic (Duty et al.9-28.7 (11..1 (11.5-99.3 (12.1) 24.2) 11.9 (43.6-99.3-11.6-15.0) 13.0-53.6 (57.8) 46.6) 30.6-86.4 (11.7-397) 70..9) 52.1-58.0) Selected percentiles ( 95% confidence interval) 50th 13.4-99..4 (34. 2005.5-61.8) 11.7-20.5 (56.Phthalates York City (Adibi et al.8-14.9) 24.4-102) 70.6) 58.1-27.5 (49.6-116) 74.1) 12.1 (21.4) 51..3-16.9-14.2 (40.4-60.1 (15.9) Total 14.3) 13.7 (55.3) 73.7-56. 2002).8) 34.1 (9.8) 53.8) 26.8 (64.3 (24.4) 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 12.8-13.5 (35. In NHANES 1999-2000.4 (46.0) 24.2-17.7 (13..0) 60.8-39.3) 29.4) 14. population from the National Health and Nutrition Examination Survey.8) 13.5) 16.6) 75th 25.1 (46.1 (21.8-34. 2004.4) 21.1) 142 (99.4-23.7 (18.5-57.5) 14.6) 12.9 (24.6 (34.6 (15.5-26.5) 10.6-81. interval) 14.5) 23.7 (14..5-79.5-23..4-42.2) 26.9-40.0 (10.4-142) 134 (116-176) 136 (85.5) 78.7-29.1) 23.5-31.8) 15.5) 20.7 (19.8) 33.5-29.1-125) 86.2 (56.3) 16.8) 56.4-14.4 (25.9) 42.3) 14.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.4 (21.7) 38.7 (59.3) 37.3 (13.0-26.5-213) 49.7-90.1-79.4-14.4) 60.6 (36.5 (10.7-19. 2003).3) 90.8 (11.8 (69.6 (19.7-14..5) 17.3-64.0) 11.7-20.8-80.7 (38.3) 55.6 (11.4 (10.6 (11.3) 36.3 (39.0 (12.4 (69.1 (43.0-109) 65. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2) 12.1 (13.0) 15.5 (42.0) 12.2-51.8-64.9) 12.9 (54.1-12.5) 41.3-38.0 (67.1 (21.4 (60.1 (53.1 (34. 2005).8) 53.9-115) 57.3 (15. Hauser et al.3) 21. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.1-12.8-42.5) 46.2 (41.73-12. 2006).9 (9.8-69.0 (62.4-116) 73.9 (22.9 (12.2-15.8-16.95-14.4 (12.1-35.9) 100 (80.6 (30.1 (21.8 (10.9-69.8 (57.3-34.6) 53.0 (12.1) 80.9) 12.8) 54.2) 32.8) 108 (75. 2007).1) 39.4-93.9 (51. and females compared to males (Silva et al.7-12.5 (9.9-104) 62.4-19. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.7) 19.2) 67.1 (14.7-123) 77.5 (11.9 (15.1) 27.3) 13.8-48.7-15.0-51.4) 90th 50.7 (21.8-85.7 (13.7 (54.6 (14. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.4 (33.4) 50. 2003).9-13.7-19.7) 46.5 (10..2) 15. and in a small sample of German residents (Koch et al.5) 95th 77.6-40.1 (23.6 (22.8-13.3 (60.2-57.0 (41.1-120) 77. In an annual sample of German university students.4) 12.3) 12.9) 11.4) 104 (89.7 (11.9-83.4 (11.5-76.5-26.0 (13.6-20.7-61. A small study of African-American women in Washington.0-27.1 (41.6 (51.0-90.2 (69.6 (30.5-58.1) 17.7-15.4) 17.2-26.8-173) 195 (121-305) 229 (99.6) 13.9-16.7-69.0-15.8) 71.9-23.3 (35.6) 25.2-13.6-12.5-16.9 (15.2-49.6-47.9) 11.4) 13.2) 11. 2002.3-73.8 (49.5 (12.8-15. 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.9) 12. Weuve et al.8-13. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.7 (12.1 (19.0) 49.9 (10. adolescents compared with adults.2) 11.4) 13.8 (13.9 (12.4-17.S.4) 28.5) 13.9 (29.7-14.0-48.5-42.4) 25.6 (11.9-62.7 (11.3 (23.5-38.3 (38.1 (13.7 (23.6 (24.4-27.2-15.1) 24.1 (25. in young Swedish men (Jonsson et al.3) 67.8) 80.6-13.1) 35.3) 18.8 (50.4-18.4-79.4 (74.1-14.3) 89.9 (24.8) 16.8-27.9) 64.4 (26.2 (27.3) 14.8-60.0 (41.2-12.2-78.0) 24.69-11.4) 44.

Butala JH. Helm D. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Atlanta (GA). Caudill SP. Ryan L. Rossbach B. Duty SM. Hu H. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Rylander L. Environ Health Perspect 2003. Jonsson BAG. Environ Health Perspect 2002.nih. Levels of seven urinary phthalate metabolites in a human reference population. Malek NA.S. Brock JW.16(4):487-493. Environ Res 2003. Singh NP. 2000 [online].18(1):122. Sampson EJ. 2005.93:177-185. Koch HM. et al. Needham LL.html. et al.111(14):1719-1722. Silva MJ.114(9):1424-1431. David RM. et al. Barr DB. Reproducibility of urinary phthalate metabolites in first morning urine samples. Camann DE. Silva MJ. Research Triangle Park (NC). Reidy JA. NTP-CERHR. Barr D. 112(5):A270]. Wiesmuller GA. Schettler T. Needham LL. Jedrychowski W. Epidemiol 2005. Hum Reprod 2007.108(10):979-982. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Available at URL: http://cerhr. Calafat AM. Silva MJ.68:309-314. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Jacek R. et al. Meeker JD. Phthalate monoesters levels in the urine of young children. Blount BC. Angerer J. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Brock JW. Hagmar L. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.210(3-4):319-333.Phthalates References Adibi JJ.110(5):515-518. Urinary levels of seven phthalate metabolites in the U. et al. Wittassek M. Dobler L. Environ Health Perspect 2000. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Hauser R.niehs. Perera FP. et al. Caudill SP. Centers for Disease Control and Prevention (CDC). Davis BJ. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Brock JW. J Androl 2004. Richthoff J.112(3):331-338. Duty S. Chen Z. Reprod Toxicol 2004. Hodge CC. 4/20/09 Silva MJ. Baird DD.25(2):293-302. Gans G. Green RA. Bull Environ Contam Toxicol 2002. et al. Environ Health Perspect 2006. Hilborn ED. Caudill SP. Weuve J. Int J Hyg Environ Health 2007. Silva MJ. Third National Report on Human Exposure to Environmental Chemicals. Calafat AM. Environ Health Perspect 2004. Ryan L. Eckard R. Sanchez GN. Hoppin JA. Giwercman A. Drexler H. Pirkle JL.22(3):688-695.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Poland. McKee RH. Prenatal exposures to phthalates among women in New York City and Krakow. Koch HM.

30) 5.40-17.46 (3. and insecticides.20-6.10-9.00) 10..5) 25.10) 3.46-5.0-14.5) 22.20 (3.60 (2.30) 10.00) 6.50) 8. 2005).5) 18.60 (8.80) 75th 5.S.1-20.1-17.60-6.1) 25. In addition.S.6 (14.3) 33. and also in some printing inks.4 (20.7 (17. Survey Geometric mean (95% conf.90-4.4) 22.10-2. mostly as MnBP (Anderson et al.3-19.97) 4.56) 3.11-3.0) 24. Hauser et al.6-26.90 (3.56-4.22 (3. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.90 (4. Following oral administration of DBP to humans.66) 2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.1) 22.7) 4.0-18. Fourth National Report on Human Exposure to Environmental Chemicals 265 .70-4.3-24.97) 2.00-6.50 (3.40-4.30 (1.30-6.20-2.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.72-3. population from the National Health and Nutrition Examination Survey.0 and 0.50-4.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.19-3.73 (2.44-2. they have been referred to as monobutyl phthalate (MBP).68 (2.20-12.9 (16.24-8.7) 14.. Koch et al.90-2.6 (9.30-7.96) 3.4-12.10) 2.0) 12.6) 17.9) 15.1 (8.7 (7.00-6.20) 7.26 (2.20) 4. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.80 (5.0) 20.22) 3.50) 7.00 (7.90) 12.49-2. 2007).00 (5.2 (8.07 (3.8) 21.50) 2.3 (19. NTP-CERHR.6 (10.60) 3. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.70-4.50 (6.55 (3.40-12.40 (6.33 (2.90-4.5) 23.6 (13. 84-74-2 Di-isobutyl Phthalate CAS No. 2004. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity. CDC. Studies of children found age-related differences in urine MBP levels.30) 6.5-16.70-8.6 (11..6) 10. interval) 2. residents (Blount et al.00) 7.50) 90th 12. Biomonitoring Information Median concentrations reported in the NHANES 19992000.Phthalates Di-n-butyl Phthalate CAS No. 2005.30-6.7-31.2) 5. When total DBP metabolites have been measured.50-10.30 (4.6 (13.40 (7.67 (5.1 (13.20-12.17 (2. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. pharmaceutical coatings.7-20..7-18.17) 4.7) 18.5) 18.50-2.00-9.73-5. in a small sample of pregnant women in New York City (Adibi et al.10 (3.3-30. 2005).40 (3.5 (20.10 (4.40-4.8 (9.30-3.2 (12.0) 13.50-6. about 65% to 80% of a dose is eliminated in urine within 24 hours.0) 9.80 (3.46) 2.30) 2.7) 7.5) 12.56 (5.3 (11.43) 6.7 (9.48 (2.60 (5.3-48.91) 4.55) 2.30-13. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.3 (16.3 (13.9-23. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.6-20.70) 5. OSHA has established a workplace air standard for external exposure to DBP.81 (3.40-3.2-14.0 (13.7) 15. 2004.80 (2...1-25.0 (19.82-3.0-38.3 (18.3 (16.00-11.5) 14.00) 4.6-14. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.6) 16.30 (3.3.0-25.80 (2.6) 16.85-6.0) 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 2.70 (5.2-33. 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.40 (2.50) 5.6-18.4) 12.2 (11.5-16.8) 40.59) 3.10 (4.40-3.30-2.5-29. in men attending a Boston infertility clinic (Duty et al.7 (16.9) 10.40) 5.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.30) 10.5 (10.60 (4.71 (2.3 (13.50) 18.6 (10.. and in a small sample of Japanese adults (Itoh et al.1) 16.3) 18.3-18.63) 3. 2001).00) 4.3) 3.6) 17.6 (29.28-5.90-7.5-24.46 (2.5 (27.3-43.40-9. DBP can produce reproductive toxicity in male rodents (McKee et al.9-14.5 (11.6-34.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.0 (13.5 (17. 2003).00-4.37) 6.56 (3.0 (11. 2005).6) 26.70 (2.6 (14.20 (7. 2003).97-7.5) 19.4 (14.30-11.10) 8.80-5.8) 677 652 703 699 1216 1088 Limit of detection (LOD.40-5.70) 3.20-9.80 (5.4) 5.7 (18.10-9.2-22.40 (2.1-12.6) 12.10) 9.02) 4. 2000. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine...20 (6.7 (17.4-27. 2000).3-20.90 (6.10) 11.9 (16.90 (4.7-31.84) 4.80-5.

15) 3.47-12.32 (3.04) 7.0-18.13-6.1) 13.83 (2.30) 2.6) 13.56-15.7) 10.65 (4.6 (10.07-5.0 (12..2-13.78) 8. 2007).56) 2.38 (6.6-19.51) 2.4) 15. the students’ median values for MiBP levels remained relatively unchanged.4) 23. interval) 2.42) 2.98 (2.7-28.56) 5.75 (4.1) 15.18 (4.74 (4.65-11.81 (3.57 (3.20-2.03-7.52) 3.43) 3..39) 5.9-16.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.9) 12.66) 10.3) 28.29-8.29-3.89 (3. 2005).2) 9.76-3.1) 11.8 (10.18) 3.84 (8.57-4.68) 5.33 (3.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.0 (8.72) 5.02 (7.94) 6.95-3. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.18-4.88 (2.20-4.54 (2.92 (7. up to four and 13 fold.7) 11.53-4.1 (10.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.11 (5.52-20.85 (2.37) 3.68 (2.00-3.75 (6.66) 4.4) 7.1) 7.6) 11.31 (7. 2007).80) 7.39-3.64-10.8) 10.74-3.7 (9.2) 8.66) 2.5 (11.21 (5.2-15.18-10.20 (2.7) 3.31) 2.8 (8.17-12.79 (4.8-13.01-2. 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.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.33) 3.0) 11.28-13.02-10.11-2. 2005).3) 18. than adults in NHANES subsamples during the same time period. samples from German university students had consistently higher median urine levels of MnBP and MiBP.64-7.03 (5. 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.20 (2.95) 2.25) 5.46-11.17) 90th 8.45) 3.6 (8.53-3.00-3.66 (8.and gender. Between 1998 and 2003.35) 3.6 (9.3 (13.13 (2.58-3.44 (3.24) 3.6) 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 2.05) 2.7 (21.5) 15.9 (9.93-6. An analysis of NHANES 2001-2002 showed similar age.8-18.19 (2.3 (17.26-2.46 (2.47 (3. Weuve et al.3) 16.20 (7.46) 3.1-24.6-19.94 (5.31) 2.64-7. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.68) 3.6 (12.81) 9.0) 7.04) 3.S.08-2.69) 6.51) 5. ranging from more than one-tenth the NHANES median (Itoh et al.72-7. Over this time.89-5.65-4.7 (11.2 (11. Survey Geometric mean (95% conf. 2002.96 (3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC. 2004).0) 3.99) 7.43) 3.18 (1.94-12.99-4.56-4.76-3.1-12.8-36.30 (6.7) 19.54 (4..26 (2. while MnBP declined (Wittassek et al.27-12.00 (3.84 (4.53-5.76-15.79-8.89) 6.09-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.8 (9.36-2.62 (6.6 (15.51) 15.95) 10.10-5. In an analysis of NHANES 1999-2000.15-4.9-40.1-25.67-5..33-9.69 (2.3) 13.1-15.73 (5.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .43) 3.08) 75th 4..07 (2.58-4.86-4.4 (12.38-10. 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.82 (4.76 (3.2) 24.5 (9.22 (2.04-5. 2006).91-6.52-3.18) 4.80-3.97-2.1) 4. 2004).69-7.78-8.20-3.28 (4. population from the National Health and Nutrition Examination Survey.6 (8.1) 10.55-6.2 (10.03-11.69) 4.3) 13.34 (3.81) 4.5-19.32 (7.52 (2.36-7..11) 5.7 (13.78) 9. 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. to about two to fourfold higher (Fromme et al.54) 2.0) 15.4-16.59 (4..14 (4.47-5.9-26.1 (11.62-12.32) 7.00-7.80 (3.33 (2.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.31 (2.41 (2.21) 10.61-3.81 (6.9 (11.9 (15.5) 13.0 (10.86) 6.82) 4.57 (3.17 (2.8-18. respectively.79-6.

0 (78.3-145) 85.1 (36.3 (60.0) 84.7-91.7 (43.7-53.3 (36.6 (19.5 (30.6 (32.7 (18.5) 26.6-44.4-25.2 (25.7-26.0-32.9) 29.7) 42.0) 30.0-24. 01-02.6) 20.7-127) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 22.9) 71.8-25.2 (58.1-51.6) 35.0) 27.4 (35.2-24.9 (79.5-44.5 (59.0) 31.1 (19.2 (17.4 (84.4 (35.2) 32.4 (71.2 (79.7) 74.2) 38.0) 120 (98.6-49.7 (28. 1.1) 30.4) 59.8) 75th 51.3) 19.3 (23.3) 26.9 (20.1 (19.1) 20. see Data Analysis section) for survey years 99-00.5) 19.3-96.7-20.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.1 (62.4-18. referred to as monobutyl phthalate (MBP).5) 36. interval) 24. population from the National Health and Nutrition Examination Survey.5) 17.6 (65.5) 95.2) 42.3 (23.1) 31.6-24.9-53.9 (17.2-87.4 (19.4 (25.6) 46.8) 19.8) 23.7 (22.3) 21.0 (20.2 (21.8) 58.8 (57.9-114) 116 (97.0 (30.0 (72.2) 20.1 (31.2 (19.5 (74.8-29.9-92.1) 19.2-56.9-101) 77.1-75.5-121) 106 (94.4-42.2 (59.0-26.1 (26.2 (75.7 (64.7-24.1-80.3 (56. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.4) 20.5 (28.2 (20.4 (36.8-119) 90.0 (15.3 (17.4 (38.1 (19.5 (59.3-60.4.7-111) 64.4 (21.6-48.9-22.7) 124 (98.7) 28.4-20.3-40.0) 20.1 (41.3) 40.3) 18.1 (34. Survey Geometric mean (95% conf.9) 21.5) 36.9-79.2-63.8-22.6) 38.0 (18.3) 36.5-60.3-67.1.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.1) 23.1 (51.5) 34.1) 46.6-31.5) 85. and 03-04 are 0.0-19.2-33.5) 37.6) 21.5-47.6-33.6-36.4-31.7-117) 118 (108-143) 93.7-42.8) 48.0) 117 (104-131) 112 (84.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.8) 43. respectively.7 (18.6) 39.5) 65.7-121) 97.3-79.1) 17.1-24.1 (18.6 (16.7 (16.5-42.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.2) 62.9) 26.3-85.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.2 (18.0 (23.6 (61.6) 80.0-51.6-113) 108 (90.2-32.0-19.1 (21.6-20.5) 21.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.5-53.9) 75.1-82.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.9-22.6) 71.4) 52.4-44.6 (48. Fourth National Report on Human Exposure to Environmental Chemicals 267 .4) 22.4 (35.7-116) 95.5) 24.1 (16.5-47.0-73.7-42.1 (19.0) 21.9.7 (19.6 (22.0-21.6 (44.4 (35.7-92.8-132) 95.3 (37.3 (42.0-24.2) 90th 98.7-106) 69.9-28.6 (55.6-37.2-23.6 (90.1) 23.9 (79.2-22.6-69.6-29.3) 23.2) 26.9) 46.6-143) 127 (99.7) 52.9-33.2 (21.6) 17.5) 47.7 (70.1) 47.5) 40.3 (30.2 (74.1 (28.0 (45.3-136) 137 (107-162) 119 (90.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1-29.1-92.4 (72.1-20.5) 31.8-123) 101 (90.4-60.9) 36.0) 38.5) 78.2-49. and 0.8) 62.1-22.1 (54.9-87.1) 23.4) 64.7 (24.2-114) 73.1 (58.5 (29.2-21.9-42.8-42.3-24.3) 24.8 (19.1) 25.4-26.2 (78.2-93.4-159) 107 (84.6-29.9) 18.3 (51.6-40.7 (33.7) 92.1) 36.3-76.0 (36.6 (26.7-34.2) 68.0 (25.0-58.2-159) 92.0 (31.0 (17.1 (17.5) 20.S.9 (17.3 (30.5-43.7 (51.5-117) 95. *In the 1999-2000 survey period.1-27.7-34.7 (38.4 (23.3-21.5-27.

3 (17.3-38.7 (28.2-106) 64.7 (43.2-22.1 (61.3-21.5 (14. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.6-32.6) 23.6) 37.3 (46.9 (30.4 (17.0-38.8-23.8) 17.7) 42. population from the National Health and Nutrition Examination Survey.6-50.3 (21.2 (35.6-24.9 (20.6 (29.2-22.0) 19.5) 39.6-27.5) 134 (93.8 (18.8) 35.4 (16.7-19.7-42.3) 52.9-34.9 (37.1) 35.4-103) 117 (83.S.1-32.7 (57.3) 19.4) 51.4) 16.6) 31.5-41.1-83.3-81.4-76.1 (21.1 (46.9) 14.2-22.3 (16.6-119) 63.6) 18.0-19.0 (18.6-44.7 (81.5-70.8 (18.3-17.3) 20.8) 75th 38.6-44.8-32.9) 19.1-99.4 (19.5 (15.4-61.3) 67.1 (56.4) 53.4) 15.5-15.5-18.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.1) 37.1) 44.6) 34.0) 94.0 (61.3-40.0 (27.6 (17.9-56.6 (72.5 (30.9 (35.4 (31. interval) 22.2 (16.6 (25.3) 35.4-164) 96.0 (43.8-24.7-20.7 (27.7 (20.7 (73.3 (19.3-32.2-85.1) 20.0) 81.9) 30.8-24.1-128) 97.8) 30.2 (38.2-73.7-78.0 (52.8 (18.0-90.8-235) 137 (108-198) 88.4 (17.3 (17.7-23.0 (16.1 (15.7) 20.3 (17.6-23.1-62.6-26.4-65.6-28.2-179) 84.4 (53.0) 41.9-70.0-47.0) 28.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.9) 62.4-131) 81.2-61.3-26.7 (16.3) 18.7-21.0-92.7-28.3-78.1) 22.8 (65.5-76.9 (64.8 (33.0-75.9 (21.1) 50.0 (19.6 (41.6) 14.5-21.2-21.8) 17.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.8-43.1-18.3 (71.2) 159 (102-263) 147 (93.4 (37.9) 49.7 (19.8) 28.6-16.5-64.4 (31.3-23.9 (58.7 (60.8) 40.2-18.6-74.2) 16.4 (47.6) 39.5) 91.2) 59.6-155) 91.4) 15.5 (18.0 (18.8 (13.2-108) 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.6-92.5-30.4) 19.6-128) 96.0) 55.5-142) 81.3-21.7) 19.0) 75.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9 (30.5) 90th 68.8 (22.8) 63.5-16.9) 24.9-49.2-48.3) 21.3-49.2 (19.8 (50.9) 91.8 (17.6) 83.5-37.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4 (23.2) 74.9) 20.5) 60.8) 17.2-86.5) 21.5 (18.0-17.9-38.0 (34.4-72.2-27.4 (56.0-113) 104 (83.7-39.5 (64.1) 20.4-47.0-60.7-51.4-24.2 (19.7-19.9-68.0 (26.0 (71.3 (48.7-37.4 (50.3 (28.6) 65.4) 20.4 (16.5-142) 89.0 (20.9) 39.4 (45.4) 21.4 (18.0) 108 (71.8) 34.1-21.6-22.2) 31.8) 22.8 (25.6 (19.9 (30.9-100) 86.9-14.6-23.4 (33.1 (29.0) 35.3) 19.4 (68.6-19.7 (14.3-18.8) 13.4) 62.7 (60.3) 33.8) 19.0-41.6) 64.6 (74.9-36.0) 29.6) 24.7-26.4 (50.3-71.0) 70.6-24.0) 53.9 (39.1-23.7 (54.8 (16.6) 25.3 (55.6) 38.4 (20.7 (12.9) 28.3 (69.9-26.6-43.2) 65.3) 33.0 (69.8) 20.6 (61.0) 59.3 (42.6-42.2-16.3 (24.6) 24.1-99.3 (60.5) 84.1) 21. 268 Fourth National Report on Human Exposure to Environmental Chemicals .3 (52.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9 (16.3-20.2-28.0 (50.3-39.1) 53.9 (35.7) 36.9-68.5 (81.6 (27.9) 52.9-105) 85.0) 26.2 (83.4-135) 71.3 (52.0) 25.9-84.5) 17. Survey Geometric mean (95% conf.2) 21.6-53.8) 34.6 (57.1) 61.3-106) 74.0 (15.7-80.6 (31.5) 82.8) 23.8) 20.9 (56.1) 17.9 (73.3 (76.5-22.4 (31.0 (70.4 (13.3) 59.5-23.6 (25.1 (32.9 (19.3) 17.1 (34.1) 42.4-34.

16(4):487-493. Meeker JD.22(3):688-695.S. Poland. Koch HM. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.111(14):1719-1722. Hilborn ED. Available at URL: http://cerhr. McKee RH. Reprod Toxicol 2004.93:177-185. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Reidy JA. Calafat AM. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Hagmar L. David RM. et al. Gans G. Levels of seven urinary phthalate metabolites in a human reference population. Perera FP. Butala JH. Drexler H. Needham LL.208:237-245. Caudill SP. Barr D. Wiesmuller GA. Eckard R. Richthoff J.68:309-314.html. Bolte G. Brock JW. Singh NP. Hauser R. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Caudill SP. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. NTP-CERHR. Sanchez GN. Angerer J.108(10)979-982. Epidemiol 2005. Yoshida K. et al.niehs. Chen Z. Environ Health Perspect 2004. et al. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. 112(5):A270].18(1):122. Anderson WA. Fromme H. Weuve J. Rossbach B. Silva MJ. Massey RC. Camann DE. Giwercman A. Bull Environ Contam Toxicol 2002. Koch HM. Drexler H. Environ Health Perspect 2003. Duty SM. Silva MJ. Int J Hyg Environ Health 2005. Calafat AM. Ryan L. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Research Triangle Park (NC). Koch HM. Jacek R. Int J Hyg Environ Health 2007. Brock JW. Jedrychowski W. 2005. Wittassek M. Environ Health Perspect 2000. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Duty S. et al. Prenatal exposures to phthalates among women in New York City and Krakow. Atlanta (GA). Centers for Disease Control and Prevention (CDC). NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Int J Hyg Environ Health 2007. Pirkle JL.25(2):293-302. Hodge CC.112(3):331-338. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.Phthalates References Adibi JJ. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Sampson EJ. Barr DB. Dobler L. et al. Itoh H. Silva MJ. Springall C.114(9):1424-1431. Blount BC. et al. Jonsson BAG. Environ Health Perspect 2006. et al. Boehmer S.nih. Rylander L.210(3-4):319-33. Environ Res 2003.gov/chemicals/ phthalates/dbp/dbp-eval. Caudill SP. Angerer J. Hu H. Phthalate monoesters levels in the urine of young children. Needham LL. Castle L. Green RA. Food Addit Contam 2001. Malek NA. Masunaga S. Third National Report on Human Exposure to Environmental Chemicals. J Androl 2004. Schettler T. et al.210:21-33.18(12):10681074. Hum Reprod 2007. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Scotter MJ. Urinary phthalate metabolites and biomarkers of reproductive function in young men. 2000 [online]. Urinary levels of seven phthalate metabolites in the U. 4/20/09 Silva MJ. Silva MJ. Ryan L. Helm D.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. and polyvinyl chloride.400 (<LOD-.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .400 (. and 0.10 (.300 (. 01-02.200-.300 (<LOD-.400 (.300 (.20) .700) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.200-.600) .300) < LOD .70) .00) . respectively.400 (.500 (.700) .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 .00 (<LOD-1.500) 1.90) .S.400) 1.600) .900-1.500 (.300-.400-.00-2.500-.Phthalates Dicyclohexyl Phthalate CAS No.500 (.80) . < LOD means less than the limit of detection.70 (1.200-. 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (<LOD-.300-.00 (<LOD-1.300 (.300 (.500 (.300-.600) .200 (<LOD-.400 (. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500) . see Data Analysis section) for Survey years 99-00.600 (.10) .500) 1. polyvinyl acetate.500) < LOD < LOD . resins.400-.400 (.200-.200-.70 (1.10 (<LOD-2.600) .500 (.300 (.400-.400-.400 (.500) .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) .400) 1.2.500 (.00-3.600) < LOD .500) 1. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.400) < LOD < LOD . only levels at or above the 90th percentile could be characterized.50) .00 (<LOD-1.300 (.300 (.300-.300-.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.500) .400-. In this Report.10 (<LOD-1. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. Survey Geometric mean (95% conf.9. 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.600) .70) .400 (<LOD-.300) < LOD .200-.500 (.10 (<LOD-1.500) .500 (.700) .3.500) < LOD < LOD .300-.300-.400 (<LOD-.300-.500) < LOD 1. population from the National Health and Nutrition Examination Survey. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample.400) < LOD 1.400-.500 (.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (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 . 0.400 (. and polymers.400-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. including nitrocellulose. and 03-04 are 0.300-.

880 (.290-.770-1.420-.530 (.10) .17) .350-.12-1.16 (<LOD-3.270) < LOD .34) .18) .770 (.470 (.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.82 (1.36-1.400-.380 (.420-.74) .530-1.05) .510 (.67 (1.00) .54) .00 (<LOD-3.53) .500 (.670 (<LOD-.530-.06) .450 (.660) .33 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 271 .260-.500) 3.590 (.770-1.620) < LOD .490) .500-.950 (.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. * 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.910 (.400-.610 (.470) 3.06) .690 (.410 (.740) .240-.250 (.910 (.54 (<LOD-2.630 (<LOD-.11) .560) 1.690-1.16) .S.54-6.690) < LOD 2.710) .910 (.770) < LOD 2.740) < LOD < LOD .830) 1.800-1.310-.43 (1.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .82) .53) . Survey Geometric mean (95% conf.910 (.390 (.370 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.420-.44) .14 (<LOD-3.480 (.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 .310) < LOD .660) < LOD < LOD .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.690) < LOD < LOD .630 (<LOD-.380-.450 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .330 (.590 (<LOD-.330 (.670-1.33) .530) 1.360-.220 (<LOD-.940 (.170-.510-.770-1.22 (<LOD-1.790-1.

population from the National Health and Nutrition Examination Survey. Biomonitoring Information MEP levels in the NHANES 1999-2000. interval) 179 (156-204) Selected percentiles ( 95% confidence interval) 50th 164 (136-201) 169 (141-194) 174 (151-208) 75th 454 (370-538) 465 (415-527) 502 (457-555) 90th 1260 (1010-1480) 1230 (1040-1440) 1380 (1170-1750) Total 178 (159-199) 193 (169-220) Sample size 2840 (2150-3770) 2536 2500 (1860-3220) 2782 2700 (2160-3310) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 91. and 0.8-111) 85. soaps.9-92.S. 0.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.. 2001-2002.2-102) 95.7) 71. 2002).. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.9 (61. colognes. 2007). and also in men attending a Boston infertility clinic (Hauser et al.1-93.. particularly those containing fragrances. respectively.4.3-103) 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. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.4 (62.7 (70. and 03-04 are 1. Products that may contain DEP include perfumes. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. and hand lotions.Phthalates Diethyl Phthalate CAS No.1 (71. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. DC (Hoppin et al.3 (74. deodorants.3 (82.9. 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. 272 Fourth National Report on Human Exposure to Environmental Chemicals . In contrast.5) 81.2. see Data Analysis section) for Survey years 99-00. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. shampoos. 2003) and African-American women in Washington. 01-02.

2004).. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Median MEP levels found in a small sample of German residents (Koch et al. In an analysis of NHANES 1999-2000. Other population estimates also differed by sex and race ethnicity (Silva et al.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.S. 2003) were slightly lower than levels found in NHANES 2001-2002. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. This age-related trend is opposite the direction seen for other phthalates.9 (82.0 (66.Phthalates 2002 (Brock et al.5-114) 101 (87.6 (65. 2005).. population from the National Health and Nutrition Examination Survey. 2002).7-110) 81. Analysis of NHANES 2001-2002 showed similar findings.9-110) 96.6 (77. 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.5-113) 122 (93.0-156) 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 .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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups.2 (66.

Drexler H. Koch HM. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Reidy JA. Phthalate monoesters levels in the urine of young children. Barr D. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Jacek R. Hum Reprod 2007. Poland. Silva MJ. Third National Report on Human Exposure to Environmental Chemicals. Hoppin JA. Perera FP. Duty S. Hauser R. Needham LL. Camann DE. Urinary levels of seven phthalate metabolites in the U. Malek NA. Caudill SP. Brock JW. Barr DB. Silva MJ. Ryan L. Jedrychowski W. Atlanta (GA). Hilborn ED. Rossbach B. Environ Health Perspect 2002. et al. Environ Health Perspect 2003.68:309-314. Davis BJ. 2005. Environ Health Perspect 2004. Baird DD. Environ Res 2003. Silva MJ. 112(5):A270]. Caudill SP. Brock JW. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.112(3):331-338. Singh NP. Angerer J. Hodge CC.S. 274 Fourth National Report on Human Exposure to Environmental Chemicals .Phthalates References Adibi JJ. Prenatal exposures to phthalates among women in New York City and Krakow. Centers for Disease Control and Prevention (CDC).111(14):1719-1722. et al. Meeker JD. Bull Environ Contam Toxicol 2002.93:177-185.22(3):688-695.110(5):515-518. et al. Reproducibility of urinary phthalate metabolites in first morning urine samples.

75-4.60) 4.82) 3.5-40.5-28.50-20.3-49.03-2.5) 40.8) 15.10) 3.40-9.10) 3.5 (20.70) 16.50-2.40 (4.40) 75th 7.6) 5. After parenteral administration.77 (2. interval) 3.4-20. 01-02.10) 2.30-13. respectively.0 (16.68 (3.3-57.40) 1.1) 29.9.50 (7.3) 13.6) 14.1 (10. and blood product storage and intravenous delivery systems.60 (6.9 (29.90) 4.60) 9.5-36.4-27.50-2.63-4.70) 2.57 (3.50 (8.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70 (7.90) 4.4) 22.70 (3.4) 22. see Data Analysis section) for Survey years 99-00. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00) 1.40) 4.70 (1.6-25. 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.1-29.1-48.4-20.21 (2.10 (6.90 (1.5-28.40) 2. Concentrations in plastic materials may reach 40% by weight.10 (3.1) 19.50-16.27) 2.6) 9.54) 4.4) 15.80-27.42) 3.6-60.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.9 (15.40-8.92) 4.3-26.00) 2.70-3.3 (24.4) 23.5 (12.0) 11.80-5.00) 2.70 (2.90-3.10-11.69) Selected percentiles ( 95% confidence interval) 50th 3.2-17.9 (29.60) 90th 14.20 (1.10) 8.00) 5.30-8.90-5.60) 8.4 (13.60-11.5 (18. 1989.00) 11.5) 37.50-11.7-18.2) 4.16-3.2 (29.10 (4.10-2. and 0. 2002.20 (3.07-4.7) 19.30 (4.5) 21.30 (7.5) 31.60) 7.92-2.50-3.10-5.87-2.70-4.0) Total 4.89-3.16 (2.70-5.10-3.61 (3.00 (2.60) 4.20 (4.6 (16.6-130) 31.2.50 (3.15 (1.7) 27.70-8.50-3.10 (2.2 (10.4) 6.9 (16.9) 5.3 (10.0-18. Peck and Albro.40 (6.1-17.6-23.79) 2.30) 2.31-4.40-1.70) 7.5 (24. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).80 (2.00-3.23) 3.5 (11. 1.9) 18.0 (13.40 (4.90-8.9) 27.70-6.10 (5.25-3.90 (3.0 (19.6) 14.40-8.49 (3.10-5. Fourth National Report on Human Exposure to Environmental Chemicals 275 .82 (3.57-7.3-64.1-17.7-32.31 (3.20 (3.84) 3.70 (8.6 (20.80-9.39) 3.50) 9.40 (4.40 (2.6 (10.1) 22.91-3.0.50-6.5 (12.19-3.35 (1.90) 7.00 (5.3) 52.67-4.4) 13.44) 4.80-3.6-28.56 (2. mainly polyvinyl chloride.4) 33.0-84.4) 5.0 (19.90-4.4-42.21 (2.24-4.1 (8.40-12.10-5.9 (17.30-6.9-29.5 (12.1) 25.00) 19.50 (2.34 (2.94-3.0 (9.3 (15. Albro and Lavenhar. DEHP has been removed from or replaced in most toys and food packaging in the United States.70 (1.0) 31.0) 39.8) 17.9 (26.2 (31.8-47