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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1.5'-Hexabromodiphenyl ether (BDE 153) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6-Pentabromodiphenyl ether (BDE 100) 2.4.4.1.html.2-Dichloropropane 2.1-Trichloroethane (Methyl chloroform) 1.5.4'.3-Dichlorobenzene (m-Dichlorobenzene) 1.2'.5'.4'.1-Dichloroethene (Vinylidene chloride) cis-1.1-Dichloroethane 1.4.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.2'. Paradichlorobenzene) 1.3.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4.2'.6-Heptabromodiphenyl ether (BDE 183) 2.What’s New in this Report What’s New in this Report In this Fourth Report.2-Dichloroethene trans-1.3-Tetramethylbutyl] phenol) Triclosan (2.4'-Tribromodiphenyl ether (BDE 28) 2. Table 1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2-Dichloroethane (Ethylene dichloride) 1.5.4.2'.2'.4’.4'-Pentabromodiphenyl ether (BDE 85) 2.2'.3.gov/exposurereport/chemical_selection.4.4'.4.4-Tribromodiphenyl ether (BDE 17) 2.5’. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.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 2.6.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .3.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4.4'-Tetrabromodiphenyl ether (BDE 47) 2.5.2’.4.2-Dichloroethene Dichloromethane (Methylene chloride) 1.1.4.4-Dichlorobenzene (p-Dichlorobenzene.6'-Hexabromodiphenyl ether (BDE 154) 2.3'.1.2'3.4'-Tetrabromodiphenyl ether (BDE 66) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.2'.4'.2.3.2'4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.3’.4. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'.cdc.4.5'-Tetrachlorobiphenyl (PCB 49) 2.2-Trichloroethane Trichloroethene (Trichloroethylene) m.5. The process for selection is described at http://www.5'-Tetrachlorobiphenyl (PCB 44) 2.2'. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4'.4’.

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

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

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

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

1987. Lewis Publishers. All data from 1999-2004 have been reanalyzed using this new procedure to handle situations where the percentile falls on a repeating value. 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. Therefore. Appendix A gives the details of the new procedure for estimating percentiles. Fourth National Report on Human Exposure to Environmental Chemicals 7 . we have improved the procedure for estimating percentiles to better handle this situation. Taylor JK. Quality Assurance of Chemical Measurements.Data Sources and Data Analysis Report. Boca Raton (FL).

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

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

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

5-80.2-91.7) 75th 79.2-77.9 (69.1) 101 (95. In humans. 2006. soil conditioners.0) 57.3 (55.0 μg/kg for adults (FAO/ WHO.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.1 (73. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. FDA.1) 53. Animal studies indicate that acrylamide is well absorbed. as an absorbent in disposable diapers.7-60.0 (67. Natural substances in the food are converted to acrylamide.4 (54.6 (81.1) 55. 2004.9 (54.8-55.S. Fennell et al.3-71. population from the National Health and Nutrition Examination Survey.9) 58.8 (81. and from dermal contact with products that contain residual acrylamide. 217 million pounds of acrylamide were produced commercially in the U.0. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2006).Acrylamide Acrylamide CAS No.6 (56.7-64.1-57.2-59.4-60. These estimated intakes are hundreds of times lower than occupational exposures.6) 73. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.6-104) 82.6) 71. and cosmetics (NTP-CERHR.1 (52. and an average daily intake is estimated as 0.2 (58. 1990.3 (53. glycidamide. EPA reference dose of 0.2-118) 98.9-61.1-61. pulp and paper production.0 (57.9-52.4-83. and in the synthesis or compounding of dye materials.4 (51.5-85. 2005). are heated at temperatures used for frying and baking. Since acrylamide has limited volatility and high water solubility.6-61. EPA.4) 100 (89. Tareke et al.1 (88.8 (91. it was discovered that acrylamide is formed when starch-rich foods.0 (53. (NTP-CERHR. and well below doses known to cause nerve damage or carcinogenicity in animals.7 (65.6-65.7 (58.9) 63.5 (52. and is either metabolized to the reactive epoxide.1 (83.0-49..1-64.4 (54.S.5 (74.4) 57.6-75.S.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61.0-66. Polyacrylamides are useful water-compatible polymers used in water treatment.4 (59.5 (79. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. but can covalently bind to form adducts with proteins. Fourth National Report on Human Exposure to Environmental Chemicals 11 . In 1997.7 (63. In the general population.2-93. Acrylamide is not thought to accumulate in the body at environmental doses.2) 57.1) 46.8-57. FAO/WHO. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.0-108) 152 (139-175) 126 (111-142) 108 (86.. Estimated intakes in children are about twice that of adults (DiNovi and Howard. in permanent press fabrics.1 (47.3) 86.8 (57.6 (51.2 (75. 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.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. 2004). the main source of exposure is from the diet.0-58.7-64.7) 96. but are generally above the U. drinking water.6) 90. interval) 61. and binding agents.3-2.9) 57.9-105) 86.1) 62.3) 70. Recently.9) 75.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. smoking. EPA. 1994).4-89.S.6-108) 61. 2005).8 (52. People may be exposed to acrylamide from foods. see Data Analysis section) for Survey year 03-04 is 3.4) 57. in some sealing grouts. mineral processing. widely distributed in tissues.1-64.2) 57.4-60.7) 58. or to glutathione conjugates (Calleman et al. such as potatoes and some grains..2 μg/kg/day (U.S.6-66. and in some cosmetics. ocular and dermal irritation from direct contact with acrylamide containing materials.4 (53.2 (62. 2005).7) 54. 2005).0) 85.7) 73. gels.0 (69. acrylamide has produced upper airway irritation following inhalation of high levels. 2005. Survey Geometric mean (95% conf.2-70.2-67.7 (55.3) 63.9 (60. Commercially.4-76. 2005). Elimination occurs mainly in the urine as mercapturic acid conjugates.5) 66.2-114) 163 (147-191) 96. 2002). acrylamide is synthesized and used in the production of polyacrylamide polymer.5) 58.5 (44.6) 50.

2006.8-48.S. 2006) have been demonstrated after acrylamide dosing.2) 55.4) 46.9-76.4) 83.1-62. Acrylamide is clastogenic and can produce dominant lethal mutations..2-68.4 (61.0 (80.8-49.5 (83. 2005) have been demonstrated in animals.3-78.5-92. 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.7) 74. fetal death. 2005.1-56. 2005. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. 2005).4 (90.1) 62.. probably through its epoxide metabolite.9 (57.. EPA.3-101) 95.2-91. Vesper et al.0 (70.1) 56. 2005.7-64.0-62.1 (70.4 (81. After exposure ceases.5-64.. EPA at: http://www.4-65.8) 45. 2006). Vesper 2005) and smoking (Bergmark.pdf.5) 87. and neuronal DNA reactivity (Doerge et al. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. 2005.9-62. 1997. Puppel et al.9-64. 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.4 (56.4 (57.7 (57. 2003. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.0-93..who. male germinal cell injury. 2008).. 2005).1 (56.7 (61.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.S. Survey Geometric mean (95% conf. 2001). Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. NTP-CERHR.8 (44. 2002. 2002.0) 118 (103-126) 121 (112-134) 113 (94.9) 65.8-61. 2006).Acrylamide occupational exposures. 2005) and sperm DNA adducts (Xie et al.4) 53. In addition.2 (72. and other sites) (FAO/WHO.9 (81. Schettgen et al. 2005..4-59.5-66.4 (51. 2005. thyroid.S...5 (56. and cancer (mammary. interval) 59.3) 85. Maniere et al.2) 87. respectively) are markers of integrated acrylamide exposure over the preceding few months. Puppel et al. 2004.7-86..3) 59.7 (84.9) 87. Glycidamide has been shown to react with DNA (Doerge et al. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2005. 2008). most non-smokers had levels less than about 100 pmol/gram hemoglobin.5) 71. reproductive effects (reduced litter size.1 (66.9-138) 143 (130-159) 96.6-64.7) 61.2 (63.5) 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.5) 75th 85.1 (82.. 2005. Klaunig et al. glycidamide (NTP-CERHR. Hagmar et al.2 (56.8 (51.8) 60. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.4-103) 79. scrotal. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).. 1997. Schettgen et al. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. IARC classifies acrylamide as probably carcinogenic to humans. 12 Fourth National Report on Human Exposure to Environmental Chemicals . to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.4-98.0-103) 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.epa.9 (58..S.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.3) 59. U.1) 60. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. EPA. presynaptic nerve terminal binding (LoPachin. U. Rice. see Data Analysis section) for Survey year 03-04 is 4.9-77.7-62. Mucci et al.6-62. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.3) 59.3 (56.9) 75.. 2005).7) 60. adrenal.9) 59. population from the National Health and Nutrition Examination Survey. dominant lethality).6 (66.7) 90.9-78.0 (52..int/ ipcs/food/jecfa/summaries/summary_report_64_final..1 (57. 2005. 2005. 2004). uterine. 2009).5 (59.0) 94. 2005.1-60.0 (75..1-70.2) 65.5-94. 2005).6-90. altered gene expression in testicular tissues (Yang et al..5 (42. although different analytic methods can affect results. Additional information is available from U.0.7 (87. Axonal degeneration.2-90..6 (90..

580(1-2):157-165.cfsan. Bridson WE. Bruze M. July.126(2):361-371. et al. Italy. 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. Survey data on acrylamide in food: individual food products. morphological and molecular endpoints in animal models. Kamendulis LM. Calleman CJ. Burgess J. and Research Strategies. Maniere I. Doerge DR. 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. 1994). da Costa GG. Metabolism and hemoglobin adduct formation of acrylamide in humans. Bergmark E.561:49-62. Scand J Work Environ Health 2001. The Updated Exposure Assessment for Acrylamide. Available at URL: http://www. Uncertainties.. Acrylamide intake through diet and human cancer risk. 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. Fennell TR. Cheong HK. J Agric Food Chem 2008. gov/~dms/acrydata. Bergmark E. Wu Y. Hagmar L. et al. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Chicago. 054472. et al. smokers and nonsmokers. Bjellaas T.27(4):219-226. Illinois. Farmer PB.pdf. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. 2005.580(1-2):131-141.niehs. Available at URL: http://cerhr. 2/3/09 Hagmar L. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Calleman CJ. In another study. 2/3/09 Perez HL. LoPachin RM. Mutat Res 2005. 2009 Jan 8.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Yang JS. Acrylamide neurotoxicity: neurological. Magnusson AL. Doerge DR. DiNovi M and Howard D. Fennell TR. Andersen M. Rosen I. smoking habits and gender. Toxicol Appl Pharmacol 1993. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. April 13-15. Alexander J.. Twaddle NC. Churchwell MI. Joint FAO/WHO Expert Committee on Food Additives. 2004. Summer SCJ. Costa LG. 2001). Spicer R. 8-17 February 2005. Paulsen JE.3:406-412. Adv Exp Med Biol 2005.561:21-37.. Wirfalt E. Churchwell MI. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.pdf. Calleman CJ. February. McDaniel LP. Mutat Res 2005. Becher G. Kautiainen A. Paulsson B. et al. He F. 1993. 2/3/09 Klaunig JE. 64th Meeting: Summary and Conclusions (FAO/WHO).10(1):78-84. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Nordander C.html#u1004.nih.who. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Toxicol Sci. [Epub ahead of print] Dybing E. Granath F.gov/chemicals/ acrylamide/Acrylamide_Monograph.. 1999). Aprea P. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Guffroy M. References Bergmark E.56. Malmberg B.580(1-2):119-129. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Osterman-Golkar S. 2006. Duale N. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. 2001.85:447-459. Mutat Res 2005. Costa LG. Godard T. Food Chem. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Rome. Toxicol Sci 2005. 6013-6019. Beland FA. Human exposure and internal dose assessments of acrylamide in food. NIH Publication No. Bergmark E. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Toxicol 2005. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers.Acrylamide In occupational settings. Available at URL: http://www.fda. Zhang S. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Tian G.43:365–410. Laurentie M. et al. He F. Axmon A. National Toxicology Program. Haugen M. Mucci LA. Chem Res Toxicol 1990. Adv Exp Med Biol 2005. Tornqvist M. Perez et al. Hagmar et al. Mechanisms of acrylamide induced rodent carcinogenesis..120(1):45-54. 2004 Acrylamide in Food Workshop: Update Scientific Issues. CFSAN/Office of Plant and Dairy Foods. Snyder RW. Wilson KM. Chem Res Toxicol 1997 Jan.Toxicol Appl Pharmacol 1994. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Food and Drug Administration (FDA). AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Tornqvist M.

Analysis of acrylamide. Toxicol Lett 2002. Puppel N. Fueller F. Available at URL: http://www.S. a carcinogen formed in heated foodstuffs.274(1):59-68. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Vesper HW. Myers GL. EPA).epa. Adv Exp Med Biol 2005. Marko D. Ospina M. Mutat Res 2005 Feb 7. Broding HC. Toxicol Lett 2006. Chemical Summary for Acrylamide. Available at URL: http://www. Lee SH. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Eriksson S.163(2):101-8. Vesper HW. Letzel S. J Agric Food Chem 2008. Gray JG. Ding X. Xie Q.56(15):6046-53.gov/iris/subst/0286.20(6):959-64. Hallmans G. Rydberg P. Fu D. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.206(1):9-14. Kutting B. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Angerer J. Agudo A. Int J Hyg Environ Health 2004. Schettgen T. Rapid Commun Mass Spectrom 2006. Schettgen T. The carcinogenicity of acrylamide.50(17):4998-5006. Drexler H. 14 Fourth National Report on Human Exposure to Environmental Chemicals .txt. Weiss T. September.207(6):531-9. Rossbach B. Office of Pollution Prevention and Toxics. Tornqvist M. J Agric Food Chem 2002.134(1-3):65-70.S. Lee MH. Reprod Toxicol 2005. Ospina M.S. 2/3/09. Angerer J. Rice JM. Environmental Protection Agency (U. Choi JH. Ingham L.580(1-2):71-80.Acrylamide glycidamide by gas chromatography-mass spectrometry. Chae C. Licea-Perez H. Angerer J. Mutat Res 2005. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Slimani N. Drexler H. Sun H. Int J Hyg Environ Health 2003.htm. Yang HJ. Drexler H. Han DU. U. Washington (DC). EPA). Schettgen T. Meyers T. Hemoglobin adducts of ethylene oxide. Tjønneland A. Anal Biochem 1999. Han CH. Acrylamide.gov/chemfact/s_acryla.epa.580(1-2):3-20. et al. Smith A. revised 1/3/06. 2/3/09 Vesper HW. 1994. Benetou V. Tjaden Z. Liu K. Jin Y.19(4):527-34. Karlsson P. propylene oxide. Meyers T. Toxicological effects of acrylamide on rat testicular gene expression profile. U. Environmental Protection Agency (U. Liu Y. et al. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells.S.561:89-96. Integrated Risk Information System (IRIS). Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Tareke E.

220) .139) * .70) 2. 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.49) 1.510 (.200) 1.630 (.540 (.054 (.77 (1.62) 2.153-. respectively.140 (.620-1.066) .630 (.44 (2.120 (.160) .75) 1.21 (.126) .230 (.108) * .040-.49) 1.110) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.09-2. and 0.20) 1.50) 3.077) .057-.14-1.080-.140-.950 (.300) .57) 2. Survey Geometric mean (95% conf.19) .131 (.140-.63-2.220-.030-.5% nicotine by weight (Kozlowski et al.01) 3.600-1. emphysema.28) .60-2.160 (.96) 2.12) 1.150) .073) < LOD .050 (.120-.21-1.42 (1.621-1.38-2.30) * .66-3.533-.99) 2.95) 1.670) .120 (.080-.770) .89) 1.167 (. 83% of measurements had an LOD of 0. DHHS.030 (. DHHS.040 (.050-.197) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.42-4.92 (1.154-.150) .060 (.70-2.50 (1.052 (<LOD-.53 (1.120-.410) .00) .00) 1.580) . 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.428-.060) .48-3.104-.140 (.075 (.111-.193) .310-1.187) .39) 3.110-.480-.68) .059-.96-4.28-1.220) .54) 1.180 (.470-. cardiovascular disease.110 (.180) .216 (.09-3.180 (.180) .02) 1.087-.12 (2.160-.78) 2.190-.087) < LOD < LOD .350 (.050) .015 ng/mL.090-.360) .260) 1.20) .430-1.49) 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. see Data Analysis section) for Survey years 99-00.45) 1.770-1.30) 2.40) .S.100-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.144 (.160 (.850 (.310-1.080 (.540-.190-.16) .23-2.047-.Cotinine Cotinine CAS No.15 (2.124 (.066 (.S.180) .130) .505 (.77 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.040-.198) * .01 (1.480-1.310) .11) .070) 75th .710 (. stroke.163) .063) .370-.660) .12-4.050 (<LOD-.26-1. which may vary for some chemicals by year and by individual sample.77 (1.32) 1.164 (.12 (1.94) 1.20-2.68 (1.120 (. Fourth National Report on Human Exposure to Environmental Chemicals 15 .17 (.302) .160 (. 1998).630 (.312) .66 (1.88 (.070-.059-.79) 3.09-3.62 (2. Cigarettes contain about 1.05.580 (.163 (.19-2.137 (.213) .076-.060 (<LOD-.55-2.22) 2.110-.960-1.080 (.090-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.050 (<LOD-.077) .110 (.920 (.81-2.201) .620 (.99) 2. population from the National Health and Nutrition Examination Survey.S. and exacerbated asthma (U.05 ng/mL.070) .21-1.110-.690 (.580-1.310) 90th 1.02) 1.15) 2.050 (<LOD-.990 (.084) .76 (1.19) 1.32-2.50-4. ** In the 2001-2002 survey period.145) .068) .050) .068) . 2006).089) Age group 3-11 years 99-00 01-02** 03-04 .234) .175 (. 2004).080-.062 (. and 03-04 are 0.180) .080-. Children exposed to ETS are at increased risk for sudden infant death syndrome.950-1.53-4.02 (.85 (1.066-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .450-.63 (2.14) .83-2.860 (.060 (<LOD-. 2004).087 (.87-3.50-1.230) .33-2.900-1.34 (1.047-.280 (.180) . acute respiratory illness.68) 2.17 (1.308 (.110 (.05) 1. maternal exposure during pregnancy can result in lower birth weight.190-. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.040 (.058 (.071) .020-.570 (.93) .23 (.54 (1.164 (.142-.506 (.910-1.740-1.088-. ear problems.053 (<LOD-.65 (1.92) 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 . and various other disorders (U.32-2.740-1.570-1.015.060 (.060-.23 (2.66) 1.070 (<LOD-.520 (.070) .47-3.930 (. and 17% had an LOD of 0.43 (1.997-3.48-2.726) .060-.060-.55 (1. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.39 (1.120) .04 (1.35 (2..080) < LOD < LOD . acute respiratory infections.030-.061) < LOD .115-.790) .086 (.350-.110 (.050-.30) 2.625) .090-.094) .14) .54 (1.188) .20 (1.44 (1.110 (.148-.17) .240 (.210 (.030-.050 (<LOD-.800 (. < LOD means less than the limit of detection.120 (.990) .260-1.052 (<LOD-.110) .84-3.18-3.20 (.080) < LOD .137-.350-.071 (.840) 3.44) 2.88 (1.320) .400-.040 (.120 (.043-.23 (1.770) .500 (.96 (1.44) 2.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .130 (.730 (.160) .106-.820) .

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

280:135-140. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Fong I. Mehta NY. Metabolism and disposition kinetics of nicotine. Department of Heath and Human Services. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Benowitz NL.S Department of Health and Human Services (U. Atlanta (GA): 2005. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Pirkle JL.S Department of Health and Human Services (U.114(6):853-858. Sosnoff CS. et al. Jacob III P. National Center for Chronic Disease Prevention and Health Promotion.nih.gov/eid/rmca/critdocs/ criteriadoc/33. Benowitz NL. 4/13/09 U. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Houseman TH. Hukkanen J. Centers for Disease Control and Prevention. Available at URL: http://monographs. National Toxicology Program (NTP). Third National Report on Human Exposure to Environmental Chemicals. 1999-2002. Trends in the exposure of nonsmokers in the U.280:152-156. Turner DM.275:1233-1240.iarc. Flegal KM. Exposure of the U. Clin Pharmacol Ther 1994. Racial/ethnic differences in serum cotinine levels among adult U. Pirkle JL. [online]. Maurer KR. Available at URL: http://monographs.18:188-204. Jacob P III. Available at URL: http:// cancercontrol. BMJ 1975. available at URL: http://mtn. Kozlowski LT. 1988-1991. the United Kingdom. Summary of Data Reported and Evaluation [online] 2004.S. Schober SE. Coordinating Center for Health Promotion. 4/13/09 Iwase A. Tob Control 2006. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Giovino GA.gov/ntp/roc/eleventh/profiles/ s176toba. Vogler GP.S. 1999.surgeongeneral. DHHS). Pechacek TF. Strauss WJ. IARC Monogr Eval Carcinog Risks Hum.94(2):314-320. J Pharmacol Exp Ther 1999. Herrera B. Caraballo R. iarc. Brody DJ. Vol 83. Respiratory nicotine absorption in non-smoking females during passive smoking. and the United States.7:369-375.57(1):79115.fr/ENG/Monographs/allmonos90. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Centers for Disease Control and Prevention.niosh.pdf. IARC Monogr Eval Carcinog Risks Hum.niehs. Warner K. Modin G. Tobacco related exposures.63:139-43. Int Arch Occup Environ Health 1991.4:313-316. National Institute for Occupational Safety and Hygiene (NIOSH). References Armitage AK.fr/ENG/Monographs/ allmonos90. 4/13/09 Centers for Disease Control and Prevention (CDC). Tob Control 1998. 2004. Pollack HA.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. JAMA 1998. Caudill SP. Vol 38. Absorption and metabolism of nicotine from cigarettes. Office on Smoking and Health [online] 2006. 1988-1991. Lewis PJ. Available at URL: http://www. Epidemiol Rev 1996. Ethnic differences in N-glucuronidation of nicotine and cotinine. Giovino G. Pharmacol Rev 2005. Herrera B.gov/library/ secondhandsmoke/. Smoking and Tobacco Control Monograph 10 [online]. Kira S. Soliman S. Sweeney CT. Bernert JT.S. Am J Public Health 2004. 4/13/09 International Agency for Research on Cancer. Dollery CT. Environ Health Perspect 2006. Richter PA. U. U. In Report on Carcinogens. Tobacco Smoke and Involuntary Smoking. Pickett MA. JAMA 1998.56:483-493. Nicotine metabolism and intake in black and white smokers. U. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.291(3):1196-1203.cdc. Available at URL: http://ntp. June. Benowitz NL. Tobacco Smoke. Summary of Data Reported and Evaluation [online] 1986. George CF. JAMA 1996. 4/13/09 Perez-Stable EJ.pdf. Benowitz NL. DHHS). Perez-Stable EJ. Benowitz NL. cigarette smokers: the Third National Health and Nutrition Examination Survey.S. Curtin LR. population to secondhand smoke: 1988-2002. Cotinine as a biomarker of environmental tobacco smoke exposure.php.15:302-307.S. 11th ed. Metabolism of nicotine to cotinine studied by a dual stable isotope method.gov/tcrb/monographs/10/. Pechacek TF. Brody DJ. Department of Heath and Human Services. Etzel RA. Coordinating Center for Health Promotion. Bernert JT.S. Jacob P III. Jarvis MJ. International Agency for Research on Cancer.php. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Jacob P. Mowery PD. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Aiba M. 1991. et al. Centers for Disease Control.cancer. Schwartz SS.S. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. 4/13/09 National Cancer Institute (NCI).

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

DEET is not genotoxic.270) 688 678 518 700 598 956 Limit of detection (LOD.110 (.120-.N.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. DEET has low acute toxicity. One survey detected DEET in 74% of sampled streams in the U.130-.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 .S. About 3-8% of dermally applied DEET is absorbed.120-.130-.N-Diethyl-meta-toluamide (DEET) N.220 (.140) < LOD .250) < LOD . General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110-.N-Diethyl-meta-toluamide (DEET) CAS No. 2003).epa.180 (.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 they range in concentration from 4% to 100%.S. which may vary for some chemicals by year and by individual sample. including seizures and encephalopathy. DEET is not a developmental or reproductive toxicant in animals (U.EPA.110 (<LOD-. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.EPA. 2003).180 (. Additional information is available from U.100-.gov/pesticides/.170 (. There are over 225 insect repellents brands containing DEET.100-.100-. Urinary N.1. DEET is also used in combination with dermal sun screens (U.520) < LOD . People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.190) < LOD .110 (<LOD-. population from the National Health and Nutrition Examination Survey.560) < LOD .160) < LOD .. Its use is recommended for prevention of several vector-borne diseases. Sudakin and Trevathan. < LOD means less than the limit of detection. (U.110 (.EPA at: http://www.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. 134-62-3 General Information N. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. Neurological effects in humans.210 (. (Kolpin et al.130) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 . 1998).140 (. have been reported as result of self-poisoning by ingestion or excessive dermal application.240) < LOD .S.100-.130-. Survey Geometric mean (95% conf. 2005). 1998).150) < LOD . 1995. 2002).100 (<LOD-.130 (. EPA.130 (. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. 2002)..S. After absorption.130 (.130-.110 (.170 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. DEET can be applied to clothing and the skin to repel biting insects.449 and 0.110-.110 (..100-.140) < LOD . DEET is not registered for use on agricultural commodities. and it has not been rated by IARC or NTP with respect to human carcinogenicity.130) < LOD .210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .180 (.180) < LOD .140) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.100-.140-.

150) < LOD .170-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.230-. 2005).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 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .150-.350-.190 (.270 (. population from the National Health and Nutrition Examination Survey. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.240-.270-.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . In this survey period.280-1.390-.140-. Urinary DEET levels as high as 5.410 (.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 .190 (.370-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .630) < LOD .190 (<LOD-.370) < LOD .200 (.270) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Biomonitoring 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..490) < LOD . Urinary N.250) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.350) < LOD . 1992). 20 Fourth National Report on Human Exposure to Environmental Chemicals .330 (.190-. representative subsamples from NHANES 2001-2002.410-.230) < LOD . Survey Geometric mean (95% conf.280 (.320 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.480 (.93) < LOD .300 (.N.330 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.500 (.250 (.S.290-.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.130 (<LOD-. 2007).230-.410 (.440) < LOD .320) < LOD ..640 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270 (<LOD-.240) < LOD .350) < LOD . Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.250-.

2005.S. 1999-2000: a national reconnaissance. Toxicity and Exposure Assessment in Children’s Health. 2005 Kolpin DW. Reregistration Eligibility Decision (RED): DEET. Human exposures to N. Available at URL: http://www.S.S. EPA. Barber LB.S. J Toxicol Clin Toxicol 2003.36(6):1202-1211. Diethyltoluamide (DEET). DEET: a review and update of safety and risk in the general population.EPA). Schoenig GP. Environmental Protection Agency (U. Meyer MT. Available at URL: http://www. Fundam Appl Toxicol 1995.S. Furlong ET. Atlanta (GA). 1993-1997.115(8):1254-1260. Thurman EM.pdf. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Barr DB. Trevathan WR.N-diethyl-mtoluamide following dermal application to human volunteers. Chemical Summary. September 1998. Smallwood AW. et al. and excretion of N. Environ Health Perspect 2007. Hartnagel RE Jr. Lowry LK. metabolism.EPA. Absorption.N. Centers for Disease Control and Prevention (CDC). U. N. hormones. pdf.gov/oppsrrd1/REDs/0002red.S.16(1):10-13. Veltri JC. Selim S. Tapia J. J Anal Toxicol 1992.epa.N-Diethyl-meta-toluamide (DEET) References Arcury TA.S. DeBord KE. 1-118.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.25:95-100. 4/9/09 U. and other organic wastewater contaminants in U. Quandt SA. Washington (DC): U. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Osimitz TG.EPA). Grzywacz JG.2:341352. Bell JW. EPA 738-R98-010. Zaugg SD.41(6):831-839. Third National Report on Human Exposure to Environmental Chemicals. Gabriel KL.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Int J Toxicol 2002. U. Pharmaceuticals. Page BC. Chen H.gov/teach/chem_summ/ DEET_summary. pp. Sudakin DL.epa. Environ Sci Technol 2002. Environmental Protection Agency (U. streams.

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

DirectorateGeneral Health and Consumer Protection.59(9):625-628.pdf. Richter CA. Needham LL. Fujii S. Wong LY. National Toxicology Program. 2008. Regul Toxicol Pharmacol 2002. 2/4/09 Ouchi K. Yoshinaga J. Bradley S. Munro IC. Park 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. Calafat AM.116(1):39-44.. 2/4/09 European Commission. May 22. Hum Ecol Risk Assess 2004. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Kim JC.113(4):391-395. Exposure of the U. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Doull J. bisphenol A glucuronide. Cohen JT.pdf . Toxicol Sci 2002. et al. Available at URL: http://cerhr.69(22):2611-2625. Available at URL: http://cerhr. Barton L. 2007.. Gender differences in the levels of bisphenol A metabolites in urine. niehs. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Barr JR.149:988-994. Myers CB. Occup Environ Med 2002. Marr MC.S. Life Sci 2001. Proc Natl Acad Sci USA 2005. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Watanabe S. Serizawa S.niehs. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite.. Matthews JB. Watanabe C.59(4):403-408.137(3):353-362. streams. Koulova AI. Barber LB. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Human Health. 5: 505-523. Zacharewski TR. Szigeti-Buck. Howdeshell KL. Kroes R. Belgium. C. Tyl RW.gov/chemicals/bisphenol/bisphenol. Endocrinology 2008. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Cunha G. T. Gray GM. Kiguchi M. Caudill SP. National Institutes of Health. 4. Ecotoxicity and the Environment (CSTEE).4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Lynch BS. November 26. Chem Res Toxicol 2001. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Thurman EM.gov/chemicals/bisphenol/BPAFinalEPVF112607.nih. Needham LL. Furukawa M. Available at URL: http://ec. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Pharmaceuticals. Rhomberg et al. et al.312(2):441-448. Yang M. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. J Am Dent Assoc 2006. Hanaoka T.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325.36(6):1202-1211.nih. Imai H. Needham LL.780(2):365-370. 2003. September. McConnell EE.J. niehs. Han SY. European Commission. MacLusky. Rat two-generation reproductive toxicity study of bisphenol A.pdf . Kolpin DW. Kuklenyik Z.145:592-603. Bisphenol A. Shin HC. vom Saal FS. August 2001.Environmental Phenols References Akingbemi BT. Chung MK. Environ Sci Technol 2002. Hara K. Sottas CM. Ema M. Tsugane S. Kawamura N. and Hardy MP.Scientific Committee on Toxicity. Rubin C. Ispra. Meyer MT. Italy. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. 32 Fourth National Report on Human Exposure to Environmental Chemicals .S. Available at URL: http://ntp. Joskow R. Koh WS. and Hajszan. Twomey K. Leranth. Nippon Eiseigaku Zasshi 2004. et al.europa.S. Ekong J. Calafat AM. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Arakawa C.35(2 Pt 1):238-254. Endocrinology 2004. An evaluation of the possible carcinogenicity of bisphenol A to humans.68(1):121-146. hormones. Haighton LA. and other organic wastewater contaminants in U. Available at URL: http://ecb. Zaugg SD. with estrogen receptors alpha and beta. Calafat AM. Barr DB. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Brussels. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Reidy JA. Kim CS. Joint Research Centre Institute of Health and Consumer Protection. Harazono A. 2002. Furlong ET. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. NC. Ikka T. In vitro and in vivo interactions of bisphenol A and its metabolite. Kim YH. 1999-2000: a national reconnaissance. Biochem Biophys Res Commun 2003. Department of Health and Human Services. Timms BG. Han SS.eu/ health/ph_risk/committees/sct/documents/out156_en. Environ Health Perspect 2008. Hughes C.jrc. K. U. National Institute of Environmental Health Sciences. Brine DR.pdf. 2/4/09 Fujimaki K. Research Triangle Park. Reidy JA. Reprod Toxicol 2001. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.14(2):149-157. Thomas BF. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Hlywka JJ.10:875-921.nih. Environ Health Perspect 2005. Pyo MY. N. Cha SW.pdf. Keimowitz AR. Ye X.102(19):7014-7019. Klinefelter GR.

Witorsch RJ.15:12811287. vom Saal FS. Csanady GA. Large effects from small exposures. Chem Res Toxicol 2002. et al. Colnot T. Wilson NK. Yang M.Environmental Phenols Volkel W. Lee SM.44(4):546-51. Vom Saal FS. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Welshons WV. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Dekant W. Sheldon LS. III. Food Chem Toxicol 2002. Kim SY.103(1):9-20. Nagel SC.147(6 Suppl):S56-69. An observational study of the potential exposures of preschool children to pentachlorophenol. Biological monitoring of bisphenol a in a Korean population. Environ Res 2007. Hughes C. Morgan MK. Arch Environ Contam Toxicol 2003. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. bisphenol-A. and nonylphenol at home and daycare. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Chang SS. Endocrinology 2006.40(7):905-12. Lordo RA. Filser JG. Kawamoto T. Chuang JC.113(8):926-33. Jang JY. Environ Health Perspect 2005. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.

497) * .600-1.900 (. to shorter chain alkylphenol ethoxylates.S.300 (<LOD-.500-1.60-3. Saito et al. In 1999-2000. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.600) 1.80) 2. Katsuda et al.400) 1.900 (. The alkylphenols can bioaccumulate in some fish.50) .10 (1. Several alkylphenols. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.80 (1.500) . which are anionic surfactants used in detergents.40 (1.00 (.369 (.389 (. and was quickly eliminated from the blood (Certa et al.400 (. 2002)..300-. The alkylphenol ethoxylates enter the environment through human use of products containing them. textiles.3.00 (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.30 (1.10-2. and to alkylphenoxycarboxylates.274-.20-2.50-3.30-2..600) .2.20-2.500) .60) 1.10) 2.299-.20-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.. < LOD means less than the limit of detection. and through manufacturing waste streams (Warhurst.10 (. leading to inhalation as another potential exposure route (Rudel et al.40) 1.. Ying et al. 2003..700-1. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).20-2.200-. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.60-3. and emulsifiers.60) 613 652 1092 Limit of detection (LOD.40) * 03-04 03-04 03-04 .Environmental Phenols 4-tert-Octylphenol CAS No.000 tons of alkylphenol ethoxylates were produced annually worldwide.70 (1. testicular atrophy. an alkylphenol. Disposition in humans has not been studied sufficiently.S. have demonstrated estrogenic effects particularly when injected at high doses in animals. including 4-tert-octylphenol.1.30 (1.300 (<LOD-.. see Data Analysis section) for Survey year 03-04 is 0. and impaired spermatogenesis (e.40) 1.30) 90th 1.300 (<LOD-.477) .60-3. 2000.20) 2. During the 1980s and 1990s. altered estrus cycles and reproductive outcomes.600-1. Urinary 4-tert-Octylphenol (4-[1. altered neonatal sexual development. is used to manufacture alkylphenol ethoxylates.g. impaired steroidogenesis.20-2.300-.800-1.400 (. and some personal care products..30 (1..60) .60-3.600-1.40) 2. over 500. 2002).60-3.90) 2.20) 1. 34 Fourth National Report on Human Exposure to Environmental Chemicals .50) . 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 . Less frequently.268-..600-1.5% of 139 U.500) . which may vary for some chemicals by year and by individual sample.900 (.90) 2.600-1.600-1.g.50-2. 140-66-9 General Information 4-tert-Octyphenol.900 (.600) . Indoor and to a lesser extent. Bian et al. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.00 (.70 (1.30) 2.500-1. 1997. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.50) 1.00) 1229 1288 03-04 03-04 03-04 * .300 (<LOD-. and some of their degradation products are toxic to aquatic life. Laws et al.400 (. 1996).30 (. pesticides.50) 1.500 (..70 (1.30) 1. and from contact with some personal care products and detergents. streams in 30 states (Kolpin et al. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.30 (1.20 (1.20) 314 715 1488 03-04 03-04 * * .900 (. fish) and drinking water. industrial cleaners. the various alkylphenols have also been used as emulsifiers and modifiers in paints. orally administered 4-tert-octylphenol was well absorbed.80 (1.50) 1.10 (. and the polyethoxy chain may consist of up to 50 ethoxy units.50 (1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.500) 75th .20-2.70 (1. 1995.200-.80 (1.357 (. Blake and Boockfor. 2006.40) 2. In rats.300 (<LOD-.600) . Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) 1.507) * < LOD . did not bioaccumulate. 2000.60-3. In the 1990s. 2004). through sewage.

160-.78) 1228 1286 03-04 03-04 03-04 * . 2005.00) 2.03-6. Tyl et al.910 (.570) . population from the National Health and Nutrition Examination Survey.337-.78) 3.43) 1.460 (.17 (.S. Kawaguchi et al.50 (2.29) 2. Urinary 4-tert-Octylphenol (4-[1.53-3.199-.. Nagao et al.. IARC and NTP have not rated octylphenol.470-1.33 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33) 3.62 (1. 2004).25) 90th 1.03 (1.62 (1.3. 4-tert-Octylphenol is not considered directly genotoxic.43) 1.85 (1.450) 1.384) * .610) .24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.03 (1. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.00) 1.25-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.890-2. Fourth National Report on Human Exposure to Environmental Chemicals 35 .500-1. representative subsample of NHANES 2003-2004.67-2.62) .11-2. 2000. 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..270 (.02-4.170-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.530) .96-4.320 (<LOD-.78 (1.300 (<LOD-.640-1. or their corresponding ethoxylates with respect to human carcinogenicity.40-4.Environmental Phenols Myllymaki et al. It is unclear if estrogenic or other effects occur in animals through oral dosing.730-1. Survey Geometric mean (95% conf. 2001).59 (1.00) 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 . Calafat et al.08) 1.14) 314 713 1487 03-04 03-04 * * .280-.18-4. Yoshida et al.420) .270 (.620) .270-.25) 2.620-1.73) 2.54) * 03-04 03-04 03-04 .269 (..06 (2. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure. at lower or environmentally relevant doses (Blake et al.560) .11) 2.380 (<LOD-.43-3.1.68) 2..550-1.22) .349) * < LOD .S.850 (.15) 1.59) 1.860 (. nonylphenol. 2001.00 (.31 (1.65-3.71) 2.00) 2.00 (.770 (.260 (<LOD-.450) .11) 1.31-2.60 (1.740 (..36-3. In a small number of adult Japanese volunteers. 1999).05-2.435 (.370 (<LOD-.40 (1.410 (. 2003.740 (. Sweeney et al.207-.276 (.64 (.68-2. 2004.470) 75th .3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.10-2.470-1.540-1.630-1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al. Biomonitoring studies on levels of 4-tert-octylphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 4-tert-octylphenol than are found in the general population.20 (1.81 (1.76 (2.41) .400) .

Camann DE. Sweeney T. Kookana R. Boockfor FR.uk/resource/reports/ethoxylates_alkylphenols. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Zaugg SD. Toxicol Appl Pharmacol 2000. Watanabe G. Estrogenic activity of octylphenol. Calafat AM. Carey SA. alkylphenols. Rudel RA. Warhurst AM. Toxicol Appl Pharmacol 2005. Regul Toxicol Pharmacol 1999. Reprod Toxicol 2004. Toxicol Lett 2001. Ferrell JM. streams. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Reprod Toxicol 2001.Environmental Phenols References Bian Q. Kawaguchi M. and testosterone. Fail PA.57(2):255-266. Kawaguchi M. et al. Taya K. Raychoudhury SS. Phthalates. Yoshida M.28(3):215-226. Toxicol Sci 2000.18(1):43-51. hormones. Environ Health Perspect 2008. Indoor air pollution by alkylphenols in Tokyo. and other organic wastewater contaminants in U. Usumi K. Pharmaceuticals. Bodman GJ. Katsuda S.S. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Watanabe G. and other endocrine-disrupting compounds in indoor air and dust. Cooper RL. Endocrinology 2000. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Maekawa A.pdf. Myers CB. Millette CF. Wiegand HJ. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats.44(8):1355-1361. Tyl RW. Haavisto TE.co. prolactin. Sakui N. J Chromatogr B Analyt Technol Biomed Life Sci 2004.15(6):683-692. Korn LR. Ono H. Toppari J. Karjalainen M.799(1):119-125. Horie M. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.116(1):39-44. Saito Y. Boockfor FR. Wong LY. Kolpin DW. Williams B. Anal Chim Acta 486:41-50. Biol Reprod 1997. nonylphenol. Roche JF. Barber LB. Myllymaki SA.foe. polybrominated diphenyl ethers. Two-generation reproduction study with para-tert-octylphenol in rats. Paranko J. and sertoli cell number. Nair-Menon JU. Maekawa A. Needham LL.37(20):4543-53.121(1):21-33. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Brooks AN. Ito R. Muller AM. Brody JG. Katsuda S. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Bolt HM. Saito I.S.141(7):2667-2673. Environ Sci Technol 2003.54(1):154-167. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.folliclestimulating hormone. Ye X. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Xu L. Inoue K. Wang X. Reidy JA.207(1):59-68. et al. 2/4/09 Ying GG. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review.36(6):1202-1211. et al. Yoshida M. Spengler JD. Onuki A. 2003. bisphenol A and methoxychlor in rats. Blake CA. Izumi S. Available at URL: http:// www. Makino T. 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. Seto H. Arch Toxicol 1996. Seely JC. Nagao T. Environ Int 2002. Chen J. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. pesticides. Furlong ET. Meyer MT. Thurman EM. Yoshimura S.71(1-2):112-122. Marr MC. Laws SC.165(3):217-226. Yoshimura Y. Nakagomi M. Okada F. Environ Sci Technol 2002. Nicol L. Exposure of the U. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. 1995. Blake CA. 1999-2000: a national reconnaissance. Qian J. Song L. testis size. Food Chem Toxicol 2006. et al. Fedtke N. Brine DR.14(5):325-332. Taya K.30(2 Pt 1):81-95. Indoor Air 2004. Certa H. Takai N. Takenaka A. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. McCoy GL. Inoue K.

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

86-12.8) 9.6-37.8 (21.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.20 (7.7 (28.7 (11.4) 51.5 (11.2-46.82 (8.80 (5.6 (10.2 (13.6) 12.5) 13.9) 7.1 (45. Survey Geometric mean (95% conf.1) 9.5) 11.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .3 (9.0) 65.10) 84.1) 9.4 (11.5) 66.50-10.6) 90th 212 (172-241) 03-04 03-04 03-04 9.6-15.0) 49.8-127) 37.6 (12.9) 8.21 (6.1) 9.10-9.2 (27.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.45-10.6 (9.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.7) 292 (151-432) 132 (78.45-13.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6) 39.2) 12.9 (8.90-10.2-58.6) 10.74 (5.1) 13.8) 116 (39.8-63.4 (38.16 (6.3 (8.5-14.20 (7.9 (11.3-67.4) 357 (225-456) 203 (87.1) 9.7) 123 (36.2 (25.5-86.S.22-10.6) 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 9.70-16.55 (4.1) 50.3) 6.9-61.4 (12.20-13.40-17.3 (26.3-31.20-10. see Data Analysis section) for Survey year 03-04 is 2.4) 73.72-13.11-11.1-39.0-19.2 (37.29-12.0 (26. Urinary Triclosan (2.4) 90th 249 (188-304) 03-04 03-04 03-04 8. interval) 13.9) 75th 47.2) 13.1 (8.48-10.7) 10.6-111) 33.8-85.4) 75th 43.3-35.2-58.6-65.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.60 (6.8) 7.9-236) 193 (90.3) 47.8-112) 30.4-19.4-18.3-15.6-14.94 (7.6 (30.00 (4.92-12.8-60.1) 11.30-14.7 (14.2 (11.93 (7.9 (33. interval) 12.2 (10.4 (32.38-18.7 (9.4) 317 (231-433) 144 (96.6-20.1) 7.0 (8.32-14.3) 10.0) 9.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (36.0 (34. population from the National Health and Nutrition Examination Survey.Environmental Phenols Urinary Triclosan (2.4.4) 7.00-8.7 (39.2-14.1) 14.0-73.6-14.1 (15.4) 25.6) 31.18 (5.43-13.2) 9.48 (8.54 (8.60 (8.1) 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 9.89-11.50) 10. population from the National Health and Nutrition Examination Survey.0-15.S.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.0-15.45 (5.40-11.4.20-11.3. Survey Geometric mean (95% conf.0 (11.5) 20.9) 32.9 (50.3 (11.8) 14.

Windham G. Toxicology of 2. hormones. Lyman FL.S. Levy SB. Pharmacokinetics of triclosan following oral ingestion in humans. Wigmore H.24(3):209-218. Okui T. Barber LB. Pharmaceuticals.45 Suppl 2:S137-S147. Larson EL.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Moss T. Bodey GP. Br J Clin Pharmacol 1987. Mezcua M. Chemosphere 2007.38(4):361370. Benson WH. Ye X. Howes D. Environ Health Perspect 2008. 4. Aguera A. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. streams. J Toxicol Environ Health A 2006. Readman JW. Fourth National Report on Human Exposure to Environmental Chemicals 39 . population: 2003-2004.69(20):1861-1873.67(4):532-537. Kolpin DW. Pinney SM. Photolytic degradation of triclosan in freshwater and seawater. Kaneshima H. Thurman EM. Chelimo C. Adolfsson-Erici M.S.524:241-247. Hernando MD. Williams FM. and phenols in girls. Environ Sci Technol 2002. Environ Health Perspect 2007.83(1):84.36(6):1202-1211. Fernandez-Alba AR. Sandborgh-Englund G. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Urinary concentrations of triclosan in the U.80(3):217-227. Furia T. Ogawa H. phthalates. Watanabe N. Gilbert RJ. Britton JA. Aranami K. Calafat AM.23(5):579-583. Bennett ER.28(9):1748-1751. Leonard PA. Katsura E. Ishibashi H. Foran CM.115:116-121.116(3):303-307. Gunderson MP. and other organic wastewater contaminants in U. Meyer MT. Ebersole R. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Teitelbaum SL. Am J Infect Control 1996. Skirrow RC.4’-trichloro-2’hydroxydiphenyl ether). Gomez MJ. Wong LY. Aquat Toxicol 2006. Furlong ET. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. et al.38(2):64-71. J Invest Dermatol 1976. Ekstrand J. Reidy JA. Clapson DJ. Veldhoen N. Percutaneous penetration and dermal metabolism of triclosan (2. Ferrer I. Wolff MS.4. Nagao Y. The oral retention and antiplaque efficacy of triclosan in human volunteers. Zaugg SD. Evidence of 2.66:1052-1056.. et al. 1999-2000: a national reconnaissance.7/2. Shiratsuchi H. Hirano M. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Hong HC. Osachoff H. Williams PE. Matsumura N.50(1-5):153-156. Triclosan: applications and safety. Needham LL. Bhargava HN. Odham G.17(5):637-644. Arch Environ Contam Toxicol 1988. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. et al. Biol Pharm Bull 2005. 4’-trichloro-2’-hydroxydiphenyl ether. et al. Erratum in: Aquat Toxicol 2007. Food Chem Toxicol 2000. Mar Environ Res 2000. IMS Ind Med Surg 1969.Environmental Phenols References Aiello AE. Anal Chim Acta 1004. Pilot study of urinary biomarkers of phytoestrogens. Kanetoshi A.

and metabolic acidosis were observed in CAS No.51) 1.350 (.78) 1.350 (. are eliminated in the urine. < LOD means less than the limit of detection.350 (.. After a single dose.94 (1. hypertension.48-2. PCP is degraded by sunlight and metabolized rapidly by microorganisms.94 (1. Effects including hyperthermia.350) < LOD . Since 1984.73 (1. To-Figueras et al. plants.350-2. Acute.10) 1.390 (. algaecide and insecticide.350) < LOD . 40 Fourth National Report on Human Exposure to Environmental Chemicals .70) 2.10 (1.54-2.32 (.42) 696 680 521 696 603 951 Limit of detection (LOD.30 (1. population from the National Health and Nutrition Examination Survey.350-.350 (.58-2.350) < LOD < LOD 75th .350 (.350-. 1976. with repeated or chronic exposure.75) 2.350) < LOD .350-. PCP is eliminated over a few days (Braun et al.50) 1.g.350 (. General population exposure to PCP may occur by inhalation of contaminated air. ingestion of contaminated food or water.350-.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .S.00 (.350 (.350 (.350-.990-2. 1986). along with small amounts of tetrachlorohydroquinone and conjugates.350-..350-.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-2.350) 90th .960) 1.47-5.91 (1.47-3.350-. the elimination half-life may be a week or more (Uhl et al.350-.350-.650 (. Survey Geometric mean (95% conf.680-1.350 (.10 (. air.350-1.890-1.350-1.350-.860-2. Human exposure to PCP has become less common.350-.350 (. has been restricted.350 (.770 (.76) 1.67) 1. and dermal contact with PCP-treated products.350) < LOD . and possibly of lindane (IPCS. which may vary for some chemicals by year and by individual sample. mollusicide. 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.37) .890 (.30) 1.350 (.350) < LOD .45-2.350-2.33) .350) < LOD .350) < LOD .530) 1.350-.660 (.83 (2. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.64) 1. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.23 (.350 (.350 (. In the environment. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350) < LOD . 1979).53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350-.350) < LOD .350 (. PCP is absorbed rapidly and well by all exposure routes.30 (.60) 1.65 (.350-2.350) < LOD .350-.350) .350-. PCP is distributed to most tissues and is not extensively metabolized. 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.630 (.350) < LOD .650) 1.350) < LOD .01 (<LOD-1.76) .350-.350-.98 (1.33-2.350) < LOD .350 (. PCP cannot be used on wood in residential or agricultural buildings.500-2.350-.350 (. and it is used primarily as a preservative for wood to be used outdoors (e. 2002.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Kohli et al.90) 2. PCP has been detected in soils.18 (<LOD-1.350-1...10) 1.350 (.350) < LOD .90) 1. so it is relatively non-persistent.350-1..510-3.350) < LOD .30) . PCP use in the U. After absorption.350) < LOD .08-3.350-2. herbicide.350 (.80) . other polychlorinated benzenes.70) .390 (.350 (. water and sediments because of the large amounts that were produced and used historically. 1997).60) 1.25 and 0.62 (.510-5.10 (<LOD-1.350-.850-2. bactericide.590-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350-.65 (.5.40 (.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 .00) 2. The parent compound and conjugates.480-2.00) 1.00) 1.90 (1.990 (<LOD-2.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .09) .48 (.37 (. utility poles and fence posts).30 (.58-2.350 (. and animals.980 (.350-.04) 1.30) 1.

350) < LOD .700-2.40) 1..290-.990 (.40) 1.19) 2. 1989). 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.84 (1.30-2. 2003).55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . In animals.25 (1.650 (. inhalation.S.84) 1. carcinogenic. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.92) 1.420) < LOD .82 (1.430-.320) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1..18) .16 (.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 .920 (.470 (.950-1.. EPA at: http://www.gov/ pesticides/ and from ATSDR at: http://www.440 (. 2004. 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. and adversely affected thyroid function (U. population from the National Health and Nutrition Examination Survey. environmental levels) and health effects is available from the U.75 (<LOD-2.30 (.21-2.26 (1.780-1.83 (1.09 (<LOD-2. 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.950-1.40) 1.500 (.51) 1.00-1.490) < LOD .590-1.710-1.340-.10-2.78) 1.900-1.35) 1.55) 1.S. EPA has developed standards for PCP in drinking water and the environment.Fungicides adults and children severely exposed to PCP through ingestion.25-1.26 (1.250 (.40) 1. In NHANES 2001-2002 subsamples.67-3.35-2.52 (1.780) < LOD .34 (. 1991). and the FDA has established a standard for bottled water.atsdr.910-1.330-. Death can result from seizures and cardiovascular collapse.370 (.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .21 (.280) < LOD .gov/ toxpro2.570 (. respectively) (Seifert et al.40-2.25-2.52) 1.67 (1. children in the 1980’s.310-. Survey Geometric mean (95% conf.36) .300 (.e.270-.84-4.320 (.360 (.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * ..16-1.19) 2. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.270-.18 (1.78) 1.69 (1.260 (.30) 1.800) < LOD 1.S.cdc.S. 1995).06-3.250 (.94 (1.06) 1.67-2.19) 2.630 (.56) 1.510-.290-.650) 90th 1.30) 1.310) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 41 .290) < LOD .90) 1.94 (1.560) < LOD .08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00-1.79) 1.13 (.67 (1.19 (1.320) < LOD < LOD 75th .73 (1.300 (.360-.430) < LOD .0 mg/L.95) 3.380-.6 and 14. 2003). 1989).08 and 5.10 (1.html.75) 1.25) 1.220-.S.25 (1.06 (. More information about external exposure (i.52 (<LOD-1.82) 1.300 (.650 (. van Raaij et al.09-1.57 (.57 (1. 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.830) < LOD .500-.950-1.epa.320) < LOD .500-1.67 (1.510-. Among adults in the NHANES 1999-2000 subsample. 2000). the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. 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. or skin absorption.560-.850 (.800-1.40) 1. OSHA has established an occupational standard..EPA. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al. chronically administered high doses of PCP were hepatotoxic. The U. Pentachlorophenol is not mutagenic or teratogenic.94-3.29-3.760 (.730) < LOD .560) < LOD .35) 1.00) 1.25-2.220-.35-2.240-.610 (.67 (1.67-3. respectively) (Becker et al.52 (<LOD-1.67 (1..9 mg/L.11) 2.400 (..48-2. In a small sample of U..580-.590) < LOD .

To T.18:475-481. Available at URL: h t t p : / / w w w. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Head SL. Otero R. Environ Health Perspect 1997. Hill RH. Sala M. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Hill RH Jr. et al. Cline RE.org/documents/jmpr/jmpmono/2002pr08. Phillips DL. Bailey SL. Schlatter C. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Shealy DB. hair. et al. Gregg M. 2002. Dev Toxicol Environ Sci 1979. Safe A. Pesticide residues in urine of adults living in the United States: reference range concentrations. Seiwert M. PCP: Human Risk Characterization [online]. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Fast DM. 4/21/09 van Raaij JA. Needham LL. 4/21/09 Kohli J. available at URL: http://www. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Int J Hyg Environ Health 2003. house dust. 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. van den Berg KJ. htm.10:552-65.S. Needham LL. Engel R. Baker S.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Smith SJ. Schulz C. Lindane.4:289296. Can J Biochem 1976. Helm D. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Notten WR. References Becker K. drinking water and indoor air. Santiago-Silva M. Seiwert M. Environ Res 1995. Uhl S. Arch Toxicol 1986.58:182-186. r e g u l a t i o n s .105(1):78-83. Toxicology 1991: 67(1):107-16. Holler JS. Schmid P. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402.18(4):469-474. International Programme on Chemical Safety (IPCS).71:99108. Barrot C. Arch Environ Contam Toxicol 1989. Braun WH. Blau GE. The metabolism of higher chlorinated benzene isomers.S. EPA). The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. U. Arch Environ Contam Toxicol 1989. To-Figueras J. Environmental Protection Agency (U. et al. Chenoweth MB. urine. Seifert B. J Expo Anal Environ Epidemiol 2000. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Becker K. 42 Fourth National Report on Human Exposure to Environmental Chemicals . 11/30/2004. Rodamilans M. Kaus S. Seifert B.inchem. Schulz C.54(3):203-208. Hill RH Jr. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Bragt PC. Jones D. 206:15-24. Pharmacokinetics of pentachlorophenol in man. Krause C.

30) < LOD 90th 1.493 (..17 (.497 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops.450 (<LOD-.466 (.490 (<LOD-.20) < LOD 1.90 (1.50-2.Fungicides ortho-Phenylphenol CAS No.50) < LOD .520 (.30-7.50 (1. Available evidence suggests that OPP does not accumulate in the body.590-2. and sanitizers. 2006). General population exposure can occur via dermal. or apply these chemicals may be more highly exposed than the general population.07 (.28-3.90) .00 (1. Survey Geometric mean (95% conf. inhalational.40-5. fungicides. 2002.10) .40-2.10) .61) 2.600-1.540-2.600) < LOD . formulate.410-. < LOD means less than the limit of detection.60-3.350-1. whereas SOPP is not volatile and is more water soluble.50) < LOD .496 (.630) < LOD .570 (..710) 3.00 (1.950) < LOD .740 (. OPP is volatile. 2006).00) < LOD .60 (1.420 (<LOD-.480-1.880-2. such as fruits and vegetables.690) < LOD . it was used in home sanitizers for surfaces.780) < LOD .552 (.389-.20 (.570-. however.14 (<LOD-3. Workers who manufacture.498 (.28 (.10-2. Estimated human intakes have been below recommended intake limits (U.34) 1.80 (2.40-5.490 (<LOD-..390-.600) < LOD .570-2.610 (. 2006). and it has limited water solubility. or 2-phenylphenol) and its water-soluble salt.770 (.508 (.560-8.10) .50) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) < LOD 1.3 and 0. 2006).10) 2.19 (.640) < LOD .10 (1.696) * .27 (.638) * . Cnubben et al. but OPP and SOPP are still used on pears and citrus (U.33 (.EPA. in paints.600) < LOD 1.509 (. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. SOPP is applied topically to the crop and then rinsed off. and as a wood preservative.760-2.00 (1.S.364-.670) 2.490 (<LOD-. Both chemicals degrade within hours to weeks in the environment (U.03) 1.750-2.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .20 (1.40 (.10) 1.88) 1.370-.600-1.370-.636) * .S.690-1.970 (.20) 2.632) Selected percentiles ( 95% confidence interval) Sample 95th 2. population from the National Health and Nutrition Examination Survey.450 (<LOD-.370-.389-.30) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. EPA.710-2.550-1.836) * .645) * . 1998.600) < LOD 75th .50) < LOD .90) .930 (.23) 695 680 520 695 603 953 Limit of detection (LOD.50-3.20-2.20 (1.60-2.92 (. 1998).90) 2.50 (1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al. interval) .500-2.50-4.00 (1.386-.790) 2.10 (1. 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.90) 1. sodium ortho-phenylphenate (SOPP).S.770 (.30-2.00) . Timchalk et al. Most agricultural food applications have been revoked.610-1.890 (.00-2.85) 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) 1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .10-1.80-3.85) 2.820 (.433-.450 (<LOD-.490 (<LOD-.90 (1. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.80) 1. 1989).402-.570-1. which may vary for some chemicals by year and by individual sample.890 (. OPP is still used as a disinfectant fungicide for industrial applications. In the past.470 (<LOD-.S.50) 1.621) * . leaving the chemical residue OPP.60 (1.02) 1.349-.60 (1.09) 2. on ornamental plants and turfs. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.20) < LOD 2.76) 1. Fourth National Report on Human Exposure to Environmental Chemicals 43 . are antimicrobial agents used as bacteriostats.850 (.30) 1.600-1.840-1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.570 (.860 (.800-3.00) .830 (.22) 2.3. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.890) 1.580-1.30 (1.EPA.80) 1.50 (1.22 (.40-7.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . OPP is considered to be moderately toxic after acute oral doses in animal studies.567 (.624) * .742) * . 90-43-7 General Information Ortho-phenylphenol (OPP.20-3.490 (<LOD-.

410 (<LOD-. interval) .560) < LOD 75th .61 (.484) * .950) < LOD .580) < LOD . and it has classified OPP as not classifiable with respect to human carcinogenicity.900-1.24-2.750-2.21 (.470 (<LOD-.670 (.89 (1. Biomonitoring Information Urinary OPP levels reflect recent exposure.473) * .320 (<LOD-.570) < LOD 1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone..07) 2. 2002.93 (1.860 (.09-3.96) 1. or.656) * . 1997.455-. leading to production of two metabolites.670 (.S.990) < LOD . 1993.06-5.75 (1. 1992.21) 1.910-1.11) < LOD 90th 1.59) .53) 1.28 (<LOD-4. 1999. Brusick.28 (2. Volunteers exposed to 0. 2005).11-1.EPA 2006). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09 (1.78 (2.20) < LOD 3.91 (1.S.248-.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.. reproductive. Smith et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.666) * .910 (<LOD-1.568) * .810-1.480-.75 (1.61 (2.360 (<LOD-.04-4.0) 1.420 (<LOD-.43-2. population from the National Health and Nutrition Examination Survey. but no neurologic. 1984.38-3.84 (1.18) 2.620-1.403-.96 (1.33) .980 (.410 (<LOD-.S.750 (.29) 1.385 (.440 (.32) 3. or developmental toxicity was observed (Bomhard et al.11 (.610) < LOD 1.S.311-.05-2.21-2.510 (<LOD-.690 (.650-1.510-.24-2.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .840 (.. 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.970) 1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.40-13.11) 4.epa.33-2.380 (. U. Bomhard et al.460-.329-.Fungicides anemia.780 (.93) 1. Ito et al.343 (.96 (1.93) .96-4.353-.780-14.. 1999. less likely. 1998. In high dose animal studies.59) 1.52 (. Detectable levels were seen in over half the U.670) < LOD .361-..62) . Kwok et al. 2002).08-1.26) 1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.770-2.46) < LOD 1.93) .620-1.420 (<LOD-.291-.470) < LOD . population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.940-2. Murata et al.500) < LOD .382 (.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .. Zhao et al.81) 1.640-1.09-6.514 (.600-1..17 (.11 (. U.31) < LOD .550 (.13) 1.44 (1.43) 3. 2002.17 (.860 (. 1984.02 (.EPA 2006). 2000.301-.444 (.900) < LOD . 2005.38) 1. 44 Fourth National Report on Human Exposure to Environmental Chemicals .496 (. Pathak and Roy.12-2.gov/pesticides/..4) 3.51-3.750 (.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .43-2. Nakagawa et al.32) 1.58) 2. 1986).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 . Additional information is available from U. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.580-1.47) .550) < LOD .560-2.86 (1.980 (<LOD-1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.00 (.97 (2.25-6.508) * .810) < LOD .01) 1.EPA at: http:// www.74 (1.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.910 (.S.43 (1.880-1.88-4.29) 1.08-2.64 (2.270-. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (1.69 (1.800-1.12) < LOD 1. 2005).. IARC has classified SOPP as a possible human carcinogen.38) 2. CDC. Survey Geometric mean (95% conf. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.17) 2. by possible genotoxic mechanisms (Hagiwara et al.453 (..590) * . OPP was not found to be mutagenic.550-.06-4.08) 1.791) * .27) < LOD .06 (1.61 (1.

van de Sandt JJ. Smith RA. Moore GA. Murata M. 90-43-7) in Swiss CD-1 mice (dermal studies). Brzak KA.17(8):411-417. Ito N. Moriya K. Inoue S. Buchholz BA. Herbold BA. Richter M. Roberts AL. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol.32(6):551-625.43(7):14311437. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Brendler-Schwaab SY.286(2):309-319.50(11):3351-3358. Arch Toxicol 2000. Timchalk C. St John MK. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Available at URL: http://ntp. Nakagawa Y. 2006.gov/ntp/htdocs/LT_ rpts/tr301. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. J Chromatogr B Biomed Sci Appl 1997. Coelhan M. Identification of SARA compounds in adipose tissue. Christenson WR.S. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Pathak DN. Biochem Pharmacol 1992. Brusick D. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Turteltaub KW..(56):399-407. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Carcinogenesis 1999. et al. EPA-560/5-89-003. Hagiwara A. Toxicol Appl Pharmacol 1998. Hirose M.nih. The carcinogenicity of the biocide ortho-phenylphenol. Narang A.epa.S.703(12):97-104. Selim S. Meuling WJ.S. Fukushima S.159(1):18-24. Zhao S. Ito N. Shirai T. rat and man. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Elliott GR. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Food Chem Toxicol 1984. Timchalk C.54(16):5731-5735. Bartels MJ. Kawanishi S. Cnubben NH. National Toxicology Program (NTP). Vogel JS. Kwok ES. Christenson WR.28(6):579594.74(2):61-71. Environmental Protection Agency (U. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Bormett GA. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. food additives and natural products as promoters in rat urinary bladder carcinogenesis.EPA). Sangha G. Comparative metabolism of orthophenylphenol in mouse. 1989. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes.20(5):851-857. Mendrala AL. Roy D.pdf. J Agric Food Chem 2006. Leser KH. Hum Exp Toxicol 1998. Available at URL: http://www. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Xenobiotica 1998. Environ Mol Mutagen 2005. Eadon G. Fukushima S. Centers for Disease Control and Prevention (CDC). Atlanta (GA). Bromig KH. Environmental Protection Agency (U. Mutat Res 1993.22(10):809-814. Imaida K. U. Toxicol Appl Pharmacol 1999. 4/9/09. Moldeus P. Bartels MJ. Cano M. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers.35(2 Pt 1):198-208. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Arnold LL. U. Hagiwara A. EPA). 4/13/09 Onstot JD. July 28. Hakkert BC.Fungicides References Appel KE. Crit Rev Toxicol 2002. McNett DA. Gierthy J. Bomhard EM. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Office of Toxic Substances. EPA 739 R-06004. 2005. et al.niehs. Tayama S. Drugs. Shibata M.gov/oppsrrd1/REDs/ phenylphenol_red.45(5):460-481. Bartels MJ.S. Sangha GK. Regul Toxicol Pharmacol 2002.pdf. Stanley JS. IARC Sci Publ 1984. Freyberger A. J Agric Food Chem 2002. Bartels MJ. March 1986. Glas K. Eastmond DA. Third National Report on Human Exposure to Environmental Chemicals.150(2):402-413.

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

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006). 2000). Jefferies et al. 2000. General population exposure to acetochlor may occur through diet or drinking water. Hladik et al.EPA considers acetochlor likely to be carcinogenic in humans. 2005).. and has been detected in watersheds of agricultural lands (Battaglin et al.EPA. and it is unlikely to be genotoxic at relevant doses (Ashby et al.. but it has produced testicular atrophy.EPA.e. environmental levels) is available from U. Fourth National Report on Human Exposure to Environmental Chemicals 47 . Plants can degrade acetochlor to 2-ethyl-6-methylaniline.. Acetochlor is not mutagenic. NTP and IARC do not have ratings regarding human carcinogenicity. remains in soils for up to 3 months. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. which are often more prevalent in the environment. Acetochlor is moderately toxic to fish and honey bees.S.S. 2000. Additional information about external exposure (i. renal injury. 2006). Kolpin et al. and neurologic movement abnormalities (U. Urinary acetochlor mercapturate levels of 0.0 μg/L (Curwin et al. Biomonitoring studies on levels of acetochlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acetochlor than are found in the general population. and hydroxymethyl ethyl aniline (U.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al.S. 1996).Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. 2006). Feng and Wratten. in some species and at doses above maximum tolerated doses. CAS No. U. Acetochlor is microbiologically degraded.. 2-hydroxyethyl-6-methylaniline. Acetochlor has low acute toxicity. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect.S. however. Davison et al..EPA. 2005.S. Estimated human intakes of acetochlor have been below recommended limits (U.S. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. 2006). People exposed to acetochlor will excrete acetochlor mercapturate in their urine. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. mainly corn. In animals.EPA 2000. 1994. 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. It is absorbed by plants and inhibits plant protein synthesis. EPA at: http://www..gov/ pesticides/.. animals have demonstrated tumors of the lung. nasal epithelia. and thyroid (U.. 1989.. including one that produces 2-methyl-6ethylaniline and its reactive metabolite.. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. 1998). but other pathways occur. However. 2000. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. 2007). 2005).epa. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. the latter which may account for some observed effects (Coleman et al. a major pathway for acetochlor metabolism involves mercapturate conjugation.

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

Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Striley CA. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. 5/30/06 U. EPA). Reynolds SJ. Roberts AL. et al. Barr DB. Number 15. Feng PCC.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Third National Report on Human Exposure to Environmental Chemicals. Casida JE. Davison KL. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Jefferies PR. Coleman S. Furlong ET.37(4):10881093. EPA). Larsen GL. Atlanta (GA). epa. J Expo Sci Environ Epidemiol 2007. EPA 738-R-00-009. Heederik D.17(6):559-566. Kinney PL. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.15(6):500-508.39(17):6561-6574.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Barr DB.248(2-3):115-122. Occurrence of sulfonylurea. Acetochlor (Harness) Pesticide Petition Filing 1/00. Linderman R. March 2006. Environmental Protection Agency (U. 1998. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.S. Linhart SM. Volume 65. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Available at URL(non U. Andrews HF. and other herbicides in rivers. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Lefevre PA. Hines CJ. Dialkylquinonimines validated as in vivo metabolites of alachlor. Peter CJ. et al. acetochlor. Barr DB.cce.15(9):702-735. Comparative metabolism and elimination of acetanilide compounds by rat. Federal Register: January 24. Available at URL: http://www. Burkhardt MR. Thurman EM. Sci Total Environ 2000.11(4):353359. Sanderson WT. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Rose RL. Xenobiotica 1994. Kier L. Wilson AG.cornell. 5/30/06. Hum Exp Toxicol 1996. reservoirs and ground water in the Midwestern United States. Wratten SJ. pages 3682-3690. Environ Health Perspect 2003. Hsiao JJ.108(12):1151-1157.111(5):749-756.S. Battaglin WA. Hladik ML. Deddens JA. sulfonamide. 2005.24(10):1003-1012. Green T. Olsson AO.EPA): http://pmep. Hodgson E. 2000. Ward EM. Environ Sci Technol 2005. Fourth National Report on Human Exposure to Environmental Chemicals 49 . J Agri Food Chem 1989. Bravo R.html. Quistad GB. Environmental Protection Agency (U. Alavanja MC. Curwin BD.pdf. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Feil VJ. Tinwell H.S. Camann DE.S. U. Sci Total Environ 2000. Barr JR. Hein MJ.Herbicides References Ashby J. Environ Health Perspect 2000. Kolpin DW. Centers for Disease Control and Prevention (CDC). and metolachlor herbicides in rats. Whyatt RM. et al. Chem Res Toxicol 1998. imidazolinone.S.248(2-3):123-133. J Expo Anal Environ Epidemiol 2005.

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

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

Chem Res Toxicol 1998. Geological Survey (USGS). Biagini R. Environ Health Perspect 2003. Dialkylquinonimines validated as in vivo metabolites of alachlor. EPA).S.248(2-3):123-133. 1998. Feil VJ.inchem. Tolos W. reservoirs and ground water in the Midwestern United States.37(4):10881093. Tessier DM. Available at URL: http://www. Martens MA. Brown KK. et al. who. Supplemental Technical Information (available on-line only). Striley CA. Camann DE. Thake DC.11(4):353359. 1999. Centers for Disease Control and Prevention (CDC). Heydens WF. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Life Sci 1988. Linhart SM. Kolpin DW. Henningsen G. Occurrence of sulfonylurea.47(6):503-517. California.43(9):2504-2512. Davison KL. Hum Exp Toxicol. Kier LD. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. imidazolinone.php.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. sulfonamide.S. Environ Sci Technol 2005. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.epa. Circular 1291. Shoemaker DA. ALACHLOR. No. Larsen GL. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Reregistration Eligibility Decision (RED) Alachlor.39(17):6561-6574. DNA adduct formation by alachlor metabolites. revised February 15. Available at URL: http://www.395(2-3):159-171.usgs. Hull RD. Kinney PL. Quistad GB.Herbicides References Battaglin WA. Roberts AL.htm. Third National Report on Human Exposure to Environmental Chemicals. 2/27/09 Jefferies PR. Feng PCC. Sci Total Environ 2000. Hines CJ.18(6):363-391. Burkhardt MR. Whyatt RM. acetochlor. Lau H. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Quistad GB. Geological Survey (USGS). Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Ann Occup Hyg 2003. Erratum in: Life Sci 1989. and metolachlor herbicides in rats. Sci Total Environ 2000. Shealy DB. Furlong ET. Am Ind Hyg Assoc J 1995.111(5):749-756. Barr DB. Sacramento.56(9):883-889. December 1998. International Programme on Chemical Safety (IPCS).pdf. Hladik ML. et al. WHO/ FAO Data Sheets on Pesticides. Kolpin DW. J Ag Food Chem 1995. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.pdf.int/water_sanitation_health/dwq/chemicals/en/alachlor. 1997. Xenobiotica 1994. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. World Health Organization (WHO). Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. March 2006.43(25):2087-94. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. EPA 738R-98-020. 1996. Biagini RE. 4/2/09 U. Clark JM. Casida JE. Mutat Res. Deddens JA. Available at URL: http://water. Wilson AG. Kimmel EC. Thelin GP. Geneva. Hill AB. Driskell WJ. 86. World Health Organization.248(2-3):115-122. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.44(18):1325. Alachlor in Drinking-water. U. Jefferies PR. Casida JE. Comparative metabolism and elimination of acetanilide compounds by rat.org/documents/pds/pds/pest86_e. J Agri Food Chem 1989. Available at URL: http:// www. 2003.S. Brown MA. Atlanta (GA). Wratten SJ. Thurman EM. Casida JE. 2/27/09 U. Hsiao JJ. 2005. Peter CJ. Bull Environ Contam Toxicol 1996. 98-4245 (by Barbash JE. Sanderson WT.gov/oppsrrd1/ REDs/0063. Barr JR. Hines CJ. Gilliom RJ).56(6):853-859. Background document for development of WHO Guidelines for Drinking-water Quality. Environmental Protection Agency (U. MacKenzie B. 2007. 1992-2001. 1999.S. and other herbicides in rivers.24(10):1003-1012. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Andrews HF. Hill RH Jr.

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

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

htm. J Toxicol Environ Health 1994. 3/11/09 Arcury TA. World Health Organization. Jones AD. Mendoza M. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Blewett C. diamino-S-chlorotriazine and hydroxyatrazine.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Reynolds SJ. 1993). Perry et al. Laws SC. et al.53(2):297-307. Ferrell JM.atsdr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pfeifer KF.64(9):672-678. Gillis JH. Saiz SG. Stoker TE. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Hermaphroditic. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Toxicol Lett 1993. In a study of 60 farm worker children.47(6):503-517. 1996. Lioy PJ. WHO/ FAO Data Sheets on Pesticides. J Expo Anal Environ Epidemiol 2005. McElroy WK. Cottica D. J Agric Food Chem 1982. Fleenor-Heyser DG.. Freeman NC. Barbieri F. Pest Manag Sci 2005.58(2):366-376.gov/toxprofiles/tp153. et al. Barr DB.115(8):1254-1260. Agency for Toxic Substances and Disease Registry (ATSDR). In small studies of Maryland residents in 19951996 (MacIntosh et al. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.43(2):155-167.. Sanborn JR.43(2):155-167. 2005.76(1):190-200. Available at URL: http:// www. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Deddens JA. 2000). International Programme on Chemical Safety (IPCS). Toxicol Sci 2000. Stuart AA. Eldridge JC. Cooper RL. 82. No. Heederik D. Proc Natl Acad Sci USA 2002.. Striley CA. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Atlanta (GA). Gillis JH. Stoker TE. Tyrey L. Hines CJ. 2007). Ann Occup Hyg 2003. In a small number of field workers.. Moseman RF. Aldous CN. Goldman JM. Cooper RL. Third National Report on Human Exposure to Environmental Chemicals. Simpkins JW. Eberly LE. Available at URL: http://www. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.inchem. Quandt SA. Maroni M. Barr DB. References Adgate JL. Lucas AD. Eldridge JC. Wetzel LT.org/documents/pds/pds/pest82_e. Breckenridge CB. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. 2001). 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. Environ Health Perspect 2007. Chen H. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. levels of atrazine mercapturate were generally not detectable (CDC. Ferioli A. Sanderson WT.html. Shoemaker DA. 3/11/09 Laws SC. Centers for Disease Control and Prevention (CDC). et al. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Steroids 1999. Curwin BD. Wetzel LT. Clayton CA. J Toxicol Environ Health 1994. Carr WC Jr. Cooper RL. Stoker TE. Brown KK.69(2):217-222. A risk assessment of atrazine use in California: human health and ecological aspects. Geneva. The geometric mean of urinary atrazine mercapturate was 1. atrazine was detected in only four children (Arcury et al. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Bersani M. Vonk A.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Toxicol Sci 2000. Goodrow MH. et al.. et al. Environ Health Perspect 2001. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.61(4):331-355.30(2):244-247. Toxicological profile for atrazine. Barr DB. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Hein MJ. 2001 [online]. 2005).. 2005). Collins A. Ferrell JM. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Gammon DW.. Biagini RE. Bradway DE. et al. Lee M. Noriega N. Extrom PC. Toxicol Sci 2003. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.99(8):5476-5480. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Catenacci G. Stevens JT. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.15(6):500-508. Grzywacz JG. Biological monitoring of human exposure to atrazine. 2003. Schmid J.cdc. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. In the NHANES 2001-2002 subsample.109(6):583-590. ATRAZINE. Hayes TB. Tapia J. Seiber JN.

Toxicol Sci 2002. The Quality of Our Nation’s Waters. 1992-2001.epa. Available at URL: http://water. Ann Epidemiol 2000.182(1):44-54.S. U. Toxicology 1990. A longitudinal investigation of selected pesticide metabolites in urine. Boerma J. Stevens JT. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Crit Rev Toxicol 1997. Urinary biomarkers of atrazine exposure among farm pesticide applicators. A risk characterization for atrazine: oncogenicity profile.gov/oppsrrd1/REDs/ atrazine_ired.php.56(2):69-109. Hammerstrom KA. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Pesticides in the Nation’s Streams and Ground Water. Dagenhart D. Lansbergen GW.S. Wood C. Office of Prevention. Ryan PB. Singzoni B. 2007. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. EPA). Breckenridge CB. J Expo Anal Environ Epidemiol 1999.S.9(5):494-501. Cooper RL. Sanderson JT. EPA). Guidici DL. Circular 1291.67(2):198-206. Laws SC.Herbicides development of a biomarker of exposure.pdf. Pesticides and Toxic Substances.27(6):599612. Laws SC. White paper on potential developmental effects of atrazine on amphibians.61(1):27-40.usgs.S. Fenton SE. Interim Reregistration Eligibility Decision For Atrazine. Geological Survey (USGS). Stoker TE. Cooper RL. Environmental Fate and Effects Division. Toxicol Sci 2000. Christiani D.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.6(1):107-116. revised February 15. 3/11/09 U. A review of epidemiologic studies of triazine herbicides and cancer. Kastl PE. Timchalk C. Sathiakumar N.58(1):50-59. Delzell E. Available at URL: http://www. Guidici DL. Available at URL: http://www. Supplemental Technical Information (available on-line only).pdf. Wetzel L. March 2006. 6/1/09 U. Toxicol Appl Pharmacol 2002. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Osborne DW. Environmental Protection Agency (U. Dryzga MD. Langvardt PW. J Toxicol Environ Health A 1999. MacIntosh DL. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Chem Res Toxicol 1993. May 2003a. Washington (DC).epa. Rayner JL. Tortorelli J. Environmental Protection Agency (U. van den Berg M.195(1):23-34. Toxicol Appl Pharmacol 2004. Stoker TE. 0062.10(7):479. EPA Office of Pesticide Programs.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Needham LL. Case No. Perry M. 2003b.S.

24 (.16) < LOD .43) 1. 2007).890 (. Once absorbed.420) < LOD .02-1.370-. 1977). Similar to other chlorophenoxy herbicides. dizziness.55 (1.440-1.10 (<LOD-1.51 (1. Fourth National Report on Human Exposure to Environmental Chemicals 57 . < LOD means less than the limit of detection. 2. abdominal pain.60) 1.260 (<LOD-.22) < LOD .05-2. 2005). but at higher levels they are herbicidal.930 (.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .210 (<LOD-.490) < LOD < LOD < LOD .690 (.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-D have been below recommended intake limits (U.660) 1.230-. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. It is not well absorbed through the skin.420-.00-2.760 (. and mecoprop). nausea.680-1. 1989.03) 695 659 520 668 589 892 Limit of detection (LOD.20 (<LOD-1. the chlorophenoxy herbicide 2. It is poorly bound in soils.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.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 .690 (.610-.4-D may occur during residential applications.EPA in 1948.S.670-1. Recent estimates of chronic intakes of 2. 2.250 (<LOD-. and delayed Urinary 2.210-. renal and hepatic injury.910) < LOD .310 (.4-dichlorophenoxyacetic acid (2. 2. and by consuming food or drinking water contaminated with 2..560-1.. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.EPA.952 and 0. Human health effects from 2.960-1.S.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. It is rarely detected in ground waters (USGS.550-1. with a half-life of several days to several weeks.27 (1. headache.560-.4-D is rapidly absorbed via oral and inhalation routes.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Herbicides 2.4-D has low acute toxicity.410) < LOD .330 (. which may vary for some chemicals by year and by individual sample.540-.10) < LOD 1.690-1.08) < LOD . It was first registered with U.350) < LOD < LOD < LOD . and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.S.490 (.910) 1. 1974. these herbicides can enhance plant growth. 94-75-7 General Information Widely used throughout the United States.400) < LOD . hypotension.80) 1.4-D) controls broadleaf weeds in residential.320) 90th .20 (.13) < LOD . agricultural.2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.30 (<LOD-2. 2. myotonia.810-1.48) < LOD 1. and aquatic environments.10 (<LOD-1.4-D or exposed for prolonged periods. in 2001 (U.4-D were used in the U. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.890) < LOD .EPA.740 (.610 (. 4-D. As much as 62 million pounds of 2. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.27-2. 2004).690 (.40) 1..930-1.730 (.70) 1.66) < LOD 1.250 (<LOD-.27 (. General population exposure to 2. it acts as a plant growth hormone.4-D can be applied either as an aqueous salt or as oil-soluble esters.4-Dichlorophenoxyacetic Acid CAS No.21) 1. MCPA.310) < LOD . At low levels. Kohli et al.S. Survey Geometric mean (95% conf.07 (.S.32 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.230 (<LOD-. Sauerhoff et al. by direct contact with agricultural and residential areas after applications.

1995).gov/pesticides/. IPCS..670 (. 58 Fourth National Report on Human Exposure to Environmental Chemicals .680) < LOD .570) < LOD .810-1. IPCS. developmental. or teratogenic effects in chronic rodent studies (Charles et al.EPA. Survey Geometric mean (95% conf. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 1996. Knopp et al. 1980. U. 1985.S. Post-application levels in farmers and home gardeners were dependent on Urinary 2. population (Hill et al.610-. 2.410 (<LOD-.480 (.670 (<LOD-1. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. liver..390) < LOD < LOD < LOD .550-.490 (.410) < LOD < LOD < LOD .4-D does not have significant reproductive.440 (.08 (.780-1.EPA.S.EPA.39) < LOD 1. U.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .720 (. 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.S.08 (.Herbicides neuropathy (Bradberry et al.270-.3.. Epidemiological studies have reported associations of several types of cancer.27-1. 1992).EPA at: http://www. eyes.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 . and of adults and children (Baker et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1995. 1994). 2005). IPCS.EPA 2005). CDC. In previous samples of the U.24) 1. 2002. Frank et al.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1989).380 (<LOD-.660 (. 2001.610-.13 (.40) 695 659 520 667 589 892 < 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.330-.4-D production plant workers and a few forestry workers spraying 2.17 (. 2004). 2005.4-D levels were detectable in less than a quarter of the individuals studied. Kolmodin-Hedman and Erne.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. Biomonitoring Information Urinary levels of 2.380 (<LOD-.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. Acute high doses administered to laboratory animals produced ataxia.4-D reflect recent exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.740 (.930-1.580-. 2005). other exposures.590 (<LOD-1. U.820-1. adrenals and gonads (NTP.810-1. 2.700 (.790) < LOD . It is unclear whether these associations are related to the chlorophenoxy herbicides..780 (.270 (<LOD-.S.920) < LOD 1.. Pearce and McLean.73) . 2002.780) .560-.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 2006. IOM.14 (.13 (.S.4-D are eye irritants..560-.08 (.790) 1. 2005).620-. Additional information is available from U.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .670 (. 2.4-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. 2005). The acid and salt forms of 2..41 (1.890-1.590 (<LOD-1.410) 90th . Average post-application urinary levels of 2.350 (<LOD-.640 (.35) < LOD .16) 1. 2005.980) < LOD 1.. thyroid. Kutz et al. 2003. or to contaminants in the herbicide formulations (specifically 2.520-. 1996. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. in small samples of children (Hill et al. myotonia. 2005.990-1.660) < LOD .56) .470) < LOD .S. 2005.410) < LOD 1.epa. 1996.340-.19) ... and evidence of histological injury to the kidneys.890) < LOD 1. 2000).32 (<LOD-2. urinary 2.380) < LOD .340 (. U.05) . Hill et al.850) < LOD .380-.7.S.

51(3):152-159. Harris SA. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Arch Environ Contam Toxicol 1985.4-D were highest in the farmers who applied the 2. Baker BA.4-D and 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fast DM. J Expo Anal Environ Epidemiol 2005 Nov. Tables.18(4):469-474.niehs. Shealy DB.4-D will result in an adverse health effect. the number of acres to which it was applied (Curwin et al. Smith SJ.27(1):23-38. Arnold EK. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .. Gregg M. Kolmodin-Hedman B. Ritter L. Xenobiotica 1974.15(6):500-508. Mandel et al.edu/catalog.nap. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.php?record_id=10603. Beasley VR. Available at URL: http://ntp. Atlanta (GA). Arch Environ Contam Toxicol 1989. Dichlorophenoxyacetic acid. Gupta BN. In farm families. Kohli JD.. Available at URL: http:// www. Veterans and Agent Orange: update 2002.4-D than levels found in the general population. Curwin BD. Dhar MM. Pesticides residues in food: 1996 evaluations Part II Toxicology. Exposure of homeowners and bystanders to 2. general population..4. Needham LL. 1992).nih. Campbell RA.4-dichlorophenoxyacetic acid (2. Holler JS. Garabrant DH. Philbert MA. Harris et al. Survival and Growth Curves from NTP Toxicity Studies. et al.31 Suppl 1:98-104. Kutz FW. Hein MJ. Erne K. Absorption and excretion of 2. Arch Toxicol Suppl 1980. 2005. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Driskell WJ. Honeycutt R. Carter-Pokras OD.31(2):121-125.htm. To T. J Toxicol Environ Health 1992. Bailey SL. 2003. the amount of pesticide applied. Third National Report on Human Exposure to Environmental Chemicals.4-dichlorophenoxyacetic acid (2. Pesticide residues in urine of adults living in the United States: reference range concentrations. TOX-63: TOXICITY REPORT CURVES. Crit Rev Toxicol 2002. 2005 Charles JM. Sirons G J. Sanderson WT. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. et al. Sircar KP. Selected pesticide residues and metabolites in urine from a survey of the U.4-D in urine does not mean that the level of the 2.4-dichlorophenoxyacetic acid in man. Centers for Disease Control and Prevention (CDC).31 Suppl 1:90-97.4 dichlorophenoxyacetic acid (2. Needham LL. Beeson MD. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Hill RH Jr. Ripley BD. 2005). Alexander BH. et al.4:427-435. Vet Hum Toxicol 1989. Mandel JS. Scand J Work Environ Health 2005.4-Dichlorophenoxyacetic Acid).4:97-100. Baker SE.5-T). Barr DB. Occup Environ Med 1994. Toxicol Sci 2001. 2. Chapman P. Barr DB. 914.4-D) epidemiology and toxicology. J Expo Anal Environ Epidemiol 2000. 2005). Available at URL: http:// www. Murphy RS. International Programme on Chemical Safety-INCHEM (IPCS). geometric mean urinary levels of 2. Acquavella JF. J Environ Sci Health B 1992. Assessment of exposure to 2.inchem.Herbicides the time since application. Biomonitoring studies of 2. Washington (DC): National Academies Press. Finding a measurable amount of 2. Frank R. References Arbuckle TE.10(6 Pt 2):789-798. Updated March 7. Khanna RN.37(2):277-291. Review of 2..60(1):121-131. Forestry workers involved in aerial application of 2. Baker S.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. Cook BT. Board on Health Promotion and Disease Prevention.4:318-321.4-dichlorophenoxyacetic acid and its forms. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.4-D.org/documents/jmpr/jmpmono/v96pr04. Stephenson GR.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. and the use of protective clothing or equipment (Arbuckle et al. Heederik D. Head SL. Estimation of occupational exposure to phenoxy acids (2. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Environ Res 1995. Tandon JS. Wilson RD. Hanley TR Jr.4-D): exposure and urinary excretion. Biomonitoring for farm families in the farm family exposure study.gov/index. Biomonitoring of herbicides in Ontario farm applicators. Solomon KR.32(4):233-257. National Toxicology Program (NTP). TOX-63 Peroxisone Project (2. 3/17/09 Knopp D. Bus JS.4-D). Hill RH Jr.4-. 3/17/09 Institute of Medicine (IOM). Reynolds SJ. Brody D.71(2):99-108. 2005.S. Cole DC. Scand J Work Environ Health 2005. 2006. Developmental toxicity studies in rats and rabbits on 2. van Ravenzwaay B.

S. March 2006.epa. 60 Fourth National Report on Human Exposure to Environmental Chemicals .epa. Blau GE.S.4-D RED Facts. 3/17/09. Toxicology 1977.EPA). Office of Prevention Pesticides and Toxic Substances.EPA. The Quality of Our Nation’s Waters. Supplemental Technical Information (available on-line only).Herbicides Sauerhoff MW.S. Environmental Protection Agency (U. 2. 3/17/09 U.4-D) following oral administration to man. Available at URL: http://water.pdf. 2004.4-dichlorophenoxyacetic acid (2. The fate of 2. 4/2/09 U.S. S. revised February 15. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www. 1992-2001.htm. EPA 738 F-05-002.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Pesticide industry sales and usage . Available at URL: http://www. June 2005. Environmental Protection Agency (U.2000 and 2001 market estimates. Geological Survey (USGS).usgs.S.gov/oppsrrd1/ REDs/factsheets/24d_fs. Circular 1291. 2007.EPA).php. May. Washington (DC): U.8:3-1U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Braun WH. Gehring PJ.

Feng and Wratten. 2000. 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. Hines et al.S. and convulsions were observed at lethal doses in animal studies. lacrimation..S.S. General population exposure may occur through the consumption of contaminated food or drinking water. metolachlor levels in water have exceeded lifetime human health advisory levels (U. 1995. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. In animal studies.. Occasionally in the past. Fourth National Report on Human Exposure to Environmental Chemicals 61 . In animals. USGS.. Estimated human intakes have been below recommended limits (U. and field workers may have significant exposures via this route. It is absorbed by plants and inhibits plant protein synthesis. WHO. soybeans. WHO. Kolpin et al. metolachlor was quickly absorbed after dermal or oral doses. 2005. The geometric mean metolachlor mercapturate was 4.. so applicators. 2000. including corn.Herbicides Metolachlor available from U.S. and eliminated in urine and feces over two to three days (WHO. 2003). Hladik et al.. EPA at: http://www. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure.EPA. Gilliom. 1999. formulators. 2007.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. NTP and IARC do not have ratings regarding human carcinogenicity. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al.epa.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al.EPA.gov/pesticides/. in both ground and surface waters (Battaglin et al.S. mercapturate conjugates were the predominant metabolites. and on non-crop land for general weed control. 2007. U. and it was not mutagenic in mammalian cells (U. 2005). (2003) showed that 2. 2003).EPA considers metolachlor to be a possible human carcinogen. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. 1998). 1995). 1995). whereas 60% of applicators had detectable amounts. Metolachlor has low potential for acute toxicity (U. 1989. Metolachlor is well absorbed dermally. though the 95th percentile for males was 0. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. Salivation. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.EPA. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. 51218-45-2 General Information Metolachlor is a chloroacetanilide type herbicide that is applied for preemergent control of grasses and broadleaf weeds on agricultural crop land. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. sorghum and other crops. Biomonitoring Information CAS No. 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. 1994. Jefferies et al. 1995). This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. EPA.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Davison et al. 2003). People exposed to metolachlor will excrete metolachlor mercapturate in their urine.S.200 μg/L (CDC. 2005)..

S.240) 679 701 957 Limit of detection (LOD.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.S. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.670 (<LOD-.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. which may vary for some chemicals by year and by individual sample. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.440 (<LOD-.200 (<LOD-. Survey Geometric mean (95% conf.200 (<LOD-. < LOD means less than the limit of detection. 62 Fourth National Report on Human Exposure to Environmental Chemicals .

Xenobiotica 1994.24(10):1003-1012. Comparative metabolism and elimination of acetanilide compounds by rat. Third National Report on Human Exposure to Environmental Chemicals.47(6):503-517. Environmental Protection Agency (U.int/water_sanitation_health/dwq/chemicals/ metolachlor. Heederik D. Linhart SM.248(2-3):123-133. Dialkylquinonimines validated as in vivo metabolites of alachlor. Available at URL: http://water. 2005.gov/nawqa/ pnsp/pubs/wrir984245/text. Quistad GB. Geological Survey (USGS). Occurrence of sulfonylurea.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Pesticides in U. Deddens JA.php. et al. Camann DE.41:3409-3414.pdf. Sanderson WT. Available at URL: http://water. Brown KK. Davison KL. 1992-2001. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Geological Survey (USGS). Supplemental Technical Information (available on-line only). usgs.pdf.39(17):6561-6574.S. Circular 1291.108(12):1151-1157.gov/oppsrrd1/ REDs/0001. Hladik ML.S.Herbicides References Battaglin WA. Available at URL: http://water. Biagini RE. R. 1998. Striley CA. 98-4245 (by Barbash JE. Feil VJ. Reregistration Eligibility Decision (RED) Metolachlor. Ward EM. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Andrews HF. Environ Sci Technol 2005. J Agri Food Chem 1989.11(4):353359.epa. Coleman S.pdf 3/30/09 Hines CJ. California. Environ Health Perspect 2003. revised February 15. 2003. Barr DB.usgs.248(2-3):115-122. imidazolinone. Background document for development of WHO Guidelines for Drinking-water Quality.ESTfeature_gilliom. EPA). Hein MJ. Environ Sci Technol 2007. Environ Health Perspect 2000.who.S. 1999. Linderman R. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Hsiao JJ. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Thurman EM. and other herbicides in rivers. Reynolds SJ. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Peter CJ. Sci Total Environ 2000. EPA 738R-95-006. March 2006.37(4):10881093.S. Kolpin DW. 6/1/09 Whyatt RM. streams and groundwater. J Expo Anal Environ Epidemiol 2005. Wratten SJ. World Health Organization (WHO). April 1995. and metolachlor herbicides in rats.S. Sacramento. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Kinney PL. Barr DB. Available at URL: http://www. reservoirs and ground water in the Midwestern United States. Barr JR. Metolachlor in Drinkingwater. 4/2/09 U. U. Sci Total Environ 2000. Curwin BD. 2007. acetochlor. Gilliom RJ). Kolpin DW.usgs. Chem Res Toxicol 1998. Hodgson E. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Ann Occup Hyg 2003. Gillion. Casida JE. Larsen GL. Furlong ET. Alavanja MC. et al. Shoemaker DA.gov/nawqa/pnsp/pubs/files/051507. Roberts AL.15(6):500-508. Centers for Disease Control and Prevention (CDC). Burkhardt MR.html. sulfonamide. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. 3/26/09 U. Rose RL. Thelin GP. Jefferies PR. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Available at URL: http://www. Feng PCC. Atlanta (GA).111(5):749-756.

5-Trichlorophenoxyacetic Acid CAS No.3.4. < LOD means less than the limit of detection.4.4.4.g. Given the commercial unavailability of 2.4. 2. myotonia. Epidemiological studies have reported associations of several types of cancer. 93-76-5 General Information 2. renal and hepatic injury. Survey Geometric mean (95% conf.5-T. abdominal pain.4. The half-life of 2. 2007). dizziness. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Mohammad and St. 1992). 1989.5-T degrades to 2. these herbicides can enhance plant growth.. Human health effects from 2. but higher levels are herbicidal. Agent Orange). 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.5-T in soil varies with conditions.4. the general population is unlikely to be exposed to it.4.5-T and 2. Ester forms of 2.4. which may vary for some chemicals by year and by individual sample. and concern about contamination with 2. Omer. it is not well absorbed through the skin.4.. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.5T is rapidly absorbed via oral and inhalation routes.4. population from the National Health and Nutrition Examination Survey. Kohli et al. ranging from several weeks to many months. Once absorbed into the body.Herbicides 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals ..5-trichlorophenol and other degradates.7. Although 2.4. 2004).4.1.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4.5-T is eliminated mostly unchanged in the urine..4. headache.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Nelson et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.4.5-T was once applied as either an aqueous salt or as an oil-soluble ester. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. hypotension. 1986.5-T has been rarely detected in ground waters (USGS. nausea.4-D were used as defoliants in the Vietnam War (e.2 and 0. 1992.. At low levels. and delayed neuropathy (Bradberry et al. 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S.5-T (Holson et al. with an elimination half-life of approximately 19 hours (Arnold et al.5-Trichlorophenoxyacetic acid (2. 2.5-T use as a herbicide in 1985. 2. Chlorophenoxy herbicides act as plant growth hormones. 1974).

4.4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 1996. IOM. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.3.5-T were generally below the limit of detection. in which urinary levels of 2.4. Biomonitoring studies on 2.gov/pesticides/.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.EPA. 2005.5-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. 1992). similar to results of NHANES II (19761980).5-T also were below the limit of detection (Kutz et al. population from the National Health and Nutrition Examination Survey.5-T reflect recent exposure.4. 2005).5-T itself is not mutagenic. Survey Geometric mean (95% conf..S.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.EPA at: http://www. IPCS. Biomonitoring Information Urinary levels of 2. Mean urinary levels of 2. 2003. Pearce and McLean. or to contaminants in the herbicide formulations (specifically 2. urinary levels of 2.Herbicides or contaminated herbicides. other exposures. Finding a measurable amount of 2.4. 2.7.S. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. Fourth National Report on Human Exposure to Environmental Chemicals 65 .5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.S.5-T than levels found in the general population.5-T does not mean that the level will result in an adverse health effect. Urinary 2. 2004).4.4. It is unclear whether these associations are related to the chlorophenoxy herbicides.4. Additional information is available from U. 1980). 2002. U.epa.

Environmental Protection Agency (U. Fundam Appl Toxicol 1992.5-trichlorophenoxyacetic acid (2. St Omer VE. Vale JA.31 Suppl 1:1825. 2003. 210:250-255. et al.5-T). Board on Health Promotion and Disease Prevention. Washington (DC): U. Philbert MA. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Gaines TB.4-D/2. II. Nelson CJ. Agricultural exposures and non-Hodgkin’s lymphoma.org/documents/jmpr/jmpmono/v96pr04.4. LaBorde JB. Third National Report on Human Exposure to Environmental Chemicals. Dichlorophenoxyacetic acid. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Veterans and Agent Orange: update 2002. Developmental toxicity of 2. McCallum WF. Review of 2. Vet Hum Toxicol 1989.4.S. Nelson CJ. 2005. Crit Rev Toxicol 2002. et al.S.4-dichlorophenoxyacetic acid (2.nap.php?record_id=10603. Atlanta (GA).EPA).37(2):277-91. Dhar MM. Garabrant DH.4.4-. Scand J Work Environ Health 2005.Herbicides References Arnold EK. Proudfoot AT.8(5):551-60. Erne K. Sheehan DM. May. Absorption and excretion of 2. Mohammad FK. 3/17/09 Institute of Medicine (IOM). 2. Estimation of occupational exposure to phenoxy acids (2. Available at URL: http://www.19(2):286-297. Arch Int Pharmacodyn Ther 1974. Pesticides residues in food: 1996 evaluations Part II Toxicology. Tandon JS. Office of Prevention Pesticides and Toxic Substances. J Toxicol Environ Health 1992. McLean D.htm. Developmental toxicity of 2. Holson JF.pdf.epa. I. Fundam Appl Toxicol 1992. Poisoning due to chlorophenoxy herbicides. Toxicol Rev 2004. Kolmodin-Hedman B. 914. Pearce N.edu/catalog.inchem. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Bradberry SM. International Programme on Chemical Safety-INCHEM (IPCS). Murphy RS.5-trichlorophenoxyacetic acid (2. Available at URL: http:// www.5-t mixture. LaBorde JB.31(2):121-125. Centers for Disease Control and Prevention (CDC). Gaines TB. Carter-Pokras OD. Arch Toxicol Suppl 1980. gov/oppbead1/pestsales/01pestsales/market_estimates2001.19(2):298-306.5-T). Gaylor DW. Available at URL: http:// www. 2004. Wolff GL. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4:318-21.5-T in four-way outcross mice.4-D) epidemiology and toxicology. 3/17/09 Kohli JD. Pesticide industry sales and usage . Selected pesticide residues and metabolites in urine from a survey of the U.4.32(4):233-257.EPA. Brody D. Neurobehav Toxicol Teratol 1986.S.4. Cook BT. Khanna RN. general population.5-trichlorophenoxy acetic acid in man. Behavioral and developmental effects in rats following in utero exposure to 2.2000 and 2001 market estimates.4-D and 2. Sircar KP. Multireplicated dose-response studies with technical and analytical grades of 2. Washington (DC): National Academies Press.4. Kutz FW. S.5-T).4. Gupta BN. discussion 5-7. Holson JF. Beasley VR. U.23(2):65-73.4.

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

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

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

116) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.109-.101) .0 (11.4) 539 456 484 487 980 885 Limits of detection (LOD.090-.8 (11.242) .102 (.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.110-.0 (15.4-17.112) 95th .4) 20.6-24.8-17.0) 21.5 (<LOD-11.80 (<LOD-10.124) .120 (.056-.3 (18.0 (10.8) 14.054-.075) < LOD . see Data Analysis section) for survey years 01-02 and 03-04 are 10.9 (12.1) 13.3 (14.147 (.0) < LOD 9.4 (12.117) < LOD .5 (16.80-10.8.070) .7 (15. < LOD means less than the limit of detection.086-.140 (.120) .100-.130-.070-.1-24.100 (.190) . Survey years 01-02 03-04 Geometric mean (95% conf.4) 95th 20.100-.160) .50 (8.8-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (9.103 (.098 (.1-16.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .9 (14.00-14.080) .110 (.2) 12.4) 21.7-19.1) 15.7 (14.S.058) < LOD .053 (<LOD-.060) .3-21.90) 90th 15.8) 15.7 (<LOD-15.6 (15.2) 15.3 (13.160 (.1) 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 9.170) .40-9.120 (.0) 19.6) 19.112-.103 (. Survey years 01-02 03-04 Geometric mean (95% conf.088-.120-.5-15.113 (.160 (.062-.054-.108-.4) 19.190) .8-25.130) .070 (<LOD-.062 (.4) < LOD < LOD 16.4 (12.100) .6) 9. population from the National Health and Nutrition Examination Survey.9-23.4-18.0-25.130-.090-.S. 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.1 (18.2) 11.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .60-10.150 (.6-24.064 (.10 (<LOD-16.150 (.9-38.2) 14.5) 15.9 (12.049-.0-21.093) .138 (.073-. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .00 (8.7) 15.9 (13.138) .70 (7.149) .180) .080 (.3 (19.4) 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 8.140) .130-.110) .7-22.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.109-.4) 14.130 (.6-33.8-19.50) 15.084-.064) 90th .120 (.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.6 (15.6 (14.40-10. population from the National Health and Nutrition Examination Survey.1-18.080-.100) .130) .1) 14.096-.8 (18.5) 19.090 (<LOD-.1-19.9 (13.139 (.054-.6) 16.055 (.090-.30 (8.80-9.158) .110) .083-.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. which may vary for some chemicals by year and by individual sample.5-17.109 (.1) 10.180) .090 (.110 (.2-15. which may vary for some chemicals by year and by individual sample.140-.30 (8.147) 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 .089 (.9-22.059 (.5) 21.069) < LOD < LOD .1) < LOD 9.5-17.8) < LOD 8.139 (.0 (10.100-.077-.062 (.3 (18.8-17.048 (<LOD-.130) .110 (.063-.5 and 7.1 (13. Fourth National Report on Human Exposure to Environmental Chemicals 79 .1) 20.077 (.

Environ Health Perspect 2001. Frey JM. Revised Feb.109(Supp1):113-139. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress.91(1):122-126. 4/21/09 Bates MN. Facca A. Effect of occupational exposure to aldrin on urinary D-glucaric acid. 15. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.103(Suppl 7):113-122. Pesticides in the Nation’s Stream and Ground Water. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. David VL. United States Geological Survey (USGS). Available at URL: http://www. Ellis H. Kitzazwa M. Corrigan FM.inchem.html. Jorgensen T. et al.66(4):229-234. Kanthasamy AG. Lancet 1998. Toxicol Lett 1992. Grajewski B. Demographic and seasonal influences on human serum pesticide residue levels. Anantharam V. Andersen A. PA.26:701-719.gov/ circ/2005/1291/. VT.150:263-271. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Smith AG. Available at URL: http://www.9:1357-1367. Turner W. Mumtaz MM. Needham LL. 80 Fourth National Report on Human Exposure to Environmental Chemicals . September 2002. Available at URL: http://www. Sanchez-Ramos J. In Hayes WJ. Exp Neurol 1998. Serrano FO. Neurotoxicol 2005. Priestly BG. Ginsburg KS. Fernandez MG.14:95-102. 4/21/09 Jorgenson JL. Garrett N. New York. Roy ML. bioaccumulation. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Vol. plasma dieldrin. toxicology. Wienburg CL.47:1059-1087. Toxicological profile for aldrin/dieldrin [online]. Int Arch Occup Environ Health 1994. pp. Food and Drug Administration (FDA).htm. Chlorinated Hydrocarbon Insecticides. Six high-priority organochlorine pesticides. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Mink PJ.gov/toxprofiles/ tp1. Rosellini RA. Jr and Laws ER. Stehr-Green. J Occup Environ Med 2005.cdc. August 2008. Available at URL: http://pubs. Edwards JW. 1992-2001. are nonestrogenic in transfected HeLa cells. Aldrin and dieldrin: A review of research on their production environmental deposition and fate.59:229-234. Carlson JN. Basit A.html. Olea N. Aldrin and Dieldrin [online]. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Teta MJ. Patterson DG Jr. Reprod Toxicol 2000. Finley B. and epidemiology in the United States. J Toxicol Environ Health. and lymphocyte sister chromatid exchange. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Cancer Epidemiol Biomarkers Prev 2000.atsdr.gov/~dms/ pesrpts. Handbook of Pesticide Toxicology. 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. 731-915. Organochlorine exposure and risk of breast cancer. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. 1989. Narahashi T. 1991.org/documents/ehc/ ehc/ehc91. Brock JW. 2007 [online]. Eds. Cox. Psychopharmacology (Berl) 1987.fda.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). 2 Classes of Pesticides. 4/21/09 Hoyer AP. 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. Kanthasamy A. Song S.64-65 Spec.cfsan. Chung KL. J Toxicol Environ Health 1989. Grandjean P. Academic Press. Soto AM. Part A 2000. Hartvig HB. Chapin RE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.54:1431-1443. Buckland SJ. 6/1/09 Ward EM. Tully DB. Inc. No:429-436. Daniel SE. International Programme on Chemical Safety (IPCS). Schulte P. Sonnenschein C. Environ Health Perspect 1995. Mann D. Shore RF. References Agency for Toxic Substances and Disease Registry (ATSDR). McIntosh LJ. Jr.352:1816-1820. Environmental Health Criteria 91. Patterson DG Jr. Li AA.usgs.27:405-421. Chemosphere 2004. et al. either singly or in combination.

8-42.3) 18.9 (29. 57-74-9 Heptachlor CAS No.3) 10.6-53.1) 16.6) 9.1 (<LOD-12.5 (41.3) 37. and 03-04 are 14.2) 33.7 (17.69-10.6-12.3-45.6) 48.6-24.5-41.2) 46.5-65.8-43.4-21.5-40.2-56.5) < LOD < LOD 9.6) 36. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.0 (32. Fourth National Report on Human Exposure to Environmental Chemicals 81 .7 (43.S.37 (8.5) 56.0-12. the technical grade product of each chemical contains 10%-20% of the other chemical.8-73. buildings.4) 37.6) 39.3-49.10 (8.5-13.9 (11.3 (25.5-43.8 (18.8) 44.1 (27.9-21.30-11.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.9) 11. 1994). heptachlor use has been limited to treatment of fire ants near power transformers.5-38.7 (19.0-61.2 (37.7) 28.3 (26.3) 10.9) 23.8-23. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.5 (34.1) 30.0-33.2) 34.2 (21.8 (10. 10.0 (26.6-24.8-33.8-61.3 (27.8.4 (31.2-26.10-11.4) < LOD 11.9) 13.4-45.9) 36. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.7 (34.9-40.5 (31.8) 52.4) 22.9 (26.3 (20.5) 9.2) < LOD 11.3) 18.9 (31.3 (28.4) < LOD < LOD < LOD 23.7-14.1 (15.1-25. fish.9) 31.8 (17.S.2) 37.0) 37.8) 52.7) 19.2) 22.4 (22.7) 9. chlordane was used to kill termites and other insects on agricultural crops. Chlordane is not currently produced or used in the U.1) 22.6) 20.4) 18.4-40.1 (17.4 (35.3 (11.8-32.89-10.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.1) * 11.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Technical grade chlordane had contained 7% trans-nonachlor.4 (10. and in soil.5-44.7 (34.20-11.6 (25.7-39.9 (15.6) < LOD 11. < LOD means less than the limit of detection.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.0) 27.6-45.1-50. 2007).0) 21.5) 38.5 (33.5) 21.2 (28.6) 9.9) 10.8) 53.3) 41. respectively.9 (26.6 (9.1 (40.6) 49.6 (43.2) < LOD 11.1) < LOD < LOD < LOD < LOD < LOD 8. 2007).6-18.8 (10.7) 35.8-33. and 7.2-28. see Data Analysis section) for Survey years 99-00.9-42.4-14.3 (21.6) 23.2) 36.10-18.1 (<LOD-12.9-38.0 (<LOD-12. Since 1992.63 (8.3 (<LOD-19.5) 10.5) 37.3-24.9-21.20 (<LOD-11.9) 11.2 (41. Consequently.8) 27.7 (<LOD-32.7-12. foods high in fat such as meat.8 (17.9 (11.9 (15.4 (<LOD-12.3-43.0) 31.3-45.9 (36.6 (16.7 (42.2 (10. which may vary for some chemicals by year and by individual sample.0-18.0 (20.0 (16.7 (32.7) 19. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.5.8 (40.7) 42.5-32.7-56.6) 48.6) 11.0-25.0) 20.9) 17.0-13.Organochlorine Pesticides Chlordane CAS No.1 (25. from the early 1950’s until the mid-1980’s.5-42.1 (16.6) 8.1 (<LOD-12.1-51.4-51. 1994.4) 12.8-31.7-25. 01-02.1-15.9) 37..7 (10.90 (8.7-70. in addition to trace amounts of numerous other related compounds (ATSDR.4 (30.20-10. 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.1-25.0) 75th 20. 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.2) * 12.4) 29.7 (<LOD-13.8) 18. Survey Geometric mean (95% conf.1) * 11.8 (42.2-21.S.2-49.7) 31.5.5) 44.2 (39.0-67.1-65.9) 47. 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.82-11.3-32.70 (<LOD-10.2 (9.1-19.8-20.2-49.1 (11.9 (21.3 (9. lawns.2 (36.74 (<LOD-10. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.36-11.9) 39.5) 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 (44. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and dairy products are the usual sources of exposure to these chemicals in the general population. population from the National Health and Nutrition Examination Survey.0) 41.5 (<LOD-12.9 (17.5 (8.1) 90th 34.4) 39.9) 23. As a result of the manufacturing process.0 (37.9 (18.5) < LOD < LOD < LOD < LOD 13. Until 1988.1 (20.4 (30.5-47.1) 30.6 (9.

130-.140 (.090) .150-.077) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.207 (.140) .100-.136) .410) .090) . 1977a.253-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300) .230-.130 (.300 (.280 (.146) < LOD < LOD .070 (.063) * .070 (<LOD-.150) .091) .079) < LOD < LOD < LOD .066-.270 (.300-. Chlordane and heptachlor are absorbed after oral.S.189 (..063 (.300) .068) 75th .061-.280 (. Smith.320 (.077) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.286 (. 1981).120-.286 (. neonatal mortality..290-.300) .430) .100 (<LOD-.250 (.180-.115-.070) . dermal.290-. 2002.210-.083) .380) .340) .150 (.130-.310-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . IARC.070 (<LOD-.057 (.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.S.079) .110-.240 (.058 (. and the U.130-.207) . heptachlor.450) .245-.170) . 2007.108-.170) .250 (.106-.510) .069 (<LOD-.149 (.055-.320) .160) .430) ..062) < LOD .360) .150 (.050 (<LOD-.056 (.280-.170) .240-.320 (. 2006).280-.057-.128 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.058-.063-.048-.070-. 1996.140-.230 (.050-.290) .104) . 1991.130 (.170) .242-.053-.119 (.290 (.100 (. Survey Geometric mean (95% conf. characterized by seizures and paralysis.200 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.068-.560) .190-.200-.373) . FDA established allowable residues of chlordane. 1986). 2007).216-.230) .310 (.146) .S.270 (.320) .148) .148-.287) . 1991).063) .370 (.204 (.210 (.280) .370 (. 1977b.180) .065-.060 (<LOD-.092) .160) .070-.315 (.070 (<LOD-.330 (.057) * .269 (.047 (<LOD-.080) .271 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.071 (.199-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .083 (. and heptachlor epoxide in foods and bottled water.340) . The U. which is also persistent in the body (ATSDR.280-.260 (.063 (.165-.133) 90th . and breast milk is a major excretion route in lactating women. chronic doses of heptachlor have produced liver enlargement and injury.320 (.115 (.220-.225 (.150 (.400) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.450) .126) .350) .064) < LOD .310) .220-.074-. and inhalation exposure.189-.270 (.140 (.053-. OSHA has established occupational exposure criteria.168-.260 (.350 (.250-.049 (<LOD-. and alterations in immune function of offspring.082 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.130-. Acute.230-.260-.066 (.066-.104-. Elimination of all these chemicals from the body occurs over months to years.120-.210 (.120 (.180-.370 (. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.200-.068) .200-.070 (<LOD-.130) . which may vary for some chemicals by year and by individual sample. to heptachlor.240-.077) .077) .080 (.126 (.067 (.130 (.213) * .258-.130) .070) < LOD < LOD < LOD < LOD < LOD .Organochlorine Pesticides (Dallaire et al.227) < LOD .080 (.290-.063 (. 2001.058-. 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. 1986).300) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .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 * * * * . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.348) .063 (. Shindell and Ulrich.260 (. The major metabolite of heptachlor is heptachlor epoxide.160 (.076) < LOD .208 (.240) .073) < LOD < LOD < LOD < LOD . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.170) .223) . Rogan. Takahashi et al. EPA has established environmental criteria for chlordane and heptachlor. population from the National Health and Nutrition Examination Survey.190-.075 (.160) .120-.073 (.320 (.231) . In laboratory animal studies.400) .066 (<LOD-.230 (.350 (.130-.090-.290) .140-.140 (.190-.258 (.080) .110 (<LOD-.087-.203-.070-.100-.440) . Le Marchand et al.310) .220 (..140 (.080) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .180) .230-.310) .302) .246-.170-.112 (.

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

6-21.1) 13.9-29.3) 27.9) 15.6) 13.90 (<LOD-9.5 (<LOD-32.5) < LOD 14.8-23.0 (11.8) 14.7 (10.8) 13.9-29.8 (18.8-24.5 (<LOD-21.4 (<LOD-54.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.4 (11.6 (13.4) 18. Survey Geometric mean (95% conf. 10.S.8) 19. respectively.2) 15.2) 13.0-54.2) 20.4 (11.8) 20. and 03-04 are 14.3-18.6 (16.0 (15.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (10.2 (<LOD-62.5 (18.1-38.8-24.5 (11.8) 21.9-23.50) < LOD < LOD < LOD 17. and 7.3 (13.20 (<LOD-9.8 (13.9 (15.7-25.0-16.3) 16.1-29.1 (19.10-13.9-16.6 (<LOD-27.5) 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 7.6 (14.4 (<LOD-19.8) 16.5) 19. 84 Fourth National Report on Human Exposure to Environmental Chemicals .8) 19.2-27.7 (13.2) 26.3 (<LOD-25.3) 18.40) 15.8) 14.2-27.2 (18.7-18.8) 13.1-15.8) 15.9) * * * 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. population from the National Health and Nutrition Examination Survey.6-17.9-25.0-19.4 (15.0) 13.1 (16.0-17.3) 22. which may vary for some chemicals by year and by individual sample.7 (16.1) 23.1-16.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.0-17.8 (15.9 (12.2 (<LOD-25.2 (<LOD-16. < LOD means less than the limit of detection.5 (11.2-17.4) 21.7-19.3) 18.3) 18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 22.8 (<LOD-23.8 (18. 01-02.6 (8.6) 14.8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.8 (13.8-24. see Data Analysis section) for Survey years 99-00.1) 20.8-46.3) 10.6 (11.6) < LOD < LOD < LOD 27.2-16.6 (16.3) 23.6 (12.5.0) 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.

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

7) 56.8.6) 60.7 (35.3) 19.9) 51. < LOD means less than the limit of detection.5-17.9-22.1) 14.5.9 (28.9-36.5) 48.9-89.0 (16.5) 20.2 (14.6 (16.3) 36.0-113) 68.6-22.3 (14.0) 13. and 03-04 are 14.9-64.6-20.8 (28. respectively.5) 90th 55.9) 51. 86 Fourth National Report on Human Exposure to Environmental Chemicals .0) 40.1-20.2 (26.5) 77.7-34.2 (59.0 (42.7-23.0) 49.0) 18.8 (17.5) 14.1 (48.1-34.4) 16.5-69.3 (14.S.7) 78.2) 17. which may vary for some chemicals by year and by individual sample.8 (49.2-16.8-77.1-22.86-13.9 (51.9) 14.4) 48.2 (60.8 (71.2) 20.3-86.3-32.9 (66.2) 19.2-17.3) 16.8-21.9-65.3) 32.4-52.0 (13.5) 19.8-16.3) 32.1) 17.6 (12.8-90.9) 14.4-36.6 (15.7 (59.6) 54.7) 52.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.7-32.3 (49.6) 25.8) 47.1-28.4-22.8 (19.4 (45. see Data Analysis section) for Survey years 99-00.8) 80. 01-02.5 (45.0) 19.8-110) 59.0-93.7 (30.3) 25.7-77.8 (11.3-21.0) 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) 82.4 (28.0-143) 112 (68.2 (64.1 (22.5-19.9-45.2) < LOD 10.6) 13.6) 84.1-16.1) 78.6 (32.0 (42.4) 107 (84.7 (16.9 (36.6-54.0 (15.1) 62.6-66.0-93.8 (28.0-59.0-24.0 (13.7) 17.8-19.2 (19.4 (12.7) 73.3-74. population from the National Health and Nutrition Examination Survey.6-88.8 (13.6) 34.1) 16.1-18.6) 56.3) 30.2 (36.1-34.1) 17.3 (58.5 (25.2 (15.5-95.1 (17.8-16.7 (18.7-29.0) 75th 31.3 (17.70 (<LOD-12.9-69. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) 18.2 (27.9-58.4) 19.0-38.9 (16.7-160) 86.0-68.1 (10.5 (15.9 (19.5 (15.0) < LOD < LOD 8.3-58.4 (67.7) 35.5) 30.1) 31.2 (7.1 (41.7-113) 68.8 (26.5-111) 68.7-35.0-22.1) 30.6) 56.3) 18.0 (29.8-90.8 (26.2 (14.8) 19.3 (56.2-88.0 (19.5) 78.1-51.3) 15.8 (<LOD-20.5 (44.8-19.5) 22.8 (26.0 (62.4-35.4 (30.4-18.6-82.7-18.7-21.2) 34.3 (45.6 (57.1) 18.7-38.6 (56.1) 17.3 (16.9 (29.1-55.2-37.9) < LOD < LOD < LOD 20.8 (42.3) 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.10 (<LOD-11.9-65.2-18.2) 39.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.8-129) 74.2-18.4) 55.7-22.9-35.7 (74.6 (50. and 7.3-57.8-67.7) 15.9-40.0 (14.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.8-41.8 (12.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.1) 32.7) 14.4 (11.1) 17.0-123) 74.5.1-16.8) 51.9 (47.8 (15.8-79.4) 59.4-67.0) 33.5-36.6 (52.1) 78.8 (13.0-20.0-23.1) 17.3-30.4-62.9 (15.9 (51.2) 30.0-37.5-87.1) 17.0-23.5 (13.2 (25.7) 28. Survey Geometric mean (95% conf.9-20.9 (15.1) 17.1 (47.0 (48.7 (28. 10.3-39.0 (60.1-126) 67.2) 59.2-23.5) 35.5) 14.1) 18.7 (11.4-23.6-19.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.8 (45.6) 10.7 (13.7) 59.7-17.5) 36.6 (56.5-20.3) 30.5) 26.7-20.8 (28.9 (<LOD-14.8 (16.3-50.0 (16.3) 18.6 (<LOD-14.5) 9.8 (30.0 (15.2-21.7 (59.7) 78.1 (65.4) 20.4 (16.

565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .114) .110 (.594) .450) .240-.202 (.409-.220 (.600 (.145-.110 (.590 (.397-.106 (.470-.110-.760 (.360-.210 (.240) .490 (.099-.080-.280) .210) .099-.440) .279-.630) .100-.520) .080 (.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 . interval) .288 (.960) .140) .420) .370 (.367) .565) .150) .470 (.100-.096-.211) 90th .116-.112 (.440-.150) .497-.113) < LOD .210) .355 (.090-.105 (.090-.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.081 (.130) .390 (.930) .110) .286-.270-.830) .210-.109 (.070 (.260) .100-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .190-.119) Selected percentiles ( 95% confidence interval) Sample 95th .090-.097) .240) .290-.220 (.272-.092 (. population from the National Health and Nutrition Examination Survey.327 (.130 (.310-.220 (.190-.108) .090-.089 (.260) .400-.113) .120) .680) .410-1.285-.330-.177-.134) .090 (<LOD-.104-.069) .096-.060) .071 (<LOD-.500) .078 (.190-.186-.310-.520 (.085-.210 (.084-.330 (.310-.395-.220 (.119) < LOD < LOD < LOD .380 (.242) .047-.171-.340-.109 (.250) .600) .120-.190-.310) .110 (.080) .180-.120-.220 (.130) .350-.080-.161) .301-.135 (.470 (.183 (.091) .098-.400 (.116) .237) .250) .120-.210 (.093-.460) .103 (.510 (.125 (.090-.095-.128 (.080-.130) .120 (.098 (.220 (.191 (.081-.060 (<LOD-.237) .158-.458 (.540) .240 (.130) .405) .350 (.460) .190-.430-.220 (.124) .220) .120 (.091-.390 (.116 (.470 (.127) < LOD < LOD .800) .090-.310 (.640 (.559) .680 (.580 (.141) .060-.370 (.120 (.414 (.630) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .129) .210-.840) .580 (. which may vary for some chemicals by year and by individual sample.170 (.324 (.390 (.371) .490-.360-.480) .125) .340-. Survey Geometric mean (95% conf.390-.310-.092 (.082) .461 (.090) .126) .098) .161-.430-.630) .130 (.098 (.573 (.240) .110 (.085-.430-.100-.093) .111-.100 (.320-.160 (.490) .108) 75th .510-.085-.490 (.117) .130) .520 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .420 (.400 (.111 (.061-.120) .141) .300) .317 (.062 (.090 (.080-.054-.320-.093-.220 (.108 (.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.110 (.390) .590) .400) .180-.112 (.343 (.173-.205 (.160-.130) .590 (.S.830) .106 (.096) .210) .684) .180-.690) .340) .250) .041 (<LOD-.234) .110 (.093-.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190-.232) .417 (.186 (.103 (.330-.580 (.087 (.390) .079-.550 (.410-.651) .131) .122) .079-.470-.078-.288-.395) .106 (.120) .104 (.690) .069-.460-.100 (.230 (.122) .068-.055 (<LOD-.120) .400-.094 (.130) .20) .390 (.

pdf. Wohlleb JC. 4/21/09 James RA. Sci Total Environ 2004. Eds. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Granath F.inchem. Smith AG.niehs. Barker J. Bioassay of chlordane for possible carcinogenicity.150:981-990. Odland JO. Glynn AW. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. 2001. Bull Environ Contam Toxicol 1981:27:506-511. Available at URL: http://www.org/documents/iarc/ vol79/79-12. Covaci A. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Keller JA. 4/21/09 Dallaire F. Environ Res 2000.gov/ntp/ htdocs/LT_rpts/tr008. Hertz-Picciotto I. 1993. Vol.8:1-123. New York. Head SL. Takahashi W.111:349355. 1979-1980. J Occup Med 1986. 4/21/09 Baker DB. Atuma S. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Vol.330:55-70. LeMarchand L. Stehr-Green P. gov/toxprofiles/tp12.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Hawaii Med J 1991. Kolonel LN. May 1994. Mortality of workers employed in the manufacture of chlordane: an update. 2006. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Chlorinated Hydrocarbon Insecticides. Organochlorine exposures and breast cancer risk in New York City women. August 2007. Gilman A. Organochlorines in Swedish women: determinants of serum concentrations. Jr and Laws ER.org/site/foundation/ research/projects2.inchem. Sci Tot Environ 2006. Organochloride pesticide residues in human milk in Hawaii. Siegel BZ.org/ documents/cicads/cicads/cicad70.atsdr.html.gov/toxprofiles/tp31. Inc. National Toxicology Program (NTP). Ayotte P. 6/1/09 Rogan WJ. 1991 pp. 9/25/07 International Programme in Chemical Safety (IPCS). Arch Pediatr Adolesc Med 1996. Voorspoels S. A Report to the Hawaii Heptachlor Research and Education Foundation. Jr. Loo S. Tartter P. Arch Environ Health. Chlordane and heptachlor [online]. Toxicological profile for heptachlor and heptachlor epoxide [online]. Distribution of polychlorinated biphenyls. 79. Charles MJ. Canada). Brower S.Summaries & Evaluations. et al.html. 2 Classes of Pesticides. Royce W.heptachlor. Handbook of Pesticide Toxicology. Shindell S and Ulrich S. et al. Wolff MS. 6/1/09 National Toxicology Program (NTP). Pollutants in breast milk. Saidein D. 1994-1997 organochlorine compounds.9:1-109. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Willman E. Available at URL: http://www. Available at URL: http://ntp.110:617-624.cdc. Lulek J. Baker DB.28:497501. Bleiweiss IJ. International Agency for Research on Cancer (IARC) . Berkowitz GS. Natl Cancer Inst Carcinog Tech Rep Ser 1977b.372:20-31. Aune M. Hansen JC. Senie R. Bioassay of heptachlor for possible carcinogenicity. Environ Health Perspect 2003. maternal serum and milk from Wielkopolska region. Drews K. Lawrence River (Quebec. Darnerud PO.htm. Available at URL: http://www. Chashchin V. Wong L. In Hayes WJ. Van Oostdam JC. 1986. Academic Press. Toxicological profile for chlordane [online].41:145–148.110(8):835-838. Dewailly E. Takei G. Poland.pdf. Concise International Chemical Assessment Document 70 Heptachlor [online].htm. International Agency for Research on Cancer (IARC). Available at URL: http://www. Available at URL: http://www. et al. Dendle WH. JAMA 1988. Dewailly E. KalubaSkotarczak A.50(3):108-118. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Jaraczewska K.gov/ntp/ htdocs/LT_rpts/tr009. Bjerselius R. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Environ Health Perspect 2002. 88 Fourth National Report on Human Exposure to Environmental Chemicals .nih. et al. 1963-1967. Circumpolar maternal blood contaminant survey. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.nih.259(3):374-377.cdc. Laliberte C. Muckle G.atsdr.84:151-161.html. Available at URL: http://ntp. 731-915.niehs. Environ Health Perspect 2002.

7) 12. 1991). In the body.8-26.3 (<LOD-21.10 (<LOD-12.3 (27.9 (10.S.0-35.1’-(2.2 (<LOD-40. Food imported from countries that still use DDT may contain the chemical or its residues.2-95.0 (18.0 (18. continues to be the primary source of DDT exposure.4) < LOD 17.3) 21.p’-DDT (15%-21%).0-37.9) 17.70 (8. or dermal exposure.8) 15. and trace amounts of several related compounds.0) 20.7-16.8-17.2-65. The biodegradation half-life of DDT in soil varies from 2 to 15 years. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) < LOD < LOD 9. Survey Geometric mean (95% conf.9-34. Only a small proportion of DDT is metabolized and excreted (Smith. In the general U. DDT usually refers to the technical product.7) < LOD 18.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. fish. inhalation.1’-dichloro-(2.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.3-236) 24.1) 31.6 (<LOD-25.7 (15.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.0) 19.5) < LOD < LOD 9.1 (23.6 (25.5-54. DDT is converted in the environment to other more stable chemical forms.7 (19. Smith. These chemicals are highly persistent in soil.7. o. 2008.3-590) 293 (104-541) 48. food. population from the National Health and Nutrition Examination Survey.0-15.6 (31. and water.5 (14. see Data Analysis section) for Survey years 99-00.3) 28. Both Serum p. Fourth National Report on Human Exposure to Environmental Chemicals 89 .8-23.0 (21.9 (<LOD-20.0) 40.2) < LOD < LOD 9. p. 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. It is still used in some countries.1 (<LOD-39.9-28.0 (10. and 03-04 are 20.10-13.8) 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 8.5 (23.7) 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 10.3-16. population.0-53.8-39.3 (<LOD-31.6 (9.8) 30.9 (21.4 (23.3) 22.9 (10. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.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.S. particularly meat.4.1 (33.9) 14.p’-DDD (4% or less). sediments. including 1.1-71.4) < LOD < LOD < LOD 61.2) 155 (59.8) 36. 2002. and dairy products.00 (<LOD-10.9) 29. DDT can be absorbed after ingestion. DDT and DDE can cross the placenta. although DDT and DDE intakes have decreased over time (FDA. 1991).0-155) 83.9 (10.2 (11.6 (22.0) 26. after World War II until 1972. 01-02. 1988).50-11. DDT is converted to DDE and several other metabolites.6-33.8. It was produced and used in the U.S.3) 21.2) 30.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.5-36.1-27.5 (15. and 7. 17. air. particularly for endemic vector and malaria control. respectively.p’-DDT (65%-80%).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. when virtually all use of it was banned.2-bis(p-chlorophenyl) ethane (DDD). as well as in plant and animal tissues. < LOD means less than the limit of detection. which is a mixture containing p.5 (23.5) 25. DDT was used at one time as a treatment for head and body lice.0-27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.90 (<LOD-12. Gunderson. which may vary for some chemicals by year and by individual sample.5) 23. resulting in fetal exposure. depending on conditions.

059-.061) < LOD < LOD < LOD .170-.078-.120 (<LOD-.150 (<LOD-.570-4.140) .240 (..290) .260) .130 (<LOD-. 2006). other organochlorines..074-. and duration of lactation.142 (.530) . 2002.112 (.106-.62 (.150) .190 (... have not been consistently demonstrated (Beard. In laboratory animals. overt signs of acute human toxicity include vomiting. 1995. Mariussen and Fonnum. 2002.01) .084 (.343) < LOD .00 (. 2000. and leukemia have also been inconclusive (ADSDR.220) .. 2001).230) . 2002.180 (.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. 2004.120-. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. Beard. Animal studies reported reduced fertility. Studies of DDT exposure and pancreatic cancer. 90 Fourth National Report on Human Exposure to Environmental Chemicals .p’-DDD and p.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 . 2001). Hayes et al.132-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.200 (.068-.220) .34) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2002. Reproductive effects in humans affecting birth weight. 2006).054-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. Longnecker et al. resulting in exposure to nursing infants (Rogan. 2001).130 (<LOD-.143) < LOD < LOD . lung cancer..201 (.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.190-1.075) 1. premature delivery.420) .. Survey Geometric mean (95% conf.530 (.160-.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .071 (..S..170 (. dioxins and furans). A workplace standard for DDT has been established by Serum p.150-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 1997).095) < LOD . and seizures. 1998).g.071-.170) .190 (.180) .078 (.069) .189-.114-. Jusko et al.400 (. 2006. tremor.00) .313 (.180 (.Organochlorine Pesticides chemicals are excreted in breast milk.130-... and altered behavior after neonatal exposure (Eriksson and Talts.130 (<LOD-.250 (.105-. Snedeker.150-. which may vary for some chemicals by year and by individual sample.26) 1. fertility.064 (.250-1.128 (.051 (<LOD-.106) . Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. 2006).080-.106) < LOD < LOD . Gray et al. accidental exposures.048 (<LOD-.140-.098-.180) .p’-DDE can produce anti-androgenic effects (Gray et al.079) < LOD < LOD .150 (<LOD-.230) .. In high dose. population from the National Health and Nutrition Examination Survey.086 (. 1996).240) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .180-.330-4. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR.203) .065-.146 (.108 (. 1956). 2006. Gladen and Rogan.627) . Calle et al. and o. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2001). 2006.063 (<LOD-.087 (. polychlorinated biphenyls. DDT may bind to estrogen receptors (Chen et al.400) . reproductive organ abnormalities.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 .189) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Jusko et al.146 (.

1989).7-119) 113 (100-140) 93. population from the National Health and Nutrition Examination Survey.e. 2003. In general. and 03-04 are 18.. 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.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.p’-DDT) as a possible human carcinogen. Compared to females in the NHANES 1999-2000 subsample.gov/ toxpro2. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.cdc. Stehr-Green. environmental levels) and health effects is available from the U... 1998..S. see Data Analysis section) for Survey years 99-00. 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 (84.6 (81. 2003). 8.8.0-114) 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. Fourth National Report on Human Exposure to Environmental Chemicals 91 .7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.html. Survey Geometric mean (95% conf. IARC classifies DDT (p. 01-02... mean serum levels of DDT and DDE in the U.S. Smith.. In a population-based sample of men and women from eastern Slovakia. 2004). for males and females in the NHANES 19992000 subsample (Pavuk et al. 2002. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Since the 1970’s. Link et al. EPA at: http://www. More information about external exposure (i. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.6. 1991). compared to levels observed in this Report (Anderson et al. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.gov/ pestcides/ and from ATSDR at: http://www.. respectively.epa.3. population declined by about fivefold to tenfold. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. 2005). 2004). respectively. Biomonitoring Information DDE persists in the body longer than DDT.atsdr. 2002. 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. and 7. NTP considers DDT as being reasonably anticipated to be a human carcinogen. Declining DDE levels over time have also been observed in the German population. Heudorf et al.S.

3) 10. 2001-2002 and 2003-2004 subsamples.994-2.69 (.1 (8.5) 5.26-10.58) 75th 3.48-4.39 (3. considerably higher than levels in this Report (Smith.726) .680-1.90-8.52 (1.63 (1.71 (5.46 (1.49 (1.5) 16.69 (1.8 (9.59 (1.8) 15.15-4.85-10.49) 8.49 (6. 2004).56-3.56-2.72) 1.430-.3-43.860 ng/L) and DDE (about 14.24-17.32-9.730) .26-2.32-1.34 (7.12 (6.77 (1.3) 16.01) 1.557) 1.43 (5.4 (12.4 (8.6 (17.890-1.46 (1.25) 1.25 (1.81-18.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.12 (.65 (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.4) 13.385-.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.7) 9. serum levels of o.48 (6.51-15.88 (2.57 (3.38 (1.3 (8. Finding a measurable amount of p.72) 1.92 (3.91-2.30 (1.46-2.456 (.39) 1.62-6.37-4.13-2.38 (1.80) 1.40-4.16-1.2 (19.11 (2. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al. or p.26) 3.01-5.01) 1.64-2. In a subsample of NHANES II (19761980) participants.69 (2.65) 1.75) 6.p’-DDT.419-.76-3.52-6.05) 1.78 (4.18-4.14) 2.45 (1.68) 2.03-4.39-1.520 (.70-3.40-4.84 (3.31-2.00 (.31-12.06) 3.51-49.93 (7..6 (7.1) 7.01-15.14 (1.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.36) 3.63-15.51 (1.22-1.S.85 (1.2 (9. 2005).37-16.35) 1.30 (1.7-20.41 (1.37-10.611-1.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 . High mean levels of whole blood DDT (about 3.81-5.14-1.47 (1.6) 12.30-1.10) .6) 9.600) .70) 1..963-1.2 (6.34) 6.91 (6.623 (.96) 1.05 (3.82 (1.488-.41-12. Serum p.24) 1.1) 12.22) .50-17.01-1.34-11.p’-DDT.23 (7.01-11.32-1.81) 11.7) 16.91-3.27) 3.40 (3.64) 3.71) 32.07 (5.34) 2. 1971).57-3.18) 1.30-1.796 (.53) 7.76) 1.53-15.58) 1.39-2.561 (.6 (9.21) 3.07) 1.87 (5.24 (1.66) 3.33-1.03-1.53 (2.13) 4.02) 1.3) 13.36-2.68 (2.07) 1.79) 4.9-38.4) 9.8 (13.80) 1.7 (8.49 (1.40-8.0) 2.80) 3.965-1.71 (6.91) 3.52 (3.84-3.12-1.43-4.43-8.54) 8.10-1.6 (8.63 (1.01-1.6) 13.29 (1.66-17.09-1.19) 4.6) 11.60-13.870 (.53) 1.54-7.97 (3.51) 3.19-14..6) 9.87-16.9-17.76 (2.14-9. population from the National Health and Nutrition Examination Survey.88-35.5) 22.6) 9.36-11. o.7-19.635) 1.59) 6. 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.4) 14.90) 22.06) 1.34-3.16 (2.92 (3.516 (.18 (6.6) 9.2) 19.25-14.75 (8.57-13.28) 1.36-1.8 (13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.59 (4.0 (9.57 (1. 1989).54 (1.2) 26.02-8.11-1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.18-3.36 (3.1 (9.71) 12. 2004).00 (6.10) 2.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.81 (1.9 (26.83 (1.66) 4.10-5.820-1.59 (1.4-19.81 (7.18-1.37-1. 1991).8-90.69) 8.9 (15. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.20 (.p’-DDT (Stehr-Green.25) 8.01-11.04 (6.21) 90th 7.0) 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 .75) 1.17-3.69) 4.32) 1.57) 2.9) 7.25-16. Survey Geometric mean (95% conf.66) 1.2 (9.66-4.32 (1.18-1.45 (1.p’-DDT were below the limits of detection.0 (12.14) 2.97-4.32 (1.85-4.82) 1.22 (7.2-32.66-2.13 (1.3 (9.27-1.31 (1.57 (1. 309 versus 268 ng/g lipid.5) 7.77 (1.646) .61 (1.25 (. less than one percent had detectable serum levels of o.66) 1.99) 1.9) 5.6) 8.5) 10.26 (1.50 (2.56) 2.61-2.02 (2.55 (2.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.76) 1.1) 40.63 (6..75) 2. In the NHANES 1999-2000.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.17 (3.55-9.7-48.80 (2.44) 1.56-6.58) 1.68-4.8 (14.37 (1.92) 1.00) 7.75 (4.Organochlorine Pesticides nearby agriculture (Botella et al.7) 13.500-.43-4. interval) 1.590 (.534-.51) 1.00-1.04-1.96) .47) 3.59) 3.51-8.57-2.

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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organochlorine Pesticides Serum o. respectively.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. and 03-04 are 20. and 7. Survey Geometric mean (95% conf. 17. Fourth National Report on Human Exposure to Environmental Chemicals 93 .S.4. < LOD means less than the limit of detection.7. 01-02.8. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00.

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

Baker RJ. Becker K. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. J Assoc Off Anal Chem 1988. Falk C. Effects of environmental antiandrogens on reproductive development in experimental animals.21(1-2)37-48. FDA total diet study.17(6):692-700. selected elements. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Sci Tot Environ 2006. CA Cancer J Clin 2002.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Durham WF. The Great Lakes Consortium.fda. Eriksson P. Jr. Greenfield TA. hexachlorobenzene. Hediger ML. Piechotowski I. Henley SJ. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Available at URL: http://www. Garrett N. 4/21/09 Gladen BC.html.58:1185-1201. Zhou H. Int J Hyg Environ Health 2002. Jusko TA. Environ Res 2005. Lancet 2001. Davis MD. Am J Epidemiol 2002. Brock JW. DDE. Glynn AW. Hanrahan L. Herrman T. DDT and human health. Bull Environ Contam Toxicol 2004. Heudorf U. Lepom P. Charles MJ. Zhou H. Zaidi SS. Calle EE.atsdr.355:7889. Maternal serum level of 1.53(8):1161-1172. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. JAMA 1956. Paepke O. Int J Hyg Environ Health 2003.72:261265.1-dichloro2.206:485-491.155(4):313-322. Drexler H.111:349355.52:301-309. et al. Barr DB. Wolf CJ. Longnecker MP. Atuma S. Klebanoff MA. Frumkin H. Klebanoff MA. Maternal DDT exposures in relation to fetal and 5-year growth.162:890-897. lindane (g-HCH). Bloom MS. Cerrillo I. Olea-Serrano MF. Botella B. et al. et al. and HCB residues in human blood in Ahmedabad. Needham LL.97(2):178192.gov/ toxprofiles/tp35. Gunderson EL. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Notides AC. Swanson MK.106(5):279-289. Longnecker MP. Kaus S. Willman EJ.cdc. Bates MN. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Organochlorines in Swedish women: determinants of serum concentrations. Ellis H. Patterson DG Jr. Parks L. 4/21/09 Anderson HA. Gladen BC. Olea N. Moysich KB. and polythelia among male offspring. Vorojeikina DP. Neurotoxicol 2000.54:1431-1443. Biomonitoring of persistent organochlorine pesticides. Arnold SF. Environ Health Perspect 2003.85:504508.. Epidemiology 2006. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Rogan WJ.112(17):1761-1767. Chen CW. Thun MJ. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Levels of DDT. Talts U. et al. Schulz C.gov/~dms/ pesrpts. Aune M. Burse VW. Environ Res 2004. Needham LL. Food and Drug Administration (FDA). et al. Lambright C. Exposure of women to organochlorine pesticides in Southern Spain. and other chemicals. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Link B. Granath F.358:110-114. Bhatnagar VK.205:297-308. Kashyap R. Gray LE Jr. Biochem Pharmacol 1997. and DDD [online]. Rivas A. Gabrio T. Available at URL: http://www. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Hurd C. Koepsell TD. Hayes WJ. Saiyed HN. September 2002. Angerer J. Needham LL. Olson JR. Hum Reprod Updat 2001. Zoellner I. et al. Toxicological profile for DDT. Ostby J. HCH. Seiwert M.96:34-40. Brock JW. dichlorodiphenyldichloroethylene.html. and dichloro(diphenyl)ethylene (DDE).7(3):248-264. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. DDE and shortened duration of lactation in a northern Mexican town. Chemosphere 2005. Chemosphere 2004.71(6):1200-1209. Am J Public Health 1995. Jr. India. Environ Health Perspect 2004. et al. Savitz DA. Buckland SJ. Klebanoff MA. Crespo J. et al. Katz SH. Profiles of ortho-polychlorinated biphenyl congeners. Olson J. Bjerselius R. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. hypospadias. Environ Health Perspect 1998. Kulkarni PK.cfsan. Darnerud PO. Vena JE. Organochlorines and breast cancer risk. Krause C. August 2008. Furr J.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. et al. Cueto C. Beard J. April 1982 to 1984. dietary intakes of pesticides. Gray KA.

Vol. Chemosphere 2004.Organochlorine Pesticides Mariussen E. Fox S.109:35-47.150:981-990. Rogan WJ. Chlorinated Hydrocarbon Insecticides.36:253-589. Smith AG. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Jr and Laws ER. Cerhan JR. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Demographic and seasonal influences on human serum pesticide residue levels. Fonnum F. 1991 pp. Toxicol Appl Pharmacol 1971. Thomas PE. Handbook of Pesticide Toxicology. New York. Reddy AB.27:405-421. Schecter A. children and newborn infants. Inc. Stehr-Green. Astolfi E. Rey AA. et al. Deichmann WB. 731-915. J Toxicol Environ Health Part A 1998. 2 Classes of Pesticides. and dieldrin.53:455-477. Pollutants in breast milk. Comparative pharmacodynamics of CYP2B induction by DDT. Chovancova J. Nims R. Lubet R. and DDD in male rat liver and cultured rat hepatocytes. Jones CR. Academic Press.20(2):186-193. J Toxicol Environ Health 1989. Lynch CF. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Eds. Pesticides and breast cancer risk: a review of DDT. Environ Health Perspect 2001. In Hayes WJ. Arch Pediatr Adolesc Med 1996. Petrik J. et al. Crit Rev Toxicol 2006.54:1509-520. Snedeker SM. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Pavuk M. DDE. PA. Jr. DDE. Radomski JL.

1991). and occasionally at low levels in sediment and surface waters. IPCS. 1991). Endrin does not accumulate in body tissues (IPCS. 1979. 1992). Fourth National Report on Human Exposure to Environmental Chemicals 97 . which may vary for some chemicals by year and by individual sample.50) < LOD < LOD < LOD 5. anti-12hydroxyendrin. interval) Selected percentiles ( 95% confidence interval) Sample 95th 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. 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..30 (<LOD-6. or discarded. 1987).S.S. population from the National Health and Nutrition Examination Survey. 1992). Smith. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. inhalation or dermal exposure routes. a stereoisomer of dieldrin. 1981). Hepatic effects of endrin exposure have included necrosis.20 (<LOD-5. endrin can persist for years. is no longer manufactured in the U. total diet surveys (FDA. 1992. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. Endrin was used as an insecticide.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. Depending on soil conditions. endrin is converted rapidly to its major metabolite.20 (<LOD-5. 1996.30) < LOD 5. Endrin is absorbed rapidly after ingestion. Over time. fatty infiltration. Endrin has been detected in soils.40 (<LOD-6. endrin has been detected with declining frequency in U. Survey Geometric mean (95% conf. At high doses. or from contact with contaminated soils and sediments in areas where endrin was applied. and inflammation (Smith. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. 1992). 2008).40-5. have been cancelled by the U. endrin usually is not detected in serum of exposed individuals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Ketoendrin is a major photodegradation product (IPCS.09 and 7. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. All uses of the pesticide in the U.. Kavlock et al.. rodenticide and avicide. manufactured. In the body. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. largely the result of historical agricultural application or run off from contaminated soils (ATSDR.S. unless the dose is high and the exposure is very recent.S. Because it is metabolized so rapidly. EPA. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.Organochlorine Pesticides Endrin CAS No.S..50) < LOD 5. An epidemic of acute endrin poisoning. unlike aldrin and dieldrin.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. Endrin was not widely used as a termiticide. 72-20-8 General Information Endrin.10 (<LOD-5. < LOD means less than the limit of detection.8.60 (5.

. Workplace exposure standards for endrin have been established by OSHA.020 (<LOD-.020 (<LOD-. 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. 2000). Information about external exposure (i. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Ward et al..020) < LOD < LOD < LOD . with the highest value 6.S.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 .S. 98 Fourth National Report on Human Exposure to Environmental Chemicals . serum levels of endrin were below the limit of detection.020) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020-.cdc.. EPA has established environmental standards for endrin. 2004. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.html.020 (<LOD-. environmental levels) and health effects of endrin is available from ATSDR at: http://www.atsdr. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.020 (.24 ng/g of serum) (Botella et al.020 (<LOD-.020) < LOD . Survey Geometric mean (95% conf.. IARC has determined that endrin is not classifiable with regard to human carcinogenicity. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. In a small study of Spanish women hospitalized for elective surgery. endrin was detected in 9% of serum samples. This finding is consistent with other general population studies (Bates et al.Organochlorine Pesticides The U. and the FDA monitors foods for pesticide residues.gov/toxpro2. 2004).24 ng/mL (about 6.e.020 (<LOD-.020 (<LOD-.020) < LOD . Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.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 . Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level.

Patterson DG Jr.gov/~dms/ pesrpts. 4/21/09 International Programme on Chemical Safety (IPCS).96:34-40. Burse VW. Buckland SJ. Andersen A. Rogers E. August 2008. Fetotoxic effects of prenatal exposure in hamsters. Ward EM. Handbook of Pesticide Toxicology. Needham LL. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 1991.cdc.htm. Convulsions caused by endrin poisoning in Pakistan.9:1357-136. Environmental Health Criteria 130.html. Olea-Serrano MF. et al. Toxicology 1981. Fetotoxic effects of prenatal exposure in rats and mice. Toxicological profile for endrin [online].inchem. Gray J. Rowley DL. 4/21/09 Bates MN. Available at URL: http://www. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Chernoff H. In Hayes WJ. 1992. Academic Press.13:155-165. Roy ML. Jr. et al. Frey JM. Schulte P. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.cfsan. Patterson DG Jr. Liddle J. Gray JA. et al. Fourth National Report on Human Exposure to Environmental Chemicals 99 .org/documents/ehc/ehc/ ehc130. Kavlock RJ. Rivas A. Available at URL: http://www. Exposure of women to organochlorine pesticides in Southern Spain. August 1996. Cerrillo I.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Gray LE.79(6):928-934. Inc. Toxicol Lett 1992.html. Gray LE.64-65 Spec. I. Chlorinated Hydrocarbon Insecticides. Turner W. Rab MA. Narahashi T. Smith AG. Perinatal toxicity of endrin in rodents. Crespo J. 2 Classes of Pesticides. Chernoff N. Environ Res 2004.21:141-150. 4/21/09 Kavlock RJ.fda. No:429-436. Endrin [online]. Hardjotanojo W. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Vol. Perinatal toxicity of endrin in rodents.54:1431-1443.atsdr. Garrett N. Sokal D. Ginsburg KS. Hanisch RC. Eds. Hanisch RC. Saleem M. Botella B. pp. Pediatrics 1987. Olea N. New York. Whitehouse DA. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. et al. Jr and Laws ER. Ellis H. II. 731-915. Cancer Epidemiol Biomarkers Prev 2000. Food and Drug Administration (FDA). Available at URL: http://www. Grajewski B. Toxicology 1979. Chemosphere 2004.gov/toxprofiles/tp89.

4 (22.0) < LOD < LOD 15. 100 Fourth National Report on Human Exposure to Environmental Chemicals .2) < LOD < LOD 29. primarily as a fungicide and seed treatment until the U.7 (15.3 (16.8-15. 2. 1997).8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.0 (14.7 (15.4) < LOD < LOD 33.5-18.0) < LOD < LOD 24.4) < LOD < LOD 22.0-19.5 (14.. 2002).3 (14.0) < LOD < LOD 15.3 (22..6 (23.7-16.0 (18.6-44. or game taken from areas with HCB contamination.4 (18.4) < LOD < LOD 18.5-15. and 03-04 are 118.9) < LOD < LOD 20. Gunderson. breast milk is an additional route of elimination in nursing women.7-15. Urinary metabolites include pentachlorophenol (PCP).8 (15.0-28. and sediment (Barber et al.5-TCP) and 2.3-20. measuring HCB in serum is a specific indicator of exposure to the parent Serum Hexachlorobenzene (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0 (25.2 (14.. Although it is not manufactured as an end-product in the U.4-15.9) 19.5 (13.9) < LOD < LOD 19.7 (27. < LOD means less than the limit of detection. distributes widely throughout the body.6) < LOD < LOD 14.9 (25.2-15.7-21.8 (26.4.2) < LOD < LOD 13.9 (14.8. air.2-15.3) < LOD < LOD 29.6) < LOD < LOD 26. 31.2 (14. and foods with a high fat content.6-TCP) (To-Figueras et al.7) < LOD < LOD 24. Survey Geometric mean (95% conf. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. water.3) * * 15.2 (13. and 7.9-17.6) < LOD < LOD 25.3-26. and accumulates in fatty tissues where it persists for years.1 (14.S.4.3) 24.9 (23. HCB is slowly metabolized.Organochlorine Pesticides Hexachlorobenzene CAS No.4) < LOD < LOD 23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Therefore.1 (13.7-30.4. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.6 (24.9) < LOD < LOD 28.0.S.6 (21.9) < LOD < LOD 20.3 (22. The FDA dietary surveys have shown that over time. EPA cancelled its use in 1984.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.7-26. HCB has been detected in fewer foods since the 1980s (FDA.0) * * 15.7-22.6-26.5-15.5-trichlorophenol (2.1-16.9-15.2 (17.5 (13.2 (24.3 (12.6-33.6) < LOD < LOD 24.4.0-16. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28..5-33.2-31. 1976).7) < LOD < LOD 75th < LOD < LOD 90th * * 15.S.3 (20.5-14.0 (18. population from the National Health and Nutrition Examination Survey.6-32. particularly by consuming fish. 1988).8) < LOD < LOD 27. 2005).5-14.4 (11.1 (17.4) < LOD < LOD 19.6-trichlorophenol (2. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4-16.1) * * 15.1) < LOD < LOD 15.0-25. 2008.4.3) < LOD < LOD 20.3-22.4 (18. see Data Analysis section) for Survey years 99-00. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.9) < LOD < LOD 15. and has been detected in soil.1-20.9-24. and elimination occurs by renal and fecal routes.7-16.9-30.9-32.7-29.9 (25.1 (14.8 (22. respectively. wildfowl. The general population may be exposed to HCB through diet.S. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.9-20.7 (19.6) < LOD < LOD 26. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. HCB is well absorbed after oral administration.5) < LOD < LOD 18.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9) < LOD < LOD 16.4) < LOD < LOD 14.6-19.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.7) * * 14.7) 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. 01-02. which may vary for some chemicals by year and by individual sample.

which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.155) < LOD < LOD .176) < LOD < LOD .130) < LOD < LOD .163-. Survey Geometric mean (95% conf.094) < LOD < LOD . as well as hypertrichosis.095) * * .125 (.092 (.111) < LOD < LOD .090 (.S. More information about external exposure (i.203) < LOD < LOD .gov/toxpro2.086) < LOD < LOD . Chronic feeding studies in animals have demonstrated kidney injury.159-. With chronic exposure.147-.091-.092-.077-.094 (.148-.141) < LOD < LOD .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . population from the National Health and Nutrition Examination Survey.090 (.123 (.152) < LOD < LOD .099) < LOD < LOD .102 (. 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.126) . IARC classifies hexachlorobenzene as possibly carcinogenic to humans.095) < LOD < LOD 75th < LOD < LOD 90th * * .114-.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 * * .099) < LOD < LOD . The U.104 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .171 (.095 (.147 (. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.e. very high.156 (.129) < LOD < LOD .114-.143-. In humans.078 (.258) < LOD < LOD .097) < LOD < LOD .081 (.100) < LOD < LOD .123 (.072-.069) < LOD < LOD .163 (. 2002).086-.html.088-.073-.135-.107) < LOD < LOD . 1982.083) < LOD < LOD . EPA at: http://www.163) < LOD < LOD . environmental levels) and health effects is available from the U.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .060-.169-.087 (.118-. anorexia.179 (.097 (. arthritis.191 (.157-.092 (. and many died before 2 years of age (Peters et al.S.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. immunologic abnormalities. and the FDA has established a bottled water standard for HCB. Infants were exposed transplacentally and through breast milk.118-.186 (.203) < LOD < LOD . Schmid..atsdr.178-.065 (.196) < LOD < LOD .088-.145-.062-.090 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/pesticides/ and from ATSDR at: http://www.069) * * . and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.225 (.090-.127-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.115 (. HCB interferes with normal heme synthesis.064 (.095-.122) < LOD < LOD .082-.107-.182 (.102) < LOD < LOD .113-.167 (.123 (.092 (. 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.099) < LOD < LOD . This condition.095 (.081-. acute doses produce central nervous system depression and seizures. and liver and thyroid cancers (ATSDR.175) < LOD < LOD .089-.157 (. Biomonitoring Information Serum concentrations reflect the body burden of HCB.085) * * . which may vary for some chemicals by year and by individual sample. ACGIH has developed workplace exposure limits for HCB. 1960). reproductive and developmental toxicities.079 (.140 (.088-.cdc. EPA has established a drinking water standard.118) < LOD < LOD .145-.176-.S.epa. and weakness.086-.121 (.085-.190 (..111-.097) . Fourth National Report on Human Exposure to Environmental Chemicals 101 .109) * * .173) < LOD < LOD .Organochlorine Pesticides chemical.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 * * . thyromegaly.174-.089-.120 (.160 (.098 (.132) < LOD < LOD .

Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Lecha M.html. Schulz C. Sala M. et al.349:144. Available at URL: http://www. Jones D.. J Exp Sci Environ Epidemiol 2007.81(2):82-85. HCB levels were directly related to age. Hexachlorobenzene in the global environment: emissions. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al.44 mg/L. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Gocmen A. Lackmann.205:297-308.58:1185-1201.cdc. Atuma S.9% of participants had quantifiable levels (Stehr-Green. Barr DB. Lepom P. 2002. FDA total diet study. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Dogramaci I. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. April 1982 to 1984.. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.. Lackman. Muckle G.71(6):1200-1209. In a representative sample of the 1998 German adult population. 2002.77:173182.. Toxicological profile for hexachlorobenzene update [online]. 1989). Seiwert M.cfsan.. Chemosphere 2005. HCB detection in serum also was proportional to age. The metabolism of higher chlorinated benzene isomers. Arch Neurol 1982. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. more HCB levels were quantified. 2002. In Spain.. 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. Food and Drug Administration (FDA). Bryan GT. selected elements. 2002) and among children (Link et al. Bradman A. 4/21/09 Glynn AW. Otero R. 4/21/09 Barber JL. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. and other chemicals. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Bradman et al. Holland NT.. Schwartz JM. Granath F.gov/ toxprofiles/tp90. Dallaire F.fda. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Darnerud PO. Santiago-Silva M. Cripps DJ. 2006). Herrero C.. August 2008. As a result of the lower limit of detection in NHANES 2003-2004. Dewailly E. 2002). Int J Hyg Environ Health 2002. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. dietary intakes of pesticides. only 4.. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.111:349355. Environ Health Perspect 2003. Sci Tot Environ 2005.. Kemper FH. Gunderson EL. In the 1976-1980 NHANES subsample. Kaus S.gov/~dms/ pesrpts. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Bertram et al. 102 Fourth National Report on Human Exposure to Environmental Chemicals .54(3):203-208. Link et al. Zoellner I. et al. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. 2003). FDA Pesticide Program Residue Monitoring 1993-2006 [online]. IARC Sci Publ 1986. respectively. Arch Dermatol 1999. Sweetman AJ. 1986. J Assoc Off Anal Chem 1988. Available at URL: http://www. and the geometric mean concentration of HCB in whole blood was 0. Krause C. September 2002.html. Safe A.39(12):744-749. Biol Neonate 2002. Kohli J. Lawrence River (Quebec. however. Ayotte P. Becker K. References Agency for Toxic Substances and Disease Registry (ATSDR). German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 2005. 2005). but overall. Organochlorines in Swedish women: determinants of serum concentrations. Bertram HP. Laliberte C.. Jones KC. levels. Gabrio T. Peters HA. Muller C. Environ Health Perspect 2002. Paepke O. Fenster L.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. 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. Aune M. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Lackmann GM.135(4):400404. Glynn et al.atsdr. Over the past two decades. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Reference values updated.110(8):835-838. Piechotowski I. et al. Herrman T. 2002. Bjerselius R. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Eskenazi B. van Wijk D. trends and processes. 1999). Biomonitoring of persistent organochlorine pesticides. Ozalla D. distribution. Canada). 2005). Can J Biochem 1976. Link B.17:388–399.

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

2-52.0 (37.9) 17.9 (40.9) 15. and 7.6-37.60-13. In 2006.9-56.9-51.3 (62.04-10.8) 7.9-24.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.2 (29.S. so they can accumulate in fatty tissues of animals.7-69.4 (11. However.2-20.76.0-23.5 (43.9 (32.3) 25.3 (42.5 (16.4-111) 84.2) 36.1 (9.7 (<LOD-16.4 (52.87 (9. which may vary for some chemicals by year and by individual sample. containing about 64% alpha and 10%-15% gamma isomers.0 (19.6-20. 2005).7 (29.7) 23.6 (16.8) 12.6-42.8-16.4 (50.3-56.9 (26.4 (8.1 (11.0) 71.1) 31.3) 14.1 (18.7 (35. 608-73-1 beta-Hexachlorocyclohexane CAS No.3) 34.4-50.7) 56.5) 67.43 (<LOD-9.6) 16.5 (24.1-36.7 (62.3 (13. including alpha.5-29.9 (62.46-11.8 (64.2-67.6-135) 69. respectively.7-166) 70.7) 73.6 (33.6-47.7) 10. see Data Analysis section) for survey years 99-00.5) 14. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.4) 21.3 (26.6-62.5) 11.8) 39.4) 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. beta.89 (<LOD-9.1 (12. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.6) 47.5 (11.4) 901 1067 952 992 1224 1007 Females 11.S.2 (50.2 (9.5528.0-20.7 (53. EPA cancelled agricultural uses of lindane (ATSDR.9 (50.4-45.0-34.6 (17.6) 18. 104 Fourth National Report on Human Exposure to Environmental Chemicals .66-12.7) 18.0 (8.5) 22.1-16.70-19.5) 90th 42.6-18.0 (<LOD-12.9-21.90-8.8) 95th 68.0-70.5 (8.8 (10.8) < LOD 10.70-12. interval) 9. formerly referred to as benzene hexachloride.0) 8.8) 52.0 (14.1 (30.3) 51.70 (8. soil.70 (6.8 (33.0 (33.90) 7.9-81. the U.6) 35.0) 7.8-199) 134 (85. environmental levels declined. and sediment as a result of historic production and use.6) 50.0) 17.1-49.8 (23.3 (42. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.1) 13.4) 51.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.2-55.30-11.5 (37. and 03-04 are 9.4 (16.2 (18.4) < LOD < LOD < LOD 46. Lindane has a half-life of about two weeks in soils and water.6-89.9) 45.3) 37.4) < LOD 9.8-54.2-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.56-12.9 (11.1-15.4) 10. and delta. The other isomers can be formed during the synthesis of lindane.7) 10. HCH isomers are lipophilic.2-22.9 (30.8-68. exists in several isomeric forms.2-98. **In survey period 2001-2002.8 (32.2-42. 319-85-7 gamma-Hexachlorocyclohexane CAS No. each result has been multiplied by 1.2) 142 (99.1-32. 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. particularly alpha and gamma have been detected widely in air.1 (27.5) 40.0-21.5) 16.6 (22.2 (48.8 (17.2 (31.2) 62. The gamma isomer.6 (40.0-70. It is no longer produced or sold in the U. 2005).2) 13.8) * * * * * * 15.2-87.8 (9.6-14. See the section “What’s New” at the beginning of this Report for details.8 (21. 01-02.2-46.61-12.2) 9.4) 27.0-111) 70.1) 71.Organochlorine Pesticides Hexachlorocyclohexane CAS No.7-26.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.68 (<LOD-10. and have been used either as fungicides or to synthesize other chemicals.5 (14.36.20-16.8.8-87.7 (25.3-85.7-20. population from the National Health and Nutrition Examination Survey.80 (6.6 (10.S. HCH isomers.9) 81.4 (12.7 (30.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.0 (35.6) 36.90-8.7) 27.6) 653 758 589 1240 1533 1370 20 years and older 10.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.1 (9.7-69.5-123) 49.8-19. water. Technical grade HCH is a mixture of all four isomers.1-37.1 (21. As pesticide applications of HCH were increasingly restricted or eliminated.80 (<LOD-14. commonly known as lindane.1) 12. < LOD means less than the limit of detection.4-73.9-14.1-32.5) 29.4) 44.0) 35.9-178) 48.7-96. 6.7) 97.7 (13.1-27.50) 8.9 (9.2 (34.0) 41. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. gamma. 58-89-9 General Information Hexachlorocyclohexane (HCH).7) 32.3-38.4) 11.1) 12.8) 27.1 (16.7-96.

FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.067) .290 (. After dermal application of lindane 1% lotion.062 (.080-.220) .5528.400) ..250 (.580 (.S.130 (.290) .140) .057-..058 (<LOD-.260-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.910 (.270 (.140) .057-.690) .700) .710) ..300-.360 (. Distribution is mainly to fatty tissues.297-.191-. The beta isomer accumulates in fatty tissues and is metabolized more slowly.305) .221-.120-.086) < LOD < LOD < LOD < LOD < LOD < LOD .372 (.S.090 (.170-.280-.230-.090-. Rogan. respectively.070 (.210 (.080) * * * * * * .077) < LOD .250-.057 (<LOD-.560 (. OSHA and ACGIH have established workplace standards and guidelines. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.570 (.120) .050-. **In survey period 2001-2002.146-.103-.120-.160) . tremors.170-.37) 1.040-.175 (.200-. 2008.250 (. When animals were chronically fed lindane at high doses.287 (.050 (<LOD-. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.080 (.150 (.190) . which may vary for some chemicals by year and by individual sample.050-. 1983). each result has been multiplied by 1.410) .210) .290) .340) .05) .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 . HCH isomers are absorbed after inhalation.080-.059-.420-.083) . paresthesias.083 (. or dermal exposure.Organochlorine Pesticides exposure to HCH is through the diet.103) 90th .308-.410 (. 1977). EPA has established a drinking water standard.240 (.051-. The U.125) < LOD < LOD < LOD .118 (.319) .144 (.190-.089) .814) .140) .092 (.047-.460 (.460) .077) < LOD .510) .210 (.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .310 (. 2002).100-.050 (<LOD-. ataxia.220-.290 (.250) .110) .140 (.210-..065 (.091) .234 (. 1981).680) .480) .450 (.072 (.056-.110) .064 (.480 (. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.100-.587) 653 758 589 1240 1533 1370 20 years and older .100 (.090 (.124-.. Gunderson 1988). ingestion.450) .620) .120-.320 (.173-.294-.139 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. enlarged livers. See the section “What’s New” at the beginning of this Report for details.501) .070) .370-.600) .120) .069) .410-.260) .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.840) .080 (.100) .150) .281 (.330 (.090 (.130) . interval) .110) .254) 95th .661) 901 1067 952 992 1224 1007 Females .096) .260) .580-1.480 (.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.120 (.470) .410) .070-.220-.131-.068-.130-.118-.073-.32) .330-. Saxena et al. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.310) . resulting in a half-life of about seven years. 1971.220 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.560) .119) .190-1.050-. and FDA has established a bottled water standard and food residue tolerances for lindane.280-.048 (<LOD-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.081-.078 (. Workers who directly handled HCH have complained of headache.450-.382-.390-. hepatic enzyme induction.240-.100-.120 (.167 (.620-1. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity. and seizures. and memory loss (Nigam et al. Fourth National Report on Human Exposure to Environmental Chemicals 105 .150) .290 (.098 (.310) .360) .222 (.521 (. probably by blocking inhibitory neurotransmitters in the central nervous system.214) .470 (.110-.244-.331 (. population from the National Health and Nutrition Examination Survey.056-.060) .180-.191-.S.390 (.160 (.150-.250-.360-.065 (.070 (.200-.412 (. the serum half-life was about 20 hours among children (Ginsburg et al.160-.050-.080-.070-.350) .067 (.01 (.051 (<LOD-.089-. 1986).350 (.380 (.174) .050 (.103 (.400) .200 (.070-.442 (.216 (.190) .050 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .100 (.120 (.050) .064) . for lindane.404) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th . 1996.100) .062 (.080) . U. and nephropathy developed (IPCS.340-.

1998. EPA at: http://www. 1991. 2005.5. 10. 2002. Becker et al. male sex. 2004. the maximum and 95th percentile beta-HCH values.. 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. serum levels of lindane were generally below the limits of detection. respectively. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al.html. 2001-2002. In recent years. were similar to the 95th percentiles in this Report. Radomski et al. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens... Stehr-Green. and 03-04 are 14.e. Sturgeon et al. 1989. Link et al. 1971.. see Data Analysis section) for Survey years 99-00. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al.. 1998). 2004) and India (Bhatnagar et al.. 2004). Survey Geometric mean (95% conf.cdc.. In an earlier (1996-1997) sample of German children. Kutz et al.. In NHANES 1999-2000.5. More information about external exposure (i. 2002). and 7. and 2003-2004.gov/pesticides/ and from ATSDR at: http:// www.epa. aged 9-11 years. Biomonitoring Information Because of its longer half-life. 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. 106 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Additional factors associated with higher beta-HCH levels include rural residence. 1989). beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. < LOD means less than the limit of detection.. respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. older age.8.gov/toxpro2. population from the National Health and Nutrition Examination Survey. environmental levels) and health effects is available from the U..S. Bates et al. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR.atsdr. 01-02. and a diet that includes meat (Becker et al. In populationbased studies of New Zealand adults and German adults and children.S. Kutz et al..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. which may vary for some chemicals by year and by individual sample. 1991.. Stehr-Green.

S. Radomski et al. in this Report (Nigam et al. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. Fourth National Report on Human Exposure to Environmental Chemicals 107 .. which may vary for some chemicals by year and by individual sample. Beta-HCH and lindane levels in workers involved in HCH production have been more than 1000-fold higher than the 95th percentile and limit of detection (lipid adjusted). the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. 1986. Survey Geometric mean (95% conf. 2003)... population from the National Health and Nutrition Examination Survey. In a small study of adults who consumed sport fish from the Great Lakes. 2005). respectively. 1971). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 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. 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.Organochlorine Pesticides 2001-2002 survey period (Link et al. 1998).

9(4):417-424. Stehr-Green. Aune M. Arch Toxicol 1981. Arch Pediatr Adolesc Med 1996.52(1):59-67. Link B.106(5):279-289. Gunderson EL. Atuma S. org/documents/jmpr/jmpmono/2002pr08.54:1431-1443.71(6):1200-1209. Available at URL: http://www. Biomonitoring of persistent organochlorine pesticides. Maass R. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Int Arch Occup Environ Health 1986. et al. Granath F. Reisch JS.html. Needham LL. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.20(2):186-193. Occupational exposure to hexachlorocyclohexane. selected elements. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 4/21/09 Anderson HA. J Toxicol Environ Health 1989. Olea-Serrano MF.48:127-134. et al. Burse VW. Int Arch Occup Environ Health 1983. Glynn AW.205:297-308. Bull Environ Contam Toxicol 2004. HCH. Bhatnagar VK.96:34-4Food and Drug Administration (FDA). Organochlorines in Swedish women: determinants of serum concentrations. Piechotowski I. Heinrich R. Zaidi SS. Int J Hyg Environ Health 2002. Chemosphere 2004. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Deichmann WB.cdc.72:261265. Lindane. Demographic and seasonal influences on human serum pesticide residue levels. Potischman N. The Great Lakes Consortium. Visweswariah K. Krause C. Zoellner I. Bates MN.120:1-82. VI. Radomski JL. Needham LL. 2002. Brock JW. Raju GS. 4/21/09 Kutz FW. Pollutants in breast milk. Saiyed HN.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Darnerud PO. Astolfi E.atsdr. Rev Environ Contam Toxicol 1991. et al. Garrett N. Seiwert M.cfsan. August 2008. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Environ Health Perspect 2003. August 2005. Bottimore DP. Rey AA. Kashyap R. Metabolism of gammahexachlorocyclohexane in man. International Programme on Chemical Safety (IPCS). Nigam SK. Siddiqui MKJ. Toxicological profile for hexachlorocyclohexanes update [online].111:349355. Angerer J. et al.27:405-421.htm. Lowry W. Becker K. J Assoc Off Anal Chem 1988. Bai KM. J Pediatr 1977. Rogan WJ. Patterson DG Jr. PA. gov/toxprofiles/tp43.57(4):315-320.91:998-1000. and HCB residues in human blood in Ahmedabad. April 1982 to 1984. Olson J. Brinton LA. et al. Falk C. Botella B. Available at URL: http://www. et al.gov/~dms/pesrpts. Majumder SK. Bjerselius R. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. dietary intakes of pesticides.inchem. Lepom P. Exposure of women to organochlorine pesticides in Southern Spain. Ellis H. Needham LL. Bhargava AK. and other chemicals. Saxena MC.fda. Kutty D. available at URL: http://www. Cerrillo I. Environ Res 2004. Herrman T. Environ Health Perspect 1998. Karnik AB. Gabrio T. Buckland SJ. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Absorption of lindane (g benzene hexachloride) in infants and children. Chemosphere 2005. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Rothman N. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Sturgeon SR. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Toxicol Appl Pharmacol 1971. Hanrahan L.150:981-990. Olea N. Rivas A. children and newborn infants. Crespo J. India.58:1185-1201. Schulz C. Paepke O.html. Wood PH. 4/21/09 Ginsburg CM. Krishna Murti CR. Kulkarni PK. Levels of DDT. et al. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). FDA total diet study. Kaus S. Placental transfer of pesticides in humans. Cancer Causes and Control 1998.

Formerly. Occupational exposure is limited to workers at sites where mirex contamination is present.8 (12. water. where it has a half-life of 12 years.7 (<LOD-47. especially those from persons living in the southeastern U. population from the National Health and Nutrition Examination Survey..S. resulting in exposure to newborns and nursing infants.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. 2385-85-5 General Information Mirex has not been produced or used in the U. and 7.2-230) 13. Mirex has been detected in air.6 (<LOD-23. and foods. Mirex binds strongly to soil. which may vary for some chemicals by year and by individual sample. and 03-04 are 14. mirex was detected in human adipose samples. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. 1995).70-24.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. where it was applied directly to soil and by aerial spraying.6 (<LOD-31.0) * * * 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 19.1 (8. Fourth National Report on Human Exposure to Environmental Chemicals 109 . 1991).6 (<LOD-108) 9. Survey Geometric mean (95% conf. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8) < LOD 15. Some states and the U.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..S. 1985.0 (14. after which it is widely distributed in the body and stored in fat.6-305) 15.40 (<LOD-13.5 (<LOD-115) 153 (30.S.S.S.7) 8.6) 9.1) 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. 01-02. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. sediments.2) 51. animals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Mirex is not metabolized in the body. (Kutz et al.8 (<LOD-73. see Data Analysis section) for Survey years 99-00.0 (<LOD-108) < LOD < LOD 50. or pesticide application.10-37.5-291) 11.5 (<LOD-42.2 (7.5 (9.5-425) 40.90-29.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.Organochlorine Pesticides Mirex CAS No. 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.4 (8.8.5-82.6.3 (15.0 (12.10 (<LOD-15. it is a highly persistent chemical in the environment.4) < LOD 15. < LOD means less than the limit of detection. since 1977.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.1 (<LOD-65. respectively. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. disposal.70 (<LOD-15.6) < LOD < LOD < LOD < LOD 71.3-225) 15.70-40.7 (12.4) < LOD 63.1 (13.7) < LOD 66. Mirex can cross the placenta and be excreted in breast milk.3 (15. Mirex is absorbed through the skin and from the gastrointestinal tract.0-374) 11. soil. aquatic organisms. 10. In studies conducted in the 1970’s and 1980’s.5.4-230) 18.

170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .077 (<LOD-. environmental levels) and health effects is available from the ATSDR at: http://www. EPA has established environmental standards for mirex. 1991). More information about external exposure (i.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 . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.053-. 110 Fourth National Report on Human Exposure to Environmental Chemicals .310 (.41) . which may vary for some chemicals by year and by individual sample.html.610) < LOD < LOD < LOD < LOD . IARC classifies mirex as possibly carcinogenic to humans.055-.Organochlorine Pesticides exposures are unknown.106) < LOD .100 (<LOD-. In addition.635) < LOD .064 (<LOD-.690) . 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.02) .268) < LOD .cdc.052-.08 (.79) . Biomonitoring Information In the NHANES 1999-2000.080-1.470) ...73) . The U.062-.gov/toxpro2. 7.106 (. The geometric mean mirex levels of the Inuit mothers were 8.090 (<LOD-. Laboratory animals fed high doses developed liver enlargement and liver tumors.108 (.070-1. 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.. reproductive toxicity included decreased fertility and testicular damage.090-1.174) 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.470 (.089-.090-1. 1989).430 (. and 4.370 (.170) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. 2005).102) < LOD < LOD < LOD < LOD .100 (<LOD-.92) .450) 1.220) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .37) . as well as in a subsample of NHANES II (1976-1980) participants.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 . serum mirex levels were generally below the limits of detection (Stehr-Green.79) .112 (. Smith.110 (<LOD-.093 (. Survey Geometric mean (95% conf.080-1. 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. 2001-2002.090 (<LOD-.059 (<LOD-.090-1.079 (<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.256 (.e.090 (<LOD-.470) . and NTP classifies mirex as reasonably anticipated to be a human carcinogen.140 (<LOD-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.510) < LOD < LOD . In samples obtained between 1994 and 1997. 2004).7 ng/g of lipid.054 (<LOD-.450 (. and 2003-2004 subsamples.atsdr.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 .170-3.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .220 (<LOD-.410 (.8. population from the National Health and Nutrition Examination Survey. 1995.S.

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

Survey Geometric mean (95% conf.0) < LOD 5.00 (2.0) 2.0) < LOD 21.0 (8.0) < LOD 11.6-TCP).40-18.950 (<LOD-1. Trichlorophenols are no longer manufactured commercially.40 (2.5-Trichlorophenol CAS No.10-3.27) 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 1.72) < LOD 1.8) 21.50 (1.40 (1.42 (<LOD-12.60 (2.19 (<LOD-6.00-3.50-63. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.20 (4.30-27.50) < LOD 1.30-44.50 (2.4.0 (5.0 (4.40-11.40 (1.5-Trichlorophenol 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..0) < LOD 11.50-16.4.0) 2.0) 2. 1999).40) < LOD 4. 112 Fourth National Report on Human Exposure to Environmental Chemicals .20) < LOD 90th 5. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.50 (.00 (3.5TCP and 2.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.80-41.0) < LOD 5.42 (<LOD-8.30-27. EPA. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0 (3.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.50-25. surface water. 2006). however.20) < LOD 1.9 and 0.6-TCP were used as intermediates in the production of certain pesticides.6-Trichlorophenol CAS No.00-8. are metabolites of several organochlorine chemicals.40) < LOD 6.60-8. Formation of 2.0) < LOD 5. which may vary for some chemicals by year and by individual sample.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .5-TCP) and 2.30) < LOD 4.40 (2. Both chemicals have been detected in air.4.20-71.9. population from the National Health and Nutrition Examination Survey. public drinking water systems did not detect 2.4.30-40. including hexachlorobenzene and hexachlorocyclohexanes. 95-95-4 2. Historically.30 (.31 (<LOD-9.60) < LOD 8.900-2.4.980-3.40 (2. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.S. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.40 (2. soils.0) 14.63) 18.20) < LOD 5. other organochlorines.20-36. < LOD means less than the limit of detection. 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.71 (<LOD-8. 2. recent sampling of U.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.40 (. 1976). and sediments.4.60 (4.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.30-3.4.57 (<LOD-15.71 (<LOD-8.80 (1.0) 2.5-trichlorophenol (2.S. and polychlorinated benzenes (Kohil et al. may occur by inhalation or dermal routes.30) < LOD < LOD < LOD < LOD < LOD 1.30-27.6-trichlorophenol (2.4.80 (2.Organochlorine Pesticides 2.S.27) 696 661 521 696 603 939 Limit of detection (LOD.5-trichlorophenol. 2.80) < LOD 1. 1999).6-TCP in any of the samples (U. Such workers would probably Urinary 2.30-11. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. 2.0) 2.9 (<LOD-121) 9.0 (4. Exposure to trichlorophenols also may result from metabolism of lindane.920-3.980-3.03) 9.7) 24.0 (3. usually at herbicide production or waste incineration facilities.4.60-18.0) 5.00-3.940-3.3.60 (.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7.0 (4.4. Occupational exposures.40) < LOD 1.90-33. hexachlorobenzene.4.0) 2.40 (.

interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. 1989). 2003.86 (3.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Neither 2.29 (1.24) < LOD 1..4.5-TCP and limited for 2.82 (<LOD-32.9) 12.4.88-16. At lower doses. environmental levels) and health effects is available from ATSDR at: http://www.6) 4.69-18.4.S. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.13-13.4.6-TCP. More information about external exposure (i.55 (4. animals showed hepatocellular abnormalities.4.3 mg/L reported in German adults aged 18-69 years (Becker et al.67 (1. Fourth National Report on Human Exposure to Environmental Chemicals 113 .80 (1.02-3.05-8.37) 16.53-3.16) < LOD 90th 5.33) < LOD < LOD < LOD < LOD < LOD 2.6-TCP had increased rates of hepatic tumors.79-4. population from the National Health and Nutrition Examination Survey..62-20.69 (2.5-TCP or 2.43) < LOD 12.78) < LOD 1.00) < LOD 4.93-11.15) < LOD 2.. However.0) 7.6-TCP as reasonably anticipated to be a human carcinogen.4) 5.920-2.44 (.17) 9.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .4. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.02) < LOD 7.95 (3.44 (1.28-25.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).atsdr. 2004).4. furans. in addition to dioxins.78-19. 2003). which includes trichlorophenols.5) 11.4.820-2. the 95th percentile urinary 2.1) 2.8) < LOD 9. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.73 (<LOD-8.19-12.4. Human health effects from 2.83-12.4) < LOD 3.47-8. In the same 2-6 year old children.90 (4.19-4.24-11.0 mg/L.4.html.57 (3. and other chlorinated compounds.67 (1.00-29.6) 4. 7.24) < LOD 6.24 (3.53-3. Laboratory animals chronically fed high doses of 2.. urinary 2.5-TCP.81 (<LOD-9.6-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.75 (3.8) 4.2) 2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary 2.9 (5.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.32) < LOD 4.50) < LOD 2. The 95th percentiles for 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.4) < LOD 3.20-6.43 (2. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.e.68-4.4. 1995) and up to 19 times higher than the 95th percentile value of 1.Organochlorine Pesticides be exposed to mixtures of chlorophenols.60-3. 1989). NTP classifies 2. and lymphomas. leukemias.4 (6.74) 11.64 (4.24) < LOD 5.37-11. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.6) 4.68 (<LOD-8.27-17.8 (5.75 (<LOD-6.46 (1.2) < LOD 5.5-TCP nor 2.6-TCP levels at the 95th percentile were up to eight times higher than 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.16 (..980 (<LOD-1. IARC classifies combined exposures to polychlorophenols.7 (4. Radon et al.gov/toxpro2. 2003).3 (5.78 (3.. Survey Geometric mean (95% conf.36 (1.31) < LOD 2.5) < LOD 12.cdc.4.4. as being possibly carcinogenic to humans. 1995) were similar.1 (<LOD-58.57 (<LOD-7.00-19.49 (1.05-17.2 (2.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2..57 (<LOD-7.. the 95th percentile urinary 2. Among 6-11 year old children in NHANES 1999-2000..

6 mg/g creatinine) and 2.40 (2.69 (3.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.0) 11.6-TCP (0.80-20.36 mg/g creatinine.40-2.1-25. 2003).5 mg/g creatinine) were similar to the limit of detection for 2.80-7.50-5.6TCP causes an adverse health effect.20) 4.8-24.45 (5.0 (14.4 (8.7-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.98-11.0 (14.60-21.48-26.92 (2.55-3.6-TCP level.40-32.52 (2.8) 18.9) 13.5-TCP and to the median 2.52-3.78 (2.53) 4.4.18-3.00 (4.0) 10.0) 12. the median urinary 2.70-6. In harbor workers exposed to chlorophenol-contaminated river silt.0) 7.30-2.70) 3.66 (8.4.89-6.40-4.0 (8.4. which may vary for some chemicals by year and by individual sample. Biomonitoring data will also help scientists plan and conduct research about 2.60 (3.67) 4.04) 2.53) 2.0) 14.4.70-6.12) 2.7 (9.47 (3.40) 2.14 (2.40-2.3) 23.4.90-8.57 (<LOD-2.0 (15.10 (5.08 (2.0) 13.54) 6.20 (3.51-12.07 (<LOD-3.40) 2.59-6..0) 13.40) 3.65) 15.23) 3.0 (14.40) 4.5-46.90) 2.70 (2.80) 1.1 (10.0) 14.01-6.30-33.4.06) * 2.4.70) 1.30) 4.30-11.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.28) * 2.58-3.8 (9.20 (3.87-14.0 and 1.40 (2.0) 19.0 (8.00 (1.4. < LOD means less than the limit of detection.35-3.70 (2.60-37.80 (2.84) 2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.4. was about six times lower than the median urinary levels for males in this Report (Radon et al.60 (3.4.5-TCP and 2.10-2.0 (6.31 (3.56 (3.0-37.4.0-54.0-38.85 (2.0 (13.4. Biomonitoring studies on levels of 2.95) 3. population from the National Health and Nutrition Examination Survey.0 (20.5-TCP (0.80-25.28) 24.7 (13.6 (11.5-TCP or 2.90 (4.32-4.26 (2.0) 19.63) 90th 15.5-TCP level of 0.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.00 (2.4 (9.4.4 (17. Urinary 2.0-44.32) 3.3) 20.3.95-6.60) < LOD 5.74 (2.6-TCP in urine does not mean that the level of 2.89 (3.0 (11.S. Survey Geometric mean (95% conf.7-3.10) 2. 2004).58 (1.6 (12.0) 17.8) 32.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.6) 21.6-19.4.45-9.44) 75th 4.33-4.80-6.90 (3.2) 12.1 (8.7) 33.02) 2.0-18.60) 6.79 (5.4.4 (10.30-2.0) 9.70-3.9 (13. 1998).45) < LOD 11.32) * 3.91-4.10) 6.2 (14.99) 6.6) 26.9) 694 677 519 696 602 931 Limit of detection (LOD.6TCP values.3 (11.23-2.0 (6.00-21.20-23.76) 3.0-50.0) 17.4.0) 15.70) 5.4.0 (4.4. Urinary 2.0) 7.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.0) 6.9 (11.3 (11.36 (1. Mean values of 2.5-TCP or 2.5-TCP or 2.50 (2.3-17. respectively. interval) 2.0 (9. similar to the limit of detection for this Report (Anderson et al.0 (16.7) 21.65 (5.40-7.25-11.20-6.59) 4.0-41.73-9.3-26.2-0.5-TCP or 2.0 (20.0-43.6-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.8-15.0) 13.0 (12.75 (8.09-7.4-17.10-3.40-14.72-10..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 2.70) 5.98-7.45 (2.7 mg/L.20-3.3) 37.09) 15. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.2) 25.36-5.0 (15.4.0) 9.68 (<LOD-2.80 (3.74-3.95 (4.6-TCP than are found in the general population.1) 16.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.0) 10.80 (2.46-3. 0.0) 11.0-68.23) 2..60-3. 1991).. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60 (2.78 (2.6-TCP exposure and health effects.0 (7. for males in NHANES 19992002 (Agramunt et al.85) * 3.0-38.6-22.6-17.31) * 2.0 (6.24 (2.4.8-13.49 (6.0) 13.00-4.67-12. 114 Fourth National Report on Human Exposure to Environmental Chemicals . Finding a measurable amount of 2.10-3.5-TCP and 2.

41 (3.91 (7.42) 2.8) 12.0) 8.50 (2.1) 14.15 (1.10-9.87) 2.55-2.5-28.77-4.53-11.9) 8.4.00 (2.3-37.06-2.6) 8.81) 2.16-10.9) 7.65-2.51-21.3 (9.26 (6.00 (3.70-9.65-21.53) * 2.88) 4.40 (7.6 (9.22 (3.9-64.23) 4.83-5.30-2.76-8.19-5.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.32-19.33 (7.91-2.73-22.2 (8.25-15.2 (12.02) 3. Survey Geometric mean (95% conf.33 (1.66-4.8) 21.51 (2.32 (2.04-2.88) 4.13 (1.72) 32.94-13.62-15.04-16.35 (3.67-17.52) 2.28-4.8 (8.53 (3.60 (4.98 (1.88) 1.9-32.95-2.63) 4.4) 8.82-2.90) 2.1-32.9 (9.10 (6.0) 10.3) 8.00) 4.63) * 4.5) 11.43 (2.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.5) 8.33) * 2.8) 19.53) 4.25 (3.72-16.2 (13.63-15.18-4.76) 1. interval) 2.0 (6.6) 12.41-6.76) 4.90 (1.0 (9.00) 4.18-2.3-23.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.56) < LOD 11.06) 4.2) 19.1-21.1 (8.52 (5.1 (13.8 (7.7) 25.9-29.73) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.52 (3.78) 2.81-9.50-8.82 (8.6 (5.22 (<LOD-2.60-2.5) 9.56-5.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.21-11. population from the National Health and Nutrition Examination Survey.1) 11.98) 10.51) 18.9-34.99-2.5 (10.91 (3.40 (2.88-7.5 (8.87-7.09-3.83-6.88) * 2.6 (10.4) 9.77) 2.14-13.27-9.26-13.02 (1.54 (2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.4) 4.17-4.6) 13.96) < LOD 4.25-2.59 (2.63-13.76) 2.83 (3.89) 10.6 (9.5 (7.9 (9.14-2.46-14.65) 2.7 (14.10) 4.05 (3.68) 2.65) 18.56 (7.4 (11.38) 22.5) 11.23 (1.22-2.44 (3.49-3.11) 10.75) 75th 4.29 (6.7-36.82 (3.S.43-7.13-6.78) 90th 12.43 (<LOD-2.87-6.25-17.17) 2.9) 19.08-2.82) 2.6 (6.48-2.52) 2.15 (6.83-6.42 (2.88) 5.20-2.24 (1.49) 4.87) * 2.58 (4.05 (6.0 (11.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.5) 12.79-17.63 (2.9) 8.4 (12.7) 6.6 (12.25 (3.38-5.71 (3. Fourth National Report on Human Exposure to Environmental Chemicals 115 .22-9.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.29-4.92) 4.38 (4.6-31.2 (7.33-2.68) 2.29-4.01 (3.8) 11.47-5.Organochlorine Pesticides Urinary 2.63 (<LOD-2.87 (3.89-2.22 (1.78 (2.06) 11.17) 13.88 (2.6 (22.38 (2.

S. 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]. Domingo A. Hanrahan L. Toxicological profile for chlorophenols [online]. The Great Lakes Consortium. Poschadel B. U. Shealy DB. Head SL.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Environ Res 1995.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).pdf. Int Arch Occup Environ Health 1991. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.146:83-91. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Domingo JL. Chlorophenol exposure in harbor workers exposed to river silt aerosols.gov/toxprofiles/tp107. Available at URL: http://www. Baur X. July 1999. Heinrich-Ramm R.106(5):279-289. Available at URL: http://www. Urinary excretion of chlorinated phenols in saw-mill workers. Fast DM. Needham LL. et al. Lindroos L. Hill RH Jr. 206:15-24. 4/21/09 Agramunt MC. Environ Health Perspect 1998. Burse VW. Anderson HA. Seifert B. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Wegner R. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .45:440-445. Jarvisalo J. Jones D. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Baker S. The metabolism of higher chlorinated benzene isomers. Smith SJ.71:99108.cdc. Aitio A.18(4):469-474. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Szadkowski D.epa. Arch Environ Contam Toxicol 1989. December 2006 Draft.EPA). Holler JS. Gregg M. Becker K. Toxicol Lett 2003. Seiwert M. et al. Kohli J. Int J Hyg Environ Health 2003.S. Pekari K. Schulz C. Luotamo M. Corbella J.atsdr. Can J Biochem 1976. Environmental Protection Agency (U. Needham LL. Radon K. html. Safe A.63:57-62.54(3):203-208. Am J Ind Med 2004. Bailey SL. To T. Falk C. Olson J. Kaus S. Hill RH Jr.

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

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

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

and 03-04 are 0.70) .0-27.4 (7.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3) 14.99 (5.00-19.90) 3.14) * * .2.4 (7.93 (4.955 (.72) 5.70 (4.91) 4.1-23. population from the National Health and Nutrition Examination Survey.55-8.2) 16.80-24.80-22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 9.74 (8.89) 9.8) 7.52) * * 1.10) < LOD .0 (12.55-6.00-27.90-4.0 (6.70) < LOD < LOD 1.42-3.4) 18.34-7.20 (.19) 9.30-4.8 (9.8-32.90 (1.97) 8.757-2.840-1.717-1.37 (3.30 (2.34-3.0 (9.82-12. which may vary for some chemicals by year and by individual sample.579-1.0) 11.53) 4.81) 11.13 (2.20-30.40-14. 01-02.70-11.54 (3.780) < LOD 3.98-12.2 (7.0 (8.60) .600 (<LOD-1.3) 17.9-18.12) 4.2 (9.50 (2.1) 13.74 (8.23-5.2) 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 1.00-12.4) 17. and 0.94) 3.79 (5.16) 4.2.13-2.750-1.830 (<LOD-3.50 (4.8) 11.4 (9.00) 3.71-9.08-15.90-5.90) 2.670-1.81) 1.80) 3.758-1.6) 18.0) 6.50) 2.0) 11.2) 14.42) .61) 4.0 (5.40-1.30 (2.01) * * 1.39 (8.79-7.8) 19.29) * * 1.4 (9.3) 16.40-19.08-2.80) 2.50-36.12-19.70 (2.2) 471 576 308 664 822 701 814 1122 922 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.81) 11. respectively.33-18.21) 9.20 (.0 (7.0) 10.0 (4.740-2.0) 5.8 (12.83 (5.10 (.0) 10.490-2.00-7.44 (2.26 (5.290 (<LOD-.0) 11.56 (4.50 (.0 (9.6) 7.32) 1.16 (2.80) 11.0) 20.0 (8.03 (.2 (11.0) 5.S.86 (1.33 (5.0 (8.07-10.1.981 (.0) 10.40-11.60 (1.40 (.10 (.26-8.68-7.05-7.40-16.96-3.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.80) 4.623-1.40-5.0 (6.76 (2.00 (1.97) 90th 7.20 (.0) 10.95) 5.43-12.27-3.17-3.98-5.30 (4.80-4.44-38.0) 12.58 (5.04) < LOD 1.32 (.970-2.2 (14. 120 Fourth National Report on Human Exposure to Environmental Chemicals .0 (7.11 (.20-4.80 (2.58 (3.890 (<LOD-2.86-15.70-14.58 (2.94) * * .47) 5.30-6.67) 3. < LOD means less than the limit of detection.02) 4.13 (2.36-4.2) 16.954 (.15-12.56 (6.8) 7.0) 6.93-24.00 (5.66) * * 1.56-13.00 (4.0) 10.0-28.45 (2.46) 10.70) < LOD < LOD 75th 3.22 (.2 (7.26-6.52-11.1-17.5-17.5) 15.7 (12.810-1.530 (<LOD-2.0) 11.28) 1.80) . see Data Analysis section) for Survey years 99-00.35-16.39 (3.21 (.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.85 (3.1 (9.50-5.00-12.10 (2.27-15.56 (1.7 (14. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80) 2.20 (.61 (3.35-12. interval) 1.599-1.51) 2.5 (8.60-18.71 (2.00) 3.7) 11.9) 8.60-11.1) 95th 13.20-7.70-19.02-5.10-7.57-7.52) 6.290 (<LOD-1.2 (9.4) 20.44-3.700-1.8 (14.0) 15.0) 5.9) 14.00-27.20 (2.1) 10.80 (4.3-15.5) 20.5 (11.82) 10.10) < LOD < LOD 4.48-7.860-2.2 (14.620-1.73) * * .80) .0) 7.5-16.9 (8.08 (<LOD-2.2-20.60) < LOD < LOD 4.1 (10.63) 1.47) * * 1.80) 2.70-23.35-11.0) 6.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60-25. 0.2 (7.8 (8.15) 14.0 (7.60 (5.10 (2.0 (7.38-5.

98-5.55-20.47) 2.533-1.89) * * 1.5) 8.6) 13.430-1.88-15.15-10.40 (3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.89-3.8 (10.62-5.95 (3.98) 9.9-28.860 (.34 (6.39 (2.42 (3.71-2.510-1.67) 1.8) 16.2) 95th 12.82-6.3) 15.67-19.09 (.29) * * .56) 4.56) .52) 4.996 (.500-1.23) 4.37-3.790 (.2) 8.04-6.66 (5.9 (9.88-10.04 (1.80) 9.87 (1.1) 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 1.81 (1.66 (2.0) 7.8) 8.30 (1.54-4.57-10.60) * * .7 (8.83 (7.90-8. interval) .9) 16.10-13.02-14.5-16.6) 9.10 (3.3) 5.37) 9.574-1.00 (4.00) 8.95) 2.4 (9.13) 4.06-2.03) 2.81-5.32-12.6 (9.633-1.14 (3.2) 13.00 (4.4) 4.47 (3.66 (1.78 (2.46) 2.00-19.98) .27) < LOD 2.43 (3.6) 8.7) 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.94-10.69 (4.1 (8.40-28.5 (4.82-14.855 (.37-5.9) 12.21-23.43) 2.6) 11.37 (5.9 (5.57 (4.03-6.94 (4.80 (7.54-2.02 (2.570-1.79-9.750 (<LOD-1.924 (.75) 14.03 (7.54-11. population from the National Health and Nutrition Examination Survey.20-8.93-9.34) * * .650-1.60-9.28 (2.94-9.1) 4.05) .5) 7.51-5.2) 9.900 (.00-13.3) 12.61-29.94 (2.4 (4.83) 8.54) .920 (.710 (<LOD-1.34) < LOD < LOD .38 (1.7 (10.40-14.8) 6.41) Selected percentiles ( 95% confidence interval) Total * * 50th .0) 6.69-10.9) 11.45-11.75) 2.2 (6.43 (.98) .620-1.608-1.66-15.29 (2.549-1.6 (10.58) * * 1.0 (8.68) < LOD < LOD 3.85) 2.40) 4.57) 4.92-5.1 (7.820 (.11-6.84 (5.28 (4.53 (6.870-2.69) 4.87-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.56) 7.7) 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 .35) < LOD < LOD 3.18 (.440 (<LOD-2.75 (3.3) 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 1.00-17.890 (<LOD-1.5) 12.9 (9.84) 7.94-22.74) 90th 7.03) 2.25) < LOD .47) * * .28 (5.960 (. Fourth National Report on Human Exposure to Environmental Chemicals 121 .57 (6.34 (6.883 (.31-14.1 (11.92-2.82-14.45-5.818 (.7) 18.53) 9.98-22.88 (5.780 (<LOD-1.35 (1.98 (3.8) 12.1) 4.5-32.19 (4.45-5.62) .64-5.5-13.85 (6.47 (3.75 (7.7) 12.31 (3.53-11.93) 9.28-9.24-3.540-1.40) < LOD < LOD 75th 2.2) 5.40-3.1-15.773-1.560-1.2) 5.77 (6.830-1.1 (9.73 (1.2) 7.7 (9.36) * * 1.1 (6.44 (2.09-11.566-1.1 (10.8) 7.25) 6.23 (4.05 (.02-2.82-26.94-23.40-12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09) 2.5-20.30) 2.50) 7.61-13.5) 7.72) 11.7) 5.80 (6.71) 10.2 (8.5) 11.S.74) 4.93-5.76) < LOD .40-5.05 (1.56-13.54-15.01-2.75-7.03 (2.88) 2.87 (3.28) 10.2 (10.4) 13.79-3.68-4.41) .26) * * .38) .61 (1.66-34.42) 12.80 (2.69) 2.60) 2.07 (.4) 4.61 (1.932 (.90-5.76-4.46-5.3) 16.41-12.67) 4.37 (4.47 (1.02 (7.960 (<LOD-2.890 (<LOD-1.

90 (6.88) 3.00-4.86-10.10) 6.95-9.39-13.00) 3.6) 14.61 (3. 0.30) 3.49-4.22-12.8 (12.60 (2.3 (11.80-8.1 (10.72) 2.10 (<LOD-1.9) 16.8) 8.10-4.5.3 (9.20 (<LOD-2.80-21.6) 14.0 (7.8-20. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.73) 7.8 (12.3) 10.01 (2.70) 2.7) 10.90-15.0) 14.22) 8.40) < LOD < LOD 75th 2.90 (2.45 (3.22 (6.3) 20.90 (1.7 (10.0) 7.50-5.3 (9.82) 8.0) 6.0-24.31-12.60) < LOD < LOD 2.0-24.77-14.7 (11.6) 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 * * * 1.17 (7.24-5.70 (8.40 (2.95 (5.50) .80 (5.9-15.20-4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .3) 22.58.62-17.46-4.5-26.27 (3.970 (<LOD-2.74) * * * * * 1.6 (10.20) 3.670 (<LOD-1.0-29.3 (6.7) 16.6) 18.7-21.14 (6.16-1.0) 9.0) 23.4 (10.2) 14.15-6.80-6.0-19.97-4.0 (5.59-3.80-14. respectively. see Data Analysis section) for Survey years 99-00.78) 5.04 (3.4-17.2 (7.53 (3.64) 10.30) 3.67) 4.70-5.5.60 (5.6) 11.58 (1.31) 1.80-4.80) 5.10-15.50) 3.77-3.66) 4.41) 3.0) 14.9) 9.1 (10.4 (14.3 (7.0) 13.5 (9.0) 13.20-18.3) 8.20) 3.99 (3.81-6.910 (<LOD-2.67) 3.670 (<LOD-1.39 (5.3 (12.5 (8.95 (2.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.37 (3. 01-02.0) 12.0) 18.30) < LOD < LOD 4.70 (1.89) 2.00) 3.12 (4.00-4. and 0.580-2.650-1.90) 8.52 (6.28 (7.27) 9.9) 95th 14.96) 3.34-10.47-6.0 (9.27 (7.90 (5.4) 11.34-5.9) 10.1) 11.90-31.8-21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.31-7.5 (8.0-33.3) 14.15-2. 122 Fourth National Report on Human Exposure to Environmental Chemicals .9 (7.34 (6.0 (9.7-19.06 (2.90-15.00) 8.67-10.80) .0) 19.41-5.7) 15.90 (6.10-10.35 (6.92) 9.670 (<LOD-1.46-28.51) < LOD 1.5) 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 * * * * * * .24 (2. and 03-04 are 0.61-32.30) < LOD < LOD .00-18.75 (3.80 (2.98-9. < LOD means less than the limit of detection.22 (6.90 (2.42 (1.84-4.35) 4.80 (2.10 (.0 (10.29) < LOD < LOD < LOD < LOD 3.00 (.7) 14.90 (2.00-18.1-23.0) 11.0) 12.00-9.00-16.60 (6.20-8.5) 21.29-4.90 (6.20) .740 (<LOD-1.0 (15.50-4.7) 22.25 (2. which may vary for some chemicals by year and by individual sample.0 (13.34-3.80) .6-19.4 (10.S.670 (<LOD-1.80-12.9-17.27) 4.27) .8) 9.6-41.00) 7.0 (14.96) 90th 7.11-6.8) 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 1.90) 4.0) 9.4) 7.0) 11.40 (2.90 (6.8-20.00) < LOD .63-14.70-8.70-9.37) 2.790 (<LOD-1.80-3.2 (9.0 (8.66-13.30) 8.6 (10.88) 10.90-9.33-11.35-3.8-17.92-17.680 (<LOD-1.18) * * * * * * * * 1.18 (3.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.70-9.89 (2.0 (10. population from the National Health and Nutrition Examination Survey.75 (2.50) 5.9 (12.0) 12.9-14.

37) 3.6) 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 1.6) 6.1 (19.72) 4.4-15.0-21.810 (<LOD-1.7) 15.760 (<LOD-1. population from the National Health and Nutrition Examination Survey.55) 16.89 (2.52-3.07) 2.00 (<LOD-1.6 (13.67 (1.69-11.6) 7.95) 90th 8.4) 15.42) 7.37-5.02-4.95) 3.920 (<LOD-1.63 (2.34) < LOD < LOD < LOD < LOD 3.4-16.78) 4.0 (11.4) 9.9 (9.94 (5.7) 14.27) * * * * * * * * 1.88 (1.9 (9.93 (2.03 (2.04) 9.54) 9.2) 16.7 (10.55) .82-8.28 (1.61 (2.34-18.0 (10.6 (11.690 (.54 (7.50 (6.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .27) 5.3-17.92 (5.1) 20.96-11.28-12.78-10.6 (12.51-10.7 (8.910 (<LOD-1.19) 3.8 (8.3-34.91) 3.8 (10.55 (2.5-17.97) < LOD .9 (9.7-23.83 (7.71 (1.86 (3.00 (2.2) 15.03 (6.68-10.7) 12.0 (8.09-11.850 (<LOD-1.5) 10.27-13.99 (4.43 (2.00 (<LOD-1.86) 9.8) 11.77 (2.940) < LOD < LOD 1.8) 14.45) 6.89-3.64-11.0 (13.78 (6.25-9.590 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 123 .2 (9.38) 1.67 (7.82-11.95 (2.53-8.4) 7.30) 2.1) 10.96-10.12) < LOD < LOD 4.0-19.2-15.42-19.78 (4.05-3.4) 6.00 (5.00) 8.27) 1.20-3.12 (7.620 (<LOD-.36 (2.07) 2.72-4.9-17.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.15 (1.3) 8.33-10.89 (3.4-18.29-2.41 (7.09-11.89) 5.5) 13.50-17.1) 13.2) 8.4) 7.3-21.30-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.14 (2.86-3.03) 3.4) 16.47-9.06) .68) .5 (11.73 (5.79-9.6) 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 * * * .89-10.530-1.11-3.63 (6.91-9.85-8.30) 7.68-19.5 (9.70-2.27) < LOD .6) 12.54-5.32-8.59-3.89-3.9) 19.29 (5.1 (13.15) < LOD < LOD 75th 2.6 (10.2-30.7 (10.18) 2.6-19.S.3) 12.21-21.2) 10.89-13.94-14.75-3.0) 14.42) 8.6) 13.6) 95th 16.77) 3.16-14.30) 8.28) 6.71) < LOD < LOD 2.950) .85-17.75-3.8) 16.3 (7.06 (<LOD-1.07 (5.58 (4.29 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .5 (8.23-3.45) 3.00 (7.68-4.74-4.5 (10.99) 2.92) 3.48 (2.93 (6.01-5.44-6.11 (5.3) 9.4-16.07-3.25 (4.973 (.74-19.80) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.16 (3.6) 14.9) 16.97-4.21) * * * * * 1.00 (3.38 (1.3) 6.38 (.5) 8.7) 14.4) 7.87 (3.39-17.79-6.83 (6.7-19.00) 2.93 (<LOD-2.93-10.33) 3.88-7.6 (11.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.7 (11.29) 3.9-25.70-35.2) 19.1 (8.6 (13.38-13.2) 12.4 (11.7) 9.81 (7.780-1.38 (2.2 (9.3-15.77 (2.890-2.3-17.2) 12.32) 2.51-7.2) 12.5) 22.5 (15.

17) 1.90) 3.930-1.30-3.37-2.35) 1.46) 1.94) .10) 1.17-4.34) 2.340-.49) .33-2.89-6.79) .80) 5.25-1.880) < LOD 75th .80) 3.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.01) .22-3.820 (.20 (2.13) 2.80 (1.40 (1.960) .20) 2.27 (3.15) 2.S.73 (2.79) .560-.960) .960-1.467 (.350-.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 * .70 (1.690-.10-1.570) * .50 (1.48 (2.587) * * .86) 3.910) 1.850) < LOD .780 (.570 (<LOD-. respectively.54 (2.940) < LOD .29) 1.930) 1.388-.80) 3.590-.670) .19-1.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.46 (1.750) 1.13) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (.58 (1.89) 1.760 (.720 (.740 (.59-2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .750-1.09 (.720-1.710) .390-.980) 1.22 (1.64 (1.29-2.14-1.930) < LOD .380-.22-8.97 (2.50) 1.680-1.46 (2.98 (2.950) 90th 1.73 (1.570-1.57 (2.78) 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 * .710 (.45 (1. 0.600-1.210 (<LOD-.57 (1.353-.10-1.11-3.570 (. interval) Selected percentiles ( 95% confidence interval) Total * .36-4.31-3.510 (<LOD-.700) .86 (1.47) 2.20) 2.20) 1.50 (1.30 (.60) 3.17) 1.90) 2.510 (.83) 1.83 (2.42-2.78) .730) .60) 2.00-2.20-1.650-.453 (.549 (.810) .30 (.20 (1.1. see Data Analysis section) for Survey years 99-00.759) * .720-1.201-.95 (2.592-.960 (.449 (.00 (1.740-1.80) 3.20) 3.880 (.98-3.94 (3.990-1. 01-02.45-4.70 (1.95) 2.960) 1.54-2.45 (1.68-5.96-5.98) .21) 3.620-1.47 (1.55 (3.680-1.740 (.15) 2.280-.38) 1.970) .23-3.45 (2.14 (1.41-5.20-2.48 (1.700) .77-2.592) * .90) 2.400) .50-2.50 (1.83 (2.490 (<LOD-.26) .500 (<LOD-.00) 2.01-1.20-3.09.16-3.32-1.75 (2.61 (1.30-3.49) 2.690) .20) 3.800 (.740-.91) 2.160 (<LOD-.930 (.73-5.70-2.584) .20) 1.457 (.30) 4.450 (<LOD-.41 (2.83) 2.18 (1.540 (.749 (.2.08 (2.382-. which may vary for some chemicals by year and by individual sample.26 (2.505 (.96-3.840 (.70-7.50 (1.30) 2.350-.39) 2.343 (.76-6.580-1.780) .74) 3.260 (<LOD-.83) .65 (2.69-4.31-3.830 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30 (.585) * * .336-.550 (.32 (1.90-4.425 (.690 (.22-2.00) 1.08 (2.05-2.80) 2.90 (1.592) * 50th .600 (<LOD-.710 (.16) 2.30) 4.75-2.87-3.34) 2.657) * * .16) 1.22-3.820 (.380) .50 (1.80) 2.88) 1.31) 95th 2.10) 3.455 (.359-.00-4.570 (<LOD-. and 0.70 (1.63 (1.910-1.76 (1.618) * .550 (.89) . < LOD means less than the limit of detection.398-. population from the National Health and Nutrition Examination Survey.910 (.04) 1.30 (1. and 03-04 are 0.40 (1.31) 2.440-.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 * .597) * .27 (2.240 (<LOD-.30-1.30) 1.303-.54) .11-3.50-2.380-.390-.60 (2.94 (2.01-3.460-.77 (1.18 (.20 (1.80 (2.790 (.690-1.46-3.10) 1.59-6.20 (1.03) 1.459 (.32) 3.949) .60-4.10) 1.880) < LOD .74-5.600-.970) 1.580-.95-5.05-3.860) < LOD < LOD .570 (.20-2.04) .

38-3.92) 3.760) .510-. interval) Selected percentiles ( 95% confidence interval) Total * .60 (2.43) 2.390-1.400) .06-2.591 (.99) 1.230 (<LOD-.71) 2.590 (.39 (1.07) 1.20-2.850) 1.71 (1.700 (.47 (1.660-.950-2.79 (1.444-.13 (1.390) .280 (<LOD-.92-8.448 (.58 (1.69 (1.06) 4.77-4.910) < LOD .372 (.310 (<LOD-.00 (3.97) 1.25-3.23) 1.29-4.11 (.66 (2.72-4.840) .490 (.42) .305 (.820) .630) * .690) < LOD < LOD .370-.180 (<LOD-.680 (.16) 1.710 (.89 (1.04-5.89-3.900) 1.44) 2.42-8.08-3.52) 3.94) .980-1.49 (1.270-.742) * * .22-3.24) 4.07) 1.552 (.136-.590) * 50th .520-.05-2.34 (1.67) .S.597) * .91 (1.43) 1.67) 1.47 (1.76) 1.590-1.79) 1.61-3.57-2.41 (.840) 1.57-4.22) 1.73 (2.75-3.470) .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.377-.460-1.800) < LOD .60) .99) 2.77-3.08-2.22 (2.640 (.380-1.88 (1.530 (.66) .98) 1.688) * .84 (2.43) 2.790 (.33 (1.285-.32) 2.348-.62 (2.920) .830) 90th 1.82 (2.30-2.440-1.870) .45 (2.61-3.07) 5.710 (.61 (3.14 (2.07-3.20-7.84-6.535 (.580-.52 (1.97) 2.33) .930-1.720-1.05) 1.50 (1.02-3.470 (<LOD-.640 (.550-.739) * .32 (.509 (.00-1.90) 2.88) .32) 5.67 (1.550-1.57 (3.20) 1.03-2.471-.44-2.61) 2.05) < LOD .08-3.10) 2.11-2.330-.08-3.58) 3.03-1.700 (.75 (2.87 (2.67-3.92 (1.350) .460) .250 (<LOD-.39) 2.300-.70 (2.23 (.08) 1.250 (<LOD-.720 (.64 (2.453 (.97 (1.16-2.42 (.47-4. population from the National Health and Nutrition Examination Survey.393 (.447 (.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.740) .17) 2.07) 1.97 (1.08 (2.670 (.380) .550) .81) 2.58-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.08-3.820) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.880) 1.08-2.335-.400-1.640 (.65) 2.840) 1.75) 6.500-.00-3.320-.485) * * .02-6.22-2.560 (.08) 2.480-1.28 (1.22) 4.72 (1.73-3.95) 1.04-1.480) .08 (.310-.69 (3.67 (1.790) .320-.45 (1.560-.08-2.645) .64 (2.760) < LOD 75th .300 (<LOD-.09) .36) 3.32) 1.580 (.70 (3.55-3.38 (1.412-.19 (1.730) .30) 3.830 (.42-6.98) 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 * .62 (1.800-1.49-4.38 (2.07 (.80) 471 575 296 664 821 689 814 1122 918 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .580) .72) 1.63 (1.55 (1.750 (.270-.22-3.940-1.60 (1.31-1.22) .510 (.234 (.16-1.75 (1.460 (.02-3.550-.710 (.72 (2.17) 2.23) 3.560-.05-4.77 (3.05 (1.253-.318-.380-.18-2.53) .82) 2.80) 2.43 (1.403) .870 (.520 (.57 (1.740) < LOD 1.990-1.368) * .750 (.07-2.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .700 (.330 (<LOD-.04) 95th 2. Fourth National Report on Human Exposure to Environmental Chemicals 125 .78) 3.11) 1.515) * * .71) .510 (.23) 2.23) 2.50) 1.60) 1.540-.270 (<LOD-.17-2.32-1.310 (<LOD-.

90) 11.6-54.0-43.46-2.0-110) 42.530-4.19) 2.40-16.5 (24.3) 28.50-20.8) 62.0-62.61 (1.80) < LOD 1.3 (12.10) .98) * 2.3 (14.0) 16.10-13.6 (11.80-2.8) 32.06) * 2.0) 15.0) 3.6 (15.7) 20.0) 30.53) * 2.29-4.70 (1.19-2.2-27.00 (.80-18.20) 1.0 (38.5) 30.59 (1.3) 33.6-22.0-31.0-41.1) 18.83-2.18) 6.7 (12.3) 38.60 (2.20 (2.92) * 2.4-22.79 (1. see Data Analysis section) for Survey years 99-00.85) * 2.6-27.7 (12.0) 8.48-2.14) 5.S.86-3.1) 38.91 (4.71) 5.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.79-2.53) 1.11) 2.06 (1.96) 5.16) 2.95 (5.41 (1.2-62. population from the National Health and Nutrition Examination Survey.20-4.36-2. 0.77) 38.8-24.8 (26.0) 15.23-2.40) < LOD 2.21 (1.50-2.0 (8.0-53.3 (24.0) 33.64-8.0) 17.0) 32.0 (6.6-45.0 (38.80) 90th 38. interval) 1.8 (22.41-4.10 (1.53) 40.0 (26.0 (20.41) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (32.0 (17.67 (1.49-2.0-92.0 (38.0) 20.0-110) 34.12) 1.2-26.470 (<LOD-1.0) 6.83 (1.76 (2.9) 18.4 (10.40) < LOD 1.610 (<LOD-1. respectively.88) 1.0 (20.0-50.23) 9.830-3.97) 6.10 (1.1 (26.0 (25.6) 52.29) 2.0) 3.12 (3.5-45.41) 5.3) 26. < LOD means less than the limit of detection.04 (<LOD-2.1-47.53 (1.690-3.70 (.71-2.70 (1.70-6.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.18.70-17.29-9.13) 12.80) 1.64-3.5-74.70 (7.0 (38.60) < LOD 1.4 (15.2 (19.0 (24.30-14.0-230) 35.0 (13.86 (1.90 (1.33 (5.52 (4.0-58.3) 31.0-62.48-2.50-5.10 (7.0-41.32 (2.26) 75th 11.16) * 1.44) Selected percentiles ( 95% confidence interval) Total * 2.0 (21.600-2.9-51.13 (1.0-39. and 03-04 are 0.2) 31.0 (19.79 (2.7-22.41) 1.0) 31.8-21.88) 3.1 (10.4.9) 48.0) 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 2.76 (2.83-2.9 (19.50-7.82 (1.46-6.0) 18.1-40.1 (11.31-6.13 (1.6 (9.1) 38.57-2.90-8.00 (.90 (1.0 (38.7) 47.59 (1.8) 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 1.1) 140 (46.63-6.72 (1.94 (1.3 (23.1 (22.4-76.85 (1.8 (12.7 (28.9 (23.81-2.09 (4.54 (3.2-39.0) 4.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.5-40.81-3.9-21.30) 4.0 (8.46 (.660-2.54 (1.1) 95th 48.9 (27.61-2.5-27.0-49.0) 45.65 (4.0-41.77 (1.10 (1.5-20.8) 39.26 (.0 (37.70) 1.35-6.44) 2.70) 5.44-7.0) 4.4) 38.0) 19.0 (7.0) 16.66-5.0-260) 34.1-20.6 (26.0-52.1 (25.1-25.0) 17.45) 2.0-69.93-3.0 (38.9 (19.78 (1.0 (8.74-2.0) 3.0) 4.0) 28.07-5.00-24.04) 3.30 (.18) 20.05) * 2. and 0.23-2.21 (3.0-29.30) 11.8 (12. which may vary for some chemicals by year and by individual sample.0) 5.25-3.2-47.27-6.05-3.9 (10.75-14.9) 17.0 (11.04-8.48) 5.43-7.80) .99 (2.2-80. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-33.4) 19.5) 69.2) 16.42) 1.57-2.2-27.0-58.70) 1.10-4.830-4.40) 50th 2.2 (12.10 (1.83 (3. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0-47.11 (4.0) 3.98 (1.3 (10.3 (12.0 (33.1 (25.7-41.45) 2.0) 42.0) 20.40-4.69) 2.44) 3.78) 9.9) 38.50-17.10) 39.0 (40.0-39.5.87-7.1-46.0-53.1-19.0) 28.18) 14.4 (19.0) 13.17-2.21 (4.05) 1.71 (4.02 (2.8) 41.58-2. 01-02.50 (2.58) 16.0 (38.92-5.

2 (22.4 (12.6) 7.16-2.86) * 2.08 (1.91 (6.890-4.19) 5.1 (34.18-1.7) 95th 51.9 (19.8) 11.14-8.7) 66.35) 1.4-71.5 (15.09 (5.4-21.2) 13.9) 24.15 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33) < LOD 1.3) 13.40 (2.0 (19.37-2.4 (21.5-97.97 (1.8 (7.53) 1.4) 12.7-20.7 (10.3) 28.22-2.6-51.0) 25.870-3.750 (<LOD-1.6-38.4 (25.64 (1.41 (2.21 (4.7 (11.16 (1.91-2.5 (15.83) .0 (23.57 (6.46-22.2 (8.6 (11.7-43.95) 90th 32.1 (33.18) * 2.3 (8.20-5.1) 13.7-47.40 (5.2) 13.93) 5.50 (2.9 (39. interval) 1.88 (1.8-34.8-26.5 (17.0 (14.5 (8.17) 2.7-37.0 (6.36) 10.2) 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.19-6.7) 30.6 (7.66 (1.8) 32.00) 6.7 (18.35) .14 (.95-16.80 (1.08) 1.2 (16.61-22.19 (1.4) 3.71 (1.27) 10.1 (39.68 (1.5-43.5 (41.2 (21.0) 48.0) 13.66) 8.35 (2.56) 1.9 (10.1) 13.94) 19.9) 24.62) 4.82 (2.4 (25.30) 28.9) 3.32-3.0) 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 1.7 (24. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-18.5-190) 30.68) 47.4-39.2) 33.47 (3.51) < LOD 1.58-17.0) 10.7 (18.9-52.67-16.8) 3.59-2.03) 1.4-67.67 (1.12) 3.1) 15.8-45.43-12.5) 27.40-4.0 (25.62 (2.76-2.2-70.52-4.02) * 1.7-109) 22.37 (1.70-4.5 (6.33-5.6) 3.22 (2.67 (1.82) 1.40-7.11-2.46) 1.6 (24. population from the National Health and Nutrition Examination Survey.26-4.26-2.9 (7.2 (15.1) 52.0) 30.06) 1.9-41.01 (.3 (10.8) 15.0-70.1-63.45 (1.7) 15.00 (4.8) 31.4 (5.75) * 1.8) 23.9) 3.6) 11.71) 8.60 (.51) .3 (9.06) 75th 9.12 (1.36-13.7) 61.860 (<LOD-1.9) 12.0-40.0 (39.7) 23.1 (25.75-6.07) 9.3-42.1-60.3 (20.9 (13.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.11) < LOD 1.7-38.94-20.17-3.870-3.43-2.870-3.07-2.70 (1.23) 37.47-17.2-34.5) 70.28 (1.8-43.1-22.00-16.90 (.02) 1.930 (<LOD-1.96-16.48 (4.72) 2.9 (26.899-2.56 (2.3-27.1) 36.55 (2.66 (1.16 (1.888-1.5 (34.59-15.680-4.39 (1.6) 3.58-2.1) 25.88 (4.38-5.46-5.4) 14.8-37.7-19.2-28.69-18.75 (1.84-13.0 (17.18) 3.19-14.22 (.03-2.19) 5.80-8.38-1.00) 1.88 (1.9-36.27) 50th 2.6-49.22-3.6) 19.27 (6.4-34.5 (13.36 (4.20) Selected percentiles ( 95% confidence interval) Total * 1.4) 12.1) 27.54-2.7) 26.61-2.46-6.0 (23.2) 4.6-32.63-5.29-5.38 (3.4 (11.45-1.02 (.16 (1.0) 3.61 (1.4 (9.2-38.5-36.71-2.79 (2.1) 25.25-3.86) * 3.43) * 2.S.99-4.6) 112 (40.54-15.79-17.6 (27.67-3.24 (1.33) 2.9-37.59-2.2) 36.96) 2.1) 17.06) 1.33) 1.9-95.670-1.47 (1.4 (19.52 (1.95 (2.69-5.0-118) 29.57) 4. Fourth National Report on Human Exposure to Environmental Chemicals 127 .1 (12.95-16.27-3.3 (10.83 (.60) 4.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.38) 5.0 (32.0-71.06-1.9) 54.48) 1.28) 1.75 (1.07-2.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.2) 41.44) 9.32 (3.2-47.88 (4.1 (50.23-1.3-22.50-5.1) 27.0) 47.34) * 1.31) 2.6) 23.7) 34.94) 1.3-19.23) < LOD 2.2 (9.

610 (.430-. and 03-04 are 0.540 (<LOD-.390 (.860) .290 (<LOD-.10) .280) < LOD < LOD < LOD < LOD .090 (<LOD-.130 (.610-1.530-.870 (.200) < LOD < LOD .410-1.540) 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 * * * * * * * * * .440-1.820 (.1.700) 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 . which may vary for some chemicals by year and by individual sample.720 (.220 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .310 (.090 (<LOD-.300-.42) .100 (.390) < LOD < LOD .680-1.230) .270 (. 01-02.380-.290) < LOD < LOD < LOD < LOD 90th .610 (.470-1.140) .410-.850 (.640 (.720-1.120 (<LOD-.60) 1.650 (.240 (<LOD-.870 (.13) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.130) .370-.870) < LOD .42) .760) < LOD .190 (.320 (.160) .220 (<LOD-.03) .700-1.740) < LOD .090 (<LOD-.860-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .15) .990) .20) .05.700-1.58) .680) .490 (.400-.210 (.32) .360-.640) .150 (<LOD-.330-. see Data Analysis section) for Survey years 99-00.180) .900 (.380-.450 (.162) * * * * * .610-.870 (. respectively.450 (.310) < LOD < LOD < LOD < LOD .00) .170-.160) . and 0.090 (<LOD-.420-.580) 471 576 310 664 822 717 814 1118 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .830) < LOD .690-1.470 (.370-.640-1.310 (.10) .430 (.940 (.080 (<LOD-.S.140-.450 (.230-.410) < LOD < LOD < LOD < LOD .30) .720) .730) .870 (.1.410-.310) < LOD < LOD < LOD < LOD .730-.30) .870 (.36) .460-.350) .930 (.540) .550) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.140-.460 (.084-.850) < LOD .650-1.190 (.570) .990 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.050-.630 (.680-1.260 (.380-.620 (.10 (.770) < LOD 95th .360-.640) .110-. 0.120-. population from the National Health and Nutrition Examination Survey.350) < LOD < LOD < LOD < LOD .171) * * .990) .30) .320-.660 (.130-.650) .830) .090 (<LOD-.830 (.10) .190 (.130) .310-.650-1.560 (.630 (.140-.130-. < LOD means less than the limit of detection.700-1.560 (.300-1. 128 Fourth National Report on Human Exposure to Environmental Chemicals .090 (<LOD-.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.40) .680 (.600 (.840) .160-.850 (.130-.830 (.650) .780) < LOD 1.540) .150) .210 (.700-1.117 (.840) .080 (<LOD-.290) < LOD < LOD < LOD < LOD .099-.510-1.120-.770 (.820 (.12 (.

070 (<LOD-.670 (.29 (.110) .330-.110) .09) .230 (<LOD-.560 (.070 (<LOD-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.300-.330 (.600-1.860 (.870) .450) .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 * * * * * * * * * .700 (.161) * * .180-.410) .410-.200 (.330-.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 .14) 1.36 (1.110) .24 (.090 (.410-.440 (.500 (<LOD-.78) .380-.700 (.460 (.470 (<LOD-.170 (.990) .060-.710-1.100 (<LOD-.800-1.780) < LOD 1.140-.580 (.050 (<LOD-.740) < LOD 1.670-1.360-.070 (<LOD-.220 (.960) .500) .540 (.720 (.520-.360-.12) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (.730) .500-1.550 (.450 (.86) .140-.290) < LOD < LOD < LOD < LOD 90th .230) < LOD < LOD < LOD < LOD .570-1.140-. Fourth National Report on Human Exposure to Environmental Chemicals 129 .750) < LOD 95th .730) .360 (.740 (.100-.080) .00) < LOD .110) .43) .38) 1.300 (.230-.700) .03 (.890 (.170) < LOD < LOD .111) * * * * * . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.200 (.250-.310) < LOD < LOD < LOD < LOD .860 (.02-1. population from the National Health and Nutrition Examination Survey.400) .270 (.650) < LOD .880 (.190-.67) .650-1.260) .370 (<LOD-.03 (.140-.510-.660-1.110-.120) .090 (<LOD-.190 (.19 (.66) 1.20) 1.670 (.380-.700-1.410 (.490-1.170 (.340-.070 (<LOD-.440-1.400 (<LOD-.580) .570-.580 (.270) < LOD < LOD < LOD < LOD .330 (.120) .580) < LOD .640-1.03 (.190 (.410 (.S.720 (.380-.330-.390-.240-.600) .02) .990) .86) .150-.550 (.540 (.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.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 * * * * * * .300-.140) .080 (<LOD-.380 (.057-.850 (.60) .360) < LOD < LOD < LOD < LOD .380-1.320 (<LOD-.540) .390-.260-.760) .570 (.220) < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .940) .810 (.780 (.24) .730 (.58) 1.03) .140-.084-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .62) 1.880-1.280) < LOD < LOD < LOD < LOD .610-1.080 (.01 (.940) .860-2.580-1.970) .730) .116 (.410) < LOD < LOD .

47 (3.29-10. and 03-04 are 0.960 (.32 (1.00 (.82-4.35) 5.10 (.70) 2.00 (1.97) 20.90-28.63) 32.800) 90th 13.80 (4.14) .110 (<LOD-.870) < LOD < LOD .70-50.880) 5.360-1.0-38.05-3.55-4.40-4.0 (17.30 (1.40-7.30 (.42) 2.330 (<LOD-1.0) 4. 0.18) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (5.960 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.83-3.800) 17.48 (2.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.30-7.590 (.480-.610) < LOD < LOD < LOD < LOD < LOD 2.1.10-3.07-3.87) 12.61 (1. 130 Fourth National Report on Human Exposure to Environmental Chemicals .750-2.850) 16.0) 2.53-7.50) .0 (6.48) 13.30 (1.10-3.6) 5.24-7.40-8.20-17.94 (1.45 (2.620-1.10-9.1.40 (1.36-3.14-5.0) 5.0 (16.640 (.49) 17.0) 5.0) 2.0) 5.83) 2.07 (3.96 (1. < LOD means less than the limit of detection. 01-02.0 (4.12-1.0) 2.05 (2.20 (1.0 (17.840 (<LOD-1.07 (3.00) .49 (1.0 (13.39) .70-17.10 (3.38-3.01) 5.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .51 (2.190-1.0) 3. which may vary for some chemicals by year and by individual sample.0 (5.425-1.800-4.350-.42) .840-3.87) 5.52 (1.750-1.60) 1.0-44.28) .97) 20.55-8.51-8.90 (2.03 (.15) 14.0 (17.62) 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 * * * * * * .40) 1.370-.15) 19.510-.43-4.0 (5.99 (1.730 (.53 (2.63 (3.07-3.32-9. see Data Analysis section) for Survey years 99-00.70-7.52 (1.0) 4.36-3.30-6.07 (1. respectively.90-20.0) 2.770 (<LOD-1.0) 7.11) .52) 5.94-8.35) 11.85-3.90) .00-17.83-3.0) 4.21-3.0) 2.0-38. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) .12) * * * * * * * * .99) 19.08.610 (.07) 1.00-17.0) 5.0 (5.0 (17.40 (1.20-4.31-10.99) 11.0-38.0-40.50) 2.14) 2.40-20.770) 2.30-3.30) .380-.890 (.28) 1.21) 3.260-.31) .39 (2.250 (<LOD-.0) 2.S.67 (2.10 (3.70-3.62-8.210-1.691 (.400-1.170-1.830 (.11 (1.33 (4. and 0.94-3.90) .65) 1.60) .76 (1.74) 5.080-1.910) 2.90-9.0-40.13 (3.40) 2.30) 95th 19.53) 20.20) < LOD < LOD < LOD < LOD < LOD 1.28-9.37) .30 (2.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.67) .580 (.49 (1.90-37.74 (3.20 (1.59-5.05 (3.740 (.26 (2.600 (.0) 2.00) 1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (4.00) .0 (3.86) 4.0 (5.23-6.66) 4.840 (.690 (. population from the National Health and Nutrition Examination Survey.350-.30 (1.20-4.640 (.900 (.46 (1.0 (7.0) 4.68) 2.11) 13.720) 2.16) 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 (17.88-3.0-39.90 (1.70-30.67 (1.35-10.

7) 3.33-3.71 (2.540-1.260-.25 (1.670 (.07-21.748 (.890 (. population from the National Health and Nutrition Examination Survey.9) 5.370 (.0 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.85-3.31) .690-5.630-1.33-4.44) .56) .31-18.8) 4.45 (1.5 (9.8) 2.730-3.580-1.53) 27.270 (<LOD-.43) .7 (12.1 (7.25-9.540 (.47) 5.430) 1.85 (1.700) < LOD < LOD < LOD < LOD < LOD 1.50) 11.5 (8.48-42.770) .21-3.430 (<LOD-.67 (2.48-7.51-4.50 (4.320-1.360 (.60 (1.850-3.52 (.40-2.90-6.61) 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 .59 (1.700) 6.790 (.02-4.02) .22-27.470 (.09-3.340-.01 (1.67) 2.83-11.1) 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.14 (1.150 (<LOD-.2 (8.81-17.57 (.88 (.02 (1.03) 2.11) .33 (3.51-44.10 (2.03) 16.2-38.66-47.710 (<LOD-1.580) 16.340-.31) .27 (2.97) .55) 21.29 (4.4) 2.91) 2.590) 2.36 (.370) < LOD < LOD < LOD < LOD < LOD 1.330-1.390-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.620-3.5) 2.56 (1.0 (9.48 (4.17 (1.650) 90th 10.86 (3.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.4 (4.5) 7.83 (4.10) 2.7) 6.12 (4.47) .840-3.32-6.33-5.47-10.89 (2.65 (2.62 (1.500 (.00) .73 (4.7) 5.820) .69) 2.08) .39) 20.4-34.02 (.960 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.560 (.50) .310-.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 * * * * * * * * * .57-40.82-11.80 (.660) < LOD < LOD .69-7.18) 95th 21.580) 1.650 (.41 (4.84) 9.18) * * * * * * * * .41) 18.96) 2.12-4.820 (.75) 5.10-3.17) 5.8 (20.04-16.44-11.860-2.00-19.33 (1.29-4.8) 1.8) 7.970-3.38 (2.8) 7.830 (.96-8.05) .79 (.5 (11.57) 8.06 (.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.49-2.3) 2.13 (2.67-6.55) 21.790) 11.1) 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 * * * * * * .40 (.31-7.340 (.88 (2.80) 3.1) 2.71 (.24) 3.7) 4.5-40.37) 4. Fourth National Report on Human Exposure to Environmental Chemicals 131 .340-.50 (2.23-7.88-3.260-.580 (.47-10.250 (<LOD-.64-4.98 (4.35 (.56) 2.940-4.91-4.370-1.07 (2.1 (5.55 (3.740-1.0) 4.67) 1.86) .30 (4.930) .800-2.40-12.62-17.14-6.9 (11.780-4.600 (<LOD-1.28-6.32) 9.9) 6.474-1.S.74 (2.11-5.5) 2.57) 1.18) 1.190-1.15) 9.22) 2.830-3.53) .64) 30.8) 2.88) 17.240-.8-33.7 (6.270-.92 (2.96-25.77 (.04 (1.3) 3.40) 1.450 (.25-38.

Peterson JC. neurophysiological. Vaughan TL. Charnley G.14(6):869-889. Bozzi N. Bradman A. Bouvier G. Castorina R. Farahat TM. Sci Total Environ 1996. Angerer J. Kissel JC. Abdel-Azis M.16(5):417-426. Young AD. Krieger RI. Garrison RP. Fenske RA. Eaton DL. Keifer MC. Anger WK.59(1):217-228. Fenske RA. Chevrier J. Leffingwell JT. Lu C. Miller M. Ann NY Acad Sci 1997. 132 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2005. Kelly-McNeil K. Am J Ind Med 1997. Franklin CA. Momas I. Amr MM.113(12):1802-1807. Regul Toxicol Pharmacol 2003. Bravo R. Barr DB. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Robinson LR. Environ Res 1992.177:37-41.32(5):487-496. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. et al.110(8):829-833. J Toxicol Environ Health 1981. J Expo Anal Environ Epidemiol 2005. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Novelli MT. 2005. Elgethun K. Greenhalgh R. Engel LS. Fenske RA. Buchanan D. Arch Environ Health 1998. J Occup Environ Med 2004. Seta N. Checkoway H. Aprea C. Shebl MM.59(7):434-441. Eskenazi B. Gillham RA.111(3):377382. Curl CL. Environ Health Perspect 2000. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.37(3):382-395. Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion. and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides. Heudorf U. Pilkington A. Arcury TA. Surveillance of occupational. Boccalon P. Grzywacz JG. The relationship between maternal and fetal effects following maternal organophosphate exposure during gestation in the rat.15(2):164-171. accidental. Neurobehavioural effects among workers occupationally exposed to organophosphorous pesticides. Orsi D.60(4):279-286. Fenske RA. Freshwater KJ. McKone TE. A clinical neurological.46(4):367-378. Lunghini L. Toxicol Ind Health 1998b. Kissel JC. Curl CL. Third National Report on Human Exposure to Environmental Chemicals. Sartorelli P. Barr DB. Koch D. Quandt SA. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides. Sartorelli E.108:521-525. Berent S. Occup Environ Med 2002. Fiedler N. Chukwudebe A. Hansen S. Astroff AB. Bradman A. et al. Regul Toxicol Pharmacol 2003. Sciarra G. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Duggan A. Denley HV. Eskenazi B. Davis SW. Environ Health Perspect 2002. Abdelrasoul GM.38(1):91-97. Neuropsychological performance among agricultural pesticide applicators. Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort. Blanchard O. Atlanta (GA). et al. Garabrant DH.837:257-268. Organophosphate urinary metabolite levels during pregnancy and after delivery in women living in an agricultural community. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. Barnhart S. Demers P. Barr DB. Astroff AB. Environ Health Perspect 2003. Griffith W. 86:80-87. Farahat FM.12(6):619-645. Fisker-Andersen J. J Expo Sci Environ Epidemiol 2006. Aprea C. et al. Mathieu L. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Environ Health Perspect 2003. Occup Environ Med 2003. Am J Ind Med 2006. Kedan G. Eigenberg DA.49(9):751-760. Harnly ME. Castorina R. Schweitzer SJ. Jamal GA. Costa LG. Davies JE. et al. Hawk R. Centers for Disease Control and Prevention (CDC). Daniell W. Barr DB. Kipen H. Urinary excretion of alkylphosphates in the general population (Italy). Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Chen W. Reprod Toxicol 1998a. et al. Giordani B. Strambi M.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW.111(13):1640-1648. Fenske R. Richardson RJ. Environ Res 2001. Jolley L. Lu C. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. Neurophysiological function in farm workers exposed to organophosphate pesticides. Long-term use of organophosphates and neuropsychological performance. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State.53(1):714. Curl CL. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children.7(5):715-731.

Arch Environ Health 1975. low-level organophosphate exposure on delayed recall. Pesticide industry sales and usage . A behavioral evaluation of pest control workers with short-term.S.30(2):98-103. Stokes L. Rohlman D.345(8958):11351139. Kidd M.nap.pdf. Stark A.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Buchanan D. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. van der Hoek W. S. Salvini S. Claypoole K. Lancet 1995. 2004. Chronic central nervous system effects of acute organophosphate pesticide intoxication.43(1):38-45. Heaton RK. 1991. Thompson ML. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Frasca G.php?record_id=2126&page=1. Neurotoxicity among pesticide applicators exposed to organophosphates. Bravo R. EPA). The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Burcar PJ. Saieva C. Neurotoxicology 2005. Lancet.epa. Narang A. Scherer J. Wickremasinghe AR. Lu C. Lasarev M. U. Muniz J. Keefe TJ. et al. National Research Council (NRC). et al. Ames RG. Smit LA. Stephens R. Nell V. Bull Environ Contam Toxicol 1994. Jenkins B. Neurotoxicol Teratol 1998.S.12(2):153-172. 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. discrimination. Marshall E.2000 and 2001 market estimates.26(2):199-209. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Rodnitzky RL. Arch Environ Health 1988. Environ Health Perspect 2006. Aprea C.52(10):648-653. Masala G. Occup Environ Med 1995. Irish RM. Effects of long-term organophosphate exposures on neurological symptoms.113(4):504-508. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Daniell WE. Buccafusco JJ. Office of Prevention Pesticides and Toxic Substances. Gillham R.58(11):702710. 1993 [online]. Environmental Protection Agency (U. Bradman A. Eskenazi B. 4/7/09 Young JG. Berry H. Rothlein J. The Pesticide Health Effects Study Group. et al. Washington (DC): U.44(4):352-357.38(4):546-563. et al. 1/12/09 Peiris-John RJ. and cholinesterase status of date dusters and harvesters in California. Rosenstock L. May. J Toxicol Environ Health A 2005. Am J Ind Med 1987. Phillips J. Effects of chronic. Jamal GA.84(5):731-736. Seiber J. vibration sense and tremor among South African farm workers. National Academy of Sciences.12(2):134-141. Caltabiano LM. Dinoff TM. Schenker M. Barr DB. Occup Environ Med 2001. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Scand J Work Environ Health 1998. McConnell R.20(2):115-22. Available at URL: http://www. McCauley L. Am J Public Health 1994. Sci Total Environ 2004. London L. Keifer M. Muniz J. Spurgeon A. Visuthismajarn P. Washington (DC). Ruberu DK. J Occup Environ Med 2002. Arch Environ Contam Toxicol 2000. Lasarev M. Santana J. Malathion deposition. Environ Health Perspect 2005.338(8761):223-227. Mounce LM. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Pesticides in the Diets of Infants and Children. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Chronic neurological sequelae to organophosphate pesticide poisoning. Weerasekera G. Available at URL: http://books. Petchuay C. gov/oppbead1/pestsales/01pestsales/market_estimates2001. EPA.114(5):691-696. Hansen S. et al. Weisskopf C. Rothlein J.52(2):190-195. and spatial learning in monkeys and rats. Samuels S. Johnson C. Prendergast MA. Int J Occup Environ Health 2006. Hore P.edu/ openbook. Chrislip D. Vitayavirasak B. Lambert WE. Savage EP. Myers JE. Steenland K. Robson MG. Levy LS. metabolite clearance. Takamiya K. low-level exposure to the organophosphate diazinon. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Russo J. Pilkington A.68(3):209-227 Maizlish N. O’Malley M. Calvert IA. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Gladstone EA. Terry AV Jr.332(1-3):71-80. Tumino R. Lewis JA.24(1):18-29. Beach J. Pedersen L.

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 . These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. malathion is metabolized to malathion dicarboxylic acid.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. In addition to reflecting exposure to the parent insecticide.5. For example. For general information about the organophosphorus class of insecticides.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3. parathion and methyl parathion are metabolized to para-nitrophenol. the level may reflect exposure to the environmental degradation products of these pesticides.

37) 5.68 (7.13-3.7-23.00) 2.10) 6.04-10.0) 18.0) 12.50 (1.70-15.95) 7.28) 2.40-13. 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.40) 9.46-2.63 (8.66-15.44-5.10 (5.0 (7.37 (4.17 (1.02 (7.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 5.90 (1.40-2.68-2.34) 1.01) 1.80) 1.05) 1. and is infrequently detected in ground water (IPCS.90-7.50 (1.20-11.53 (1.24-1.03) 1. dermal. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators. For instance.97) 2.70) 1.0 (10.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.26) 7.50-14.84) 1.20-16.40 (5.0 (7.0) 10.10 (3.04-10.0 (7.90 (1.76 (1.74 (1.9) 11.67 (1. and sprayed to kill mosquitoes.97) 7.15 (1.70 (1.20) 2.80 (7.98-15.30-9.0 (9.66-4.3) 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 1.76 (1.5 (8.47-13. Exposure can also result from contact with contaminated surfaces.50 (2.30-11.40 (6. air.0) 8. Approximately 21-24 million pounds per year were used domestically from 1987-1998.0) 15.30) 4.30-5.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.S.77-15.20-3.6) 7.0) 8. in 142 urban homes and preschools in North Carolina.3) 8.30 (2. but can be detected in streams receiving runoff from application sites.31-2.44-2.90 (3.71 (6.3 (10.50 (2.0) 12.9 (7.20) 2. 2005).89 (2. and inhalation routes.80) 2.20 (4.30) 4.0 (7.70 (1.8) 9.80 (1.5-24.19-3.90-2.3 (11.20) 4.40) 2.25) 1.80) 4.57 (2.0) 7.47) 1.80-10.20-2.4-15.05-5.29-1.90 (2.79-2.EPA.35) 1.77) 1.77-6.9 (10.97) 4.0) 11.39) 4.1) 5. USGS. chlorpyrifos was no longer registered for indoor residential uses in the United States.20 (2. 2002). Estimated intakes from diet and water have not exceeded recommended intake limits.4 and 0.30-1.30-12.20) 10. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.7) 9.0) 14.0) 12. and on plants for days to several weeks.47-9.50-4.63 (1. 2007).61 (1.40-10. Survey Geometric mean (95% conf.87-6.9-18.90) 7.70-16.44 (3.60 (2.8-15.0) 9.35) 2.90-8.10) 2.45 (1.09 (3. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.50 (2.64) 3.3 (8.30 (2.5.28-3.97) 2.81-2.47 (4.22 (1.62-2.90 (6.0) 10. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.5) 7.0 (13.8) 10.60 (4.32-1. applied to structures to kill termites.27 (7.40-26.24-3. Chlorpyrifos is Urinary 3.09 (2.000 pounds are used per year.30 (4.0 (7.74-9.0) 10.51 (1.63 (2.2 (10.EPA.83) 1.00-24.30) 5.96) 3.50-2.25) 3.7) 8. population from the National Health and Nutrition Examination Survey.67 (2.0) 12.13 (1.59) 2.67 (2. Approximately 80.60-2.0-28.02 (1.10-17.50-4.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.70-17.00) 3. 2002).91) 16.86) 4.60-4.9 (9.02) 1.9) 697 660 521 701 602 947 Limit of detection (LOD.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.72) 2.5.95 (4. After 2001.10 (1.92 (1.60 (5.00) 1. Fourth National Report on Human Exposure to Environmental Chemicals 135 . 5598-13-0 General Information The chemical 3.89-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10. 2921-88-2 Chlorpyrifos-methyl CAS No.22) 2.51) 1.0) 6.0) 12.43-2. 1999.55-5.16) 2.52-12.7) 13..99-4.50-2.S.and post-construction structural applications for termite control were to be phased out by 2005 (U.88 (1. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.60-3.00-8. and dust.47-11.51-2.80) 12.4 (10.40 (5.20-14.37 (1.4 (9.32) 2.80-8.4.52-2.10 (4. staying bound to soil particles.90-4.20-4.71 (1.31-2.50-8. It has low leachability.43-2.94 (4.19 (1. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.97-7. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.61) 75th 3.38 (3.30-2.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.36 (4.4 (8.60-3.39-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.72-4.S.50-5. pre.21) 3.1-16.29) 90th 7. interval) 1.70-11. The general population may be exposed to chlorpyrifos via oral. It also has been applied directly on animals to kill mites.91 (1.59-2.70-5.71 (2.90) 3.78 (7.61-7.77 (1.

30-1.5) 5.01) 3.57-2.88-10.66) 1.23) 14.09 (1.89) 4..33 (5.98 (7.06-4. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.24) 75th 2.41 (1.5.49-2.2) 6.62) 90th 5.05-1. 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.46 (2.69 (1.56 (4.14-8.64 (1. Once absorbed.24-4.1-21.6-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.64-7.27-1.55) 1.49-2.5 (6.57-2.3) 8.79-13.25-11.09-2.44 (1.44 (1.44 (6.99) 1.74) 1.86 (1.05-4.19) 3.97) 3.90-9. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.19) 6.83-11.52 (5.7) 7.58-5..23-1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.35-1.01) 1.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.56) 2.58 (1.81) 2.94-14.66-11.14) 1..65-15.91) 1.00-8.15 (4. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.35) 2.33 (1.85) 1.42-2.34-1. 2006. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.38) 3.44-6. 2005.91 (3.03) 1.72-2.44 (5.17-4.88 (1.05) 3.3) 8.68) 6.88-8.62-7..80-6.29 (3.54 (2.88-8.92-2.95 (1. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.3) 9. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. TCPy is more persistent in the environment than chlorpyrifos itself (U. 2005.32) 1.76 (3. 2002).75 (1.91) 10.07) 1.85 (2.58) 1. 2005.72) 2.93 (4.01) 3.93 (1.22 (6.940-1.63 (5.85-4.58) 5.43 (4. Thus.22 (4..00-13. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.8) 9.75) 6. The metabolite TCPy does not inhibit acetylcholinesterase enzymes. resulting in excess acetylcholine at nerve terminals.39 (4.93 (2.72) 1.80) 3.16) 6. cholinergic effects.48 (2.54) 5.31-1.37 (1..55 (4.64-2.1-38.91-13.53-5.S.49-2. and seizures.21-6.45-1.46 (1.92 (1.35) 1.45 (1.50 (4.96) 3. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.68) 1.12) 1.1 (7.98 (6.73 (1.6) 9.01) 99-00 01-02 99-00 01-02 99-00 01-02 3. population from the National Health and Nutrition Examination Survey.81 (3.11-9.24 (1.47 (1.11 (2.22) 1.80-11.58 (1.84-6.EPA.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.11) 7.33) 2.6) 10.49 (1.22-6. 2000). and other metabolites.82 (3. neurotransmission.80-4.77) 1.82 (2.93) 5. Roy et al.0) 10.56 (1.51 (1.78 (1.76 (2.30-4.85) 4.2 (7.60-3. vomiting.91-4.20-1.07) 5..56-2.33 (..31) 1. Slotkin et al.20 (2.16 (4.39) 6.09-3.59-2. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.00 (7. In pesticide applicators.24-1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).91 (4.4) 4.82-4.63 (4.71 (1.92) 3. Based on animal data and human cholinesterase monitoring during occupational exposure. paralysis.93) 2..9 (12.57) 2.11 (2. 2006a.56) 5.63-2.97-3. Ricceri et al.36) 1.88 (1.0) 16.66 (1.39 (2.05-3.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .47-2.65-11.71) 3. Metabolic hydrolysis leads to the formation of TCPy.09-1.17-4.31-4.58 (4.08) 6.1 (10.33-7.24) 5.12-3. 2006b).86 (3.53 (2.28) 2. interval) 1.02) 7. TCPy can also occur in the environment from the breakdown of the parent compounds.25-1.91) 2. 2006.00) 1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.82) 8.44 (5.47 (1.97) 3.62) 1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.0) 12. Urinary 3. 1984).0) 6.06 (5.87-3.24-24.83-2.88) 6.88-9.26-14.70-4.95 (3. weakness.57) 9.43-10.42 (5.86 (1.97 (2.48 (1.19-1. and producing acute symptoms such as nausea.S.47 (5.06 (1.83) 1.40) 1.99-8.94-12.3 (7. Survey Geometric mean (95% conf.24-5.21-1.05-8.55 (1.59) 3. Betancourt et al.25-12.97 (3.19-2.39-1.42 (6.28) 2.60 (1. Howard et al.27-7.12-1.91) 1.02 (5.85 (3.

Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 2004). median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. Magnaghi S. 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. Slotkin TA. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.EPA. Barisano A. Burns CJ. et al. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.. EPA at: http://www.atsdr. Whyatt et al. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. 2005).. environmental levels) and health effects is available from ATSDR at: http://www. 2005. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.Organophosphorus Insecticides: Specific Metabolites 2004.. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. References Adgate JL. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Catenacci G.. Following crack-and-crevice application of chlorpyrifos in their homes. Lotti A. 2002). but levels were roughly four to six times higher than the geometric means in the U. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Occup Environ Med 2006. 2005).S.. but not chlorpyrifos. Barr DB. et al. Koch et al... In a probability-based sample of 102 Minnesota children aged 3-13 years.S.. population (CDC. urinary TCPy levels in children were reported not to have increased (Hore 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. In Iowa farm families using several different pesticides.. 2005). 2004). Biomonitoring Information Urinary TCPy levels reflect recent exposure. 2000).e.html and from U.63(3):218220. 2005). Fourth National Report on Human Exposure to Environmental Chemicals 137 . Toxicol Sci 2006. Perera et al.. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. Eberly LE. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Curwin et al. Chlorpyrifos exposure and biological monitoring among manufacturing workers.S. 1992. Albers JW. 2005).. 2001). In Minnesota and South Carolina farmers who used chlorpyrifos.. representative subsample of NHANES 19992000 (CDC. 1999).gov/pesticides/.S. Garabrant D.S.cdc. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Betta A. Freeman NC. Seidler FJ. 2001) and Italy (Aprea et al. et al. Meyer A.5.109(6):583-590. Levels of TCPy in the U. Environ Health Perspect 2005.. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Burgess SC.92(2):500-506. Carr RL. Betancourt AM. Of 482 pregnant women living in an agricultural community.Reference values of urinary 3.. 2006). J AOAC Int 1999. the geometric mean urinary TCPy levels were similar in parents and children. Clayton CA. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. 2007). 2005). Additional information about external exposure (i. 2005.epa. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.. CDC. Haidar S.gov/toxpro2. MacIntosh et al. U. Aprea C. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.82(2):305-312. 2005. Lioy PJ. Aldridge JE.113(8):1027-1031. Environ Health Perspect 2001. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Berent S. Giordani B.. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al.

Int J Hyg Environ Health 2001. Rick DL. Capone F. Edwards RD. et al. Yang D.31 Suppl 1:98-104. Available at URL: http://www.207(2):112-124. Neurologic function among termiticide applicators exposed to chlorpyrifos.73:8-15. Toxicol Appl Pharmacol 1984. International Programme on Chemical Safety-INCHEM (IPCS).113(2):211-219. Slotkin TA. Bucelli R. Brain Res Dev Brain Res 2005. et al. Curwin BD. Meeker JD. Scand J Work Environ Health 2005. Honeycutt R. et al. Barr D.6-trichloro-2-pyridinol. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. MacIntosh DL. et al. Kinney P. Slotkin TA. Baker S.S. Wartenberg D. Slotkin TA. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Rauh V.93(1):105-113. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Ryde IT. Howell RJ. Harley K. Environ Res 1995. Freeman N. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. 4/7/09 Perera FP. Levin ED. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. et al.155(1):71-80. Reid TM. Chrislip DW. J Expo Anal Environ Epidemiol 2005. Lioy PJ. chlorpyrifos.114(10):1542-1546. Lorenzini P. Chlorpyrifos. et al. Hardt J. Kromhout H.nih. Camann D.5. Jett DA. Environ Health Perspect 2000. Alexander BH.114(5):746-751. Fortuna S. Seidler FJ. et al.51(1):53-65. Angerer J. A longitudinal investigation of selected pesticide metabolites in urine.org/documents/jmpr/jmpmono/ v99pr03. 1999. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Hammerstrom KA. Bailey SL. National Toxicology Program (NTP). Pellizzari E. et al. Freshour NL.71:99108. Jewell NP. 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. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Robson M. Zhang J. Head SL. 1992.15(3):271-281. Barr DB.112(10):1116-1124. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Biomonitoring for farm families in the farm family exposure study. Herrick RF. Weltzien E. Acquavella JF. Ozkaynak H. Saunders JH. Chapman P. Eskenazi B. Mandel JS.niehs. Jones PA. Steenland K. Barr DB. Environ Health Perspect 2006. Chuang JC. Howard AS. Bravo R. Bravo R. Cometa MF.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Exposures of preschool children to chlorpyrifos and its degradation product 3. Tsai WY.S. 4/7/09 Koch HM. Sharma V. Ryan PB.111(2):201-205. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. EPA). Nolan RJ. Lein PJ. Morgan MK. Heederik D. Gurunathan S.204(2-3):175-180. mothers and fathers living in farm and non-farm households in Iowa. gov/ntpweb/index. Bruun D. U. Roy TS. Fenske RA.6-trichloro 2-pyridinol in their everyday environments. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Shealy DB. 2921-882. Barr DB. Available at URL: http://ntp. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Croghan CW. Chlorpyrifos: pharmacokinetics in human volunteers. Pesticide residues in urine of adults living in the United States: reference range concentrations. Hore P. Environmental Protection Agency (U. Ricceri L. Environ Health Perspect 2006b. Interim registration eligibility decision for chlorpyrifos. Dick RB. Needham LL.5.inchem. Irish R. Environ Health Perspect 2005. Environmental Health Criteria 198. Sanderson WT. Environ Health Perspect 2006a. Hines CJ. Freeman N. Lu C. Seidler FJ. Striley C. J Expo Anal Environ Epidemiol 2005. Adgate JL. Gregg M. Sheldon LS. Third National Report on Human Exposure to Environmental Chemicals. Ryan L. Venerosi A. Hill RH Jr. Bradman A. Ann Occup Hyg 2007.9(5):494-501.10(4):327-340. Executive summary of safety and toxicity information. et al.15(4):297-309. Tate CA. et al. February 5. Toxicol Appl Pharmacol 2005. Levin ED. Toepel K. Seidler FJ. Robertson GL. 2005. Baker BA. Hein MJ.114(2):260-263. J Expo Anal Environ Epidemiol 2000. Urinary pesticide concentrations among children.htm. Environ Health Perspect 2004. Bennett DH. Atlanta (GA). Toxicol Sci 2006. Environ Health Perspect 2003. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. J Expo Anal Environ Epidemiol 1999.108(4):293-300.

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

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

< LOD means less than the limit of detection. Survey Geometric mean (95% conf.380 (<LOD-.270) < LOD 659 701 920 Limit of detection (LOD.200 (<LOD-.2.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 141 . see Data Analysis section) for Survey year 01-02 is 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.S.200 (<LOD-. population from the National Health and Nutrition Examination Survey.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * 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.670 (<LOD-1. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 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 .

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

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. 2007). Most granular formulations. an organophosphorus insecticide that is used to control insects on nuts. It is also used for cattle ear tag applications to control flies and ticks and. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. Once absorbed.S. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. diazinon was widely used in residential and garden application.2 and 0.45 (<LOD-3. diazinon cannot be sold for residential use. Diazinon is not well-absorbed through the skin. which may vary for some chemicals by year and by individual sample.EPA. Prior to 2000. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. and forage crops. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. fruits. 1998. 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. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks.EPA. 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. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 143 . 2004). and particularly when it was ingested in granular form. 2004). 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. Estimated intakes from diet and water do not exceed recommended intake limits (U. population from the National Health and Nutrition Examination Survey. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. vegetable. 1998). seed and foliar applications are planned to be phased out (U. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. in the past. aerial. 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.49 (<LOD-2. in some pest strips. It is toxic to birds. but these uses have been phased out. diazinon produced wild bird kills before use restrictions were in place. USGS.S. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine.7. since 2004. Before these restrictions. Inhalational and dermal routes of exposure can be significant for pesticide applicators.S. but is rapidly absorbed orally (IPCS. and other metabolites.

..49 μg/L. 2000. resulting in excess acetylcholine at nerve terminals. Diazinon has moderate acute toxicity in animal studies.cdc. vomiting. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate.EPA considers diazinon unlikely to be carcinogenic in humans. animal carcinogen. Thus.S. Intoxications in humans from intentional overdose. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. In the U. Survey Geometric mean (95% conf.S. EPA at: http://www. agricultural. diazinon does not accumulate in tissues (IPCS. Seifert and Pewnim. The U.e. subsamples of NHANES 1999-2000 and 20012002.epa. 1992). respectively. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. Olsson et al. and producing acute symptoms such as nausea. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. weakness.gov/pesticides/.atsdr. 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 two nonrandom samples of United States adults and children.. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. population from the National Health and Nutrition Examination Survey. Additional information about external exposure (i. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2003). respectively (Baker et al.S. 1998).Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..45 and 1. 144 Fourth National Report on Human Exposure to Environmental Chemicals . teratogen.html and from U.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 1.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.76 (<LOD-3.S. and seizures.. In addition to being a human metabolite of diazinon.. paralysis.72 (<LOD-4. In animals. Diazinon is not considered to be a mutagen. 1986 Rajendra et al. or reproductive toxicant (IPCS. and indoor applications have been documented. 2002).gov/toxpro2. cholinergic effects. 1998). in the 2001-2002 subsample (CDC. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. 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. environmental levels) and health effects is available from ATSDR at: http://www. 1986. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. At high doses.

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

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

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

metabolite clearance. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Environ Health Perspect 2004. Pluth JM. Goldhaber M. 2007 [online]. Kedan G. et al. Sharma GD. Jaloszynski P. and cholinesterase status of date dusters and harvesters in California. Genetic toxicity of malathion: a review.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Trzeciak A.gov/oppsrrd1/REDs/ malathion_red. Clayton CA. U. Giri S. Jewell NP.114(2):260-263. Samuel O.inchem. Dumoulin MJ. Toepel K. 2005. Gosselin NH. Barr DB.132(4):794-795. Rappaport E. et al. Grether JK. The Quality of Our Nation’s Waters. Ryan PB.S. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo.epa. Reregistration eligibility decision (RED) Malathion.gov/circ/2005/1291/. 1992-2001. Brunet RC. Eskenazi B. Hertz-Picciotto I. Griffith W. Fenske RA. Carrier G. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. EPA). Hammerstrom KA. Malathion (addendum). 4/7/09 Kissel JC. Reproductive outcome in women exposed to malathion. Swan SH. Am J Epidemiol 1990. Szyfter K. Lu C. Harris JA.109(6):583-590. Geological Survey (USGS).S. revised February 15. Lioy PJ. Barr DB. Prasad SB. Erratum in: Toxicol Sci 2003 Aug. Neutra R.77:1009-1010. July 2006.pdf. Giri A. O’Neill JP. 6/1/09 U. A longitudinal investigation of selected pesticide metabolites in urine. Thomas D. Curl CL.73(1):182-94. Freeman NC. Pesticides in the Nation’s Streams and Ground Water. Third National Report on Human Exposure to Environmental Chemicals. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers.514(1-2):223231. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Mutat Res 1999. International Programme on Chemical Safety-INCHEM (IPCS). htm. Lu C. J Expo Anal Environ Epidemiol 1999. Flessel P. MacIntosh DL.112(10):1116-1124. Eberly LE. Irish R. Petitti D. Toxicol Sci 2003 May. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Atlanta (GA). Environ Health Perspect 2006.usgs. Am J Public Health 1987. Barr DB. EPA 738-R06-030. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.56(10):2393-2399. Quintana PJ. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.9(5):494-501.org/documents/jmpr/jmpmono/v2003pr06.38(4):546-553.22(1):7-17. Mutat Res 2002. Blasiak J.S. Centers for Disease Control and Prevention (CDC). Cancer Res 1996. Krieger RI. Albertini RJ. Environ Health Perspect 2001. Weltzien E. Available at URL: http://www.74(2):following table of contents. Arch Environ Contam Toxicol 2000. Harley K. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Bradman A. Dinoff TM.15(2):164-171. Environmental Protection Agency (U. J Expo Anal Environ Epidemiol 2005. Malathion deposition. Needham LL. Environ Mol Mutagen 1993. March 2006. Nicklas JA. Barr DB. Available at URL: http://pubs. Available at URL: http://www.445(2):275-283. Bravo R. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Hooper K. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Bouchard M.

20-5.34 (3. 2003).40-4.70 (2.0) 2.90-9.33 (1.45) 5.10) 4. fish.50 (1.30 (1.EPA.700 (<LOD-. and oral routes can occur in pesticide and agricultural workers (Muttray et al.12) < LOD < LOD 1.300-.61) < LOD 1.50 (2.46 (3. and to a lesser extent.48) 90th 2. Once absorbed.85 (2.70 (2.0) 3. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.910) < LOD < LOD . O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.80 (2.0) 3.60) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.09-1.910) < LOD .60-19.02-6.66 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. Methyl parathion is not registered for residential use in the United States. 2006). It had been applied to cotton.910) < LOD < LOD < LOD 1.50-9.10 (<LOD-6.71 (2.940 (<LOD-2.47) 2.92-2.91-3.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. Survey Geometric mean (95% conf.70-6.80 (1. Estimated intakes from diet and drinking water have been below recommended limits.20 (2. Many previous registered agricultural uses of methyl parathion have been cancelled (U. 1977).990-1.37-4. first registered in 1948.01-4. methyl parathion was rapidly absorbed after ingestion.0) 4. peak domestic use was as high as 5-6 million pounds per year.00 (2. more slowly absorbed through the skin.41-4.00 (2.37-2. Methyl parathion has low water solubility.40-3.40-4.21 (2. binds tightly to soils resulting in low leachability.27) 2.70) 2.67) < LOD 1.01) 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.13-1.61) < LOD 1.10 (3. and of the chemical nitrobenzene.8 and 0.01) 695 660 518 679 603 941 Limit of detection (LOD.18-3. Fourth National Report on Human Exposure to Environmental Chemicals 149 .32-3.30-3.74) 5. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.33) 2. Increased risk of exposure via dermal.11-4.90-11.50) 3. was once a restricted-use insecticide with limited applications on certain agricultural crops.0 (3. pulmonary.36-1.70-3.69 (2.30-5.32-1.00) 3. Methyl parathion use is highly restricted.80) 2.50) 3. but by 2003.21-1.15-3. with limited applications in agriculture.40) 2.45 (1. Given its limited use.40 (1.16) < LOD 1. Both are toxic to birds.71 (3.67 (1. Morgan et al.28 (1.50 (1.50 (2.S.32-1.20) 5. 2007).28-4. population from the National Health and Nutrition Examination Survey.19 (.70 (3.1. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.32 (1.90 (1.50) 1.57) 1. Ethyl parathion. which may vary for some chemicals by year and by individual sample.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. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.80 (2.50-14.70) 2.44) 2.70) 2.0) 3.40) 4.850) < LOD .50 (1.0) 3.S.62 (1.860 (<LOD-1.37-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. on cereal grains.10) 22. and eliminated rapidly from the body after absorption (Kramer et al. In the 1990s. < LOD means less than the limit of detection.60-5. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.20 (<LOD-2. 2000).10-1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .22-3.28 (1.37) 2.298-00-0 Ethyl Parathion CAS No.30 (2.S.70 (2. In animal studies.10 (3.. all registered uses were voluntarily cancelled (U.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Methyl Parathion..79) 4.EPA.26 (1.89 (2. and has a short half-life in soils and on plants.0) 3. 2002. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.50 (1.730 (<LOD-.790 (<LOD-.60-36.72 (3.92) 5.. and aquatic invertebrates.70-6.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .50) 2.05) 4.57-4. ethyl parathion.58) 3.770 (.10-11.11) 2.49 (1.60 (4.40) 1.69) 4.30-16.70 (<LOD-3.60-24.70-3.70-6.

33-6. but lists ethyl parathion as a possible human carcinogen.940 (<LOD-1.23) 1.930 (. accidental exposure.25 (2..87 (1.790-. EPA at: http://www. paralysis. Orsorio et al.S. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2004). Additional information about external exposure (i.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .S.31-3. gov/toxpro2.39 (1.840 (.720 (<LOD-.970 (.790-1.08-3. and seizures.Organophosphorus Insecticides: Specific Metabolites Metabolites”). environmental levels) and health effects is available from ATSDR at: http://www.440 (<LOD-.14-3. gov/pesticides/.1) 2.30-1. teratogenic.90 (1.7) 3.500) < LOD < LOD .60-2. vomiting.38-3..78-2.72-2.67 (3.35-3. The metabolite.83 (1.690-1. 150 Fourth National Report on Human Exposure to Environmental Chemicals .33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .44-3. In large doses.29) 2.430 (.08) < LOD .3) 2.05) 4. Parathion and methyl parathion have high acute toxicity in animal testing. Zurich et al. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.48-4.730-1.20) 3. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.cdc.97 (2. U.97-10. resulting in excess acetylcholine at nerve terminals.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 .41-2.78 (2.20) .09) 2.55 (<LOD-3.88) 1.10) 90th 2..15) 3. Slotkin et al.60) 2.00 (1.97 (<LOD-4.880 (.720-1. Jaga and Dharmani.20 (3. 2006.10 (1.9) 1.56-2.96 (1.30) 3.e.73 (1.950) < LOD .00 (1.epa. 1995.61) 4.400 (<LOD-. Methyl parathion is not considered genotoxic..95) 1. Thus. 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.01-3.33-3.57-2.82) < LOD .EPA considers methyl parathion unlikely to be carcinogenic to humans. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.93 (2.77-7.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. paranitrophenol.55) 2.2) 2.25) 1.79) 1.07) 2.86 (2.79 (1.33-3.980 (. does not inhibit acetylcholinesterase enzymes. ethyl parathion.13-12.01 (2. WHO.88 (1. 1978.67-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.31) < LOD . Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.04 (2.310-.26 (1.89 (2. Survey Geometric mean (95% conf. 1991).640) < LOD < LOD 1.2) 2.4 (3.07 (1. methyl parathion.91) 1.530) < LOD < LOD < LOD .60 (1. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.970 (.94-47.94-4.830-1.78) 2.21) 1. population from the National Health and Nutrition Examination Survey.00) 2. and unintentional acute or chronic high-level occupational exposure (Hill et al.atsdr.21-21.92 (2.57-7.89 (2.37-1. 1990.04) 1..870) < LOD . or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. 2006.35-3..16-4.39) 1. 2003.91 (1.17-4. 1995).80 (1. Karanth and Pope et al.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .800-1.29) 1.930 (.29 (2.11) 1.71) 1.01 (.70) 3.57) 6.59 (1.98-7.370 (<LOD-..26) 17. and producing acute symptoms such as nausea.71 (1.82 (2.540) < LOD .80 (1. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.84) 3.850-1.43) 4. weakness.96 (1.76-14.78-2..08 (1.S. and other metabolites.html and from U. In addition to being a metabolite of methyl and ethyl parathion.17) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.44-3. 2005.680 (<LOD-1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13) 4. 2004).11-4. Methyl Parathion. At high animal doses of methyl parathion. Lores et al.15-10. cholinergic effects.

2005). Baker SE.112(10):1116-1124. Pathak S. Arch Environ Contam Toxicol 1977. Pesticide workers may have much higher levels following pesticide applications. In a study of workers who handle parathion.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. oral or dermal administration. Bailey SL. 2005. Leng G.S. Barr DB. Hill et al. 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. 1995). Lin LI. Kissel JC. Baker S. Rubin et al. Alley CC. Barr DB.21(1):5767. 2004).5 mg (500 µg)/g creatinine for workers at the end of shift. Pope C.. et al. 2002. Atlanta (GA). Hill RH Jr. Lewalter J. 2005. References Barr DB.110 Suppl 6:1085-1091. Weltzien E. Environ Health Perspect 2004. Karanth S. Rev Environ Health 2006. Jewell NP. Needham LL. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. McCann KG. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. et al. Dharmani C. Lu C. Environ Health Perspect 2002.56(7):449553. Barr JR. Clark JM. 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. population (Olsson et al. Environ Health Perspect 2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.org/documents/jmpr/jmpmono/v95pr14..htm. Kedan G. and levels were similar or slightly lower that those in a small convenience sample of the U. Runkle KD.15(2):164-171. Laboratory investigation of a poisoning epidemic in Sierra Leone. and many residents were symptomatic (Barr et al. 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. Rockhold RW. J Biomed Sci 2002. Cline RE. 2005). Turner WE. J Anal Toxicol 1990.. Costa LG. Neurotoxicol Teratol 2003. Methyl parathion: an organophosphate insecticide not quite forgotten. Moomey CM. 2002). Hill RH Jr. McCann et al. Slach EF. et al. Barr DB. Bradway DE.. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Chicago area methyl parathion response. et al. Head SL. Centers for Disease Control and Prevention (CDC). Lores EM. Eskenazi B.S.inchem. Baker RC. 2005.33(5):270-276. Pesticide residues in urine of adults living in the United States: reference range concentrations. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. 1999). Fourth National Report on Human Exposure to Environmental Chemicals 151 . 1995.71:99108. Giordano G. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect.215(3):182-190. Guizzetti M. Curl CL. general population (CDC. Pharmacokinetics of methyl parathion: a comparison following single intravenous.. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Harley K. McClure PC.110 Suppl 6:1075-1078. a range of values several hundred times higher than levels found in the U. 2002.. Ashley DL. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.14(4):213-216. Third National Report on Human Exposure to Environmental Chemicals. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Gregg M. Wellman SE.6(2-3):159-173. Moseman RF. ACGIH recommends a BEI of 0.9:311-320. Environ Res 1995. Occup Environ Med 1999. Toxicology 2005. International Programme on Chemical Safety-INCHEM (IPCS). et al.25(5):599-606. DiPietro E. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Morgan DP. 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. Head SL.. 4/7/09 Jaga K. Kramer RE. Bradman A. CDC. Parathion-Methyl (addendum). Griffith W. Hetzler HL. Shealy DB. Available at URL: http:// www. Hryhorczuk DO. Arch Environ Health 1978. J Expo Anal Environ Epidemiol 2005. Role of individual susceptibility in risk assessment of pesticides. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter.

Monnet-Tschudi F. Dunlop B. Available at URL: http://www. Esteban E. pdf. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. U. Honegger P.20(4):533-546. Hill RH Jr. Seidler FJ. Yacovac R. Available at URL: http://www.376(6):808-815. EPA). Tate CA. Methyl parathion in drinking water.epa. 5/19/09 Zurich MG.S. Facts.D. Costa LG. WHO/SDE/WSH/03. Pesticides in the Nation’s Streams and Ground Water. Schilter B. revised February 15.S.110 Suppl 6:1047-1051.gov/circ/2005/1291/. Am J Ind Med 1991. Environ Health Perspect 2002. Hill G.S. 6/1/09 World Health Organization (WHO).04/106.usgs. 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. 1/14/09 U. Jung D. Investigation of a fatality among parathion applicators in California.Organophosphorus Insecticides: Specific Metabolites Muttray A.pdf.epa. March 2006. Slotkin TA. Ryde IT. 2007 [online].who. 1/12/07 U.pdf. Backer G. The Quality of Our Nation’s Waters. Rubin C. EPA). Ames RG.int/water_sanitation_health/dwq/chemicals/ methylparathion.201(2):97-104. Olsson AO. Osorio AM.S. Geological Survey (USGS). Letzel S. et al. Barr DB. May 2003. Anal Bioanal Chem 2003. External and internal exposure of wine growers spraying methyl parathion. Environ Health Perspect 2006. Environmental Protection Agency (U. gov/oppsrrd1/REDs/methylparathion_ired. Case No. Nguyen JV. Toxicol Appl Pharmacol 2004. 2004. Ethyl parathion.114(10):1542-1546.162(2-3):219-224. 0153. Kieszak S. Interim reregistration eligibility decision (IRED) for Methyl Parathion. 1995-1996. Environmental Protection Agency (U. Rosenberg J.S. Toxicol Lett 2006. Mengle DC. 1992-2001.gov/oppsrrd1/REDs/factsheets/0155fct. Available at URL: http://www. EPA-738-FOO-009. R. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Available at URL: http://pubs. Ohio.E. 152 Fourth National Report on Human Exposure to Environmental Chemicals . September 2000. Sadowski MA. Levin ED.

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

820) < LOD < LOD .700-.780 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .580-1. Survey Geometric mean (95% conf.55) .S. interval) Selected percentiles ( 95% confidence interval) Sample 95th .27) .670 (<LOD-1. see Data Analysis section) for Survey year 01-02 is 0.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .300-1.740-1.700-1.2.210-1.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-. Survey Geometric mean (95% conf.780 (.210 (<LOD-.410 (<LOD-1.17 (.430 (<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 .15) < LOD .07) .500 (.850 (.680 (<LOD-. which may vary for some chemicals by year and by individual sample.470 (.610 (<LOD-1. population from the National Health and Nutrition Examination Survey.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.780 (<LOD-1.31) . 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. population from the National Health and Nutrition Examination Survey.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.250 (<LOD-.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .21) < LOD .840) 669 687 929 Limit of detection (LOD.950) < LOD < LOD 1.64) .840 (. < LOD means less than the limit of detection.670) 567 810 1104 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.780 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .210-. 154 Fourth National Report on Human Exposure to Environmental Chemicals .S.760 (<LOD-.94) .

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

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

Eriksson and Fredriksson..gov/toxprofiles/ tp155. 2002). neurochemical changes in cholinergic. et al. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. 2003. 1998. Thomson BM. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. 2004. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.. Kim et al. McCarthy AR. Kunimatsu T. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.. Wang SL. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Kang IH. Pogo BG. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Neurotoxicol Teratol 2001. Ose K. 2005).. Kuhn K. 2005). Kim TS. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. 2005). 2000. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Garey J.8(1):197-202.cdc. Shukla Y. EPA at: http://www. Lee SJ. and permethrin) in the Hershberger and uterotrophic assays. and striatal dopamine levels in male and female rats. Pauluhn J. Ranft U. McCarthy et al. Shafer. Toxicol Appl Pharmacol 2006. Go V. Varoli FM. Hu et al. 1991. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Leng A. Bernardi MM. Fredriksson A. Wolff MS. Leng G. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Idel H. Wolff MS. Kuhn KH. 1999. 2001. Shaw IC.. Yamada T. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Pyrethroid pesticide-induced alterations in dopamine transporter function. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002.1/15/09 Aziz MH. Caudle WM. Neurosci Lett 2001. 2002). Adhami VM. Shin JH. Abell AD. Leng G. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays.. Additional information about pesticides is available from U.html. Okuno Y. Zhao RC. Guillot TS. Levsen K. cdc. 2003. Int J Hyg Environ Health 2002. Neurotoxic effects of two different pyrethroids. Ray et al. tremor. WHO. References Agency for Toxic Substances and Disease Registry (ATSDR). Hu JY. Cruz-Casallas PE. epa. Garey and Wolff. Elwan MA. Lazarini CA. Moniz AC. Toxicol Appl Pharmacol 1991.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. et al. Indoor pyrethroid exposure in homes with woollen textile floor coverings. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. 2006). Leng G. Available from URL: http://www. Richardson JR. Miller GW. Environ Health Perspect 1999. Lazarini et al. Regul Toxicol Pharmacol 2002.62:101-108. Kunimatsu et al. Florio JC. Lemonica IP. 2003. Estrogenic and antiprogestagenic activities of pyrethroid insecticides.211(3):188-197.50(2):245-255. Soderlund et al. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.8(1):18-21. Bernardi MM. Sunami O. salivation. Moniz et al. Agrawal AK. motor activity.27(4):609-614. Wieseler B. J Reprod Dev 2004. hypersensitivity. Neurotoxicol Teratol 2005. Elwan et al. No relationship of indoor air or housedust concentrations of permethrin and irritant symptoms was found in a study of urban residents in 80 private homes (Berger-Preiss et al. 2001. Toxicological profile for pyrethrins and pyrethroids. on immature and adult mice: changes in behavioral and muscarinic receptor variables. J Environ Monit 2006. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Kamita Y. Generally. 2006. Estrogenicity of pyrethroid insecticide metabolites. Eriksson P. fenvalerate.107(3):173-177. Idel H.205(6):459-472. Go et al.. September 2003. Spinosa HS.35(2 Pt 1):227-237. et al. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.. Bull Environ Contam Toxicol 1999. Xenobiotica 1997.gov/pesticides/ and from ATSDR at: http://www. Salzgeber SA.108(1):78-85. choreoathetosis.300(3):161-165. 2006. and seizures (ATSDR.. In California. Song L. Berger-Preiss E. 2002. et al. 2003.. Yang J. dopaminergic. Fourth National Report on Human Exposure to Environmental Chemicals 157 . 2005). Seth PK. Lewalter J.atsdr.html.27(12):1273-1283.23(6):665-673.. Biochem Biophys Res Commun 1998. Sugiri D.gov/toxpro2. In developing rodents. Garey J..251(3):855-859. bioallethrin and deltamethrin.. Chen JH. Kim IY. Kim HS.atsdr.S.

April 2002. Pyrethroid insecticides: poisoning syndromes. Available at URL: http://www. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .htm.S. O’Malley M. 5/26/09 U. EPA).Pyrethroid Pesticides Ray DE. Available at URL: http://whqlibdoc.38:95-101. 19962002.usgs. Shafer TJ. Meyer DA. EPA). Available at URL: http://www. resmethrin. Piccirillo VJ. Pyrethroid illnesses in California. June 2006b. J Toxicol Clin Toxicol 2000. EPA).113(2):123-136. Available at URL: http://pubs. Soderlund DM.epa.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Geological Survey (USGS). synergies. Crofton KM. Spencer J. Rev Environ Contam Toxicol 2006.gov/ circ/2005/1291/.who. Environmental Protection Agency (U. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Environ Health Perspect 2005. Revised February 25. 5/26/09 U. Forshaw PJ.epa. Environmental Protection Agency (U. March 2006. Xenobiotica 1992.S.171:3-59. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).S. June 2006a.pdf. Laird WJ.htm. Permethrin. Clark JM.S. Available at URL: http://www.S. Reregistration Eligibility Decision for Cypermethrin.S. Lesser JE. Sheets LP.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Marsh JR. Pesticide and Evaluation Scheme. Mullin LS. sumithrin synthetic pyrethroids for mosquito control. 5/26/09 Woollen BH. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. U.gov/oppsrrd1/REDs/cypermethrin_red.22(8):983-991. 2007. 2005. 5/26/09 U. 1992–2001.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Pesticides in the Nation’s Streams and Ground Water.epa.S. pdf. Safety of pyrethroids for public health use. et al.10.186:57-72. and therapy. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Sargent D. Environmental Protection Agency (U. World Health Organization (WHO). Toxicology 2002.

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

Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 160 Fourth National Report on Human Exposure to Environmental Chemicals .S.2.2 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 831 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 701 594 957 Limit of detection (LOD.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.

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. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 161 . Survey Geometric mean (95% conf.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 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.

162 Fourth National Report on Human Exposure to Environmental Chemicals . Drexler H. Hoppe HW. Rev Environ Contam Toxicol 2006. Seiwert M. Angerer J. Olsson AO. Heudorf U. Becker K. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Sugiri D. 2005. Hadnagy W. Ball M. Williams RL. 19962002.77(1):67-72. Atlanta (GA). Pyrethroid illnesses in California. J Expo Anal Environ Epidemiol 2003. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Environ Health Perspect 2001. Angerer J. et al. Angerer J. Heudorf U. Arch Environ Contam Toxicol 2004.206(2):85-92.209(3):221-233. Int Arch Occup Environ Health 2004. Third National Report on Human Exposure to Environmental Chemicals. Spencer J. Int J Hyg Environ Health 2006. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Angerer J.109(3):213-217. Barr DB. Centers for Disease Control and Prevention (CDC). Schulz C. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.Pyrethroid Pesticides References Baker SE. O’Malley M. Leng G. Int J Hyg Environ Health 2006. Idel H.46(3):281-288. Butte W. Bernard CE. Krieger RI. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ranft U.209(3):293-299.186:57-72. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Berger-Preiss E. Kolossa-Gehring M. Int J Hyg Environ Health 2003.13(2):112-119. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Heudorf U.

280-.670 (..570 (.730 (.230) .43) . ciscypermethrin and cis-cyfluthrin.710-1.630-.460 (.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.600) .630 (. Generally.510 (.210) .330 (.460-.960 (.490-1.11) .380-.630) .2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.730 (.610) . transcypermethrin and trans-cyfluthrin.430-. The presence of cis-3-(2. 1999).690) .670-1.2-dichlorovinyl)-2..210-.2-dichlorovinyl)-2. but it can also reflect exposure to cis-3-(2.120-.340) . Cyfluthrin.300-.740-2.2dichlorovinyl)-2.610) .47 (.2-dichlorovinyl)-2. the presence of trans-3-(2.370-.520) .or trans-3-(2.24) 1.270-.710) . trans-permethrin. Kuhn et al.28) 671 680 518 701 591 957 Limit of detection (LOD.300 (.420-.880 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.340-.120-.580) 1.1 and 0. cis-permethrin.890 (.500 (.202 (.12 (.340) .890 (.110 (<LOD-.35) 1. but can also reflect exposure to trans-3(2.53) .330) . 52315-07-8 CAS No. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.530 (.580-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.670-1.260 (.900 (.470 (.180) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.270 (.80) .680-3.820 (.110-.950-2.630) .220-.350) .200-.220) .240) . In the body.110-.200) .160 (.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.910-5.510 (. and trans-cyfluthrin.650-1.210) 90th .770-1.250-.640 (.770) .670-2.380-.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .140 (<LOD-.730 (.440 (.68) .2-dichlorovinyl)2.270 (.600 (.160 (<LOD-.120-.410) . 1985. population from the National Health and Nutrition Examination Survey.310) . which may vary for some chemicals by year and by individual sample.740) 1. cis-3-(2.280 (.200) .2-dichlorovinyl)- CAS No.380-.07 (.740 (.68 (.790-1.790 (.550) .32) .21) .1.200 (.180 (.2-Dichlorovinyl)-2. 1985.460-1.170 (.490-.S.220-.490-1.870) 1. Kuhn et al.68359-37-5 Cypermethrin Permethrin CAS No.790) . trans-cypermethrin.380) .370 (.44 (.700) .490-.77 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.50) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.600-1.250 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.510 (.140 (.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 .68) .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .850 (.300 (.35) .380 (.570-.400-.and trans-isomers.240) .740-1.08) . 1999).160 (.2dichlorovinyl)-2.220-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.920) 1. Biomonitoring Information Urinary levels of cis. cis-cypermethrin.15) .13 (.150 (. more of the trans-metabolite than Urinary cis-3-(2.54) .155-. The chemical trans-3(2.200-.780) .680 (.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.200-. Fourth National Report on Human Exposure to Environmental Chemicals 163 . and ciscyfluthrin.120-.262) * * * < LOD < LOD .470-1.200) < LOD < LOD < LOD . Similarly.410) .500 (.790-1. Survey Geometric mean (95% conf.270 (.220-.300-.

2006) and 1177 urban adults and children (Heudorf et al.390 (.300 (.24) .360-1.160 (<LOD-.11) .190 (.580) .120 (.320) .150-. 164 Fourth National Report on Human Exposure to Environmental Chemicals . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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 . 2006. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240 (<LOD-.2-dichlorovinyl)-2..530 (.750 (.710-3.440 (. median urinary levels of trans-3-(2.230-.350 (.540 (.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 * * .260-.530 (.33) .230-. post- Urinary cis-3-(2.290 (.380-.Pyrethroid Pesticides 2.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.250) .450-1.31) .150-.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al..104-.230-..190) .170 (..700) .250) 90th . 2002). Cyfluthrin.260 (.300) .300 (.170) < LOD < LOD < LOD .290-.450-.430 (.400-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1..59) .270) .260) . 2003).810 (. 2001.840 (.370-. Survey Geometric mean (95% conf.67) . Studies in Germany of 396 children and adolescents (Becker et al.300) .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.220) . 2004).200 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.780) 1. 2006).570) . 2001) showed urinary levels of cis.180-. 2006).12-2.2-dichlorovinyl)-2.11) .2-dimethylcyclopropane carboxylic acid did not increase.390-.750-1.138 (.S.550-1.640-1.840 (.700-2.220 (.2-dichlorovinyl)-2.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC. Other studies have provided evidence that urinary levels of cis.540 (.560) 1.350) .2dichlorovinyl)-2.890 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.400 (.920 (.33 (.270 (.690-1.550-1.450 (.130-.150-.290) .440-.320-.830) .and trans-3-(2. Lu et al.440 (.270) .800 (.260 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .410) .590) . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.59 (1.250-.210-.250) ..190) .680 (.182) * * * < LOD < LOD . urinary levels of cis-3-(2.080-.550 (.540) .780 (. In a study of urban residents in Germany (Berger-Preiss et al.600 (.900 (.640 (.2-dichlorovinyl)-2.710 (.700) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.680-1. 2004. representative NHANES 2001-2002 subsample (CDC. population from the National Health and Nutrition Examination Survey.250 (<LOD-.250-.890) .180 (...140-..270-.340) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. 2006.430-1.640-1. 2003).280-. In a study of volunteers.300-. 2005).49) .80) .550) .380 (.S.370-.340) .470-1. urinary trans-3-(2.29 (.580-1.640-.420 (.390-.11 (.290) . the median and 95th percentile of urinary levels of cis-3-(2.200) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. 2005).880) .59) .220 (.and trans-3(2.500 (. In these volunteers.. Schettgen et al.21) .260 (.250-.67 (. In the same residents. 2005).640) 1. 2002).200-.2dichlorovinyl)-2.550) .430-.37) .03) 1. 2005).2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.590 (. 2005) In a small group of indoor pest-control operators.380) .370-.340-.440-.510-1.560) .200-.230 (.280 (.170 (.680-1. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al..2-Dichlorovinyl)-2.11) 1.12 (.

500 (.08-4.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .40 (1.410 (<LOD-.69) 1.730) .26 (.55-4. population from the National Health and Nutrition Examination Survey.670) .610) 1.07 (1.23) 2.680-1.68) 1.69 (1.620) < LOD 2.460-.560 (.95) 2.14-2.09 (.17 (.4 and 0.470 (.87 (1.19 (2. Fourth National Report on Human Exposure to Environmental Chemicals 165 .840-1.970 (.2-dichlorovinyl)-2.550 (.08-6.S.48) 4.7) 2.670) .780 (.56) 2.39 (1.19) 1.97-11.01 (1.77 (1.490-1.530) .56 (1.60) 1. however.560 (.60-4.5) 2. 2005).920-1.64-4.23 (.08) 1.63) 1. Biomonitoring studies on urinary levels of cisor trans-3-(2.760) .84 (1.700) .55-5. Finding a measurable amount of cis.77) 1.50 (1.42 (2.54 (1.27 (1.11-1.11-2.400-.10) 2.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.41 (1.14) 1.81) 2.710 (.59 (1.820) .800-1.580 (.85) 4.54) 4. which may vary for some chemicals by year and by individual sample.17-1.410 (<LOD-.750) .56) 2.and trans-3-(2.910-1.520-. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.60) . The maximum post-application urinary levels.28 (1.03-1.810-1.460-.66) .91 (1.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.76-3.95) 3.2dichlorovinyl)-2.Pyrethroid Pesticides application median urinary levels of summed cis.49-5. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.49-3.470 (<LOD-.17 (.400 (<LOD-.16) 1.22 (1.20 (.37 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.700-1.07-3.520) .2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin. < LOD means less than the limit of detection.68) 1.42) 1.25 (1.66) 691 680 518 690 595 954 Limit of detection (LOD. trans-Cypermethrin.860) . Urinary trans-3-(2.4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005).850-1.28 (2.77) 2.41-14.2-dichlorovinyl)-2.68) 2.39-5.440 (<LOD-.55-3.830-1.or trans-3-(2.01) 4.63) 1.14-6.560 (.570) 90th 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.910-1.56 (1.35) 1.94 (1.660) 1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .90) 1.500) .2-Dichlorovinyl)-2.43) 2.68-2. Survey Geometric mean (95% conf.03-1.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .19 (3.410-.76-4.480-.420 (<LOD-.20 (.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.25-3.940 (. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.20 (.500-.410-.89 (2.49-3.490 (<LOD-.62 (1.68-3.13) .12-6.

850-3.60 (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 .20-2.Pyrethroid Pesticides Urinary trans-3-(2.02-1.850) .700 (.15 (1.34-3.00 (1.880-1.89) 2.57 (1.30-3.15-3.35 (1.26 (1.08 (.770) < LOD 2.930-1.42) 1.00) 1.65) 1.47-2.800-1.410-.760 (.75 (1.470-. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.07-2.33-2.570 (<LOD-.750) .780) 90th 1. trans-Cypermethrin.15-3.S.55 (2.570 (.730) . 166 Fourth National Report on Human Exposure to Environmental Chemicals .970 (.45 (1.19) .610-.30-6.880 (.35) 1.640) .33 (1.880 (<LOD-1.87-8.74) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.34-4.44) 2.29) 1.91-11.2-Dichlorovinyl)-2.740) .19 (1.64 (1.91) 1.45-2.560 (.70 (.55 (2.80) 1.48-2.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .12 (.81 (2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.40-2.07-1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey.60) 2.720-1.37 (1.800-1.87) 1.47 (1.480-.13) 1.42 (.87) 1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .36 (1.57) 3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.74) 2.20 (1.48 (1.15) 2.67 (2.15-3.31 (.33-1.39) 1.47-2.87 (1.530 (.91 (1.39 (1.27-2.540) .55 (2.00) 5.3) 2.520 (<LOD-.780) .700-.36) 2.580 (.780 (<LOD-.61) 1.670) .56-5.68) 3.22-2.60) 2.27-2.00) 1.41) 1.12-1.31 (2.87-3.65 (2.11) .56-2.530 (<LOD-.08 (.07-3.07) 2.700 (.900 (<LOD-1. Survey Geometric mean (95% conf.580) .440-.22) 1.98 (1.56 (1.86 (2.22-1.15) 3.470 (.16 (1.07) 2.13) .720-1.00-5.570-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.660) .500-.720 (<LOD-.31) 1.28) 2.850) 1.820-2.

Idel H. Leng G. Drexler H. Angerer J. Biological monitoring of workers after the application of insecticidal pyrethroids. Leng G. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Idel H. Heudorf U.68(6):1160-1163. George DA.209(3):221-233. Levsen K. Kolossa-Gehring M. Ranft U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Atlanta (GA). Int Arch Occup Environ Health 2003. Heudorf U. Wieseler B. Int J Hyg Environ Health 2006. Barr DB. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Ranft U. Leng G. Int J Hyg Environ Health 2003. Idel H. Hardt J. Angerer J. Int J Hyg Environ Health 2002. Drexler H. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides.205(6):459-472. Angerer J.134(1-3):141-145. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Heudorf U.Pyrethroid Pesticides References Becker K. Kuhn K.209(3):293-299. Environ Health Perspect 2001. Third National Report on Human Exposure to Environmental Chemicals.62:101-108. Bull Environ Contam Toxicol 1999. Schettgen T. Int Arch Occup Environ Health 2004. Pearson M.76(7):492-498. 2005. Angerer J. Bartell S. Seiwert M. Hadnagy W. Butte W. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.114(9):14191423. Int J Hyg Environ Health 2006. et al. Berger-Preiss E. Angerer J. Heudorf U. Sugiri D.77(1):67-72. Sugiri D. Berger-Preiss E. Hoppe HW. Permethrin and its two metabolite residues in seven agricultural crops. Schulz C. Environ Health Perspect 2006. Centers for Disease Control and Prevention (CDC).109(3):213-217. Lu C. Bravo R. Ball M. J AOAC 1985.206(2):85-92. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Indoor pyrethroid exposure in homes with woollen textile floor coverings.

.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.39 µg/L. in detection of cis-3-(2. 2005).2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. 2005). In an analysis of 217 urine specimens from a nonrandom sample of United States residents. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. In the NHANES 2001-2002 subsample.2-dibromovinyl)-2.2-dibromovinyl)-2. Biomonitoring Information Urinary levels of cis-3-(2. in some situations replacing the use of DDT.2-dibromovinyl)-2. mean peak urinary levels of cis-3-(2. Urinary levels for adults and children in these studies were similar (Heudorf et al..2-dimethylcyclopropane carboxylic acid of 0.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dibromovinyl)-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Pyrethroid Pesticides Deltamethrin CAS No.S.2-dibromovinyl)-2. 168 Fourth National Report on Human Exposure to Environmental Chemicals ... 2005). Finding a measurable amount of cis-3-(2. 2006) and 1177 urban adults and children (Heudorf et al.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dibromovinyl)-2. Outside the U.2-dibromovinyl)2.2-dibromovinyl)-2. Deltamethrin can degrade to cis-3(2. urinary levels of cis-3-(2.5 μg/L) than the detection limit (0. (2004) reported a geometric mean concentration of cis-3(2. Baker et al. 1990).2-dimethylcyclopropane carboxylic acid in the environment (IPCS.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.3-0. 2001) showed that urinary levels of cis-3-(2. 2001. deltamethrin has been used against mosquitoes that carry malaria. 52918-63-5 General Information Cis-3-(2.. Thus. 2004). Studies in Germany of 396 children and adolescents (Becker et al.. Following residential spraying with deltamethrin for malaria protection in Mexico.2dimethylcyclopropane carboxylic acid formed in the environment.

Survey Geometric mean (95% conf.1. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 169 . 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.Pyrethroid Pesticides Urinary cis-3-(2.1 and 0. population from the National Health and Nutrition Examination Survey. 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-Dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin 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.

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

Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Batres LE. Angerer J. Environ Health Perspect 2001. 2005.209(3):293-299.113(6):782-786. Angerer J. Schulz C.org/documents/ehc/ehc/ ehc97. Int J Hyg Environ Health 2006. Environmental Health Criteria 97. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Heudorf U. Torres-Dosal A. et al.htm. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Ball M. Angerer J. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2006. Seiwert M.Pyrethroid Pesticides References Becker K. Lopez-Guzman OD. Available at URL: http://www.inchem. Kolossa-Gehring M. Deltamethrin. Carranza C. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Drexler H. and genotoxicity in exposed children. 5/26/09 Ortiz-Perez MD.209(3):221-233.77(1):67-72. Environ Health Perspect 2005. et al. [online] 1990. toxicokinetics.109(3):213-217. Hoppe HW. Heudorf U. International Programme On Chemical Safety (IPCS). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Butte W. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). Heudorf U. Int Arch Occup Environ Health 2004. Grimaldo M.

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

18 (2.200-.230 (.27-2.360) .273 (.292 (.27-11.590 (.42-2.352-.233-.240 (.246-.05) 1.470-.507 (.760 (.434) .27-2.65-2.277-.46) .610) .35 (2. Deltamethrin.226-.390) .260-.36) 1.550-.63-3.810) 1.288 (.29-1.78 (1.430-.38 (2.320) .270 (.227-.750) .26) 2.267 (.373) .940) 1.427) .276-.71 (1.62-6.56-5.298 (.64) 697 680 524 701 603 957 Limit of detection (LOD.730 (.49-2.314) .650 (.39) 2.288-.35) 1.325 (.48-2.23 (2.02-6.290 (.253-.510-.250 (.450 (.630) .49 (1.78) 1.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .570-1.25-1.69) 3.700 (.190-.30 (.1.25 (2.78) 1.311 (.33) .800 (.570-.28) 1.1 and 0.490-.292-.800) 1.490) .780) 4.600 (.16-1.230 (.16) 1.260 (. Fourth National Report on Human Exposure to Environmental Chemicals 173 .369) .250 (.315 (.295) .960 (.340) .62-8.26) 2.230-.710 (.595) .92-3.34-6.314 (.48-2.210-.81 (1.45 (2.18 (1.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .336 (.300 (.30 (1.220-.32 (2.320 (.1) 3.26-2.700-1.69 (1.830-2.41 (1.33 (1.75 (1.530-.41) 3.200-.51-6.52-5.63 (3. Survey Geometric mean (95% conf.740 (.430-.250-.210-.46) 2.428-.S.355) .530-.35) 2.41-3.271-.330) .16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .04) .300) .590-.330) .25-7.45-5.180-.49-2.353 (.260 (.990) .72 (1.820) .740 (.03 (3.12) 4.454 (.50 (2.51-3.340) 1.25 (2.560-1.200-. population from the National Health and Nutrition Examination Survey.560-.300 (.41-2.34) 8.586) .300 (.35 (1.640 (.35) 2.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.270) .13 (.350-.250 (.320) .53-3.38 (2.320) .190-.520 (.05) .32 (1.240 (.247-.321 (.362) .417 (.850) .54) 1.620-1.820) . interval) .750-1.55 (1.60) .830) 90th 1.73) 1.560-.870 (.238-.420) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.89-71.406) .1) 3.21 (2.49 (1.62) 5.13) .43) 3.1) 3.364) .90) 1.680 (.44) 5.230-.670 (.83-11.52-4.260 (.33 (2.266-.160-.280 (.76 (1.510-.14-6.190-.230-.8) 3.601) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.387) .750) .297 (.93 (1.320) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .328 (.12 (.04-5.12) .79) 3.160-.850) .340) 75th .86 (1.384) .190-.34 (2.440) .65 (1.30) 3.710 (.01 (1.25-4.53) 1.840-1.370) .32-21.265-.78) 6.

40) 2.330 (.03 (.150-.05-3.740) .10 (2.810) 1.387) .530-.335-.280) .420-.49 (1. population from the National Health and Nutrition Examination Survey.234 (.440-.94 (1.19-6.309) .401) .534) .202-.200-.370-.13 (.650) .280 (.410-. interval) .860-1.81 (1.410) .290) .310) .630) .02-1.73-4.226-.44) 2.610 (.19 (2.670) 3.560 (.860 (.00) 1.440-.200-.270 (.490-.190-.372) .275 (.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .240 (.400-.04 (3.280-.312 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.07) 2.270-.230) .580) .240-.75-8.370 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.02 (2.210-.09) 3.43 (1.54 (1. Survey Geometric mean (95% conf.83 (1.450 (.540 (.271-.190-.590) .64-5.670) .320) .720) 90th 1.240 (.225-.73) 1.60) 1.220-.17-1.677) .37 (1.299-.17 (.224-.330) 75th .400-.227 (.274-.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.13-1.264 (.173-.250) .91 (2.95) 1.240-.52) 2.510 (.330) .S.460-.280 (.278) .15-2.550 (.91) .316 (.44 (1.63) 1.43) 1.88) 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 .309 (.74) 3.960-1.330) 1.91) 9.460-.55 (1.720 (.261 (.09 (.350 (.362 (.200-.570) .730) .67 (1.210 (.04 (.88-5.48 (1.09-2.230-.40 (1.35 (1.240-.07-5.67 (1.35) 1.55) 3.35-3.210 (.25) 2.730-1.357) .480-.61-2.311 (.378 (.530-.96 (1.272) .700-1.321-.760) .90) 3.51-7.06-3.590) .03-1.930) 1.22 (1.437) . Deltamethrin.270) .49) 1.480 (.240 (.67) 1.63-3.72 (1.49) 3.49-2.25-2.246 (.62) 1.840-1.270 (.09-2.229-.250 (.261-.13-1.43-64.240 (.21-4.550 (.510 (.160-.83) 1.272 (.00) 1.446) .290-.220 (.270) .91-4.36-6.329) .11 (.80) 4.41) 1.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .216-.178-.16-4.35) .39) 1.27) 1.190 (.390-.640 (.300-.490 (.200-.323 (.240-.25-5.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .930) .300-.590-1.0) 3.330) .274 (.238-.37) 1.250 (.490 (.423 (.280 (.290) .19) 2.328) .350) .84 (1.365) 99-00 01-02 99-00 01-02 99-00 01-02 .580 (.329) .62) .253) .21 (1.53 (1.86 (1.510 (.52 (1.860-1.640 (.32 (2.36 (1.730) .00) 5.440-.11 (.280) .590) .41-4.43 (2.550 (.60-4.380-.380 (.500) .750-1.230-.400) .

Environ Health Perspect 2006. Int J Hyg Environ Health 2002. Angerer J.205(6):459-472. Atlanta (GA). Idel H. Deych E. Ranft U. Pearson M. Becker K. Berger-Preiss E. Lapinski R. Bartell S. Olsson AO. Liu Z. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int J Hyg Environ Health 2006. Lopez-Guzman OD. Seiwert M. Idel H. Arch Environ Contam Toxicol 2004. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2003. Ranft U.111(1):79-84. Batres LE. Barr DB. Obel J. Kolossa-Gehring M. Biological monitoring of workers after the application of insecticidal pyrethroids. Int Arch Occup Environ Health 2003. Hadnagy W. Berkowitz GS. Centers for Disease Control and Prevention (CDC). Angerer J.46(3):281-288. Leng G.206(2):85-92. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.113(6):782-786. Sugiri D. 2005. Ball M. Torres-Dosal A. Levsen K. Sugiri D. Indoor pyrethroid exposure in homes with woollen textile floor coverings. et al. Barr DB. Leng G. Hardt J. urban cohort. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Hoppe HW. Bravo R. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. et al. Berger-Preiss E. Environ Health Perspect 2005.114(9):14191423. toxicokinetics. Grimaldo M. Fourth National Report on Human Exposure to Environmental Chemicals 175 .209(3):221-233. and genotoxicity in exposed children.Pyrethroid Pesticides References Baker SE. et al. Carranza C. Godbold J. Environ Health Perspect 2003. Lu C. Exposure to indoor pesticides during pregnancy in a multiethnic. Ortiz-Perez MD. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.76(7):492-498.

440) .175 (.117-.207) .220) 95th .230-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.080) .180) .390-.360) . The absorption. ammunition.220-.280 (.270 (.470) .410-.210 (.420) .390) .150-. from air and drinking water.120-.140) .105 (. It is also used in paints.160-.170) .110 (. People are exposed to antimony primarily through food and.169 (.122 (.070 (<LOD-.110-.119-.430 (.100) .300-.160 (.390-.330 (.170-.090) 75th .180 (.157) .160-.140) .126 (.120-.140) .320) .130 (.108 (.130) .180 (. enamels.390) .280-.310 (.460) .240 (.270 (.440) .137) .190-.080-.260 (.103) .250-.150 (.220-.470 (.260) .390-.134 (. ceramics.115) .310 (.400) .109-.128 (.130 (.310-.230-.087-. or other substances containing antimony is another means of exposure.470) .300) .110-.150) 90th .330) .130) < LOD .220) .300 (. sheet and pipe metal.230-.154) .240-.134-.210) .200) .190-.200 (. interval) .210) .180 (.137) .260) .340 (.133) * .230) .400 (.120 (.290 (.150) .150-.250 (.560) .093 (.250 (.160 (.210 (.079-.390) .320) 316 368 290 663 762 725 1297 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .120-.095-.180-.132 (.280) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .350-.350-.200-.360 (.136-.350) . respectively. Stibine is a metal hydride form of antimony used in the semiconductor industry.710) .220) . water.S.164-.350) .320-.130 (.180) .117-.158 (. to a lesser extent. metal bearings.180-.160) .130) .132 (.120-.500) .160) .160) .126-.460 (.110-.190 (.140) .07.270 (.160) .260-.098-.140) .176 (. 01-02.190 (.400 (.310) .100 (.280-.197) .210) . 7440-36-0 General Information Antimony is found in ores or other minerals.140 (.120-.099 (.100-.270-.140-.Metals Antimony CAS No.190 (.161) .350) .140 (.190 (.340) .330-.136) * .400 (.100-. and 03-04 are 0.190-.200 (.330) .230 (.300-.570) .130 (.190 (.430 (.200) .360-.260 (.150 (.150-.148-.156-.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 (.250-.500) . see Data Analysis section) for Survey years 99-00.310) .070-.150-. solder.220 (.088-. castings.320 (.530) .120) .240 (.230 (.135) * .140) .154) .240-.310-.130 (.130 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.300-. population from the National Health and Nutrition Examination Survey.330) . which may vary for some chemicals by year and by individual sample.220-.260-. Antimony can exist in one of four valences in its various chemical and physical forms: -3.170 (. coal-fired plants.170 (.320) Total .230) . and 0. and pewter.131-. 0.280-. fireworks.190-.330 (.220-.120-.300 (.200) .090 (<LOD-.184) .400-.160-.100 (.123 (.210-.125 (.130 (.180-.220 (.190) .130-.260) .141-. and +5.120-.270 (.115-. and as a fire-retardant in textiles and plastics.210-.230-.200-.410) .128 (.130-.400) .240 (.120) .108-.240 (.200 (.330 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.150) .110-.114) .250) .160-.280-.130-.112-.120 (.143 (.180 (.280) .180-.280) .120 (. and glass.600) .04.090-.04.240 (. 0. storage batteries.130) . Workplace exposures can occur at smelters.310 (. and excretion of antimony vary depending on its oxidation state.080) .190-.160 (.140 (.350 (.130-. Dermal contact with soil.170-.210) .350-.070 (<LOD-.320-.510) .360) .110) . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite. 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.200-.290-.220) .220-. It is used in metal alloys.300) .190) .260 (.220-.250-.170-.230 (.370) .310 (.160) .230) .095 (.250 (. Antimony enters the environment from natural sources and from its use in industry.410) .330) . +3.130-.230-.145) Selected percentiles ( 95% confidence interval) 50th .370-.290-.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 .154-.120 (.180 (.180-.350 (.320-.200-.240) . distribution.130-.150-.120) .190) .080 (<LOD-.142 (.460 (.150) .350 (.330-. < LOD means less than the limit of detection.320 (.130-. and refuse incinerators that process or release antimony.490) .090-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.210) .400) .150 (.090 (.270) .119) .280 (.190) .130 (.120) .300) .350 (.140 (.200 (.180 (.200) .340 (.146 (.440 (.120 (.144) .390) .270) .145 (.120-.460 (.200 (.490 (.350) .430 (.320-.280-.250-.390 (.190) .170-.170-.200 (.120-.178) .360 (.

and gastrointestinal symptoms such as vomiting.075 (.295 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.320) .333-1.098) . liver. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.230-. and kidney have been demonstrated in high dose animal studies depending on the dose.238) .226 (.154-. 1986).125 (.228-.233 (.248-.185 (.130) .160 (.238) .137 (.233-.112 (.120 (.206-.176 (.086 (..135 (.338 (.136) .107-.277 (.176 (.119 (.250-.135 (.129) * .092-.380 (.308) .266 (.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. Histopathologic inflammatory and degenerative changes in the lung.186) .086) 75th .129 (.228 (.245) .159-.191 (.161) .150-.146) .109-.195-.173) .429 (. 1954).144-.129) . 1944).098-.256 (. Ming-Hsin et al.102-.131-.133) .196 (.185-.320 (.207) ..135) .217 (.480) .130) .134) .S.298 (.167-.214) .113-.138) * .131) .205-.096-.421) .300) .333 (. 1986).099-.198) .315) .250 (.352 (.204-.192-.112-.092) .102-.371 (.192 (.116 (.250-.485) .253 (.071-.188-.120 (.220) .138 (.147) .263 (.203) .164) .113) .338 (.176-.333-.236 (.447 (.438) .333 (.114 (.163 (.308-.429) .119-. skin.104-.103-.Metals than for trivalent compounds (Elinder and Friberg.099-.269 (.115 (.143) 90th .250-.318-.333-.124-.069-.081 (<LOD-.175 (.127) .242-.317) .414) .080 (.199-.138-.30) .130) .087) . Inorganic antimony salts irritate the mucous membranes.310 (. species.150-.124 (. and ulcers (Werrin.227-.163 (.444) .267 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.233) .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 .200) .300) . 1962).194-.320-.139 (.261) .117-.156-.111 (.391) .280 (.320 (.471 (.247) .100 (.310) ..118 (. population from the National Health and Nutrition Examination Survey.128-.222 (.268) .140) < LOD .500) .080 (<LOD-. 1953).253-.117-.164 (. 1958) and occupational exposures (Briegner et al.259 (.112 (. 1995).333 (.167 (.126 (.121 (.126) .188) .097-.182 (.061-.286 (.225 (.183) .082) .343 (.364 (.115 (.138-.318-.149) .357-.126-.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 .373) .185 (. diarrhea.107-.173 (.124-.444) .241-.333) .471) .250-.167 (.187) ..122 (. myocardium..123 (.098-.250) .727) .107-.357) .074 (.281-.239-.152) .400 (.139 (.147-.131 (.317) .103-.211) .132 (.108-.095-.200-.127 (.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 . 1973).116-.108-.172-.135) .385 (.200-.153-.120 (.195-.130 (.391) .257) .075 (.209) .310) .200-.127) .338) .089) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .125-.162-. and route of exposure (Elinder and Friberg.189 (.225) .193) .213 (.108-.095-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.156 (.109 (.135) .127) .148) * .417) .145) . and eyes.132) .167 (.267) .278 (.115 (.121) .430) . Acute antimony poisoning may cause a metallic taste.159-.255) .209 (.173-.123) .193 (.077) .082 (<LOD-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.181) .178-.195 (.084) .230) 95th .294) Total .117-.352) . abdominal pain.417) .079 (<LOD-.317) .224 (.143) Selected percentiles ( 95% confidence interval) 50th .069-.149-.288 (.082) .114 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.146-.114 (.085) .265 (.143) .741 (.272) .280-.104-.120 (.161) .173 (.255-.106-.119-.244-.265-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.741) .263-.171) .148-.278) .333-.179-.143 (.113-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.068-.115) .153 (.192) .170 (.203) .151) .405) .208 (.111-.181) .122 (.248) .127) .140) .159-.208-.313-.364 (.238 (.068 (.235-. 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.209) .146-.106-.076-.124) .241-.267-.115-. interval) .076-.178 (.276 (.250 (.209-.129 (.148-.105-.228 (.146-.229-.081) .152) .320-.121 (.164-.271-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.078 (.300 (.115-.118 (.425) .321) .181) .143) .108 (.109 (. 1988.

and a drinking water standard has been established by the U. Apostoli P.67:119-123. J Clin Pathol 1998. population. Suchenwirth R. 20012002. Arsine. Int Arch Occup Environ Health 1987. Nau CA. Schacke G. Pozzoli L. Information about external exposure (i. Wade A. 26-42. Stocks J. even when exposure levels were below workplace air standards (Bailly et al. Element reference values in tissues from inhabitants of the European community. Industrial Medicine 1944. HH. Chia-Yu H.. Kiberd B. Yu H-S.S. Buchet JP. Antimony trioxide is rated by IARC as a possible human carcinogen. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. 1987). 1998) or compiled reference ranges (Hamilton et al. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . 1998. Matthews T. Cheng-Wei L.64(2):182-185. Int Arch Occup Environ Health 1995. Dernehl CU. Fuchs A. Mahieu P. Pietra R. Atlanta (GA). Review of elements in blood. New York: Elsevier. respectively.html. Kentner et al. pp. Ming-Hsin H. eds. and future strategies. 1998). Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Wu M-T.. Cullen A.48:93-97. Dunkelberg...Metals to antimony have been established by OSHA and ACGIH. Paschal et al. Leinemann M. Trace element reference values in tissues from inhabitants of the European community I. Mayne P. Iavicoli I. 1990. Luedersdorf R. Bolten C. Rev Infect Dis 1988. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. 1994) have reported values slightly higher than those in this Report. 1986. Minoia C.46:931-936. Briegner H.. VI.13:361-362. Delves HT.51:238-240. clinical efficacy. Piatnek DA. Konings J. Pilgrim L. Friberg L.76(2):103-115. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. EPA. Chest 1973. J Trace Elem Med Biol 2002. Stead FM.16: 33-39. Liao Y-H et al. gov/toxpro2. et al. environmental levels) and health effects is available from ATSDR at: http://www. Br J Ind Med 1991. Earlier measurements in general populations (Minoia et al. Lenert G.atsdr.106:33-39. Antimony.. Nordberg GF. gallium. 2nd ed. Environ Health Perspect 1998. Biological assessment of exposure to antimony and lead in the glass-producing industry. Mayer P. 1997).. Weltle D. arsenic. Biological monitoring of exposures to aluminum. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Chen J-R. Stone FD. Arch Dis Child 1997. Van der Venne MT. Carelli G. which may be due to methodologic. 2004.. Petrucci F. Gebel TW. indium. Ju-Sun P. 1995. Antimony in blood and urine of infants.76:432436. Third National Report on Human Exposure to Environmental Chemicals. J Occup Environ Med 2004. Elinder CG. Ho C-K. Semisch CW. Shao-Chi C.cdc.521-523. Bailly R. In: Friberg L. Sabbioni E. Centers for Disease Control and Prevention (CDC).. Delves HT. Dezateux et al. and antimony in optoelectronic industry workers.. et al. Biomonitoring of a worker population exposed to low antimony trioxide levels. et al. Costeloe K.59:469-474. Sabbioni E. Vouk VB. O’Regan M. Handbook on the toxicology of metals. Industrial antimony poisoning. Dezateux C. or exposure differences. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kuo-Juie Y. Iavicoli et al. stibine. 2005. and 2003-2004. References Berman JD. and hydrogen sulfide. 1991. plasma and urine and a critical evaluation of reference values for the United Kingdom population. 2002.158:165-190. Alimonti A. External and internal antimony exposure in starter battery production.. Hamilton EI. Caroli S. Lauwerys R. Chin Med J 1958. Gallorini M.)1954. Urinary antimony in infancy.. Industrial Medicine and Surgery (Dec.e. Pulmonary edema of environmental origin. Liao Y-H. Stasney J. Roland H. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Ludersdorf et al. Chemotherapy for leishmaniasis: Biochemical mechanisms. Sci Total Environ 1994. Yang C-Y. 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. Kentner M. Skulsukai G. Cordasco EM. Schaller KH.10(3):560-586.

Werrin M. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Quarterly Bulletin of the Association of Food and Drug Officials 1962. Trace metals in urine of United States residents: reference range concentrations. Antimony poisoning in industry. Chemical food poisoning. Paschal DC. Morrow JC. et al.95:89-105.Metals in urine. Sampson EJ. 27:38-45.76(1):53-59. Pirkle JL. Ting BG. Renes LE. Jackson RJ. Sci Total Environ 1990. blood. Industrial Hygiene and Occupational Medicine 1953.99-108. Environ Res 1998. and serum of Italian subjects.

90-8.10) 10.0-19.9-34.8 (48. gaseous hydride manufactured in small quantities for use in the semiconductor industry. cacodylic acid.2-93.4) 60. Survey years 03-04 Geometric mean (95% conf. alloys.5 (14.20 (8.9-46. and.4 (7.6) 11.5-178) 46.4 (24.5) 43.4 (31. or rarely as elemental metalloids (yellow.2-61.90) 16. The United States no longer produces arsenic from mining but imports about 22.08 (5.6-141) 53.5) 95th 65.S. 180 Fourth National Report on Human Exposure to Environmental Chemicals . grain.12-10.3-19.6 (32. and in lead-acid storage battery grids. and indium arsenides are used in the semiconductor industry.4) 13. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.8) 34. lead. 2005).8) 7. 2001). CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. Since the 1940s.7) 65.0 (43.0 (11.5 (40. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.5-19. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.9 (8.25-9. pesticides. Arsenic and its compounds have had many uses in the past and present as medicines. and arsenates (oxidation states of -3.34-10. Water sources contain mostly inorganic arsenate. the smelting of copper.90 (5. Also.02-8.7) 24. such as arsenopyrite (FeAsS) and realgar (As4S4).7) 90th 37.4 (26.1) 15. and gray forms).90-11. as alloy in metal bearings.6-43. it is found in over 200 crystalline or mineral forms. referred to as inorganic arsenic compounds. arsenites. Arsenic is measurable in most soils.1-40.12 (6. sodium arsenite.34-9. Gallium. ocean and fresh waters. Various arsenic compounds were used in paint pigments and for tanning animal hides.50 (8.8) 17.2 (41. +3 and +5).9) 68.57) Selected percentiles ( 95% confidence interval) 50th 7.30 (6.77) 6.70 (6.30) 17.6 (9. retaining walls.000 metric tons annually. arsenic compounds. to a lesser extent. and arsenosugars.3-15. and foods.66-8. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. copper arsenates. black. though in some locations arsenite may be prevalent (WHO.3-111) 78.84) 8.2) 46.90) 75th 16.0 (15.7-95.5) 66.10 (6. arsenic as elemental metalloids may be used in some ammunition.1) 290 725 1542 03-04 03-04 9. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. arsenocholine.8) 30.3) 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. In the last century.9-62.6) 618 722 1074 Limit of detection (LOD. lead hydrogen arsenate.5 (23.74.29 (8.8) 29.90 (7. Before the 20th century. from coal burning.8) 7.Metals Arsenic CAS No. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.3) 10.1 (38.6 (15.30 (7. In nature.80 (5.90-8.4) 40.84) 8. and produce.5-52. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) 8.13-8.55 (7. mostly for use in wood preservation (ATSDR.1) 7. and as a cosmetic to lighten complexion.9 (17. meats. and as homicidal poisons.2) 15.00-9.2 (13.0 (14.8-61.80-9.5 (34.27) 9.90-14.00 (6.90 (7. psoriasis. semiconductors. see Data Analysis section) for Survey year 03-04 is 0.40) 7. trimethylarsine oxide.1) 1281 1276 03-04 03-04 03-04 9.7-83.50-14. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. Arsenic trioxide is approved to treat acute promyelocytic leukemia. mental disorders.9) 21.7 (11.5-41. population from the National Health and Nutrition Examination Survey.5) 41.2 (12. were used as treatments for syphilis.80) 6.0 (22.10-10.70) 8. Although it is still widely used in the United States.0-60.41 (7.5 (36.2-17.8-77. and play sets.1 (32. cancers. solders.70-9. and other metals. to a lesser extent.8) 33. aluminum.10-7. particularly arsenic trioxide. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.1-18.2 (51.90-7.6-35.4 (48. Arsenic trioxide (As2O3.19-9.4-65.6 (13. Arsine (AsH3) is a reactive.2-20.97) 8. General population exposure to inorganic arsenic can occur through consumption of drinking water and.

35) 7. Chowdhury et al.88 (5.0) 14.0 (17. EPA’s maximum contaminant level (Hughes.47 (7. In aquatic sediments.18 (5.0) 1281 1276 03-04 03-04 03-04 8.3) 9.6 (10.5 (9.45) 5.3-53.3 (27.38-10.04) 7.10-16.1) 58.51) 75th 14. 2001).33 (6.0 (31.4 (11.7) 28.3-41. so exposure to the general population is extremely limited.47-6.5-17. Steinmaus et al.4 (42. but is poorly absorbed dermally (WHO.44) 6.8 (12.4 (26. are used in enclosed ultraclean operations within the semiconductor industry. 2007. interval) 8.86-17.1) 6.S.7-34. dust..4 (40. age.6 (17. 2006. Extremely high groundwater arsenic levels.6 (35.06 (4.61 (7. 2001. 2001).2-46. have caused clinical arsenic poisoning. 2001).40) 8.75) 13. 2001).01) 7. WHO.2-15.47 (6.2) 15. and contact with CCA-preserved wood structures.7-188) 27. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.1-36.13) 8.5-120) 40.9) 13. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.44-11.8 (27. 2001. Smoking tobacco is also a source of inorganic arsenic.8 (20. 2001).7-18.0-69.76 (6.1 (11. and some other seafood can contain organic forms of arsenic including arsenobetaine.2) 90th 30.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .33-10.3-62. 2007.8-75.3) 6.24 (7. kelp.5) 17.75 (5. shellfish. WHO.1) 7. Tseng.9-56.99-9.64 (7.0) 12.S.20-9. gallium arsenide and indium arsenide.4-64. Children may have additional exposures from ingestion of contaminated soils (e.8) 27.10-8.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.59) Selected percentiles ( 95% confidence interval) 50th 7. as observed in Bangladesh where millions of people have been exposed. 2001).30-9.0-26.4 (12.1) 8.9 (45.2 (12.5) 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 8.8 (11.9) 53.4) 54. Direct exposure to DMA and MMA may result from use of the two pesticides. U.28-7.66 (7. arsenic does not show biomagnification in the food chain (WHO.6-17.32 (5.11 (5. population from the National Health and Nutrition Examination Survey. Though modest bioconcentration occurs in some aquatic life.8 (21.50 (6. organic arsenic can be converted back to methylated and inorganic arsenic.04 (5.3 (24.01) 11. 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. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.5) 290 725 1542 03-04 03-04 8. and arsenosugars. Inorganic forms of arsenic demonstrate high acute toxicity. Survey years 03-04 Geometric mean (95% conf..g.58-10. selenium.. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. 2006. mine tailings).66-8. 1988).0) 33.81-9.2) 40. dose level.3-64.0-38.0) 26.7-17.12-10.. and folate status (Chen et al. After absorption.4) 32. 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. The semiconductor dopants. EPA.41) 6.23-7. 2003. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.25 (6. arsenocholine. NRC.1) 24.07-9. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. Fish. Gamble et al.7 (25.1 (14.4 (24.00 (6. inorganic arsenic is widely distributed within the body.66-8.7 (9. 2007.8-62. though some reduction may occur in the gut prior to absorption.88) 7.25-9.S.93-8. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.0-18.7 (11. 2001).6) 45.0) 42. 2001). Arsenate is reduced in the body to arsenite (oxidation state +3).7-35.31 (6. cacodylic acid and monosodium methyl arsenate. In aquatic organisms.8-32.93-9.7) 95th 50.. trimethylarsine oxide (TMAO).96) 12.8) 22.

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

. 2008). Vahter et al.. 2001). 2008. 2006. 2006). DMA produced bladder cancer in some chronic rat studies (Cohen et al. 1999. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2006). 2000. Josyula et al. In animal studies.. 2006. Calderon et al.. WHO.50) 1. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. population (Rubin et al.00) 1. In a Nevada town where groundwater levels were naturally elevated.html.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Caldwell et al. 2001).... Levels of total urinary arsenic in the U. 1986)..S..41) 3. 1999. Shalat et al.33 (<LOD-3. and the FDA has established a bottled drinking water standard.S. 2006).. Pellizzari and Clayton.. 2001).. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. environmental levels) and health effects is available from ATSDR at: http://www. 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.cdc.S.. had decreased since the prior 1990– 1992 survey. although urinary arsenic levels were not associated with CCA contact (Shalat et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. Pellizzari and Clayton.75 (<LOD-2.75 (<LOD-2. In the German Environmental Survey III of 1998. median urinary total arsenic levels in 4052 adults varied with seafood intake. 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. Compared with this Report. 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. but generally only at maternally toxic doses (WHO. Fourth National Report on Human Exposure to Environmental Chemicals 183 .33 (<LOD-3. 2007.61 (<LOD-3. Pellizzari and Clayton 2006).80 (<LOD-4. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. Survey years 03-04 Geometric mean (95% conf. 2008).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. Consequently... 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. Meza et al. and were about two-fold lower than those for the U. Valenzuela et al.atsdr. Caldwell et al. 2004. population in NHANES 2003–2004 (Schulz et al.18 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. 1992. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2000).Metals compounds.19) 3. 1999). 2006)...04 (<LOD-3.18) 3. 2006.. arsenic has been fetotoxic and teratogenic. Additional information about external exposure (i. 2003. 2007.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.. Shalat et al.e. 1998. gov/toxpro2.69 (<LOD-3. Offergelt et al. 2004.95) 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. 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.. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.

29 (1.8) 35.00 (1. 2000.S. Arsenate.90-29. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.70 (3. Caldwell et al.30) 2.00-1.40-6.871-1.. respectively. Caldwell et al. Aposhian et al.9 (6.90-7. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.6. geometric mean levels were about 70-fold higher than for the U. arsenocholine.20-3.55 (1.80 (.9-23. Individually measurable species resulting from inorganic arsenic exposure are arsenate. arsenite. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.70-21.7) 15. and TMAO were detected in only 7.10 (4. 2008). Chowdhury et al. Some noncancer effects of arsenic (e. Measurable organic arsenic species in this Report are three biologically generated environmental forms.. population (Ahsan et al.. population showed a higher contribution of arsenobetaine (Caldwell et al. 2000.74 (1.6.800 (..4 (16.40) 75th 5. Tseng et al.05) < LOD .00-12..00-4. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. In most human studies.S..8 (12.500-1..4-35. and 0. and other factors such as nutrition. 1990. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. 2007) with higher levels of arsenic in the drinking water. 2008).. Valenzuela et al.0) 4.8 (17.1-25.. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. Blom et al.9) 13. After recent seafood ingestion.e. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-23.6 (25.28) 1. China.20) 3..20 (2. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.0 (26. 1985.4) 31. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. MMA.g. population (Sun et al.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 * * 1.20) 18. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.5) 29.3) 95th 35.93) 1.37 (1.5) 621 725 1078 Limit of detection (LOD.0 (27..8-40.3) 1284 1284 03-04 03-04 03-04 1.1) 45.5) 292 728 1548 03-04 03-04 1.S.900-1. Survey years 03-04 Geometric mean (95% conf. WHO. DMA and MMA.70) 6.60-3. dermal keratosis. see Data Analysis section) for Survey year 03-04 is 0. with DMA.S. Pellizzari and Clayton.20 (1.Metals other areas of the world (Ahsan et al.600 (. 2005. which may vary for some chemicals by year and by individual sample.17-1.6-44. In the residents of a Chilean town who consumed water with high levels of arsenic.48-2.20) 7. The higher percentiles of total urinary arsenic levels in the U.8-50.0) 29. and TMAO.400-. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.700-1.. 2006).10) 4.2-38.. 2003).50) 90th 16. Caceres et al.800-4. when seafood organic arsenic is subtracted).900 (. 2005.. 2007). methylation capacity.3 (9. 4.2 (6.10) 8.83) Selected percentiles ( 95% confidence interval) 50th 1. 2000. 2008. 2008).2-35.6 (11. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.62) 2. and two methylated metabolic products. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40) 5.. 2001). arsenocholine.80) 1.800 (.3) 35. 1996.6 (13.3 (21.7 (13. 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.31-1. In the late 1980s.00-6. 2005. These associations are stronger at higher urinary levels.700-1. population in the NHANES 2003–2004 subsample.80 (4.S.11-1.00 (.50) .20 (.3% of a representative sample of the U.43-1...8. 2008. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. population from the National Health and Nutrition Examination Survey.3-39. vasospasm.80 (3. interval) 1. Also. in NHEXAS 1995–1996.7-22.7) 13.5 (14. and duration of exposure are also considered important.800) 1. 1.4) 23. 2001. arsenobetaine.30) 10. < LOD means less than the limit of detection.68) .19 (.. Caldwell et al.80-5. Sun et al.60) 1.9 (7.1) 18.70 (5.5 (26. 2008).20 (4.30 (1.4. When seafood intake is avoided.50-6.800-1.1-51.50) ..7 (21.30 (2.45 (1.70-21.5) 32.20-190) 31. 184 Fourth National Report on Human Exposure to Environmental Chemicals .66 (1.. arsenite.1-94.40-7.20-25.00) 3. For residents of Inner Mongolia.

50-7.36) 2.82) 4. 1992.28) 1.6-32.7) 9. 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.1) 26.25-7.44 (1.3-24.91) 90th 16.9-18.5 (18.786-1. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.2 (12.25 (. Fourth National Report on Human Exposure to Environmental Chemicals 185 .67) 4.4 (11. Vahter et al.93 (1.50-15. population for the sum of inorganic related species was 18.78-5.68 (1.4) 13.40 (1..76-27.3) 1284 1284 03-04 03-04 03-04 1..4 (24. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.53 (.9) 14.82) Selected percentiles ( 95% confidence interval) 50th 1.32-7. 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.Metals as with DMA.6 (9. 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. Information about the biological exposure indices is provided here for comparison..6) 19.05 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18-1.13-39.400-. 1998.3 (10.12) < LOD .43) 14.40) 1. The 95th percentile of the U.39-3.9 (25.88) 2.72) 12.55) 1.5 (18.938-1.64-29.833-1.51-2. 2007).1 (26.4-82. 2001).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 * * 1.80) .81 (4.70) 5. Sun et al.88 (5.7) 17. 2001)..959-1.67) 1. 2008).901-2.91 (4.612-1.5) 26. WHO.6-46.1-36.16 (.1-18.78 (3.2 (13.5) 17.00 (1.. interval) 1.29-14. 1986.83) 8.0 (9..2 (4. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.00 (3.47 (2.9) 32.638) 1.73-6.29 (4.8) 29.531 (.15-1.80-153) 17.S.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.877 (.14 (1.7) 30. 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.0-36.4) 292 728 1548 03-04 03-04 1.05) 1..19-2.15-4.37-2.58 (3.S.21) 5.3 (10.6-29. Caldwell et al.65 (1..5-20.54 (1.909-1.15-1.51) 5. 2008).9 μg/L.9 (13.11 (. Offergelt et al.43) 75th 5.2 (12.79 (1. population from the National Health and Nutrition Examination Survey. In recent years.4) 32.4-28.30-1.83) 2.45) 1.3) 95th 29.4-21. 2003.62-6. 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.61-6. Survey years 03-04 Geometric mean (95% conf. not to imply a safety level for general population exposure.6 (6. which is below the ACGIH BEI (Caldwell et al.30) 1. 2006. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.47 (1.10 (.

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

population from the National Health and Nutrition Examination Survey.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. population from the National Health and Nutrition Examination Survey.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (<LOD-1.S.08 (<LOD-4.76) < 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. which may vary for some chemicals by year and by individual sample.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 187 .20 (<LOD-1.00 (<LOD-3. see Data Analysis section) for Survey year 03-04 is 1. Survey years 03-04 Geometric mean (95% conf. Survey years 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.95 (<LOD-2. < LOD means less than the limit of detection.00) 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.00 (<LOD-2.80) < LOD 621 725 1078 Limit of detection (LOD.44) 2. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

22) 4.00 (7.69 (3.00) 7. interval) 3.03-6.7) 13.00-15.5 (11.1 (8.49-4.00-7.0-17.16 (2.00-12.0) 10.69 (3.9 (11.12-4.0 (8.00 (5.06) 5.90) 2.00 (3.60-6.14) 3.0 (12.80) 2.80-5.0) 17.6 (9. population from the National Health and Nutrition Examination Survey.45) 8.0-16.00) 90th 11.2) 10.80) 7.74 (2.48 (3.00 (5.00) 4.0) 95th 16.00-4.65-8.6-18. population from the National Health and Nutrition Examination Survey.0) 16.34) 3.32 (8.98) 4.31-4.09 (7.0 (10.84-8.86-7.00 (7.05) 10.8) 7.44 (2.00 (5.25 (4.9) 13.0-16.0 (8.00-15.00 (3.00 (6. Survey years 03-04 Geometric mean (95% conf.0) 292 728 1548 03-04 03-04 4.94) 3.20-12.00-4.0 (12.6) 1284 1284 03-04 03-04 03-04 4.70-12.27 (3.S.30 (7.1-15.0) 14.61-11.48 (2.57 (3.00-7.0) 13.88 (4.33-4.50-5.7.27-5.00) 3.0 (13.0) 11.34 (3.34-4.0) 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 Sample size 2568 03-04 03-04 03-04 4.00-4.29-4. Survey years 03-04 Geometric mean (95% conf.00-22.32-10.92-12.7) 1284 1284 03-04 03-04 03-04 4.7-16.08 (2.00-11.37 (3.78) 4.00-3.4 (7.86 (2.90) 5.24-4.0) 9.03 (3.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .00 (6.00-15.33) 3.3 (8.71) 3.82-9. see Data Analysis section) for Survey year 03-04 is 1.80-3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.78 (4.00 (3.86-21.67) 9.95-6.70 (3.60-3.69-6.20) 11.0 (9.5) 95th 13.82) 3.45) 3.16 (4.0 (10.71 (3.30) 3.17-4.19) Selected percentiles ( 95% confidence interval) 50th 3.00 (5.37 (2.90 (3.00) 6.16-11.3 (7.95 (4.5) 12.00 (3.9) 5.80-6.0 (10.0-19.00) 5.0 (9.00) 6.15) 4.34 (3.0) 9. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00-7.6) 292 728 1548 03-04 03-04 3.79 (3.00) 6.00) 6.00) 12.00 (6.0) 13.10) 6.27 (2.70-3.50 (4.00-11.12 (3. interval) 3.52) 3.10) 3.7 (10.1-18.00-4.00-5.0-12.84-18.94-3.00 (5.0-25.60-4.00 (3.0) 11.89 (3.95-4.97-3.18 (6.45 (8.0) 16.46 (4.59 (6.95-3.71-4.60-7.55 (2.00-4.81 (5.1-22.05) 3.14) Selected percentiles ( 95% confidence interval) 50th 3.00-11.0 (11.9 (7.38 (3.0 (9.0) 17.00-7.00) 4.S.42) 3.92) 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 3.73) 6.61-16.70) 5.17 (2.62) 4.9) 11.69-3.73 (3.50-15.00) 9.00-8.0-18.3 (8.0) 9.00-13.77 (3.9) 12.72 (4.57-5.00) 75th 6.32 (4.8) 7.70-4.28) 2.11) 4.31) 4.44) 5.20-4.39-3.74) 90th 9.7) 12.85 (3.0 (10.80 (4.24) 3.82-5.0) 12.65-6.0) 621 725 1078 Limit of detection (LOD.0 (14.27-2.34-4.11 (3.00-10.91) 75th 5.00 (4.00-9.49) 10.0 (13.13-4.05) 5.17-6.00-3.71 (4.00) 3.0-17.00-12.00 (3.67) 8.00-4.

30-1.05-1.30) 1.61) 2.07) 2.23) 1.90) 2.70-3.50 (<LOD-1.00 (<LOD-1.40-3.46-2.70-2.20 (1.82-2.70-2.10 (.60) 1.35-3.00-4.10-3.80) 1.57) 95th 2.86) 3.00-2.84-3.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.70) 2. < LOD means less than the limit of detection.31 (1.90) 1.80 (1.40) 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-1.40-2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.28 (1.86 (2.10 (1.40) 1.00 (1.50) 1.80) 1.22 (1.20 (1.30) 1.20-3.46 (1.16 (2.40-2.60-2.53 (1.45) 3.00 (2.50) 621 725 1077 Limit of detection (LOD.40-3.20 (1.00) 1.90) 2.00) 1.50 (1.54) 90th 2.28 (1.853-1.86 (2.10) 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .70-2.82-2.80-2.00) 2.30 (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 1.30) 2.79) 2.985) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample.20 (1.S. population from the National Health and Nutrition Examination Survey.86) 2.40) 2.62) 2.36 (1.34) 2.58) 2.14-1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (1.10 (1.07 (1.18-1.96-2.900-1.80 (2.80-2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10-1.30 (1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10-1.85) 1.20-1.00-1.40 (1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30) 90th 1.33 (1.88 (1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.36) 1.43-3.15-1.07-3. Survey years 03-04 Geometric mean (95% conf.90 (1.80 (1.20 (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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33 (1.85) 2.71-2.37 (1.63 (<LOD-1.22) 3. Survey years 03-04 Geometric mean (95% conf.00) 1.93) .81) 1.60 (2.88-2.50-2.60) 2.10) 95th 2.73-2.00-2.30 (2.88 (1.30 (1.77) 1.10 (<LOD-1.60) 2.18-1.816 (<LOD-. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.11-1.53-2.S.9.10 (.52 (2.00 (2.30-1.50 (2.60 (1.20) 2.30-2.70-2.00) 2.17) 2.90 (2.80 (1.00 (<LOD-1.20 (1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.61-3.80 (1.40 (2.31-3.

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

98(2):151-159. Toxicological profile for arsenic. et al. Chem Res Toxicol 2000. Kalman DA. Rahman MM. Gamble MV. Eldan M. September 2005 [online]. Hudgens E. Calafat AM. Kalman DA. International Agency for Research on Cancer (IARC). Matczak W. Roy S. Fourth National Report on Human Exposure to Environmental Chemicals 191 . DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh. Environ Health Perspect 1990. and biotransformation involved in cellular response and toxicity.8(2):119-127. Liu X. Parvez F. Lodh D. Blom S. Perrin M. Biomarkers of exposure: a case study with inorganic arsenic.38(1):87-113. and lung cancer risk: a follow-up study in arseniasis-endemic areas in Taiwan. Annu Rev Pharmacol Toxicol 2007. McClellen H. Needham LL.13(8):693697. Wong LY. Gurzau A.216(1):69-79. Biggs ML.gov/toxpro2. Caceres DD.iarc. Crit Rev Toxicol 2006. Chen CL. Eblin KE. Chowdhury UK. J Expo Anal Environ Epidemiol 2003.cdc. transcription factor. arsenate. Sengupta MK.41(10):2399-2428. Hall M. Arnold LL. Beck BD. Wu MM.24(3):298304. Coble K. Hysong TA.pdf. Reidy JA. Gurzau ES. et al. Lu X. Pilsner JR. Hopenhayn-Rich C. J Occup Environ Med 2000. Atalah E. A prospective study of blood selenium levels and the risk of arsenic-related premalignant skin lesions. Sandstrom M. Moore LE. Hughes MF. Gandolfi AJ. Le XC. placebocontrolled folic acid-supplementation trial in Bangladesh. Available at: http://www. American Conference of Government Industrial Hygienists (ACGIH). Smith AH. Moldeus P. Cellular metabolism of arsenocholine.47:243-262.84(5):1093-1101. Aposhian HV. Methylated arsenicals: the implications of metabolism and carcinogenicity studies in rodents to human risk assessment. Environ Health Perspect 2006. Razniewska G. Pino P. Documentation of biological exposure indices.107(8):663-667. Calderon RL. Burbacher T. Jakubowski M.42(12):1195-1201. Graziano JH. Poplin GS. Stute M. Some Drinking-water Disinfectants and Contaminants.71 Suppl:S29-32. Chen Y. Norin H. Amigo H. Clinical and neurophysiological studies. Biological monitoring of occupational exposure to arsenic by determining urinary content of inorganic arsenic and its methylated metabolites. Arsenic: signal transduction. Folate and arsenic metabolism: a double-blind. Monomethylarsonous acid induces transformation of human bladder cells.116(7):893-897. Cebrian Garcia ME. J Appl Toxicol 1988. Hughes J. Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Slavkovich V. Cancer Epidemiol Biomarkers Prev 2007. Cohen SM. Ye X. 7th edition. Excretion of arsenic in urine as a function of exposure to arsenic in drinking water.292(24):2984-2990. Exposure to inorganic arsenic in drinking water and total urinary arsenic concentration in a Chilean population. Environ Res 2005.104(11):1200-1207.11(4):265-269. Lewis AS. Ryhage R. MMA(V). Kurzius-Spencer M. Ilievski V. Ingested arsenic. Lagerkvist B. J Health Popul Nutr 2006. et al. Burgess JL. Linderholm H. Montesinos N. Environ Health Perspect 1999. Reduction in urinary arsenic with bottled-water intervention. Zheng Y. J Environ Sci Health A Tox Hazard Subst Environ Eng 2006. Volume 84. et al. Kumagai Y. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003-2004.html. The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species. Liber K. Chen SY. 8/7/07. Healy SM. Ahsan H. et al. Christakopoulos A.fr/ENG/Monographs/vol84/ volume84. Available at URL: http://monographs.13(3):211-218. Slavkovich V. Bhattacharya P. Int Arch Occup Environ Health 1998. Kapaj S.36(2):99-133. Bolgiano D. Hsu LI. Josyula AB. House dust and inorganic urinary arsenic in two Arizona mining towns. Jagadish B.16(2):207-213. Parvez F. Thor H. cigarette smoking. Sturup S. O’Rourke MK. Peterson H. Schreinemachers D.114(11):1790-1796.atsdr. Le XC. Bredfeldt TG. Cincinnati (OH): ACGIH Worldwide. Arsenic methylation patterns before and after changing from high to lower concentrations of arsenic in drinking water. Trzcinka-Ochocka M. 8/7/08 Ahsan H. Summary of Data Reported and Evaluation. Arsenic exposure to smelter workers. Environ Health Perspect 2008. van Geen A. van Belle G. et al. Toxicol Appl Pharmacol 2006. Thomas DJ. Loomis D. Chiou HY. Mash EA. Environ Health Perspect 1996. including Arsenic. Human health effects from chronic arsenic poisoning--a review. Associations between drinking water and urinary arsenic levels and skin lesions in Bangladesh.89:145-151. Pattern of excretion of arsenic compounds [arsenite.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Sumi D. JAMA 2004. et al. Chanda CR. Scand J Work Environ Health 1985. 2001. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Am J Clin Nutr 2006. et al. Hsueh YM. J Environ Sci Health A Tox Hazard Subst Environ Eng 2003. Rahman A. Hysong TA. Updated September 2004 [online].

20(8):1120-1125. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. et al. Jhangri GS. inorganic. Borja-Aburto VH. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. National Research Council (NRC).25(1):1-22.210(3-4):271-297. Toxicol Appl Pharmacol 2007. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. using a routine LC-ICP-MS method. Int Arch Occup Environ Health 1986. Arsenic exposure. Ferreccio C. Steinmaus C. Fleming LE. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. Rubin CS.115(1):151-157. Nygren A.inchem. Environmental Health Criteria 224. CruzGonzalez MB. Lewis Publishers. Schulz C.epa. Environmental Protection Agency (U. Raml R. Kopplin MJ. Hoet P.49(6):387-393. Br J Ind Med 1992. Rey OA. Seiwert M.222(3):374-380. Vahter M. Available at URL: http://www. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Buckley BT. Huang YL. Becker K. et al. Naranmandura H. Conrad A. Garcia-Montalvo EA. Meza MM. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Washington (DC) National Academy Press. et al. Lauwerys RR. J Anal Toxicol 2006. Kolossa-Gehring M.gov/safewater/arsenic/regulations_factsheet. 1998 [online]. Boca Raton (FL). Biggs ML.114(8):1293-1296.57(2):79-91.112(14):1375-1380. Sci Total Environ 2006. Friberg L. Boeckx M. Vahter M. Toxicol Appl Pharmacol 2005.S. J Toxicol Environ Health A 2007.96(2):119126.epa. Environ Health Perspect 2005. Available at URL: http://www. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS).Metals Kwon E. Gandolfi AJ.htm. Wang Z. Marshall G. 2001. Francesconi KA. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells. Environ Health Perspect 2007. et al. Pellizzari ED. Arsenic. Environ Res 2004.S. Sonora. Seifert B. Li B. Fok N. Burgess JL. et al. Shalat SL. Black K. et al. Arsenic on the hands of children after playing in playgrounds. World Health Organization (WHO). Integrated Risk Information System. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Rahnster B. Environ Health Perspect 2006. et al. Environ Health Perspect 2006. Tseng CH. Chen CJ. urinary arsenic metabolites and human diseases: current perspective. Goessler W. Flanders WD. Shipp M. Morton J. html. Valenzuela OL.206(3):299-308.367(1):80-88. Kalman D.gov/iris/subst/0278.K. Sun G. GSTM1 and T1. Arsenic in Drinking Water. Zhang H. A pilot study of children’s exposure to CCAtreated wood from playground equipment. and metabolism of arsenic. Jones RL. urinary arsenic speciation. Clayton CA. 8/7/07. Suzuki KT. Chung CJ. Jin Y. Fact Sheet: Drinking Water Standard for Arsenic. Arsenic and Arsenic Compounds. Environmental Protection Agency (U. Environ Health Perspect 2004. Chem Res Toxicol 2007.htm. Ibata K. Environ Health Perspect 2007. Investigating childhood leukemia in Churchill County. Nolinder P. Nevada. Mason H. Rumpler A. EPA). Guidelines for Biological Monitoring. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Buchet JP. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. Xu Y. 8/7/07 U. Arsenic methylation. Available at URL: http://www. Erratum in: Toxicol Appl Pharmacol 2006. Holmes AK. Smith AH.113(3):250-254. Arsenic in drinking water-2001 update. Yang MH. Moore LE. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals .115(4):648-652. Kieszak SM. Offergelt JA. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan.114(2):220-227. Yuan Y. Jimenez M. Solo-Gabriele HM. Sun X. Ochi T.S.70(2):159-170. EPA). Liaw J. Tseng CH. U. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. Genetic polymorphisms in MTHFR 677 and 1298. pp. Geneva 2001. Belson MG.211(2):175. January 2001 [online]. von Ehrenstein O. Roels H. Lauwerys R. Arsenic.org/documents/ehc/ ehc/ehc224. Garcia-Vargas GG. 2nd ed.30(5):293-301. Huang YK. Int J Hyg Environ Health 2007. China. In:Industrial Chemical Exposure. Calderon-Aranda ES. Mexico.36-37. 3rd Ed. EPA 815-F-00-015. Li L. 2001.S. Li X. Lu X.

74) 3.37-1.90) 2. depilatories.35) 5. such as barium chloride.70) 1.76) 1. In nature.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. water. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Metals Barium CAS No.30) 8.33 (1. and 0.46-1.00) 6.50 (5.11 (3.62) 1.12.50 (1.19) 2.9) 5.50-6.88 (5. barium sulfate and barium carbonate).08-8.50) 2.27) 2.80-5.40) 7.43 (1.8 (6.30-1.50 (4.28) 90th 5. 01-02.87-14.44-5.86 (4.72) 1.70) 3.g.56 (1.14-6.43) 6.24 (4. Fourth National Report on Human Exposure to Environmental Chemicals 193 .49 (1.20-8.70 (1.12 (2.65-1.80 (2.60-2.80 (1.32) 8.54) 1.15-11.80-3.30-5.87-7.14-1.10-5.4) 6.26) 5.63 (5.92) 2.66) Selected percentiles ( 95% confidence interval) 50th 1.65-8.71) 95th 6.50) 1.03 (1.35-1.71 (2.21 (1.88) 1.39 (1.87 (5.82) 1.86-4.78) 1.30) 4.54-8.90) 1.37) 5.70-2.20-8.17-1.70-5. 2001).72) 75th 3.38) 8.57-7.62 (1.01-7.30) 5.20 (3.75-3.10) 5.40 (4.95-6.78-2.49-1.70-3.55-7.47-1.10 (4.4) 7.36-1.36 (4. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.78) 1.40 (5.54 (2.11 (3.38 (1.14 (6. bricks. fireworks.95 (4.76-7.56) 1.12) 6.59) 3.41-3.30-1.50-1. 0. Workers employed by industries that make or use barium compounds can be exposed to barium dust.80 (1.10 (3.43 (1.41) 1.70) 7.30) 5.31-2.60 (1.22) 6.09 (2.73 (5.09 (1.60) 1.73 (6.37-8.65 (5.87-9.39) 1.06-1. population from the National Health and Nutrition Examination Survey.49) 4.24-1.94-6.74-3.1) 9.72) 4.30 (1.99-5.64-3.77) 1.61 (2.86-5.61 (5.77-3.20-1.43 (5.87 (6.45) 7.35-1.60-6.98) 1.74-2.45 (1.50 (1.30 (3.24-1.00 (1.81-2.05% of the earth’s crust.80-2.04-2.15-1.40) 7.80) 1.80 (2.93 (4.30) 3.55-3. glass.48) 1.31.46) 1.18) 3.62) 1.4) 9. The general population can be exposed to low amounts of barium in air.85) 1.56 (2.38 (1.22-1.47-1.30 (2.85 (2.82) 2.73) 1.00-8.63) 1.50 (4.50-1.40) 3.56 (6.11-1..70-6.52 (4.00-3.91) 2.34 (1.43) 2.63) 1. interval) 1.60-3.54) 2.02 (7.50 (2. In single dose animal studies. it combines with other chemicals such as sulfur or carbon and oxygen.70) 1.90) 2.63 (1.48) 1.50) 2.S.99 (4.86 (4.54 (6.70) 5.00 (2.48 (6.10-4.75) 2.56) 4.51 (1.22-1.52 (1.53) 2.88) 4.49) 8.12 (2.26-1.76 (3.11 (2.40 (1.90 (4.80 (1.80) 6.90 (6.31 (2. Some barium salts are freely soluble in water.56 (1.93-2.57) 3. Certain foods.29-5.30 (5.15-1.87-3.60) 3.53-5.20-5. Barium compounds are used by the oil and gas industries to make drilling muds.91 (2. are high in barium (Genter. whereas others are practically insoluble (e.44 (1. soluble forms of barium.26) 2. rubber.12) 7.20-1.20 (4.00) 1.51) 7.81-3.32-7.26-7.82-6.64 (1.57 (5.10 (2.68 (1.54) 1. Small amounts of barium can be released into the air during mining and other industrial processes.28-1.48-4.80-7.63) Total 1.30) 2.64) 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 2.51) 1.54-1.16) 5.69 (1.77 (3.30-2.85) 1.30) 5.76-2.60) 4.20) 2.16 (1.73) 3.60) 1.71) 2.30 (5.40 (1.90) 4.35 (3.47) 4.18 (6.2) 6. such as brazil nuts.40 (5.80) 7.67) 6.70 (5.88) 7.20-1. and food.25-11.27 (1.30-2.84) 5.90 (1.61 (3.8) 9.50 (1.29) 5.25-1.61 (1.21-2.35 (2.37) 1. and ceramics.06-2.49) 11.90-9.8) 5.44-2.39) 4.15 (1.36 (1. respectively.48-4.97 (1.30-3.07 (2. Barium salts have also been available as rodenticides.20-8.50 (4.50 (3.46) 1.78-3.54-1.63 (8.70) 4.65-5.15 (2.12.05-2.50 (6.29-1.21-8.20-1.12-1.35-4.59-11.20 (1.08 (6.60 (2.66 (4.93-8.60-6.36-1.00) 4.51) 2.15 (6.61 (1.50 (1.49-9.10) 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 1.39 (1.21 (1.71) 1.76-3.65) 1.40 (1.39-1.81-2.27 (1.42 (1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.18-1.38) 2.70-8.90-2.15) 5.32-1.91) 6.50 (1.50-6.86) 6.87) 7.34 (1.71-9.65) 3.34) 2.80 (5. see Data Analysis section) for Survey years 99-00.49) 2.65) 1.53) 1.41-1.10) 3.96-2.35 (1.00) 1.00-76.19-1.40 (5.20-6.01 (4.61-8.90-13.70-2.73-5. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).62 (1.25 (1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Barium compounds are also used commercially in paint.37 (4. 7440-39-3 Medically.36) 5. tiles.34 (2. and 03-04 are 0.40-13.60-10.04-6.50) 4.63 (2.

28-6.30) 2.29 (1.14-2.91 (3. vomiting.49-1.77) 1.96) 4. 1985.46) 2.57-5.74) 1.04 (2.02) .08-1.54) 2.04) 5.47-8. Chronic high doses in animals resulted in kidney damage (McCauley et al.49 (1.92 (4.31-1.38 (4.76) 2.55-5.38-5.55 (1.59 (1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.20 (1.41) 5.80) 4.00) 4.46) 3. chemical form.64) 7.32 (1.45-8.45) 1.49 (1. Following intravenous injection in animals.00 (3.33 (1.75) 1.75) 2.91) 2.64 (1.89) 90th 4.84 (3.24 (5.62 (2.36 (1.79) 1.52) 7.03-1.20) 4.72) 4.881 (.68 (3.35-1.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 7.38 (1.31 (4.38) 4.66 (1. 1989).89 (2.43-6.24 (3.40 (1.03) 1.68-3.64 (1.34 (1.97-4.56 (1.37) 2.92) 2.2) 6. Barium blocks cellular efflux of potassium resulting in profound hypokalemia. water solubility.0) 5. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.4 (5.48-1.24-3.36 (3.16 (1.36-1.58) 4.45 (1.61) 2.03) 3.29-1. in urine.31 (1.00 (5.76 (4.10) 3.51-3.99 (2.36-1.01) 1.96-6.24-1.41) 4.39-5.26-1.58-6.52-4.11) .73-2.09) 6.20-8.26-4.54 (1.65 (2.70) 10.81-6.50 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48) 2.80-6.28-11.36 (3.68 (3.55 (4.37-1.38) 1.40 (1.39 (2.51) 6.43) 1.28 (1.90-2.86) 5.52 (3.27) 7.76) 2.20-2.21 (1.76 (2.33-1.56-3. Perry et al.00) 4.57-7.29-7.921 (.38 (4.39 (2.2) 5.55) .24) 3.59) 2.44 (1. 1994.49-1.51 (1.62 (4.75) 1.777-1.86-7.8) 4.59-7.55-6. weakness.53-21.75-22.98 (2.50) 1.33-4.24-6.36 (5.15-4.45-6.00 (2.963 (.78 (2.26) 4.48 (1.41 (1.29-4.44-2.99 (4.51 (1. diarrhea.58) 75th 2.40 (1.96) 7.42 (4.10-1.3 (6.47) 10.38) 1.47) 4.79-5.34-5.52) 1.62) 2.891 (.00-7.08-2.16) 11. 1986).84) 2.56 (1.46) 1.31-1.19-1.28-1.754-1.81-6.84-2. Wones et al.91-2.88 (2.76) 1.29 (3.49-1.60 (2.74) 1.39-10.33 (5.58 (4. such as those used in medical radiographic procedures.77) Total 1.65 (5.48-3.4) 5.68) 3.36-2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.39 (3.19-2.29-4.44-2.73-4.56) 4.46-22.60) 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. Symptoms following acute high dose include perioral paresthesias.47) 1.10-2.06) 2.24-11. Toxicity from soluble barium salts is rare.710-1.59) 1.34-3.50) 2.72 (2.39 (2.27-3.27-1.47 (2.39) 4.53) .84-5. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.96 (4.25) 4.97 (5. and cardiac dysrhythmias.24-1.45-1.0) 6.10) 6.29) 1.29-3.63-4. a benign condition that may occur among barite ore miners.96 (4.80) 3.38 (1.25 (1.35-1.33 (1.68-3..03-1.41 (2. 1990).06) .68) 1.03) 2.39-1..22-2.82) 1.26-1.56) Selected percentiles ( 95% confidence interval) 50th 1. are not absorbed when administered.53 (2.40-1.58) 1. population from the National Health and Nutrition Examination Survey.42) 1.Metals was eliminated primarily in feces and to a lesser extent. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.42) 1.60 (5.59) 1.74 (5.33) 1.82) 1.86 (2.88 (6.19-1.41 (1.3) 6.32 (2.45) 95th 6.69-9.38-1.54 (2.02-5.01 (5.26-1.75) 2.71 (5. 2001).25-11.30 (1.48-5.57 (6.00 (3.60 (2.52-10.02) 4.76 (3.880-1. Barium is not rated for human carcinogenicity.45 (3.48 (1.55 (5. 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.11-2.57) 2.97-3.51) 4.62 (1.35-3.38-7.77) 5.57-10.34) 1. and route of exposure.30 (1.26-1.16-1.91 (3.23-2.915 (.54) 1.70) 1.50) 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 1.47) 1.13-2.97 (4.52) 2.37 (1.73) 2.68 (2.83) 3.00-1.77-5.18 (1.77) 1.69 (5.19-1.23-5.60 (1.22-1.58 (2.51) 4.31) 5.23-1.01 (4.64 (1.28) 5.32 (1.99) 1.32) 2.18 (1.832-1.50) 1.22-4.76-3.703-1.33) 6.85-5.02 (3.75-3.39-1.10 (6.37-2.64) 7.00) 1.22-1.45-1.905 (.2 (3.70) 4. The health effects of exposure to barium compounds depend on the dose.20-1.S.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 .24-6.37 (1.51 (3.32) 2.67-6.63) 1. hypertension.34-1.05-1.97) 1.64 (1. interval) 1. NTP.47 (5.27 (2.46 (2.59 (1.81-7. paralysis.61 (4.83) 2.87) 1. 1984.13-3.36 (1.00) 6.04) 1.72) 6.12) 2. Insoluble barium salts.96) 4.77) 1.28-7.96) 4.55 (1.11) .60 (1.48 (1.31-1..

atsdr.niehs. Lack of effect of drinking water barium on cardiovascular risk factor.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en.. Pirkle JL. Jr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Howerton K. Princeton NJ: Princeton Scientific Publications. Levy.e. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Princeton (NJ): Princeton Scientific Publications.nih. Sci Total Environ 1990. Information about external exposure (i. et al. PS. Laurie RD. et al. 1994. Available at URL: http://ntp.64(1):13-23. Ash KO. Trace element reference values in tissues from inhabitants of the European community I. patient population and literature reference intervals for urinary trace elements. Patty’s toxicology. Advances in modern toxicology. 2001.gov/toxpro2. et al.296(1-2):71-90.85:355-359.. Sabbioni E. and serum of Italian subjects. 2000) to levels in NHANES 1999-2000 and 2001-2002. 2001-2002.76(1):53-59. J Toxicol Environ Health.cdc. Third National Report on Human Exposure to Environmental Chemicals. 1984. References Brenniman GR. [online]. p. 84-94. NTP. 221-252 Komaromy-Hiller G. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. blood. Centers for Disease Control and Prevention (CDC). Biomonitoring studies of levels of barium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of barium than are found in the general population. Barium. Minoia C. 1992).28(3):373-388. Gallorini M.. Ting BG. In Friberg L. and a drinking water standard has been established by U. 1998).gov:8080/cs. 1989. Inc. 1990. EPA..S. Genter MB. Clin Chim Acta 2000. Pietra R. Weltle D. p. Cohressen B. Paschal et al. Vouk VB. barium. strontium. Douglas BH. Jackson RJ. Comparison of representative ranges based on U. 1985. New York: Elsevier. Biomonitoring Information Levels of urinary barium reflect recent exposure. p. 1986. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Nordberg GF. ed. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report... Frohman.. Costa R. Environ Res 1998. 2nd Ed. Atlanta (GA). the welders had no obvious adverse clinical effects (Zschiesche et al. In: Inorganics in drinking water and cardiovascular disease. 4/8/09 Paschal DC.html?charset=iso-88591&url=http%3A//ntp. environmental levels) and health effects is available from ATSDR at: http://www. Handbook on the Toxicology of Metals. Epidemiological study of barium in Illinois drinking water supplies. 2005. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. eds. Int Arch Occup Environ Health 1992.. Reeves AL. and radium In: Bingham A. Magnesium.nih. A study of 46 elements in urine. Sampson EJ. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). 2005. Investigations into the effect of drinking water barium on rats. Trace metals in urine of United States residents: reference range concentrations. Stadler BL. pp. eds. and 2003-2004 (CDC. LA. et al. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Perry HM. Calabrese EJ. New York: John Wiley & Sons.95:89-105.html. ed. Schaller KH. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. National Toxicology Program (NTP). 5th ed.S. In: Calabrese EJ. Morrow JC. 231-249. Vol 2: Specific Metals.niehs. calcium. Minoia et al.gov/ntp/htdocs/LT_rpts/tr432.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA..197210. Pozzoli L. McCauley PT. Exposure to soluble barium compounds: an interventional study in arc welders. Powell C. Apostoli P. Kopp SJ. Environ Health Perspect 1990. Wones RG. Perry EF. Zschiesche W.

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

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

95:89-105.S. Levels of beryllium in urine for the U. Minoia et al. Third National Report on Human Exposure to Environmental Chemicals. Sabbioni E. Hamilton EI.Metals (i. and the 95th percentile for males in NHANES 2001-2002. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. blood.. Environmental Health Criteria. Costa R. Pietra R.13 μg/L. 0. Centers for Disease Control and Prevention (CDC). 1998). Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. less than 0.e. Hamilton et al.76(1):53-59. International Programme on Chemical Safety (IPCS).atsdr.html. plasma and urine and a critical evaluation of reference values for the United Kingdom population.158:165-190. Andrew M.. Available at URL: http://www.inchem.e. Ting BG.. Trace metals in urine of United States residents: reference range concentrations. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Genetic and exposure risks for chronic beryllium disease. 106.. 198 Fourth National Report on Human Exposure to Environmental Chemicals . 20012002. Atlanta (GA) 2005.S. A study of 46 elements in urine.htm. References Apostoli P. They reported urinary beryllium levels ranging from 0. Maier L. population are lower than levels in workers. Comparison of representative ranges based on U. Kriess K. Trace element reference values in tissues from inhabitants of the European community I. 3/27/08 Komaromy-Hiller G. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. HLA-DPB1 and chronic beryllium disease: a HuGE review.1 μg/L). Environ Res 1998. Sci Total Environ 1994. Beryllium [online]. Paschal et al.23:827-839. Paschal DC. Minoia C. Sampson EJ.cdc. 2001). and serum of Italian subjects. Sci Total Environ 1990. it is likely that urinary beryllium levels in the U. VI.296(1-2):71-90. Weston A. Schaller KH. Int Arch Occup Environ Health 2001. Howerton K. et al. et al. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Review of elements in blood. In other studies.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Sabbioni E. Clin Chest Med 2002. McCanlies EC. Morrow JC. which approximate this Report’s limit of detection. Jackson RJ.org/documents/ehc/ehc/ ehc106. 1990.S. Apostoli P. 2000. 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. Pirkle JL. Given these results. Element reference values in tissues from inhabitants of the European community. Van der Venne MT. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. and the fact that most NHANES participant levels were undetectable.. population were generally undetectable in NHANES 1999-2000. Gallorini M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Clin Chim Acta 2000. patient population and literature reference intervals for urinary trace elements. and 2003-2004. environmental levels) and health effects is available from ATSDR at: http://www. 1990. Am J Epidemiol 2003.12 to 0.gov/toxpro2. Pozzoli L.74:162-166.157:388-398. Ash KO.

600 (.400-.800-1. population from the National Health and Nutrition Examination Survey.20) 1.600 (.700) .300-.800 (.395 (.400) .300) .378 (.00) .10 (1.600-1.500 (.10) 1.300-.60-1.00 (.337) .300-.20) 1.500-.600 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 0.400) . see Data Analysis section) for Survey years 99-00.400 (.500-.700-1.900-1.30) 1.600 (.900-1.400) .400 (.300-.400) .20-1.80) 1.304 (.400) < LOD < LOD < LOD .S.366) * * .3.400-.00-1.400) .300 (.300-.700) .400 (.500 (.500-.10 (1.10) 1.400-.00 (.359-.40 (1.300-.10 (1. cadmium use has declined in response to environmental concerns (http:// minerals. and nonferrous alloys.300) .235 (.900 (.300) .600 (.00 (1. EPA.40 (1.400-.600) . < LOD means less than the limit of detection.30-1.50 (1. during refining of lead and copper from sulfide ore.600 (.40) 1.60 (1.400 (.10) 1.50 (1.200) .500-.800) 1.900-1.300) .40-1.600) .40) 1.300 (<LOD-.400 (.20) 1.600 (.362-.900 (.300-.283 (.400) .426-.600 (.20) 1.30 (1.70) 1.50-1.300 (<LOD-.300) 75th .400) .500-.300) .400) .700) .400 (.30-1.50) 1.400-.300) 1.14.20) .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 * * * * * * .216-.398) < LOD < LOD < LOD < LOD < LOD < LOD .00 (.00 (.300 (.400) < LOD .500-.326 (.usgs.378-.266-.400) .400-.368-.600) .800 (.500) .361-.200 (.600 (.400) < LOD .00 (.60 (1.400) . lead.300-.600) 1.300-.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .00 (.600) .500-.500 (.50 (1.20-1.30-1.00 (.00-1.400 (.400) . interval) . malleable.300 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300 (.10) 1.300-.500) .40 (1.900-1.403) .424) * .400 (.800) .400-.Metals Cadmium CAS No.700) .700-1.10) 1.300) .20 (1.90) 1.30) 1.300-.296-.300-.60 (1.3.289-.304 (.200 (<LOD-.468 (.300 (.900-1.10) 1.00-1.20-1.500) .20) 1.441) * .400 (.00-1.400) < LOD .10 (1.300 (.50) 1.421 (.00 (1.400 (.600-.200-.20) 1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20) . Since 2001.60) 1.300 (.60 (1.500 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.40 (1.200-.00-1.376-.400-.900-1.20-1.500 (.700-1.600) .60) 1.700 (.452) .382 (.367-.300 (.500-. respectively.600) .300-. as zinc sulfide) and to a lesser extent.10) 1.386-.500 (.300-.500-.600) .10 (1.700) .400 (.600-.00) .500) .20-1.50) 1.500-.300 (<LOD-.500-.500-.200-.400 (.20) 95th 1.30) .400 (.40 (1.425 (.304-. 7440-43-9 General Information Cadmium is a soft.400) .60) Total * .600 (.700) .30-1.S.00-1.300) .300-.400-.800-1.300 (.449) Selected percentiles ( 95% confidence interval) 50th .300-.500-.20 (.10 (.600 (.10 (1. 01-02.300-. coatings and plating.700) 1.20) 1.331) .500-.80 (1.800) .300-.600 (.10) 1.255) .60) 1.300 (.470) * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.393 (.600) 90th 1.600) .60 (1. U.500 (.427) * .300) .300) .700) . and 03-04 are 0.275-.00-1.500) . The predominant commercial use of cadmium is in battery manufacturing.200 (.00-1.500) .700) .300 (.309-. and 0.400) .30) 1.500-.500) .50-1.600) .400 (.gov/minerals/pubs/commodity/cadmium).00 (.200-.50-1.80) 1.600 (.500-.403 (.300-.500-.513) .400 (.70) 1.50 (1. Cadmium also may be emitted into the air from zinc.460) .600-.200-.00 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.400-.313 (. or copper smelters (U.300-.500 (. and incineration of municipal waste materials.300) .300-.900-1.40 (1.200 (<LOD-.300) .S.300 (.412 (.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 .900-1.900-1. which may vary for some chemicals by year and by individual sample.300) .344) .40-1.300 (.30-1.300 (.300 (<LOD-.10 (1.300-. plastic stabilizers.20-1.420 (.400) .500-. Other uses include pigment production.400-.70) 1.300) .40 (1.00-1.400 (.333 (.20-1.500 (.200) .70) 1.400 (.900-1.20) 1.50-1.00 (.200 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .600 (.

241) .178-.229) .316 (.13-1.279 (.078 (.211 (.249-.262) .261-.855-1.210) .326) .447 (.870) .372) .540) .204 (.800 (.20-1.362) .820-1.Metals 2000).977) .500) 90th .090) .433-.890 (.589 (.130 (.607) .440-. 2003).462 (.285-.151-.886-1.15) 1.817 (.366-.530) .04 (.330-.189-.207-.270 (.633 (.28-1.37) 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 .092) .299) .171-.216 (.243-.202 (.366-.430-.238) .890-1.198) .452 (.195-.492 (.498-.820 (.963-1.875 (.466 (.203) .490) .753-.858 (. an inducible metal binding protein.219 (.705-.22 (1.160-.167-. 2003.308) .730-.455 (.238-.196-.060-.231) .623) .06) .806) .277 (.230) 75th .748-1.960) 1.234 (. copper) and protein. Renal tubular and glomerular damage.43) 1.980) .733) .290-.322 (.200 (.211-.519) ..519) .210 (.192-..530 (.175 (.880) .110-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .255) .680 (.261-.17) .47) 1.813 (.214-.17 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.482) .700-.354) .820) 1.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .112-.148) .580) .350 (. however.387) .209 (.700-.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.52 (1.300) . 2003).226) .109 (.115-.17 (.150-. potatoes..220) .329 (.257) .221) . 2001). see Data Analysis section) for Survey years 99-00.189-. calcium.01) .180 (.220-.120 (.257-.38) .10 (1.265) .500) .310 (.24) 1.170-.980-1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR..01-1.255) .081) .220-.03) .550 (.281 (.848 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.249) .06.210 (.02-1.12 (.232 (.381-.232) .700-. Horiguchi et al.818 (. interval) .22 (.148-.223 (.20 (1.160) .390 (.918-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.539) .100-.282 (.559 (.219 (.101) .41 (.265 (.067-.255) . population from the National Health and Nutrition Examination Survey.300 (.193-.177-. 1994).360) .28) 1.192-.S. For nonsmokers who are not exposed to cadmium in the workplace.210 (.810-1.190-.061 (<LOD-.** Survey Geometric mean (95% conf.892-1.253-.302 (.320) .239 (.160) .226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .596) .247) .206) .400-.741-1.440 (.06-1.109-.201 (.200 (.38) 1.393-.839 (.219 (.203 (.790 (.221 (.766 (.179-.717-.436-.220 (.763-.817 (.714-1.456-.136) . and 03-04 are 0.450 (.790 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.190-. **All results are corrected for molybdenum oxide interference in the ICP-MS method. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.551 (.733-.640) .114-. Kikuchi et al.430) .313) .222) . zinc. Diamond et al.128 (.57) 1.72) 1.423-. With chronic exposure.165-.989-1.800-.184-. and various seeds.190-. 0.270 (.390-. To a lesser extent.229) .080 (.960 (.74) 1.38) 1.990) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.82) 1.233) .200-.087-.107-.210 (.272-.15) .240) .980) .980-1.077 (.426 (.260-. 2004a.83) 1.980 (.12-1.233) .480) .04 (.336) .34) 1.551) .230) .06.06-1. wheat.475 (.875) .157) .175 (.06.470-.134) .440 (.633-1.20 (1.520-.972 (..15 (.260-.51 (1.235) .310) .181 (.141 (.28 (1.206 (.686-.169-.090) .860) 1.306 (.339) .476-.183-.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 .351-.260 (.251) .191-.445 (.07-1.121 (.135 (.919) . Cadmium in soil is absorbed by plants.140 (.229-.273 (.199 (.09-1. 1999.48 (1.067-.13) .210) . Cadmium absorption may be increased with iron deficiency (Berglund et al.30-1.38) . drinking water is a source for cadmium intake. Cadmium is absorbed via inhalation and ingestion.230 (.210 (.836-1.153-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.135-.240-.227 (.173) .170 (.157-.194-. whose body burdens of cadmium can be approximately twice that of nonsmokers.150) .610) .220) Selected percentiles ( 95% confidence interval) Sample 95th 1.295) .400-.510-.892 (. and 0.940-1.481) . including many food crops such as cereal grains.170-.412) .187 (.545 (.191-.843-1.061-.390-.208-. respectively.077 (.366) .713) . 2003).394-.289-.237-. 01-02.458 (.32 (1.36) 1.284) .445 (.065-.160 (. ingestion through food is the largest source of exposure.126) .20) 1.246) .202-.191 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.17 (.510) .01 (.490) 1.493-.283 (.189) .19) 1.200-.193 (. rice.886) .25 (1. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.20 (1..13 (.25) 1.263) .388-.450 (.280 (.507) .327 (.479) .092 (.

176 (.712 (.906) .185) .507-.171-..210) .159 (.727-.156-.224 (.297) .187) .850) .156 (.444-.247-.S.856) . 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.222-.192) .472) .206-.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.985 (.551) . 2003.234 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.873 (.802 (.479 (..691-.718 (.806-1.398-. At lower environmental exposures.288) . 2000.209) .979 (.204-.813-1. 2002.300-.084-.113-.404) .449) .382-.545) .325 (.421 (.261-.470) .075 (<LOD-.107) .827) .205 (.828) .919 (.647-.197-.. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.075-.693 (.242) .686 (.940 (.876-1.288 (.667) .156) .131-.998) .184-.241) .084 (.700 (.067-.500-.784) . 1996.839) .431) .830-1.245 (. During the 1950’s and 1960’s.112) ..433-.253) .136-.063-. interval) .283 (.184-.175 (.708-1.336-.175 (.181) .536 (.071 (.143-. Noonan et al.38) .267 (.100 (.274) 1.293-.093 (.645-.531 (.181-.783 (.434 (.176 (.240) .614) .198) .191-.830) .106) .16) .147-.189-.338 (.335 (.316 (.233 (.184) .228-.104) .818) .729 (.078 (.767 (.340) .090 (.078-.432 (.653) .700) .183 (.865 (.051-.716-. Horiguchi et al.144-.135) .10) 1.414-.850) .740 (.288-.261) .202 (.143-.199 (.159 (.270 (.470) .754) .917 (.196 (.281) .719 (.281) .533) .484 (.137-.148 (.668-. Olsson et al.191 (.289) .166 (.06 (.311) .560-. can result from high dose chronic exposure.501 (.157-.209) Selected percentiles ( 95% confidence interval) Sample 95th ...210 (.158-.111-.163) .178) .630-.779 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.387 (.207-.687-.147 (.308) .096) .690 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .909-1.085-.00 (.364) .182) .140-.208-.537-.304) .146-.163 (. 2004b).316) .207) .377-.211 (. Staessen et al.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.234-.318 (.412 (. However.722-.562-.559-.229) .607) .308 (.077-.140-. 2002..438) 90th .097) .687 (.631) .178-.688-.473 (. 1999).173-.278) .813-.07) .261 (.941 (.423 (.296 (.187-.182) .173 (.273 (.** Survey Geometric mean (95% conf.343-.190 (.391-.266) ..194-.491-.884) .104) .137 (.239-.226) 75th .716) .00 (. 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.240) .225) .931 (.219 (.181 (.201-.223) . 1999).678-.874-1.440) .690-.917) . 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.215 (.161-.220 (.856 (.518) .175-.154-.091) ..247-.387-.174-.350) .927-1.331 (.17) .304-.216-.235) .441-.266-.666-.789 (.183) ..181 (.256-.162 (.122 (. 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.757 (.157-.247-.170-.415) .221 (.238) .02 (.252 (.303) .818) .221-.757) .232) .236-.143) .086 (.085 (.238-.185 (.292) .725-1.255-.268 (.250) .696-. most often a result of occupational exposure (Roels et al.094) .833-1.199-.321) .795) 1.267 (.414 (.516-.388-.091 (.225) .123-.263 (.232) .190 (. 2002. population from the National Health and Nutrition Examination Survey.282 (.826-1.622 (.289) .329 (.101) .280 (.154 (.440) .177) .200 (.253 (.212 (.227-.210 (.263-.147-.426-.218) .438-.09 (.690-.767) .168-.792 (.783) .678 (.16) 1.208 (.098) .826-1.074-.481 (.487 (.591 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .541) .382) .126 (.123-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .13) .091 (.136-.962) .191) .234) .940-1.05) 1.663 (. 2004).08) . Jarup et al. 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.674-1.170 (.950) .352) .418) .418-.538) .381-.130-.490 (.168-.650-.929) .168 (.182) .12) 1.423-.617 (.446) . 1999).07 (.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 .150-.083-.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 .476) .404 (.219 (.769 (.

Moriguchi et al... Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al.. Noonan et al. as may occur from welding cadmium-alloyed metals.. 2002). 2003. 2002). CDC. 2002). Creatinine-corrected urine cadmium values in U. For NHANES 19992000.... approached these values associated with subclinical changes in renal function and bone mineral density.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven 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. Friedman et al. has resulted in severe.. Staessen et al. Becker et al. Olsson et al.. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. Ezaki et al. 2006).. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. 2004. respectively. Jarup et al. 2002.e. 2003. 2004. 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).. 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. 1988).. 2003.. 2006.. 2002.. 2002. 2000.S. 2002)... blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. environmental levels) and health effects is available from ATSDR at: http://www. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen 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. 2000). urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. 2005... not to imply a safety level for general population exposure.. maternal blood or maternal urine and birth weight (Nishijo et al. Jin et al.. respectively. 2002. 1999. Horiguchi et al. Women had higher blood and urine cadmium levels compared to men of similar ages. Zhang et al.46 mg/gram of creatinine) (Ezaki et al. Blood and urine cadmium levels are typically higher 202 in cigarette smokers.. 1996. 2002.S. Olsson et al. 2003). Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood... Cadmium can produce lung....gov/ toxpro2... potentially fatal pneumonitis (Fernandez et al. In postmenopausal women. 2004.. Wennberg et al. However. Acute and heavy exposure to airborne dusts and fumes. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. EPA.. 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. 2006). 2004. Ezaki et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Wilhelm et al. Staessen et al. 1996). Staessen et al.. Salpietro et al. 2005. Mannino et al. 2002.26 and 3. 2004b. In adults aged 60 years and older. Komaromy-Hiller et al.. 2003. 2003.. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles.cdc. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Jarup et al. 2000. 2002) and length at birth (Nishijo et al. In the typical environmental exposure.atsdr.. Olsson et al. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Wennberg et al. 2000. Becker et al. Suwazono et al. 2004).. 2003. 2005). 1999).S. Animal studies have demonstrated reproductive and teratogenic effects. Information about external exposure (i. data (CDC. 1999). Further research is needed to address the public health consequences of such exposure in the United States.. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . intermediate in former smokers and lower in never-smokers (Becker et al. and drinking water and environmental standards have been established by U. Both IARC and NTP consider cadmium a human carcinogen. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 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..html. Horiguchi et al. 2002). Occupational standards are provided here for comparison only. with peak values observed in the fifth to sixth decades (CDC. 2004b). Becker et al. 2006. 2005.. 2005...1 mg/L (Alfven et al.

76:186-196. Bregante G. possibly better than b2microglobulin. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lancet 1988. Chislovska NV. Clin Chim Acta 2000. Seiwert M. Savage-Brown A. Komaromy-Hiller G. Ye T. Tsukahara T. 196:114-123. Neurotoxicology 2003. Tsukahara T. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey.45:43-52. Berglund M. Seiwert M. Schulz C.S. Lundh T. Chiappino G. et al. Mucha A. Nordberg G. Thorax 2004. Vahter M. Hotz P.gov/toxprofiles/tp5. Kumagai N. Ezaki T. Ezaki T. Bernard A. Lepom P. Horiguchi H.96:353-359. Grubb A. Kaus S.html. Environ Res 2004b. environmental. Moriguchi J. Horiguchi H. Zhu G.59:497].atsdr. J Toxicol Environ Health 2003. Schulz C. Miyamoto K. Environ Health Perspect 1994. Olfactory function in workers exposed to moderate airborne cadmium levels. Environ Health Perspect 2005. Oguma E. et al. Hellstrom L. et al. Akesson A. Elinder CG. Kundiev YT. Serra J. Miyamoto K. Jarup L. Takebayashi T. population. Mannino DM.354:1508– 1513. Atlanta (GA). Available at URL: http://www.59:194-8. Lidfeldt J. Consonni D. Environ Res 2004.102:83-89. Toxicol Lett 2004.296(1-2):71-90. Vahter M. Okamoto S. et al. Venables KM. Lison D. Davison AG. Lauwerys R. Palomar M. Toffoletto F. Ikeda Y. Toxicol Appl Pharmacol 2004a. Stock AL. Diamond GL. Bellerup P. et al. Lukyanova EM.66(Pt A):2141-2164. Toxicological profile for cadmium update. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Int J Hyg Environ Health 2002. et al. et al. Fernandez MA. Agency for Toxic Substances and Disease Registry (ATSDR). Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Krause C. Comprehensive study of the effects of age. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Lancet 1999. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10.46:372-374. Centers for Disease Control and Prevention (CDC). Furuki K. 102:10581066. Furuki K. Persson B. Int Arch Occup Environ Health 2003. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Darbyshire J. Jin T. Fukui Y. Mascagni P.205:297-308. Alfven T. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China.000 women in the Japanese general population: a nationwide large-scale survey. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Becker K. diabetes mellitus. Sasaki S.13(11):1627-1631. Buchet JP. 2005. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. et al. Occup Environ Med 2000. 4/8/09 Alfven T. Greves HM. Cadmium fume inhalation and emphysema. Uemura T. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Machida M. Gadea E. 206:15-24. Kikuchi Y. Fukui Y. et al. ShkiryakNizhnyk AZ.110:699-702. Int J Hyg Environ Health 2003. Moriguchi J. Environ Res 2006. Wang H. Machida M.95:20–31.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. patient population and literature reference intervals for urinary trace elements. Carlsson MD. Becker K. Sanz P. Taylor AJ. References Akesson A. Ikeda Y. Comparison of representative ranges based on U. Environ Health Perspect 2002. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Fatal chemical pneumonitis due to cadmium fumes. iron deficiency. Ukai H. Fayers PM.1(8587):663-667. Jarup L. Pickering CA. Choudhury H.S. Bo M. J Occup Health 2003. et al. Third National Report on Human Exposure to Environmental Chemicals. Howerton K. et al. Dekio F. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Costa R. Nomiyama T. Sasaki S. Kaus S.24:717-724. Nermell B. Friedman LS. Holguin F. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Occup Med 1996. Thayer WC. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U.57:668-672. Seifert B. Oguma E.148(1-2):11-20.cdc. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. 1999 [online]. Jones RL. Ash KO. Anthropometric. Nerbrand C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.

30(5):395-399.39:2507-2515. Ottosson H.209:301305. et al. Environmental exposure to cadmium. Fan YG.110:151-155. Minciullo PL. Wennberg M. Arch Environ Health. Nakagawa H. Japan. Revised and new reference values for arsenic. Zhang YL. J Perinat Med 2002. Roels H. Tanebe K. Kathman SJ. Time trends in burdens of cadmium.59:394-397. Merlino MV. Olsson IM. Bensryd I. Thijs L. Liu QF. Nogawa K. Environ Res 2000. et al.110:1185-1190. Biological monitoring of cadmium. eds. 2004. Oskarsson A. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. created 1992. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk.Metals Nishijo M. Kobayashi E. Nakagawa H. Nordberg M. Biological monitoring of toxic metals. Int J Hyg Environ Health 2006. dietary intake. Kuznetsova T. Environ Health Perspect 2002. Nordberg GF. Environ Res 2006. Bergdahl IA.html.59(1):22-25. Stegmayr B. Vangronsveld J. Stelitano A. Nakagawa H. Cadmium carcinogenesis. Tanebe K. Zhao YC. Mutat Res 2003.84 (Section A):4455. J Cardiovasc Risk 1996.3:26-41.gov/ttn/atw/ hlthef/cadmium. 151-168.533(12):107-120. Roels HA. Salpietro CD. Zhu HD. Suwazono Y. Schultz C. Friberg L. and mercury in the population of northern Sweden. Skerfving S. Buchet JP. Lauwerys R. Lundh T. et al. In: Clarkson TW.100:330-338. 4/8/09 Waalkes MP. Usefulness of biomarkers of exposure to inorganic mercury. EPA). Noonan CW. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium.21(3-4):251-262. Honda R. lead. cadmium. J Environ Sci Health B 2004. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Mueller PW. Bruiglia S. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. et al. or cadmium in controlling occupational and environmental risks of nephrotoxicity. New York: Plenum Press. Kido T. iron status. Hazard Summary. Lijnen P. Revised 2000 [online]. Sager PR. Cadmium in blood and urine – impact of sex.epa. Lybarger JA. Wilhelm M. et al. Lancet 1999. Honda R. Staessen J. age. Ginucchio G. Lundh T. Roels HA. Gallmans G. Tawara K.353:1140-1144. Relationship between newborn size and mother’s blood cadmium levels. lead. Schwenk M. Wang JX. Staessen JA. Campagna D. Okubo Y. 2001. Jansson J-H. 2000. Cadmium compounds. et al. Available at URL: www. Nordberg GF. Saito S. Gangemi S. pp. Hoet P. Ren Fail 1999. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Lison D. Toyama. forearm bone density. and risk of fractures: prospective population study. Nishijo M. 204 Fourth National Report on Human Exposure to Environmental Chemicals . and former smoking – association of renal effects. Occup Environ Med 2002. United States Environmental Protection Agency (U. Environ Health Perspect 2002. Emelianov D.S. lead. Sarasua SM. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan.

scintillation counters.44 (8.0) 10.34 (4.5) 9.20-7.29 (4.80 (8.73-5.25 (3.31-8.59) 7.80 (4.3) 9.38) 5.89) 5.53 (6.9) 11.82-4.23) 9.50-7.64-10.27 (7.93 (4.30) 7.27-5.56 (4.83-4.1-12.4-13.64) 4.59-5.73-11.13 (5.84 (4.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8) 12.55 (4.9) 12.76-6.80-10.27) 4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.70-5.8-13.0) 11.3-13.0) 12.17 (6.80) 7.86-11.4) 12.81) 4.40-5.13 (7.08 (7.3 (8.90) 5.05) 5.8 (11.40-5.79 (4.1) 11.60 (7.70) 5.95 (3.7) 10.1-13.04) 7.14.42) 7.40-5.90) 4.81-14.3) 10.77 (9. soil. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.81 (4. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.00) 6.33-5.64 (4.8) 11.94 (4.74 (4.00-4.2) 12. For absorbed cesium salts.12-5.3) 12. photographic emulsions.01) 7.1 (10.70 (8.35 (4.1 (9.80-11.64) 5.1 (11.00-9.56 (4.6) 11. and 03-04 are 0.20) 5.97) 4.87 (4.72-7.70 (6. see Data Analysis section) for Survey years 99-00.03 (4.30 (6.5 (8.36) 3.25-5.32) 4.00-8.59-5.87 (4.30 (6.5-14.60) 7.5-14.70-8.49) 75th 7.8) 9.10-8.25) 4.10-7.20) 4.64) 5.98 (7.54-11. 2004).90-8.97 (7.90-12.20) 7.50 (4.00-10.90) 9.71-9.39-4.20-5.90) 5.02 (4.90 (6.Metals Cesium CAS No.33 (5. Radioactive 137Cs has been used medically to treat cancer.3-13.30) 5.8) 12.63) 6.35 (4.50) 5.29) 4. nausea. and 0.40) 5.9 (10.3) 10.39) 7.86-12.50) 9.00-8.70 (6.4 (9.6) 10.43-8.59-5. 01-02.55 (7.21 (4.60-6.6 (11.10-9.12 (4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 4.88 (8.9 (10.8) 11.71) 4.80 (4.42-7.71 (4.84) 5.10 (6.30-10.72) 4.84-9.62 (5.74) Selected percentiles ( 95% confidence interval) 50th 4.0-15.6 (9.84-5.49 (4.0 (9.56-11.99-11.77 (9.S.3-15.5-13.90-10.15-8.17) 4.16-6.5) 12.87 (4.3) 10.2-12.2) 11.6 (9.6 (9.80 (8.08-5.20-8.0-13.21) 90th 9. interval) 4.86 (7.80-10. However.7 (9.62 (5.77 (4.80-10.60-5.40) 7.7 (8.47-8.09) 5. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.26-11.80 (4.05-5.22 (4.45-8.2 (9.90) 7. and cardiac arrhythmia (ATSDR.99) 9.4) 10.34) 9.16-6.80-13.08) 7.43 (5.2-14.99) 7.8) 12.23-4.7) 10.71-5.40-11.14.4) 10.87-7.9 (11. semiconductors.35-5.7) 11.7-14.80-6.94 (4.0) 12.95-4.9) Total 4.70) 5.71-8.00 (7. cesium hydroxide is corrosive and irritating at high concentrations.70) 7.60-12.4) 95th 11.26) 7.7 (11. and as polymerization catalysts.2-13.10-5.09-5.3 (8.7 (10.91 (7.60-7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.42) 6.4 (10.94) 4.22-4.8 (10.52) 7.49) 4.14 (4.89) 4.81) 9.63-4. Little is known about the health effects of this metal.71 (8.20 (4.70 (4.12-11.56) 5.50 (6.40 (4.90-10.10 (8.55-11.60) 5.5) 10.9 (11.9) 8.68) 9.60-7.97) 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 4.60 (8. and high-power gas-ion devices.5 (10.26) 4.13 (8.89-5.63 (4.54) 4.10 (6.70 (8.4 (9.05) 5.3) 10.8 (10.4) 11.00) 7.99-11.07-11.60-6. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.4) 12.92-13.40-7.5-16.9 (11.99-6. respectively.84) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (10.50 (7. Whether cesium compounds are carcinogenic is unknown.59 (5.24) 4.94-4.04 (4.66 (7.36 (3.96 (6.0) 12.13-8.6 (9.08 (6.49 (5.69-6.57-5.7) 11.67 (4.01-6.7 (9.81) 4.46) 7.82) 5.26 (3.00) 4.36 (6.50 (4. infrared lamps.70 (5.2 (9.62) 4.68 (7.40-11.90 (4.03-4.8) 9.20) 8.1) 10.50 (4.53-11.08-5. 0.32-5.7 (9.9 (11.98 (7. Most human exposure to cesium occurs through the diet.2. population from the National Health and Nutrition Examination Survey.95) 5.30-5.7 (10.4) 9.2-13.37) 5.37) 7.20-4. Fourth National Report on Human Exposure to Environmental Chemicals 205 .64-5.10 (8. diarrhea.1-12.74-5. although cesium was generally of low toxicity when given to animals.70 (9.77-8.80 (8.90-10.01-8.40) 5.07) 4.91-8.20 (6.40-5.6 (11.2-13.87) 5.32 (3.97-7.47-4.12) 5.33 (6.7 (10.05-5.1) 9.61) 7.61-6.0) 11. and clay.17-6.83) 6.0) 9.60) 7.1) 9.45-5.90-12.52-9.1) 11.03 (4.9) 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.

25) Selected percentiles ( 95% confidence interval) 50th 4.50 (7.24-10.50 (5.42-4.96-4.48) 90th 7.19-6.53) 6.49) 3.67) 5.43) 8.26 (3.14) 4.46 (8.73 (3.95) 10.43 (8.20-4.20-4.40) 7.16-8.95 (5.09) 4.29) 5.14-7.56) 3.5 (9.93-9.81 (4.41 (4.43 (3.50) 4.7-12.51 (4.10 (5.91) 5.6 (9.84-9.9) 10.50 (6.24 (3.5) 9.96) 4.3-15.66 (5.92 (5.47) 6.51 (3.08) 4.33 (5.00) 6.73-4.68) 4.63 (4.7) 10.27 (6.03) 6. population.28 (5.16) 5.10 (3.63-6. Two small studies of European populations reported urinary cesium levels similar to U.63) 6.21 (2.27-4.95 (3.27 (6.99-9.84-11.61 (7.97-4.03-5.14-4.51) 4.50-5..51 (3.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.39) 5.29-3.36-3.75 (6.04-5.47 (4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al. population from the National Health and Nutrition Examination Survey.27-6.77-5.42 (4.01-8.8) 5.99-9.53 (6.41) 4.64-6.00-5.60 (5.42-6.46-4.51 (7.83) 8.41-4.1) 11.8) 10.74 (5.99-4.33-3.0) 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 .29) 4.48) 7.40) 6.58-5.55) 4.74 (4.71) 6.78) 4.80) 6.66-6.87 (5.04) 5.65-4.8 (9.95-6.00-9.48-6.68-11.26-6.00-4.88-10.07-4.34 (5.59-8.47) 7.85-4.44-5.95) 8.37-3.14) 4.56-10.22 (3.06 (3.06) 5.11 (5.77 (6.06 (5. Minoia et al.47) 6.38 (3.8) 6.13-9.15) 95th 8.46-8. 2004).91-9.97) 8.88-4.03-6.S.17) 9.07) 8.97-5.65-3.47) 4.96 (4.04-11.72) 4.56) 4.16-5.28 (4.30-4.05-3.12 (3.9 (10.70) 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.28) 8.30) 10.77 (4.64) 4.94 (5.98 (6.83-7.35-7.53 (4.58 (4.00 (8.31-4.08 (5.63 (7.75-11.18-6.84-7.15-4.78 (3.76-6.S.68 (4.74) 3.60 (3.14 (6.20) 5.84-9.53) 3.79) 4.41 (5.3 (8.52-5.72 (4.35) 3.90-3.63-6.0 (7.33-8.70) 6.98 (7.91) 5.60-20.6) 6.72-5..10) 7.03) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.33 (5.13 (3.45-6.55-5.30 (7.38) 10.22-11.30) 10.18-7.14-6.37) 4.42-4.41 (8.00-5.92) 3.90 (7.42 (5.09) 8.98) 5.79 (5.17 (6.43 (4.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.76-9.05) 6.10 (3.77 (7.04) 6.07 (5.79) 9.78) 4.12-6.81 (4.44 (4.08) 3.47 (7.05-3.84-7.99) 4.70 (7.54 (4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.08-3.36-6.58) 3.25) 4.57) 3.35 (3.22) 6.38 (3.3 (10.12) 3.6 (9.44) 3.68) 3.64 (4.39) 8.91) 4.50) 8.18) 8.28) 7.79) 6.74-11.07) 8.43-6.13-9. population results shown in this Report (Alimonti et al.91-7.05) 3.55 (3.91-6.87) 5.06) 4.46 (7.79-5.96-4.82) 7.3) 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 3.17-4.23 (7.41) 9.11 (5.2 (8.67 (5.2) 11.08 (3. Using clinically submitted specimens.87-4.21-4. and were also roughly similar to those in this Report.3 (9.17) 4.39 (5.36-10.50) 4.94) 7.02-4.98) 5.44 (8.27) 4.82-4.91 (5.00-8. 2005.85) 4.21-3.4) 10.41-7.35 (4.15 (7.60) 3.24-4.43 (4.95) 4.15-11.86 (4.38-7.35-11. interval) 4.61-3.2 (8.13) 7.56 (4. Komaromy-Hiller et al.90-8.63 (6.9 (9.10-4.58) 8.30 (4.60-10.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.64 (8.0) Total 4.30-4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.26 (4.05-4.09 (4.5) 9.5) 7.38-12.05 (4.83-6.29) 4.62) 5.58 (6.99 (3.18 (7.3) 11.56) 4.19-3.77) 4.54 (5. 1990).95-12. (2000) found urinary cesium levels that were slightly lower than those reported for the U.20-8.85) 5.96) 4.43-11.91 (5.31 (4.51 (4.27 (8.74) 75th 5.0) 7.3) 9.90-8.S.54 (4.44-9.40-5..67 (6.20-4.02 (5.08-7.54 (3.65 (6.59) 4.7) 10.00-10.45 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31 (4.89-4.64) 9.66 (5.93-7.71 (7.64) 5.78 (3.50) 4.16-8.66 (6.68) 6.29-3.75 (7.08 (6.21-5.46) 6.62-8.08) 4.31-6.30 (3.

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

630 (.890-1. and kitchenware. shiny.350-.03-1.690 (.405-.550 (.25-1.870 (. 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.890) 95th 1.380 (.355-.47 (1.29 (1.24 (.610-. steel-belted radial tires.820 (.39) 1.581) .430 (.20 (1.680) .770) .850) 1.564) .339 (.313) .750 (.570) .64) 1.05 (.890-1.431) .03 (.15 (1.320 (.370-.333-.650-.830-1.47 (1.790) .03) 1.410 (.880-1.305-.S.56) 1.33 (1.16 (1.390-.350-.930-1.26) Total .336-.338-.23-2. large appliances.26-1.660-. and in synthesizing polyester and other materials.460) .550) 90th .530 (.410-.28 (1.291-.920) 1.583) .690-.16-1.380-.370) .373) .372) .850-1.530-.23) .630 (.343 (.02-1.13) 1.410) .47) 1.610) .434 (.890-1.520) .333-.331-.330-.502) .04 (.430 (.32 (1.540) 1.820 (.520-.50) 1.340-.431) .01 (.01 (.04-1.33-1.45 (1.890) .550-.460) .543) .460-.490-.540-.348-.454 (.460 (.420) .418 (.259-.360-.500 (.352 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.430) .01-1.460 (.327-.330) .340 (.380 (.900-1. Cobalt is used as a drying agent in paints.410-. industry is imported or obtained by recycling scrap metal that contains cobalt.370 (.910-1.463-.28 (1.620-.48) 1.920-1.950 (.50 (1.398 (.388-.32) 1.14) .790 (.496) .03 (.270-.26-2.09) .870 (.980) .460) .680) .570-.487) .430 (.404) .427-.399) .04) 1.359 (.60 (1.410) .940-1.450-.360-.340) .570) .394) .670 (. diamond-polishing wheels.400-.700) .670-.42) 1. interval) . see Data Analysis section) for Survey years 99-00.520 (.07-1.390 (.523) .960-1.450) .850) .410-.04-1.26) 1. Usual human exposure is from food sources.740 (. and magnetic recording media.32-2.330 (.03) .01-2.860 (.334) .461 (.520 (.490-.300 (.790-.420) .22) 1.32) 1.65) 1.310 (.48) 1.630-. and 03-04 are 0.21) 1.52 (1.810) .36) 1.16 (1.440-.435 (.520-.379 (.420 (.870-1.750 (.S.367 (.620-.92) 1.590-.710) 1.930 (.14-1.28-2.430-.308-.950) .465) .08.515 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.760) . 0. hard metal (alloys of cobalt and tungsten carbide).414) .17 (1.580 (. varnishes.520 (.730) 1.81) 1.580 (.67) 1.360-.37-1.350) 75th .600) .710 (.12) 1.640) .398) .47) 1.670 (.540-.424) .370-.470) . The cobalt used in U.519 (.540-.05 (.610 (.950 (.640) .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 .540-.350 (.75 (1.820 (. Cobalt compounds are used as catalysts in producing oil and gas.Metals Cobalt CAS No.07-1.900) .390) .450) .450-.590-.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 .369 (.06 (.24 (1.364-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.750 (.680 (.00) .319) .16) 1. and soil. and inks. and fertilizers.44) 1.940 (.800-. 01-02.22 (1.59 (1.417) .428-.710) .810) . blue-colored pigments.660) .373-.340) .310-.499 (.08-1.580 (.04-1.760 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.590) .380-.800) .950-1.469-.340-.900) .290-.68 (1.285 (.450) .316 (. respectively.374 (.07. automobile airbags.850-1.375 (.07.940-1.900) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.840) .410 (.700) .650 (. It is emitted into the environment from burning coal and oil and car and truck exhaust. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.99) 1.390 (.680 (.06 (.950-1.16-1.393-.301 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .12) 1.410 (. Cobalt occurs naturally in airborne dust.810-.07 (.350-.22-1.600 (.419) Selected percentiles ( 95% confidence interval) 50th . seawater. and 0.590 (.270-.470 (.430) .980-1.520-.670-.410 (.610) .560 (.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 .900-1.740-.650 (.53) 1.294 (.480 (.28 (1.390 (. population from the National Health and Nutrition Examination Survey.380 (.270-.480-.81) 1.570 (.670 (.16 (.750-.500) .17 (.620-.450) .280-.620) .05) 1.08) .316-.690-.300-.371 (.510) 1.570-.19) .73) 1.452 (.386) .530) .880 (.03) 1.09 (.600-.800-.370-.46 (1.520 (.06-1.660) .640) .377-.348-.379 (.410 (.520) .32 (1.930) .09 (.740-.416) .17-1.480 (.520-. hard metal or in combination with other elements. Cobalt compounds are also used in manufacturing battery electrodes.16) 1.15-1.17 (1.

821 (.533 (. 2003).781-1.294-.608 (.303-.343-.03-1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.04-1.662) .407) .391) Selected percentiles ( 95% confidence interval) 50th .872 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.301) .248-.500 (.983) .560-.777-. respectively.361-.848 (.363) .316 (.286) .278 (.314 (.513-.368) ..737 (.317 (.00) .964 (.479-.313-.304-.313-.362-.10) Total .471-.542 (.362) .296-.457-.282 (.419) .50 (1.368 (. in the feces.36) 1.534 (.461) .421) .932-1.275-.27) 1.313 (.523 (.57) 1.407 (.388 (.273 (. A portion of cobalt retained for long periods is concentrated in the liver.505) .365-.00 (..19) .723 (. cobalt is excreted predominantly in the urine.334) .329-.774 (.55) .543) .488) .11-1.781) 95th 1.616-.387) .333 (.290 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.349) .792-1.727 (.343 (.728) .33) .438) .503-.352 (.380-.378-.24) .487-.304) .900-1.50) 1.667-1. 1972).691 (.29 (1.669) .268 (.611) .306) 75th .550-.844 (.25 (.513 (.384) .44 (. Smith et al.03 (.562) .963-1.847) . 1994.352 (.562) .515 (.425-.850 (.861-1.310) .396) .388 (.850-1.599) .400 (.700 (.10-1.634-.481) 90th .476-.256-.394) .830 (. Exposure in the workplace may come from electroplating.990-1. or using diamond-polishing wheels that contain cobalt metal.581) .281) .938-1.753-.679-.333-.29) 1.378-.344-.753) 1.382-.337 (.378 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.00-1.963-1.372) . Once absorbed and distributed in the body.733-1.396) .635 (.552 (.786-.417) .595) .257 (.508-.358 (.324) .17) . with pulmonary clearance half-lives of from one to two years (Hedge et al.247 (.290 (.523 (.361 (.290 (.495 (.905) .60) 1.804) 1.297-. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.937 (.278-.333-.27) 1.861 (.938) .00 (.360) .272-.257-.361-.49) 1.442-.694) .248-.879-1.667-1.829-1.239-.392 (.329 (.259 (.16 (.952 (.949) .425) .479) .756 (.640) .279) . 1994).738 (.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 .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 .368) .428-..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 .300) .331-.703-.842) .500-.792 (.348) .33) 1.324-.393 (.35) .750) .02 (.700 (.29 (1.Metals fabricated from cobalt alloys (Lhotka et al.313-.16) .361 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.83) 1.352) .417 (.740-1.554 (.10 (.00 (. 1979).547 (.647) ..251-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.963) .297) . population from the National Health and Nutrition Examination Survey.455 (.660-.271 (.16 (1.475 (.738 (.393-. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).554 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.750-.548 (.895-1.376 (.851 (.402 (.829) .689 (.404-.457 (.259) .250) .736-.335 (.54) 1.976 (.73) 1.471-.757-1.302-.313-.365) .00) .457) ..630-.60) 1.833-1.306 (.328 (.513) .522) .561) . using hard metal cutting tools.04 (.277-.955) .313-.439) .704-.582-.23 (1.467-.534-.824 (.708) .289) .09) 1.327 (.301-.00 (.838 (.237-.06 (.975 (.468) .683-.309) .275-.626-.826-1. an essential human nutrient.574-.785) .296) .615) .327-.346 (. 1972).29 (1.11-1. refining or processing alloys.707) .326-.353 (.369 (.591 (.353-.391 (.30 (1.760-1.434-.328) .386 (.744) 1.990) .29) .279 (.895-1.15 (.16 (.585) .600-.606 (.298 (.630-.243-. interval) .821-3.898 (.282-.593) .12-1.319-.14 (.362 (.469-.381) .409) .328 (. and to a lesser extent.435 (.280-.333-.435-.955) .463-.594) .378-.611) .35) 1.12 (.487-.323) .449) .25 (.355) .337) .50) 1.342-.598 (.963) .960 (.917) .983-1.529 (.857-1..15) 1.291 (.408 (.429) 1.673-.444 (.36) 1.S.274-.644 (.234 (.462) . Cobalt is absorbed by oral and pulmonary routes.452-.638-1.449-.293 (.433) .339-.259-.10) .500-.609) .911-1.471 (.632-.537 (.563-.728 (.215-.426 (.929) .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 .28) 1.

1988). Am J Med 1972. population results in this Report (Kristiansen et al. 2003.50(13):95-104. Lauwerys and Hoet.. 210 2006. Linnainmaa and Kiilunen. Dunstan et al.. Morgan WKC. 2001... Poulsen OM. Third National Report on Human Exposure to Environmental Chemicals. 2003). A 1982-1992 surveillance programme on Danish pottery painters. 1993). with mean levels that were about 15-20 times higher than in the general U. population (CDC. Atlanta (GA). Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. not to imply that the BEI is a safe level for general population exposure. 1972). Perkins DG. Lisi. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Blood and urinary concentrations as estimators of cobalt exposure.. 1998). 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al.S. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. has been associated with exposure to dusts that contain cobalt. although substantial occupational exposures have produced elevated urinary levels for many weeks. Cugell DW. For workers exposed to cobalt in the air. 1989). Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. Iavicoli et al.. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. Information about external exposure (i. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. environmental levels) and health effects is available from ATSDR at: http://www. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al.html. 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. Thomassen et al. “Hard metal” disease. usually in combination with tungsten carbide (Cugell et al. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans.... 2005 [online].gov/toxpro2. Daniel et al. 1955). 2005. 1997). Roycroft JR. References Alexander CS.49:56-67. 2001).43(4):299-303.. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al.... Arch Environ Health 1988. 1988). A clinical and pathological study of twenty-eight cases.. Available at URL: http://www... Toxicol Sci 1999. 2001. Rubin A. Alexandersson R. 1994. Bucher JR. Cobalt was once added as a foaming agent to beer. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. 1994. 1997.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. et al. 2006. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. 2003.. White and Sabbioni.. Centers for Disease Control and Prevention (CDC)... Cobalt-beer cardiomyopathy. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al.53:395417. 1990). Hailey JR. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Sci Total Environ 1994. 1998). A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al.. Shirakawa et al. 1992)... 1994). 1993). Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Lison et al. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al.e. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations.atsdr.cdc. MacDonald et al.cdc. 4/3/08 Christensen JM. Swennen et al. Sills RC.. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Information about the BEI is provided here for comparison. 1999). a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. 2001..S. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary measurements mainly reflect recent exposure. Haseman JK. 1985.gov/ exposurereport/. Grumbein SL. Krause et al.

36:732-734. oxides. Christensen JM. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Pradhan C. salt. Iversen BS.51(7):447450.50(9):835-842.406:282-296. Co-sensitivity between cobalt and other transition metals. Kiilunen M. J Occup Med 1992. Health Phys 1979. Mosconi G. Kriss JP. et al. 3rd ed. Fujimura N. Chest 1989.20(1):25-31. Kusaka Y. Robinson C. cobalt salts. Occup Environ Med 1994.22:359367. Alessandrelli M. Molders J. a study of 13 elements in blood and urine of a United Kingdom population. 1985. Schramel P. Hoher T. Kato M. Thakker DM. Schaller KH. Ichikawa Y. Radulescu M. Zhuber K. Bacis M. Am J Ind Med 2003. Kraus T.28(5):1121-1128. Szekeres T. Uitti J. Zobelein P. McMinn DJ. Boca Raton (FL): Lewis Publishers. Cobalt and antimony: genotoxicity and carcinogenicity. Bourne RB.21(2):189-195. Hoet P. et al. Epidemiological survey of workers exposed to cobalt oxides.88(4):443448. Lhotka C. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. J Bone Joint Surg Br 2006.148:241-248. Lasfargues G. Kuska Y. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Heki S. Daniel J. McCalden RW. Meyer zum Buschenfelde K-H. J Trace Elem Med Biol 2006. Smith T. Cresti R. A report of two cases from mineral assay laboratories and a review of the literature. Lauwerys RB. Linnainmaa M. Dunning SP. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Zweymuller K. Edmonds CJ. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Lauwerys R. Barnaby CF. Vitali MT. Kirsch-Volders M. and cobalt metals. Stanescu D. et al. Clin Orthop Relat Res 2003. Goto S. Iavicoli I. Bozec C. Goldberg MA.34:620-626.” Contact Dermatitis 2001.44:124-132. Lison D. Lung cancer risk in hard-metal workers. Buchet JP. Rorabeck CH. Sci Total Environ 1998. Dickel H. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Dunstan E. Chess DG. Am J Epidemiol 1998. Leghissa P.150. Hedge AG. Gross RT. Weyher I. Biological monitoring of workers exposed to cobalt metal. Weber A. Bunn HF. Int Arch Occup Environ Health. Salama A. Zedda S. Lauwerys R. Carnes WH. Int Arch Occup Environ Health 1997. Angerer J. Ziaee H.242:1412-1415.204:147-160. Moulin JJ. Sabbioni E. De Boeck M. Palmroos P.48:172-173. Pisati G. Linna A. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Swennen B.95:29-37. Sanghrajka AP. Kristiansen J.69(3):193-200. Diepgen TL. HoffmannB. Br J Ind Med 1993. Meier R. Sci Total Environ 1994. Thabe H.55(4):269-276.(1-3):133-139.150:177-183. et al. Contact Dermatitis 2003. Sabbioni E. Mutat Res 2003. Arch Intern Med 1990. Romazini S. Thomassen H.45:246-247. DeSantis V. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Unwin P. J Rheumatol 2001. Steffan I. Salvatori S. Ghat IS. Sci Total Environ 1994. Cleland D. and hard metal dust. Health Phys 1972. Schank M. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements.157:117121. Outcome of occupational asthma due to cobalt hypersensitivity. Occupationallyinduced “isolated cobalt sensitization. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group.216:253-270. Trace element reference values in tissues from inhabitants of the European Union. Tilley S. Sci Total Environ 1997.150(1-3):167-171.87(5):628-631. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Jarvis JQ. Hammon E. Swennen B. Sabbioni E.533:135-152. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Peltier A. J Orthop Res 2003. Buchet JP. et al. J Bone Joint Surg Br 2005. Science 1988.58(10):631-634. Roto P. Lison D. Cobalt cardiomyopathy.Metals effects of cobalt. X. Respiratory health of cobalt production workers. et al. Occup Environ Med 2001. Lisi P. The release of metals from metal-onmetal surface arthroplasty of the hip. Wild P. MacDonald SJ. Shirakawa T. Goto S. Blunn G. Cannon SR. Absorption and retention of cobalt in man by whole-body counting. Fourth National Report on Human Exposure to Environmental Chemicals 211 . 2001. Lison D. Falcone G. Oksa P. White MA. Laippala P. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Long-term clearance of inhaled 60Co.

30-1.10) 2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .50-3.40-1.70-1.75-2.60 (2.00 (1.10-3.71-1.20 (3.80) 2.900 (.37 (1.Metals Lead CAS No.65 (1.10) 3.00 (3. Elemental lead can be combined with other elements to form inorganic and organic compounds.90-4.04-1.43-1.50) 1.80 (2.86) 1.60) 4.80) 1.30) 2.60-4.50-2. 01-02.80) 1.53) 1.40-6. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.70 (2.40 (4.00) 2. interval) 1.50 (4.46 (1.20 (1. blue-gray metal that occurs naturally in soils and rocks.20-2.50-5.87) 1.60) 2.70 (1.20 (1.00) .60) 1.40-3.30 (1.10-2.50-1.77 (1.30-1.60-3.60-1.80 (1.60 (1.60) 5.50-1.30-1.10 (1.52-1.09) 1.90) 2.10-3.90-4.70-2.80-4.60 (3.10 (2.20 (1.40-2.30-1.90 (3.70-1.52-1.40-2.90) 3.20-2.30-1.30 (3.87 (1.60 (1.30 (2.60 (2.30 (2.60) 1.40 (3.50-2.60) 3.50-1.40-1.80) 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 1.60) 4.90 (3.80 (1.80 (1.00) 3.70 (5.49-1.00) 1.3.32-1.30-4.942 (.90 (2.30-6.90) 1.40) 2.40-3.60) 1.90-2.60-1.50-5. Lead has a variety of uses in manufacturing: storage batteries.80 (4.80 (1.30-2.40-3.10) 1.20 (1.40) 1.30 (1. respectively.50-6.10) 1.50-4.70) 4.00 (2.80-3.60 (3.50-2.30) 2.899-.70 (2.878-1. plastics.40) 5.40-1.00) 1.19 (1.40-5.80) 3. ceramic glazes.10 (2.96-2.00-1.80-3.00-6.70) 1.39) 1.90) 1.43) 1.10) 3.S.00) 4.10-2.36-1. brass.10 (4.80) 1.10 (1.40 (5.70 (1. and 0.70) 1.83 (1. see Data Analysis section) for Survey years 99-00.20) .40) 1.30-2.50 (4.75-1.60) 2.20-1.20-3.30) 1.43 (1.20) 4.43 (1.39-1.80 (2.40) Total 1.00-4.10 (2.80-3.S.30 (2.10) 1.62 (1.20-6.55-1.14-1.80 (5.50-2.80-2.60 (2.80 (1.10-2.60 (1.40) 2.70 (3.66) 1.20) 5.40-1.00-4.70) 4.10-6. metal alloys (e.80) 2.50-4.30-1.50-1.20) 3.60-1.00) 2.50 (3.40 (2.90 (2.20 (3. and for radiation shielding.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.90-2.30) 2.00) 4.62) 1.01 (1.10-3.60 (1.60-2. In the past.14-1. ammunition.10-2.50) 4.28.80 (5.90 (3.80 (1.10-2.20) 2. antique-molded or cast ornaments.70) 3.60 (1.30-5. lead was added to gasoline and residential paints and used in soldering the seams of food cans.14-1.50 (1.946 (.37 (1.20 (1.20) 90th 3.40-6.50-3.62-1.43) 1.30 (4.20) 3.69 (1.70-4. and 03-04 are 0.36-1.50) 3.90) 2.20-4.50 (2.25 (1.20 (2.00) 1. leaded glass.60) 4.50 (1.02) 1.70 (2.70-1.56 (1.90) 2.00) 1.10 (3.10) 2.10-1.10-4.70-5.60 (3.50 (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.50) 2.25 (1.70) 3.50) 75th 2.90-3.30 (2.800-1.66 (1.60) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90-6.20 (3.00 (4.12-1.40 (2.30) 95th 5.70) 3.40) 1.10-3.20 (3.30 (4.70-2.80-4.40) 4. 0.80) 1.80 (4.90 (4.80) 1.90-4.10) 3. the main source of lead exposure for the general U.70) 4.60) 3.00-4.50-1.20-3.40-2.90 (1.70) 1.40 (1. Lead was used in plumbing for centuries and may still be present.91) 1.30 (2.52 (1. Since lead has been eliminated from gasoline.50 (2.22 (1.40) 3.31) 1.986) .30 (2.20-3.900 (.50 (2. bronze).30 (1.20 (3. 7439-92-1 General Information Elemental lead is a soft.50) 1.40 (1.00) 2.90) 1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.00) 6.30 (4.10-1.60) 2.60-6.60) 3.60) 4.60 (1.55-1.50) 1.20) 1.69) 1.10-6.72) Selected percentiles ( 95% confidence interval) 50th 1.48) 1.10-2. population from the National Health and Nutrition Examination Survey.90-4.34-1.10) 5. solders.40 (1.30 (1.40 (1.20-1.32-1.50) 2.90) 2.20) 3.20 (4.40-1.93-2.40) 2.60 (4.90-2.70 (3.50 (2. Lead is most often mined from ores or recycled from scrap metal or batteries.50) 5.60) 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 2.90) 5.00 (4.00-5.60-2.81) 1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70) 4.50 (1.90) 3.30) 5.51 (1.60) 2.3.50) 5.60) 1.90 (1.60 (2.00) 1.50 (1.20) 3.10) 4.78 (1.00-2.40-4.80) 2.80 (3.20 (3.60 (3.00-1.g.50) 1.70) 1.69) 1.45-1. Before the 1980’s.17) .80) 2.40) 2.80-4.00) 5.50) 7.900-1.69 (1.00) 3.37-1.00 (5.36) 1.60 (2.80-3.75 (1.30 (2.51) 1.70-2.70-6.60-4.60-1. malleable.00) 2.90) 2.20 (2.25) 1.50 (2.45 (1.75) 1.70) 2.70) 1.30-2.68-1.50) 4.60 (1.60) 1.00 (1.90 (3.20 (3.00 (6.89) 1.70 (1.70-3.20-3.10-4.60) 2.20) 4. such as lead phosphate and tetraethyl lead.95) 1.10-8.10 (1.40-1.30-2. dense.60 (2.55 (1.70 (1.80 (2.90 (3.80-5.23 (1.90-2.10-1.60) 3.

40 (2.50) 3.659 (.40) 2.900-1.59-2.955-1.90 (1.90 (2.80) 3.10 (1. lead-based painted surfaces undergoing renovation or demolition.833 (.86 (1.13-3.50) 1.700 (.579-.30-1.900-1.840 (.900) .700 (.70) 1. and 0.86) 1.80) 2.604 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.10-1.600-.610 (.31-3.02) 1.30 (3.20) . lead-contaminated dust in indoor firing ranges.13) .30-3.60-3.700-1. CDC.50 (1.60 (1.688 (.10-5.935) 1.30-2.00) .40) 2.642 (.20) .749) .590 (.30-1.40-3.10) 2.00 (1.700-.20 (1.808 (.20 (1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.00-1.10-3.931) .00) 1.616) .19 (1.04) .23) .09) 1.40 (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 .80) 2.10 (. or water contaminated by mining or smelting operations.20 (3.800-.33.78-2.20 (2.833-1.600-..573 (.70) 1.30 (1.625 (.572-.30) 2.50 (2.700 (.20-1.900 (.40) 1.90-2.00-2. and contact with soil.580-.29 (2.20 (1.700-.80) 2.500-.44-2.90 (1.10) 2.785) . 01-02.560-.960-1.556-.75) 3.00 (1.30) 1.636 (.1.52-1.50-3.30 (2. Fourth National Report on Human Exposure to Environmental Chemicals 213 .10-1.637-.795 (.810-1.558 (.589-.800 (.50 (1.915-1.04) 2.00 (1.66 (2.80) 1.70) 3.40) 1.30-1.753 (.700 (.90-4.40) 3.729-.50) 2.20) 1.04 (.03 (1.900) .600) .900) .90 (2.90-2. population from the National Health and Nutrition Examination Survey.540-.00 (.625-.70 (1.27 (1.40 (1.86-2.923 (.506-. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.620) 1.600) . 1991).82 (1.03-2.90 (1.640 (.50-1.80) 2. pewter utensils and drinking vessels.40-1.40) 2.30) 2.33 (2.30-5.10-3.04-2.691-.80) 3.32 (1.50) 1.40 (1.20 (2..822-1.20) .80-2.480-.857) .60-2.710-.766 (.10-1.80 (1.90-3.07-1.651) .31 (1.700) 1.50-2.90) 2.526-.900) .72) 1.00) 2.773) .752 (.570-.940 (.20) 1.50) 1.600-.990) 1.80 (2.1.680-.40-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.50-2.738) .900-1.600 (.20) .60-2.800) .535-. 0.30-1. interval) .80) 2.40 (2.40 (2.757-.20-2.800) .17 (1.800-.40-1.595-.75) 4.800 (.70) 2.40-5. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.10 (1.671-.11) 2.90) 1.731 (.07 (.64) 2.900) . or after soluble lead compounds are ingested.10-1.70 (2.800) . stained glass framing.680-.10-1.40 (1.613) .920 (.986) .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 1.90 (2.50 (2. In the blood. see Data Analysis section) for Survey years 99-00.640-.89) 2.20-1.701) .S.628) 1.00 (2.710-1.700-.21 (2.680) .14 (1.660) .06) .90-2.790 (.591 (. Approximately half of the absorbed lead may be incorporated into bone.g.12) 90th 2.30) 1.11 (1.20-2.20 (2.18-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.818) . which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.674) 1.600 (.10) .540 (.82 (2.600-.800-1.690) 75th 1. 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.900 (.40-2. older plumbing systems with leaded pipes or lead soldered connections.66 (2.90-2.40) 1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.920 (.02 (.86) 95th 2.60 (1.815 (.620 (.630 (.10) 1.22) 1.70) 1.40-1.20 (1.30) 1.60-3.35 (.90) 2.52-1.700 (.745-.800) .00-1.70) 3.10) . dust.70-2.30) 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 1.00 (1.40) 1. 2007.00-1.14-1.80 (1.52 (1.862) .49 (1.00-2.800-1. lead-containing folk remedies and cosmetics.20 (1.62-4. and 03-04 are 0.80-2.20) 1.600-. bullet fragments retained in human tissue.800 (.700 (.62) Total .14 (1.20 (1.00) .10 (1.Metals occupational (e.700) .60 (1.41) 2. battery and radiator manufacturing) and recreational sources.50-2.80-3.960 (.70-3.00-2.80) 1.848 (.40 (1.60) 2.29) 2.850 (.661-.27) 1.78-2.20-1.828) Selected percentiles ( 95% confidence interval) 50th .800) .708-.900 (.30) 2.970-1.605) .50) 2.10 (.90) 2.910-.650) 1.60-1.990) 2.700-.10 (1.97) 4.700-.50 (2.30) 1.40 (2.579-.900-1.60 (1.60 (2.553-.677 (.800 (.00) .40) 2.70 (2.30) .90-3.78-2.564 (. However.40) 1.730 (.70 (2.00) .00) 2.960-1. respectively.641-.10 (.900) .73 (1.23-4.59) 1.80) 1.10-3.718) .820-1.30) 1. 2000). imported children’s trinkets and toys.70 (2.91) 2.33-2.24-1.04 (.695 (.941) .51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.

50 (1.469 (.683-.601-.72) .47 (1.S.559-.708 (.31 (1.97-18.56 (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 .77) 2.893) .62-2. 1991.712 (.887 (.03 (.957-1.644 (.703) .64) 2.94 (1.718) 1.914 (. CDC.592-.698) .755 (.623 (.11) 1.19) 1.583-.739) .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 .938 (.914-1.43 (1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.609 (.593 (.61) 1.15) 1.Metals 90% of the body lead burden in most adults.731-.52 (1. the Centers for Disease Control and Prevention (CDC) established a BLL of 10 Urinary Lead (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1993). population from the National Health and Nutrition Examination Survey. O’Flaherty.98-2.725) .876-1.569 (.926 (.938-1.702) .20-3.781-1.05 (1.496 (.11 (.551-.20) . with a half-life of years to decades.18) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.718) .07 (.990 (.617-.08-2.72-2.667-.55 (1. through the inhibition of certain enzymes.746) .67-4..696 (.15) 1.27 (1.725) .654) .693 (.383-.37-1.79 (1.679-.571-.23 (1.997-1.46 (1.65 (1. kidney injury.22-2.45 (1.603-.10 (1.31 (2.851) .679) 1. 2007).07-1.85-2. based on prospective population studies.00 (1.796-1.404 (.977) 1.79) 1.668-.97) 1.47) 1.44 (1.541-.56-3.14) 1.587-.586-.98 (1.649 (.64 (1.734) .29 (1.645-.19-5.63) 4. 1993.40-1.64-2. The skeleton acts as a storage depot. seizures.03) .41) .65-2. interval) .720 (.55 (1.10 (.677 (.86 (1.36-2.03 (.51) 1.623 (.88) 2. and paralysis.24 (1.39-1.670) 1.61) 3.11 (1.992-1. encephalopathy.648 (.69 (1. Lead can cross the placenta and enter the developing fetal brain.88-2.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.608-.432 (.05-1.677) . 2004.963-1.00 (1.946-1. Schwartz.702) .588-.632 (.722 (.43 (2.992-1.686) . and nails (Leggett.11 (1.667) . hair.03 (1.645-.78-4.810 (.09-1.94-2.25-1.48 (1.08) .658 (.31) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.730) 1.03) 2.31) 1.28) 2.22) 1. 1995).404-.428) .882-1.900 (.641 (.43) 2.53) 1. abdominal pain.44 (1.47 (2.606-.03-2.682) .50) 1.22) . and iron.571-.64) 95th 2.50-2.510-.721 (.33) 1.31 (1.707 (.11 (.853-1.79) 2.790) .898) . zinc.88 (1.579-.603 (.96 (1.720 (. In 1991.33) 2.71 (1.461) .03 (.492-.03) 1.38 (2.03) .33 (1.671 (.44) 1.673) .667-.97) 1.981-1.460-.605-.594-. 1995.00 (1.58) 1.701 (.710) .50-1.72-2. 2003.594-.89-5.37-1.342-.52) 1.07) .20) .793-1.400) .46 (2.00) .89-2.62-3. with lesser amounts eliminated via the feces.0) 3.62) 2. scant amounts are lost through sweat.588-.659-.18) 2.979 (. Nash et al.933) .51 (1.681-.56-2. The toxic effects of lead result from its interference with the physiologic actions of calcium.638 (.639 (.62-1.17-1.85) 1.608 (.61) 1.22) 1.920-1.621 (.33-1.15-2.05 (.375 (.98) 2.83 (2.03) 90th 1.00 (.635 (.22-1.49 (1..800-.862-.78 (2.603-.66 (1.63) 1.644) .83) 1.66 (1.615 (. 1996).09) 1.66) 2.828) .14 (1. and through binding to ion channels and regulatory proteins.702-.38 (2. BLLs and associated toxic effects differ in children and adults.50-2.18 (1.742) .18) 1.26) 2.677-.01 (.639 (.03) 2.20) 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 .05-1.765) .92) 2.676) .09-1.61) 1.12-1.988 (.962 (.68 (1.688) .11) .70 (1.25-1.633 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.73) 2.28) .709 (.82) 1.838) .43-1.436) .75 (2.87) 1.655-.698) .15-2.28-1.841-1.763) .56) 3. Approximately 70% of lead excretion occurs via the urine.655) .08) .61) 1.535) .612-. Staessen et al.26) Total .10) 1..11-1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.701) .618 (.652 (.34-1.681-.71-2.73-2.774 (.41-1.04) 2.615 (.529-.59-3.917-1.758) .74 (1.43) 1.97 (1.09-1.722 (.625 (.639 (.914 (.622 (.04-3.408-.508) .02-1. For instance.41 (1.639) .06 (.06) 1.975-1.404 (.35) 2. Large amounts of lead in the body can cause anemia.918 (.988-1.06) .88) 1.17 (.03) 1.50-2.75-2.933-1.02) 1.742) Selected percentiles ( 95% confidence interval) 50th .88) 2.971 (.870 (.06 (1.828-1.18) 1.15-3.753) .657) 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.940 (.85-2.01) .561-.700-.604-.38 (2.380-.918-1.85 (1.812-1.53-1.607-.655) 75th 1.

5 per 100. In NHANES 1999-2002 in children 1-5 years old. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. which is an 84% decline. urban residence. 2002. EPA.4% of children had BLLs of 10µg/dL or higher (CDC..S.. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. lead in women may be associated with hypertension during pregnancy. with overt encephalopathy.gov/toxpro2.. Schwartz et al. 1995. 2009). 2005b). and decrease fertility (Alexander et al.xls).html. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR.6% in NHANES 1988-1991 to 1. and spontaneous abortion (Baghurst et al. Surveillance data reported by U.. At low environmental exposures. The U...21% of approximately 3. High dose occupational lead exposure. 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.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 2003).S. premature delivery.S.75 µg/dL in U. higher than 100-200 µg/dL). In occupationally exposed adults.0 µg/dL in females (Soldin et al. adults in the 19992000 NHANES sample (Apostoli et al. Staessen et al.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample.. 1998). A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Pirkle et al. including minority race or ethnicity. Korrick et al.. and organic lead compounds not classifiable with respect to human carcinogenicity. approximately 11. seizures. Telisman et al.07 µg/dL (Becker et al.. Both drinking water and ambient air standards for lead have been established by the U. Bellinger 2005.4% in NHANES 1999-2004...S. 2001).cdc. 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. almost double the geometric mean of 1. 2005b. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.. environmental levels) and health effects is available from ATSDR at: http://www. reduce sperm count. 2003. the prevalence rate has declined annually since 1994 (CDC. Fourth National Report on Human Exposure to Environmental Chemicals 215 . 2006). Urine levels may reflect recently absorbed lead. 1984. 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.7 µg/dL and 4.atsdr.. and low family income (CDC. usually with BLLs greater than 40 mg/dL. CDC.6%) were lower than those from NHANES 1991-1994. Overall. However. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. Schwartz.S. 1999).. More recently. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al... Jones et al.3 million children tested had BLLs of 10 mg/dL or higher (http://www.. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. 1987. the geometric mean BLL was 3. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.g. and peripheral neuropathy generally occurring at much higher levels (e.. both the geometric mean (1. 2005a).Metals µg/dL or higher as the level of concern in children. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. For example. adults in the 1999-2000 NHANES sample. 2006). 2003. 1994)..9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. Lanphear et al. 2002). Information about external exposure (i. residing in housing built before the 1950’s. 1996. particularly in the skeleton. 1996. Data submitted through state public health programs from 2006 showed that 1. 2003.S. state childhood lead programs also show a decline in the percentage of children younger than 6 years of age who had BLLs of 10 mg/dL or higher. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. 2002a). Borja-Aburto et al. adult residents.2 µg/dL in males and 3.. Muntner et al. 2007). A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. Payton et al. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 1996. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.e. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. 1999). 1991.000 adults. 2000). when the geometric mean BLL was 2.. IARC considers inorganic lead compounds probable human carcinogens. may alter sperm morphology. 2000). respectively. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC...cdc.

Hu H. Neurotoxicol Teratol 2004. Pediatrics 2004. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Acquisition and retention of lead by young children. Environ Res 2000.cdc.150(6):590-597. Chiodo LM.htm. MMWR Morb Mortal Wkly Rep 2006. The relationship of bone and blood lead to hypertension. Environ Health Perspect 1993. Henderson CR. 4/14/09 Centers for Disease Control and Prevention (CDC).gov/nceh/lead/ CaseManagement/caseManage_main.26:359-371. Hu H. Aug 2007 [online]. gov/mmwr/preview/mmwrhtml/mm5420a5. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Bellinger D. Lanphear BP.55(32):876-879. Mantere P. 4/14/09 Centers for Disease Control and Prevention (CDC).html. Available at URL: http://www. McMichael AJ. Pirkle JL. Lanphear BP. Lead and hypertension in a sample of middle-aged women. Stanek KL. et al. Teratogen update: lead and pregnancy. Brody DJ. Cox C.275:1177-1181. Sparrow D.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. Manton WI. Becker K.cdc. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Vimpani FB. Ga. Blood lead levels measured prospectively and risk of spontaneous abortion. Birth Defects Research (Part A). Kaus S.54(20):513-516. Seiwert M. Reese YR.53:411-416. Ronchi L. Scand J Work Environ Health 1984. et al. Atlanta.10:43-50. Jacobson SW. Schulz C. Neri A. Rotnitzky A. Bellinger D. Intellectual impairment in children with blood lead concentrations below 10 µg/dL.205:297-308. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. et al. Available from URL: http://www. Angle CR. Wager C.89:330-335.htm. Adult blood lead epidemiology and surveillance—United States. Borja-Aburto VH. Lead. Rojas LM. 2005b.cdc. Semen quality of men employed at a lead smelter. 4/14/09 Alexander BH. Jusko TA. 2005. Hunter DJ. Kaufman JD. 2002 [online].101(7):598-616. Checkoway H. Krause C.1542/peds:2007-3608. Korrick SA. Neurodevelopmental effects of postnatal lead exposure at very low levels. doi:10. Dietrich K. Kim R. Batuman V. Baghurst PA. MMWR Morb Mortal Wkly Rep 2005a. Neurotoxicol 1987.cdc. Meyer PA. Lepom P. Available at URL: http://www. Farias P. Coresh J. Jacobson JL.gov/mmwr/preview/mmwrhtml/ mm5532a2. Hu H. Hertz-Picciotto I.123:e376-e385. Auinger P. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.cdc. 4/14/09 Centers for Disease Control and Prevention (CDC). Atlanta (GA). Payton M. Available at URL: http://www. Cory-Slechta DA. Blood lead levels—United States. et al. Muller CH. Occup Environ Med 1996. Kuehnemann TJ.87:1-471. Am J Epidemiol 1999. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 4/14/09 Centers for Disease Control and Prevention (CDC). Rios C. Ganzi A.htm.115:521-529. Am J Public Health 1999. Homa DM. Preventing Lead Poisoning in Young Children. Korrick S. Third National Report on Human Exposure to Environmental Chemicals. Aro A. et al. Apostoli P.113(4):1016-1022. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Leggett RW. Blood lead reference values: the results of an Italian polycentric study. Inorganic and Organic Lead Compounds. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. van Netten C. 1991 [online]. Blanco J.gov/toxprofiles/tp13. IARC Monogr Eval Carcinog Risks Hum 2006. Vupputyuri S. Age-specific kinetic model of lead metal in humans. Atlanta (GA). A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Hänninen H. N Engl J Med 2003. Pediatrics 2009. 2003-2004. Weiss ST. Sparrow D. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. JAMA 1996. Robertson EF. Caldwell KL. Canfield RL. Sci Total Environ 2002. JAMA 1996.287:1-11. Muntner P.atsdr.348:15171526. Int J Hyg Environ Health 2002. Luukkonen R.275(15):1171-1176. Wigg NR. Weiss ST. Ewers TG. Roberts RR. Hernberg S. Cox C.73:409-420.gov/nceh/lead/publications/ books/plpyc/contents. Available at URL: http://www. CDC. Managing Elevated Blood Lead Levels Among Young Children. Toxicological profile for lead. Baj A. References Agency for Toxic Substances and Disease Registry (ATSDR). Bavazzano P. Centers for Disease Control and Prevention (CDC).82:60-80. 1999-2002. Rotnitzky A. Speizer FE.htm.8(3):395-401. Jones RL. 1988-2004. Public Health Rep 2000.

cadmium. Environ Health Perspect 1998. IV. Brody DJ. J Hum Hypertens 1995. Blood lead concentrations in children: new ranges. Osterloh JD. JAMA 2003.289(12):1523-1531.S.327:109-113.106:745-750.140:821-829. and copper in men. Telisman S. Environ Health Perspect 1996. Am J Epidemiol 2001. Hwang KY. zinc. Rocic B. Lead. population to lead: 1991-1994. Smith DR. blood pressure and cardiovascular disease in men.209:301305. Pizent A. Flegal AR. Low-level lead exposure and renal function in the Normative Aging Study. Roels H. dimercaptosuccinic acidchelatable lead. Gavella M. Schulz D. Paschal DC. Arch Environ Health 1995. et al. Lee BK. Lee GS. blood pressure. Hu H.104(1):60-66. Sparrow D. Kinetics of lead disposition in humans. Lustberg M.9:303-327. Soldin SJ. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Hickman T.63:1044-1050. Use of endogenous. Low-level lead exposure and blood pressure. et al. stable lead isotopes to determine release of lead from the skeleton. Physiologically based models for bone-seeking elements. Schwartz J.108(1):45-53. Exposure of the U. Gunter EW. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Int J Hyg Environ Health 2006. Soldin OP. Kaufmann R. Stewar WF. Revised and new reference values for arsenic. Schwenk M. Magder L. Kidney Int 2003. Nash D. Clin Chim Acta 2003. 50:31-37.153(5):453464.118:16-29. Pirkle JL. and tibia lead with neurobehavioral test scores in South Korean lead workers. Semen quality and reproductive endocrine function in relation to biomarkers of lead. and hypertension in perimenopausal and postmenopausal women. Sherwin R. Lauwerys RR. Am J Epidemiol 1994. Wilhelm M. Schwartz BS. Rubin R. Toxicol Appl Pharmacol 1993. cadmium. Blood lead. Jurasovic J. O’Flaherty EJ. Cvitkovic P. Weiss ST. Lee SS. Kaufmann RB. Environ Health Perspect 2000. lead. Hanak B.Metals results from NHANES III. Amery A. Association of blood lead. Staessen JA. Payton M.

Hursh et al.80) 3.20 (2.g. mercuric chloride).300 (.400 (.40 (3.70 (4.80) 4.500 (. thermometers.927) .. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.400-.877 (.00 (.60) 1.. Elemental mercury is a shiny. Atmospheric elemental mercury can be deposited on land and water.g.700-.700-.490 (.700) . electrical lamps. thimerosal.Metals Mercury CAS No.776 (. and organic forms.20-4.40 (3. or oxygen.70 (3. and dental amalgam. The ingestion of methyl mercury.60) 2085 2293 3478 Limit of detection (LOD.30-4. which create an episodic potential for volatization and inhalation of mercury vapor.40-1.50) 5.00 (2.900) .80) 1. synthetic organomercury compounds were once used in pharmaceutical applications.40-2.300) .70 (1.. to form inorganic mercury compounds or salts. Some cosmetic skin creams from countries other than the U.20) 2.60 (2.900) 1.00) 4. and is distributed to most tissues. Survey years 03-04 Geometric mean (95% conf.753-1. Accidental spills of elemental mercury.. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).700-.12) .60-2. 218 Fourth National Report on Human Exposure to Environmental Chemicals .00) 3.90 (4.80 (1.689-. elemental mercury is absorbed mainly by inhaling volatilized vapor.800-1.80 (3. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. 1993).574) .40-2.800 (.90) 3.00 (.700-.40 (4.900) 75th 1.70) 911 856 2081 4525 03-04 03-04 .S..400-.10-3.60) 1.326 (.20-4.20-3. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. IARC.2.714-.363-.40) 1. 1994.30) 4132 4241 03-04 03-04 03-04 .814 (.30-6.800-1.419 (.00) 1. sphygmomanometers and barometers. Also.00 (2.600 (.285-.g.979 (.781 (. 1998.30 (1.40) 3. In addition. which can bioaccumulate in aquatic and terrestrial food chains.800 (. population from the National Health and Nutrition Examination Survey.S.50) 2.60-3.40-1.80 (1. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.60-6. may contain inorganic mercury.300-. interval) .50) 1. 2007).40 (4. solid-waste incineration.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 . Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.703-. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. see Data Analysis section) for Survey year 03-04 is 0.00-1. merbromin).g.60-5.80 (1.600) 1.797 (. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.30) 3. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.. predominantly from fish and other seafood.500 (. The kinetics of the different forms of mercury vary considerably.800-1.30) 3.800 (.563 (.372) . 1980.900 (. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.00) .484) . After elemental mercury is absorbed.02) .919) . and mining and smelting. phenylmercuric acetate) or topical antiseptics (e.90) 95th 4.500) .90 (1.800-1.472-. and mercury compounds are still used as preservatives (e.860-1.50-3..900) 1. constitutes the main source of dietary mercury exposure in the general population.00-5.30) 1. such as chlorine (e.00 (.60 (1.700) .500-.50-1.90) 90th 3.672) .00) 1. have often required public health intervention (Zeitz et al.00 (1.30 (2. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.00 (2. Other major uses include electrical equipment (e.500-.30-2. sulfur.70 (1. 2002).30) 5. Kingman et al. Poorly absorbed from the gastrointestinal tract.60 (1. 1999 .00 (.10) .800 (..900) 1.60-6.655-.90 (1.30-5.. with the highest concentrations occurring in the kidneys (Barregard et al.800-1. inorganic.50-2. Apart from methyl mercury.90-3.50) 4.418-.40-3.700-.70-2. an organic form of mercury. thermostats and switches).30) 1.886) .903) Selected percentiles ( 95% confidence interval) 50th .700 (. Woods et al.

60 (1.70) 4..400-.800 (.90 (1. interval) Selected percentiles (95% confidence interval) 50th . 1994.30 (1.50) 95th 2.. 1992).40-2.600) .20) .200 (. 1998).90) 2.500-.329 (.70-3...541-.00 (2.60) 3.30-4.60) 1.825-1.800-1.60) 2.60 (2.90 (4. Geometric mean Survey years (95% conf.700-1.343 (.944 (.40 (1.30-3.700-1.90) 5.30-2. Jonsson et al.90) 2. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.00 (1. Methyl mercury enters the brain and other tissues (Vahter et al. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .70 (1.300) .40-1..200-.700 (.00-1.200 (. Sandborgh-Englund et al.35 (1.02 (..307 (.10 (1.90) 3.S.80) 1.700 (.. 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.700) 2.300) .30) 1.317 (.. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al. Myers et al.10 (5.50) 2.300 (. 1969.70-6.00) 1.300) .3) 4.30-6.900-1. Suzuki et al.. Miettinen et al. Fourth National Report on Human Exposure to Environmental Chemicals 219 .70-5.29) ..Metals the tissues to mercurous and mercuric inorganic forms.80-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1993).500-. 1995..500 (. 2004.30 (1.297-.900 (.50) 1.10 (3.300 (. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.30-11.800) 75th .70-3.00 (2.10) 1.300 (.40) 1. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.374) .600 (.40-2.60 (1.00 (2.940) Race/ethnicity (females.30 (.800) 1.90) 90th 1.20-3. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations. Vahter et al.377 (.50 (1.300) .833 (.50-3.20-11.700-. 1996.900 (.475) .10) .500-. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.30 (1.10-3. Methyl mercury is incorporated into growing hair.80) 579 527 370 436 588 806 Limit of detection (LOD. 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.800) .60) 1. Smith et al.265-. 1975.300) . and a useful marker of exposure in epidemiologic studies (Grandjean et al.00) 4.664-1.800 (..200-.200-.900-1. for both acute and chronic exposures.800-1..20 (2.73) 1.820 (.10 (.70-5.20-3..90 (1.395) . 1994) and then undergoes slow dealkylation to inorganic mercury. National Health and Nutrition Examination Survey. McDowell et al. 1971).10 (.20) .70) 1.27) .0) 4.871-1.00-2.14 and 0.60 (3.738-.00) 2.00-3..299-. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.50-12. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al. After exposure to elemental mercury.80 (3.30-5.00) 6.407) .40) 2. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.. 2003).00) .06 (.200-.10-1. 2003).30-6.00-6.06-1. population.268-. 1992 and 1999.10 (1.. 1991.200-.30-4. 1996).369) 1. 1993).800-1.700 (.90 (4.23) .726-1.00-2.30-6.. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.824) 1.200-.20-3.60 (1.800) .30) 3. 1999). 1984.70 (1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.30) 1.300) .. with most elimination occurring through in the feces (Sherlock et al.50) 3.500-1.377) . 1992.919) .70 (1.697-. Smith and Farris.90 (3.20-2. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al. 1998).50 (2.00-2.600) . thereafter.900 (..80 (1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith. 1994).60 (3.10) .70) 4.20) 1.40 (1.00) 7.318 (.7) 4.700 (.269-.50) 1.667 (. Vimy et al.50-2.20 (.10 (1. a measure of accumulated dose (Cernichiari et al.00 (3.500-.700-. 1973).500 (.40) 5.256-.300 (. 1990).01) . 1999-2002.800) 1.14.00) 1.. 2005).800 (..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 .500-. Excretion occurs by renal and fecal routes.

700-.600) . particularly irritability. limb deformities..600-. and cerebral palsy (NRC. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. and sleep disturbance (Bidstrup et al. 1963)..700-.500-. 2000). Salonen et al.. Sakamoto et al. 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.500-.. sensory impairments.500-.600 (. insomnia. 2005. 2003).600 (. 2004.600 (. 2006. maculopapular rash.500 (<LOD-. Once absorbed. 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.700 (. ataxia. < LOD means less than the limit of detection..600) . Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.. irritability. The constellation of findings may include anorexia. interval) Selected percentiles ( 95% confidence interval) Sample 95th . and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 2004). 1970. Smith et al. causing parasthesias.700 (. which may vary for some chemicals by year and by individual sample. 2006.700) 2007 2240 3406 Limit of detection (LOD. short-term memory loss. Vupputuri et al. see Data Analysis section) for Survey year 03-04 is 0.600-.700 (. 2000. dysarthria. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) . 220 Fourth National Report on Human Exposure to Environmental Chemicals .. 1983). Acute. 1998. and neurocognitive and behavioral disturbances. anorexia.600) .600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Sakamoto et al. Drexler and Schaller.700-. 1995. 1996). depression.600) . 1993). overt signs and symptoms of chronic inhalation may include tremor.. 2000. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.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 .500 (.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . pain in the extremities. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. DeRouen et al.800) . Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. 2002.700 (..500-.600) .600) . 2004.600 (. Bellinger et al. the existence of a causal relation is unresolved (Chan and Egeland. Inorganic mercury exposure usually occurs by ingestion.. and progressive constriction of the visual fields. population from the National Health and Nutrition Examination Survey.600 (. Rice. 2004).600 (. fatigue.700 (.600-. and pinkish discoloration of the hands and feet (Tunnessen et al. hypertension. Factor-Litvak et al...600) . high-dose exposure to elemental mercury vapor may cause severe pneumonitis.500-. At levels below those that cause acute lung injury. Smith et al. Stern 2005. typically after a latent period of weeks to months. In recent epidemiologic studies.600 (. 1987).42. Rissanen et al.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500 (.. Oskarsson et al.S.800) .500-. cerebellar ataxia. Survey Geometric mean (95% conf.. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. 1995. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. hearing impairment.500-.. dysarthria. 2005). Overt poisoning from methyl mercury primarily affects the central nervous system. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.600) .500 (<LOD-.700 (. altered physical growth..700) .500-.500) ..Metals may be more efficient for inorganic mercury (Grandjean et al.600 (.600-. 1951.. gingivitis.500-.

00) 1.58 µg/L for 4645 adults.97) 2.840-1. Biomonitoring Information In the general population.07 (.405-.700 (.476 (.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 . Fourth National Report on Human Exposure to Environmental Chemicals 221 .09 (2.440 (.89) 3.63-2.213-.88 (1. Among the three racial/ethnic groups. 2003).26 (1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC..460) .55 µg/L.08 (1.406-.atsdr.442-. average age 9. Schober et al.13-2. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.. In Germany the geometric mean for blood mercury was 0. EPA at: http://www. 2002).610-1. population from the National Health and Nutrition Examination Survey.870-1. see Data Analysis section) for Survey year 03-04 is 0. EPA. total blood mercury increased with age. who participated in a 1998 representative population survey (Becker et al. interval) . the total blood mercury concentration is due mostly to the dietary intake of organic forms.570) .30) 3.700-1.410-.530) .370) .54 (2.960 (.S.46) 3.549) .350-.509) .S.e.360-.890 (..20 (1.770-1.67-3.940 (.290-. From 1996 through 1998.382-.31) 2.46 µg/L for children. 1998).18) 2. Mahaffey et al. Information about external exposure (i.408) ..33 (2..304) .330-.280-.530-..160-.330 (. Total blood mercury levels increase with greater fish consumption (Dewailly et al.396-. During the same survey periods.9 years).88) 287 722 1529 03-04 03-04 . 2004.840-1..463) .250) .16 (. range 40 years to 78 years) had an average total blood mercury concentration of 2.68 (2.96 (1. 2001. 2009). Grandjean et al..85-2. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. 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. However.19 (1. slightly higher total blood mercury levels were found in U. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.05) 3.358 (.78-2.76-3.430) .65) 1.430 (. 758 children. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.88-3. aged 18 to 69 years. A cohort of 1127 U.60 (1.03-4. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.S.580) . 1998)..400 (.433 (.340-.24 (2. military veterans (mean age 52. et al. particularly methyl mercury.gov/toxprofiles.23) .90) 2.19 (2. 2001.8 years. 1997.520) .840) 1.05) 1.S.360 (.534) .gov/mercury and from ATSDR at: http:// www. Over the NHANES 1999-2006 survey periods.61) 1.31) 1266 1272 03-04 03-04 03-04 . environmental levels) and health effects is available from the U..Metals standard for inorganic mercury has been established by U. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.14) 90th 2.60-2.78 µg/L for adults and 0. In NHANES 19992002. 2003).254 (.460 (. Sanzo et al.52) 2.492) Selected percentiles ( 95% confidence interval) 50th .67-2..313-. 1995.447 (.509) .430 (.39-3.42) 95th 3.200 (.01 (.480 (...66) 3.14. 2009).S. and increased slightly in non-Hispanic white children (Caldwell.77-2.413-.330-.34-3.99-6.cdc.08 (1.29) 1.60) 619 713 1066 Limit of detection (LOD.555) . and the age-related changes differed across the groups (Caldwell et al. average age 33 years.870-1.420 (.530) .416 (. 2000).12 (.00 (. adult women in several ethnic subgroups (Hightower et al. These distinctions can help interpret mercury blood levels in people.76-4. 2006).epa.93 (1.495 (.23) 2.14-2. total blood mercury geometric mean levels in females aged 16-49 years did not change.16 (1.76-3. Kingman et al. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. Survey years 03-04 Geometric mean (95% conf. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.360-.441 (.420 (.96 (1.24) 1. the median concentration of blood mercury was 0.28) 1.930-1. Benes et al..480) 75th 1.330-.

522-.368) .620-.297 (.365 (.619-.498) 75th .00) 286 722 1529 03-04 03-04 .333-.25 (..63) 1.404-. Urine mercury and the number of dental amalgams were correlated. interval) .35 (1.41-2. Levels in U.79) 1.208-.347) .S. Survey years 03-04 Geometric mean (95% conf. military veterans with dental amalgams.714-1.525 (.768 (.362 (.04-3. An expert-panel report recently prepared for the U. Information about the biological exposure indices is provided here for comparison. DeRouen et al.11) 2.485 (.S.447-.S. 2002) adult population surveys were similar to those in a U.588) .392-.11-2.480) .62 (1.384 (.00 (.964-1.289) .87) 2.875-1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. and Italian (Apostoli et al.301-.1 µg/L.07) 1.358) .13 (1.265-.455-.06 (..275) .667-1.. In the study of U.508 (.343 (. and on average. Czech (Benes et al.61) 1.400) .S.385-.566) . Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. et al.40 (1.970 (.09) 1.784) 1.276 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.01) 2.307-.464 (. Department of Health and Human Services noted that several studies have observed a modest.32-2.455-.255 (.391-.587 (.30) 1.78-4. 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. women of childbearing age have generally been much lower than these levels (CDC. 1988.18-1.85) 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 .417) .03) 2.280-. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.67 (1.87 (1.391) .86) 95th 2.56) 1266 1271 03-04 03-04 03-04 .652) ..400-.969-1.532 (.16) 1.616) . 2009). Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.21) 1.696 (.309-.217 (. mean urinary mercury was 3.40-1. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.31 (1.472-. reversible increase in urinary N-acetyl-glucosaminidase.S.909 (.630) . Langworth et al.785-1.463 (.88-2.88 (1. 2002). 2003). Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell..00) 90th 1.46-2.599) .65 (1.11) 1. 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. population from the National Health and Nutrition Examination Survey.545 (.306 (. Urinary mercury levels in recent German (Becker et al.443 (.365 (.476 (.196-.447 (. not to imply a safety level for general population exposure..537) .486) Selected percentiles ( 95% confidence interval) 50th . 1992).455) .13-2.79 (1. the urine mercury increased by approximately 0. a biomarker of perturbation in renal tubular function.51-2...32 (1.225-.376-. 2005).1 µg/L for each surface with a dental amalgam (Kingman et al.800-1. 2006.Metals 2000).76 (1.28 (.88-2.06 (.. et al.64-2. 2009). 1998).12-3.687) . ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.535) 1.54 (2.67 (1.246-. 2006).23-2.44) 1.39) 1.990) ..30) 2.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .77 (2.

387-.760 (.616-.45-2.50-4.569-.07-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.84 (2.710 (.32) 2.580-.824) .92) 4.799) .930) .23-1.35) .596 (.892) .94) 1.61) 1.774) .664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .691) .04-1.04-10.76 (1.17) 95th 5.13 (2.3) 5.502-.686) .580 (.81 (3.721 (.27 (1.624-.14) 3.592 (.709) . National Health and Nutrition Examination Survey.62 (4.637) .742-1.657 (.46 (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.41 (2.632 (.710) 1.51) .850-1.27-1.631-.475-.70 (2. population.85) 4.53-3.65) 1.14.30 (1.719 (.620 (.966) .772 (.10-4.910) .47) 1.62 (1.69-3.50 (2.91-7.565 (.97) 2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .636-.68) 3.21 (2.35 (1.99 (2.23-1.81-6. Geometric mean (95% conf.16) 5.28 (1. 1999-2002.77) 1.87-4.84 (2.18) 3.650) 1.00) 2.68 (3.46-4.420-.41 (1.45) 95th 3.83-3.13-4.500-.03-2.38) 4. National Health and Nutrition Examination Survey.14 and 0.46) 3.03 (.56) 3.560-.54) 595 531 381 442 594 826 Limit of detection (LOD.553-.42) 2.00 (2.07) 1.24) 6.05 (3.32 (1.18 (3.622-.870) .79) 3.09-1.42-3.45 (1.699) 1.670) 75th 1.21-3.99 (3.47) 1.65-4.522 (.85-3.92) 3.31 (1.806) .639 (.97) 2.56) 4.09-1. 1999-2002. population.744) 1.520-.790) .450-.15-1.S. interval) Selected percentiles (95% confidence interval) 50th .516 (.650 (.740 (.723 (.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females. 16-49 years) 99-00 01-02 .S. 16-49 years) 99-00 01-02 .809) .63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.30 (2.32-3.24-1.600 (.06 (.540-.832-1.685 (.76-5.56 (1.606 (.426-.14-1.Metals Urinary Mercury−Females Aged 16-49 Years Old.77) 2.610-.578-.42) 90th 2.410-.98 (5.41-6.22 (.62 (3.41 (1.833) .92) 2.59-5. Geometric mean Survey years (95% conf.31-1.520-.501-.810) .540 (.22-3. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.95 (2.39-3.831) .846) .526-.579-.45) 2.50 (1.51 (3.557-.05 (2.560 (.91 (2.55-3.57-4.706 (.07-5.508-.72) 1.99-2.582-.37) 1.909-1.25) 2.16-5.724 (.831) .650 (.43-1.89 (2.21 (1.15 (2.03) 1.69 (1.37 (1.14-2.00 (3.61-6.68-3.52) 3.10-2.30-2.658 (. interval) Selected percentiles (95% confidence interval) Survey years 50th .665) .99) 1.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .605-.76) 2.27 (2.655 (.656-.79) 1.664) .97 (1.48 (2.710 (.97) 2.45) 2.615 (.709) 75th 1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.55) 90th 3.03 (.30 (2.44) 3.45-3.

Levallois P. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Chronic mercury poisoning in men repairing direct-current meters. Martins IP. Bidstrup PL. Daniel D. Metabolism of methyl mercury (203Hg) compounds in man.33:1-9. Bonnell JA. Snihs JO.7(3):176-184. Jorgensen PJ.77(2):124-129. Videro T. Seiwert M. Int J Hyg Environ Health 2009. selenium. Environ Health Perspect 2005. Luis H. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Int Arch Occup Environ Health 1999. Cianciola ME. Mortensen ME. Chan JM. Debes F. Weihe P. Cu. Becker K. Echeverria D. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Grandjean P. Niklasson B.212:588-598. Drexler H. Third National Report on Human Exposure to Environmental Chemicals. Kline J. Kinetics of mercury in blood and urine after brief occupational exposure. et al. Sallsten G. Impact of maternal seafood diet on fetal exposure to mercury. Myers GJ.56(4):350-357. Rosenbaum G. Biennow M. Schuzt A. Marsh DO. Barregard L. Arch Environ Health 1969. 2005. Pb. Arch Environ Health 2001. Jacobs D. Leitão J. Ekman L. Seiwert M. Persson G. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Atlanta (GA). ACGIH.289:1324. Total blood mercury concentrations in the U. and heart diseases. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Roels H. Hultberg B. Cernichiari E. Mangili A. Sandborgh-englund B. Lauwerys RR. Schaller KH. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. Ayotte P.2:856-861. et al. Vahter M.62(2):68-72. Sallsten G.111:719-723. Fawcett J. Lebel G. Benes B. Kaus S.19:478-484. Bates MN. Cortesi I. et al.16(4):705-710. Cutress T. Neurotoxicology 1995. and Se in blood of the population in the Czech Republic. Lapham LW. Harvey DG. I. Spevackova V. Berglund B. Cardenas A. Budtz-Jorgensen E. Bruneau S. Br J Ind Med 1993. White RF. Locket S. Int J Hyg Environ Health 2003. Apostoli P. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Garrett N. Begg M. Krause C. Attewell R. Elia G. 2007 TLVs and BEIs. population: 19992006. Osterloh JD. Zn. Environ Health Perspect 2003. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. J Toxicol Environ Health 1997. Fish consumption. Nutr Rev 2004. Hasselgren G. Arch Environ Health 1992.S. Martin MD.205:297-308. Am J Epidemiol 1999. Drago I. Weihe P. Geier J. 52:19-33. Int J Epidemiol 2004. Lepom P. et al. Barregard L. Bernard AM.47(3):185-195. JAMA 2006. Aposian HV. Jarvholm B. Dewailly E. Cerna M. Grandjean P. Cernichiari E. et al. Bernardo M.149:301-305. Jorgensen PJ. Bjornberg KA. Martin MD. Health effects of dental amalgam exposure: a retrospective cohort study. Sallsten G. Barbon R. Schulz C.. Buchet JP. Schulz C. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Application to workers exposed to mercury vapour. and lead. Factor-Litvak P. Cent Eur J Public Health 2000. Gagliardi T. mercury exposure. Kaus S.72:169-173. Cejchanova M. Townes BD. Arch Environ Health 1992. Tissue levels of mercury determined in a deceased worker after occupational exposure. Kjellstrom T. Enzymuria in workers exposed to inorganic mercury. Seifert B. Cernichiari E. Brewer R. Subrt P.Metals References Aberg B. Bellinger DC. Smid J. et al. Weber JP. Egeland FM. DeRouen TA. et al. Mercury derived from dental amalgams and neuropsychologic function. Skerfving S. Cincinnati (OH): Signature Publications. Centers for Disease Control and Prevention (CDC). Jones RL. Tavares M. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Res 1998. Woods JS.113(10):1381-1385. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Caudill SP. Cox C. Castro-Caldas A.61:65-69. Hg. Int JHyg Environ Health 2002. Clarkson T. Woods JS. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Markers of early renal changes induced by industrial pollutants. Trachtenberg F. Schutz A. Caldwell KL.50:17-27.295(15):1775-1783. JAMA 2006. Lancet 1951. Leroux BG. Conradi N. Int Arch Occup Environ Health 1988. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. McKinlay S. Barregard L. The concentration levels of Cd.295(15):17841792. 206:15-24. Becker K.8(2):117-119. Greitz U. Falk R. Sci Total Environ 2002. Barregard L.

51(3):234-241. Nakamoto S. Nyyssonen K. Lauwerys RR.70(5):310-314. Nakano A. Nyyssonen K. IARC Monographs on the Evaluation of Risks to Humans. J Dent Res 1998. Amalgam tooth fillings and man’s mercury burden. Ann Clin Res 1971. and Exposures in the Glass Manufacturing industry.49(6):394-401. Rahola T. et al. Environ Res 1995. Elimination of 203Hg-methyl mercury in man.48:247-53. Elinder CG. Declining risk of methylmercury exposure to infants during lactation. and the risk of myocardial infarction and coronary.95:406-13. Rissanen T.114(2):173-175. J Dent Res 1998. Myers GJ. National Research Council (NRC). Bodurow CC. Lagerkvist BJ. Miettinen JK. Elimination of free and protein-bound ionic mercury (203Hg2+) in man. et al.php. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population.50(9):814-821. Volume 58. 1993. and any death in eastern Finnish men. Burse VW. Kingman A. children and women of childbearing age: reference range data from NHANES 1999-2000. Langworth S. 2000. Seppanen K.90:185-189. Cadmium. Hum Exp Toxicol 1994. The distribution and biological half-time of 203 Hg in the human body according to a modified whole-body counting technique.361:1686-1692. Adachi T. Relation of a seafood diet to mercury. Environ Physiol Biochem 1975. Osterloh J. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. A compartmental model for the kinetics of mercury vapor in humans. Albertini T. Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey. Hirayama K. Sakamoto M.91:645655.112(11):1165-1171. Sallsten G. Clarkson TW. Bolger PM.S. Satoh H. et al. Available at URL: http:// monographs. Hattula T. Langworth S. 7/15/09 Jonsson F. Vesterberg O. Hernandez GT. Mercury. Sandborgh-Englund G. Halbach S. Kantola M.77(3):461-467. Cernichari. Environ Health Perspect 2006. Davidson PW. Circulation 1995.103:2766-2679. Circulation 2000. Mehaffey KR. Native American.iarc. The US EPA reference dose for methyl mercury: sources of uncertainty.77(4):615-624. Beryllium. Oskarsson A. McDowell MA. Hair mercury levels in U.3(2):116-122.5:252-257. docosahexenoic acid and docosapentaenoic acid. Br J Ind Med 1993. Rice DC. Hattula T.fr/ENG/Monographs/vol58/index.3dimercaptosuccinic acid (DMSA). Brown LJ. Shamlaye CF. Schutz A. Intake of mercury from fish.71(1):29-38.13:496-501.112(5):562-570. The effect of ethanol on the fate of mercury vapor inhaled by man.59(5):692-706. Liu XJ. Blood mercury reporting in NHANES: Identifying Asian. Ekstrand J. Renal and immunological effects of occupational exposure to inorganic mercury. Nakai K. Dillon CF. Allen J. J Pharmacol Exp Ther 1980. Miettinen JK. Sundquist KG. Lakka TA. Johanson G. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers. Pellizzari E. lipid peroxidation. Murata K. Needham LL. Barregard L. Environ Res 2002. Palumbo D. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. Sakamoto M. and polychlorinated biphenyl and other organochlorine concentrations in human milk. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Rahola T. Br J Ind Med 1992. Fernando R.5:214-219. arsenic. Kauhanen J.155(2):161-168. Hallen IP. Pacific Islander.38:3860-3863. Arch Environ Health 1996. cardiovascular. Ceulemans E. Cox C. Environ Sci Technol 2004. Yasutake A. and the risk of acute coronary events— The Kuopio Ischaemic Heart Disease Risk Factor Study. Washington (DC). Tillander M. Boeckx M. Weihe P. Urinary excretion of mercury after occupational exposure to mercury vapor and influence of the chelating agent meso-2. Rahola T. Skerfving S. Environ Health Perspect 2004. methylmercury transport across the placenta via neutral amino acid carrier. Roels HA. Kubota M. Greenwood MR. Arch Toxicol 1996. International Agency for Research on Cancer (IARC). Demuth S. Kubota M. Matsumoto S. Lancet 2003. et al. Clickner RP. Sanchez-Sicilia L. Schultz A. Hursh JB. Sandborgh-Englund G. Hightower JM. selenium. National Academy Press.Metals Grandjean P. Toxicological effects of methylmercury. Ann Intern Med 1963. Mercury in biological fluids after amalgam removal. Patterson DG Jr. Ohlin B. Br J Ind Med 1991. Salonen JT. Hattula T. Sampson EJ. O’Hare A. KajiwaraY. Schutz A. Ann Clin Res 1973. Akagi H. Elinder CG. Korpela H. Seto DS. Korolainen A. Kolff WJ. Toxicol Appl Pharmacol 1999. Environ Health Perspect 2004. Salonen JT. Fish oil-derived fatty acids. and multiracial groups. Rissanen K. 1999 and 2000. Environ Res 2004. Fourth National Report on Human Exposure to Environmental Chemicals 225 . Acute mercurial intoxication treated by hemodialysis.214(3):520-527. Voutilainen S.

79:786789. Vimy MJ. Newton G. Dorronsoro M. Stern AH. Am Ind Hyg Assoc J 1970. Kaye WE. Langolf GD. Amiano P.40:413-419. Fisher HL. Arch Environ Health 1993. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Friberg L. Environ Res 2005. Pediatrics 1987. et al. Vupputuri S.124:221-229. Woods JS. et al. Smith RG. Guo S. Environ Health Perspect 2003.Metals Sanzo JM. Public Health Nutr 2001. Osterloh J. Shen DD. Blood mercury levels in US children and women of childbearing age. et al. DeRouen TA. JAMA 2003. Yoshinaga J. Smith JC. Allen PV. Aguinagalde FX. Mottet NK. The hair-organ relationship in mercury concentration in contemporary Japanese. Goldberg J. Farris FF. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Am J Physiol 1990.98(1):133-142.2:117-131. 1999-2000. Effects of exposure to mercury in the manufacture of chlorine. Smith AE. Sandler DP. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Hongo T. Toxicol Appl Pharmacol 1996.4(5):981-988. Sherlock J. Hislop D. Turner MD.115(10):1527-1531.31:687-700. Baser M. Stern AH. Effects of occupational exposure to elemental mercury on short term memory. Leitao JG.97(2):195-200. Burbacher T. Patil LS. Methyl mercury pharmacokinetics in man: a reevaluation. Lorscheider FL. Nakazawa M. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Acrodynia: exposure to mercury from fluorescent light bulbs. Orr MF. Matsuo N. Hum Toxicol 1984. Bernardo MF. Longnecker MP.37:245-252. The kinetics of intravenously administered methyl mercury in man. Topping G. Leroux BG. Zeitz P. Daniels JL. Most B. Vahter M. Schober SE.289(13):1667-1674. Bolger PM. Vorwald AJ. Mooney TF. Smith JC.111(12):1465-1470. Toxicol Appl Pharmacol 1994. Amurrio A. Environ Res 2005. Br J Ind Med 1983. Hall LL.258(4 Pt 2):R939-945. Takahashi Y.48(4):221229. Martin MD. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Suzuki T. Imai H. Lind B. Toxicol Appl Pharmacol 1994.128(2):25125-25126. Environ Health Perspect 2007. Smith PJ. McMahon KJ. Sinks TH. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Whittle K. Jones RL. The contribution of dental amalgam to urinary mercury excretion in children.110:129-132. Environ Health Perspect 2002. Tunnessen WW. McDowell M. Azpiri MA. 1993-1998.

5 (37.7-39.6 (55.8-108) 87.3 (79.7-105) 69.9 (73.9 (44.0) 84. chemical reagents in hospital laboratories.5 (67.6) 71.4) 52.3) 85.6-62.1-63.4 (79.1-55.6) 51. 0.7) 51.1-48. At a daily oral molybdenum dose of 24 µg.9-83.7-96.4) 49.8) 48.8.3-91.0-62.1-59.1 (91.9 (37. semiconductor and battery industries have begun to use molybdenum. hydrogenation catalysts.2-53.0-71.3 (55.2-59.7) 78.7-92.2) 79. which exert homeostatic regulation over molybdenum balance.S.3) 37.2) 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. lubricants.7) 75th 84.0 (48.5-52.9-109) 97.0 (41.7 (73.5 (41.8-46. 1996).4-82.5) 85.8.4) 42.0-100) 63.0-110) 90.2-79.5 (74. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5 (41.6) Selected percentiles ( 95% confidence interval) 50th 50.3 (71.8-94.6 (52.0) 55. Compounds of molybdenum are also used as corrosion inhibitors.0-56.7-60.0 (42.0) 54.1 (34.6) 93. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. 01-02.6 (55.3) 65.Metals Molybdenum or ore deposits.9-55.0-65.9 (32.7-122) 93.3-47.5-91. and in pigments for ceramics.9-56.7 (37.0-38.0-101) 82.6-46.7 (51.2) 53.3) 54.6) 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 (99.1-51.1-52.2 (49.9-82.2 (40. Fourth National Report on Human Exposure to Environmental Chemicals 227 . and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.4) 41.0 (42.7-73.1 (38.9-55.2) 41.9 (52.9-85.8 (82.1-88.8) 75. 2001).0 (81.3 (38.3 (64.2 (56.9 (40.4) 45.5-66.4-61.6 (43.2 (49. urinary excretion over six days CAS No.3 (55. 2001.1) 46.3 (73.1 (71.4 (80.5 (81.7) 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 78.1) 59.7) 45. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8 (85.2-59.8-90.4-52.7) 46.2) 40.0) 39. and 1.3) 41.7 (44.0) 97.4) 76.7 (71.3 (46.8) 40. Excretion occurs predominantly via the kidneys. In humans. and paints.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.7 (45.7-50.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.2 (69.8 (67.7-41.8) 46.7-68.6-55.1-52.0) 62.6 (73.8-106) 88.7) 78. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.9) 34. and 03-04 are 0.2-37.7) 86.7-84.5-65.0 (43.8 (42.0-77.8-49.3) 47.4 (48.5-68.3-115) 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. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.2) 48.0-53.2 (38.5-41.3-75. aldehyde dehydrogenase. inks. More recently.5) 80.0 (76. 7439-98-7 General Information Elemental molybdenum is a silver-white..3 (47.4 (34.7) 57.6 (40.7-51.1) 35. see Data Analysis section) for survey years 99-00.4 (72.0) 60.9 (78.7 (36.9 (34.6) 53.2 (63.4-75.2 (83.5) 80.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.9) 62.0 (46.3-108) 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. respectively.8) 44.5) 47.5-46.3-44.2 (55.1-44.7-91.5-52. and xanthine oxidase (Kisker et al.2-70.5) 60.4) 56. The recommended dietary allowance for adult men and women is 45 µg/day (IOM. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.5.5 (49.5) 44.7 (50.6-42.5 (48.1) 126 (106-147) 109 (94.5 (43.2-42.3 (37.2 (61.1) 82.7-47.4 (48.9 (33.6 (40.6-58.2-91. WHO. 1997).9) 67.3 (53.0-85.3 (84.6-72.0) 45.7) 77.6-82.8) 39. population from the National Health and Nutrition Examination survey.5-124) 108 (92.1) 60.7 (58.2) 37.6) 71. interval) 45.2) 52.1) 57.3) 83.6-96.

2) 37.7-100) 77. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.5 (65.5 (41.4 (59.3-115) 98.2-121) 107 (92.2) 38.0) 39.4) 122 (107-133) 109 (99. Based on studies finding adverse reproductive effects in rats and mice.5 (54.4) 40. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5-46.6-63.3-141) 109 (81.4-66.9-71.7) 75th 63.7-93.4 (56. 1993).0 (58.4) 77.9-61.5-119) 90.5 (39.0) 53..3) 61.3 (37.1 (38.9-68.2) 43. 1999).1-112) 78.4-185) 106 (94. EPA.5) 63.5) 71.1-45.8) 71.8 (37.5-97.6-88.2 (37..8-66.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5) 72.4) 61.3 (71.5 (34.9) 31.0) 33.5 (50.9 (39.3-43. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.5) 60.1-43.3) 57.9-41.2-40.5) 73.8-118) 81.5 (38.0) 88.4) 58.6-78.8-67.1 (39.2-96.3) 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 85.3) 43.5-69.2 (36.6-76. respectively.6 (38.5 (37.3) 40.7-38.3-46.7) 41.7-137) 129 (109-155) 112 (97.0-41.4-106) 85.9-45.8) 62.6 (59.1-100) 86.1-34.6 (42.2-65.8) 37.3-52.6-61.2 (40.4 (55.2) 39.4) 60.2 (69.5-92.S.3 (36.8-42.0) 72.0-103) 103 (90.9 (64.7) 115 (93.6) 43.3-68.0) 44.1 (33.5-60.8) 38.2) 39.1) 40.2-96.5 (39.1) 37.7) 112 (95.1 (42.4) 47.9-96.3-102) 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 40.5 (78.4 (37.2) 58.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.9 mg/kg/day and established a tolerable upper intake level of 0.1 (54.5 (80.0 (35.1 (40.6) 48.5-62.9 (49.7) 62. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-35.2 (57.5 (59.9) 40.1-79. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0 (80.8-46.6-63.1-81.4-39.2-49.7-62.7-44.0-38.9 (73.9 (39.4 (40.6) Selected percentiles ( 95% confidence interval) 50th 41. 1997).4-76.1-127) 90.2 (52.8-47.1 (30. interval) 43.6 (36.9) 79.3 (83.9 (79.2 (33.9 (40.7 (77.S.3) 56.7 (66.0-120) 85. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.1) 65.3-45.0-46.3) 64.4-118) 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 . 1995).6) 39. 2001).1 (38.1 (49.03 mg/kg/day in humans (IOM.3-44.5 (40.5 (37.8) 61.3 (36.8 (90.9) 44.8) 45.6-45.8) 39. at daily oral doses of 95 µg and 428 µg.0-133) 119 (88.8) 79. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.5 (83.5-48.9 (64.0) 39.1 (44.0) 36.4 (78.2 (43.0-56.4) 116 (101-126) 104 (88.5) 90th 108 (97.1-109) 89.5-44.2) 37.5-50.9-42. but available epidemiologic data are scant.8 (57.5 (65.2) 42.1-39.6) 36.1-43.1) 43.8 (75.Metals was 18% of the ingested dose.3) 41.0) 38.7-52.6-41.5-70. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4-42.3 (37. U.2-46.2 (40.4 (44.7) 45.9-117) 57.1-41.4-41.5 (79.7) 42.4 (53.1-39. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.6 (57.3 (53.5 (35.7-120) 87. Molybdenum is generally considered to be of low human toxicity.8) 38.4) 44.7 (75.2 (73.9) 41.9) 92.5 (35.7) 57.7 (30.8 (56.0 (74.3 (58.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.5 (36.5 (40.3 (71. population from the National Health and Nutrition Examination survey.5-99.2) 55.9-87.4) 89.9-118) 91.6 (36.7) 53.5-45.3 (55.6) 39.2-80.7-43. and urinary levels reflect intake from all sources..8 (36.4 (67.3) 37.1) 101 (83.1) 56.2-47.7-40.6-61. and clinical or epidemiologic evidence of adverse effects is limited.5 (41.1) 37.1 (82.4-120) 101 (84.2 (50. urinary excretion over six days rose to 50% and 67%.8-65.9-45.9 (36.3) 44.4-107) 85.0) 62.3-59.1 (37.0-46.8-52. Biomonitoring Information Molybdenum is an essential element for health.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.9-40.2) 42. of the ingested dose (Turnlund et al.3 (51.4) 48.1-67.6 (71. In industry. 1961.8-84.2-41.9 (35.2 (40.1-40.3-56.1-38.8-47.

TR-462. White MA. Trace element reference values in tissues from inhabitants of the European Union. 4/14/09 Sievers E. 2001.216:253-270. 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. Molybdenum in infancy: methodical investigation of urinary excretion. References Centers for Disease Control and Prevention (CDC). Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Available at URL: http://books. J Trace Elem Med Biol 2001. Van Meerbeeck JP. 2005).niehs. copper. Weyler JJ. Gatti A. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. boron. nickel. silicon.S. edu/openbook.22(3):179-191. vanadium. Available at URL: http://www.S. Ronchi A. National Toxicology Program (NTP).S. Schindelin H. iodine. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum.htm.gov/iris/ subst/0425. 144-154.gov/index. van Sprundel MP. et al.nap. Molybdenum 1993 [online]. Droste JHJ. 16:1313-1319. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Food and Nutrition Board. Turnlund JR. Kisker C. Kristiansen J. pp. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Analyst 1998. Koval’skiy GA. World Health Organization (WHO).Metals in urine for the U. Turci R. X. 4/14/09 Iversen BS. White and Sabbioni. 1998. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Available at URL: http://ntp. Yarovaya GA. A study of 13 elements in blood and urine of a United Kingdom population. Washington. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. manganese. Occupational risk factors of lung cancer: a hospital based case-control study.php?record_id=10026&page=420. Rapid Comm Mass Spectrom 2002. Sabbioni E. Atlanta (GA). iron. Sabbioni E. Peiffer GL. Schleyerbach U. Dietary reference intakes for vitamin A. 56:322-327. Shmavonyan DM. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Rees DC. and zinc: a report of the Panel on Micronutrients. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC.15(2-3):149-154. Environmental Protection Agency (U. Molybdenum absorption. Sci Total Environ 1998.. Sciarra G. molybdenum. 420-441.62(4):790-796. Minoia et al. Zhurnal Obshchey Biologii 1961. Geneva: WHO..66:233-267. 4/14/09 White MA. pp. Molybdenum. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. chromium. 1998). 2005. Vermeire PA. Molybdenum-cofactorcontaining enzymes: structure and mechanism. 2002. In: Trace elements in human nutrition and health. Menne C. EPA).123(1):81-85. vitamin K.epa. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No.. Ann Rev Biochem 1997. Am J Clin Nutr 1995. U. (DC): National Academy Press. 1996. Christensen JM. arsenic. Minoia C. Institute of Medicine (IOM).nih. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Third National Report on Human Exposure to Environmental Chemicals. 2001). excretion. Aprea C. Keyes WR. Schaub J. Occup Environ Med 1999.

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

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

1991 [online]. eds. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Kuster W. Kelly J. 2001). Carelli G.. Boos KS. osmium. Herr et al. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Arch Environ Health 2001..207(1):69-73. Wilhelm et al. In: Bingham E. Fruhmann G. Levels of platinum in urine for the U. Platinum concentrations in urban road dust and soil. 1997.org/documents/ehc/ehc/ehc125. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Schierl R. Hebert R. 2004. Saindelle A. Schulz C. Occup Environ Med 2004.htm... Nowak D. 1998). Biomonitoring Information Urinary platinum levels reflect recent exposure. Huber R. Raab W. which elevate urinary platinum by five to twelve-fold (Begerow et al. population were below the limit of detection (0.61(7):636-9.76(1):5-10. ruthenium. Seifert B. Int Arch Occup Environ Health 2003. Ruff F: Platinum and platinosis. Available at URL: http://www. 1999. Urinary platinum levels associated with dental gold alloys. Schulz C. Blanks R. Allergy and histamine release due to some platinum salts. Bocca B. 5th ed. Ewers U. Hauff K. Duneman L:Long-term urinary platinum.htm. Hall L. Br J Pharmacol 1969.9:152-158. 2003. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.10:63-71. Int Arch Occup Environ Health 1997. Powell CH. Saindelle A. Patty’s Toxicology. Ensslin AS. Pethran et al. Stilianakis NI. 2000. Fries HG. 2004)... Kulka U. Thornton I. Environ Res 1975a. Schierl. 2003). Parrot JL.S. Pethran A. Analyst 1998. Schierl R.55(2):138-140. Czerczak S.01 µg/L (Becker et al.4(1):27-36. Nickel. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 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. Wilhelm M.Metals the International Programme on Chemical Safety at http:// www. 1998).. et al. Seiwert M. Environ Health Perspect 1975b. 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. Senofonte O. 289-380. Rommelt H. Occup Environ Med 1998.13(1):24-30. New York: John Wiley & Sons. et al. rhodium. Influences on human internal exposure to environmental platinum. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Schierl et al. Hysell D.org/documents/ehc/ehc/ ehc125. Campbell K. Iavicoli I.. and gold excretion of patients after insertion of noble-metal dental alloys. Urinary excretion of platinum from platinum-industry workers.56(3):283-286. Moore W Jr. 206:15-24.. Hysell D. Int J Hyg Environ Health 2004. palladium.inchem. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. and platinum. 3/31/08 Moore W Jr. Begerow J. Schierl R. palladium. Grimm CH. Angerer J.123(3):451-454. Schierl R. Alimonti A. Jankofsky M. Uptake of antineoplastic agents in pharmacy and hospital personnel.70(3):205-208. Petrucci F.35:313-321. Part 1: monitoring of urinary concentrations.inchem. et al..04 µg/L) in this Report. and in blood and urine in the United Kingdom. Herr et al. Biomarkers 1999. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Ruff F: Histamine release by sodium cholorplatinate. Turfeld M. 2003. Kazantzis G. Farago ME. Neuendorf J. Platinum. 2003. Kavanagh P.. International Journal of Hygiene and Environmental Health 2003. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.005 µg/L (Iavicoli et al. Several studies have shown that background concentrations in general populations were usually less than 0. pp. International Programme on Chemical Safety (IPCS). Biomonitoring of traffic police officers exposed to airborne platinum. Gieler U. Gromiec JP. Kaus S. Arch Environ Health:1969. Environmental Health Criteria 125. Crocker W. van de Weyer C. J Expo Anal Environ Epidemiol 2003.19:685-691. 2004) or less than 0. Pethran A. et al. References Becker K. Cohrssen B. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Herr CE.

190 (.440 (.340-.240) .290) 90th .197 (.390-.260-.210) .320 (.560) .370 (.500) .170-.230-.350-.440 (.440 (.167-.02.170-.300 (.159 (.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 . and 03-04 are 0.490) .390) .300 (.202 (.170) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.180-.330) .250-.380-.150-.162-.172 (.220) .410 (.420) .240) .470) .300-.145-.217 (.220) .280-.260-.187-.330-.192) Selected percentiles ( 95% confidence interval) 50th .290-.250-.350-.520) .300) .430-.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 .183) .420-. thallium was obtained as a by-product of smelting other metals.320) .200) .270 (.420-.160-.400) .250-.206) .190 (.135-.410-.630) .420) .180 (.480) .410 (. and 0.390 (.390) .200) .350-.170-.250-.450 (.280) .310 (.350-.260-.280) .290 (. thallium readily crosses the placenta and also distributes into breast milk.340-.133-.290 (.190 (.380 (.450 (.430) .200) .310 (.184 (.370 (.350) .440) .137-.180 (.460) .410-. Thallium disappears from the blood with a half-life of several days.330-.200) .200 (.310-.165 (.200) .300 (.400) .370-. it has not been specifically mined or refined in the United States since 1984.250-.156) .196) .220 (.160 (.450 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.220) . however.260 (.220 (.170-.260-.156) .147-.260-.480) .330-.300) .170) . 0.188) .490 (.450 (.148-. interval) .400 (.360 (.410-.550 (. 2005).450 (.239) .470) .200 (.480) . representing distribution into other tissues. Fourth National Report on Human Exposure to Environmental Chemicals 233 .201 (.183) .460 (.370 (.200-.170 (.270 (.690) .280 (.400 (.175) .170 (.400 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.163) .220-.215) .177) .250-.180) 75th .420) .200 (. In the United States.200 (.230) .210 (.410) .360-.350 (.370-.290) .380-.500 (.340-.330-.290) .370 (.173) . population from the National Health and Nutrition Examination Survey.360 (.146 (.400-.290) .150-.160 (.270 (.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 .330-.400-.02.290 (.430-.185-.270-.390-.160 (.520) .170-.450 (.210 (.196) .191 (.410-.200-.370 (.350) .197-.179-.420 (.440 (.280 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.410 (.290 (.230) .330-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.220 (.158) .290) .430 (.200) ..150-.155 (.170) . From these and other sources.270-.590) .370 (.156-.160 (.160 (.220 (.330) .181-.490) Total .450 (.150-.450) .230 (.190 (.280) .280 (.176 (.340 (.02. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.160-.180 (.440-.520) .590) .390) .320-.390-.360 (.220) .270 (.250) .370-.180-.172) . 01-02.440) .144 (.S.145-.390 (.450 (.190 (. see Data Analysis section) for Survey years 99-00.420) .350-.500) .400-.178) .380) .280-.190-.370 (.320) .400) .360-.410 (.420-.218) . respectively.490) .510 (.420) .200-.520 (.200 (.310) .410 (.340-.220 (.217) .230) .430 (. In the past.182-.360-.360 (.410-.430) .243) .180-.149 (.400-.330) .240-.153-.159 (.270 (.173-.150-.167 (.400) 95th .310 (.210-.320) .400-.150-.480) .330) .140-.430-.470) . 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.230-.450 (.360-.250-.200 (.260 (.240) .400 (.218) .390-.410 (.260) .240-.340) .420-.360) .167-.440) .250 (.300) .173) .370-.170 (.240-.290 (.330-.160-.340) .230-.270) .202 (.159 (.225) .460-.380 (. Human health effects from thallium at low environmental CAS No.134-.420) .350 (.400) .180) .420) .160-.220) .430 (.480) .360-.350-.202) .147-.Metals Thallium depilatory cosmetics.170-.157-.185 (.171 (.430 (.220) .147-.180-.270) . In addition.145 (.470 (.270-.510) .200-.640) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.201 (.390) . the latter being the current major industrial consumer of thallium in this country.370) .260 (.400 (.410-.470 (.250 (.172 (.250-.300) .190 (.160-.230) .290 (.154-.490) .290-.170-.500) .370) .

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

et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Sabbioni E. 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. White MA. A study of 13 elements in blood and urine of a United Kingdom population.S. Sci Total Environ 1998. 1998.. Pirkle JL. Int Arch Occup Environ Health 1980. Pozzoli L. Sabbioni E. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Available at URL: http://www.5 μg/L.. 2005. 2005) and are shown with results from NHANES 2003-2004 in this Report.. population) are thought to correspond to workplace exposures at the threshold limit value of 0.113(1):47-53.47(3):223-231. Sampson EJ. Dolger R. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Investigations of thallium-exposed workers in cement factories. 1980. Celier D.atsdr. Martin J-C. 1981. 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. 2005. A study of 46 elements in urine.95:89-105. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Brockhaus et al. Raithel HJ. blood. Challeton-de Vathaire C. Buhlmeyer G.. Environ Res 1998. Paschal DC. Ewers U. Jackson RJ.265 people living near a thallium-emitting cement plant in Germany. J Soc Occup Med 1985. and serum of Italian subjects.76(1):53-59. Paschal et al. Minoia C. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Schaller KH. Schmidt M. White and Sabbioni. Boisson P. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. 1985). with concentrations ranging up to 76.Metals (CDC. Pietra R. Schaller et al. X. Toxicological profile for thallium.cdc. Kramer U. Radiat Prot Dosim. Minoia et al. Trace element reference values in tissues from inhabitants of the European Union. et al. 1990. Sci Total Environ 1990. Valentin H. Manke G. Gallorini M.html. Trace element reference values in tissues from inhabitants of the European community I. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Int Arch Occup Environ Health 1981. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium.1 mg/m3 (Marcus.216:253-270. Centers for Disease Control and Prevention.35(1):4-9. Morrow JC. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. 7/15/09 Blanchardon E. Marcus RL. Soddemann H. Cassot G. Brockhaus A. 1998). Investigation of a working population exposed to thallium. Trace metals in urine of United States residents: reference range concentrations. et al.gov/toxprofiles/tp54. (1981) studied 1. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Wiegand H. Ting BG. Apostoli P.48(4):375-389. 1992 [online].

082-.060 (.380 (.130-.170) .180 (.330) .340-.080 (. Tungsten compounds are used as lubricating agents.460) .050-.220) .510-1.380 (.060-.420-.110) .400 (.120-.170) .160-. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone. 236 Fourth National Report on Human Exposure to Environmental Chemicals .100-.077-.690) .380) .340) .570 (.130-.460 (.056-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.360 (.290) .093) .069-. Little information is available on the toxicity of tungsten.560) .S.400 (.066-.230-.190-.430 (.110-.190-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350) .310-.550 (.550) .260 (. see Data Analysis section) for Survey years 99-00.370) .580) .470-.130) .130 (.073-.068) .350) .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 .101 (. and 03-04 are 0. 01-02.00) .800) .150 (.180) .190 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.180-.204) .360) .260-.230-. respectively.140 (.460) .110 (.071 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.410 (.250) .120) .105) .080-.160 (.170) .230 (.140) 90th .430) .300 (.620) .200) .320 (.230) .088 (.160) .390 (.340-.092 (.270 (.170 (.430-.050-.230-.550) .560 (. 0.087-.100-.450-.093-.950) .080-.250-. population from the National Health and Nutrition Examination Survey.065-.190) .210 (.480) Total . which are used in rock drills and metal-cutting tools.110 (.460 (.630) .310) .290 (.100 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.160 (.380-.330-.133) .151) .100-.Metals Tungsten CAS No.370 (.070-.53) .290-.090 (.190 (.090-.082 (.090 (.180-.550) .410-.160-.120) .590) .120-.250-.310-.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 .120 (.380-.320 (.070) .810) .270-.100) .290) .150-.240 (.120-.530 (.074-.370-.130 (.113 (.250) .380-.140-.082 (.250) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).090-.460 (.069) .058-.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 .092) .210 (.120-.158 (.100 (.290-.130) .092 (.073-.080 (.270-.250) .560) .300 (.180) .090-.230-.400 (.050-.126) . and for producing ferrotungsten.090-.510-.800) .280 (.04.113 (.060 (.570 (.090-.300 (.060 (.500 (.350) .300) .180 (.490 (.104) .200-.310-.080) .140-.100) Selected percentiles ( 95% confidence interval) 50th .070 (.060-.110 (.210-.420-.380-.120) .370 (.140 (.070-.110 (.070) .062 (.087) .086 (.530 (.100) .450 (.290-.430-.076 (.060-.093 (.105 (.04.520) .230) .070) .500) .100) .320-.080 (.350 (.210) .060 (.160) .830) .090-.090-.084 (.330) .080) .070-.360-.560) .470) .370-.084) .330-.060-.260-.071-.280 (.210 (.210 (.130-.090) .130) .100 (.270-.430 (.430 (.065 (.109) .530 (.620) .130) .120) .060 (.140 (.097-.135) .180) .310-.320-.091) .210 (.470 (.101-.078-.120-.160 (.140 (.330 (.190-. and as catalysts in the petroleum industry.130-.470 (.180-.062 (. mainly as scheelite (CaWO4).080 (.310-.160-.110-.400-.770 (.073) .100 (.095-.081 (.270 (.064-.300-.110) .110-.120-.088) .110 (.260-.060-.132) .370 (.116) .220-.070) .620 (.360 (.050-.310 (.250) .073 (.090 (.160-.220 (.150 (.084-. which is used in the steel industry.070 (.440) .076 (.080-.080) 75th .360 (.100) . Occupational exposure is from dusts released during grinding or drilling of hard metals.090-. filaments for incandescent lamps.070 (.280-.400) .640 (.150) .090) .500 (.180) .300) 95th . Evidence is lacking for the carcinogenicity of tungsten.080 (.320) .122) .090) .107 (.260) .100) .270 (.400 (.096 (.170-. bronzes in pigments.095-. Tungsten is used mainly for producing hard metals.090) .270-.04.520) .250) .670) .123-.220) .130) . and 0.490) .180-.520) .170) .070-.111-.650) .160 (. interval) .220) .070-.510 (.160 (.560) .190-.170 (.350-1.056-.240-.113 (.200 (.060 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.390) .060-.113 (.470) .150 (.260 (.137 (.080) .790) .120) .082) .360-.096-.120) .340-.

554) .092) .077-.253) 95th .073 (.340 (.133) .237-.150-.059-.066 (.385 (.083) .094) .186 (.111 (.061-.063 (.066 (.255-.083) .333 (.286-.074 (.538) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.078 (. 2001-2002.381) .250-.073 (.059 (.347 (. interval) .739) .181 (.090-.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 .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH. 2001).245-.064-.258 (.108-.187) .197 (.158) .133) .240-.287) .100 (.453) . 1997).216-.070 (..088) .083 (.095) Selected percentiles ( 95% confidence interval) 50th .098-.061-.168 (.199 (.053-.136-.080 (.136 (.068 (.253-.231-.208-.167) .364 (. (1987) found possibly due to methodologic.108) .158) .331-.091) .439) Total .106 (.497 (.069-.054-.170-.315-.S.308) .059-.267) .075) .358) .255 (.086-.179-.174) .049-.121 (.078) .153-.096) . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.279 (.078 (.148 (.272-.146) .150 (.100) .079 (.104-.412 (.105 (.065) .067 (.144-.333) .880) .077-.084 (.082 (.139 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.065-.154) .667 (.233-.095-.085) . Nicolaou et al.379 (.063 (.085 (. population.167-.306) .410-.146 (.098 (.279 (.080-.139) .084) .439 (.084 (.133) 90th .107-.091) .165) .582) .375) .216 (.081 (.261-.431) .200-.200-.103-.253 (.452-.341 (.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 .086) .090-.197) .500) . measure urinary tungsten. similar to those in this Report (Schramel et al.088) .482 (.179-.215 (.197-.300-.089 (.116) .056-.065 (.216-.119 (.301) .130-.062 (.333-.317 (.605) .283) .071 (.126-.158 (.344-.071) .075) .250 (.091 (.465) .174 (.214-.294 (.065-.436) .201) .169) . 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.211 (.339 (.054-.130 (.075 (.176-.079) .136-.214) .079) .060-.064-.293 (.S.138 (.28) .(Kraus et al.155-.063-.089) .122-.176-.317-.224) .426) .151 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.082) .124 (.116-.153) .080 (.333-.167-.333 (.484 (.057-.121-.063-.158) .091) .143-.354-.098-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U. or exposure that a control group of non-metal workers had mean levels differences.098-.071 (.109-.068-.093) .299 (.145 (.122 (.119-.083 (.091) .167) .117 (.333) .084) .057-.100) .082) .067-.317) .154) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.215) .206-.360 (.222-.072 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.074) .217-.138) .465) .205-.797) .161) .459) .152-.087) .333 (.301) .270 (.727) .284) .078) .222) .125) .198) .075-.075 (.055-.431) .217-.359 (.197) .125 (.060 (.237) .267-.823) .067 (.120) .078-.063-.164 (.077) .329-.199 (.198-.144 (.117) ..086) .383 (.094) . 1998).426) .285) .354) .169 (.071) . population (CDC. Using neutron activation analysis to 2000.302-.555 (.216 (.061-.278-.484) .265 (.075-.333 (.071 (.056-.180-.074) 75th .086) .326) .209-. population from the National Health and Nutrition Examination Survey.436-1.190) .414) .072-.080-.065 (.157) .300) .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 .105 (.074-.148) .073 (.S.079 (.072-.139-.065-.059-.120) .081-.122-.339 (.099-.462) .136-.250 (.386) .188-.301) .077) .093-.138 (.060-.116 (.308) .074-.634 (.353 (.109 (.091 (.353 (.279 (. 2003.667) .431) .231 (.237) .136-.079) .071) .087 (. 2005).085-.081) .201 (.146 (. Patients with medically-inserted tungsten found at increased levels in drinking water.070 (.073 (.094-.069 (.359 (.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 .079) .063-.302-.216-.300 (.203-.071-.098) .258-.218 (.392) ..058-. and 2003-2004 (Paschal et al.131-.083-.275 (.150-.081 (.300-.124-.069 (.329 (.255 (.184 (.143 (.439 (.

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

030) .006-.049) .037) .026) .032 (.036) .026) .028 (.009) . 235U (about 0.007 (.038 (.008) . 0.033 (.006-.011-.054) .008-.007 (. and 03-04 are 0.025-.010) .027 (.029 (.008-.017 (.005.056) . respectively.065) .008 (.049) .037) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .069) .009) .012 (.034-.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 .053 (.009 (.024-.029-.009 (.022-.006-.026-.008 (.047 (. interval) .022) .012-.008) .027-.010) .009 (.011) .016-. In workplaces that involve uranium mining.033) .006-.035) .013 (.026-.016-.279) .088) .006 (.009-.010 (.007) .009) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.013 (.004.010) . nuclear fuel.035) .013) .018 (.008) .051) .038) . 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.011) .007-.007 (.027-. and 234U.048 (. 01-02.056) .008-.019-.011 (.019-.007-.007-.007-.006-.065) .016) .010) * . milling. including nuclear weapons.029-.009-.067) .012 (.018) .023-.045) .036-.009 (.022-.027 (.009-.017-.027 (.067) .009 (.016) .030 (.010-.007-.006-.007) .046 (.031-.041 (.012-.019-.006 (.012-.021-.021 (.012-.046 (.014 (.015) .030 (.010-.008 (.012) .015 (.020-.005-.007-.013) 90th .007 (.012) .010 (.008 (.023-.023) .010-.009) .127) .021-.053) .020-.007 (.011) .016) .027) .017) .016) .028 (.008) .028-.011-.013 (.020-.009-.043) .012) .007 (.007-.017) .011-.006 (. Variable concentrations of uranium occur naturally in drinking water sources.007-.007-.046) .014 (.009 (.018 (.008 (.72%). in some ceramics.034-.020-.015) .023 (.027) .054-.046 (.008-.021 (.009) * .072) .062) .015-.013-.034) .008 (.008-.021 (.010-.006-.026 (.026) 95th .060 (.009-.010) .011-.031 (.008 (.017) .007-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).010) .046 (.018) . see Data Analysis section) for Survey years 99-00.009) .007 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.014 (.028 (.027-.004.007) .014 (.036-.023-.036 (.009 (.040) .008 (.023) .043 (.008 (.017-.039-.007 (.030-.017) .007-.114 (.016-.007 (.Metals Uranium CAS No.008-.016 (.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 .008 (.015 (.012 (.033 (.024-.037 (.008 (.011) .012 (.042 (.009) .009) .040 (.S.046-.158) .023-.015 (.031 (.054) .008 (.015 (.013 (.026 (.020) .013-.009) .010) .013 (.011) .009) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.014 (.040-.007-.020-.019 (.028-.005-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.022-.007-.027 (.050) .023) .018) .012 (.018-.007-.023 (.017-.014 (.023 (.021) .012) .009) .009-.019-.006-.037-.012-.066) .007-.020 (.024-.006-.007) .041 (. population from the National Health and Nutrition Examination Survey.013 (.017-.006-.017 (.010) .036) .030 (. Thus.009 (.011) .039) .033-.008-.011-.008) .010-.017) .006-.006 (.009-. human exposure occurs primarily by inhaling dust and other small particles.064 (.039) .012 (. Uranium has many commercial uses.010) .010-.010) * .007-.010 (. Since the 1990’s.050) .009) .012-.024 (.010 (. and 0.027) .021) .009 (.020) .040) .005-. 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.021) .010 (.022 (.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 .073) .007-. or processing.026 (.017-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.045) .008 (.027) .009 (.006-.037) .009-.048) .031 (.007-.005-.031 (.031 (.052 (.040 (.011-.009-. and as an aid in electron microscopy and photography.036 (.016) .008 (.008 (.007 (.040-.016) .044 (.063) .009) .006-.018) .011-.008-.007) .035-.007) 75th .007 (.013 (. 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.013-.011) .009) Selected percentiles ( 95% confidence interval) 50th .008 (.055 (.009-.037) Total .017-.011 (.042) .008 (.009) .005-.

042) .029 (..006-.033 (.019-.005-.025 (.037 (.039) Total .013) .039) .022 (.025-.009-.016) .034-.004-.030) .047) .Metals impact.009) .007 (.006 (.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 .007) .008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .. In cases of retained DU shrapnel.010) .014-.008-.008 (.007 (.024) . 2005).006-.005 (.024) .014) .019 (.006-.010) * .006) .011) .006-.007-.015-.009-.007 (.006 (.007 (.005-.020 (. which can occur occasionally from high occupational exposure.026-.015) .027 (.039) .031-.011-.020) .006-.008 (. low level exposure.005-.016) .007 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.007-.035 (.026 (.008) 75th .014 (.006-.006) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.028 (.019-.006-.010-.034 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.006-.019-.015) .010) .009) .016) . Depending upon the specific compound and solubility.013 (.011-.030) .008) .048) .025 (.016) .008 (.010-.012 (.008) .015-.025-.014 (.044) .010 (.053) .022 (.013 (.012) .029) .024) .005 (. 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.012) .007) .058) .012-.017) .022-.007 (.016) .012 (.007 (.013 (.027 (.030-.006-.006-.007-.021-.012) .016-.027) .008) .028-.025) 95th . interval) .033 (.007-.013 (.015 (.012 (.007 (.009) . Inhaled uranium-containing particles are retained in the lungs.018-.022) .006-.010-.050) .024) .005 (.022-.012 (.074) .050) .007 (.010) .024-.016) .029) .009) .042-.018-.020-.006 (.067) .007 (.015 (.010 (.009 (.017 (.008) .008) .009-.008 (.008) .019 (.008-.011-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.034 (.011) * .023-. 2003).020-.009-.015-.006-.006-.045 (.009-.006-.034 (.030 (.013) .006) .024 (.034 (.007-.011-.033) .006 (.007 (.051) .080) .010) .017-.028) .014) .022-.027 (.008 (.011) .009-.011-.010) .021 (.009 (.014) 90th .009) .013 (.146) .013 (.027-.010-.008) .007-.019-.006 (. which represents distribution and excretion.009) .024 (.008) .012 (.016) .054) .012-.042) .031 (.005-.021) .010-.020 (.017-.008-.. kidneys.010) . the shrapnel acts as a source of chronic.014-.013-.010-.024-.006-.010 (.033 (.029) .028) .005-.019) .021 (.006) .017 (.028) .016) .020 (.008 (.006-.008) .025-.013 (.008) .007 (.030 (.077) .008 (.100 (.018 (.020-.006) .034) .007-.018) .029 (.010 (.028) .006-. After exposure to soluble uranium salts. 240 Fourth National Report on Human Exposure to Environmental Chemicals .027-.017-.019-.058) .020-.009) .008-.010-.021 (.012 (.027-.016-.009) * .006-.007-.015 (.1%-6% of an ingested dose may be absorbed.018-.051) .034-.008 (.018-.009 (.008 (.017) .011 (.012 (.026 (.010 (.006-.035 (.021 (.006-.008-.051 (.014-.014) .013 (. Health effects from uranium exposure result from chemical toxicity to the kidney.007 (. Radiation risks from exposure to natural uranium are very low.026) .005 (. Uranium is eliminated in feces and urine.029 (.007 (.013 (.015) .009) .011-. 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.040 (.007 (.015) .009) . 1992).006-.011-.009) Selected percentiles ( 95% confidence interval) 50th .039) .016-.015 (.007) .006 (.024-.032) .048) .010-.010-.004-. After inhalation.007 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.009 (. where limited absorption occurs (less than 5%).019) .050 (.041) .270) .030-.063) .015-.061) .056) .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.015-.008 (.013 (.007-.024 (.008) .017-.024) .010-.007 (.011-.034 (.027-.013) .011 (.S.017) .051) .018-.043 (.026 (.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 . liver.019 (.016 (.009) .006-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.007 (.005-.011) .053) .032) .029) .006-.059 (.027) . population from the National Health and Nutrition Examination Survey.006-.008-.009 (.007 (.033 (.030 (.016-.010-.005-.007 (.009) .025-. with much slower elimination from bone.011-.022 (.007 (. After long term or repeated exposure.028 (.007-.

S. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. the median urinary uranium concentration was 2. Horan P. urinary levels of uranium were as high as 9. had a mean urinary uranium concentration of 0. 2002). A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Zimmerman I. and 2003-2004 (Dang et al. Centers for Disease Control and Prevention (CDC). Hamilton et al. the median urinary concentration was 0. (May et al. The U. 2006). Stradling GN. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Fourth National Report on Human Exposure to Environmental Chemicals 241 .gov/ toxpro2. Dietz LA. 1991. 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. environmental levels) and health effects is available from ATSDR at: http://www. 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. Thomas RG. Kent (England): Nuclear Technology Publishing. 1992.. Komaromy-Hiller et al.110 to 45 μg/L (Ejnik et al. 1978). In a study of 105 persons exposed to natural uranium in well water. and no consistent effects on multiple endpoints of kidney function were found.S.107:143-157. 2006. IARC and NTP have no ratings for uranium human carcinogenicity. Squibb K. Uranium content of blood.. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. with emphasis on quality control. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 2002. or wound contamination. pp. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.55 μg/L (median 0. Galletti. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Six workers in a depleted uranium program showed concentrations of 0. 28 soldiers who may have been exposed to DU by inhalation. respectively. soldiers evaluated before. 2004). McDiarmid et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Drinking water and other environmental standards have been established by U.. Pillai KC. Sci Total Environ 1991.. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Atlanta (GA). Metivier H. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.. 1-49. Pullat VR.e.html.. 2004). the geometric mean urinary uranium concentration was 0.. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 2006). 2004).1992. McDiarmid M.S.. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. in that the levels were below their respective detection limits (Byrne et al.078 μg/L (ranging up to 5. 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. Benedik L.. 2005. et al.78:143-146. Dang HS. 2003.1996. NRC. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.. Health Phys 2000. 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. Carmichael AJ.. In 17 U. Byrne AR. Third National Report on Human Exposure to Environmental Chemicals.atsdr.066 μg/g creatinine (Gwiazda et al. 41 (1). population. although slightly increased during and after deployment. Hamilton MM. Durakovic A. Vol. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. 1994. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.. Information about external exposure (i.S. ingestion..011 μg/L (McDiarmid et al. Mil Med 2003.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Muggenburg BA..S.168(8):600-605. 2001-2002. 2006). during.65 μg/L). In: Gerber GB. EPA. A cohort of 46 U. eds. 2000). 2000).. but in whom no shrapnel was embedded.. Ejnik JW. 2006).162 μg/L) (Orloff et al. Volf V. References Bhattacharyya MH.. Boyd P.. Breitenstein BD. Tolmachev et al. (Kurttio et al. In the same study. Health Phys 1992.62:562-566.cdc.S.61 μg/g creatinine. Karpas et al. 2004). Radiation protection dosimetry.

plasma and urine and a critical evaluation of reference values for the United Kingdom population. Pirkle JL. Marko R. Review of elements in blood. Nuclear Regulatory Commission (NRC) Guide 8. Sci Total Environ 1994.Metals Galletti M. Costa R. Englehardt SA. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. J Toxicol Environ Health A 2004. et al. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Engelhardt SM. U.47(6):972-982. Element reference values in tissues from inhabitants of the European community. Shelly T.S. Wilson PD. Cremisini C. Ash KO. Komulainen H.85:228-235. concentration and daily excretion of uranium in urine of Japanese. Int Arch Occup Environ Health 2006. Scott K. Gucer P. Health Phys 1996. Smith D. Pekkanen J.110(4):337-342.82(4): 527-532. Oberbroekling KJ. rapid. Sampson EJ. Saha H. Gwiazda RH. et al. Health Phys 2004. Orloff KG. Hollriegl V. Saha H. Heller J. Charp P. Paretzke HG. Clin Chim Acta 2000. Ting BG. et al. McDiarmid MA. Biologic monitoring for urinary uranium in Gulf War I veterans. Squibb K. Auvinen A. May LM. Makelainen I. McDiarmid MA.S. Jackson RJ. Harmionen A. Kurttio P. 242 Fourth National Report on Human Exposure to Environmental Chemicals .87:51-56. Environ Health Perspect 2002. Uranium and thorium in urine of United States residents: reference range concentrations. Renal effects of uranium in drinking water.44:29-40.81:45-51.86:12-18. et al. Environ Res 1999. Ough EA. et al. Nuclear Regulatory Commission (U. Salonen L.S. Karpas Z. Paschal DC. Sabbioni E. Metcalf S.S. Radiat Environ Biophys 2005.94:319-326.22–Bioassay at uranium mills. Halicz L. Kane R. Pinto V. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Kidney toxicity of ingested uranium from drinking water. McDiarmid M. Auvinen A.158:165-190. Ejnik J. Jarrett JM. Kalinsky V. patient population and literature reference intervals for urinary trace elements.91(2):144-153. Karpas Z. Health Phys 2006. Noguchi H. Komaromy-Hiller G. Human exposure to uranium in groundwater. Health Phys 2003. Andrews WS. Roth P. et al. Hamilton EI. Washington (DC): NRC. Oliver M.296(1-2):71-90. Tolmachev S. Mistry K. Marino R. Hancock RG. Lorber A. Squibb K. Bennett LG.79(1):11-21. Am J Kidney Dis 2006.71(6):879-85. Lewis BM. Katorza E. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Salonen L.67(8-10):697-714. Oeh U. NRC). Roiz J. Kurttio P. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Inductively coupled plasma mass spectrometry as a simple. Environ Res 2004. Kuwabara J. July 1978. Wahl W. Biokinetic modeling of uranium in man after injection and ingestion. Health Phys 2002. U. Howerton K. Cordero S. Health Phys 2004. VI. Li WB. Comparison of representative ranges based on U. Van der Venne MT. Uranium daily intake and urinary excretion: a preliminary study in Italy. D’Annibale L.

0 (13. 2005).90) 6.90-11. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.50) 5.65) 3. and reducing agents.30 (5.50-3. laboratory analysis.07-4.70-5.0 (11. 2007).0 (8.50) 6.60 (4.20 (2.30) 6.79 (2.0) 14.50-4.60) 5.0 (11.30-7.88) 3.40 (3.20 (4.89-3.90 (5.00-6.60-7.Perchlorate Perchlorate (Urbansky.0-15. but has strong oxidant properties in the presence of concentrated acids.0-17..0-17.01 (2.19 (3.18-3.87-3. milk.81) Selected percentiles ( 95% confidence interval) 50th 3. Drinking water.90-12. Other manufactured uses include fireworks.05 and 0.10 (6. or ammonium salt.51 (3.40-5.70-11.0 (9.70-12.80-12.05 (2.11) 3.60 (4.51 (3.30) 6.0-20.0 (11.80-6.20-4. 1998).0 (9.40) 6.0 (9.5 hours and has a small estimated volume of distribution (Crump and Gibbs.0 (8.44-4.90-10.47-4.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.40) 90th 10.20) 3.70-3.80 (6.0) 708 617 681 652 1228 1092 Limit of detection (LOD.67-5.40 (5.30 (2.30-6.80-8.30 (5.EPA.80) 75th 6. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms..80-4.0) 11.05.10 (5.0 (8.16) 3.20 (6.10-12.49-3.0-15. It is normally found and produced as the anion of a sodium.09) 3.40) 4.20-11.10) 5.00) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.54 (3.93-4.0-17.0) 19.40 (3.10-11.68) 4.70-9.0) 9. 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.08-3.0) 13. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .38) 5.80 (7.0 (11.20-4.20) 4.0-18.50 (5.0) 10.93 (4. matches.00) 7.0) 16.20 (5.90-3.10) 3.0) 13.0) 13. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.22 (2.0 (11.74-3.40 (4.84) 14.80 (3. 2002).0) 14.0) 13.29-3.0) 15.20 (7.96 (3.30-7.40) 3.0 (8.60) 8.40 (4. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.76) 4.80 (3. Survey years 01-02 03-04 Geometric mean (95% conf.12) 3.50-7.70-7.32 (3.90 (2.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0 (11.90-9.0 (11.0 (12.0-23.80) 7.70 (3.21 (2.02 (3. and electroplating. and certain plants with high water content (e.40) 3.20 (2.80) 3.S.0 (9.0 (12.0 (9.10 (2.10 (7.10) 5.0) 9.50) 3.10) 3.0) 8.50) 5.00) 4. interval) 3.0) 12.50 (3.70-6.0) 13.50 (8. potassium.0-17.70 (3.76 (3.0-17. and limited applications in pharmaceutics.50) 11.70) 3.66) 3.90 (5.0) 9.26 (2.46) 3.0 (11.56) 3.90-11.75-3.0) 10.0-17.0 (12. leather tanning.0 (9.70-3.40 (8. lettuce) can be the main sources of intake for humans (FDA.40 (5. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.80) 12.0) 9.0) 11. 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) 15.0 (11.0) 95th 14.0-29.60) 3.45-4.90 (4.90 (3.35 (3.10-11.0 (12. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 8.00) 3.10-4.80-15.70 (3.62 (3.0) 13.g.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.00-6.0 (11.10 (6.90-6.50-11.60-6.40-4.31) 2.40-7. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0-19. Perchlorate was added to the U.40-6.22-5.30-17.03) 3.0) 9.30 (2.0 (8.20-12.90 (5. In addition.40) 2.40-4.0) 13.0-14.93-3.60 (7.0-18. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.S. Perchlorate is stable under most environmental and physiological conditions.75 (3.30-19.0 (9.11) 4.40 (5. certain catalytic metals.0) 10.00-5.20 (8.40-11.S. population from the National Health and Nutrition Examination Survey.0) 11.20) 7.0-18.90) 5.81-16. 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 (10. 2005).10-7.40-13.0) 9.0) 13.19-4.00) 5.40) 3.90-9.20-3.80-4.0) 14.39-4.50-4. fabric dyeing.10) 12.90-3.20 (4.

menopausal status.45-2.4 (8.2) 8.20 (4.90 (4. 1999. Lawrence et al.71 (5. During gestation and infancy.00) 4.30) 3.2) 8.0 (11.84) 2.46 (3.90-15. Greer et al.70 (2.82 (5.46-13.64-3.35 (2.3) 11. chronicity of exposure.35) 3.20 (6. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.40 (7.32) 5.90-3.05 (4.30 (6.26) 4.50) 2.76 (3. perchlorate is negative in most genotoxic assays (U.30-5. women with urinary levels of iodine less than 100 micrograms per day.1-16. 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).73) 3.20 (7. Lamm and Doemland.25) 5. in a representative sample of U.5) 8.39 (3.0) 7. age.10-3. levels and sufficient in most participants (Tellez et al.54 (2.00-2.40 (3.93-7.60-8.56 (3. However.16-3.20 (3. Also. In the U.0 (9.96) 2.10) 3.75) 3. gender. 2005).30) 75th 5. medications).33-12.0) 12.Perchlorate inhibition (RUI).S.39) 2.S.S.09) 3.0) 13..00-11.10 (1.90 (2.76-3.20-3.99-3.0 (8.44-6.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.. dietary iodine intake.90-20.22-4.40-10.64) 5. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.. 2005).86) 4.10 (2.04-3.0) 12.80 (4.50) 5.4 (11.0) 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 .0) 9.93-5.70-15.90) 5.20) 8. Steinmaus et al.95 (2.50 (6.08 (3.20-3.39-4. interval) 3.30 (3.50-9.36 (8.45) 3.4 (11.00 (4.00-3.52-9.50-3.S.97-5.90 (2.0) 12. 2000). 2003.07 (2..80 (7.10) 4.S. and the presence of other substances known to affect thyroid function (e. Many factors may be important in consideration of perchlorate action on the thyroid: dose.34-3.59) 3.99 (5. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.50) 6.3-14.90-9.20-4. population from the National Health and Nutrition Examination Survey.1) 8. 2006.74) 7.30) 5.60) 10.1-22.10-7.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3..50 (3. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.40 (4.10 (6.60-11.20 (2.0) 13.18-3.37 (4.33-6.0-44.4) 8.54 (3. 2005. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.58) 2.66) 3.52 (8.30 (5.33 (7.g.46-4.10) 6.70 (2.EPA.70) 2.80-3.61-5.30) 90th 9.02-4.87) 7.0) 4.50) 95th 12.0) 9.20-10.20-9.6) 12.60-5.0-17.10 (4.04-3.47) 2.4-16.29) 2.25) 5.08) 3.1 (8.09 (7..00) 3.20) 3..4) 13.40) 17.60-5. 2001.0) 12. U. nitrate.40) 3.37-13.1-13.0-19.0 (11.3) 8.26 (3.8 (11.51-4.6) 20.3 (10. 2007). NAS.60-6.61 (5.61-10.0 (11.0) 10.89 (2. 2002)..00 (2.70-4. although iodine intake was higher than U.0) 14.35 (4.81-3.60) 3.3) 12.60 (3.53 (2.S.51 (3.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.50-5. levels.80-3.91) 4. thiocyanate.93-8.0 (9.4 (10.60) 8.10 (4.6-17. 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.70-3.S.70-5. 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.80 (7..22-4.0) 11.00) 9.93-5.90-11.03 (2.15-12.25 (3.40 (3.87) 2.7 (11.98) 3.93) 3.0-14.90 (7. 2002.77 (3.60-11. 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.56-3.0 (10.0 (8.29-6. Li et al.10) 13.0-14.1 (11.12-2. 2002.24 (4.72 (3.21 (2.70) 10. Survey years 01-02 03-04 Geometric mean (95% conf.02) 3.43) 6.44) 3.87 (5..0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.89-3.40) 5.12 (6.1-14. up to 68% RUI has been demonstrated.0) 6.19-6. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.30-5.22-6. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.19-10.60-15.60-3.00 (6.60-8. 2005.90-2.0 (9.25) 5.24-2.87 (7.50) 9.5 (13.67) 5.14 (2.83 (5.50) 2.EPA.22 (2.41-9.30-10.80) Selected percentiles ( 95% confidence interval) 50th 3.42 (3.87-3.70 (4.

and environmental perchlorate exposure among residents of a Southern California community.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Jackson WA.90(2):700-706. et al. Biomonitoring studies of urinary perchlorate provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of perchlorate than levels found in the general population. thiocyanate.114(12):1865-1871. Low dose perchlorate (3 mg daily) and thyroid function.113(8):10011008. Braverman LE. Miller MD.S.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Pino S. Analysis of relative source contributions to the food chain. J Clin Endocrinol Metab 2005.. Gibbs JP.htm. Blount BC. 2005). Blount et al. most of the population is considered to be below the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Cross M. CFSAN/Office of Plant & Dairy Foods. and nitrate on thyroid function in workers exposed to perchlorate long-term. Goodman G. Pirkle JL.html and from ATSDR at: http://www. Steinmaus C. Magnani B. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.gov/safewater/ccl/perchlorate/perchlorate. Sesser DE.. Kelsh MA. J Expo Sci Environ Epidemiol 2007. et al. Primary congenital hypothyroidism. Deyhle GM. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Osterloh JD. Kirk AB.10(8):659-663. Lamm SH. Perchlorate in the United States.11(3):295. et al. Braverman LE. Available at URL: http://www. Environ Health Perspect 2002.fda. Environ Sci Technol 2006. 2001-2002. Lau EC. Pleus RC. Mauldin JP. Food and Drug Administration (FDA).110(9):927-937. Braverman LE. Thyroid 2001. newborn thyroid function.17(4):400-407.gov/toxpro2. Landingham CB. Osterloh JD. National Academy of Sciences (NAS).41(5):409-411. Perchlorate Exposure of the US Population. EPA reference dose (Blount et al. Caldwell KL. 6/2/09 Greer MA.115(9):1333-1338. 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.S.cdc. Howd R. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Abarca CR. Health Implications of Perchlorate Ingestion.EPA at: http://www.html. References Blount BC.. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. epa. population. Pirkle JL. Lamm S. Rutherford GW. Neonatal thyroxine level and perchlorate in drinking water. Environ Health Perspect 2007. He X. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Daaboul JJ. Erratum in: J Occup Environ Med 2004. et al. National Research Council of the National Academies. J Occup Environ Med 2003. Crump KS. Environ Health Perspect 2006. 2007). Li Z. 2005. Lawrence JE. Greer SE.40(21):6608-6614. 2005). Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Also. Dyke JV. Crump KS. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Barnard JC. Page Last Updated: 05/28/2009. Skeels MR.45(10):1116-1127.42(2):200-205. Doemland M. Chacon PM. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. J Occup Environ Med 2000. Valentin-Blasini L. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Benchmark calculations for perchlorate from three human cohorts. Dasgupta PK. Byrd D. Additional information about exposure and health effects is available from the U. (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. Li FX.46(5):509. Valentin-Blasini L. May 2007.atsdr. The effect of perchlorate. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Richman K. Buffler PA. Thyroid 2000. Blount BC. Pino S. Erratum in: Environ Health Perspect 2005. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Environ Health Perspect 2005. Tellez RT.S. Lamm SH. Lamm SH.113(11):A732. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Washington (DC): National Academy Press. Lawrence J. 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.

S. Environ Sci Pollut Res Int 2002.1/15/06 U.9(3):187-192. Environmental Protection Agency (U. Revised 2/11/05. Integrated Risk Information System (IRIS). 246 Fourth National Report on Human Exposure to Environmental Chemicals . Perchlorate as an environmental contaminant.gov/iris/quickview. U.S. Doc. Urbansky TF.Perchlorate pregnancy and the neonatal period.15(9):963-975. Environmental Protection Agency (U. EPA).epa. Drinking Water Contaminant Candidate List. EPA/600/F-98/002 Washington (DC). Available from URL: http://cfpub. No. Perchlorate. 1988.S. cfm?substance_nmbr=1007. EPA).S. Thyroid 2005.

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

or effects of other PFCs. 1995. approximately 4. thymus and spleen. pancreas.. may metabolize or degrade to PFOA (Dinglasan et al. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al...... C5. Unlike many organohalogen contaminant chemicals.. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. Lau et al.. 2004). U. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. Kannan et al. Tittlemier et al. Vanden Heuvel et al.8 years (Olsen et al. PFOA is mostly excreted in the urine in animal studies.5 years and for PFOS. 2004. 2003).. 1993). Taniyasu et al. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. 2005.4. 2007). The elimination half-life of PFOA in humans is roughly estimated to be 3. 2004. 2003a and 2004a). and in offspring. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. by high protein binding in plasma and other proteins. 2003. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. hepatotoxicity.. 2004. 2006a. 2002.. the 8-2 telomer. but probably include dietary sources (Kannan et al. and in human blood and semen (Calafat et al. population from the National Health and Nutrition Examination Survey. 2004. In some cases. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al.. C7).S. 2000.. which may vary for some chemicals by year and by individual sample... 2004). 2003). there is limited information on the sources.. environmental fate. 1990).. Bookstaff et al. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. The PFCs often measured in human serum are listed in the table. Survey Geometric mean (95% conf. Prevedouros et al.. in part. Keller et al.. 248 Fourth National Report on Human Exposure to Environmental Chemicals . 2007a). 2005. 2005). All sources of human exposure are uncertain. heptadecafluoro-1-decanol. 2005). human toxicokinetics.. PFOA has been reported to cause liver. 2005. 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. see Data Analysis section) for Survey year 03-04 is 0. in a wide variety of marine and land animals (Kannan et al. C6. Guruge et al. endocrine and immune effects.e. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. 2006.. and β-oxidation of lipids (Kudo et al. EPA. peroxisomal proliferation... For instance. Excepting PFOS and PFOA.. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. Olsen et al.S. growth retardation and delayed sexual maturation (Kennedy et al.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). Lau et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. but still can have long residence times in the body. kidney. environmental breakdown products of the telomers used to make fluoropolymers or the metabolic products of fluorochemicals in the body can produce PFCs that are measured human blood. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. 2005). including immunologic effects and tumor induction. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. < LOD means less than the limit of detection. Some of the effects in animals may be mediated through peroxisomal proliferation. It is unclear if environmentally degraded telomer products are a major source of other PFCs.

10) .00) . monkeys. 2003. In such studies.. PFOS.300 (<LOD-. 1999. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. and changes in thyroid hormone concentrations (Grasty et al. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11... thyroidal). 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.. 1992.600 (..500) .108 times higher than background serum levels in humans (Butenoff et al.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . 2004.500) . Kennedy et al. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. hepatotoxicity. 2001.80) 485 538 962 Limit of detection (LOD.. PFOS. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. and there was no clear evidence of excess all-cause or diseasespecific mortality. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. Olsen et al.400) . A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal... At doses causing maternal toxicity.80) 640 1454 03-04 03-04 * * < LOD < LOD . or increased cancer rates (Alexander et al.400-1. 2007).20) . Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. In comparing three separate reports on adults.400 (<LOD-. 2007a. Olsen et al..500) . 2005).900 (.10) * 03-04 03-04 * * < LOD < LOD < LOD .00) .S. 2003a). interval) Selected percentiles ( 95% confidence interval) Sample 95th .S. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. see Data Analysis section) for Survey year 03-04 is 0. possibly related to lung immaturity (Lau et al.600-2.500-1. 2004).500-1..S. PFOA.. 2003). which may vary for some chemicals by year and by individual sample. 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.500) 90th .40) .Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900 (. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.500-3. perfluorohexanesulfonate (PFHxS).50) .500-1. PFOA.. 2005).400-.500 (. the potential to estimate risks to humans from animal doses is uncertain. U.. Fei et al..700 (. 2007. Fourth National Report on Human Exposure to Environmental Chemicals 249 . reproductive. 2004).. At high but non-toxic maternal doses of PFOS.500 (<LOD-1.400-1.800) 1.400-1.3. Lau et al.600 (. Thibodeaux et al.400 (<LOD-.10) .S.400 (<LOD-. 2003a. U.10 (. However. 2007a. Cook et al.400-.300 (<LOD-.800 (. 2004a.. EPA.500-. 2007b.700) . 2004.500 (. and humans.300-1.00) . Harada et al. Olsen et al. population from the National Health and Nutrition Examination Survey. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.400-1. 2003).600 (.900 (. 2003a. 2003.500-1. EPA. development in offspring was stunted and hypothyroxinemia was observed. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 2004b).800 (. Animal studies of PFOS have demonstrated weight loss. Survey Geometric mean (95% conf. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. 2003. population. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.400-1.. 2003).800 (..00 (. 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.. elderly and children. 2007b). 2003a). developmental and teratogenic effects were demonstrated in offspring.300 (<LOD-.800 (..500) . < LOD means less than the limit of detection. 2003a.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .800) 1.

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

interval) Selected percentiles ( 95% confidence interval) Sample 95th . see Data Analysis section) for Survey year 03-04 is 1.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .300 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 251 .400) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.500 (<LOD-. < LOD means less than the limit of detection.500) 485 538 962 Limit of detection (LOD. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .0. population from the National Health and Nutrition Examination Survey.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0.S.400 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300-. 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. Survey Geometric mean (95% conf.500-.3.600 (.600) < LOD . which may vary for some chemicals by year and by individual sample.S.400 (.300 (<LOD-. < LOD means less than the limit of detection.900) < LOD . which may vary for some chemicals by year and by individual sample.400 (<LOD-.

10) 1053 1041 03-04 03-04 03-04 .00) 1.90 (4.14 (.10) 8.87-2.30-6.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.56-1. population from the National Health and Nutrition Examination Survey.689 (.40) 640 1454 03-04 03-04 1.80 (4. population from the National Health and Nutrition Examination Survey.966 (.90) 1.800 (.50) 2.60-3. Survey Geometric mean (95% conf.800-1.20-1.80-8.10-5.20 (1.05-2.80-3.70-2.70) 1.50 (1.40 (1.80-3.20 (6.70-6.700 (.90-19.40) 4.73-2.10) 75th 1.60-7.10 (.08) 2.50 (1.834-1.30) .6) 7.40-1.10) 1.50) 6.816-1.30) 03-04 03-04 .20-2.80) 3.600-.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.90-2.50 (6. 252 Fourth National Report on Human Exposure to Environmental Chemicals .30 (3.80-6.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.1.30 (7.40 (1.67-2.77-2.10) 5.60 (6.80) 4.50) 2.60-3.S.40 (1.60 (1.50 (6.00 (.80 (1.30-2.92 (1.00 (1.900 (.50 (1.900-1.01 (1.852 (.00-1.50-10.861 (.900) 1.50 (2.90 (2.40-1.00 (1.10 (1.30-12.90) 3.90) 8.90) 90th 5.10) 6.30 (2.60) 2.20) 03-04 03-04 2.50-6.40) 640 1454 03-04 03-04 2.80-12.10) 1.40 (2.00 (5.00 (2.00) 3.54) .10-9. Survey Geometric mean (95% conf.17 (1.697-1.86 (1.12) .60-2.26) 2.04) .00 (1.80) 1.30) 3.70-2.60-2.5) 8.60-8.00 (.20-1.30) 3.30 (1.30 (1. interval) .10 (4.90 (4.80 (1.80-4.72 (1.10 (4.3.20) 1.912-1.70) 2.3 (9.835-1.20 (1.70) 3.30) 3.70-5.00) 1.721-1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) 75th 3.900-1.40) 1.60 (1.20 (1.44 (2.80-2.20-1.30 (6.30 (1.90 (1.70) 1.1) 485 538 962 Limit of detection (LOD.80) 5.70) 2.50 (4.30 (2.60) 1.80-7.20) .90-10.70) 13.984 (.00-7.20) 485 538 962 Limit of detection (LOD.900-1.90) 1.20 (1.900-1.5) 5.62-2.27) 1. see Data Analysis section) for Survey year 03-04 is 0.91) 2.50 (1.20-1.70-7.700-1.10-9.70 (1.20 (6.20-3.70 (2.10) 4.80-8.S.963 (.809) 1.00-8.03) 1.40 (1.20) 2.50-3. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40-3.80) 90th 2.72) 1.826-1.0) 8. interval) 1.51) 1.90 (1.60-4.30 (1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.00-1.60-4.10) 6.10) 4.90) 1.80-7.90 (1.900-1.586-.60) 3.10 (.10 (.00-6.00) 2. see Data Analysis section) for Survey year 03-04 is 0.90 (1.00 (1.20) 1.70-10.40) .17-1.50 (4.80-4.60 (1.09 (.60) 9.42 (1.50-6.93 (1.0) 1053 1041 03-04 03-04 03-04 1.40) 2.16) .80-4.30-9.60-2.40) 1.900-1.900 (.

9) 27.10 (3.7 (35.5 (28.30-6.20-5.1) 57.2) 30.18 (3.5) 18.9-19.4 (19.2 (28.00 (5.40) 3.5 (28.70-7.1-24.50-4.5-62.90 (5.80 (7.50 (3.40-14.80 (6.3) 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.1 (19.2) 640 1454 03-04 03-04 4.50-13.20 (4.3 (35.7-23.9) 22.40) 90th 7.3 (28.9-23.07-4.47 (4.3-22.8-78.30 (3.40-10.50 (4.30 (3.99-3.70) 4.4) 640 1454 03-04 03-04 23.5-33.5-21.47-4.8-81.30-3.3) 42.2-22.5) 1053 1041 03-04 03-04 03-04 14.4. interval) 20.90-12.6 (35.1 (23.40-17.30-5.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.0-20.7-53.S.9 (19.60 (6.6) 35.0) 23.90) 6.4) 21.9 (22.0) 485 538 962 Limit of detection (LOD.00 (5. see Data Analysis section) for Survey year 03-04 is 0.30-11.0-70.6) 9.2 (18.90-4.96 (3.20) 5.2) 45.3) 41.84-3.0) 36.8-30.8 (37.60-9.6) 1053 1041 03-04 03-04 03-04 3.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.1-33.3 (44.20-9.30-8.0) 21.8-22.9 (13.80-12.S.85-4.21-3.7-69. Survey Geometric mean (95% conf.60-13.10 (3.65-4.4 (17.8-22.00) 3.10 (6.6) 7.7-49.6 (44.90-4.40-6.3) 28.20-4.4 (23.3 (17.8-22.20) 10.82) 4.20 (4.91) 3.1-35. Survey Geometric mean (95% conf.80-4.1-25.37 (2. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.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 21.0 (20.30) 6.60 (4.60-6. interval) 3.4 (28.7-30.7 (19.60) 03-04 03-04 3.0 (27.4-25.60 (3.89 (3.6 (19.70) 6.40 (4.4) 75th 30.7 (35.4-42.27) 4.0) 43.9 (17.40 (6.5) 32.70 (5.2 (19.7-33.50) 4.8 (34.70-10.10-3.0) 21.90 (7.2) 30.70 (5.80-9.7 (7.0) 90th 41.80 (5.8) 27.40) 75th 5.30) 7.2-57.70-9.5-23.5) 19.8-35.20) 7.20) 5.6 (42.9-38.6) 62.1.6-45.80) 8.60 (6.6) 18.7 (43.00 (3.8) 32.6) 42.53) 3.70-5.80 (6.10) 5. Fourth National Report on Human Exposure to Environmental Chemicals 253 .0) 03-04 03-04 19.1) 15.11 (2.90 (7.20) 4.60-14.4) 56.4 (19.5) 7.60) 8.0-16.95 (3.1 (24.4) 20.2 (27.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.9) 9.7 (13.3-61.90 (7.1-36.2 (21.8) 46.40-6.67-4.50) 7.6-24.40) 5.1-52.70-7.7 (43. population from the National Health and Nutrition Examination Survey.7) 39.5) 8.5) 57.6) 21.3 (35.5) 9.60 (5. see Data Analysis section) for Survey year 03-04 is 0.79) 4.50-6.60 (7.9) 22.20) 7.30 (5.8 (45.70) 3.4-17.0-66.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.70 (3.35) 3.2 (16.6-50.

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

10 (1.600 (<LOD-1.10 (.700) 90th 1.700 (<LOD-.10) . see Data Analysis section) for Survey year 03-04 is 0.20-1.10 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900) 1.10) 1.700 (<LOD-.00 (.900-1.30) 1.900-1. < LOD means less than the limit of detection.40) 1.600 (<LOD-1.10) .900 (<LOD-1.700 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 255 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.6.30 (1.30 (1.700) 1.00 (. which may vary for some chemicals by year and by individual sample.00 (.50 (1.900 (.10-1.700) 1. which may vary for some chemicals by year and by individual sample.400 (<LOD-1.300 (<LOD-.800) .80) 1.700 (<LOD-.900) .10) 1. population from the National Health and Nutrition Examination Survey.700 (<LOD-.300-2.600 (<LOD-.S. Survey Geometric mean (95% conf.70) 1.900-1.900-1.3.60) 640 1454 03-04 03-04 * * < LOD < LOD .50 (1.80) 1.90) .10-1. Survey Geometric mean (95% conf.00) < LOD .900-1.900) 485 538 962 Limit of detection (LOD. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700 (<LOD-.300 (<LOD-1.40) < LOD < LOD . population from the National Health and Nutrition Examination Survey.900-1.10-1.20 (1.10 (. see Data Analysis section) for Survey year 03-04 is 0.30) 1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .20) 1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .700) .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 .700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .60) 485 538 962 Limit of detection (LOD.400 (<LOD-.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .00-1.500 (<LOD-.30 (1.10) * 03-04 03-04 * * < LOD < LOD .800 (<LOD-.800) .700 (<LOD-2.900-1. < LOD means less than the limit of detection.30) .00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .10-1.600 (<LOD-1.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.600) .

Keller JM. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Kuklenyik Z.134(1):18-25.S. Chemosphere 2006b. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Sasaki S. Kumar KS. Perkins RG. Kennedy GL Jr.60(1):44-55. Arendt MD. Reidy JA. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States.68(6):465-471.38(17):4489-4495. Liu RC. Perfluorinated chemicals in selected residents of the American continent. Tully JS. Moore RW. O’Connor JC. Kawashima Y. The toxicology of perfluorooctanoate.40:21282134. Aguilar-Villalobos M. et al. Olsen GW. Seacat AM. Mandel JH. Jarnberg U. Morikawa A. Environmental and toxicity effects of perfluoroalkylated substances.60(10):722729. Environ Sci Technol 2004.115(11):1670-1676. Inoue K. et al. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Inoue K. Olsen GW. Wijeratna S. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. The influence of time.39(3):363-380. Mandel JH. Reidy JA. O’Connor JC. Fei C. Toxicol Appl Pharmacol 1990. Butenhoff JL. Yoshinaga T.179:99-121. Kuklenyik Z. et al. Katakura M.S. Occup Environ Med 2003. Yoshinaga T. Hurtt ME. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries.39(1):80-84. Hekster FM. Needham LL. Kannan K. Fillmann G. Falandysz J. Bandai N. Yamashita N. Kuklenyik Z. Calafat AM. Hurtt ME. Frame SR. Characterization of risk for general population exposure to perfluorooctanoate. Environ Sci Technol 2004. Calafat AM. Yun SH. Guruge KS. Crit Rev Toxicol 2004. Cook JC. et al.39(23):9101-9108. Dinglasan MJ. Biegel LB. J Environ Monit 2005. Needham LL. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Koizumi A. Kudo N.1968--2003. Rev Environ Contam Toxicol 2003. Bignert A. Birth Defects Res B Dev Reprod Toxicol 2003. Suzuki E. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Herbstman JB. Toxicol Sci 2001. Ingall GB. Kamiyama S. Environ Sci Technol 2006a. Caudill SP. Reidy JA. Apelberg BJ. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. in vivo. Holmstrom KE. Saito N. Watanabe T. Chem Biol Interact 2000. Calafat AM. Toxicol Appl Pharmacol 1992. Burris JM. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Olsen J. Taniyasu S. Tully JS. Ye Y. Frame SR. Polyfluoroalkyl chemicals in the U. Environ Sci Technol 2007a. Environ Health Perspect. et al. Calafat AM.115(11):1677-1682. Halden RU. Chlorinated. et al. Kuklenyik Z. Lau CS. Grasty RC.46(2):141-147.124(2):119-132. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Mandel JS.Perfluorochemicals References Alexander BH. Caudill SP. Day RD. Needham LL. Corsolini S. Murray SM. Kannan K. and ex vivo studies. Environ Health Perspect 2007. Toxicol Appl Pharmacol 1995. Biegel LB. Environ Health Perspect 2007. Rogers JM. McLaughlin JK. Tarone RE. Environ Sci Technol 2005. Saito N. Mabury SA. J Occup Health 2004.99(2):253-261. Butenhoff JL.Koizumi A. Kannan K. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility.7(4):371-377. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Peterson RE. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000.115(11):1596-1602. Harada K. Environ Sci Technol 2005. Taniyasu S. Androgenic deficiency in male rats treated with perfluorodecanoic acid. de Voogt P. Evans TJ. Reidy JA. brominated. Fluorotelomer alcohol biodegradation yields poly. Calafat AM. Wong LY. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort.and perfluorinated acids.38(10):2857-2864. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Needham LL. Laane RW. Environ Sci Technol 2005. Gaylor DW.63:490496. Olsen GW. Mohotti KM.39(23):9057-9063. Loganathan BG. 2007b. Edwards EA.104(2):322-333. Cook JC.113(2):209-217. Environ Res 2005. and perfluorinated contaminants in livers of polar bears from Alaska.34(4):351-384. Moore JA. Hurtt ME. Witter FR. Yamashita N. et al. Bookstaff RC. Seneviratne HR. Regul Toxicol Pharmacol 2004. Grey BE. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Harada K.41:2237-2242. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Rodricks J. Cook JC. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.

Toxicol Sci 2002. Froehlich JW. Gamo T.37(12):2634-2639. Peterson RE. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Olsen GW. Burris JM. Butenhoff JL. Biochim Biophys Acta 1993. Rogers JM. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. EPA). Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Lundberg JK.Perfluorochemicals Kudo N.111(16):1892-1901. Lau C. 2003a. fish. Prevedouros K. I: maternal and prenatal evaluations. Olsen GW. U. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Hansen KJ. Hansen KJ. Taniyasu S. Thomford PJ. Butenhoff JL. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Butenhoff JL. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors.gov/opptintr/pfoa/pfoara. Thibodeaux JR. Burris JM.epa. Environ Health Perspect. Pepper K. J Children’s Health 2004b. Lau C.45(3):260-270. Horii Y. Available from URL: http://www. Hansen KJ. van Belle G. Environ Sci Technol 2003. Hanari N. Yamashita N. J Occup Environ Med 1999.82(1):359. Larson EB. birds. 2007a. Kannan K. et al. Nesbit DJ. Environ Health Perspect 2003a. and perfluorooctanoate in retired fluorochemical production workers.115(9):1298-1305. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Half-life of serum elimination of perfluoroo ctanesulfonate. and food items prepared in their packaging. Ellefson ME. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. et al. Rogers JM. Kawashima Y. Ehresman DJ. Olsen GW. Seymour C. Olsen GW. Mair DC. Olsen GW. Hansen KJ. Petrick G. Lundberg JK. Fourth National Report on Human Exposure to Environmental Chemicals 257 .51(8-12):658-668.68(1):249-264. Butenhoff JL.41(9):799-806. Mandel JH. Biol Pharm Bull 2003. Grey BE. Olsen GW. Taniyasu S. Bronson R. (Erratum in: Environ Health Perspect. Korzeniowski SH. Richards JH. Helzlsouer KJ. Buck RC. Olsen GW. Hanson RG.S. A global survey of perfluorinated acids in oceans. J Ag Food Chem 2007. Mandel JH. 2003. Rogers JM. Washington. Butenhoff JL. Case MT.) Tittlemier SA. Church TR. Olsen GW. Seacat AM. Zobel LR. fate and transport of perfluorocarboxylates.2(1):53-76. Huang HY.111(16):1900) Olsen GW. Moisey J. Yamashita N. Mandel JH.54(11):1599-1611. Chemosphere 2007b. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Seacat AM.198(2):231-241. Church TR. Barbee BD. Toxicol Sci 2003.26(1):47-51. htm. Church TR. perfluorooctanoate andother fluorochemicals in human blood. Burris JM.68:105–111. Cousins IT. fish. II: postnatal evaluation. Sources.74(2):369-381. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. 1/15/06 Vanden Heuvel JP. (Erratum in: Toxicol Sci 2004. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. et al. et al. Kannan K. Environ Sci Technol 2006.perfluorohexanesulfonate. et al. Stanton ME. Hanson RG.55:3203-3210. Mar Pollut Bull 2005. Environ Health Perspect 2005. Butenhoff JL. Cao XL et al.. Coordinate induction of acyl-CoA binding protein. Burris JM. Miller JP. Sterchele PF. Reagen WK. Burris JM. fast foods. Grey BE. Horii Y. Historical comparison of perfluorooctanesulfonate.74(2):382-392. The developmental toxicity of perfluoroalkyl acids and their derivatives. Mandel JH. et al. Environmental Protection Agency (U. J Occup Environ Med 2003b.1177(2):183-190.113(5):539-545.S. Chemosphere 2004a.40(1):32-44. Toxicol Appl Pharmacol 2004. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Burlew MM. Hansen KJ. Toxicol Sci 2003. and humans from Japan. Thibodeaux JR. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Ehresman DJ.

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. inhalation. 1985. to a lesser extent. 1982. blood product storage bags. corresponding monoester metabolites.. Pan et al. 2001). Various phthalate esters have been measured in specific foods. followed by inhaling indoor air. vinyl tiles and flooring. lubricating oils. For the general population. Phthalates are metabolized and excreted quickly and do not accumulate in the body (Anderson et al. Human milk can be a source of phthalate exposure for nursing infants (Calafat et al. intravenous medical tubing. and toys (ATSDR. Human health effects from phthalates at low environmental doses or at biomonitored levels from low environmental exposures are unknown. in humans. 2002). excreted in urine largely as glucuronide conjugates (Albro et al. Dirven et al. 2000. Okubo et al. water sources. and teratogenicity. Infants may have relatively greater exposures from ingesting indoor dust containing some phthalates (Clark et al. fragrances. Absorbed monoester metabolites are usually oxidized in the body and. inflatable recreational toys. 2001.. 1998). and sediments (Clark et al. lotions. such as plastic bags.. Phthalates have low acute animal toxicity. Mortensen et al. but in vivo studies did not support phthalates having estrogenic effects (Milligan et al. 2005).. several of the phthalates produced testicular injury. indoor and ambient air. Phthalates are often used in polyvinyl chloride type plastics. and nail polish. Nielsen et al. In chronic rodent studies. automotive plastics.. some medical devices and pharmaceuticals... and other oxidized metabolites included in this Report. Albro and Lavenhar. 1985. In vitro studies showed that certain phthalates can bind to estrogen receptors and may have weak estrogenic or anti-estrogenic activity (Coldham et al... urinary metabolite and air phthalate concentrations are roughly correlated (Liss et al. shampoo. Parks et al. but these effects either have not been demonstrated when tested in non-human primates or are yet to be studied. detergents. Zacharewski et al. such as soap. 1995). and personal-care products. There are numerous products that contain phthalates: adhesives. dietary sources have been considered as the major exposure route. Harris et al.. 1997. not all phthalates Phthalates and Urinary Metabolites in this Report Phthalate name (CAS number) Benzylbutyl phthalate (85-68-7) Dibutyl phthalates (84-74-2) Dicyclohexyl phthalate (84-61-7) Diethyl phthalate (84-66-2) Di-2-ethylhexyl phthalate (117-81-7) Abbreviation BzBP DBP DCHP DEP DEHP Urinary metabolite (CAS number) Mono-benzyl phthalate (2528-16-7) (some mono-n-butyl phthalate) Mono-isobutyl phthalate Mono-n-butyl phthalate (131-70-4) Mono-cyclohexyl phthalate (7517-36-4) Mono-ethyl phthalate (2306-33-4) Mono-2-ethylhexyl phthalate (4376-20-9) Mono-(2-ethyl-5-hydroxyhexyl) phthalate Mono-(2-ethyl-5-oxohexyl) phthalate Mono-(2-ethyl-5-carboxypentyl) phthalate (40809-41-4) Mono-isononyl phthalate Mono-methyl phthalate (4376-18-5) Mono-(3-carboxypropyl) phthalate Mono-n-octyl phthalate (5393-19-1) Abbreviation MBzP MiBP MnBP MCHP MEP MEHP MEHHP MEOHP MECPP MiNP MMP MCPP MOP Di-isononyl phthalate (28553-12-0) Dimethyl phthalate (131-11-3) Di-n-octyl phthalate (117-84-0) DiNP DMP DOP 258 Fourth National Report on Human Exposure to Environmental Chemicals . Phthalates are also used as solubilizing and stabilizing agents in other applications. solvents. however. 1993). 2004. Ingested phthalate diesters are initially hydrolyzed in the intestine to the corresponding monoesters. hair spray. The intravenous or parenteral exposure route can be important in patients undergoing medical procedures involving devices or materials containing phthalates. indoor dust. which are then absorbed (Albro et al. Jobling et al.. and. deodorants. 2003). In settings where workers may be exposed to higher air phthalate concentrations than the general population. dermal contact with products that contain phthalates.. phthalates can be released into the environment during use or disposal of the product.. The table shows the phthalate diesters. 2003). 2003.. 1997.. 1989). 2006). liver cancer. People are exposed through ingestion.. garden hoses. plastic raincoats.. liver injury.. Because they are not chemically bound to the plastics to which they are added. 1998. 1982.

gov/toxpro2. Kessler et al. Available at URL: http://www. Pharmacokinetics.. Matthews HB. Rhodes et al. References Agency for Toxic Substances and Disease Registry (ATSDR). 2006). 2004).. NTP-CERHR. Castle L. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Coldham NG. Also. 2007). Drug Metab Rev 1989.nih. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. pp.45:19-25. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. Slakman AR. Population estimates of concentrations of specific phthalate metabolites may differ by age. Environ Health Perspect 1997. 2002). A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Schroeder JL. Springall C. Herbert AR. 2007. 1985. Cousins IT. van der Broek PH. Anderson WA. 2001. 2002). 1986). Hauser et al. Mackay D. Lovekamp-Swan and Davis. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels.. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Clark K.. which may be a pathway to the development of liver toxicity and cancers in these animals. Environ Health Perspect 1982.. 2004. Connor C.e.gov/toxprofiles/ tp135. 4/20/09 Albro PW. Dave M. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 227-262. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. 2001. Peck and Albro. and Sertoli cell abnormalities in the male animals and. Information about external exposure (i. 2004. reducing estrogen production... J Chromatogr B 2004. Toxicological profile for di-n-butyl phthalate update [online]. 1982. 2003. Hoppin et al. variation also occurs in the same person during repetitive monitoring (Fromme et al. 2001).html.atsdr. dibutyl phthalate (DBP). 1982). Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. Silvapathasundaram S. 2000a..html. Springer. 2000c. phthalates have been shown to induce peroxisomal proliferation in rodents. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Metabolism of di(2-ethylhexyl) phthalate. Available at URL: http://www. However. Jongeneelen FJ. Scotter MJ. 2005). McDonnell DP..3.21:13-34. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 2000b.html). at very high levels. Food Addit Contam 2001.atsdr. 2004. but there are known species-related differences in the hydrolysis of diester phthalates. These differences may contribute to species-specific differences in toxicity (ATSDR. and race/ethnicity (Silva et al.cdc.. Corbett JT. 2003. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . and extent of metabolite conjugation to glucuronide (Albro et al. Sauer MJ.gov/ reports/index... phthalates produced anti-androgenic effects by reducing testosterone production and. Jordan S. In animals. testicular atrophy. 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. Silva MJ.. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Albro PW and Lavenhar SR. at higher doses..805:49-56.cdc. McKee et al. Dirven HA. ovarian abnormalities in the female animals (Jarfelt et al. In Staples CA (ed).html.cdc. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. 105:734-742. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Calafat AM.. Hauser et al. 2005.18(12):10681074. efficiency of intestinal absorption. Part Q: Phthalate Esters. The Handbook of Environmental Chemistry. 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.gov/ toxprofiles/tp9. 2006). 2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Vol. gender. 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. Evaluation of a recombinant yeast cell estrogen screening assay. atsdr. Assessment of critical exposure pathways. Massey RC. High doses of di2-ethylhexyl phthalate (DEHP). 2004.niehs.Phthalates and metabolites have been tested.. interactions with macromolecules and species differences in metabolism of DEHP.New York. Needham LL.

Research Triangle Park (NC).niehs. Koch HM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Skerfving S. consumer milk. Filser J.25(2):293-302.niehs. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.gov/chemicals/dehp/dehp-eval. Park S. Kessler W. Int J Hyg Environ Health 2007.Phthalates in human urine samples. Hoppin JA. Jarfelt K. Jacobsen H. Liss GM. Meeker JD. 2006 [online].gov/chemicals/ phthalates/dbp/dbp-eval. Reynolds T.niehs. Akesson B. Hass U.105:802-811. Int Arch Occup Environ Health 1993. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). et al.18(1):122. Environ Health Perspect 2002. Research Triangle Park (NC). David RM. Hagmar L. et al.nih. Kalita JC. 6/2/09 NTP-CERHR. Sumpter JP. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Am Ind Hyg Assoc J 1985. 2000b [online]. Hanaoka T. Hartle RW. Duty S. Available at URL: http://cerhr. Balasubramanian AV. Sumpter JP. Toxicol Appl Pharmacol 2004. Jonsson BAG. Singh NP. Mortensen GK. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Milligan SR.110(5):515-518.niehs. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Stringer WT. Numtip W.106(1):23-26. Parker MG. Ryan L. Meeker JD. J Androl 2004. Harris CA. Environ Health Perspect 2004.nih. Brock JW. Yokoyama Y.nih.46(11):643-647. Kano K.nih. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). 2000c [online]. Duty SM. Leffers H. Research Triangle Park (NC). Skakkebaek NE. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate.26(8):1219-24. Reprod Toxicol 2004. Ladefoged O. Scand J Work Environ Health 1985. Reprod Toxicol 2005.112(17):1740]. Lovekamp-Swan T. Reproducibility of urinary phthalate metabolites in first morning urine samples. Available at URL: http://cerhr. Kano I. Drexler H.382:10841092.103:582-587. Pan G.html. Environ Health Perspect 1995. Davis BJ. Baird DD. and infant formula by tandem mass spectrometry (LC-MS-MS). Andersson A-M. Determination of phthalate monoesters in human milk. Davis BJ. Hum Reprod 2007. Available at URL: http://cerhr. et al.22(3):688-695. Tsukino H. 6/2/09 NTP-CERHR.112(17):1734-1740. McKee RH. Nielsen J. 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 . Dalgaard M.64(8):555-560. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Mechanisms of phthalate ester toxicity in the female reproductive system. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Brock JW. Fromme H. Available at URL: http://cerhr. 6/2/09 NTP-CERHR. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hauser R. White R. Butala JH. Gans G.11(5):381-387. Silva MJ. 6/2/09 Okubo T. Borch J. Suzuki T. Henttu P.195:142-153. Jobling S.210:21-33. et al.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. 2000a [online]. Environ Health Perspect 2003. Boehmer S. Park MG. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Wang P. Zhang S. Richthoff J. Bolte G. Calafat AM. NTP-CERHR. Calafat AM.16(4):487-493. Research Triangle Park (NC). Biol Pharm Bull 2003. Anal Bioanal Chem 2005.19(4):505-515. Environ Health Perspect 1997. Grote K. Yoshimura M. Hauser R. Ryan L. Main KM. Rylander L. Csanády G.html. gov/chemicals/dehp/dehp-eval. Angerer J. Silva MJ. Silva MJ. Epidemiol 2005.html. Environ Health Perspect 1998. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Chahoud I. Occurrence and daily variation of phthalate metabolites in the urine of an adult population.html. Albro PW. Giwercman A. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Chen Z. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.111(2):139-145. The estrogenic activity of phthalate esters in vitro.

Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Toxicol Sci 2000. 112(5):A270]. Environ Health Perspect 2006. Caudill SP. Peck CC. Ostby JS. Pratt IA. Barr DB. Abbott BD. Reidy JA. Toxicol Sci 1998. Albro PW. Urinary levels of seven phthalate metabolites in the U. et al. Zacharewski TR. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Fielden MR. Cunningham ML. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. et al. Barlow NJ. Clemons JH.36:459-479. Wu ZF. Parks LG. Crit Rev Toxicol 2006. Peters JM. et al.46:282-293.114(11):1643-1648.45:11-17.58:339349.Phthalates phthalate (DEHP): a cross-sectional study in China. Silva MJ. Batten PL. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Hodge CC. Meek MD. Matthews JB. Jackson SJ. Lambright CR. Environ Health Perspect 2004.65:299-308.112(3):331-338. Environ Health Perspect 1986. Orton TC. Malek NA. Bratt H.S. Environ Health Perspect 1982. Rusyn I. Rhodes C. Klinefelter GR.

1 (58.4) 71.9-62.9) 14.1-38.8) 24.6) 14.3 (12.0 (33.3-74.6) 16.2-17.5-145) 138 (106-241) 143 (127-179) 120 (99.7) 38.3) 23.7-35.8 (10.1 (10.8) 14.5 (13.9-47. 0.3) 54.9 (13.5 (57.5-94. including MBzP.2-20. BzBP can be released into the environment during its production and. some personal care products.5 (66. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.9 (16.6-17.1) 14.4 (29. interval) 15.0-26.8-17.7-58.8-18.9) 13.5-33.4 (63.4) 81.0 (55.2) 14.6-150) 94.7 (13. Food crops take up BzBP.3) 13.3) 37.3-27.1) 13.1 (14.9 (39.4 (13.7 (53.0 (34. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.6) 24.4-16.0) 23.3 (54.0-106) 58.3 (13.3-130) 122 (88. it can be released into the ambient air during use or disposal of the products.9 (70.8) 33.4 (53.5-14.4 (32.8-41.8 (80.7-15.4) 35.0 (23.8-72.7-172) 103 (74.1) 31.3-21.4 (27.6) 37.8 (14.9-49. particularly male animals (McKee et al.7-16.2-19.2) 14.1) 76.2-40.3-88.6 (32.4-25.2) 69.0 (27.7-119) 99.3.3-18.9-30. NTPCERHR.Phthalates Benzylbutyl Phthalate CAS No.8 (28.7) 23.1-18.1) 12.4-120) 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. 2000). and 03-04 are 0.4-127) 80.8-17.4 (53. sealants.6) 14.8-76.5) 16.6 (41.0) 32.9-190) 86.7-16.2 (25.5 (67.9 (21.6-38.6) 25.6-29.8-48.4) 12.2) 22.7-16.8-16.7-13.4 (10.5) 27.8 (71.2) 78.0) 70.6-92.4) 75th 35..1-35.3 (30.6-72.7-170) 169 (134-198) 152 (99.4 (68.6-132) 103 (84.2-155) 91.3-75.8 (30.8-133) 89.2) 32.5-36.3-34. respectively..0) 16.1) 29.7 (82.6 (66.6 (12.6 (13.0 (14.7 (51.1-16.5 (47.9) 14.6 (21.7 (70.2-31.1-61.4 (59.9-87. 2001-2002.3-82.1) 68.0 (12.8-121) 79.2-16.6) 50.8-64.7-14.5-84.6 (13. car care products. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (15.0-85.7-82.8 (53.3-12.8 (71. see Data Analysis section) for Survey years 99-00.0) 24.4) 108 (96.6-116) 122 (102-142) 101 (85.9-28.4 (31.6 (53. High dose BzBP and its monoester metabolites.8.6) 95th 103 (94.9) 15.3-161) 99.2) 15.0 (30.4-62.6 (13.8-35.9-14.7) 40.0 (26.4 (48.4) 51. and 2003-2004 were generally similar those reported in U.1-116) 122 (93.0 (20.2 (10.8 (21.5-36.2 (14.1 (55.6) 35.3 (12.4-92.4) 35.1-16. and to a lesser extent.2 (43.6 (13.2-183) 101 (78.2-115) 113 (91.6) 63.3 (33.9 (12.1 (13.8 (38.4-24.4) 49.1 (14.5 (61.1-120) 52. 01-02.2-116) 122 (102-143) 101 (84.9) 11.9 (11.3-18.5-41.2) 17.0) 34. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.2 (19.8-14.3-125) Total 15.8-13.9) 43. 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.5-97. 2000).2 (11.7-17.1) 67.2) 66.3 (44.3 (29.0 (43.9) 49.1 (32.7-25.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.0) 33.1) Selected percentiles ( 95% confidence interval) 50th 17. 2004.0 (15.6) 13.3 (29.4-15.1-90.2-38.8) 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 16.1 (13.3-91.2) 13. and diet is the major source for general population exposure.7 (80.3-43.1.1 (20.5-35.S. can produce developmental and reproductive toxicity in rodents.0) 90th 67.6-18.8-14.5) 65.1-15.9 (12.5 (27.5) 15.7 (11.3) 15.9) 12.2-16.5-25.4 (32.8 (12. because it is not bound to products in which it is incorporated.3) 94.6-79.3 (12.4) 80.4) 14.9-27.1-15.2 (19.5) 15.7 (12.6) 67. vinyl tile.0-55.6-43.1-214) 166 (116-191) 145 (110-213) 88.0 (11.6) 15.1-39.5-40.1) 32.2) 33.2-39.6-39.5) 55.8 (50.5 (76.3) 13.5 (26. 262 Fourth National Report on Human Exposure to Environmental Chemicals .0 (30.9 (22.5 (55.2) 12.8) 63.0 (15. population from the National Health and Nutrition Examination Survey.3) 63. IARC considers BzBP not classifiable with respect to human carcinogenicity.8-16.9-16.4) 98.0) 20.1-43.9 (28.8-98.9) 18.S.8) 28.1 (19.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5) 23.3 (22.5) 82.4) 129 (98.4 (10.6) 13. and 0.5-18.4) 33.2-33.0-130) 101 (86.6) 35.6-92. residents (Blount et al.4) 38.5-62.4) 65.5) 30.6) 29.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.2 (47.8 (86.

9-104) 62.0-51.6) 53.7) 25.9) 11.6-12.0 (67.3) 21.6-47.6 (36.8) 24.7-20.7 (54.6-13. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.1 (21.9 (15.9 (12.7 (18.8) 33.5) 46.5-16.8 (46.1 (21.7 (38.9-14.1 (18.5) 14.4-19.4) 50.4 (69.6) 12.6 (14. Hoppin et al.9-40.1-29.5-26. 2007).1 (21.8) 68.2-12.6) 58. 2002)..Phthalates York City (Adibi et al.8) 71.0 (10.3) 55.1-14.0 (12.4) 15.4) 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 12.2 (69.8) 13.7) 11.4-15.4-27.7-29.3-73.9 (9.4) 51.7 (13. and females compared to males (Silva et al.1 (13.1 (14.9 (54.3-34.8) 54.9 (39.0 (41.8 (49.0) 15.1 (11.2-17.8) 26.5-26.0-53.4 (21.5-29.8) 11.9) 12.1 (41..0) Selected percentiles ( 95% confidence interval) 50th 13.8-13.4 (12.7-14.2-13.7 (11.7 (55.4 (33.8-34.1 (15.1-12.5-58.7 (23.1-125) 86.8) 15.1 (23.5 (9.1 (53.8) 33.5 (56.6) 13.1 (46.5-213) 49.6) 30.2) 12.9 (24.8-39.2-49.7) 38.4-42.7) 19.6) 75th 25.6-15. in men attending a Boston infertility clinic (Duty et al.6 (30.4-99. 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.8-42..4-23.8-69.3) 13.4-142) 134 (116-176) 136 (85.4-14.2-78.4 (25..8-13..9-13.3 (15.7-56.9-28.7 (12.5) 41.5-42.5) 17.4-93.6-99.5 (10.7-61.3) 90.8-14.3) 16.3 (12.2) 32.3 (23.9 (15.0 (13.3) 13.2) 15.6 (24.4-102) 70.2-13.0) 11.0) 24.0 (33.8) 56.0 (38.2-15.3-38.5) 13.7-31.9 (55.3) 12. 2004). the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.S.0) 13.3) 73.5 (12. 2007).1) 142 (99.1) 27.9) 100 (80.4) 104 (89.6) 25.3) 14.69-11.6 (11.9-23.6 (15.8) 53.1-120) 77..95-14.9 (10.3) 18.2-51.4 (11.3-16.3 (13.9) 64.4) 60.4) 13.2-117) 95.4 (60.4 (10.8) 80.5) 20.4) 21.4-116) 73. A small study of African-American women in Washington.8-14.4 (11.6 (34.3 (35.9 (12.1 (25.7 (21.2 (40.5 (49. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-76..7-123) 77.5) 78.3-64.4 (11.6 (19.8) 34.0 (62.7) 46.3) 67.5 (10.8 (30.73-12.5-57.4-18.1 (19.2) 11.1 (34.8-15.8 (10.9) 52.9-13.7 (14.7) 56.4-14.5 (11.2 (56.1) 80.1 (13. Weuve et al.0-27.4-79.4) 44.8) 53.8-173) 195 (121-305) 229 (99.2-57.2) 11.9) 12.0-26.9) 24.3) 14.8-15.5-13.5-61.8 (12.9-69.7-14.3) 29.0 (41.8) 46. 2003).8 (64. 2002.9 (10.8-85.0-15.4) 28.9-16.7-12.7 (11.9 (43.5-58.5-38.6-20.0 (49.9) Total 14.4) 13.7-20.2-15.0) 49.5-79.4 (34.4 (63.1) 12.4 (26.9-83.2 (41.5 (42.5-99.8-27.1 (21..9 (22.5-31.. In NHANES 1999-2000. population from the National Health and Nutrition Examination Survey.9 (29.2) 26.6) 73.9) 42.5-23.5) 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 .6 (11.7-19. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6-81. and in a small sample of German residents (Koch et al.8-64.2 (27.6-26.8-60.6-116) 74. adolescents compared with adults. 2004. interval) 14.8) 108 (75.1-79.8 (50.2) 11.7-15. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.8-80.0-48.9-62.3 (38.8 (57.2) 67.7 (19.7) 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 40.4 (74.7-69.0) 24.4 (13.7 (59.1-27..1) 39.4-17.3) 89.7-90.5 (35.4) 25.8-48.9 (24.7-15.6 (22.0-90.9) 11.7 (11. Hauser et al.5) 95th 77.1) 24.2-21.0 (11.7 (13.8 (11.4) 17. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.4) 12.6 (51.5) 16.1) 23.9-115) 57. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3 (60.0) 60.6 (30.8) 16.3) 37.6-40.5) 10.1-35.1) 24.3 (24.4 (46.0-109) 65.6) 12.1 (43.4) 14.6 (57.1 (9. In an annual sample of German university students.8 (13. in young Swedish men (Jonsson et al.6-86.0 (12.9) 12.1-12.1-58.8-16. 2005.5) 23.6 (11.3-11.1) 17.3 (39.4-60.3) 13.0) 12. 2005). DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC. 2006).1) 35.2-26.4) 90th 50.7-19.8-13.5 (48.3) 36.6) 38.8 (69.9 (51. 2003).4-90.7-397) 70.2) 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.

Reidy JA.Phthalates References Adibi JJ. NTP-CERHR. Brock JW. Int J Hyg Environ Health 2007. Sanchez GN. Green RA.16(4):487-493. Wiesmuller GA.114(9):1424-1431. Levels of seven urinary phthalate metabolites in a human reference population. Research Triangle Park (NC). Urinary levels of seven phthalate metabolites in the U. Caudill SP. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Epidemiol 2005. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. et al. Reprod Toxicol 2004. Environ Res 2003. Jonsson BAG.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Environ Health Perspect 2003. Jedrychowski W. et al. Gans G. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Silva MJ. Brock JW. et al. Blount BC. Duty S. Environ Health Perspect 2002. Hauser R. 264 Fourth National Report on Human Exposure to Environmental Chemicals .html. Wittassek M. J Androl 2004. Ryan L. Jacek R. Environ Health Perspect 2004. Hilborn ED. Barr DB. Environ Health Perspect 2006. Helm D. Hodge CC. Centers for Disease Control and Prevention (CDC). Needham LL. Sampson EJ. Dobler L. Caudill SP. Weuve J. Perera FP. Brock JW.93:177-185. Koch HM. et al. Giwercman A. McKee RH.108(10):979-982. Calafat AM.25(2):293-302. et al. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Koch HM. Silva MJ.111(14):1719-1722. Environ Health Perspect 2000. Meeker JD. et al.68:309-314. Needham LL. Barr D. Caudill SP. Richthoff J. Duty SM.110(5):515-518. Atlanta (GA). Chen Z. Baird DD. Available at URL: http://cerhr. Hu H. Silva MJ. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.S. Poland. Prenatal exposures to phthalates among women in New York City and Krakow. et al. Drexler H. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. 2005. 4/20/09 Silva MJ. Eckard R.22(3):688-695. Camann DE. Calafat AM. Hagmar L.112(3):331-338. Bull Environ Contam Toxicol 2002. Phthalate monoesters levels in the urine of young children. Third National Report on Human Exposure to Environmental Chemicals. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Malek NA. Rylander L. David RM. Ryan L. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. 2000 [online]. Silva MJ.210(3-4):319-333. Reproducibility of urinary phthalate metabolites in first morning urine samples. Hum Reprod 2007. Rossbach B.niehs.nih. Angerer J. Singh NP. Schettler T. Hoppin JA. Pirkle JL. Davis BJ. Butala JH.18(1):122. 112(5):A270].

46-5.9) 15.97) 4.80 (5.40 (2.50) 8.90-2.80 (5. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.37) 6.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.7) 15.40-3. and insecticides.30-3.60 (5.6 (11.6 (10.6 (9.S. When total DBP metabolites have been measured.30 (1.0 (13.10 (4. mostly as MnBP (Anderson et al. Survey Geometric mean (95% conf.30-2.10) 3..3) 18. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.55) 2.7 (9.3 (11.70 (5.50-2.70-4.3.6) 17.50-10..80) 75th 5.40-9.9-23.46 (2. 2003).66) 2.10) 11.6) 12.5 (27. 2003).50) 18.30) 5.10) 9. in a small sample of pregnant women in New York City (Adibi et al.3 (13.2-33.50) 5.19-3.2 (8.73 (2.5-16.70-4.0) 20.3 (13.6-26. 2005). People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine. interval) 2.90 (4.80 (2.20 (7.00 (5.1) 25.96) 3. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.2-14.10) 2.90) 12.00-6. 2000).85-6. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.80-5.0 (11.60 (2.3 (16.6) 16.40-4.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.20-9.0) 24. Biomonitoring Information Median concentrations reported in the NHANES 19992000.55 (3.S. Following oral administration of DBP to humans.10-2.80-5.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.1-17.50-4.4) 5.90 (3.81 (3. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.46) 2.02) 4.7 (16.30 (4.30-11.28-5.17 (2.00-4.4 (20.9 (16. about 65% to 80% of a dose is eliminated in urine within 24 hours.2 (12.4 (14.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.20) 4.1-25.. and also in some printing inks.0) 9.30) 10.97) 2.3) 33.70) 5.6 (14. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.30) 10..8 (9.7) 4.90-4..22 (3.7-31. Koch et al.30) 2.0) 12.17) 4.80 (3.50) 2.5-24. residents (Blount et al.0 and 0. 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.20-12.3 (18.40 (3.7) 7.40-4.00-6.82-3. 84-74-2 Di-isobutyl Phthalate CAS No.1) 16.00-11.7-18.40 (2.56 (5.26 (2.40-12.6) 16.22) 3.68 (2.71 (2.60 (8.56) 3.6) 17.3) 3.3-30.56 (3.50-6.5-29.8) 21.7 (17.30-13.60-6.5) 18.7) 18.59) 3.7 (7.60) 3. 2001).9 (16.3-20.70 (2. Hauser et al.44-2.3-43.20 (6.0 (19.2-22..46 (3.40 (7.00) 7.48 (2.24-8. Fourth National Report on Human Exposure to Environmental Chemicals 265 . 2004. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.70) 3.9) 10.20-12.3 (16.84) 4.6 (13.40 (6.2 (11.6 (14.0-25.7-31.50) 90th 12. CDC.00) 4.5 (11.3-48.30) 6. population from the National Health and Nutrition Examination Survey.30-6.4) 12.5-16.10-9. and in a small sample of Japanese adults (Itoh et al.10) 8..4-12. DBP can produce reproductive toxicity in male rodents (McKee et al.1 (13.8) 40.5) 19.90 (4.0 (13.6) 26.9-14.90 (6.0-14..3 (19.6-18. see Data Analysis section) for Survey years 01-02 and 03-04 are 1. In addition.63) 3. OSHA has established a workplace air standard for external exposure to DBP.90-4.40-17.7 (17.50) 7.2) 5.33 (2.91) 4.70-8.5) 25.80 (2.6-14. 2007).00-9.5) 18. NTP-CERHR.5 (17. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.6) 10. 2004.1-20.8) 677 652 703 699 1216 1088 Limit of detection (LOD.3-24.4) 22.0-18..30-7.00) 4.6 (29. pharmaceutical coatings.43) 6.0-38.6 (13.90-7.49-2.00) 10.7 (18.5 (20.7) 14.5) 23.56-4.20) 7.5) 14. 2005. Studies of children found age-related differences in urine MBP levels.1) 22.6-20.97-7.10-9.00) 6.7-20.5) 12. 2005).Phthalates Di-n-butyl Phthalate CAS No. they have been referred to as monobutyl phthalate (MBP).72-3.5 (10.1-12.40-5.10 (3.07 (3.40) 5.60 (4.50 (3.5) 22.1 (8.0) 13.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.73-5.6 (10. 2005). NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.67 (5.3-18.10 (4.4-27.3-19.30 (3.6-34.50 (6.20 (3.30-6.20-2.11-3. 2000.00 (7. in men attending a Boston infertility clinic (Duty et al.20-6.40-3.

69) 6.29-8.81) 4. 2004).1) 15.2) 24.65-4.17 (2.6) 13.0) 3.17) 90th 8.33-9.42) 2.92 (7.94-12..64-10.03-7.6-19. 2007).68) 5.30 (6.6) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.61-3.09-2.44 (3.51) 5.38-10.4 (12.22 (2.58-4.20-3.76-3.18 (1.81 (6.34 (3. Weuve et al.7 (13.76 (3.9) 12.8 (9.0 (10.20-4.86-4.03-11.9-40.46-11.1-15.52 (2.07-5.13-6.28 (4.0 (8.18-4.18) 4.04) 7. than adults in NHANES subsamples during the same time period.68 (2.21 (5.78-8. interval) 2. respectively. 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..37) 3. Biomonitoring studies on levels of MnBP and MiBP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of dibutyl phthalates than are found in the general population.69) 4.76-15. 2006).1) 7.80) 7.89) 6.32 (7.75 (4.75 (6.56-15.02-10.46) 3.20 (2.15) 3. 2004).31 (7.31 (2.3) 18.28-13.94 (5.11 (5. population from the National Health and Nutrition Examination Survey.96 (3.78) 9.2 (10.57-4.6 (10.7) 19.53-4.66 (8.85 (2. In an analysis of NHANES 1999-2000.99) 7.0-18.00-3.02 (7.21) 10..56) 5.3 (17.79 (4.5-19.3) 13.89-5.2) 8.78) 8.72) 5.1 (10. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.01-2.79-6. Between 1998 and 2003.31) 2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .57 (3.62-12. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.33 (3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.15-4. samples from German university students had consistently higher median urine levels of MnBP and MiBP.24) 3.18) 3.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.64-7.66) 4.97-2.9 (15.95) 10.5 (9. Over this time.93-6.84 (8.25) 5.0) 11.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.1 (11.1) 4.3 (13.26-2.14 (4. the students’ median values for MiBP levels remained relatively unchanged.74 (4.17-12.80 (3.36-7.4) 7. 2007). Survey Geometric mean (95% conf.11-2.98 (2.20 (2.66) 2.0) 7.11) 5.4) 23.6 (8.91-6.51) 2.69-7.20-2.51) 15.9-16.13 (2.36-2.31) 2.73 (5.41 (2.00-7.99-4.1) 13.7) 3.55-6.07 (2.86) 6.4-16.1) 10.62 (6. 2002.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.04) 3.7) 10.39-3.81) 9.1-12.64-7.8 (10.08-2.80-3.29-3.30) 2.8-13.7-28.18-10.66) 10.74-3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.9 (9.6 (12.39) 5.53-3.79-8.95) 2.83 (2.S.26 (2.6 (9.2-13.and gender.47 (3. 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.1) 11.9-26.33 (2.3) 13.6) 11. 2005).89 (3.38 (6.7) 11.20 (7.88 (2.3) 16. ranging from more than one-tenth the NHANES median (Itoh et al.5) 13.57 (3.1-25.69 (2.58-3.2 (11.47-5.32 (3. 2005).82) 4.46 (2.43) 3.45) 3.03 (5.8-36.7 (11.65 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.56-4.52) 3.35) 3.27-12.18 (4.6 (8.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.68) 3.8 (8.00-3.81 (3.05) 2.43) 3..33) 3.3) 28.52-3.5 (11. while MnBP declined (Wittassek et al.52-20.43) 3.59 (4.67-5.54 (2.2) 9.54) 2..8-18.47-12.6 (15..76-3.1-24.7 (21.82 (4.56) 2.65-11.7 (9.53-5..32) 7. to about two to fourfold higher (Fromme et al.0 (12. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.2-15.04-5.0) 15.8-18. up to four and 13 fold.08) 75th 4.19 (2.00 (3.8) 10.6-19.84 (4.95-3.54 (4.9 (11. An analysis of NHANES 2001-2002 showed similar age.5) 15.4) 15.10-5.72-7.94) 6.

4 (21.6) 46.5) 34.9-92.2) 68.7-34.9.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.3-145) 85.4) 64.4 (84.5 (59.9 (20.7-92.5 (30.6 (61.5-43.7 (33.5) 37.0-24.5-42.9) 46.1 (19.2) 42.5 (29.4 (38.1 (17.1 (54.5 (28.5 (74.5) 26.2 (79.6) 17.3-96.9) 21.7) 28.5-53.1 (58.1 (16.0-51.6) 80.4-18.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.9-101) 77.3 (60.7-91.0) 20.2-21.5) 36.0) 27.3-60. interval) 24.7-26.8-29.5-47.3 (42.1-51.3-21.5 (59.2-22.2 (18.4 (36.2 (74.3 (23.3-136) 137 (107-162) 119 (90.0-26.0) 31.2 (75.5-44.3) 36.1) 46.7 (16.7-116) 95.9-87.2-56.3 (17.7 (19.8) 62.6-29.0 (17.4) 20.0-21.1-92.1 (36.2-114) 73.9 (17.8-22.7-127) 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. Fourth National Report on Human Exposure to Environmental Chemicals 267 .1-29.4 (25.4) 59.0) 117 (104-131) 112 (84.6 (22.4 (35.7) 52.6-48.3-24.3 (30.3 (51.6) 38.9 (79.9) 71.6 (65.1-20.3) 26.4-20.6-24.0 (36.6) 39.7) 92. population from the National Health and Nutrition Examination Survey.7-121) 97.8-25.8) 43.7-20.2-49.4) 52.5) 19.1-80.2-33.1 (28. 01-02.8 (19.2) 32.9) 75.6-31.0-58.4-26.7 (28.2 (59.9) 36.6 (55.1 (19.1) 23.4-25.2 (25.7 (38.7) 124 (98.8-132) 95.0) 21.4.5) 21.9 (17.4 (35.9-22.8-111) 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 23.1 (26.7-42.S.9) 26.7 (22. 1. *In the 1999-2000 survey period.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.4 (35.0) 38.1 (19.2-93. respectively.1) 23.6 (16.1 (18.1 (19.1) 36.5) 78.3) 19.2 (78.8) 58.7) 42.2) 38.9-79.6-29.9 (79.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.0) 84.1 (21.3) 23.8 (57.7-111) 64.6-113) 108 (90. see Data Analysis section) for survey years 99-00.0 (18.6 (48.7-42.0 (20.2-63.2 (21.2) 62.5) 36.0 (78.1.5) 40.3) 24.1 (34.8) 48.7-117) 118 (108-143) 93.8-123) 101 (90.5-27.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.7-24.7) 74.3 (23.1) 19.4 (35.4 (72.6-49.1-82.1 (31.5-117) 95.1 (41.6-33.4 (23.5) 17.1 (51.6 (90.2 (21.0) 120 (98.5) 95.0 (15.4-42.9-42.2-87.2) 20.6) 21.6-37.0 (72.6 (26.7 (43.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1) 25.8-42.8-119) 90. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value. and 03-04 are 0.0 (25.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.6) 71.2-23.5) 24.4 (19.9-28.7 (64.1) 20.6-20.0 (45.4 (71.3) 18.6 (32.4) 22.1-22.0) 30.2-159) 92.7 (18.9) 29. Survey Geometric mean (95% conf.5-121) 106 (94.5) 47.6 (19.1) 17.6 (44.7 (24.1-24.2 (58.6) 35.3 (37.5) 20.3-85.6-143) 127 (99.1 (62.2 (19.7 (18. referred to as monobutyl phthalate (MBP).2 (17.3-76.5-47.0 (30.4-44.6-69.9-22.9) 18.9-114) 116 (97.5) 85.0 (23.6) 20.4-60.2) 90th 98.7-34.7-106) 69.0-24.5) 65.6-40.8) 19.3) 40.9-33.7 (51.1) 47.0 (31.3 (36.6-44.6-36.4-31.3) 21.5-60.9-53. and 0.1-27.8) 75th 51.3 (30.2-32.1) 31.7 (70.0-19.8) 23.0-19.0-73.3-40.3-79.1) 30.0-32.3-67.7-53.2) 26.1) 23.3 (56.5) 31.2 (20.4-159) 107 (84.2-24.1-75.

4) 16.3 (76.7 (73. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.7 (43.0 (34.0-92.0) 70.3 (71.8 (22.6 (41.1) 21.8) 17.7-39.1) 53.6-24.0 (69.1-23.6-16.3 (52.1) 20.3 (17.1) 22.7 (60.8 (33.6) 65.3-26.3) 20.6-92.1-83.9-56.8) 17.2 (19.0 (19.0) 28.8-235) 137 (108-198) 88.3-21.8-32.3 (21.7 (19.9-34.2-28.6) 37.5-76.2 (16.4 (53.4 (18.3) 21.3-81.3) 35.1 (46.4 (17.2-106) 64.5 (18.1) 35.2-73.6) 31.5) 90th 68.0) 55.3-114) 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 17.4 (50.3) 19.1) 61.5 (14.7 (81.0-90.6-22.0-17.1) 37.8) 28.7-37.5) 84.1-99.7) 36.2-22.4) 21.7-28.8) 63.6 (61.1) 17.8 (16.5-30.9-38.0 (70.5-15.0) 26.1 (61.3) 67.6 (31.9) 19.7-78.7-42.2) 74.8) 13.6 (72.0 (27.4 (16.1 (15.1 (29.7) 20.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.5-23.5-37.2) 59.9 (20.6-23.3 (28.4 (56.6-32.9 (21.6 (74.2) 31.S.0 (43.8-24.2-61.3-23.2 (83.5 (64. interval) 22.8 (13.1) 44.7 (16.2 (19.4-131) 81.3-21.5 (81.2-22.4 (68.7-19.6) 34.8) 35.0 (71.3 (42.1) 50.3 (55.5 (18.0) 41.9 (37.4 (31.4) 20.3) 52.1-18.9-105) 85.6) 23.2-16.6) 25.3 (24.8) 19.4 (13. 268 Fourth National Report on Human Exposure to Environmental Chemicals .2 (38.7 (28.4 (33.5) 134 (93.8) 23.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 (20.6-19.4-24.0-60.4-103) 117 (83.7-51.8-23.0) 53.5-41.8) 20.2-179) 84.8-43.2-21.8 (18.0) 81.0 (15.0-75.8-24.3-17.4) 53.9 (39.0) 59.8) 34.4-164) 96.6-28.5) 17.5) 60.5 (15. Survey Geometric mean (95% conf.6) 14.9 (16.4-61.3 (69.1-21.4-34.1 (56.1) 20.8) 17.2) 21.0) 94.7 (14.9 (30.6 (19.4-76.6-43.6) 64.4) 51.7) 19.5) 82.9-68.3-71.0 (52.6) 38.8 (25.3) 18.9 (30.9 (19.0 (26.9-68.7 (12.3-40.8) 40.6) 24.3) 33.9 (35.7-23.9-70.4 (31.4 (47.6-42.3-39.2-48.0 (61.3 (19.3) 59.3-78.9) 49.7-80.3) 19.4) 62.6-155) 91.7 (60.4-65.9-36. population from the National Health and Nutrition Examination Survey.4 (17.6-44.0-19.0 (18.8 (65.2-18.1 (32.9) 20.7-19.9 (73.7 (54.8) 75th 38.3-38.0-38.5) 21.4-72.9) 62.0-113) 104 (83.6-44.4) 15.6-74.2-27.1-128) 97.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.6 (25.0 (18.9 (35.5) 91.0-41.4 (23.1 (34.0 (50.0) 35.5-142) 81.3-32.1-32.6 (17.5-64.0) 19.5) 39.2-85.9) 30.9 (56.3) 17.5-70.2 (35.5-142) 89.0 (20.6-128) 96.6-27.9-14.8) 34.3-20.9) 52.3-106) 74.8) 20.3 (17.2-86.0) 25.9-100) 86.9-84.3-18.6-23.3 (46.3-49.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9-26.4 (37.5-16.7-20.6-26.2) 159 (102-263) 147 (93.9) 28.2) 65.7 (20.0) 75.6-50.4) 15.8) 22.6) 18.1-99.7 (57.7) 42.0 (16.6-24.4 (45.8) 30.6) 24.7-21.9) 39.6) 83.8 (18.5-22.6-53.9-49.6 (27.3 (60.2) 16.5 (30.0) 108 (71.8 (17.2-22.2-108) 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.7-26.1) 42.7 (27.9 (58.0) 29.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9 (30.4 (31.4) 19.5-18.3 (52.3 (48.9) 24.1 (21.3 (17.8 (50.6) 39.4 (50.9 (64.4 (16.9) 91.8 (18.1-62.4-135) 71.4 (19.0-47.6-119) 63.3 (16.9) 14.5-21.6 (29.4-47.3) 33.6 (57.6 (25.

Sampson EJ. Caudill SP. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.111(14):1719-1722. Calafat AM. Bull Environ Contam Toxicol 2002. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.93:177-185.112(3):331-338. Silva MJ. J Androl 2004. Dobler L. Ryan L. Available at URL: http://cerhr. Wittassek M.108(10)979-982.114(9):1424-1431.nih. Phthalate monoesters levels in the urine of young children. Fromme H. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Barr DB.gov/chemicals/ phthalates/dbp/dbp-eval. Massey RC. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Hagmar L. Bolte G. Springall C. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Angerer J. Reidy JA. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. et al. Brock JW. Food Addit Contam 2001. Epidemiol 2005.Phthalates References Adibi JJ. Urinary levels of seven phthalate metabolites in the U. Int J Hyg Environ Health 2005. Prenatal exposures to phthalates among women in New York City and Krakow. Malek NA. Poland. Meeker JD.210:21-33. Int J Hyg Environ Health 2007. et al. Duty S. Schettler T. Helm D. David RM. Jonsson BAG. Research Triangle Park (NC). Barr D. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hu H. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Int J Hyg Environ Health 2007. Castle L.18(1):122.68:309-314. Angerer J. Caudill SP. Hodge CC. et al. Eckard R. et al.niehs.25(2):293-302. Giwercman A. Brock JW. Green RA.210(3-4):319-33. Duty SM. Singh NP. 2000 [online]. Yoshida K. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.208:237-245. Koch HM. Needham LL. Silva MJ. Caudill SP. NTP-CERHR. Camann DE. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). et al. Environ Health Perspect 2000. Chen Z. Butala JH. Needham LL. McKee RH. Hilborn ED. Rossbach B. Koch HM. Pirkle JL. Scotter MJ. Masunaga S. Hum Reprod 2007. Weuve J. Richthoff J. Drexler H. Gans G. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Boehmer S.18(12):10681074. Ryan L. Silva MJ.16(4):487-493. Jedrychowski W. 2005. Blount BC. Koch HM. Environ Health Perspect 2003.22(3):688-695. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.S. Silva MJ. Anderson WA. Wiesmuller GA. 112(5):A270]. Sanchez GN. et al. Levels of seven urinary phthalate metabolites in a human reference population. et al. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Perera FP. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Environ Res 2003. Drexler H. 4/20/09 Silva MJ. Calafat AM. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2004. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Rylander L. Itoh H.html. Reprod Toxicol 2004. Hauser R. Environ Health Perspect 2006. et al. Jacek R.

70 (1.500) < LOD < LOD . 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) .300 (.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300-.400 (.200-.500 (.200-.400 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400 (<LOD-.900-1.300 (.00 (<LOD-1.300 (.9.10 (<LOD-2.400-.400-.200-.600) .500 (.200 (<LOD-. and 0. and polyvinyl chloride.00 (<LOD-1.600) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500) 1.300-.600) .400-.S.10 (. which may vary for some chemicals by year and by individual sample.400 (.700) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .200-.600) < LOD . Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. 0.700) .00) .00 (<LOD-1.500-. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500 (.600 (.Phthalates Dicyclohexyl Phthalate CAS No.10 (<LOD-1.400-.300-.400-.400) < LOD 1.300-.500) < LOD < LOD .70) .400 (.400 (. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. 270 Fourth National Report on Human Exposure to Environmental Chemicals .00-3. respectively.400 (<LOD-.70 (1.10 (<LOD-1.300-.300 (.400) 1.10) .400-. In this Report.300-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.500) .700) .3.500 (.500) 1. 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. < LOD means less than the limit of detection. resins. only levels at or above the 90th percentile could be characterized. Survey Geometric mean (95% conf.300 (<LOD-.300-.500) .90) . including nitrocellulose.500 (. polyvinyl acetate. see Data Analysis section) for Survey years 99-00.300) < LOD .400) 1.2.50) . 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.00-2. 01-02.500) < LOD 1.500 (.500) .400) < LOD < LOD .70) .400 (<LOD-.500) 1. and 03-04 are 0.500 (.600) .500) .400 (.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300-.50) .400 (.300-.80) .20) .400-.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. and polymers.200-.300 (.500 (.300) < LOD .500 (.300-.300 (.200-.

12-1.770 (.530-1.800-1.16 (<LOD-3.450 (.690) < LOD 2.54 (<LOD-2.910 (. population from the National Health and Nutrition Examination Survey.74) .290-.470 (.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .380 (.18) .270) < LOD .880 (.410 (.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 1.53) .470) 3.620) < LOD .330 (.710) .33 (<LOD-3.36-1.830) 1.420-.610 (.690) < LOD < LOD .67 (1.310-.44) .11) .54-6.530) 1.370 (<LOD-.740) < LOD < LOD .690-1.500) 3.630 (<LOD-.770-1.360-.740) .530 (.350-.330 (.82 (1.14 (<LOD-3. Survey Geometric mean (95% conf.00 (<LOD-3.480 (.33) .390 (.500 (.590 (.420-.510 (.670-1.770) < LOD 2.590 (<LOD-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .770-1.16) .53) .400-.S.34) .54) .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 .22 (<LOD-1.43 (1.910 (.510-.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.250 (.10) .670 (<LOD-.400-.770-1.450 (.500-.690 (.530) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.530-.00) .06) . Fourth National Report on Human Exposure to Environmental Chemicals 271 .790-1.420-.17) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.380-.560) 1.220 (<LOD-.940 (.660) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170-.910 (.260-.950 (.910 (.630 (<LOD-.660) .310) < LOD .490) .240-.82) .06) .05) .

84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. 2001-2002. DC (Hoppin et al. population from the National Health and Nutrition Examination Survey.7 (70.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. 2003) and African-American women in Washington.4. and 0. In contrast.3 (74. see Data Analysis section) for Survey years 99-00. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 272 Fourth National Report on Human Exposure to Environmental Chemicals . 01-02.Phthalates Diethyl Phthalate CAS No.9-92.8-111) 85. 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. 0.3-103) 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. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.4 (62. and 03-04 are 1. Biomonitoring Information MEP levels in the NHANES 1999-2000. 2002).5) 81. respectively.. 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. Products that may contain DEP include perfumes. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. 2007).. 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. particularly those containing fragrances. and also in men attending a Boston infertility clinic (Hauser et al.3 (82.9. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.1-93.1 (71. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-102) 95. deodorants.S.7) 71. and hand lotions. soaps.. shampoos.9 (61.2. colognes.

Median MEP levels found in a small sample of German residents (Koch et al.7-110) 81.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. Analysis of NHANES 2001-2002 showed similar findings. 2005). 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. 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. Other population estimates also differed by sex and race ethnicity (Silva et al. 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.6 (65..3-105) 87.6 (77.5-113) 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 . In an analysis of NHANES 1999-2000. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2002). population from the National Health and Nutrition Examination Survey. 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. 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 92.5-114) 101 (87. This age-related trend is opposite the direction seen for other phthalates.9-110) 96. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Phthalates 2002 (Brock et al.2 (66. 2003) were slightly lower than levels found in NHANES 2001-2002.0 (66. 2004)..9 (82.

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

6) 39.3 (24.00-5.0-29. and 0.50-6.50-2.80-3.31-4.80 (1.7) 6.40) 9.26-2.7-32.90-4.37-4.40-8.30-11.90 (3.80) 9.9-26.6-130) 31.3 (15.40) 75th 7.1982).5 (12.0 (14.90) 4.0-84.70-5.7) 19.82) 3.46) 3. and blood product storage and intravenous delivery systems.00 (2. 1.70-3.40) 4. respectively.9) 13.2) 29.6 (10.3 (11.9 (29.00) 5.50-20.42-5..16 (2.4) 5.40-11.5-36.70 (1.4) 20.60) 4.2) 6. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.0.50-2.9 (13.00-3.90) 3.00) 3.10 (4.90) 1.70-2.10-5.60 (6.9-19.30-13. 1989.92) 4.56 (2.0) 23.31 (3.6) 14.85) 4.9-28.60) 90th 14.0) 35.41) 3.87-2.4-40.94-3.70-8.25-3.30 (3.00) 1.30 (6.20 (3.91-3.44) 4.0) 23.00) 19.0 (19.80-5.92-2.60) 3.40) 11.82 (3.10) 3.30 (4.5) 21.0-18.7) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.70-5.5-28.4-20.3-57.10 (4.6) 95th 23.84 (2.90-8.5) 37. population from the National Health and Nutrition Examination Survey.9 (15.03-2.35) 4.7 (14.20 (3.15 (1.70 (1.6-38.27) 2.50-8.1-17.16-3.6 (16.00 (4.3-26.70-6.9 (29.20 (1.4) 15.80-9.60) 7. 2002.50 (7.10 (6. see Data Analysis section) for Survey years 99-00.60) 8.70) 16.9) 27.5-40.00) 2.10) 3.1) 25.50-3.1-48.4-20.70-4.50-6.92-5.3-64.14 (1.6-60.1) 29.0 (17.9) 13.96-5.6 (41.9 (26.6 (11.0) Total 4.86) 2.3 (19.50 (3.6) 14.67-4.19-3.40-8.70 (7.3) 52.3) 13.0 (19.50 (7.80-27.9) 15.9-49.2.12 (4.34 (2.40 (4.10) 2.90-11.9) 5.9.70 (2.0) 23. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).7 (17.60-7.90-5.90-3.40-12.90) 4.4) 6.00) 2.40) 4.30 (7.9-29.0 (21.7) 35.10-5.6) 5.6-25.00) 1.2-39.9-48. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).79) 2.3-25.80-8.3) 28.0-19.5 (20.75 (3.4) 13.5 (31.23 (3.5-41.2-28.10-4.5) 40.07-4.5) 23.61 (3. Albro and Lavenhar.63-4.1 (11.70 (3.85 (3. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.0 (18.1) 19.7) 18.00-4.83) 2.Phthalates Di-2-ethylhexyl Phthalate CAS No. Peck and Albro.0) 39.50-3.8 (19.5-17.4-27.5-28.2-17.10) 4.84) 3. Fourth National Report on Human Exposure to Environmental Chemicals 275 .50-5.70) 2.23) 3.7) 8.50) 9.90 (4.4 (13.86) 2.40) 1.60) 10.50 (2. 01-02.9 (17.8) 15.5 (24.98) 2.2) 42.90) 4.10-3.6-23.80 (4.1