2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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2'.4'.4.2'.2-Dichlorobenzene (o-Dichlorobenzene) 1.4'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.5'.1.5.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.5'-Tetrachlorobiphenyl (PCB 44) 2.6'-Hexabromodiphenyl ether (BDE 154) 2.3.1.2'.2'4.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'.4'-Tetrabromodiphenyl ether (BDE 66) 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4.4'. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1. The process for selection is described at http://www.2'3.3-Tetramethylbutyl] phenol) Triclosan (2.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4.5'-Tetrachlorobiphenyl (PCB 49) 2.4-Tribromodiphenyl ether (BDE 17) 2.4'.5’.4.What’s New in this Report What’s New in this Report In this Fourth Report.2'.1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1. Paradichlorobenzene) 1.cdc.2-Dichloroethene trans-1. Table 1. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.5-Pentabromodiphenyl ether (BDE 99) 2.4-Dichlorobenzene (p-Dichlorobenzene.4.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dichloroethane (Ethylene dichloride) 1.3’. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4’.2.4.3.2-Dichloropropane 2.4.4.5.4'.1-Trichloroethane (Methyl chloroform) 1.html.4'-Tribromodiphenyl ether (BDE 28) 2.5'-Hexabromodiphenyl ether (BDE 153) 2.5.4'-Tetrabromodiphenyl ether (BDE 47) 2.1-Dichloroethene (Vinylidene chloride) cis-1.1.2'.6.5.4.4.6-Pentabromodiphenyl ether (BDE 100) 2.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4.3.2-Dichloroethene Dichloromethane (Methylene chloride) 1.6-Heptabromodiphenyl ether (BDE 183) 2.2’.4’.2'.1-Dichloroethane 1.2'.3-Dichlorobenzene (m-Dichlorobenzene) 1.gov/exposurereport/chemical_selection.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 2.3.3'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2'.4.

Details of this procedure are provided in Appendix A. Fourth National Report on Human Exposure to Environmental Chemicals 3 . and these data will be included in the next release of the Report.4-dichlorophenol and 2. Percentiles for all three NHANES survey periods (1999-2000.g..g. five results that all have the value 90.. urinary 2. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. 2003-2004) have been re-computed by use of this improved procedure. Explanations for each change are provided in Appendix B. the presence of an interference) that produced results of inadequate quality. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. 2001-2002. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available.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.5-dichlorophenol for the 1999-2002 survey periods. Data for other pesticides are included only for 1999-2000 and 2001-2002.1).

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

Other racial/ethnic groups are sampled. serum levels are presented per gram of total lipid and per whole weight of serum. Census Bureau estimates of the U. These compounds are lipophilic and concentrate in the body’s lipid stores. Serum levels reported per gram of total lipid reflect the amount of these compounds that are stored in body fat. Ninety-five percent confidence intervals around this Fourth National Report on Human Exposure to Environmental Chemicals 5 .. Useful unit conversions are shown in Table 2. but the proportion of the total population represented by other racial/ethnic groups is not large enough to produce valid estimates. and race/ethnicity as defined in NHANES.Data Sources and Data Analysis metabolites in blood.cdc. state. population. The geometric mean is influenced less by high values than is the arithmetic mean. Units of Measurements and Abbreviations Unit liter deciliter milliliter gram milligram microgram nanogram picogram femtogram Abbreviation L dL mL g mg µg ng pg fg Value 10 liters -3 10 liters 10 grams -6 10 grams -9 10 grams -12 10 grams -15 10 grams -3 -1 Geometric means: A geometric mean provides a better estimate of central tendency for data that are distributed with a long tail at the upper end of the distribution. results are given for the total population as well as by age group. if one person has consumed more fluids than another person. or region. Guidelines for the analysis of NHANES data are provided by NCHS at http://www. probability-cluster design. Results are reported here using standard units. The Report presents descriptive statistics on the blood. 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.S.0. and urine were based on isotope dilution mass spectrometry. Sample weights also are used to adjust for possible bias resulting from nonresponse and are post-stratified to U. serum. sample weights must be used to adjust for the unequal probability of selection into the survey. levels are presented two ways: per volume of urine and per gram of creatinine. and organochlorine pesticides. including tolerance limits for operational parameters. Laboratory measurements underwent extensive quality control and quality assurance review.e.g. For example. micrograms per liter). Table 2. seasons of the year. In each table. stratified. 2002) and the statistical software package SUDAAN (SUDAAN Release 8. Other racial/ethnic groups are included in estimates that are based on the entire population sample. Data Analysis Because the NHANES is a complex. Statistics include unadjusted geometric means and percentiles with confidence intervals. including the lipid in serum. or by use of particular products. Units of measurement are important. Levels per gram of creatinine (i. or graphite furnace atomic absorption spectrometry. creatinine corrected) adjust for urine dilution. Other mostly non-lipophilic chemicals measured in serum are expressed per liter of serum (e. Geometric means were calculated by taking the log of each concentration and then computing the weighted mean of those log-transformed values using SUDAAN software.S. PCBs.gov/nchs/nhanes/ nhanes2003-2004/analytical_guidelines. his or her urine output is likely higher and the urine more dilute than that of the other person. non-Hispanic black. Data were analyzed using the statistical software package Statistical Analysis System (SAS) (SAS Institute Inc. the measurement of quality control samples in each analytical run to detect unacceptable performance in accuracy or precision. 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. Age groups are as described for each chemical in each data table. Urinary levels are expressed both ways in the literature and used for different purposes. 2001).htm.. or urine levels for each environmental chemical. SUDAAN uses sample weights and calculates variance estimates that account for the complex survey design. generally conforming to those most commonly used in biomonitoring measurements. References for the analytical methods used to measure the different chemicals are provided in Appendix C. inductively coupled plasma mass spectrometry. For these analyses. proximity to sources of exposure. furans. serum.. race/ethnicity is categorized based on the sample design as Mexican American. Gender is coded as male or female. gender. multistage. and nonHispanic white. and verification of traceable calibration materials. For dioxins. Units: For chemicals measured in urine. Acrylamide and glycidamide adducts are expressed as the picomoles per gram of blood hemoglobin to which the adduct is bound. This design does not permit straightforward analysis of exposure levels by non-targeted strata such as locality. This type of distribution is common in the measurement of environmental chemicals in blood or urine.

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

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

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

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

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

8 (52. and binding agents.. Survey Geometric mean (95% conf. or to glutathione conjugates (Calleman et al. 2006. FAO/WHO.7) 73.4-76. Acrylamide is not thought to accumulate in the body at environmental doses.0-66.4 (53. Estimated intakes in children are about twice that of adults (DiNovi and Howard.5-80.2-118) 98.3-2.9 (60.3 (53.2 (75. smoking.9) 58.8 (91.2-70.2-59. acrylamide is synthesized and used in the production of polyacrylamide polymer.8 (57.4) 100 (89.6) 73.7-64.7 (55.1 (73. mineral processing.6-61.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.7) 58.7 (65. Since acrylamide has limited volatility and high water solubility.S.1) 46. pulp and paper production.1-61. 2005).4-60.7) 54.6-65. 1994).2 μg/kg/day (U.0-49.5) 58.1-64.7-64.9) 57. 217 million pounds of acrylamide were produced commercially in the U.6-108) 61.2 (58.6) 50.7 (58. but can covalently bind to form adducts with proteins. interval) 61.6) 90.S.1-57.9 (69.0-58. 2005). such as potatoes and some grains. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.9-52. and cosmetics (NTP-CERHR. and in some cosmetics. see Data Analysis section) for Survey year 03-04 is 3.4 (54.8 (81.1 (52. as an absorbent in disposable diapers. and well below doses known to cause nerve damage or carcinogenicity in animals.6-75.0 (67.4-60. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61.1 (83. FDA. Fourth National Report on Human Exposure to Environmental Chemicals 11 .4 (54.9-105) 86. are heated at temperatures used for frying and baking.2-77. widely distributed in tissues. ocular and dermal irritation from direct contact with acrylamide containing materials.1 (47..8-55.5) 66. acrylamide has produced upper airway irritation following inhalation of high levels. People may be exposed to acrylamide from foods.4) 57.2) 57. (NTP-CERHR.6 (51.7) 75th 79. EPA.7 (63.0 (69.0) 85. Recently. but are generally above the U. These estimated intakes are hundreds of times lower than occupational exposures. Commercially. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. 2002).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 54.0 μg/kg for adults (FAO/ WHO.8-57.4-83. Tareke et al. drinking water.6) 71.S.3) 86.4 (59. Elimination occurs mainly in the urine as mercapturic acid conjugates.4 (51. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.3-71.1) 55.2-114) 163 (147-191) 96. and an average daily intake is estimated as 0.5 (44.0 (57. Fennell et al. and is either metabolized to the reactive epoxide.2 (62. 2004). In humans. Animal studies indicate that acrylamide is well absorbed.1 (88.3 (55. in some sealing grouts. and in the synthesis or compounding of dye materials. In 1997. it was discovered that acrylamide is formed when starch-rich foods.2-93.5 (74. EPA. glycidamide. the main source of exposure is from the diet.0) 57. 2005.1-64.7) 96. 2005).6 (56.6 (81.2) 57.Acrylamide Acrylamide CAS No.2-67.6-104) 82.9 (54.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. Natural substances in the food are converted to acrylamide. Polyacrylamides are useful water-compatible polymers used in water treatment. In the general population.9) 63.7-60.2-91. 1990..0-108) 152 (139-175) 126 (111-142) 108 (86. gels.4-89. in permanent press fabrics. EPA reference dose of 0.3) 63.S.0 (53. 2006). population from the National Health and Nutrition Examination Survey.S. 2005).5 (79.5-85.3) 70.9) 75. and from dermal contact with products that contain residual acrylamide.1) 101 (95.6-66. 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.5 (52. soil conditioners. 2005).9-61.0. 2004.4) 57.1) 53. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.1) 62.

5-92.7-86. 2005.2-68.2 (56.1) 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. most non-smokers had levels less than about 100 pmol/gram hemoglobin.6 (66. 2005.2-90.9) 65.. After exposure ceases.7-62. altered gene expression in testicular tissues (Yang et al. 2005).S. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.8) 60.7) 90.7 (87.9 (81. AHA levels have been shown to increase with dietary intake (Hagmar et al. population from the National Health and Nutrition Examination Survey.0) 118 (103-126) 121 (112-134) 113 (94. Survey Geometric mean (95% conf.1 (66. 2005. Acrylamide is clastogenic and can produce dominant lethal mutations. Puppel et al. EPA.9) 59.3-101) 95. 2005.0-62. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.7) 60. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.3) 59..S..1 (82.3-78. presynaptic nerve terminal binding (LoPachin.6 (90. and cancer (mammary.0 (75.0. male germinal cell injury. reproductive effects (reduced litter size. 2002.8 (51. respectively) are markers of integrated acrylamide exposure over the preceding few months.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.5 (42. 2005) and sperm DNA adducts (Xie et al.5) 87. 2008).1-62.3) 85.2 (63.4 (51. 1997.pdf.. interval) 59. Schettgen et al. 2005. 2005. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).1-60. although different analytic methods can affect results. 2005).2-91. uterine. and other sites) (FAO/WHO.4) 83. 2006).0) 94. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. 2006)..4-59. Glycidamide has been shown to react with DNA (Doerge et al.Acrylamide occupational exposures.0 (70.2) 55. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al..7 (61.0 (52.9 (57. 2008). thyroid.5 (56. EPA. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. Maniere et al.7) 61.5-66.S.1 (70.2 (72. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.3) 59. fetal death.4 (90. glycidamide (NTP-CERHR.1-56.. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al. U..8 (44. In addition.9-138) 143 (130-159) 96.0-93.1) 56. see Data Analysis section) for Survey year 03-04 is 4.4 (57. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.5) 75th 85.epa.9 (58.9) 75.3) 59.7) 74. Axonal degeneration.2) 65..who. Klaunig et al.5) 118 (110-129) 121 (108-140) 136 (124-149) 152 (135-170) 159 (129-204) 172 (157-194) 1841 1954 3044 Limit of detection (LOD. 1997.8-49.9-64. 2002.0-103) 136 (123-148) 125 (116-135) 126 (119-135) 141 (126-157) 146 (123-169) 187 (169-204) 129 (111-141) 174 (157-197) 159 (143-175) 411 784 1931 2623 1529 3604 3674 03-04 03-04 03-04 64..4) 53. EPA at: http://www.8-61. 2005.7 (84.4 (81. 2005)..... 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.9) 87. Rice.. scrotal. NTP-CERHR. Additional information is available from U..6-90. 2005..1 (57.5-64. 2005).5-94. 2005) have been demonstrated in animals. 2006) have been demonstrated after acrylamide dosing. 2005. probably through its epoxide metabolite.4) 46.5 (59..4-98.1-70.1) 62. adrenal.5 (83.4 (61.5) 71.int/ ipcs/food/jecfa/summaries/summary_report_64_final.6-64.4-103) 79.S.7 (57.4-65. IARC classifies acrylamide as probably carcinogenic to humans..9-76. 2005.0 (80. 2004). and neuronal DNA reactivity (Doerge et al. 2003.8-48. 2009). 2001). 12 Fourth National Report on Human Exposure to Environmental Chemicals .9-78. 2005. Mucci et al.4 (56.. Vesper 2005) and smoking (Bergmark. Schettgen et al. dominant lethality). U. Hagmar et al.9-77.8) 45. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.2) 87.9-62.7-64. 2006.3 (56. Puppel et al.1) 60.6-62.1 (56. Vesper et al. 2004.

Osterman-Golkar S. Illinois. 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.580(1-2):119-129. Mechanisms of acrylamide induced rodent carcinogenesis. CFSAN/Office of Plant and Dairy Foods.Toxicol Appl Pharmacol 1994. Toxicol Sci. Haugen M. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. February. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Andersen M. Maniere I. Tornqvist M. Tian G. Kamendulis LM. DiNovi M and Howard D. Mucci LA. In another study. 2004 Acrylamide in Food Workshop: Update Scientific Issues. References Bergmark E. 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. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. 1994). Duale N. Calleman CJ. Burgess J. Perez et al. et al. Zhang S.56.who. Toxicol Appl Pharmacol 1993. Available at URL: http://www. Paulsen JE.niehs. Bridson WE. J Agric Food Chem 2008. Bergmark E. smoking habits and gender. Kautiainen A. Toxicol 2005.85:447-459. 2/3/09 Perez HL. [Epub ahead of print] Dybing E. Farmer PB.cfsan. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Chicago. 2001). Aprea P. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Mutat Res 2005.120(1):45-54.561:21-37. Chem Res Toxicol 1990. Doerge DR. gov/~dms/acrydata. and Research Strategies. Bruze M. smokers and nonsmokers. 2005. 2006. 2009 Jan 8.. Laurentie M. Wilson KM. Tornqvist M. Calleman CJ. 6013-6019. Hagmar et al. Granath F. Italy. July. 2001. April 13-15. 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. Wirfalt E.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Fennell TR. Bergmark E. Mutat Res 2005. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 2004. 2/3/09 Klaunig JE. Churchwell MI. Metabolism and hemoglobin adduct formation of acrylamide in humans. 2/3/09 Hagmar L. Cheong HK.10(1):78-84. Twaddle NC. 8-17 February 2005. Snyder RW. Bergmark E. et al. Joint FAO/WHO Expert Committee on Food Additives. Acrylamide neurotoxicity: neurological. He F. Adv Exp Med Biol 2005. Uncertainties. Costa LG. Guffroy M. He F.43:365–410. Food and Drug Administration (FDA).pdf.nih.. morphological and molecular endpoints in animal models.gov/chemicals/ acrylamide/Acrylamide_Monograph. NIH Publication No. Spicer R. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Hagmar L. Alexander J. Malmberg B.126(2):361-371. da Costa GG.580(1-2):157-165. Calleman CJ. 054472. Rosen I. National Toxicology Program. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Godard T. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Human exposure and internal dose assessments of acrylamide in food. Adv Exp Med Biol 2005. Mutat Res 2005. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Toxicol Sci 2005. et al. Available at URL: http://www. 64th Meeting: Summary and Conclusions (FAO/WHO).fda. Survey data on acrylamide in food: individual food products. Yang JS. Available at URL: http://cerhr. Acrylamide intake through diet and human cancer risk.580(1-2):131-141. et al.27(4):219-226. 1993. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.3:406-412.pdf. Axmon A. Churchwell MI.. Rome. McDaniel LP..Acrylamide In occupational settings. Chem Res Toxicol 1997 Jan. Food Chem. Beland FA. Costa LG. Becher G.html#u1004. Summer SCJ. et al. Fennell TR. Scand J Work Environ Health 2001. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.561:49-62. Wu Y. Bjellaas T. Magnusson AL.. Doerge DR. 1999). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. LoPachin RM. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Paulsson B. Nordander C. The Updated Exposure Assessment for Acrylamide.

Angerer J. Fueller F. Gray JG. Sun H. Hallmans G. Eriksson S. Rossbach B.19(4):527-34. 14 Fourth National Report on Human Exposure to Environmental Chemicals .56(15):6046-53. Drexler H. Rapid Commun Mass Spectrom 2006. 2/3/09 Vesper HW.580(1-2):71-80. Schettgen T.207(6):531-9. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.htm. Integrated Risk Information System (IRIS). Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Liu K. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.561:89-96. Meyers T. EPA). Lee MH. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.20(6):959-64.S. Int J Hyg Environ Health 2004. Jin Y.206(1):9-14.134(1-3):65-70. Choi JH. et al. Angerer J. U. Chemical Summary for Acrylamide. revised 1/3/06. Fu D. Ospina M.S. 2/3/09.Acrylamide glycidamide by gas chromatography-mass spectrometry. Drexler H. Tjønneland A. Hemoglobin adducts of ethylene oxide. Smith A. propylene oxide. Reprod Toxicol 2005. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Toxicol Lett 2002. Benetou V. Drexler H.epa.S. Yang HJ. Broding HC. Han DU. EPA). Chae C. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Acrylamide. Rydberg P. Schettgen T. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Marko D. Office of Pollution Prevention and Toxics.gov/chemfact/s_acryla. Toxicol Lett 2006. Available at URL: http://www. Karlsson P. Analysis of acrylamide. Int J Hyg Environ Health 2003. Vesper HW. Tornqvist M. Slimani N. Adv Exp Med Biol 2005.163(2):101-8. Kutting B. Meyers T. September. Xie Q. Washington (DC). Available at URL: http://www.S. 1994. Mutat Res 2005 Feb 7. Ingham L. Toxicological effects of acrylamide on rat testicular gene expression profile. Ding X. The carcinogenicity of acrylamide.50(17):4998-5006. Schettgen T.txt. a carcinogen formed in heated foodstuffs. J Agric Food Chem 2002.274(1):59-68. Tareke E.gov/iris/subst/0286. U. Environmental Protection Agency (U. Anal Biochem 1999. Lee SH. Licea-Perez H. Weiss T. et al. Environmental Protection Agency (U. Tjaden Z. J Agric Food Chem 2008. Agudo A.epa. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Rice JM. Ospina M. Liu Y.580(1-2):3-20. Mutat Res 2005. Puppel N. Myers GL. Letzel S. Angerer J. Han CH. Vesper HW.

2004). cardiovascular disease.110 (.308 (.094) .066 (.520 (.060-.20) .140 (.910-1.050) .153-.088-.050 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120 (.79) 3.15 (2.77 (2. 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.66 (1.18-3.690 (.350-.080) < LOD < LOD .50 (1. which may vary for some chemicals by year and by individual sample.164 (.142-.28) .047-.050 (<LOD-.058 (.800 (.080) < LOD .140-.084) .96 (1.066) .12 (2.071) .197) .900-1.312) .076-.100-.030-.33-2. maternal exposure during pregnancy can result in lower birth weight.770) .163) .230 (.85 (1.120-.630 (.60-2.015 ng/mL.040 (.180) .49) 1.120) .115-.21 (.063) .620 (.920 (.5% nicotine by weight (Kozlowski et al.19) .216 (.506 (.15) 2.00) .180 (.00) 1.20-2.16) .42-4.230) .02) 1.30) * .630 (.860 (.145) .580-1.87-3.144 (.070) 75th .950 (.120 (.23 (.154-.300) .080 (.470-.140 (.050 (<LOD-. and various other disorders (U.04 (1.193) .48-2. ear problems.42 (1.310) 90th 1. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. 2004).148-. respectively.770) .120-.02) 1.54 (1.480-1.180) . stroke.620-1.S.175 (.201) .500 (.740-1.130) .077) .22) 2.32-2.068) .39) 3.88 (.108) * .110 (.32-2.111-.131 (.053 (<LOD-.09-2. see Data Analysis section) for Survey years 99-00.060) .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 .050 (<LOD-.53 (1.630 (.190-.110 (.050 (.320) .198) * .070) .068) .075 (.180 (.057-.220-.040 (.060 (<LOD-.120 (.061) < LOD .137 (.280 (.70) 2.140-.050) .040-.066-.030-.043-.62) 2.570-1.090-.44) 2. DHHS.080-.310-1. and 03-04 are 0.70-2.110 (.580) .139) * .770-1. ** In the 2001-2002 survey period.950-1.09-3.060-.50) 3.160 (.071 (.14) .080 (.070) .428-.12 (1.180) .75) 1.88 (1. and 0.130 (.850 (.040-.54 (1.19-2. 83% of measurements had an LOD of 0.210 (. DHHS.089) Age group 3-11 years 99-00 01-02** 03-04 .180) .63-2. Children exposed to ETS are at increased risk for sudden infant death syndrome.81-2.730 (.S.26-1.48-3.059-.84-3.060 (<LOD-.30) 2.190-. emphysema.44 (2. and exacerbated asthma (U.68) 2.167 (.17) .39 (1.410) .960-1.68 (1.44) 2.350 (.17 (1.93) .015.370-.110) .21-1.43 (1.01) 3.57) 2.12-4.28-1.32) 1.080-.997-3.054 (.63 (2. acute respiratory infections. and 17% had an LOD of 0.66) 1. population from the National Health and Nutrition Examination Survey.77 (1.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .187) .190-.23 (2.080-.621-1.740-1.49) 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.060 (.126) .240 (.726) . Cigarettes contain about 1.077) .23-2. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.160 (.087-.54) 1.030 (.76 (1.160-.83-2.430-1.35 (2.150) .02 (.14) .77 (1.260-1.570 (.44 (1.200) 1. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.20 (.124 (.11) .087) < LOD < LOD .21-1.505 (.086 (.450-.160) .164 (.059-.360) .05.104-.533-.213) .45) 1..820) .120 (.50-4.087 (.080-.020-.150) .66-3.625) .17 (.110-.073) < LOD .310-1.96) 2. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.540-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.090-.710 (.350-.110-.55 (1.050-.99) 2.120 (.99) 2.53-4.030-. 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.302) .540 (.12) 1.110) .930 (.110 (.990) .510 (.050-.89) 1.180) .070 (<LOD-.20 (1.62 (2.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .65 (1.78) 2.220) .94) 1.160) .40) .220) .234) .34 (1. 2006).047-.160 (.68) .260) 1.060-.188) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.01 (1. acute respiratory illness. 1998).110-.790) .14-1.480-.30) 2.23 (1.060 (.38-2.92 (1.070-.163 (.310) .106-. < LOD means less than the limit of detection.05 ng/mL.09-3.660) .S.137-.040 (.840) 3.55-2.052 (<LOD-.49) 1. Survey Geometric mean (95% conf.19) 1.600-1.Cotinine Cotinine CAS No.062 (.580 (.090-.47-3.670) .990 (.50-1. Fourth National Report on Human Exposure to Environmental Chemicals 15 .400-.95) 1.052 (<LOD-.20) 1.05) 1.96-4.

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

Kira S.S Department of Health and Human Services (U.niehs. 4/13/09 Perez-Stable EJ. Pechacek TF.15:302-307.fr/ENG/Monographs/allmonos90. U. Richter PA. Jacob P III. Available at URL: http://www.gov/tcrb/monographs/10/. National Institute for Occupational Safety and Hygiene (NIOSH). Respiratory nicotine absorption in non-smoking females during passive smoking. Hukkanen J.php. National Center for Chronic Disease Prevention and Health Promotion. cigarette smokers: the Third National Health and Nutrition Examination Survey. Department of Heath and Human Services. 4/13/09 National Cancer Institute (NCI). 4/13/09 Iwase A. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Cotinine as a biomarker of environmental tobacco smoke exposure. 4/13/09 International Agency for Research on Cancer. Ethnic differences in N-glucuronidation of nicotine and cotinine. Jarvis MJ. Caudill SP. Warner K.php. Vogler GP. International Agency for Research on Cancer. Centers for Disease Control and Prevention. Available at URL: http://monographs. Etzel RA.18:188-204.S. Trends in the exposure of nonsmokers in the U. Bernert JT. Environ Health Perspect 2006. Clin Pharmacol Ther 1994. Mehta NY. Racial/ethnic differences in serum cotinine levels among adult U. Vol 83.291(3):1196-1203. Tobacco Smoke. Tobacco related exposures.fr/ENG/Monographs/ allmonos90.gov/eid/rmca/critdocs/ criteriadoc/33. Flegal KM. BMJ 1975.surgeongeneral.iarc. Pirkle JL.56:483-493. Pickett MA.4:313-316. Available at URL: http://monographs. Maurer KR. Pharmacol Rev 2005. Metabolism and disposition kinetics of nicotine. Pechacek TF. Brody DJ. Strauss WJ. Benowitz NL. Pirkle JL. Lewis PJ. Am J Public Health 2004. 2004. Atlanta (GA): 2005. Mowery PD. Benowitz NL. Aiba M. IARC Monogr Eval Carcinog Risks Hum. JAMA 1998. U.280:135-140. the United Kingdom. Office on Smoking and Health [online] 2006. Curtin LR.gov/library/ secondhandsmoke/. Houseman TH. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Tob Control 1998. IARC Monogr Eval Carcinog Risks Hum. and the United States. Caraballo R. Sosnoff CS. iarc. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .63:139-43. References Armitage AK. 4/13/09 U. Vol 38. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Soliman S. Jacob P. et al. Int Arch Occup Environ Health 1991. Jacob III P.S. 1999. Centers for Disease Control and Prevention.niosh. Centers for Disease Control. Herrera B. George CF. Pollack HA. Dollery CT. Absorption and metabolism of nicotine from cigarettes. 1988-1991.S. JAMA 1996. Tobacco Smoke and Involuntary Smoking.280:152-156. Giovino GA. DHHS). Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. June. Summary of Data Reported and Evaluation [online] 2004. Available at URL: http://ntp. J Pharmacol Exp Ther 1999.cdc. Benowitz NL. Available at URL: http:// cancercontrol.S. National Toxicology Program (NTP). Tob Control 2006. Schwartz SS. Sweeney CT. Schober SE.S. Department of Heath and Human Services.S Department of Health and Human Services (U. 1988-1991. Epidemiol Rev 1996. Coordinating Center for Health Promotion. Herrera B. [online]. Benowitz NL. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.pdf. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Smoking and Tobacco Control Monograph 10 [online]. Exposure of the U.57(1):79115. et al. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Nicotine metabolism and intake in black and white smokers. available at URL: http://mtn. 1991. DHHS). U.7:369-375. 1999-2002. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. In Report on Carcinogens.nih. Bernert JT. Perez-Stable EJ. Jacob P III. Turner DM. Benowitz NL. 11th ed. Giovino G. Fong I. Coordinating Center for Health Promotion. Summary of Data Reported and Evaluation [online] 1986.275:1233-1240.94(2):314-320. Third National Report on Human Exposure to Environmental Chemicals.pdf. JAMA 1998. population to secondhand smoke: 1988-2002.cancer. Brody DJ. Kozlowski LT.114(6):853-858. Modin G.gov/ntp/roc/eleventh/profiles/ s176toba. 4/13/09 Centers for Disease Control and Prevention (CDC).S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.S. Metabolism of nicotine to cotinine studied by a dual stable isotope method.

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

S. Urinary N.160) < LOD .130-.220 (.180 (.210 (.EPA at: http://www.S.110 (<LOD-.130 (.180) < LOD .110 (.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. including seizures and encephalopathy.EPA.130) < LOD . Sudakin and Trevathan.gov/pesticides/. and it has not been rated by IARC or NTP with respect to human carcinogenicity. DEET can be applied to clothing and the skin to repel biting insects. DEET is not genotoxic.S.130-.140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . About 3-8% of dermally applied DEET is absorbed. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample..S.100-. Neurological effects in humans.100-.100-.S.140) < LOD .250) < LOD . population from the National Health and Nutrition Examination Survey.110 (<LOD-. There are over 225 insect repellents brands containing DEET.150) < LOD .120-.N-Diethyl-meta-toluamide (DEET) CAS No. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. 1998).100-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .EPA.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. 2003). 2002). 1998).110 (. and they range in concentration from 4% to 100%.180 (. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.100 (<LOD-.N-Diethyl-meta-toluamide (DEET) N.140 (.140-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. One survey detected DEET in 74% of sampled streams in the U. DEET is also used in combination with dermal sun screens (U. have been reported as result of self-poisoning by ingestion or excessive dermal application.110 (.110-.130-.120-. 2003).520) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD. Its use is recommended for prevention of several vector-borne diseases.140) < LOD . 134-62-3 General Information N. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170 (. DEET is not a developmental or reproductive toxicant in animals (U. 1995.190) < LOD .1. DEET has low acute toxicity. Additional information is available from U. (Kolpin et al.. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.130) < LOD .130 (. DEET is not registered for use on agricultural commodities.S. 2005).N. EPA.N-Diethyl-meta-toluamide (DEET) 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. (U.180 (.100-.170 (.130-. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.130 (.100-.110 (.epa.110-.560) < LOD .140) < LOD .240) < LOD .449 and 0.220) 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 . Fourth National Report on Human Exposure to Environmental Chemicals 19 . After absorption. 2002).210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

N.280 (.500 (.230-.440) < LOD .270 (.170-.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.640 (.410-..370) < LOD . Urinary N. 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.150-.190 (.270) < LOD .370-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.93) < LOD . the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. Survey Geometric mean (95% conf.350-.410 (.190 (<LOD-.330 (.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.350) < LOD .S.290-.150) < LOD .130 (<LOD-.250) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.230-. 1992).690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.240) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.270 (<LOD-.230) < LOD .190-.140-. Urinary DEET levels as high as 5.200 (.410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .320 (.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 .270-.S.480 (.490) < LOD .250-. In this survey period.280-1.330 (.190 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .240-.390-.320) < LOD .300 (. 2007). Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U. representative subsamples from NHANES 2001-2002..250 (.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 . 2005).N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.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 .630) < LOD .350) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

epa. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. 1993-1997. Sudakin DL. Atlanta (GA). Chemical Summary. Osimitz TG.gov/teach/chem_summ/ DEET_summary. DeBord KE.S. 4/9/09 U. Available at URL: http://www. U.S.S. 1999-2000: a national reconnaissance. DEET: a review and update of safety and risk in the general population. Chen H. Centers for Disease Control and Prevention (CDC). Page BC. Meyer MT. Veltri JC. EPA. Environmental Protection Agency (U. pp. Toxicity and Exposure Assessment in Children’s Health.N-diethyl-mtoluamide following dermal application to human volunteers. Washington (DC): U. Grzywacz JG.115(8):1254-1260. Environ Health Perspect 2007. Thurman EM. Smallwood AW.epa.pdf.gov/oppsrrd1/REDs/0002red. 2005 Kolpin DW. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . and excretion of N.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.EPA). and other organic wastewater contaminants in U. Bell JW. Gabriel KL. metabolism. Schoenig GP. streams. Int J Toxicol 2002. J Anal Toxicol 1992. Barr DB. Fundam Appl Toxicol 1995. 2005.EPA).N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Available at URL: http://www. Environ Sci Technol 2002.EPA.S. et al. Human exposures to N. Absorption. Lowry LK. N. Zaugg SD. Diethyltoluamide (DEET).25:95-100. 1-118.S. Environmental Protection Agency (U. Pharmaceuticals. September 1998. Hartnagel RE Jr. Quandt SA. Tapia J. pdf. hormones.N-Diethyl-meta-toluamide (DEET) References Arcury TA.2:341352.36(6):1202-1211. EPA 738-R98-010.S.N. U.S.41(6):831-839. Barber LB.16(1):10-13. Furlong ET. Trevathan WR. Selim S. Third National Report on Human Exposure to Environmental Chemicals. J Toxicol Clin Toxicol 2003. Reregistration Eligibility Decision (RED): DEET.

Disinfection By-Products (Trihalomethanes)

Disinfection By-Products (Trihalomethanes)
Bromodichloromethane CAS No. 75-27-4 Dibromochloromethane (Chlorodibromomethane) CAS No. 124-48-1 Tribromomethane (Bromoform) CAS No. 75-25-2 Trichloromethane (Chloroform) CAS No. 57-57-8 General Information Disinfection by-products (DBP) are a class of chemical by-products also referred to as trihalomethanes (THMs), formed when chlorine or bromine interacts with the natural organic materials found in water. DBPs also include other formed products, such as haloacetic acids, haloacetonitriles, haloketones, and chlorophenols. The composition and levels of specific DBPs are determined by water quality, water treatment conditions, and disinfectant type (IPCS, 2000). Primary sources of DBPs are chlorinated drinking water and recreational water bodies, such as swimming pools.

In drinking water, trichloromethane is the predominant DBP, usually found at much higher levels than bromodichloromethane; tribromomethane is the least abundant (Krasner et al., 1989). DBPs are volatile at room temperature and can be detected in ambient air during activities such as showering, bathing, dishwashing, and swimming (Backer, et al., 2000; Gordon et al., 2006). Trichloromethane has industrial applications and is used to produce refrigerants and feedstock. It may be released into the environment where chlorine-based chemicals are used for bleaching and disinfecting processes or disposed at hazardous waste sites (IPCS, 2004; LaRegina, et al. 1986). Tribromomethane has limited industrial uses, mainly in geological assaying, electronics manufacturing, and as a solvent in laboratory analyses (ATSDR, 2005). DBPs tend not to bioaccumulate in aquatic organisms or persist in open or surface waters or soils, but they can remain in water within closed pipe systems. Workplace exposure may occur during the production of trichloromethane or tribromomethane, or in workplaces where DBPs may be generated, such as pulp or paper manufacturing, swimming pools, and water treatment plants (IPCS, 2004). General population exposure to DBPs occurs primarily through ingesting chlorinated water and inhaling the water

Blood Bromodichloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 2.21 (1.65-2.97)

Selected percentiles
( 95% confidence interval)

50th 2.30 (1.56-3.21) 1.40 (1.10-1.90)

75th 4.63 (3.24-6.20) 3.40 (2.60-4.20)

90th 8.45 (5.86-12.0) 6.20 (5.30-7.00)

95th 12.0 (7.68-19.2) 9.50 (7.00-12.0)

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

1.50 (1.20-1.86)

Sample size 785 1322

01-02 03-04

2.21 (1.65-2.97) 1.50 (1.20-1.86)

2.30 (1.56-3.21) 1.40 (1.10-1.90)

4.63 (3.24-6.20) 3.40 (2.60-4.20)

8.45 (5.86-12.0) 6.20 (5.30-7.00)

12.0 (7.68-19.2) 9.50 (7.00-12.0)

785 1322

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

2.19 (1.60-3.00) 1.48 (1.18-1.85) 2.24 (1.66-3.01) 1.51 (1.21-1.90)

2.31 (1.63-3.21) 1.40 (.940-2.00) 2.28 (1.49-3.24) 1.50 (1.10-1.90)

4.64 (3.21-6.08) 3.40 (2.60-4.30) 4.63 (3.09-7.01) 3.30 (2.50-4.20)

7.96 (5.74-15.3) 6.60 (5.40-7.20) 8.62 (5.26-12.9) 6.10 (4.69-7.30)

13.0 (6.93-20.5) 11.0 (7.20-14.0) 11.1 (7.68-25.0) 7.80 (6.40-12.0)

382 650 403 672

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

3.28 (2.29-4.68) 1.65 (1.15-2.38) 2.32 (1.82-2.94) 1.56 (1.15-2.13) 2.02 (1.42-2.87) 1.42 (1.11-1.81)

3.32 (2.19-4.70) 1.60 (.820-2.80) 2.50 (1.56-3.55) 1.70 (1.10-2.20) 2.16 (1.36-3.09) 1.30 (.850-1.90)

6.81 (3.71-10.4) 3.50 (2.60-4.90) 4.57 (3.60-5.56) 2.90 (2.15-3.80) 4.34 (2.92-6.01) 3.30 (2.30-4.40)

10.8 (8.24-14.7) 7.30 (4.50-10.0) 8.69 (5.63-9.49) 5.10 (3.80-6.60) 7.33 (4.72-15.3) 6.20 (5.20-7.20)

14.7 (11.1-20.5) 10.0 (7.30-11.0) 10.0 (5.89-13.5) 6.60 (4.90-13.0) 11.1 (6.01-26.1) 9.80 (6.70-13.0)

227 244 130 290 365 684

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.233 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

22

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

vapor. Dermal absorption also may occur during bathing and swimming (ATSDR, 1997, 2005; Dick, et al., 1995; Leavens et al., 2007). Each of the DBPs is rapidly absorbed and distributed widely throughout the body. In animals, these chemicals undergo hepatic metabolism to reactive chemicals, which can bind to cell macromolecules and be toxic in large amounts (IPCS, 2000). Ultimately, DBPs are metabolized to carbon dioxide, which is eliminated in exhaled air within a few hours. Only a small amount of each DBP is eliminated unchanged in urine. Elimination halflives for these chemicals are less than four hours (ATSDR, 2005; Leavens et al., 2007). Human health effects from DBPs at low environmental doses or at biomonitored levels from low environmental exposures are unclear or unknown. Humans exposed to massive levels of trichloromethane or tribromomethane develop central nervous system depression and hepatotoxicity (ATSDR, 2005, 1997). Acute animal toxicity studies of each of these chemicals have found central nervous system depression, liver and renal damage or necrosis, and occasionally, cardiac depression and arrhythmias (IPCS, 2000). In studies of rodents chronically fed high doses of either trichloromethane or bromodichloromethane, carcinomas occurred in the liver and kidney; large intestine tumors and

polyps were also noted with bromodichloromethane (NCI, 1976; NTP, 1987). Chronic feeding studies in rodents with either dibromochloromethane or tribromomethane showed inconsistent evidence of carcinogenicity across species and genders. The DBPs did not produce reproductive or developmental effects in animals unless maternal toxicity was present, but bromodichloromethane altered sperm motility (IPCS, 2000). Numerous epidemiologic studies of the relationships between chlorinated water source and various cancers, adverse reproductive outcomes, and cardiovascular disease have been inconclusive (IPCS, 2000). IARC classified trichloromethane and bromodichloromethane as possible human carcinogens, and NTP determined that these chemicals are reasonably anticipated to be human carcinogens. However, IARC found dibromochloromethane and tribromomethane to be unclassifiable regarding human carcinogenicity. The U.S. EPA has established drinking water and environmental standards for “total THMs.” OSHA and ACGIH have established workplace standards and guidelines, respectively, for trichloromethane and tribromomethane. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at: http://www.atsdr.cdc.gov/toxpro2.html.

Blood Dibromochloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) .867 (.521-1.44)

Selected percentiles
( 95% confidence interval)

50th .780 (.340-1.90) < LOD

75th 2.61 (1.22-4.38) 1.30 (1.00-1.80)

90th 5.46 (3.53-9.71) 3.60 (2.70-4.80)

95th 8.96 (5.04-12.9) 7.20 (4.80-8.60)

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

*

Sample size 781 1333

01-02 03-04

.867 (.521-1.44) *

.780 (.340-1.90) < LOD

2.61 (1.22-4.38) 1.30 (1.00-1.80)

5.46 (3.53-9.71) 3.60 (2.70-4.80)

8.96 (5.04-12.9) 7.20 (4.80-8.60)

781 1333

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

.850 (.481-1.50) * .884 (.550-1.42) *

.730 (.300-2.25) < LOD .820 (.340-1.69) < LOD

2.66 (.960-4.38) 1.30 (1.00-1.90) 2.54 (1.37-4.31) 1.30 (1.00-1.80)

4.77 (3.33-9.20) 3.70 (2.70-5.70) 6.30 (3.28-10.1) 3.60 (2.50-4.80)

8.06 (4.31-14.6) 7.20 (5.20-8.60) 9.91 (5.02-13.0) 6.60 (3.80-9.20)

371 657 410 676

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

1.61 (.843-3.06) 1.20 (.963-1.50) 1.03 (.505-2.09) * .736 (.413-1.31) *

1.49 (.670-3.99) 1.10 (.810-1.40) .930 (.530-2.03) < LOD .640 (<LOD-1.93) < LOD

4.59 (1.93-8.89) 2.30 (1.50-4.10) 2.03 (.770-7.06) .970 (.650-1.60) 2.49 (.870-4.27) 1.30 (.950-1.80)

9.26 (5.21-12.1) 5.20 (3.80-6.90) 4.22 (2.01-10.5) 1.90 (1.20-3.20) 4.57 (3.00-7.12) 3.30 (2.50-4.60)

12.0 (9.63-16.1) 7.70 (5.20-11.0) 8.09 (2.80-16.5) 3.20 (1.80-5.20) 6.98 (4.27-11.1) 6.60 (3.70-9.20)

233 256 128 288 357 685

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.271 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

23

Disinfection By-Products (Trihalomethanes)

Biomonitoring Information Levels of blood DBPs reflect recent exposure. Geometric mean blood trichloromethane levels were 0.039 and 0.043 ng/mL among non-smoking and smoking adults, respectively, in a subsample of NHANES 1999-2000 participants (Lin et al., 2008), which were at least twice as high as comparable levels in NHANES 2001-2002 and 2003-2004. In a non-representative sample of NHANES III (1988-1994) participants, the geometric mean and median blood trichloromethane levels, respectively, were 0.043 and 0.023 mg/L (Churchill et al., 2001). Similar median blood trichloromethane levels were reported in smaller studies of U.S adults (Ashley et al., 2005; Backer et al., 2000; Buckley et al., 1997) and in this Report. Immediately following bathing or showering with chlorinated water, median blood levels of trichloromethane, dibromochloromethane, and bromodichloromethane can increase two to four times over baseline levels, and then return to baseline rapidly during the next one to two hours (Ashley et al., 2005; Backer et al., 2000). Finding a measurable amount of one or more of these THMs in blood does not mean that the level of THMs causes an adverse health effect. Biomonitoring studies of blood

THMs can provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of THMs than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Blood Tribromomethane (Bromoform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 1.57 (1.07-2.31)

Selected percentiles
( 95% confidence interval)

50th 1.39 (.960-2.02) < LOD

75th 2.78 (1.76-4.63) 1.80 (<LOD-2.80)

90th 6.05 (2.92-29.2) 3.74 (2.30-7.10)

95th 15.5 (3.68-85.4) 6.40 (3.60-14.0)

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

*

Sample size 774 1310

01-02 03-04

1.57 (1.07-2.31) *

1.39 (.960-2.02) < LOD

2.78 (1.76-4.63) 1.80 (<LOD-2.80)

6.05 (2.92-29.2) 3.74 (2.30-7.10)

15.5 (3.68-85.4) 6.40 (3.60-14.0)

774 1310

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

1.49 (.944-2.34) * 1.67 (1.17-2.39) *

1.29 (.850-1.98) < LOD 1.46 (1.05-2.21) < LOD

2.65 (1.49-5.05) 1.90 (<LOD-2.87) 2.86 (1.89-4.57) 1.72 (<LOD-2.65)

6.12 (2.26-33.9) 4.00 (2.40-6.80) 5.69 (3.30-27.5) 3.20 (1.93-7.70)

14.9 (2.79-69.9) 6.50 (4.00-13.0) 22.2 (5.09-49.6) 6.10 (3.10-31.0)

374 645 400 665

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

2.34 (1.15-4.77) * 1.51 (.857-2.67) * 1.47 (.980-2.22) *

1.66 (.990-3.38) 1.60 (<LOD-3.10) 1.47 (.780-3.15) < LOD 1.29 (.840-2.06) < LOD

4.03 (1.42-36.5) 3.30 (<LOD-9.40) 2.58 (1.39-4.64) 1.60 (<LOD-2.30) 2.58 (1.51-4.91) 1.70 (<LOD-2.90)

28.3 (4.39-49.2) 7.60 (3.60-14.0) 4.34 (2.57-8.48) 2.50 (1.80-3.20) 5.69 (2.84-21.2) 3.50 (2.00-7.70)

40.8 (31.5-57.9) 11.0 (5.60-210) 6.27 (3.28-15.2) 3.20 (2.40-6.10) 11.0 (3.30-69.9) 5.90 (3.30-21.0)

234 242 121 289 362 680

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.596 and 1.5. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

24

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

Blood Trichloromethane (Chloroform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 16.6 (13.0-21.1)

Selected percentiles
( 95% confidence interval)

50th 16.1 (11.9-22.2) 10.0 (8.50-13.0)

75th 31.7 (23.9-40.4) 20.0 (17.0-24.0)

90th 55.5 (44.5-68.6) 35.0 (29.0-40.0)

95th 72.1 (57.3-105) 50.0 (37.0-65.0)

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

10.2 (8.56-12.2)

Sample size 744 1222

01-02 03-04

16.6 (13.0-21.1) 10.2 (8.56-12.2)

16.1 (11.9-22.2) 10.0 (8.50-13.0)

31.7 (23.9-40.4) 20.0 (17.0-24.0)

55.5 (44.5-68.6) 35.0 (29.0-40.0)

72.1 (57.3-105) 50.0 (37.0-65.0)

744 1222

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

16.8 (12.0-23.5) 10.1 (8.43-12.1) 16.4 (13.4-20.1) 10.4 (8.41-12.7)

16.1 (11.0-24.8) 10.0 (7.90-14.0) 16.6 (12.0-21.5) 10.0 (8.40-13.0)

34.3 (22.4-48.7) 20.0 (17.0-25.0) 29.2 (24.0-36.5) 20.0 (16.0-23.9)

57.0 (39.9-76.4) 36.8 (29.0-49.0) 53.5 (38.4-68.9) 33.0 (26.0-40.0)

75.2 (54.5-156) 53.0 (36.8-69.0) 69.5 (53.3-104) 46.0 (35.0-65.0)

358 599 386 623

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

17.0 (10.5-27.6) 9.17 (7.45-11.3) 19.1 (12.9-28.1) 11.8 (9.54-14.6) 15.6 (12.0-20.2) 9.84 (8.09-12.0)

14.5 (10.0-32.7) 9.30 (7.60-11.0) 20.9 (9.28-37.4) 12.0 (8.90-15.0) 15.2 (11.2-20.5) 10.0 (8.10-13.0)

35.1 (18.6-57.6) 19.0 (15.0-24.0) 38.4 (27.7-46.0) 20.0 (15.0-30.0) 26.8 (20.4-39.5) 20.0 (16.0-23.0)

60.7 (41.5-100) 34.0 (24.0-44.4) 55.9 (45.5-69.8) 35.0 (28.0-59.0) 53.5 (35.3-72.1) 33.8 (27.0-40.0)

93.0 (49.7-243) 44.4 (30.0-59.0) 68.9 (51.9-74.0) 61.0 (34.0-100) 69.5 (53.5-105) 47.0 (35.0-67.0)

223 225 116 272 348 630

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 2.37 and 2.11. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

Fourth National Report on Human Exposure to Environmental Chemicals

25

Disinfection By-Products (Trihalomethanes)

References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for chloroform update. 1997 [online]. Available at URL: http://www.atsdr.cdc.gov/toxprofiles/tp6.html. 4/26/09 Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for bromoform and chlorodibromomethane. 2005 [online]. Available at URL: http://www.atsdr.cdc.gov/ toxprofiles/tp130.html. 4/26/09 Ashley DL, Blount BC, Singer PC, Depaz E, Wilkes C, Gordon S, et al. Changes in blood trihalomethanes concentrations resulting from differences in water quality and water use activities. Arch Environ Occup Health 2005;60(1):7-15. Backer LC, Ashley DL, Bonin MA, Cardinali FL, Kieszak SM, Wooten JV. Household exposures to drinking water disinfection by-products: whole blood trihalomethane levels. J Expo Anal Environ Epidemiol 2000;10(4):321-326. Buckley TJ, Liddle J, Ashley DL, Paschal DC, Burse VW, Needham LL. Environmental and biomarker measurements in nine homes in the lower Rio Grande Valley: multimedia results for pesticides, metals, PAHs and VOCs. Environ Int 1997;23(5):705732. Churchill JE, Ashley DL, Kaye WE. Recent chemical exposures and blood volatile organic compound levels in a large populationbased sample. Arch Environ Health 2001;56(2):157-166. Dick D, Ng KM, Sauder DN, Chu I. In vitro and in vivo percutaneous absorption of 14C-chloroform in humans. Hum Exp Toxicol 1995;14: 260-265. Gordon SM, Brinkman MC, Ashley DL, Blount BC, Lyu C, Masters J, Singer PC. Changes in breath trihalomethane levels resulting from household water-use activities. Environ Health Perspect 2006;114(4):514-521. International Programme on Chemical Safety (IPCS). Environmental Health Criteria 216. Disinfectants and Disinfectant By-Products. 2000 [online]. Available at URL: http://www. inchem.org/documents/ehc/ehc/ehc216.htm.4/26/09 International Programme on Chemical Safety (IPCS). Concise International Chemical Assessment Document 58. Chloroform. 2004 [online]. Available at URL: http://www.inchem.org/ documents/cicads/cicads/cicad58.htm. 4/26/09 Krasner SW, McGuire MJ, Jacaugelo JG, Patania NL, Reagan KM, Aieta EM. The occurrence of disinfection by-products in US drinking water. J Am Water Works Assoc 1989;81:41–53. LaRegina J, Bozzelli JW, Harkov R, Gianti S. Volatility organic compounds at hazardous waste sites and a sanitary landfill in New

Jersey. An up-to-date review of the present situation. Environ Prog 1986;5:18-27. Leavens TL, Blount BC, De Marini DM, Madden MC, Valentine JL, Case MW, et al. Disposition of bromodichloromethane in humans following oral and dermal exposure. Toxicol Sci 2007;99(2):432-445. Lin YS, Egeghy PP, Rappaport SM. Relationships between levels of volatile organic compounds in air and blood from the general population. J Expo Sci Environ Epidemiol 2008;18(4):421-9. National Cancer Institute (NCI). Report on the carcinogenesis bioassay of chloroform (CAS No. 67-66-3). National Cancer Institute Carcinogenesis Technical Report Series March 1, 1976. [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/htdocs/ LT_rpts/trChloroform.pdf. 4/26/09 National Toxicology Program (NTP). Carcinogenesis studies of bromodichloromethane (CAS No. 75-27-4) in F344/N rats and B6C31F mice (gavage studies). Technical Report Series No. 321. 1987 [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/ htdocs/LT_rpts/tr321.pdf. 4/26/09

26

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

Benzophenone-3
CAS No. 131-57-7 General Information Benzophenone-3 (2-hydroxy-4-methoxybenzophenone) occurs naturally in some flowering plants. It is commercially synthesized as a sunscreen for use in lotions, conditioners, and cosmetics. It is also used as a UV stabilizer in plastic surface coatings and polymers. Benzophenone-3 is a common ingredient in sun-blocking agents. People may be exposed through dermal application of sunscreens and cosmetic products. Small amounts of benzophenone-3 can be absorbed through human skin and excreted in the urine, mostly as a glucuronidated conjugate (Gonzalez et al., 2006; Gustavsson et al., 2002; Janjua et al., 2004; Ye et al., 2005). After dermal application of a 4% lotion over the entire body daily for 5 days, one study found that 1.2-8.7% of the applied benzophenone-3 amount was recovered in the urine (Gonzalez et al., 2006). Human health effects from benzophenone-3 at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Following dermal application, some cases of photoallergy or allergy to benzophenone-3 have been reported. Male reproductive toxicity has been inconsistently reported in chronic high dose animal studies (Daston et al., 1993; French, 1992). Benzophenone-3 has weak estrogenic activity or weak anti-androgenic activity (French, 1992; Schlecht et al., 2004; Schlumpf et al., 2001; Schreurs et al., 2005). No human hormonal changes were observed during four days of application of 10% benzophenone-3 lotion (Janjua et al., 2004). Benzophenone-3 is not considered mutagenic (Robison et al., 1994). IARC and NTP have no ratings as to human carcinogenicity of benzophenone-3. Biomonitoring Information Urinary benzophenone-3 levels include both conjugated and unconjugated forms and reflect recent exposure to the chemical. The NHANES 2003-2004 levels of urinary benzophenone-3 have been described by Calafat et al. (2008). The analysis showed that female participants had slightly higher urinary levels than males and that nonHispanic whites were more likely than non-Hispanic blacks to have levels above the 95th percentile of the overall population. In a study of 90 U.S. females aged 6-8 years, the median urinary benzophenone-3 level of 14.7 µg/L was comparable to the median level of children 6-11 years of age (17.2 µg/L) in the NHANES 2003-2004 subsample (Calafat

et al., 2008; Wolff et al., 2007). Total benzophenone-3 urinary concentrations were detectable in 90% of a small sample of adults in whom the values ranged up to 3000 μg/L (Ye et al., 2005). Following short-term application of 10% benzophenone-3 lotion, men and women had mean urinary levels of 140 and 60 μg/L, respectively (Janjua et al., 2004). Finding a measurable amount of benzophenone-3 in urine does not mean that the levels of benzophenone-3 cause an adverse health effect. Biomonitoring studies on levels of benzophenone-3 provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of benzophenone-3 than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Fourth National Report on Human Exposure to Environmental Chemicals

27

Environmental Phenols

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone)
Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.9 (18.1-28.9)

Selected percentiles
( 95% confidence interval)

Sample 95th 1040 (698-1390) size 2517

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

years 03-04

50th 18.1 (15.5-23.2)

75th 94.0 (67.5-123)

90th 370 (225-570)

03-04 03-04 03-04

21.2 (16.4-27.3) 22.9 (18.0-29.3) 23.1 (18.0-29.6)

17.2 (14.9-25.9) 20.1 (16.1-25.1) 18.1 (14.7-23.3)

66.7 (38.7-102) 67.1 (45.2-93.8) 109 (72.1-140)

158 (106-246) 170 (137-240) 450 (315-733)

246 (154-618) 407 (183-717) 1220 (769-1750)

314 715 1488

03-04 03-04

16.8 (13.2-21.3) 30.7 (23.7-39.8)

13.7 (11.4-16.8) 26.0 (20.2-34.1)

55.3 (33.2-86.6) 137 (106-172)

178 (134-324) 596 (403-769)

567 (238-1350) 1340 (776-1790)

1229 1288

03-04 03-04 03-04

16.5 (10.9-25.1) 12.8 (9.38-17.4) 27.7 (20.3-37.8)

11.9 (8.50-18.3) 10.2 (7.40-14.4) 24.4 (16.8-32.0)

45.5 (25.9-78.2) 34.3 (22.8-50.6) 121 (83.6-162)

178 (76.4-412) 127 (90.8-176) 507 (316-769)

412 (178-2180) 247 (143-499) 1340 (733-2070)

613 652 1092

Limit of detection (LOD, see Data Analysis section) for Survey year 03-04 is 0.3.

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) (creatinine corrected)
Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.2 (17.6-28.0)

Selected percentiles
( 95% confidence interval)

Sample 95th 1080 (686-1600) size 2514

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

years 03-04

50th 16.2 (12.7-21.6)

75th 82.0 (58.7-108)

90th 415 (283-577)

03-04 03-04 03-04

25.8 (19.5-34.1) 17.2 (13.7-21.5) 22.8 (17.8-29.1)

22.4 (14.4-33.7) 12.9 (10.4-16.5) 16.2 (12.7-21.9)

84.6 (41.0-131) 43.6 (29.5-57.7) 93.2 (66.0-130)

171 (132-365) 136 (91.7-239) 491 (361-700)

427 (171-710) 350 (173-646) 1330 (880-1880)

314 713 1487

03-04 03-04

13.6 (10.8-17.1) 35.5 (27.1-46.4)

10.3 (8.36-12.9) 28.2 (20.2-37.0)

40.0 (24.9-62.5) 144 (101-224)

169 (93.3-316) 686 (491-1130)

381 (229-685) 1850 (1220-2580)

1228 1286

03-04 03-04 03-04

15.1 (9.44-24.0) 8.78 (6.49-11.9) 28.3 (20.6-38.8)

11.1 (6.95-16.0) 6.80 (5.27-9.00) 22.0 (14.6-32.7)

40.7 (18.3-85.8) 19.7 (13.5-33.4) 116 (73.5-175)

158 (87.4-362) 79.8 (46.8-139) 510 (380-760)

595 (118-1860) 185 (79.8-536) 1330 (852-2410)

612 651 1091

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Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

References Calafat AM, Wong LY, Ye X, Reidy JA, Needham LL. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003--2004. Environ Health Perspect 2008;116(7):893-897. Daston GP, Gettings SD, Carlton BD, Chudkowski M, Davis RA, Kraus AL, et al. Assessment of the reproductive toxic potential of dermally applied 2-hydroxy-4-methoxybenzophenone to male B6C3F1 mice. Fundam Appl Toxicol 1993;20(1):120-124. French JE. NTP technical report on the toxicity studies of 2-hydroxy-4-methoxybenzophenone (CAS No. 131-57-7) Adminstered topically and in dosed feed to F344/N Rats and B6C3F1 mice. National Institutes of Health Publication No. 923344, October 1992 (also Toxic Rep Ser. 1992 Oct;21:1-E14). Gonzalez H, Farbrot A, Larko O, Wennberg AM. Percutaneous absorption of the sunscreen benzophenone-3 after repeated whole-body applications, with and without ultraviolet irradiation. Br J Dermatol 2006;154(2):337-340. Gustavsson Gonzalez H, Farbrot A, Larko O. Percutaneous absorption of benzophenone-3, a common component of topical sunscreens. Clin Exp Dermatol 2002;27(8):691-694. Janjua NR, Mogensen B, Andersson AM, Petersen JH, Henriksen M, Skakkebaek NE, et al. Systemic absorption of the sunscreens benzophenone-3, octyl methoxycinnamate, and 3-(4-methylbenzylidene) camphor after whole-body topical application and reproductive hormone levels in humans. J Invest Dermatol 2004;123(1):57-61. Okereke CS, Barat SA, Abdel-Rahman MS. Safety evaluation of benzophenone-3 after dermal administration in rats. Toxicol Lett 1995;80(1-3):61-67. Robison SH, Odio MR, Thompson ED, Aardema MJ, Kraus AL. Assessment of the in vivo genotoxicity of 2-hydroxy 4-methoxybenzophenone. Environ Mol Mutagen 1994;23(4):312317. Schlecht C, Klammer H, Jarry H, Wuttke W. Effects of estradiol, benzophenone-2 and benzophenone-3 on the expression pattern of the estrogen receptors (ER) alpha and beta, the estrogen receptorrelated receptor 1 (ERR1) and the aryl hydrocarbon receptor (AhR) in adult ovariectomized rats. Toxicology 2004;205(12):123-130. Schlumpf M, Cotton B, Conscience M, Haller V, Steinmann B, Lichtensteiger W. In vitro and in vivo estrogenicity of UV screens. Environ Health Perspect 2001;109(3):239-244. Erratum in: Environ Health Perspect 2001;109(11):A517. Schreurs RH, Sonneveld E, Jansen JH, Seinen W, van der Burg B. Interaction of polycyclic musks and UV filters with the estrogen

receptor (ER), androgen receptor (AR), and progesterone receptor (PR) in reporter gene bioassays. Toxicol Sci 2005;83(2):264-272. Ye X, Kuklenyik Z, Needham LL, Calafat AM. Quantification of urinary conjugates of bisphenol A, 2,5-dichlorophenol, and 2-hydroxy-4-methoxybenzophenone in humans by online solid phase extraction-high performance liquid chromatographytandem mass spectrometry. Anal Bioanal Chem 2005;383(4):638644.

Fourth National Report on Human Exposure to Environmental Chemicals

29

Environmental Phenols

Bisphenol A

CAS No. 80-05-7 General Information Bisphenol A is a phenolic chemical which has been used for over 50 years in the manufacture of polycarbonate plastics and epoxy resins; in thermal paper production; and as a polymerization inhibitor in the formation of some polyvinyl chloride plastics. Polycarbonates are used to make products such as compact discs, automobile parts, baby bottles, plastic dinnerware, eyeglass lenses, toys, and impact-resistant safety equipment. Epoxy resins containing bisphenol A are used in protective linings of some canned food containers, wine vat linings, epoxy resin-based paints, floorings, and some dental composites. In recent years, about 5-6 billion pounds of bisphenol were produced annually worldwide. Bisphenol A may enter the environment from industrial sources or from product leaching, disposal, and use. In 1999-2000, bisphenol A was detected in 41.2% of 139 U.S. streams in 30 states (Kolpin et al., 2002). Bisphenol A can be biodegraded and does not bioaccumulate significantly in aquatic organisms. Some invertebrates may be sensitive and show reproductive effects (European Commission, 2003).

component of total exposure estimates (Wilson et al., 2007. In animal and human studies, bisphenol A is well absorbed orally. In humans, little free bisphenol A circulates after oral absorption due to the high degree of glucuronidation by the liver. The glucuronidated bisphenol A is excreted in the urine within 24 hours with no evidence of accumulation (Volkel et al., 2002).

Human health effects from bisphenol A at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Occupational exposure of epoxy workers to bisphenol A dust may produce eye irritation and skin sensitization. In animal studies, bisphenol A has low acute toxicity. It is not considered a teratogen (Kim et al., 2001). Bisphenol A is rated as weakly estrogenic (Matthews et al., 2001). Some reproductive or developmental changes are observed at high doses in standard experimental animal studies (e.g., delayed vaginal opening and preputial separation) (Ema et al., 2001; Tyl et al., 2002; NTPCERHR, 2008). Reproductive and neurodevelopmental effects of bisphenol A at low doses in animals, including environmental doses potentially relevant to humans, have been the subject of ongoing scientific reviews and study (European Commission, 2002; Gray et al., 2004; NTP, 2001; NTP-CERHR, 2007 and 2008; vom Saal and Hughes, 2005 Welshons et al., 2006; Witorsch, 2002). Examples General population exposure to bisphenol A may occur of recent animal studies which suggest possible low dose through ingestion of foods in contact with bisphenol A effects include altered development of the fetal prostate containing materials. For small children, hand-to-mouth and mammary gland, inhibition of postnatal testosterone and direct oral contact with materials containing bisphenol production, and changes in neurodevelopment (Akingbemi A are possible. Exposure from indoor air is a small et al., 2004; Leranth et al., 2008; NTP-CERHR, 2007;

Urinary Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane)
Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 2.64 (2.38-2.94)

Selected percentiles
( 95% confidence interval)

Sample 95th 16.0 (14.4-17.2) size 2517

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

years 03-04

50th 2.80 (2.50-3.10)

75th 5.50 (5.00-6.20)

90th 10.6 (9.40-12.0)

03-04 03-04 03-04

3.55 (2.95-4.29) 3.74 (3.31-4.22) 2.41 (2.15-2.72)

3.80 (2.70-5.00) 4.30 (3.60-4.60) 2.60 (2.30-2.80)

6.90 (6.00-8.30) 7.80 (6.50-9.00) 5.10 (4.50-5.70)

12.6 (9.50-15.1) 13.5 (11.8-15.2) 9.50 (8.10-11.3)

16.0 (11.5-23.3) 16.5 (15.2-20.9) 15.2 (12.4-18.1)

314 715 1488

03-04 03-04

2.92 (2.63-3.24) 2.41 (2.11-2.75)

3.20 (2.70-3.60) 2.50 (2.20-2.80)

6.10 (5.40-6.60) 5.00 (4.20-6.20)

10.4 (9.50-11.6) 10.6 (8.70-12.5)

16.0 (12.7-17.6) 15.9 (13.5-20.1)

1229 1288

03-04 03-04 03-04

2.58 (2.15-3.08) 4.24 (3.73-4.82) 2.51 (2.26-2.79)

2.60 (2.10-3.20) 4.30 (3.80-5.10) 2.70 (2.50-3.00)

5.20 (4.40-6.50) 8.20 (7.10-9.80) 5.20 (4.70-5.80)

9.90 (7.30-13.9) 14.2 (11.7-16.9) 9.60 (8.30-10.9)

15.4 (10.2-19.7) 20.6 (14.9-25.2) 15.1 (12.6-16.7)

613 652 1092

Limit of detection (LOD, see Data Analysis section) for Survey year 03-04 is 0.4.

30

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

Timms et al., 2005). Bisphenol A is not considered mutagenic and is unlikely to be a carcinogen, although it may form DNA adducts in vitro and inhibit mitotic spindle activity (Haighton et al., 2002). IARC and NTP do not have ratings for bisphenol A with respect to human carcinogenicity. The epoxy resin oligomer, bisphenol A diglycidyl ether, has limited evidence of animal carcinogenicity and is not classifiable as a human carcinogen by IARC. Biomonitoring Information Urinary levels of bisphenol A include both conjugated and unconjugated forms and reflect recent exposure to the chemical. In the participants of NHANES 20032004, prevalent exposure to bisphenol A in the U.S. population was demonstrated with children, females, and lower income strata having slightly higher urinary levels (Calafat et al., 2008). This study confirmed levels seen in an earlier smaller sample of 394 U.S. residents (Calafat et al., 2005). Several previous small studies in Japanese pregnant women, Japanese university students, and Korean residents have found mean urinary bisphenol A levels to be similar or up to several times higher than those in the U.S. representative NHANES 2003-2004 subsample (Fujimaki et al., 2004; Kim et al., 2003; Ouchi and Watanabe, 2002), although one study of 73 Koreans found levels that averaged seven times higher than median levels in the NHANES 2003-2004 subsample (Yang et al., 2003; Calafat et al., 2008). Applications of certain dental sealants were shown to increase urinary levels of bisphenol A for 24

hours (Joskow et al., 2006). Hanaoka et al. (2002) studied workers with exposure to bisphenol A diglycidyl ether and found mean urinary levels of bisphenol A about double that of unexposed workers. Finding a measurable amount of bisphenol A in the urine does not mean that the levels of bisphenol A cause an adverse health effect. Biomonitoring studies on levels of bisphenol A provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of bisphenol A than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Urinary Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane) (creatinine corrected)
Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 2.58 (2.36-2.82)

Selected percentiles
( 95% confidence interval)

Sample 95th 11.2 (9.78-12.4) size 2514

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

years 03-04

50th 2.50 (2.31-2.80)

75th 4.29 (3.88-4.75)

90th 7.67 (6.62-8.66)

03-04 03-04 03-04

4.32 (3.63-5.14) 2.80 (2.52-3.11) 2.39 (2.17-2.64)

4.29 (3.63-5.23) 2.74 (2.35-3.22) 2.36 (2.15-2.59)

7.14 (5.83-9.56) 4.74 (4.21-5.09) 3.93 (3.44-4.33)

12.2 (9.84-14.8) 7.79 (6.41-8.87) 6.64 (5.97-7.74)

15.7 (12.2-23.2) 11.8 (8.05-14.2) 10.0 (9.01-11.4)

314 713 1487

03-04 03-04

2.38 (2.15-2.63) 2.78 (2.50-3.08)

2.31 (2.08-2.70) 2.68 (2.40-2.94)

4.19 (3.81-4.64) 4.41 (3.81-5.15)

7.10 (6.41-8.28) 7.93 (6.48-10.2)

9.94 (9.06-11.7) 12.4 (9.29-18.2)

1228 1286

03-04 03-04 03-04

2.34 (2.02-2.71) 2.92 (2.58-3.32) 2.58 (2.37-2.81)

2.38 (2.00-2.65) 2.95 (2.51-3.27) 2.55 (2.32-2.80)

3.85 (3.24-4.55) 4.90 (4.07-6.13) 4.30 (3.93-4.67)

7.09 (5.00-9.04) 8.64 (7.53-9.63) 7.58 (6.32-8.87)

10.9 (8.50-14.3) 11.9 (10.2-13.3) 11.0 (9.34-12.4)

612 651 1091

Fourth National Report on Human Exposure to Environmental Chemicals

31

pdf.116(1):39-44. Arakawa C. Yoshinaga J. Endocrinology 2008. et al. Ecotoxicity and the Environment (CSTEE). Belgium. Needham LL. 2007.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Environ Sci Technol 2002.pdf .S. Cunha G.pdf. Rubin C. Pyo MY. Lynch BS. Joskow R. 2008. Barber LB. Leranth. 2003. 5: 505-523.69(22):2611-2625. National Institutes of Health.. bisphenol A glucuronide.10:875-921. Koh WS. November 26. Department of Health and Human Services. Biochem Biophys Res Commun 2003..59(4):403-408. Szigeti-Buck. September.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Furlong ET. Keimowitz AR. May 22. C. with estrogen receptors alpha and beta. Pharmaceuticals. Reidy JA. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. J Am Dent Assoc 2006. Hanaoka T. Life Sci 2001. National Institute of Environmental Health Sciences. Gender differences in the levels of bisphenol A metabolites in urine. Twomey K. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Matthews JB. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Ikka T. K.113(4):391-395. 2/4/09 European Commission. T. 2/4/09 Fujimaki K. and other organic wastewater contaminants in U. Kawamura N. Human Health. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Available at URL: http://cerhr.68(1):121-146. Hum Ecol Risk Assess 2004. Shin HC. Harazono A. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. McConnell EE. Italy. August 2001. Calafat AM. Zaugg SD. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. and Hajszan. Ispra. Barr DB. Han SS.J. Brine DR. Available at URL: http://ec. Watanabe S. National Toxicology Program. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Han SY. Available at URL: http://cerhr. MacLusky.pdf . NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Marr MC. Tsugane S.149:988-994.europa. Cohen JT. Imai H. Furukawa M. Thurman EM. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.35(2 Pt 1):238-254. vom Saal FS.jrc. Koulova AI. Zacharewski TR. Calafat AM. Kiguchi M. 4.nih. Available at URL: http://ntp. Needham LL. Kolpin DW. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite.59(9):625-628.137(3):353-362. 2002. Proc Natl Acad Sci USA 2005.niehs. European Commission. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Serizawa S. Environ Health Perspect 2008.pdf. Bisphenol A. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Hara K. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Barton L. Chung MK. 1999-2000: a national reconnaissance. Regul Toxicol Pharmacol 2002. Reidy JA.S. Cha SW. Timms BG. N. Richter CA. hormones. Endocrinology 2004. Hlywka JJ. Kim YH.Scientific Committee on Toxicity. Rhomberg et al.145:592-603. Tyl RW. Wong LY. Ema M. Available at URL: http://ecb.nih. et al.eu/ health/ph_risk/committees/sct/documents/out156_en. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Occup Environ Med 2002. Doull J. Sottas CM. Klinefelter GR. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.36(6):1202-1211. Park S. Reprod Toxicol 2001. Brussels.gov/chemicals/bisphenol/bisphenol. Rat two-generation reproductive toxicity study of bisphenol A. Ekong J.S. Nippon Eiseigaku Zasshi 2004. streams. Caudill SP. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. niehs.nih. Joint Research Centre Institute of Health and Consumer Protection.14(2):149-157. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Yang M.Environmental Phenols References Akingbemi BT. Barr JR. Environ Health Perspect 2005. Kuklenyik Z. Chem Res Toxicol 2001. An evaluation of the possible carcinogenicity of bisphenol A to humans. Haighton LA. Watanabe C.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. 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. 2/4/09 Ouchi K.102(19):7014-7019. Kim JC. Fujii S. Gray GM.. DirectorateGeneral Health and Consumer Protection. NC. Needham LL. Calafat AM. Exposure of the U.312(2):441-448. Kim CS.gov/chemicals/bisphenol/BPAFinalEPVF112607.780(2):365-370. Bradley S. U. Meyer MT. Myers CB. Ye X. et al. Kroes R. Hughes C. Research Triangle Park. Thomas BF. and Hardy MP. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Toxicol Sci 2002. In vitro and in vivo interactions of bisphenol A and its metabolite. Howdeshell KL. Munro IC. niehs.

Food Chem Toxicol 2002. Dekant W. Colnot T. III. Sheldon LS. bisphenol-A. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. and nonylphenol at home and daycare. Welshons WV. Lordo RA. vom Saal FS. Jang JY. Csanady GA. Chuang JC. Lee SM. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. et al. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Vom Saal FS. Hughes C.103(1):9-20. Morgan MK.113(8):926-33. Nagel SC. An observational study of the potential exposures of preschool children to pentachlorophenol. Arch Environ Contam Toxicol 2003. Kawamoto T. Witorsch RJ.Environmental Phenols Volkel W.44(4):546-51. Biological monitoring of bisphenol a in a Korean population.15:12811287. Environ Health Perspect 2005. Filser JG. Environ Res 2007. Yang M. Wilson NK. Endocrinology 2006.147(6 Suppl):S56-69.40(7):905-12. Kim SY. Large effects from small exposures. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chang SS. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Chem Res Toxicol 2002.

497) * . Urinary 4-tert-Octylphenol (4-[1. 2004).Environmental Phenols 4-tert-Octylphenol CAS No. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (1. through sewage. which may vary for some chemicals by year and by individual sample. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.80 (1.50) ..3.S.S. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.389 (.500-1.00 (.60-3.477) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.70 (1. < LOD means less than the limit of detection. is used to manufacture alkylphenol ethoxylates. did not bioaccumulate.10-2.300-. Disposition in humans has not been studied sufficiently.900 (.900 (. to shorter chain alkylphenol ethoxylates.600-1.50-2. population from the National Health and Nutrition Examination Survey.60-3.70 (1.40) 2. 1997.30 (1. Survey Geometric mean (95% conf.90) 2. In the 1990s.500) . textiles..500) . 2000.10 (1.5% of 139 U. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.900 (.300 (<LOD-.20-2. 2002).20-2. In 1999-2000. and the polyethoxy chain may consist of up to 50 ethoxy units.g. leading to inhalation as another potential exposure route (Rudel et al.300 (<LOD-.g.90) 2.50) 1.00 (1.20) 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 .600-1. 140-66-9 General Information 4-tert-Octyphenol. fish) and drinking water.200-. and impaired spermatogenesis (e.60) 613 652 1092 Limit of detection (LOD. 1995.30 (1.30) 1.20) 1.500-1..40) 1. 2006. and some personal care products. Saito et al. see Data Analysis section) for Survey year 03-04 is 0.10 (.10) 2.40) * 03-04 03-04 03-04 .30 (..300 (<LOD-. and was quickly eliminated from the blood (Certa et al.600) . Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.50 (1.2. 2002).800-1.60-3.60-3. and through manufacturing waste streams (Warhurst.900 (.80) 2.10) 1.500) .30-2.400 (. Indoor and to a lesser extent..700-1.40 (1.10 (. 34 Fourth National Report on Human Exposure to Environmental Chemicals .299-. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). an alkylphenol.80 (1. impaired steroidogenesis.30 (1.50) 1.20-2.40) 1.80 (1.60-3. altered estrus cycles and reproductive outcomes. the various alkylphenols have also been used as emulsifiers and modifiers in paints. 1996).40) 2.00 (. The alkylphenol ethoxylates enter the environment through human use of products containing them.500) 75th .600) .50) 1. including 4-tert-octylphenol.00) 1229 1288 03-04 03-04 03-04 * .000 tons of alkylphenol ethoxylates were produced annually worldwide.1.600-1.268-. altered neonatal sexual development. In rats.600) .300 (<LOD-.900 (.20-2. Katsuda et al.300 (<LOD-. and to alkylphenoxycarboxylates. pesticides. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. streams in 30 states (Kolpin et al. Blake and Boockfor.369 (. which are anionic surfactants used in detergents.20-2.60) 1.600-1.400 (.274-. 2003. 2000. During the 1980s and 1990s.20) 2. over 500.400) 1. orally administered 4-tert-octylphenol was well absorbed. Several alkylphenols. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.20) 314 715 1488 03-04 03-04 * * .. industrial cleaners. 4-octylphenol monoethoxylate was detected in 43. and from contact with some personal care products and detergents. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.50-3. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. Ying et al..507) * < LOD . The alkylphenols can bioaccumulate in some fish. and emulsifiers.60-3. and some of their degradation products are toxic to aquatic life.600) 1. have demonstrated estrogenic effects particularly when injected at high doses in animals.70 (1.600-1.50) .30) 2.400 (..357 (.600-1. Less frequently.60) .300-.30) 90th 1.70 (1.20-2.30 (1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression..3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. testicular atrophy.. Bian et al.200-.500 (. Laws et al.

78) 1228 1286 03-04 03-04 03-04 * .170-. In a small number of adult Japanese volunteers..384) * .31-2.270-. Nagao et al.337-.269 (.96-4.460 (.S. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.550-1.410 (.29) 2.160-. Sweeney et al.41) .25) 2.11-2.770 (. IARC and NTP have not rated octylphenol.910 (.500-1.17 (. 2001).300 (<LOD-.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.470-1. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.06 (2.Environmental Phenols Myllymaki et al.380 (<LOD-.. 2004.53-3.740 (.00) 2.25) 90th 1.81 (1. Tyl et al. representative subsample of NHANES 2003-2004.1.860 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000.62 (1.03-6.260 (<LOD-.40-4. 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. It is unclear if estrogenic or other effects occur in animals through oral dosing.33 (2.276 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.20 (1.10-2.76 (2.420) .03 (1.450) 1.470-1.25-2.36-3. 2001.64 (.270 (. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Yoshida et al.31 (1. Survey Geometric mean (95% conf.620) .630-1.00 (.68-2. 4-tert-Octylphenol is not considered directly genotoxic. Biomonitoring studies on levels of 4-tert-octylphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 4-tert-octylphenol than are found in the general population.00) 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 . Urinary 4-tert-Octylphenol (4-[1.199-..73) 2. Fourth National Report on Human Exposure to Environmental Chemicals 35 .62 (1.620-1.560) .640-1.730-1.62) . or their corresponding ethoxylates with respect to human carcinogenicity.610) . 2005. Kawaguchi et al. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure. 1999).67-2.78) 3.400) .50 (2.11) 1.15) 1. 2003. Calafat et al..14) 314 713 1487 03-04 03-04 * * .05-2.54) * 03-04 03-04 03-04 .71) 2. nonylphenol.11) 2.349) * < LOD . at lower or environmentally relevant doses (Blake et al.60 (1.740 (.570) .435 (.68) 2.00) 2.43-3.18-4...08) 1.370 (<LOD-.3.00) 1.02-4.43) 1.530) .00 (.270 (.540-1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.22) .280-. population from the National Health and Nutrition Examination Survey.03 (1.470) 75th .890-2.43) 1.207-.S.850 (.320 (<LOD-.59) 1.40 (1.59 (1.65-3.33) 3.85 (1.78 (1.450) .

2/4/09 Ying GG. Kawaguchi M. Fedtke N.pdf. Environ Int 2002. Kookana R. Qian J. Myllymaki SA. Takenaka A. Two-generation reproduction study with para-tert-octylphenol in rats. Kawaguchi M. Thurman EM. Usumi K. Seely JC. Boockfor FR. Reprod Toxicol 2004. Meyer MT. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Nagao T.15(6):683-692.36(6):1202-1211. Korn LR. and other endocrine-disrupting compounds in indoor air and dust. Toxicol Appl Pharmacol 2005.799(1):119-125. McCoy GL. Wiegand HJ. Toxicol Sci 2000.44(8):1355-1361.121(1):21-33. Katsuda S. Makino T. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Yoshida M. Estrogenic activity of octylphenol. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Boockfor FR. Ito R. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Sweeney T. Environ Sci Technol 2002. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Ye X.207(1):59-68. Carey SA. Indoor air pollution by alkylphenols in Tokyo. Toppari J. 1999-2000: a national reconnaissance. Wong LY.141(7):2667-2673. Nakagomi M. nonylphenol. Yoshimura S.116(1):39-44. Taya K. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. testis size.18(1):43-51. streams. Cooper RL. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Watanabe G. Blake CA. Fail PA. Environ Sci Technol 2003. Brine DR. Katsuda S. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Camann DE.S.Environmental Phenols References Bian Q. Food Chem Toxicol 2006. Phthalates.folliclestimulating hormone. Needham LL. Chen J.71(1-2):112-122. Nair-Menon JU. Exposure of the U. et al.foe. Saito Y. Ono H.uk/resource/reports/ethoxylates_alkylphenols. Onuki A. Bolt HM. Zaugg SD. Seto H.37(20):4543-53. Brody JG. Wang X. Nicol L. Available at URL: http:// www.30(2 Pt 1):81-95. prolactin. Haavisto TE. Ferrell JM. et al. Environ Health Perspect 2008. Bodman GJ.54(1):154-167.28(3):215-226. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry.co. Anal Chim Acta 486:41-50. Taya K. Roche JF. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Sakui N. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Lett 2001. Spengler JD. Inoue K. and other organic wastewater contaminants in U. Yoshida M. Saito I. Calafat AM. pesticides. Laws SC. Muller AM. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. 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.57(2):255-266. Reidy JA. Horie M. 1995. Williams B. et al. Yoshimura Y. 2003. Toxicol Appl Pharmacol 2000. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Myers CB. hormones. Song L. Millette CF. Watanabe G.14(5):325-332. Indoor Air 2004. bisphenol A and methoxychlor in rats. Reprod Toxicol 2001. Inoue K. Certa H. Maekawa A. Maekawa A. and testosterone. Marr MC. Kolpin DW. Izumi S. Pharmaceuticals. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. alkylphenols. Tyl RW. Warhurst AM. Brooks AN. polybrominated diphenyl ethers. Takai N. Raychoudhury SS.165(3):217-226. Xu L. et al. Biol Reprod 1997.S. Blake CA. Rudel RA. Endocrinology 2000. Karjalainen M. Arch Toxicol 1996. Paranko J. Barber LB. Okada F. Regul Toxicol Pharmacol 1999. and sertoli cell number. Furlong ET.

and wound disinfection solutions. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. General population exposure results from dermal and oral use of products containing triclosan.Environmental Phenols Triclosan CAS No. 1996. it has low acute toxicity. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. 2007. 2000)..S. Moss et al. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2000. 2007. Lyman and Furia. In animal and human studies. mouthwashes. In 1999-2000. (Sandborgh-Englund et al. toys. Triclosan is not considered teratogenic at maternally toxic doses. the median urinary triclosan level of 7. In a study of 90 U.. triclosan was found in 57. Triclosan can be absorbed across skin into the blood stream. 2007). deodorants. Fourth National Report on Human Exposure to Environmental Chemicals 37 . 2008). Triclosan enters the aquatic environment mainly through residential wastewaters. representative subsample of NHANES 2003-2004.. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. toothpastes.. Matsumura et al. In a U. 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. Veldhoen et al. streams sampled in 30 states (Kolpin et al. Calafat et al. 1988. 1976.. Triclosan formulations may rarely cause skin irritation. 2008 has shown higher levels during the third decade of life and among people with the highest household income. In the body it is conjugated to glucuronides and sulfates (Bodey et al. IARC and NTP do not have ratings with respect to human carcinogenicity.. It acts by inhibiting bacterial fatty acid synthesis. 2007). young girls.. and has also been impregnated into some kitchen utensils. Some reports show endocrine effects are observed in amphibians and fish (Foran et al.8-dichlorodibenzo-p-dioxin (Aranami et al.. Triclosan has a low bioaccumulation potential in fish. and medical devices. 1969).. Calafat et al.2 µg/L was comparable to the median level (8.6% of 139 U. 2005. 1987). Mezcua et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006). It can be photochemically and biologically degraded.. a process that can result in the formation of small amounts of 2. In animal studies.. 2002). and has not been considered mutagenic or carcinogenic (Bhargava and Leonard.. 2004). Biomonitoring Information Urinary triclosan levels reflect recent exposure.. but not by race/ethnicity and sex. Triclosan has been added to soaps. acne medications...2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al.S. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al.S. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent.

9) 32.4) 357 (225-456) 203 (87.90-10.16 (6.48 (8.20-11.20-10.00-8.4) 90th 249 (188-304) 03-04 03-04 03-04 8.8) 14.2-46.8 (21. interval) 12.0 (11.2) 9.89-11.10) 84.6-65.7) 10.1) 11.5) 11.2-58.38-18.6-37.45-13.10-9.6) 10.7) 123 (36.30-14.20 (7.7 (39.6) 90th 212 (172-241) 03-04 03-04 03-04 9.4) 73.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.54 (8.6-20.2-14.6 (9.1-39.32-14.0 (8.0) 65.20-13.7 (11.8) 116 (39.0 (34.4.6) 12.86-12.4 (12.9) 7.6) 31.5) 20.5 (11.48-10.70-16.1) 14.0-19.4 (32. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.0-73.2-58.2 (25. Urinary Triclosan (2.9) 75th 47.1) 7.45 (5.20 (7.4) 7.6 (10.8-60.Environmental Phenols Urinary Triclosan (2.0) 9.2 (37.9 (50.93 (7.29-12.50-10.3.3 (11.55 (4.6 (30.18 (5.80 (5.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.3-67.8) 9.4) 51.3) 6. see Data Analysis section) for Survey year 03-04 is 2.2 (10.50) 10.4) 317 (231-433) 144 (96.4.00 (4.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.2 (11.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.3 (9.9) 8.4-19. population from the National Health and Nutrition Examination Survey.S.1) 9.0) 49.0-15.3) 10.5) 13.2) 12.21 (6.92-12.1 (45.1) 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 9.5-86.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .6) 39.43-13. interval) 13.40-17.1) 9.94 (7. Survey Geometric mean (95% conf.3 (8.8) 7.5-14.5) 66.3) 47.60 (6.2 (27.0 (26.4) 75th 43.40-11.3-15.2 (13.3-31.1) 9.6-14.4-18.1) 13.7 (14.6-15.4) 25.1 (15.7) 292 (151-432) 132 (78.8-85.74 (5.60 (8.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.9 (11.6-14.3 (26.7 (28.22-10.9-61.82 (8.4 (38.6 (12.9 (8.7 (9.0 (36.72-13.0-15.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3-35.1 (8.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4 (11.8-63.1) 9.6-111) 33.9-236) 193 (90.1) 50.S.11-11.8-112) 30.2) 13.45-10.9 (33.8-127) 37.

524:241-247. J Toxicol Environ Health A 2006. Foran CM. et al. Triclosan: applications and safety. Moss T. Nagao Y. Windham G. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Evidence of 2. Developmental evaluation of a potential non-steroidal estrogen: triclosan. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Mezcua M.67(4):532-537. Wolff MS. Food Chem Toxicol 2000. and other organic wastewater contaminants in U.17(5):637-644. J Invest Dermatol 1976. Clapson DJ. Environ Health Perspect 2007.. Wigmore H. Br J Clin Pharmacol 1987.S. Erratum in: Aquat Toxicol 2007. Anal Chim Acta 1004. Wong LY. Ebersole R. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.23(5):579-583. Gomez MJ. Shiratsuchi H. Leonard PA. Ferrer I. Hirano M. Pinney SM. Matsumura N. Pilot study of urinary biomarkers of phytoestrogens. Fernandez-Alba AR.45 Suppl 2:S137-S147. Percutaneous penetration and dermal metabolism of triclosan (2. et al. Gilbert RJ. and phenols in girls. Hernando MD.80(3):217-227.115:116-121. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Calafat AM. Odham G. Environ Sci Technol 2002. population: 2003-2004. 4. Pharmaceuticals. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Bhargava HN. Skirrow RC.38(2):64-71. Environ Health Perspect 2008. Mar Environ Res 2000. Williams FM. Urinary concentrations of triclosan in the U. Bodey GP. 4’-trichloro-2’-hydroxydiphenyl ether. Kanetoshi A.4. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Aguera A.50(1-5):153-156. Thurman EM. Ishibashi H. Photolytic degradation of triclosan in freshwater and seawater. Barber LB. Teitelbaum SL. Biol Pharm Bull 2005. Okui T. Howes D. Levy SB. Sandborgh-Englund G. Williams PE.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Watanabe N. Veldhoen N. Am J Infect Control 1996.7/2. Readman JW. Ye X.36(6):1202-1211.116(3):303-307.66:1052-1056. streams. Meyer MT. Kolpin DW. Britton JA.S. Aranami K. phthalates. Osachoff H. et al. Adolfsson-Erici M. Larson EL.69(20):1861-1873. Zaugg SD. Arch Environ Contam Toxicol 1988. Chemosphere 2007. Furia T. Bennett ER.83(1):84. Ogawa H. Furlong ET. Aquat Toxicol 2006. 1999-2000: a national reconnaissance. Benson WH. The oral retention and antiplaque efficacy of triclosan in human volunteers. Kaneshima H. Chelimo C.24(3):209-218. Toxicology of 2.28(9):1748-1751.4’-trichloro-2’hydroxydiphenyl ether). Gunderson MP. Ekstrand J. hormones. et al. IMS Ind Med Surg 1969.38(4):361370. Katsura E. Needham LL.Environmental Phenols References Aiello AE. Reidy JA. Lyman FL. Hong HC. Pharmacokinetics of triclosan following oral ingestion in humans.

09) . Kohli et al.350) < LOD .350-.350 (.08-3. so it is relatively non-persistent.850-2.350-2.350 (.980 (.630 (.64) 1.25 and 0.350 (.350-. After a single dose.90) 1. PCP use in the U.350 (.350-2.350-1. 1976.350) < LOD . and animals.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-.94 (1.350 (.350-.510-3.67) 1.30 (1.350) < LOD .350-.00) 1.350) 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. PCP is absorbed rapidly and well by all exposure routes.390 (.350-2.890 (.62 (.350 (.60) 1.350) < LOD .350-. air.660 (. Survey Geometric mean (95% conf.350 (.30) .47-3. 1986).58-2.73 (1..350-.350 (.40 (.18 (<LOD-1.45-2.350-2. PCP has been detected in soils.90 (1.590-1.78) 1. General population exposure to PCP may occur by inhalation of contaminated air. bactericide. algaecide and insecticide.75) 2. The parent compound and conjugates.30 (.76) . utility poles and fence posts).76) 1. 1979).350 (.5.83 (2.37) .650 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .990 (<LOD-2..94 (1.350 (..350 (.350) < LOD < LOD 75th . other polychlorinated benzenes.350 (.10 (<LOD-1.350-.80) .350-1. Human exposure to PCP has become less common.350-1. 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.30) 1.350 (.350-. 1997).91 (1.01 (<LOD-1.65 (. and possibly of lindane (IPCS. water and sediments because of the large amounts that were produced and used historically.30) 1.530) 1.54-2.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350) < LOD . plants.350-. Acute.70) 2.10) 1. and dermal contact with PCP-treated products.350) < LOD .350) < LOD .960) 1.42) 696 680 521 696 603 951 Limit of detection (LOD.350-.70) .10 (1.. along with small amounts of tetrachlorohydroquinone and conjugates. In the environment.51) 1.890-1.10) 1.350-2. After absorption.350) < LOD .65 (.350) .350 (.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 .23 (.990-2.47-5.98 (1. with repeated or chronic exposure.350-. To-Figueras et al.350-.350) < LOD . and metabolic acidosis were observed in CAS No.350-. mollusicide.33) .S. PCP is distributed to most tissues and is not extensively metabolized.350-.350 (.350-.33-2. 2002.770 (. which may vary for some chemicals by year and by individual sample. PCP is degraded by sunlight and metabolized rapidly by microorganisms.650) 1.860-2. are eliminated in the urine.32 (.S. ingestion of contaminated food or water..390 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350) < LOD . and it is used primarily as a preservative for wood to be used outdoors (e.50) 1.350-.350-1.00) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.g. PCP cannot be used on wood in residential or agricultural buildings.510-5.500-2. hypertension.350) < LOD .90) 2.480-2. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350 (. Since 1984.04) 1.10 (.350) < LOD . herbicide.60) 1. the elimination half-life may be a week or more (Uhl et al.350 (.350) < LOD .350) < LOD .37 (. < LOD means less than the limit of detection. has been restricted.350-.350-. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350-.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .48 (. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350 (.58-2.350 (. Effects including hyperthermia. PCP is eliminated over a few days (Braun et al.00) 2.350 (.350) < LOD .00 (.48-2.350-.350-.680-1.350) < LOD .30 (. population from the National Health and Nutrition Examination Survey.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .

.290-.240-.19) 2.430-.29-3.25-1.920 (.800-1.67 (1.90) 1. 2003). environmental levels) and health effects is available from the U.360 (.650 (.75 (<LOD-2. In animals.11) 2. population from the National Health and Nutrition Examination Survey. van Raaij et al.gov/ pesticides/ and from ATSDR at: http://www.700-2.560) < LOD .40) 1. 2003).570 (.75) 1.380-.67-3..epa.25-2.84-4. carcinogenic.40) 1.990 (.79) 1.950-1. OSHA has established an occupational standard.760 (.300 (.78) 1.67-3.html.650) 90th 1.250 (.06) 1.780) < LOD .69 (1.950-1.610 (.500-1.280) < LOD .830) < LOD .00-1.18 (1.84 (1.220-.300 (. children in the 1980’s.330-.52 (<LOD-1.35-2.510-. 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) 1.25 (1.Fungicides adults and children severely exposed to PCP through ingestion.18) . Pentachlorophenol is not mutagenic or teratogenic.40) 1. chronically administered high doses of PCP were hepatotoxic.40) 1.710-1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.26 (1.370 (. respectively) (Becker et al. 2000).270-.13 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.25 (1.S.S..55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .420) < LOD .590-1. Death can result from seizures and cardiovascular collapse.19) 2.320) < LOD . respectively) (Seifert et al.6 and 14.gov/ toxpro2.09-1.850 (.48-2. The U.94 (1.06 (.82) 1.52 (<LOD-1.310-.580-.290-.630 (.560-.650 (.e.360-.10 (1.94-3.21-2.16 (.51) 1.67 (1.35) 1. 1991).cdc. EPA has developed standards for PCP in drinking water and the environment. 1995).10-2.67-2.260 (.250 (.36) .94 (1.950-1. 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.52 (1. Survey Geometric mean (95% conf.270-. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.06-3.95) 3.25) 1. and adversely affected thyroid function (U.67 (1.730) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 41 .560) < LOD .30) 1.EPA.320) < LOD < LOD 75th .30-2.340-.35) 1.320 (.92) 1.30) 1.510-.320) < LOD .0 mg/L.490) < LOD .430) < LOD .9 mg/L.21 (.34 (.19) 2.900-1.57 (..09 (<LOD-2.82 (1.30 (.290) < LOD ..08 and 5..470 (.00) 1.40) 1..52) 1.40-2. 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.350) < LOD .67 (1.atsdr.910-1. EPA at: http://www. More information about external exposure (i.26 (1.500 (.83 (1.590) < LOD . 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..220-. inhalation.16-1.S.19 (1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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.25-2.800) < LOD 1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .400 (.310) < LOD .S. 1989).780-1. and the FDA has established a standard for bottled water.500-. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In NHANES 2001-2002 subsamples.440 (.00-1.56) 1.78) 1.300 (.35-2. In a small sample of U.67 (1.S.57 (1.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th . Among adults in the NHANES 1999-2000 subsample. 1989). or skin absorption.55) 1.73 (1. 2004.

J Expo Anal Environ Epidemiol 2000. Gregg M. Otero R. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Toxicology 1991: 67(1):107-16. Safe A. Cline RE. U. Hill RH Jr. To T.S. Bailey SL. hair. Needham LL. Becker K.4:289296.54(3):203-208. Seiwert M. drinking water and indoor air. PCP: Human Risk Characterization [online]. Int J Hyg Environ Health 2003. Pentachlorophenol measurements in body fluids of people in log homes and workplaces.S.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Schlatter C. Krause C. Uhl S. Santiago-Silva M. Helm D. Fast DM. et al. r e g u l a t i o n s . Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995. Shealy DB. Chenoweth MB. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Holler JS.inchem. Arch Environ Contam Toxicol 1989. Phillips DL. Engel R. The metabolism of higher chlorinated benzene isomers. 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-2004-0402.10:552-65. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Baker S. 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. Can J Biochem 1976. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Arch Environ Contam Toxicol 1989. Lindane. Hill RH Jr. 11/30/2004. Needham LL. Available at URL: h t t p : / / w w w. Bragt PC. To-Figueras J. Seiwert M. Schulz C. Smith SJ. Jones D. 4/21/09 van Raaij JA. Notten WR. International Programme on Chemical Safety (IPCS). urine. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects.71:99108. Barrot C. Sala M. Environmental Protection Agency (U. Arch Toxicol 1986. Schulz C. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Blau GE. Seifert B. Schmid P. Environ Health Perspect 1997. house dust. 4/21/09 Kohli J. Dev Toxicol Environ Sci 1979. Braun WH. Head SL. van den Berg KJ. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Hill RH. available at URL: http://www.org/documents/jmpr/jmpmono/2002pr08. Rodamilans M.58:182-186. EPA).105(1):78-83.18:475-481. References Becker K. Seifert B. et al. htm. Kaus S. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. et al. 206:15-24. 2002.18(4):469-474. Pharmacokinetics of pentachlorophenol in man.

85) 2.490 (<LOD-.580-1. OPP is volatile.466 (.820 (.20-3.850 (.402-.80 (2. Both chemicals degrade within hours to weeks in the environment (U. whereas SOPP is not volatile and is more water soluble.390-. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.389-.50-3.600) < LOD 1.50-4. sodium ortho-phenylphenate (SOPP).60-3.07 (.90) . 90-43-7 General Information Ortho-phenylphenol (OPP.490 (<LOD-.40-7. Fourth National Report on Human Exposure to Environmental Chemicals 43 .50 (1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .03) 1. Both have been used in agriculture to control fungal and bacterial growth on stored crops.27 (.80) 1.23) 695 680 520 695 603 953 Limit of detection (LOD.50) < LOD .570-2.20 (.90 (1.90) 1.710) 3.570 (.480-1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. 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 (1.780) < LOD .550-1.500-2.420 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2006).00 (1.EPA.30) 1.50) < LOD . 2002.690-1.490 (<LOD-.950) < LOD . and as a wood preservative. formulate.50 (1. on ornamental plants and turfs.690) < LOD .30 (1. 1998).670) 2.433-.20 (1.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .570 (. Workers who manufacture.493 (.60-2.497 (.20 (1.370-. such as fruits and vegetables.76) 1.60 (1. < LOD means less than the limit of detection.22) 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 .624) * .00 (1.20) < LOD 2.3.3 and 0.28-3.970 (.10 (1.S.S.09) 2.Fungicides ortho-Phenylphenol CAS No.840-1.710-2.890) 1. Estimated human intakes have been below recommended intake limits (U.552 (.770 (.EPA. Most agricultural food applications have been revoked.80) 1.742) * .600-1.20-2.30-7.40 (.600-1. and it has limited water solubility. 2006).90) 2.364-.560-8.790) 2.90) .61) 2.800-3.50-2. SOPP is applied topically to the crop and then rinsed off. Timchalk et al.00) < LOD .50) .770 (.570-.10-1.760-2.80-3.600) < LOD 75th ..600) < LOD .20) < LOD 1. 1989). Survey Geometric mean (95% conf.88) 1.750-2.509 (. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1998.386-. population from the National Health and Nutrition Examination Survey.60 (1. are antimicrobial agents used as bacteriostats. and sanitizers.S. In the past.10 (1.640) < LOD . which may vary for some chemicals by year and by individual sample.621) * .30-2.890 (.02) 1. in paints.450 (<LOD-.30) < LOD .17 (.610-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.880-2.520 (.645) * . leaving the chemical residue OPP.S. however.490 (<LOD-.50) < LOD .590-2.600-1.496 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.50) 1. OPP is still used as a disinfectant fungicide for industrial applications.349-.638) * .00) . it was used in home sanitizers for surfaces.10-2.40-5.00 (1.930 (.890 (..636) * .410-. but OPP and SOPP are still used on pears and citrus (U.60 (1.50 (1.00-2. EPA. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. or apply these chemicals may be more highly exposed than the general population.370-.836) * .28 (.389-. interval) .450 (<LOD-.10) 1.470 (<LOD-.630) < LOD .498 (.540-2.450 (<LOD-.10) .40-2. Available evidence suggests that OPP does not accumulate in the body.30) < LOD 90th 1.570-1.20) 2. 2006).33 (.696) * .00 (1.508 (.830 (..14 (<LOD-3.600) < LOD .10) . inhalational.34) 1.40-5.610 (.10) 1. 2006). OPP is considered to be moderately toxic after acute oral doses in animal studies. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.30) < LOD 1. fungicides.92 (.567 (. General population exposure can occur via dermal.22 (.00) .490 (<LOD-.370-.10) 2.350-1. Cnubben et al.19 (. or 2-phenylphenol) and its water-soluble salt.10) .91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .860 (. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.740 (.

01) 1.46) < LOD 1.96 (1.21 (.470 (<LOD-.75 (1. Survey Geometric mean (95% conf.EPA 2006).EPA 2006).88-4.620-1.00 (1.00 (.11-1.43 (1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.382 (. but no neurologic.96-4.38-3.09-3. IARC has classified SOPP as a possible human carcinogen.990) < LOD .12) < LOD 1.33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .670 (.Fungicides anemia.11) 4.17 (.666) * . OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.420 (<LOD-.840 (.74 (1. reproductive.18) 2.910 (<LOD-1.86 (1.900-1.950) < LOD . Biomonitoring Information Urinary OPP levels reflect recent exposure. In high dose animal studies.4) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.33) .32) 3.470) < LOD .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.58) 2.84 (1. Bomhard et al.970) 1.38) 1.444 (.980 (<LOD-1. U.810) < LOD .496 (.780-14.53) 1. Kwok et al.514 (.291-..560-2.09-6.270-.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .880-1..500) < LOD .33-2.484) * ..380 (.27) < LOD .93) 1. Nakagawa et al.453 (. 1992. CDC. Smith et al. 2002.750 (.S.29) 1.900) < LOD .59) .61 (1.09 (1.96) 1.560) < LOD 75th .750-2. Pathak and Roy.81) 1.940-2.51-3..38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .860 (.550-.568) * . 1998.S. leading to production of two metabolites. 2005.89 (1.28 (2.47) .61 (.440 (.550 (. 1986). 1999.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.510 (<LOD-.93) . and it has classified OPP as not classifiable with respect to human carcinogenicity.93) . Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.361-.640-1. Volunteers exposed to 0.750 (.62) .43-2.91 (1.21) 1. 2002. U.97 (2. 2005).800-1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.11) < LOD 90th 1.31) < LOD .26) 1.780 (.29) 1.59) 1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.69 (1.620-1.455-.690 (.385 (.06 (1.S. by possible genotoxic mechanisms (Hagiwara et al..403-.329-.860 (.570) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..0) 1.44 (1.93 (1.360 (<LOD-. Brusick.20) < LOD 3. OPP was not found to be mutagenic.410 (<LOD-.02 (.508) * .25-6.61 (2.311-.28 (<LOD-4.07) 2.17) 2.04-4.gov/pesticides/.11 (.08) 1.38) 2.353-.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) .770-2.32) 1. 1984.S. Additional information is available from U.40-13.06-5.980 (. or developmental toxicity was observed (Bomhard et al. Zhao et al.52 (.550) < LOD .43) 3..06-4. 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.. 1993.S.24-2.910-1.343 (..75 (1.78 (2.910 (.510-.05-2. 1999.580) < LOD .08-1.301-.12-2.11 (.480-. 1984.17 (.epa.670 (.473) * .43-2.08-2.64 (2.460-.248-.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .96 (1. 2000.13) 1.320 (<LOD-.EPA at: http:// www.791) * . Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Murata et al.810-1. 1997.580-1. or.410 (<LOD-.24-2.650-1. Detectable levels were seen in over half the U. Ito et al.590) * ..21-2.656) * . 2005). population from the National Health and Nutrition Examination Survey.670) < LOD . 44 Fourth National Report on Human Exposure to Environmental Chemicals .600-1. 2002).610) < LOD 1. less likely.420 (<LOD-.

pdf. Moriya K. Available at URL: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Bromig KH. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Bomhard EM. Drugs.32(6):551-625. Freyberger A. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Sangha G. Coelhan M. IARC Sci Publ 1984. Vogel JS. Sangha GK. van de Sandt JJ. Centers for Disease Control and Prevention (CDC). Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Environmental Protection Agency (U. Roy D. Regul Toxicol Pharmacol 2002. Timchalk C.703(12):97-104. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. 4/13/09 Onstot JD. Cnubben NH. 2006. Moldeus P. Narang A. Hagiwara A. Pathak DN. Christenson WR. rat and man. Food Chem Toxicol 1984. Biochem Pharmacol 1992. Stanley JS. U. McNett DA.50(11):3351-3358. Timchalk C. Bartels MJ. Arnold LL. Inoue S. Shirai T.Fungicides References Appel KE. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol.150(2):402-413. National Toxicology Program (NTP). Richter M. Mutat Res 1993.epa. Third National Report on Human Exposure to Environmental Chemicals. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Toxicol Appl Pharmacol 1999. Fukushima S. Nakagawa Y. food additives and natural products as promoters in rat urinary bladder carcinogenesis.S. EPA 739 R-06004. Arch Toxicol 2000. Zhao S.(56):399-407. Hakkert BC. July 28.pdf. Bartels MJ. Murata M. Carcinogenesis 1999. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Brendler-Schwaab SY. Comparative metabolism of orthophenylphenol in mouse. Kwok ES. Available at URL: http://ntp. Xenobiotica 1998. Eastmond DA.nih.22(10):809-814.niehs.S. Brusick D. Shibata M.gov/ntp/htdocs/LT_ rpts/tr301. Toxicol Appl Pharmacol 1998.S.gov/oppsrrd1/REDs/ phenylphenol_red. 2005. Ito N.74(2):61-71. J Agric Food Chem 2002. 4/9/09.286(2):309-319.20(5):851-857. U. Gierthy J. The carcinogenicity of the biocide ortho-phenylphenol. 1989. Smith RA. J Agric Food Chem 2006. Crit Rev Toxicol 2002. Tayama S..159(1):18-24. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Kawanishi S. Glas K. Bartels MJ. Environmental Protection Agency (U.54(16):5731-5735. Fukushima S. EPA-560/5-89-003.45(5):460-481. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. St John MK. 90-43-7) in Swiss CD-1 mice (dermal studies). Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Meuling WJ. Elliott GR. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Hagiwara A. Herbold BA.EPA). et al. Selim S. Moore GA.S.28(6):579594. Imaida K. Cano M. Buchholz BA. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Atlanta (GA). Bormett GA. Turteltaub KW.35(2 Pt 1):198-208. Hirose M. Identification of SARA compounds in adipose tissue. March 1986.43(7):14311437.17(8):411-417. Environ Mol Mutagen 2005. Roberts AL. Christenson WR. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Bartels MJ. Office of Toxic Substances. EPA). Leser KH. et al. Eadon G. Mendrala AL. Ito N. Hum Exp Toxicol 1998. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Brzak KA. J Chromatogr B Biomed Sci Appl 1997.

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

EPA. Urinary acetochlor mercapturate levels of 0. a major pathway for acetochlor metabolism involves mercapturate conjugation..EPA.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. but other pathways occur.S..EPA 2000.S. 1989. 1996).EPA. Acetochlor is moderately toxic to fish and honey bees. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. Kolpin et al. animals have demonstrated tumors of the lung. Acetochlor is microbiologically degraded. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. It is absorbed by plants and inhibits plant protein synthesis. Additional information about external exposure (i. however. 2005). In animals. 2006). and has been detected in watersheds of agricultural lands (Battaglin et al. 2006). 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. However. and hydroxymethyl ethyl aniline (U. 2006).e. Acetochlor is not mutagenic. 2005). in some species and at doses above maximum tolerated doses. 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..EPA considers acetochlor likely to be carcinogenic in humans. the latter which may account for some observed effects (Coleman et al. EPA at: http://www. mainly corn. Davison et al. and it is unlikely to be genotoxic at relevant doses (Ashby et al. Acetochlor has low acute toxicity. and neurologic movement abnormalities (U.S. 2006). nasal epithelia.S. Jefferies et al.. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. 2-hydroxyethyl-6-methylaniline. which are often more prevalent in the environment.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid.epa.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Hladik et al. but it has produced testicular atrophy. 2000. 2000).. U. environmental levels) is available from U. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. Feng and Wratten. Estimated human intakes of acetochlor have been below recommended limits (U. 1994. including one that produces 2-methyl-6ethylaniline and its reactive metabolite. CAS No. 2000. NTP and IARC do not have ratings regarding human carcinogenicity. remains in soils for up to 3 months. and thyroid (U. 1998).S.. 2005. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8.0 μg/L (Curwin et al. 2000.. Fourth National Report on Human Exposure to Environmental Chemicals 47 .. renal injury.gov/ pesticides/. People exposed to acetochlor will excrete acetochlor mercapturate in their urine.S. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. General population exposure to acetochlor may occur through diet or drinking water. 2007).

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

Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Rose RL.S.248(2-3):115-122. Reynolds SJ. Roberts AL. Kier L. Furlong ET. Occurrence of sulfonylurea.S. 2005. et al. Heederik D. Hines CJ.S.S. Wratten SJ. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Federal Register: January 24. Barr DB. Andrews HF. Barr DB. Larsen GL.111(5):749-756. Third National Report on Human Exposure to Environmental Chemicals. Hum Exp Toxicol 1996. EPA). Available at URL(non U.108(12):1151-1157. Atlanta (GA). Finding minimal herbicide concentrations in ground water? Try looking for their degradates.11(4):353359. Sci Total Environ 2000. pages 3682-3690. Burkhardt MR. Striley CA. epa.cce. J Agri Food Chem 1989. Whyatt RM.pdf. Peter CJ. and metolachlor herbicides in rats. Barr DB. Number 15. 2000. Ward EM. Environmental Protection Agency (U.Herbicides References Ashby J. Environmental Protection Agency (U. J Expo Sci Environ Epidemiol 2007.39(17):6561-6574. Olsson AO.cornell. Davison KL. Centers for Disease Control and Prevention (CDC).37(4):10881093. et al. Kinney PL. Camann DE. Lefevre PA. Coleman S. imidazolinone. Linderman R. and other herbicides in rivers. Quistad GB.html. U. Xenobiotica 1994. Bravo R. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.17(6):559-566. Feng PCC. Hsiao JJ. Green T. et al. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Sci Total Environ 2000. EPA 738-R-00-009. Environ Health Perspect 2003. Acetochlor (Harness) Pesticide Petition Filing 1/00. 5/30/06 U. Casida JE. Hladik ML. Comparative metabolism and elimination of acetanilide compounds by rat. acetochlor. Hein MJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. J Expo Anal Environ Epidemiol 2005. Feil VJ. reservoirs and ground water in the Midwestern United States. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.24(10):1003-1012. Sanderson WT. March 2006. 5/30/06. Environ Sci Technol 2005. Kolpin DW. EPA). Tinwell H. Available at URL: http://www. Linhart SM. Chem Res Toxicol 1998. Curwin BD. Dialkylquinonimines validated as in vivo metabolites of alachlor. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. sulfonamide.S. Battaglin WA. Alavanja MC.15(9):702-735. Jefferies PR. Fourth National Report on Human Exposure to Environmental Chemicals 49 .EPA): http://pmep. Environ Health Perspect 2000.15(6):500-508. Volume 65.248(2-3):123-133. Barr JR. Deddens JA. 1998. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Wilson AG. Hodgson E. Thurman EM.

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

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

Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Kier LD. 1999. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes.43(9):2504-2512. Thake DC.S. Geological Survey (USGS). Davison KL. acetochlor. Thelin GP. Tolos W. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Tessier DM. EPA). Biagini R. 1998. Geological Survey (USGS). Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Casida JE. Casida JE.18(6):363-391. Background document for development of WHO Guidelines for Drinking-water Quality. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Hsiao JJ. 1992-2001. Life Sci 1988. Brown KK. Kimmel EC. Hill RH Jr. Kolpin DW. Dialkylquinonimines validated as in vivo metabolites of alachlor. Atlanta (GA). California. 2/27/09 Jefferies PR. Wilson AG. Alachlor in Drinking-water.int/water_sanitation_health/dwq/chemicals/en/alachlor. Reregistration Eligibility Decision (RED) Alachlor. Barr JR. Chem Res Toxicol 1998. Burkhardt MR. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. DNA adduct formation by alachlor metabolites.pdf. Furlong ET. MacKenzie B. Striley CA. Circular 1291. Feng PCC. Camann DE. 2/27/09 U. Bull Environ Contam Toxicol 1996.htm. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. An evaluation of the carcinogenic potential of the herbicide alachlor to man. who. Available at URL: http://www. Gilliom RJ). EPA 738R-98-020.gov/oppsrrd1/ REDs/0063. Hull RD. Occurrence of sulfonylurea. et al.php. Supplemental Technical Information (available on-line only). The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. 4/2/09 U. ALACHLOR.43(25):2087-94. 1999. Wratten SJ. Mutat Res. Martens MA. 2007. 86. Centers for Disease Control and Prevention (CDC). Quistad GB. et al. Xenobiotica 1994. Sci Total Environ 2000. Available at URL: http:// www.37(4):10881093. Clark JM. revised February 15. World Health Organization.56(6):853-859. Environ Health Perspect 2003. Larsen GL. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor.S.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Erratum in: Life Sci 1989.Herbicides References Battaglin WA. Hines CJ.epa. Kolpin DW. Heydens WF.pdf. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Henningsen G. Environmental Protection Agency (U. International Programme on Chemical Safety (IPCS). Sanderson WT. Peter CJ. Linhart SM.11(4):353359. WHO/ FAO Data Sheets on Pesticides. Biagini RE. Sacramento. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.44(18):1325. 2003.usgs. Kinney PL.org/documents/pds/pds/pest86_e. Hill AB. Comparative metabolism and elimination of acetanilide compounds by rat. Available at URL: http://water.S.39(17):6561-6574. Lau H. Roberts AL. Thurman EM. 98-4245 (by Barbash JE. Geneva. March 2006. December 1998. U. imidazolinone.56(9):883-889.47(6):503-517. Driskell WJ. Shoemaker DA. Deddens JA.395(2-3):159-171. 1996.111(5):749-756. Whyatt RM. No. Jefferies PR. Casida JE. and metolachlor herbicides in rats. 2005. and other herbicides in rivers.248(2-3):115-122.248(2-3):123-133. Sci Total Environ 2000.S. Environ Sci Technol 2005. Ann Occup Hyg 2003. 1997.24(10):1003-1012. sulfonamide. Shealy DB. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. J Ag Food Chem 1995. reservoirs and ground water in the Midwestern United States. Andrews HF. J Agri Food Chem 1989. Hines CJ. Feil VJ. Hladik ML. Available at URL: http://www.inchem. Quistad GB. World Health Organization (WHO). Am Ind Hyg Assoc J 1995. Brown MA. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Hum Exp Toxicol.

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

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

Toxicol Sci 2000. Vonk A. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. J Toxicol Environ Health 1994. atrazine was detected in only four children (Arcury et al. Pfeifer KF. Ferrell JM. Simpkins JW. Lioy PJ. Deddens JA. Chen H.30(2):244-247.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. 2003. Cooper RL. Shoemaker DA. Carr WC Jr.. Barr DB.. Eberly LE. In a study of 60 farm worker children.99(8):5476-5480. Biological monitoring of human exposure to atrazine. Biagini RE. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Agency for Toxic Substances and Disease Registry (ATSDR). Collins A. Hein MJ.atsdr.61(4):331-355. McElroy WK.. Extrom PC. Aldous CN. 2001 [online].. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Centers for Disease Control and Prevention (CDC). Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Tyrey L.47(6):503-517. Hayes TB.html. Lee M. et al. Eldridge JC. Barbieri F. Clayton CA. Barr DB. diamino-S-chlorotriazine and hydroxyatrazine.gov/toxprofiles/tp153.. Ferioli A. Toxicol Sci 2000. Schmid J. 1993). In the NHANES 2001-2002 subsample. et al. Gillis JH. 1996. J Agric Food Chem 1982. Grzywacz JG. Eldridge JC. 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.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.15(6):500-508. Cottica D. Toxicol Sci 2003. 2001). Environ Health Perspect 2007. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.org/documents/pds/pds/pest82_e. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Stuart AA. Heederik D. World Health Organization. Sanborn JR.109(6):583-590. J Expo Anal Environ Epidemiol 2005.64(9):672-678. 2000).inchem. ATRAZINE. The geometric mean of urinary atrazine mercapturate was 1.58(2):366-376.. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Saiz SG. Striley CA.htm. Goldman JM. 3/11/09 Arcury TA. Toxicological profile for atrazine. 82. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Cooper RL. Mendoza M. A risk assessment of atrazine use in California: human health and ecological aspects. WHO/ FAO Data Sheets on Pesticides. Third National Report on Human Exposure to Environmental Chemicals. Cooper RL. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Available at URL: http://www. 2005. Quandt SA.115(8):1254-1260. Perry et al. Lucas AD. Laws SC. Breckenridge CB. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Freeman NC. In a small number of field workers. Proc Natl Acad Sci USA 2002. Gillis JH. Hines CJ. Wetzel LT. Environ Health Perspect 2001. et al. Barr DB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pest Manag Sci 2005.cdc. 2007). Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Hermaphroditic. Jones AD. Steroids 1999. Tapia J. Gammon DW. No. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 3/11/09 Laws SC. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 .43(2):155-167. levels of atrazine mercapturate were generally not detectable (CDC. et al. Brown KK. Stoker TE. Toxicol Lett 1993. Ferrell JM. Seiber JN. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Available at URL: http:// www.. Reynolds SJ. 2005).69(2):217-222. Ann Occup Hyg 2003.53(2):297-307. Maroni M. Goodrow MH. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. References Adgate JL. Catenacci G. Stevens JT. J Toxicol Environ Health 1994. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Stoker TE. 2005). Sanderson WT. Fleenor-Heyser DG. Stoker TE. et al. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Bersani M. In small studies of Maryland residents in 19951996 (MacIntosh et al. Atlanta (GA). et al. Wetzel LT.43(2):155-167. Geneva. International Programme on Chemical Safety (IPCS). Curwin BD. Noriega N. Bradway DE. Moseman RF.76(1):190-200. Blewett C.

J Expo Anal Environ Epidemiol 1999. Pesticides and Toxic Substances. Toxicol Sci 2002. 2007. Laws SC. Sathiakumar N. March 2006. Langvardt PW.usgs. van den Berg M. Circular 1291. Fenton SE. Crit Rev Toxicol 1997. Case No. Cooper RL. Available at URL: http://water. White paper on potential developmental effects of atrazine on amphibians. The Quality of Our Nation’s Waters.gov/oppsrrd1/REDs/ atrazine_ired. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Interim Reregistration Eligibility Decision For Atrazine. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.195(1):23-34. Wood C.S. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www. Urinary biomarkers of atrazine exposure among farm pesticide applicators.Herbicides development of a biomarker of exposure. Dagenhart D. Kastl PE. Geological Survey (USGS).S. EPA Office of Pesticide Programs. Cooper RL.S. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Sci 2000. Rayner JL. Washington (DC). Sanderson JT. EPA). U. Hammerstrom KA.27(6):599612. Delzell E. A risk characterization for atrazine: oncogenicity profile. 6/1/09 U.6(1):107-116.S.pdf. revised February 15.58(1):50-59.61(1):27-40. Tortorelli J. Supplemental Technical Information (available on-line only). Osborne DW. 0062. Stoker TE.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.pdf. Stoker TE. Laws SC. EPA). Boerma J. Toxicol Appl Pharmacol 2002. Guidici DL. Ryan PB.10(7):479. Christiani D.epa. J Toxicol Environ Health A 1999. Wetzel L. Breckenridge CB. MacIntosh DL.182(1):44-54. Available at URL: http://www. Guidici DL. 1992-2001.56(2):69-109. Singzoni B.epa. Toxicol Appl Pharmacol 2004.S. Chem Res Toxicol 1993. Perry M. 3/11/09 U. A review of epidemiologic studies of triazine herbicides and cancer. Toxicology 1990. Ann Epidemiol 2000. Lansbergen GW. Environmental Fate and Effects Division. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. 2003b. A longitudinal investigation of selected pesticide metabolites in urine. Stevens JT. Environmental Protection Agency (U. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Office of Prevention. Timchalk C. Dryzga MD. Environmental Protection Agency (U.php.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Needham LL. May 2003a.67(2):198-206.9(5):494-501.

32 (1.690 (..10 (<LOD-1.250 (<LOD-.930-1. with a half-life of several days to several weeks.60) 1. 1974.690 (.4-D or exposed for prolonged periods. renal and hepatic injury.610-.40) 1.4-Dichlorophenoxyacetic Acid CAS No. 2007).EPA.24 (.51 (1.440-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. 1977). 2005).690 (.55 (1.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .S.740 (. As much as 62 million pounds of 2. agricultural.670-1.560-1. 2004).370-. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.00-2. it acts as a plant growth hormone.22) < LOD .4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.48) < LOD 1.890 (. these herbicides can enhance plant growth.03) 695 659 520 668 589 892 Limit of detection (LOD.730 (.490 (.310 (. At low levels.43) 1.260 (<LOD-.27-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4-D has low acute toxicity. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.310) < LOD . Recent estimates of chronic intakes of 2.4-D) controls broadleaf weeds in residential.S.4-D were used in the U.S.960-1.660) 1. in 2001 (U.27 (.560-. by direct contact with agricultural and residential areas after applications. the chlorophenoxy herbicide 2.37) 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 .930 (.S.05-2.4-D can be applied either as an aqueous salt or as oil-soluble esters.320) 90th . 2.S.20 (.250 (<LOD-..230-. abdominal pain.10) < LOD 1. dizziness.13) < LOD .70) 1. < LOD means less than the limit of detection.890) < LOD . 2.490) < LOD < LOD < LOD . Similar to other chlorophenoxy herbicides. MCPA.910) < LOD .760 (. but at higher levels they are herbicidal.EPA in 1948. and mecoprop). General population exposure to 2. It is not well absorbed through the skin.10 (<LOD-1.400) < LOD .30 (<LOD-2. headache..420) < LOD . hypotension.4-D is rapidly absorbed via oral and inhalation routes. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4-D have been below recommended intake limits (U.550-1. and aquatic environments.330 (. Fourth National Report on Human Exposure to Environmental Chemicals 57 .Herbicides 2.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.07 (.4-D may occur during residential applications. 4-D.21) 1.210 (<LOD-.230 (<LOD-.20 (<LOD-1. It is rarely detected in ground waters (USGS.66) < LOD 1. Sauerhoff et al. and delayed Urinary 2.610 (.410) < LOD . 1989.4-dichlorophenoxyacetic acid (2.27 (1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . nausea.02-1. Once absorbed.80) 1. myotonia.350) < LOD < LOD < LOD .540-.210-.EPA. Human health effects from 2. Kohli et al. and by consuming food or drinking water contaminated with 2.680-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. 2.08) < LOD . 2. 94-75-7 General Information Widely used throughout the United States.2.952 and 0.16) < LOD . population from the National Health and Nutrition Examination Survey.420-.910) 1.690-1. It was first registered with U.810-1. which may vary for some chemicals by year and by individual sample. It is poorly bound in soils.

4-D production plant workers and a few forestry workers spraying 2.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.820-1.EPA. Post-application levels in farmers and home gardeners were dependent on Urinary 2.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 2005.EPA.EPA 2005).380 (<LOD-. 1989).410 (<LOD-.32 (<LOD-2. or teratogenic effects in chronic rodent studies (Charles et al.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . It is unclear whether these associations are related to the chlorophenoxy herbicides. 2004).810-1.850) < LOD .19) . 1994). Frank et al.S. 58 Fourth National Report on Human Exposure to Environmental Chemicals .EPA.620-.S. 2006.41 (1.35) < LOD .410) < LOD 1.680) < LOD . population (Hill et al..560-.13 (.4-D levels were detectable in less than a quarter of the individuals studied. 2005.08 (. U. liver. 1996. 1995. and of adults and children (Baker et al.. 2.. IPCS.17 (.330-.660) < LOD .S. 2005).05) .. Survey Geometric mean (95% conf.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .720 (..350 (<LOD-.. In previous samples of the U.580-.700 (.930-1. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. other exposures.780) . eyes. 2003. Pearce and McLean.980) < LOD 1.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .73) .920) < LOD 1.660 (.410) < LOD < LOD < LOD .56) ..640 (. Epidemiological studies have reported associations of several types of cancer. 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. 2.380 (<LOD-. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2.. and evidence of histological injury to the kidneys.EPA at: http://www.550-.27-1.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. U.4-D reflect recent exposure. 2002.S. or to contaminants in the herbicide formulations (specifically 2.7. 1996.670 (.790) 1. thyroid.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 . 2001.39) < LOD 1. myotonia.08 (. IOM. Additional information is available from U.470) < LOD .440 (.270-.780 (. 2005. 2005). 2000). U. 2005.780-1.4-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..410) 90th . population from the National Health and Nutrition Examination Survey.S.340-.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.390) < LOD < LOD < LOD . Acute high doses administered to laboratory animals produced ataxia. developmental.08 (. Biomonitoring Information Urinary levels of 2.670 (<LOD-1.S.480 (. U.560-.490 (. 2002.270 (<LOD-.epa.520-.790) < LOD .3.16) 1.4-D does not have significant reproductive. IPCS.740 (. 1995). Kutz et al. 1980.590 (<LOD-1. in small samples of children (Hill et al. urinary 2.610-. IPCS.Herbicides neuropathy (Bradberry et al.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. The acid and salt forms of 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. 1992).610-. Hill et al. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result..570) < LOD . 2005). Average post-application urinary levels of 2.24) 1. 1996.810-1.13 (.670 (. 1985. CDC.890-1.4-D are eye irritants. Kolmodin-Hedman and Erne.990-1.340 (. Knopp et al.890) < LOD 1. adrenals and gonads (NTP.14 (.S.380-.gov/pesticides/.590 (<LOD-1.380) < LOD .

Finding a measurable amount of 2. 2005. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Shealy DB. Centers for Disease Control and Prevention (CDC).inchem. Kolmodin-Hedman B.4-D than levels found in the general population. Biomonitoring of herbicides in Ontario farm applicators. Pesticides residues in food: 1996 evaluations Part II Toxicology. Hill RH Jr. Pesticide residues in urine of adults living in the United States: reference range concentrations. Developmental toxicity studies in rats and rabbits on 2. Hein MJ. Curwin BD.. Third National Report on Human Exposure to Environmental Chemicals.org/documents/jmpr/jmpmono/v96pr04. Khanna RN.4-D in urine does not mean that the level of the 2. Alexander BH. Atlanta (GA). Crit Rev Toxicol 2002.31 Suppl 1:90-97. J Expo Anal Environ Epidemiol 2000. Mandel JS.4-. National Toxicology Program (NTP). et al. Hill RH Jr.4:97-100.4:427-435. Review of 2.nih. Survival and Growth Curves from NTP Toxicity Studies. Brody D. et al. Ritter L.32(4):233-257. 2005). the number of acres to which it was applied (Curwin et al.nap. Holler JS. Hanley TR Jr. Murphy RS. Exposure of homeowners and bystanders to 2. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Heederik D. 3/17/09 Institute of Medicine (IOM).4 dichlorophenoxyacetic acid (2. Veterans and Agent Orange: update 2002. Stephenson GR. Beasley VR. References Arbuckle TE.Herbicides the time since application.gov/index. Driskell WJ. Kohli JD.htm. Solomon KR. Carter-Pokras OD.4-dichlorophenoxyacetic acid and its forms. Tables.4-dichlorophenoxyacetic acid (2. Gupta BN. Philbert MA. Fast DM.4-D were highest in the farmers who applied the 2. Scand J Work Environ Health 2005. Biomonitoring studies of 2. Washington (DC): National Academies Press. Barr DB. Dichlorophenoxyacetic acid. geometric mean urinary levels of 2.. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. J Toxicol Environ Health 1992.71(2):99-108. 2003. Harris et al. J Expo Anal Environ Epidemiol 2005 Nov.37(2):277-291. Honeycutt R. Chapman P. Head SL.4-D). 2005). Scand J Work Environ Health 2005. Xenobiotica 1974. Reynolds SJ.niehs. Wilson RD.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 2.18(4):469-474.4-dichlorophenoxyacetic acid (2.4:318-321. Toxicol Sci 2001. general population. 2005 Charles JM.4-D) epidemiology and toxicology. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 2. Gregg M. 2006.4. Kutz FW. Acquavella JF. Smith SJ.27(1):23-38. Sanderson WT. Baker BA. Erne K. Arch Environ Contam Toxicol 1989. Bailey SL. Absorption and excretion of 2.. Cook BT. Barr DB. In farm families. Assessment of exposure to 2.15(6):500-508. Mandel et al. Selected pesticide residues and metabolites in urine from a survey of the U. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Needham LL. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.4-D. Forestry workers involved in aerial application of 2. Dhar MM. van Ravenzwaay B. 914.31(2):121-125.. International Programme on Chemical Safety-INCHEM (IPCS). Baker SE. Available at URL: http://ntp. Environ Res 1995. To T. Biomonitoring for farm families in the farm family exposure study. 2005. Campbell RA.edu/catalog. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.51(3):152-159. 3/17/09 Knopp D. Tandon JS. the amount of pesticide applied.4-D will result in an adverse health effect. Updated March 7. Board on Health Promotion and Disease Prevention. Baker S. et al.31 Suppl 1:98-104.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Garabrant DH. Sircar KP. Ripley BD. Arch Environ Contam Toxicol 1985.php?record_id=10603. Available at URL: http:// www. Estimation of occupational exposure to phenoxy acids (2. Sirons G J.S.4-D): exposure and urinary excretion. Frank R. TOX-63: TOXICITY REPORT CURVES. Bus JS.4-Dichlorophenoxyacetic Acid). Needham LL. Vet Hum Toxicol 1989. Beeson MD. J Environ Sci Health B 1992. Available at URL: http:// www.4-dichlorophenoxyacetic acid in man.10(6 Pt 2):789-798. Harris SA. Arch Toxicol Suppl 1980.4-D and 2. Arnold EK. TOX-63 Peroxisone Project (2. Cole DC. and the use of protective clothing or equipment (Arbuckle et al. 1992).60(1):121-131. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-T). The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Occup Environ Med 1994.

Pesticides in the Nation’s Streams and Ground Water.pdf. March 2006. Gehring PJ. revised February 15. Environmental Protection Agency (U. Braun WH. 2007. The fate of 2. Available at URL: http://www. Available at URL: http://www. 4/2/09 U.4-dichlorophenoxyacetic acid (2. 1992-2001.4-D) following oral administration to man.S. 60 Fourth National Report on Human Exposure to Environmental Chemicals . Washington (DC): U.4-D RED Facts.EPA. 2004. Geological Survey (USGS).8:3-1U.php.EPA). 3/17/09 U. 2.S. 3/17/09. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Blau GE. June 2005. EPA 738 F-05-002.epa.epa. Office of Prevention Pesticides and Toxic Substances. Available at URL: http://water.htm.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.EPA).S.Herbicides Sauerhoff MW. The Quality of Our Nation’s Waters. S. Pesticide industry sales and usage .usgs. Environmental Protection Agency (U.S. Toxicology 1977. May.S. Supplemental Technical Information (available on-line only).gov/oppsrrd1/ REDs/factsheets/24d_fs.2000 and 2001 market estimates. Circular 1291.

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

population from the National Health and Nutrition Examination Survey.670 (<LOD-.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2. 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 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. < 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.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .240) 679 701 957 Limit of detection (LOD. Survey Geometric mean (95% conf.440 (<LOD-. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 01-02 is 0.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 62 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.200 (<LOD-.200 (<LOD-.S. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Kinney PL.S. Heederik D. Thurman EM. and metolachlor herbicides in rats. Xenobiotica 1994.111(5):749-756.usgs.41:3409-3414. Environ Health Perspect 2003. et al. Pesticides in U. Quistad GB. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . 1998. Davison KL. Sacramento. Reynolds SJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Ann Occup Hyg 2003. Available at URL: http://www. 98-4245 (by Barbash JE.37(4):10881093. Roberts AL. Peter CJ.S.int/water_sanitation_health/dwq/chemicals/ metolachlor. Feil VJ. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Andrews HF.gov/oppsrrd1/ REDs/0001. Linhart SM. Hsiao JJ. Environ Sci Technol 2007. 1999.ESTfeature_gilliom. streams and groundwater. Dialkylquinonimines validated as in vivo metabolites of alachlor. Environ Sci Technol 2005.248(2-3):123-133. Wratten SJ. Brown KK. R. Metolachlor in Drinkingwater. Alavanja MC. Kolpin DW. and other herbicides in rivers. reservoirs and ground water in the Midwestern United States. 2007. Available at URL: http://water. Burkhardt MR.epa. Hein MJ.24(10):1003-1012. imidazolinone. Barr JR. revised February 15. Larsen GL. EPA 738R-95-006. et al. Chem Res Toxicol 1998. Centers for Disease Control and Prevention (CDC). Gillion. Hladik ML. Barr DB. sulfonamide. Thelin GP. Kolpin DW. Background document for development of WHO Guidelines for Drinking-water Quality. Camann DE. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. acetochlor. Ward EM. World Health Organization (WHO). 2005. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Atlanta (GA). Curwin BD. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes.php. Environ Health Perspect 2000. Sanderson WT. Casida JE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Feng PCC.248(2-3):115-122. Available at URL: http://water. Available at URL: http://www.S. Deddens JA. J Expo Anal Environ Epidemiol 2005. Barr DB. Jefferies PR. March 2006.S. Available at URL: http://water.pdf 3/30/09 Hines CJ. 6/1/09 Whyatt RM.who. April 1995. Reregistration Eligibility Decision (RED) Metolachlor.Herbicides References Battaglin WA. 4/2/09 U. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.47(6):503-517. usgs. Gilliom RJ).pdf.pdf. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. 2003.39(17):6561-6574.gov/nawqa/ pnsp/pubs/wrir984245/text.usgs. Sci Total Environ 2000. Third National Report on Human Exposure to Environmental Chemicals. Comparative metabolism and elimination of acetanilide compounds by rat. Furlong ET. Linderman R. Circular 1291. Environmental Protection Agency (U. Geological Survey (USGS). Coleman S.108(12):1151-1157. Striley CA.html. 3/26/09 U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.11(4):353359. Hodgson E. Supplemental Technical Information (available on-line only). California.S.gov/nawqa/pnsp/pubs/files/051507. Occurrence of sulfonylurea. EPA). J Agri Food Chem 1989. Sci Total Environ 2000. Shoemaker DA. Geological Survey (USGS). Biagini RE. Rose RL. 1992-2001.15(6):500-508. U.

At low levels. Omer.5-T and 2... Chlorophenoxy herbicides act as plant growth hormones.4.4. nausea. abdominal pain. it is not well absorbed through the skin.4.4..4. and concern about contamination with 2. ranging from several weeks to many months.5T is rapidly absorbed via oral and inhalation routes. with an elimination half-life of approximately 19 hours (Arnold et al.5-Trichlorophenoxyacetic acid (2.S. Given the commercial unavailability of 2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2.4.5-T has been rarely detected in ground waters (USGS.4.5-T (Holson et al. and delayed neuropathy (Bradberry et al. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Human health effects from 2.Herbicides 2. 1974).5-T was once applied as either an aqueous salt or as an oil-soluble ester. population from the National Health and Nutrition Examination Survey. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. hypotension.4. 1986. Epidemiological studies have reported associations of several types of cancer. 1989.4.4. which may vary for some chemicals by year and by individual sample. 2004).5-T in soil varies with conditions. 1992. Kohli et al.4-D were used as defoliants in the Vietnam War (e. 1992). see Data Analysis section) for Survey years 99-00 and 01-02 are 1.5-T.3..5-trichlorophenol and other degradates. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.4.g.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. renal and hepatic injury. headache.4. Ester forms of 2. Mohammad and St. 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals .5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. 2007). < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD. 2.4.5-T use as a herbicide in 1985.4. these herbicides can enhance plant growth. dizziness. Nelson et al.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2..5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. Survey Geometric mean (95% conf.7.1.5-Trichlorophenoxyacetic Acid CAS No. Although 2.5-T is eliminated mostly unchanged in the urine.4. The half-life of 2. but higher levels are herbicidal.2 and 0. myotonia. Once absorbed into the body. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. 93-76-5 General Information 2. Agent Orange). 2. the general population is unlikely to be exposed to it.5-T degrades to 2.

S. 2004). Survey Geometric mean (95% conf.5-T reflect recent exposure.4.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. Biomonitoring studies on 2. urinary levels of 2. 2003. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary 2. 2005). 1980). Biomonitoring Information Urinary levels of 2.4. Finding a measurable amount of 2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Additional information is available from U.5-T than levels found in the general population.7. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. U. population from the National Health and Nutrition Examination Survey. 1992). Mean urinary levels of 2. 2005.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. IOM.4. Fourth National Report on Human Exposure to Environmental Chemicals 65 .5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. Pearce and McLean. in which urinary levels of 2. similar to results of NHANES II (19761980). It is unclear whether these associations are related to the chlorophenoxy herbicides.EPA at: http://www.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. or to contaminants in the herbicide formulations (specifically 2. 1996.EPA.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.5-T does not mean that the level will result in an adverse health effect.4.Herbicides or contaminated herbicides.5-T itself is not mutagenic.4.4.5-T were generally below the limit of detection. 2002.3.gov/pesticides/.epa.5-T also were below the limit of detection (Kutz et al. 2. IPCS. other exposures.4.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-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.

Tandon JS. Philbert MA.4. Third National Report on Human Exposure to Environmental Chemicals. Crit Rev Toxicol 2002.4. I.4:318-21. 2005.4. International Programme on Chemical Safety-INCHEM (IPCS). Selected pesticide residues and metabolites in urine from a survey of the U.32(4):233-257.4.EPA. Garabrant DH.4. Arch Int Pharmacodyn Ther 1974. Gupta BN.4-dichlorophenoxyacetic acid (2. Fundam Appl Toxicol 1992. Board on Health Promotion and Disease Prevention. Khanna RN. Vet Hum Toxicol 1989.5-T in four-way outcross mice.epa. Kolmodin-Hedman B. McCallum WF. Kutz FW. 210:250-255. Carter-Pokras OD. Bradberry SM. Fundam Appl Toxicol 1992. Erne K. Office of Prevention Pesticides and Toxic Substances. Atlanta (GA). 3/17/09 Kohli JD.23(2):65-73. Gaines TB. S.nap. II. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Sircar KP.5-T). Scand J Work Environ Health 2005. Centers for Disease Control and Prevention (CDC). 2004. Brody D. Available at URL: http:// www.4. 2. Multireplicated dose-response studies with technical and analytical grades of 2.4-. Proudfoot AT.31 Suppl 1:1825. Mohammad FK. Pesticide industry sales and usage . Developmental toxicity of 2.4-D/2.5-trichlorophenoxyacetic acid (2. LaBorde JB. Poisoning due to chlorophenoxy herbicides.4. Available at URL: http:// www.5-T). Absorption and excretion of 2.edu/catalog. Beasley VR. Dichlorophenoxyacetic acid.EPA). et al.pdf. Gaines TB. Neurobehav Toxicol Teratol 1986.org/documents/jmpr/jmpmono/v96pr04. Nelson CJ. Pearce N. Washington (DC): National Academies Press.2000 and 2001 market estimates. J Toxicol Environ Health 1992. Nelson CJ. Estimation of occupational exposure to phenoxy acids (2. 3/17/09 Institute of Medicine (IOM). discussion 5-7.37(2):277-91.5-t mixture.31(2):121-125. Toxicol Rev 2004. general population. May. Washington (DC): U.5-T). Dhar MM.S.php?record_id=10603. Environmental Protection Agency (U. Holson JF. Cook BT. U.8(5):551-60. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Wolff GL. St Omer VE. Behavioral and developmental effects in rats following in utero exposure to 2. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Gaylor DW. 914. Agricultural exposures and non-Hodgkin’s lymphoma.5-trichlorophenoxyacetic acid (2. McLean D. et al.inchem. Review of 2. Pesticides residues in food: 1996 evaluations Part II Toxicology. 2003. Veterans and Agent Orange: update 2002.S. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Arch Toxicol Suppl 1980. Holson JF.S.4. Available at URL: http://www. Developmental toxicity of 2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4-D) epidemiology and toxicology.5-trichlorophenoxy acetic acid in man. Murphy RS.19(2):298-306.4-D and 2. Sheehan DM.htm.19(2):286-297.Herbicides References Arnold EK. Vale JA. LaBorde JB.

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

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

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

9 (13.9 (14.2) 14.073-.4) 539 456 484 487 980 885 Limits of detection (LOD.8-17.5-15.150 (.0) 19.086-. which may vary for some chemicals by year and by individual sample.9-22.054-.117) < LOD .5 (16.140-.110 (.8-24.100-.055 (.2-15.5) 19.9 (13.7) 15.9-23. Fourth National Report on Human Exposure to Environmental Chemicals 79 .096-.054-.090 (<LOD-. which may vary for some chemicals by year and by individual sample.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.1) < LOD 9.0-25.090-.102 (.140) .130-.6) 19.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .6-24.100-.1-16.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.113 (.120-.50 (8.5) 15.8-25.077-.3 (18.110) .1-19.5) 21.160) .1-24.2) 11.8 (11.1 (18.1 (13.1) 20.4 (12.8 (9.124) .109 (.40-9.30 (8.180) .147 (.060) .80-10.2) 12.130) .3-21.080) .4) 95th 20.9-38.100 (.170) .063-.3 (19.4) 19. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for survey years 01-02 and 03-04 are 10.054-.4) 21.8.139 (.093) .062 (.00-14.130 (. population from the National Health and Nutrition Examination Survey.190) .103 (.120 (.30 (8.8-19.130-.101) .3 (13.150 (.100-.083-.S.0) < LOD 9.130) .190) .5 (<LOD-11.049-.084-.158) .064) 90th .138) .6) 9.064 (.S.0-21.8) 14.00 (8.5 and 7.109-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130) .140 (.7 (15.7-22.40-10. Survey years 01-02 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70 (7.242) .112) 95th . 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 .077 (.090-.090-.4) 14.4) 20.80-9.60-10.1) 10.80 (<LOD-10.130-.7 (<LOD-15.0 (10.5-17.075) < LOD .10 (<LOD-16.110) .088-.100) .089 (.6) 16. < LOD means less than the limit of detection.8-17.9 (12.090 (.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .8) 15.7-19.058) < LOD .1) 15.180) .1) 13. Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.0 (11.4) 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 8.120) .7 (14.160 (.062-.120 (.1-18.6-24.080-.069) < LOD < LOD .5-17.90) 90th 15.3 (14.048 (<LOD-.50) 15.098 (.149) .0 (10. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD 9.080 (.103 (.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 .112-.116) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.0) 21.056-.109-.062 (. Survey years 01-02 03-04 Geometric mean (95% conf.1) 14.8 (18.110-.8) < LOD 8.138 (.160 (.070) .9 (12.4) < LOD < LOD 16.110 (.070-.6 (15.4-18.070 (<LOD-.0 (15.108-.6-33.2) 15.1) 15.100) .6 (15.6 (14.4 (12.4-17.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.053 (<LOD-.139 (.110 (.059 (.120 (.3 (18.

McIntosh LJ. pp. Basit A. 15. Mumtaz MM. are nonestrogenic in transfected HeLa cells.54:1431-1443. Edwards JW. J Toxicol Environ Health 1989.64-65 Spec. Pesticides in the Nation’s Stream and Ground Water. David VL. Shore RF. Carlson JN. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.109(Supp1):113-139. 2007 [online]. Environ Health Perspect 2001. 731-915. Olea N. Stehr-Green. plasma dieldrin. Needham LL. Neurotoxicol 2005.htm. Tully DB. Garrett N. Serrano FO. Environmental Health Criteria 91. September 2002. Brock JW. Priestly BG. 1992-2001. References Agency for Toxic Substances and Disease Registry (ATSDR).352:1816-1820. Handbook of Pesticide Toxicology. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Six high-priority organochlorine pesticides. Lancet 1998.103(Suppl 7):113-122. Narahashi T. Andersen A. Anantharam V. 1991. Daniel SE. bioaccumulation. Jorgensen T. Cox. Patterson DG Jr.html. Sonnenschein C.9:1357-1367. Ginsburg KS. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Toxicological profile for aldrin/dieldrin [online].fda. Available at URL: http://www. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. 4/21/09 Hoyer AP. Demographic and seasonal influences on human serum pesticide residue levels.org/documents/ehc/ ehc/ehc91. Song S. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 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. 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.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).91(1):122-126. Int Arch Occup Environ Health 1994. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Grajewski B. International Programme on Chemical Safety (IPCS). New York. Rosellini RA. Turner W. Available at URL: http://www. Grandjean P. Kanthasamy A. Facca A. Mink PJ. Environ Health Perspect 1995. Organochlorine exposure and risk of breast cancer.27:405-421. Hartvig HB. Finley B. Teta MJ. 1989. Fernandez MG.26:701-719. and lymphocyte sister chromatid exchange.cfsan. Li AA.atsdr. Chlorinated Hydrocarbon Insecticides. et al. Toxicol Lett 1992. Food and Drug Administration (FDA). Wienburg CL. Chung KL. et al. J Occup Environ Med 2005.66(4):229-234. Sanchez-Ramos J. Reprod Toxicol 2000.59:229-234. Psychopharmacology (Berl) 1987. Academic Press. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Ellis H.gov/ circ/2005/1291/. Jr. 6/1/09 Ward EM. PA.html. either singly or in combination.cdc. Cancer Epidemiol Biomarkers Prev 2000. Patterson DG Jr. Kitzazwa M.usgs. Aldrin and Dieldrin [online]. Available at URL: http://pubs. Part A 2000. In Hayes WJ. Corrigan FM. Roy ML.47:1059-1087. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. 2 Classes of Pesticides. Buckland SJ. Inc. August 2008. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 4/21/09 Bates MN. Smith AG. Kanthasamy AG. Eds. Vol. Chemosphere 2004. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www.gov/~dms/ pesrpts. toxicology. Revised Feb. Exp Neurol 1998. Jr and Laws ER. and epidemiology in the United States. J Toxicol Environ Health. Soto AM. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. VT. Schulte P. No:429-436. 4/21/09 Jorgenson JL.14:95-102. United States Geological Survey (USGS). Chapin RE.inchem.gov/toxprofiles/ tp1. Mann D.150:263-271. Frey JM. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.

6) 48.8) 52.5) < LOD < LOD < LOD < LOD 13.3-45. and 7.6-53.5-47.5-65.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.5) 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 * * * * 11.20 (<LOD-11.5-42. population from the National Health and Nutrition Examination Survey.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.8 (40.9) 11.10-11. Fourth National Report on Human Exposure to Environmental Chemicals 81 .6) 9.5 (41.1 (15. heptachlor use has been limited to treatment of fire ants near power transformers.8 (10.89-10.1 (17. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.7 (<LOD-32.6 (25.0) 20.1 (40.7-39. fish.2 (36.3) 10.9 (36.4) 18.5 (<LOD-12.9) 47.5) 44. Survey Geometric mean (95% conf.0 (37.8-42.0) 21.3 (20.1-51.2) < LOD 11.9) 23.1 (<LOD-12.7 (34.6) 39.2 (9.82-11. Technical grade chlordane had contained 7% trans-nonachlor.4 (22.6 (9. 2007).2) 34.3-45.9 (17.Organochlorine Pesticides Chlordane CAS No.1) 22. 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.4 (35.9-40.1 (16.4-21.1-50. which may vary for some chemicals by year and by individual sample.2-28.4 (10.9) 31.5-44.6) 11.2) < LOD 11. 1994.1-65.9-21.8-61.4 (30. 01-02.6) < LOD 11.7) 31. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7-12.1) 30. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.3-32.9) 39.9) 17.5 (31.0) 37.2) * 12.0 (<LOD-12.1-15. 57-74-9 Heptachlor CAS No.6 (16. Chlordane is not currently produced or used in the U.8-20.6-45.4-14.1) 90th 34.S.2 (10.2) 33.9 (31.9) 37. As a result of the manufacturing process.8-32.69-10.74 (<LOD-10.4) 37.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 1994).7 (42.2) 36. the technical grade product of each chemical contains 10%-20% of the other chemical.2 (28.2-49.6 (9.37 (8.8) 44.0-33.7 (32.5-40.2-56.5-38.6-12.1-19.1 (<LOD-12.3 (11.1) < LOD < LOD < LOD < LOD < LOD 8.0 (16.S.70 (<LOD-10.36-11.63 (8.7 (<LOD-13. Since 1992.9-21.9 (18. in addition to trace amounts of numerous other related compounds (ATSDR.5) 10.2 (21.7-70.0-67.20-11.5 (34.8) 18.2) 46. foods high in fat such as meat.7) 19.4-51.5) 56.8 (42.3 (<LOD-19.8 (17. chlordane was used to kill termites and other insects on agricultural crops.9) 23. and dairy products are the usual sources of exposure to these chemicals in the general population.7-25.8) 53.4-45.0-12.6-24..5 (8.0) 41.6-24.4) 29.0) 31.6) 48.6) 20.0-18.7) 19.1) 16.0 (32.4) < LOD 11.8) 52. lawns. and 03-04 are 14. from the early 1950’s until the mid-1980’s.0-61.4 (31.8-23.2 (41. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988. buildings.9-42. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.8) 27.6-18.1 (25.9 (29.5-43.0 (20.8.30-11.3-49.2 (39.9 (26.5.3) 10.2-21.7 (10.7) 42.8-73.4) < LOD < LOD < LOD 23.8 (10.0 (26.3 (28.9) 11.0-25.9) 10.2-49.10 (8.9-38.5-13.4) 12.5) < LOD < LOD 9.0) 27.4-40.3 (25.9 (15.6) 36.1 (20.3) 37. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.6) 8.9 (11.5) 37.5) 9.5) 21.8 (17.3-24. 10.7 (17.10-18.3 (27.3) 41.90 (8.1 (<LOD-12. see Data Analysis section) for Survey years 99-00.9 (26.9 (21. respectively.1 (27.5 (33.1) 30.9 (15.4) 22.5.4) 39.5-41.1 (11.3 (9.8-33.1 (44. Consequently. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.7-14. 2007).3) 18.7 (43.7) 9.20-10.1) * 11.6 (43.1) * 11.6) 49.7 (34.6) 23.9) 13.9) 36.3 (26.4 (<LOD-12.0-13.3-43.5) 38.0) 75th 20.2) 22.2 (37. < LOD means less than the limit of detection.1-25.2) 37.3 (21.7) 28. Until 1988.6) 9.4 (30.3) 18. and in soil.S.7 (19.8-31.7) 35.8 (18.8-33.2-26.9 (11.8-43.7-56.5-32.1-25.

Elimination of all these chemicals from the body occurs over months to years.053-. 2007. EPA has established environmental criteria for chlordane and heptachlor.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .070 (<LOD-.208 (.066-. Smith.290-.050 (<LOD-.220-.Organochlorine Pesticides (Dallaire et al.106-.200-.070-.064) < LOD .076) < LOD .130-.130-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.058-. Takahashi et al.100 (<LOD-.240-.450) .058 (.140 (.240-.287) .133) 90th .430) .066-. 1981).320 (.170) .189-.112 (.225 (.047 (<LOD-.120-.280-.250 (.270 (.430) .380) .050-. chronic doses of heptachlor have produced liver enlargement and injury.210 (.071 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . OSHA has established occupational exposure criteria.. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.079) .200 (.240 (.079) < LOD < LOD < LOD .230 (.269 (.080) .223) .115-.230-.057 (.199-. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. and inhalation exposure.320) .180) .063 (.280-.310) .130 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .370 (.077) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.057) * .066 (<LOD-.062) < LOD . Information Serum Oxychlordane (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.170) .290) ..300) .320) .104) .270 (.245-. neonatal mortality.140 (.320 (.270 (. 1986).230) .160) .216-.280) . 2007).067 (.150 (.320 (. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. FDA established allowable residues of chlordane.077) .286 (.258-.350 (.080) . 2001.280 (.100 (.260 (.100-.048-.140 (..315) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.165-.348) . population from the National Health and Nutrition Examination Survey.083 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.074-.400) .140 (.213) * . 2006). Chlordane and heptachlor are absorbed after oral.220 (.315 (.091) .057-.140) .060 (<LOD-.300) . 1986). 2002.242-. 82 Fourth National Report on Human Exposure to Environmental Chemicals . The U.049 (<LOD-.075 (.310) .360) .070) .150 (.160) .068) .130-.126 (.207 (.146) < LOD < LOD .310) .373) .286 (.120-. to heptachlor.160) . which may vary for some chemicals by year and by individual sample.120-.148) .080 (.110-.150-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .260 (.058-.160 (.136) .070 (<LOD-.340) . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.230-.350) .340) .146) .070 (<LOD-.092) .240) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.330 (.180-. 1977b.073) < LOD < LOD < LOD < LOD .119 (.370 (.130 (.180) .063 (. 1977a.250-.280-. Survey Geometric mean (95% conf.300 (.126) . Acute. and alterations in immune function of offspring.061-.087-.069 (<LOD-.S.320 (.271 (.056 (.120 (.073 (.082 (.260-.302) . heptachlor.207) .110 (<LOD-.200-.290-.077) .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 * * * * .189 (.190-.066 (.150 (.100-.063 (.090-..130 (.070 (<LOD-.231) .055-.090) . The major metabolite of heptachlor is heptachlor epoxide.300) .080 (.204 (. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al. Le Marchand et al.104-.149 (.140-. 1991.063) .280 (. 1991).130-.310 (.070) < LOD < LOD < LOD < LOD < LOD .400) .115 (.220-.077) .128 (.310-.130-.260 (.290) .150) .065-. and breast milk is a major excretion route in lactating women.200-.090) . and the U.230 (. and heptachlor epoxide in foods and bottled water.170) .300-.190-. which is also persistent in the body (ATSDR. In laboratory animal studies.510) .300) .S.258 (.190-. dermal.350 (.253-.130) .210-. Shindell and Ulrich.170-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.246-.290-.070-. characterized by seizures and paralysis.230-.148-.450) .083) .070-.290 (.108-.170) .210 (. 1996.063) * .180-.063 (. IARC.070 (.140-.068) 75th .440) .410) .130) .227) < LOD .250 (.168-.068-.370 (.063-. Rogan.170) .053-.080) .560) .203-.

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

8) 14.6) 13.8-24.4 (11.0-17. see Data Analysis section) for Survey years 99-00.3 (13.2-16.6.0 (15.1) 13.6 (8.9 (12. respectively.3) 18.2 (<LOD-62.8) 19.6-17. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.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.3) 16.8 (13.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 13. 84 Fourth National Report on Human Exposure to Environmental Chemicals .2) 15.8 (<LOD-23. population from the National Health and Nutrition Examination Survey.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.8 (15. 01-02.7 (13.5 (<LOD-21.9-23.9 (15.3) 10.4 (<LOD-19.3) 18.1) 23.1-38.9-29.8) 19.2-27.1 (19. which may vary for some chemicals by year and by individual sample.1-29.0 (11.8-46.9-29.5.6) 22.0-54.5) 19.0) 13.5) < LOD 14.6 (16. 10.8) 20.4 (<LOD-54.6 (11.3) 18.8) 21.10-13.7 (10.8-23. Survey Geometric mean (95% conf.4 (11.9) * * * 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 8.1) 20.3) 27.0-16.8 (18.6 (<LOD-27.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.8.6 (16.2 (18. and 03-04 are 14.7 (16.1-16.6 (13.S.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.6-21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-17.8) 14.50) < LOD < LOD < LOD 17.3 (<LOD-25.8-24.6) 14.5 (10.5 (11.2) 26.1-15.5 (<LOD-32.8) 15.6 (12.2 (<LOD-25.40) 15.3) 23.2-27.1 (16.8 (18.9-25.4) 21.7-19.8) 13.8) 13.4 (15.3-18.20 (<LOD-9.6 (14.2 (<LOD-16.4) 18. < LOD means less than the limit of detection.3) 22.5 (18.2) 20.8 (13.7-25.7-18.9-16. and 7.6) < LOD < LOD < LOD 27.8-24.9) 15.90 (<LOD-9.2-17.5 (11.0-19.8) 16.

150 (.087 (.135 (.108) .101 (.094 (.170 (.097) < LOD .107-.200) .113) .090-.098 (.180) .120 (<LOD-.220) .200 (.157) .100-.110-.Organochlorine Pesticides Serum Heptachlor epoxide (whole weight) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.150 (<LOD-. Survey Geometric mean (95% conf.170 (.110 (<LOD-.063) < LOD < LOD < LOD .116) < LOD < LOD < LOD .053-.190 (.100-.090-.090 (<LOD-.130) .190) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .100 (<LOD-.071-.180) .069 (.130-.120-.170) .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .200) .130 (.170 (.063) .090-.100 (.130-.108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .117) .101 (.111) .070-.240) .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.100 (.113-.120) .140) .173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .077-.111-.082-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.126 (.110 (.094 (.110-.180 (<LOD-.110 (<LOD-.130 (<LOD-.140-.133 (.110) .180 (.130-.170) .076-.180) .310) .067-.135 (.106-. Fourth National Report on Human Exposure to Environmental Chemicals 85 .180) .190) .110) .100 (.310) .130) .074-.140) .104) .130-.077-.170) .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 .100 (.120 (<LOD-.055 (<LOD-.270) .150 (.108-.096 (.090-.120 (. population from the National Health and Nutrition Examination Survey.S.190) .170 (<LOD-.110 (.149) .128 (. which may vary for some chemicals by year and by individual sample.090-.380) .090-.120) .057 (<LOD-.090 (.

7 (35.1 (65.6 (56.0) 49.4-67.1) 31.1-22.6 (16.9) 51.2 (26.8 (<LOD-20.2) < LOD 10.9 (28.7) 28.8-67.8 (11.1-34.0 (42.3 (17.3-39.9) 14.0) < LOD < LOD 8.9-89.3) 36.1) 17.1) 17.3) 16.8-79.8-90.1 (22.8 (16.0 (48.8) 80.3 (14.4-36.6-54.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.3) 19.8 (71.8-90.4 (45.1) 30.5) 90th 55.9 (51.5 (13.1 (48.5) 19.0 (19.0-37.0 (42.4 (11.9-22.6-19.2-17.6-88.6-66.8 (13.9-40.7-20.1) 17.3) 18.8 (17.7-160) 86.1) 18.0) 75th 31.8-16.2) 19.6) 56.6 (56.5-17.3-32.7) 52.4 (16.7) 59.9-64.8 (13.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.8-16. < LOD means less than the limit of detection.0 (60.7-38.0 (29.5-69.7) 15.0-68.8-19.6 (57.8 (28.1 (10.2-18.5) 36.9-58.1-16.3) 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.0-93.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.5 (45.0-22.6) 10.0) 13.2 (60.3 (49.9) 14.3-50.3-58.6 (15.3 (14.4 (67.5-36.7 (30.2 (25.4 (30.5) 78.2-23.7-22.1) 62.2) 39.2 (64.5) 20.5) 14.8) 47.1 (41.2) 30. interval) 18.2 (36.3-74.9-45.4) 48.7 (59.7 (74.1) 17.6) 60.0 (13.7 (16.0-123) 74. respectively.3-86.7) 14.8-21.5) 14.3) 32.5-87.7-18.S.1) 78.7 (28.8 (15.2 (15.3-57.1) 17.3) 25. 01-02.7 (18.6 (12.1 (47.3) 18.2 (27.3) 30.8 (26.9) < LOD < LOD < LOD 20.8-129) 74.70 (<LOD-12.5 (25.1-126) 67.4 (28.8) 51.6) 54.1-34.2-37.6-22.7) 78.8 (26.7) 56.8 (28.5. 86 Fourth National Report on Human Exposure to Environmental Chemicals .0 (16.0-23.0) 19.5) 9.2 (7.3-21.8-110) 59.1) 17.4) 55. population from the National Health and Nutrition Examination Survey.5-20. Survey Geometric mean (95% conf.4-23.9) 51.1) 16.7-21.9 (15.0-93.0-38.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.7-77. which may vary for some chemicals by year and by individual sample.7 (11. see Data Analysis section) for Survey years 99-00.0 (62.1) 14.0-23.8 (49.3) 30.7-23.0 (13.2-18.0-113) 68.2) 17.3 (56.1) 18.7) 78.9 (15.6-20.9 (29. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-82.6) 82.2) 59.9 (16.5-19.4) 59.0-143) 112 (68.2-21.0-24.2) 34.4 (12.5) 22.5. and 7.1) 32.1-51.10 (<LOD-11.5) 30.2-88.5 (15.4) 19.7-35.1 (17.4) 107 (84.8 (12.0-59.2 (14.3 (58.8-41.8-19.5) 26.1-28.8 (19.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.0) 40.6) 84.9 (51.5-95.5) 48.9-65. and 03-04 are 14.2 (19.6) 13.7-29.7) 17.2) 20.7) 73.1) 17.5) 77.3 (16.4-22.3) 32.2 (14.8-77.3) 15.5-111) 68.0) 33.3 (45.9-36.4-18.5 (15.1-55. 10.4) 20.9-65.6 (50.9-69.4) 16.6 (<LOD-14.9 (19.1-20.7 (59.8 (42.8 (26.6) 56.7-17.9 (66.6 (52.0) 18.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.86-13.8 (30.3-30.0-20.4-52.9-20.7-113) 68.0 (15.9 (<LOD-14.2 (59.4-35.5) 35.1) 78.6) 34.6 (32.9 (36.0 (14.7-34.0 (16.1-18.5 (44.1-16.9-35.7 (13.7-32.4-62.9 (47.7) 35.8.8) 19.8 (28.0 (15.2-16.6) 25.8 (45.

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

Jaraczewska K. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. et al. Toxicological profile for heptachlor and heptachlor epoxide [online]. Hertz-Picciotto I. 1979-1980.84:151-161.html. 1993. maternal serum and milk from Wielkopolska region. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Covaci A. Charles MJ.heptachlor. Kolonel LN. Stehr-Green P.pdf. Organochlorine exposures and breast cancer risk in New York City women.gov/ntp/ htdocs/LT_rpts/tr008.inchem.niehs.41:145–148. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Res 2000. Toxicological profile for chlordane [online]. Bjerselius R. Jr and Laws ER. et al.cdc. LeMarchand L. Hawaii Med J 1991. Available at URL: http://www. In Hayes WJ. Wohlleb JC. Available at URL: http://www. Shindell S and Ulrich S.150:981-990. Senie R. Environ Health Perspect 2002. 2001. Available at URL: http://www. Dendle WH. International Agency for Research on Cancer (IARC). Jr.330:55-70.8:1-123.htm. Environ Health Perspect 2002. Sci Tot Environ 2006.htm. Saidein D. 2006. Bioassay of heptachlor for possible carcinogenicity.pdf. 731-915. 6/1/09 National Toxicology Program (NTP).atsdr. Darnerud PO. Mortality of workers employed in the manufacture of chlordane: an update. Odland JO. Available at URL: http://ntp. KalubaSkotarczak A. May 1994. Gilman A.gov/toxprofiles/tp31. Berkowitz GS.inchem. Glynn AW. et al.html. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Pollutants in breast milk. Drews K. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR).259(3):374-377. 4/21/09 Baker DB. Atuma S. gov/toxprofiles/tp12. Available at URL: http://www. National Toxicology Program (NTP). Bioassay of chlordane for possible carcinogenicity. Chashchin V. International Agency for Research on Cancer (IARC) .111:349355. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.gov/ntp/ htdocs/LT_rpts/tr009.9:1-109. Takahashi W. Vol. Chlordane and heptachlor [online]. Available at URL: http://www. Available at URL: http://ntp. Organochlorines in Swedish women: determinants of serum concentrations. Concise International Chemical Assessment Document 70 Heptachlor [online]. Ayotte P. Smith AG. Wolff MS. Muckle G. Distribution of polychlorinated biphenyls. 4/21/09 Dallaire F. Environ Health Perspect 2003. Chlorinated Hydrocarbon Insecticides.html. Tartter P. New York. Hansen JC. Canada).org/documents/iarc/ vol79/79-12. Baker DB. Voorspoels S. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Poland. Keller JA. 4/21/09 James RA. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. 9/25/07 International Programme in Chemical Safety (IPCS). A Report to the Hawaii Heptachlor Research and Education Foundation.28:497501. Lawrence River (Quebec. Wong L.110(8):835-838. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.atsdr. Laliberte C.372:20-31.50(3):108-118. Willman E. Arch Pediatr Adolesc Med 1996.nih. 1991 pp. 2 Classes of Pesticides. 1963-1967. August 2007. Granath F. Takei G.org/ documents/cicads/cicads/cicad70. Royce W.Summaries & Evaluations. Inc.cdc. Bleiweiss IJ. Circumpolar maternal blood contaminant survey. Aune M. Van Oostdam JC. Arch Environ Health. Handbook of Pesticide Toxicology. Lulek J. et al. Siegel BZ. Dewailly E. Eds. 6/1/09 Rogan WJ.niehs. Organochloride pesticide residues in human milk in Hawaii.nih. Head SL. Vol. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. J Occup Med 1986. Bull Environ Contam Toxicol 1981:27:506-511. 79. Sci Total Environ 2004. 1994-1997 organochlorine compounds. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Academic Press. JAMA 1988. Dewailly E. Brower S. Barker J. 1986.110:617-624. Loo S.org/site/foundation/ research/projects2.

70 (8.S.0-35.1 (<LOD-39. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.0-53.5 (15.1 (33.3 (<LOD-21. after World War II until 1972.3) 28.S.2-95.9 (21.5 (14.3-16. population.1-27.1) 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 12.4) < LOD 17. DDT and DDE can cross the placenta.5) < LOD < LOD 9. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.1 (23. Both Serum p.5) 23.6 (25. food. depending on conditions.1’-(2.6-33.3 (<LOD-31. inhalation.7) 12. The biodegradation half-life of DDT in soil varies from 2 to 15 years. Smith. and 7.9 (10.8-39. 1991).2 (<LOD-40.1) 31.0-27. It was produced and used in the U.p’-DDT (65%-80%).9 (10. In the general U. although DDT and DDE intakes have decreased over time (FDA. It is still used in some countries.10-13.8) 30. 2002. DDT can be absorbed after ingestion.S.2) 155 (59.90 (<LOD-12.2-65.7.9-34. sediments.9-28.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.4.6 (22.3) 22. p.3) 21. and 03-04 are 20. Gunderson. particularly meat. 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. Fourth National Report on Human Exposure to Environmental Chemicals 89 .0) 26. or dermal exposure. 1991).0-155) 83.7 (19. which may vary for some chemicals by year and by individual sample.50-11.3) 21.8) 15. 17. fish.8-26.4 (23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Only a small proportion of DDT is metabolized and excreted (Smith.3 (27.0-37.2) < LOD < LOD 9. as well as in plant and animal tissues.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. population from the National Health and Nutrition Examination Survey.9 (<LOD-20. and water.5 (23.0) 20.0 (10. when virtually all use of it was banned.3-236) 24.8. particularly for endemic vector and malaria control.7-16. 01-02.0-15.5-54.p’-DDD (4% or less).8-23. air. o.6 (<LOD-25.00 (<LOD-10.1’-dichloro-(2.5) 25.9) < LOD < LOD 9.0) 40. which is a mixture containing p.7) < LOD 18.3-590) 293 (104-541) 48. DDT usually refers to the technical product.0 (18.6 (31.10 (<LOD-12. see Data Analysis section) for Survey years 99-00. 1988).Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.7 (15.1-71.5 (23.8) 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. resulting in fetal exposure. DDT was used at one time as a treatment for head and body lice. DDT is converted to DDE and several other metabolites.0 (21.8-17. Survey Geometric mean (95% conf.9) 14.7) 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 10.2 (11.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.9) 17.5-36. DDT is converted in the environment to other more stable chemical forms. and trace amounts of several related compounds.4) < LOD < LOD < LOD 61.0) 19. < LOD means less than the limit of detection. continues to be the primary source of DDT exposure.6 (9.p’-DDT (15%-21%). These chemicals are highly persistent in soil. In the body. 2008. and dairy products.2-bis(p-chlorophenyl) ethane (DDD).8) 36.9) 29. including 1. respectively.9 (10.0 (18. Food imported from countries that still use DDT may contain the chemical or its residues.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 30.

220) . polychlorinated biphenyls. 90 Fourth National Report on Human Exposure to Environmental Chemicals .064 (. reproductive organ abnormalities.200 (. and altered behavior after neonatal exposure (Eriksson and Talts. lung cancer.054-.180) . dioxins and furans).120-.290) .260) . both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.250 (. In high dose. Mariussen and Fonnum.330-4. and leukemia have also been inconclusive (ADSDR.106) . overt signs of acute human toxicity include vomiting. 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..130-. premature delivery. 2006).143) < LOD < LOD .146 (.068-.108 (.078-.048 (<LOD-..130 (<LOD-. 2006).140-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.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 . 2004.130 (<LOD-.150-. 2001). 2002.087 (.130 (<LOD-. 1997). Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.189-. Animal studies reported reduced fertility.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.Organochlorine Pesticides chemicals are excreted in breast milk.051 (<LOD-. and duration of lactation.106-. 2001).071 (.069) . have not been consistently demonstrated (Beard.220) .167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. DDT may bind to estrogen receptors (Chen et al.086 (. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.34) .084 (. Longnecker et al.106) < LOD < LOD .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.570-4.190 (. 1996).150) .240 (.240) .01) .059-.170) . Survey Geometric mean (95% conf.065-.343) < LOD .150 (<LOD-. 2001). Reproductive effects in humans affecting birth weight. tremor.p’-DDE can produce anti-androgenic effects (Gray et al. 2002. 1956). 2006). A workplace standard for DDT has been established by Serum p.071-. 1995.313 (. Gray et al.132-.p’-DDD and p.170 (.203) . Jusko et al.190 (. and o.26) 1. 2006. population from the National Health and Nutrition Examination Survey.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 .. 2002. 2001).420) . Calle et al..142 (.230) .180) .150 (<LOD-. accidental exposures..120 (<LOD-.146 (.160-. Hayes et al. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. Gladen and Rogan..061) < LOD < LOD < LOD . 1998).00) .250-1.190-1.189) 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 .140) . which may vary for some chemicals by year and by individual sample.095) < LOD ..400) .180 (. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.170-. Studies of DDT exposure and pancreatic cancer. and seizures.00 (.112 (. resulting in exposure to nursing infants (Rogan.098-. fertility. Beard. Jusko et al. Snedeker.079) < LOD < LOD .201 (. In laboratory animals.230) .074-.114-.. 2000.063 (<LOD-.180-..128 (..62 (.530 (. 2002..078 (. 2006.080-.627) . other organochlorines. interval) Selected percentiles ( 95% confidence interval) Sample 95th .530) .180 (..150-.400 (. 2006.g.105-.075) 1.

. In a population-based sample of men and women from eastern Slovakia.7-119) 113 (100-140) 93. mean serum levels of DDT and DDE in the U.. Compared to females in the NHANES 1999-2000 subsample.Organochlorine Pesticides OSHA and a guidance established by ACGIH.S. and 03-04 are 18.S. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. population declined by about fivefold to tenfold.. 2002. IARC classifies DDT (p.p'-Dichlorodiphenyldichloroethene (DDE) (lipid adjusted) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 8.. 1991).6.epa. 2005). Link et al. 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.gov/ pestcides/ and from ATSDR at: http://www. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. 2002. Smith. respectively. compared to levels observed in this Report (Anderson et al.. 2003. 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. 01-02. 1998. More information about external exposure (i.S.8. Fourth National Report on Human Exposure to Environmental Chemicals 91 . mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.html. In general. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. EPA at: http://www. Declining DDE levels over time have also been observed in the German population. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Biomonitoring Information DDE persists in the body longer than DDT.0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD.6 (81. environmental levels) and health effects is available from the U. 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.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. Since the 1970’s. 2004). and 7.3.gov/ toxpro2. 1989)...p’-DDT) as a possible human carcinogen. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. 2004). Stehr-Green. 2003). NTP considers DDT as being reasonably anticipated to be a human carcinogen.. see Data Analysis section) for Survey years 99-00. Heudorf et al.e. respectively.atsdr. for males and females in the NHANES 19992000 subsample (Pavuk et al.cdc.

75) 6.18-4.01-11.68-4.9 (26.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.82) 1.6) 13.430-.91) 3.9) 5.32-1.13 (1.53-15. In the NHANES 1999-2000.14 (1.69 (.34-3.37 (1.820-1. 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.28) 1. 2005). 2001-2002 and 2003-2004 subsamples.4) 9.72) 1.24-17.10-1. interval) 1.11 (2.01-1.80) 1.64) 3.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 . Survey Geometric mean (95% conf. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.70) 1.03-1.4) 13.81 (7.70-3.25) 8.34 (7.870 (.4 (12.40 (3.79) 4.46 (1.57 (1.66-17.22) .37-4.20 (.561 (.91 (6.25-16.01-15. serum levels of o.14-9.62-6.36-1.611-1. considerably higher than levels in this Report (Smith.9-17.92 (3.623 (.456 (.45 (1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.500-.796 (.04-1.15-4.65 (1.10) 2.00 (6. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.8) 15. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.36 (3.69) 4.01-5.80) 1.5) 22.66-2.2-32.80 (2.33-1.39 (3..7) 16.19-14.63 (1.75 (4.17-3.58) 1.99) 1.32 (1.51) 1.76) 1.80) 3.38 (1.43 (5. 1989).385-.76-3.59) 3.13) 4.51-49.50-17.890-1. In a subsample of NHANES II (19761980) participants.14) 2.6) 12.6 (8.69) 8.51) 3.726) .9) 7.1 (8.75) 1.5) 7.47 (1.12 (.9-38.77 (1.6 (9.40-4.26-2.p’-DDT.50 (2.48 (6.25 (.76 (2.4) 14.63 (6.7-19.1 (9.60-13.71 (5.1) 40.19) 4.22-1.88 (2.59 (1.37-16.44) 1.54 (1.49 (1.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.02 (2.78 (4.64-2.16-1.14-1.7) 9.21) 90th 7.37-10.49 (6.8 (9.p’-DDT were below the limits of detection.45 (1.68 (2.81 (1.48-4.27-1.S.58) 1.57-2.6) 11.30-1.01-1.6) 9.66) 3.12 (6.51 (1.36-2.06) 3.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.56-6.23 (7.29 (1.3 (9.516 (.25 (1.730) .41-12..2 (6.2) 19.06) 1.85 (1.8 (14.72) 1.37-1.6) 8.87 (5.04 (6.7 (8.0) 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 .32-1.6) 9.54) 8.91-2.26 (1.56-3.963-1.07 (5.Organochlorine Pesticides nearby agriculture (Botella et al.84-3.680-1.p’-DDT.47) 3.57 (3. o.39-2.557) 1.02) 1.18-1.18-1.57 (1.3-43.12-1.75) 2.77 (1.36) 3.7-48.34) 6.84 (3.26-10.24) 1.31-12.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.81-18. 2004).55-9.46 (1.69 (1.7-20.10-5.25-14.56-2.34-11.00) 7.82 (1.13-2.63 (1.53 (2. less than one percent had detectable serum levels of o.4-19.63-15.17 (3.61-2.994-2.52 (3.53) 1.68) 2.66) 1.69 (2.96) 1. or p.646) .1) 7.6 (7.56) 2.7) 13.90) 22.03-4.40-8.83 (1.53) 7.3 (8.59 (4. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.88-35.55 (2.965-1.18 (6.3) 10..p’-DDT (Stehr-Green.81-5.8-90.534-.520 (.10) .419-. 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.30 (1.6) 9.51-15.43-4.0 (9.02-8.6 (17.488-.43-4.93 (7.57-3.57) 2.91-3.11-1. High mean levels of whole blood DDT (about 3.0 (12.43-8.22 (7.21) 3.38 (1.66-4.92 (3.6) 9. Serum p.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.24 (1..71 (6.07) 1.30 (1.0) 2.00 (.25) 1.16 (2.52-6.96) .92) 1.31-2.01) 1.2 (9.18) 1.90-8.54-7. population from the National Health and Nutrition Examination Survey.59) 6.01-11.5) 16.2 (19. 1991).860 ng/L) and DDE (about 14.30-1. 1971).09-1.35) 1.26) 3.01) 1.8 (13. 309 versus 268 ng/g lipid.34) 2.87-16.31 (1.5) 10.66) 1.46-2.51-8.2) 26.8 (13.36-11.76) 1.5) 5.97-4.71) 32.39) 1.61 (1.00-1.1) 12.49) 8.57-13. 2004).32-9.4 (8.40-4.85-4.2 (9.3) 16.27) 3.85-10.18-3.14) 2.58) 75th 3. Finding a measurable amount of p.32) 1.41 (1.07) 1.59 (1.65) 1.05 (3.590 (.635) 1.05) 1.600) .75 (8.81) 11.52 (1.9 (15.32 (1.66) 4.39-1.71) 12.97 (3.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.3) 13.49 (1.

which may vary for some chemicals by year and by individual sample.8. 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.Organochlorine Pesticides Serum o.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 01-02.7. Fourth National Report on Human Exposure to Environmental Chemicals 93 . Survey Geometric mean (95% conf. respectively. 17. and 03-04 are 20.4. see Data Analysis section) for Survey years 99-00. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 7.

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. population from the National Health and Nutrition Examination Survey.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Survey Geometric mean (95% conf. 94 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides Serum o.S. 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.

Baker RJ.96:34-40. Brock JW. Klebanoff MA.cfsan. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Environ Res 2004. Am J Epidemiol 2002. April 1982 to 1984. Hum Reprod Updat 2001. Thun MJ. dichlorodiphenyldichloroethylene.112(17):1761-1767. et al. Hurd C. Talts U.106(5):279-289. Parks L. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Botella B. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Olea-Serrano MF.162:890-897. Rogan WJ.html. Gabrio T. Bhatnagar VK. Becker K. 4/21/09 Gladen BC. Chemosphere 2004. Environ Health Perspect 2003. Gray KA. Bjerselius R. Arnold SF. et al. FDA total diet study. Toxicological profile for DDT.. Am J Public Health 1995.58:1185-1201. Gunderson EL.7(3):248-264. dietary intakes of pesticides. Eriksson P. Granath F. Maternal DDT exposures in relation to fetal and 5-year growth. Int J Hyg Environ Health 2002. et al. India.358:110-114. CA Cancer J Clin 2002. and other chemicals. Vorojeikina DP. Herrman T. Available at URL: http://www. Lepom P. The Great Lakes Consortium. DDT and human health. Hayes WJ. et al. Biomonitoring of persistent organochlorine pesticides. Wolf CJ. Zhou H. Fourth National Report on Human Exposure to Environmental Chemicals 95 .111:349355. Longnecker MP. Int J Hyg Environ Health 2003. Longnecker MP. hexachlorobenzene.53(8):1161-1172.97(2):178192. HCH. Exposure of women to organochlorine pesticides in Southern Spain. Neurotoxicol 2000. Chen CW. Vena JE. Zoellner I. September 2002. Savitz DA.205:297-308. Bates MN. Bull Environ Contam Toxicol 2004. Beard J. Davis MD.21(1-2)37-48. lindane (g-HCH). Furr J. Gray LE Jr. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Calle EE. Falk C. Rivas A. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Notides AC. Hediger ML. Darnerud PO. Cueto C.206:485-491. Crespo J. Hanrahan L. Atuma S. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.85:504508. DDE. Piechotowski I. Koepsell TD. Saiyed HN. Heudorf U. Olson J. Schulz C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.fda. Environ Res 2005. 4/21/09 Anderson HA. et al. Food and Drug Administration (FDA). Sci Tot Environ 2006. Available at URL: http://www. Lambright C. Zhou H. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.52:301-309. Klebanoff MA.72:261265. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Ostby J. et al.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Cerrillo I. Profiles of ortho-polychlorinated biphenyl congeners. Link B. Brock JW. Patterson DG Jr. Zaidi SS. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Needham LL. and dichloro(diphenyl)ethylene (DDE). Swanson MK. Chemosphere 2005. DDE and shortened duration of lactation in a northern Mexican town. Needham LL. Bloom MS. Durham WF. Kulkarni PK. Environ Health Perspect 1998.gov/ toxprofiles/tp35. Willman EJ. Buckland SJ. and polythelia among male offspring. Epidemiology 2006. Barr DB. Garrett N. Aune M. Organochlorines in Swedish women: determinants of serum concentrations.cdc. Jr. Jusko TA. et al. Greenfield TA. JAMA 1956. Needham LL.155(4):313-322. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Henley SJ. Levels of DDT. Krause C. Seiwert M. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Lancet 2001. Olson JR. and DDD [online]. Moysich KB. and HCB residues in human blood in Ahmedabad.17(6):692-700. Organochlorines and breast cancer risk.gov/~dms/ pesrpts. Olea N. Paepke O. Maternal serum level of 1. Kashyap R. Environ Health Perspect 2004.355:7889. et al. hypospadias. August 2008. selected elements. Effects of environmental antiandrogens on reproductive development in experimental animals.54:1431-1443. Glynn AW.html.71(6):1200-1209. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT).Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).atsdr. Drexler H. Ellis H. Frumkin H. Angerer J. Jr. Katz SH. Charles MJ. Burse VW. J Assoc Off Anal Chem 1988. Klebanoff MA. Biochem Pharmacol 1997.1-dichloro2. et al. Gladen BC. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Kaus S.

Comparative pharmacodynamics of CYP2B induction by DDT. Radomski JL. and DDD in male rat liver and cultured rat hepatocytes. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Chovancova J. Thomas PE. Chlorinated Hydrocarbon Insecticides. Academic Press. Jr. Astolfi E. Fonnum F. Chemosphere 2004.109:35-47. 731-915. Lynch CF. Pavuk M. Reddy AB. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health Part A 1998. Crit Rev Toxicol 2006. In Hayes WJ. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Jones CR. Toxicol Appl Pharmacol 1971. Eds. Cerhan JR. Smith AG. Lubet R.150:981-990. Environ Health Perspect 2001. Snedeker SM. 2 Classes of Pesticides. Rey AA. DDE. Petrik J.20(2):186-193. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. 1991 pp. PA. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Stehr-Green. Handbook of Pesticide Toxicology. and dieldrin. Fox S.54:1509-520. Nims R. New York. Pollutants in breast milk. Inc.53:455-477. Deichmann WB.36:253-589.27:405-421. Vol. Arch Pediatr Adolesc Med 1996.Organochlorine Pesticides Mariussen E. Jr and Laws ER. Pesticides and breast cancer risk: a review of DDT. Rogan WJ. Schecter A. et al. et al. DDE. J Toxicol Environ Health 1989. children and newborn infants.

or from contact with contaminated soils and sediments in areas where endrin was applied. Because it is metabolized so rapidly. An epidemic of acute endrin poisoning. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1996. Ketoendrin is a major photodegradation product (IPCS. Endrin was used as an insecticide. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. All uses of the pesticide in the U. Survey Geometric mean (95% conf. and occasionally at low levels in sediment and surface waters.50) < LOD 5.50) < LOD < LOD < LOD 5. inhalation or dermal exposure routes. 1992). endrin has been detected with declining frequency in U. In the body. endrin usually is not detected in serum of exposed individuals. endrin is converted rapidly to its major metabolite. Depending on soil conditions. or discarded. Endrin does not accumulate in body tissues (IPCS. rodenticide and avicide.S. IPCS. 1979. manufactured. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.10 (<LOD-5.40 (<LOD-6. 1981).10 (<LOD-5.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. Endrin was not widely used as a termiticide. < LOD means less than the limit of detection. endrin can persist for years. 1987). 1992)..30 (<LOD-6. 1991).20 (<LOD-5. anti-12hydroxyendrin. Endrin is absorbed rapidly after ingestion. unlike aldrin and dieldrin. Fourth National Report on Human Exposure to Environmental Chemicals 97 . interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.60 (5. 1992.S. fatty infiltration. which may vary for some chemicals by year and by individual sample.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. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. 72-20-8 General Information Endrin. 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. 2008).09 and 7. Smith. Endrin has been detected in soils.S. a stereoisomer of dieldrin.. unless the dose is high and the exposure is very recent. Hepatic effects of endrin exposure have included necrosis.Organochlorine Pesticides Endrin CAS No.. have been cancelled by the U.40-5. total diet surveys (FDA. Kavlock et al. At high doses. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and inflammation (Smith.S. EPA.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. Over time.20 (<LOD-5. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. 1991). is no longer manufactured in the U.. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.8.30) < LOD 5. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. 1992).S.

Workplace exposure standards for endrin have been established by OSHA. 2004.cdc. and the FDA monitors foods for pesticide residues. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. serum levels of endrin were below the limit of detection.. Survey Geometric mean (95% conf. 98 Fourth National Report on Human Exposure to Environmental Chemicals . environmental levels) and health effects of endrin is available from ATSDR at: http://www.html. population from the National Health and Nutrition Examination Survey.020 (<LOD-.020) < LOD .020 (<LOD-..020 (<LOD-..020) < LOD . In a small study of Spanish women hospitalized for elective surgery.020 (<LOD-.020) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020-.S.020) < LOD < LOD < 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.020 (<LOD-.24 ng/mL (about 6. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020 (. Ward et al. IARC has determined that endrin is not classifiable with regard to human carcinogenicity. with the highest value 6.020) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020 (<LOD-.020) < LOD < 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 . 2000).24 ng/g of serum) (Botella et al.Organochlorine Pesticides The U. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. EPA has established environmental standards for endrin. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.e.atsdr..S.gov/toxpro2. which may vary for some chemicals by year and by individual sample. This finding is consistent with other general population studies (Bates et al.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. 2004). endrin was detected in 9% of serum samples. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Information about external exposure (i.

Toxicology 1981. Rivas A. Turner W.21:141-150. Chernoff H. Inc. et al. Hanisch RC. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Frey JM.96:34-40. Endrin [online]. Needham LL. Whitehouse DA. Gray LE. Smith AG. et al. et al. Fetotoxic effects of prenatal exposure in hamsters. II. Rowley DL. Garrett N. Perinatal toxicity of endrin in rodents. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Academic Press. Available at URL: http://www.inchem. Food and Drug Administration (FDA).gov/toxprofiles/tp89. Cerrillo I. I. Andersen A.htm. Vol. Narahashi T. Saleem M.9:1357-136. Chernoff N. Rogers E. In Hayes WJ.cfsan. Olea-Serrano MF. 4/21/09 Kavlock RJ. Ward EM.cdc. Botella B. Jr. 2 Classes of Pesticides.html.54:1431-1443. Exposure of women to organochlorine pesticides in Southern Spain. Grajewski B. Toxicological profile for endrin [online]. Rab MA.html. Jr and Laws ER. Chemosphere 2004. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. pp. 4/21/09 International Programme on Chemical Safety (IPCS). Liddle J. Roy ML. Ellis H. August 1996. Buckland SJ.13:155-165. 1991. Gray JA. Perinatal toxicity of endrin in rodents. Cancer Epidemiol Biomarkers Prev 2000. Hardjotanojo W. Crespo J. et al. Handbook of Pesticide Toxicology. Sokal D. Eds. New York.atsdr. Environmental Health Criteria 130.79(6):928-934. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. 731-915. 4/21/09 Bates MN.64-65 Spec. Patterson DG Jr. Toxicology 1979. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Fetotoxic effects of prenatal exposure in rats and mice.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Gray LE. Pediatrics 1987. Patterson DG Jr. Burse VW. Ginsburg KS. Hanisch RC.gov/~dms/ pesrpts. Available at URL: http://www. Gray J.org/documents/ehc/ehc/ ehc130. Toxicol Lett 1992. August 2008. Convulsions caused by endrin poisoning in Pakistan. Environ Res 2004. No:429-436. Schulte P. Available at URL: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Kavlock RJ. Chlorinated Hydrocarbon Insecticides. 1992.fda. Olea N.

2-31.8 (22.3 (20.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.6) < LOD < LOD 14. 2.3) 24.7-16.0-28.2) < LOD < LOD 29. Although it is not manufactured as an end-product in the U. HCB has been detected in fewer foods since the 1980s (FDA.6 (21.3-22.5-14.1-16. < LOD means less than the limit of detection.3) * * 15.1 (17. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.7-29.7 (19.6-33.5-trichlorophenol (2.9 (25.S. EPA cancelled its use in 1984.4. The FDA dietary surveys have shown that over time. breast milk is an additional route of elimination in nursing women. HCB is slowly metabolized. population from the National Health and Nutrition Examination Survey.1) * * 15.1 (14. Therefore.9) < LOD < LOD 20. 1976).8 (15.9) < LOD < LOD 28.3-26.3 (14.0-19.4) < LOD < LOD 14.4) < LOD < LOD 33.0.S.9-17. 2002).3-20.4) < LOD < LOD 19.6) < LOD < LOD 25.7-21.2-15.3 (12. and foods with a high fat content.7-22. Urinary metabolites include pentachlorophenol (PCP). Survey Geometric mean (95% conf. distributes widely throughout the body. and sediment (Barber et al.4 (11.5-18. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. 100 Fourth National Report on Human Exposure to Environmental Chemicals .7 (15. The general population may be exposed to HCB through diet.3 (16.6) < LOD < LOD 26.6) < LOD < LOD 26. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.0) < LOD < LOD 15.6-32.9) < LOD < LOD 20.3 (22..7-16.2-15.1-20.2 (14.7) * * 14.0 (14.8. or game taken from areas with HCB contamination.1 (13.6-TCP) (To-Figueras et al.7-26.6-trichlorophenol (2.5-33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..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 * * 16.9) < LOD < LOD 15. 1997).2 (14.5-14.5 (13. 31..9-15.9) 19.7 (15. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.8) < LOD < LOD 27.4. water. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.8 (26.5 (14. see Data Analysis section) for Survey years 99-00. and elimination occurs by renal and fecal routes.0-25.6-26.0-16.0 (18.4 (22. HCB is well absorbed after oral administration.4.9-30.8-15.6 (24. Gunderson.4 (18.2 (17.7-15.9) < LOD < LOD 19.7 (27.5) < LOD < LOD 18.0) < LOD < LOD 24.4.0) * * 15. and accumulates in fatty tissues where it persists for years.0 (18.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.9 (14.9-24.2) < LOD < LOD 13.6-19. wildfowl.4-16.7) < LOD < LOD 24.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. air.6) < LOD < LOD 24.0 (25.3) < LOD < LOD 20. 2005).4. and has been detected in soil. and 7.4) < LOD < LOD 22. respectively.2 (24.3) < LOD < LOD 29.4) < LOD < LOD 23.9 (25.2 (13.4-15.1) < LOD < LOD 15.6-44..9-32.4 (18.5-15.9 (23.Organochlorine Pesticides Hexachlorobenzene CAS No.1 (14. and 03-04 are 118. 2008. particularly by consuming fish.4) < LOD < LOD 18. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. which may vary for some chemicals by year and by individual sample.7-30.S.S.0) < LOD < LOD 15.9) < LOD < LOD 16.9-20. 01-02. 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. primarily as a fungicide and seed treatment until the U. 1988).5-15.5 (13.3 (22.6 (23.5-TCP) and 2.

123 (.190 (. ACGIH has developed workplace exposure limits for HCB.148-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity. and liver and thyroid cancers (ATSDR. which may vary for some chemicals by year and by individual sample.125 (.107) < LOD < LOD .atsdr. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.095-. anorexia.069) * * .090-.113-.104 (.098 (.163-. EPA at: http://www.145-.176) < LOD < LOD .173) < LOD < LOD .186 (.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 * * . Fourth National Report on Human Exposure to Environmental Chemicals 101 .107-.088-.079 (.157-.086-.163 (.Organochlorine Pesticides chemical.115 (.087 (.085) * * .082-. and many died before 2 years of age (Peters et al.072-.141) < LOD < LOD .147 (.225 (.174-.159-.258) < LOD < LOD . and the FDA has established a bottled water standard for HCB. In humans.078 (. 1982.091-. and weakness.121 (.069) < LOD < LOD .086-.157 (.114-.epa.102 (.132) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .095 (.118-.064 (. Chronic feeding studies in animals have demonstrated kidney injury. 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.092 (.123 (.127-. thyromegaly. 1960). Infants were exposed transplacentally and through breast milk.126) .081 (..095 (.089-. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.gov/toxpro2.176-. population from the National Health and Nutrition Examination Survey.145-.179 (.html.095) * * . The U.065 (. More information about external exposure (i.077-.178-.S.095) < LOD < LOD 75th < LOD < LOD 90th * * .143-.081-.109) * * . environmental levels) and health effects is available from the U.118) < LOD < LOD .100) < LOD < LOD .152) < LOD < LOD .171 (.122) < LOD < LOD .111-.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.062-.123 (.089-.114-.073-.203) < LOD < LOD . EPA has established a drinking water standard. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.094 (.085-. HCB interferes with normal heme synthesis.097) . reproductive and developmental toxicities.099) < LOD < LOD .092 (.102) < LOD < LOD .088-.092 (.cdc.120 (.S.111) < LOD < LOD . Survey Geometric mean (95% conf.129) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.156 (.155) < LOD < LOD . immunologic abnormalities.160 (.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 * * .083) < LOD < LOD . With chronic exposure.094) < LOD < LOD . Biomonitoring Information Serum concentrations reflect the body burden of HCB.147-.097) < LOD < LOD . Schmid.092-.135-.086) < LOD < LOD .gov/pesticides/ and from ATSDR at: http://www.191 (.140 (.167 (. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.118-.097 (.099) < LOD < LOD .090 (.196) < LOD < LOD . arthritis.182 (.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD ..088-. This condition.203) < LOD < LOD .060-. 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.090 (. acute doses produce central nervous system depression and seizures. 2002).090 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD . as well as hypertrichosis.169-.130) < LOD < LOD . very high.099) < LOD < LOD .175) < LOD < LOD .S.e.163) < LOD < LOD .

Lackmann. and other chemicals. Zoellner I. Eskenazi B. et al. trends and processes. Dallaire F. Kemper FH. et al. Biomonitoring of persistent organochlorine pesticides. Santiago-Silva M. more HCB levels were quantified. et al. April 1982 to 1984.. but overall. Darnerud PO. Sala M.81(2):82-85. Seiwert M. September 2002. Environ Health Perspect 2003. Schulz C. Link et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Gabrio T. Hexachlorobenzene in the global environment: emissions. and the geometric mean concentration of HCB in whole blood was 0. Laliberte C.205:297-308. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. dietary intakes of pesticides.html. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Bradman et al.71(6):1200-1209. Ayotte P.cfsan. Organochlorines in Swedish women: determinants of serum concentrations.135(4):400404. Lepom P. Piechotowski I. Muller C. Sweetman AJ.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Toxicological profile for hexachlorobenzene update [online]. 2002. Bryan GT. respectively. Bertram et al. Available at URL: http://www. Bertram HP.. HCB detection in serum also was proportional to age. Jones D. 2006). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.. 1986. Lackmann GM. Biol Neonate 2002. August 2008.. Kohli J. van Wijk D. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al.. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002.. The metabolism of higher chlorinated benzene isomers. Reference values updated.fda. et al. Link B. Available at URL: http://www. only 4. selected elements.atsdr. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Peters HA. however. Krause C.cdc.9% of participants had quantifiable levels (Stehr-Green. 2002. 2002) and among children (Link et al.html. Fenster L.39(12):744-749. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. J Assoc Off Anal Chem 1988.110(8):835-838.gov/ toxprofiles/tp90.54(3):203-208. Chemosphere 2005. Sci Tot Environ 2005.44 mg/L.gov/~dms/ pesrpts. Dogramaci I. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. 2005). Food and Drug Administration (FDA). Schwartz JM.. 1989). In Spain.. Herrman T.349:144. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. IARC Sci Publ 1986. FDA total diet study. Granath F. As a result of the lower limit of detection in NHANES 2003-2004. 2002). Environ Health Perspect 2002. 2005). Can J Biochem 1976. Lawrence River (Quebec. 2002. Glynn et al. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Gunderson EL. Bjerselius R. 4/21/09 Glynn AW. In the 1976-1980 NHANES subsample. 4/21/09 Barber JL. Holland NT. Paepke O. J Exp Sci Environ Epidemiol 2007. Int J Hyg Environ Health 2002. Arch Dermatol 1999. Herrero C.. Atuma S. Jones KC.17:388–399. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. levels. Over the past two decades. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Ozalla D. Barr DB. 2005. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. 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.. 1999). 102 Fourth National Report on Human Exposure to Environmental Chemicals . In a representative sample of the 1998 German adult population.. Becker K. Cripps DJ. References Agency for Toxic Substances and Disease Registry (ATSDR). Aune M. Canada). Safe A.58:1185-1201. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Lecha M. HCB levels were directly related to age. Arch Neurol 1982. Kaus S. 2002. Dewailly E. Otero R. Gocmen A. distribution. Bradman A.111:349355. Lackman.77:173182. 2003). Muckle G. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. the more recent values in these studies were similar to the lipid adjusted limit of detection in NHANES 1999-2000 and 2001-2002 (Dallaire et al.

Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Barrot C. Otero R. PA.Organochlorine Pesticides Schmid R. Stehr-Green.105(1):78-83. Santiago-Silva M. Cutaneous porphyria in Turkey. Fourth National Report on Human Exposure to Environmental Chemicals 103 .27:405-421. N Engl J Med 1960. Rodamilans M. To-Figueras J. Sala M. Environ Health Perspect 1997. J Toxicol Environ Health 1989.263:397-398. et al. Demographic and seasonal influences on human serum pesticide residue levels.

4-73.6-42.8-19.46-11. HCH isomers are lipophilic. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. see Data Analysis section) for survey years 99-00.9-24.7) 10.3 (62.8) 12.3 (42.6) 36.0-23. exists in several isomeric forms.4-111) 84.8. EPA cancelled agricultural uses of lindane (ATSDR. each result has been multiplied by 1.0) 41.2) 142 (99.2) 36.0 (8.4) 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 21.5 (24.0 (33. containing about 64% alpha and 10%-15% gamma isomers.1) 71.6-62.87 (9.04-10.1-32.0-70.8) 7.9-21.1-32.3-38.0 (35.1) 12.5) 90th 42.2-67.2 (31.7) 73.6) 47.8) 95th 68.2 (18.7 (13.3 (13.90-8.0-20.8) 52.4-45.9-81.5 (11.1 (18.6 (33.1 (11. formerly referred to as benzene hexachloride.7) 18. Technical grade HCH is a mixture of all four isomers.Organochlorine Pesticides Hexachlorocyclohexane CAS No.9 (40. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.1-49.3) 51.1-15.8 (21.7 (29.7-166) 70. commonly known as lindane.4 (50.2-20.S.0-111) 70.1 (9.5) 11.8 (23.9-14.2-87. See the section “What’s New” at the beginning of this Report for details.7) 97.4) < LOD 9.70-19.5) 67.0) 8. 01-02.3 (42.0 (<LOD-12.1) 13.1 (30.5 (16.8) 27. 2005).4) 901 1067 952 992 1224 1007 Females 11.4 (12.0-21.6) 50.9 (11.5-123) 49. < LOD means less than the limit of detection.9-51.7-69.0-34.6-37.80 (6. 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.7) 27.9 (30.6) 653 758 589 1240 1533 1370 20 years and older 10. **In survey period 2001-2002. The gamma isomer.3 (26. respectively.2-22.70 (8. and 7. 319-85-7 gamma-Hexachlorocyclohexane CAS No.4 (11. The other isomers can be formed during the synthesis of lindane.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-199) 134 (85.2-17.S.9 (50.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.6 (40. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.36.3) 34. gamma.5) 40.8 (17.5 (43.4-50.43 (<LOD-9. It is no longer produced or sold in the U.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.20-16.5 (14.7-26.7 (<LOD-16.0) 17.1-37.0-70.9 (26.8-16. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.0 (14.7-96.6-18.2 (9.7-96.1-16.5 (37.0) 7.8) 39.4) < LOD < LOD < LOD 46. environmental levels declined.1 (16.9) 15.70 (6.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.1) 12.8 (64.9) 81. and sediment as a result of historic production and use.6 (22.5528.4) 10.7 (30.4) 51.2-98.6 (17.2-55. and delta.89 (<LOD-9.6-135) 69.8 (10. and have been used either as fungicides or to synthesize other chemicals.0 (37.4) 27.8-87. the U.2) 13.7-20.3) 37.1 (12.90) 7.68 (<LOD-10. 58-89-9 General Information Hexachlorocyclohexane (HCH).7 (62. 6.7 (35.8) < LOD 10.6 (10.8) * * * * * * 15.S.1 (21.61-12. 2005).9-56.2 (34.1-36.5) 14.8 (32.50) 8.6 (16.9 (32.9) 17.66-12. HCH isomers.2-52.7 (25. 104 Fourth National Report on Human Exposure to Environmental Chemicals .5) 29.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.9 (9.56-12.30-11.7 (53.2 (50.3-85. interval) 9.1 (9.0 (19. Lindane has a half-life of about two weeks in soils and water. soil.4 (8. so they can accumulate in fatty tissues of animals.90-8. including alpha.6-20. 608-73-1 beta-Hexachlorocyclohexane CAS No.4) 11.0) 71.2 (29.60-13. However.7) 56. In 2006.4) 21. population from the National Health and Nutrition Examination Survey.6) 35.3) 14.3-56.9-178) 48.80 (<LOD-14.6-89.2-46. beta.2) 62. and 03-04 are 9.8 (33. As pesticide applications of HCH were increasingly restricted or eliminated.8 (9. water.4) 44.5) 16.6) 16.70-12.7) 10.5) 22. which may vary for some chemicals by year and by individual sample.1) 31.5 (8.6-47.4 (52.7-69.9) 45.1-27.2-42.2) 9.7) 23.6) 18.76.0) 35.3) 25.7) 32.4 (16. particularly alpha and gamma have been detected widely in air.8-68.2 (48.5-29.1 (27.8-54.6-14.9 (62.

330 (.170-.110) .057-.290) .580 (.190-.057 (<LOD-.280-.200-.470 (.100 (.680) .060) . Saxena et al. 1996.470) .410-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.521 (.103 (.080-.118 (.078 (..330-.372 (.051-.410) .175 (.100-.587) 653 758 589 1240 1533 1370 20 years and older . which may vary for some chemicals by year and by individual sample.140) .080-.480 (.174) .290) . 1981).250-.281 (.057-.190-1...300-.110) .620-1.460 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. 1977).290 (.040-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .S. 1983).070-.051 (<LOD-.480) .124-.062 (.067) . HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.460) .083) .250 (.050-. each result has been multiplied by 1.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .144 (.305) .180-. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.110-.280-.S.146-.086) < LOD < LOD < LOD < LOD < LOD < LOD .210 (. tremors.090-. and FDA has established a bottled water standard and food residue tolerances for lindane.310 (. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.210) . After dermal application of lindane 1% lotion. 1971.047-.250) .290 (.480 (.091) .S.270 (. or dermal exposure.140) . paresthesias. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.350) .080-.090 (.150) .120) .077) < LOD .600) .080 (.120 (.710) .260) . When animals were chronically fed lindane at high doses. enlarged livers.400) .382-.390 (.140) .173-.814) . respectively.050 (.260-.450) .220-.230-. resulting in a half-life of about seven years.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .380 (.120-.620) .050 (.160) .240-.340-.350 (.200 (.910 (.080) * * * * * * .310) . HCH isomers are absorbed after inhalation.064 (.070-. U.5528. 2008.070 (.058 (<LOD-. IARC classifies Serum beta-Hexachlorocyclohexane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.560 (.073-.081-. The beta isomer accumulates in fatty tissues and is metabolized more slowly. See the section “What’s New” at the beginning of this Report for details. the serum half-life was about 20 hours among children (Ginsburg et al.150-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.120 (.080 (.250-. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.130) .125) < LOD < LOD < LOD .050) .120-.062 (.331 (.090 (.287 (.410) .320 (. and nephropathy developed (IPCS.220 (.048 (<LOD-.059-. and memory loss (Nigam et al.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.070-.089-.120) . Gunderson 1988).560) .340) .412 (.191-.160-.214) .098 (.065 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.290 (.103-.360-.065 (. and seizures.103) 90th .092 (.077) < LOD .360 (. Distribution is mainly to fatty tissues.404) .068-.370-.170-.131-.067 (.308-.200-.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 .050-. 2002).130 (.260) .570 (.118-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane. ingestion.050 (<LOD-.37) 1.297-.. interval) .221-.191-. The U. Rogan. Workers who directly handled HCH have complained of headache.Organochlorine Pesticides exposure to HCH is through the diet.450 (.050 (<LOD-.070) .240 (.120 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .216 (.160 (.690) . hepatic enzyme induction.130-.110) .360) . probably by blocking inhibitory neurotransmitters in the central nervous system.080) .310) .661) 901 1067 952 992 1224 1007 Females .056-.05) .501) .190) .072 (.089) .150) .190) .050-.120-.083 (. 1986).150 (..069) .056-.090 (. ataxia. **In survey period 2001-2002.294-.064) . OSHA and ACGIH have established workplace standards and guidelines.050-.450-.580-1.510) .100) .319) . for lindane.100 (.070 (.420-.234 (.100) .140 (. EPA has established a drinking water standard.254) 95th .210 (.096) .32) .840) .167 (.700) .222 (.220) .250 (.139 (.100-.400) .410 (. population from the National Health and Nutrition Examination Survey.250 (.100-.210-.01 (.390-.220-.244-.442 (.119) .

environmental levels) and health effects is available from the U. 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. More information about external exposure (i. In NHANES 1999-2000. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al.cdc. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers..html. 01-02. Survey Geometric mean (95% conf. 1989. respectively. 2002.. aged 9-11 years. 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. In an earlier (1996-1997) sample of German children...5. Kutz et al. Bates et al. were similar to the 95th percentiles in this Report.epa.8. 2004) and India (Bhatnagar et al. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. and a diet that includes meat (Becker et al. In populationbased studies of New Zealand adults and German adults and children. 2005. male sex. 1998). 2004). serum levels of lindane were generally below the limits of detection.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. < LOD means less than the limit of detection.. Stehr-Green. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al... and 03-04 are 14. Sturgeon et al.gov/toxpro2. older age. In recent years. 1991. and 7. the maximum and 95th percentile beta-HCH values. and 2003-2004.. 1991. 2004. * 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. EPA at: http://www. 1971. 2002). Additional factors associated with higher beta-HCH levels include rural residence.S.atsdr. Biomonitoring Information Because of its longer half-life. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. 2005.gov/pesticides/ and from ATSDR at: http:// www. 1998. 10.. Stehr-Green. Becker et al. 2001-2002. 1989). 106 Fourth National Report on Human Exposure to Environmental Chemicals . Kutz et al. Link et al. which may vary for some chemicals by year and by individual sample.5...e. respectively.S. Radomski et al. population from the National Health and Nutrition Examination Survey..

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

Organochlorines in Swedish women: determinants of serum concentrations. et al. children and newborn infants. Toxicological profile for hexachlorocyclohexanes update [online]. The Great Lakes Consortium. PA. Lindane.52(1):59-67. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Radomski JL. Herrman T. Brinton LA.gov/~dms/pesrpts. Kashyap R. 4/21/09 Ginsburg CM. Environ Health Perspect 1998. and other chemicals. Available at URL: http://www. Rev Environ Contam Toxicol 1991. Chemosphere 2005. Krishna Murti CR. Environ Res 2004. Placental transfer of pesticides in humans. available at URL: http://www. Nigam SK. gov/toxprofiles/tp43. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.atsdr. Gabrio T. Kulkarni PK. Available at URL: http://www. August 2005. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. dietary intakes of pesticides. Granath F. et al. Reisch JS. Saxena MC. Rothman N.91:998-1000.cfsan.111:349355.72:261265. Kutty D. Arch Pediatr Adolesc Med 1996. Pollutants in breast milk. Atuma S.cdc.150:981-990. Bull Environ Contam Toxicol 2004. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Raju GS.htm. Lepom P. Falk C. Int J Hyg Environ Health 2002. et al.fda. August 2008. International Programme on Chemical Safety (IPCS). Majumder SK. Schulz C. Needham LL. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. 2002. Link B. Ellis H. Int Arch Occup Environ Health 1983. Brock JW. et al. Visweswariah K. Karnik AB. J Toxicol Environ Health 1989. et al. Maass R. 4/21/09 Anderson HA. Arch Toxicol 1981. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Stehr-Green.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).58:1185-1201. Bhargava AK.106(5):279-289. Piechotowski I. Needham LL.20(2):186-193. Aune M.205:297-308. Cerrillo I. Absorption of lindane (g benzene hexachloride) in infants and children. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Kaus S. Environ Health Perspect 2003. et al.9(4):417-424.54:1431-1443. Rivas A. Siddiqui MKJ.96:34-4Food and Drug Administration (FDA). Levels of DDT. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Deichmann WB. Zaidi SS. Garrett N. April 1982 to 1984. Becker K. Biomonitoring of persistent organochlorine pesticides.48:127-134. Botella B. Heinrich R. Chemosphere 2004. Toxicol Appl Pharmacol 1971.html. Cancer Causes and Control 1998. Buckland SJ. 108 Fourth National Report on Human Exposure to Environmental Chemicals . India. Int Arch Occup Environ Health 1986. J Assoc Off Anal Chem 1988. Rogan WJ. Krause C. Demographic and seasonal influences on human serum pesticide residue levels. VI. Bjerselius R. 4/21/09 Kutz FW. Needham LL. Lowry W. Wood PH. and HCB residues in human blood in Ahmedabad. Sturgeon SR. Olea N. Saiyed HN. Angerer J. Olea-Serrano MF.120:1-82.inchem. Patterson DG Jr. Bai KM. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Bates MN. Occupational exposure to hexachlorocyclohexane. Gunderson EL. Burse VW. Glynn AW. Metabolism of gammahexachlorocyclohexane in man. Crespo J. Potischman N. Paepke O. Rey AA. Bhatnagar VK. Seiwert M. Astolfi E. Olson J.27:405-421.71(6):1200-1209. et al. HCH. Hanrahan L. org/documents/jmpr/jmpmono/2002pr08. Bottimore DP.57(4):315-320. FDA total diet study. Exposure of women to organochlorine pesticides in Southern Spain. J Pediatr 1977. Zoellner I. selected elements. Darnerud PO.html.

EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.8 (<LOD-73. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.6) 9.7) 8. Fourth National Report on Human Exposure to Environmental Chemicals 109 . 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.40 (<LOD-13.5-82. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. sediments.6 (<LOD-108) 9. see Data Analysis section) for Survey years 99-00.. water.4 (8. after which it is widely distributed in the body and stored in fat. respectively. since 1977. Mirex is not metabolized in the body. disposal.7 (12.1) 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 16.0-374) 11. Formerly.6-305) 15.Organochlorine Pesticides Mirex CAS No.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 (<LOD-104) < LOD < LOD < LOD < LOD 39.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 1995).3-225) 15.6 (<LOD-31..5.3) 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 13.8 (12.3 (15.S.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. and foods.4) < LOD 63. 2385-85-5 General Information Mirex has not been produced or used in the U.10-37.2-230) 13. Mirex has been detected in air. it is a highly persistent chemical in the environment. especially those from persons living in the southeastern U.0 (12. < LOD means less than the limit of detection.S. In studies conducted in the 1970’s and 1980’s.8) < LOD 15. where it has a half-life of 12 years.2) 51.6. (Kutz et al.1 (8. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. 1991). Mirex can cross the placenta and be excreted in breast milk. aquatic organisms. soil.4) < LOD 15.5-291) 11. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.8.90-29.5 (<LOD-115) 153 (30. and 03-04 are 14. 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. which may vary for some chemicals by year and by individual sample.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.S. 1985. Mirex is absorbed through the skin and from the gastrointestinal tract. resulting in exposure to newborns and nursing infants.7 (<LOD-47. where it was applied directly to soil and by aerial spraying.4-230) 18.5 (<LOD-42. or pesticide application.S.0 (<LOD-108) < LOD < LOD 50. and 7.5 (9. Occupational exposure is limited to workers at sites where mirex contamination is present.0 (14. 10.6) < LOD < LOD < LOD < LOD 71. mirex was detected in human adipose samples.3 (15.70-40. population from the National Health and Nutrition Examination Survey.1 (<LOD-65. Some states and the U. animals. Survey Geometric mean (95% conf.6 (<LOD-23. Mirex binds strongly to soil.2 (7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (<LOD-15.70 (<LOD-15.7) < LOD 66.S.1 (13.5-425) 40. 01-02.70-24.

112 (. In addition.cdc. 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.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.100 (<LOD-.370 (. serum mirex levels were generally below the limits of detection (Stehr-Green.090 (<LOD-.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .077 (<LOD-. as well as in a subsample of NHANES II (1976-1980) participants.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 .02) .106 (..070-1..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 . Biomonitoring Information In the NHANES 1999-2000. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.090-1.090-1.html.S.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .79) .102) < LOD < LOD < LOD < LOD . reproductive toxicity included decreased fertility and testicular damage.140 (<LOD-.470) .170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . IARC classifies mirex as possibly carcinogenic to humans.059 (<LOD-.080-1.170-3.450 (. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.090 (<LOD-. EPA has established environmental standards for mirex.8.atsdr.054 (<LOD-. Smith. 1995. 7.470) .052-. 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.268) < LOD .106) < LOD . The geometric mean mirex levels of the Inuit mothers were 8.7 ng/g of lipid. 2001-2002.08 (.108 (. population from the National Health and Nutrition Examination Survey. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.064 (<LOD-.73) . and 2003-2004 subsamples. 2005).062-.110 (<LOD-.635) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Laboratory animals fed high doses developed liver enlargement and liver tumors.. 1991).510) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.79) .41) .470 (. 2004).080-1. which may vary for some chemicals by year and by individual sample.090 (<LOD-.690) .100 (<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.430 (.610) < LOD < LOD < LOD < LOD .Organochlorine Pesticides exposures are unknown.gov/toxpro2.053-.310 (.e.450) 1. The U. In samples obtained between 1994 and 1997.089-.079 (<LOD-.220) . and 4.37) .055-. 110 Fourth National Report on Human Exposure to Environmental Chemicals .090-1.093 (.256 (. More information about external exposure (i.220 (<LOD-.S.170) < LOD .410 (. 1989). 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.92) . environmental levels) and health effects is available from the ATSDR at: http://www.

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

5-Trichlorophenol CAS No. Both chemicals have been detected in air. usually at herbicide production or waste incineration facilities.920-3.27) 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 1.20) < LOD 90th 5.5-TCP) and 2.63) 18.0) 5. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.0) 2.71 (<LOD-8. recent sampling of U. Exposure to trichlorophenols also may result from metabolism of lindane.42 (<LOD-8.40 (2.30-27. Survey Geometric mean (95% conf.S.6-TCP in any of the samples (U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.20 (4.40) < LOD 6.27) 696 661 521 696 603 939 Limit of detection (LOD.40 (2.4.0) 14.0) < LOD 11.30-27.4.42 (<LOD-12. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.940-3. public drinking water systems did not detect 2.6-Trichlorophenol CAS No.8) 21.0) < LOD 21.3.9 (<LOD-121) 9.4.50) < LOD 1. 1999).72) < LOD 1. may occur by inhalation or dermal routes.0) 2. soils.0 (4.40) < LOD 4.0) 2. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.40 (1.4. EPA.0) < LOD 5.40 (1. Occupational exposures..9 and 0. however.30-11. 2.Organochlorine Pesticides 2.40-18.30-44. including hexachlorobenzene and hexachlorocyclohexanes.30) < LOD < LOD < LOD < LOD < LOD 1.0 (3.0 (3.4.30 (.00-3.00-8.80-41. 1976).50-25.50 (1. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.50-63. Such workers would probably Urinary 2.6-TCP were used as intermediates in the production of certain pesticides.0) 2.50 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.4.00 (2.5TCP and 2.7) 24.S.60 (4.0 (5.20) < LOD 5.6-trichlorophenol (2.60 (.30-3.19 (<LOD-6. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.40 (2. 2006).20-36.60) < LOD 8.60-8.950 (<LOD-1.00 (3.0) 2.0) < LOD 5. and polychlorinated benzenes (Kohil et al.0 (8.40-11.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.57 (<LOD-15.50 (2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.50-16.30-40.40 (2.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. which may vary for some chemicals by year and by individual sample. other organochlorines. Historically. Formation of 2.30-27.80 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 112 Fourth National Report on Human Exposure to Environmental Chemicals .5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40 (.0) < LOD 11. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. hexachlorobenzene. and sediments.80) < LOD 1.5-trichlorophenol.0 (4. 2.4.7.4. surface water.0) 2.5-trichlorophenol (2.980-3.0) < LOD 5.40) < LOD 1.20-71. < LOD means less than the limit of detection.60-18.90-33. population from the National Health and Nutrition Examination Survey.4.4. 1999). Trichlorophenols are no longer manufactured commercially.80 (2.0 (4.900-2.31 (<LOD-9.4. 95-95-4 2.40 (.03) 9.6-TCP). are metabolites of several organochlorine chemicals.980-3.60 (2.00-3. 2.20) < LOD 1.10-3.S.4.9.71 (<LOD-8.30) < LOD 4.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .

4) < LOD 3.33) < LOD < LOD < LOD < LOD < LOD 2.27-17.4.24) < LOD 5.6) 4.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.19-12.S.78) < LOD 1. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2.74) 11.1 (<LOD-58..5-TCP and limited for 2.24-11.0) 7.43 (2.20-6.4..4..81 (<LOD-9.83-12.50) < LOD 2.55 (4.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.53-3.24) < LOD 1.82 (<LOD-32.4.8) < LOD 9.78-19. 2003).37-11.cdc.atsdr.62-20.5) 11. and lymphomas.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.57 (<LOD-7. Radon et al.05-17. which includes trichlorophenols..6-TCP levels at the 95th percentile were up to eight times higher than 3.73 (<LOD-8. Fourth National Report on Human Exposure to Environmental Chemicals 113 .4. 2003. More information about external exposure (i.2 (2. environmental levels) and health effects is available from ATSDR at: http://www.980 (<LOD-1. Among 6-11 year old children in NHANES 1999-2000.. urinary 2.43) < LOD 12.6-TCP as reasonably anticipated to be a human carcinogen.28-25.1) 2.93-11.4.4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.95 (3. Urinary 2.5-TCP or 2.e.88-16.57 (3. the 95th percentile urinary 2. Neither 2..5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. as being possibly carcinogenic to humans.02) < LOD 7.4.29 (1. leukemias.6) 4.html.31) < LOD 2. 7.5) < LOD 12.13-13.4. the 95th percentile urinary 2.3 mg/L reported in German adults aged 18-69 years (Becker et al.49 (1.7 (4.gov/toxpro2. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. 1995) and up to 19 times higher than the 95th percentile value of 1.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .4) < LOD 3.2) < LOD 5.00) < LOD 4.36 (1.75 (<LOD-6. 1995) were similar.32) < LOD 4.00-19.Organochlorine Pesticides be exposed to mixtures of chlorophenols.46 (1.78 (3.02-3.3 (5.44 (1..16) < LOD 90th 5.4. 2004).5-TCP.37) 16. Human health effects from 2.4) 5.00-29. 2003).69 (2. population from the National Health and Nutrition Examination Survey..90 (4. At lower doses.820-2. NTP classifies 2.24 (3.86 (3.16 (. Laboratory animals chronically fed high doses of 2.6-TCP had increased rates of hepatic tumors.47-8.69-18.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6) 4. furans. in addition to dioxins. IARC classifies combined exposures to polychlorophenols. However.67 (1.0 mg/L. animals showed hepatocellular abnormalities.64 (4.4.9 (5.24) < LOD 6.9) 12.05-8. 1989). Survey Geometric mean (95% conf..6-TCP level was approximately eight times higher than the corresponding percentile in a small group of 2-6 year old children living near an herbicide manufacturing facility: 33 versus 4 mg/L (Hill et al.4.68-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75 (3.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.67 (1.2) 2.17) 9.53-3.5-TCP nor 2.8) 4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). 1989). In the same 2-6 year old children. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.19-4.4.57 (<LOD-7.8 (5.44 (.79-4.6-TCP. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.920-2.15) < LOD 2. The 95th percentiles for 2. and other chlorinated compounds.80 (1.60-3.68 (<LOD-8.4 (6.

45 (2.58-3.0) 9.90 (3.00 (2.4..0 (20. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.0 (6.0 (8.3.3) 37.40-4.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.6-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.02) 2.23-2.7) 33.01-6.4.0) 13.5-TCP or 2.8-13.4.0) 7.7 (13.6 mg/g creatinine) and 2.4 (17.06) * 2.0-38.00-4.3) 23.5-TCP and 2.58 (1.60) 6.0) 17.59-6.0) 12.4.6-TCP level.0-38.60) < LOD 5.2) 12.98-7.32) * 3.00 (4.44) 75th 4.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.80-25.4.40) 4.49 (6..0) 6.0) 9.9) 694 677 519 696 602 931 Limit of detection (LOD.6-TCP than are found in the general population.6-TCP (0.30-2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.78 (2.20-6.70-6.70) 5.0 (6.6) 26.20) 4.6-19.7 (9.5-TCP or 2.4.0) 14.00-21. Survey Geometric mean (95% conf. In harbor workers exposed to chlorophenol-contaminated river silt.0) 11.45 (5.40) 3.4.8-24.40 (2.10-3.10 (5.23) 3. < LOD means less than the limit of detection.32) 3.S.6TCP values.40-7.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0 (14.0 (11.0-37.6-TCP in urine does not mean that the level of 2.1 (10.07 (<LOD-3.0 (16.74 (2.46-3. Finding a measurable amount of 2.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.67) 4.6 (11.30-2.30) 4. Urinary 2.89 (3.4.54) 6.75 (8.98-11.85) * 3.47 (3.95 (4.52 (2. Biomonitoring data will also help scientists plan and conduct research about 2.50-5.40-14.4.10) 2.80 (2.35-3.31 (3.60-21.1) 16.65 (5.1 (8.5-TCP and 2.80-20.9 (13. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.3) 20.8-15. 0. for males in NHANES 19992002 (Agramunt et al.0 (9.14 (2.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.60-3.5-TCP and to the median 2.0-18.40) 2.66 (8.8) 18.65) 15.0 (7.0 (15.0) 15.2-0.28) * 2. 2004).0 (13.92 (2.0) 13.0 (14.10) 6.70 (2.0) 17.73-9.0 (4.70-3.5-TCP or 2. respectively.0) 10.70 (2.51-12.3-26.. population from the National Health and Nutrition Examination Survey. 1991).5 mg/g creatinine) were similar to the limit of detection for 2.3-17.40-32.95-6.40-2.4.76) 3.8 (9.89-6.7-3.36 (1.7) 21.6-22.12) 2.45-9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28) 24.5-TCP or 2.45) < LOD 11.40) 2.30-11.78 (2.5-46.4.09) 15.0 (20.4.70-6.0-68.99) 6.5-TCP (0.20 (3.55-3..6TCP causes an adverse health effect.4 (10.26 (2.4 (9.08 (2. similar to the limit of detection for this Report (Anderson et al.8) 32.80-7.0) 7.4.50 (2.53) 4.0) 13.4.10-2.00 (1.20-3.95) 3.3 (11. the median urinary 2.24 (2.57 (<LOD-2.2) 25.67-12.59) 4.0-43.0 (14.40-2.04) 2.53) 2.70) 1.69 (3.4.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.9 (11.36-5.09-7.0 (15.20-23.80) 1.0-54. which may vary for some chemicals by year and by individual sample.0 (8.70) 5. 2003).84) 2.4.18-3.56 (3.9) 13.0 and 1.31) * 2.33-4. Mean values of 2.72-10.0-41.60-37.6 (12.4.20 (3.91-4.6-TCP exposure and health effects.79 (5.0 (12.0) 13.0) 19.60 (3.2 (14.5-TCP level of 0. Biomonitoring studies on levels of 2.40 (2.74-3.52-3.4.85 (2.6-17.0) 19.90) 2.6) 21.10-3.36 mg/g creatinine.4. interval) 2.0) 10. was about six times lower than the median urinary levels for males in this Report (Radon et al.25-11.80 (2.4.90 (4.87-14.0) 11.80 (3.70) 3. 114 Fourth National Report on Human Exposure to Environmental Chemicals .48-26.30-33.63) 90th 15.3 (11.7-16.60 (2. Urinary 2.4 (8.7 mg/L.0-44.60 (3.0) 14.0 (6.32-4.1-25.90-8.0-50.80-6.68 (<LOD-2. 1998).4-17.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.23) 2.

29 (6.9-64. interval) 2.53) 4.81-9.30-2.9) 8.95-2.53) * 2.22 (<LOD-2.17-4.15 (1.0 (6.59 (2.06) 4.65) 18.73) 5.5 (10.89-2.92) 4.8) 11.1 (13.40 (2.76) 1.0) 10.70-9.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.56) < LOD 11.52) 2.76) 4.83-6.18-2.02) 3.26-13.46-14.02 (1.1-21.23 (1.65) 2.1-32.35 (3.67-17.5-28.19-5.6 (9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18-4.83 (3.91-2.52 (5.00) 4.63-15.4 (12.72-16.2 (12.3) 8.6 (12.17) 13.65-2.50 (2.88) 5.90 (1.54 (2.88-7.S.5 (7.10) 4.56-5.63 (2.9-34.1) 14.4) 4.68) 2.50-8.3-23.38-5.13-6.91 (7.63) * 4.25 (3.52) 2.0 (11.87-7.43 (<LOD-2.2 (13.4) 9.8) 21.04-2.98) 10.87) * 2.8 (8.1) 11.82-2.22-2.0) 8.76) 2.33 (1.42) 2.4 (11.2 (7.29-4.88) * 2.33-2.5) 11.63-13.60-2.82) 2.7) 25.7-36.25-15. Survey Geometric mean (95% conf.88) 4.17) 2.65-21.55-2.25 (3.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.60 (4.27-9.68) 2.2) 19.6) 8.14-13.51-21.2 (8.10-9.22 (3.9) 8.5) 12.99-2.9) 19.00) 4.29-4.4.58 (4.6 (6.51) 18.0 (9.09-3.49) 4.76-8. Fourth National Report on Human Exposure to Environmental Chemicals 115 .26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.32 (2.88) 1.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.7 (14.3-37.4) 8.Organochlorine Pesticides Urinary 2.81) 2.32-19.82 (8.38 (4.96) < LOD 4.51 (2.33) * 2.66-4.15 (6.14-2.10 (6.49-3.23) 4.08-2.41 (3.43 (2.6) 12.78 (2.16-10.77) 2.63) 4.9-29.8 (7.6) 13.47-5.9 (9.87 (3.62-15.72) 32.8) 12.44 (3.6-31.9) 7.00 (3.38) 22.9 (9.9-32.20-2.28-4.41-6.6 (9.01 (3.25-2.53-11.91 (3.38 (2.71 (3.94-13.5) 11.52 (3.22-9.82 (3.73-22.24 (1.7) 6.05 (6.6 (10.77-4.6 (5.56 (7.83-6.79-17.22 (1.78) 90th 12.78) 2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.06) 11.04-16.63 (<LOD-2. population from the National Health and Nutrition Examination Survey.6 (22.87) 2.53 (3.88 (2.13 (1.83-5.43-7.40 (7.33 (7.42 (2.11) 10.3 (9.21-11.98 (1.88) 4.00 (2.87-6.6) 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 2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.06-2.90) 2.1 (8.5) 9.48-2.75) 75th 4.8) 19.26 (6.5) 8.05 (3.5 (8.25-17.89) 10.

Int Arch Occup Environ Health 1991. Domingo A. Int J Hyg Environ Health 2003. Environ Res 1995. Safe A. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Pekari K. The metabolism of higher chlorinated benzene isomers. Urinary excretion of chlorinated phenols in saw-mill workers.epa. Hill RH Jr. To T.gov/toxprofiles/tp107. 4/21/09 Agramunt MC. Bailey SL.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Needham LL. Pesticide residues in urine of adults living in the United States: reference range concentrations. Am J Ind Med 2004. Schulz C. Baker S. S. Holler JS. Becker K. Available at URL: http://www. Aitio A. Smith SJ.146:83-91. Szadkowski D. et al. Can J Biochem 1976. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Olson J. Radon K. et al. December 2006 Draft. Gregg M. Available at URL: http://www. Seifert B. 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]. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Hill RH Jr. Toxicol Lett 2003. U. Shealy DB. Jarvisalo J. Arch Environ Contam Toxicol 1989. Lindroos L. Toxicological profile for chlorophenols [online].Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 206:15-24. Anderson HA. Domingo JL.106(5):279-289. Corbella J. Jones D. Fast DM. Wegner R. Kohli J. Luotamo M. Environ Health Perspect 1998.71:99108. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.63:57-62. Kaus S.cdc. Head SL. Poschadel B. Seiwert M.45:440-445. Falk C. html. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. The Great Lakes Consortium. Baur X. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . July 1999.pdf. Needham LL.EPA). Hanrahan L.54(3):203-208. et al.atsdr. Heinrich-Ramm R. Environmental Protection Agency (U. Burse VW.18(4):469-474.S.

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

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

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

4) 18.00) 3.53) 4.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.11 (.5) 15.39 (3.42) .5-16.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.89) 9.0) 11.0) 11.66) * * 1.80-4.95) 5.599-1.51) 2.08-15.82) 10.9-18.0 (9.0 (5.47) 5.0 (8.0) 10.0) 5.7 (14.17-3.50 (4.80) 2.40 (.00-27.14) * * .8) 11.0 (7.290 (<LOD-1.20 (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 1.3-15.10) < LOD .9) 14.6) 7.90) 3.42-3.00 (1.20 (.48-7.0) 9.5-17.81) 11.70) < LOD < LOD 75th 3.00) 3.0 (4.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.0 (8.8) 19.26 (5.56 (4.80) 4.71 (2.40-5.2) 16.35-12.60-11.99 (5.61) 4.02-5.290 (<LOD-.34-7.0) 5.5 (11.40-14.00-19.00-7.21) 9.1-23. respectively.54 (3.32 (.0) 10.2 (14.80-24.08 (<LOD-2.0 (8.96-3. 120 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.8 (12.4 (9.0 (12.9) 8.4 (7.9) 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 1.15) 14.63) 1.12-19.0) 20.30 (2.45 (2.30-6.52) * * 1.0) 6.19) 9.83 (5.4 (7.00 (5.58 (5.93-24.20 (.10 (.0) 11.50-5.530 (<LOD-2.43-12.35-11.0) 11.90-5.2 (11.4) 20.80) 2.10) < LOD < LOD 4.44 (2.55-6.0) 7.80) .50 (2.3) 14.13 (2.0) 6.5 (8.98-5.80) 11.1.60-18.94) * * .33 (5.0) 12.810-1.2 (7.93 (4.16 (2.03 (.70) < LOD < LOD 1.30 (4.954 (.12) 4. < LOD means less than the limit of detection.8 (14.860-2.40-11.02) 4.30-4.07-10.80 (4.73) * * .0-27.0 (7.56 (6.80) .40-1.86-15. interval) 1.38-5.22 (.1) 10.0) 15.750-1.2 (7.30 (2.74 (8.490-2.13-2.26-6.68-7.7 (12.79-7.717-1.600 (<LOD-1.97) 8.1-17.623-1.1 (10.21 (. see Data Analysis section) for Survey years 99-00.0) 6.86 (1.81) 1.67) 3.8 (9.70 (2.23-5.0-28.0 (7.71-9.13 (2.29) * * 1.57-7.90) 2.01) * * 1.08-2.3) 16.670-1.70-14. 0.26-8.20-7.44-38.00-27.10 (2.47) * * 1.8 (8.60) < LOD < LOD 4.80) 2.94) 3.80 (2.2-20.90 (1.58 (2.740-2.757-2.0 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2.44-3.55-8.620-1.33-18.04) < LOD 1.52) 6.52-11.90-4.2) 14.56 (1.700-1.890 (<LOD-2.10-7.4) 17.70-11.36-4.20-4.5) 20.35-16.0 (7.20-30.00-12.7) 11.76 (2.60 (5.81) 11.3) 17.10 (.27-15.1) 13.70-19.981 (.00 (4.0) 5.8) 7.56-13.6) 18.60) .82-12.85 (3. and 03-04 are 0.58 (3.70 (4.0 (6.9 (8.74 (8.50-36.37 (3.2) 16.20 (.91) 4.0 (9.39 (8.2 (14.28) 1.40-16.830 (<LOD-3.1 (9.8) 7.16) 4.0) 10.970-2.0) 10.00-12. and 0.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15-12.2 (9.80) 3.50) 2.2 (7.72) 5.98-12.32) 1.40-19.8-32.4 (9.0) 10.46) 10.60-25.10 (2.70-23.780) < LOD 3.S. population from the National Health and Nutrition Examination Survey.2 (9.05-7.70) .579-1.80-22.27-3.1) 95th 13.34-3.840-1. 01-02.50 (.79 (5.97) 90th 7.61 (3.2) 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 1.20 (.955 (.758-1.60 (1.

56) 7.890 (<LOD-1.00-13.98 (3.40-5.4) 13.02 (7.43 (3.3) 12.21-23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40-3.75) 14.61 (1.66-15.6) 13.37 (5.41) Selected percentiles ( 95% confidence interval) Total * * 50th .03-6.19 (4.84) 7.79-9.38) .40) 4.03) 2.54-4.90-5.40-28.37-5.566-1.5-20.75) 2.64-5.549-1.00 (4.94-22.94-10.60) 2.0) 7.57) 4.45-5.02-14.03) 2.818 (.1 (10.09 (.03 (2.98) .89) * * 1.7) 5.94-9.95) 2.440 (<LOD-2.3) 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 1.3) 5.80 (6.53 (6.6) 9.9 (9.77 (6.75-7.2) 9.1) 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 1.66-34.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.92-2.80) 9.2) 95th 12.88 (5.9 (9.8) 12.790 (.960 (<LOD-2.5-16.1 (9.773-1.67) 4.1 (6.18 (.1 (8.82-14.820 (.57-10.4) 4.69) 4.11-6.93) 9.650-1.87 (3.46-5.53) 9.28 (4.05 (.54-15.95 (3.85 (6.2) 5.37) 9.7) 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 .88) 2.6) 11.870-2.510-1.4) 4.40) < LOD < LOD 75th 2.42 (3.66 (1.960 (.7 (8.8) 6.09-11.05) .0) 6.8) 7.40-14.58) * * 1.8) 8.39 (2.20-8.69-10.860 (.52) 4.88-10.54) .89-3.28 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.69 (4.56) .7 (9.41) .2) 7.61-13.37-3.890 (<LOD-1.7) 12.27) < LOD 2.41-12.34 (6.66 (2.29 (2.3) 16.2 (6.62) .25) < LOD .01-2.72) 11.13) 4.28 (5.74) 90th 7.1) 4.67) 1.46) 2.36) * * 1.61-29.574-1.9 (5.54-2.34) < LOD < LOD .5 (4. population from the National Health and Nutrition Examination Survey.47) 2.38 (1.60-9.920 (.9) 12.05 (1.533-1.73 (1.28) 10.02 (2.35 (1.90-8.10 (3.855 (.37 (4.92-5.5) 7.71) 10.34 (6.10-13.69) 2.34) * * .83 (7.932 (.47) * * .98-22.7) 18.57 (4.06-2.608-1.53-11. Fourth National Report on Human Exposure to Environmental Chemicals 121 .750 (<LOD-1.43) 2.87-5.78 (2.67-19.8 (10.82-6.30) 2.14 (3.71-2.55-20.830-1.9) 11.74) 4.6 (9.5) 12.35) < LOD < LOD 3.5) 7.04 (1.4 (4. interval) .00 (4.1 (7.00-19.09) 2.4 (9.2) 13.5) 8.0 (8.93-9.6 (10.02-2.80 (7.04-6.3) 15.98) .29) * * .68-4.84 (5.62-5.5-13.780 (<LOD-1.23) 4.40-12.94 (2.2 (8.50) 7.40 (3.76) < LOD .82-26.633-1.2 (10.7) 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.S.00-17.98-5.45-11.1-15.60) * * .32-12.9-28.620-1.57 (6.87 (1.996 (.75 (3.98) 9.81 (1.47 (3.75 (7.45-5.81-5.85) 2.883 (.5-32.88-15.47 (1.94-23.56-13.7 (10.03 (7.43 (.56) 4.80 (2.900 (.23 (4.82-14.1) 4.68) < LOD < LOD 3.24-3.31-14.560-1.2) 5.2) 8.47 (3.31 (3.54-11.570-1.5) 11.79-3.42) 12.83) 8.44 (2.25) 6.28-9.66 (5.26) * * .430-1.710 (<LOD-1.61 (1.924 (.30 (1.6) 8.9) 16.94 (4.00) 8.76-4.500-1.8) 16.15-10.93-5.51-5.07 (.1 (11.540-1.

9-15.5.27 (3.740 (<LOD-1.89 (2.92-17.67) 3.2) 14.46-28.0) 9.7-19.4 (10.00) 7.20 (<LOD-2.92) 9.90 (6.51) < LOD 1.S.7) 10.72) 2.910 (<LOD-2. which may vary for some chemicals by year and by individual sample.7) 22.8 (12.18) * * * * * * * * 1.20-18.4) 11.8) 8.50) .35 (6.0) 13.60) < LOD < LOD 2.0 (15.78) 5.84-4.3 (11.2 (9.70 (8.34-10.3) 8.90 (2.90) 8. respectively.6) 18.0-29. and 0.20) 3.27) 4.66-13.28 (7.80) .90-15.00-4.670 (<LOD-1. 0.66) 4.88) 3.80-12.60 (5.70-9.81-6.99 (3.17 (7.95 (5.8 (12.0 (7.18 (3.3 (12.41) 3.0) 11.10 (<LOD-1.00) < LOD .10-15.98-9.3 (9.9) 16.0) 6.80-14.04 (3.20) .70-9.0) 12.53 (3.12 (4.70-5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) 3.39-13.6-19.6) 14.77-3.34-5.70-8.4 (10.10-10.30) 3.0) 14.40) < LOD < LOD 75th 2.6) 11.1) 11. and 03-04 are 0.0-24.3) 14.0 (10.0) 9.90) 4.9-17.7-21.70) 2.60 (6.90-31.67) 4.75 (2.4-17.39 (5.0) 12.90 (6.1 (10.9) 9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .8-20.00) 3.9 (7.22) 8.6) 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 * * * 1.10-4.0 (5.8) 9.47-6.15-2.30) < LOD < LOD .58 (1.11-6.16-1.00-18.90 (6.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80 (5.00-4.680 (<LOD-1.30) 3.74) * * * * * 1.46-4.31-12.95 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (9.6 (10.9) 95th 14.6-41.7) 16.49-4.8-21.80) .30) 8.88) 10.580-2.96) 90th 7.37) 2.20) 3.77-14.3) 20.06 (2.29) < LOD < LOD < LOD < LOD 3.90 (2.10) 6.670 (<LOD-1.62-17.24 (2.0) 11.0 (14.9) 10.34 (6.80-4.14 (6.90-9.40 (2. < LOD means less than the limit of detection.00-18.75 (3.31) 1.1-23.00-16.58.0 (13.90 (5.70 (1.0-33.80-6.0) 7.90-15.35-3.30) < LOD < LOD 4.29-4.0) 18.5) 21.970 (<LOD-2.7 (11.61-32.0 (10.7) 15.90 (1.9 (12.22 (6.670 (<LOD-1.97-4.10 (.22 (6.00) 8.50-4.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.86-10.5-26.50-5.0-24.0 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (2.0) 19.0) 14.80-21.27) .24-5.96) 3.45 (3.15-6.6 (10.31-7.64) 10.80 (2.9-14.0) 13.95-9.5 (8.4) 7.35) 4.27 (7.90 (6.0 (9.41-5.00-9.3) 22.2 (7.80-8.50) 3.27) 9.63-14.61 (3.25 (2.60 (2.20-4.82) 8.80-3.00 (. see Data Analysis section) for Survey years 99-00.0) 12.50) 5. population from the National Health and Nutrition Examination Survey. 01-02.3 (6.8-20.790 (<LOD-1.3 (9.4 (14.37 (3.3) 10.34-3.7 (10.90 (2.8-17.5 (8.650-1.52 (6.67-10.59-3.80) 5.33-11.670 (<LOD-1.3 (7.0) 23.0-19.89) 2.20-8. 122 Fourth National Report on Human Exposure to Environmental Chemicals .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 * * * * * * .01 (2.6) 14.22-12.5.7) 14.42 (1.80 (2.73) 7.1 (10.5 (9.

1 (13.4-18.5) 8.6) 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 * * * .27) 1.21) * * * * * 1.3) 6.6) 6.9 (9.75-3.29 (2.690 (.2) 19.2) 12.94-14.12 (7.69-11.3 (7.3) 12.7 (10.18) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.890-2.72) 4.04) 9.2) 12.2) 8.96-10.25-9.8 (8.7) 14.6 (11.9 (9.4) 15.79-9.920 (<LOD-1.12) < LOD < LOD 4.67 (7.8 (10.80) 3.6) 14.93-10.28) 6.78 (6.83 (6.92) 3.27) < LOD .74-19.6 (12.7) 12.27) * * * * * * * * 1.15) < LOD < LOD 75th 2.3-15.0 (10.530-1.91) 3.63 (2.06) .7 (8.55) .06 (<LOD-1.30) 8.36 (2.6) 7.52-3.59-3.43 (2.77 (2.6-19.89 (2.54-5.4-16.7-23.1) 10.9) 16.5 (15.3-17.6) 13.78) 4.27) 5.54) 9.28-12.0 (8.68-4.4) 7.42) 7.03 (6.03) 3.00 (<LOD-1.19) 3.68) .6) 95th 16.61 (2.4) 16.00 (<LOD-1.95 (2.87 (3.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .16-14.05-3.58 (4.91-9.34) < LOD < LOD < LOD < LOD 3.6 (13.97-4. Fourth National Report on Human Exposure to Environmental Chemicals 123 .910 (<LOD-1.3-34.810 (<LOD-1.1 (19.45) 3.54 (7.55) 16.950) .82-8.4) 9.3-17.67 (1.68-19.7) 14.07) 2.0-21.38 (.4) 6.1) 20.07) 2.41 (7.34-18.07 (5.2) 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.00 (3.16 (3.75-3.4 (11.940) < LOD < LOD 1.88-7.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.89) 5.95) 3.38 (2.590 (<LOD-.4) 7.00) 2.55 (2.2) 10.38 (1.S.78 (4.82-11.07-3.7 (11.89-3.4) 7.3-21.29-2.89-10.44-6.27-13.0 (13.68-10.1 (8.88 (1.7) 9.8) 11.85-17.23-3.21-21.47-9.96-11.73 (5.5 (11.74-4.7) 15.97) < LOD .09-11.03 (2. population from the National Health and Nutrition Examination Survey.79-6.51-7.4-15.89 (3.0 (11.01-5.94 (5.2) 16.2-30.620 (<LOD-.99) 2.30) 2.78-10.86) 9.5 (9.99 (4.93 (2.780-1.2) 15.760 (<LOD-1.53-8.81 (7.00 (7.30) 7.6 (13.20-3.89-13.8) 16.6 (10.5) 13.3) 9.51-10.2 (9.5-17.0-19.1) 13.5 (10.86-3.25 (4.5) 22.64-11.00) 8.2-15.29) 3.7-19.38-13.89-3.11-3.8) 14.70-35.14 (2.33) 3.70-2.63 (6.72-4.86 (3.9-25.850 (<LOD-1.00 (5.93 (6.45) 6.02-4.11 (5.71) < LOD < LOD 2.77) 3.38) 1.2) 12.77 (2.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.6 (11.15 (1.9-17.5) 10.83 (7.50 (6. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .33-10.50-17.37) 3.9 (9.4-16.5 (8.7 (10.9) 19.92 (5.29 (5.30-5.71 (1.42) 8.95) 90th 8.42-19.32-8.3) 8.39-17.37-5.2 (9.6) 12.93 (<LOD-2.00 (2.85-8.973 (.32) 2.09-11.28 (1.48 (2.0) 14.

59-6.30-3.80 (2.58 (1.65 (2.75-2.450 (<LOD-.83) 2.759) * .90-4.11-3.160 (<LOD-.550 (.50 (1.880 (.650-.16-3.60) 2.90 (1.63 (1. < LOD means less than the limit of detection.570-1.76 (1.79) .80 (1.18 (.49) 2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.585) * * .336-.343 (.22-3.850) < LOD .455 (.440-.90) 2.60 (2.01-3.14 (1.670) .570 (<LOD-.240 (<LOD-.490 (<LOD-.22-3.47 (1.710) .657) * * .30 (.34) 2.54) .20) 3.970) .540 (.930-1.64 (1.16) 1.570 (.680-1.20) 2.20-3.11-3.27 (3.350-. and 03-04 are 0.618) * .73-5.89) .16) 2.05-3.830 (.20-1.380) .380-.69-4.30-1.280-.457 (.740-1.50-2.2.592-.13) .810) .31-3.80) 3.780) .720-1.39) 2.20) 1.560-.587) * * .50 (1.54-2.949) .70 (1.91) 2. which may vary for some chemicals by year and by individual sample.55 (3.20 (1.57 (2.760 (.505 (.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 * .460-.57 (1.20) 2.750-1.960-1.15) 2. interval) Selected percentiles ( 95% confidence interval) Total * .700) .50-2.710 (.94) .780 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10-1.930) < LOD .94 (2.20) 3.910) 1.740 (.83) 1.46-3.83) .600-.89-6.950) 90th 1.14-1.800 (. population from the National Health and Nutrition Examination Survey.70 (1.08 (2.398-.350-.33-2.960) .353-.32 (1.80) 5.45-4.10-1.78) .960 (.40 (1.690-1.87-3.29-2.74) 3.13) 2.01) .749 (.20) 1.820 (.600 (<LOD-.00 (1.550 (.570 (<LOD-.388-.01-1.390-.690) .31) 95th 2.22 (1.90) 2.10) 1.10) 3.30) 4.98 (2.32-1.00-4.54 (2.98) .970) 1.80) 3.18 (1.45 (1.1.960) 1.41-5.86 (1.94 (3.48 (1.510 (<LOD-.70-2.201-.31-3.720-1.820 (.30) 2.35) 1.549 (.449 (.840 (.83 (2. and 0.59-2.580-1.26) .359-.00) 1.620-1.20-2.60) 3.95-5.21) 3.720 (.95 (2.88) 1.03) 1.50) 1.680-1.31) 2.597) * .08 (2.880) < LOD 75th .510 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.467 (.89) 1.860) < LOD < LOD .390-.46 (2.584) .500 (<LOD-.95) 2.20-2.96-5.80) 3.98-3.22-2.05-2.930) 1.400) .10) 1.22-8.36-4.17) 1.38) 1.00) 2.30 (1.30 (.590-.25-1.77-2.20 (2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .790 (.47) 2.303-.34) 2.210 (<LOD-.80) 2.740 (.32) 3.740-.20 (1.04) .50 (1.10) 1.580-.S.570 (.50 (1.380-.48 (2.30-3.17) 1.910-1.73 (2.459 (.73 (1.70-7.80) 2.60-4.600-1.990-1.690 (.41 (2.23-3.46) 1.97 (2.30 (.50 (1.382-.76-6.04) 1.27 (2.90) 3.86) 3.83 (2.690-.61 (1.49) . see Data Analysis section) for Survey years 99-00.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.30) 1.37-2.46 (1.592) * 50th .710 (.79) .15) 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 * .730) .910 (. 0.940) < LOD .17-4.930 (.09.29) 1.750) 1.19-1.40 (1.780 (.09 (. 01-02.260 (<LOD-.77 (1.70 (1.96-3.340-.960) .42-2. respectively.74-5.700) .00-2.880) < LOD .453 (.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 * .45 (2.30) 4.980) 1.45 (1.68-5.20 (1.26 (2.592) * .570) * .75 (2.425 (.

688) * .318-.07-3.32) 2.19 (1.13 (1.52) 3.453 (.285-.250 (<LOD-.45 (2.04-1.98) 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 * .07) 1.99) 2.07) 1.43) 1.05 (1.400) .720-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .740) < LOD 1.67) .16-2.92) 3.460) .820) 1.730) .590-1.60 (1.07-2.597) * .590 (.30-2.660-.550-.97) 2.372 (.58 (1.710 (.640 (.520-.49 (1.97) 1.22) .94) .42 (.412-.57 (3.67-3.08-2.920) .950-2.25-3.335-.57-4.75-3.350) .62 (1.77-3.23) 1.560 (.700 (.38-3.71) 2.05-2.57 (1.72-4.377-.32 (.790 (.20-2.22-3.500-.08-3.43) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.22-2.79 (1.61-3.270-.33 (1.08) 2.08 (.480-1.43 (1.460 (.77 (3.930-1.53) .530 (.330 (<LOD-.320-.234 (.67 (1.300 (<LOD-.87 (2.S.76) 1.81) 2.44) 2.23) 3. interval) Selected percentiles ( 95% confidence interval) Total * .300-.250 (<LOD-.480) .470) .510-.400-1.560-.23 (.20) 1.23) 2.02-3.490 (.64 (2.08-2.800) < LOD .88 (1.06-2.03-2.16-1.580) .71 (1.67) 1.42) .39) 2.55 (1.11) 1.230 (<LOD-.70 (3.540-.79) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.720 (.710 (.04) 95th 2.00-3.08 (2.73 (2.75) 6.73-3.61) 2.310 (<LOD-.380-1.78) 3.43) 2.740) .38 (1.22) 4.58) 3.05) 1.84-6.71) .50) 1.393 (.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 * .70 (2.00 (3.447 (.280 (<LOD-.88) .22-3.22) 1.830) 90th 1.52 (1.91 (1.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .50 (1.471-.44-2.940-1.690) < LOD < LOD .82) 2.66 (2.820) .790) .75 (2.550) .67 (1. population from the National Health and Nutrition Examination Survey.41 (.69 (1.32) 1.90) 2.72 (1.742) * * .700 (.77-4.750 (.448 (.06) 4.560-.380-.32) 5.535 (.89-3.92 (1.470 (<LOD-.520 (.02-3.69 (3.17) 2.640 (.57-2.700 (.28 (1.17-2.580 (.670 (.840) 1.550-.05-4.590) * 50th .510 (.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.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.61-3.591 (.82 (2.45 (1.07 (.47 (1.305 (.460-1.10) 2.739) * .08-2.680 (.02-6.61 (3.830 (.253-.23) 2.89 (1.11-2.136-.710 (.92-8.330-.24) 4.348-.390) .66) .370-.63 (1.62 (2.440-1.07) 1.60) 1.80) 2.310 (<LOD-.08-3.760) .60) .20-7.05) < LOD .870 (.645) .84 (2.29-4.03-1.64 (2.910) < LOD .72) 1.310-.17) 2.08) 1.800-1.32-1.42-8.04-5.270-.270 (<LOD-.60 (2.630) * .870) .750 (.95) 1.840) .550-1.180 (<LOD-.16) 1.34 (1.980-1.840) 1.58-6.515) * * .880) 1.47 (1.552 (.55-3.14 (2.99) 1.900) 1.444-.49-4.47-4.38 (2.390-1.640 (.65) 2.72 (2.97 (1.98) 1.33) .30) 3.08-3.368) * .36) 3.11 (.509 (.403) .22 (2.485) * * .760) < LOD 75th .510 (.07) 5.39 (1.850) 1.990-1.97 (1.380) .09) .75 (1.42-6.320-.18-2.08-3.580-.00-1.31-1.

40) 50th 2.92) * 2.12 (3. < LOD means less than the limit of detection.67 (1.7-41.8 (22.3 (12.10 (1.1) 38.0 (17. 126 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.5-40.0-31.42) 1.0 (38.54 (1.44-7.0) 15.41 (1.0 (37.3) 26.30-14.6-45.5 (24.76 (2.0) 16.48) 5.0) 3.00 (.93-3.6 (15.07-5.0 (11.18) 20.87-7.9 (27.26) 75th 11.2) 31.66-5.78 (1.80) 1.20-4.0 (21.0) 32.6 (11.0-29.0-53.57-2.0 (38.3 (10.00-24.2-33.0) 33.0-41.41) 1.79 (2.77 (1.10) .48-2.5-45.5) 30.7 (28.2) 16.70 (1.16) * 1.23-2.8-21.21 (4.54 (3. see Data Analysis section) for Survey years 99-00.10-4.5.45) 2.61 (1.50-2.0) 4.13 (1.71) 5.41-4. and 0.41) 5.12) 1.98) * 2.1) 18.0 (13.7) 47.0-69.26 (.79-2.6-22.05) * 2.70 (7.0-41.2-62.98 (1.660-2.31-6.83 (3.9-21.80) .0 (38.43-7.9) 17.0) 8.59 (1.86 (1.10-13.0-230) 35.49-2.6 (26.30) 4.77) 38. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.21 (3.4 (19.44) 3.19-2.0-110) 42.33 (5.10 (1.9 (19.86-3.23) 9.0) 18.8) 39. 0.90) 11.36-2.27-6.83-2.1 (25.0 (38.0-39.23-2.58) 16.6-27.6 (9.06) * 2.88) 1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.60) < LOD 1.0) 15.0) 3.0-53.0) 28.53) 1.0-260) 34.70) 1.17-2. 01-02.81-2.9) 48.06 (1.97) 6.0 (40.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 16.50-20.0 (33.4-22.0) 31.1-19.0 (24.0 (32.1) 140 (46.80-2.0) 30.3) 33.80) < LOD 1.1-47.65 (4.0-43.60 (2.4.9 (10.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30 (.90-8.0) 4.0-62.0) 42.64-3.53 (1.0 (25.10 (1.71 (4.82 (1.2 (19.0-39.0) 20.3) 28.2-27.1-25.46-6.40-16.7 (12.9 (19.0) 5.830-3.90 (1.0-41.1 (22.57-2.1 (25.S.85 (1.9) 18.72 (1.830-4.9-51.8 (26.45) 2.48-2.14) 5.46-2.0 (20.40-4.0-49.1 (10.1) 38.2 (12.0-58.0) 4. which may vary for some chemicals by year and by individual sample.0-50.90 (1.0) 19.8) 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 1.05-3.3 (23.0-58.0) 3.19) 2.18) 6.4 (10.0 (6.8 (12.53) 40.29) 2.80) 90th 38.85) * 2.70-6.2-39.0) 28.96) 5.83-2.0 (8.3 (14.09 (4.02 (2.610 (<LOD-1.18) 14.5) 69.1-20.1 (26.0 (26.6-54.64-8.58-2.41) 1.88) 3.7-22.0-62.94 (1.79 (1.9) 38.53) * 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3 (24.44) 2.0 (38.61-2.25-3.35-6.40) < LOD 1.52 (4.20 (2.8 (12.50-17.9 (23.80-18.40) < LOD 2.05) 1.1 (11.18.530-4.13 (1.32 (2.2-47.95 (5.11) 2.30) 11.70) 1.600-2.8) 41.83 (1.3) 38.4-76.00 (.70 (1.16) 2.6) 52.21 (1.92-5.10 (1.0) 17. respectively.0) 20.7) 20.8-24.690-3.50-5.0 (8.99 (2.71-2.13) 12.69) 2.74-2.2-80.8) 32.4 (15.29-4.5-20. and 03-04 are 0.04 (<LOD-2.2-27.3 (12.0 (20.1-40.0 (19.04) 3.3) 31.8) 62.5-74.0-52.50-7.470 (<LOD-1.29-9.20) 1.0 (8.2-26.04-8.0) 17.70 (.76 (2.0 (38.70) 5.0-47.0 (7.4) 19.70-17.0) 6.75-14.0) 3.0-92.63-6.91 (4.0) 45.4) 38.7 (12. interval) 1.1) 95th 48.0-110) 34.11 (4.81-3.1-46.50 (2.10 (7.78) 9.0) 13.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.0 (38.44) Selected percentiles ( 95% confidence interval) Total * 2.59 (1.5-27.46 (.10) 39.

94) 19.0-118) 29.91 (6.0 (14.56 (2.38) 5.1) 15.5 (15.06) 1.88 (1.60) 4.63-5.96-16.96) 2.37-2.2 (15.3 (10.18) 3.41 (2.38-5.680-4.75-6.1) 25.29-5.1 (50.93) 5.1-60.7 (10.14-8.7) 95th 51.4-71.2) 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.0 (6.27-3.1) 13.47-17.9-52.22-3.45 (1.95 (2.54-2.7-37.2) 13.14 (.43-12.07) 9.33) 1.97 (1.0-40.23) < LOD 2.670-1.1-22.79 (2.09 (5.08) 1.75) * 1.34) * 1.8-37.2-47.4) 3.27 (6.3 (8.9-37.3 (20.4 (11.21 (4. population from the National Health and Nutrition Examination Survey.70 (1.9 (39.2) 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 1.5 (8.58-2.45-1.67-16.2) 36.4-34.69-18.33) 2.9) 54.22-2.7 (18.12) 3.7-20.40 (5.7-38.8) 3.27) 50th 2.46) 1.00 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1.2-34.9 (13.57 (6.02) * 1.95) 90th 32.67 (1.57) 4.0-70.64 (1.47 (1.61-22.48 (4.02) 1.40-4.19) 5.76-2.S.11-2.36-13.7) 15.0) 48.03-2.888-1.2 (22.6) 23.9-36.20) Selected percentiles ( 95% confidence interval) Total * 1.5 (41.12 (1.79-17.6) 3.8-34.37 (1.82 (2.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.43-2.36 (4.68) 47.8-43.6 (27.51) < LOD 1.33-5.6 (24.71) 8.1) 27.06-1.28 (1.95-16.5 (34.860 (<LOD-1.19-6.4) 14.75 (1.75 (1. Fourth National Report on Human Exposure to Environmental Chemicals 127 .0-71.08 (1.7) 66.51) .9 (7.18) * 2.2) 4.3 (10.19 (1.18-1.22 (.19-14.94) 1.82) 1.5-190) 30.1 (25.3-27.54-15.0 (25.1 (12.7 (18.5 (6.2) 33.31) 2.2) 13.3-22.8) 23.60 (.870-3.4 (21.62 (2.15 (.83 (.35 (2.7) 26.9-41.40 (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 2.17) 2.8) 11.4-39.2) 41.1) 13.59-2.30) 28.3 (9.6-49.06) 75th 9.2 (9.46-22.5) 70.72) 2.2-70.50 (2.17-3.0) 47.0) 10.43) * 2.4 (25.7) 34.07-2.66 (1.66 (1.03) 1.53) 1.899-2.16 (1.3-42.7-47.68 (1.16-2.16 (1.38-1.2 (8.26-4.9 (26.5-36.99-4.32-3.8) 32.61 (1.00) 6.1) 25.06) 1.8) 15.56) 1.8) 31.27) 10.8-45.0 (39.86) * 2.40-7.44) 9.52 (1.9) 24.33) < LOD 1.1) 52.35) .4-21.59-15.28) 1.2-38.61-2.58-17.0 (32.38 (3.9) 3.20-5.39 (1.07-2.9-18.870-3.1 (39.6-38.50-5.69-5.35) 1.6) 3.2-28.0) 13.16 (1.62) 4.1) 27.9) 3.19) 5.7 (11.9) 12.23-1.3) 13.7) 61. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8 (7.4 (19.84-13.7) 23.930 (<LOD-1.70-4.23) 37.4 (5.6) 7.7) 30.0) 3.7-109) 22.870-3.1) 17.1-63.67-3.6 (7.0 (19.36) 10.22 (2.9) 24.95-16.0 (23.890-4.6) 11.0) 30.7-43.4 (12.02 (.83) .46-6.1 (34.80-8.5 (15.90 (.6-51.4-67.0) 25.94-20.7-19.5 (13.2 (16.1 (33.67 (1.4) 12.5-43.6) 112 (40.47 (3.26-2.8-26.4) 12.55 (2.00-16.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.7 (24.80 (1.32 (3.5) 27.6) 19.9-95.6 (11.46-5.1) 36.3-19.91-2.5 (17. interval) 1.01 (.88 (1.24 (1.9 (19.71-2.86) * 3.4 (9.71 (1.48) 1.4 (25.750 (<LOD-1.0 (23.88 (4.66) 8.0 (17.5-97.3) 28.9 (10.25-3.2 (21.88 (4.6-32.52-4.59-2.

310 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .090 (<LOD-.130-.990) .30) .560 (.410) < LOD < LOD < LOD < LOD .200) < LOD < LOD .760) < LOD .870 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.700-1.870 (.870) < LOD .450 (.080 (<LOD-.570) .820 (.220 (.620 (.310) < LOD < LOD < LOD < LOD .850 (.230) .830) .090 (<LOD-.930 (.990) .700-1.650) .380-.840) .160) .360-. see Data Analysis section) for Survey years 99-00.320 (.270 (.640 (.540 (<LOD-.190 (.490 (.084-.450 (.820 (.470-1.320-.860-1.05.540) .090 (<LOD-.190 (.080 (<LOD-.860) .380-.117 (.730-.10) .830) < LOD .050-. and 0. 0.640) .1.640-1.720 (.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 * * * * * * * * * .120-.630 (.280) < LOD < LOD < LOD < LOD .210 (.58) .090 (<LOD-.650-1.090 (<LOD-.850) < LOD .370-.220 (<LOD-.00) .160-.830 (.310) < LOD < LOD < LOD < LOD .300-1.30) .150 (<LOD-.390) < LOD < LOD .720) .10 (.120-.680-1.140-.350) < LOD < LOD < LOD < LOD .610-1.680-1.510-1.420-.290 (<LOD-.140) .870 (. < LOD means less than the limit of detection.130-. population from the National Health and Nutrition Examination Survey.180) .130-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.680) . 01-02.780) < LOD 1.990 (.160) .870 (.540) .12 (.630 (.690-1.090 (<LOD-.1.380-.660 (. which may vary for some chemicals by year and by individual sample.850 (.190 (.150) .390 (.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 * * * * * * .170-.740) < LOD .60) 1.360-.130) .470 (.460 (.530-.610 (.550) .290) < LOD < LOD < LOD < LOD 90th .430 (. respectively.310 (. and 03-04 are 0.140-.770 (.10) .720-1.260 (.870 (.700-1.410-1.40) .240 (<LOD-.140-.700-1.900 (.130 (.840) .370-.400-.460-.610-.S.730) .610 (.210 (.650) .650 (.03) .430-.560 (.440-1.310-.162) * * * * * .130) .10) .30) .42) .36) .290) < LOD < LOD < LOD < LOD .680 (.15) .600 (.650-1.300-.410-.770) < LOD 95th .230-.830 (.450 (.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. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .100 (.110-.42) .410-.640) .32) .20) .940 (.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 .120 (<LOD-.171) * * .099-.350) .13) .330-.

200 (.170 (.450) .360) < LOD < LOD < LOD < LOD .510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .540 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .02) .170) < LOD < LOD .330 (.140-.400 (<LOD-.100-.730) .860 (.440 (.210 (.38) 1.600-1.570 (.320 (<LOD-.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .760) .057-.220) < LOD < LOD < LOD < LOD .330 (.410-.490-1.700 (.550 (.960) .140-.230 (<LOD-.24 (.340-.740 (.050 (<LOD-.330-.080) .730) .290) < LOD < LOD < LOD < LOD 90th .190 (.66) 1.190-.58) 1.00) < LOD .330-.580-1.360-.36 (1.570-1.850 (.750) < LOD 95th .660-1.080 (.560 (.260-.300-.070 (<LOD-.410) .230-.730 (.390-.710-1.810 (.510-.860-2.410) < LOD < LOD .12) < LOD .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .260) .410-.540) .070 (<LOD-.310) < LOD < LOD < LOD < LOD .670 (.090 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.740) < LOD 1.380-1.78) .870) .580 (.240-.190 (.470 (<LOD-.86) .02-1.161) * * .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.110) .090 (.370 (<LOD-.700) .500 (<LOD-.380-.170 (.500) .270 (.500-1.20) 1.940) .880-1.540 (.43) .400) .080 (<LOD-.09) .890 (.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 .070 (<LOD-.110) .100 (<LOD-.650) < LOD .670-1.700-1.410 (.200 (.19 (.990) .03) .380-.730) .580 (.330-.520-.62) 1.120) .220 (.360-.01 (.S.110-.084-.140) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (.780) < LOD 1.580) < LOD .670 (.720 (.86) .380-.780 (.720 (.24) .800-1.460 (.880 (.140-.230) < LOD < LOD < LOD < LOD .450 (.60) .600) .03 (.410 (.29 (.970) .14) 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.67) .250-.300-.120) .180-. population from the National Health and Nutrition Examination Survey.440-1.610-1.03 (.570-.150-.116 (.580) .550 (.060-.270) < LOD < LOD < LOD < LOD .360 (.990) .860 (.070 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .140-.280) < LOD < LOD < LOD < LOD .110) .111) * * * * * .300 (.650-1.110) .03 (.940) .380 (.640-1.140-.390-.

interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.35) 11.0) 2.55-8.21-3.87) 12.600 (.0 (4.70) 2.691 (.580 (.15) 14.01) 5.0-40.68) 2.28) 1.690 (.60) 1.750-1.10 (3.10-3.400-1.70-17.0) 4.10-3.20-17.90 (2.30 (1.42) 2.51-8.590 (.620-1.21) 3.20 (1.74 (3.0) 2.00 (1.24-7.960 (.90) .0 (6.350-.10 (3.840 (<LOD-1.10-9.0-39.90) .40) 2.0 (17.425-1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90-20.110 (<LOD-.07) 1.90-9.96 (1.40-20.830 (.30-3.23-6.0-38.49 (1.0 (4.880) 5.850) 16.800-4.87) 5.39) .08.63 (3.66) 4.55-4.43-4.510-.90-28.40-7.20) < LOD < LOD < LOD < LOD < LOD 1.640 (.0 (17.51 (2.260-.610) < LOD < LOD < LOD < LOD < LOD 2. and 03-04 are 0.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .86) 4.12-1.750-2.67 (2.03 (.720) 2.70-50.59-5.50) .70-7.0) 3.0 (17.00) . which may vary for some chemicals by year and by individual sample.0) 7.53) 20.00) 1.0) 4.52 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.800) 90th 13.740 (.48) 13.80 (4.11 (1.33 (4.610 (.40) 1.0 (3.94-3.83-3. respectively.S.36-3.0 (5.770 (<LOD-1.31) .800) 17.30-7.1.28-9.870) < LOD < LOD .14-5.47 (3.330 (<LOD-1.94 (1.35) 5.0) 5.0) 2.36-3.190-1.0 (17.890 (.370-.38-3.07 (1.20 (1.90) .170-1.52 (1.30) 95th 19.0) 4.11) .0-38.14) 2.0) 5.0) 5.31-10.50) 2.42) .49) 17.70-30.20-4.20-4.0 (5.210-1. population from the National Health and Nutrition Examination Survey.52) 5.0 (13.40 (1.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .32-9. 01-02.90 (1.840-3.840 (.00 (.65) 1.0) 2.40-4.13 (3. < LOD means less than the limit of detection.0-38.30 (2.00-17.30-6.45 (2.960 (<LOD-1.40 (1.0) 2.12) * * * * * * * * .07-3.48 (2.28) .49 (1.0 (17.97) 20. and 0.770) 2.0-44.11) 13.15) 19.0) 5.46 (1.480-.0 (5. see Data Analysis section) for Survey years 99-00.67 (1.18) 1.61 (1.0) 4.0 (7.74) 5.30) .07 (3.05 (3.14) .40-8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.99) 19.900 (.0-40.0 (16.53-7.00) .350-.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 .82-4. 130 Fourth National Report on Human Exposure to Environmental Chemicals .97) 20.910) 2.250 (<LOD-.88-3.0 (5.63) 32.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.62-8.30 (.37) .94-8.99) 11.30 (1.83-3.70-3.53 (2.90-37.60) .80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.1.380-.0 (5. 0.0) 2.0) 2.99 (1.05-3.67) .83) 2.07-3.32 (1.30 (1.26 (2.730 (.76 (1.35-10.29-10.07 (3.39 (2.05 (2.080-1.360-1.6) 5.85-3.640 (.00-17.10 (.

6) 952 1187 934 997 1330 993 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .67-6.60 (1.850-3.83-11. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.44) .24) 3.40-12.5 (8.80) 3.00-19.10 (2.84) 9.260-.85-3.690-5.1) 672 678 497 509 694 551 595 947 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40-2.580) 1.55 (3.88 (.01 (1.1) 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 * * * * * * .32) 9.660) < LOD < LOD .7) 4.56) .83 (4.650 (.9) 5.748 (.56) 2.23-7.03) 16.830 (.4) 2.0 (9.47) 5.1 (7.670 (.14 (1.830-3.17) 5.67) 2.05) .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.5) 2.22-27.92 (2.41 (4.13 (2.71 (2.36 (.37) 4.8) 7.69) 2.0) 4.80 (.7 (12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.260-.48 (4.57-40.3) 3.86) .48-42.7) 5.150 (<LOD-.88-3.75) 5.4 (4.600 (<LOD-1.49-2.18) 95th 21.73 (4.57) 8.4-34. Fourth National Report on Human Exposure to Environmental Chemicals 131 .28-6.96-25.270-.1) 2.33-3.07 (2.390-.12 (4.67) 1.85 (1.55) 21.790) 11.66-47.96-8.65 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (9.14-6.59 (1.45 (1.48-7.41) 18.1 (5.02) .2 (8.5) 7.780-4.31) .340-.21-3.450 (.3) 2.580) 16.88 (2.650) 90th 10.960 (.81-17.61) 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 .29 (4.33 (3.370) < LOD < LOD < LOD < LOD < LOD 1.22) 2.71 (.5 (11.43) .35 (.18) * * * * * * * * .33-5.9) 6.02 (.38 (2.57 (.02 (1.800-2.330-1.50) .730-3.770) .820 (.31-7.8) 2.5) 2.5-40.0 (4.86 (3.500 (.90-6.52 (.560 (.9 (11.790 (.7 (6.340 (.2-38.620-3.370-1.47-10.29-4.430) 1.91-4.51-4.04-16.270 (<LOD-.540-1.53) .40) 1.17 (1.50) 11.540 (.430 (<LOD-.50 (4.340-.57) 1.06 (.940-4.15) 9.07-21.474-1.8) 1.250 (<LOD-.33 (1.930) .700) < LOD < LOD < LOD < LOD < LOD 1.7) 6.10) 2.64) 30.310-.32-6.240-.27 (2.02-4.S.91) 2.18) 1.31-18.04 (1.08) .33-4.53) 27.47-10.700) 6.62-17.88) 17. population from the National Health and Nutrition Examination Survey.62 (1.8-33.40 (.47) .8) 4.39) 20.7) 3.44-11.360 (.03) 2.630-1.320-1.590) 2.56 (1.740-1.98 (4.860-2.25 (1.580-1.74 (2.25-38.30 (4.11) .470 (.69-7.970-3.12-4.11-5.55) 21.97) .10-3.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.580 (.820) .8 (20.67 (2.340-.840-3.31) .00) .370 (.79 (.890 (.25-9.8) 2.50 (2.51-44.710 (<LOD-1.190-1.77 (.64-4.82-11.09-3.96) 2.89 (2.8) 7.

Bradman A. Richardson RJ. Eaton DL. Bozzi N. Peterson JC. Momas I. Robinson LR. Aprea C. Jamal GA. Fenske R. Giordani B. Surveillance of occupational. Curl CL.49(9):751-760. Freshwater KJ.12(6):619-645. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Barr DB. McKone TE. Fisker-Andersen J.837:257-268. Jolley L.59(7):434-441. Garrison RP.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. Hansen S. Elgethun K. Reprod Toxicol 1998a. Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion.32(5):487-496. Krieger RI. Pilkington A. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides. A clinical neurological. Kipen H. Young AD. Novelli MT. Duggan A. and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides. Vaughan TL. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Occup Environ Med 2003. Curl CL. Neuropsychological performance among agricultural pesticide applicators. Blanchard O. Sci Total Environ 1996. Kissel JC. Chukwudebe A. Environ Res 1992. Fenske RA.37(3):382-395. et al. Abdel-Azis M. Arcury TA. Bouvier G. Schweitzer SJ.53(1):714. Bradman A. Barnhart S. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Checkoway H. Gillham RA. Environ Health Perspect 2000. Neurobehavioural effects among workers occupationally exposed to organophosphorous pesticides. Leffingwell JT. Castorina R. Sartorelli E. Curl CL. Quandt SA. Long-term use of organophosphates and neuropsychological performance.38(1):91-97. Aprea C. Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort. J Expo Anal Environ Epidemiol 2005. Eigenberg DA.60(4):279-286. Angerer J. Amr MM. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. Am J Ind Med 2006. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. Demers P. Organophosphate urinary metabolite levels during pregnancy and after delivery in women living in an agricultural community. Farahat FM.46(4):367-378. Castorina R. Environ Res 2001.110(8):829-833. Costa LG. Davis SW. Koch D. Keifer MC. Fenske RA. Kedan G. J Occup Environ Med 2004.111(13):1640-1648. Shebl MM. Chen W. Greenhalgh R. Farahat TM. Am J Ind Med 1997. Hawk R.59(1):217-228. et al. Lu C. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Harnly ME. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. Griffith W. Miller M. Third National Report on Human Exposure to Environmental Chemicals. Bravo R. Fenske RA.177:37-41. Engel LS. Environ Health Perspect 2002. Anger WK. Sciarra G. et al. Denley HV. Toxicol Ind Health 1998b. Seta N. Arch Environ Health 1998.111(3):377382. Regul Toxicol Pharmacol 2003. Barr DB. 86:80-87. Davies JE. Fiedler N. et al. Daniell W. Chevrier J. Neurophysiological function in farm workers exposed to organophosphate pesticides.113(12):1802-1807. Lu C. Berent S. Mathieu L. Regul Toxicol Pharmacol 2003. et al. Environ Health Perspect 2005. 132 Fourth National Report on Human Exposure to Environmental Chemicals .7(5):715-731. Abdelrasoul GM. 2005.15(2):164-171. Centers for Disease Control and Prevention (CDC). Atlanta (GA). Lunghini L. Kelly-McNeil K. Occup Environ Med 2002. Barr DB. Environ Health Perspect 2003. accidental. Eskenazi B. Charnley G. et al. Astroff AB.108:521-525.16(5):417-426. Heudorf U. Ann NY Acad Sci 1997. The relationship between maternal and fetal effects following maternal organophosphate exposure during gestation in the rat. Kissel JC. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Orsi D. J Expo Sci Environ Epidemiol 2006. Franklin CA. Environ Health Perspect 2003. J Toxicol Environ Health 1981. Fenske RA. Barr DB. Boccalon P. Strambi M. Urinary excretion of alkylphosphates in the general population (Italy). Buchanan D. Grzywacz JG. Garabrant DH. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Eskenazi B.14(6):869-889. Sartorelli P. Astroff AB. neurophysiological.

J Occup Environ Med 2002. Weerasekera G. Seiber J. Prendergast MA. Wickremasinghe AR. Rothlein J. Lu C. Marshall E. Rodnitzky RL. Pilkington A. et al. Muniz J. Eskenazi B. Dinoff TM. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Neurotoxicol Teratol 1998. Daniell WE.pdf. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. McCauley L. Lancet.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Phillips J. Environ Health Perspect 2006. Pesticides in the Diets of Infants and Children. Saieva C. Steenland K. et al. National Academy of Sciences. Occup Environ Med 2001. low-level exposure to the organophosphate diazinon. 4/7/09 Young JG.58(11):702710. Office of Prevention Pesticides and Toxic Substances.30(2):98-103. Neurotoxicology 2005. Occupational exposure to organophosphate pesticides: a neurobehavioral study.68(3):209-227 Maizlish N. McConnell R. and cholinesterase status of date dusters and harvesters in California. Sci Total Environ 2004.52(2):190-195. Smit LA. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Robson MG.52(10):648-653. Chronic neurological sequelae to organophosphate pesticide poisoning. Neurotoxicity among pesticide applicators exposed to organophosphates. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Available at URL: http://books.24(1):18-29. Bull Environ Contam Toxicol 1994. Scherer J. Burcar PJ. Terry AV Jr.113(4):504-508. Vitayavirasak B. Keifer M. Bravo R. Lewis JA. Chrislip D. Mounce LM.114(5):691-696. gov/oppbead1/pestsales/01pestsales/market_estimates2001. et al. Ruberu DK. Pedersen L. Rosenstock L. Scand J Work Environ Health 1998.12(2):134-141. Masala G. Stephens R. 1/12/09 Peiris-John RJ. J Toxicol Environ Health A 2005. Lasarev M. Kidd M. Berry H.332(1-3):71-80. Stokes L. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. EPA. EPA). Int J Occup Environ Health 2006. Beach J. Washington (DC). Washington (DC): U.php?record_id=2126&page=1.26(2):199-209.S.2000 and 2001 market estimates. Jenkins B. Thompson ML.nap. 1991. Jamal GA. Arch Environ Health 1975. Caltabiano LM. Arch Environ Contam Toxicol 2000. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Effects of long-term organophosphate exposures on neurological symptoms. Schenker M. London L. Lancet 1995. 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.edu/ openbook. Irish RM. 1993 [online]. Heaton RK.44(4):352-357. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Arch Environ Health 1988. Johnson C. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Environmental Protection Agency (U. Malathion deposition.43(1):38-45. Tumino R. Buccafusco JJ. U. Gladstone EA. Lambert WE. Hansen S. discrimination. Narang A. National Research Council (NRC). Myers JE. Keefe TJ. Levy LS. Salvini S.12(2):153-172. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Calvert IA. and spatial learning in monkeys and rats.338(8761):223-227. Pesticide industry sales and usage . Weisskopf C. et al. S. Gillham R. A behavioral evaluation of pest control workers with short-term.epa. Environ Health Perspect 2005. van der Hoek W.84(5):731-736. Visuthismajarn P. Rohlman D. Russo J. metabolite clearance. Frasca G. Available at URL: http://www. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Effects of chronic. Aprea C. Takamiya K. Occup Environ Med 1995. Buchanan D.38(4):546-563. Barr DB. Ames RG. Am J Public Health 1994. O’Malley M. vibration sense and tremor among South African farm workers. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Samuels S. Muniz J. The Pesticide Health Effects Study Group. Spurgeon A. Bradman A. low-level organophosphate exposure on delayed recall. Stark A. Lasarev M. Petchuay C. et al. May. Santana J. Savage EP.345(8958):11351139. Claypoole K.S. Nell V. Hore P. 2004. Am J Ind Med 1987. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Rothlein J.20(2):115-22.

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

66-15.60 (4.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 7. Approximately 21-24 million pounds per year were used domestically from 1987-1998.70-16. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.5-24.9 (9. The general population may be exposed to chlorpyrifos via oral.5. population from the National Health and Nutrition Examination Survey.76 (1.20-4.59-2.31-2.71 (6.50-5. 2921-88-2 Chlorpyrifos-methyl CAS No.40-2.30-9. For instance.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. in 142 urban homes and preschools in North Carolina.47-9.28) 2. Survey Geometric mean (95% conf.4 and 0.44-2.20) 10.7) 9.10 (4.63 (2.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.04-10.60-3. applied to structures to kill termites.68-2.5. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.22) 2.35) 2. and is infrequently detected in ground water (IPCS. 2005).97) 2.9) 11.0) 10.S.04-10.EPA. 5598-13-0 General Information The chemical 3.30 (2.37 (4.67 (2.50-2.61-7.72-4.31-2.S.80-8.00) 3.0) 15.90-4.7) 13. chlorpyrifos was no longer registered for indoor residential uses in the United States.67 (2.0) 18.50 (2.80 (7.60 (5.36 (4.67 (1.1) 5.20-3.4 (8.97) 7.74 (1.63 (8.4 (10.4 (9.0) 6.59) 2. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al. It also has been applied directly on animals to kill mites.77-15.40-26.22 (1.0 (7.40 (5.96) 3.EPA.20-11.37 (1. Fourth National Report on Human Exposure to Environmental Chemicals 135 .76 (1.40-10.9) 697 660 521 701 602 947 Limit of detection (LOD.02) 1.5 (8.81-2.97-7.47-11. pre.91 (1.53 (1.0) 10. After 2001.77 (1.98-15.97) 4.72) 2.10 (5.3 (11.40) 9.50 (1.83) 1.20 (2. 2007).29-1.8) 10.60-4.9 (10.30-1. air.50 (2.89 (2.30-2.87-6.90-7. and sprayed to kill mosquitoes.27 (7.60) 5.0 (9.20) 2.30) 4.80) 1.47-13.9 (7.40-13.3 (10.and post-construction structural applications for termite control were to be phased out by 2005 (U.70-5.19 (1.10-17.43-2.30) 4.90) 3.30-12.35) 1.70-15.10) 6.61) 75th 3.44-5.90 (3.68 (7.64) 3.80) 12.78 (7.80) 2.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.47 (4.1-16.6) 7.0) 8.80-10.70) 1.2 (10.40) 2.91) 16.0) 10.70-17.0) 12.95 (4.46-2.0 (7.0) 12.16) 2.01) 1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.38 (3.17 (1.70 (1. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.9-18.25) 1. staying bound to soil particles. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.0) 11.90) 7. dermal.13-3.63 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.20) 2.13 (1.90-2.3) 8.4.55-5.51) 1.29) 90th 7.09 (3.000 pounds are used per year. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.70-11.7-23.24-1. It has low leachability.50 (1. interval) 1.99-4.20-2.94 (4.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.21) 3.24-3.00) 1.25) 3. and on plants for days to several weeks.80) 4.43-2. 2002). Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.20-16.30 (4.09 (2.20 (4. Approximately 80.32-1.60-3.00-24. Exposure can also result from contact with contaminated surfaces.0) 8.0) 12.77-6.05-5.3 (8.10 (1.03) 1.62-2.60 (2.90 (6.70 (1.02 (7.0 (13.4-15. but can be detected in streams receiving runoff from application sites.7) 8.39) 4.40 (5.50 (2.19-3.50-2.61 (1.52-2.88 (1.20) 4.50-4.95) 7.86) 4.26) 7.50-14.50-8.80 (1.10) 2.57 (2.77) 1.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.51 (1.0 (10. Estimated intakes from diet and water have not exceeded recommended intake limits.90 (1.39-2.60-2.40 (6.0-28. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.0 (7.0 (7.45 (1. Chlorpyrifos is Urinary 3.0) 9.32) 2.8) 9.30-5.44 (3.0) 14.74-9. and inhalation routes.5) 7.15 (1.S.97) 2.90 (2.10 (3.50-4.20-14.37) 5.00) 2.92 (1.0 (7.30) 5.89-2..51-2. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.79-2.30 (2.84) 1.28-3. and dust. 2002).34) 1.8-15.30-11.52-12.66-4.05) 1.02 (1. USGS.90 (1.0) 12.00-8.71 (1.47) 1. 1999.0) 12.90-8.71 (2.

Urinary 3. 2005.3) 8.80) 3. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.31-1..80-11. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.S.39-1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).79-13.2) 6.5 (6. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.62) 90th 5.35-1.72-2.59) 3.5.85-4.2 (7.19-2.49-2.84-6.93) 5.75 (1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.33) 2.32) 1.44 (1.07) 5.82 (2.11 (2.1-38.97 (3.39 (4.30-4.94-14.58 (1. neurotransmission.83-11.22-6.40) 1.64-2. TCPy is more persistent in the environment than chlorpyrifos itself (U.0) 10.0) 12.94-12.03) 1.91-4.34-1.65-11.62) 1.77) 1.00) 1.14) 1.47-2.97) 3.05) 3.16 (4. 2006.33 (.86 (3.71 (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.01) 3. and producing acute symptoms such as nausea.28) 2.38) 3.91) 2.57-2.92 (1.05-8.08) 6.45-1.66) 1.80-6.88-9.27-7. 2006.30-1.23-1. Betancourt et al. Based on animal data and human cholinesterase monitoring during occupational exposure.12-3.48 (2.17-4.940-1.00 (7.44 (1.42 (5.36) 1.88-8. 2005.49-2.58) 5.39) 6.93 (2.05-3.59-2..02 (5.0) 16.88) 6.48 (1.64 (1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.37 (1.1 (7.31-4.64-7.43 (4.22 (6.50 (4.02) 7. Howard et al.3) 9. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.S.6) 10.87-3.88-10.06 (1.19-1.85) 4.09-1.01) 1.44-6. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.01) 3.35) 1.5) 5.11 (2.33 (5. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.88-8.68) 6. Thus.44 (5.68) 1.6) 9.19) 6.76 (2.85 (3.11) 7.29 (3. weakness.46 (2. and seizures.9 (12.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.05-1..24-5.47 (1.33-7.70-4.99) 1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.71) 3.12-1.24-1.41 (1.95 (3.91) 1. Metabolic hydrolysis leads to the formation of TCPy.24) 75th 2.24-24.66 (1.58 (1.55) 1.60-3.85) Selected percentiles ( 95% confidence interval) Sample 95th 8. TCPy can also occur in the environment from the breakdown of the parent compounds.90-9.92) 3.55 (4..14-8. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.80-4. 2002).92-2. In pesticide applicators.62-7.93 (4.78 (1.44 (6.8) 9.28) 2..4) 4. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. cholinergic effects.24 (1. paralysis.83) 1.60 (1.75) 6.09-2.33 (1.81 (3.22) 1.98 (7.82 (3.54 (2.86 (1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.05-4..31) 1.63-2.82) 8.99-8.82-4.52 (5.74) 1.91 (4.06-4.56) 2.72) 2.55 (1.25-12.97) 3.66-11. Roy et al.56-2.35) 2.23) 14.95 (1. 2006b).85 (2.3) 8.0) 6.00-13.88 (1.72) 1.69 (1. resulting in excess acetylcholine at nerve terminals.20 (2.86 (1.57-2..01) 99-00 01-02 99-00 01-02 99-00 01-02 3.39 (2.63 (4.25-11.49 (1. Survey Geometric mean (95% conf.06 (5.00-8. and other metabolites.24) 5.46 (1.43-10.27-1.56) 5.1 (10.91 (3.54) 5. Ricceri et al. vomiting.58-5.7) 7.97 (2. Once absorbed.91) 1. 2000).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 1.58 (4.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.42-2.88 (1.97-3.58) 1.1-21.85) 1.11-9.89) 4.51 (1.21-6.98 (6.73 (1.56 (1.EPA.93) 2.53-5. Slotkin et al.15 (4.83-2.47 (5.22 (4.3 (7.6-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.45 (1.47 (1.16) 6. interval) 1.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. 2005.49-2.57) 9..96) 3.09-3.20-1.44 (5.12) 1.19) 3.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals . 1984).65-15.93 (1.76 (3. 2006a.09 (1.26-14.25-1.63 (5.57) 2.81) 2.42 (6.21-1..53 (2. population from the National Health and Nutrition Examination Survey.07) 1.91) 10.17-4. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.91-13.24-4.56 (4.

Organophosphorus Insecticides: Specific Metabolites 2004.S. Curwin et al. Betancourt AM. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al.S. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. In a probability-based sample of 102 Minnesota children aged 3-13 years. Haidar S. Barisano A. 1999). urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. 2005. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Carr RL. 1992. Whyatt et al. Lioy PJ. but not chlorpyrifos.. representative subsample of NHANES 19992000 (CDC. environmental levels) and health effects is available from ATSDR at: http://www.. 2005). Giordani B. Occup Environ Med 2006. 2005). Betta A. et al.cdc. U. Berent S.. 2003.82(2):305-312. et al. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Magnaghi S.S..109(6):583-590.gov/pesticides/. 2005.epa. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al.Reference values of urinary 3.. Garabrant D.. 2001).S. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Albers JW. population (CDC.5.. Burgess SC.. urinary TCPy levels in children were reported not to have increased (Hore et al. Environ Health Perspect 2001.S.EPA. 2007). Meyer A.92(2):500-506. Freeman NC. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. CDC. 2006). References Adgate JL. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al.atsdr. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. Seidler FJ. Eberly LE.. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Slotkin TA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2002). Biomonitoring Information Urinary TCPy levels reflect recent exposure. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.. Additional information about external exposure (i. Of 482 pregnant women living in an agricultural community.. Environ Health Perspect 2005. Burns CJ. 2004). 2005). 2005). Chlorpyrifos exposure and biological monitoring among manufacturing workers. Levels of TCPy in the U. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. 2005). 2004).. In Iowa farm families using several different pesticides. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. Lotti A. EPA at: http://www. Following crack-and-crevice application of chlorpyrifos in their homes. 2001) and Italy (Aprea et al. MacIntosh et al. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.63(3):218220. 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. 2005).html and from U. Catenacci G.. 2000). J AOAC Int 1999. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Aldridge JE. Fourth National Report on Human Exposure to Environmental Chemicals 137 .. 2005. et al. Clayton CA. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al.. Perera et al.. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.e. the geometric mean urinary TCPy levels were similar in parents and children.113(8):1027-1031. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. In Minnesota and South Carolina farmers who used chlorpyrifos. Toxicol Sci 2006. but levels were roughly four to six times higher than the geometric means in the U. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Aprea C. Barr DB.gov/toxpro2. Koch et al. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.

Adgate JL. gov/ntpweb/index. et al.nih. Barr DB. Seidler FJ. Rauh V.204(2-3):175-180. National Toxicology Program (NTP). Bailey SL. Seidler FJ. Bucelli R.114(2):260-263. Croghan CW. Sheldon LS. Harley K. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Bravo R. Levin ED.73:8-15. et al. Morgan MK. Tate CA.15(3):271-281. Gregg M. et al. J Expo Anal Environ Epidemiol 2005. Lioy PJ. Biomonitoring for farm families in the farm family exposure study. 2921-882. Toepel K.108(4):293-300. Angerer J.6-trichloro 2-pyridinol in their everyday environments. Jett DA. Eskenazi B.6-trichloro-2-pyridinol.inchem. Fortuna S. Roy TS. Yang D. Chrislip DW. 1999. Scand J Work Environ Health 2005.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Kromhout H. Pellizzari E. Jewell NP. Hein MJ. U. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Meeker JD. Camann D. MacIntosh DL. Jones PA. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals .S. Environmental Health Criteria 198. Chuang JC. Sharma V. 2005. Toxicol Sci 2006. Lu C. Head SL. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Bradman A. Ann Occup Hyg 2007. February 5. Third National Report on Human Exposure to Environmental Chemicals.114(10):1542-1546.51(1):53-65. et al. Slotkin TA. Environ Health Perspect 2005. Hore P. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Kinney P. Environ Health Perspect 2006a.org/documents/jmpr/jmpmono/ v99pr03. Barr D.207(2):112-124. Fenske RA. Bruun D. Hill RH Jr. Hardt J.93(1):105-113. Ricceri L. Herrick RF. Atlanta (GA). Sanderson WT. Environ Health Perspect 2004. Environ Health Perspect 2006b. Robson M. Striley C. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Toxicol Appl Pharmacol 1984. Barr DB. Hammerstrom KA. Available at URL: http://ntp.htm. Cometa MF. Available at URL: http://www. Robertson GL. et al. Wartenberg D. 4/7/09 Perera FP. Pesticide residues in urine of adults living in the United States: reference range concentrations. Chlorpyrifos. Edwards RD. Freeman N. Nolan RJ. Neurologic function among termiticide applicators exposed to chlorpyrifos. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Seidler FJ. Curwin BD. Environ Health Perspect 2003. Bennett DH. mothers and fathers living in farm and non-farm households in Iowa.5.15(4):297-309. Rick DL.niehs. Environ Res 1995.71:99108.5. Mandel JS. International Programme on Chemical Safety-INCHEM (IPCS).S. Slotkin TA. J Expo Anal Environ Epidemiol 2000. Zhang J. Bravo R. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Honeycutt R.10(4):327-340. Baker BA. chlorpyrifos. Brain Res Dev Brain Res 2005. Environ Health Perspect 2000. Freeman N. Alexander BH. J Expo Anal Environ Epidemiol 1999. Hines CJ. Irish R. Acquavella JF. Heederik D. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Ryan L. Environmental Protection Agency (U. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Ryde IT. Gurunathan S. Chlorpyrifos: pharmacokinetics in human volunteers. Levin ED. A longitudinal investigation of selected pesticide metabolites in urine. et al. Weltzien E. Shealy DB.31 Suppl 1:98-104. 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. Saunders JH. Howard AS. et al. Lorenzini P. Barr DB. Chapman P. Environ Health Perspect 2006. Exposures of preschool children to chlorpyrifos and its degradation product 3. EPA). Baker S. Needham LL. Dick RB. et al. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Ozkaynak H. Urinary pesticide concentrations among children. Ryan PB. Toxicol Appl Pharmacol 2005.113(2):211-219. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Interim registration eligibility decision for chlorpyrifos.155(1):71-80. Reid TM. Lein PJ. Int J Hyg Environ Health 2001. Executive summary of safety and toxicity information.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Steenland K.114(5):746-751.9(5):494-501. Slotkin TA. 1992. Capone F. Venerosi A. J Expo Anal Environ Epidemiol 2005.112(10):1116-1124. et al. Howell RJ. Tsai WY.111(2):201-205. 4/7/09 Koch HM. et al. Freshour NL.

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

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

200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 01-02 is 0.2. 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. population from the National Health and Nutrition Examination Survey.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 .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. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 141 .270) < LOD 659 701 920 Limit of detection (LOD.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.380 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.670 (<LOD-1. which may vary for some chemicals by year and by individual sample.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (<LOD-.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 .S.

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

05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. in some pest strips. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. about 13 million pounds of diazinon were used annually on agricultural sites in the United States.S.2 and 0.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.S. population from the National Health and Nutrition Examination Survey. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Estimated intakes from diet and water do not exceed recommended intake limits (U.EPA. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. fruits.45 (<LOD-3. but is rapidly absorbed orally (IPCS. USGS. seed and foliar applications are planned to be phased out (U. but these uses have been phased out. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. It is toxic to birds. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. It is also used for cattle ear tag applications to control flies and ticks and. Prior to 2000.49 (<LOD-2. Inhalational and dermal routes of exposure can be significant for pesticide applicators. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. since 2004.EPA. Fourth National Report on Human Exposure to Environmental Chemicals 143 . and particularly when it was ingested in granular form. Most granular formulations. diazinon produced wild bird kills before use restrictions were in place. 1998. diazinon was widely used in residential and garden application. 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. * 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. Once absorbed. 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. 2004). Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. 2004). and other metabolites. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. 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.S. aerial. 2007). It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. 1998). in the past.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. Before these restrictions. vegetable. and forage crops. Diazinon is not well-absorbed through the skin.7. an organophosphorus insecticide that is used to control insects on nuts. diazinon cannot be sold for residential use.

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

Semen quality in relation to biomarkers of pesticide exposure. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Oloffs PC.usgs. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses.50(5):505-515. Environ Health Perspect 2006.376(6):808-815. Barr DB. 1/14/09 U. Environmental Health Criteria 198.S.gov/circ/2005/1291/. 1992-2001. EPA 738-R-04-006. Environ Health Perspect 2003.S. Atlanta (GA). Diazinon. 2005. Seifert J. 4/7/09 Lu C.. Redmon JB. 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. Beeson MD. Irish R. Oloffs PC. Drobnis EZ. Garfitt SJ.pdf. Available at URL: http://www. J Expo Anal Environ Epidemiol 2000. Pesticides in the Nation’s Streams and Ground Water. Third National Report on Human Exposure to Environmental Chemicals. Rajendra W.9(2):117-131. 2007 [online]. In 54 Canadian greenhouse workers. 2006).gov/ oppsrrd1/REDs/diazinon_ired.S. Kruse RL. Cocker J. Carrier G. Centers for Disease Control and Prevention (CDC).134(1-3):105-113. U. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. References Anthony J. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. International Programme on Chemical Safety-INCHEM (IPCS). Barr DB. Banister EW. Ann Occup Hyg 2006. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicol Lett 2002. Anal Bioanal Chem 2003. Environmental Protection Agency (U. EPA). Bull Environ Contam Toxicol 1986. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Jones K. Swan et al. Effect of sublethal levels of diazinon: histopathology of liver. Barr DB. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon.org/documents/ehc/ehc/ehc198. Available at URL: http://www.inchem. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Olsson AO. Available at URL: http://pubs.111(12):1478-1484. March 2006. Study for Future Families Research Group. Bouchard M. Brunet RC. Baker SE. Mason HJ. Barr DB.44(11):2243-2250.10(6 Pt 2):789-798. Toepel K. In 23 children. 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.114(2):260-263. Swan SH. Biochem Pharmacol 1992. Diazinon. The Quality of Our Nation’s Waters. In a small number of men visiting fertility clinics in Missouri and Minnesota. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .37(4):501-507.epa.Organophosphorus Insecticides: Specific Metabolites 2005). Banister E. Needham LL. Interim reregistration eligibility decision (IRED.htm.. Bravo R. 1998. Nguyen JV. Liu F. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Driskell WJ. May 2004. Noisel N. Fenske RA. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Pewnim T. revised February 15. 2006). Drug Chem Toxicol 1986. Geological Survey (USGS). Dumas P. Sadowski MA.

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

a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. IARC considers malathion not classifiable as a human carcinogen. 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. Flessel et al. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. 2001. Pluth et al.gov/pesticides/.atsdr. Thomas et al.S. 2005. representative subsample from NHANES 19992000 (Adgate. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 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. Toxicity from unprotected bystander exposure during applications is rare (U.cdc. population from the National Health and Nutrition Examination Survey. Human studies of single oral doses between 0.EPA. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 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.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. 2006).html and from U. 2004)... Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. 2003).. 2005).S. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. 2006). but cholinesterase activity was not affected. 1999).... Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al.S. Survey Geometric mean (95% conf. 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. CDC.S. 2006). 2002... 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. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 1987. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. Fourth National Report on Human Exposure to Environmental Chemicals 147 . 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.gov/toxpro2. 1996.50) < 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. Of 382 pregnant women living in an agricultural community.epa. and it is not considered an animal teratogen or a reproductive toxicant.. Giri et al.e.EPA. Additional information about external exposure (i. 1993. EPA at: http://www. 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.. but isomalathion. 1990). 2000).5 and 5. Malathion itself has not been considered genotoxic (U..S. 1999. Lu et al. 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.74 (<LOD-5. environmental levels) and health effects is available from ATSDR at: http://www.

Lioy PJ. Toepel K. Goldhaber M. Available at URL: http://www. Lu C. Environ Mol Mutagen 1993. Nicklas JA. Giri S. et al. Kedan G. Gosselin NH. Griffith W. 6/1/09 U.pdf. Fenske RA. Thomas D. Albertini RJ.S. 1992-2001. Dinoff TM. Samuel O. Am J Public Health 1987. Malathion (addendum).9(5):494-501.15(2):164-171. Freeman NC. July 2006.114(2):260-263. Prasad SB.73(1):182-94. Toxicol Sci 2003 May. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Malathion deposition. Neutra R. Curl CL. Trzeciak A. htm. Reregistration eligibility decision (RED) Malathion. Swan SH. Harley K. Environ Health Perspect 2004. Clayton CA. revised February 15. Hammerstrom KA. Eskenazi B. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Erratum in: Toxicol Sci 2003 Aug. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. and cholinesterase status of date dusters and harvesters in California. Third National Report on Human Exposure to Environmental Chemicals. Grether JK. Brunet RC.77:1009-1010. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Hertz-Picciotto I. MacIntosh DL. Carrier G.usgs.S. Arch Environ Contam Toxicol 2000. Barr DB. Lu C. Needham LL. EPA). Bravo R. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Environmental Protection Agency (U. Bouchard M. Ryan PB. Environ Health Perspect 2001.22(1):7-17. Dumoulin MJ. Reproductive outcome in women exposed to malathion. metabolite clearance. et al.514(1-2):223231. Harris JA. O’Neill JP.38(4):546-553. Jewell NP. Irish R. 2007 [online]. The Quality of Our Nation’s Waters. Blasiak J. et al. Am J Epidemiol 1990.epa. International Programme on Chemical Safety-INCHEM (IPCS). A longitudinal investigation of selected pesticide metabolites in urine. Weltzien E. Mutat Res 2002.S.org/documents/jmpr/jmpmono/v2003pr06. Pesticides in the Nation’s Streams and Ground Water. Petitti D. U. Hooper K. Barr DB. Eberly LE. Environ Health Perspect 2006. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Genetic toxicity of malathion: a review. Flessel P. Available at URL: http://www. Jaloszynski P.gov/oppsrrd1/REDs/ malathion_red. Barr DB. Bradman A. 2005. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Krieger RI. Giri A.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Szyfter K.inchem. March 2006.109(6):583-590.56(10):2393-2399. J Expo Anal Environ Epidemiol 2005. J Expo Anal Environ Epidemiol 1999.gov/circ/2005/1291/. Atlanta (GA).132(4):794-795. Barr DB. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Mutat Res 1999. Available at URL: http://pubs. Cancer Res 1996. 4/7/09 Kissel JC. Centers for Disease Control and Prevention (CDC). Pluth JM. Quintana PJ. Sharma GD.112(10):1116-1124.74(2):following table of contents. Rappaport E. Geological Survey (USGS). EPA 738-R06-030. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.445(2):275-283.

with limited applications in agriculture.40-3.27) 2.50) 3.80 (2.70-3.80 (2.50) 2. Morgan et al.37) 2. peak domestic use was as high as 5-6 million pounds per year.30 (1.S.60-24. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.37-4.90-11.85 (2.13-1.58) 3.298-00-0 Ethyl Parathion CAS No.01) 4. It had been applied to cotton.70 (2.910) < LOD < LOD . the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.21-1.10-1.EPA.89 (2.850) < LOD .61) < LOD 1.700 (<LOD-.02-6.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 2007).50-14.37-2. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. Methyl parathion is not registered for residential use in the United States. and oral routes can occur in pesticide and agricultural workers (Muttray et al.90 (1.50-9.30-16.11) 2. and aquatic invertebrates.32-1.0) 2.79) 4.00 (2. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides. more slowly absorbed through the skin.12) < LOD < LOD 1.790 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.34 (3.50 (1.00) 3..00 (2. ethyl parathion.50 (1. fish.EPA.910) < LOD < LOD < LOD 1.60-36..20) 5.70 (2.70-3.32-1.50 (1.69 (2.940 (<LOD-2.45 (1.20-5.28 (1.10 (3. 1977).30-3.05) 4. binds tightly to soils resulting in low leachability.30-5.0) 3.74) 5.10 (<LOD-6.28-4.32 (1.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .60) 1.50 (1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .860 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. population from the National Health and Nutrition Examination Survey. 2002.70) 2.30 (2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.60 (4.18-3.40) 1.10) 22. 2003).71 (2. and eliminated rapidly from the body after absorption (Kramer et al.80 (1.49 (1.S.15-3.300-.90-9.62 (1.46 (3.70 (2.44) 2.11-4. In the 1990s.70-6. Methyl Parathion.0) 3.41-4.40-4.0) 3.70) 2.32-3.80) 2. 2006).70) 2. and of the chemical nitrobenzene. In animal studies. was once a restricted-use insecticide with limited applications on certain agricultural crops.10-11.50) 3.01) 695 660 518 679 603 941 Limit of detection (LOD.10 (3. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.91-3.990-1.16) < LOD 1.67 (1.66 (2.8 and 0..70-6.0 (3.36-1.61) < LOD 1. but by 2003.92-2.60-5.910) < LOD . all registered uses were voluntarily cancelled (U. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.50 (2.71 (3. first registered in 1948. Methyl parathion use is highly restricted. and to a lesser extent.40 (1. Once absorbed.33) 2.40) 4.26 (1. Methyl parathion has low water solubility.40) 2. Given its limited use.730 (<LOD-.01-4.21 (2.00) size 1989 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.20 (2. Both are toxic to birds. 2000). and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and has a short half-life in soils and on plants.57) 1.0) 4.28 (1.50) 1.1.20 (<LOD-2. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.60-19. methyl parathion was rapidly absorbed after ingestion.45) 5.70-6.92) 5.0) 3.72 (3.47) 2.70 (3.09-1.50 (2. on cereal grains.37-4. Survey Geometric mean (95% conf.70 (<LOD-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.0) 3. which may vary for some chemicals by year and by individual sample. Ethyl parathion.69) 4. < LOD means less than the limit of detection. Estimated intakes from diet and drinking water have been below recommended limits.33 (1.S. Increased risk of exposure via dermal.67) < LOD 1. pulmonary.10) 4.48) 90th 2.57-4.19 (. Many previous registered agricultural uses of methyl parathion have been cancelled (U.770 (.22-3. Fourth National Report on Human Exposure to Environmental Chemicals 149 .40-4.

25 (2. At high animal doses of methyl parathion.39 (1.33-3. In addition to being a metabolite of methyl and ethyl parathion.91) 1.950) < LOD .93 (2. 1978.39) 1.07) 2.440 (<LOD-. U.76-14.05) 4.13) 4.530) < LOD < LOD < LOD . resulting in excess acetylcholine at nerve terminals.79 (1.370 (<LOD-.720 (<LOD-. environmental levels) and health effects is available from ATSDR at: http://www.77-7. 150 Fourth National Report on Human Exposure to Environmental Chemicals .82) < LOD .08) < LOD .2) 2.9) 1. Thus. Additional information about external exposure (i.. 2003.3) 2. The metabolite.680 (<LOD-1.33-6.80 (1.20) 3.96 (1.epa.00 (1.S.84) 3.55 (<LOD-3.60) 2.26) 17.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . EPA at: http://www. 2006.880 (. and seizures. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.7) 3.15-10.08-3.2) 2. 1991). weakness. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.10) 90th 2.790-1.59 (1. vomiting.EPA considers methyl parathion unlikely to be carcinogenic to humans.21) 1.. 1990.37-1.09) 2..970 (.98-7. 1995).57-7.640) < LOD < LOD 1.90 (1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .30) 3.29) 2.60-2. Karanth and Pope et al. Survey Geometric mean (95% conf.540) < LOD . ethyl parathion.850-1. does not inhibit acetylcholinesterase enzymes.4 (3.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Lores et al.14-3.23) 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 .21-21. and producing acute symptoms such as nausea.17) . Jaga and Dharmani.S.830-1.94-4.78-2.13-12.08 (1.980 (.atsdr. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion. Methyl Parathion.79) 1.00) 2. cholinergic effects.1) 2. Orsorio et al.33-3. Methyl parathion is not considered genotoxic.840 (.940 (<LOD-1.500) < LOD < LOD .29 (2.56-2.97-10.97 (2.20) . In large doses.82 (2.11) 1. 2005.cdc.89 (2.73 (1. Parathion and methyl parathion have high acute toxicity in animal testing.71) 1.23) 1.95) 1.400 (<LOD-.91 (1.67 (3. Zurich et al.96 (1.01-3.87 (1. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.430 (.870) < LOD . the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.38-3. and unintentional acute or chronic high-level occupational exposure (Hill et al. accidental exposure.31-3.00 (1.07 (1. gov/pesticides/.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. WHO. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4..e..35-3. teratogenic.31) < LOD .17-4.72-2.10 (1.11-4.94-47.30-1.78-2.16-4.78 (2.70) 3.15) 3.61) 4. paralysis. 2004).57) 6.25) 1.29) 1.41-2..55) 2.57-2.01 (2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).80 (1. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.310-. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.44-3.60 (1.26 (1.800-1. 2006.86 (2.970 (.04) 1. methyl parathion.43) 4.html and from U. population from the National Health and Nutrition Examination Survey.71 (1.790-.930 (.44-3. 2004). paranitrophenol.730-1.89 (2.83 (1. but lists ethyl parathion as a possible human carcinogen. and other metabolites. 1995.04 (2.92 (2.48-4. gov/toxpro2.. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.930 (. Slotkin et al.88) 1.97 (<LOD-4.78) 2.35-3.67-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.88 (1.20 (3.690-1. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al.720-1.01 (.

Lin LI. Griffith W.. Curl CL. McCann KG. 2002. Pesticide workers may have much higher levels following pesticide applications. 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. Kedan G. 1995). Baker SE. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Runkle KD. J Anal Toxicol 1990. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 2005. Kissel JC. oral or dermal administration.110 Suppl 6:1075-1078. Rubin et al. Centers for Disease Control and Prevention (CDC).15(2):164-171.14(4):213-216. 2005. International Programme on Chemical Safety-INCHEM (IPCS). Head SL.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion.5 mg (500 µg)/g creatinine for workers at the end of shift. Lores EM. Karanth S. Moomey CM. Arch Environ Health 1978. Barr DB. Methyl parathion: an organophosphate insecticide not quite forgotten. Alley CC. and many residents were symptomatic (Barr et al. Baker RC. 1999). Fourth National Report on Human Exposure to Environmental Chemicals 151 . Neurotoxicol Teratol 2003. Lu C. Jewell NP. et al. Barr DB. population (Olsson et al. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Pesticide residues in urine of adults living in the United States: reference range concentrations. Bradman A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.org/documents/jmpr/jmpmono/v95pr14. Head SL. Environ Health Perspect 2002. 2005. 2004).33(5):270-276. et al. Atlanta (GA).. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Toxicology 2005.inchem. Lewalter J. 2005). 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. Kramer RE. Environ Health Perspect 2002. 2002. and levels were similar or slightly lower that those in a small convenience sample of the U. Occup Environ Med 1999.6(2-3):159-173.S. general population (CDC. a range of values several hundred times higher than levels found in the U. 4/7/09 Jaga K.. References Barr DB. Arch Environ Contam Toxicol 1977.9:311-320.. Environ Res 1995. Weltzien E. Laboratory investigation of a poisoning epidemic in Sierra Leone. Harley K. Eskenazi B. Slach EF. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Pharmacokinetics of methyl parathion: a comparison following single intravenous. In a study of workers who handle parathion. et al. Giordano G. Morgan DP..110 Suppl 6:1085-1091. Shealy DB. Role of individual susceptibility in risk assessment of pesticides. Costa LG. Barr JR. Hill et al. ACGIH recommends a BEI of 0.21(1):5767. DiPietro E.S. Ashley DL. J Expo Anal Environ Epidemiol 2005. Clark JM. Moseman RF. McClure PC. 2002). Available at URL: http:// www.. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation.htm. Bradway DE. 2005). Rockhold RW. J Biomed Sci 2002. Pathak S. Baker S. et al.56(7):449553. Hetzler HL. Chicago area methyl parathion response. Pope C. Leng G.71:99108.. Environ Health Perspect 2004. Hryhorczuk DO. Third National Report on Human Exposure to Environmental Chemicals. McCann et al.112(10):1116-1124. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Turner WE. Hill RH Jr. Cline RE. Hill RH Jr. 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. CDC. Gregg M.25(5):599-606. Parathion-Methyl (addendum). Wellman SE. 1995. Barr DB. Guizzetti M. 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. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Needham LL. et al. Bailey SL.215(3):182-190. Dharmani C. Rev Environ Health 2006.

S.04/106. Sadowski MA.int/water_sanitation_health/dwq/chemicals/ methylparathion. Yacovac R. Environ Health Perspect 2002. Ames RG.E. Interim reregistration eligibility decision (IRED) for Methyl Parathion.376(6):808-815. R. Rosenberg J. Rubin C.20(4):533-546. Geological Survey (USGS). Environmental Protection Agency (U.Organophosphorus Insecticides: Specific Metabolites Muttray A. Letzel S. September 2000. Backer G. Available at URL: http://www.usgs. Osorio AM.S. 1/14/09 U. Schilter B. Hill RH Jr.S. Costa LG. Toxicol Appl Pharmacol 2004. Ryde IT. 0153. 2004. Slotkin TA.114(10):1542-1546. Olsson AO. Monnet-Tschudi F. gov/oppsrrd1/REDs/methylparathion_ired.gov/oppsrrd1/REDs/factsheets/0155fct. WHO/SDE/WSH/03. Facts. U. Methyl parathion in drinking water. 5/19/09 Zurich MG. External and internal exposure of wine growers spraying methyl parathion. Available at URL: http://pubs. 1/12/07 U. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Hill G. Jung D. 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.gov/circ/2005/1291/. Barr DB. EPA).110 Suppl 6:1047-1051. Available at URL: http://www. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. March 2006. Ethyl parathion. The Quality of Our Nation’s Waters. Tate CA.epa. Environ Health Perspect 2006.who. Mengle DC. Ohio. Case No.201(2):97-104.S.epa. 1992-2001. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. 2007 [online].S. 1995-1996. Honegger P. Levin ED. Am J Ind Med 1991. Environmental Protection Agency (U. revised February 15. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. May 2003. Seidler FJ.162(2-3):219-224. Pesticides in the Nation’s Streams and Ground Water.pdf. 6/1/09 World Health Organization (WHO).pdf. Dunlop B. Kieszak S. Investigation of a fatality among parathion applicators in California. Anal Bioanal Chem 2003. Toxicol Lett 2006. EPA-738-FOO-009. EPA). pdf. Nguyen JV. et al. Esteban E.D. Available at URL: http://www.

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

780 (<LOD-1.740 (. Survey Geometric mean (95% conf.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.07) .820) < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0. 154 Fourth National Report on Human Exposure to Environmental Chemicals .740-1. Survey Geometric mean (95% conf.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 .780 (<LOD-1.780 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .760 (<LOD-. < LOD means less than the limit of detection.210-1.94) .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th .840 (.300-1.410 (<LOD-1.15) < LOD .250 (<LOD-.S.27) .64) .17 (. which may vary for some chemicals by year and by individual sample.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .700-.670 (<LOD-1.580-1.2.430 (<LOD-.21) < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.55) .470 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .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 .500 (. population from the National Health and Nutrition Examination Survey.200-.210 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .780 (. 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.210-.S.840) 669 687 929 Limit of detection (LOD.31) .680 (<LOD-.950) < LOD < LOD 1.610 (<LOD-1.700-1.850 (.

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

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

Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. McCarthy AR. et al. EPA at: http://www. Richardson JR. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Idel H. et al.27(4):609-614. Xenobiotica 1997. Kunimatsu et al. Garey and Wolff. WHO. 2003. Okuno Y. Miller GW.html. Elwan MA. Kim et al. Leng G. Effects of prenatal exposure to deltamethrin on forced swimming behavior.8(1):18-21.1/15/09 Aziz MH.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Berger-Preiss E. J Reprod Dev 2004. Moniz AC. J Environ Monit 2006. Kim TS. Yamada T.S. Kamita Y.gov/toxprofiles/ tp155. Spinosa HS.8(1):197-202.211(3):188-197. Fourth National Report on Human Exposure to Environmental Chemicals 157 . References Agency for Toxic Substances and Disease Registry (ATSDR). In California. 1999.atsdr. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. and seizures (ATSDR. Toxicol Appl Pharmacol 2006. Kuhn K. et al. Wolff MS. Elwan et al. on immature and adult mice: changes in behavioral and muscarinic receptor variables. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Toxicol Appl Pharmacol 1991.62:101-108. Kim IY. tremor. Wolff MS. Eriksson P. Go et al.. Abell AD. choreoathetosis. Lazarini et al. Pogo BG. Kang IH.. Chen JH. bioallethrin and deltamethrin. 2006. September 2003. 2002). Bernardi MM. Salzgeber SA. In developing rodents. Leng G. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Kuhn KH. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Leng A. McCarthy et al. 2005). Pyrethroid pesticide-induced alterations in dopamine transporter function. Soderlund et al.gov/pesticides/ and from ATSDR at: http://www.35(2 Pt 1):227-237. Eriksson and Fredriksson. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides.. Lee SJ. 2003. 1991. motor activity. 2004.300(3):161-165. fenvalerate. Shukla Y. neurochemical changes in cholinergic. Agrawal AK. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Leng G. 2003. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Idel H.. Toxicological profile for pyrethrins and pyrethroids.27(12):1273-1283. epa. 2002). Kunimatsu T. Lemonica IP.. Lazarini CA. salivation. Wieseler B. 2000. Wang SL. Lewalter J. Go V. 2006). Environ Health Perspect 1999. Additional information about pesticides is available from U. Shaw IC.108(1):78-85. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Neurosci Lett 2001. Garey J. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. 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.. Int J Hyg Environ Health 2002. Regul Toxicol Pharmacol 2002. and striatal dopamine levels in male and female rats.23(6):665-673.. 2002. Neurotoxicol Teratol 2001. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Varoli FM. Thomson BM. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.html. Shafer. Sugiri D. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Zhao RC. Adhami VM. Florio JC.205(6):459-472. Seth PK. Cruz-Casallas PE. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR.atsdr.. Estrogenicity of pyrethroid insecticide metabolites. 2001. Kim HS. 2005). 2006. Sunami O.251(3):855-859. Caudle WM. Yang J. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. 2001... dopaminergic. Biochem Biophys Res Commun 1998. Levsen K.. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Guillot TS. Moniz et al. Fredriksson A. Hu JY. 1998. Bernardi MM.107(3):173-177. and permethrin) in the Hershberger and uterotrophic assays. Ose K. 2003.50(2):245-255. Neurotoxic effects of two different pyrethroids.. 2005). Ranft U.gov/toxpro2. Pauluhn J. et al. Generally. Garey J. Song L. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation.. hypersensitivity. 2005). Neurotoxicol Teratol 2005. Available from URL: http://www. Bull Environ Contam Toxicol 1999. Ray et al.cdc. cdc. Shin JH. Hu et al.

Sargent D. Revised February 25.htm. synergies. Environmental Protection Agency (U.Pyrethroid Pesticides Ray DE. pdf.S.epa. 2005. 5/26/09 U. Sheets LP. Available at URL: http://www.htm. 1992–2001.epa. Environ Health Perspect 2005. EPA).S.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.S. Spencer J.who.usgs. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Shafer TJ. Mullin LS. Toxicology 2002. Crofton KM.186:57-72. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Piccirillo VJ. EPA).gov/ circ/2005/1291/. Available at URL: http://whqlibdoc.38:95-101. and therapy.gov/oppsrrd1/REDs/cypermethrin_red. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Reregistration Eligibility Decision for Cypermethrin. March 2006. Marsh JR.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. U.S. 19962002. Available at URL: http://pubs. Meyer DA.S. Clark JM. Safety of pyrethroids for public health use. 2007.10. Rev Environ Contam Toxicol 2006. et al. Pyrethroid insecticides: poisoning syndromes. 5/26/09 Woollen BH. Available at URL: http://www. Xenobiotica 1992. June 2006b. Pesticide and Evaluation Scheme. Geological Survey (USGS). J Toxicol Clin Toxicol 2000. Soderlund DM. Available at URL: http://www. World Health Organization (WHO).int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Pesticides in the Nation’s Streams and Ground Water. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).pdf. April 2002. Environmental Protection Agency (U. resmethrin.epa. Permethrin. O’Malley M.113(2):123-136.S. Pyrethroid illnesses in California.S. 5/26/09 U. sumithrin synthetic pyrethroids for mosquito control. Lesser JE.22(8):983-991. Forshaw PJ. Environmental Protection Agency (U. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. June 2006a. Laird WJ. EPA). 5/26/09 U.171:3-59.

.. Studies in Germany of 396 children and adolescents (Becker et al. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. representative subsample in NHANES 2001-2002 (CDC. 2003). 2005). Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population. 2003).S.Pyrethroid Pesticides Cyfluthrin CAS No. 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. 2004). Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S.. Baker et al... representative 2001-2002 NHANES subsample (CDC.. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2005). 2006) and 1177 urban adults and children (Heudorf et al. Cyfluthrin is rapidly metabolized and eliminated from the body. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). 2001. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Thus. Fourth National Report on Human Exposure to Environmental Chemicals 159 . Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0.95 µg/L. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. Following an indoor application exposure. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. most of which were dermal and respiratory irritations (Spencer and O’Malley.2 μg/L) in the U. 2006). the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. 2005. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. 2003). Finding a measurable amount of 4-fluoro-3-phenoxybenzoic acid in urine does not mean that the level will result in an adverse health effect.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment.

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

population from the National Health and Nutrition Examination Survey. 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. Fourth National Report on Human Exposure to Environmental Chemicals 161 . Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.

Int J Hyg Environ Health 2006. Rev Environ Contam Toxicol 2006. Olsson AO. Third National Report on Human Exposure to Environmental Chemicals. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Ball M.Pyrethroid Pesticides References Baker SE. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. 2005. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Arch Environ Contam Toxicol 2004. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Int J Hyg Environ Health 2006.206(2):85-92. Heudorf U. Barr DB. Angerer J. Angerer J.13(2):112-119. Hoppe HW. Seiwert M. Heudorf U. O’Malley M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Ranft U. Schulz C. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J.77(1):67-72. Heudorf U. Butte W. Int J Hyg Environ Health 2003. J Expo Anal Environ Epidemiol 2003.109(3):213-217. Idel H. Pyrethroid illnesses in California. Drexler H. Environ Health Perspect 2001. Sugiri D. Leng G. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Int Arch Occup Environ Health 2004. Atlanta (GA). Spencer J. Krieger RI. et al. Bernard CE. Centers for Disease Control and Prevention (CDC).209(3):221-233. Berger-Preiss E. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.46(3):281-288. Hadnagy W.209(3):293-299.186:57-72. Williams RL. Kolossa-Gehring M. Angerer J. Becker K. 19962002.

280-.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin. cis-3-(2.600) .77 (. Biomonitoring Information Urinary levels of cis.150 (.08) .24) 1. ciscypermethrin and cis-cyfluthrin. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.200-.68) .270-.2-dichlorovinyl)-2.1 and 0. In the body.510 (.230) . trans-permethrin.770) .340-.490-.380-.500 (.730 (.200) < LOD < LOD < LOD . 52315-07-8 CAS No.430-. 1999).530 (..680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .10) size 1951 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .262) * * * < LOD < LOD .300-. population from the National Health and Nutrition Examination Survey. 1999).200 (.630) .32) .510 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George. more of the trans-metabolite than Urinary cis-3-(2.610) .2-Dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.520) .790 (.580) 1.730 (. and trans-cyfluthrin. Kuhn et al. < LOD means less than the limit of detection.490-1. Fourth National Report on Human Exposure to Environmental Chemicals 163 . but it can also reflect exposure to cis-3-(2.380-.and trans-isomers.570 (.180) .220-.580-1.54) .21) .690) .710-1.110-.270 (. Kuhn et al.11) .600-1.160 (.630) .460-1.670 (. The chemical trans-3(2.260 (.270 (.740-2. Cyfluthrin.220-.202 (.2-dichlorovinyl)-2.2dichlorovinyl)-2. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.370-.240) .220-. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.370 (. trans-cypermethrin.950-2.900 (.350) .170 (.140 (.220) .630-.470 (.160 (<LOD-.47 (.07 (. and ciscyfluthrin.550) .2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.210-.28) 671 680 518 701 591 957 Limit of detection (LOD.880 (.68359-37-5 Cypermethrin Permethrin CAS No.610) .500 (.110-.68 (.490-.340) .240) .180 (.15) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-. the presence of trans-3-(2. which may vary for some chemicals by year and by individual sample.310) .200-.300 (. 1985. cis-permethrin.280 (.250-. 1985.80) .670-1.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .650-1.470-1.920) 1.S.250 (.960 (.44 (. Generally.680-3.50) .53) .380) .410) .890 (.210) 90th .380 (.440 (.35) 1..160 (.300-.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.330) .28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .330 (.790-1.120-.460-.220-.490-1.740-1.890 (.300 (. transcypermethrin and trans-cyfluthrin.420-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.2dichlorovinyl)-2.740 (. Survey Geometric mean (95% conf.340) .270 (.410) .780) .710) .670-2. but can also reflect exposure to trans-3(2.570-.640 (.400-.2-dichlorovinyl)2.850 (.140 (<LOD-.12 (.630 (.68) .Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.110-.120-.35) .120-.460 (.670-1.210) .200) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.200-.200) .110 (<LOD-.790) . cis-cypermethrin.510 (.600 (.13 (.2-dichlorovinyl)-2.680 (.380-.910-5.790-1.870) 1.740) 1.or trans-3-(2. The presence of cis-3-(2. Similarly.770-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.730 (.700) .155-.2-dichlorovinyl)- CAS No.1.43) .820 (.

800 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.430 (.29 (.370-.11) .340-.170 (. 2006).200 (.560) .750 (. 2006.300 (.260 (.840 (.11) 1.920 (. 2002).890 (.550) .810 (.400-1. Other studies have provided evidence that urinary levels of cis.270-.420 (.290) .250-.320-.710 (.450 (.440-. Lu et al. population from the National Health and Nutrition Examination Survey..510-1.150-.59 (1.67) . In a study of volunteers.270) .410) .750-1. median urinary levels of trans-3-(2. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.250-.2-dimethylcyclopropane carboxylic acid did not increase.2dichlorovinyl)-2.33 (.240 (<LOD-. 2006) and 1177 urban adults and children (Heudorf et al.370-.2-dichlorovinyl)-2. 2002).710-3.130-.12 (.290) .690-1.190 (.640-1.11) .250 (<LOD-.104-.290-.390 (.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.S.500 (.150-.390-.700-2.2-dichlorovinyl)-2. 2003). 2005).14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. Studies in Germany of 396 children and adolescents (Becker et al.200-.150-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.138 (.640-1.12-2.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC. 2005).170 (.380 (.080-.220 (.580-1. 2003).450-1.2dichlorovinyl)-2. post- Urinary cis-3-(2.550 (. urinary levels of cis-3-(2.470-1.220 (.360-1.260 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.31) .2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.140-.300) .880) .550-1.230-.350) .600 (.49) .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .560) 1.190) . 2005).170) < LOD < LOD < LOD .190) .430-1. urinary trans-3-(2. the median and 95th percentile of urinary levels of cis-3-(2.380-.11 (.Pyrethroid Pesticides 2. 2001) showed urinary levels of cis.03) 1. representative NHANES 2001-2002 subsample (CDC.250) 90th .830) .640-.59) ...200) .230-.270) ...2-dichlorovinyl)-2.2-Dichlorovinyl)-2.450-.680-1.59) .300 (. 2006.580) . Cyfluthrin.200-.540 (.37) .and trans-3(2.21) .2-dichlorovinyl)-2.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.780) 1. In a study of urban residents in Germany (Berger-Preiss et al.290 (. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.550) .390-.640 (. 2005).680 (.400 (. 2005) In a small group of indoor pest-control operators.380) . 2004).24) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC..270 (.540) .840 (.530 (.700) .320) .900 (.182) * * * < LOD < LOD .520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .570) .80) .780 (.230 (.340) .260 (.540 (.530 (. In the same residents. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.300) .250) .260) .440 (.160 (<LOD-.370-. Survey Geometric mean (95% conf. 2004.260-.300-. In these volunteers.180 (.230-.590 (.250-..120 (.430-. 164 Fourth National Report on Human Exposure to Environmental Chemicals .S..700) .210-.220) .67 (.350 (.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 .340) .and trans-3-(2.890) .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.550-1. Schettgen et al..250) .2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.280-.640) 1.440-. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al..590) .180-.280 (. 2006).680-1.33) . 2001.440 (..2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.

08-4.59 (1.10) 2.55-3.68) 2.550 (.670) .20 (.410 (<LOD-.68) 1.660) 1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect. 2005).620) < LOD 2.610) 1.37 (1.500) .94 (1.56) 2.and trans-3-(2.60-4.08-6.77 (1.730) .28 (1.03-1.81) 2.50 (1.520) .01) 4.07 (1.97-11. trans-Cypermethrin. Fourth National Report on Human Exposure to Environmental Chemicals 165 .570) 90th 1.4.710 (.860) .2-Dichlorovinyl)-2.01 (1.91 (1.39-5.14-6.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.560 (.830-1.90) 1.54 (1.23 (.470 (.49-5.56 (1.25-3.460-.910-1.2dichlorovinyl)-2. however.440 (<LOD-.2-dichlorovinyl)-2.55-5.07-3.77) 1.76-3.23) 2.Pyrethroid Pesticides application median urinary levels of summed cis.41-14.S.17 (.970 (.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.410 (<LOD-.750) .410-.66) 691 680 518 690 595 954 Limit of detection (LOD.56) 2.25 (1.500-.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .26 (. 2005).520-.64-4. Survey Geometric mean (95% conf.55-4.11-2.03-1.28 (2.20 (.68-2.460-.670) .or trans-3-(2.08) 1.580 (. The maximum post-application urinary levels.2-dichlorovinyl)-2.410-.14-2. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC. which may vary for some chemicals by year and by individual sample.42) 1.60) 1.68) 1.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th . were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.19) 1.500 (.76-4.490 (<LOD-. Finding a measurable amount of cis.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .27 (1.17-1.85) 4.920-1.19 (2.16) 1.800-1.12-6.940 (.66) .480-.11-1.40 (1.49-3.13) .89 (2.420 (<LOD-.4 and 0.95) 3.700) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.19 (3. 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.54) 4.35) 1.43) 2.560 (. < LOD means less than the limit of detection.820) .39 (1.400 (<LOD-.09 (.470 (<LOD-.69) 1.840-1.95) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.530) .42 (2.700-1.22 (1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.84 (1.780 (.20 (.400-.810-1.560 (.49-3.62 (1.490-1.910-1.63) 1.60) . population from the National Health and Nutrition Examination Survey.7) 2.5) 2.17 (.69 (1.760) .56 (1. Urinary trans-3-(2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.41 (1.14) 1. Biomonitoring studies on urinary levels of cisor trans-3-(2.77) 2.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .87 (1.850-1.48) 4.680-1.68-3.63) 1.

3) 2.580 (.31 (2.20-2.470 (.500-.15 (1.540) .15-3.20 (1.970 (.30-6.48-2.56-2.570 (.45-2.610-.00) 1.15) 3.57) 3.22-2.750) .42 (.48 (1.900 (<LOD-1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.770) < LOD 2.07-3.37 (1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .70 (.28) 2.Pyrethroid Pesticides Urinary trans-3-(2.00-5.22) 1.86 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1.35) 1.08 (.75 (1.36) 2.520 (<LOD-.440-.570-.60 (1.480-.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .S.700-. trans-Cypermethrin.700 (.60) 2.850) .15-3.410-.87-3.930-1.34-4.67 (2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.530 (<LOD-.74) 2.34-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.2-Dichlorovinyl)-2.740) .13) 1.87 (1.22-1.720-1.81 (2.19 (1.02-1.89) 2.31 (.33-2.27-2.640) .700 (.65 (2.800-1.800-1.56-5.39) 1.33 (1.47-2.42) 1.07-2.720-1.07) 2.880 (<LOD-1.55 (2.91-11.19) .64 (1.39 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.91) 1.45 (1.560 (.660) .68) 3.470-.15-3.16 (1.56 (1.87) 1.820-2.47 (1.13) .12-1.35 (1.00) 1.530 (.87-8.10) 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 .570 (<LOD-.60) 2.07) 2.91 (1.730) . population from the National Health and Nutrition Examination Survey.87) 1.00) 5.98 (1.36 (1.780 (<LOD-.670) .27-2.00 (1.880-1.880 (.12 (.40-2.31) 1.780) 90th 1.760 (.580) .26 (1.08 (.65) 1.55 (2.47-2.61) 1.29) 1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .41) 1.74) .30-3.44) 2.57 (1.07-1.780) .720 (<LOD-.55 (2.33-1.850) 1.850-3.15) 2.11) .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin. Survey Geometric mean (95% conf.

Bartell S.77(1):67-72. Environ Health Perspect 2001. Angerer J. Int J Hyg Environ Health 2006. Pearson M. Bravo R. Leng G. Hadnagy W. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.Pyrethroid Pesticides References Becker K. Int J Hyg Environ Health 2003. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. 2005.76(7):492-498. Heudorf U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Atlanta (GA). Heudorf U.209(3):293-299. Butte W. Schulz C. Int Arch Occup Environ Health 2004. Ranft U. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Int J Hyg Environ Health 2006. et al. J AOAC 1985. Third National Report on Human Exposure to Environmental Chemicals. Leng G. Heudorf U.205(6):459-472. Berger-Preiss E. Barr DB. Hardt J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Seiwert M.62:101-108. Sugiri D. Berger-Preiss E. Kuhn K. Wieseler B. Centers for Disease Control and Prevention (CDC).68(6):1160-1163. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Hoppe HW. Schettgen T. Biological monitoring of workers after the application of insecticidal pyrethroids. Drexler H. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.209(3):221-233. Lu C.134(1-3):141-145. Drexler H. George DA. Idel H. Bull Environ Contam Toxicol 1999. Idel H. Leng G. Angerer J.206(2):85-92. Heudorf U. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Levsen K.109(3):213-217. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Ball M. Ranft U. Sugiri D. Kolossa-Gehring M. Permethrin and its two metabolite residues in seven agricultural crops.114(9):14191423. Angerer J. Environ Health Perspect 2006. Angerer J. Angerer J. Int Arch Occup Environ Health 2003. Angerer J. Idel H. Int J Hyg Environ Health 2002.

Outside the U. 2005).2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 2006) and 1177 urban adults and children (Heudorf et al.. In the NHANES 2001-2002 subsample. 168 Fourth National Report on Human Exposure to Environmental Chemicals ..2dimethylcyclopropane carboxylic acid formed in the environment..2-dibromovinyl)2. Thus. 2001. in detection of cis-3-(2.39 µg/L.S. Following residential spraying with deltamethrin for malaria protection in Mexico. 2005). mean peak urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. (2004) reported a geometric mean concentration of cis-3(2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dibromovinyl)-2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dibromovinyl)-2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Baker et al.Pyrethroid Pesticides Deltamethrin CAS No.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. in some situations replacing the use of DDT.2-dibromovinyl)-2.. 2004).2-dibromovinyl)-2. 1990). Deltamethrin can degrade to cis-3(2. deltamethrin has been used against mosquitoes that carry malaria.. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dimethylcyclopropane carboxylic acid of 0.2-dibromovinyl)-2. Biomonitoring Information Urinary levels of cis-3-(2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of cis-3-(2.2-dibromovinyl)-2..2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.3-0.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. 2005). Studies in Germany of 396 children and adolescents (Becker et al.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2. urinary levels of cis-3-(2.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2.5 μg/L) than the detection limit (0.

which may vary for some chemicals by year and by individual sample.S.Pyrethroid Pesticides Urinary cis-3-(2. < LOD means less than the limit of detection.1 and 0.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin 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 0.2-Dibromovinyl)-2.1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 169 . population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. Survey Geometric mean (95% conf.

2-Dibromovinyl)-2. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 830 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 700 527 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 170 Fourth National Report on Human Exposure to Environmental Chemicals .Pyrethroid Pesticides Urinary cis-3-(2.S. population from the National Health and Nutrition Examination Survey.

Torres-Dosal A. Angerer J. Angerer J. Kolossa-Gehring M. [online] 1990. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.inchem.htm. Angerer J. Ball M. toxicokinetics. International Programme On Chemical Safety (IPCS). Environmental Health Criteria 97. Butte W. Centers for Disease Control and Prevention (CDC). Carranza C. and genotoxicity in exposed children. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Int J Hyg Environ Health 2006. Int Arch Occup Environ Health 2004. Atlanta (GA). Schulz C. Heudorf U. Available at URL: http://www. Lopez-Guzman OD. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Seiwert M. Environ Health Perspect 2001. et al. Third National Report on Human Exposure to Environmental Chemicals.209(3):221-233. Batres LE. Heudorf U. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.113(6):782-786. 2005. Deltamethrin.77(1):67-72. Environ Health Perspect 2005.org/documents/ehc/ehc/ ehc97. Hoppe HW. Grimaldo M. Drexler H. Int J Hyg Environ Health 2006. Heudorf U.209(3):293-299. Angerer J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. et al. 5/26/09 Ortiz-Perez MD.Pyrethroid Pesticides References Becker K.109(3):213-217.

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

53) 1.298 (.590 (.38 (2.270) .89-71.230 (.507 (.340) 75th .300 (.65-2.340) .630) .05) 1.311 (.490) .220-.830) 90th 1.48-2.69) 3.297 (.54) 1.35 (1.55 (1.29-1.26) 2.300 (.586) .81 (1.240 (.04) .34 (2.373) .69 (1.288 (.760 (.384) .05) .49-2.35 (2.227-.288-.73) 1.160-.355) .18 (1.26) 2.01 (1.300 (.440) .63-3.320) .36) 1.62-6.1) 3.13) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.320 (.700-1.271-.62) 5.820) .49-2.1 and 0.352-.321 (.246-.25 (2.353 (.560-.230-.428-.03 (3.370) .595) .93 (1.250 (.04-5.510-.92-3.450 (.740 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .374) 99-00 01-02 99-00 01-02 99-00 01-02 .314 (.315 (.230-.387) .850) .30) 3.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.340) 1.1) 3.53-3.320) .250 (.320) .390) .27-2. Fourth National Report on Human Exposure to Environmental Chemicals 173 .200-.680 (.49 (1.190-. interval) .210-.430-.45-5.33 (1.8) 3.75 (1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.39) 2.35) 1.23 (2.63 (3.60) .32 (1.292-.570-.470-.28) 1.64) 697 680 524 701 603 957 Limit of detection (LOD.277-.46) .560-.750) .670 (.49 (1.369) .364) .940) 1.78) 1.362) .32 (2.71 (1.12 (.34) 8.25) 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 .260 (.16-1.260 (.247-.200-.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .253-.360) .417 (.810) 1.434) .290 (.33) .270 (.13 (.740 (.S.25 (2.800 (.300) .650 (.190-.52-4.160-.21 (2.510-.38 (2.56-5.840-1.260 (.330) .30 (.292 (.190-.406) .780) 4.330) .27-11.51-3.79) 3.1.800) 1.65 (1.25-4. population from the National Health and Nutrition Examination Survey.83-11.454 (.12) .610) .233-.266-.62-8.260-.33 (2.870 (.960 (.190-.76 (1.210-.530-.25-1.48-2. Survey Geometric mean (95% conf.34-6.530-.238-.1) 3.280 (.520 (.45 (2.230 (.710 (.570-1.226-.14-6.325 (.12) 4.35) 2.990) .250 (.314) .26-2.44) 5.02-6.328 (.830-2.42-2.601) .18 (2.265-.750) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.32-21.41-3.78) 1. Deltamethrin.90) 1.41 (1.52-5.41-2.200-.78 (1.250-.427) .550-.180-.240 (.30 (1.640 (.820) .27-2.320) .490-.590-.750-1.43) 3.710 (.430-.51-6.276-.273 (.41) 3.730 (.78) 6.560-1.420) .295) .25-7.350-.50 (2.700 (.850) .336 (.72 (1.46) 2.35) 2.16) 1.86 (1.267 (.600 (.620-1.230-.

320) .350) .410) .190 (.190-.370-.15-2.61-2.09) 3.09 (.270 (.83) 1.860-1.200-.S.173-.510 (.272) . interval) .330) 75th .48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .02 (2.380-.220-.49-2.640 (.280) .810) 1.11 (.73) 1.03-1.60) 1.37 (1.21 (1.860 (.43 (1.37) 1.238-.280) .81 (1.240 (.62) .730-1.580 (.67) 1.91 (2.534) .700-1.240-.670) .760) .202-.36 (1. population from the National Health and Nutrition Examination Survey.280 (.53 (1.11 (.0) 3.490 (.440-.225-.590) .423 (.35) .930) 1.446) .590) .25-2.75-8.420-.720) 90th 1.740) .210 (.64-5.329) .160-.13 (.328) .323 (.530-.510 (.32 (2.40) 2.362 (.17-1.730) .94 (1.840-1.03 (.35-3.21-4.550 (.560 (.271-.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .227 (.95) 1.550 (.02-1.370 (.540 (.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 . Deltamethrin.400) .530-.35) 1.480-.04 (.960-1.480 (.250 (.220 (.316 (.311 (.400-.216-.19-6.270) .309) .730) .13-1.80) 4.280-.210-.178-.07-5.387) .07) 2.67 (1.25) 2.229-.650) .329) .372) .860-1.510 (.210 (.96 (1.930) .380 (.670) 3.224-.05-3.27) 1.590) .09-2.270) .74) 3.41) 1.09-2.677) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.390-.290-.460-.630) .300-.330) 1.264 (.240 (.49 (1.640 (.365) 99-00 01-02 99-00 01-02 99-00 01-02 .150-.230-.60-4.500) .410-.450 (.84 (1.378 (.274-.401) .39) 1.580) .490-.51-7.88) 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 .91) 9.13-1.570) .00) 1.226-.25-5.330) .52 (1.610 (.550 (.49) 1.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.240 (.253) .400-.63-3.250 (.350 (.230) .321-.490 (.16-4.17 (.270-.91-4.280 (.234 (.86 (1.190-.357) .309 (.63) 1.43-64.290) .83 (1.48 (1.90) 3.312 (.200-.43) 1.270 (.310) .278) .290) .73-4. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.72 (1.91) .230-.88-5.460-.40 (1. Survey Geometric mean (95% conf.250) .261 (.44) 2.36-6.43 (2.330 (.00) 5.299-.54 (1.240-.04 (3.41-4.22 (1.275 (.10 (2.19) 2.00) 1.330) .280 (.440-.240-.200-.55) 3.246 (.44 (1.300-.750-1.35 (1.52) 2.19 (2.49) 3.55 (1.590-1.67 (1.335-.274 (.240 (.272 (.437) .06-3.200-.720 (.62) 1.440-.240-.261-.

GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ortiz-Perez MD. toxicokinetics. Int J Hyg Environ Health 2006. Exposure to indoor pesticides during pregnancy in a multiethnic. Leng G. Becker K. Leng G. Fourth National Report on Human Exposure to Environmental Chemicals 175 . et al. Atlanta (GA).111(1):79-84. Idel H. Lu C. Sugiri D. Environ Health Perspect 2006. Grimaldo M. Godbold J. Centers for Disease Control and Prevention (CDC).206(2):85-92. Hadnagy W. Carranza C. and genotoxicity in exposed children. Hardt J. Seiwert M. Levsen K.Pyrethroid Pesticides References Baker SE. Sugiri D. Ball M. Bravo R. Int J Hyg Environ Health 2002. Berger-Preiss E. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Int J Hyg Environ Health 2003. Obel J. Barr DB. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Batres LE. Lopez-Guzman OD.46(3):281-288. Int Arch Occup Environ Health 2003. Angerer J. Deych E. et al. Arch Environ Contam Toxicol 2004. Berkowitz GS. Pearson M. 2005. Biological monitoring of workers after the application of insecticidal pyrethroids. Environ Health Perspect 2003.113(6):782-786.205(6):459-472. urban cohort. Ranft U. Ranft U. Lapinski R. Kolossa-Gehring M. Olsson AO. Environ Health Perspect 2005.114(9):14191423. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Third National Report on Human Exposure to Environmental Chemicals. Hoppe HW. Liu Z. Angerer J. et al. Barr DB. Torres-Dosal A. Idel H.209(3):221-233. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.76(7):492-498. Berger-Preiss E. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Bartell S.

or other substances containing antimony is another means of exposure.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 .110 (.130 (.200-.310) .160-.240) .220 (.133) * .130-.120-.390-. enamels.350-.260 (.270) .440) .400) .230) . solder.280-.130) .120-. Workplace exposures can occur at smelters.170-. castings. which may vary for some chemicals by year and by individual sample.160 (.131-.197) .130) < LOD .200 (.130 (.490) .S.230) .120) .490 (.330-.090-.04.154) .340 (.260 (.190-.230 (.190) .400) .180 (.120-.04.430 (.460 (.390) .350-.140 (.250 (.280 (.220) .079-.169 (.128 (.340) .120 (. 0.093 (.280) .270-.125 (.117-.320-.080) .200) .230) .230-.120 (.154-.120 (.330 (. and +5.220-.300) .210 (.126-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.600) .132 (. It is also used in paints.070 (<LOD-.710) .141-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. ammunition. population from the National Health and Nutrition Examination Survey.110) .190) . storage batteries.150) .190 (.145 (.07.135) * .140) .280-.190-.270 (.320-.440) . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.310-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.180 (.122 (.220-. 01-02.070 (<LOD-. Antimony enters the environment from natural sources and from its use in industry.210) .160) .103) .164-.150) . and refuse incinerators that process or release antimony.184) .300) .250) .140 (.160-. metal bearings.156-.300 (.300 (.180 (.150-.190) .140) .220-. < LOD means less than the limit of detection.280) .290-.400 (.260 (.114) .320 (.430 (.240 (.130-.180-.220-.570) .088-.460) .190-.230 (.250-.250 (.220 (.160) .360) .130-.130) .230-.410) .190-.080) . +3.119-.110-.250 (.134 (.207) .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 (.140) . coal-fired plants.280-.350) .136-.260-.130-.090 (<LOD-.176 (.270 (. ceramics.150) 90th .123 (.240 (.150-.320) .120-.120-. 0. respectively.350 (. Stibine is a metal hydride form of antimony used in the semiconductor industry.130 (.180-.087-.100-.260) .108 (.130 (.240-.320) Total .160-.160 (.320-.300-.220-.190 (.144) .200-.150-.250-.095 (.143 (.148-.370) .300-.210) .270 (. water.330) .290-.390 (.180) .470) .190-.330 (.109-.280-. from air and drinking water.150 (.280) .120 (. and excretion of antimony vary depending on its oxidation state.070-.350 (.120-.190 (.160) .210) .126 (.170) .190) .136) * .360-.134-.170-.090-.160 (.350 (. and 03-04 are 0.210-.146 (.240 (.120) .170 (.470) .200 (.220) .500) .137) .390) . sheet and pipe metal.350) . Urinary excretion appears to be greater for pentavalent antimony Urinary Antimony Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.115-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.390) . People are exposed to antimony primarily through food and.130-.200) .180 (.330-.142 (.400-.300) . distribution.310-. and pewter.220) 95th .360 (.157) . The absorption.240-.105 (.Metals Antimony CAS No.180) .230-.300-.560) .240 (.170-.210) .510) .230-.200 (.110-.120) .220) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.130 (.350 (.250-.160) .200 (.112-. to a lesser extent.160) .310 (.180 (.117-.260) .150-.132 (.200-.310) .160-.120-.130) .220-.210-.150 (.230-.310 (.190 (.360) .160) .100-.330 (.270 (.390) .180-.130 (.440 (. see Data Analysis section) for Survey years 99-00.290 (.470 (.400 (.330) .430 (. fireworks.175 (.140) .150) .280-.137) .260-.090 (.120) .390-.390-.310 (.180-.170-.260) .130 (.110-.120-.115) .098-. interval) .370-.140 (.180 (.200) .130 (.100 (.161) .190) .270) .200-.080-.530) .120-.170 (.210) .410-.400 (.340 (.310 (.119) .170-.400) .150-.178) .420) .110-.330) .230 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .190 (.500) . and glass.250-.140 (.140-.210 (.330) . 7440-36-0 General Information Antimony is found in ores or other minerals.180-.090) 75th .140) . and 0.128 (. and as a fire-retardant in textiles and plastics.130-.150 (.130-. It is used in metal alloys.100 (.140) .320 (.350) .120 (.280 (.240 (.410) .200 (.460 (.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 .108-.280) .154) .080 (<LOD-.099 (.200 (.320-. Dermal contact with soil.200) .158 (.100) .145) Selected percentiles ( 95% confidence interval) 50th .460 (.360 (.350-.095-.350) .

161) .173 (.115) .256 (.267-.188) .298 (.209) .265-.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 .320) .417) .320-.195-.134) ..164) .128-.194-.143) 90th .144-.183) .104-.130 (.338 (.159-.235-.414) . abdominal pain.214) .149-.245) .102-. and route of exposure (Elinder and Friberg.069-. and kidney have been demonstrated in high dose animal studies depending on the dose.130) .095-.106-.078 (.139 (.300) .278 (.115 (.225) .438) .135) .120 (.086 (.126-.118 (.121) .228 (.080 (<LOD-. liver.126) .108-.146-.247) .226 (.447 (..143) .357) .233) .163 (.480) .320-.391) .265 (.133) .136) . 1986).333 (.118 (.244-.167 (.107-.250 (.098-.176 (.152) .250-. resulting in hemolysis with abdominal and back pain (Dernehl et al.122 (.317) .105-.115-.124-.196 (.391) .238) .280-.206-.117-.471 (.104-.175 (.255) .233 (. Ming-Hsin et al.209) .109-.185-.120 (.068-.143) Selected percentiles ( 95% confidence interval) 50th . species.147-.318-.176-.333) 1132 1334 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . and ulcers (Werrin.191 (.220) .138) * .333-.208-.167-.250-.129 (.181) .129) .276 (.129) * .400 (.313-.069-.148) * .061-.200-.132) .364 (.108 (.179-.333-.176 (.125 (.164 (. 1944).193) .278) .S.099-.103-.115 (. 1954).352 (.203) .317) .115-.074 (.230) 95th .200) .187) .444) .193 (.147) .500) .239-.146-.126 (.160 (.075 (.127 (.277 (.137 (.100 (. 1962).114 (.085) .281-.317) .178-. 1973). and gastrointestinal symptoms such as vomiting.229-.263-.429 (.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. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.098-.310) .741) .238 (. diarrhea. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.185 (.241-.156 (.092-..082) .119-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.198) .272) .081 (<LOD-.308) .068 (.113) .112 (.146) .253-.Metals than for trivalent compounds (Elinder and Friberg.266 (. population from the National Health and Nutrition Examination Survey.741 (.267 (.343 (.124 (.352) .089) .224 (.122 (.425) .131-.421) .156-.161) .123 (.079 (<LOD-.125-.071-.250 (.109 (.132 (.164-.095-.248) .181) .098) .267) .152) .115 (.471) .333-. myocardium.112-.268) ..364 (.192) .081) .138-.338) .444) .173-.230-.163 (.129 (.170 (.288 (.108-.143) .124) .271-.075 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.109 (.385 (.099-.200-.171) .096-.417) .145) . Acute antimony poisoning may cause a metallic taste.167 (.310 (.204-.127) .076-.124-.238) .107-.200-.153-.173 (.209 (.111 (.138 (.192 (.111-. and eyes.373) .130) .294) Total .092) .151) .131) .233-.127) .255-.295 (.241-.211) .135 (.236 (. Inorganic antimony salts irritate the mucous membranes.263 (.242-.333 (.338 (.189 (.154-.213 (.113-.121 (.333-1.405) .127) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .146-. 1995). Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 .082 (<LOD-.121 (.259 (.087) . 1988.250-.321) .195-.250-.250) .269 (.108-.225 (.116-. skin.138-.084) .140) .357-. 1953).186) .080 (.253 (.195 (.209-.117-.150-. 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.148-.248-.082) .153 (.205-.227-.119-.086) 75th .430) .114 (.135) . interval) .261) .178 (.300) . 1986).130) .127) .199-.107-.192-.333 (.120 (.097-.257) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.172-.485) .139 (.320 (. 1958) and occupational exposures (Briegner et al.280 (.119 (.310) .123) .113-.308-.217 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.135 (.371 (.103-.131 (.380 (.159-.181) .150-.162-.188-.315) .159-.208 (.203) .140) < LOD .185 (.143 (.102-.076-.228-.429) .727) .077) .106-..114 (.167 (.207) .116 (.300 (.318-.173) .117-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.135) .222 (.228 (.30) .112 (.286 (.120 (.320 (.333) .149) . Histopathologic inflammatory and degenerative changes in the lung.182 (.148-.

48:93-97. J Clin Pathol 1998. Delves HT. Ju-Sun P. Lenert G. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. and hydrogen sulfide. Ming-Hsin H. 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. Earlier measurements in general populations (Minoia et al. Sabbioni E. 26-42. Atlanta (GA). 1987). Fuchs A.76:432436. Mayne P. Sci Total Environ 1994. Roland H. and 2003-2004.. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Bailly R. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Wu M-T. Nau CA. Environ Health Perspect 1998. Trace element reference values in tissues from inhabitants of the European community I. and antimony in optoelectronic industry workers. Cheng-Wei L.521-523. indium. VI.106:33-39. Industrial antimony poisoning. New York: Elsevier. Paschal et al. Pilgrim L. Schaller KH. or exposure differences. J Occup Environ Med 2004. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Liao Y-H. Yang C-Y. Carelli G. Int Arch Occup Environ Health 1995.. arsenic. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Third National Report on Human Exposure to Environmental Chemicals. 1998. respectively. Antimony. Kentner et al.. Dezateux et al. Matthews T.e. 1990. O’Regan M.76(2):103-115. 1994) have reported values slightly higher than those in this Report. Industrial Medicine 1944. Information about external exposure (i. Br J Ind Med 1991.. Cordasco EM. Nordberg GF. pp. eds. Kiberd B. Caroli S. Dernehl CU. Dunkelberg..cdc. even when exposure levels were below workplace air standards (Bailly et al. Antimony trioxide is rated by IARC as a possible human carcinogen.S. References Berman JD. Stocks J. 2nd ed. In: Friberg L. Ho C-K. Chia-Yu H. Antimony in blood and urine of infants. Dezateux C. Kuo-Juie Y. Biological assessment of exposure to antimony and lead in the glass-producing industry. Mahieu P.46:931-936.64(2):182-185. Konings J. Schacke G. Lauwerys R. Gebel TW. population. Element reference values in tissues from inhabitants of the European community. Review of elements in blood. et al. 1997). Int Arch Occup Environ Health 1987. Arsine. Centers for Disease Control and Prevention (CDC). Liao Y-H et al. Piatnek DA.atsdr.. gallium.59:469-474. 1998) or compiled reference ranges (Hamilton et al. Iavicoli I. 20012002. HH. Delves HT. Biomonitoring of a worker population exposed to low antimony trioxide levels. et al. Mayer P. 1998). Vouk VB. 2004.. Petrucci F. 1995. Alimonti A. 1991. Stasney J. Wade A. Chen J-R. stibine. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Briegner H. 2002. clinical efficacy. Bolten C.13:361-362.10(3):560-586. Pietra R.. Semisch CW. Yu H-S. Elinder CG. Minoia C. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Leinemann M. Hamilton EI. Apostoli P. and a drinking water standard has been established by the U. environmental levels) and health effects is available from ATSDR at: http://www. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . EPA. Luedersdorf R. 2005. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Costeloe K. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Biological monitoring of exposures to aluminum. Weltle D. Kentner M.51:238-240. Iavicoli et al. J Trace Elem Med Biol 2002.html. 1986.. gov/toxpro2. Urinary antimony in infancy.. Buchet JP.158:165-190. External and internal antimony exposure in starter battery production. Chest 1973.67:119-123. Sabbioni E.16: 33-39.. Friberg L.. Pulmonary edema of environmental origin. Gallorini M. Arch Dis Child 1997.)1954.Metals to antimony have been established by OSHA and ACGIH. Suchenwirth R. et al. Stone FD. and future strategies. Cullen A. Chin Med J 1958. Stead FM. which may be due to methodologic. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Handbook on the toxicology of metals. Industrial Medicine and Surgery (Dec. Ludersdorf et al. Rev Infect Dis 1988. Chemotherapy for leishmaniasis: Biochemical mechanisms. Skulsukai G. Van der Venne MT. Shao-Chi C. Pozzoli L.

et al. Environ Res 1998. Renes LE. Werrin M.76(1):53-59. Jackson RJ. Sampson EJ. Trace metals in urine of United States residents: reference range concentrations. Chemical food poisoning. 27:38-45.95:89-105. Ting BG. Antimony poisoning in industry. Morrow JC.99-108. Fourth National Report on Human Exposure to Environmental Chemicals 179 . blood. and serum of Italian subjects. Paschal DC. Industrial Hygiene and Occupational Medicine 1953. Pirkle JL.Metals in urine. Sci Total Environ 1990. Quarterly Bulletin of the Association of Food and Drug Officials 1962.

The United States no longer produces arsenic from mining but imports about 22.90-8.80) 6.5 (23.6) 618 722 1074 Limit of detection (LOD.6-141) 53.1-40.40) 7. black.1) 1281 1276 03-04 03-04 03-04 9.2 (51. In nature.3-111) 78.12 (6.97) 8. Since the 1940s.0 (15. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. arsenites.Metals Arsenic CAS No. Gallium.10-10. 2001).90-8.90-11. gaseous hydride manufactured in small quantities for use in the semiconductor industry. and. as alloy in metal bearings.5) 66. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.5 (36.70-9. aluminum.2 (12.0 (22. were used as treatments for syphilis.50 (8. +3 and +5).12-10. meats.0 (11.34-9.00 (6.9-34.1 (32. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9) 68.2 (41. the smelting of copper. copper arsenates. retaining walls.8) 7.3-15.2) 46.8) 34.66-8. and arsenates (oxidation states of -3.20 (8. particularly arsenic trioxide.1) 7.27) 9. lead.9 (17. and play sets. see Data Analysis section) for Survey year 03-04 is 0.90) 75th 16. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. 2005).90 (5.90-14. Although it is still widely used in the United States. and as homicidal poisons.000 metric tons annually.29 (8. such as arsenopyrite (FeAsS) and realgar (As4S4).S.1 (38.10 (6. lead hydrogen arsenate.8) 17. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.1) 15. and gray forms).2-20. ocean and fresh waters.5 (14.70 (6.9) 21.4) 60. grain.90 (7. to a lesser extent.90) 16. and indium arsenides are used in the semiconductor industry. Also. mental disorders.5) 41. and as a cosmetic to lighten complexion.2-93.6-35.9-62.0 (14.7-95. from coal burning.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. mostly for use in wood preservation (ATSDR.41 (7. Arsenic is measurable in most soils.5 (34.5 (40.8) 30. Arsenic trioxide (As2O3. or rarely as elemental metalloids (yellow. referred to as inorganic arsenic compounds. alloys.6) 11.8-61. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.4) 40. trimethylarsine oxide.74.90-7. psoriasis.6-43.19-9.4-65. arsenic compounds. Various arsenic compounds were used in paint pigments and for tanning animal hides.5) 95th 65. Before the 20th century. and produce.80-9.7) 65.10-7.34-10. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.5-19.10) 10. to a lesser extent. Water sources contain mostly inorganic arsenate.55 (7.5) 43.7) 24. 180 Fourth National Report on Human Exposure to Environmental Chemicals .1) 290 725 1542 03-04 03-04 9.7 (11.4 (48. and arsenosugars. and in lead-acid storage battery grids.2) 15. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.4 (24.50-14.6 (9. population from the National Health and Nutrition Examination Survey.4 (7.7) 90th 37.2-17.0-19. Survey years 03-04 Geometric mean (95% conf. Arsenic trioxide is approved to treat acute promyelocytic leukemia. cancers.00-9.4) 13.84) 8.8-77. and foods. cacodylic acid. sodium arsenite.5-41.5-178) 46. solders.13-8.6 (15.25-9.7-83. In the last century. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.8 (48.57) Selected percentiles ( 95% confidence interval) 50th 7.84) 8.2 (13.30 (7.6 (13.5-52. it is found in over 200 crystalline or mineral forms.0 (43.4 (26. semiconductors. General population exposure to inorganic arsenic can occur through consumption of drinking water and.0-60.2-61. arsenocholine.8) 33. though in some locations arsenite may be prevalent (WHO. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.9 (8. interval) 8.9-46.30) 17.02-8.4 (31.8) 29.3) 10.1-18.8) 7. pesticides.80 (5.77) 6.08 (5. Arsine (AsH3) is a reactive.3-19.6 (32. Arsenic and its compounds have had many uses in the past and present as medicines. and other metals.90 (7.30 (6. arsenic as elemental metalloids may be used in some ammunition.70) 8.

interval) 8. shellfish.33-10. Tseng.47 (7.4) 54.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.28-7. 2001). 2001).7 (11..66 (7. arsenic does not show biomagnification in the food chain (WHO. 2007. 2003.13) 8.76 (6.4 (24.32 (5. dose level. Survey years 03-04 Geometric mean (95% conf.24 (7. Children may have additional exposures from ingestion of contaminated soils (e. In aquatic organisms.0) 33.61 (7. Arsenate is reduced in the body to arsenite (oxidation state +3).7 (25. 2001). with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.0-69.0 (17.06 (4. The semiconductor dopants. and contact with CCA-preserved wood structures. 2001). WHO.6) 45.2-46.5-17. 2001). NRC.0-38.04) 7.93-8.58-10.3-53. Direct exposure to DMA and MMA may result from use of the two pesticides.2 (12.6 (17.2) 90th 30. have caused clinical arsenic poisoning.0-26.9) 53.88) 7. EPA. inorganic arsenic is widely distributed within the body. trimethylarsine oxide (TMAO).44) 6.2) 40.5) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 8.51) 75th 14. WHO.9-56. gallium arsenide and indium arsenide. as observed in Bangladesh where millions of people have been exposed.18 (5.10-16.1) 58.8-32.8) 27.4-64. are used in enclosed ultraclean operations within the semiconductor industry.5) 17.64 (7. Steinmaus et al.1 (14.30-9. 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.31 (6.0) 42.g.5 (9. Inorganic forms of arsenic demonstrate high acute toxicity.66-8.8 (11. Extremely high groundwater arsenic levels.2) 15. In aquatic sediments.40) 8.7) 95th 50. 2001).S. 2007..8-62. U.7) 28. 2001). selenium.99-9.8 (27. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. 1988).0) 26.. 2007.3 (24.4 (26.4 (11. Smoking tobacco is also a source of inorganic arsenic.7-35.10-8.3) 6. mine tailings).23-7.1 (11.59) Selected percentiles ( 95% confidence interval) 50th 7. Fish. cacodylic acid and monosodium methyl arsenate.6 (35. 2006. 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. 2001.0-18.96) 12.41) 6.7-34. Though modest bioconcentration occurs in some aquatic life. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.4 (12.4 (42.2-15.7 (9. and folate status (Chen et al.75 (5.07-9.0) 12.8 (12. EPA’s maximum contaminant level (Hughes.81-9.1) 24. arsenocholine.50 (6. After absorption.93-9. 2001).3) 9.3-62.. Gamble et al. and arsenosugars. organic arsenic can be converted back to methylated and inorganic arsenic. so exposure to the general population is extremely limited.1) 7.47 (6.8 (21..3-41.12-10. though some reduction may occur in the gut prior to absorption. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. age.4 (40.8 (20.4) 32.38-10.1) 6.88 (5.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . and some other seafood can contain organic forms of arsenic including arsenobetaine.S.9) 13.33 (6. Chowdhury et al.7-18.5-120) 40.11 (5. but is poorly absorbed dermally (WHO. kelp. 2006.6 (10. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.86-17.8-75.25-9.9 (45.8) 22.35) 7.5) 290 725 1542 03-04 03-04 8. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.7-17.01) 7.47-6.S.20-9. dust.04 (5.0 (31. population from the National Health and Nutrition Examination Survey.44-11.25 (6.75) 13.1-36. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.3-64. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.7-188) 27.0) 14.1) 8..00 (6.01) 11.66-8.3 (27.0) 1281 1276 03-04 03-04 03-04 8.6-17.45) 5. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. 2001.

which may vary for some chemicals by year and by individual sample. hypertension..50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Chronic elevated arsenic intakes have been associated with diabetes. can cause peripheral sensorimotor neuropathies. arsenic trioxide) includes hemorrhagic gastritis with nausea. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. WHO.10 (<LOD-1.. WHO. and production of glutathione may be affected as well. gluconeogenesis. 182 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey year 03-04 is 1. and childhood neurodevelopmental effects in observational human studies. Acutely. NRC.50) 621 725 1078 Limit of detection (LOD. 2001). food residue.S. leading to a decrease in adenosine triphosphate energy production. 1998. Chronic arsenic exposure in humans is considered to be a cause of skin. 2001). U. 2007. 2007). and diarrhea.20 (<LOD-1..10 (<LOD-1. With chronic exposure. interference in signal transduction pathways. 2001). Arsenic has many actions demonstrated in cellular studies.10 (<LOD-1. lung. 2001. hyperkeratosis. hematocytopenias. Bredfeldt et al.EPA has established drinking water..g. 2006) or when exposure occurs in smokers (Chen et al. < LOD means less than the limit of detection. 2001. 2004. 2007. substitution in phosphate metabolism.80) 1.50) 1. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.60) 1.. Bangladesh. but additional or confirmatory research is needed (Kapaj et al. cytotoxicity. 2004).S.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Raml et al. 2000.. respectively. apoptosis.30) 1. 2006. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.20 (<LOD-1. and hyperpigmentation of the skin (NRC..60) 1.. The U. 2001). Such actions may lead to decreased energy production. 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. 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. Survey years 03-04 Geometric mean (95% conf. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. WHO. including inhibition of numerous enzymes.. Taiwan. and bladder cancer (IARC. and it also will inhibit succinate dehydrogenase. some of these effects may take years to develop. The organic forms of arsenic occurring in seafood have little known toxicity. Chronic human intake of arsenic at less than acutely toxic doses.0. cell transformations. including drinking water sources with elevated arsenic levels (e. 2001). Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. and endothelial injury (Kumagai and Sumi.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.EPA.g.10 (<LOD-1. Chile). noncirrhotic portal hypertension. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. Although arsenate is reduced in the body to arsenite. renal failure. Cohen et al. drinking water have not been associated with increased cancer rates (Schoen et al. 2001). and by uncoupling oxidative phosphorylation (NRC.S. vomiting. which can lead to dehydration and shock. fatty acid oxidation.10 (<LOD-1. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 2006.20 (<LOD-1.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. hepatotoxicity. Cardiac arrhythmias. 2006. WHO. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.20 (<LOD-1. peripheral vascular disease. increased oxidative stress... NRC. Studies of arsenic at levels typical of U. and altered gene expression. and DNA repair inhibition (Cohen et al. 2004). Cellular glucose uptake.S.

2000).00) 1. Valenzuela et al.. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al..S. In animal studies. 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. 2001). 2007.18 (<LOD-3. 2006. 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.80 (<LOD-4. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.41) 3. DMA produced bladder cancer in some chronic rat studies (Cohen et al. 1999. Calderon et al. 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 3.61 (<LOD-3.33 (<LOD-3. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.75 (<LOD-2. arsenic has been fetotoxic and teratogenic.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.69 (<LOD-3. had decreased since the prior 1990– 1992 survey. Meza et al. Offergelt et al. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. In the German Environmental Survey III of 1998.33 (<LOD-3.. Additional information about external exposure (i. 2006)..18) 3.. 2008).. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.19) 3.. and the FDA has established a bottled drinking water standard. population from the National Health and Nutrition Examination Survey.75 (<LOD-2.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2008. median urinary total arsenic levels in 4052 adults varied with seafood intake. Caldwell et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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. 2004.S. 1986). 2007. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.. although urinary arsenic levels were not associated with CCA contact (Shalat et al.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2006). Survey years 03-04 Geometric mean (95% conf. 2006. Pellizzari and Clayton. In a Nevada town where groundwater levels were naturally elevated.. 2003. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. but generally only at maternally toxic doses (WHO. Shalat et al. 2000.S. Consequently.. population (Rubin et al.. 1999. Levels of total urinary arsenic in the U.. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al. 1999)... Though CCA-treated wood contains several thousand times more arsenic than untreated wood.. 2008). 2006. Pellizzari and Clayton. 2006).70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2... 2001).Metals compounds. 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.50) 1.. environmental levels) and health effects is available from ATSDR at: http://www. 1998. Fourth National Report on Human Exposure to Environmental Chemicals 183 ... 2001). WHO.cdc.S. Shalat et al. 2004. population in NHANES 2003–2004 (Schulz et al. Compared with this Report. 2006).atsdr. Josyula et al. gov/toxpro2.04 (<LOD-3. Vahter et al.html.e. 1992. Pellizzari and Clayton 2006). and were about two-fold lower than those for the U.. Caldwell et al..

. 4.871-1. Blom et al.7) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (14. 1.0 (27.0 (26.800-4. WHO. population showed a higher contribution of arsenobetaine (Caldwell et al.70-21. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.11-1.g. 1996.. and duration of exposure are also considered important. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.80 (.900-1.5) 292 728 1548 03-04 03-04 1.1-51..40) 75th 5. In the late 1980s.6 (25. 2005. 2000. 2003).7) 15. 2008). dermal keratosis.S. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.3 (21. 2008). Sun et al.43-1.66 (1.48-2. Valenzuela et al.1) 18.70) 6. see Data Analysis section) for Survey year 03-04 is 0.S. and two methylated metabolic products.29 (1.2-35.. Caldwell et al.68) . 1985..0-23. 2008.00 (1. China..50) .80) 1.800 (.9) 13.0) 4.83) Selected percentiles ( 95% confidence interval) 50th 1.40) 5.30) 2.70 (3.50) 90th 16. population in the NHANES 2003–2004 subsample.1) 45.400-.2-38. population (Sun et al.. When seafood intake is avoided. geometric mean levels were about 70-fold higher than for the U. Tseng et al.4) 31.8. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Individually measurable species resulting from inorganic arsenic exposure are arsenate.00-12.00-4.10) 4.3) 35... Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. 2007)..70 (5.S.45 (1. which may vary for some chemicals by year and by individual sample.62) 2.00) 3.55 (1.3) 95th 35.70-21.80-5. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.S. 2005.8-50. arsenobetaine.28) 1. For residents of Inner Mongolia. 2008.1-25. Caceres et al.60) 1.9-23. Caldwell et al. 2001).6 (11. 2000.7-22. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.40-6. 2005. Also.5 (26. Aposhian et al. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. population (Ahsan et al. 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. and 0.20-190) 31.8 (12.3 (9. The higher percentiles of total urinary arsenic levels in the U.20-3. Survey years 03-04 Geometric mean (95% conf.500-1.. 2000. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. Pellizzari and Clayton. and TMAO were detected in only 7.7 (13.60-3. methylation capacity.700-1. respectively. < LOD means less than the limit of detection.00 (.800 (.20 (1.50) . DMA and MMA. 2007) with higher levels of arsenic in the drinking water.30) 10..90-7. 1990.4 (16.20 (.19 (.20 (4.4-35. vasospasm.1-94. and other factors such as nutrition. In most human studies.10) 8..6-44.800-1.700-1. Arsenate.20) 18..00-6.7 (21. interval) 1. Chowdhury et al.900 (.10 (4.9 (7. population from the National Health and Nutrition Examination Survey.50-6. 2001.e..80 (3. when seafood organic arsenic is subtracted).6.0) 29. Measurable organic arsenic species in this Report are three biologically generated environmental forms. arsenocholine. MMA. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.800) 1..90-29. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.93) 1. Caldwell et al. 2006).6 (13.Metals other areas of the world (Ahsan et al.8 (17.8-40.30 (2.20 (2.20-25..31-1. arsenocholine.05) < LOD .74 (1..5) 32.600 (.3) 1284 1284 03-04 03-04 03-04 1. and TMAO.6.S.80 (4. After recent seafood ingestion. in NHEXAS 1995–1996. with DMA.4.37 (1. 184 Fourth National Report on Human Exposure to Environmental Chemicals . In the residents of a Chilean town who consumed water with high levels of arsenic..17-1.5) 29.4) 23. arsenite. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.30 (1.00-1. 2008).20) 3. Some noncancer effects of arsenic (e.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) 7. arsenite.3-39.9 (6.2 (6.40-7. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. 2008).5) 621 725 1078 Limit of detection (LOD.3% of a representative sample of the U. These associations are stronger at higher urinary levels.8) 35.

00 (1..80-153) 17.81 (4.7) 9. In recent years.76-27.13-39.612-1.14 (1..4) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1.65 (1.45) 1.9 μg/L. interval) 1.1 (26.5-20. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.44 (1. Sun et al.901-2.15-4.5) 26. Offergelt et al.531 (.05 (.62-6.0-36.36) 2.9 (13.21) 5.3 (10.3) 1284 1284 03-04 03-04 03-04 1.0 (9.72) 12.50-7.30) 1.64-29.4 (11.400-. Vahter et al. 2008). WHO.15-1.2 (4.18-1..43) 14.78 (3.1-36.47 (2.5 (18.79 (1.93 (1.67) 1.51-2. population for the sum of inorganic related species was 18.6 (9.833-1. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.5) 17. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30-1. which is below the ACGIH BEI (Caldwell et al.91) 90th 16..55) 1. Survey years 03-04 Geometric mean (95% conf.80) .877 (.1-18. 2003.3 (10.8) 29.28) 1. The 95th percentile of the U. 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.4 (24.959-1.61-6.16 (.Metals as with DMA.7) 17.83) 8.6-46.88) 2.12) < LOD .39-3.9) 32. Information about the biological exposure indices is provided here for comparison.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.91 (4.68 (1.29 (4.638) 1.58 (3.83) 2.78-5.786-1. 1998.15-1.67) 4.82) Selected percentiles ( 95% confidence interval) 50th 1.32-7. 1986.. Caldwell et al.S.S.4-82.3-24. 2008).43) 75th 5.2 (12.2 (12.19-2..40) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.51) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-18.3) 95th 29. population from the National Health and Nutrition Examination Survey.47 (1.10 (.909-1.50-15. 2001).6) 19.82) 4.9) 14. Fourth National Report on Human Exposure to Environmental Chemicals 185 .9 (25.00 (3. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.40 (1. 2006.2 (13.53 (. 1992.4) 32..11 (.4-28.6-32.70) 5. 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.73-6.25-7.5 (18.54 (1.1) 26.37-2. not to imply a safety level for general population exposure.938-1.29-14. 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.05) 1.6 (6.88 (5. 2007).4) 292 728 1548 03-04 03-04 1.4-21.25 (.6-29. 2001).. 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.7) 30.4) 13.

6. see Data Analysis section) for Survey year 03-04 is 0. Survey years 03-04 Geometric mean (95% conf. 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. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. Survey years 03-04 Geometric mean (95% conf. 186 Fourth National Report on Human Exposure to Environmental Chemicals .Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.S.

Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.00) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95 (<LOD-2.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. which may vary for some chemicals by year and by individual sample.20 (<LOD-1.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.00 (<LOD-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40 (<LOD-1. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.08 (<LOD-4.00 (<LOD-3.80) < LOD 621 725 1078 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf.2.S. see Data Analysis section) for Survey year 03-04 is 1. Survey years 03-04 Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 187 .44) 2.

0 (8.0) 10.0-12.94-3.0 (11. see Data Analysis section) for Survey year 03-04 is 1.5 (11.00-11.00 (5.60-6.00 (7.6) 292 728 1548 03-04 03-04 3.49) 10.65-8.14) 3.48 (2.00-4.82-9.05) 5.20-12.00-10.00-4.70-3.1-18.50-5.0) 95th 16.00-3.81 (5.00 (7.69-6.00 (3.34 (3.32-10.59 (6.00) 6.27-2.69 (3.8) 7. Survey years 03-04 Geometric mean (95% conf.74 (2.0-17.79 (3.5) 95th 13.70) 5.45) 8.34-4.17-6.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .70-12.0) 13.11 (3.60-3.3 (8.77 (3.34 (3.61-16.18 (6.97-3.0 (9.00) 6.84-8.0) 16.55 (2.03-6.71 (3.00 (4.17-4.12-4.70 (3.00-4.65-6.00-8.17 (2.84-18.1-22.6) 1284 1284 03-04 03-04 03-04 4.00 (5.0) 14.6-18.30 (7.69-3.72 (4.00 (3.00) 90th 11.9 (11.0-17.00-15.00 (6.69 (3.0 (12.80-5.24) 3.98) 4.00) 5.00) 12.10) 6.9) 12.00-5.44 (2.80-6.29-4.61-11.73 (3.19) Selected percentiles ( 95% confidence interval) 50th 3.9 (7.52) 3.00 (3.0 (10.00-7.42) 3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (9.0-16.10) 3.7) 1284 1284 03-04 03-04 03-04 4.08 (2.00) 4.80 (4.9) 13.92) 3.60-7.7-16.0 (9.0) 292 728 1548 03-04 03-04 4.00) 9.38 (3.00-9. Survey years 03-04 Geometric mean (95% conf.0-18.0) 9.0) 12.57-5.27-5.0) 13.71) 3.67) 9.30) 3.00-7.0-25.00) 3.00-11.9) 11.00 (3.50 (4.82-5.00) 6. population from the National Health and Nutrition Examination Survey.24-4.00) 7.5) 12.0-16.0 (10.00-12.48 (3.90) 2.92-12.86-7.00 (3.32 (8.90) 5.3 (8.8) 7.78 (4.00 (6.00-4.25 (4.00-11.33-4.0) 11.00-3.45) 3.57 (3.16 (4.88 (4.16-11.74) 90th 9.00) 4.00-4.9) 5.0) 9.20) 11.0 (10.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.S.00-4.00 (3.00-15.05) 3.16 (2.00-15.00) 3.00 (5.78) 4.28) 2.00 (5.95-6.0) 16.37 (3. 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. interval) 3.70-4.0) 9.31-4.0 (12.03 (3.0) 17.34) 3.0) 17.62) 4.73) 6.91) 75th 5.11) 4.89 (3.80-3.95-3.32 (4.22) 4.00-7.0-19.00 (6.95 (4.95-4.3 (7. interval) 3.15) 4.94) 3.49-4.80) 2.50-15.00-13.27 (2.00-12.8) 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 3.7 (10.05) 10.13-4.2) 10.71 (4.31) 4.0 (13.80) 7.00-22.7.82) 3.0 (9.46 (4.67) 8.60-4.S.90 (3.85 (3.1 (8.7) 13.14) Selected percentiles ( 95% confidence interval) 50th 3.0) 11.27 (3.4 (7.86 (2.0 (14.71-4.1-15.33) 3.0 (13.0) 621 725 1078 Limit of detection (LOD.34-4. population from the National Health and Nutrition Examination Survey.7) 12.39-3.09 (7.44) 5.45 (8.12 (3.86-21.06) 5.20-4.0 (10.00) 6.37 (2.00) 75th 6.00 (5.0 (8.

86) 3.40-2.88-2.82-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.85) 1.00 (2.18-1.10) 95th 2.900-1. 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. population from the National Health and Nutrition Examination Survey.22) 3.85) 2.07) 2.10 (.70-2.70-2.985) 1. Survey years 03-04 Geometric mean (95% conf.58) 2.853-1.40-2.80) 1. Survey years 03-04 Geometric mean (95% conf.80) 1.20 (1.80-2.14-1.9.90) 2.35-3.81) 1.88 (1.50 (<LOD-1.40) 2.00) 2.31-3.10 (1.80 (1.00) 1.36 (1.00 (<LOD-1.28 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.70-3.40) 1.10 (1.80-2.30) 90th 1.60) 1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.61) 2.S.30 (1.53-2.10) 2.00-1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (2.45) 3.20 (1.93) .70-2.30-2.46-2.80 (1.00 (<LOD-1.80 (1.00) 1.816 (<LOD-.05-1.10 (<LOD-1.60) 2.33 (1.07-3.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.33 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.37 (1.30) 1.00-1.40-3. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 189 .63 (<LOD-1.90) 1.52 (2.11-1.86 (2.53 (1.07 (1.77) 1.34) 2.40) 1.30) 2.50 (2.23) 1.30-1. which may vary for some chemicals by year and by individual sample.50-2.17) 2.20-3.16 (2.46 (1.36) 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.96-2.20-1.57) 95th 2.70-2.28 (1.88 (1.30-1.43-3.30 (1.62) 2.90 (1.90) 2.00-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30) 1.60) 2.61-3.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.50) 1.20 (1.79) 2.00) 1.20 (1.15-1.18-1.40 (2. see Data Analysis section) for Survey year 03-04 is 0.60 (1.31 (1.73-2.00 (1.82-2.90 (2.10-1.10-3.50 (1. population from the National Health and Nutrition Examination Survey.00) 2.40-3.60 (2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.30 (1.86) 2.00-4.10 (.40 (1.86 (2.20) 2.84-3.S.00-2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.50 (1.50) 621 725 1077 Limit of detection (LOD.20 (1.20 (1.30 (2.60-2.80 (2.10-1.22 (1.54) 90th 2.70) 2.71-2.80 (1.

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

Hudgens E. Crit Rev Toxicol 2006. Slavkovich V. Chowdhury UK. Environ Res 2005. 7th edition. A prospective study of blood selenium levels and the risk of arsenic-related premalignant skin lesions.41(10):2399-2428. Available at: http://www. Perrin M. Am J Clin Nutr 2006.fr/ENG/Monographs/vol84/ volume84. placebocontrolled folic acid-supplementation trial in Bangladesh. Needham LL. Reidy JA. Linderholm H. Parvez F. et al.pdf.36(2):99-133. Ryhage R. Liu X. Gamble MV. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Lu X. JAMA 2004. Sumi D. Josyula AB. Toxicol Appl Pharmacol 2006. Atalah E. Ingested arsenic.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Arsenic methylation patterns before and after changing from high to lower concentrations of arsenic in drinking water. Pilsner JR. Hughes MF. Blom S. Biological monitoring of occupational exposure to arsenic by determining urinary content of inorganic arsenic and its methylated metabolites.114(11):1790-1796.98(2):151-159. Int Arch Occup Environ Health 1998. J Environ Sci Health A Tox Hazard Subst Environ Eng 2006. Thomas DJ. McClellen H. Jakubowski M. Folate and arsenic metabolism: a double-blind. Bredfeldt TG. Arsenic exposure to smelter workers. Chiou HY. Aposhian HV. Cincinnati (OH): ACGIH Worldwide. Burgess JL. Stute M. Available at URL: http://monographs.iarc. Chen Y.104(11):1200-1207.16(2):207-213. Hsu LI. Hysong TA. Methylated arsenicals: the implications of metabolism and carcinogenicity studies in rodents to human risk assessment. Mash EA. et al. DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh. Eldan M. transcription factor. Zheng Y. O’Rourke MK. Kalman DA. Jagadish B. Cancer Epidemiol Biomarkers Prev 2007.gov/toxpro2. September 2005 [online]. Montesinos N. Associations between drinking water and urinary arsenic levels and skin lesions in Bangladesh. Ahsan H. Slavkovich V. Biggs ML. Healy SM. et al.107(8):663-667. Hysong TA. Gandolfi AJ. Kalman DA. J Expo Anal Environ Epidemiol 2003.292(24):2984-2990. Excretion of arsenic in urine as a function of exposure to arsenic in drinking water. Gurzau ES. Cohen SM. 8/7/07. Eblin KE. Monomethylarsonous acid induces transformation of human bladder cells.216(1):69-79. J Appl Toxicol 1988.47:243-262. Trzcinka-Ochocka M. American Conference of Government Industrial Hygienists (ACGIH). J Health Popul Nutr 2006. Moore LE.13(8):693697. Human health effects from chronic arsenic poisoning--a review. and biotransformation involved in cellular response and toxicity. J Environ Sci Health A Tox Hazard Subst Environ Eng 2003. Lagerkvist B. et al. Summary of Data Reported and Evaluation. Arsenic: signal transduction.11(4):265-269. Amigo H. van Belle G.13(3):211-218. Razniewska G. Smith AH. Sandstrom M. Clinical and neurophysiological studies. International Agency for Research on Cancer (IARC). van Geen A.116(7):893-897. Wu MM. Caceres DD. Cebrian Garcia ME. Coble K. Sturup S. Pattern of excretion of arsenic compounds [arsenite.38(1):87-113. Roy S. House dust and inorganic urinary arsenic in two Arizona mining towns. Gurzau A. Parvez F. Hughes J. Pino P. Toxicological profile for arsenic. Chem Res Toxicol 2000. Rahman MM. Ye X. Poplin GS. Le XC. et al. Chen CL. Documentation of biological exposure indices. Le XC. Environ Health Perspect 2008. Updated September 2004 [online]. Moldeus P. including Arsenic. Wong LY. arsenate.atsdr. et al.24(3):298304. Scand J Work Environ Health 1985. et al.84(5):1093-1101. Ilievski V. Lodh D. Loomis D. Bhattacharya P.html. Reduction in urinary arsenic with bottled-water intervention. Exposure to inorganic arsenic in drinking water and total urinary arsenic concentration in a Chilean population. 8/7/08 Ahsan H. and lung cancer risk: a follow-up study in arseniasis-endemic areas in Taiwan.42(12):1195-1201.89:145-151. Volume 84. Beck BD. Some Drinking-water Disinfectants and Contaminants. Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Kapaj S. Burbacher T. MMA(V). Norin H. J Occup Environ Med 2000. Calafat AM. Graziano JH. Environ Health Perspect 1990. Liber K. Environ Health Perspect 2006. Biomarkers of exposure: a case study with inorganic arsenic.cdc. Lewis AS. Bolgiano D. Annu Rev Pharmacol Toxicol 2007. Sengupta MK. Hopenhayn-Rich C. Schreinemachers D. Environ Health Perspect 1999. Cellular metabolism of arsenocholine. Matczak W.71 Suppl:S29-32. Chanda CR. Hall M. cigarette smoking. et al. The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species. Thor H. Peterson H. Christakopoulos A. Arnold LL.8(2):119-127. Calderon RL. Chen SY. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Fourth National Report on Human Exposure to Environmental Chemicals 191 . Rahman A. Environ Health Perspect 1996. Hsueh YM. Kurzius-Spencer M. Kumagai Y. 2001.

Goessler W. Lauwerys R. et al. Guidelines for Biological Monitoring. Br J Ind Med 1992. Available at URL: http://www.inchem. 2nd ed. J Anal Toxicol 2006. Sun X. National Research Council (NRC). Becker K. Solo-Gabriele HM. Belson MG. Tseng CH. et al. Environmental Health Criteria 224. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. EPA). Environmental Protection Agency (U. urinary arsenic metabolites and human diseases: current perspective.epa. CruzGonzalez MB. Xu Y. Tseng CH. Buchet JP.gov/iris/subst/0278. Chung CJ. Chen CJ. Offergelt JA.49(6):387-393.57(2):79-91. 8/7/07. J Toxicol Environ Health A 2007. Pellizzari ED. Arsenic. Shalat SL. Boeckx M.210(3-4):271-297.25(1):1-22.org/documents/ehc/ ehc/ehc224. Borja-Aburto VH. Morton J. Black K. Burgess JL.20(8):1120-1125. 2001. Liaw J. EPA). Ibata K. Environ Res 2004. Rey OA. 2001. Biggs ML. Available at URL: http://www. and metabolism of arsenic. Arsenic. EPA 815-F-00-015. A pilot study of children’s exposure to CCAtreated wood from playground equipment. Fact Sheet: Drinking Water Standard for Arsenic. Rumpler A. Nygren A.96(2):119126. Roels H. Gandolfi AJ. Yuan Y. Valenzuela OL. Investigating childhood leukemia in Churchill County. Int Arch Occup Environ Health 1986. Geneva 2001. Vahter M. Environ Health Perspect 2006. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Arsenic in Drinking Water. Sun G. inorganic. Nolinder P. In:Industrial Chemical Exposure. Nevada. Calderon-Aranda ES. Environ Health Perspect 2007. et al. Kalman D.211(2):175. Li L.115(1):151-157. Toxicol Appl Pharmacol 2005. Integrated Risk Information System. Clayton CA. Environ Health Perspect 2005. Ochi T. Friberg L. Garcia-Vargas GG. China. Moore LE. GSTM1 and T1. Raml R.222(3):374-380. Fok N. Marshall G.112(14):1375-1380. Arsenic in drinking water-2001 update. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Smith AH. html. Holmes AK.S. Ferreccio C. Genetic polymorphisms in MTHFR 677 and 1298.htm. Arsenic on the hands of children after playing in playgrounds. Arsenic methylation. Francesconi KA.S.S. Mason H. Seiwert M. Rubin CS. et al. Meza MM. Jimenez M. 8/7/07 U. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. World Health Organization (WHO).36-37.gov/safewater/arsenic/regulations_factsheet. Li X. Environ Health Perspect 2007. Boca Raton (FL). Schulz C.113(3):250-254. Vahter M.114(8):1293-1296.206(3):299-308. Fleming LE. January 2001 [online]. Int J Hyg Environ Health 2007. Jhangri GS. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. von Ehrenstein O. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Jin Y. Shipp M. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U.30(5):293-301. Environ Health Perspect 2006. Jones RL. using a routine LC-ICP-MS method. et al. Arsenic and Arsenic Compounds.115(4):648-652.epa. Lewis Publishers. Hoet P.114(2):220-227. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. pp. Seifert B. Naranmandura H. Sci Total Environ 2006. Steinmaus C. Yang MH.K. Toxicol Appl Pharmacol 2007. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Chem Res Toxicol 2007. Kieszak SM. Huang YL. Arsenic exposure. U. Lu X.Metals Kwon E.70(2):159-170.htm. 1998 [online]. Garcia-Montalvo EA. Suzuki KT. Sonora. Washington (DC) National Academy Press. Buckley BT. Conrad A. Lauwerys RR. Zhang H. et al. Rahnster B. Kopplin MJ. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals . Erratum in: Toxicol Appl Pharmacol 2006. et al. Wang Z. 3rd Ed.S. Available at URL: http://www. Environmental Protection Agency (U. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS). Kolossa-Gehring M. Li B.367(1):80-88. Environ Health Perspect 2004. Flanders WD. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. urinary arsenic speciation. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Huang YK. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells. Mexico.

4) 6.31 (2.70-6.87-14.25-1.45) 7.37-8.28) 90th 5.80 (1.63) 1.30) 5.10 (3.00-76.11-1.09 (2.15-1.11 (3.26) 2.50 (2.74-2.43 (5.60-6.33 (1.78-3. are high in barium (Genter.93 (4. depilatories.42 (1. such as brazil nuts.30) 2.69 (1.76-3.99 (4.09 (1.60-2.80-7.20-8.59-11.65-5. In nature.14 (6.08 (6.71) 2.51) 1. In single dose animal studies.26-1.90) 2.60 (1. rubber.21-8.40 (1. bricks. The general population can be exposed to low amounts of barium in air.39) 1.90-2. and food.60 (2.90-13.76-2.30 (5.70) 3.00-8.80) 1. and 0.80 (2.46-1.63) 1.40 (5.20 (1.20-6.71 (2.54 (2.32-7.34 (1.56) 1.16 (1.47) 4.37) 1.54) 1.74-3.80) 7.20-5.50 (1.50 (4.48) 1.15-1.52 (4.2) 6.77 (3.64-3.99-5.34 (2.86 (4.90) 1.27 (1.67) 6.87-7.88) 7.30-1.30 (3.12 (2.22-1.8) 9.43) 2.82) 2.61 (2.50 (3.40 (5.19-1. barium sulfate and barium carbonate). Barium compounds are used by the oil and gas industries to make drilling muds.60-10.39) 4.43 (1.93-8. soluble forms of barium.78) 1.12.35 (3.12.49-1.12) 7.45 (1.73) 3.85) 1.61 (5.20) 2.39 (1.90 (1.85 (2.91) 6. interval) 1.37 (4.30 (5.04-2.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.63 (8.48) 1.50-6.73 (6.35) 5.36 (4.48-4.29) 5.15) 5.53) 1.30-3.72) 4.47-1.50 (1.19) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.49) 4.22-1.01 (4.76-7.75-3. Barium salts have also been available as rodenticides.56 (1.66 (4.82-6.18) 3.24 (4.39 (1.75) 2.70-5.50 (1.56 (2.50 (1.88) 4.50) 2. glass.Metals Barium CAS No. population from the National Health and Nutrition Examination Survey.56 (6.51) 7.48-4. respectively.80 (1.35-4. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).25 (1. Small amounts of barium can be released into the air during mining and other industrial processes.53) 2.65) 1.40 (1.24-1.30-2.87 (5.05% of the earth’s crust.16) 5.55-7.54-1. 2001).62) 1.95-6.50-6.74) 3.06-2.30) 5.92) 2.80) 6.80 (2.36-1.36 (1. it combines with other chemicals such as sulfur or carbon and oxygen.53-5.57 (5.10-5.26-7.64 (1.98) 1.38) 2.66) Selected percentiles ( 95% confidence interval) 50th 1.20-1. tiles.30-5.46) 1.60-6.71) 95th 6.21 (1.77-3.73 (5.21 (1.44 (1.70) 1. Workers employed by industries that make or use barium compounds can be exposed to barium dust.10 (2.40 (1. 0. fireworks.63 (2.43) 6.50) 2.50-1.11 (3.50-1.70) 5.40) 7.44-5.35-1.20-1.20-1.06-1.S.55-3.85) 1.97 (1.39-1.54-1.g.20-1.60) 3.70) 4.62) 1. Certain foods..57) 3.57-7.25-11.71) 1.32-1.65) 3.62 (1.34) 2.22) 6.50) 1.90-9.50 (6.35-1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.80-3.03 (1.70) 7.30) 3.18 (6.40) 3.18-1.41-1.20-8.96-2.70 (1.60) 1.65-8.65-1. and ceramics.78-2.8) 5.81-3.46) 1.87-3.61-8.70-2.05-2.40) 7.90) 4. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.49) 8.65 (5.91) 2.27 (1.56) 4.51 (1.50 (4.1) 9.00-3.15 (2.11 (2.10) 5.30-1.86-4.54-8.00) 1.54) 1.44-2.30) 5.91 (2.77) 1.30) 8.00) 4.00) 1.81-2.4) 7.76) 1.86) 6.37-1.86 (4.10 (4.30-2.29-1.20 (3.70-3.73) 1.15 (1.90) 2.24-1.00) 6.17-1.02 (7.14-1.70) 1.70-8.21-2.49) 11.10) 3.72) 1.60-3.63) Total 1.82) 1.4) 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 1.28-1.20 (4.60) 4.32) 8. whereas others are practically insoluble (e.52 (1.38 (1. 7440-39-3 Medically.61 (1.60) 1.78) 1.30) 4. Fourth National Report on Human Exposure to Environmental Chemicals 193 .95 (4. Barium compounds are also used commercially in paint.72) 75th 3.90 (6.63 (1.01-7.63 (5.41) 1.35 (1.12) 6.35 (2.61 (3.14-6.68 (1.40-13.80 (1.73-5.70 (5.36-1.54) 2.49) 2.51) 2.07 (2.10-4. and 03-04 are 0.56 (1. such as barium chloride.54 (6.30 (2.15-11.62 (1.9) 5.49-9.47-1. see Data Analysis section) for Survey years 99-00.37) 5.65) 1.87) 7.26) 5.40 (4.90 (4. Some barium salts are freely soluble in water.50) 4.20-8.76 (3.27) 2. 01-02.87-9.88) 1.87 (6. water.50 (4.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.38 (1.31-2.93-2.70-2.59) 3.80-2.08-8.88 (5.86-5.48 (6.84) 5.50 (1.00 (1.8 (6.30 (1.34 (1.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.43 (1.04-6.38) 8.00 (2.94-6.81-2.80 (5.31.12-1.71-9.80-5.41-3.49 (1.61 (1.50 (5.36) 5.15 (6.12 (2.40 (5.29-5.

06) .27 (2.58-6.41) 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.68-3.38 (1. Insoluble barium salts.20-8.881 (.15-4.68-3.03) 2.4 (5.8) 4.777-1.38 (1.48-5.34-1.68 (3.60 (1.97 (5.84) 2.24-1.61 (4.60 (2.45-1.51-3.55 (1.24-11.921 (.59 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.754-1.48 (1.03-1.36 (3.31-1.58 (4.10) 3.19-1. 1994.37 (1.13-3. such as those used in medical radiographic procedures.39) 4.90-2.44-2.45 (1.69 (5.03) 3.31-1.21 (1.27) 7.43-6.62) 2.49-1.01 (5.55 (1.02) 4.56 (1.52-4.65 (2.31-1.72) 4.69-9.00) 1.98 (2.96 (4.68) 3.51 (1. are not absorbed when administered.51) 4. Chronic high doses in animals resulted in kidney damage (McCauley et al.45 (3.96) 7. 1986).36-1.39 (2.25-11.48-1.52-10.19-1.76 (3.39 (3.32) 2.703-1.11-2.45) 95th 6.70) 10.38-1.85-5. 1985.24-3.33) 1.48 (1.40-1.20-2.3) 6. NTP.87) 1.76) 2.75) 1.76 (4.55-6.02-5.97-3. water solubility.22-1.32 (1.34-3.4) 5.Metals was eliminated primarily in feces and to a lesser extent.77) 1.89) 90th 4.23-2..32 (1.91) 2.41 (1.22-4.63) 1.47) 1.80-6. in urine.64 (1.54) 1. a benign condition that may occur among barite ore miners. Toxicity from soluble barium salts is rare.39-1.59) 2.68) 1.52 (3.64) 7.0) 5.29-3.97-4.12) 2.00) 4.41 (1.86) 5.84-5.55 (4.52) 7.36 (1.45-6.43) 1.46-22.51) 4.29-4.33) 6.77) 1.35-1.57 (6.24-6.59-7.34) 1.73-4.32) 2.29) 1.51 (3.29-7.05-1.34 (1.67-6.63-4.41 (2.50) 1.66 (1.09) 6.45) 1.28) 5.42) 1.10) 6.10-2. 1990).04) 1.75) 1.96) 4.47 (5.18 (1. Perry et al.40 (1.47) 1.29 (3.75) 2.56) 4.00-1.10-1.23-5. and cardiac dysrhythmias.03) 1. interval) 1.48-3.73-2.26-4.39-5.47 (2.79) 1.76 (2.77-5.24) 3.46) 2.68 (2.46 (2.38-7.55) .80) 3.16-1.880-1.88 (6.50) 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 1.36-2.33 (5.06) 2.25 (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 .22-1.92 (4. Following intravenous injection in animals.47) 10.40 (1.710-1.50) 1.56-3.70) 1.38 (4.68 (3.31 (1.29 (1.64 (1.28-6.00 (2.55-5.45-1.91-2.51 (1.27-3.77) 5.50 (4.28-1.60) 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 2.58) 75th 2.96 (4.33-4.30) 2.70) 4.08-2.33-1.84 (3.915 (.49 (1.91 (3.00 (3.64 (1.81-6.36 (1.45-8.00 (3.59) 1.57-7.33 (1.38) 4.34-5.2) 6.2) 5.57-5.39 (2. weakness. chemical form. The health effects of exposure to barium compounds depend on the dose.84-2.58 (2.11) .78 (2.62 (1.04 (2.29-4.49 (1.37 (1.83) 2..0) 7. Wones et al.54 (2.75-22.38-5.42 (4.58) 1.26-1.99 (2.89 (2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.24-6.76) 2.76) 1.55 (5.72 (2.77) Total 1.91 (3.30 (1.832-1.18 (1. 2001).64 (1.30 (1.42) 1.52) 2.75) 2.38 (4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.27-1. paralysis.82) 1.26-1.26-1.46) 3.14-2.00) 6.62 (2.53-21.02) .83) 3.60 (5.28-11. 1989).65 (5.48 (1.32 (2.57) 2.00 (5.28-7.41) 4.0) 6.40 (1.44-2.38) 1.96) 4.86 (2.24-1.97 (4.39 (2.60 (2.50) 2.51) 6.86-7.47) 4.49-1.26-1.62 (4..03-1.29-1.56) Selected percentiles ( 95% confidence interval) 50th 1.13-2.53) .20-1.16) 11.36-1.39-10.963 (.64) 7. Barium is not rated for human carcinogenicity.59 (1.35-1.76-3.74) 1.10 (6.99 (4.891 (.81-7.26) 4.73) 2.59) 1.11) . Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.97) 1. hypertension. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.35-3.44 (1.02 (3.74 (5.96-6.04) 5.81-6. 1984.20) 4.2 (3.56 (1. and route of exposure.99) 1.48) 2.61) 2.79-5. diarrhea.60 (1.19-1.39-1.905 (.23-1.28 (1.00) 4.52) 1.33 (1.19-2.54) 2.01) 1.00-7.82) 1.22-2. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.57-10.71 (5.88 (2.72) 6.53 (2.49-1.58) 4.25) 4.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.80) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.16 (1. vomiting.54 (1.46) 1.08-1.75-3.74) 1.3 (6.01 (4.96) 4.36 (3.38) 1.31) 5.77) 1.36 (5.37) 2.47-8. population from the National Health and Nutrition Examination Survey.24 (3.31 (4.37-2.20 (1. Symptoms following acute high dose include perioral paresthesias.24 (5.37-1.92) 2.

Apostoli P.e.S. Sci Total Environ 1990. Investigations into the effect of drinking water barium on rats.85:355-359. Third National Report on Human Exposure to Environmental Chemicals. Stadler BL. Barium. [online]. Costa R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Exposure to soluble barium compounds: an interventional study in arc welders. Princeton NJ: Princeton Scientific Publications. environmental levels) and health effects is available from ATSDR at: http://www.. Schaller KH. Epidemiological study of barium in Illinois drinking water supplies. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. 2001. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. 5th ed. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Inc. et al. Gallorini M. et al. Genter MB. patient population and literature reference intervals for urinary trace elements. Pozzoli L. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Ting BG. and serum of Italian subjects. Zschiesche W. Pirkle JL. Powell C. Comparison of representative ranges based on U.197210. PS. Wones RG. ed. p. Environ Res 1998. et al.. 2005. J Toxicol Environ Health. strontium. 2005. Kopp SJ. NTP. et al. National Toxicology Program (NTP). Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. calcium. Patty’s toxicology. Information about external exposure (i. Biomonitoring Information Levels of urinary barium reflect recent exposure. the welders had no obvious adverse clinical effects (Zschiesche et al. and a drinking water standard has been established by U. 1992).296(1-2):71-90. Jackson RJ.html. Vol 2: Specific Metals.. New York: John Wiley & Sons.S.nih.gov/toxpro2. Jr.gov/ntp/htdocs/LT_rpts/tr432. Levy. 1998). A study of 46 elements in urine. Weltle D.76(1):53-59. Reeves AL. Perry HM. Calabrese EJ. Atlanta (GA)..niehs. Minoia et al.nih. 1994. Morrow JC. Howerton K. Princeton (NJ): Princeton Scientific Publications. 1990. Lack of effect of drinking water barium on cardiovascular risk factor. LA. References Brenniman GR. p. Int Arch Occup Environ Health 1992. In Friberg L. 2nd Ed. 1984. and 2003-2004 (CDC.niehs.. EPA. In: Calabrese EJ. Handbook on the Toxicology of Metals. Douglas BH. Available at URL: http://ntp.atsdr. 84-94. 221-252 Komaromy-Hiller G.95:89-105. p. Frohman. blood. Sabbioni E. McCauley PT. Ash KO. ed. eds. barium. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). 4/8/09 Paschal DC. Magnesium.. Perry EF. Nordberg GF. Vouk VB. 2000) to levels in NHANES 1999-2000 and 2001-2002. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Trace element reference values in tissues from inhabitants of the European community I.28(3):373-388. Minoia C. Centers for Disease Control and Prevention (CDC). Clin Chim Acta 2000..html?charset=iso-88591&url=http%3A//ntp. 1989. Advances in modern toxicology.gov:8080/cs. Laurie RD. New York: Elsevier. 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.. Pietra R.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. In: Inorganics in drinking water and cardiovascular disease. 2001-2002.64(1):13-23. pp. Trace metals in urine of United States residents: reference range concentrations. Paschal et al. eds. and radium In: Bingham A. Cohressen B. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA..cdc. 1986. Environ Health Perspect 1990. Sampson EJ. 231-249. 1985.

130 (<LOD-. and refined beryllium is used in mirrors and special metal alloys for the automobile. bertrandite and beryl. or drinking water containing the metal. 196 Fourth National Report on Human Exposure to Environmental Chemicals . computer. population from the National Health and Nutrition Examination Survey. Low-level beryllium exposure in the general population can occur through breathing air. x-ray machines. respectively.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. see Data Analysis section) for Survey years 99-00. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. which may vary for some chemicals by year and by individual sample. and from breathing tobacco smoke. Exposure to beryllium occurs mostly in the workplace. Beryllium compounds are commercially mined.130 (<LOD-. 7440-41-7 General Information Pure beryllium is a hard gray metal. coal.140 (<LOD-.13.170) < 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. soil. and machine-parts industries. are mined for commercial recovery of beryllium. and 0.Metals Beryllium CAS No. electrical. near some hazardous waste sites. In medicine. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and can be found in mineral rocks. In studies of laboratory animals.13. eating food. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. and dental bridges. beryllium is used in instruments. aircraft. Two types of minerals.13. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. and volcanic dust. 0. nuclear. 01-02. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 03-04 are 0. < LOD means less than the limit of detection.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 . the lightest of all metals.

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

html. population are lower than levels in workers. Int Arch Occup Environ Health 2001. Van der Venne MT. 1990. 3/27/08 Komaromy-Hiller G. 2000. Apostoli P. References Apostoli P... Levels of beryllium in urine for the U. 1998). Trace element reference values in tissues from inhabitants of the European community I. Centers for Disease Control and Prevention (CDC). Minoia C.76(1):53-59. In other studies.. Sabbioni E. Am J Epidemiol 2003. 20012002. Given these results.htm. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Hamilton et al. Biomonitoring studies on levels of beryllium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of beryllium than are found in the general population. blood. less than 0. Paschal DC. Clin Chim Acta 2000.S. Andrew M. 106. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www.. and serum of Italian subjects.e. Jackson RJ.13 μg/L.S. Third National Report on Human Exposure to Environmental Chemicals. 0.atsdr. 1990. Comparison of representative ranges based on U.1 μg/L). Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Paschal et al.org/documents/ehc/ehc/ ehc106. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. VI.95:89-105.23:827-839. and the 95th percentile for males in NHANES 2001-2002. Schaller KH. Pozzoli L.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. HLA-DPB1 and chronic beryllium disease: a HuGE review.inchem.296(1-2):71-90.74:162-166.S. Hamilton EI. it is likely that urinary beryllium levels in the U. Gallorini M. Minoia et al. Ting BG.157:388-398.158:165-190. Sabbioni E. et al. which approximate this Report’s limit of detection. 2001).Metals (i. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Morrow JC. Beryllium [online]. population were generally undetectable in NHANES 1999-2000.gov/toxpro2. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. and 2003-2004. Clin Chest Med 2002.e. Sci Total Environ 1994. Howerton K. Sampson EJ. McCanlies EC. Pirkle JL. patient population and literature reference intervals for urinary trace elements. International Programme on Chemical Safety (IPCS). Element reference values in tissues from inhabitants of the European community. Weston A.. They reported urinary beryllium levels ranging from 0. Sci Total Environ 1990. Environ Res 1998. et al. Atlanta (GA) 2005. Pietra R. Costa R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.12 to 0. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Maier L. Environmental Health Criteria. environmental levels) and health effects is available from ATSDR at: http://www. A study of 46 elements in urine. Genetic and exposure risks for chronic beryllium disease. and the fact that most NHANES participant levels were undetectable.cdc. Trace metals in urine of United States residents: reference range concentrations. Review of elements in blood. Kriess K. Ash KO.

00 (1.400 (.20-1.500) .200-.50 (1. interval) .400) < LOD . coatings and plating.337) .300) .400-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.425 (. plastic stabilizers. lead.600 (.500-.900-1.300-.362-.300-.400 (.500-.700-1.900-1.800) .500-.400-.366) * * .10 (1.800-1.500-.20-1.300 (.60 (1.00 (1.500-.500 (.300) .20) 1.600) 90th 1.300) .500) .300) .600) .70) 1.600-.200) .400) .S.40) 1.300 (<LOD-.500-.400 (.10 (1.800) 1. cadmium use has declined in response to environmental concerns (http:// minerals.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 .10 (1.usgs.900-1.500) .300-.30 (1.500 (. respectively.800 (. see Data Analysis section) for Survey years 99-00.20-1.300-.216-.400-.00-1.00-1.300 (.500-.400 (.378 (.300-.300-.300-.600 (.20) 1.600) .20) 1.20) .400-.400) < LOD < LOD < LOD .10 (.400 (.00 (. population from the National Health and Nutrition Examination Survey.00 (.20) 1.10) 1.400) .800 (.500-.500 (.200-.700 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .500-.200 (.300-.300 (.40 (1.600) .50-1.300-.344) .400) .00) .50 (1.700) .200 (<LOD-.70) 1.900-1.500-.10 (1.500) .900-1.300 (. 0.S.400) .700) .470) * .400 (.300 (.50 (1.700) .00-1.400) .331) .00 (.500-.359-.40 (1.368-.500-.50-1.400 (.427) * .304 (.50 (1.600) .400 (.20) 1. 01-02.296-.80) 1.700) .300 (<LOD-.300 (.80 (1. as zinc sulfide) and to a lesser extent.60 (1.00) .300-.400 (.300-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. < LOD means less than the limit of detection.600 (. U.400 (.40 (1.50) 1.300) 75th .400) .200 (.400-.500 (.395 (.00 (.30-1.500) .20 (. Other uses include pigment production.235 (.400 (.14.300-.50) 1.200-.300) .300 (.513) .700) 1.900 (.800) .300-.600 (.600) .300) .40-1.500-.300 (.40 (1.900-1.500-.400 (.300) .60 (1.600-.460) .400) .00-1. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.400) . or copper smelters (U.10 (1.10) 1.300 (.30) 1.378-.600 (.300-.300) 1.382 (.20-1.300-.400-.700) .20) 95th 1.283 (.412 (.500-.400) .00-1.20-1.50) 1.300) .20 (1.300 (.600 (.00 (.386-.400 (.304-.400) .400 (.20) .309-.00 (.40 (1.20) 1.10) 1.600) 1.333 (.10 (1.20-1.700-1.40 (1.300) .400) .300-.400) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400-.468 (.200 (<LOD-.00-1. The predominant commercial use of cadmium is in battery manufacturing. which may vary for some chemicals by year and by individual sample.600) .426-.400) < LOD .60) 1.421 (.gov/minerals/pubs/commodity/cadmium).400) . during refining of lead and copper from sulfide ore.300 (<LOD-.00 (.400 (.300 (<LOD-. and incineration of municipal waste materials. EPA.900 (.367-.500) .900-1.60) 1.800-1.376-.600-.700) .30-1.289-.600 (.300 (. 7440-43-9 General Information Cadmium is a soft.400-.10 (1.420 (.300) .30-1.10) 1.900-1.00-1.361-.60 (1.60) 1.300) .300) .00 (.300-.500 (.00 (.300 (.700) .200) .30) .3.500-.30-1.20) 1.400) < LOD .424) * .00-1.600 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .400-.10) 1.200-.60) Total * .90) 1.600 (.326 (. malleable.600) .313 (.30-1.10) 1.600) .300 (.300-.452) .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 . Cadmium also may be emitted into the air from zinc. and 0.275-.500) . and nonferrous alloys.600-1.3.441) * . and 03-04 are 0.403) .70) 1.600 (.40 (1.200 (.449) Selected percentiles ( 95% confidence interval) 50th .60-1.600 (.50-1.00-1.40) 1.255) .600 (.400 (.500 (.Metals Cadmium CAS No.700) .500 (.300 (.400) .20-1.30) 1.300) .266-. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.403 (.900-1.400 (.300-.600 (.500-.500 (.700-1.393 (.50-1.500-.500 (.400-.300-.S.20) 1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .200-.70) 1.400-.600) .304 (.10) 1.80) 1.600 (.900-1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300-. Since 2001.00 (.40-1.60 (1.300-.30) 1.10) 1.

167-.892-1.38) .211-.423-.28) 1.272-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .336) .972 (.173) .366-.790 (.545 (.241) . 2003).255) .329 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.194-.239 (.800-.316 (.412) .06) .192-.189-.390-.492 (.320) .445 (.120 (. To a lesser extent.680 (.20 (1.730-.640) . 1994).38) 1..313) .201 (. Diamond et al.277 (. respectively.200 (.890-1. whose body burdens of cadmium can be approximately twice that of nonsmokers.400-.763-.475 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.440-.255) .110-.067-.270 (.262) .210 (.260 (.090) .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.498-. Renal tubular and glomerular damage.326) .255) .870) .381-.607) .290-. potatoes.306 (.177-.57) 1. Cadmium in soil is absorbed by plants.482) .230 (.810-1.190-.456-.339) .886-1.880) . Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.229) .100-.265) .191-.300) .490) 1.10 (1.135 (.551 (.170-.204 (.181 (.223 (.390 (.210 (.232) .190-.360) .191-. 2001).540) .06.101) .25 (1.466 (.279 (. and various seeds. Cadmium is absorbed via inhalation and ingestion.114-.077 (. drinking water is a source for cadmium intake.234 (.47) 1.067-. Kikuchi et al.** Survey Geometric mean (95% conf.282 (.530) .510) . calcium.210) .713) .741-1..480) .087-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.860) 1.843-1.235) .820) 1.243-..219 (.189-.219 (.15 (.963-1.06.387) . and 03-04 are 0.28-1.22 (.12-1.06-1.01) .171-.183-.733-.430) .208-.270 (.462 (.220 (.115-.28 (1.596) .107-.198) .210 (.17) .589 (. 0.07-1.214-. however.200 (. zinc.090) .184-.231) .179-..209 (.366) .500) .219 (.493-.220-.170 (.203 (.06.34) 1.06-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.354) .519) .350 (.200-.452 (.230) 75th .237-. population from the National Health and Nutrition Examination Survey.330-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.440 (.322 (.12 (.273 (.980-1.507) .175 (. including many food crops such as cereal grains.806) .351-.251) .02-1.766 (.187 (.52 (1.940-1.134) .20-1.249) .74) 1. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.25) 1.458 (.394-. an inducible metal binding protein.753-.230) .261-.38) .700-.886) . 01-02.390-.550 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.180 (.141 (.157) .284) .500) 90th .858 (.530 (.169-. 2004a.580) .310) .519) .510-.15) .283 (. and 0.220-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .061 (<LOD-.206 (.01 (.206) .112-.229-.280 (.299) .479) .232 (.800 (.38) 1.490) .714-1.03) .160) .092 (.836-1.121 (.246) .289-.01-1.203) .440 (. 2003).51 (1.263) .151-.875) .623) .077 (.989-1.705-.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 .327 (.126) . 1999.733) .36) 1.240-.17 (. wheat.160-.281 (.790 (.260-.717-.128 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.04 (.820-1.17 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.633 (.450 (. For nonsmokers who are not exposed to cadmium in the workplace.433-.160 (. see Data Analysis section) for Survey years 99-00.150) .216 (.19) 1.308) .41 (.610) .257-.081) .300 (. copper) and protein.30-1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.148) .960) 1.220) .445 (.990) .455 (.165-.818 (.227 (.153-.175 (.890 (..240) .13) .447 (.210 (.233) .233) .855-1.450 (.960 (.178-.400-.366-.170-.109-.388-.210) .196-.140 (.72) 1.476-.222) .211 (.238) .302 (.32 (1.817 (.249-.160) .092) . ingestion through food is the largest source of exposure.82) 1.20 (1.202-.247) .426 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.520-.080 (.061-. 2003.20 (1.372) .210 (.193-.060-.559 (.24) 1.253-.470-.820 (. With chronic exposure.S. rice.135-.875 (.700-.157-.22 (1.148-.980 (.83) 1.226) .261-.109 (.980-1.919) .436-.191 (.193 (.150-.285-.229) .136) .393-.17 (.13-1.202 (.189) .15) 1.265 (.362) .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 .207-. interval) .848 (.817 (.700-.190-.199 (.481) .04 (.221 (.980) .686-.977) .48 (1.130 (.195-.551) .748-1.539) .065-.257) ..13 (. Horiguchi et al.200-.192-.310 (.43) 1.09-1.078 (.221) .238-.260-.918-1. 2003).20) 1.839 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .430-.892 (.633-1.980) .Metals 2000).813 (.295) .

154 (.091 (.687-.688-.091 (.184) .174-.209) Selected percentiles ( 95% confidence interval) Sample 95th . During the 1950’s and 1960’s.690-.210 (.479 (.415) .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..431) .441-.148 (.653) .783) . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.224 (.150-. 1999).225) . 2003.191-.940 (.240) .931 (.181-.377-.175-.250) .962) .700 (.263-.130-.123-.404 (.740 (.192) .423-.388-.700) .215 (.387 (.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.238-.839) .667) .289) .178) ..156 (.085-.876-1.173 (.297) .084-.178-.100 (.123-.288) .104) .414-.200 (.232) .163) . interval) .197-.08) .227-.663 (.440) . 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.210 (.175 (.754) .063-.927-1.241) .02 (.321) .722-.716-.727-.240) .827) .233 (.111-.446) .208-.818) .168-.767) .261) .170-.303) .183 (. population from the National Health and Nutrition Examination Survey. 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. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.470) .187) .185 (.769 (.940-1.229) .182) .263 (.856) .112) .267 (.674-1.181 (..101) .225) .487 (.813-1.288 (.067-. Jarup et al.412 (. 2002.418) .198) .289) .051-.252 (.783 (.093 (.690 (.208 (.718 (.481 (.813-.234 (.137-.784) .414 (.168-.906) .352) .316) .075 (<LOD-.210) .235) .708-1.074-.678-.311) .850) . 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.159 (.211 (.207) .757 (.631) .253) .500-.472) .501 (.418-.17) .650-.. 1999).090 (.792 (.434 (.184-.340) .278) .607) .617 (..07 (.826-1.491-.382) .381-..168 (.247-.106) .261 (.221 (.729 (.083-.533) .137 (.199 (.712 (.536 (.13) .140-.154-.268 (. At lower environmental exposures.173-.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 .476) . 1999).219 (.077-.444-.280 (.156) .343-.686 (.518) .919 (.202 (.147-.645-.245 (.364) .421 (.205 (.941 (.551) .181) . 2000.16) 1.490 (.795) 1.873 (.185) .170 (.175 (.850) .144-. can result from high dose chronic exposure.157-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .979 (.162 (.12) 1.146-.156-.591 (.537-.998) .690-.806-1.449) .950) .078-.541) .470) .545) .281) .687 (.757) .136-.398-.191) .182) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.181 (.176 (.917) .331 (.216-.562-.221-.136-.00 (.143-.296 (.630-. 2004).122 (.833-1..507-.270 (.05) 1.234-.438) 90th .281) .00 (.438-.143) .316 (.219 (.387-.07) .282 (.300-.828) .329 (.242) .308) .716) .614) .622 (.668-.336-.404) .909-1. Noonan et al.071 (.S.094) .929) .283 (.261-.830-1.917 (.078 (.. However.255-.559-.238) .075-.802 (.779 (.159 (.719 (.147 (.199-.184-.166 (.267 (.234) .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 .830) .171-.253 (.884) .204-.826-1.143-. 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.538) .473 (.426-.222-.207-.382-.696-. most often a result of occupational exposure (Roels et al.220 (.161-.104) .183) .247-.274) 1.177) . 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.196 (.187-.432 (.157-.318 (.325 (.304-.484 (.693 (.. Fourth National Report on Human Exposure to Environmental Chemicals 201 .865 (.266-.098) . 1996.10) 1.678 (..194-.16) .304) .288-.113-.06 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .223) .666-.985 (.874-1.107) .560-.256-.189-.423 (.** Survey Geometric mean (95% conf. 2004b).147-.190 (.856 (.212 (. 2002.140-.338 (.084 (.206-.433-.308 (.691-.182) .647-.09 (.266) .163 (.228-.135) .236-.209) .440) .725-1.086 (. Staessen et al.096) .516-.239-.818) .232) .335 (.293-.176 (.292) .789 (.247-.097) . Horiguchi et al.531 (.158-.218) .201-.350) .085 (.226) 75th . 2002.190 (.131-.191 (.391-.091) .767 (.273 (.126 (.38) . Olsson et al.

Becker et al. Wennberg et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Staessen et al.. Cadmium can produce lung. 2004. EPA. and drinking water and environmental standards have been established by U. 2004b.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.S. 2003.. 2003. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. For NHANES 19992000. Olsson et al. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. Becker et al. 2003. 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. Women had higher blood and urine cadmium levels compared to men of similar ages. Both IARC and NTP consider cadmium a human carcinogen.. Moriguchi et al. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine). with peak values observed in the fifth to sixth decades (CDC.gov/ toxpro2. 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. Jarup et al.. 2002. 2005.1 mg/L (Alfven et al.. 2005. Information about external exposure (i. 2002.. Zhang et al. 2003). 2002. Animal studies have demonstrated reproductive and teratogenic effects. Horiguchi et al. Acute and heavy exposure to airborne dusts and fumes. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. respectively. 2005). Staessen et al. 2006. 2003. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. 1996..46 mg/gram of creatinine) (Ezaki et al.. 2002). 2002. 2002). pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. 1988). 2002. 1996). In the typical environmental exposure.. Becker et al.atsdr.. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. Jarup et al. 2003. Mannino et al.. 2003. 2006). approached these values associated with subclinical changes in renal function and bone mineral density. 2005. CDC.. 1999). 2006... In adults aged 60 years and older...S. Noonan et al.. Further research is needed to address the public health consequences of such exposure in the United States.. maternal blood or maternal urine and birth weight (Nishijo et al. two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al... data (CDC. 1999. 2000.. 2006). Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. 2002).. Occupational standards are provided here for comparison only... 2004. 2002). 1999)..cdc. 2002). 2000. intermediate in former smokers and lower in never-smokers (Becker et al. not to imply a safety level for general population exposure. 2004). 2004b). Ezaki et al..26 and 3... urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. 2002) and length at birth (Nishijo et al. Creatinine-corrected urine cadmium values in U. 2005. 2000).. However.S. Suwazono et al. Komaromy-Hiller et al. Olsson et al.. In postmenopausal women. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al.html. has resulted in severe. respectively. Horiguchi et al. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. environmental levels) and health effects is available from ATSDR at: http://www. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.. Staessen et al.. potentially fatal pneumonitis (Fernandez et al.. 2000.. Olsson et al... 2004. Wennberg et al. as may occur from welding cadmium-alloyed metals.e. Friedman et al. Ezaki et al. Salpietro et al. 2002. Wilhelm et al. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles.. 2004. 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.. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Jin et al.

Ye T. Bellerup P. Seiwert M. Int J Hyg Environ Health 2002. Int Arch Occup Environ Health 2003. Seiwert M. Kikuchi Y. et al. Machida M. Vahter M. Howerton K. Kundiev YT. Ezaki T. Wang H. Grubb A. 2005. 102:10581066.S.atsdr. Alfven T. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Bregante G. Toxicol Lett 2004. Lison D. Fayers PM. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. et al. Environ Health Perspect 2002. Nordberg G. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Berglund M. Clin Chim Acta 2000. Schulz C.354:1508– 1513. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Chiappino G.59:194-8. Environ Health Perspect 1994. Kaus S. Taylor AJ. Comparison of representative ranges based on U. Uemura T. Tsukahara T. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U.148(1-2):11-20. Komaromy-Hiller G. Serra J. 1999 [online].205:297-308. Choudhury H. Environ Res 2004b. Jarup L.110:699-702. Kaus S. et al.296(1-2):71-90. Nerbrand C. J Occup Health 2003. Diamond GL. et al.1(8587):663-667. Palomar M. Fatal chemical pneumonitis due to cadmium fumes. Sasaki S. Persson B. Sasaki S. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Lancet 1999. Ezaki T. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. et al.html. Ukai H.66(Pt A):2141-2164.102:83-89. Schulz C.45:43-52. Occup Med 1996. 4/8/09 Alfven T. et al. Centers for Disease Control and Prevention (CDC).24:717-724. Dekio F. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Tsukahara T. Costa R. Bo M. environmental.76:186-196. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. patient population and literature reference intervals for urinary trace elements. possibly better than b2microglobulin.gov/toxprofiles/tp5. Jin T. Carlsson MD. Krause C. Atlanta (GA). Friedman LS. Okamoto S.S. Thayer WC. Lauwerys R. Becker K. Miyamoto K. Lepom P. Available at URL: http://www. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Lukyanova EM. Machida M. Fernandez MA. Environ Res 2006. Kumagai N. Pickering CA.57:668-672. Mascagni P.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. Davison AG. Thorax 2004. Mucha A.59:497]. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. 196:114-123. diabetes mellitus. Becker K. Olfactory function in workers exposed to moderate airborne cadmium levels.46:372-374. et al. Lancet 1988. Anthropometric. Agency for Toxic Substances and Disease Registry (ATSDR). Oguma E. Seifert B. Vahter M. Jarup L. Oguma E. Gadea E.13(11):1627-1631. ShkiryakNizhnyk AZ. Toxicological profile for cadmium update. Moriguchi J. Fukui Y.96:353-359. Cadmium fume inhalation and emphysema. 206:15-24. Moriguchi J. Third National Report on Human Exposure to Environmental Chemicals. Toffoletto F. Holguin F. Fukui Y. Takebayashi T. J Toxicol Environ Health 2003. Buchet JP. Horiguchi H. Environ Health Perspect 2005. Lidfeldt J. Ikeda Y. Chislovska NV. Int J Hyg Environ Health 2003. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Zhu G. Nermell B. Hellstrom L. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Darbyshire J. et al. References Akesson A. Horiguchi H. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Elinder CG. Savage-Brown A. Bernard A. Furuki K. iron deficiency. Comprehensive study of the effects of age. Occup Environ Med 2000. Akesson A. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Ikeda Y. Mannino DM. Furuki K.cdc. Miyamoto K. Toxicol Appl Pharmacol 2004a.000 women in the Japanese general population: a nationwide large-scale survey. Sanz P. Jones RL. et al. et al. Environ Res 2004. Consonni D. et al. Nomiyama T. Neurotoxicology 2003. Greves HM. Ash KO. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers.95:20–31. Lundh T. population. Stock AL. Venables KM. Hotz P. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002.

Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Bensryd I.3:26-41. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Usefulness of biomarkers of exposure to inorganic mercury. Wennberg M. iron status. Kathman SJ.110:1185-1190. Revised and new reference values for arsenic. Cadmium compounds. Nogawa K. Environ Res 2006. 204 Fourth National Report on Human Exposure to Environmental Chemicals . created 1992. 4/8/09 Waalkes MP. Lison D. Zhu HD. J Perinat Med 2002. Bergdahl IA. Schwenk M. Noonan CW. Toyama. lead. Zhang YL. Friberg L.epa. Gallmans G.S.html. Vangronsveld J. Occup Environ Med 2002. Lancet 1999. Biological monitoring of toxic metals.59:394-397. Revised 2000 [online]. Environmental exposure to cadmium. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Tanebe K. pp. Stegmayr B. Kido T. cadmium. Staessen J. Roels HA. Campagna D. et al. New York: Plenum Press. In: Clarkson TW. dietary intake. United States Environmental Protection Agency (U. Emelianov D. Skerfving S. Environ Health Perspect 2002. Nakagawa H. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Schultz C.533(12):107-120. Nakagawa H. and risk of fractures: prospective population study. Tawara K. Available at URL: www. Thijs L. Honda R. et al. Merlino MV. Japan. EPA). Salpietro CD. Mutat Res 2003. Mueller PW. Jansson J-H.110:151-155. Arch Environ Health. Environ Health Perspect 2002.Metals Nishijo M. Stelitano A. Nordberg GF. Effects of exposure to low levels of environmental cadmium on renal biomarkers. lead. et al. Ren Fail 1999. 2004. Bruiglia S. Roels HA. Saito S. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. eds. Lybarger JA. Nordberg GF. Tanebe K. 2000.353:1140-1144.30(5):395-399.gov/ttn/atw/ hlthef/cadmium. Time trends in burdens of cadmium. Ottosson H. and mercury in the population of northern Sweden.39:2507-2515. Cadmium in blood and urine – impact of sex. Nakagawa H. Biological monitoring of cadmium. Nishijo M. Lundh T. et al. Buchet JP. Olsson IM.209:301305. Sager PR. Roels H. Lundh T. et al. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. 151-168. Honda R.59(1):22-25. Staessen JA. Cadmium carcinogenesis.84 (Section A):4455. Int J Hyg Environ Health 2006. Minciullo PL.100:330-338. Kobayashi E. Fan YG. Zhao YC. Wilhelm M. Ginucchio G. Nordberg M. age. Lauwerys R. Relationship between newborn size and mother’s blood cadmium levels. Gangemi S. Oskarsson A. Hoet P. lead. J Environ Sci Health B 2004. et al. 2001. and former smoking – association of renal effects. Hazard Summary. Lijnen P. Environ Res 2000. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. forearm bone density. Kuznetsova T. Sarasua SM. Liu QF.21(3-4):251-262. Wang JX. Suwazono Y. J Cardiovasc Risk 1996. Okubo Y.

70 (8.60-5.03 (4. photographic emulsions.67 (4.76-6.3) 10.55-11.4) 12.70) 7.07) 4.60 (7.2-12.83-4.43 (5.7 (10.56-11.5) 12.0-15.81) 4.87-7.42-7.1 (10.8 (10.34 (4.1) 11.90) 5.20) 5.99) 9.20-7.61) 7.50 (6. infrared lamps.32 (3. and cardiac arrhythmia (ATSDR.2) 12.83) 6.12 (4.35-5. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 7.26 (3.60-6.10-5.95) 5. and high-power gas-ion devices.70) 5.37) 7.30-10.8) 9.1 (9.49 (5.20 (4.60-6.47-4. see Data Analysis section) for Survey years 99-00.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.8) 11.00 (7.3 (8.3-13.71) 4.59 (5.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.29 (4.Metals Cesium CAS No.00) 4. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.50 (4.70 (6.4) 95th 11.91 (7.62) 4.63 (4.1 (11.38) 5.12-5.74-5. and 0.64-5.05-5.08-5.1-13.0) 11.70 (8.55 (4.86-12.90-12.59) 7.10 (6.77 (9.63-4.30-5.9) 11.2-13.21) 90th 9.00-8.60-12.94-4.20) 8.54-11.S.8) 12. scintillation counters.1) 10.87 (4.2. although cesium was generally of low toxicity when given to animals.26-11.77 (9.80 (4.9 (11.9) 8.84-9. Radioactive 137Cs has been used medically to treat cancer.72-7.22 (4.87 (4.00) 6.52) 7.5-13.49) 75th 7.36 (6.90-10.70 (4.53 (6.02 (4.56) 5.6 (9.89) 4. respectively.09-5.50 (7.84) 5.71 (4.10-9.92-13.30) 5.64) 5.32) 4.3 (8.70 (9.50) 9.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.42) 6. population from the National Health and Nutrition Examination Survey.0 (9.90 (4.30) 7.1) 9.60) 5.7) 11.8) 12.99-11.94 (4.80 (8.98 (7.10-8.1) 9.81) 9.90-12.5 (10.12-11.7 (9.00-8.5-14.66 (7. and clay.25) 4.39-4.95 (3.7 (10.34) 9.1-12. 01-02.59-5.33-5.0-13.10 (8.4-13.7) 10.69-6.7 (9. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. interval) 4.10 (6.4) 10.0) 12.8 (11.99-6.80-10.5) 10. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.64-10.3-15.3) 10.7 (9.9 (11.80-11.91-8.80 (4.9 (10.7) 11.80 (8.1) 11.27 (7.26) 4. semiconductors.5) 9.71-5.90) 7.00) 7.59-5.50 (4.21 (4.08 (7.97) 4.70 (5.70-8.20 (6.6) 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 4.90 (6.40-11.26) 7.13-8.6 (11.6 (9.77-8.90) 5. However.89) 5.3) 10.8 (10.42) 7.80-6.94) 4.08 (6. Fourth National Report on Human Exposure to Environmental Chemicals 205 .95-4.5 (8.4) 11.87) 5.01) 7.8) 9.40) 7.40) 5.84 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 11.4 (9.2) 11.73-11.35 (4.4 (10.80-10.9 (10.1-12.4) 10.55 (7.97 (7.30 (6.81) 4.45-8. Little is known about the health effects of this metal.84) 8.56 (4.0 (10.33 (5.47-8. diarrhea.6) 10.32-5.90) 9.49 (4.00-9.45-5.61-6.17-6.74) Selected percentiles ( 95% confidence interval) 50th 4.71 (8.9) 12.71-8.43-8.30 (6.50-7.25 (3.49) 4.86-11.68 (7.33 (6.40) 5.0) 12.6 (11.20-4.4) 9.16-6.29) 4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.63) 6. Most human exposure to cesium occurs through the diet.90-10.64) 5.98 (7.39) 7.25-5.08) 7.40-5.27-5.05-5.82-4.80 (4.60-7.62 (5.99-11.16-6.3-13.5-16.71-9.31-8.57-5.5-14.40-5.44 (8.01-8.7 (10.00-4.70 (6.40-7.90) 4. soil.50 (4.12) 5.4 (9.03-4.01-6.10-7.64 (4.20-5.05) 5.90-10.40-5.37) 5.80-13.27) 4.74 (4.97-7.96 (6. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.8) 12.24) 4. Whether cesium compounds are carcinogenic is unknown.90-8.07-11.93 (4.54) 4.09) 5.89-5.7 (8.82) 5.84-5.17 (6.9 (11.08-5. and as polymerization catalysts.70-5.8-13.36) 3.68) 9.14.6 (9.40-11.0) 9.2-14.8) 11.13 (5.79 (4.13 (8.20-8. cesium hydroxide is corrosive and irritating at high concentrations.52-9.40 (4.46) 7. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.03 (4.05) 5.80 (8.53-11.04 (4.20) 7.4) 12.87 (4.72) 4.20) 4.50) 5.14.62 (5.3) 12.35 (4. and 03-04 are 0.99) 7.0) 12.7-14.94 (4.59-5.81 (4.81-14. nausea.64) 4.10 (8.88 (8.17) 4.6 (9.56 (4.9 (11.80-10.36 (3.86 (7. 0.7 (11.2 (9.0) 10.70) 5.15-8.60 (8.04) 7.13 (7.2 (9.77 (4.80) 7.60) 7.23) 9.22-4.00-10.40-5.2-13. For absorbed cesium salts.14 (4.3) 10.73-5. 2004).3) 9.2-13.9) Total 4.6) 11.60-7.23-4.7) 10.

90-8.29) 4.79 (5.50 (5.66-6.27 (6.82) 7.30 (7.91 (5.77) 4.8) 10.29-3.6) 6.0) Total 4.05) 3.98) 5.50 (7.6 (9.42 (4.79) 9..04-5.14-7.09 (4.39) 5.13) 7.63 (4.08) 3.06) 5.19-3.51 (3.63-6. 2005.00) 6.95-6.87 (5.54 (3.10-4.24 (3.65-3.63) 6.97-5. 2004).73 (3.38) 10. Two small studies of European populations reported urinary cesium levels similar to U.5) 7.05-3.16-8.53) 6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.91-6.26 (4.10 (3.58 (6.35 (4.58) 3.92) 3.66 (6.45-6.00-10.24-10.31-4.22 (3.22-11.20-4.58-5.26-6.43-6.48-6.70 (7.58 (4.36-10.0) 7.78 (3.86 (4.98 (6.85) 4.60 (3.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.75 (7.41) 4.00 (8.09) 8.5) 9.51 (4.30-4.18) 8.15-4.78) 4.60-10.08) 4.17) 9.04) 6.42 (5.33-3.7) 10.95 (3.40-5.96-4.68) 4.47) 7.33-8.31-6.00-8.75 (6.07) 8.54 (4.08 (5.39 (5.5 (9.27 (8.11 (5.79-5.05) 6.74-11.56-10.55-5.94 (5.03-6.30) 10.84-7.72-5.59) 4.92 (5.43 (8.68) 6.97-4.67 (6.15 (7.00-5.90 (7.98) 5.58) 8.00-4.13-9. 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.43-11.41-7.2) 11.41 (5.38-12.11 (5.41-4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.61 (7.17) 4.43 (4.34 (5. Using clinically submitted specimens.64) 5.41) 9.12-6.51 (3.43 (4.13-9.06 (5.10) 7.6 (9.97) 8.91) 4.81 (4.93-9.16) 5. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.16-5.50) 4.83) 8.53 (4.67) 5. population results shown in this Report (Alimonti et al.38-7.83-6.90-8.87) 5.27 (6.27-6.21-3.16-8.51 (4.20-8.19-6. (2000) found urinary cesium levels that were slightly lower than those reported for the U.78 (3.35) 3.47) 4.21-4.99) 4.44-5.14) 4.76-9. and were also roughly similar to those in this Report.27-4.53) 3.70) 6.S.37) 4. Minoia et al.91-9.4) 10.46-8.09) 4.3) 11.2 (8.5) 9.17-4.17 (6.14 (6.2) 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 3.36-6.99-4.82-4.74) 3.84-11.8 (9.8) 5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.21 (2.28) 8.10 (3.64-6.S.3 (8.31 (4.14) 4.3) 9.7-12.96-4.68-11.31 (4.26 (3.35 (3.14-6.3-15.08) 4.08 (6.75-11. population.40) 7.56) 4..50-5.57) 3.71 (7.67 (5.03) 6.60 (5.06) 4.95) 8.99-9.53 (6.18-6.48) 7.56 (4.18-7.38 (3.02-4.42-4.S.88-10.35-11.88-4.63 (6.87-4.20-4..89-4.76-6.72 (4.91) 5.03) 5.43) 8.38 (3.65 (6.41 (4.30) 10.84-9.63 (7.43 (3.68 (4.29-3.62-8.66 (5.54 (4.9) 10.35-7.44-9.00-9.62) 5.52-5.50) 4.14-4.84-9.55 (3.08 (3.0 (7.59-8.47) 6.61-3.05 (4.12 (3.07-4.30 (3.42-4.87) 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 5.12) 3.05-4.60-20.64 (4.70) 7.44 (4.95) 10.56) 4.51) 4.30 (4.22) 6.44 (8.99 (3.46-4.63-6.00-5.50) 4.80) 6.96) 4.77 (6.90-3.81 (4.29) 4.77 (4.48) 90th 7.28) 7. Komaromy-Hiller et al.93-7.68) 3.25) 4.23 (7.95-12.1) 11.15-11.78) 4.91) 5.83-7.66 (5.30-4. interval) 4.73-4.94) 7.28 (5.13 (3.96 (4.04) 5.28 (4.77-5.47 (4.36-3.07) 8.74 (4. 1990).9 (9.18 (7.24-4.96) 4.84-7.03-5.41 (8.46 (8.47) 6.27) 4.9 (10.42-6.10 (5.44) 3.51 (7.79) 4.65-4.46 (7.25) Selected percentiles ( 95% confidence interval) 50th 4.71) 6.47 (7.49) 3.60) 3.06 (3.95 (5.2 (8.7) 10.85) 5.99-9.74 (5.77 (7.8) 6.08-7.46) 6.04-11.50) 8.40) 6.64 (8.20) 5.3 (9.98 (7.07 (5. population from the National Health and Nutrition Examination Survey.95) 4.55) 4.79) 6.20-4.50 (6.01-8.45 (4.72) 4.33 (5.0) 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 .54 (5.3 (10. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.33 (5.37-3.39) 8.91 (5.64) 4.05-3.02 (5.08-3.21-5.85-4.74) 75th 5.15) 95th 8.56) 3.29) 5.64) 9.91-7.

blood. Apostoli P. and serum of Italian subjects. Gallorini M. Voorhees RE. et al. Available at URL: http://www. Wood CM. Pietra R. Wolfe MI. Sci Total Environ 1990. Fourth National Report on Human Exposure to Environmental Chemicals 207 .S.296(1-2):71-90.19:3131-3138. Mott JA. Atlanta (GA) 2005. et al. Howerton K.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Clin Chim Acta 2000.atsdr.gov/toxprofiles/tp157. Forte G.html. Paschal D. Comparison of representative ranges based on U. Sabbioni E. patient population and literature reference intervals for urinary trace elements. J Expo Anal Environ Epidemiol 2004. New Mexico. Komaromy-Hiller G.2004 [online]. Trace element reference values in tissues from inhabitants of the European community I. Assessment of urinary metals following exposure to a large vegetative fire. Mincione G.95:89-105. Ronchi P. 2000. Rapid Commun Mass Spectrom 2005. Spezia S. Minoia C. Sewell CM. Pozzoli L. Costa R. Centers for Disease Control and Prevention (CDC). Ash KO. cesium. Third National Report on Human Exposure to Environmental Chemicals. antimony and tungsten. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium.cdc. 4/8/09 Alimonti A. et al. Gatti A.14:120-128. A study of 46 elements in urine. Toxicological profile for cesium.

620-.470 (.377-.470) .33-1.301 (.460 (.950 (.490-.390-.65) 1. Cobalt compounds are also used in manufacturing battery electrodes.650 (. diamond-polishing wheels.09) .16 (.47) 1.386) .327-.270-.890) 95th 1.340 (.630-.930 (.374 (.360-.03-1.430) .25-1.416) .308-.890-1.880 (.67) 1.960-1.610) . Cobalt is used as a drying agent in paints.370-.47 (1.750-.08-1.398) .910-1.05 (.417) .19) .680 (.660) .405-.03 (.14-1.450-.330-.316-.890) .340) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .33 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.17-1.610 (.510) 1.410 (.480 (.01-1.450) .850-1.540-.450) .380 (.04-1.09 (.Metals Cobalt CAS No.07-1.900) .370 (.39) 1.870-1.14) .81) 1.350-.430 (.460) .590) .S.452 (.348-.840) .03) .47 (1.390) .310 (.640) .379 (.515 (.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 .880-1.59 (1.860 (.336-.26) 1.17 (1.430 (.46 (1.07-1. Cobalt occurs naturally in airborne dust.56) 1.15 (1.350 (.950-1.26-2.394) .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 .338-.285 (.630 (.469-.590-.371 (.348-.410 (.620) .01 (.390 (.463-.372) .02-1.367 (.259-.980) .03) 1.294 (.388-.460 (.316 (.650 (.50 (1.519 (.60 (1.680 (.460-.05 (.487) .305-.670 (.500) .610-.460) .390 (.600) .820 (.410-.20 (1.340-.29 (1.940-1.380 (.800-.530) .99) 1.465) .15-1.03 (.330) .583) .379 (.930) .S.17 (1.06 (.940-1.22 (1.980-1.950 (. 0.740-.461 (.540-.790 (.480-. industry is imported or obtained by recycling scrap metal that contains cobalt.930-1.380-.520 (.581) . and 0. and magnetic recording media.900) .670-.414) .434 (.570) .730) 1.530-.300-.430) .410 (.333-.750 (.710 (.428-. and 03-04 are 0.390 (.460) .45 (1.690-.04 (.04-1.740-.340) .300 (.32) 1.520-. and soil.01 (.750 (.36) 1.900-1.640) .06-1.47) 1. Usual human exposure is from food sources. and inks.270-. and kitchenware.950) .313) .410 (.92) 1.690-.291-.37-1.343) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .570-.16-1. large appliances.564) .520-.400-.790) .540) 1.370) .760 (.22-1.359 (.660) .28-2.48) 1.600-.310-. It is also a component of porcelain enamel applied to steel bathroom fixtures.520-.364-.690 (.427-. respectively.419) Selected percentiles ( 95% confidence interval) 50th .810) . seawater.550-. 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.499 (.73) 1.12) 1.520 (.350-.280-.920) 1.360-.680) .590 (.480 (. The cobalt used in U.420 (.24 (1.50) 1.800) .355-.380 (.68 (1.750 (.543) .430 (.610) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.81) 1.44) 1.670-.330 (.420) .520 (.399) .502) .710) 1.290-.670 (.32 (1.12) 1.16 (1.410-.820 (.48) 1.32 (1.900) .570 (.04) 1.640) .630 (.660-.52 (1.500 (.08.04-1.410) . hard metal or in combination with other elements.810-.380-.620-.431) .850) 1.370-.32) 1.520) .23-2. Cobalt compounds are used as catalysts in producing oil and gas.398 (.331-.01-2.26-1.580 (. interval) .670 (.07.540-.75 (1.23) .890-1.410 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray. 01-02.850-1.450) .334) .580 (.850) .450) .870 (.620-.373) .435 (.810) .369 (.21) 1.940 (.03) 1.520-.431) .440-.680) .520) . hard metal (alloys of cobalt and tungsten carbide).700) .590-.270-.16) 1.580 (.600 (.800-.530 (.350) 75th .830-1.16-1.570) .00) . population from the National Health and Nutrition Examination Survey.17 (.430-.26) Total .420) . varnishes.320 (.450-.07.373-.64) 1.13) 1.339 (. and in synthesizing polyester and other materials.520 (.950-1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines. see Data Analysis section) for Survey years 99-00.06 (.22) 1.410-.352 (.760) .550) 90th .24 (.404) .08) .07 (. shiny.53) 1.418 (.496) .393-. It is emitted into the environment from burning coal and oil and car and truck exhaust.900-1.454 (.333-.790-. automobile airbags.424) .560 (.16 (1.05) 1.28 (1.920-1.09 (.350-.370-.550 (.343 (. and fertilizers.490-.890-1.28 (1.410) .540-.340-.42) 1.375 (.319) .360-.32-2.870 (.650-.523) . blue-colored pigments.28 (1.740 (.16) 1.710) .570-. steel-belted radial tires.770) .700) .820 (.

237-.547 (.313-.391 (.895-1.279) .378-.313 (.282 (.54) 1. A portion of cobalt retained for long periods is concentrated in the liver.457) .503-.900-1.429) 1.821-3.00 (.829) .30 (1.361 (.738 (.16 (.630-.316 (.850 (.361-.378 (.792 (.06 (.872 (.11-1.12 (.333 (.361-.57) 1.328) .435 (.960 (.239-.392 (.378-.955) .667-1.257 (.804) 1.259) .833-1.615) .306 (.990) .737 (.386 (.522) .861-1.24) .380-.33) 1. 1979).10-1.50) 1.36) 1.847) .280-.700 (.479-.561) .821 (. 2003).04-1.15) 1.669) .309) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.500-.355) .55) .963) .606 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.487-.785) .Metals fabricated from cobalt alloys (Lhotka et al.215-.638-1.434-.495 (.421) .302-.426 (.462) .611) .861 (.11-1.708) .44 (.552 (.402 (.707) .469-.327-.574-.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 .00) .349) .683-.694) .542 (.616-.301) .407 (.963-1.830 (.10) Total .00) .274-.756 (.523 (.842) .313-.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 .28) 1.328 (.740-1.848 (.562) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al. using hard metal cutting tools.955) . 1972).634-. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.348) .388 (.333-.760-1.16 (.417) .560-.291 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).248-.27) 1.36) 1.337) .393 (.938) .365-.353 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.278 (.508-.362 (.286) .850-1.467-.50 (1.29 (1.598 (.394) .898 (.554 (.562) .644 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.600-. respectively.640) .00 (.313-.365) .963) .259-.777-.17) . Once absorbed and distributed in the body.00 (.33) .449) .505) .19) .60) 1.488) .543) .388 (.310) .500 (.438) . 1972).297) .626-.786-.594) .733-1.781) 95th 1.363) .857-1.328 (.608 (.963-1.548 (.381) .259 (.952 (. 1994.976 (. population from the National Health and Nutrition Examination Survey.35) 1.368) .333-.457-.534-.611) . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.324-.368) .826-1.304) .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 .523 (.838 (.476-.452-.290 (.346 (.824 (.314 (.727 (.938-1.500-. interval) .12-1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.774 (.296-.728 (.10) .25 (.343-.983-1.457 (.442-.728) .404-.04 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.294-.83) 1.317 (.673-.360) .293 (.278-.352) .250) .329 (.439) .323) .275-.662) .382-.09) 1.352 (.279 (.03 (.335 (.513-.792-1.407) .303-.700 (.319-.251-.757-1.911-1.444 (.353-.534 (.400 (.281) .73) 1.50) 1.35) .361 (.00 (.306) 75th .14 (..393-.376 (.463-.358 (.932-1.585) .60) 1.744) 1.301-.10 (.975 (.337 (.529 (.599) .15 (.905) .290 (.582-.461) .781-1. refining or processing alloys.487-.929) .475 (.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 .313-.368 (.282-.326-.425) .396) .468) .27) 1.990-1.689 (.829-1. an essential human nutrient.591 (.513) .595) .513 (.419) .339-.515 (.481) 90th .417 (.964 (.723 (..428-.273 (.324) .949) ..449-.537 (. in the feces. and to a lesser extent.635 (. Smith et al.704-.257-.290 (.362) .753) 1.243-. 1994).23 (1. Cobalt is absorbed by oral and pulmonary routes.844 (.29) 1.391) Selected percentiles ( 95% confidence interval) 50th .25 (.738 (.362-.563-.304-.333-.331-.667-1..329-.396) . with pulmonary clearance half-lives of from one to two years (Hedge et al.271 (.471-.554 (.632-.879-1.750-.750) .433) .296) .344-.234 (.247 (.435-.00-1.917) .533 (.334) .327 (.268 (.275-.471 (.49) 1..703-.29 (1.29) .272-.289) .851 (.248-.352 (.550-.372) .471-.16) .425-.647) .408 (.S.630-.895-1.256-. cobalt is excreted predominantly in the urine.02 (.753-.736-.409) .581) .277-.16 (1.29 (1.479) .369 (.343 (.313-.593) .983) .298 (.342-.455 (.03-1.691 (.384) .378-. or using diamond-polishing wheels that contain cobalt metal..297-.937 (.609) .300) .679-. Exposure in the workplace may come from electroplating.660-.387) .

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

Sci Total Environ 1994. Heki S. Salvatori S. Lung cancer risk in hard-metal workers. Alessandrelli M. Lauwerys R. Cobalt cardiomyopathy. Vitali MT. Cleland D. and hard metal dust. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Christensen JM.(1-3):133-139. salt. Zweymuller K. Unwin P. Falcone G.95:29-37. Lauwerys RB. A report of two cases from mineral assay laboratories and a review of the literature. Bozec C. Sci Total Environ 1998. Sci Total Environ 1994. Linnainmaa M. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Ichikawa Y.216:253-270. Zedda S. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Co-sensitivity between cobalt and other transition metals. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. J Trace Elem Med Biol 2006.48:172-173. Daniel J. Sanghrajka AP. Clin Orthop Relat Res 2003. Leghissa P. J Orthop Res 2003. Lison D. X. Goldberg MA. Steffan I. Oksa P.55(4):269-276. Kuska Y.150:177-183. Palmroos P.50(9):835-842. Hammon E. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Bunn HF. Pisati G. Angerer J.28(5):1121-1128. Edmonds CJ. Fujimura N.157:117121. Meier R. Health Phys 1972. Sabbioni E. Moulin JJ. Ziaee H. Dunning SP. Kirsch-Volders M. Int Arch Occup Environ Health 1997. Kusaka Y. Zobelein P. Epidemiological survey of workers exposed to cobalt oxides. a study of 13 elements in blood and urine of a United Kingdom population. et al. Biological monitoring of workers exposed to cobalt metal. Sci Total Environ 1997. Lhotka C. J Bone Joint Surg Br 2005. Sabbioni E. Health Phys 1979. Tilley S. Blunn G. Stanescu D.87(5):628-631. Boca Raton (FL): Lewis Publishers. Hedge AG. Meyer zum Buschenfelde K-H. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Occupationallyinduced “isolated cobalt sensitization.58(10):631-634.21(2):189-195.69(3):193-200.45:246-247. Mutat Res 2003. Lisi P. J Bone Joint Surg Br 2006.148:241-248. Iavicoli I. 1985. Lison D. Kiilunen M.Metals effects of cobalt. Weyher I. Pradhan C. Occup Environ Med 2001.204:147-160. Occup Environ Med 1994. et al.34:620-626. Mosconi G. Outcome of occupational asthma due to cobalt hypersensitivity. Schramel P. Iversen BS. Kristiansen J. HoffmannB. Chest 1989. 3rd ed. Cobalt and antimony: genotoxicity and carcinogenicity. et al. Weber A. Respiratory health of cobalt production workers. De Boeck M. Molders J. Dickel H. Long-term clearance of inhaled 60Co. Barnaby CF.533:135-152. Dunstan E. Absorption and retention of cobalt in man by whole-body counting.51(7):447450.20(1):25-31. et al. DeSantis V. Robinson C. Zhuber K. Shirakawa T. Trace element reference values in tissues from inhabitants of the European Union. Lison D. et al. Swennen B.150. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Contact Dermatitis 2003. Lasfargues G. McCalden RW. Romazini S. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Goto S. Lauwerys R. Gross RT. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Szekeres T. Hoet P. Cresti R. Bourne RB. et al. Chess DG. Kato M. 2001. MacDonald SJ. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.150(1-3):167-171. Wild P.” Contact Dermatitis 2001. Thakker DM.36:732-734. Bacis M. Kraus T. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Roto P. Salama A.406:282-296. The release of metals from metal-onmetal surface arthroplasty of the hip. Science 1988. Ghat IS. Goto S. Carnes WH. Radulescu M. Schaller KH. Arch Intern Med 1990. cobalt salts. Thomassen H. Schank M. Diepgen TL. Br J Ind Med 1993. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Int Arch Occup Environ Health. oxides. White MA. Am J Ind Med 2003. Sabbioni E. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Hoher T. Kriss JP.22:359367. Buchet JP. and cobalt metals. Buchet JP. Peltier A. J Rheumatol 2001. Rorabeck CH. Thabe H. Swennen B.44:124-132.242:1412-1415. J Occup Med 1992.88(4):443448. Am J Epidemiol 1998. Cannon SR. Uitti J. McMinn DJ. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Smith T. Laippala P. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Linna A. Jarvis JQ.

80-3.40-2.50-1.00) 1.20 (1.53) 1.50) 7.30-2.60 (4.10) 2.40 (1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.36) 1.80-4.10) 2.10-1.80) 2.90) 1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.28.50-1.00-4.40-3.00 (1.80-4.10 (3.14-1.04-1.30-6.20) .30-2.17) .30) 1.60 (3.10-6.00-4.80) 1.50 (2.81) 1.30-4.00) 1.90) 2.50) 3.00) 2.10-6.90) 1.87) 1.40-4.10-3.30 (2.60) 2.70 (1.50-3.30) 2.50-1.40-1.00) 2.00) 5.70-2.00-4.60 (1.56 (1.71-1.10-2.10-2.80 (4.75) 1.70-6.40-3.70-4.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.70) 3.20 (2.50 (3.50 (2.3.60) 1.10 (1.80) 2.90 (2.14-1.40) 2.90-4.20) 90th 3.70 (1.60) 4.51) 1.60) 3.20 (1.70 (5.40) 1.83 (1.60) 2.10-3.90-2.00) 2.10 (4.91) 1.10) 3.62-1.49-1.50 (4.50) 2.10) 5. interval) 1.22 (1.39-1. and 0.40-1.37-1.30) 2.30) 5.60 (2.80 (2.80-3.80) 3. respectively.20-1. the main source of lead exposure for the general U.70 (3.60-2.30-1. Elemental lead can be combined with other elements to form inorganic and organic compounds.60) 5.80 (5. and 03-04 are 0.10-2.50) 5.50) 1.20 (1.40) 5.00) 1.93-2.30 (2.70) 4.40-2.25 (1.70 (2.30-1.50-2.30 (1.32-1.00 (1.60 (2.30 (3.20 (3.00 (5.30 (2.90) 2.50-5.60-4.50-1.40-3.50) 4.50-4.986) .10) 3. leaded glass.90-4.20-2.60-3.87 (1. antique-molded or cast ornaments.10-2.60) 2.50) 1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.32-1.60-4.37 (1.70) 4.66 (1.60 (1.60) 3.60 (2.50 (1.60 (2.45-1.80 (2.70) 1.50-2.40-5.30 (1. solders.10 (2.20-3.70) 2.60-1.30-1.90 (3.00-1.50-6. blue-gray metal that occurs naturally in soils and rocks.942 (.66) 1.60) 2. dense. Lead has a variety of uses in manufacturing: storage batteries.80 (5.30 (4.10-3.50) 75th 2.40-2.72) Selected percentiles ( 95% confidence interval) 50th 1.70) 4.20 (3.80-2.20-3.10-8.80 (1.50-1.69) 1.80) 1.10-4. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.90 (2.00-5.50 (1. Lead is most often mined from ores or recycled from scrap metal or batteries.50 (1.20) 4.80 (3.40 (3.00 (3.30 (2.60 (2.00) 4.946 (.40) Total 1.60 (1.50 (3.90 (3.900 (. 7439-92-1 General Information Elemental lead is a soft.70) 3.50-3.39) 1.20) 3.40) 2.10 (1.80-3.30-5.70-1.40-6.00) 2.20-3.20) 2.70 (1.70 (2.69 (1.60) 1.70-2. and for radiation shielding.90 (1.10 (1.00-6.00 (4.40 (1.30-1.40) 2.20-4.60 (1.02) 1.20 (3.10) 4.30) 2. In the past.90-4.00) 6.10 (2.80 (1.60 (1. Since lead has been eliminated from gasoline.20 (1. ceramic glazes.878-1.50 (2.60) 1.90) 3.900 (.65 (1.70) 3.40-1.60 (1.20) 3.70 (1.70) 1.30 (2. population from the National Health and Nutrition Examination Survey.48) 1.20 (3.75 (1.50-2.50) 1.25) 1.40 (2.80-5.40-1.30 (2.30-1. plastics.30 (2.10-1.30) 95th 5.60 (2. such as lead phosphate and tetraethyl lead.60 (1.50) 1.70) 1.25 (1.20) 3.80) 2.30-2.40-1.70) 1.10-2.40 (5.70-5.90-2.70 (2.30 (4.90-4.80) 1.50) 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 2.60 (3.69) 1.60-1.20 (3.80 (1.55-1.68-1.60) 3.30-1.50 (1.20-6.00) 1.80-4.90 (3.34-1.70-2. Lead was used in plumbing for centuries and may still be present.60) 5.10 (2.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.60 (3.60) 4.40) 2.45 (1.60) 1.55 (1.43) 1.20 (4.20) 3.40 (2.00-2.62 (1.10) 1.70) 4.10-1.90-2.90 (4.90-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 4.70-1.90) 5.60) 4.90) 2.20 (2.80 (1.90) 2.900-1.20-2.19 (1.37 (1.10-2.75-2.52-1.00-1.40) 1.80 (1.36-1.50-4.69 (1.90 (3.50) 5.40) 1.20-3.20-1. brass.09) 1.60) 2.50) 4.90-6.96-2.30 (1.800-1.89) 1.23 (1.Metals Lead CAS No.75-1.60-2.50 (2.00) 1.40 (4.78 (1.70-1.60-1.00 (2.60) 3.20) 4.40-1.36-1.00) 3.86) 1.60) 1.90) 1.52 (1. ammunition.43 (1.55-1.60-1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.43-1.20) 1.00) .77 (1. Before the 1980’s.80-3.43) 1.90 (3.00 (6.40) 3.10-4.20) 5.60) 4.30 (4.3.10) 1.40 (1.S.95) 1.14-1.80) 2.01 (1.70-3.43 (1.30-2.90 (1.31) 1. bronze).30 (1.90-2.60 (3.90) 2.10-3.50 (2.50-2.S.00) 3.20 (3.10) 3.50-5.00 (4.50 (4.60-6. 01-02.50) 2.80 (2.80 (1.70) 1. see Data Analysis section) for Survey years 99-00.20 (3.70 (3.10) 1. 0.40-6.46 (1.80 (4.g.90) 3.62) 1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .52-1.40 (1. metal alloys (e. malleable.80) 1.12-1.899-.00) 4.51 (1.80) 1.20 (1.

840 (.600-.820-1.24-1.745-.10-5.900) .40) 1.800 (.600) .90-2.09) 1.30) 1. stained glass framing.30-3.30-1..59) 1. 0.80) 1.30-2.900) .70 (1.616) .800 (.86-2.S.910-.20 (1.931) .20 (1.50-2.40) 1.00) 2.62) Total .20 (1.941) .900) .80) 2.30-5.80) 2.60-2.620 (.20) .60 (1.10-3.72) 1.708-.700 (.20 (2.731 (.20) .30 (2.700-.40 (1.90) 2.10-1.900 (.600-.850 (. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.29) 2.960-1.833-1.00) 2.700) 1.701) .10 (.40-1.60-3.700 (.690) 75th 1.680) .52-1.900) .52-1.10) 2.600 (.60 (2.80 (2.30 (3.580-.986) .80) 2. However.80) 2. Approximately half of the absorbed lead may be incorporated into bone.70) 1.70-2. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.800-1.680-.50) 1.03-2. dust.700-.80 (1.22) 1.89) 2.10-3.700-.07-1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.20 (1.70) 1.60-3.800) . which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (1.40-2.40-1.14 (1.90 (1.815 (.07 (.800) .60 (1.90 (2.628) 1.40) 2.640 (.00-2.20 (2.00-1.605) .50 (2.70 (2.579-.900-1.558 (.572-.20-2. CDC. and 0.10-1.80-2.20) 1.62-4.49 (1.40) 1.600-.700-.13-3.90 (2.70 (2.40) 2.11 (1.27) 1.637-.800-1.20-2.40 (1.78-2.64) 2.700 (.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.Metals occupational (e.04) .1.13) .700 (. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.688 (.671-.753 (.10) .10 (1.86) 95th 2. 01-02.20-1.625 (.00) .1.600-.00) 1.40) 3.40) 1.86) 1.31-3.818) .80-3.60 (1.828) Selected percentiles ( 95% confidence interval) 50th .920 (.30) .00 (1.04 (.10-1.40-3.04) 2.970-1.75) 4.570-.589-.66 (2.04-2.50-1.900) .700 (.535-.10 (1.60-2.604 (.82 (2.595-.795 (.40) 2.40) 1.90 (1.738) .900-1.560-.10-3.g.90-3.50-2.60-1.20) .90 (2. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.50-3.14 (1.50 (1.00 (2.20) 1.06) . see Data Analysis section) for Survey years 99-00.80) 3.800-.40-5.00 (1.800) .90) 1.540-.23) .21 (2.12) 90th 2.40 (2. 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.41) 2.630 (.04 (.691-.10) 2.900 (.591 (.790 (. interval) .78-2.900-1.960 (.00) .90 (1.50) 1.700) . imported children’s trinkets and toys. In the blood.00-1.940 (.640-. 2007. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. and 03-04 are 0.600 (. battery and radiator manufacturing) and recreational sources.40-1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30-1.30-1.33-2.729-.44-2.40 (2.800) . bullet fragments retained in human tissue.19 (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 .661-.17 (1.20) .757-.14-1.680-.20 (1.31 (1.20 (2. older plumbing systems with leaded pipes or lead soldered connections.600) .40-1.800 (. Fourth National Report on Human Exposure to Environmental Chemicals 213 .91) 2.915-1.660) .752 (.920 (.40 (1.10 (1.923 (.785) .32 (1.30 (1.40 (2.800) .10) 1.506-.90-3.718) .00) .90-2.40 (2. lead-containing folk remedies and cosmetics.808 (.30) 1.990) 1.50 (2. lead-based painted surfaces undergoing renovation or demolition.10-1..33.80) 1.800-.10 (.00 (. 2000).90) 2.40 (1.33 (2.00-2.822-1.00 (1.70) 1.642 (.20) 1.90-2.90) 2. or after soluble lead compounds are ingested.540 (. and contact with soil.29 (2.70-3.78-2.700-.75) 3.00-1.700-1.70) 2.02) 1.625-.10 (.857) .613) .30-1.600-.935) 1.50 (2.674) 1.810-1.18-1.695 (.30) 1.700 (.27 (1.80-2.50) 3.80) 2.50) 2.651) .20-1.35 (.20-1.773) .900) .90-4.52 (1.60 (1.97) 4.677 (.730 (.60) 2.80) 1.70 (2. population from the National Health and Nutrition Examination Survey.659 (.30) 2.833 (.82 (1.70) 3.710-1.862) .11) 2.573 (. lead-contaminated dust in indoor firing ranges.590 (.66 (2.00-2.00 (1.960-1.50) 2.766 (. respectively.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 1.848 (.86 (1.50) 1.579-.70 (2.30) 1.50 (1. 1991).59-2.955-1.620) 1.03 (1.30) 2.610 (. pewter utensils and drinking vessels.641-.556-.636 (.10-1.20 (3.80) 3.749) .30) 1.564 (.650) 1.23-4.40 (1.30) 2.02 (.553-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50-2.40) 2.710-.90-2. or water contaminated by mining or smelting operations.73 (1.70) 3.900-1.990) 2.20 (1.500-.00) .800 (.526-.10) .900 (.480-.10 (1.

04-3.851) .621 (. scant amounts are lost through sweat.920-1.654) . In 1991. with a half-life of years to decades.592-. Lead can cross the placenta and enter the developing fetal brain.648 (.75-2.62) 2.605-.601-.08) .18) 1. 1995).793-1.862-.946-1.20) .677 (.71 (1.28-1.09) 1.603-. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.97) 1.64) 2.603 (.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 . Approximately 70% of lead excretion occurs via the urine.342-.22) .53) 1.571-.701) . BLLs and associated toxic effects differ in children and adults.38 (2.682) .55 (1.31 (1.702) .755 (.763) .742) Selected percentiles ( 95% confidence interval) 50th .17-1. CDC.594-.88 (1.853-1.94-2.633 (.37-1. 2003.01) .681-.838) .977) 1.10 (1.404-.571-.40-1.79) 2.655-.679) 1.992-1.510-.03 (.758) .83) 1.971 (.00 (1.33-1.82) 1.44 (1.688) .49 (1.61) 1.36-2.06 (.71-2.70 (1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.15-2.47 (1.870 (.15) 1.828) .50-2.460-. abdominal pain.508) .Metals 90% of the body lead burden in most adults.00) .709 (.375 (.588-.51) 1.731-.03) 2.561-.541-.677) .52 (1.03) 90th 1.979 (.569 (.683-..644 (.10) 1.97) 1.679-.428) .03 (.19-5.18 (1.69 (1.623 (.24 (1.898) .404 (.00 (1. 2007). zinc.65 (1.917-1.701 (.670) 1.07 (.61) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.639 (. encephalopathy.78-4.657) 1.609 (.46 (1.10 (.50-2.673) .608-.604-.89-5.734) ..26) Total .67-4.68 (1.27 (1.85 (1.48 (1.50 (1.03) .790) .62-2.703) .681-.15-2. through the inhibition of certain enzymes.08-2.14) 1.31) 1.887 (.796-1. 1995.41) .20) . 2004.98 (1.22) 1. Large amounts of lead in the body can cause anemia.667) .918-1.559-.607-.19) 1.655) 75th 1.593 (. and paralysis.06) 1.28) .61) 1.603-. 1993.97 (1.97-18.588-.65-2.893) .56 (1.644) . Schwartz.89-2.18) 2.50) 1.72-2.10) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites 214 Fourth National Report on Human Exposure to Environmental Chemicals . kidney injury.66 (1.753) .11-1.11) 1.615 (.461) ..03) 1.92) 2.800-.43) 2.59-3.659-.47 (2.990 (.583-.18) 1.981-1.66) 2.43 (1.31 (1. hair. and nails (Leggett.77) 2.66 (1.710) .88) 2.08) .586-.535) .765) .918 (.56) 3.62-3.29 (1.15) 1.529-.686) .79) 1.01 (.676) . interval) .55 (1.963-1.606-.11) .35) 2. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.74 (1.667-.02-1.85-2.44 (1. population from the National Health and Nutrition Examination Survey.85-2.662) 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 1.400) .86 (1.639 (.43-1.668-.58) 1.774 (.810 (.63) 1.718) 1.725) .63) 4.56-3.926 (.652 (.25-1. Staessen et al.957-1.933-1.641 (.50-1.579-.02) 1.22-2.88-2.618 (.408-.61) 1.635 (.20-3.17 (.432 (.72-2.667-. seizures.612-.18) .594-.25-1.44) 1.62-1.492-.96 (1.720 (.658 (.85) 1.07) .708 (.52) 1.33) 1.938 (.47) 1.781-1.75 (2.730) 1.09-1.83 (2.914-1.608 (.712 (.933) .623 (.702-. 1996).655) .38 (2.15-3.876-1.22) 1.73-2.720 (.622 (.87) 1.03) .841-1.914 (.04) 2.638 (.05 (.677-.41-1.05-1.51 (1.649 (.469 (. 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.72) .23 (1.56-2.693 (.707 (.09-1.03 (. The skeleton acts as a storage depot.06) .88) 1.725) .43 (2.45 (1.00 (.721 (.03) 2.05-1.28) 2.742) .722 (.14 (1.12-1.64) 95th 2.700-.94 (1. O’Flaherty.98-2.645-.26) 2.551-.988-1.404 (.938-1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.64-2. Nash et al.03-2. The toxic effects of lead result from its interference with the physiologic actions of calcium. 1993).718) .73) 2.828-1.587-.06 (1.03) 1.11 (1.03 (1.31) 1.79 (1.617-.639) .746) .632 (.31 (2.698) .22-1.61) 3.436) .07-1.702) .98) 2.05 (1.33) 2.78 (2.41 (1.812-1.88) 2. based on prospective population studies.696 (.50-2.383-.11 (.940 (. For instance.11 (.11 (1.33 (1.00 (1.962 (.38 (2.53-1.43) 1.0) 3.914 (. and through binding to ion channels and regulatory proteins.900 (.639 (.64 (1.997-1.496 (.671 (.37-1.625 (. with lesser amounts eliminated via the feces.992-1.09-1.34-1.739) .882-1.S.615 (.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 .39-1.645-.975-1.46 (2. and iron. 1991.722 (.380-.988 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.698) .

. and spontaneous abortion (Baghurst et al.atsdr. For example. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. including minority race or ethnicity. 1996. with overt encephalopathy.S.5 per 100. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.7 µg/dL and 4.75 µg/dL in U. Telisman et al. In NHANES 1999-2002 in children 1-5 years old. approximately 11..4% in NHANES 1999-2004. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.. may alter sperm morphology. 1995.07 µg/dL (Becker et al. both the geometric mean (1.. and organic lead compounds not classifiable with respect to human carcinogenicity. 2003. 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. respectively.xls). particularly in the skeleton. and low family income (CDC. residing in housing built before the 1950’s. Schwartz et al.. environmental levels) and health effects is available from ATSDR at: http://www. when the geometric mean BLL was 2. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. IARC considers inorganic lead compounds probable human carcinogens.gov/toxpro2. 2005b. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.. 1996.0 µg/dL in females (Soldin et al.3 million children tested had BLLs of 10 mg/dL or higher (http://www. lead in women may be associated with hypertension during pregnancy. 2000). though there is greater individual variation in urine lead than in blood and greater potential for contamination. Fourth National Report on Human Exposure to Environmental Chemicals 215 . 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. Jones et al. which is an 84% decline. and decrease fertility (Alexander et al. Information about external exposure (i.. However. 2003. More recently.Metals µg/dL or higher as the level of concern in children.. 1999).S.000 adults. 2003).S.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. Bellinger 2005. and peripheral neuropathy generally occurring at much higher levels (e. 2000). higher than 100-200 µg/dL). 2007). usually with BLLs greater than 40 mg/dL. Urine levels may reflect recently absorbed lead. premature delivery. 2002. Payton et al. EPA. 1991. 1999). adults in the 19992000 NHANES sample (Apostoli et al. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.cdc. seizures. 2002). The U. Borja-Aburto et al.. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Pirkle et al. 2002a). adult residents. the geometric mean BLL was 3.cdc..S. Overall. 1984. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. Staessen et al. BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist..21% of approximately 3. 2006).6% in NHANES 1988-1991 to 1. Schwartz.6%) were lower than those from NHANES 1991-1994. 2006)..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. 1994). 2003. reduce sperm count. Both drinking water and ambient air standards for lead have been established by the U... Data submitted through state public health programs from 2006 showed that 1. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. In occupationally exposed adults. urban residence.html. 2009). 1996.. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. High dose occupational lead exposure. Surveillance data reported by U. almost double the geometric mean of 1..g.S.. 1998).S. Muntner et al. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. adults in the 1999-2000 NHANES sample... CDC. 2005b). At low environmental exposures.. the prevalence rate has declined annually since 1994 (CDC. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.4% of children had BLLs of 10µg/dL or higher (CDC. Lanphear et al. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors..2 µg/dL in males and 3. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH.e. 1987. 2005a). Korrick et al. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. 2001)..

Hu H. Farias P. Kuehnemann TJ.gov/mmwr/preview/mmwrhtml/ mm5532a2. Batuman V. Borja-Aburto VH.287:1-11.123:e376-e385. Hertz-Picciotto I. Hu H. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Semen quality of men employed at a lead smelter. Pirkle JL. Kaufman JD.gov/nceh/lead/publications/ books/plpyc/contents. Atlanta (GA). Atlanta. Public Health Rep 2000. Lepom P. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. et al. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Kim R. Wager C. Teratogen update: lead and pregnancy. Becker K. Birth Defects Research (Part A).89:330-335. 4/14/09 Alexander BH. Payton M. Weiss ST. Lead. doi:10. Vupputyuri S. Blanco J.26:359-371. Vimpani FB. Neurotoxicol 1987. et al. N Engl J Med 2003. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Ewers TG. Meyer PA. MMWR Morb Mortal Wkly Rep 2005a. Ganzi A. 2005b. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Managing Elevated Blood Lead Levels Among Young Children. Jacobson SW. IARC Monogr Eval Carcinog Risks Hum 2006. Mantere P. Blood lead levels measured prospectively and risk of spontaneous abortion. Canfield RL.101(7):598-616.53:411-416. Aro A. Checkoway H. JAMA 1996.cdc.205:297-308. Environ Res 2000. 4/14/09 Centers for Disease Control and Prevention (CDC).gov/toxprofiles/tp13. Pediatrics 2009. van Netten C. 2002 [online]. Available at URL: http://www. Available at URL: http://www.cdc. Aug 2007 [online]. 4/14/09 Centers for Disease Control and Prevention (CDC). Rios C.htm. Acquisition and retention of lead by young children. Bellinger D. Lanphear BP. Henderson CR. Speizer FE. Seiwert M.115:521-529. gov/mmwr/preview/mmwrhtml/mm5420a5. CDC. Am J Epidemiol 1999. Age-specific kinetic model of lead metal in humans.73:409-420. Environ Health Perspect 1993.html. Apostoli P. Occup Environ Med 1996. Coresh J. Rotnitzky A.htm.348:15171526. Ga. Am J Public Health 1999. Brody DJ.cdc. 2005. Homa DM. Muntner P.82:60-80. Wigg NR. Hu H. Cory-Slechta DA. Centers for Disease Control and Prevention (CDC).8(3):395-401.1542/peds:2007-3608. Baghurst PA.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. Ronchi L. Scand J Work Environ Health 1984.cdc. Inorganic and Organic Lead Compounds. Kaus S. Lanphear BP. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1999-2002. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Third National Report on Human Exposure to Environmental Chemicals. Adult blood lead epidemiology and surveillance—United States. Bavazzano P. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. The relationship of bone and blood lead to hypertension. Luukkonen R. Jones RL. JAMA 1996. Auinger P. References Agency for Toxic Substances and Disease Registry (ATSDR). Preventing Lead Poisoning in Young Children. Reese YR.54(20):513-516. Blood lead reference values: the results of an Italian polycentric study. Neri A. Caldwell KL. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Rojas LM. Available from URL: http://www.atsdr.55(32):876-879. 2003-2004. Dietrich K.cdc.htm. Available at URL: http://www. Bellinger D. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. et al. et al.gov/nceh/lead/ CaseManagement/caseManage_main. Korrick SA.htm. 1991 [online]. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Leggett RW. Korrick S. Pediatrics 2004. Jacobson JL. MMWR Morb Mortal Wkly Rep 2006. Roberts RR. Stanek KL. Cox C. Robertson EF. Sci Total Environ 2002. Manton WI. Chiodo LM. Baj A. Sparrow D. Atlanta (GA). Muller CH. Hunter DJ. Toxicological profile for lead. 1988-2004. Rotnitzky A.87:1-471.275(15):1171-1176. Int J Hyg Environ Health 2002. McMichael AJ.150(6):590-597. Cox C. Blood lead levels—United States. 4/14/09 Centers for Disease Control and Prevention (CDC). 4/14/09 Centers for Disease Control and Prevention (CDC). Krause C.10:43-50. Lead and hypertension in a sample of middle-aged women. Neurotoxicol Teratol 2004. Weiss ST. Hänninen H. Schulz C. Angle CR. Available at URL: http://www.275:1177-1181. Sparrow D. Neurodevelopmental effects of postnatal lead exposure at very low levels. Hernberg S.113(4):1016-1022. et al. Jusko TA.

Fourth National Report on Human Exposure to Environmental Chemicals 217 .289(12):1523-1531. Roels H. Kidney Int 2003. Schwartz BS. Pizent A. Kaufmann RB. Gunter EW. Gavella M. Rocic B. and copper in men. Low-level lead exposure and blood pressure. Association of blood lead. Hickman T. Amery A. Hu H. Environ Health Perspect 1996. IV. cadmium.Metals results from NHANES III. Flegal AR. Revised and new reference values for arsenic. Schwenk M. Kaufmann R. and hypertension in perimenopausal and postmenopausal women.106:745-750.9:303-327. Lead. Rubin R.108(1):45-53. Exposure of the U. Stewar WF. 50:31-37. Nash D. Lee GS. Schwartz J. Telisman S.153(5):453464.209:301305. et al.S. J Hum Hypertens 1995. Physiologically based models for bone-seeking elements.104(1):60-66. blood pressure and cardiovascular disease in men. Magder L. blood pressure. Am J Epidemiol 2001. Blood lead. Blood lead concentrations in children: new ranges. JAMA 2003. Pirkle JL.118:16-29. et al. Am J Epidemiol 1994. Use of endogenous. Int J Hyg Environ Health 2006. Smith DR. Hanak B. Cvitkovic P. Low-level lead exposure and renal function in the Normative Aging Study. Lauwerys RR.63:1044-1050. Paschal DC. Payton M. Lee SS. Toxicol Appl Pharmacol 1993. Schulz D. stable lead isotopes to determine release of lead from the skeleton. Arch Environ Health 1995.327:109-113. Brody DJ. cadmium. Hwang KY. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Environ Health Perspect 1998. Lee BK. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Osterloh JD. Clin Chim Acta 2003. Wilhelm M. zinc. Weiss ST. dimercaptosuccinic acidchelatable lead. and tibia lead with neurobehavioral test scores in South Korean lead workers. Lustberg M. Kinetics of lead disposition in humans. population to lead: 1991-1994. Soldin SJ.140:821-829. Environ Health Perspect 2000. Jurasovic J. Sparrow D. O’Flaherty EJ. Soldin OP. Sherwin R. lead. Staessen JA.

500) . In addition.10) .70 (1. have often required public health intervention (Zeitz et al.30 (1.574) .40 (3..600) 1.700-.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 .800-1.927) . with the highest concentrations occurring in the kidneys (Barregard et al. Elemental mercury is a shiny.400-.80) 3.20) 2.500 (.30) 4132 4241 03-04 03-04 03-04 .60-2. Accidental spills of elemental mercury.903) Selected percentiles ( 95% confidence interval) 50th .00 (.50-2.Metals Mercury CAS No.90) 95th 4.40-1.700-.80) 4.00-5.797 (.g. Some cosmetic skin creams from countries other than the U. 1980.80) 1.776 (.20-4.2.563 (.814 (. predominantly from fish and other seafood.g. electrical lamps.30) 1.60) 1.363-.30-4.40-2. an organic form of mercury.12) . Apart from methyl mercury. 1998. mercuric chloride).30-5.. such as chlorine (e.30 (2.00 (.60 (2.400 (..S.20 (2.877 (. to form inorganic mercury compounds or salts.00 (2.30-2.800-1.979 (. IARC.60 (1.326 (.800-1.40) 1.02) .60-6. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. and mining and smelting. solid-waste incineration.90 (4. 218 Fourth National Report on Human Exposure to Environmental Chemicals . 1993).900) 75th 1. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.. Atmospheric elemental mercury can be deposited on land and water. elemental mercury is absorbed mainly by inhaling volatilized vapor.490 (.40-2. Survey years 03-04 Geometric mean (95% conf. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. or oxygen. Other major uses include electrical equipment (e.714-. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).30-6.800 (.50) 1.70 (1. phenylmercuric acetate) or topical antiseptics (e.655-. and dental amalgam. Hursh et al.372) .00 (.60 (1.00) 4.00) .472-. sulfur.00-1.300 (.672) .g.484) .90) 90th 3. thimerosal.300-.30) 5.00 (2. synthetic organomercury compounds were once used in pharmaceutical applications. thermometers.900) 1.80 (1. The ingestion of methyl mercury.80 (1.40 (4.419 (.30) 3.800 (. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.919) .70 (4.753-1.700) . may contain inorganic mercury. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).900 (. 1994.40-3.00) 1.700) .500-.60) 2085 2293 3478 Limit of detection (LOD.50) 2. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.70-2.781 (. 1999 .900) . Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. which can bioaccumulate in aquatic and terrestrial food chains.S.700-.30) 3. The kinetics of the different forms of mercury vary considerably. population from the National Health and Nutrition Examination Survey. Woods et al.285-.60-6. 2007).g. inorganic. which create an episodic potential for volatization and inhalation of mercury vapor..50) 4.80 (1.800-1. merbromin).00 (2. Also.600 (.300) .800 (..900) 1.40) 3.50-3.10-3. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges. see Data Analysis section) for Survey year 03-04 is 0. Poorly absorbed from the gastrointestinal tract.00) 1.703-..800-1.00 (1.50) 5. After elemental mercury is absorbed. Kingman et al.60) 1.900) 1. sphygmomanometers and barometers.860-1. interval) .20-3.50-1.60-3. thermostats and switches).800 (.886) .00 (. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. and is distributed to most tissues.00) 3.90 (1.30) 1. and mercury compounds are still used as preservatives (e.. 2002).400-.90-3.689-.20-4.700-.40 (4.500-.70 (3.90) 3.40-1.700 (.90 (1..60-5.70) 911 856 2081 4525 03-04 03-04 .40 (3.700-.500 (. and organic forms. constitutes the main source of dietary mercury exposure in the general population.80 (3.418-.

.297-.377) . Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. 1973).800-1. 1995.820 (.90 (1.800) 75th .800) .300) .00-6.30-4. 1999). After exposure to elemental mercury.700 (.90) 2.10-3.00 (2..919) .50) 3. Jonsson et al. 1971).500 (. Fourth National Report on Human Exposure to Environmental Chemicals 219 .50-2.3) 4.200-.00) 2. Myers et al.10-1.30-6. Smith and Farris..70) 4. with most elimination occurring through in the feces (Sherlock et al. 1991.30) 3. Methyl mercury enters the brain and other tissues (Vahter et al.00) 1. Miettinen et al.700 (.30-11.10 (5.329 (.697-..800-1.40 (1.343 (. 1999-2002..300) .70) 1. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.200 (.70 (1. 1998).300) .20) .10 (1...20-11.70-5.300 (. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.60 (3.30-6.700-.500-.265-.700) 2..80 (1.317 (.825-1.70 (1.318 (.00 (2.940) Race/ethnicity (females.500-1.50-3.500 (. 1996).871-1. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. 1994) and then undergoes slow dealkylation to inorganic mercury.29) .200-.377 (.200-. 1996. Vahter et al.10) 1.40) 2.944 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50) 2.10 (1.70-3.700-1.40) 1.50 (2.. 1992).30 (. 1975.. for both acute and chronic exposures.50 (1.600) .30-4.40-1.73) 1. 2004.20-3.369) 1.27) . The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.800) 1.900-1.00) 7..10 (.800) 1. 1994).10 (3.200-.256-. population. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.00 (2.60 (1.30 (1.30-3.800 (. 2005).14 and 0.800 (.60) 1.667 (.738-.60) 3.. thereafter.50-12.S.60 (1.60 (1.. the transfer Total Blood Mercury−1999-2002 Geometric mean and selected percentiles of blood concentrations (in µg/L) for males and females aged 1 to 5 years and females aged 16 to 49 years in the U.70-5.300) .900 (.50) 95th 2.00) 4.90) 5.80-3.00) 6.20) 1. 1993). Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.00-2. Smith et al.30 (1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.. 1969.0) 4.299-.500-.700-.90) 2.20 (.400-. 2003).20) .664-1.300 (.40 (1.10 (.30-5. 2003).30-2. 1992 and 1999.60) 1. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.00-2.7) 4.726-1.10) . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.395) . Vimy et al.23) ..541-.00) .90 (4.300) . a measure of accumulated dose (Cernichiari et al.200 (.00 (1.40-2.475) .20-3.60) 2.80) 1. Geometric mean Survey years (95% conf.30 (1. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.00-1.500-.Metals the tissues to mercurous and mercuric inorganic forms..20-2.800-1.268-. Excretion occurs by renal and fecal routes.60 (3.10 (1.20-3. Suzuki et al.14.50) 1. 1998).10) .407) . 1992. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations. McDowell et al..02 (.600 (.374) ..70) 4.300 (.90 (3.35 (1.90 (4.824) 1.700 (.70-6. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days..900 (. and a useful marker of exposure in epidemiologic studies (Grandjean et al.00-2.90) 90th 1.300) .70 (1.30) 1. 1993).700-1.30) 1.600) .00 (3. 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.40) 5.500-.800 (. National Health and Nutrition Examination Survey.20 (2.200-.80) 579 527 370 436 588 806 Limit of detection (LOD.00-3..06 (.90) 3.200-.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 .300 (.01) .700 (.50) 1. 1990). Sandborgh-Englund et al. interval) Selected percentiles (95% confidence interval) 50th .269-. 1984.900 (.30-6.60 (2.90 (1.70-3.500-. 1994.900-1.80 (3.00) 1. Methyl mercury is incorporated into growing hair.06-1.40-2.307 (..833 (.

2004.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .700 (. and neurocognitive and behavioral disturbances.500 (.. the existence of a causal relation is unresolved (Chan and Egeland. Rissanen et al..Metals may be more efficient for inorganic mercury (Grandjean et al.600) . Salonen et al. and sleep disturbance (Bidstrup et al.500-.600) . 2004). Inorganic mercury exposure usually occurs by ingestion.600-.600 (.600) . particularly irritability.500-. 1951.500 (. depression. maculopapular rash. overt signs and symptoms of chronic inhalation may include tremor. Drexler and Schaller. typically after a latent period of weeks to months.500) . Sakamoto et al. < LOD means less than the limit of detection. 2006. Sakamoto et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . ataxia.600-. fatigue.700 (.... Factor-Litvak et al.. 2003). Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. Smith et al. and cerebral palsy (NRC. dysarthria.42. altered physical growth. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.700 (. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700-. 220 Fourth National Report on Human Exposure to Environmental Chemicals .700) 2007 2240 3406 Limit of detection (LOD. 2005). 2004).800) . Acute.600 (..600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Oskarsson et al.700-.600 (. sensory impairments. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. 2000.600-. 1970.. pain in the extremities. insomnia.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .700) . 2006.600) . dysarthria. Vupputuri et al. anorexia.. cerebellar ataxia. Survey Geometric mean (95% conf.600) . the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Overt poisoning from methyl mercury primarily affects the central nervous system. 1998.600-. limb deformities. Once absorbed.600 (. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas 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-. 2005... 1995. see Data Analysis section) for Survey year 03-04 is 0. 1995. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al..500-.600 (. 2000).600) . and progressive constriction of the visual fields. 1987). 1963)..500 (<LOD-. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.500-. short-term memory loss. 2000.500-. 1983).700 (. At levels below those that cause acute lung injury.700) size 8147 Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .700 (.500-. Bellinger et al.500 (<LOD-. Stern 2005. hypertension. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.600 (.. Smith et al..600 (.600 (. 2004. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.500-.600) .. 1993). gingivitis. DeRouen et al. In recent epidemiologic studies.500-. 2002. causing parasthesias.700-. hearing impairment.700 (. irritability. 1996). Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.800) .600) . Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. The constellation of findings may include anorexia. and pinkish discoloration of the hands and feet (Tunnessen et al.S.600) . Rice.

840-1.530-.441 (.76-3.330-...430 (.250) . 1998). aged 18 to 69 years.. 2003).68 (2. During the same survey periods.700 (.400 (. Survey years 03-04 Geometric mean (95% conf.01 (. particularly methyl mercury.S. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.65) 1.78 µg/L for adults and 0.530) . range 40 years to 78 years) had an average total blood mercury concentration of 2.360 (. These distinctions can help interpret mercury blood levels in people.atsdr. 2003).09 (2. average age 33 years. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.463) .476 (. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.304) .S. EPA at: http://www.396-.330 (. adult women in several ethnic subgroups (Hightower et al.88) 287 722 1529 03-04 03-04 .509) .14. Benes et al. Fourth National Report on Human Exposure to Environmental Chemicals 221 .29) 1.840-1. 2004.360-.534) . environmental levels) and health effects is available from the U.13-2. Kingman et al. slightly higher total blood mercury levels were found in U. the median concentration of blood mercury was 0.66) 3.S.gov/toxprofiles. 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. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females..433 (.24 (2.33 (2.14-2. et al.480 (. 1997.290-.99-6.. EPA.430) .940 (.8 years.88 (1.360-. From 1996 through 1998.509) .570) .14) 90th 2.340-.416 (..05) 3.280-..61) 1.00) 1.330-. interval) . see Data Analysis section) for Survey year 03-04 is 0. Biomonitoring Information In the general population.76-3. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.24) 1.67-3. 758 children. Information about external exposure (i.770-1.epa.160-.382-.9 years).960 (..410-. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.480) 75th 1.46 µg/L for children.77-2.60-2.60) 619 713 1066 Limit of detection (LOD.700-1. 2001..cdc.46) 3.890 (.67-2. Total blood mercury levels increase with greater fish consumption (Dewailly et al.870-1.495 (.420 (. 2000). Mahaffey et al.85-2. the total blood mercury concentration is due mostly to the dietary intake of organic forms.30) 3. However.96 (1. In Germany the geometric mean for blood mercury was 0.34-3.610-1.313-. Schober et al. Grandjean et al.213-.870-1. A cohort of 1127 U.07 (.31) 1266 1272 03-04 03-04 03-04 . 2006).549) .460 (.12 (.93 (1.16 (1.840) 1.420 (. Over the NHANES 1999-2006 survey periods. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. average age 9.89) 3.405-.23) 2.580) .930-1.200 (. population from the National Health and Nutrition Examination Survey.28) 1.350-.358 (.90) 2. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.530) .18) 2.16 (.08 (1.03-4. and increased slightly in non-Hispanic white children (Caldwell.408) .555) .05) 1.370) .76-4.19 (1.. In NHANES 19992002.460) .413-.gov/mercury and from ATSDR at: http:// www. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. 2009).88-3. who participated in a 1998 representative population survey (Becker et al.S.96 (1.442-.00 (.31) 2.26 (1..52) 2. 2002).. 1998). 2001.54 (2. total blood mercury geometric mean levels in females aged 16-49 years did not change. and the age-related changes differed across the groups (Caldwell et al.492) Selected percentiles ( 95% confidence interval) 50th .60 (1.440 (. military veterans (mean age 52. 2009).e.42) 95th 3.406-.S.330-.97) 2.19 (2.430 (...254 (.39-3.08 (1.20 (1.58 µg/L for 4645 adults. Among the three racial/ethnic groups.55 µg/L.23) . Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.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 . total blood mercury increased with age.Metals standard for inorganic mercury has been established by U.447 (.78-2.520) . Sanzo et al. 1995.63-2.

76 (1.32 (1. 1998).667-1.464 (.246-..301-.309-. 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..417) . the urine mercury increased by approximately 0..04-3.87) 2.463 (.77 (2.S.67 (1.969-1. not to imply a safety level for general population exposure.800-1.275) ..44) 1.S. interval) .25 (.630) . and on average. 2009).00 (.400-.208-.40-1.620-.23-2.362 (.41-2.358) .545 (.289) .00) 90th 1.785-1. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.599) .18-1. 2003).333-.11) 2.87 (1. 2009).443 (.. Department of Health and Human Services noted that several studies have observed a modest.392-.343 (. a biomarker of perturbation in renal tubular function. population from the National Health and Nutrition Examination Survey.498) 75th .11-2. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.714-1. and Italian (Apostoli et al.56) 1266 1271 03-04 03-04 03-04 .616) . 2002).12-3.39) 1. et al.619-.. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.525 (.1 µg/L for each surface with a dental amalgam (Kingman et al.78-4.01) 2.32-2.217 (.225-.652) .455-. An expert-panel report recently prepared for the U.31 (1.368) .28 (. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.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 ..404-.455-.306 (.537) .64-2. military veterans with dental amalgams.40 (1. Information about the biological exposure indices is provided here for comparison.07) 1. 1992).51-2.S.522-.587 (. Survey years 03-04 Geometric mean (95% conf.535) 1.Metals 2000).476 (.06 (.06 (.447 (.35 (1.964-1. et al. 2002) adult population surveys were similar to those in a U.63) 1.566) .455) .990) .307-. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.472-.508 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.276 (.79 (1. 1988..687) .297 (.196-.46-2.265-.65 (1.13-2.13 (1.00) 286 722 1529 03-04 03-04 .54 (2.03) 2.486) Selected percentiles ( 95% confidence interval) 50th .90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .S. Czech (Benes et al.16) 1.970 (.909 (.67 (1.30) 1. Urinary mercury levels in recent German (Becker et al.61) 1.11) 1.875-1.376-.391) . Langworth et al.365 (. 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.79) 1. 2005). Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. mean urinary mercury was 3.480) .09) 1. women of childbearing age have generally been much lower than these levels (CDC.1 µg/L.365 (..30) 2.86) 95th 2.347) .255 (. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.532 (.400) .62 (1.384 (.21) 1.385-.391-. DeRouen et al. Urine mercury and the number of dental amalgams were correlated.768 (.447-.485 (.. reversible increase in urinary N-acetyl-glucosaminidase.88 (1.88-2. Levels in U. 2006).588) .280-.696 (. In the study of U.S.784) 1. 2006.88-2.

580-.52) 3. 16-49 years) 99-00 01-02 .69-3.22-3. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.850-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S.650) 1.Metals Urinary Mercury−Females Aged 16-49 Years Old.31 (1.97) 2.632 (.560 (.810) .68 (3.79) 1.636-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .910) .833) .724 (.622-.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.14.610-.31-1.579-.68-3.624-.42) 2.06 (.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.83-3.966) .07-5.65) 1.25) 2.94) 1. interval) Selected percentiles (95% confidence interval) Survey years 50th .21-3. population.578-. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for females aged 16 to 49 years in the U.772 (.03 (.76 (1.04-1.43-1.61) 1.39-3.832-1.930) .56) 4.99) 1.99 (2.657 (. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.95 (2.606 (.41-6.30-2.540 (.596 (. 1999-2002.30 (2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .04-10.47) 1.76) 2.24-1.799) .526-.81 (3.59-5.92) 2.09-1.691) .85-3.55) 90th 3.600 (.740 (.42) 90th 2.92) 3. population.27 (2.14 and 0.13-4.35) .557-.664) .21 (1.699) 1.650 (.501-.637) .03 (.38) 4.500-.03-2.37) 1.47) 1.00) 2.84 (2.99-2.615 (.30 (1. 1999-2002.650 (.45-2.46) 3.30 (2.50 (2.709) . Geometric mean (95% conf.450-.420-.665) . National Health and Nutrition Examination Survey.592 (.723 (.24) 6.721 (.656-.475-.41 (2.55-3.760 (.07-2.91 (2.32 (1.16-5.09-1.580 (.61-6.508-.831) .774) .631-.710) 1.15-1.17) 95th 5. Geometric mean Survey years (95% conf.50-4.32-3.57-4.16) 5.10-2.92) 4.23-1.35 (1.410-.56 (1.710 (.3) 5.81-6.91-7. National Health and Nutrition Examination Survey.45-3.806) .790) .22 (.45) 2.655 (.23-1.72) 1.10-4.42-3.892) .77) 1.909-1.32) 2.565 (.846) .706 (.99 (3.07) 1.65-4.79) 3.44) 3.520-.00 (3.41 (1.51 (3.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .45) 2.56) 3.426-.21 (2.605-.62 (4.68) 3.46 (1.28 (1.62 (1.670) 75th 1.97) 2.520-.05 (3.50 (1. 16-49 years) 99-00 01-02 .03) 1.809) .15 (2.77) 2.686) .744) 1.516 (.502-.97 (1.540-.620 (.14) 3.76-5.00 (2.97) 2.710 (.560-.41 (1.522 (.87-4.742-1.18) 3.553-.569-.48 (2.45) 95th 3.831) .70 (2.69 (1.824) . interval) Selected percentiles (95% confidence interval) 50th .387-.709) 75th 1.582-.62 (3.27-1.84 (2.51) .53-3.639 (.98 (5.616-.13 (2.05 (2.719 (.658 (.870) .685 (.14-1.54) 595 531 381 442 594 826 Limit of detection (LOD.S.45 (1.85) 4.27 (1.37 (1.18 (3.14-2.89 (2.46-4.

77(2):124-129.7(3):176-184.19:478-484.295(15):17841792. Lapham LW. Bidstrup PL.113(10):1381-1385. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Spevackova V.295(15):1775-1783. Centers for Disease Control and Prevention (CDC). Weihe P. Trachtenberg F. Mangili A. Gagliardi T. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. Rosenbaum G. Biennow M. Schaller KH. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Martin MD. Cent Eur J Public Health 2000. Leitão J. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Becker K. Cernichiari E. et al. Total blood mercury concentrations in the U. mercury exposure. Environ Health Perspect 2003.111:719-723. Chronic mercury poisoning in men repairing direct-current meters. Jorgensen PJ. Sandborgh-englund B. Dewailly E. Br J Ind Med 1993. Arch Environ Health 1992. Garrett N. Luis H. Geier J. Mercury derived from dental amalgams and neuropsychologic function. Caldwell KL. JAMA 2006. Krause C. Attewell R. Environ Res 1998. Lancet 1951. Cernichiari E. Levallois P. 2007 TLVs and BEIs. JAMA 2006. Videro T. Becker K. Myers GJ. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Martin MD. Drago I. Neurotoxicology 1995. Application to workers exposed to mercury vapour. Berglund B. Niklasson B.149:301-305. Cortesi I. Elia G. Barbon R. selenium. The concentration levels of Cd. Budtz-Jorgensen E. Woods JS. Pb. 206:15-24. Snihs JO. Schuzt A. Tissue levels of mercury determined in a deceased worker after occupational exposure. Enzymuria in workers exposed to inorganic mercury.212:588-598. Int JHyg Environ Health 2002. Cernichiari E. Greitz U. Martins IP. Am J Epidemiol 1999. Lebel G. Int Arch Occup Environ Health 1999. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Chan JM. Ekman L. Fish consumption. Apostoli P. Kaus S. Int Arch Occup Environ Health 1988. Zn.61:65-69. Drexler H. Hultberg B. Jarvholm B. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Benes B. population: 19992006. Tavares M. Sallsten G. Mortensen ME.S. Grandjean P. Egeland FM. Seifert B. Begg M.8(2):117-119. et al. Vahter M. Kinetics of mercury in blood and urine after brief occupational exposure. 2005. Third National Report on Human Exposure to Environmental Chemicals. White RF.50:17-27. Schulz C. Osterloh JD. Jacobs D. Hasselgren G. Brewer R. Cutress T. Markers of early renal changes induced by industrial pollutants. Jorgensen PJ. et al.62(2):68-72. Buchet JP.205:297-308. Lepom P. Cianciola ME. Factor-Litvak P.Metals References Aberg B. Barregard L. Sallsten G. Castro-Caldas A. Arch Environ Health 1969. Cox C.47(3):185-195. Locket S. Cu. Sallsten G. Kjellstrom T. McKinlay S.2:856-861. Cejchanova M. I. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Metabolism of methyl mercury (203Hg) compounds in man. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Leroux BG. ACGIH. Bernard AM. Ayotte P. Roels H. Int J Epidemiol 2004. Fawcett J. Falk R. Daniel D.16(4):705-710. Aposian HV. Skerfving S. Seiwert M. Bjornberg KA. Kaus S.56(4):350-357. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. J Toxicol Environ Health 1997. and heart diseases. Arch Environ Health 1992. Int J Hyg Environ Health 2009. Schutz A. Schulz C. Grandjean P.33:1-9. Townes BD. Weber JP. Caudill SP. Persson G. Harvey DG. Smid J. Bellinger DC. Woods JS. et al. Int J Hyg Environ Health 2003. Bonnell JA. Health effects of dental amalgam exposure: a retrospective cohort study. and Se in blood of the population in the Czech Republic. Bernardo M. et al. Hg.72:169-173. et al. Bruneau S.. 52:19-33. Jones RL. DeRouen TA. Barregard L. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Subrt P.289:1324. Echeverria D. Sci Total Environ 2002. Impact of maternal seafood diet on fetal exposure to mercury. Cerna M. Marsh DO. Lauwerys RR. Barregard L. Cardenas A. Arch Environ Health 2001. Cincinnati (OH): Signature Publications. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Atlanta (GA). et al. and lead. Weihe P. Barregard L. Seiwert M. Environ Health Perspect 2005. Kline J. Bates MN. Nutr Rev 2004. Clarkson T. Conradi N. Debes F.

Skerfving S. Beryllium. Albertini T.38:3860-3863. Patterson DG Jr.70(5):310-314. Ann Intern Med 1963. Environ Health Perspect 2004. Fourth National Report on Human Exposure to Environmental Chemicals 225 . 1993. J Dent Res 1998. Nakai K. Fernando R. Salonen JT. 1999 and 2000. 2000. Salonen JT. Sampson EJ. Lancet 2003. Hattula T. Sundquist KG. Arch Toxicol 1996. Voutilainen S. Ekstrand J. J Pharmacol Exp Ther 1980. Sakamoto M. Kubota M. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. Kantola M. Pacific Islander. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers. Urinary excretion of mercury after occupational exposure to mercury vapor and influence of the chelating agent meso-2. Kolff WJ. Kubota M. Environ Health Perspect 2006. Davidson PW. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population.php.95:406-13. Adachi T. Demuth S. Burse VW. Allen J. et al. 7/15/09 Jonsson F. Osterloh J.59(5):692-706. Sallsten G. Relation of a seafood diet to mercury. National Academy Press. et al. docosahexenoic acid and docosapentaenoic acid. lipid peroxidation. Br J Ind Med 1991. and Exposures in the Glass Manufacturing industry. Akagi H. Hirayama K. Circulation 1995. Vesterberg O.112(5):562-570.91:645655.iarc.77(4):615-624. Nyyssonen K.Metals Grandjean P. Rice DC. Matsumoto S. Elimination of 203Hg-methyl mercury in man. Lakka TA. Elimination of free and protein-bound ionic mercury (203Hg2+) in man.214(3):520-527. arsenic. J Dent Res 1998. cardiovascular. International Agency for Research on Cancer (IARC).114(2):173-175. Kingman A.49(6):394-401. Kauhanen J. KajiwaraY. Satoh H. Halbach S. Lagerkvist BJ. A compartmental model for the kinetics of mercury vapor in humans. Mercury in biological fluids after amalgam removal. Dillon CF. Blood mercury reporting in NHANES: Identifying Asian.48:247-53. O’Hare A. Shamlaye CF. Volume 58. Environ Health Perspect 2004. Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey. Hursh JB. Environ Res 1995.77(3):461-467. Hightower JM. Yasutake A. Br J Ind Med 1992. IARC Monographs on the Evaluation of Risks to Humans.112(11):1165-1171. and the risk of myocardial infarction and coronary. Hattula T. Clickner RP. Declining risk of methylmercury exposure to infants during lactation. Cox C.5:214-219. Clarkson TW. Korpela H. Mercury. Korolainen A. Barregard L. Greenwood MR. Environ Sci Technol 2004. Rissanen T. Tillander M. The US EPA reference dose for methyl mercury: sources of uncertainty. Johanson G. Elinder CG. Schultz A. Murata K.3(2):116-122. Amalgam tooth fillings and man’s mercury burden.361:1686-1692. Nakamoto S. Cadmium. Washington (DC). Toxicological effects of methylmercury. Miettinen JK. Bodurow CC. methylmercury transport across the placenta via neutral amino acid carrier. Environ Res 2004. Br J Ind Med 1993. Boeckx M. Acute mercurial intoxication treated by hemodialysis.90:185-189. Intake of mercury from fish. Cernichari.5:252-257. Mehaffey KR. Ann Clin Res 1971. et al. Available at URL: http:// monographs. Sandborgh-Englund G. et al.3dimercaptosuccinic acid (DMSA). Hernandez GT. Environ Physiol Biochem 1975. Palumbo D.13:496-501. and multiracial groups. children and women of childbearing age: reference range data from NHANES 1999-2000. Hair mercury levels in U. National Research Council (NRC). The distribution and biological half-time of 203 Hg in the human body according to a modified whole-body counting technique. Nakano A. Elinder CG. Needham LL.S. Schutz A. Myers GJ. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Oskarsson A. Environ Res 2002. Sakamoto M.71(1):29-38. Ann Clin Res 1973.fr/ENG/Monographs/vol58/index. Liu XJ. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. and any death in eastern Finnish men. Bolger PM. Miettinen JK. The effect of ethanol on the fate of mercury vapor inhaled by man. Circulation 2000. Renal and immunological effects of occupational exposure to inorganic mercury. Sanchez-Sicilia L. selenium. Rahola T. Roels HA. Sandborgh-Englund G. McDowell MA. Rahola T. Langworth S. Pellizzari E. Toxicol Appl Pharmacol 1999.50(9):814-821. Rahola T. Arch Environ Health 1996. Langworth S. Fish oil-derived fatty acids. Seto DS. Schutz A. Ceulemans E. Hallen IP. Rissanen K.155(2):161-168.51(3):234-241. Nyyssonen K. Native American. Lauwerys RR. Hum Exp Toxicol 1994. Ohlin B. Seppanen K. Hattula T.103:2766-2679. and polychlorinated biphenyl and other organochlorine concentrations in human milk. Weihe P. Brown LJ. and the risk of acute coronary events— The Kuopio Ischaemic Heart Disease Risk Factor Study.

Nakazawa M.4(5):981-988. Farris FF. Amurrio A. Whittle K. Orr MF.111(12):1465-1470. Vorwald AJ. Hislop D. Effects of occupational exposure to elemental mercury on short term memory. Am J Physiol 1990. Longnecker MP. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Osterloh J. Toxicol Appl Pharmacol 1994. JAMA 2003. Suzuki T.115(10):1527-1531. Lind B.98(1):133-142. Smith PJ. Stern AH. Mottet NK. Matsuo N.97(2):195-200.48(4):221229. Environ Res 2005. et al. McDowell M. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Environ Health Perspect 2007. Environ Health Perspect 2002. Shen DD.110:129-132. 1993-1998. Sandler DP. Goldberg J. Topping G.2:117-131. Leitao JG. Hum Toxicol 1984.128(2):25125-25126. et al.31:687-700. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Smith AE. Friberg L. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Takahashi Y. Zeitz P. Public Health Nutr 2001. Newton G.79:786789. Hongo T. Smith JC. Schober SE. Martin MD. Yoshinaga J. The contribution of dental amalgam to urinary mercury excretion in children. Methyl mercury pharmacokinetics in man: a reevaluation. Tunnessen WW. et al. Mooney TF. Hall LL. Sinks TH. Effects of exposure to mercury in the manufacture of chlorine. Environ Health Perspect 2003.289(13):1667-1674. Imai H. Smith JC. Vimy MJ. Vupputuri S. Kaye WE. Patil LS. Stern AH. Turner MD.37:245-252. Leroux BG.124:221-229. Blood mercury levels in US children and women of childbearing age. Aguinagalde FX. Bernardo MF. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Guo S. Fisher HL.258(4 Pt 2):R939-945. The kinetics of intravenously administered methyl mercury in man. Dorronsoro M.40:413-419. Langolf GD. 1999-2000. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Pediatrics 1987. Daniels JL.Metals Sanzo JM. Toxicol Appl Pharmacol 1994. Woods JS. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Am Ind Hyg Assoc J 1970. Smith RG. Most B. Toxicol Appl Pharmacol 1996. The hair-organ relationship in mercury concentration in contemporary Japanese. Bolger PM. Sherlock J. Br J Ind Med 1983. Arch Environ Health 1993. Baser M. Burbacher T. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Jones RL. McMahon KJ. Lorscheider FL. Azpiri MA. Acrodynia: exposure to mercury from fluorescent light bulbs. DeRouen TA. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Amiano P. Vahter M. Environ Res 2005. Allen PV.

0 (81.6-72. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2 (69.1-44.1 (38.9 (33.9-55. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.6 (40. 0.1-48. aldehyde dehydrogenase.6-96.8-106) 88.5) 47.7-60. Compounds of molybdenum are also used as corrosion inhibitors.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 47.2) 48.7-47.2-59. and in pigments for ceramics.8) 75..5) 80.2-91.8-94. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.3 (55.0-77.5 (41.3 (47.0) 39.8.3) 54.7 (58.0 (46.9-83.5) 60.0-38.5) 44.8) 48.1 (91.7-73.6-55.9) 67.3 (37.9 (78.1 (71.2 (56.0 (41.6-62.1) 46.3) 37. 2001.2) 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 (98.2) 41.4 (48.1) 57.8-108) 87.9 (52.6) 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. inks.8.4 (34.6-46. More recently.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.1-88.7) 45.7 (45.5-124) 108 (92.9 (34. and 1. Excretion occurs predominantly via the kidneys.0) 60.8-49. urinary excretion over six days CAS No.2-79.3 (46.1-63.5) 80.0-65. respectively.5 (81.7-105) 69.8 (42.8 (85.7) 51.7 (44. 01-02. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9) 34.7) 78.2-42. 2001).0 (42.6) 71.0-85. and xanthine oxidase (Kisker et al.1) 60.4) 45.7) 75th 84.9-85.7 (73.3-115) 152 (120-217) 177 (142-207) 152 (141-169) 206 (150-274) 166 (147-170) 156 (135-175) 187 (146-223) 152 (134-180) 130 (119-142) 780 683 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.5-66.0-101) 82.3-91.4) 76.0-62.5-46.5-91.4 (80.9) 62.0) 55.8 (67.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.8) 39.6 (55.2-59.5 (37.7 (71.5.1) 82.9 (40.6 (43.3 (84.3 (53.6-42.7-122) 93.7-50. population from the National Health and Nutrition Examination survey. interval) 45.0 (48.2 (49.8 (82.6) 93. 7439-98-7 General Information Elemental molybdenum is a silver-white.6) 53.7) 57.4) 41.1) 59.0 (43. chemical reagents in hospital laboratories.1) 126 (106-147) 109 (94.8) 40.3 (64.9-55. see Data Analysis section) for survey years 99-00.3) 47.9 (37.0-71.2 (61.6 (73.8-90. hydrogenation catalysts.2 (83.0) 54. lubricants.7-96. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.6-58.5-52.4) 52.4-61.6) Selected percentiles ( 95% confidence interval) 50th 50.5 (67.7-41.1-52.0 (76. semiconductor and battery industries have begun to use molybdenum.6) 51.4-52.3 (73.3 (38. which exert homeostatic regulation over molybdenum balance.8) 44.0) 62.6-82. At a daily oral molybdenum dose of 24 µg.0 (42.3) 85.4 (79.5-65.3 (71. and paints.0) 84.7) 78.6) 71.2 (49.9 (73.3 (79.2) 52.0) 45.1-59. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.4) 42.1-55. WHO.2-53.7 (51.0-53.5-68.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.4) 49.7 (50.7-39.1-52. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2 (40.3) 65.7 (37.6 (55.5 (43.4 (72. 1996).7 (36. and 03-04 are 0.0-56.5 (49.7-51.4) 56.3-44.7) 46.1) 35.1-51.0) 97.2) 40.9 (32.9-109) 97.2-70.3) 41.1 (34.5 (74.2 (63.6 (52. In humans.0-110) 90.4-82.3-75.5) 85.5-41.3 (55.8-46.3) 83.2 (38.7-68.5 (41. Fourth National Report on Human Exposure to Environmental Chemicals 227 .5 (48.4-75.7-92.S.2) 79.7) 77.2) 37.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.9 (44.3-47.5-52.2 (55.9-56.7-84.4 (48. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.0-100) 63.9-82.7-91.2) 53.7) 86.8) 46. 1997).Metals Molybdenum or ore deposits.6 (40.2-37.

6 (38.2-65.1-39.4) 58.0 (74.5-119) 90. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.7) 112 (95.1 (49.8-66.4) 122 (107-133) 109 (99.5-69.5-60.1-79.6 (42.9 (64.9) 31.2) 43.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.5 (50.9 mg/kg/day and established a tolerable upper intake level of 0.5 (83.2) 55.7 (66.8-42.4) 77.8) 61.3-45.9-42.7-120) 87.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.3-102) 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 40.1-100) 86.3 (55.0) 39.6-63.1-45.8-67.0 (58.3 (58.9-118) 91.3-44.6) 39. urinary excretion over six days rose to 50% and 67%.1) 40.2 (69.3) 40. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.1) 37.2-47.0) 38.4) 89.7-100) 77.4-106) 85.7) 75th 63.4) 116 (101-126) 104 (88.9-45. 2001).5 (40.3 (71.0-103) 103 (90.03 mg/kg/day in humans (IOM.9) 44.7-93. population from the National Health and Nutrition Examination survey.2 (40.9-96.1-38.9-71.5 (36.3) 57.6 (57.1-40.6-88.5-62.0) 53.9-41. and clinical or epidemiologic evidence of adverse effects is limited.Metals was 18% of the ingested dose.0) 39.7-40.1 (42.7 (30.4 (55.0 (80.3-141) 109 (81.0) 88.0) 44.3 (51.6-61.1 (30.4 (78.3-52.8) 38.1 (37.1-109) 89. at daily oral doses of 95 µg and 428 µg.8) 79. 1961.8-84.7-43..2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.3-115) 98. 1999).2) 42.4) 44.S.6-78.2 (57.5 (80.5 (54.5) 90th 108 (97.5 (39.9) 92.8-46.2) 39.2 (37.1-41.1) 101 (83.7 (77.1 (38.8) 71.2) 37. Molybdenum is generally considered to be of low human toxicity.1-81.1 (40. of the ingested dose (Turnlund et al.6 (36.4-118) 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 .0-38.3 (53.5) 63.5 (38.5 (79.8 (36.8) 37.2-46.9 (36.4 (67.9) 79.7-137) 129 (109-155) 112 (97.2 (36.1) 65.3 (83..2-96.6) 39.9 (35.6-41.1 (38.5 (65. 1995).3) 44.4) 48.5-70.5 (39.5-99.5 (41.5-46.0) 36.4) 61.1 (44.9-68. Based on studies finding adverse reproductive effects in rats and mice.0-120) 85.7) 41.3) 43.0-46.6 (71.4 (59.9 (49.2) 38.2) 39.1-34.9 (39.4-120) 101 (84.7-62.2-96.3) 56. EPA. 1993).6 (59.5 (65.4) 47.4 (56.9) 40.6) 36.5-45. Biomonitoring Information Molybdenum is an essential element for health. and urinary levels reflect intake from all sources.9 (40.1 (82.2 (40.2) 42.6-61.2 (50. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5-44. 1997).9 (79.5) 73.1-127) 90.4-41.8-52.0-133) 119 (88.9-117) 57.6) Selected percentiles ( 95% confidence interval) 50th 41.5 (37.8-65.7 (75.0 (35.7) 45.6) 48.5) 60.5 (78.4 (37.5-97.1 (54.7) 57.7) 42.2) 37.1-112) 78.8 (90.6-76.3-59.9 (64. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2-40.1 (39.3-43.8 (57.5 (35.2) 58.4) 60.8 (56.8 (37.4-107) 85.5-35.0) 33.3-68.8-47. In industry. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.7) 53.9-45.2 (52.3 (71.9) 41.5 (59.1 (33.3) 41.6-45.8) 38. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.3 (36.1) 37. respectively.8-118) 81.5) 71. but available epidemiologic data are scant.1) 43.2-49.5-50.9-61. interval) 43.1-43.7) 115 (93.5-92.5) 72.2-80.4-76.8 (75.3) 64.5 (34.4) 40.8) 45.0) 72.7-38.8-47.3) 37.0) 62.9 (73.5 (35.2-121) 107 (92. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.2 (33.2-41.3 (37.4 (40.4-66.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.8) 39.2 (43.3 (36.2 (40.4-39.0-46.9 (39.3 (37.5 (40.S..1-39.5 (41.3-46.5 (37.6-63.7-52.7) 62.6) 43. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-87.1-67.1) 56.3-56.0-56. U.4 (53.6 (36.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.2 (73.4-185) 106 (94. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.7-44.3) 61.8) 62.0-41.4 (44.9-40.4-42.5-48.1-43.

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

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

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

Blanks R. Stilianakis NI.123(3):451-454. and gold excretion of patients after insertion of noble-metal dental alloys. Urinary excretion of platinum from platinum-industry workers. Pethran et al. Herr et al.htm. Nowak D.55(2):138-140. Fruhmann G. 2003.76(1):5-10. 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. Hysell D. 2000. Alimonti A. Duneman L:Long-term urinary platinum.htm. Platinum concentrations in urban road dust and soil. Kaus S. and platinum. Fries HG. Environ Health Perspect 1975b. Seiwert M. Kelly J. Hysell D.01 µg/L (Becker et al. Petrucci F. Crocker W. rhodium. 206:15-24. 1999.04 µg/L) in this Report. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.10:63-71. Herr et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Environmental Health Criteria 125. 2003.35:313-321. Gromiec JP. New York: John Wiley & Sons. and in blood and urine in the United Kingdom. Environ Res 1975a. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Iavicoli I. Campbell K. Schierl R.. et al. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.005 µg/L (Iavicoli et al. 2003). 289-380. Bocca B.70(3):205-208. Part 1: monitoring of urinary concentrations. Saindelle A. Occup Environ Med 1998. Hauff K. Jankofsky M. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Schierl. Pethran A. 2003.. Thornton I.. Urinary platinum levels associated with dental gold alloys. Carelli G. Platinum. Uptake of antineoplastic agents in pharmacy and hospital personnel. 3/31/08 Moore W Jr. International Programme on Chemical Safety (IPCS). Huber R.13(1):24-30. Turfeld M. Schierl R. Available at URL: http://www. Modest (ten-fold or less) elevations in urinary platinum concentrations were associated with handling of cisplatin and carboplatin by pharmacy and other hospital personnel (Ensslin et al. population were below the limit of detection (0. Schierl et al.S.. 2004) or less than 0. et al.org/documents/ehc/ehc/ ehc125. Ensslin AS. Grimm CH. 2001). Seifert B. Farago ME. Occup Environ Med 2004. Patty’s Toxicology. Arch Environ Health:1969. Raab W. 1998).. Kazantzis G. Wilhelm M. Biomonitoring of traffic police officers exposed to airborne platinum. Int Arch Occup Environ Health 1997. Hebert R. palladium. Biomarkers 1999. Schulz C. Senofonte O.. Br J Pharmacol 1969. Herr CE. Schulz C. Schierl R.inchem.Metals the International Programme on Chemical Safety at http:// www. et al. 1998).61(7):636-9. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. ruthenium. Cohrssen B. Int J Hyg Environ Health 2004. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. van de Weyer C.. 1997. Ruff F: Platinum and platinosis. pp. Pethran A. Kulka U. Nickel. Saindelle A. Wilhelm et al. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Levels of platinum in urine for the U. Angerer J. Neuendorf J. Arch Environ Health 2001.56(3):283-286. Allergy and histamine release due to some platinum salts. Hall L. Powell CH. 1991 [online]. Rommelt H. Kavanagh P. osmium. References Becker K. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..19:685-691. 2004. et al.9:152-158. Int Arch Occup Environ Health 2003. In: Bingham E... Several studies have shown that background concentrations in general populations were usually less than 0.. Czerczak S. International Journal of Hygiene and Environmental Health 2003. Schierl R. Biomonitoring Information Urinary platinum levels reflect recent exposure. Boos KS.org/documents/ehc/ehc/ehc125. 5th ed. Parrot JL. Influences on human internal exposure to environmental platinum. which elevate urinary platinum by five to twelve-fold (Begerow et al. Kuster W.inchem. 2004). Gieler U.4(1):27-36. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Ewers U. Analyst 1998. J Expo Anal Environ Epidemiol 2003. Begerow J. eds. palladium.207(1):69-73. Moore W Jr. Ruff F: Histamine release by sodium cholorplatinate.

490 (.200 (.220 (.218) .200) .440 (.196) .470) .160-.270) .420-.150-.450 (.145-.170 (.200-.180 (.310 (.160-.210 (.160 (.500) . and 03-04 are 0.170 (.240) .360-.147-.390) .450 (.250-.330-.220-.490) Total .243) .400) 95th .185 (.185-.410-.400) .430-.170-.490) . In the United States.220) .218) .300) .200-.270 (.179-.160 (.200 (.190 (.202 (.400 (.300 (.400) .200) .156) .170) .400 (.370 (.520) .184 (.157-.170 (.260-.240) .330) .360-.460-.170-. it has not been specifically mined or refined in the United States since 1984.160-.201 (.410) .210 (.200) .360-.410-.170-.350) .440 (. respectively.290 (.150-.200) . Human health effects from thallium at low environmental CAS No.370) .202 (.430 (.290 (.270) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.220) .260-.450 (.380-.270 (.520) .191 (.350-.300-.370 (.450 (.220 (.690) .187-.145 (.206) .410-. see Data Analysis section) for Survey years 99-00.220 (.410 (.390 (.190 (.500) .360 (.217 (.370-.180 (.350-.370 (.330) .300 (.200 (.250 (.320) .390) .250-.239) .230 (.280) .260 (.360-.430) .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 .240-.440) .380-.400-.300) .181-.320) .480) .430-.470 (.450) .156-.135-.173) .400 (.201 (.290-.160 (.340) . representing distribution into other tissues.02.270-.330-.410-.260) .150-.280 (.188) .183) .370 (.150-.240-.230) .640) .360 (.330-.370 (.430 (.180-.360-.290) .260-.400) .220) .290 (.290) .370 (.217) .410-.410 (.230-.180-.S.330) .171 (. From these and other sources.Metals Thallium depilatory cosmetics.590) .159 (.400-.200-.260-.200 (.370-.144 (.430 (.270-.390-.420-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.420) .290-.420-.190 (.460) .220 (.320 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.390-. In the past.380 (.215) .470 (.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 .180 (.173) .630) .172 (.158) .280 (.320-.450 (.300) .450 (.150-.163) .160-.350-.310 (.190 (.550 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 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.400) .170) .160 (.430 (.170) .155 (.167-.178) .175) .250-.510 (.137-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.490) .420) .190-.330-.290) . In addition.290 (.410 (. the latter being the current major industrial consumer of thallium in this country.440-.02.02.560) .410 (. 01-02.290) 90th .230) .196) .330-.340-.350-.390-.250-.340-.159 (.240) .340-. however.200 (.148-.180-.146 (.162-.410-.290 (.440 (.500) .260 (.470) .197 (.340-.360 (.320) .230) .270-.200) .210-.156) .182-.260 (.340 (.360 (.160-.147-.290 (.310-.280) .330-.172 (.165 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al..360) .460 (.390) .220) .430-.410 (.330-.440) .450 (.192) Selected percentiles ( 95% confidence interval) 50th .390) .270 (.160 (.180) 75th .420) .430) .173-.400 (.167-.440 (.250-.200 (.172) .510) .380) .350 (. Thallium disappears from the blood with a half-life of several days.480) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.500 (.200) .250-.400-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .310) .170-.220 (.159 (.520) .390-.250-.230-.420) .225) .280 (.220) .149 (.200-.180) .133-.480) .480) .183) .176 (.170-.177) .250-.280-.420) .400 (.230) .330) .220) .340) .470) .490) .370) .380 (.420-.480) . 2005).147-.370-.440) .370-.400-.170-.140-.153-. thallium readily crosses the placenta and also distributes into breast milk.210) .410 (. and 0.350 (.250) .390 (.270 (. 0.280) .450 (.260-.240-.150-.280-.370 (.190 (.420 (.190 (.167 (.590) .460) 336 362 290 697 746 725 1380 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .450 (.145-.134-.154-.290) .420) .202) .230-. thallium was obtained as a by-product of smelting other metals.300 (.400-.420) .270 (.350-.350) .197-.350-.250 (.520 (.170-.310 (.180-.300) . interval) . population from the National Health and Nutrition Examination Survey.

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

2005. 1985). X. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Morrow JC. 2005) and are shown with results from NHANES 2003-2004 in this Report. Trace element reference values in tissues from inhabitants of the European Union. Sabbioni E. Schaller KH.S. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. with concentrations ranging up to 76. Pozzoli L. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging.html. Celier D. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Cassot G. Pietra R. Kramer U.95:89-105. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.76(1):53-59. Schmidt M. A study of 46 elements in urine. Brockhaus et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Jackson RJ. Minoia C. 7/15/09 Blanchardon E. Sci Total Environ 1990.. Available at URL: http://www. et al. Buhlmeyer G. 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. Sci Total Environ 1998.gov/toxprofiles/tp54. et al.48(4):375-389. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. A study of 13 elements in blood and urine of a United Kingdom population. 2005. Sampson EJ. Raithel HJ. Atlanta (GA). Gallorini M.216:253-270. Environ Res 1998. Paschal et al. Marcus RL. Valentin H. White MA.265 people living near a thallium-emitting cement plant in Germany. 1980. Challeton-de Vathaire C. and serum of Italian subjects. Third National Report on Human Exposure to Environmental Chemicals. Manke G. 1990.. Sabbioni E. Apostoli P. Wiegand H.. 1998. Int Arch Occup Environ Health 1981.113(1):47-53. Toxicological profile for thallium.47(3):223-231. 1992 [online]. Centers for Disease Control and Prevention.atsdr.Metals (CDC. Dolger R. Trace element reference values in tissues from inhabitants of the European community I. Pirkle JL. Brockhaus A. Trace metals in urine of United States residents: reference range concentrations. Ewers U. Minoia et al.5 μg/L. Investigations of thallium-exposed workers in cement factories. Int Arch Occup Environ Health 1980. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. 1981. Soddemann H. population) are thought to correspond to workplace exposures at the threshold limit value of 0. et al. Paschal DC.. 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 and Sabbioni. blood. Investigation of a working population exposed to thallium.35(1):4-9.1 mg/m3 (Marcus. Ting BG. (1981) studied 1. 1998). Radiat Prot Dosim. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Boisson P. Martin J-C. Schaller et al. J Soc Occup Med 1985.cdc.

300) 95th .170 (.060 (.180) .260) .056-.105) .090-.084 (.220 (.080) .113 (.082) .300-.110-.180 (.430 (.160-.135) .100-.120-.250-.470) .370 (.390 (.250-.105 (.650) .070) .130-.100-.580) .270-.120) .470) . interval) .056-.133) .100 (.220-.120) .109) .100 (. which are used in rock drills and metal-cutting tools.220) .204) .400 (.300 (.077-.400 (.520) .360-.111-.130) .060 (.073 (.110-.310-.100) .110 (.100 (.210 (.310-.350-1.160-.110) . and 0.380) .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 .170-.520) . which is used in the steel industry.340-. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.120-.400 (.080-.53) .120-. Tungsten is used mainly for producing hard metals.080 (.270 (.090-.210) .800) .130) . Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.093) .060-.140-.190-.450 (.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 .080 (.550) .071 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.065-.084) .150 (.270-.530 (.120-.084-.151) .113 (.290) .190-.300 (.550) .S.062 (.210 (.180 (.380-.800) .120) .360 (.340-.150 (.160 (.170) .690) .090-.310 (.810) .132) .120) .068) .158 (.320) .130 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.250) .130-.340-.060 (.420-.470-.070) .082 (.560) .140 (.290-.510 (.090) . mainly as scheelite (CaWO4).400-.04.530 (.101-.107 (.100-.330 (.360 (.062 (.090 (.080-.380 (.330-.082-.060-. and as catalysts in the petroleum industry.830) .070-.060 (.088) .460) .430 (.091) .100) .070-.250) .250) .050-.090) .090 (.140 (.126) .080) .090-.050-. Occupational exposure is from dusts released during grinding or drilling of hard metals.330) .350) .570 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).140 (.058-.101 (.00) .04.490) .350) .260 (.370 (.530 (.060 (.190-.230-.260-.360) . bronzes in pigments.280-.160 (.080) 75th .170 (.180-.092 (.160) .380-.140 (.350 (. respectively.122) .270 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350) .130) .550) .100) .620) .087-.620) .130-.090-.069) .560 (.230) .120) .460 (.450-.470 (. Little information is available on the toxicity of tungsten.110-.460) .620 (.086 (.380 (.220) .066-.190 (.076 (.060-.110 (.082 (.104) . and for producing ferrotungsten.380-.064-.210-.190-.180) .065 (.074-.270 (.110 (.100) Selected percentiles ( 95% confidence interval) 50th .480) Total .510-.078-. 0.330) .093 (.310-.220) .113 (.073) .470 (.430) .160 (.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 .140-.070-.070) .280 (. 01-02.073-.200) .120 (.320 (.180-.080 (.430-.370-.320-.092 (.110) .120-.230-.460 (.069-.950) .380-.150-.120-.400 (. population from the National Health and Nutrition Examination Survey.640 (.090-.390) .420-.630) .070 (.060-.090) .210 (.071-.090-.060-.170) .330-.300) .320-.310-.770 (.130) .113 (.123-.04.270-.060 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .110 (.070) .230) .130-.Metals Tungsten CAS No.500 (.210 (. Evidence is lacking for the carcinogenicity of tungsten.560) .116) .500 (.460 (.160 (.410-. see Data Analysis section) for Survey years 99-00.310) .130 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.410 (.200 (.240 (.200-.290-.180) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.095-.137 (.095-.073-. and 03-04 are 0.100 (.560) .230 (.070-. filaments for incandescent lamps.430-.250) .140) 90th .270-.790) .090-.160-.490 (.300 (.370) .230-.060-.150 (.230-.080) .440) .081 (.050-.070-.070 (.087) .520) .093-.096 (.250) .510-1.170) .190 (.500) .290 (.280 (.400) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.670) .160 (.170) .550 (.180) .260-.160) .050-.290-.590) .180-.110 (.570 (.070 (.130) .100) .190) .370-.080-.560) .260-. Tungsten compounds are used as lubricating agents.260 (.120) .210 (.150) .340) .090 (.097-.088 (.076 (.370 (.100) .360-.360 (.430 (.310-.160-.290) .080 (.080 (.096-.240-.092) .090) .180-.250) .320 (.

300-.096) .108-.354-.143 (.084 (.153) .169) .739) .436-1.199 (.083 (.079) .497 (.217-.063-.119-.333) .379 (.158) .109 (.061-.077) .300 (.075 (. 2001). and 2003-2004 (Paschal et al.414) .150-.081 (.344-.161) .060-..074-.063-.124-.091) .186 (.111 (.364 (.214-.253 (.071) .091) .065 (. 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.072-.071 (.279 (.059 (.28) .439) Total .150-.265 (.073 (.098-.064-.139 (.077-.431) .070 (.333-.217-.S.167-.222) .300) .131-.667) .158 (.465) .383 (.333 (.302-.093-.206-.098) .255 (.300-.078) .214) .174 (.201 (.093) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.329-.059-.090-.340 (. interval) .634 (.130 (.339 (.144 (.105 (.085) .079) .133) .301) .285) .066 (.216 (.317) .381) .064-.727) .092) .081 (.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 .146) .067 (.086) .074) .049-.179-.120) .055-.176-.061-.079 (.086-.167) .075 (.124 (.057-.066 (.067 (.360 (.190) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.081-.554) .308) .465) .333 (.165) .119 (.302-. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.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 .146 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.100 (.426) .072 (.278-.133) .094-.187) .065 (.333-.180-.088) .086) . (1987) found possibly due to methodologic.084) .082) .255-.315-.555 (.095) Selected percentiles ( 95% confidence interval) 50th .283) .074-.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 .122-.164 (. Using neutron activation analysis to 2000.071-.329 (.453) .116-.089) . population from the National Health and Nutrition Examination Survey.231-.073 (.083-.197) .500) .176-.091 (.880) .065-.065-.158) .326) .154) .075) .069 (.120) .116) .063-.056-.089 (.317-..088) .074 (.233-.439 (.065-.152-.205-.538) .198-.237) .082 (.062 (.126-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.079) .063 (.392) .216 (.157) .279 (.071) .105 (.431) .107-.169 (. or exposure that a control group of non-metal workers had mean levels differences.375) .080 (.339 (.353 (.353 (.130-.065) .203-.261-.087) .200-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.068 (.121-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.158) .199 (.125 (.341 (.080 (.452-.208-.077-.267) . population (CDC.083) .154) .138 (.484) .482 (.136 (.426) .250-.061-.060-.150 (.184 (.358) .146 (.279 (.167-.099-.100) .258-.103-.085 (.094) .197) . 1997).106 (.136-.054-.359 (.385 (.275 (.255 (.179-.073 (.198) .439 (.073 (.216-.272-.237-.301) .181 (.222-.308) .287) .100) .170-.104-.267-.090-.077) .167) .078) .431) .098-.155-.085-.197-.484 (.067-.143-.462) .253) 95th .148) . 2005).080-.823) .109-.078-.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 .071 (.080-.218 (.078 (.200-.S.095-.331-.237) .168 (.063 (.250 (.094) .053-. similar to those in this Report (Schramel et al.148 (.284) .333 (.084 (.086) .091 (.116 (.306) .667 (.138) .201) .216-. 2003.317 (.386) .122 (..079) .(Kraus et al.070 (.075) .059-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.059-.231 (.068-.216-.215) .286-.174) . Patients with medically-inserted tungsten found at increased levels in drinking water.098 (.108) .224) .354) .083) .058-.138 (.083 (.069-. 1998).270 (.253-.301) .117 (.136-.145 (.459) .133) 90th .188-.412 (.084) .136-.060 (.091) .211 (.410-.087 (.197 (.293 (.144-.359 (.091) .056-.250 (.117) .071) .151 (.240-. measure urinary tungsten.136-.605) . 2001-2002. population.082) .079 (.081) .582) . Nicolaou et al.071 (.294 (.245-.347 (.S.075-.333) .122-.063-.072-.075-.139) .797) .153-.209-.333 (.436) .098-.139-.299 (.078 (.121 (.258 (.215 (.069 (.054-.125) .074) 75th .057-.

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

009-.011-.009 (.012 (.054-.009 (.012 (.043) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.127) .033 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.021 (.012) .033-.010-.031 (.016-.011) .015 (.012 (.007-.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .041 (.007-.039) .007 (. milling.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 .049) .010) .027 (.006-.050) .016) .065) .009 (.047 (.007 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks. 01-02. including nuclear weapons.008) .016) .012 (.008-.012 (.039) .051) .030) .013 (.010) * .007 (.022) .027 (.007-.026 (.009) .037) .021 (.022 (.048 (.008 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).024-.006 (.025-.046 (. and as an aid in electron microscopy and photography.063) .019-.009) .279) .006-.009 (.009) .011) .023) .007 (.016 (.017) .027 (.046 (.007-.019-.013-.036) .031 (. and 234U.015 (.026-.004.015-.006-.023) .067) .011-.021) .008-.017-.008 (.006-.030 (. and 0. 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.023 (.038) .036 (.072) .Metals Uranium CAS No.010 (.014 (.020) .012) .010) .007 (.019-.011 (.031 (.009) .008 (. Thus.009 (.008 (.013 (.006-.005-.014 (.005-.011) .015) .007-.069) .009) .040-.007-.022-.015 (.015) .013-.037 (. in some ceramics.009 (.008) .021-.006-.041 (.032 (.009-.067) .009-.009 (.010-.007-.039-.010-.046) .020 (.009 (.017 (.011-.031 (.007 (.034-.053) .016) .008 (.011-.019-.010) .006-.012 (.034-. respectively.040 (.007 (.042 (.088) .023-.005.007-.054) .012-.030 (.016-.007 (.037) .009-.008 (.011) .014 (.007-.040 (.014 (.024-.040-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.007) .008-.020-.013 (.008-.017-.008-.046 (. human exposure occurs primarily by inhaling dust and other small particles.040) .008 (.158) .014 (.052 (.007 (.009 (.027 (.056) .010) .009-.024 (.060 (.017) . Variable concentrations of uranium occur naturally in drinking water sources.006-.72%).046 (.007-.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .009) .017) .044 (.018) .028 (.036-.021 (.016) .013) .009) .007) .008 (.035) .008) .010) .034) .006 (.019 (.009-.031 (.S. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.043 (.010-.011 (.014 (.021) .008 (. nuclear fuel.010-.020-.064 (.016) .036) .013 (.006-.012-. and 03-04 are 0.007-.010 (.037-.023-.035) .009-.062) .017 (.040) .004.008 (.053 (. or processing.045) . In workplaces that involve uranium mining.012) .007 (.018) .017-.009) .023) .007) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .007-.008-.013) 90th .009) .023 (.006-.013 (.020-.010) * .023-. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00.020) .027) .020-.009) .007) .005-.008) .006 (.026) 95th .055 (.011-.026 (.026) .013-.007) 75th .054) .021-.022-.065) . Since the 1990’s.022-.026 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.008-. Uranium has many commercial uses.008 (.030-.018) .009-.009) Selected percentiles ( 95% confidence interval) 50th .010) .007-.042) .018-.046-.026) .007-.010) .008) .007 (.009 (.029 (.006 (.006-.009) * .114 (.012-. Depleted uranium (DU) refers to uranium in which the proportions of 235U and 234U isotopes have been reduced compared with the proportion in natural uranium.031-.045) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.008-.027) . interval) .009) .017-.008 (.010 (.010 (.028 (.007-.033) .023 (.038 (.049) .012-.027-.012) .027-.009) .030 (.006-.008 (.007-.011) .029-.013 (.012-.037) Total .027) .027) .035-.011-.016) .005-.015 (.009) . 235U (about 0.007-.048) .029-.005-.010 (.026-.011-.010-.024-.017) .012-.023-.056) .017-.017-.008 (.073) .008 (.006-.013 (.036-.011) .008 (.028-.020-.018 (.050) .011) .009-.028 (.033 (.028-.036 (.066) .018 (.010) .008 (.017) .007) .016-.007-.021) .018) .037) . 0.009-.027-.

006-.026-. with much slower elimination from bone.015 (.010) .020 (.019 (.015-.012-.009 (.053) .020 (.013) .007-.017-.007 (. 2003).019-.021 (.024) .030 (.010) .011-.007 (.005 (.010 (.009) .022 (. 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.006) .027-.030-.019) .006-.010 (.009) .005-.008) . After exposure to soluble uranium salts.033 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.010 (.008) .051) .006-.012 (.077) .007) .008 (.007-.007-.006-.007 (.007 (.033 (.015-.017-.1%-6% of an ingested dose may be absorbed.009) .034-.030 (.027 (.018-.008 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.010 (.015) .030-.011-.039) Total .018) .027-.067) .033 (.019-.011-.100 (.058) .024-.005 (. liver. 240 Fourth National Report on Human Exposure to Environmental Chemicals .013-.012) .024-.013 (..040 (.054) .017 (.045 (.006 (.023-.008-.006-.016) .012) .010-.006 (. 1992).008 (.270) .027) .033 (.048) .053) .007-.034) .007 (. 0.016) .017) .022-.013 (.007 (.024 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006-.059 (.039) .009-.048) .010) .008-.028) .011) .009 (.058) .007-.012 (.008) . kidneys. which represents distribution and excretion.006 (.006-.011-.015-.063) .011) .015) .013 (.034-.018-.005 (.006 (.038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .035 (.074) .025) 95th .024) .014) .027-.034 (.012) .007-.008) . Radiation risks from exposure to natural uranium are very low.031 (.006-.007 (.008 (.011 (.009) .026) .043 (.016) .042) .008-.009) Selected percentiles ( 95% confidence interval) 50th .029) .021-.022 (.008 (.037 (.006) .009) .008 (.019 (.008 (.024) .018-.027) ..013) .007 (.042) .061) .010-.007 (.027 (.034 (.020-.008-. Uranium is eliminated in feces and urine.010 (.012 (.014-.007 (.005-.009) .028 (. population from the National Health and Nutrition Examination Survey.017) .011) .146) .024 (.044) .008 (.034 (.009 (.020 (.030 (.009-.010) .012 (.025-.017-.019) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.013 (.015 (.021 (.029) .025-.017) .007-.015-.032) . which can occur occasionally from high occupational exposure.008) .012-.013 (.020-.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 .039) .008) .026 (.016-.020-.028) .025-.021) .029) .006-.006 (.035 (.016) .006-.007 (.015 (. low level exposure.004-.016-.041) .024 (. where limited absorption occurs (less than 5%).022-.019-.031-.010) .007 (.009) .006-.030) .010-.021 (.009 (.014) 90th . Depending upon the specific compound and solubility.010) .006) .008) .021 (.016) .008-.016-.039) .006-.019-.009) .029) .010-.013) .009-.010-.011-.013 (.050) .024) . Inhaled uranium-containing particles are retained in the lungs.006-.010-.006-.015) .006) .010-..042-.007 (.005-.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.013 (.008) .006-.010-.016) .008) .018-.009-.006 (.051) .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 .029 (.026 (.011) * .034 (.011-.S.051) .006-.010-.019 (.018 (.022 (.007 (.050 (.030) .006-.019-.006) .009) .018-.006-.005 (.Metals impact.024-.047) .005-.008) .022) .028-.008) .032) .024) .006-.010-.020) .005-.010-.034 (.007 (.028) .028) .027 (.012 (. Health effects from uranium exposure result from chemical toxicity to the kidney. the shrapnel acts as a source of chronic.006-. After inhalation.007 (.007 (.017 (. In cases of retained DU shrapnel.004-.015) .029 (.016 (.029 (.025 (.007) .011-.014 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.007-.013 (.017-.007 (.014-.014 (.008-.009) .005-.016) .009-.013 (.007 (.009-.028 (.015-.016) .016-.056) .006-.051 (.007-.010) * .006-.007 (.080) .011-.013 (.026 (. 2005).012 (. After long term or repeated exposure.014) .009 (.007 (.011 (.008) 75th .005-.033) .025-.014) .050) .027-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.011-.008 (.006-.009) * .020-.006-.009) .025 (.015 (.008 (.012 (.014-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.007) .022-.007-. interval) .

Pillai KC. Carmichael AJ.. Third National Report on Human Exposure to Environmental Chemicals. Horan P. Galletti.78:143-146. Durakovic A. EPA. Ejnik JW. (May et al. soldiers evaluated before. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 28 soldiers who may have been exposed to DU by inhalation. in that the levels were below their respective detection limits (Byrne et al. or wound contamination..Metals injury associated with elevated urinary uranium levels (Kurttio et al. pp. 2006.. Vol. during.S. Information about external exposure (i. Hamilton et al. eds. In a study of 105 persons exposed to natural uranium in well water... Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. 2006). Uranium content of blood. 41 (1). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Pullat VR. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000...168(8):600-605..S.atsdr. environmental levels) and health effects is available from ATSDR at: http://www.. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U.61 μg/g creatinine. (Kurttio et al.162 μg/L) (Orloff et al. Stradling GN. 2000).cdc. Sci Total Environ 1991. ingestion. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 2001-2002.S. Metivier H. 2000). Hamilton MM.gov/ toxpro2.55 μg/L (median 0. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Tolmachev et al. Health Phys 2000. respectively. Muggenburg BA.S. Centers for Disease Control and Prevention (CDC). NRC. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Byrne AR.62:562-566. Drinking water and other environmental standards have been established by U. The U. 2006). 2002. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 2006).. urinary levels of uranium were as high as 9.e. Squibb K.. Dietz LA. Boyd P. Breitenstein BD. IARC and NTP have no ratings for uranium human carcinogenicity.1996. Atlanta (GA). had a mean urinary uranium concentration of 0. 2003. In: Gerber GB.078 μg/L (ranging up to 5.. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. 1978).066 μg/g creatinine (Gwiazda et al. Radiation protection dosimetry. A cohort of 46 U. Karpas et al.html.011 μg/L (McDiarmid et al. the median urinary uranium concentration was 2. and no consistent effects on multiple endpoints of kidney function were found. 1992. 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. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. although slightly increased during and after deployment. et al. Guidebook for the treatment of accidental internal radionuclide contamination of workers.. 2002). 2006). but in whom no shrapnel was embedded. 2004). Thomas RG. 1994. 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. McDiarmid et al. Komaromy-Hiller et al.. 2004). the median urinary concentration was 0.1992. and 2003-2004 (Dang et al. 1-49.S. 2004).110 to 45 μg/L (Ejnik et al. Zimmerman I. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Volf V. 1991.65 μg/L). Health Phys 1992. Benedik L. 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. References Bhattacharyya MH.. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Dang HS. 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. with emphasis on quality control. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. the geometric mean urinary uranium concentration was 0. McDiarmid M.107:143-157. In the same study. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Kent (England): Nuclear Technology Publishing. 2005. 2004). Six workers in a depleted uranium program showed concentrations of 0. Mil Med 2003. In 17 U..S.. population.

Kane R. Komulainen H. Sabbioni E. rapid.94:319-326. Makelainen I. U. Metcalf S. concentration and daily excretion of uranium in urine of Japanese. Salonen L. Shelly T. Wahl W. Environ Res 1999. 242 Fourth National Report on Human Exposure to Environmental Chemicals . McDiarmid MA. Ough EA. Environ Res 2004. Uranium daily intake and urinary excretion: a preliminary study in Italy.S. Heller J. Sci Total Environ 1994. Clin Chim Acta 2000. Am J Kidney Dis 2006. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Noguchi H. Lorber A. Karpas Z. et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population.86:12-18. Kalinsky V. Lewis BM. Tolmachev S. Nuclear Regulatory Commission (NRC) Guide 8. Kidney toxicity of ingested uranium from drinking water. Sampson EJ. Li WB. Pirkle JL. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Karpas Z.79(1):11-21. Gwiazda RH. Health Phys 2003.85:228-235.87:51-56. et al. Smith D. Bennett LG. Auvinen A. Pinto V.158:165-190. Oeh U. Charp P. Harmionen A. Komaromy-Hiller G. Paretzke HG. Wilson PD.44:29-40. Human exposure to uranium in groundwater. Health Phys 2004. Nuclear Regulatory Commission (U. Health Phys 2004. Int Arch Occup Environ Health 2006. Biologic monitoring for urinary uranium in Gulf War I veterans. McDiarmid M. Gucer P. Jackson RJ. et al. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Kuwabara J. Halicz L. Biokinetic modeling of uranium in man after injection and ingestion. Scott K. Jarrett JM. Review of elements in blood.47(6):972-982. Oliver M. Health Phys 2006. Howerton K. Cordero S. VI. Military deployment human exposure assessment: urine total and isotopic uranium sampling results.S.S. Van der Venne MT. Radiat Environ Biophys 2005. Pekkanen J.91(2):144-153.S. Englehardt SA. May LM. Renal effects of uranium in drinking water. J Toxicol Environ Health A 2004.82(4): 527-532.81:45-51. Squibb K. McDiarmid MA. Washington (DC): NRC. Ting BG. Squibb K. Orloff KG. Engelhardt SM. Kurttio P. Environ Health Perspect 2002. Saha H. Kurttio P. July 1978.110(4):337-342. Mistry K. Uranium and thorium in urine of United States residents: reference range concentrations. et al. Marino R. Oberbroekling KJ.Metals Galletti M. et al. Roth P.22–Bioassay at uranium mills. Cremisini C. U. Comparison of representative ranges based on U. Saha H. Hancock RG. Auvinen A. Ash KO. D’Annibale L. Costa R.67(8-10):697-714.71(6):879-85. Salonen L. Element reference values in tissues from inhabitants of the European community. Hamilton EI. Health Phys 2002. Inductively coupled plasma mass spectrometry as a simple. patient population and literature reference intervals for urinary trace elements. Katorza E.296(1-2):71-90. Ejnik J. Health Phys 1996. NRC). et al. Roiz J. Andrews WS. Marko R. Hollriegl V. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Paschal DC.

0) 708 617 681 652 1228 1092 Limit of detection (LOD.90 (3.0 (10.0) 13.90-3.40 (4.90 (5.00) 7.50) 11.70-3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.60-7.20-4.62 (3.80) 7.90-12. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0 (12.70-5.40) 3.60 (7.0 (8.74-3.10 (7.11) 3.26 (2.0) 19.20 (4.0) 9.20 (5.39-4.70-12.30-19.0 (9. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0-17.0) 14.40-11.90 (5.00) 3.0) 11. Perchlorate was added to the U.0 (11.81-16.05 (2.60) 3.0-18.90 (5.0-15.70-9.10) 12. 2002). certain catalytic metals.0) 15.0 (9. and certain plants with high water content (e.10-11.0) 13.10-11.20) 7.0-20.84) 14.0) 15.40 (5.51 (3.49-3.70 (3.0) 13.10 (6.50) 6.30 (5.40) 4.00) 4.01 (2.45-4.90-11.0 (8.35 (3.09) 3.0-18.47-4...75 (3.0-23. 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.0 (11. population from the National Health and Nutrition Examination Survey.05 and 0.80) 75th 6.54 (3. 2005).02 (3.0) 10.0) 10.20-3.0 (11.40 (3.20 (7.20-4. interval) 3.90-3.0) 9.00-6.0-17.0 (11. and electroplating.10) 3.30-7.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3. 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.75-3.0 (8.20 (2.40-13.40-4.0 (13.70) 3.66) 3.67-5.31) 2.0-29. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant. potassium.0 (12.79 (2.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.40-5. or ammonium salt. It is normally found and produced as the anion of a sodium.40) 3.0) 9. 1998). 2005).10 (5.80 (3.0 (9.88) 3.30-7.10) 5.76) 4.20) 3.80) 3.16) 3.19 (3.96 (3.0) 13.EPA. leather tanning.40) 3. but has strong oxidant properties in the presence of concentrated acids.0) 13.50 (5.70 (3.81) Selected percentiles ( 95% confidence interval) 50th 3.40 (5.89-3. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.60 (4.0 (9.0 (11.03) 3.50 (8.10) 5.20-11.80-6.0) 9.0-18.30 (5.10 (6. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0) 8.05. Survey years 01-02 03-04 Geometric mean (95% conf.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 13.76 (3. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.70-11.30 (2.20 (8.40 (8.0-17.29-3. laboratory analysis.87-3.22-5.80-12.40 (3.80) 12.21 (2.80 (3.0-14.0) 9. Drinking water.70-6.20 (2.0 (11.0-17.50-11.40) 90th 10.80-15.60-6.0 (12.10 (2.00) 3.12) 3.50-4.0) 10. 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) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0) 9.51 (3.40 (4.0 (11.0 (11.0-15. Perchlorate is stable under most environmental and physiological conditions. lettuce) can be the main sources of intake for humans (FDA.0 (9.30-17. fabric dyeing.0) 12.65) 3.22 (2.0-17. Other manufactured uses include fireworks.07-4. and limited applications in pharmaceutics.0) 13.32 (3.19-4.00) 5.0) 11.30) 6.50) 5.40-4.0) 14.0) 95th 14.11) 4.90 (4.g.80 (6.0 (11.44-4.56) 3.0 (8.80 (7.50) 3.50-4.30-6.50-3.70-7. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.10) 3.90-6.S.46) 3. 2007).68) 4.10-12.90 (2.40-6.08-3.90-9.90) 6.93-3.20 (6.0 (12.0-17.60) 5.40 (5.0 (9.93-4.0) 14.20) 4.70 (3.80-8.0-19.80-4.40) 2.90-10.90-9.60) 8.38) 5.5 hours and has a small estimated volume of distribution (Crump and Gibbs. matches.0) 11.50 (3.40) 6.00-5.S. milk. and reducing agents.70-3.0 (8.40-7.90-11.10-7.0) 13.00-6.20-12.0) 8.30 (2.0 (11.50) 5.Perchlorate Perchlorate (Urbansky.10-4.93 (4. In addition.0 (9.80-4.20 (4.50-7.30) 6.0) 16.90) 5.18-3.60 (4.S.

00) 3.74) 7.4) 13.50-5. chronicity of exposure.10 (2. although iodine intake was higher than U.70) 2. 1999.10-3. 2005.60 (3.09 (7.50) 2.0) 11.S..90 (2.20) 8. dietary iodine intake.87 (5.0 (9.12 (6.S. 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.51 (3.97-5.90 (4.50 (6.. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.6-17.81-3. gender.60-5.50) 6. Steinmaus et al.71 (5.0 (11.60-8.59) 3.08 (3.00 (4.87) 2.24-2. Li et al.40 (3.93-5.g.29-6.1 (11.70-5.30) 3. in a representative sample of U.10-7.0 (11.2) 8.70) 10.0) 10.4 (11.25) 5.25) 5.70-4.61-10.0 (9.70-3. levels.0) 9.70 (2.EPA. perchlorate is negative in most genotoxic assays (U.80 (4.4 (11.1-14. interval) 3.50) 95th 12.Perchlorate inhibition (RUI).70-15.30) 75th 5.90 (7.S.61-5.60-6.1) 8. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.80-3.54 (3.42 (3. 2002).41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.46-4.33-12.45) 3.60-11. 2002. population from the National Health and Nutrition Examination Survey.64-3.58) 2.02) 3.76-3.00) 4.36 (8.30 (5.91) 4.S. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.03 (2.39) 2.08) 3. nitrate.5) 8. 2005.90-20.0 (8.0) 14.0 (10.30) 5. 2000).10 (1.56-3. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures.67) 5.25 (3.40) 17. 2005).34-3.12-2.77 (3.33 (7.52 (8.00) 9.20-4. In the U.75) 3..56 (3.19-6.60) 3.90-9.02-4.S.45-2.7 (11.1-16.22 (2. up to 68% RUI has been demonstrated.30-5.33-6.20-3. 2005).52-9.0 (9.0-14.21 (2..10 (6.47) 2.83 (5.72 (3.93-7..46-13. Lamm and Doemland. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.4) 8.35) 3.54 (2. Also.96) 2.00-11.22-6.93-5.95 (2.50-3.3) 12.35 (2. 2007).0) 7.0) 13. 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.20-3.89-3. NAS.87) 7.50 (3.0) 13.00-2.39 (3.09) 3.14 (2.20-10..20) 3.60) 8.37 (4.2) 8.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.0) 12.29) 2.99 (5.0-19.20-9.18-3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.3) 11.32) 5.40 (4.51-4.30-10.35 (4.8 (11.80 (7.44) 3.6) 12.10) 4. Lawrence et al. menopausal status.22-4. 2006.89 (2..50) 9.60-3.44-6.43) 6.60-5.93) 3.3 (10.50-9.90) 5.40 (7.50) 2.0) 9..46 (3.00 (6.90-2.24 (4.60) 10.4-16.20 (7.0) 12.0 (8.61 (5.0 (11.20 (3.6) 20.37-13.39-4.0) 12. 2002.30) 90th 9.60-8.10 (4.20 (6.10) 13.66) 3. 2005).4 (10. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.16-3.80) Selected percentiles ( 95% confidence interval) 50th 3. thiocyanate. levels and sufficient in most participants (Tellez et al. age.30 (6.20 (4.98) 3. medications).84) 2.40 (3.99-3.15-12.EPA.80 (7.S.26) 4.0-14.5 (13.40) 5.00-3.25) 5.70 (2.07 (2.60-11.30-5.0-44.05 (4.53 (2.90-11.20 (2.40) 3.10) 3. Many factors may be important in consideration of perchlorate action on the thyroid: dose.0) 12.26 (3.0) 6.0-17.93-8. U.90-3. women with urinary levels of iodine less than 100 micrograms per day.40-10.90-15.3) 8.4 (8.1-13.0) 4.80-3.30 (3.90 (2. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.1-22.1 (8.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.64) 5.00 (2.04-3.22-4.73) 3.87 (7.3-14.87-3.41-9.86) 4.60-15. Survey years 01-02 03-04 Geometric mean (95% conf. 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.10 (4. Greer et al.70 (4.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals . and the presence of other substances known to affect thyroid function (e.04-3.19-10.50) 5. During gestation and infancy.S... 2003. 2001.10) 6.76 (3. However.82 (5.

National Research Council of the National Academies. (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. He X. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. May 2007. Pirkle JL.11(3):295. Also. Neonatal thyroxine level and perchlorate in drinking water. Available at URL: http://www.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653.EPA at: http://www. thiocyanate. J Expo Sci Environ Epidemiol 2007. Landingham CB. epa.41(5):409-411.46(5):509. Doemland M. Valentin-Blasini L.html and from ATSDR at: http://www. Steinmaus C. Washington (DC): National Academy Press. population. Lamm SH. 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.. Page Last Updated: 05/28/2009. Tellez RT. Buffler PA. Thyroid 2001. Lau EC. 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. Greer SE. Dasgupta PK. Dyke JV. Crump KS.114(12):1865-1871. Environ Health Perspect 2002.. J Occup Environ Med 2003.115(9):1333-1338. most of the population is considered to be below the U. et al. Miller MD.html. Pino S.42(2):200-205. Kelsh MA. Environ Health Perspect 2007. Low dose perchlorate (3 mg daily) and thyroid function.40(21):6608-6614. Lamm SH. The effect of perchlorate. Sesser DE. Valentin-Blasini L. Braverman LE. Skeels MR. and nitrate on thyroid function in workers exposed to perchlorate long-term. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect.S. Braverman LE. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Goodman G. Erratum in: Environ Health Perspect 2005. J Occup Environ Med 2000. 2007). Li Z. Gibbs JP.90(2):700-706. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.45(10):1116-1127. Biomonitoring Information Urinary perchlorate levels reflect recent exposure.113(11):A732. Deyhle GM. Jackson WA. Crump KS. References Blount BC. Blount BC. Additional information about exposure and health effects is available from the U.htm. Osterloh JD. 6/2/09 Greer MA. Perchlorate Exposure of the US Population. Mauldin JP. Byrd D. Pino S. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.17(4):400-407. Abarca CR. Daaboul JJ.atsdr. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . newborn thyroid function. Environ Health Perspect 2005. Environ Sci Technol 2006. Blount BC. Lamm SH. Li FX. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. National Academy of Sciences (NAS). Analysis of relative source contributions to the food chain. and environmental perchlorate exposure among residents of a Southern California community. Cross M. 2005. Primary congenital hypothyroidism. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. et al. Perchlorate in the United States. Kirk AB. Magnani B. Environ Health Perspect 2006. Thyroid 2000.cdc..113(8):10011008. Braverman LE. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Chacon PM. Rutherford GW. EPA reference dose (Blount et al. Howd R. et al. Food and Drug Administration (FDA). Pirkle JL.fda. J Clin Endocrinol Metab 2005.S. Caldwell KL. 2001-2002. Lawrence JE. Lamm S. Pleus RC. et al.gov/toxpro2. 2005).S.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Erratum in: J Occup Environ Med 2004. Benchmark calculations for perchlorate from three human cohorts. CFSAN/Office of Plant & Dairy Foods.10(8):659-663.gov/safewater/ccl/perchlorate/perchlorate. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Blount et al. Osterloh JD. Richman K. 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.110(9):927-937. Health Implications of Perchlorate Ingestion. Barnard JC. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.

Drinking Water Contaminant Candidate List. No. EPA/600/F-98/002 Washington (DC).epa. 246 Fourth National Report on Human Exposure to Environmental Chemicals . Perchlorate as an environmental contaminant. Available from URL: http://cfpub.1/15/06 U. Integrated Risk Information System (IRIS). Thyroid 2005. Perchlorate. Environmental Protection Agency (U.S. Environ Sci Pollut Res Int 2002. 1988.gov/iris/quickview.Perchlorate pregnancy and the neonatal period. Revised 2/11/05. Urbansky TF. U.S. Environmental Protection Agency (U. EPA).S.15(9):963-975. EPA). cfm?substance_nmbr=1007.9(3):187-192.S. Doc.

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

PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. 2006. Bookstaff et al. Some of the effects in animals may be mediated through peroxisomal proliferation. 2004). Vanden Heuvel et al. may metabolize or degrade to PFOA (Dinglasan et al. by high protein binding in plasma and other proteins. 2004. 2000.S. 1990). 2004. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.. 2005). see Data Analysis section) for Survey year 03-04 is 0.. C6. peroxisomal proliferation. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. EPA.... pancreas.. hepatotoxicity. 2007a). C7). The PFCs often measured in human serum are listed in the table.4. Lau et al. Tittlemier et al. 2005). The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. in part. or effects of other PFCs.. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. PFOA has been reported to cause liver. and in human blood and semen (Calafat et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. It is unclear if environmentally degraded telomer products are a major source of other PFCs. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. in a wide variety of marine and land animals (Kannan 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. Prevedouros et al. kidney. 2007). Olsen et al.8 years (Olsen et al.. Lau et al. 2005.. For instance. Kannan et al.. growth retardation and delayed sexual maturation (Kennedy et al. human toxicokinetics.e. and β-oxidation of lipids (Kudo et al.. U. the 8-2 telomer.. 2006a.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). Unlike many organohalogen contaminant chemicals.5 years and for PFOS. there is limited information on the sources.. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. < LOD means less than the limit of detection. 2004. but still can have long residence times in the body.. Keller et al. C5. 2003a and 2004a). but probably include dietary sources (Kannan et al.. 2003. Excepting PFOS and PFOA. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. All sources of human exposure are uncertain.. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al.. 1993).S. endocrine and immune effects. 2004. thymus and spleen. which may vary for some chemicals by year and by individual sample. 2005. 2004).. 2005. In some cases. environmental fate. 2003). and in offspring. PFOA is mostly excreted in the urine in animal studies.. 2005)... population from the National Health and Nutrition Examination Survey.. 2002. Taniyasu et al. including immunologic effects and tumor induction. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. The elimination half-life of PFOA in humans is roughly estimated to be 3. 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. 2003). Guruge et al. heptadecafluoro-1-decanol. 1995. 248 Fourth National Report on Human Exposure to Environmental Chemicals ... approximately 4.

In such studies. elderly and children.300 (<LOD-.500) .500 (<LOD-1. 2001. Animal studies of PFOS have demonstrated weight loss. 2004..500) . 2007. Survey Geometric mean (95% conf. At high but non-toxic maternal doses of PFOS. EPA..20) . reproductive. development in offspring was stunted and hypothyroxinemia was observed.108 times higher than background serum levels in humans (Butenoff et al. Cook et al. Harada et al.800) 1.40) .Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 2003a. 2004). 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.. hepatotoxicity.00) . Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. EPA.. 1999.700 (.. At doses causing maternal toxicity.600 (. Olsen et al. U.900 (.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .900 (.. 2003a).400 (<LOD-...10) . Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. see Data Analysis section) for Survey year 03-04 is 0. Fourth National Report on Human Exposure to Environmental Chemicals 249 .. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80) 485 538 962 Limit of detection (LOD. 2005).800) 1..10) . 2004b).500-1. In comparing three separate reports on adults.. Fei et al.600 (.. Olsen et al.500) . monkeys. PFOA.400-1.300-1. 2003. 2004a. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.300 (<LOD-..400-1. Thibodeaux et al.00 (.. 2003a. perfluorohexanesulfonate (PFHxS).400) .400 (<LOD-.800 (. 2007a.50) . 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. developmental and teratogenic effects were demonstrated in offspring. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.300 (<LOD-. < LOD means less than the limit of detection.600 (.400-1.. population from the National Health and Nutrition Examination Survey. 2003).500-3.400-. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. Lau et al. population.10) * 03-04 03-04 * * < LOD < LOD < LOD . However.400-1.500-1.800 (. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. and changes in thyroid hormone concentrations (Grasty et al. 2003).800 (. thyroidal)..500-1.. or increased cancer rates (Alexander et al. 2007b).3. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. 2007b. possibly related to lung immaturity (Lau et al.S. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. the potential to estimate risks to humans from animal doses is uncertain.00) .500-1.400-1.500) 90th . 2005).80) 640 1454 03-04 03-04 * * < LOD < LOD .. PFOS. 2003a. PFOA.400 (<LOD-.500-. 2003).400-. 2004).500 (. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Kennedy et al.500 (.700) . and humans. 2003. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. 2003a). U. 2003.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample.S. 2004.800 (. Olsen et al. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U..00) .80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .500) . and there was no clear evidence of excess all-cause or diseasespecific mortality. 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.S. 2007).900 (. 1992. 2007a.S.600-2.10 (. PFOS.. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. interval) Selected percentiles ( 95% confidence interval) Sample 95th .

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

300 (<LOD-. < LOD means less than the limit of detection.600) < LOD .500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .500-.600 (.300 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 251 .500 (<LOD-. see Data Analysis section) for Survey year 03-04 is 1. which may vary for some chemicals by year and by individual sample.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.S.500) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (<LOD-. population from the National Health and Nutrition Examination Survey.900) < LOD .400 (.300-. < LOD means less than the limit of detection.S.0. population from the National Health and Nutrition Examination Survey.3. Survey Geometric mean (95% conf. * 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. 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.400) . see Data Analysis section) for Survey year 03-04 is 0.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.

30-12. 252 Fourth National Report on Human Exposure to Environmental Chemicals .50 (4.04) .20-1.600-.00-1.16) .861 (.816-1.6) 7.27) 1.20 (1.S.70-7.984 (.20 (6.852 (.40 (1.20 (1.40 (2.900-1.10) 4.30) 3.900-1.586-.40-1.80-4.60-4.90-2.834-1.00-6.40) 4.20) 1.80-4.44 (2.70-2.10) 4.900-1.10) 6.10) 75th 1.26) 2.90) 8.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.10 (4.1. see Data Analysis section) for Survey year 03-04 is 0.70) 13.900-1.10) 8.50 (2.70-6.60-4.60-2.5) 5.40 (1.40) 640 1454 03-04 03-04 2.809) 1.01 (1.80-7.20 (6.20) 03-04 03-04 2.10 (.50) 2.70) 3. interval) 1.00 (2.00) 3.50-6.30 (1.70) 2.50) 2.08) 2.30 (2.00) 1.80-3. Survey Geometric mean (95% conf.40-3.00 (5. population from the National Health and Nutrition Examination Survey.10 (.50) 6.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.90 (2.20 (1.30) 03-04 03-04 .60 (1.20) .60 (6.20-3.67-2.54) .93 (1.912-1. see Data Analysis section) for Survey year 03-04 is 0.00) 1.30-6.87-2.80) 1.721-1.80-3.70-5.00 (1.10 (.697-1.10) 1.80-2.56-1.0) 8.00 (1.40 (1.72) 1.62-2.20-1.90) 3.10-9.10) 5.10) 1.50 (1.50 (1.60) 1.40 (1.30-9.60-3.50 (1.86 (1.689 (.700 (.92 (1.90) 1.835-1.30 (3.00 (.40) 640 1454 03-04 03-04 1.30 (1.60-2.30 (1.80 (4.00 (1.80-4.30 (6.80 (1.90-10.20-1.3 (9.05-2.800 (.90 (4.30) 3.60-3. interval) .00) 2.50-3.90 (1.10-9.90) 1.50 (6.90 (4.10) 75th 3.70-10.60) 9.5) 8.900 (.10) 1053 1041 03-04 03-04 03-04 .40-1.73-2.00-8.70 (2.40) 2.90) 90th 5.03) 1.72 (1.09 (.10) 6.50-10.70) 1.S.826-1.30 (2.20) 2.20-1.50 (6.700-1.80 (1.50 (4.30-2.17 (1.10 (4.70) 2.90 (1.60 (1.30) 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 1.80) 5.00-1.10 (1.963 (.80) 4.40) 1.80-12.70) 1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.77-2.800-1.0) 1053 1041 03-04 03-04 03-04 1.42 (1.10-5.60-8.900 (.60-2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.80) 90th 2.1) 485 538 962 Limit of detection (LOD.20) 1.60) 3.14 (.00-7.60) 2.30 (1.900-1.30) .90) 1. Survey Geometric mean (95% conf.51) 1.12) .Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.90-19.90 (1.20 (1.17-1.80-7.40) .60-7.30 (7.70-2.80-8.900-1.80-8.40) 1.50-6.20) 485 538 962 Limit of detection (LOD.3.00 (1.60 (1.900) 1.50 (1.80) 3.00 (.90 (1.20-2.966 (.91) 2. population from the National Health and Nutrition Examination Survey.70 (1.

3 (44.4 (19.5 (28.47-4.7 (19.7 (43.27) 4.10) 5.20 (4.7-69.60 (6.50) 7.37 (2.20) 10.1) 57.20) 5.82) 4.2 (16.5-21.60 (4.1-25.80 (5.4 (19.1 (24.0) 90th 41.7-53.5) 32.90-4.9) 22. population from the National Health and Nutrition Examination Survey.7 (35.S.5 (28.4.9-19.8) 46.2) 30.0) 36.1-52.8-78.90-12.9 (22.60 (3.5) 19.20) 7.00 (5.35) 3.4 (28.80) 8.10 (6.6-50.6 (35.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.70 (5.96 (3.30 (3.5-62.3) 485 538 962 Limit of detection (LOD.6 (44.5-33.65-4.0) 23.0) 43.4) 21.9) 9.8-81. see Data Analysis section) for Survey year 03-04 is 0.90 (7.6) 62.1-36.80-4.4-25.30-6.0) 21.20) 4.5) 8.9-38.4 (23.50 (3.6) 18.91) 3.85-4.80 (6.30 (3.10-3. Fourth National Report on Human Exposure to Environmental Chemicals 253 .30) 7.30-5.2) 30.5) 18.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.8-35.3) 41.9-23.9) 22. interval) 3.2-57.47 (4.7-49.1 (19.80 (7.7-33.00 (3.20) 5.20) 7.3 (17.5) 9.2) 640 1454 03-04 03-04 4.70) 4.90) 6.5) 7.40 (6.60 (5.79) 4.8) 27.1-33.2) 45.7-30.6 (42.1-35.70) 6.1) 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 4.6 (19.7 (13.5) 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 21.0-70.7 (35.53) 3.70-9.50-6.84-3.3) 42.30 (5. Survey Geometric mean (95% conf.4) 56.18 (3.07-4. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.0-20. interval) 20.80-12.70-7.0-16.7 (7.2 (18.8) 32.2 (21.70-7.8-22.3 (28.6-24.40 (4.30-11.3-61.3 (35.2 (27.80 (6.8 (34. see Data Analysis section) for Survey year 03-04 is 0.3) 28.90 (7.0) 03-04 03-04 19.8 (45.7 (43.80-9.50-13.8-22.50-4.40-14.0-66.6) 9.60) 03-04 03-04 3.30-8.20-5.00 (5.70) 3.10 (3.5-23.6) 35.67-4.95 (3.40) 90th 7.0) 485 538 962 Limit of detection (LOD.2 (19.11 (2.4) 75th 30.4) 20.40-6.70 (5.90 (5.40-10.20 (4.10 (3.40) 75th 5.6) 21.40) 5.20-9.1-24.4-17.60-6.4) 640 1454 03-04 03-04 23.4 (17.8 (37. Survey Geometric mean (95% conf.4-42.30-3.60) 8.40) 3.2 (28.6) 1053 1041 03-04 03-04 03-04 3.6) 42.90 (7.1.00) 3.3 (35.6-45.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.0 (20.1) 15.70-10.7-23.1 (23.5) 1053 1041 03-04 03-04 03-04 14.7) 39.9 (19.60 (6.70 (3.89 (3. population from the National Health and Nutrition Examination Survey.3-22.0 (27.5) 57.40-6.8-22.60-9.99-3.0) 21.60-13.60 (7.9 (17.9 (13.30) 6.50 (4.S.8-30.60-14.70-5.9) 27.20-4.21-3.40-17.2-22.90-4.6) 7.50) 4.

S.200-. population from the National Health and Nutrition Examination Survey.300-. < LOD means less than the limit of detection. 254 Fourth National Report on Human Exposure to Environmental Chemicals .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.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 (.300 (.500) < LOD 485 538 962 Limit of detection (LOD.400 (<LOD-. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 0.500) . Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.300 (.200-.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.300) .4.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-. 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 (.300-.300) .300 (.500) 485 538 962 Limit of detection (LOD.300 (.300) .200-.500) .300) .300 (.S.200-.300-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-.200 (<LOD-. < LOD means less than the limit of detection.300-. Survey Geometric mean (95% conf.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.200-.300) .300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (. which may vary for some chemicals by year and by individual sample.2. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300) .500) .300 (.200-. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0. which may vary for some chemicals by year and by individual sample.300 (.300) .

10-1.500 (<LOD-.10-1.700 (<LOD-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-1.700 (<LOD-.700 (<LOD-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th .50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .90) .900-1.80) 1.400 (<LOD-1.800 (<LOD-.30) .30 (1. < LOD means less than the limit of detection.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10 (.10 (.10-1.700 (<LOD-.900-1. which may vary for some chemicals by year and by individual sample.400 (<LOD-.900 (<LOD-1.900) .40) 1.700) 1.700 (<LOD-.50 (1.10) * 03-04 03-04 * * < LOD < LOD .600 (<LOD-1.10) .700) 1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900-1.900 (.30) 1.800) .60) 640 1454 03-04 03-04 * * < LOD < LOD .S.30) 1.600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) < LOD < LOD .900-1.20-1. < LOD means less than the limit of detection.900-1.900) 1. see Data Analysis section) for Survey year 03-04 is 0.600 (<LOD-1.10 (. which may vary for some chemicals by year and by individual sample.00 (. Survey Geometric mean (95% conf.10 (1.800) .300 (<LOD-.10-1.700) 90th 1.00) < LOD .00 (.900-1.00-1.3.6. Fourth National Report on Human Exposure to Environmental Chemicals 255 . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.700) .00 (.20 (1.80) 1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .10) .00 (. Survey Geometric mean (95% conf.600 (<LOD-.60) 485 538 962 Limit of detection (LOD.900) 485 538 962 Limit of detection (LOD.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .70) 1.30 (1.30 (1.20) 1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) 1. population from the National Health and Nutrition Examination Survey.600 (<LOD-1.700 (<LOD-.10) 1.900-1.300-2.50 (1. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.700 (<LOD-.300 (<LOD-1.

Toxicol Appl Pharmacol 1995.38(10):2857-2864. Herbstman JB. Kannan K.46(2):141-147.39(3):363-380. Yoshinaga T. Bandai N. Hurtt ME.1968--2003. Perkins RG. Needham LL. Environ Sci Technol 2005. Saito N. Caudill SP. Mohotti KM. Butenhoff JL. Calafat AM. Kudo N. Liu RC.Koizumi A. Grey BE. Loganathan BG. Biegel LB. and perfluorinated contaminants in livers of polar bears from Alaska.68(6):465-471. Characterization of risk for general population exposure to perfluorooctanoate. Hurtt ME.38(17):4489-4495. in vivo. Reidy JA. O’Connor JC. Reidy JA. Rodricks J. Regul Toxicol Pharmacol 2004. Environ Health Perspect. Koizumi A. Burris JM. Butenhoff JL. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Taniyasu S. Moore JA. Guruge KS. Bignert A. McLaughlin JK. Harada K. Wijeratna S. Cook JC. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000.S. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Seacat AM.179:99-121. Needham LL. Hurtt ME. Gaylor DW. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Needham LL.41:2237-2242. Lau CS. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Birth Defects Res B Dev Reprod Toxicol 2003.60(1):44-55. Environmental and toxicity effects of perfluoroalkylated substances.124(2):119-132. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Morikawa A. Ye Y. Calafat AM. O’Connor JC.99(2):253-261.60(10):722729. Caudill SP. The influence of time. Aguilar-Villalobos M. Frame SR. Bookstaff RC.115(11):1670-1676. Environ Health Perspect 2007. Chemosphere 2006b. Ingall GB. Suzuki E. Olsen GW. Sasaki S. Olsen GW. Tully JS. Frame SR. Kuklenyik Z.39(1):80-84.63:490496. Rev Environ Contam Toxicol 2003. Harada K. Edwards EA. Halden RU.39(23):9101-9108. Tarone RE. Taniyasu S. Witter FR. Moore RW. Environ Sci Technol 2004. Yun SH. Saito N. Mandel JH.39(23):9057-9063. Mabury SA. Calafat AM. et al. Reidy JA. Environ Health Perspect 2007. 2007b.and perfluorinated acids. J Occup Health 2004. Fluorotelomer alcohol biodegradation yields poly. Chlorinated. Olsen J. Kawashima Y. Calafat AM. Grasty RC. Occup Environ Med 2003. Perfluorinated chemicals in selected residents of the American continent. Inoue K. The toxicology of perfluorooctanoate. Yoshinaga T. de Voogt P. Keller JM. Biegel LB. J Environ Monit 2005. Holmstrom KE. Cook JC. Cook JC. Corsolini S. Kennedy GL Jr. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.40:21282134. et al. Inoue K. Environ Sci Technol 2005. et al. Toxicol Sci 2001. Evans TJ.34(4):351-384. Toxicol Appl Pharmacol 1990. Rogers JM.104(2):322-333. et al. Falandysz J.134(1):18-25. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Mandel JS.115(11):1596-1602.7(4):371-377. Environ Res 2005. Kannan K. Kuklenyik Z. Kannan K.113(2):209-217. et al. Wong LY. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Watanabe T. Katakura M. Arendt MD. Kuklenyik Z. Mandel JH. Crit Rev Toxicol 2004. Fei C. Chem Biol Interact 2000. Toxicol Appl Pharmacol 1992. Yamashita N. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Peterson RE. et al. Dinglasan MJ. Kamiyama S. Environ Sci Technol 2007a. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Seneviratne HR. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Apelberg BJ. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Reidy JA. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Kumar KS. Kuklenyik Z. et al. Environ Sci Technol 2006a. Environ Sci Technol 2004. Laane RW. Day RD. Jarnberg U. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Fillmann G. Calafat AM. Murray SM. Olsen GW.115(11):1677-1682. Tully JS. 256 Fourth National Report on Human Exposure to Environmental Chemicals . brominated. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Environ Sci Technol 2005. Needham LL. Hekster FM. and ex vivo studies.Perfluorochemicals References Alexander BH. Yamashita N.S. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Polyfluoroalkyl chemicals in the U. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000.

54(11):1599-1611. Butenhoff JL.2(1):53-76. Hansen KJ. Biol Pharm Bull 2003. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Olsen GW. Barbee BD. Church TR. Butenhoff JL.1177(2):183-190. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Richards JH.. and food items prepared in their packaging. 1/15/06 Vanden Heuvel JP.perfluorohexanesulfonate. Hanson RG. Olsen GW. Zobel LR. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. fate and transport of perfluorocarboxylates.82(1):359. Mandel JH. Bronson R. Kawashima Y. Helzlsouer KJ. Rogers JM. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. et al. Mair DC.68:105–111. Thomford PJ.26(1):47-51. Horii Y. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Kannan K. Mar Pollut Bull 2005.40(1):32-44. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Rogers JM. Coordinate induction of acyl-CoA binding protein.74(2):369-381. J Children’s Health 2004b.68(1):249-264.S. Lau C.Perfluorochemicals Kudo N. Sterchele PF. Biochim Biophys Acta 1993. Grey BE. perfluorooctanoate andother fluorochemicals in human blood. Ellefson ME. Washington. Toxicol Sci 2003. Taniyasu S. Mandel JH. Hansen KJ. Olsen GW. Seacat AM. Toxicol Appl Pharmacol 2004. Cao XL et al. Half-life of serum elimination of perfluoroo ctanesulfonate. Available from URL: http://www. U. Church TR. Church TR. Olsen GW. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Olsen GW. Hansen KJ. and perfluorooctanoate in retired fluorochemical production workers. Butenhoff JL. Prevedouros K.epa.37(12):2634-2639. Seacat AM.45(3):260-270. fish. Environ Health Perspect 2003a. et al. Hanari N. et al. The developmental toxicity of perfluoroalkyl acids and their derivatives. Pepper K. Environmental Protection Agency (U. Taniyasu S. Hanson RG. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Case MT. Butenhoff JL. Ehresman DJ. J Occup Environ Med 1999. Cousins IT. Reagen WK. Hansen KJ. Environ Sci Technol 2006. Burlew MM. Lau C. I: maternal and prenatal evaluations. Korzeniowski SH.gov/opptintr/pfoa/pfoara. Larson EB.) Tittlemier SA. Lundberg JK. Environ Health Perspect 2005. Butenhoff JL. Seymour C.198(2):231-241. 2007a. fish. Mandel JH. Burris JM. fast foods. Thibodeaux JR. Butenhoff JL. Historical comparison of perfluorooctanesulfonate. Froehlich JW.74(2):382-392. II: postnatal evaluation. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Environ Health Perspect. Burris JM. van Belle G. Chemosphere 2007b. Grey BE. Burris JM. Miller JP. Gamo T. Toxicol Sci 2003. Stanton ME.115(9):1298-1305. Olsen GW. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Petrick G. Burris JM. A global survey of perfluorinated acids in oceans. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Peterson RE.55:3203-3210. et al. Nesbit DJ. Ehresman DJ. Yamashita N. Yamashita N. et al. 2003. (Erratum in: Environ Health Perspect. Kannan K. (Erratum in: Toxicol Sci 2004. J Ag Food Chem 2007. Rogers JM. Olsen GW. htm. Huang HY. Buck RC. Burris JM. Sources. Olsen GW. Lundberg JK. Environ Sci Technol 2003. Chemosphere 2004a. Thibodeaux JR. and humans from Japan. et al. Horii Y. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. EPA). birds.S. Mandel JH. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Toxicol Sci 2002.111(16):1900) Olsen GW. Hansen KJ. 2003a.51(8-12):658-668. J Occup Environ Med 2003b.113(5):539-545.41(9):799-806. Moisey J.111(16):1892-1901.

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

. High doses of di2-ethylhexyl phthalate (DEHP). Evaluation of a recombinant yeast cell estrogen screening assay.gov/toxpro2. 2003. Anderson WA. 2002). Biomonitoring studies on levels of phthalate metabolites provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of phthalates than are found in the general population. Metabolism of di(2-ethylhexyl) phthalate. Environ Health Perspect 1982..atsdr. Scotter MJ. Hauser et al.gov/ toxprofiles/tp9. 2005).html. Castle L. Schroeder JL. Silva MJ.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In Staples CA (ed). Also. 2004. Dirven HA. Toxicological profile for di-n-butyl phthalate update [online]. 2007). Assessment of critical exposure pathways. Matthews HB. 2001). Connor C. reducing estrogen production. 227-262. Springer. The monoester metabolites are thought to mediate toxic effects for some of the phthalates.. atsdr..805:49-56. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www.3. 105:734-742.. variation also occurs in the same person during repetitive monitoring (Fromme et al. Herbert AR. 2000c..Phthalates and metabolites have been tested. However. interactions with macromolecules and species differences in metabolism of DEHP. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.gov/ reports/index. 1982. 2004. Mackay D. 2006). Clark K. Pharmacokinetics. 2000a. Information about external exposure (i. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Dave M. 2004). 2001..gov/toxprofiles/ tp135.. Calafat AM. Environ Health Perspect 1997.. Available at URL: http://www. Available at URL: http://www. 1986). J Chromatogr B 2004.html). Drug Metab Rev 1989. 1985. 2000b. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Jongeneelen FJ. Food Addit Contam 2001. The Handbook of Environmental Chemistry. testicular atrophy. pp. Kessler et al.cdc. Albro PW and Lavenhar SR. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. and race/ethnicity (Silva et al. 2005. at higher doses. 2006). Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 4/20/09 Albro PW. Corbett JT. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester..New York.21:13-34. Coldham NG. 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. 2001. but there are known species-related differences in the hydrolysis of diester phthalates. Peck and Albro. dibutyl phthalate (DBP). Cousins IT. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). In animals.html.. McKee et al. 2007.18(12):10681074.e. 2004. References Agency for Toxic Substances and Disease Registry (ATSDR). Needham LL. Jordan S.. 2002. These differences may contribute to species-specific differences in toxicity (ATSDR. Rhodes et al. Slakman AR.html...atsdr.. 1982). Hauser et al. phthalates produced anti-androgenic effects by reducing testosterone production and. Springall C. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Massey RC. which may be a pathway to the development of liver toxicity and cancers in these animals.nih. 2002). Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. McDonnell DP. Sauer MJ.niehs. 2004. gender.cdc. Vol. 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. and extent of metabolite conjugation to glucuronide (Albro et al. Silvapathasundaram S. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. van der Broek PH.cdc. Lovekamp-Swan and Davis. Part Q: Phthalate Esters. phthalates have been shown to induce peroxisomal proliferation in rodents. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. Hoppin et al. ovarian abnormalities in the female animals (Jarfelt et al. Population estimates of concentrations of specific phthalate metabolites may differ by age. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . 2003.45:19-25. efficiency of intestinal absorption. NTP-CERHR. and Sertoli cell abnormalities in the male animals and. at very high levels.

Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Environ Health Perspect 1998. Sumpter JP.210:21-33. Toxicol Appl Pharmacol 2004. Milligan SR. Jarfelt K. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Hauser R. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Stringer WT. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. gov/chemicals/dehp/dehp-eval.105:802-811.nih. Rylander L.11(5):381-387.nih.gov/chemicals/dehp/dehp-eval. Silva MJ. Calafat AM. Jobling S. Ladefoged O.382:10841092. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Chen Z. Hass U. Main KM. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Filser J. Reynolds T. Ryan L. Jacobsen H. Silva MJ. Am Ind Hyg Assoc J 1985. The estrogenic activity of phthalate esters in vitro. Harris CA. Jonsson BAG. Environ Health Perspect 2003. et al. Hum Reprod 2007. 2000b [online]. Richthoff J.112(17):1734-1740. J Androl 2004. Park S. NTP-CERHR. and infant formula by tandem mass spectrometry (LC-MS-MS). Kessler W. Yoshimura M. Skakkebaek NE. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride.niehs.110(5):515-518. 2000c [online].103:582-587. Borch J. 6/2/09 Okubo T. Determination of phthalate monoesters in human milk.26(8):1219-24. Lovekamp-Swan T. Mortensen GK. Skerfving S. Anal Bioanal Chem 2005. Angerer J. Calafat AM. 6/2/09 NTP-CERHR. Akesson B. 2000a [online].46(11):643-647. David RM.18(1):122.64(8):555-560. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Davis BJ. Environ Health Perspect 2002. et al.html.112(17):1740]. White R. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Grote K. consumer milk. Park MG. Bolte G. Brock JW.Phthalates in human urine samples.niehs. Ryan L. Koch HM. Hanaoka T. Andersson A-M.195:142-153. 6/2/09 NTP-CERHR. Research Triangle Park (NC).html.niehs. Butala JH. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Nielsen J. Albro PW. Kalita JC.19(4):505-515. Hagmar L. Kano I. Singh NP. Csanády G. Baird DD. Fromme H. Davis BJ. Research Triangle Park (NC). Meeker JD. Suzuki T. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic.html. Available at URL: http://cerhr. Sumpter JP. Scand J Work Environ Health 1985. Research Triangle Park (NC).gov/chemicals/ phthalates/dbp/dbp-eval. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Available at URL: http://cerhr. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Epidemiol 2005. Zhang S.nih. Leffers H. 2006 [online]. Duty S. Available at URL: http://cerhr.106(1):23-26.25(2):293-302. Research Triangle Park (NC). Parker MG. Int Arch Occup Environ Health 1993. Boehmer S. Mechanisms of phthalate ester toxicity in the female reproductive system. Available at URL: http://cerhr. Environ Health Perspect 1995. Reproducibility of urinary phthalate metabolites in first morning urine samples. Liss GM. Int J Hyg Environ Health 2007. Meeker JD. Chahoud I. Brock JW. 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 . National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Environ Health Perspect 2004.html.16(4):487-493. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Reprod Toxicol 2005.22(3):688-695. Balasubramanian AV. Reprod Toxicol 2004.nih. Drexler H. 6/2/09 NTP-CERHR. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Duty SM. Gans G.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Numtip W. Hauser R. Silva MJ. Yokoyama Y. Wang P. Henttu P.niehs. Pan G. Giwercman A. Biol Pharm Bull 2003. McKee RH. et al. Dalgaard M. Tsukino H. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hartle RW. Kano K. Hoppin JA. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Environ Health Perspect 1997. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.111(2):139-145. et al.

et al.58:339349. Barlow NJ. Urinary levels of seven phthalate metabolites in the U. Lambright CR. Jackson SJ. Crit Rev Toxicol 2006.S. Albro PW. Fielden MR. Toxicol Sci 1998. Abbott BD. Ostby JS. Toxicol Sci 2000. Orton TC. Bratt H. et al. Klinefelter GR. Cunningham ML. Hodge CC. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Meek MD. Rhodes C.45:11-17. Malek NA. Matthews JB. Caudill SP.36:459-479. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Peck CC. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Zacharewski TR. Environ Health Perspect 1982. Pratt IA. Environ Health Perspect 2004. Reidy JA.114(11):1643-1648. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Peters JM. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Batten PL. Wu ZF. Silva MJ. Barr DB.112(3):331-338. Rusyn I. Environ Health Perspect 2006. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat.Phthalates phthalate (DEHP): a cross-sectional study in China.65:299-308. et al.46:282-293. Clemons JH. 112(5):A270]. Environ Health Perspect 1986. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Parks LG.

4 (13.6) 50.9-30.7-14.2 (47.6) 13. residents (Blount et al. can produce developmental and reproductive toxicity in rodents.2-38.4) 33.3 (44.3-43.6) 63.8 (53.1-16.6) 25.8-16.0) 34.5-33.7) 23.0 (15.0) 70.3-18.1-214) 166 (116-191) 145 (110-213) 88.9 (22.8 (38.6) 35.1) 13.4) 75th 35.1-18.5 (67.2 (14.4) 80.2 (10.3 (33.5) 82.4) 38.1) Selected percentiles ( 95% confidence interval) 50th 17.2-39.4) 129 (98.7-16.8 (30.2) 22.3-12.7-172) 103 (74.9-49.5 (66.0 (12.9-14.9 (39.3-18.4-16.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.4 (10.6 (53.3-125) Total 15.6) 24. 2000).5) 65.9-47.4) 35.3 (29.4-15.3 (12.8 (71.9-27.4) 81.9) 13.3-130) 122 (88.5) 30.4) 108 (96. population from the National Health and Nutrition Examination Survey.6-18.3) 13.8-76.6) 29.8-64.5-62.0 (20.3..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 39.8-17.8-16.0) 20.8-18.7 (11.7 (82.2 (43.1) 14.1 (20.4 (68. BzBP can be released into the environment during its production and.8-72.4 (32.3) 63.2) 13.4 (48.1) 12.4 (32.7 (53. it can be released into the ambient air during use or disposal of the products.2) 33.7-16.9-16.4 (27.5) 55.7-82.6-92.3) 94.7 (15.0) 90th 67.1 (13.4) 71. sealants.1) 67.8 (10.7-35.7 (13.0 (23.1-38.9 (13.4 (31.9 (12.S.5) 23.1) 68.7) 40.9 (21.8) 33.3) 23.5-94.1-39.3 (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 13.6) 14.1 (10.1) 29.9) 49.3 (12.1 (32.8-35.5-84.0 (27.8 (80.6-132) 103 (84. IARC considers BzBP not classifiable with respect to human carcinogenicity.9-62.7 (80. 262 Fourth National Report on Human Exposure to Environmental Chemicals .8 (12.Phthalates Benzylbutyl Phthalate CAS No.8-121) 79.8 (71.6-150) 94.2-115) 113 (91. NTPCERHR.5-36. some personal care products.1 (58.2 (19.4-24.6) 67.2 (19.3-88.2-17.9 (16.7-119) 99.4-62.5-40. High dose BzBP and its monoester metabolites.1.9) 15.5) 27.3 (54.8-98.8) 63.8) 24.2) 17.9-28.3) 54. 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.1-116) 122 (93.0 (14.0) 33.0 (30.2) 12.5-145) 138 (106-241) 143 (127-179) 120 (99.2) 15.3-34. interval) 15.2) 66.2-19.5) 15.0) 16.6 (21.3-74.5 (47.4) 35.3-91.4) 65.2-116) 122 (102-143) 101 (84.7-58.1-35.3) 37.3 (30. and 0.1 (13.5 (61.1-120) 52.7) 38.2) 69.0 (11.6-116) 122 (102-142) 101 (85.5-41.4) 98.3 (29.8) 28. particularly male animals (McKee et al.9-190) 86. and to a lesser extent.0-106) 58.1-61. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9) 14.6 (13.4 (53.4 (53.8) 14.1) 32.9 (11.6) 35.3-161) 99.8-14.1) 76.4 (63.3 (13.7 (70.7-13.0) 24.1 (19.6) 95th 103 (94.5) 15.S.4-25.9) 11.6-39.7-17.2-33.2) 14.2-155) 91.8 (21.9 (28.9-87.4) 12..4) 49.4 (29.4) 14.4) 51. see Data Analysis section) for Survey years 99-00. and 03-04 are 0. including MBzP.2-20.6) 13.2-40.7-170) 169 (134-198) 152 (99.1-43.5 (26.0-130) 101 (86.3-82. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.7-16.9) 18.3-75.7 (51.8-48.4-92.3) 13.0-55.0 (15.6-38. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.1-90. 2000).5 (27.5-35. 2001-2002.0 (34.3-27.5-25.1 (14.6) 15.6-92.6-79.3-21.1) 31.6-29.7 (12.5-18.6 (13.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.2 (11.9) 12.0) 23.5 (76.8 (14.6-72.8-133) 89. and diet is the major source for general population exposure. respectively.6) 16.0-26.0 (43.3 (22.9 (70.5 (55.2-16.1 (14.6 (41. car care products.0-85.5) 16.5-14.5-36.7-15.6 (12.2-183) 101 (78.6 (66.7-25.0 (33.4-127) 80.6) 37.5-97.1-16.0 (30.8-17.8-41.8 (50.8.8 (86.6) 14.0 (26.5 (13. 0.2) 14.3) 15.6 (13.6 (13. 01-02. because it is not bound to products in which it is incorporated.6 (32.9) 14.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6-43. vinyl tile.1-15.8 (28.4 (59.1 (55.6-17. and 2003-2004 were generally similar those reported in U.1-15.2) 78.2 (25.2) 32.0) 32.0 (55.5 (57.2-31.4 (10.8-14. 2004. Food crops take up BzBP.9) 43.2-16.9 (12.8-13.

0) 60.1 (13.6) 53.9) 11.8-15.9-13.4-15.4) 12.2) 11.9-13..0 (10.7 (13.8 (10.0 (33.4-42.9-28.5-213) 49.8) 24.9 (10.6 (11. 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 (21.8) 33.8-39.7-56.3) 13.0-90.5-16.8 (30.3) 13.8-15.6 (57.2) 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 12.5) 46. population from the National Health and Nutrition Examination Survey..3) 21.4-18.4) 17.5) 41.4 (11. 2002).0 (41.8-13.9 (51.5-79.8 (46.2) 11.8) 53.7) 11.2 (40.3) 36.4 (34.4) 60.9 (39.3 (23.1 (43.5) 23.0 (62.4) 21.1 (41.9) 64. 2007).1 (13.8 (13.6 (30.1 (21. in men attending a Boston infertility clinic (Duty et al.2-51.5 (11.2-57. A small study of African-American women in Washington.6-40.9) 52. Hoppin et al.7 (38.95-14.2-15.5-31.3) 55.9-23.5) 14.7-20.4-60.7-29.3) 73.5) 16. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 53.2) 11.5 (10.4 (13.4-14.7) 25.8) 56.8) 26.3 (35.9) 42.Phthalates York City (Adibi et al.3) 90.6) 58.2 (69.8) 68.1-14.9 (55.7-15.8-173) 195 (121-305) 229 (99.1 (53.0 (12.1 (21.4 (33.8 (69.9 (9.8) 71.4 (60.8-27.1-12.4) 13.7 (11.1-79.4) 44.3) 16.1 (15.8-69.4-90.0 (13.9-62.0) 24.5) 20.9-16.9-69.9 (24.2-78.3 (39.0 (12.0-15. 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.9 (54.2 (56.7 (14.0) Selected percentiles ( 95% confidence interval) 50th 13. 2003).6-12. Hauser et al.7-69.7-397) 70.1-58.1-35.6) 12.4) 51.4) 28.9 (15.6 (11.3 (24.6) 25.9) Total 14.1 (9.5-29.6 (51.8-14.3) 14.1) 80.3) 89. 2006).5-57.8-64.9) 12. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.2-26.7) 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 40.6 (36.7-12.0) 11..4 (10.3-16.5-23.3) 18.9-40.1) 24.6) 38.2) 26.2) 67.1-120) 77.6 (14.1-125) 86.9 (12.1 (19.4 (69.7 (19.4 (25.9-104) 62. In NHANES 1999-2000.5-99.7-14.3 (38.9 (22.4 (46.8-16.5-42.1) 24.7 (11.69-11.3) 12.8) 108 (75.4-17.1 (18.5) 78.1 (14.8-85.9-115) 57.2) 15.1) 23.4-99.4-14.6-20.9 (24.5) 95th 77.0) 13.9-83.6-47.9 (15.8-42.5-26.3 (12.9-14.8) 13. 2004).0) 49.7 (12.8) 15.9) 11.0-27.4) 13.8) 46.4) 25.6 (24.7) 19. interval) 14.0-109) 65.9) 12.8-14.0 (49.2 (41.7 (13.8 (57.5-58. In an annual sample of German university students.0-51.1 (25..3) 13.6-81.8) 33.8) 16.8) 80.2) 32.6-15.1 (21.8) 11.6) 75th 25.9 (29.8-13.8 (50.2) 12.9 (10.3-34.7 (55.8 (11..7-123) 77. 2004. in young Swedish men (Jonsson et al.7-14.3-64.1 (11.1) 12. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.S.6 (22.5-13.5-76.6) 12. 2005).3) 29.2-12.2-17.5 (9.2-49.4) 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. 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.6 (30. 2002.0-48.5 (48.4 (26.5 (10. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6) 30.4-27. and females compared to males (Silva et al.3) 37.1-12. 2007)..6 (19.7 (11. Weuve et al.7-90.7 (54.7-31.8) 54.4) 104 (89.6 (34.5 (35.8-80.6-86.0-53.0) 15.3) 14.3-38.6-13.6 (11.7-19.8-34.5-61. 2003).6 (15.9) 24.4-93.7) 46.2 (27.5) 13.5 (12.1 (21.9) 12.9 (12.0) 24.73-12.6-99.4 (12. adolescents compared with adults.5-38.4) 50.4-116) 73.2-13.1-27.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .1-29.5-58.0 (41.2-117) 95.7 (18.4 (74.3 (15.1) 142 (99.4-23.1) 17.9) 100 (80..8-13.0) 12.1) 27.0-26.7) 38.4 (63.5-26.7-19.5 (42.5) 17.3-73.4-102) 70.8-60.7 (21.6-26.5) 10.0 (67. and in a small sample of German residents (Koch et al.9 (43.0 (38. 2005.8) 34.7-61.7-15.4-79.7) 56.4 (11.2-21..8-48.3 (13.7-20.5 (56.6-116) 74.4-19..8 (49.4) 14.1 (34.2-15.4) 15.3 (60.6) 13.7 (23.3-11.6) 73. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.1) 39.4-142) 134 (116-176) 136 (85.8 (64.7 (59.1 (23.0 (11.1 (46.. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.4 (11.3) 67.1) 35.5 (49.8 (12.4) 90th 50.2-13.

Poland. Phthalate monoesters levels in the urine of young children. Wiesmuller GA. 112(5):A270].gov/ chemicals/phthalates/bb-phthalate/bbp-eval. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. David RM. Environ Res 2003. Environ Health Perspect 2002. Environ Health Perspect 2004. Brock JW. Malek NA. Int J Hyg Environ Health 2007.93:177-185.Phthalates References Adibi JJ. Urinary levels of seven phthalate metabolites in the U. Baird DD. Richthoff J. Third National Report on Human Exposure to Environmental Chemicals. Butala JH. NTP-CERHR.html. Brock JW. Koch HM. Helm D. Duty SM. J Androl 2004. Silva MJ. Singh NP. Camann DE. et al. Pirkle JL. Caudill SP. Rossbach B. Perera FP. Green RA. Needham LL.108(10):979-982. Hilborn ED. Wittassek M. Hoppin JA. Reidy JA.25(2):293-302. Hum Reprod 2007. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.112(3):331-338. Environ Health Perspect 2006. 2005. Dobler L. Environ Health Perspect 2000. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Calafat AM. Meeker JD. Epidemiol 2005. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.22(3):688-695. Needham LL.16(4):487-493. McKee RH. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.111(14):1719-1722. Blount BC. Urinary phthalate metabolites and biomarkers of reproductive function in young men. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Rylander L. Angerer J.114(9):1424-1431. Atlanta (GA). Centers for Disease Control and Prevention (CDC). Duty S. et al. Bull Environ Contam Toxicol 2002. Silva MJ. Koch HM. et al. Schettler T. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Hu H. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Levels of seven urinary phthalate metabolites in a human reference population. Caudill SP. 4/20/09 Silva MJ. Research Triangle Park (NC). Jonsson BAG.18(1):122. 2000 [online]. Barr DB. Davis BJ. Eckard R.110(5):515-518. Calafat AM. Hagmar L. Hauser R. Brock JW. Caudill SP. Available at URL: http://cerhr. Silva MJ. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Hodge CC. Reproducibility of urinary phthalate metabolites in first morning urine samples.68:309-314. et al.S. Silva MJ. Sampson EJ. Jacek R. Ryan L. Jedrychowski W. Drexler H. et al. Gans G. Giwercman A. et al. et al. Reprod Toxicol 2004. Barr D. Prenatal exposures to phthalates among women in New York City and Krakow. Chen Z. Sanchez GN. Ryan L. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Weuve J. Environ Health Perspect 2003.niehs.nih.210(3-4):319-333.

60) 3.0-25.4 (14.0 (13.30) 10.0) 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 2.10) 9.40-4.2) 5. interval) 2.. and insecticides.6) 12.7) 18.5-24.97) 2.80 (2.6) 17.10) 3.00 (5.72-3. and in a small sample of Japanese adults (Itoh et al. 2000).2-14.3.00-4.7) 14.0) 20.7 (17. Koch et al.90-7.2-33.2 (11.5-16.2-22.60 (5.00-11.96) 3.9-23.73-5.6 (10.5-16.00) 4.85-6.00 (7.97) 4. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.0) 9.5) 12.90-4.0 and 0.22 (3.37) 6.00) 6.8) 21.5-29.50) 2.30) 5. pharmaceutical coatings.7 (7.1 (13.6) 10.60 (8.3 (11.3 (13.7-31.3 (13.20 (3.10-9.0 (11.63) 3.10 (3. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.49-2.30-7.90 (3.50-6.3) 18.2 (12.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.17) 4.7) 15.10) 2.9) 10.30-6.67 (5.5 (20.0 (13.00-6..40 (7..50) 18.1-20.40-12.30-11.1) 22.50) 5.60 (2.90-4.07 (3.10-2.90) 12. 2001).30) 10.6 (13.6) 17.20-6.6 (11.50) 90th 12.70 (2.97-7.4 (20. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate. residents (Blount et al.26 (2.6 (9.91) 4. 2004.71 (2.10) 11.44-2. in men attending a Boston infertility clinic (Duty et al.56 (3.6) 26.46) 2. 2005.5 (17.30 (4. 2005).5) 25.0) 12.3 (16.7 (17.30-13.40-17.20 (7.5 (27.0-18.84) 4.00-6.5) 14.11-3.00) 4..40 (6.68 (2.. 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. 84-74-2 Di-isobutyl Phthalate CAS No. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics. in a small sample of pregnant women in New York City (Adibi et al.10 (4.1) 25.30-6. 2005)..40 (2. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.70) 5.33 (2.20-12.20-9.9) 15.00) 10.1-17.1 (8.40-5.6-14.4-27.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.7) 4. CDC.5) 18.90 (6.7) 7.00-9.48 (2.80-5.30 (1.6 (14.7-18.70) 3.4) 22.24-8..46-5.0) 24.3 (16.4) 5.30) 2.7-31.20) 4.8) 677 652 703 699 1216 1088 Limit of detection (LOD.60 (4.8) 40.17 (2.5) 19.40-4. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.70-4.6-18.10) 8.0) 13.90-2.Phthalates Di-n-butyl Phthalate CAS No.80 (5.20 (6.3) 3.30-2. Hauser et al.80 (5.10-9.56) 3. 2004.66) 2.3-48.22) 3.50-10. OSHA has established a workplace air standard for external exposure to DBP. Fourth National Report on Human Exposure to Environmental Chemicals 265 .56 (5.55 (3.S.5 (11.9 (16.3-30. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.6-34.80) 75th 5.0-14. mostly as MnBP (Anderson et al.6) 16.90 (4.50-2. 2003).7 (18.46 (2. 2000. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.9-14.3-19.3 (19.82-3.40-9. Biomonitoring Information Median concentrations reported in the NHANES 19992000.50) 8.50 (3.40) 5.5) 23.5) 18.6) 16.70 (5.1-12.0 (19.50 (6.7 (9.3-24. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.5 (10. and also in some printing inks.40-3.6 (13. they have been referred to as monobutyl phthalate (MBP). population from the National Health and Nutrition Examination Survey. 2003). DBP can produce reproductive toxicity in male rodents (McKee et al.3 (18.20-2.6 (29.20-12.59) 3.40-3.43) 6.80 (2.5) 22. When total DBP metabolites have been measured.S.0-38.4) 12.8 (9.3-20.40 (3.81 (3.20) 7.3) 33. 2007).46 (3.4-12.60-6.6 (10.7 (16. 2005).56-4.10 (4.6-20.73 (2..3-18.9 (16. Studies of children found age-related differences in urine MBP levels.02) 4.30) 6.90 (4..7-20.70-8.6 (14.55) 2.2 (8.80-5. NTP-CERHR. about 65% to 80% of a dose is eliminated in urine within 24 hours.30-3.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.40 (2. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.6-26.00) 7. Survey Geometric mean (95% conf.19-3.30 (3.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.28-5.1-25.70-4.3-43.80 (3. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.1) 16.50-4.50) 7. Following oral administration of DBP to humans. In addition.

56) 5.9) 12.43) 3. Between 1998 and 2003.0) 3.8 (10..2-13.7 (9.82 (4.78) 9.2) 8. 2004).83 (2.57-4.79-6.42) 2.00-7..1-24.04) 7.43) 3.56-4.46-11.62 (6.1) 15. 2006).64-7.28 (4.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.0 (12. population from the National Health and Nutrition Examination Survey.94 (5.3 (17.99-4.2-15.4 (12.00 (3. 2007).27-12.76-3.79-8. ranging from more than one-tenth the NHANES median (Itoh et al.9 (9.34 (3.59 (4.47 (3.95) 10.3) 18.78-8. to about two to fourfold higher (Fromme et al.4) 23.1-15.1 (11.24) 3.35) 3.11) 5.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.7) 11. In an analysis of NHANES 1999-2000. while MnBP declined (Wittassek et al.03 (5. samples from German university students had consistently higher median urine levels of MnBP and MiBP.10-5.2) 9. interval) 2. Biomonitoring studies on levels of MnBP and MiBP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of dibutyl phthalates than are found in the general population.2) 24.08-2.6 (9.69) 4.7 (13. 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.18-4.1-12.81) 9.86) 6.89 (3.3) 28..47-5.0) 15.29-8. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.66) 4.29-3.15) 3.26 (2. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al. 2004).62-12.98 (2.6-19.1) 13.17) 90th 8.11-2.36-2. An analysis of NHANES 2001-2002 showed similar age. 2002.4) 7.41 (2.56) 2.18) 3.0) 11.96 (3.00-3.6 (8.76-15.8) 10. than adults in NHANES subsamples during the same time period.0-18.8-36.52) 3.65-4.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .68) 5.31 (7.09-2.76 (3.68 (2.and gender.65 (4.78) 8.58-3.38-10.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.84 (8.6) 11.65-11.S.20-3..05) 2.20 (2.92 (7.66) 10.81) 4.73 (5.81 (6.32 (3.8-18. the students’ median values for MiBP levels remained relatively unchanged.04) 3.14 (4.1-25.75 (4.80) 7.57 (3.18 (4.31) 2.39-3.08) 75th 4.44 (3.20 (7.95) 2.17-12.18 (1.7-28.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.31 (2.19 (2.8 (8.5) 13.84 (4.7 (11. Over this time. up to four and 13 fold.9 (11.0) 7.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.02-10.07 (2.56-15.51) 5.45) 3.8-18.1 (10.6 (8.64-10.31) 2.97-2.68) 3.51) 2.69-7. respectively.99) 7.17 (2.6) 13.4) 15.3) 16.67-5.02 (7.39) 5.5-19.54 (2.72) 5.1) 11.32) 7.38 (6.58-4.94-12.64-7.6 (12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4-16.30 (6. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.2 (10.1) 4.54 (4.33 (2.66 (8.91-6.43) 3.04-5.86-4.51) 15.8 (9.07-5.9-26.89-5.20-2.25) 5. Survey Geometric mean (95% conf. Weuve et al.20-4.93-6.9-16.46 (2.69 (2.89) 6.53-5.21 (5.69) 6.36-7.13-6.22 (2.33-9.52-20.6 (15.1) 10.53-3.1) 7.6) 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 2.9 (15.00-3.3) 13.28-13.46) 3..82) 4.88 (2.75 (6.33) 3. 2007). 2005).15-4.47-12.11 (5.32 (7.5) 15.9-40.5 (9.13 (2.54) 2.18) 4.53-4.18-10.80-3.61-3.81 (3.80 (3.0 (8.57 (3.52-3.7) 10.20 (2..52 (2.79 (4.6-19.0 (10.03-7.8-13.26-2.72-7.01-2.85 (2.5 (11.21) 10.2 (11. 2005).0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2..55-6.74-3.66) 2.03-11.3) 13. 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.6 (10.76-3.37) 3.3 (13.33 (3.94) 6.7 (21.95-3.7) 19.7) 3.30) 2.74 (4.

7 (24.1) 23.6-48.0 (18.0 (31.1 (19. and 03-04 are 0.1 (17.8-22.2-33.0-21.2 (58.3-40.7-53.9) 75.7-127) 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 22.5-121) 106 (94.3) 26.3) 23.2) 20. respectively.4-159) 107 (84.1 (21.1 (62.1) 30.8-123) 101 (90.6-20.3-145) 85.5) 36.0) 84.6-40.5-47.2-56.7) 92.7-42.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2) 32.6-36.5-117) 95.9) 36.3 (30.7 (51. interval) 24.8 (19.2 (21.3 (51.6-33.5) 21.9 (79.3) 21.3-21.0-58.6) 21.1 (34.6) 39.0) 27.6 (65.5) 19.9 (17.4 (35.0) 117 (104-131) 112 (84.5) 26.7 (70.7) 42.6 (22.6-44.0) 120 (98.1) 31.0) 38.8) 43.4 (36.6) 80.6 (61.5) 31.2) 62. population from the National Health and Nutrition Examination Survey.0 (72.1-80.0 (23.1) 17.1) 36.8-42.5) 47.2 (21.7-124) 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.9) 46.8 (57.9) 21.5-44.6 (44.5) 34.7-24.4 (38.8-25.3-24.2 (19.8) 23.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9.9-79.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.0) 20.4 (25.1-75. 1.3-79.6 (55.4 (71.7) 124 (98.2 (79.7-34.2-114) 73.7-42.3) 19.1 (19.3-67.1-82.1) 23.0-51.5) 85.4 (35.2) 38.1 (58.6-29. and 0.8) 19.0-24.7-91.5) 17.5-43.9-114) 116 (97.3) 40.4-25.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.2) 26.6-49.0) 21.8) 48.7 (18.7) 74.6 (19.8-111) 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 23.4-60.2) 68. 01-02.2 (20.1-20.1 (36.5) 40.0-73.7 (64.5) 37.6) 71.8) 62.1 (31.0 (78.5) 20.4 (72.5-53.6 (32.3 (17.7-117) 118 (108-143) 93.1) 46.1 (19.9 (17.5) 95.5 (74.7-121) 97.1 (54.1-27.8) 75th 51.6-31.2-24.4 (35.9-22.4) 22.3 (30.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.5) 36.4) 52.3 (60.3 (56.8) 58.7 (43.6) 46.6-113) 108 (90.0) 30.3 (36.4-18.2) 90th 98.1 (28.6-24.1) 20.5) 24.9-28.7-20.2-32.7-116) 95.1) 25.6) 35.2-87.5 (29.9 (20.5 (59.9-33.9-53.9) 18.0 (30.4) 20.0-19.6) 20.2 (25.9) 71.7-106) 69.6 (90.0-24.6 (16. Survey Geometric mean (95% conf.0 (17.7-34.4 (84.5-60.3-60.1-51.3 (37.9-42.9-87.2-49.9) 26.5 (30.8-119) 90.0 (36.0-26.4-44.1) 47.6) 17. Fourth National Report on Human Exposure to Environmental Chemicals 267 .0) 31.2 (59.5 (59.7-26.7 (19.8-132) 95.7 (16.9-22.4-20.9 (79.S.1.4 (23.7 (22.1 (18. *In the 1999-2000 survey period.1) 19.5 (28.4) 59.7-111) 64.0-19.0 (15.4-42.9-92.4 (21.4) 64.6 (26.6 (48.3 (23.6-143) 127 (99.3) 24.2 (75.7 (18.3 (23.7) 52.0 (20.6-37.9) 29.7 (38.7 (28.5-42. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3-76.4 (19.2 (17.7) 28.0 (25.2) 42.9-101) 77.2-23.4-26.1-29.2-93.1 (51.2-63.5-27.0-32.5-47.1 (16.7-92.1 (19.1 (41.6) 38.2-22.0 (45.1-24.2-159) 92.4 (35.3-96.5) 65.4.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.3-136) 137 (107-162) 119 (90.6-29.1-92.6-69.5) 78.3) 36.2 (18.2 (74. see Data Analysis section) for survey years 99-00.2 (78.4-31.3) 18.3-85.3 (42.8-29.1 (26. referred to as monobutyl phthalate (MBP).2-21.1) 23.1-22.7 (33.

4) 21.4 (16.9) 62.9-68.2) 59.6-23.9) 49.8) 34.5-76.5) 82.8) 75th 38.0 (19.9) 19.7) 36.4 (45.2-61.3-17.4 (17.7) 42.9-34.6-27.3 (69.0) 94.S.2-28.0-17.4 (17.5) 91.1 (46.6-43.1) 35.4-47.4) 19.3) 20.6 (57.7-23.1-32.8-24.1-23.9) 28.6-32.2-22.3 (17.4) 15.7-78.8 (50.4 (23.6 (72.4-131) 81.3-18.6) 14.8) 40.0 (34.4-135) 71.5-142) 89.3 (16.6-128) 96.6 (31.9-14.1-128) 97.9) 91.9-105) 85.3-71.0 (16.8 (25.1) 61.3-38.7-80.8) 23.7) 19.9 (35.0-90.3 (19.7 (81.6-44.1) 37.0-41.1-21.8 (18.5-142) 81.5-70.4 (33.6-50.1) 53.0 (26.7-20.8) 63.3) 18.4) 16.3) 21.4) 62.8-23.4 (18.2 (83.2 (38.3) 59.2-22.0 (20.2-86.7 (28.5-21.8) 17.7 (73.4-76.4) 15.4-72.4 (47.5 (15.1) 44.3-81.3) 35.0-75.1 (56.4 (31.4 (31.4 (37.4) 51.5) 134 (93.6-19.0) 75.5 (18.4-61.1-99.8) 17.3) 19.7 (16.4-164) 96.8) 20.7-19.6) 64.7 (12.5-22.4-103) 117 (83.6) 25.3-114) 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 17.6 (17.9) 24.1 (61.8 (18.7 (54.0) 55.6 (61.0) 70.5-18.6-119) 63.2) 65.7-21.3-32.5-30.2) 159 (102-263) 147 (93.6-26.9-68.5 (14.2 (35.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.7 (20.1) 17.3-21.7 (43.5) 90th 68.0 (70.2 (16.9-70.9 (37.0) 25.6) 23.5-16.7 (14.3 (52.3-49.9 (30.9 (56. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.8) 28.4) 53.0 (15.1-83.1-99.0-113) 104 (83.8 (65.4 (20.9 (58.6-44.6-74.0 (50.7 (60.3 (42.1-18.8 (33. population from the National Health and Nutrition Examination Survey.1) 50.3-40.8 (17.2-179) 84.2-27.7-37.9-56.6) 83.3 (21.1 (34.3 (55.3 (76.4 (53.9 (73.5-23.0) 35.1 (29.7-39.3 (28.0) 41.5) 39.7-19.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.0 (52.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9 (30.1) 21.9 (21.6) 18.9) 14.0) 26.6 (74.4-24.5) 84.0 (71. 268 Fourth National Report on Human Exposure to Environmental Chemicals .9-84.1) 42.2) 31.1 (21.5) 17.2-18.1 (32.3 (17.8) 13.9) 52.8) 34.9 (39.8 (13.6) 34.4 (16.6) 24.2-85.0) 53.1 (15.4 (68.5 (64.6-23.2-16.0) 81.8-24.6) 31.8 (16.6-24.8) 35.0-38.7 (57.6) 39.9 (19.7-28.3) 33.3 (17.6 (27.3-20.2-22.6-16.5-64. Survey Geometric mean (95% conf.1-62.6-155) 91.0 (18.8-32.5-15.9 (16.3) 17.8-43.8) 22.6 (29.6 (25.1) 20.9 (20.3 (48.2-73.5) 60.7-42.8 (22.3) 33.9 (64.4) 20.6-24.3) 67.4 (50.3-21.2-108) 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.9-100) 86.2) 21.5 (30.7) 20.1) 22.5 (81.5-41.8 (18.4 (13.3 (71.4-65.2-48.6-92.2 (19.0) 108 (71.8) 30.6-42.3-39.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.6) 38.3-78.4 (56.0 (69.0 (61.6 (25.9 (35.9-49.8-235) 137 (108-198) 88.9-36.3 (60.0) 29.7-26.2 (19.0) 59.0 (43.0-60.6-22.6) 24.0 (27.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41. interval) 22.3-26.3 (46.5 (18.6-53.8) 19.6) 65.4 (50.0-92.9-26.4 (19.6-28.0 (18.6 (19.9-38.2) 74.9) 20.8) 20.0) 19.6) 37.7 (60.9 (30.5) 21.2-21.3-106) 74.4 (31.1) 20.2-106) 64.0-19.6 (41.7 (27.7-51.8) 17.5-37.3) 19.0) 28.0-47.9) 39.3 (52.4-34.3-23.3 (24.9) 30.2) 16.7 (19.3) 52.

210:21-33. Perera FP. Epidemiol 2005. Urinary levels of seven phthalate metabolites in the U. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hilborn ED. Hauser R. Caudill SP. Koch HM. Ryan L. Eckard R. Singh NP. Silva MJ. Jedrychowski W. Prenatal exposures to phthalates among women in New York City and Krakow. Green RA. Itoh H. Rossbach B. Butala JH. Springall C. Weuve J. Calafat AM. Masunaga S. Reidy JA. Barr D. Third National Report on Human Exposure to Environmental Chemicals. et al. Camann DE. 112(5):A270]. Environ Health Perspect 2004. Giwercman A. McKee RH. Duty SM.25(2):293-302. et al. Koch HM.112(3):331-338. Yoshida K. Schettler T. Centers for Disease Control and Prevention (CDC).108(10)979-982. Needham LL. 2005. David RM. Atlanta (GA). J Androl 2004. Malek NA. Hodge CC. et al.111(14):1719-1722. Barr DB. Silva MJ.210(3-4):319-33. et al. Int J Hyg Environ Health 2007. Int J Hyg Environ Health 2005. Massey RC. Meeker JD. Brock JW. Available at URL: http://cerhr. Food Addit Contam 2001. Environ Res 2003. Hum Reprod 2007.18(12):10681074. Calafat AM. Rylander L. Dobler L. Levels of seven urinary phthalate metabolites in a human reference population. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. NTP-CERHR.S. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Pirkle JL. Wiesmuller GA. Brock JW. Jonsson BAG. Drexler H. Sanchez GN. Poland. Environ Health Perspect 2000. Environ Health Perspect 2006. Silva MJ. Wittassek M. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.niehs. Bolte G.gov/chemicals/ phthalates/dbp/dbp-eval. Angerer J.22(3):688-695. Jacek R. Helm D. Hagmar L. Fourth National Report on Human Exposure to Environmental Chemicals 269 . et al. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Castle L. Chen Z.16(4):487-493. et al. Phthalate monoesters levels in the urine of young children. Hu H. Silva MJ. Duty S. Research Triangle Park (NC).nih. 4/20/09 Silva MJ.114(9):1424-1431. Sampson EJ. Environ Health Perspect 2003. Bull Environ Contam Toxicol 2002. Drexler H. Koch HM. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Caudill SP. 2000 [online]. Richthoff J.html. Reprod Toxicol 2004. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. et al. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. et al. Int J Hyg Environ Health 2007.208:237-245. Angerer J.18(1):122. Caudill SP. Gans G. Fromme H. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Blount BC.Phthalates References Adibi JJ. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Boehmer S. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Scotter MJ. Anderson WA. Needham LL. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Ryan L.93:177-185.68:309-314.

400) 1.400 (.Phthalates Dicyclohexyl Phthalate CAS No. resins.10) .90) .3.500) 1.500) .400 (.500 (.20) . < LOD means less than the limit of detection.400-.300-. 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.50) . which may vary for some chemicals by year and by individual sample. polyvinyl acetate.400) < LOD < LOD .400 (<LOD-.400) 1.500 (.10 (<LOD-1.300 (.300 (. only levels at or above the 90th percentile could be characterized.500) .900-1.500) .500 (.500 (.400 (<LOD-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.700) .300-.600) < LOD .500 (. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.400-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.70 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500-.400-.500 (.300-. population from the National Health and Nutrition Examination Survey.50) .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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.600) . Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.500 (.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 .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 .600) . and 0.10 (.300) < LOD .400-.300-.200-. In this Report.70) .200-.00) .300-.500 (.600) .300-.600 (.500 (.400 (<LOD-.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .500) < LOD < LOD .S.300 (. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.300 (.600) .200-.400 (<LOD-.700) .200-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. Survey Geometric mean (95% conf.400 (.300 (<LOD-.500) 1.9. respectively.500) .200-.70 (1.300 (. and 03-04 are 0.400-.2.500) 1.00-2.400-.80) . see Data Analysis section) for Survey years 99-00.200 (<LOD-.200-.300 (.00 (<LOD-1.300 (.10 (<LOD-1.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300-.400) < LOD 1.10 (<LOD-2. including nitrocellulose.300-.400 (.300) < LOD .500) < LOD < LOD . 01-02.00 (<LOD-1. and polyvinyl chloride. 0.400-.400 (.600) .400 (.300-.500) < LOD 1.400 (.00 (<LOD-1. and polymers. 270 Fourth National Report on Human Exposure to Environmental Chemicals .70) .00-3.700) .

10) .620) < LOD .690) < LOD 2.770-1.530-.S.630 (<LOD-.310-.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 1.330 (.33 (<LOD-3.330 (.360-.44) . Survey Geometric mean (95% conf.590 (<LOD-.800-1.420-.880 (.530 (.510 (.16 (<LOD-3.770-1.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.170-.410 (.05) .17) .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 .34) .240-.690-1.560) 1.250 (.660) .500 (.690) < LOD < LOD .740) .12-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.380 (.910 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .670-1.630 (<LOD-.830) 1.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .290-.390 (.67 (1.82) . population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 271 .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.470 (.610 (.670 (<LOD-.450 (.53) .790-1.350-.510-.00) .590 (.43 (1.450 (.22 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270) < LOD .910 (.06) .710) .370 (<LOD-.00 (<LOD-3.940 (.500) 3.400-.220 (<LOD-.530-1.260-.690 (.16) .06) .490) .740) < LOD < LOD .950 (.380-.660) < LOD < LOD .770) < LOD 2.480 (.33) .770 (.400-.310) < LOD .54) .770-1.14 (<LOD-3.420-.82 (1.74) .910 (.910 (.420-.530) 1.11) .54-6.500-.36-1.53) .18) .470) 3.54 (<LOD-2.

2.4 (62. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. 272 Fourth National Report on Human Exposure to Environmental Chemicals . In contrast. 01-02.S.9-92.. see Data Analysis section) for Survey years 99-00.5) 81. DC (Hoppin et al.2-102) 95. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.4. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. particularly those containing fragrances.9 (61.Phthalates Diethyl Phthalate CAS No.8-111) 85. 2002). Biomonitoring Information MEP levels in the NHANES 1999-2000. 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..7 (70. and hand lotions. deodorants. shampoos. 0.1 (71. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 0.3 (74.1-93. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2003) and African-American women in Washington. 2001-2002. 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 91.9.7) 71. Products that may contain DEP include perfumes. respectively. 2007).3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. population from the National Health and Nutrition Examination Survey.. and 03-04 are 1. soaps. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and also in men attending a Boston infertility clinic (Hauser et al.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.3 (82. colognes.

2004).5-114) 101 (87.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.Phthalates 2002 (Brock et al. 2003) were slightly lower than levels found in NHANES 2001-2002. This age-related trend is opposite the direction seen for other phthalates. In an analysis of NHANES 1999-2000.2 (66. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Analysis of NHANES 2001-2002 showed similar findings. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.0 (66.6 (65..7-110) 81. 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.9 (82. 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.5-113) 122 (93.. Other population estimates also differed by sex and race ethnicity (Silva et al.. population from the National Health and Nutrition Examination Survey.S. 2005). 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. 2002). with adjusted geometric mean levels of urinary MEP that increased with age (CDC.9-110) 96.6 (77. 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. Median MEP levels found in a small sample of German residents (Koch et al. 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.3-105) 87.0-156) 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 .

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

117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics. as glucuronide conjugates (Albro et al.3-49.0-19.2-39.4) 20.75-4.5) 23.1-29.6 (41.4 (21.10-3.61 (3.8 (19.6 (12.00) 19.5 (11.Phthalates Di-2-ethylhexyl Phthalate CAS No.10) 3.9) 13.0) 31.00 (5.80) 6.5 (20.3 (10.70 (1.2-17.90 (4.90) 4.7-32.2 (29.30-6.20 (1.00) 2.92) 4.70 (3.80) 13.4) 22.9-29.7) 27.50-3.80-27.80-4.30 (7.4-20.90-5.50-20.40-8.37-4.2) 23.40 (4.60) 8.20 (3.8) 15. respectively.30 (3. 1989.40) 2.10) 2.3 (19.21 (2.30 (4.0-29.6) 14.10-11.50) 4.75 (3.0) Total 4.50 (8.70-2.6-38.3 (11.2-28.10 (5.26-2.9 (26.70-5.7 (14.0 (9. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.27 (3.10 (4.63-4.31-4.5) 40. see Data Analysis section) for Survey years 99-00.50 (2.2 (10.7) 8.2) 29.5 (25.10-11.7) 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 3.10 (3.20 (3.3-64.70-2.4) 15.70-6.1982).9 (15.94-3.9-55.60 (5.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.40 (6.70-5.3-57.5 (30.9 (17.10) 4.50-16.00 (4.10 (2.40-8.00) 11.9) 27.46) 3.5 (18.70) 2.70 (2.9-19.4-40.50 (3.10-2.60 (6.54) 4.0-18.00) 5.80) 9.9-28.9 (16.6-60. toys. Fourth National Report on Human Exposure to Environmental Chemicals 275 .9 (29.96-5.50-6. and 03-04 are 1.60-7.6 (20. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.10-3.80 (2.30-11. and in humans. Peck and Albro.5) 32. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).60-11.1-17.1) 25.0 (19.98) 2.80-5.50-14.50 (7.80 (4.23) 3.00 (7.80 (1.5 (18.70 (5.0 (17.42) 3.0) 23.1 (11.50-6.5-40.0 (18.3) 13.07-4. Albro and Lavenhar.21 (2.20 (1.60) 9.8-36.6-25. 2002.4) 13.96) 4.9.5-27.2) 42.9) 15.10) 8.40-8.5-28.5-41.50-5.0. and blood product storage and intravenous delivery systems.00-5. 1982.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.7) 19. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.4-20.00) 9.0) 23.57 (3.2-35.84-4.90-3.68 (3.0 (14.4-42.10) 3.0 (13.92-2.1-27.2 (11