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-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5.4.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m. Table 1.3.1-Dichloroethene (Vinylidene chloride) cis-1.4.2-Dichloroethene Dichloromethane (Methylene chloride) 1.1-Dichloroethane 1.5’.4.1-Trichloroethane (Methyl chloroform) 1.What’s New in this Report What’s New in this Report In this Fourth Report.2'.2'4.1.4.2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.5'-Tetrachlorobiphenyl (PCB 49) 2.5.5'-Hexabromodiphenyl ether (BDE 153) 2.3.1.2-Dichloroethane (Ethylene dichloride) 1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.6-Pentabromodiphenyl ether (BDE 100) 2.3'.4'.4.6'-Hexabromodiphenyl ether (BDE 154) 2. The process for selection is described at http://www.4-Tribromodiphenyl ether (BDE 17) 2.2'.2-Dichlorobenzene (o-Dichlorobenzene) 1.3-Tetramethylbutyl] phenol) Triclosan (2.2'.2'.3-Dichlorobenzene (m-Dichlorobenzene) 1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4’.4’.4'-Tetrabromodiphenyl ether (BDE 47) 2.1.5.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4.1.2'3.3.4'-Tetrabromodiphenyl ether (BDE 66) 2.4'.4'.2-Dichloroethene trans-1.4.4.2’.6.6-Heptabromodiphenyl ether (BDE 183) 2.3.gov/exposurereport/chemical_selection.5'. 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 (2.5.2'.5-Pentabromodiphenyl ether (BDE 99) 2.2-Dichloropropane 2.4'. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4'.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.html.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4'-Pentabromodiphenyl ether (BDE 85) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4.5'-Tetrachlorobiphenyl (PCB 44) 2.2'.2'.4.2'.3’.4-Dichlorobenzene (p-Dichlorobenzene.4'-Tribromodiphenyl ether (BDE 28) 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1. Paradichlorobenzene) 1.cdc.2'.

and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Explanations for each change are provided in Appendix B.. five results that all have the value 90. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period..g.1).g. Fourth National Report on Human Exposure to Environmental Chemicals 3 . urinary 2. Percentiles for all three NHANES survey periods (1999-2000.5-dichlorophenol for the 1999-2002 survey periods. 2001-2002. Details of this procedure are provided in Appendix A. Data for other pesticides are included only for 1999-2000 and 2001-2002.4-dichlorophenol and 2. the presence of an interference) that produced results of inadequate quality. and these data will be included in the next release of the Report. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.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. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. 2003-2004) have been re-computed by use of this improved procedure.

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

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

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

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

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

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

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

People may be exposed to acrylamide from foods. Tareke et al.2 (62.S. 2006.6-65. in permanent press fabrics.1 (73.4-60. glycidamide. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.5 (44.7-64.9) 58. 2002).1 (88.1) 46.2 (58.0 (69.4) 57. In 1997. EPA.4 (54. as an absorbent in disposable diapers.1) 53. 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.6) 90.4) 57. 2006).6-61. such as potatoes and some grains. drinking water. Acrylamide is not thought to accumulate in the body at environmental doses.0-66. are heated at temperatures used for frying and baking.3-71. or to glutathione conjugates (Calleman et al.0) 57.6 (56.6) 50. in some sealing grouts. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. Elimination occurs mainly in the urine as mercapturic acid conjugates.2-118) 98.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.Acrylamide Acrylamide CAS No.7) 58.S.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.9 (54.1 (52.4) 100 (89. the main source of exposure is from the diet. and an average daily intake is estimated as 0.9-61. Since acrylamide has limited volatility and high water solubility. widely distributed in tissues.4 (53. Estimated intakes in children are about twice that of adults (DiNovi and Howard.6-66. and binding agents. FDA.0 (53.8-57.5-80. and is either metabolized to the reactive epoxide. These estimated intakes are hundreds of times lower than occupational exposures.1) 101 (95.4 (51. it was discovered that acrylamide is formed when starch-rich foods.5 (74.6) 73.0-49.3 (55.S. 1994). ocular and dermal irritation from direct contact with acrylamide containing materials.6-75.6) 71.4) 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 (67.1) 62.1-64.9 (69.3) 70.S..5) 66.7) 75th 79. Survey Geometric mean (95% conf.4 (59. but can covalently bind to form adducts with proteins.2-77.4-83.8 (57. but are generally above the U. Fourth National Report on Human Exposure to Environmental Chemicals 11 . 2005)..0 μg/kg for adults (FAO/ WHO.6 (51.8 (81.0 (57. Commercially.5 (52.6-108) 61. and cosmetics (NTP-CERHR.7 (63.9) 75.4-60.7) 54.1-57.1 (83.5-85. 1990. 2005).4-76. interval) 61. In humans.2-91.9 (60. Animal studies indicate that acrylamide is well absorbed. In the general population.0-58.4 (54.2-114) 163 (147-191) 96.2 (75.5) 58.0-108) 152 (139-175) 126 (111-142) 108 (86.7 (58.5 (79.0-104) 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. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. and from dermal contact with products that contain residual acrylamide.2) 57.1) 55.S.2-70. gels.3-2.7-60.0) 85. 217 million pounds of acrylamide were produced commercially in the U.2-93.9-105) 86. and in some cosmetics.2-67. and in the synthesis or compounding of dye materials.3) 86. 2005).3) 63. 2005.6 (81. Fennell et al. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. EPA reference dose of 0.2) 57. smoking.9) 57. Recently.6-104) 82. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.7 (65.7-64. acrylamide has produced upper airway irritation following inhalation of high levels. and well below doses known to cause nerve damage or carcinogenicity in animals.1 (47.9-52. soil conditioners.9) 63.0.2 μg/kg/day (U. 2004). EPA. 2005).3 (53.7 (55. pulp and paper production.1-64. population from the National Health and Nutrition Examination Survey. FAO/WHO.8 (91.1-61.8 (52.7) 73.. 2004.4-89. Polyacrylamides are useful water-compatible polymers used in water treatment. acrylamide is synthesized and used in the production of polyacrylamide polymer.2-59. 2005).7) 96. see Data Analysis section) for Survey year 03-04 is 3. mineral processing.8-55. Natural substances in the food are converted to acrylamide. (NTP-CERHR.

8-61. fetal death. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.2 (72.7) 61.. Rice. Maniere et al.0 (80. 2005.9-77. Acrylamide is clastogenic and can produce dominant lethal mutations.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) 53.4-59. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2005. 2005.7-86. 2006).7) 60.5) 71.4 (56.9 (57.2) 55. 2005)..2 (63.. EPA.1 (66.S. Schettgen et al. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).5-66.6-62. 2005.. probably through its epoxide metabolite. and neuronal DNA reactivity (Doerge et al.3) 59.8-48.6 (90. In addition. 2005) and sperm DNA adducts (Xie et al.0..1 (56..2) 65..0) 118 (103-126) 121 (112-134) 113 (94. glycidamide (NTP-CERHR. Hagmar et al.9 (58.7) 90. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.7) 74. male germinal cell injury. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.. NTP-CERHR.4 (61.8) 45.1) 56. 2005.. 2005.7 (61. Vesper 2005) and smoking (Bergmark..5-92.1) 62. interval) 59.4) 83.5 (56.5) 118 (110-129) 121 (108-140) 136 (124-149) 152 (135-170) 159 (129-204) 172 (157-194) 1841 1954 3044 Limit of detection (LOD. 2005.6 (66.4 (57. 2008). and other sites) (FAO/WHO.4 (90.. see Data Analysis section) for Survey year 03-04 is 4.7-64.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.5) 87.9) 87.1-60. After exposure ceases. EPA. U.int/ ipcs/food/jecfa/summaries/summary_report_64_final. thyroid. 2008). 2005. 2005).7-62. most non-smokers had levels less than about 100 pmol/gram hemoglobin. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. respectively) are markers of integrated acrylamide exposure over the preceding few months. 2002. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.9-64.5) 75th 85. Schettgen et al. U.1) 60.1 (70.3) 85. and cancer (mammary.2-91. altered gene expression in testicular tissues (Yang et al. 2002. IARC classifies acrylamide as probably carcinogenic to humans. Additional information is available from U.epa. scrotal. 2009).3-101) 95.. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.who.2-68.0) 94.9-78. adrenal.Acrylamide occupational exposures. Mucci et al.5 (42.9) 75....9-76. Glycidamide has been shown to react with DNA (Doerge et al.8 (51. 2003. 2005..7 (84. dominant lethality). population from the National Health and Nutrition Examination Survey..5 (83.3) 59.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59. 2006).pdf. 2006. 2005) have been demonstrated in animals. EPA at: http://www. 2001).8-49.7 (57.3-78.9-138) 143 (130-159) 96.9 (81.4 (51. although different analytic methods can affect results. Klaunig et al. Puppel et al. uterine. 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.1-70.5-94. reproductive effects (reduced litter size..1 (57.1-56.4-65. Puppel et al. presynaptic nerve terminal binding (LoPachin.4-103) 79. 1997.8) 60. 2005).2-90.0-62.6-64. 2005. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. 1997.0-93.9) 59.0 (70.7 (87.0 (75.9) 65.2) 87.8 (44. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.3) 59. 2004).4 (81. 2005). Axonal degeneration. Survey Geometric mean (95% conf. 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.S. 2006) have been demonstrated after acrylamide dosing.. 12 Fourth National Report on Human Exposure to Environmental Chemicals .9-62.S.1 (82.. 2004.5 (59.5-64.6-90.S.0 (52. 2005.2 (56. Vesper et al.1-62.3 (56.4) 46.4-98.

References Bergmark E. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.126(2):361-371.pdf. Costa LG. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. February. Yang JS. 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. Hagmar L. Kautiainen A. Paulsson B.561:21-37.. July. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.Toxicol Appl Pharmacol 1994. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Granath F. Toxicol 2005. 6013-6019. and Research Strategies. Tornqvist M. 2009 Jan 8. McDaniel LP. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Costa LG. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Adv Exp Med Biol 2005. Wu Y. Tornqvist M. Paulsen JE. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Bergmark E. Illinois. NIH Publication No. Tian G. Uncertainties. 2005. Mutat Res 2005. Andersen M. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Food and Drug Administration (FDA). Adv Exp Med Biol 2005. 1993. Available at URL: http://www.27(4):219-226.html#u1004. Nordander C. 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.. 2/3/09 Klaunig JE. Rosen I. Fennell TR. Haugen M.3:406-412. Hagmar et al. et al.who. Food Chem. Calleman CJ. Wirfalt E.10(1):78-84. Scand J Work Environ Health 2001. LoPachin RM. Toxicol Sci 2005.Acrylamide In occupational settings. Toxicol Sci. Beland FA.cfsan. Maniere I.pdf. Available at URL: http://cerhr. Zhang S. Acrylamide intake through diet and human cancer risk. morphological and molecular endpoints in animal models. J Agric Food Chem 2008. He F. Mechanisms of acrylamide induced rodent carcinogenesis. Italy. et al. Toxicol Appl Pharmacol 1993. DiNovi M and Howard D.561:49-62. Summer SCJ. Perez et al.120(1):45-54. Bridson WE. et al. Becher G. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Farmer PB. 2001. Fennell TR.int/ipcs/ food/jecfa/summaries/summary_report_64_final. [Epub ahead of print] Dybing E. Joint FAO/WHO Expert Committee on Food Additives. gov/~dms/acrydata. Mutat Res 2005. 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. Rome. Calleman CJ. Chem Res Toxicol 1997 Jan.43:365–410. Burgess J. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Snyder RW. Churchwell MI. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Survey data on acrylamide in food: individual food products. Osterman-Golkar S. Bergmark E. Mucci LA. smoking habits and gender. 8-17 February 2005. Duale N. Churchwell MI. Aprea P. Godard T.. 1994). Available at URL: http://www. Axmon A. 054472.85:447-459. 1999).. 2004. Human exposure and internal dose assessments of acrylamide in food. Metabolism and hemoglobin adduct formation of acrylamide in humans. National Toxicology Program. Bjellaas T. 2006. Laurentie M. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Kamendulis LM. 2/3/09 Perez HL. Bruze M. 64th Meeting: Summary and Conclusions (FAO/WHO). Bergmark E.. April 13-15. Doerge DR. He F. Twaddle NC. Chicago. Mutat Res 2005. In another study. Magnusson AL. Wilson KM.nih.niehs. Malmberg B. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Alexander J. Acrylamide neurotoxicity: neurological. 2001). Chem Res Toxicol 1990. Doerge DR. Calleman CJ. Guffroy M.fda. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. et al. 2/3/09 Hagmar L. smokers and nonsmokers.56. da Costa GG. CFSAN/Office of Plant and Dairy Foods.580(1-2):131-141. The Updated Exposure Assessment for Acrylamide. Cheong HK.gov/chemicals/ acrylamide/Acrylamide_Monograph. 2004 Acrylamide in Food Workshop: Update Scientific Issues. et al.580(1-2):157-165. Spicer R.

163(2):101-8. Myers GL. Drexler H. Smith A. Analysis of acrylamide. Ospina M. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.50(17):4998-5006. Karlsson P.gov/chemfact/s_acryla.Acrylamide glycidamide by gas chromatography-mass spectrometry. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.19(4):527-34. Licea-Perez H. Int J Hyg Environ Health 2003. Hemoglobin adducts of ethylene oxide. et al. et al. Jin Y. Meyers T. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Broding HC. Tjønneland A. Mutat Res 2005. Puppel N. Chemical Summary for Acrylamide. Int J Hyg Environ Health 2004. a carcinogen formed in heated foodstuffs. 2/3/09. Rice JM.274(1):59-68. Liu Y. Slimani N. Available at URL: http://www. Available at URL: http://www. Lee MH. J Agric Food Chem 2002. J Agric Food Chem 2008.580(1-2):3-20.580(1-2):71-80.207(6):531-9. Han CH. 14 Fourth National Report on Human Exposure to Environmental Chemicals .206(1):9-14. Schettgen T. Tjaden Z. Meyers T. Vesper HW.epa. Tareke E. Rydberg P. Environmental Protection Agency (U. Fu D. September. Agudo A.txt. Tornqvist M. Vesper HW. EPA).htm. Letzel S. Toxicological effects of acrylamide on rat testicular gene expression profile. Choi JH. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. U. Fueller F. Han DU.561:89-96. Schettgen T. Ding X. revised 1/3/06. Kutting B. Acrylamide. Mutat Res 2005 Feb 7. Angerer J. 1994. Sun H. Adv Exp Med Biol 2005. propylene oxide. U. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Office of Pollution Prevention and Toxics.S. 2/3/09 Vesper HW. Drexler H. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Yang HJ.epa. Reprod Toxicol 2005. Drexler H.gov/iris/subst/0286. Hallmans G. Ingham L. Weiss T. Ospina M.S. Schettgen T. Rapid Commun Mass Spectrom 2006. Anal Biochem 1999. Benetou V. Eriksson S. EPA). Rossbach B. Integrated Risk Information System (IRIS). Lee SH. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Toxicol Lett 2002. Angerer J. Xie Q. The carcinogenicity of acrylamide. Angerer J. Washington (DC). Liu K.S.20(6):959-64. Chae C. Toxicol Lett 2006.S. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Environmental Protection Agency (U. Gray JG. Marko D.56(15):6046-53.134(1-3):65-70.

77 (1.310-1.540 (. population from the National Health and Nutrition Examination Survey.00) .160) .080 (.197) .180) .960-1.110 (.95) 1.50 (1.02) 1.950-1.62) 2.92) 1174 1415 1252 1773 1902 1783 3052 3502 3285 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 20 years and older Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 .65 (1. DHHS.054 (.050 (.630 (.360) .520 (.42 (1.950 (.17 (.580-1.990) .187) .050 (<LOD-.40) .080-.188) .23-2.63-2.110 (.030-.710 (.130 (.21-1.071) .120 (.150) .15) 2.059-.131 (.094) .060) .110 (.140 (.126) .140-.66 (1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U. 2004).770) .060 (<LOD-.860 (.310) .09-3.49) 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.93) .20) .120-. which may vary for some chemicals by year and by individual sample.84-3.140 (.35 (2.55-2.230) .120 (.030-.077) .080 (.106-.108) * .160) .45) 1.430-1.071 (.505 (.110-.S.480-1.062 (.19) .060-.23 (1.14) .44) 2.070 (<LOD-.96) 2.040-.015 ng/mL.997-3.060-.20-2.047-.32) 1.S.087) < LOD < LOD .12 (2.770-1.87-3.180) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28-1.040 (.080-.54 (1.620-1.308 (.20) 1.920 (.060 (.48-2.38-2.180) .540-. DHHS.23 (2.740-1.05.193) .70) 2.94) 1.23 (.39 (1.050 (<LOD-. ear problems.110-.090-.075 (.44 (2.148-.580) .057-.96 (1.60-2.145) .060 (.506 (.79) 3. ** In the 2001-2002 survey period.910-1. and 03-04 are 0.300) .09-3.30) * . < LOD means less than the limit of detection.220-.85 (1.740-1.16) .180 (.130) .040-. 1998). 2006). and exacerbated asthma (U.04 (1.20 (1.110 (.05 ng/mL. and various other disorders (U.900-1.063) .47-3.153-.Cotinine Cotinine CAS No.175 (.302) . stroke.350-.070) 75th .310) 90th 1.090-.080) < LOD .470-.26-1.57) 2.260-1.087-.030 (.77 (2.39) 3.110) .30) 2.5% nicotine by weight (Kozlowski et al.19-2. Children exposed to ETS are at increased risk for sudden infant death syndrome.18-3.580 (.220) . producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.820) .040 (.480-.625) .144 (.077) .20 (. see Data Analysis section) for Survey years 99-00.533-.55 (1.83-2.28) .34 (1.163 (.99) 2.02 (.068) .49) 1.48-3. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.120 (.81-2.050) .047-.220) .53-4.198) * .09-2.00) 1.89) 1.14-1.99) 2.370-. Survey Geometric mean (95% conf.44) 2.770) . acute respiratory illness.190-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.060-.150) .234) .400-.216 (.800 (.154-.726) .086 (.660) .210 (.21 (.850 (.01 (1.059-.280 (.68) .33-2.060 (<LOD-.066) .05) 1.068) .137-.75) 1.17) .213) .22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .090-.080-.990 (.15 (2.70-2.570-1.68 (1.115-.163) .050) .180) .052 (<LOD-.88 (.137 (.180) .040 (.77 (1.54) 1.17 (1.02) 1.120 (.670) .96-4.42-4.230 (.110 (.44 (1.43 (1.53 (1.050 (<LOD-.100-. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.160 (.190-.142-.052 (<LOD-.50-4.089) Age group 3-11 years 99-00 01-02** 03-04 .88 (1.066 (. maternal exposure during pregnancy can result in lower birth weight.14) . acute respiratory infections.350-.49) 1.620 (.21-1.570 (. and 17% had an LOD of 0.201) .690 (.160-.124 (.020-.30) 2.200) 1.140-.164 (.50) 3..840) 3.058 (.110-.190-. 83% of measurements had an LOD of 0.S.070-.160 (.12 (1.62 (2.310-1. respectively.066-.78) 2.043-.930 (.66) 1.63 (2.410) . and 0.111-. emphysema.260) 1.164 (.22) 2.015.12) 1.11) .450-. Fourth National Report on Human Exposure to Environmental Chemicals 15 .180 (.500 (.350 (.104-.160 (.076-.312) .080) < LOD < LOD .50-1.32-2.630 (.120-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .12-4.32-2. Cigarettes contain about 1.19) 1.510 (.730 (. 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.621-1.080-.050-.084) .68) 2.54 (1.630 (.053 (<LOD-.428-.030-.120 (. cardiovascular disease.073) < LOD .050 (<LOD-. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.240 (.600-1.070) .061) < LOD .070) .92 (1.320) .01) 3.120) .050-. 2004).76 (1.088-.66-3.087 (.110) .790) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.139) * .167 (.

1999). In homes with one or more smokers. 1975. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. 2004). salivation. 2005).nih. Children are primarily exposed to ETS by parents and caregivers who smoke. 2006). is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. html.. Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. 2005.3 to 30 µg/m3. 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. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans. and hair. Acute tobacco or nicotine intoxication can produce dizziness. and peppers. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005. with higher levels measured in restaurants and bars. craving. nicotine has a half-life in blood plasma of several hours (Benowitz. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. 2005). Wilson et al. The IARC and the NTP consider tobacco smoke to be a human carcinogen. 1991). 1999. 1996).nida. nasal sprays. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. Measuring cotinine is preferred over measuring nicotine because cotinine persists longer in the body with a plasma half-life of about 16 hours (Benowitz and Jacob..Cotinine 1994. 1996). Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. with heavy exposure to ETS producing levels in the 1–10 ng/mL range. 1998). contains nicotine in larger amounts than other nicotine-containing plants.. Once absorbed.. 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. More information about the effects of smoking and nicotine can be found at: http://www. Over the previous decade...gov/researchreports/nicotine/nicotine. Hukkanen et al. Iwase et al. which include potatoes. 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. The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. and death.. chewing tobacco.. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al. Cotinine can be measured in serum. Symptoms of 16 nicotine withdrawal include irritability. the primary metabolite of nicotine.. 2004).. Serum cotinine has been measured in many studies of nonsmoking populations. Hukkanen et al. nausea. 2005. saliva. (CDC. variable changes in blood pressure and heart rate. 1998). urine. Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. 1999. Perez-Stable et al. The tobacco plant. or chewing gum. Soliman et al. mean air concentrations typically range from 2 to 14 µg/m3 (NTP. For an adult. During each previous NHANES survey.. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration.. 1994). 2005).. a process involved in the development of addiction. Pirkle et al. or skin patches that contain nicotine. 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. diarrhea. diaphoresis. 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. cognitive and sleep disturbances. Nicotiana tabacum. and increased appetite. non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al. Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. vomiting.. eggplants. Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al.. tomatoes. 2006. 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. 2006). However. Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al. seizures. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. NCI. Cotinine.

Giovino GA.S. DHHS).56:483-493. Hukkanen J. [online]. population to secondhand smoke: 1988-2002.cdc. Benowitz NL. Racial/ethnic differences in serum cotinine levels among adult U.nih. et al. 11th ed.57(1):79115.fr/ENG/Monographs/ allmonos90. Richter PA. Jacob III P. Pirkle JL. Third National Report on Human Exposure to Environmental Chemicals. 4/13/09 U.S.gov/eid/rmca/critdocs/ criteriadoc/33. Schwartz SS. Pechacek TF. Sosnoff CS. Pickett MA. Sweeney CT. Jarvis MJ. International Agency for Research on Cancer. References Armitage AK. 1999-2002.php. Caraballo R. Coordinating Center for Health Promotion. Benowitz NL. Jacob P III.275:1233-1240. Atlanta (GA): 2005. In Report on Carcinogens. National Institute for Occupational Safety and Hygiene (NIOSH).niosh. Caudill SP.cancer. U. Department of Heath and Human Services. Flegal KM. Brody DJ.gov/ntp/roc/eleventh/profiles/ s176toba. Lewis PJ. Coordinating Center for Health Promotion. 4/13/09 Iwase A. Benowitz NL. Curtin LR. Mowery PD. 4/13/09 Centers for Disease Control and Prevention (CDC). Metabolism and disposition kinetics of nicotine. Available at URL: http://www.94(2):314-320. Tobacco related exposures. Herrera B. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Exposure of the U.surgeongeneral. Turner DM. JAMA 1998.pdf. Nicotine metabolism and intake in black and white smokers. 2004. Vogler GP.S.php. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.63:139-43. Available at URL: http://monographs.iarc. Bernert JT. Houseman TH. National Center for Chronic Disease Prevention and Health Promotion. J Pharmacol Exp Ther 1999.4:313-316. Soliman S. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. U. National Toxicology Program (NTP). Pirkle JL. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .gov/tcrb/monographs/10/. Mehta NY. cigarette smokers: the Third National Health and Nutrition Examination Survey. Trends in the exposure of nonsmokers in the U. Brody DJ.S Department of Health and Human Services (U. and the United States. Department of Heath and Human Services. DHHS). Schober SE. Kira S. Tobacco Smoke. Jacob P III. JAMA 1998. Available at URL: http://ntp. IARC Monogr Eval Carcinog Risks Hum. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. available at URL: http://mtn. Modin G. the United Kingdom. Herrera B.114(6):853-858. Pharmacol Rev 2005.7:369-375. IARC Monogr Eval Carcinog Risks Hum. Strauss WJ. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. 1991. George CF. Benowitz NL. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Centers for Disease Control. Available at URL: http://monographs. 4/13/09 National Cancer Institute (NCI).291(3):1196-1203. Respiratory nicotine absorption in non-smoking females during passive smoking. Tobacco Smoke and Involuntary Smoking.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Vol 83. Kozlowski LT. Summary of Data Reported and Evaluation [online] 2004. Cotinine as a biomarker of environmental tobacco smoke exposure. June.S.S. Aiba M. Int Arch Occup Environ Health 1991.S. Perez-Stable EJ. Bernert JT. Benowitz NL. Office on Smoking and Health [online] 2006. Ethnic differences in N-glucuronidation of nicotine and cotinine. 4/13/09 International Agency for Research on Cancer.pdf.gov/library/ secondhandsmoke/. Maurer KR. 1988-1991. Giovino G. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. et al. Etzel RA. 1988-1991. Vol 38. Pollack HA. Smoking and Tobacco Control Monograph 10 [online]. Available at URL: http:// cancercontrol. Warner K.S.niehs. 4/13/09 Perez-Stable EJ. Environ Health Perspect 2006. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. U. Tob Control 1998. Am J Public Health 2004. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Jacob P. 1999. Fong I. BMJ 1975. Centers for Disease Control and Prevention. Summary of Data Reported and Evaluation [online] 1986. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Pechacek TF. Clin Pharmacol Ther 1994. Tob Control 2006.280:135-140. iarc. Dollery CT. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.15:302-307. Epidemiol Rev 1996. Absorption and metabolism of nicotine from cigarettes. Centers for Disease Control and Prevention.280:152-156.fr/ENG/Monographs/allmonos90. JAMA 1996.18:188-204.S Department of Health and Human Services (U.

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

DEET can be applied to clothing and the skin to repel biting insects.110 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.170 (.S. 2002).240) < LOD .140) < LOD .190) < LOD .N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.1. (U.100 (<LOD-.EPA.270) 688 678 518 700 598 956 Limit of detection (LOD. 2003). Additional information is available from U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.140-.N.130-.130-. 1995. including seizures and encephalopathy.110 (.N-Diethyl-meta-toluamide (DEET) N.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.520) < LOD .110 (<LOD-.170 (. Survey Geometric mean (95% conf.120-.100-.130 (.epa. and they range in concentration from 4% to 100%.130-. 2003). 1998).150) < LOD .S.EPA at: http://www.560) < LOD .180) < LOD .250) < LOD . 2002).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 . Neurological effects in humans.100-. About 3-8% of dermally applied DEET is absorbed.130-.220 (. Sudakin and Trevathan. DEET is not a developmental or reproductive toxicant in animals (U. 1998). population from the National Health and Nutrition Examination Survey. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Its use is recommended for prevention of several vector-borne diseases.140) < LOD . have been reported as result of self-poisoning by ingestion or excessive dermal application.EPA.110 (.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. Urinary N.. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. DEET is not registered for use on agricultural commodities. which may vary for some chemicals by year and by individual sample.100-. DEET is also used in combination with dermal sun screens (U.110-. After absorption. < LOD means less than the limit of detection. DEET is not genotoxic. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. (Kolpin et al. DEET has low acute toxicity.100-.110-. and it has not been rated by IARC or NTP with respect to human carcinogenicity. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.180 (. One survey detected DEET in 74% of sampled streams in the U.180 (.210 (. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.130 (..180 (.449 and 0.160) < LOD .110 (.130 (.S.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th ..130) < LOD . 2005).100-. EPA.S.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .gov/pesticides/.130) < LOD .110 (<LOD-. There are over 225 insect repellents brands containing DEET.120-.100-.N-Diethyl-meta-toluamide (DEET) CAS No.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 . 134-62-3 General Information N. Fourth National Report on Human Exposure to Environmental Chemicals 19 .140 (.140) < LOD .

Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.440) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.140-.330 (.170-.350) < LOD .330 (.240-.270 (<LOD-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .350) < LOD ..290-.250 (.150-.410-.150) < LOD .480 (. 2007).550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.350-.N.190 (<LOD-.230-.190 (.270 (.270) < LOD .230) < LOD .280 (.320 (.200 (. Urinary DEET levels as high as 5.190-.130 (<LOD-.240) < LOD .500 (.640 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . In this survey period.410 (.500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect. 1992).630) < LOD .370-.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure. 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.S.93) < LOD .490) < LOD .390-.250) < LOD . 2005).370) < LOD .250-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.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 . 20 Fourth National Report on Human Exposure to Environmental Chemicals .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.190 (.320) < LOD .410 (.230-.280-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .S.300 (. representative subsamples from NHANES 2001-2002. population from the National Health and Nutrition Examination Survey. Urinary N.270-.

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

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

and other organic wastewater contaminants in U. bisphenol A glucuronide. Research Triangle Park.jrc. Environ Health Perspect 2005. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.68(1):121-146. Gender differences in the levels of bisphenol A metabolites in urine. Italy. Chem Res Toxicol 2001.nih.. Koulova AI.14(2):149-157.59(9):625-628. Ye X. Matthews JB.S. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Regul Toxicol Pharmacol 2002. Thomas BF.europa. National Toxicology Program.145:592-603. Shin HC. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Kiguchi M. In vitro and in vivo interactions of bisphenol A and its metabolite. niehs. National Institute of Environmental Health Sciences. Proc Natl Acad Sci USA 2005. Ema M. Bisphenol A. Serizawa S. Marr MC. Belgium. Han SS.113(4):391-395. Ikka T. Meyer MT. with estrogen receptors alpha and beta.nih. Zaugg SD.gov/chemicals/bisphenol/BPAFinalEPVF112607. Needham LL. Chung MK. September. An evaluation of the possible carcinogenicity of bisphenol A to humans. Keimowitz AR.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Rhomberg et al. 2002. Ispra.pdf . Imai H. Watanabe C. Kim CS. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Lynch BS. Kroes R.S. Barr DB. Yoshinaga J.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Kawamura N. Twomey K. Reidy JA. Human Health.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Ekong J. Calafat AM.10:875-921. Joint Research Centre Institute of Health and Consumer Protection. 5: 505-523. Szigeti-Buck. Furlong ET.149:988-994. streams. Calafat AM. Yang M.312(2):441-448. NC. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.gov/chemicals/bisphenol/bisphenol. Kim JC. Hlywka JJ. Fujii S. Sottas CM. Arakawa C. N. Exposure of the U. Klinefelter GR. Gray GM. Brussels. Wong LY. MacLusky. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. T. Endocrinology 2008. National Institutes of Health. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Caudill SP. McConnell EE. Tyl RW. 2/4/09 Fujimaki K. Doull J. 2003. European Commission. K. DirectorateGeneral Health and Consumer Protection. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. 2007. et al. Endocrinology 2004.137(3):353-362. Leranth. 4. Cunha G. Environ Health Perspect 2008. Furukawa M. et al. Toxicol Sci 2002. Life Sci 2001.59(4):403-408. Richter CA.Environmental Phenols References Akingbemi BT. Timms BG. Park S.pdf. Kolpin DW. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Koh WS. Calafat AM.116(1):39-44. Watanabe S. Rat two-generation reproductive toxicity study of bisphenol A. Hum Ecol Risk Assess 2004.S. and Hardy MP. Kuklenyik Z. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Reprod Toxicol 2001.niehs. Bradley S. Nippon Eiseigaku Zasshi 2004. Han SY.J. Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Available at URL: http://ntp. Hara K. Ecotoxicity and the Environment (CSTEE). and Hajszan. Barr JR. Munro IC. Harazono A. Biochem Biophys Res Commun 2003. Cohen JT. August 2001. Rubin C. Howdeshell KL. C. Joskow R.102(19):7014-7019. et al. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Occup Environ Med 2002. J Am Dent Assoc 2006.eu/ health/ph_risk/committees/sct/documents/out156_en. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.69(22):2611-2625. Brine DR. hormones. May 22.Scientific Committee on Toxicity.780(2):365-370.. Thurman EM. Available at URL: http://ec. Pyo MY. Reidy JA. Needham LL.35(2 Pt 1):238-254. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Hanaoka T. 2/4/09 European Commission. Available at URL: http://cerhr. U.pdf .36(6):1202-1211. Environ Sci Technol 2002.pdf. vom Saal FS. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Department of Health and Human Services. 2008.nih. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). niehs.. Haighton LA. Cha SW.pdf. Barber LB. Tsugane S. 1999-2000: a national reconnaissance. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Myers CB. Available at URL: http://ecb. 2/4/09 Ouchi K. Available at URL: http://cerhr. Hughes C. Kim YH. Needham LL. November 26. Barton L. Pharmaceuticals. Zacharewski TR.

Lordo RA.15:12811287. Hughes C.40(7):905-12.103(1):9-20. Endocrinology 2006. bisphenol-A. Dekant W. Jang JY. Filser JG. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Food Chem Toxicol 2002. Lee SM. Chang SS. Chuang JC. Arch Environ Contam Toxicol 2003. Environ Health Perspect 2005. Biological monitoring of bisphenol a in a Korean population. vom Saal FS. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Chem Res Toxicol 2002.147(6 Suppl):S56-69. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Morgan MK. Yang M.113(8):926-33. Environ Res 2007. Wilson NK. Vom Saal FS. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Colnot T. Nagel SC. Csanady GA. Large effects from small exposures. Witorsch RJ. Welshons WV. et al. Sheldon LS. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure.44(4):546-51. Kawamoto T.Environmental Phenols Volkel W. and nonylphenol at home and daycare. Kim SY. III. An observational study of the potential exposures of preschool children to pentachlorophenol.

70 (1. population from the National Health and Nutrition Examination Survey.20-2.40) * 03-04 03-04 03-04 . over 500. and impaired spermatogenesis (e.477) . 1995.30 (.10-2.80) 2.00 (. and to alkylphenoxycarboxylates. which may vary for some chemicals by year and by individual sample. 140-66-9 General Information 4-tert-Octyphenol.400 (. In rats. fish) and drinking water..80 (1.10 (1. Laws et al. 2000.70 (1. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. and the polyethoxy chain may consist of up to 50 ethoxy units.20-2. altered estrus cycles and reproductive outcomes. Blake and Boockfor.299-.900 (.20-2.10) 1. 34 Fourth National Report on Human Exposure to Environmental Chemicals . Less frequently.500 (.20) 2.497) * . industrial cleaners.900 (.900 (.30-2. is used to manufacture alkylphenol ethoxylates.40) 2.500-1. 4-octylphenol monoethoxylate was detected in 43.268-.60-3. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers..50) 1.60-3. 2003.40 (1. 1997.60-3.5% of 139 U. In 1999-2000.60-3. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.00 (.50) . did not bioaccumulate.60) .400) 1.300 (<LOD-.Environmental Phenols 4-tert-Octylphenol CAS No.500) . 2002). 2000. and was quickly eliminated from the blood (Certa et al.369 (.50) . through sewage. Bian et al. 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. and some of their degradation products are toxic to aquatic life.200-.60) 613 652 1092 Limit of detection (LOD. pesticides.30 (1..70 (1.40) 1.50-3.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Ying et al.389 (. 1996). Disposition in humans has not been studied sufficiently. Several alkylphenols.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 . 2006.600-1. which are anionic surfactants used in detergents.80 (1.60-3.10 (.00) 1229 1288 03-04 03-04 03-04 * .20) 314 715 1488 03-04 03-04 * * .g.500) .30 (1.g. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.600-1.300-.600) 1.30) 90th 1. < LOD means less than the limit of detection.40) 2.30) 2.500-1.S.20) 1.274-. and emulsifiers.. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.20-2.80 (1.60-3.600) . to shorter chain alkylphenol ethoxylates.2.. In the 1990s.600-1.20-2.900 (.600) . 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (<LOD-..S.300 (<LOD-.90) 2.00 (1.30 (1.10) 2. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.800-1. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.300 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.50 (1. including 4-tert-octylphenol.50) 1.30) 1.600-1.40) 1.. have demonstrated estrogenic effects particularly when injected at high doses in animals.600) . Katsuda et al. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. leading to inhalation as another potential exposure route (Rudel et al.400 (. Indoor and to a lesser extent. 2002). Saito et al.200-. see Data Analysis section) for Survey year 03-04 is 0.300-.90) 2. and through manufacturing waste streams (Warhurst.500) 75th .700-1. impaired steroidogenesis. and from contact with some personal care products and detergents. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).600-1.. Survey Geometric mean (95% conf.507) * < LOD .400 (. The alkylphenols can bioaccumulate in some fish.50) 1...20 (1. altered neonatal sexual development.10 (.60) 1.20-2.50-2. streams in 30 states (Kolpin et al.900 (. textiles.70 (1.357 (.30 (1.3. orally administered 4-tert-octylphenol was well absorbed. and some personal care products. Urinary 4-tert-Octylphenol (4-[1. During the 1980s and 1990s. an alkylphenol. testicular atrophy. The alkylphenol ethoxylates enter the environment through human use of products containing them.300 (<LOD-.600-1.1. the various alkylphenols have also been used as emulsifiers and modifiers in paints.500) .000 tons of alkylphenol ethoxylates were produced annually worldwide.

40-4. 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.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.610) .269 (.40 (1.280-.08) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.380 (<LOD-.60 (1..270-.530) . 2001. Kawaguchi et al.54) * 03-04 03-04 03-04 .740 (.64 (.03-6.59 (1. or their corresponding ethoxylates with respect to human carcinogenicity. 1999).207-.00) 1.450) 1. 2001).50 (2.78) 1228 1286 03-04 03-04 03-04 * ..85 (1.740 (. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.29) 2.400) .00) 2.31 (1.1.Environmental Phenols Myllymaki et al.620-1.850 (.S.337-.14) 314 713 1487 03-04 03-04 * * . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.17 (.62) .53-3.25) 90th 1.43-3.96-4.570) . Tyl et al.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 . IARC and NTP have not rated octylphenol. at lower or environmentally relevant doses (Blake et al..25) 2. 2000. Fourth National Report on Human Exposure to Environmental Chemicals 35 .71) 2.00) 2.65-3. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.18-4..76 (2. population from the National Health and Nutrition Examination Survey.11) 1. Calafat et al. 2005.68) 2. In a small number of adult Japanese volunteers.630-1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.540-1.62 (1.06 (2.410 (.320 (<LOD-.. representative subsample of NHANES 2003-2004.450) . 2004.59) 1. Nagao et al.73) 2.10-2..770 (.62 (1.11) 2.276 (.270 (.349) * < LOD .03 (1.199-.160-.435 (.43) 1.170-.620) . nonylphenol.500-1.05-2.81 (1.22) .860 (.S. It is unclear if estrogenic or other effects occur in animals through oral dosing.02-4.68-2.460 (. 4-tert-Octylphenol is not considered directly genotoxic.00 (.15) 1.33 (2.00 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25-2.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270 (.550-1.11-2.640-1.3. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.260 (<LOD-.20 (1.67-2.78 (1. 2004).730-1.41) .78) 3.470) 75th .384) * .910 (.43) 1.370 (<LOD-.420) . Urinary 4-tert-Octylphenol (4-[1.33) 3. Survey Geometric mean (95% conf.03 (1.470-1. 2003.890-2. Yoshida et al.36-3.31-2.300 (<LOD-.560) .470-1. Sweeney et al.

Ito R. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Wiegand HJ. Nair-Menon JU. Reidy JA. Regul Toxicol Pharmacol 1999. Toxicol Lett 2001. Boockfor FR. Williams B. Brooks AN. Two-generation reproduction study with para-tert-octylphenol in rats. 2003. Taya K. Barber LB. alkylphenols. Katsuda S. hormones. Nagao T. Katsuda S. Millette CF. Yoshida M. Tyl RW. Kawaguchi M. Pharmaceuticals. Taya K.15(6):683-692. Korn LR. testis size.folliclestimulating hormone. Takai N.uk/resource/reports/ethoxylates_alkylphenols. streams. Raychoudhury SS.S.57(2):255-266. pesticides.Environmental Phenols References Bian Q. polybrominated diphenyl ethers. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. et al. McCoy GL. Watanabe G. Sakui N. Myllymaki SA. Exposure of the U. 1999-2000: a national reconnaissance.28(3):215-226. Toxicol Appl Pharmacol 2000. Brody JG. and other endocrine-disrupting compounds in indoor air and dust. Kawaguchi M. Reprod Toxicol 2004.54(1):154-167. Seely JC.121(1):21-33.116(1):39-44. Environ Int 2002. and other organic wastewater contaminants in U. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Izumi S. prolactin. Warhurst AM. Onuki A. Arch Toxicol 1996.S. and sertoli cell number. Indoor air pollution by alkylphenols in Tokyo.44(8):1355-1361. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Blake CA. Song L. Maekawa A. Calafat AM. Okada F. Toxicol Appl Pharmacol 2005. Anal Chim Acta 486:41-50. et al.30(2 Pt 1):81-95. Meyer MT. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Boockfor FR. Bolt HM. Laws SC.165(3):217-226. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression.18(1):43-51. Furlong ET. Zaugg SD. Endocrinology 2000. Carey SA. Needham LL. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Sweeney T. Toppari J. Horie M. Available at URL: http:// www. Reprod Toxicol 2001. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Makino T. Yoshida M. Saito I. bisphenol A and methoxychlor in rats. Inoue K. Estrogenic activity of octylphenol. 1995.co.pdf. nonylphenol. Brine DR. Spengler JD. Certa H. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Thurman EM. Yoshimura Y. Watanabe G. Blake CA.foe. Paranko J. Haavisto TE. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Yoshimura S. 2/4/09 Ying GG. Toxicol Sci 2000. Environ Sci Technol 2002. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Maekawa A. Usumi K. Saito Y. Roche JF. Seto H. et al. Takenaka A. Marr MC. Rudel RA. Environ Health Perspect 2008. Camann DE. et al. Fail PA. Kookana R. Nakagomi M. Food Chem Toxicol 2006.37(20):4543-53. and testosterone. Indoor Air 2004.71(1-2):112-122. Karjalainen M. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Wong LY. Phthalates. Ye X. Kolpin DW. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Myers CB.141(7):2667-2673. Qian J. Cooper RL. Xu L. Bodman GJ. Chen J.799(1):119-125. Inoue K. J Chromatogr B Analyt Technol Biomed Life Sci 2004. 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.36(6):1202-1211. Environ Sci Technol 2003. Nicol L. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Ferrell JM. Biol Reprod 1997. Ono H.207(1):59-68. Fedtke N. Muller AM. Wang X.14(5):325-332.

and has also been impregnated into some kitchen utensils. mouthwashes. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. 2007.. In animal and human studies. 2008 has shown higher levels during the third decade of life and among people with the highest household income. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. Triclosan is not considered teratogenic at maternally toxic doses. but not by race/ethnicity and sex. 2005. In the body it is conjugated to glucuronides and sulfates (Bodey et al. 2004).. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. In 1999-2000. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. 2008). Mezcua et al. the median urinary triclosan level of 7. 2007). 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. 2007). deodorants. it has low acute toxicity..S. In animal studies. Triclosan enters the aquatic environment mainly through residential wastewaters.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. In a U. 1976. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. toothpastes. Moss et al. Triclosan can be absorbed across skin into the blood stream. toys. Triclosan has a low bioaccumulation potential in fish. Triclosan has been added to soaps. and medical devices.. 2002).Environmental Phenols Triclosan CAS No. 1996. acne medications. a process that can result in the formation of small amounts of 2. General population exposure results from dermal and oral use of products containing triclosan. 2000).S.6% of 139 U. triclosan was found in 57... 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. 1988. Triclosan formulations may rarely cause skin irritation.. Veldhoen et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Calafat et al.. (Sandborgh-Englund et al. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. 2000. 1969). 2007.8-dichlorodibenzo-p-dioxin (Aranami et al. streams sampled in 30 states (Kolpin et al.. It acts by inhibiting bacterial fatty acid synthesis.S. Calafat et al. 2006).. young girls. It can be photochemically and biologically degraded.2 µg/L was comparable to the median level (8.. and wound disinfection solutions. In a study of 90 U. Matsumura et al.. Biomonitoring Information Urinary triclosan levels reflect recent exposure. Fourth National Report on Human Exposure to Environmental Chemicals 37 ... IARC and NTP do not have ratings with respect to human carcinogenicity.. Lyman and Furia. 1987).

50) 10.7) 123 (36.7) 292 (151-432) 132 (78.1) 50.20-10.0 (34.9 (11.8-85.60 (6.8) 116 (39.38-18.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.Environmental Phenols Urinary Triclosan (2.6) 39.4) 317 (231-433) 144 (96.45 (5.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.8-112) 30.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2 (37.7) 10.4 (12.92-12.4 (32.1) 7.7 (14.1) 9.43-13.8-60.22-10.7 (9.2 (25.20 (7.6 (30. interval) 12.1 (45.2-46.3) 6.0 (8.72-13.11-11.70-16.0-213) 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 .5) 13.18 (5.3-67.9 (50.8-63.7 (11.0 (26.3) 10.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.6-65.4) 73.94 (7.45-13.0) 9.0-73.60 (8.5) 20.5) 66.6 (12.10-9.54 (8.6-14.1 (15.29-12.3-15.2) 12.5) 11. Survey Geometric mean (95% conf.1) 9.93 (7.48-10.5-14.6-15.1) 11.50-10.8) 7.2 (27.45-10.20-11.1) 13.82 (8.6) 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 9.6 (9.6) 10.4-19.86-12.00-8.3 (9.40-11.8 (21.7 (39.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2) 9.4 (11.4-18.6) 31.1) 9.32-14.0-19.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.3 (11.0-15.2) 13.0) 49.20 (7.4) 25.0 (11.90-10.3-35.3 (26.3-31.6-111) 33.S.S.2-58.4.7 (28.9-236) 193 (90.55 (4.8-127) 37.2 (10.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.4.4) 7.0) 65.00 (4.48 (8. population from the National Health and Nutrition Examination Survey.6) 90th 212 (172-241) 03-04 03-04 03-04 9.6-14. see Data Analysis section) for Survey year 03-04 is 2.1) 14.5-86.0 (36.4) 357 (225-456) 203 (87.4) 90th 249 (188-304) 03-04 03-04 03-04 8. population from the National Health and Nutrition Examination Survey.6-37.1) 9.2-58.9-61.6-20.8) 14.2 (11.1-39.9) 75th 47.30-14. interval) 13.4 (38.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.2-14. Urinary Triclosan (2.9) 7.9 (8.2 (13.6) 12.16 (6.9 (33.80 (5.3 (8.1 (8.4) 51.9) 8.89-11.74 (5.6 (10.0-15.3) 47.9) 32.20-13.4) 75th 43.10) 84.40-17.3.8) 9. Survey Geometric mean (95% conf.5 (11.21 (6.

Reidy JA.28(9):1748-1751. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice.4. Hernando MD. Am J Infect Control 1996. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Pinney SM. Matsumura N.24(3):209-218. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Katsura E. Needham LL. Watanabe N. Aranami K. phthalates.4’-trichloro-2’hydroxydiphenyl ether).69(20):1861-1873. Percutaneous penetration and dermal metabolism of triclosan (2. Barber LB. Aguera A. Ogawa H. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Odham G. Foran CM.50(1-5):153-156. hormones. et al. Wong LY. Bodey GP. Fernandez-Alba AR. Osachoff H.. J Toxicol Environ Health A 2006. Thurman EM. Adolfsson-Erici M. Toxicology of 2.66:1052-1056. Br J Clin Pharmacol 1987. Hirano M.38(2):64-71. Anal Chim Acta 1004. Williams FM. Ishibashi H. Hong HC. 1999-2000: a national reconnaissance. Ekstrand J. Wolff MS. Lyman FL.45 Suppl 2:S137-S147. Gomez MJ. Aquat Toxicol 2006. and phenols in girls. Erratum in: Aquat Toxicol 2007. Kaneshima H. Benson WH. Evidence of 2. Meyer MT. Skirrow RC. Bennett ER.83(1):84. Williams PE. Environ Health Perspect 2008. Mezcua M. Chemosphere 2007.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Clapson DJ. Arch Environ Contam Toxicol 1988. Sandborgh-Englund G. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Moss T. Chelimo C. Calafat AM. Triclosan: applications and safety. Teitelbaum SL.17(5):637-644.38(4):361370. Kolpin DW. Kanetoshi A.Environmental Phenols References Aiello AE. streams. Wigmore H. Pilot study of urinary biomarkers of phytoestrogens. et al.116(3):303-307. Food Chem Toxicol 2000. Furia T. Nagao Y. and other organic wastewater contaminants in U. Furlong ET. Biol Pharm Bull 2005. Bhargava HN. Mar Environ Res 2000. Photolytic degradation of triclosan in freshwater and seawater. Urinary concentrations of triclosan in the U. Shiratsuchi H. Gilbert RJ. Levy SB. Ferrer I. Larson EL. Environ Health Perspect 2007.7/2.36(6):1202-1211. Ebersole R. et al. Windham G. Veldhoen N. Pharmaceuticals. 4. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Readman JW.23(5):579-583. Zaugg SD. Environ Sci Technol 2002.S. Gunderson MP.67(4):532-537. Ye X. Howes D.524:241-247. et al. Pharmacokinetics of triclosan following oral ingestion in humans. Leonard PA. Okui T. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Britton JA.80(3):217-227. 4’-trichloro-2’-hydroxydiphenyl ether. J Invest Dermatol 1976. population: 2003-2004.115:116-121. The oral retention and antiplaque efficacy of triclosan in human volunteers. IMS Ind Med Surg 1969.S.

390 (.10 (<LOD-1. air. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.00) 2.18 (<LOD-1.350 (. Since 1984. In the environment.350) < LOD .350-.76) .30 (.58-2.58-2.S. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350 (.30 (1.350-2.770 (.350 (.08-3.350) < LOD . PCP is absorbed rapidly and well by all exposure routes.350) < LOD . 1986).40 (.350-.78) 1.350-. ingestion of contaminated food or water.350-.350-2.350 (.350-1.590-1.350) < LOD .350-1.65 (.350-2. PCP use in the U. 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.350-.70) 2. algaecide and insecticide.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) 90th . and metabolic acidosis were observed in CAS No.65 (.650) 1. mollusicide.23 (. Survey Geometric mean (95% conf.350 (.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.S. PCP is distributed to most tissues and is not extensively metabolized.350-2.890 (.350) < LOD .990 (<LOD-2. To-Figueras et al.350 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. the elimination half-life may be a week or more (Uhl et al.350) < LOD . and it is used primarily as a preservative for wood to be used outdoors (e.350 (.350 (.500-2.50) 1.350 (. PCP cannot be used on wood in residential or agricultural buildings.390 (.350-.650 (.76) 1.990-2.10) 1.890-1.g.350-2.51) 1. 1979).73 (1.350) < LOD .5. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown..350) < LOD .54-2.01 (<LOD-1.850-2.350) < LOD .94 (1.10 (. bactericide.32 (. along with small amounts of tetrachlorohydroquinone and conjugates. After a single dose.00) 1.37 (.350) . population from the National Health and Nutrition Examination Survey. 2002. utility poles and fence posts). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.00 (.530) 1.350) < LOD .350 (. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.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 . plants.350-. so it is relatively non-persistent..350) < LOD .67) 1.350-. Effects including hyperthermia.350 (. After absorption.350) < LOD . 1997). and animals.350 (.48-2.. are eliminated in the urine.350-.45-2..350-.350 (.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . PCP has been detected in soils.510-3.350-.960) 1.33) . Acute.90) 2.30) .83 (2.10) 1.70) .98 (1.350 (.480-2. hypertension.350-.350-.60) 1.350) < LOD .37) . 1976.47-3. which may vary for some chemicals by year and by individual sample.350-.04) 1.350) < LOD . PCP is eliminated over a few days (Braun et al.350 (.47-5.350-1.42) 696 680 521 696 603 951 Limit of detection (LOD.350-.94 (1.350-. 40 Fourth National Report on Human Exposure to Environmental Chemicals .680-1.980 (.75) 2.00) 1.64) 1.350 (.90 (1. General population exposure to PCP may occur by inhalation of contaminated air.33-2.350-.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Kohli et al.510-5.660 (.630 (. with repeated or chronic exposure.350-.350-.350 (.350 (. PCP is degraded by sunlight and metabolized rapidly by microorganisms.48 (..350 (. and dermal contact with PCP-treated products. has been restricted.10 (1.25 and 0. other polychlorinated benzenes. 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. and possibly of lindane (IPCS.91 (1. water and sediments because of the large amounts that were produced and used historically. Human exposure to PCP has become less common.350-1.80) .350) < LOD < LOD 75th .09) .60) 1.62 (.90) 1.350) < LOD .30 (.350 (.350-. < LOD means less than the limit of detection.350-.350) < LOD .30) 1.350-. The parent compound and conjugates.860-2. herbicide.30) 1.

69 (1.16-1.370 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003).950-1.220-.470 (.67 (1.950-1.35) 1.40) 1.82) 1.67 (1.6 and 14.75 (<LOD-2.700-2.08 and 5.S.320) < LOD < LOD 75th . 1995).36) . 1991).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.78) 1.440 (.650 (.30) 1.270-.40) 1.09-1.94 (1.67-2.atsdr. In animals.330-.40) 1.990 (.19) 2.25-2.510-. chronically administered high doses of PCP were hepatotoxic.730) < LOD .11) 2.94-3.240-.910-1. and adversely affected thyroid function (U.500 (.760 (.25-2. or skin absorption.35-2..84) 1.95) 3. carcinogenic.84-4.EPA. environmental levels) and health effects is available from the U. IARC has determined that pentachlorophenol is possibly carcinogenic to humans. Death can result from seizures and cardiovascular collapse.30-2.35) 1.21-2.52 (<LOD-1..500-.S.300 (.610 (.19 (1.00) 1.52 (1.gov/ pesticides/ and from ATSDR at: http://www.290-.55) 1.html. respectively) (Seifert et al.800) < LOD 1.26 (1.30 (.73 (1.570 (. and the FDA has established a standard for bottled water. inhalation.e.250 (.06-3.gov/ toxpro2.epa.560-.51) 1. Pentachlorophenol is not mutagenic or teratogenic.79) 1.290) < LOD . 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.18 (1. 1989). In NHANES 2001-2002 subsamples.13 (.40) 1.40) 1..06 (.. respectively) (Becker et al.00-1.94 (1.280) < LOD .S.220-.780) < LOD .67-3.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..310) < LOD .92) 1.360 (.29-3.83 (1. children in the 1980’s.21 (. 2004.52) 1. More information about external exposure (i.830) < LOD . 1989).9 mg/L.75) 1.710-1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.19) 2.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .430-.82 (1.320) < LOD .84 (1.16 (.590-1.780-1..10 (1.650) 90th 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .S.56) 1.78) 1.510-. OSHA has established an occupational standard.06) 1.52 (<LOD-1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.360-. Survey Geometric mean (95% conf.10-2.19) 2.09 (<LOD-2.500-1.650 (.57 (1.420) < LOD .560) < LOD .26 (1.580-.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 .290-. 2000). In a small sample of U.560) < LOD .850 (.cdc.800-1.25 (1.67 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 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.320 (.67 (1. EPA at: http://www.300 (. population from the National Health and Nutrition Examination Survey.320) < LOD .380-.18) .490) < LOD .35-2.30) 1.350) < LOD . van Raaij et al.Fungicides adults and children severely exposed to PCP through ingestion.25) 1.S.90) 1.900-1. EPA has developed standards for PCP in drinking water and the environment. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.920 (.57 (..310-.300 (.430) < LOD .0 mg/L.67 (1. 2003).25-1.270-.48-2.630 (. Fourth National Report on Human Exposure to Environmental Chemicals 41 .40-2.590) < LOD . Among adults in the NHANES 1999-2000 subsample.340-.25 (1.400 (.34 (.250 (..67-3.260 (. The U.00-1.

r e g u l a t i o n s . Notten WR.105(1):78-83. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Toxicology 1991: 67(1):107-16. Arch Toxicol 1986. Seiwert M. Hill RH. To-Figueras J.S.10:552-65.58:182-186. Arch Environ Contam Toxicol 1989. Schulz C. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. International Programme on Chemical Safety (IPCS). et al. Barrot C. Kaus S. et al. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Arch Environ Contam Toxicol 1989. Helm D. Environ Health Perspect 1997. Becker K. Hill RH Jr. Bragt PC. 4/21/09 Kohli J. Lindane. Hill RH Jr. Seifert B. Pharmacokinetics of pentachlorophenol in man. U. Cline RE. Baker S. van den Berg KJ. house dust. Fast DM.inchem. Available at URL: h t t p : / / w w w. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Needham LL. Schmid P. available at URL: http://www. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Krause C. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Seifert B.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Jones D. Holler JS. 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. et al. Bailey SL. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. PCP: Human Risk Characterization [online]. Pesticide residues in urine of adults living in the United States: reference range concentrations. Otero R. Smith SJ. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Rodamilans M. To T. Needham LL. Blau GE. Sala M. htm. Engel R. Braun WH. Dev Toxicol Environ Sci 1979.org/documents/jmpr/jmpmono/2002pr08. 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. Seiwert M. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. EPA). 11/30/2004. Gregg M. 2002. Shealy DB. Environ Res 1995. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Head SL. 206:15-24. Schulz C. Phillips DL. 4/21/09 van Raaij JA. Environmental Protection Agency (U. Chenoweth MB. References Becker K.S.4:289296. hair. Santiago-Silva M.18:475-481.71:99108. The metabolism of higher chlorinated benzene isomers. Safe A. Schlatter C. drinking water and indoor air.18(4):469-474. J Expo Anal Environ Epidemiol 2000. Uhl S. urine. Can J Biochem 1976.54(3):203-208. Int J Hyg Environ Health 2003.

S.00-2.850 (.770 (. which may vary for some chemicals by year and by individual sample.621) * .710-2.10-1.22 (. 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.76) 1.23) 695 680 520 695 603 953 Limit of detection (LOD. OPP is volatile. whereas SOPP is not volatile and is more water soluble.00) < LOD . In the past.60 (1. Both chemicals degrade within hours to weeks in the environment (U. sodium ortho-phenylphenate (SOPP).480-1.420 (<LOD-. however.600-1.10) 1.390-.690-1.50-4.386-. population from the National Health and Nutrition Examination Survey.60-3.490 (<LOD-.498 (.570-.800-3.33 (.10) .28 (.03) 1.490 (<LOD-.645) * .570 (.30) 1.00 (1.500-2.20) 2. 1998).50) 1.509 (.90) .85) 2.00 (1.50) .508 (. 2006).10 (1.40-5.836) * .07 (. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.Fungicides ortho-Phenylphenol CAS No. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50 (1.00) .638) * .880-2.30) < LOD 90th 1.364-. < LOD means less than the limit of detection.40-7.S.590-2.570-2. formulate.552 (.88) 1.610-1.40 (.860 (.690) < LOD .02) 1.890 (.14 (<LOD-3.370-.60 (1..490 (<LOD-. OPP is considered to be moderately toxic after acute oral doses in animal studies.890) 1.450 (<LOD-.40-2.600-1. Workers who manufacture. Timchalk et al.10) 1.742) * .890 (. Fourth National Report on Human Exposure to Environmental Chemicals 43 .80) 1. 2006). Most agricultural food applications have been revoked.20-2. EPA. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.20 (1. in paints. Available evidence suggests that OPP does not accumulate in the body.30-7.61) 2. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. are antimicrobial agents used as bacteriostats. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.496 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. General population exposure can occur via dermal. 1989).50) < LOD .EPA.50-3. OPP is still used as a disinfectant fungicide for industrial applications.540-2.580-1.636) * .600-1.60 (1. interval) .S. and as a wood preservative.950) < LOD .632) Selected percentiles ( 95% confidence interval) Sample 95th 2.00) .370-.30 (1.20-3.60-2.600) < LOD 1.19 (.567 (.370-.30) < LOD 1.27 (.466 (.696) * .10) 2. 2002. such as fruits and vegetables.50 (1.600) < LOD 75th ..710) 3.770 (.470 (<LOD-.490 (<LOD-.3 and 0.760-2. SOPP is applied topically to the crop and then rinsed off..28-3.840-1.30-2.790) 2.90 (1.600) < LOD .550-1.10-2.389-.490 (<LOD-.80 (2.560-8.3.00 (1.50-2.90) 2.30) < LOD .780) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or apply these chemicals may be more highly exposed than the general population. fungicides.22) 2. Cnubben et al. leaving the chemical residue OPP. Survey Geometric mean (95% conf.433-. 2006).624) * .930 (.00 (1.450 (<LOD-.740 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops.20) < LOD 1.630) < LOD .389-. or 2-phenylphenol) and its water-soluble salt.90) .670) 2.80-3.450 (<LOD-.20 (1.497 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . inhalational.640) < LOD .90 (1.50 (1. it was used in home sanitizers for surfaces.570-1.600) < LOD .349-.610 (.92 (. and sanitizers.402-.40-5.820 (.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 . 2006).17 (.20) < LOD 2. Estimated human intakes have been below recommended intake limits (U.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .50) < LOD .EPA.410-.90) 1.10 (1.10) .493 (.10) .570 (.520 (. on ornamental plants and turfs. 90-43-7 General Information Ortho-phenylphenol (OPP.50) < LOD . but OPP and SOPP are still used on pears and citrus (U.830 (. and it has limited water solubility.970 (.S.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 . 1998.20 (.09) 2.350-1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.80) 1.34) 1.750-2.

656) * . 2005).791) * . 1998. U. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. 1986).353-. In high dose animal studies.510 (<LOD-.96 (1.496 (..46) < LOD 1.Fungicides anemia. Kwok et al.473) * . population from the National Health and Nutrition Examination Survey.epa.31) < LOD .58) 2.33) 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 .32) 3.980 (<LOD-1.514 (.343 (..81) 1.550) < LOD . IARC has classified SOPP as a possible human carcinogen.620-1.580) < LOD .01) 1. Zhao et al.26) 1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 ..13) 1.560) < LOD 75th .950) < LOD . Volunteers exposed to 0.750-2.900-1.910 (. Ito et al.93) 1.860 (. 1984.750 (.0) 1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.610) < LOD 1.84 (1.96) 1.04-4. 44 Fourth National Report on Human Exposure to Environmental Chemicals .620-1.444 (.93) .460-.11 (.11) < LOD 90th 1.910-1.666) * .47) .59) .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.690 (.508) * .800-1.780-14.860 (.08) 1.93 (1.S.. Murata et al.EPA 2006).403-.248-.61 (2.61 (.940-2.990) < LOD . 1993.40-13.75 (1. leading to production of two metabolites. Bomhard et al.75 (1.670) < LOD .38-3.96-4.62) .. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.980 (. OPP was not found to be mutagenic.S.810) < LOD .270-. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. Biomonitoring Information Urinary OPP levels reflect recent exposure.4) 3.09-6.S.38) 2.EPA 2006). 2002).28 (<LOD-4. 1997.580-1.09-3.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. CDC. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.810-1.43 (1.840 (.600-1.11-1.02 (.25-6.750 (.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.11) 4.670 (.382 (.640-1.21-2.64 (2.44 (1.61 (1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC. Detectable levels were seen in over half the U.470) < LOD .650-1.301-.770-2.gov/pesticides/.88-4.43-2.33) . 1992. but no neurologic.484) * .12-2.S.06-5.EPA at: http:// www.361-.329-.89 (1.320 (<LOD-..440 (.06-4. Smith et al. 2000.880-1.420 (<LOD-.17 (.24-2.28 (2..51-3.480-.780 (. 1999.560-2.385 (..38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .550 (. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.08-2.470 (<LOD-.291-.21) 1. or developmental toxicity was observed (Bomhard et al.86 (1.18) 2. 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.590) * .74 (1.59) 1. 2005. less likely.43-2.670 (.910 (<LOD-1..53) 1.455-. 2002. Nakagawa et al.43) 3. interval) .17 (.24-2.09 (1. reproductive. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. 2002.97 (2.00 (1. Pathak and Roy.S.06 (1. or.900) < LOD . and it has classified OPP as not classifiable with respect to human carcinogenicity.510-.32) 1.91 (1.550-. by possible genotoxic mechanisms (Hagiwara et al.17) 2.78 (2.420 (<LOD-.33-2.00 (.20) < LOD 3.27) < LOD .380 (. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. Additional information is available from U.453 (.568) * . 1999.29) 1.311-.07) 2.08-1..12) < LOD 1.500) < LOD .410 (<LOD-.21 (.970) 1.570) < LOD 1.69 (1.93) .11 (. Brusick.38) 1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . U.29) 1.96 (1.52 (.410 (<LOD-. 1984.360 (<LOD-.05-2.

Regul Toxicol Pharmacol 2002. Bartels MJ.pdf. J Agric Food Chem 2002. IARC Sci Publ 1984. 90-43-7) in Swiss CD-1 mice (dermal studies). Timchalk C. Brusick D. Christenson WR. Selim S.S. Comparative metabolism of orthophenylphenol in mouse. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Smith RA. 2005. Mutat Res 1993. Glas K. Hakkert BC. Atlanta (GA). EPA).32(6):551-625. Tayama S. Sangha GK. Environmental Protection Agency (U. The carcinogenicity of the biocide ortho-phenylphenol. Mendrala AL.pdf.. Fourth National Report on Human Exposure to Environmental Chemicals 45 . et al. Bormett GA. Bartels MJ. Fukushima S. Ito N. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.703(12):97-104. McNett DA. EPA 739 R-06004. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Meuling WJ. Timchalk C. 2006. Elliott GR. Carcinogenesis 1999. U. Roberts AL.niehs. 4/13/09 Onstot JD.nih. Eadon G. National Toxicology Program (NTP).S. Kawanishi S. Drugs. Moore GA. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Pathak DN. Bartels MJ. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Turteltaub KW. St John MK. Shibata M. Buchholz BA. food additives and natural products as promoters in rat urinary bladder carcinogenesis. J Chromatogr B Biomed Sci Appl 1997.150(2):402-413.gov/ntp/htdocs/LT_ rpts/tr301. March 1986. Richter M. Cnubben NH. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Inoue S. Shirai T. Bomhard EM. Environmental Protection Agency (U. Toxicol Appl Pharmacol 1999.17(8):411-417. Moldeus P. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Herbold BA. Food Chem Toxicol 1984. July 28.43(7):14311437. EPA-560/5-89-003. Gierthy J. Freyberger A.EPA). Hum Exp Toxicol 1998. Centers for Disease Control and Prevention (CDC). Eastmond DA. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Third National Report on Human Exposure to Environmental Chemicals. Xenobiotica 1998. van de Sandt JJ. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats.gov/oppsrrd1/REDs/ phenylphenol_red.22(10):809-814. Moriya K.S. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Available at URL: http://www. Crit Rev Toxicol 2002.50(11):3351-3358. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers.Fungicides References Appel KE. Roy D. U. Vogel JS. Narang A. Stanley JS.286(2):309-319.159(1):18-24. Zhao S. Bartels MJ. Arch Toxicol 2000. Bromig KH. Hagiwara A.35(2 Pt 1):198-208. Sangha G. Christenson WR. Ito N. Nakagawa Y.S. Leser KH. Available at URL: http://ntp. Kwok ES.28(6):579594. 1989. Coelhan M. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). rat and man. Imaida K. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Fukushima S. Hagiwara A.epa. Environ Mol Mutagen 2005. J Agric Food Chem 2006. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol.45(5):460-481. Brendler-Schwaab SY. 4/9/09.20(5):851-857. Biochem Pharmacol 1992. Arnold LL.(56):399-407. et al. Identification of SARA compounds in adipose tissue.74(2):61-71.54(16):5731-5735. Cano M. Brzak KA. Murata M. Office of Toxic Substances. Hirose M. Toxicol Appl Pharmacol 1998.

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

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

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

111(5):749-756. Hines CJ. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Hladik ML. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Acetochlor (Harness) Pesticide Petition Filing 1/00. acetochlor. Camann DE.cornell. Kinney PL. Alavanja MC. 5/30/06. U. Olsson AO. Atlanta (GA). Available at URL(non U. Wratten SJ. et al. et al. Furlong ET. and other herbicides in rivers.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.108(12):1151-1157. sulfonamide. EPA). Hodgson E.24(10):1003-1012. Deddens JA. Comparative metabolism and elimination of acetanilide compounds by rat.S. Peter CJ. Environmental Protection Agency (U. Number 15. J Agri Food Chem 1989. Volume 65. Bravo R.S. epa. Thurman EM. Hum Exp Toxicol 1996. Heederik D. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes.15(9):702-735. imidazolinone. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Environ Health Perspect 2003. Quistad GB. Rose RL.html. Feil VJ. J Expo Anal Environ Epidemiol 2005.248(2-3):115-122.S.15(6):500-508. Linhart SM. Whyatt RM. Wilson AG. Xenobiotica 1994. 2005. Sanderson WT. Reynolds SJ. Available at URL: http://www. Kier L. Hein MJ. Fourth National Report on Human Exposure to Environmental Chemicals 49 . In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Third National Report on Human Exposure to Environmental Chemicals. J Expo Sci Environ Epidemiol 2007.17(6):559-566. et al.S. Sci Total Environ 2000. EPA 738-R-00-009. EPA). Finding minimal herbicide concentrations in ground water? Try looking for their degradates.39(17):6561-6574. Centers for Disease Control and Prevention (CDC). Striley CA. March 2006. Burkhardt MR. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. 1998.248(2-3):123-133. Feng PCC. Curwin BD. Barr DB. Davison KL. Hsiao JJ.S. Roberts AL. Larsen GL. Tinwell H. Chem Res Toxicol 1998. 5/30/06 U. Ward EM.11(4):353359. Environ Health Perspect 2000.cce. Environ Sci Technol 2005. Kolpin DW. Sci Total Environ 2000. Battaglin WA.EPA): http://pmep. reservoirs and ground water in the Midwestern United States. 2000. Casida JE. Environmental Protection Agency (U. Coleman S. Green T. Barr DB. pages 3682-3690. Occurrence of sulfonylurea. and metolachlor herbicides in rats. Barr JR. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.Herbicides References Ashby J. Andrews HF. Barr DB. Federal Register: January 24. Lefevre PA.pdf. Dialkylquinonimines validated as in vivo metabolites of alachlor. Jefferies PR. Linderman R.37(4):10881093.

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. WHO. 1995).EPA considers alachlor to be a probable human carcinogen at high doses. 1997. soybeans. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. whereas 60% of applicators had detectable amounts. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. and uveal degeneration.EPA. IPCS. 1996. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al.EPA. In a study of applicators and workers exposed to alachlor. including corn. WHO. and on non-crop land for general weed control.. U. It is absorbed by plants and inhibits plant protein synthesis.1 to 1.. formulators. alachlor has demonstrated hepatotoxicity. but another metabolic pathway can produce 2.S. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. In animals. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates... 1988. U. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. Hines et al. Estimated human intakes have been below recommended limits (U.. 1998.S. 2003). In chronic animal testing. but shows little bioaccumulation. Hladik et al. but has not shown developmental or reproductive toxicity in mammalian systems (U. (2003) showed that 2.1 mg/L at various collection times (Sanderson et al. 1998). 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.. peanuts and other crops. corn cropland was treated with alachlor..S. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.EPA.EPA. 1998. mean values of urinary concentrations of alachlor metabolites. Alachlor itself is not considered mutagenic. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. 1989. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. NTP and IARC do not have ratings regarding human carcinogenicity. 2003). ranged from 0. 1994. 2003). 2005). Alachlor has a soil half-life of a few weeks. 1998). mercapturate conjugates were predominant metabolites. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. Feng and Wratten. the latter may account for some observed effects (Davison et al.S. hemosiderosis.gov/pesticides/.S.EPA. WHO. 1996.. Because it can be absorbed through skin. about 20-25% of the U.Herbicides Alachlor CAS No. Jefferies et al. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. U. Alachlor and its degradates are leachable from agricultural soils and have been detected in watersheds of agricultural land including ground and surface waters (Battaglin et al. Alachlor has low potential for acute toxicity. stomach.epa. In 1993-1995. 2005.6-diethylaniline and its reactive metabolite. USGS. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. 2000. 1999 and 2007. WHO. 1998. 1996). 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).S.S. 2003). Hill et al. and field workers. EPA at: http://www. Tessier and Clark. Additional information about is available from U. Kolpin et al. 50 Fourth National Report on Human Exposure to Environmental Chemicals . Since the late 1980s alachlor use has been declining. but not likely at low doses. 1999. U. 2000.S. the dermal exposure route is potentially significant for applicators.. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. In animal studies. 1995.. as measured through conversion to deethylamine.

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

org/documents/pds/pds/pest86_e. Jefferies PR. J Agri Food Chem 1989. March 2006. Geological Survey (USGS). Hladik ML. EPA). 1992-2001. and metolachlor herbicides in rats. Kolpin DW. Geological Survey (USGS). WHO/ FAO Data Sheets on Pesticides. Wratten SJ. sulfonamide. Feng PCC.S.htm. Kier LD. who. Kolpin DW. Erratum in: Life Sci 1989. 1999. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.pdf. Xenobiotica 1994. Lau H. Hines CJ. An evaluation of the carcinogenic potential of the herbicide alachlor to man. International Programme on Chemical Safety (IPCS). Burkhardt MR. Shealy DB. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Martens MA. Kimmel EC.pdf. California. U. Hum Exp Toxicol. World Health Organization. Sci Total Environ 2000. Furlong ET. et al. Available at URL: http://www. et al. Sanderson WT.18(6):363-391.S.56(9):883-889.43(9):2504-2512. Am Ind Hyg Assoc J 1995. Barr DB. Casida JE. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Third National Report on Human Exposure to Environmental Chemicals. EPA 738R-98-020. 2005.S. MacKenzie B.39(17):6561-6574. 1998. Roberts AL. Whyatt RM. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Tolos W. acetochlor. Thake DC. Available at URL: http://water. 86.usgs. Quistad GB. Quistad GB.11(4):353359. Davison KL.24(10):1003-1012. 1999.56(6):853-859. Striley CA. reservoirs and ground water in the Midwestern United States. and other herbicides in rivers.111(5):749-756. Centers for Disease Control and Prevention (CDC). Hill RH Jr. Available at URL: http://www.248(2-3):115-122. Wilson AG. 2007. Brown KK. Thelin GP. Heydens WF.44(18):1325. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Deddens JA. Larsen GL. 2/27/09 Jefferies PR. Hines CJ.php. Life Sci 1988. Henningsen G. Background document for development of WHO Guidelines for Drinking-water Quality. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Sci Total Environ 2000. Andrews HF. Environ Sci Technol 2005.248(2-3):123-133. ALACHLOR. December 1998. Hill AB. imidazolinone. Circular 1291.47(6):503-517. DNA adduct formation by alachlor metabolites. Casida JE. Shoemaker DA. J Ag Food Chem 1995. 98-4245 (by Barbash JE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Biagini RE.37(4):10881093. Biagini R. Kinney PL.inchem. Environ Health Perspect 2003. Environmental Protection Agency (U. Atlanta (GA). Brown MA. Thurman EM. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes.gov/oppsrrd1/ REDs/0063. Geneva. Supplemental Technical Information (available on-line only). Occurrence of sulfonylurea. Mutat Res. Chem Res Toxicol 1998. Camann DE. Gilliom RJ). World Health Organization (WHO). 2003. 1997. 2/27/09 U.43(25):2087-94. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. revised February 15. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. No.395(2-3):159-171. 4/2/09 U. Casida JE. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.epa. Clark JM.int/water_sanitation_health/dwq/chemicals/en/alachlor. Feil VJ.S. Hull RD. Tessier DM. Linhart SM. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Barr JR.Herbicides References Battaglin WA. 1996. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Comparative metabolism and elimination of acetanilide compounds by rat. Sacramento. Available at URL: http:// www. Dialkylquinonimines validated as in vivo metabolites of alachlor. Alachlor in Drinking-water. Bull Environ Contam Toxicol 1996. Hsiao JJ. Ann Occup Hyg 2003. Reregistration Eligibility Decision (RED) Alachlor. Driskell WJ. Peter CJ.

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

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

Available at URL: http:// www. Toxicol Lett 1993. levels of atrazine mercapturate were generally not detectable (CDC. WHO/ FAO Data Sheets on Pesticides. World Health Organization. In a study of 60 farm worker children. Tapia J. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. 2005. Curwin BD. Environ Health Perspect 2007.org/documents/pds/pds/pest82_e. Aldous CN. J Toxicol Environ Health 1994.. The geometric mean of urinary atrazine mercapturate was 1. International Programme on Chemical Safety (IPCS). Stoker TE. Jones AD. Cooper RL. Carr WC Jr. 82. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Clayton CA.61(4):331-355. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Deddens JA. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Toxicol Sci 2003. Pest Manag Sci 2005. Brown KK. Tyrey L.47(6):503-517. Toxicol Sci 2000. Reynolds SJ.htm. Sanborn JR. Barr DB.. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Barbieri F. References Adgate JL.gov/toxprofiles/tp153. et al.cdc.53(2):297-307. In the NHANES 2001-2002 subsample.99(8):5476-5480. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.. Barr DB. ATRAZINE.atsdr. Lee M.. Pfeifer KF. Hayes TB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000). Third National Report on Human Exposure to Environmental Chemicals. 2001). Barr DB. Bersani M. 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. Stoker TE. Schmid J. Gillis JH. 2003. Saiz SG. Gillis JH. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Wetzel LT. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Wetzel LT. Cooper RL. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Lioy PJ.html. McElroy WK. Freeman NC. Laws SC. Atlanta (GA).Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Striley CA. Cottica D. In small studies of Maryland residents in 19951996 (MacIntosh et al. 3/11/09 Laws SC. Maroni M. Breckenridge CB. Chen H. diamino-S-chlorotriazine and hydroxyatrazine. Proc Natl Acad Sci USA 2002. atrazine was detected in only four children (Arcury et al. Biagini RE.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Lucas AD. Goldman JM. et al. Toxicol Sci 2000. 2007). Mendoza M. In a small number of field workers.109(6):583-590. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Catenacci G.64(9):672-678. Cooper RL. et al. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.30(2):244-247.inchem. Grzywacz JG. Environ Health Perspect 2001. Hein MJ. Extrom PC. J Toxicol Environ Health 1994. 2005). J Agric Food Chem 1982. Moseman RF. Hermaphroditic. Geneva. Bradway DE. J Expo Anal Environ Epidemiol 2005. Centers for Disease Control and Prevention (CDC). 2001 [online]. Steroids 1999. Seiber JN. Eldridge JC. 2005).58(2):366-376. Blewett C. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.115(8):1254-1260.15(6):500-508. 1996. Quandt SA.. Ann Occup Hyg 2003.69(2):217-222. Ferrell JM. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Agency for Toxic Substances and Disease Registry (ATSDR). Ferrell JM. Heederik D. et al. No.. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Stuart AA.43(2):155-167. Ferioli A. 3/11/09 Arcury TA. Sanderson WT. Toxicological profile for atrazine. Collins A. et al. Goodrow MH.. Vonk A. Gammon DW. et al. 1993). Stoker TE. Stevens JT. Biological monitoring of human exposure to atrazine. Fleenor-Heyser DG. Noriega N. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Shoemaker DA. Perry et al. Eldridge JC. Hines CJ. Available at URL: http://www. Simpkins JW.76(1):190-200.43(2):155-167. A risk assessment of atrazine use in California: human health and ecological aspects. Eberly LE. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.

2007. Langvardt PW.56(2):69-109. Case No. Cooper RL. Pesticides and Toxic Substances.10(7):479.S. Geological Survey (USGS). Urinary biomarkers of atrazine exposure among farm pesticide applicators. Sathiakumar N. Ann Epidemiol 2000. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Perry M. Ryan PB. Lansbergen GW. Singzoni B. Sanderson JT.S. Available at URL: http://www. Boerma J.pdf. 6/1/09 U. 1992-2001. J Expo Anal Environ Epidemiol 1999.61(1):27-40.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. J Toxicol Environ Health A 1999. Stoker TE.php. EPA Office of Pesticide Programs.S. Needham LL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. 2003b.epa. Washington (DC). van den Berg M. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Dagenhart D. Office of Prevention. Christiani D. Available at URL: http://water.pdf. Circular 1291. Crit Rev Toxicol 1997.gov/oppsrrd1/REDs/ atrazine_ired. Breckenridge CB. Guidici DL. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Laws SC. Environmental Protection Agency (U. Cooper RL. 0062. Fenton SE. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Dryzga MD. White paper on potential developmental effects of atrazine on amphibians. Interim Reregistration Eligibility Decision For Atrazine. A longitudinal investigation of selected pesticide metabolites in urine. Hammerstrom KA.182(1):44-54.S. Guidici DL. Environmental Fate and Effects Division.epa. May 2003a. Stevens JT. Wetzel L. Stoker TE. Kastl PE.usgs. EPA). Toxicology 1990.Herbicides development of a biomarker of exposure. Toxicol Appl Pharmacol 2002.27(6):599612. 3/11/09 U. U. Tortorelli J. Delzell E.195(1):23-34. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water. Timchalk C. Toxicol Sci 2000.S.6(1):107-116. A review of epidemiologic studies of triazine herbicides and cancer. MacIntosh DL.67(2):198-206. Available at URL: http://www. Toxicol Sci 2002. Supplemental Technical Information (available on-line only). Osborne DW. Toxicol Appl Pharmacol 2004. Laws SC. Chem Res Toxicol 1993. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.58(1):50-59. March 2006. A risk characterization for atrazine: oncogenicity profile. EPA). Wood C. Rayner JL. The Quality of Our Nation’s Waters.9(5):494-501. revised February 15.

660) 1.51 (1. 1974. Fourth National Report on Human Exposure to Environmental Chemicals 57 .43) 1.4-D have been below recommended intake limits (U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.4-D can be applied either as an aqueous salt or as oil-soluble esters. 2.27-2.00-2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.610 (.560-1. abdominal pain. Human health effects from 2. 2007). it acts as a plant growth hormone.910) < LOD .410) < LOD .32 (1.760 (.07 (. 2.08) < LOD . 2.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740 (. and by consuming food or drinking water contaminated with 2.910) 1.230-. and mecoprop)..4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.EPA in 1948.60) 1.4-D is rapidly absorbed via oral and inhalation routes.690 (.250 (<LOD-. renal and hepatic injury. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.680-1. 2.S.S.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. the chlorophenoxy herbicide 2.690-1.27 (1. and delayed Urinary 2.16) < LOD .670-1.48) < LOD 1.930 (. but at higher levels they are herbicidal.420-.310 (. agricultural.27 (. As much as 62 million pounds of 2..55 (1.320) 90th .890) < LOD . hypotension.13) < LOD .490) < LOD < LOD < LOD .310) < LOD .80) 1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. which may vary for some chemicals by year and by individual sample. Kohli et al.S. MCPA.250 (<LOD-. 2004).420) < LOD .350) < LOD < LOD < LOD .610-.2.230 (<LOD-.Herbicides 2. 1977).370-..66) < LOD 1. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. dizziness.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.4-D) controls broadleaf weeds in residential.20 (. population from the National Health and Nutrition Examination Survey. General population exposure to 2. 2005).690 (. headache.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 . 94-75-7 General Information Widely used throughout the United States.4-D may occur during residential applications.890 (. Once absorbed. It is rarely detected in ground waters (USGS. It was first registered with U.20 (<LOD-1.02-1. by direct contact with agricultural and residential areas after applications.690 (.4-D were used in the U. At low levels.S. 4-D.4-D or exposed for prolonged periods.540-. Recent estimates of chronic intakes of 2. in 2001 (U. Sauerhoff et al.22) < LOD .70) 1.EPA.4-dichlorophenoxyacetic acid (2.260 (<LOD-.S.EPA. nausea.4-Dichlorophenoxyacetic Acid CAS No.210 (<LOD-.10 (<LOD-1.40) 1.05-2. myotonia.490 (. with a half-life of several days to several weeks.03) 695 659 520 668 589 892 Limit of detection (LOD. 1989. Similar to other chlorophenoxy herbicides.730 (. and aquatic environments.440-1.930-1.550-1.30 (<LOD-2.10 (<LOD-1. these herbicides can enhance plant growth. It is not well absorbed through the skin.952 and 0.24 (.560-. It is poorly bound in soils.4-D has low acute toxicity.960-1.330 (.21) 1.210-.10) < LOD 1.810-1.400) < LOD . although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

S. Kutz et al.720 (.3.590 (<LOD-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.EPA.S.EPA.560-.. Frank et al. In previous samples of the U. Pearce and McLean.550-..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 .380) < LOD .380 (<LOD-.340-.660) < LOD . 1996.S. 58 Fourth National Report on Human Exposure to Environmental Chemicals .570) < LOD .780-1.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .05) . with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.41 (1. It is unclear whether these associations are related to the chlorophenoxy herbicides.790) < LOD . 1989).470) < LOD . such as soft tissue sarcoma and non-Hodgkin’s lymphoma..EPA at: http://www.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2000).410) 90th .610-. 2.520-. 2002. 1985.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.410) < LOD < LOD < LOD . Survey Geometric mean (95% conf.08 (.56) . IPCS. U.. urinary 2. 2002. 2005. 2005.790) 1. 2005. 1994).35) < LOD .560-. Biomonitoring Information Urinary levels of 2.890-1.340 (. 1996. and of adults and children (Baker et al.480 (.330-. 1992). adrenals and gonads (NTP.4-D reflect recent exposure.17 (. eyes.740 (.32 (<LOD-2.4-D are eye irritants.990-1..390) < LOD < LOD < LOD .660 (.350 (<LOD-. other exposures. Average post-application urinary levels of 2. 2.980) < LOD 1.680) < LOD .780 (. 2001.epa.14 (.39) < LOD 1.27-1.410) < LOD 1. U.670 (.490 (.4-D does not have significant reproductive.780) .16) 1. Acute high doses administered to laboratory animals produced ataxia.820-1.S.270-.410 (<LOD-.4-D production plant workers and a few forestry workers spraying 2. 2006. IOM.19) ..850) < LOD . 2005). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. Additional information is available from U..810-1. developmental.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. Epidemiological studies have reported associations of several types of cancer.380 (<LOD-.S.380-. Kolmodin-Hedman and Erne.580-. The acid and salt forms of 2. liver.670 (.670 (<LOD-1.24) 1.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.700 (. 1995).EPA. 2004). U.. 1996. 2005).13 (.7.620-. IPCS. myotonia. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.Herbicides neuropathy (Bradberry et al. U. Hill et al. 1995. or teratogenic effects in chronic rodent studies (Charles et al. 1980..610-.S.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 2003.930-1. population from the National Health and Nutrition Examination Survey.890) < LOD 1.S. CDC.640 (. 2005).440 (.73) . Post-application levels in farmers and home gardeners were dependent on Urinary 2.810-1. population (Hill et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .590 (<LOD-1.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.4-D levels were detectable in less than a quarter of the individuals studied. IPCS. 2005). in small samples of children (Hill et al..gov/pesticides/. 2005.270 (<LOD-. and evidence of histological injury to the kidneys. 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.08 (. thyroid.08 (.EPA 2005).920) < LOD 1. Knopp et al. or to contaminants in the herbicide formulations (specifically 2. 2.13 (.

Head SL. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. geometric mean urinary levels of 2. Developmental toxicity studies in rats and rabbits on 2.gov/index.htm. Pesticide residues in urine of adults living in the United States: reference range concentrations. 914.4 dichlorophenoxyacetic acid (2. 2005).18(4):469-474. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Khanna RN. Tables. Dichlorophenoxyacetic acid.10(6 Pt 2):789-798. Crit Rev Toxicol 2002.51(3):152-159. Baker SE. Sanderson WT.5-T). Selected pesticide residues and metabolites in urine from a survey of the U.4-D and 2. Centers for Disease Control and Prevention (CDC). Hein MJ. Arch Environ Contam Toxicol 1985. Curwin BD. Environ Res 1995. Xenobiotica 1974. Arch Environ Contam Toxicol 1989. In farm families. Arch Toxicol Suppl 1980. Bus JS.4:427-435. Pesticides residues in food: 1996 evaluations Part II Toxicology. J Toxicol Environ Health 1992. Survival and Growth Curves from NTP Toxicity Studies. Barr DB. Chapman P. Vet Hum Toxicol 1989. Washington (DC): National Academies Press. Brody D. Scand J Work Environ Health 2005. Barr DB.S. 2005.31(2):121-125. Dhar MM. Atlanta (GA). 2003. Cook BT. Garabrant DH. Mandel et al. 2005 Charles JM. et al. Campbell RA. Solomon KR. Tandon JS.. the amount of pesticide applied. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5..71(2):99-108. Hill RH Jr.4-D) epidemiology and toxicology. Kutz FW. Hanley TR Jr. 1992).4-Dichlorophenoxyacetic Acid).4-dichlorophenoxyacetic acid (2.4-dichlorophenoxyacetic acid and its forms.4:318-321. Harris et al. Bailey SL. Review of 2. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .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. Assessment of exposure to 2. Biomonitoring of herbicides in Ontario farm applicators. et al. Toxicol Sci 2001.Herbicides the time since application. Fast DM. Erne K. Finding a measurable amount of 2. Honeycutt R. To T. Available at URL: http:// www.31 Suppl 1:98-104. 2006. Hill RH Jr. Scand J Work Environ Health 2005.org/documents/jmpr/jmpmono/v96pr04. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Gupta BN. Updated March 7. Ripley BD. the number of acres to which it was applied (Curwin et al. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. J Expo Anal Environ Epidemiol 2005 Nov. Arnold EK. Mandel JS.edu/catalog. Kohli JD. Heederik D.php?record_id=10603. Forestry workers involved in aerial application of 2. Harris SA.nap. Driskell WJ. Wilson RD. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children..4-D in urine does not mean that the level of the 2. Gregg M. 2. Absorption and excretion of 2. 2005.32(4):233-257.4:97-100. 3/17/09 Institute of Medicine (IOM). TOX-63: TOXICITY REPORT CURVES.niehs. Ritter L.nih. Stephenson GR. Biomonitoring for farm families in the farm family exposure study. J Expo Anal Environ Epidemiol 2000.4-D): exposure and urinary excretion. Murphy RS.4-. Philbert MA. References Arbuckle TE.15(6):500-508.4-D). Frank R. Baker BA. Available at URL: http://ntp.4.4-dichlorophenoxyacetic acid in man.4-D than levels found in the general population. Needham LL. Veterans and Agent Orange: update 2002. J Environ Sci Health B 1992. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Sirons G J. Alexander BH.. Occup Environ Med 1994. et al. Baker S.4-D. Reynolds SJ.4-D were highest in the farmers who applied the 2. Smith SJ. Exposure of homeowners and bystanders to 2. Beasley VR. Shealy DB. Biomonitoring studies of 2.37(2):277-291. Sircar KP. Acquavella JF.60(1):121-131. Carter-Pokras OD. 2005). and the use of protective clothing or equipment (Arbuckle et al. Board on Health Promotion and Disease Prevention. TOX-63 Peroxisone Project (2. International Programme on Chemical Safety-INCHEM (IPCS).inchem.4-dichlorophenoxyacetic acid (2. general population. Cole DC. Needham LL.4-D will result in an adverse health effect. National Toxicology Program (NTP).4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Third National Report on Human Exposure to Environmental Chemicals. Estimation of occupational exposure to phenoxy acids (2. Beeson MD. van Ravenzwaay B. 3/17/09 Knopp D. Holler JS. Available at URL: http:// www.27(1):23-38. Kolmodin-Hedman B.31 Suppl 1:90-97. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.

S. 4/2/09 U. Pesticides in the Nation’s Streams and Ground Water.epa. Washington (DC): U.EPA. Supplemental Technical Information (available on-line only). Circular 1291.2000 and 2001 market estimates. 60 Fourth National Report on Human Exposure to Environmental Chemicals . Braun WH. 3/17/09 U. Pesticide industry sales and usage . 3/17/09. 2004. 2. 2007.gov/oppsrrd1/ REDs/factsheets/24d_fs. Environmental Protection Agency (U. gov/oppbead1/pestsales/01pestsales/market_estimates2001.S.php. Environmental Protection Agency (U.usgs. March 2006.EPA). Geological Survey (USGS). May. EPA 738 F-05-002. The fate of 2.8:3-1U.htm. Available at URL: http://water.4-D) following oral administration to man. Gehring PJ.4-dichlorophenoxyacetic acid (2.epa.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Available at URL: http://www.S. Blau GE.pdf. 1992-2001.4-D RED Facts.S. Office of Prevention Pesticides and Toxic Substances.S. S. Toxicology 1977.Herbicides Sauerhoff MW. The Quality of Our Nation’s Waters. Available at URL: http://www. revised February 15.EPA). June 2005.

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

240) 679 701 957 Limit of detection (LOD. Survey Geometric mean (95% conf. 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 . population from the National Health and Nutrition Examination Survey.440 (<LOD-. Survey Geometric mean (95% conf. 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.200 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .200 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.2. < LOD means less than the limit of detection. 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.670 (<LOD-.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

R. Linhart SM. Larsen GL. 2005. Thurman EM.usgs.S. usgs. Shoemaker DA. California. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .pdf 3/30/09 Hines CJ.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. 98-4245 (by Barbash JE. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. revised February 15.pdf. Background document for development of WHO Guidelines for Drinking-water Quality. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Xenobiotica 1994.ESTfeature_gilliom.108(12):1151-1157. 6/1/09 Whyatt RM. Pesticides in U. Burkhardt MR. 1992-2001. Kolpin DW. J Agri Food Chem 1989. Davison KL.gov/nawqa/ pnsp/pubs/wrir984245/text. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Biagini RE. Reynolds SJ. and other herbicides in rivers.pdf. Gillion. Comparative metabolism and elimination of acetanilide compounds by rat. 2007. Feng PCC. Geological Survey (USGS). Hodgson E. Sci Total Environ 2000. Hsiao JJ. Rose RL.S. 3/26/09 U.Herbicides References Battaglin WA.37(4):10881093. Linderman R. Atlanta (GA).int/water_sanitation_health/dwq/chemicals/ metolachlor.24(10):1003-1012. Available at URL: http://water. Geological Survey (USGS).usgs. acetochlor. Available at URL: http://www.who.15(6):500-508. 2003. Jefferies PR. Barr DB. Ward EM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Casida JE. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. EPA 738R-95-006. Curwin BD. Striley CA. Available at URL: http://water. et al. Coleman S. Chem Res Toxicol 1998. Peter CJ.41:3409-3414. U. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Reregistration Eligibility Decision (RED) Metolachlor. March 2006. Kinney PL.111(5):749-756. sulfonamide. Roberts AL. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. J Expo Anal Environ Epidemiol 2005. reservoirs and ground water in the Midwestern United States. Alavanja MC.php.47(6):503-517. Environ Health Perspect 2003.39(17):6561-6574.11(4):353359.gov/oppsrrd1/ REDs/0001. Sanderson WT. World Health Organization (WHO). Andrews HF. Environ Health Perspect 2000. Quistad GB. Barr JR.html. Kolpin DW. 4/2/09 U. Dialkylquinonimines validated as in vivo metabolites of alachlor. April 1995. et al. Environmental Protection Agency (U. Centers for Disease Control and Prevention (CDC).epa. Wratten SJ. Heederik D. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.gov/nawqa/pnsp/pubs/files/051507. Available at URL: http://water. imidazolinone. Sacramento.S. Furlong ET. Barr DB. Environ Sci Technol 2007. Third National Report on Human Exposure to Environmental Chemicals. Occurrence of sulfonylurea. Supplemental Technical Information (available on-line only). 1998.248(2-3):115-122. and metolachlor herbicides in rats. Sci Total Environ 2000. Environ Sci Technol 2005. Circular 1291. Camann DE. Available at URL: http://www. 1999. Deddens JA. Feil VJ.S. Gilliom RJ). streams and groundwater. Thelin GP. Metolachlor in Drinkingwater.248(2-3):123-133. EPA). Ann Occup Hyg 2003. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Hladik ML.S. Hein MJ. Brown KK.

5-T in soil varies with conditions. which may vary for some chemicals by year and by individual sample.5-T has been rarely detected in ground waters (USGS. myotonia.g. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. Human health effects from 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..4. nausea. Epidemiological studies have reported associations of several types of cancer.4.4.5T is rapidly absorbed via oral and inhalation routes.5-T and 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. and delayed neuropathy (Bradberry et al.3. Ester forms of 2..5-T use as a herbicide in 1985.4. dizziness..1.Herbicides 2.4. 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. < LOD means less than the limit of detection. Omer. Kohli et al.4. ranging from several weeks to many months.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Chlorophenoxy herbicides act as plant growth hormones. 1992. abdominal pain. 64 Fourth National Report on Human Exposure to Environmental Chemicals . 2004). Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. The half-life of 2. Survey Geometric mean (95% conf. 1992).4. it is not well absorbed through the skin.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Agent Orange).4.4-D were used as defoliants in the Vietnam War (e.7.2 and 0.4. 1974)..5-T. 1989.4.4. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Nelson et al. 2007). population from the National Health and Nutrition Examination Survey. headache.4. and concern about contamination with 2.5-T is eliminated mostly unchanged in the urine. renal and hepatic injury. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. with an elimination half-life of approximately 19 hours (Arnold et al.4. but higher levels are herbicidal. 1986.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States..5-trichlorophenol and other degradates.5-Trichlorophenoxyacetic acid (2. Given the commercial unavailability of 2.5-T degrades to 2. the general population is unlikely to be exposed to it.4. Although 2.4. hypotension.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2.. these herbicides can enhance plant growth. 2.S. Mohammad and St. At low levels. 93-76-5 General Information 2.4.5-Trichlorophenoxyacetic Acid CAS No.5-T (Holson et al. Once absorbed into the body.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2.

2005.5-T were generally below the limit of detection. IPCS.5-T also were below the limit of detection (Kutz et al.4.4. 2005). Biomonitoring studies on 2. It is unclear whether these associations are related to the chlorophenoxy herbicides.epa.. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 1996.4. Pearce and McLean.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.gov/pesticides/.EPA.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Survey Geometric mean (95% conf. U. 2004). 2003.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.S.3.4. urinary levels of 2.4.Herbicides or contaminated herbicides.5-T than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1992). population from the National Health and Nutrition Examination Survey. IOM. Finding a measurable amount of 2. 1980). in which urinary levels of 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 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.S. other exposures.4.S. Urinary 2.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4.4.EPA at: http://www.7. Fourth National Report on Human Exposure to Environmental Chemicals 65 .5-T reflect recent exposure.5-T does not mean that the level will result in an adverse health effect.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2. 2002. 2. Additional information is available from U. Biomonitoring Information Urinary levels of 2. similar to results of NHANES II (19761980). Mean urinary levels of 2. or to contaminants in the herbicide formulations (specifically 2.4.5-T itself is not mutagenic.

International Programme on Chemical Safety-INCHEM (IPCS).4. general population.org/documents/jmpr/jmpmono/v96pr04.5-trichlorophenoxyacetic acid (2. 210:250-255. Washington (DC): National Academies Press.4. Scand J Work Environ Health 2005.epa.31 Suppl 1:1825. Mohammad FK.EPA. Holson JF. LaBorde JB. Poisoning due to chlorophenoxy herbicides.4-. Erne K. Estimation of occupational exposure to phenoxy acids (2. Washington (DC): U. McLean D.4:318-21. Third National Report on Human Exposure to Environmental Chemicals. Philbert MA. May.4-D/2.4-dichlorophenoxyacetic acid (2.S. Carter-Pokras OD. Dhar MM. Bradberry SM.19(2):286-297.5-t mixture. Available at URL: http:// www. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Absorption and excretion of 2. Holson JF.4. Veterans and Agent Orange: update 2002.4.S. Environmental Protection Agency (U. Brody D. Cook BT. Nelson CJ.19(2):298-306. U. Review of 2. 2005.Herbicides References Arnold EK. et al. Neurobehav Toxicol Teratol 1986.4.8(5):551-60. discussion 5-7. 3/17/09 Institute of Medicine (IOM).32(4):233-257. 2004. Toxicol Rev 2004. Beasley VR. Multireplicated dose-response studies with technical and analytical grades of 2. 2003.37(2):277-91. 914. Arch Toxicol Suppl 1980.5-T). Gupta BN. II. 3/17/09 Kohli JD.php?record_id=10603. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.23(2):65-73. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Available at URL: http:// www. Pesticide industry sales and usage .31(2):121-125. St Omer VE. Vale JA.S. Atlanta (GA). Tandon JS.5-trichlorophenoxyacetic acid (2. Pearce N.edu/catalog.nap. Proudfoot AT.pdf. Gaylor DW. Centers for Disease Control and Prevention (CDC).htm. Fundam Appl Toxicol 1992. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Arch Int Pharmacodyn Ther 1974. 2. Developmental toxicity of 2. Available at URL: http://www. Sircar KP. Wolff GL. Board on Health Promotion and Disease Prevention. Fundam Appl Toxicol 1992. Developmental toxicity of 2. Vet Hum Toxicol 1989.5-T). Crit Rev Toxicol 2002. Murphy RS.4. Gaines TB. Sheehan DM. Behavioral and developmental effects in rats following in utero exposure to 2.EPA).2000 and 2001 market estimates.4. S. Pesticides residues in food: 1996 evaluations Part II Toxicology.5-T in four-way outcross mice. Office of Prevention Pesticides and Toxic Substances. et al. Selected pesticide residues and metabolites in urine from a survey of the U.5-trichlorophenoxy acetic acid in man. LaBorde JB. Garabrant DH. McCallum WF. Kutz FW. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Gaines TB.4-D) epidemiology and toxicology. J Toxicol Environ Health 1992. Dichlorophenoxyacetic acid.5-T). Agricultural exposures and non-Hodgkin’s lymphoma.4. Khanna RN.4-D and 2.inchem. I. Kolmodin-Hedman B. Nelson CJ.

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

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

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

056-.190) .2) 11.7) 15.180) .150 (.9 (13.5 (16.9 (12.6-24.0 (11.S.109 (.8 (18.4-17.6) 9.130) .130 (.8-17.103 (.120) .2-15.059 (.110) .138 (.6-33. 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. population from the National Health and Nutrition Examination Survey.00-14.140 (.7 (<LOD-15.60-10.1 (18.060) .062-.139 (.S.7 (15.110 (.8.50 (8.4) 14.064) 90th .6-24.064 (.5-17. which may vary for some chemicals by year and by individual sample.110 (.090-.0) 21.080) .170) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.086-.4) 19.3 (14.3-21.5-17.063-.084-.053 (<LOD-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .7-22.089 (.116) .080 (.160 (.80-9.147) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .8-25.070 (<LOD-.8 (11.130-.147 (.0) < LOD 9.100-.8) < LOD 8.1-24.160) .080-.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 8.110 (.098 (.7-19.3 (19.40-9.117) < LOD .9-23.6) 16.80 (<LOD-10.108-.3 (18.4-18.130-.130) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.101) .1 (13.062 (.1) < LOD 9.062 (.9-38.5) 19.3 (18.048 (<LOD-.3 (13.5 and 7.8-19. Survey years 01-02 03-04 Geometric mean (95% conf.90) 90th 15.00 (8.054-.112) 95th .160 (.0 (15.4) < LOD < LOD 16.0 (10.055 (.4 (12.4 (12.9 (12.139 (.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .090 (<LOD-.109-. < LOD means less than the limit of detection.8-17.8) 15.9-22. Survey years 01-02 03-04 Geometric mean (95% conf.054-.140) .124) .2) 15.120-.80-10.4) 21.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.8 (9.5-15.058) < LOD .102 (.4) 539 456 484 487 980 885 Limits of detection (LOD.5) 15.8-24.054-.083-.6) 19.093) .6 (15.180) .40-10.30 (8.073-.138) .6 (15. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .100-.4) 95th 20.190) .075) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 79 .6 (14.088-.110-.1-18.0-25.1) 13.103 (.120 (.077-.1) 14.5 (<LOD-11.130-. 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.049-.100) .100 (.1-19.140-.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level. see Data Analysis section) for survey years 01-02 and 03-04 are 10.130) .070-.1-16.1) 15.5) 21.30 (8.110) .4) 20.090-.0 (10.150 (.50) 15.090 (.7 (14.158) .120 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 15.100-.149) .0) 19.113 (.120 (.Organochlorine Pesticides Serum Dieldrin (lipid adjusted) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0-21.10 (<LOD-16.077 (.2) 12.090-.8) 14.100) .2) 14.096-.9 (14. population from the National Health and Nutrition Examination Survey.112-.069) < LOD < LOD .9 (13.242) .109-.1) 20.70 (7.1) 10.070) . which may vary for some chemicals by year and by individual sample.

Available at URL: http://www. Patterson DG Jr. 2 Classes of Pesticides.14:95-102. Chung KL. Exp Neurol 1998. Tully DB. Chemosphere 2004. Aldrin and Dieldrin [online]. Serrano FO. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Revised Feb. 15. Song S. Jr and Laws ER.59:229-234. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. and epidemiology in the United States. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.cfsan. pp.26:701-719.150:263-271.inchem. Soto AM. Narahashi T. Cox. McIntosh LJ. David VL.atsdr. Chlorinated Hydrocarbon Insecticides. Toxicol Lett 1992. Needham LL. Frey JM. United States Geological Survey (USGS). Buckland SJ. 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. 4/21/09 Hoyer AP. PA. Smith AG. Anantharam V. Pesticides in the Nation’s Stream and Ground Water. 1989. New York. and lymphocyte sister chromatid exchange. Li AA. Available at URL: http://pubs.fda. Kanthasamy AG. 6/1/09 Ward EM. Teta MJ. 1991.cdc. Eds. Environ Health Perspect 1995.352:1816-1820. Jorgensen T.htm. Lancet 1998. Handbook of Pesticide Toxicology. Corrigan FM.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). toxicology.64-65 Spec.91(1):122-126. bioaccumulation. Available at URL: http://www. Basit A. VT. References Agency for Toxic Substances and Disease Registry (ATSDR). Grajewski B. Psychopharmacology (Berl) 1987. Food and Drug Administration (FDA). Ginsburg KS. FDA Pesticide Program Residue Monitoring 1993-2006 [online].gov/toxprofiles/ tp1. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Mann D. 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. Stehr-Green. Available at URL: http://www. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Finley B. J Toxicol Environ Health 1989. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Six high-priority organochlorine pesticides. plasma dieldrin. Mink PJ. Garrett N. Jr. Priestly BG. Rosellini RA. Environ Health Perspect 2001. International Programme on Chemical Safety (IPCS). J Toxicol Environ Health. 731-915. Patterson DG Jr. Daniel SE. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Part A 2000.103(Suppl 7):113-122. Kitzazwa M. Brock JW. Fernandez MG.html.gov/~dms/ pesrpts. Reprod Toxicol 2000. 1992-2001. Inc. Carlson JN. Cancer Epidemiol Biomarkers Prev 2000.47:1059-1087. Grandjean P. Hartvig HB. Mumtaz MM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ellis H. 4/21/09 Jorgenson JL.27:405-421.54:1431-1443. Edwards JW. 2007 [online]. August 2008. Sonnenschein C. are nonestrogenic in transfected HeLa cells. September 2002. Schulte P. et al. Neurotoxicol 2005. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Sanchez-Ramos J.9:1357-1367. either singly or in combination. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Andersen A.gov/ circ/2005/1291/.109(Supp1):113-139. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Vol. J Occup Environ Med 2005. Environmental Health Criteria 91. Facca A.66(4):229-234.usgs. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Toxicological profile for aldrin/dieldrin [online]. In Hayes WJ. Demographic and seasonal influences on human serum pesticide residue levels. No:429-436.html. Roy ML. Int Arch Occup Environ Health 1994. Wienburg CL. 4/21/09 Bates MN.org/documents/ehc/ ehc/ehc91. Kanthasamy A. Organochlorine exposure and risk of breast cancer. Turner W. Shore RF. Chapin RE. Academic Press. et al. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Olea N.

1-51.7-56. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7 (32.5-47. 1994.8 (42.5 (33.0-25.3 (26. 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.7 (43.8 (17.8 (10.5) 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 * * * * 11.3 (20. chlordane was used to kill termites and other insects on agricultural crops.9 (15.3 (25. and in soil.2-21.6) 36..1-65.6 (9.3) 37. 2007).5) 9.7) 31.2-56.5) 10.6) 8.3) 18.4-14.74 (<LOD-10.8-32.6) 9.9 (11.4 (30. Consequently.6-45.9) 31. which may vary for some chemicals by year and by individual sample.2-28.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.5) 38.3-49.10-11.7-14.2 (36.8 (40.0-67.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 27.2 (28.1 (40.9 (21.6) 48.10-18. the technical grade product of each chemical contains 10%-20% of the other chemical.8) 18.7-39.5-38.3 (28.S.20-10.30-11.1 (15.2) 33.1) 30. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44. fish.63 (8.6 (9.4-21.3 (<LOD-19.1 (16. Until 1988.0-12.5) 37.1 (44.1 (20.0) 37.8) 27.3) 10.5 (31.3-32.7-25.0-61.7 (42. population from the National Health and Nutrition Examination Survey.2-49.9 (11.9 (29. and dairy products are the usual sources of exposure to these chemicals in the general population.7) 19.2) < LOD 11.3-24.0-13.1 (<LOD-12.9) 11.3-45.9-42.2) 34.9 (18.8-42.0) 41.1) * 11.3-43.1 (<LOD-12.6) < LOD 11.5) 44. 1994).3-45.2) 46.9) 10.8-33. 2007).1-50.6 (43. 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.10 (8.6) 23.4-51.2) 22.6 (25.3 (27.4) 18. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.5 (8.1-19.20-11. heptachlor use has been limited to treatment of fire ants near power transformers. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.9) 37.9-21.9-38.7 (<LOD-32.5-40.2-49.4) < LOD 11.5-42.9) 17.7-12.2) * 12.7 (10.1 (<LOD-12.1 (27. and 03-04 are 14.5-41.4 (<LOD-12.0) 21.6 (16.4) < LOD < LOD < LOD 23.7 (34.90 (8.7 (19.6) 20.7) 42.1) 22.5-32.7) 28.9) 39.7 (<LOD-13.9) 23.8) 52. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.4 (30.5.7-70. < LOD means less than the limit of detection.2) 36.8 (17. Fourth National Report on Human Exposure to Environmental Chemicals 81 .4) 37.9 (17.6-24.0 (16.0) 20.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.4 (10.8-20.4) 39.8-23.4 (31.37 (8.0 (32.36-11.7) 9.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12. respectively.0 (20.1) 30.8) 53. in addition to trace amounts of numerous other related compounds (ATSDR.S.5) 56.0-18.2 (37.7) 35.5) 21.69-10.1-25.1-15.8-31.9 (15.9) 23.4) 12.9-21.7 (17.5) < LOD < LOD 9.9 (26.6-24.1-25. lawns.9 (26.89-10.4) 29.6) 48.0 (<LOD-12.9) 13.5 (<LOD-12.6-53. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.3 (9.4-45. buildings.2) 37.3) 18.1) < LOD < LOD < LOD < LOD < LOD 8.5-13.1 (11.2 (21. Since 1992.9 (36.4 (22. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.6-12.8 (18.6) 11.2 (9.1) * 11.2) < LOD 11.5 (41.7 (34. see Data Analysis section) for Survey years 99-00.6) 49. Survey Geometric mean (95% conf. 10.3) 41. 57-74-9 Heptachlor CAS No.5) < LOD < LOD < LOD < LOD 13.9) 36.0-33.8-33.8 (10.6) 39.1) 16.4-40. Chlordane is not currently produced or used in the U.1) 90th 34.0 (26.2 (39. from the early 1950’s until the mid-1980’s.2 (10.Organochlorine Pesticides Chlordane CAS No.2 (41.8-61.8) 52.9) 47.20 (<LOD-11.3) 10.S.0) 75th 20.0) 31.1 (25.4) 22.8-43.3 (21.1 (17.0 (37.5-43.5 (34. 01-02.8-73.9) 11.5-65.70 (<LOD-10.6) 9.3 (11.9 (31.82-11.8) 44.8.5-44.6-18.9-40. and 7.4 (35. As a result of the manufacturing process.7) 19. Technical grade chlordane had contained 7% trans-nonachlor.5.2-26. foods high in fat such as meat.

230) .070 (<LOD-.350 (. Smith.310) .053-.130) .220 (.246-.300) .160) . chronic doses of heptachlor have produced liver enlargement and injury.260 (.310 (.320) .049 (<LOD-.200 (.290-.320 (.120-.207) .286 (.068) 75th . heptachlor.080) .230-.210-.180) .245-. 1991).130-.170) .180-.231) .148) .260-.128 (.077) . neonatal mortality.090) .300 (.070 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. Survey Geometric mean (95% conf.115 (.213) * .220-. and alterations in immune function of offspring.200-.075 (.269 (.400) .258 (.200-.450) .370 (.126) . Chlordane and heptachlor are absorbed after oral.287) .058-.064) < LOD .220-.340) .130-.170-.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 * * * * . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.108-..070) .280-.250 (.189 (.290-.258-. 1996. and the U.074-.062) < LOD . 2007. which may vary for some chemicals by year and by individual sample. Acute. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.320) .080 (.203-.130 (.290) .126 (.140-.067 (.302) .077) . Rogan.Organochlorine Pesticides (Dallaire et al.076) < LOD .070 (<LOD-.055-.077) .080 (.148-.120 (.310-.063) .270 (.065-.180) . to heptachlor.119 (. 2002.063 (.091) .050 (<LOD-.271 (.290-.066 (<LOD-. 1977b.146) .160) .170) . FDA established allowable residues of chlordane.083) .373) . 1991.330 (.070-.510) . The major metabolite of heptachlor is heptachlor epoxide.320 (.280 (.350) . IARC.380) .080) .092) .130-.360) .066-.079) . 2006).150 (.210 (.150 (.130-.160 (. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.430) .208 (. and heptachlor epoxide in foods and bottled water.240-. which is also persistent in the body (ATSDR.149 (.063 (.048-.140 (.090-.240 (..130) .136) .053-.112 (.300) .100-.310) .168-.100-.S.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. 2001.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .060 (<LOD-.133) 90th .242-. characterized by seizures and paralysis.230-. 82 Fourth National Report on Human Exposure to Environmental Chemicals .070) < LOD < LOD < LOD < LOD < LOD .286 (. Elimination of all these chemicals from the body occurs over months to years. 1981).270 (.440) .340) .057 (.370 (. 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.160) .079) < LOD < LOD < LOD .230 (.110 (<LOD-.290) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.082 (.560) .120-. 1977a.146) < LOD < LOD .430) .190-.070 (<LOD-.S.350 (.223) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.450) . Le Marchand et al.073 (.070-.140 (.320 (.150) ..120-.130 (.140 (.047 (<LOD-.083 (.260 (.370 (. OSHA has established occupational exposure criteria.066-. Takahashi et al.140) .253-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.066 (.071 (.068) .250-.100 (.240-.225 (.050-.216-.068-.069 (<LOD-.204 (.150-.090) .180-.280) .106-.057-. In laboratory animal studies.104-.190-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (.190-.104) .260 (.227) < LOD .170) .058 (.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .348) .S.270 (. and inhalation exposure.061-.063-.300) .170) .170) .140 (.070 (<LOD-.073) < LOD < LOD < LOD < LOD .240) .207 (.058-.063 (.130-.200-.056 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.320 (.115-.290 (.140-.280-.150 (. and breast milk is a major excretion route in lactating women.310) .400) .077) .063 (. EPA has established environmental criteria for chlordane and heptachlor.070-.080) . 1986).300-. population from the National Health and Nutrition Examination Survey.100 (<LOD-.315 (.280-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.189-. The U. 1986).062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .250 (.410) .. Shindell and Ulrich.057) * .230 (.130 (. dermal.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .230-.199-.280 (.087-.063) * .165-.110-. 2007).

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

6-21.90 (<LOD-9.8-24.1-29.1) 23.8) 16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 (18. and 7. 84 Fourth National Report on Human Exposure to Environmental Chemicals .6-17.6 (11.6) 13.8) 19.8 (13.1 (16. population from the National Health and Nutrition Examination Survey.8) 19.4) 18.9-29.9-16. and 03-04 are 14.0-19.8) 15.3) 27.0) 13.8) 20.6 (16.2) 20.6 (14.0-54.8 (18.5 (<LOD-21.9 (15.3) 18.8) 13.3) 18.5 (10.9-25.3-18.3) 22.2 (<LOD-62.0) 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 13.1) 13.6 (16.2) 26. Survey Geometric mean (95% conf.8-46.40) 15.4 (15.7-18.5 (11. respectively.1-15.3 (13.10-13.S.7-25.8) 13.9 (12.7-19.8 (15.4 (11.8 (13.6) 14.6.3) 16.2) 15.3) 18.20 (<LOD-9.7 (10.9-23.0 (11. < LOD means less than the limit of detection.8) 21.0-17.8 (<LOD-23.1-38. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.2-17.8-24.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.5) 19.9-29. 01-02.8-24.5) < LOD 14.7 (13.0-16.6 (8.4 (<LOD-19.50) < LOD < LOD < LOD 17.1-16.5 (11.2-27.8) 14.2 (<LOD-25.3 (<LOD-25.2) 13.6) 22.4 (<LOD-54.5.1 (19.7 (16.3) 23.2 (<LOD-16.4) 21.9) 15.8) 14.0 (15. which may vary for some chemicals by year and by individual sample.6 (<LOD-27.9) * * * 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 8.2-16.8.6 (13.6 (12. 10.8 (18.6) < LOD < LOD < LOD 27.1) 20.5 (<LOD-32.0-17.3) 10.2-27.8-23.5 (18.4 (11. see Data Analysis section) for Survey years 99-00.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.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.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.

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

1-55.2 (64.8 (26.5-36.8-67.3-39.0-38.7-77.6-54.4-18.6 (16. population from the National Health and Nutrition Examination Survey.3 (14.0) 75th 31.0 (16.2 (26.4-36.7-22.0-93.9) 14.7) 28.5) 19.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.4 (16.8-19.4) 59.1 (22.2 (36.8 (71.2) 19.1-34.6) 13.0) 40.6) 10.5) 35.7 (59.0 (19.7) 59.5 (44.0-20.9) 14.6-66.6) 60.7-20.3) 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.6-88.9 (15.2 (59.5 (13.3) 25.2) 30.6 (12.1 (10.7) 78.2 (60.0 (13.8 (12.7-35.3-57.8 (15.4 (11.2-37.6 (57.8.6 (32.8 (<LOD-20.3-50.7 (18.8-90.8-79.9-20.7-32.1) 30.6 (<LOD-14.0) 18.7) 78.5-20.5) 90th 55.1-16.0 (29.9-65.2 (7.7 (13.3) 32.1) 62.4 (28.1) 16.7) 73.5 (45.9) 51.6 (15.0-37.5 (15.1 (17.6-22.2-18.2) 20.0 (42.5.0 (13.8-21.8 (17.2) 34.4) 55.9-40.5-111) 68.9-64.5 (15.6) 34.5) 9.0-59.5) 20.7) 52.4 (45.5) 14.9 (16.9-69.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.7-160) 86.3-32.9-58.0-23.9-35.6) 25.9 (28.4 (67.6 (56.1) 14.0-93.5-17.2) 17.8 (45.4-67.5 (25.4-22.1) 78.2 (14.0 (14.3-74.4) 20.8-16.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.4-35.0-22.5) 26.9) 51. 01-02.8 (13.6-19.4) 19.1) 78.9 (51.7-17.S.7 (30.8) 51.1-34.9 (<LOD-14.2 (15.8-129) 74.3 (45.1) 17.3 (56.5-87.0-123) 74.7 (74.1-16.3) 18.5) 22.7 (59. < LOD means less than the limit of detection.2-16.3) 16.9 (19.8-110) 59.0 (42.8 (26.1-22.7-18.5) 78.2) 59.5-69.0) < LOD < LOD 8.8 (19.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.8 (49.8) 47.4 (12.0-143) 112 (68. and 03-04 are 14.0 (15.4) 48.7-38.7-23. which may vary for some chemicals by year and by individual sample.0 (15.3) 18.3-30.9-65.1) 17.0 (62.8-77.7 (16.7 (11.2 (14.5) 48.2-21.1) 18.9-89.8 (28.0) 13.7) 17.3) 30.3 (17.5) 14.5) 36.0) 19.7-34.7) 35.8 (28.2-18.0 (48.2-17.1) 17.8 (26. and 7. see Data Analysis section) for Survey years 99-00.7) 14.2) 39.8 (13.2) < LOD 10.10 (<LOD-11.9-45.9 (47.3 (58.3) 30.3 (14.8 (42.0-23.1-18.1-51.4 (30.1) 17.4-23.0) 49.4) 16.6 (50.9-36.6-82. respectively.9 (51.4-62.8 (16.1 (65.7 (28.6) 84. interval) 18.8) 80.0-113) 68.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3-58.1 (47.0) 33.6) 56.1) 32. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-22.9) < LOD < LOD < LOD 20.7) 15.0-68.7-21.3) 36.8 (28.5-19.8-90.3-86.70 (<LOD-12.8 (30.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.9 (36.5) 30.1) 17.6) 82.2 (19.2-88.1) 17.7-113) 68.2 (25.3 (49.8) 19.7 (35.1) 31.3) 19.1-28.8-16.3) 32.3) 15.7) 56.6) 54.2-23.9 (66.1 (41.2 (27.0 (60.0 (16.3-21.6 (56.9 (15.5-95.4) 107 (84.4-52.0-24. 10.6) 56.5) 77.9 (29.8-41.8 (11. Survey Geometric mean (95% conf.1) 18.8-19.6 (52. 86 Fourth National Report on Human Exposure to Environmental Chemicals .86-13.1-20.1 (48.5.1) 17.1-126) 67.3 (16.7-29.6-20.

090-.128 (.343 (.490-.960) .300-.125) .260) .630) .104 (.237) .450) .103 (.470 (.390) .360-.430-.250) .397-.110) .126) .108) 75th .320-.129) .120) .160-.110 (.078-.684) .085-.220) .230 (.047-.460) .091-.210-.069-.470-.680) .125 (.093-.458 (.180-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .240) .116-.096) .113) < LOD .430-.160 (.100-.111 (.106 (.461 (.242) .680 (.120-.520) .180-.800) .120) .355 (.350-.141) .540) .110 (.220 (.420) .340) .096-.220 (.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.130 (.092 (.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 .109 (.285-.400 (.100-.371) .062 (.113) .260) .288-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .120 (.150) .089 (.171-.108) .205 (.105 (.183 (.210) .520 (.327 (.190-.324 (.830) .085-.497-.090 (.630) .510 (.S.099-.400-.111-.055 (<LOD-.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .210) .651) .400) .330 (.830) .191 (. interval) .480) .095-.079-.417 (.109 (.119) < LOD < LOD < LOD .500) . which may vary for some chemicals by year and by individual sample.279-.098 (.161) .100-.130) .091) .161-.290-.600) .690) .127) < LOD < LOD .090-.320-.310-.041 (<LOD-.286-.098) .210 (.069) .103 (.110 (.370 (.310 (.580 (.080 (.410-.085-.061-.186 (.220 (.120 (.234) .220 (.087 (.120) .470-.180-.145-.116) .490 (.141) .112 (.565) .558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .120-.240-.440) .395-.250) .340-.250) .100 (.124) .122) .240) .130) .210 (.405) .158-.440-.104-.098 (.170 (.130) .093-.300) .420 (.100 (.390 (.120-.400-.211) 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.070 (.390 (.119) Selected percentiles ( 95% confidence interval) Sample 95th .071 (<LOD-.100-.108 (.130) .054-.106 (.081 (.190-.580 (.590) .395) .186-.310) .110-.114) .280) .210) .390 (.080-.470 (.078 (.409-.330-.380 (. Survey Geometric mean (95% conf.116 (.520 (.690) .317 (.550 (.110 (.559) .310-.400 (.081-.190-.240 (.135 (.094 (.099-.110 (.130) .470 (.060) .060-.460-.414 (.096-.220 (.930) .367) .068-.760 (.272-.202 (.080-.270-.490) .090-.310-. population from the National Health and Nutrition Examination Survey.097) .510-.080-.112 (.640 (.080) .340-.120) .130 (.20) .117) .080-.060 (<LOD-.220 (.092 (.630) .093) .573 (.220 (.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.330-.210 (.131) .390) .360-.490 (.130) .134) .580 (.350 (.370 (.430-.140) .177-.460) .079-.190-.190-.130) .594) .190-.093-.390 (.840) .590 (.090-.090-.090 (<LOD-.098-.150) .122) .310-.090-.210-.220 (.410-1.232) .288 (.173-.110 (.390-.240) .120 (.301-.106 (.084-.590 (.237) .082) .090) .600 (.

et al. Lawrence River (Quebec.110:617-624. Chlordane and heptachlor [online].50(3):108-118. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Jaraczewska K. National Toxicology Program (NTP). Available at URL: http://ntp. Muckle G.330:55-70. Dendle WH. 2006. 1991 pp. J Occup Med 1986. Royce W. Keller JA.150:981-990. Bioassay of heptachlor for possible carcinogenicity. Bleiweiss IJ.41:145–148. 4/21/09 James RA. Available at URL: http://ntp. 4/21/09 Baker DB.htm.org/site/foundation/ research/projects2. Willman E. Wong L.259(3):374-377. Organochlorines in Swedish women: determinants of serum concentrations.atsdr. Barker J. et al.html. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Laliberte C.org/ documents/cicads/cicads/cicad70. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Van Oostdam JC.84:151-161. Jr and Laws ER. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.gov/ntp/ htdocs/LT_rpts/tr009. Darnerud PO. Ayotte P. Jr. KalubaSkotarczak A. 1993. Organochlorine exposures and breast cancer risk in New York City women. Pollutants in breast milk. Siegel BZ. Canada). Natl Cancer Inst Carcinog Tech Rep Ser 1977a.28:497501.gov/ntp/ htdocs/LT_rpts/tr008. Bull Environ Contam Toxicol 1981:27:506-511. Gilman A. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. JAMA 1988.inchem.Summaries & Evaluations. Hertz-Picciotto I. Baker DB. Toxicological profile for heptachlor and heptachlor epoxide [online]. Sci Tot Environ 2006. Poland. May 1994. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Concise International Chemical Assessment Document 70 Heptachlor [online]. Organochloride pesticide residues in human milk in Hawaii.372:20-31. Covaci A. Takahashi W. Sci Total Environ 2004.111:349355. Shindell S and Ulrich S. 2001. gov/toxprofiles/tp12. Eds. Drews K. 1994-1997 organochlorine compounds. Chashchin V. 1979-1980.110(8):835-838. Loo S. Academic Press. Available at URL: http://www. Environ Health Perspect 2003. Environ Res 2000. 2 Classes of Pesticides. Dewailly E. Handbook of Pesticide Toxicology. Arch Environ Health. 731-915. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Circumpolar maternal blood contaminant survey. Environ Health Perspect 2002.cdc. Voorspoels S. 1986. Bioassay of chlordane for possible carcinogenicity. Available at URL: http://www. Lulek J. Brower S. Saidein D. Wolff MS. International Agency for Research on Cancer (IARC). Takei G. Hawaii Med J 1991. Mortality of workers employed in the manufacture of chlordane: an update. Dewailly E. Arch Pediatr Adolesc Med 1996. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. In Hayes WJ.gov/toxprofiles/tp31.htm. Charles MJ. et al. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Vol. Distribution of polychlorinated biphenyls. 9/25/07 International Programme in Chemical Safety (IPCS). et al.9:1-109.cdc. 79. New York. 6/1/09 National Toxicology Program (NTP). August 2007. 6/1/09 Rogan WJ. Atuma S. Environ Health Perspect 2002. Stehr-Green P. Available at URL: http://www. Toxicological profile for chlordane [online].pdf.niehs. Available at URL: http://www. Smith AG. Aune M. A Report to the Hawaii Heptachlor Research and Education Foundation. International Agency for Research on Cancer (IARC) . 1963-1967.8:1-123.inchem. Granath F. maternal serum and milk from Wielkopolska region.heptachlor.html. Glynn AW. Odland JO.html. Wohlleb JC.pdf. Bjerselius R. Vol. 4/21/09 Dallaire F. LeMarchand L. Kolonel LN. Senie R. Hansen JC. Inc.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Berkowitz GS. Head SL.atsdr. Chlorinated Hydrocarbon Insecticides. Available at URL: http://www.nih.niehs.org/documents/iarc/ vol79/79-12. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.nih. Tartter P.

2008.0 (18. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.9) 14. These chemicals are highly persistent in soil. 2002.S. 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.9 (21. which is a mixture containing p. Both Serum p.9) < LOD < LOD 9.2) 155 (59.8) 15.1 (33. Gunderson. including 1. Only a small proportion of DDT is metabolized and excreted (Smith. o.0) 20. DDT is converted to DDE and several other metabolites.9) 29.9) 17.4) < LOD 17.5-54. and trace amounts of several related compounds.10 (<LOD-12. 17.3-590) 293 (104-541) 48. although DDT and DDE intakes have decreased over time (FDA.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. The biodegradation half-life of DDT in soil varies from 2 to 15 years. and water. 1988). DDT usually refers to the technical product.9 (10.0-53. 1991). fish. and dairy products.S.4.7.2-95.1’-(2.1 (23.5-36. Smith.1) 31. depending on conditions. 1991). population.6 (31. resulting in fetal exposure.4) < LOD < LOD < LOD 61. DDT is converted in the environment to other more stable chemical forms. Survey Geometric mean (95% conf. In the general U. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.1’-dichloro-(2.3 (<LOD-21. Food imported from countries that still use DDT may contain the chemical or its residues.5) < LOD < LOD 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9 (10.8-17.3 (<LOD-31.5 (15.8-39.S.8-26.3-16. DDT can be absorbed after ingestion.7) 12.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11. In the body. < LOD means less than the limit of detection.7 (19. 01-02.0 (21. as well as in plant and animal tissues.0-35.3) 21.1 (<LOD-39. inhalation.2-65.5 (23.8-23.1-27.8) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8. DDT was used at one time as a treatment for head and body lice. particularly meat.00 (<LOD-10. Fourth National Report on Human Exposure to Environmental Chemicals 89 .6 (25.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00.3-236) 24.0 (10. It was produced and used in the U.0) 26.0 (18.0-15.2-bis(p-chlorophenyl) ethane (DDD).9 (10.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.p’-DDD (4% or less). and 7.8.9 (<LOD-20.5) 23.8) 30.0-155) 83. It is still used in some countries.3) 28.10-13.3) 21. particularly for endemic vector and malaria control.3) 22.50-11.9-34.8) 36.5 (14.5) 25.7-16. p.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 12.9-28.p’-DDT (15%-21%). or dermal exposure. food.2) 30.6 (9.70 (8. after World War II until 1972.90 (<LOD-12.7) < LOD 18.0) 19.2 (11.0) 40.7 (15.1-71.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.6 (<LOD-25. sediments.2) < LOD < LOD 9.4 (23. and 03-04 are 20. population from the National Health and Nutrition Examination Survey. respectively. air.0-27.p’-DDT (65%-80%). DDT and DDE can cross the placenta.6 (22.2 (<LOD-40.3 (27.7) 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. when virtually all use of it was banned.5 (23.6-33. continues to be the primary source of DDT exposure.0-37.

106-.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..p’-DDE can produce anti-androgenic effects (Gray et al. In high dose.106) < LOD < LOD .048 (<LOD-. lung cancer..064 (.220) .400 (.230) . fertility.098-.189-.62 (.132-.146 (.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 .260) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.230) .074-.130 (<LOD-. other organochlorines.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 . In laboratory animals.084 (..p’-DDD and p.g.00) .220) . Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. overt signs of acute human toxicity include vomiting.180) .120 (<LOD-.01) .150 (<LOD-. and o. which may vary for some chemicals by year and by individual sample.170-.160-.200 (. and altered behavior after neonatal exposure (Eriksson and Talts. Animal studies reported reduced fertility.201 (. 2001).063 (<LOD-.087 (. A workplace standard for DDT has been established by Serum p.. Calle et al. 2002. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.170) .00 (. Mariussen and Fonnum. 2006).Organochlorine Pesticides chemicals are excreted in breast milk. 2006.34) .170 (. Jusko et al..105-. 2001). Gladen and Rogan.. 2006. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 2001). reproductive organ abnormalities.130-.078-. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.086 (. tremor.180-..130 (<LOD-.068-. and seizures. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.150 (<LOD-.400) .106) .240 (.. 2006).143) < LOD < LOD .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 .190-1.190 (.146 (.061) < LOD < LOD < LOD . 2006).142 (.140) .071-.051 (<LOD-. 90 Fourth National Report on Human Exposure to Environmental Chemicals .240) . Gray et al. Jusko et al.313 (.128 (. 2001). Snedeker. and leukemia have also been inconclusive (ADSDR.290) .250-1. premature delivery.250 (.570-4.150) .112 (.180 (.120-.054-.627) . 2002. Beard.150-.065-.150-.343) < LOD ... population from the National Health and Nutrition Examination Survey.095) < LOD .203) . 2006. Survey Geometric mean (95% conf.108 (. accidental exposures. and duration of lactation.530 (. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. 1956).140-. polychlorinated biphenyls.075) 1. resulting in exposure to nursing infants (Rogan.180) . Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR. Reproductive effects in humans affecting birth weight.S. 1996).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. 1997).059-. Studies of DDT exposure and pancreatic cancer. 2002.079) < LOD < LOD .071 (. Hayes et al. 2002. 1995.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . dioxins and furans).26) 1.078 (.180 (.530) .330-4. Longnecker et al.420) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .080-.130 (<LOD-.114-..069) . DDT may bind to estrogen receptors (Chen et al. 2000. 2004. 1998).190 (. have not been consistently demonstrated (Beard.

Biomonitoring Information DDE persists in the body longer than DDT. environmental levels) and health effects is available from the U. Heudorf et al. More information about external exposure (i.8. 1989).7-119) 113 (100-140) 93. 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.. 8. population from the National Health and Nutrition Examination Survey.p’-DDT) as a possible human carcinogen. respectively. 2002. for males and females in the NHANES 19992000 subsample (Pavuk et al.cdc.3. 2003. In general. 01-02. 1998.6 (81.. see Data Analysis section) for Survey years 99-00. IARC classifies DDT (p.atsdr.. respectively. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. Since the 1970’s.e. Fourth National Report on Human Exposure to Environmental Chemicals 91 . Survey Geometric mean (95% conf. Compared to females in the NHANES 1999-2000 subsample. mean serum levels of DDT and DDE in the U.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.S. NTP considers DDT as being reasonably anticipated to be a human carcinogen. Declining DDE levels over time have also been observed in the German population.gov/ toxpro2. 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. Smith.Organochlorine Pesticides OSHA and a guidance established by ACGIH. 1991).0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD.S. 2004).html. Stehr-Green. population declined by about fivefold to tenfold.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. In a population-based sample of men and women from eastern Slovakia. 2003). and 03-04 are 18. 2002.. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person...6. 2004). Link et al. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. compared to levels observed in this Report (Anderson et al.S. 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. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.gov/ pestcides/ and from ATSDR at: http://www. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.epa. and 7... 2005).

53 (2.8 (14. serum levels of o.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.3 (8.72) 1. 1989).51 (1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.3 (9.26) 3.39) 1.11-1.31-12. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al. 2004).26-10.90) 22.92) 1.860 ng/L) and DDE (about 14.61-2.17-3.6) 8.p’-DDT were below the limits of detection.06) 3.97 (3.78 (4.21) 3. interval) 1.6) 9.65 (1.26-2.92 (3.8 (13.66-4.80 (2.03-4.32-1.64-2.680-1.385-.21) 90th 7.34-3.18 (6.66) 1.1) 12.05 (3.18) 1.600) .48 (6.36) 3.63 (1.69 (1. o.59 (4.13-2.611-1.52 (1.02) 1.57-2.52 (3.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.84-3.58) 1.24-17.870 (.11 (2.75) 1. In the NHANES 1999-2000.34-11.9) 5.59) 6.17 (3.49 (1. less than one percent had detectable serum levels of o.51-8.01) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.46 (1.63 (1. High mean levels of whole blood DDT (about 3.58) 75th 3.557) 1.16 (2.Organochlorine Pesticides nearby agriculture (Botella et al.25-14.25) 1.6) 9.26 (1.14 (1.10) 2.51-15.19-14.70-3.53-15.81 (7.75) 6.9) 7.590 (.96) .72) 1.52-6.9 (26. Serum p.91-2.963-1.66-17.13) 4.2 (9.96) 1.p’-DDT.488-.12-1.82 (1.36-11.30-1.1) 40.35) 1.90-8.32-9.22) .32 (1.0) 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 .14) 2.32-1.0 (12.9-38.69) 4.15-4. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.40 (3.18-1.p’-DDT (Stehr-Green.80) 1.24 (1.516 (.2 (9.68) 2.77 (1.60-13.4 (8.30 (1.37 (1.1 (8.07) 1.30-1.48-4.68 (2.6) 9.24) 1.87-16.71 (5.7-20.80) 1.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .2-32.61 (1..85-10.88-35.57 (1.2) 26.18-4. 309 versus 268 ng/g lipid.7) 16.16-1.39-2.51-49.0 (9.28) 1.49 (1.75 (8.38 (1.43-4.3-43.01-1.02 (2.64) 3.49) 8.85-4.1 (9.76 (2.18-3.04 (6.69 (2.91-3.79) 4.34) 6.2) 19.32) 1.3) 13.4 (12.81-5.14) 2..59) 3.890-1.6) 11.69 (.4) 9.5) 5.70) 1.6) 9.561 (.83 (1.07 (5.6 (17.37-10.81) 11.7-48.10-1.57) 2.66) 4.6) 12.65) 1.63 (6.02-8.5) 16.796 (.71) 32.30 (1.87 (5.00-1.34 (7.2 (19.4-19.4) 14.57 (1.39-1. 2004).01-11.3) 10.01-11.456 (.41-12.14-1.29 (1.56-6.7) 13.56-3.56) 2.57-3.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.2 (6.49 (6. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.63-15.7) 9.58) 1.25 (.66-2.85 (1.6 (8.59 (1.39 (3.37-16.54) 8.S.77 (1.40-4.23 (7.47 (1.38 (1.04-1.27-1.p’-DDT.1) 7.06) 1.00 (.47) 3.44) 1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.80) 3.01-5.25-16.34) 2.81-18.25) 8. 2001-2002 and 2003-2004 subsamples.9-17.726) ..36 (3. considerably higher than levels in this Report (Smith.43 (5.22 (7.18-1.6 (9. 2005).76) 1.97-4.25 (1. Finding a measurable amount of p.91 (6.7-19.84 (3.92 (3.82) 1.09-1.0) 2.66) 3. Survey Geometric mean (95% conf.46 (1.88 (2.22-1.8 (9.7 (8.534-.5) 22.07) 1.50 (2.71 (6. population from the National Health and Nutrition Examination Survey.623 (.57 (3.6) 13.46-2.00 (6.43-4.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al..50-17.66) 1.9 (15.62-6.419-.10) .43-8.994-2.51) 3.520 (. 1971).635) 1.59 (1.03-1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.76-3.8 (13.75 (4.01-1.5) 10.75) 2.8) 15.430-.01) 1.99) 1.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.45 (1.53) 1. 1991).646) .14-9.37-4.19) 4.91) 3.500-.05) 1.54-7. or p.36-1.36-2.55-9.40-4.51) 1.31 (1.40-8. 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.37-1.69) 8.41 (1.8-90.33-1.6 (7.3) 16.32 (1.93 (7.4) 13.55 (2.45 (1.10-5.54 (1.57-13.68-4.56-2.13 (1.31-2.5) 7.00) 7.965-1.53) 7.12 (6.81 (1.76) 1. In a subsample of NHANES II (19761980) participants.12 (.01-15.820-1.20 (.27) 3.730) .71) 12.

respectively. 01-02. and 7.4.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.S.8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 93 . 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. which may vary for some chemicals by year and by individual sample. 17. see Data Analysis section) for Survey years 99-00. Survey Geometric mean (95% conf.Organochlorine Pesticides Serum o. population from the National Health and Nutrition Examination Survey. and 03-04 are 20.

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

155(4):313-322. Paepke O. Profiles of ortho-polychlorinated biphenyl congeners. Lambright C. and other chemicals. Heudorf U. 4/21/09 Gladen BC. Buckland SJ. Jr.html. et al.cdc.17(6):692-700. Katz SH. Jusko TA. Lancet 2001.21(1-2)37-48. Hurd C. Levels of DDT. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Gladen BC. Environ Health Perspect 2004. Talts U.72:261265. Falk C. Needham LL.52:301-309. April 1982 to 1984. Biomonitoring of persistent organochlorine pesticides. Savitz DA. Glynn AW.1-dichloro2. Frumkin H. Ellis H. Beard J. Am J Epidemiol 2002. Barr DB. Kaus S. Baker RJ. Bull Environ Contam Toxicol 2004. hexachlorobenzene. Willman EJ. The effect of known repeated oral doses of chlorophenothane (DDT) in man.cfsan. Effects of environmental antiandrogens on reproductive development in experimental animals. Epidemiology 2006. Bates MN.atsdr. J Assoc Off Anal Chem 1988. Olea N. Furr J. selected elements. dietary intakes of pesticides. Crespo J. DDT and human health. Saiyed HN. The Great Lakes Consortium.html. Hanrahan L. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Patterson DG Jr. Olson J. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT).96:34-40. Notides AC. hypospadias.111:349355. Parks L. Needham LL. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Greenfield TA. Hum Reprod Updat 2001. and DDD [online]. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.7(3):248-264. Cerrillo I. Biochem Pharmacol 1997. Gray KA. Environ Health Perspect 2003. Brock JW. and dichloro(diphenyl)ethylene (DDE). Maternal serum level of 1. Arnold SF.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. 4/21/09 Anderson HA. CA Cancer J Clin 2002. Zaidi SS. Brock JW. Rivas A. Piechotowski I. Chen CW. Granath F. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Available at URL: http://www. et al. Organochlorines and breast cancer risk. Garrett N. Atuma S.355:7889. Zoellner I. Wolf CJ.53(8):1161-1172. et al. Thun MJ. et al.358:110-114. Jr. et al. Kashyap R. India. Gunderson EL. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings.fda.112(17):1761-1767. Charles MJ. September 2002. Neurotoxicol 2000. Aune M. Olson JR. Zhou H. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Longnecker MP. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Chemosphere 2004. Burse VW. Swanson MK. Bloom MS. Cueto C. Seiwert M. FDA total diet study.54:1431-1443. Schulz C. DDE and shortened duration of lactation in a northern Mexican town. Needham LL. Botella B. Available at URL: http://www. Bjerselius R. Longnecker MP.58:1185-1201. Link B. Hediger ML. Becker K. Zhou H. Darnerud PO. JAMA 1956. Exposure of women to organochlorine pesticides in Southern Spain. Calle EE. Bhatnagar VK. DDE..206:485-491.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). August 2008. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.106(5):279-289. Int J Hyg Environ Health 2003.85:504508. and HCB residues in human blood in Ahmedabad. Chemosphere 2005. Organochlorines in Swedish women: determinants of serum concentrations. Krause C. Olea-Serrano MF. Rogan WJ. Maternal DDT exposures in relation to fetal and 5-year growth. et al. Eriksson P. Henley SJ. Herrman T. Environ Health Perspect 1998. Lepom P. Kulkarni PK. Davis MD.gov/~dms/ pesrpts. dichlorodiphenyldichloroethylene. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Koepsell TD. Gray LE Jr.71(6):1200-1209. et al.162:890-897. Hayes WJ.gov/ toxprofiles/tp35. Klebanoff MA. Vena JE. Am J Public Health 1995.97(2):178192. Environ Res 2005. and polythelia among male offspring. HCH. Klebanoff MA. Ostby J. Moysich KB. Sci Tot Environ 2006. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Drexler H. Angerer J. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. et al. Klebanoff MA. Durham WF. Toxicological profile for DDT. lindane (g-HCH).205:297-308. Vorojeikina DP. Gabrio T. Food and Drug Administration (FDA). Int J Hyg Environ Health 2002. Environ Res 2004. et al.

Chemosphere 2004. Comparative pharmacodynamics of CYP2B induction by DDT. Jr and Laws ER. J Toxicol Environ Health Part A 1998. Snedeker SM.20(2):186-193. Jones CR. PA. Astolfi E. and dieldrin. Vol.27:405-421. Pesticides and breast cancer risk: a review of DDT. Rogan WJ. J Toxicol Environ Health 1989. Pavuk M. Cerhan JR. Handbook of Pesticide Toxicology. Stehr-Green. Lubet R. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Jr. Deichmann WB. Toxicol Appl Pharmacol 1971. DDE. Chovancova J. Academic Press. and DDD in male rat liver and cultured rat hepatocytes.150:981-990. Arch Pediatr Adolesc Med 1996. Thomas PE. Schecter A. Lynch CF. Radomski JL. In Hayes WJ. Chlorinated Hydrocarbon Insecticides. DDE. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Reddy AB.36:253-589. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Petrik J.Organochlorine Pesticides Mariussen E. Pollutants in breast milk. Inc. Environ Health Perspect 2001. New York. Smith AG. Nims R. Fonnum F. et al. Demographic and seasonal influences on human serum pesticide residue levels. et al.109:35-47.54:1509-520. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Eds. Crit Rev Toxicol 2006. Fox S. children and newborn infants.53:455-477. Rey AA. 2 Classes of Pesticides. 1991 pp. 731-915.

S. 1979. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. Endrin was used as an insecticide. An epidemic of acute endrin poisoning. All uses of the pesticide in the U.40-5.50) < LOD 5.8.30 (<LOD-6. unlike aldrin and dieldrin. Smith. Because it is metabolized so rapidly. Endrin has been detected in soils. inhalation or dermal exposure routes. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.S.50) < LOD < LOD < LOD 5. Kavlock et al. Endrin was not widely used as a termiticide. which may vary for some chemicals by year and by individual sample. 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.S. manufactured.20 (<LOD-5. 72-20-8 General Information Endrin. Fourth National Report on Human Exposure to Environmental Chemicals 97 ..S. a stereoisomer of dieldrin. Endrin does not accumulate in body tissues (IPCS.40 (<LOD-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. 1991). see Data Analysis section) for Survey years 01-02 and 03-04 are 5. In the body. or discarded. 1981). and occasionally at low levels in sediment and surface waters. Endrin is absorbed rapidly after ingestion. or from contact with contaminated soils and sediments in areas where endrin was applied. 1992). unless the dose is high and the exposure is very recent.09 and 7.10 (<LOD-5. and inflammation (Smith. 2008). endrin usually is not detected in serum of exposed individuals. 1992. fatty infiltration.Organochlorine Pesticides Endrin CAS No. endrin can persist for years. Hepatic effects of endrin exposure have included necrosis. At high doses. Ketoendrin is a major photodegradation product (IPCS. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.10 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1992).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. Depending on soil conditions. endrin has been detected with declining frequency in U. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Survey Geometric mean (95% conf. have been cancelled by the U. EPA.. is no longer manufactured in the U. 1992)..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. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. 1991). General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used..20 (<LOD-5. anti-12hydroxyendrin. 1996. rodenticide and avicide. Over time. IPCS. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.30) < LOD 5. endrin is converted rapidly to its major metabolite.S. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. 1987).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 5.60 (5. < LOD means less than the limit of detection. total diet surveys (FDA.

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

In Hayes WJ. Gray JA. Rogers E. Rivas A. Kavlock RJ. Ward EM. pp. 4/21/09 Kavlock RJ. Fetotoxic effects of prenatal exposure in hamsters.54:1431-1443. Liddle J. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Rab MA. Gray LE. 731-915. Toxicological profile for endrin [online]. Jr. Grajewski B.atsdr. Perinatal toxicity of endrin in rodents. Toxicology 1981. Buckland SJ.htm. Burse VW. Botella B. Frey JM. Olea N. et al. Available at URL: http://www. Schulte P. II. Chernoff H. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Gray LE. Ellis H.13:155-165. Handbook of Pesticide Toxicology. Narahashi T. August 1996.79(6):928-934. Andersen A. Pediatrics 1987. Garrett N. Inc. Chernoff N. Hanisch RC.21:141-150. Chemosphere 2004.gov/toxprofiles/tp89. Rowley DL. 2 Classes of Pesticides. Available at URL: http://www. Patterson DG Jr. I.gov/~dms/ pesrpts. Needham LL.html. et al. August 2008.org/documents/ehc/ehc/ ehc130. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Toxicology 1979. Perinatal toxicity of endrin in rodents. Chlorinated Hydrocarbon Insecticides. Cerrillo I. Convulsions caused by endrin poisoning in Pakistan. Academic Press.96:34-40. Hardjotanojo W. 1992. Ginsburg KS. Sokal D. Turner W. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Environmental Health Criteria 130.cdc. No:429-436. et al. 4/21/09 International Programme on Chemical Safety (IPCS). Fourth National Report on Human Exposure to Environmental Chemicals 99 . Cancer Epidemiol Biomarkers Prev 2000. Patterson DG Jr. 4/21/09 Bates MN.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Olea-Serrano MF. Food and Drug Administration (FDA). Exposure of women to organochlorine pesticides in Southern Spain.fda. Environ Res 2004. Crespo J. Gray J.cfsan.64-65 Spec. Endrin [online]. Hanisch RC. Smith AG. Vol.9:1357-136. et al.inchem. Toxicol Lett 1992. Whitehouse DA. Roy ML. Available at URL: http://www. 1991. Saleem M. Jr and Laws ER.html. Fetotoxic effects of prenatal exposure in rats and mice. New York. Eds.

.4) < LOD < LOD 23. 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. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.0) * * 15.4) < LOD < LOD 14.3) < LOD < LOD 20.3 (14. and foods with a high fat content.4) < LOD < LOD 33. primarily as a fungicide and seed treatment until the U. see Data Analysis section) for Survey years 99-00. breast milk is an additional route of elimination in nursing women. and 03-04 are 118.S.1 (17.8 (15.2 (17.3 (12.6) < LOD < LOD 26.4 (18.1 (13.5-trichlorophenol (2.5-14.7-21.0-16. HCB is slowly metabolized. water.5-15.6-32.5 (13.4) < LOD < LOD 18.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.9) < LOD < LOD 15.1 (14.3-22. respectively.9-24.3 (22.3 (22.2 (13.0.4 (22.2 (24.7-16.7 (15.4) < LOD < LOD 22. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.4 (11.2 (14.0 (25.2 (14.. 1988).9 (25.6 (21.5-33.0 (18. or game taken from areas with HCB contamination.6 (23.3-26.3 (16.7-22. 1997). 31.3 (20.7-30. 2008. 01-02.7 (19.Organochlorine Pesticides Hexachlorobenzene CAS No.S.1-20.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.0) < LOD < LOD 15. 1976).6-TCP) (To-Figueras et al.0-25.2) < LOD < LOD 29.6-trichlorophenol (2.4.7-16.5-15.S.0) < LOD < LOD 24.1) * * 15. and sediment (Barber et al. and 7. Survey Geometric mean (95% conf. Urinary metabolites include pentachlorophenol (PCP). The FDA dietary surveys have shown that over time.1) < LOD < LOD 15.0 (18.9 (25. and accumulates in fatty tissues where it persists for years. wildfowl. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.7-26.7) * * 14.6-33.5-14.9-32.0 (14.. and elimination occurs by renal and fecal routes. 2002). HCB is well absorbed after oral administration.3) 24.2) < LOD < LOD 13. which may vary for some chemicals by year and by individual sample. 100 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection.8 (22. particularly by consuming fish.8) < LOD < LOD 27.1-16. HCB has been detected in fewer foods since the 1980s (FDA.0-28.4. distributes widely throughout the body. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.7 (27.9 (14.5) < LOD < LOD 18.3) < LOD < LOD 29.4) < LOD < LOD 19.9-30. 2.4.9 (23.1 (14.6) < LOD < LOD 26.7) < LOD < LOD 24.6) < LOD < LOD 25. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.2-15.4.5 (13.8-15. air.4 (18.8.9) < LOD < LOD 20.5 (14.2-15.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. The general population may be exposed to HCB through diet.8 (26.6) < LOD < LOD 24. Therefore.4-15.0) < LOD < LOD 15. Gunderson.4.9) < LOD < LOD 16.7 (15. EPA cancelled its use in 1984.9-15.3-20. 2005). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28..6 (24.9-17.4-16.2-31.9-20.7-15.9) < LOD < LOD 20.6) < LOD < LOD 14.S.9) < LOD < LOD 28.5-18.7-29.9) < LOD < LOD 19.6-19.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3) * * 15.6-26. Although it is not manufactured as an end-product in the U.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.6-44.0-19.5-TCP) and 2.9) 19. and has been detected in soil. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. population from the National Health and Nutrition Examination Survey.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.

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 * * .118) < LOD < LOD .099) < LOD < LOD .155) < LOD < LOD . Survey Geometric mean (95% conf.118-. population from the National Health and Nutrition Examination Survey.097) .088-.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 * * .107) < LOD < LOD . 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. thyromegaly.097) < LOD < LOD .152) < LOD < LOD .099) < LOD < LOD .167 (. immunologic abnormalities.102) < LOD < LOD .104 (.111-.156 (. ACGIH has developed workplace exposure limits for HCB.145-.081-.175) < LOD < LOD .135-.125 (.140 (.115 (.141) < LOD < LOD .060-.088-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans. environmental levels) and health effects is available from the U.126) .092 (.065 (. arthritis. as well as hypertrichosis.cdc. In humans.218) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.203) < LOD < LOD .S.143-. Schmid.171 (.102 (.114-.148-. Chronic feeding studies in animals have demonstrated kidney injury.129) < LOD < LOD .099) < LOD < LOD . EPA at: http://www.109) * * . Infants were exposed transplacentally and through breast milk.107-.097 (.163) < LOD < LOD .094 (.088-.091-.gov/pesticides/ and from ATSDR at: http://www.203) < LOD < LOD . reproductive and developmental toxicities.157-.078 (.073-.092 (.123 (. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.072-.092-.090 (..095-. anorexia.081 (.182 (.epa. 1960). and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.069) < LOD < LOD . which may vary for some chemicals by year and by individual sample. HCB interferes with normal heme synthesis.083) < LOD < LOD . This condition. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.094) < LOD < LOD .e.169-.086) < LOD < LOD .258) < LOD < LOD .089-. and liver and thyroid cancers (ATSDR.176) < LOD < LOD .114-.145-. and many died before 2 years of age (Peters et al.098 (. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.085) * * .086-.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . 2002). With chronic exposure.163-. 1982.090 (.062-.064 (.090 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 .atsdr.113-.gov/toxpro2. and weakness.100) < LOD < LOD .111) < LOD < LOD .079 (.086-.089-.130) < LOD < LOD .127-.163 (. 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.147 (.Organochlorine Pesticides chemical.157 (.090-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD . very high. Biomonitoring Information Serum concentrations reflect the body burden of HCB.225 (. acute doses produce central nervous system depression and seizures.173) < LOD < LOD .123 (.123 (.186 (. and the FDA has established a bottled water standard for HCB.095 (.118-.176-.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .S.095) * * .160 (.087 (. The U.122) < LOD < LOD .159-.html.082-.120 (.092 (. More information about external exposure (i.121 (.S.174-.077-.132) < LOD < LOD .085-..190 (.196) < LOD < LOD .095 (.069) * * .179 (. EPA has established a drinking water standard.178-.191 (.095) < LOD < LOD 75th < LOD < LOD 90th * * .147-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Over the past two decades. Holland NT.gov/~dms/ pesrpts..349:144.71(6):1200-1209. Bradman et al.111:349355. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Schulz C. Bertram HP.. Schwartz JM. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.. Biol Neonate 2002. Canada). Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Available at URL: http://www. trends and processes. Lackman. Muller C. The metabolism of higher chlorinated benzene isomers. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Bryan GT. 2002. only 4.54(3):203-208. 2002). Darnerud PO. Sweetman AJ. 2005). Lackmann GM.. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Aune M. Arch Neurol 1982.205:297-308.gov/ toxprofiles/tp90. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Dallaire F.77:173182. Herrman T. Jones KC.9% of participants had quantifiable levels (Stehr-Green. 4/21/09 Barber JL. 2005.html. Can J Biochem 1976. Muckle G. Jones D. As a result of the lower limit of detection in NHANES 2003-2004. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. et al. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Lackmann. Gocmen A. September 2002. selected elements. but overall. Available at URL: http://www. In the 1976-1980 NHANES subsample.. Eskenazi B. Gunderson EL.cfsan.. Chemosphere 2005. Lawrence River (Quebec.atsdr. Bertram et al. Lepom P. Fenster L. 4/21/09 Glynn AW. and the geometric mean concentration of HCB in whole blood was 0. distribution. Lecha M. 1986. Ayotte P. In Spain. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.17:388–399. Kemper FH.81(2):82-85. 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. Reference values updated. more HCB levels were quantified. August 2008. Hexachlorobenzene in the global environment: emissions. 2003). 2006).58:1185-1201. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. van Wijk D. et al. Atuma S. 1989).fda. Link et al. Becker K. Arch Dermatol 1999.110(8):835-838. Organochlorines in Swedish women: determinants of serum concentrations. Sala M. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. 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.. Dogramaci I. Toxicological profile for hexachlorobenzene update [online]. Santiago-Silva M. Int J Hyg Environ Health 2002. et al.. 2002. 2002.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. and other chemicals.. Paepke O. HCB detection in serum also was proportional to age. levels. Environ Health Perspect 2003. respectively. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. April 1982 to 1984. Granath F. Peters HA. IARC Sci Publ 1986. 2005). Sci Tot Environ 2005.44 mg/L. Laliberte C. J Exp Sci Environ Epidemiol 2007. Food and Drug Administration (FDA).cdc.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Barr DB. Seiwert M. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Biomonitoring of persistent organochlorine pesticides.39(12):744-749. FDA total diet study. Krause C. Kohli J. Dewailly E. Bjerselius R. Gabrio T. Bradman A. Kaus S. Otero R.135(4):400404. HCB levels were directly related to age. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. 2002) and among children (Link et al. 2002. Safe A. Piechotowski I. Cripps DJ.html. Herrero C. In a representative sample of the 1998 German adult population. J Assoc Off Anal Chem 1988. dietary intakes of pesticides. Zoellner I. Glynn et al. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Ozalla D. Link B. Environ Health Perspect 2002. however. 1999). References Agency for Toxic Substances and Disease Registry (ATSDR).

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

2 (9.20-16. Technical grade HCH is a mixture of all four isomers.2-87.9-51.9) 45. 104 Fourth National Report on Human Exposure to Environmental Chemicals .4 (11.7) 32.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.Organochlorine Pesticides Hexachlorocyclohexane CAS No.9 (50.4 (12.1-32. including alpha. 01-02.0) 7. so they can accumulate in fatty tissues of animals. However.6-37.0-20.1 (11.7) 56.0 (33.1 (12.1-32.70-12.6) 35.7 (25.S.8 (64.8.0-70.7) 10.76.8) 27.87 (9. In 2006.6 (33.4) 10. < LOD means less than the limit of detection.5) 22.4) 901 1067 952 992 1224 1007 Females 11.5-29.8) 12.9 (32.0) 17.4 (8.5528.1) 12.1-16.4) < LOD 9.7 (53.1-37.3) 34.2) 62.2 (50.2-20.0-23.8 (32. The other isomers can be formed during the synthesis of lindane. environmental levels declined.7) 97. EPA cancelled agricultural uses of lindane (ATSDR.7) 27.1-49.3) 51.1) 13.9-21.66-12.0-21.4 (52.6) 653 758 589 1240 1533 1370 20 years and older 10. 58-89-9 General Information Hexachlorocyclohexane (HCH).2) 36.3) 14.0-70.6) 18.4-111) 84.1) 31.7 (35. and 7.1 (9.0) 71.8) < LOD 10. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.6-89.8) 7.50) 8.3 (13.2 (48.7-96.8) * * * * * * 15.4-45.5 (43.1) 71.90-8. commonly known as lindane. population from the National Health and Nutrition Examination Survey.1-27.04-10.6 (10.1 (21.5) 14.4) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9 (9.1 (16.5) 67. respectively.8-54. particularly alpha and gamma have been detected widely in air.6) 47.9 (11.2-55.9-56. formerly referred to as benzene hexachloride.8-16.4 (50.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.2 (29.0 (14.1) 12. 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. and sediment as a result of historic production and use.5) 16. 608-73-1 beta-Hexachlorocyclohexane CAS No.0 (35.5 (37. water.8 (10. soil.5) 40. each result has been multiplied by 1.70 (8.7) 18.2-42.80 (<LOD-14.89 (<LOD-9.0) 8.7) 73.90) 7.8) 95th 68.9 (62. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.1-36.3) 37.7-69.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.4) 21.3) 25.3 (62.2-17.9 (40.46-11.5) 11.9) 15.4-50.9-24.3 (42. and have been used either as fungicides or to synthesize other chemicals.2) 142 (99.6) 50.7 (<LOD-16.7 (62.6 (40. interval) 9. see Data Analysis section) for survey years 99-00.5 (16.8 (21.5 (8.7) 23.2 (18. exists in several isomeric forms.S.90-8.4) 51.6 (17.0 (37.8) 52.8 (23.60-13.5) 29.7-96.36.1 (27.8-199) 134 (85. As pesticide applications of HCH were increasingly restricted or eliminated.4-73.2-67.8-87. 319-85-7 gamma-Hexachlorocyclohexane CAS No.80 (6.7-166) 70.8 (9.8-68.5 (14. containing about 64% alpha and 10%-15% gamma isomers. beta.9-81.6-14.2) 13. Lindane has a half-life of about two weeks in soils and water.68 (<LOD-10.6) 16.6-62.9 (26.8 (33.2-22.6-135) 69.0-34.0 (19.9-178) 48.6-47.9 (30.0 (8. 2005).7-69.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.9-14.6) 36.6 (16. **In survey period 2001-2002.4) 11.7 (13.1-15.5 (11.7 (30.3 (26.5-123) 49.0) 35. The gamma isomer.4 (16.8) 39.5) 90th 42.6-20.4) < LOD < LOD < LOD 46.3 (42.6 (22.4) 27.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.3-38.8 (17.7 (29.3-56. See the section “What’s New” at the beginning of this Report for details.7-26.61-12.1 (9. and delta. HCH isomers.S.3-85.7-20. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice. HCH isomers are lipophilic.0-111) 70.0) 41. gamma.5 (24.70-19.9) 81.0 (<LOD-12.2) 9.6-42.1 (30.6-18.2-46.2 (31.56-12.7) 10.4) 44. which may vary for some chemicals by year and by individual sample.2-98. It is no longer produced or sold in the U.2-52.1 (18.30-11.43 (<LOD-9.70 (6. the U. 6. 2005). and 03-04 are 9. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.9) 17.8-19.2 (34.

210 (.131-.070-.470) .254) 95th . Distribution is mainly to fatty tissues.050-.200-. The U.120-.442 (.100-.250 (.250 (.120 (.340) .090-.350) ..150 (.280-.062 (.380 (.410 (.180-.080-. 1971. Gunderson 1988).620) .390 (.191-. probably by blocking inhibitory neurotransmitters in the central nervous system.100-.350 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .120-.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 . OSHA and ACGIH have established workplace standards and guidelines.240-.160-. for lindane.150) .210 (.580-1. **In survey period 2001-2002.280-.S.070-.040-.067) .080) .700) .661) 901 1067 952 992 1224 1007 Females .167 (.297-.S.051-.070-.360 (.450 (.250-.065 (.050 (<LOD-.300-.050 (.120 (.910 (.080-.250) . 1986).051 (<LOD-.320 (. which may vary for some chemicals by year and by individual sample.083 (.460 (.050) .420-.050-. and nephropathy developed (IPCS.191-.070 (.120) .340-.047-.146-.372 (.410-.173-.5528.090 (.260) .091) .170-.190) .216 (.400) .680) . EPA has established a drinking water standard.400) .250 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.290) .050-.140 (.080 (.05) . and memory loss (Nigam et al.01 (.501) .37) 1.331 (.480 (. interval) .124-.065 (. resulting in a half-life of about seven years.100) . ingestion.220 (.089) . U.125) < LOD < LOD < LOD .064 (.200-.450) .240 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.372) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.100-.100 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.174) . Workers who directly handled HCH have complained of headache.310) .118 (.470 (.140) .089-. tremors. and FDA has established a bottled water standard and food residue tolerances for lindane.620-1.410) .480) .308-.222 (. enlarged livers.210) .058 (<LOD-.130) .120 (.294-.100) . 2002).260-.32) .060) .175 (.250-.140) .390-.110-.319) .096) .160) .118-.086) < LOD < LOD < LOD < LOD < LOD < LOD .130-.290 (. population from the National Health and Nutrition Examination Survey.139 (.057-.090 (. each result has been multiplied by 1.090 (.072 (.150-.103) 90th .069) .244-.587) 653 758 589 1240 1533 1370 20 years and older .220-.370-.070) .310 (.050 (.270 (.170-.234 (.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) .290 (.130 (.360) .048 (<LOD-.404) .050 (<LOD-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.214) . When animals were chronically fed lindane at high doses.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .057 (<LOD-. ataxia. 1977).260) .460) .120-.310) .210-.382-.081-.560) .080-.480 (.220-. the serum half-life was about 20 hours among children (Ginsburg et al. 1981).814) .098 (.510) .200 (.057-.119) .144 (. 1983).521 (.103-.560 (. After dermal application of lindane 1% lotion.580 (.290 (. hepatic enzyme induction.840) .092 (.S.330-.078 (. 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.120) . Rogan.077) < LOD .110) . respectively.281 (.305) .067 (.Organochlorine Pesticides exposure to HCH is through the diet.083) . See the section “What’s New” at the beginning of this Report for details.150) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.190-1.450-.330 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .190) .110) ..059-.230-.068-.073-.050-.062 (.056-.. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.160 (. Saxena et al. 1996.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .140) .221-.710) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.190-.287 (.412 (.570 (.080 (. or dermal exposure.056-.100 (.690) .410) .077) < LOD .360-. and seizures.290) .064) .110) . 2008. paresthesias. HCH isomers are absorbed after inhalation..080) * * * * * * .103 (.070 (.220) . The beta isomer accumulates in fatty tissues and is metabolized more slowly.

Stehr-Green. Kutz et al. Sturgeon et al. respectively.S. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. older age. Kutz et al. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers.5. the maximum and 95th percentile beta-HCH values. 1991. In recent years.8. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998).. 1971.cdc. and 7. see Data Analysis section) for Survey years 99-00. 2001-2002. male sex... respectively.. 2002. Bates et al. which may vary for some chemicals by year and by individual sample.. were similar to the 95th percentiles in this Report. In an earlier (1996-1997) sample of German children. EPA at: http://www. population from the National Health and Nutrition Examination Survey. Link et al. 1991. serum levels of lindane were generally below the limits of detection.epa. 2004) and India (Bhatnagar et al. 1989). < LOD means less than the limit of detection.S. 1998. In populationbased studies of New Zealand adults and German adults and children. Biomonitoring Information Because of its longer half-life.gov/toxpro2. 10. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. Additional factors associated with higher beta-HCH levels include rural residence. 01-02. 106 Fourth National Report on Human Exposure to Environmental Chemicals . environmental levels) and health effects is available from the U. More information about external exposure (i. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens..5..gov/pesticides/ and from ATSDR at: http:// www.e. Survey Geometric mean (95% conf. Becker et al.html. 2005. 1989. Radomski et al. aged 9-11 years. 2005. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. In NHANES 1999-2000. the 95th percentile of betaHCH levels was twofold to threefold higher than the 95th percentile of 12-19 year olds in the comparable NHANES Serum gamma-Hexachlorocyclohexane (Lindane) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 2004. and 2003-2004.. and 03-04 are 14.. 2004). Stehr-Green. and a diet that includes meat (Becker et al..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 2002)..atsdr..

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). 2003).. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005). 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. in this Report (Nigam et al. which may vary for some chemicals by year and by individual sample. respectively. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1986.S... 1971)..Organochlorine Pesticides 2001-2002 survey period (Link et al. A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. In a small study of adults who consumed sport fish from the Great Lakes. 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. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 107 . Radomski et al. 1998).

Brock JW. available at URL: http://www. Sturgeon SR. Kaus S. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Nigam SK. Rivas A.58:1185-1201. Environ Health Perspect 1998. org/documents/jmpr/jmpmono/2002pr08.54:1431-1443. Rogan WJ. Astolfi E. 4/21/09 Anderson HA. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Angerer J. and other chemicals. Bai KM. Metabolism of gammahexachlorocyclohexane in man. Hanrahan L. 2002. Botella B. Lindane. August 2005.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Ginsburg CM. Radomski JL. Arch Pediatr Adolesc Med 1996. Ellis H.gov/~dms/pesrpts. Siddiqui MKJ. International Programme on Chemical Safety (IPCS). Needham LL. Majumder SK. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Olson J. and HCB residues in human blood in Ahmedabad. Organochlorines in Swedish women: determinants of serum concentrations. Deichmann WB. et al. April 1982 to 1984. Maass R. Wood PH. Rev Environ Contam Toxicol 1991. Kashyap R. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.91:998-1000. Exposure of women to organochlorine pesticides in Southern Spain. Krause C. Available at URL: http://www. FDA total diet study. Bull Environ Contam Toxicol 2004.150:981-990. Environ Res 2004. J Pediatr 1977. Bates MN. Schulz C.inchem. HCH.20(2):186-193. Falk C. Demographic and seasonal influences on human serum pesticide residue levels.120:1-82. Needham LL. Cerrillo I.106(5):279-289.111:349355. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Int Arch Occup Environ Health 1983.27:405-421. Lowry W. Saiyed HN. Karnik AB. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Raju GS. August 2008. Kutty D. dietary intakes of pesticides.57(4):315-320.48:127-134. Levels of DDT.71(6):1200-1209. Saxena MC. et al. Darnerud PO. Paepke O.96:34-4Food and Drug Administration (FDA). 4/21/09 Kutz FW. Int J Hyg Environ Health 2002. Available at URL: http://www. Seiwert M. Granath F. Gunderson EL. Buckland SJ.atsdr. Gabrio T. Olea-Serrano MF. Link B. VI. Visweswariah K. Atuma S. Chemosphere 2005. Bottimore DP. Krishna Murti CR. Aune M.cdc. et al. Rey AA.html. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Bhatnagar VK. Herrman T. J Assoc Off Anal Chem 1988. Absorption of lindane (g benzene hexachloride) in infants and children. Bhargava AK. Glynn AW. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Lepom P. Zaidi SS. Rothman N.72:261265. 108 Fourth National Report on Human Exposure to Environmental Chemicals . et al. selected elements. Piechotowski I.fda. India. Toxicol Appl Pharmacol 1971. Burse VW. Kulkarni PK. Garrett N.html. Becker K. Arch Toxicol 1981. PA. Int Arch Occup Environ Health 1986. Zoellner I. Needham LL. Patterson DG Jr. Placental transfer of pesticides in humans. The Great Lakes Consortium.htm. gov/toxprofiles/tp43. Brinton LA. Potischman N. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Occupational exposure to hexachlorocyclohexane.9(4):417-424. Toxicological profile for hexachlorocyclohexanes update [online]. Olea N. Stehr-Green. Reisch JS. Crespo J. Cancer Causes and Control 1998.205:297-308. Environ Health Perspect 2003. Bjerselius R. J Toxicol Environ Health 1989. Chemosphere 2004. Biomonitoring of persistent organochlorine pesticides. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. children and newborn infants. Pollutants in breast milk. et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.cfsan. Heinrich R.52(1):59-67. et al.

Mirex is absorbed through the skin and from the gastrointestinal tract.7) < LOD 66. 01-02. and foods. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 13.6-305) 15.4-230) 18. Mirex can cross the placenta and be excreted in breast milk.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. after which it is widely distributed in the body and stored in fat. Survey Geometric mean (95% conf. sediments.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) < LOD < LOD < LOD < LOD 71.1 (8. (Kutz et al.40 (<LOD-13.5.1 (<LOD-65.0 (<LOD-108) < LOD < LOD 50. water. soil.6 (<LOD-108) 9. where it has a half-life of 12 years.S. it is a highly persistent chemical in the environment. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.5 (<LOD-42. 2385-85-5 General Information Mirex has not been produced or used in the U. since 1977.8 (<LOD-73.4) < LOD 15.6 (<LOD-31. 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.3 (15.S.6 (<LOD-23. or pesticide application.0 (14.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. 1985. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.6. where it was applied directly to soil and by aerial spraying.2) 51.1 (13.Organochlorine Pesticides Mirex CAS No.7) 8..7 (12. < LOD means less than the limit of detection. Mirex has been detected in air.4 (8.10-37.8) < LOD 15. In studies conducted in the 1970’s and 1980’s.5-291) 11.3-225) 15. mirex was detected in human adipose samples. 10. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. and 7. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. Mirex binds strongly to soil..0-374) 11.S.6) 9. respectively.70 (<LOD-15. resulting in exposure to newborns and nursing infants.5 (9.5-82.70-40. disposal. Mirex is not metabolized in the body.70-24. animals. 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.S. Formerly.7 (<LOD-47.2-230) 13. see Data Analysis section) for Survey years 99-00.8.5-425) 40. especially those from persons living in the southeastern U.5 (<LOD-115) 153 (30.1) 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. Fourth National Report on Human Exposure to Environmental Chemicals 109 . and 03-04 are 14. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.10 (<LOD-15.90-29.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. 1991). Occupational exposure is limited to workers at sites where mirex contamination is present.0 (12. 1995).3 (15.2 (7. Some states and the U.4) < LOD 63.S.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. aquatic organisms.8 (12.

environmental levels) and health effects is available from the ATSDR at: http://www.gov/toxpro2.220 (<LOD-.atsdr.170-3.062-.8. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. 1995. 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.090 (<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.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .170) < LOD .090-1.430 (. and 2003-2004 subsamples. Laboratory animals fed high doses developed liver enlargement and liver tumors.. as well as in a subsample of NHANES II (1976-1980) participants.470) .470 (.093 (. 1991).e.106 (.73) .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 . serum mirex levels were generally below the limits of detection (Stehr-Green. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .S.102) < LOD < LOD < LOD < LOD .79) . which may vary for some chemicals by year and by individual sample.140 (<LOD-.610) < LOD < LOD < LOD < LOD .256 (.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..92) .110 (<LOD-. 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.450 (.02) .S. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.690) . reproductive toxicity included decreased fertility and testicular damage. 7.7 ng/g of lipid.100 (<LOD-.079 (<LOD-.077 (<LOD-.080-1.470) .054 (<LOD-.Organochlorine Pesticides exposures are unknown.100 (<LOD-. and 4. IARC classifies mirex as possibly carcinogenic to humans. population from the National Health and Nutrition Examination Survey. 2005).510) < LOD < LOD .055-. EPA has established environmental standards for mirex.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. The geometric mean mirex levels of the Inuit mothers were 8.090 (<LOD-. Biomonitoring Information In the NHANES 1999-2000.450) 1.089-.cdc.220) . and NTP classifies mirex as reasonably anticipated to be a human carcinogen.79) .106) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.112 (. 2004). 1989).080-1.370 (. Survey Geometric mean (95% conf.064 (<LOD-.41) .37) .070-1.053-. More information about external exposure (i. In samples obtained between 1994 and 1997.html.059 (<LOD-..108 (. In addition. 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.090 (<LOD-.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 . 110 Fourth National Report on Human Exposure to Environmental Chemicals .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 . Smith.410 (.090-1.08 (.052-. The U. 2001-2002.635) < LOD .268) < LOD .310 (.090-1.

Toxicological profile for mirex and chlordecone [online].gov/toxprofiles/ tp66. 4/21/09 Bloom MS. Circumpolar maternal blood contaminant survey. Vol. Stehr-Green.atsdr. In Hayes WJ.cdc. J Toxicol Environ Health 1989. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Watts DL. Sci Total Environ 2004.27:405-421. Jr and Laws ER. Van Oostdam JC. Kutz FW. Odland JO.120:1-82. Demographic and seasonal influences on human serum pesticide residue levels. New York.html. J Toxicol Environ Health 1985. The human body burden of mirex in the southeastern United States. dichlorodiphenyldichloroethylene. August 1995. PA. Bottimore DP. Handbook of Pesticide Toxicology.97(2):178192. Chashchin V. Kutz FW. et al.330:55-70.Organochlorine Pesticides effect. Available at URL: http://www. Swanson MK. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Stroup CR. Smith AG. Wood PH. hexachlorobenzene. 731-915. 2 Classes of Pesticides. Moysich KB. Eds. Leininger CC. Academic Press. et al. Vena JE. Environ Res 2005. 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. Inc. Hansen JC. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Olson JR.15:385-394. Strassman SC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1994-1997 organochlorine compounds. Dewailly E. Rev Environ Contam Toxicol 1991. Chlorinated Hydrocarbon Insecticides. Gilman A. Carra JS. 1991 pp. Profiles of ortho-polychlorinated biphenyl congeners. References Agency for Toxic Substances and Disease Registry (ATSDR). Jr.

20) < LOD 1. Occupational exposures.4.980-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-3.9 (<LOD-121) 9.90-33. recent sampling of U.6-TCP).40 (2.50-63.57 (<LOD-15. 95-95-4 2. and polychlorinated benzenes (Kohil et al.4.0) < LOD 11. Trichlorophenols are no longer manufactured commercially.0 (8.4. usually at herbicide production or waste incineration facilities. are metabolites of several organochlorine chemicals.6-TCP were used as intermediates in the production of certain pesticides. including hexachlorobenzene and hexachlorocyclohexanes.0) 2.S.950 (<LOD-1.0 (4.0 (4.63) 18. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.900-2.40 (1.27) 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 1.5-trichlorophenol.0) < LOD 21.5TCP and 2. 1999).60 (.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.60 (2. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.19 (<LOD-6. soils.60) < LOD 8. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.00 (3. Survey Geometric mean (95% conf. Formation of 2.60-8. 1976).40) < LOD 1.42 (<LOD-12.30-3.50 (1.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.5-TCP) and 2.50 (2. 1999).00 (2. Such workers would probably Urinary 2. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.4. and sediments.40 (1. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.0) < LOD 5.30 (.31 (<LOD-9. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.0) 2.03) 9.4.71 (<LOD-8.0 (3. public drinking water systems did not detect 2. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) < LOD 11.6-trichlorophenol (2.30-40.60-18.20) < LOD 90th 5.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.4.30-44. 2.4.0) 2.40-18.980-3.8) 21.80) < LOD 1.30-27.Organochlorine Pesticides 2.7.S. Exposure to trichlorophenols also may result from metabolism of lindane. Both chemicals have been detected in air.40 (.3.4.40 (2.0) 2.50-16.4.50) < LOD 1.6-Trichlorophenol CAS No.00-8.S.30-27.9 and 0.0) 2. may occur by inhalation or dermal routes.72) < LOD 1.0 (3.4.20) < LOD 5.0) < LOD 5.80 (1.60 (4.30-27.27) 696 661 521 696 603 939 Limit of detection (LOD.0 (4. Historically.40 (.20-71. surface water.50 (.50-25.40) < LOD 6.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.4.7) 24.920-3.5-trichlorophenol (2. 2006).0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .30) < LOD < LOD < LOD < LOD < LOD 1.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. other organochlorines.0) < LOD 5.80-41.40 (2.0) 14.40) < LOD 4.0 (5.40 (2. which may vary for some chemicals by year and by individual sample.10-3. 112 Fourth National Report on Human Exposure to Environmental Chemicals .940-3. however.0) 2.42 (<LOD-8.00-3. < LOD means less than the limit of detection..30) < LOD 4.20 (4. hexachlorobenzene. 2. 2. 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.30-11.5-Trichlorophenol CAS No.40-11. EPA.9.20-36.0) 5.80 (2.71 (<LOD-8. population from the National Health and Nutrition Examination Survey.6-TCP in any of the samples (U.4.

Neither 2.36 (1.32) < LOD 4.02) < LOD 7.43 (2.86 (3. In the same 2-6 year old children.44 (1.19-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.e.8) < LOD 9. IARC classifies combined exposures to polychlorophenols. furans.4) 5.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9) 12.0) 7.50) < LOD 2.Organochlorine Pesticides be exposed to mixtures of chlorophenols.6-TCP. Human health effects from 2.4.55 (4. environmental levels) and health effects is available from ATSDR at: http://www.78-19.4.6) 4. Urinary 2.93-11..4 (6.95 (3.90 (4.2) 2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.81 (<LOD-9.46 (1. Fourth National Report on Human Exposure to Environmental Chemicals 113 .83-12...64 (4.60-3.1) 2.8) 4.00-29.75 (<LOD-6. animals showed hepatocellular abnormalities.5) < LOD 12.67 (1.69 (2.4.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.53-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11..37) 16.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).4.02-3.4. 1995) were similar.cdc..5-TCP or 2.4. as being possibly carcinogenic to humans..24-11.57 (3.5-TCP and limited for 2.43) < LOD 12.7 (4. 2003).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.27-17.6-TCP as reasonably anticipated to be a human carcinogen.17) 9.73 (<LOD-8. Among 6-11 year old children in NHANES 1999-2000. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.28-25.80 (1. population from the National Health and Nutrition Examination Survey. the 95th percentile urinary 2.05-8.atsdr.24 (3.4.8 (5.4) < LOD 3. Laboratory animals chronically fed high doses of 2. Radon et al. 2003. However.980 (<LOD-1. which includes trichlorophenols..79-4. 2004).20-6. NTP classifies 2. leukemias.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. 7. 1989).6) 4.57 (<LOD-7.820-2.68 (<LOD-8.31) < LOD 2.5) 11.78 (3. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.24) < LOD 6.4.4.gov/toxpro2.53-3.13-13.6-TCP had increased rates of hepatic tumors. and other chlorinated compounds.00-19..67 (1.11) 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 2.49 (1.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.4.78) < LOD 1. More information about external exposure (i.html.69-18.6) 4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.57 (<LOD-7. urinary 2.4) < LOD 3.05-17.47-8.24) < LOD 5. The 95th percentiles for 2.9 (5. At lower doses.19-4.68-4.88-16.44 (.920-2.00) < LOD 4.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.37-11.4.16 (.16) < LOD 90th 5.3 (5. and lymphomas.1 (<LOD-58.82 (<LOD-32.74) 11.15) < LOD 2.5-TCP.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1989).4.6-TCP levels at the 95th percentile were up to eight times higher than 3.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .75 (3. 2003). in addition to dioxins..S.5-TCP nor 2.2) < LOD 5. the 95th percentile urinary 2. Survey Geometric mean (95% conf.4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.33) < LOD < LOD < LOD < LOD < LOD 2. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.24) < LOD 1. 1995) and up to 19 times higher than the 95th percentile value of 1.62-20.3 mg/L reported in German adults aged 18-69 years (Becker et al.0 mg/L.29 (1.2 (2.

S.36 mg/g creatinine.00 (4. Urinary 2.20-6.7) 33.10-2. 1991).6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.30-2.60 (2.48-26.0 (12.9) 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 2.4.30-33.60) < LOD 5.32) * 3.0) 13.0) 15.7) 21.75 (8. interval) 2.80 (3.0-43.4.80) 1.53) 4.23) 3.52 (2.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.20-23.57 (<LOD-2.6 (11.99) 6.70 (2.31 (3.8-13.0-18.2) 25.3.10) 6. for males in NHANES 19992002 (Agramunt et al. was about six times lower than the median urinary levels for males in this Report (Radon et al.32) 3.3 (11.09-7.24 (2.0) 9.84) 2.4.68 (<LOD-2.5-TCP or 2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.0) 9..0) 13.1) 16.06) * 2.85) * 3. Mean values of 2.4.78 (2.6 mg/g creatinine) and 2.40) 3.3-26.36-5.0-38.80-25.7 (9.95) 3.4 (8.5-TCP (0.30) 4.0) 14.1-25.6-22.60-3.6TCP values. 1998).8) 32.2) 12.6-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. Urinary 2.85 (2. 0.80-6.98-7.0) 17.80 (2.74-3.0 (15.91-4.0) 13.36 (1.44) 75th 4.66 (8.70-6.55-3.7-3.12) 2.5-TCP and 2. Biomonitoring studies on levels of 2.6-TCP level.70-6.5-TCP or 2.8 (9..6 (12. Biomonitoring data will also help scientists plan and conduct research about 2.0-37.79 (5.20 (3.31) * 2.4.0 (16.30-2.4.3 (11. population from the National Health and Nutrition Examination Survey.00 (2.58-3.70 (2.4.6-17.56 (3.4. 114 Fourth National Report on Human Exposure to Environmental Chemicals .18-3.3) 20.35-3.6-TCP in urine does not mean that the level of 2.98-11. similar to the limit of detection for this Report (Anderson et al.0) 19.28) 24.0 (15.65) 15.70) 5.25-11.40) 2. 2004).02) 2.26 (2.59-6.90) 2.89 (3.9 (13.20 (3.60) 6. the median urinary 2.95 (4.5-TCP or 2.23-2.53) 2.1 (8.4-17. In harbor workers exposed to chlorophenol-contaminated river silt.0) 17.0) 11. 2003).59) 4.60 (3.40-14.0) 7.0 (20.0 (13.8-24.4 (10.4.04) 2.47 (3.0-54.0) 12.58 (1.0-38.78 (2.0) 14.4.69 (3.74 (2.10-3.4.6-TCP exposure and health effects. which may vary for some chemicals by year and by individual sample.33-4.2-0.4.54) 6.6) 26.0-50.5-TCP level of 0.90-8.4 (17.4.32-4.14 (2.70) 3.0 and 1.40) 2.72-10.0 (7.67-12.6-TCP (0.60 (3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.80-7.51-12.5-46.2 (14.50-5.0) 19.8) 18.7 (13.5-TCP or 2.0 (6.8-15.10) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-TCP and to the median 2.6) 21.9) 694 677 519 696 602 931 Limit of detection (LOD.0) 7.76) 3.40-7.4.0 (8.4.45 (2.92 (2.0 (14.5-TCP and 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.28) * 2.63) 90th 15.0 (11.50 (2. Survey Geometric mean (95% conf.0-41.0 (8.4.00-21.40-2.95-6.0 (14.70) 5.7-16.09) 15.01-6.0 (20..1 (10.52-3.90 (3.6TCP causes an adverse health effect.60-37.40) 4.40-2.0 (14.9 (11.00-4.20) 4.4. Finding a measurable amount of 2.4.3) 37.0-44.80-20.6-19.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.4 (9.40 (2.67) 4.23) 2.00 (1.4.9) 13.7 mg/L.08 (2.0 (9. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 10.6-TCP than are found in the general population. respectively.0) 6.46-3.0 (6.49 (6.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.65 (5.0) 10.45-9.40-4.0 (4.70-3..45) < LOD 11.0-68.0 (6.4.90 (4.10-3.3-17.10 (5.07 (<LOD-3.40-32.80 (2.0) 11.5 mg/g creatinine) were similar to the limit of detection for 2.0) 13. < LOD means less than the limit of detection.60-21.73-9.40 (2.3) 23.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.20-3.89-6.45 (5.70) 1.30-11.87-14.

65) 18.98) 10.43 (<LOD-2.49-3.88 (2.51) 18.02 (1.88-7.33 (1.81-9.5) 8.42 (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 2.0) 10.29 (6.55-2.72-16.82) 2.1) 14.9) 19.42) 2.91-2.52 (3.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.17) 2.95-2.S.48-2.98 (1.76) 2.2 (12.6 (12.6 (5.47-5.27-9.83-5.9-64.68) 2.50-8.56 (7.1-32.22-9.6-31.21-11.8 (7.2) 19.5 (10.15 (6.3-37.68) 2.83-6.6 (22.78) 2.35 (3.41 (3.16-10.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3) 8.9) 8.88) 5.6 (6.9 (9.53) 4.4 (11.10) 4.58 (4.00 (2.63 (2.2 (8.52) 2.4) 8.17) 13.32-19.9) 8.51 (2.4.0 (9.88) 1.Organochlorine Pesticides Urinary 2.5) 11.6) 13.76) 4.83 (3.14-13.11) 10.65-21.22 (1.06) 4.91 (7.25-2.06-2.81) 2.22-2. Survey Geometric mean (95% conf.13 (1.8) 11.6 (9.56) < LOD 11.87-7.78) 90th 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 8.5) 9.8) 21.82-2.79-17.0 (6.01 (3.41-6.1) 11.63) * 4.53-11.10-9.8 (8.1 (13.40 (7.88) 4.60 (4.7) 25.6 (9.29-4.46-14.33) * 2.22 (<LOD-2.24 (1.17-4.6) 8. Fourth National Report on Human Exposure to Environmental Chemicals 115 .7) 6.44 (3.23) 4.08-2.28-4.38) 22.19-5.43 (2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.8) 19.71 (3.91 (3. population from the National Health and Nutrition Examination Survey.7 (14.38 (2.89) 10.43-7.2 (13.32 (2.09-3.88) * 2.54 (2.94-13.87) * 2.29-4.15 (1.5 (8.88) 4.5) 11.33 (7.56-5.77-4.40 (2.6 (10.9-34.7-36.20-2.8) 12.63-15.99-2.73-22.50 (2.76) 1.05 (6.70-9.38 (4.38-5.62-15.53 (3.04-2.65-2.23 (1.25-15.9-29.78 (2.18-4.5-28.53) * 2.4) 9.83-6.22 (3.90 (1.82 (3.87 (3.72) 32.1 (8.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.59 (2.96) < LOD 4.3-23.18-2. interval) 2.0 (11.63-13.66-4.90) 2.04-16.30-2.89-2.1-21.51-21.82 (8.5) 12.63 (<LOD-2.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.06) 11.65) 2.9 (9.13-6.25-17.6) 12.49) 4.2 (7.00) 4.73) 5.10 (6.05 (3.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.00 (3.87) 2.02) 3.3 (9.63) 4.33-2.67-17.25 (3.00) 4.76-8.25 (3.4) 4.9) 7.5 (7.52 (5.92) 4.60-2.4 (12.52) 2.14-2.77) 2.9-32.75) 75th 4.26-13.26 (6.

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

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

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

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

60 (1.58 (5.6) 7.740-2.80-22.0) 10.96-3.79 (5.0) 10.30 (2.2 (14.21 (.50 (.620-1.8 (8.40-19.840-1.93-24.90) 3.19) 9.98-5.60) < LOD < LOD 4.80) .70) < LOD < LOD 75th 3.3) 17.08-15.13-2.0 (12.10) < LOD .21) 9.5-16.68-7.0 (6.97) 90th 7.43-12.40-14.20 (.8) 7.00 (4.52) 6.700-1.30-6.0) 15.0 (7.01) * * 1.5 (8.0 (5.00 (5.20-7.90-4.0 (6.32 (.8) 19.0 (8.S.10 (.80 (4.26 (5.7) 11.26-6.5-17.757-2.58 (3.4) 18.4 (9.12-19.27-15.0) 11.81) 11.00-7.5) 15.8 (14.0) 6.56-13.35-16.08-2.8 (12.0 (7.70) < LOD < LOD 1.4 (9.20-30.80-4.0) 6.0 (7.33 (5.0-27.1) 10.47) * * 1.70) .70-23.30-4.2 (9.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.34-7.82) 10.00-19.0) 12.70-19.5) 20.0 (8.599-1.53) 4.20 (.44-38.623-1.955 (.20 (.0) 7.23-5.02) 4.0) 11.90 (1.54 (3.490-2.80) 4.74 (8.12) 4.00-27.2) 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 1.15) 14.2 (11.3) 16.56 (1.05-7.50-36.04) < LOD 1.00-12. see Data Analysis section) for Survey years 99-00.0) 10.0 (7.6) 18.50-5.37 (3.60-11.8 (9.89) 9.60-25.98-12.81) 1.00-27.0 (4. respectively.56 (6.30 (4.61) 4.0) 10.40-1.0 (9.28) 1.7 (12. interval) 1.66) * * 1.0) 5.10 (. 01-02. population from the National Health and Nutrition Examination Survey.17-3.00) 3.97) 8.02-5.79-7.860-2.2 (14.80 (2.27-3.52) * * 1.42-3.530 (<LOD-2.61 (3.8) 11.26-8.36-4.80) 2.86 (1.94) * * .0) 10.70-11. 120 Fourth National Report on Human Exposure to Environmental Chemicals .58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.810-1.830 (<LOD-3.3-15.970-2.0 (9.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.15-12.2 (7.780) < LOD 3.39 (3.40-16.60 (5.4) 17.44 (2.91) 4.4) 20.2 (7.0) 11.60-18.07-10.4 (7.90-5.51) 2.56 (4.2) 14.39 (8.2-20.4 (7.81) 11.981 (.40 (.80) .00 (1.579-1. 0.72) 5.2 (7. and 03-04 are 0.35-11.600 (<LOD-1.0) 9.2.40-11.0) 20. which may vary for some chemicals by year and by individual sample.9-18.34-3.13 (2.1-23.80) 3.16 (2.30 (2.1-17.22 (.52-11.55-6.20-4.1) 13.86-15.46) 10.63) 1.38-5.8-32.70-14.58 (2.44-3.3) 14.99 (5.47) 5.90) 2.40-5.8) 7.35-12.08 (<LOD-2.1) 95th 13.670-1.0) 11.60) .7 (14.750-1.82-12.717-1. < LOD means less than the limit of detection.71 (2.758-1.93 (4.67) 3.290 (<LOD-1.9) 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 1.14) * * .1 (10.2 (9.03 (.13 (2.33-18.55-8.1 (9.9) 8.57-7.0) 5.95) 5.80) 2.5 (11.00-12.00) 3.50 (2.10 (2.80) 11.2) 16.2.954 (.85 (3.80-24.2) 16.16) 4.9 (8.1.29) * * 1.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.70 (2.0-28.10 (2.0) 5.80) 2.50) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.890 (<LOD-2.10-7.70 (4.42) .50 (4.9) 14.94) 3.76 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11 (.48-7.32) 1.20 (2.71-9.10) < LOD < LOD 4.0 (8.83 (5. and 0.45 (2.290 (<LOD-.73) * * .0) 6.74 (8.20 (.

93-5.04 (1.61-13.92-2.28) 10.10 (3.41-12.02 (2.1 (8.02 (7.46) 2.8) 6.5-20.9 (5.23) 4.60) 2.89) * * 1.28 (4.60) * * .560-1.47 (1.47 (3.8) 7.818 (.7) 5.51-5.35) < LOD < LOD 3.76) < LOD .566-1.21-23.8) 8.9) 16.7 (8.88-10.1) 4.75 (3.75-7.98-5.53) 9.57) 4.960 (<LOD-2.94 (2.650-1.72) 11.06-2.4) 4.94-9.82-14.820 (.80 (7.45-5. Fourth National Report on Human Exposure to Environmental Chemicals 121 .0) 7.47 (3.6 (10.42) 12.95) 2.6) 13.40-5.56) .53-11.430-1.00 (4.2) 5.66-15.85 (6.9-28.25) < LOD .5-32.900 (.27) < LOD 2.1 (10.31-14.68-4.85) 2.38) .66 (2.90-8.18 (.69 (4.94-23.890 (<LOD-1.60-9.71-2.62-5.74) 4.09 (.3) 15.14 (3.84 (5.00-13.87 (1.75) 14.94-10.1 (6.500-1.13) 4.4) 4.56-13.883 (.37 (5.58) * * 1.93) 9.03-6.94 (4.92-5.26) * * .2) 95th 12.00) 8.79-3.02-14.9) 11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.94-22.68) < LOD < LOD 3.34) < LOD < LOD .890 (<LOD-1.870-2.9 (9.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.570-1.02-2.7 (10.960 (.1) 4.5) 7.790 (.03) 2.75 (7.4 (4.83) 8.69) 2.69) 4.30 (1.5) 12.40) 4.710 (<LOD-1.75) 2.01-2.41) .40-14.2 (6.03 (7.42 (3.04-6.77 (6.2) 7.82-6.2) 8.37-3.95 (3.540-1.54) .549-1.1 (11.69-10.4) 13.29) * * .855 (.44 (2.7 (9.57-10.61 (1.2) 13.78 (2.40-12.55-20.45-11.83 (7.1 (9.54-4.07 (.0 (8.780 (<LOD-1.57 (4.23 (4.2 (10.84) 7.3) 16.54-2.54-11.62) .7) 18.3) 12.81 (1.7) 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 .8) 12.34 (6.73 (1.98) .620-1.57 (6.28 (2.34) * * .88-15.510-1.9 (9.28-9.03) 2.996 (.41) Selected percentiles ( 95% confidence interval) Total * * 50th .6 (9.47) 2.52) 4.98) .80 (6.29 (2.5) 7.5) 8.31 (3.61 (1.05 (.9) 12.54-15.750 (<LOD-1.87-5.39 (2.46-5.66 (1.05 (1.88) 2.76-4.50) 7.860 (.40 (3.4 (9.633-1.37 (4.93-9.24-3.924 (.8) 16.98 (3.43) 2.533-1.87 (3.43 (.15-10.1 (7.8 (10.830-1.45-5.90-5. interval) .67-19.66 (5.34 (6.574-1.36) * * 1.10-13.S.19 (4.32-12.82-26.0) 6.6) 9.5-16.920 (.11-6.80 (2.3) 5. population from the National Health and Nutrition Examination Survey.56) 4.6) 11.2) 9.05) .09) 2.608-1.440 (<LOD-2.25) 6.3) 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 1.5) 11.98) 9.37) 9.7) 12.74) 90th 7.00 (4.80) 9.38 (1.64-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.35 (1.67) 1.09-11.1-15.40-3.71) 10.40) < LOD < LOD 75th 2.88 (5.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.28 (5.00-19.89-3.2 (8.40-28.82-14.53 (6.61-29.00-17.2) 5.932 (.773-1.43 (3.6) 8.66-34.47) * * .03 (2.5-13.81-5.79-9.5 (4.20-8.98-22.37-5.30) 2.67) 4.56) 7.7) 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.

95-9. 0.00 (.01 (2.6 (10.8) 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 1.70) 2.34-10.75 (2.9-14.84-4.90-15.00) 8.70-5.0) 11.92-17.0 (7.75 (3.5-26.80-12.95 (2.74) * * * * * 1.53 (3.29-4.00-4.60 (2.670 (<LOD-1.47-6.5.27 (3.24 (2.90-9.49-4.0) 14.670 (<LOD-1.6) 14.2 (9.6 (10.67-10.66) 4.31-7.31) 1.90 (2.4) 7.60) < LOD < LOD 2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8-20.5.35-3.20) 3.30) < LOD < LOD .50) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.580-2.37) 2.7 (10.90 (6.14 (6.10 (.58.1 (10.27) 4.5) 21.0-29.0) 23.0) 9.61 (3.80) .4) 11.41-5. population from the National Health and Nutrition Examination Survey.15-6.15-2.7-19.3) 20.70 (1.8 (12.8 (12.37 (3.31-12.92) 9.16-1.7) 14.33-11.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.25 (2.81-6.98-9.80-21.50-4.2) 14.70-9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .3 (9. < LOD means less than the limit of detection.00-9.00) < LOD .9) 95th 14.0 (10.9 (12.59-3.39 (5.8-20.90 (5.27 (7.90-15.0 (10.10-10.80) .70 (8.8-17.28 (7.00) 3.3 (9.06 (2.740 (<LOD-1.6-19.63-14. 122 Fourth National Report on Human Exposure to Environmental Chemicals .9 (7.0 (13.7) 10.90 (1.90-31.50-5.00) 7.9) 10.80) 5.3 (11.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.22 (6.64) 10.0) 12.45 (3.82) 8.00-16.46-4.52 (6.5 (9.6) 14.18 (3.35 (6.0) 9.96) 3.790 (<LOD-1.34-3.24-5.20) .0-19.80-3.60 (6. and 03-04 are 0.90 (6.3) 22.90) 8.S.970 (<LOD-2.90 (2.10) 6.80 (2.35) 4.0) 12.10-4.80 (2.39-13.3 (7.5 (8.9) 9.22-12. and 0.34 (6.12 (4.6) 18.27) 9.0) 7.90 (6.0) 14.10-15.30) 3.8) 8.30) < LOD < LOD 4.5 (8.58 (1.80-4.9) 16.0 (14.7-21.80-6.9-17.0-24.50) .89) 2.34-5.40 (2.30) 3.4 (14.0-33.8-21.910 (<LOD-2.20-18.17 (7.96) 90th 7.0) 19.72) 2.46-28.1) 11.00-18.0) 6.00) 3.11-6.18) * * * * * * * * 1.7) 15.90 (6.97-4.6-41.40) < LOD < LOD 75th 2.650-1.22 (6.670 (<LOD-1.7 (11.22) 8.0 (5.95 (5. 01-02.20-4.4 (10.88) 3.30) 8.86-10.0) 11.90 (2.0) 12.62-17.89 (2.50) 5. which may vary for some chemicals by year and by individual sample.0) 18.61-32.27) .3 (6.10 (<LOD-1.670 (<LOD-1.80-8.4-17.0 (8.67) 3.70-8.3) 10.0) 13.0) 13.00-18.70-9.00-4.20-8.1 (10.80-14.78) 5.40 (2.0 (9.90) 4.1-23.9-15.0-24.7) 22.67) 4.41) 3.04 (3.80 (5.4 (10.99 (3.20 (<LOD-2.73) 7.7) 16.20) 3.3 (12.77-14.8) 9.5) 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 * * * * * * . respectively.6) 11.3) 14.0 (15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.77-3.2 (7.88) 10.680 (<LOD-1.29) < LOD < LOD < LOD < LOD 3.60 (5.51) < LOD 1.0 (9.42 (1.66-13. see Data Analysis section) for Survey years 99-00.3) 8.

940) < LOD < LOD 1.25-9.6 (11.5 (9.07 (5.6) 6.85-17.973 (.68-19.67 (7.32-8.93 (2.3-21.5) 8.25 (4.14 (2.9) 16.5-17.33) 3.03 (2.3-17.2 (9.34) < LOD < LOD < LOD < LOD 3.0) 14.86-3.78 (4.01-5.36 (2.91) 3.99 (4.04) 9.8) 14.620 (<LOD-.3-17.890-2.75-3.0 (11.9 (9.00 (<LOD-1.09-11.23-3.51-10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.27) * * * * * * * * 1.7-19.89-3.9 (9.760 (<LOD-1.12 (7.93-10.6) 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 1.20-3.6 (13.1 (19.86 (3.780-1.06 (<LOD-1.41 (7.7) 14.4-15.4) 15.4-16.11 (5.37-5.1 (13.15) < LOD < LOD 75th 2.5) 10. population from the National Health and Nutrition Examination Survey.68-4.7 (10.3) 6.2) 19.54) 9.1) 13.5 (11.50-17.45) 6.5 (8.910 (<LOD-1.72-4.82-8.2) 12.70-2.73 (5.29-2.78-10.92 (5.2) 12.97-4.58 (4.38 (.00 (2.85-8.94 (5.38-13.12) < LOD < LOD 4.42-19.47-9.99) 2.07) 2.30) 8.2-15.3) 8.2) 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.5) 22.96-10.6) 13.34-18.6 (12.7) 9.1) 20.07-3.6 (11.00) 2.89 (3.1 (8.21-21.850 (<LOD-1.7-23.590 (<LOD-.63 (2.59-3.0 (8.00 (7.06) .54 (7.0-19.77 (2.93 (6.2) 10.3-34.4) 16.74-19.4) 7.64-11.28-12.89-13.9 (9.S. Fourth National Report on Human Exposure to Environmental Chemicals 123 .2) 8.11-3.0 (13.80) 3.2) 12.55 (2.16-14.6-19.78) 4.44-6.42) 8.0 (10.9-17.8 (8.7 (10.7 (11.09-11.87 (3.29 (5.3-15.3) 9.29) 3.6) 14.95) 3.67 (1.1) 10.92) 3.45) 3.61 (2.3) 12.89-3.39-17.00 (5.30) 2.88 (1.920 (<LOD-1.530-1.28 (1.69-11.79-6.55) 16.6) 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 * * * .7) 15.00) 8.5 (15.2 (9.6) 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 * * * * * * .8 (10.9) 19.97) < LOD .71) < LOD < LOD 2.63 (6.6 (10.50 (6.71 (1.4) 9.5 (10.6) 95th 16.89 (2.68-10.96-11.55) .5) 13.48 (2.810 (<LOD-1.78 (6.81 (7.30-5.72) 4.94-14.7) 12.6) 12.53-8.42) 7.38 (1.690 (.70-35.93 (<LOD-2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2) 15.89-10.6) 7.28) 6.00 (3.83 (7.82-11.2) 16.03) 3.0-21.52-3.30) 7.75-3.8) 11.38) 1.95 (2.86) 9.74-4.54-5. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .9-25.38 (2.29 (2.05-3.77 (2.27) 5.77) 3.6 (13.83 (6.07) 2.33-10.68) .91-9.3 (7.89) 5.95) 90th 8.21) * * * * * 1.51-7.8) 16.4) 7.27-13.4-18.27) < LOD .15 (1.79-9.16 (3.7) 14.19) 3.88-7.27) 1.950) .7 (8.4) 6.4) 7.2-30.4 (11.37) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.03 (6.18) 2.32) 2.4-16.00 (<LOD-1.02-4.43 (2.

690-1.65 (2.455 (.41-5.16) 1.32) 3.60) 3.80 (1.549 (.49) .25-1.40 (1.570 (.16) 2.710 (. 0.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .45 (2.759) * .21) 3.388-.720 (.50-2.720-1.95) 2.04) .380-.34) 2.90) 2.490 (<LOD-.46) 1.98) .80 (2.820 (.30) 4.70 (1.01) .670) .22-3.30 (1.48 (1.30 (.592-.570) * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.33-2.18 (1.550 (.30-1.76-6.83) 1.45 (1.970) 1.550 (.47 (1.260 (<LOD-.20) 3.750-1.77 (1.457 (.38) 1.597) * .36-4.450 (<LOD-.840 (.449 (.350-.27 (2.03) 1.980) 1.90 (1.710) .95-5. and 0.22-3. respectively.380-.587) * * .17) 1.390-.46-3.86 (1. < LOD means less than the limit of detection.89) 1.57 (1.01-1.510 (<LOD-.90) 3.740 (.40 (1.00 (1.740 (.359-.80) 2.96-5.11-3.350-.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.600 (<LOD-. population from the National Health and Nutrition Examination Survey.68-5.800 (.500 (<LOD-.22 (1.760 (.20 (1.49) 2.46 (1.04) 1.30-3.749 (.08 (2.20-2.780 (.73 (2.45-4.37-2.50 (1.453 (.620-1.990-1. see Data Analysis section) for Survey years 99-00.50) 1.850) < LOD .10) 1.83 (2.20 (1.20) 2.73 (1.680-1.590-.10-1.94 (3.700) .05-2.83) 2.22-8.201-.90-4.30-3.11-3.780 (.83) .70 (1.61 (1.29-2.00-2.32-1.15) 2.960 (.14 (1.585) * * .860) < LOD < LOD .39) 2.710 (.15) 2.382-.510 (.31-3.930) < LOD .86) 3.592) * .390-.10) 1.42-2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .440-.970) .78) .48 (2.20) 1.96-3.690) .343 (.16-3.47) 2.960) 1.00-4.98-3.940) < LOD .570-1.75-2.690 (.618) * .570 (<LOD-.20-1.23-3.570 (.32 (1.80) 3.580-1.94) .69-4.20 (1.89-6.63 (1.31) 95th 2.57 (2.58 (1.380) .46 (2.80) 5.960) . interval) Selected percentiles ( 95% confidence interval) Total * .31) 2.09.26 (2.75 (2.10) 3.35) 1.740-1.87-3.50 (1.95 (2.880) < LOD 75th . which may vary for some chemicals by year and by individual sample.64 (1.30 (.960) .60-4.60) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.83 (2.00) 2.830 (.880 (.790 (.26) .30 (.240 (<LOD-.22-2.950) 90th 1.30) 4.740-.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 * .73-5.20-3.01-3.70 (1.880) < LOD .13) 2.94 (2.60 (2.08 (2.10) 1.650-.303-.400) .50 (1.27 (3.580-.54 (2.90) 2.592) * 50th .280-.54) .20) 3.50-2.S.89) .340-.17) 1.98 (2.910-1.19-1.680-1.29) 1.59-6.55 (3.50 (1.14-1.34) 2.425 (.88) 1.930) 1. and 03-04 are 0.600-1.74-5.17-4.50 (1.657) * * .97 (2.80) 2.210 (<LOD-.810) .160 (<LOD-.1.59-2.79) .600-.949) .80) 3.79) .460-.336-.467 (.780) .00) 1.730) .560-.70-7.76 (1.30) 2.18 (.31-3.20-2.20) 1.80) 3.45 (1.930 (.584) .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 * . 01-02.41 (2.910 (.720-1.77-2.09 (.20 (2.459 (.10-1.505 (.910) 1.700) .20) 2.30) 1.91) 2.13) .960-1.353-.05-3.570 (<LOD-.930-1.2.750) 1.398-.690-.820 (.74) 3.54-2.540 (.

00 (3.07) 1.08-3. Fourth National Report on Human Exposure to Environmental Chemicals 125 .00-3.13 (1.71 (1.739) * .04-5.23) 1.42) .57 (1.39 (1.22) .710 (.92 (1.11-2.99) 1.377-.372 (.08-2.61-3.11 (.820) .280 (<LOD-.320-.930-1.05 (1.66 (2.55 (1.57-4.403) .33) .580 (.830 (.11) 1.820) 1.16-2.75) 6.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .05) 1.64 (2.67-3.760) .250 (<LOD-.300 (<LOD-.72 (1.02-3.61) 2.830) 90th 1.52 (1.20-7.72-4.50 (1.400) .590) * 50th .320-.310 (<LOD-.05-2.62 (2.33 (1.640 (.69 (3.23) 3.23 (.02-3.300-.07) 5.580) .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.71) 2.07) 1.39) 2.36) 3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.700 (.60) 1.900) 1.67) . interval) Selected percentiles ( 95% confidence interval) Total * .550-.350) .41 (.680 (.32-1.52) 3.58) 3.08-3.335-.03-2.43 (1.29-4.22-3.49 (1.500-.448 (.688) * .31-1.840) 1.60) .720-1.790 (.980-1.S.370-.43) 2.62 (1.920) .81) 2.590 (.990-1.710 (.550-1.750 (.45 (1.368) * .850) 1.880) 1.591 (.07-3.25-3.400-1.07) 1.535 (.740) .310 (<LOD-.910) < LOD .690) < LOD < LOD .91 (1.73 (2.597) * .580-.06) 4.82) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.97 (1.58-6.23) 2.08-3.53) .510-.380-.640 (.19 (1.270-.95) 1.630) * .84-6.23) 2.71) .700 (.05) < LOD .75-3.00-1.09) .61-3.520-.230 (<LOD-.485) * * .07-2.08-2.870 (.43) 2.08-2.470 (<LOD-.380-1.65) 2.234 (.42-6.66) .88) .22 (2.17) 2.64 (2.480) .330-.32) 5.42 (.08) 2.73-3.30-2.710 (.87 (2.45 (2.20-2.560-.393 (.460) .510 (.67 (1.75 (1.330 (<LOD-.447 (.67 (1.70 (3.84 (2.60 (1.97 (1.34 (1.285-.10) 2.38 (2.590-1.520 (.490 (.28 (1.90) 2.530 (.07 (.17-2.270-.180 (<LOD-.99) 2.471-.79) 1.02-6.453 (.04) 95th 2.470) .49-4.390-1.08 (2.560-.480-1.92) 3.57-2.72 (2.63 (1.43) 1.22) 4.67) 1.730) .97) 2.32 (.44-2.460-1.55-3.08) 1.80) 2.136-.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 * .742) * * .720 (.38 (1.790) .800-1.870) .75 (2.840) 1.540-.800) < LOD .515) * * .94) .42-8.32) 2.89-3.88 (1.310-.57 (3.92-8.509 (.645) .97) 1.77-4.950-2.78) 3.270 (<LOD-. population from the National Health and Nutrition Examination Survey.444-.250 (<LOD-.16) 1.47 (1.660-.18-2.61 (3.77-3.58 (1.700 (.08-3.70 (2.04-1.79 (1.89 (1.22) 1.750 (.82 (2.03-1.72) 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 * .38-3.98) 1.380) .760) < LOD 75th .32) 1.670 (.77 (3.05-4.552 (.305 (.940-1.24) 4.69 (1.412-.560 (.840) .14 (2.16-1.50) 1.72) 1.440-1.08 (.22-3.47 (1.390) .17) 2.740) < LOD 1.348-.20) 1.253-.510 (.550) .76) 1.06-2.22-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.460 (.550-.47-4.60 (2.640 (.30) 3.318-.44) 2.

3 (14.48-2.12) 1.75-14.0-47.6 (9.0 (38.10-4.61 (1.1-47.17-2.7 (28.0 (8.21 (1.05) 1.0-260) 34.60 (2.43-7.660-2.79 (2.0-110) 42.1 (11.49-2.40) 50th 2.53) 1.0-39.2-80.94 (1.2-62.0-41.0) 20.13 (1.70 (1. 01-02.70 (.6-54.10 (7.1-25.92) * 2.0) 3.0 (7.470 (<LOD-1.5 (24.1) 140 (46.04 (<LOD-2.0) 15.600-2.85) * 2.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.86 (1.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-21.41 (1.0) 42.35-6.5-20.0) 28.0) 17.96) 5.18) 20.58-2.2 (19.0 (20.830-4.1-19.8 (26.0-58.0-110) 34.88) 3.2) 31.70 (1.46-2.8 (12.6 (26.70) 1.1 (26.18) 6.0 (38.88) 1.80-18.46 (.4-76.41) 1.13 (1.19-2.50 (2.4.1-20.67 (1.8) 32.79 (1.0 (40.41-4.30) 11.90-8.0 (21.8 (12.90 (1.3 (12.9) 17.61-2.1) 38.00-24.0 (38.6) 52.70) 5. 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.72 (1.77) 38.50-5.0-53.7-41.0-92.1-40.00 (.0) 4.3 (24.4 (10.7) 47.53) * 2.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 (17.70 (7.0-62.12 (3. and 03-04 are 0.81-2.9 (23.06) * 2.1 (22.0-62.0 (24.0) 3.0-53.64-3.70-17. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.3 (12.42) 1.40) < LOD 2.0 (38.1) 95th 48.19) 2.9 (10.98) * 2.83 (1.1) 38.44) 3.0) 33.00 (.80-2.23-2. and 0.41) 1.9) 38.0) 8.8) 62.11) 2. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0) 4.80) .97) 6.52 (4.0-58.2-26.83-2.3) 33.45) 2.5.23) 9.1 (10.50-7.0) 3.5) 30.0) 18.2-47.0 (38.7-22.0-69.74-2.04) 3.0) 16.S.0 (33.7 (12.50-17.20) 1.59 (1.18) 14.3) 31.0) 32.48) 5.0 (8.0 (38.71-2.26 (.79-2.46-6.44) 2.25-3.0 (38.5-74.0) 6.05-3.0) 4.0) 16.65 (4.4) 38.90 (1.14) 5.10 (1.0-29.9 (19.93-3.66-5.32 (2.10-13.5-45.0) 30.0-50.8) 41.71) 5.9) 48.02 (2. respectively.0-39.0 (37.9) 18.70-6.04-8.41) 5.0 (13.69) 2.06 (1.63-6.0-31.59 (1.40) < LOD 1.0 (11.9 (27.2-27.690-3.05) * 2.4 (19.3 (10.26) 75th 11.27-6.54 (1.80) < LOD 1.10 (1.29) 2.4 (15.0 (6.4-22.87-7.0) 20.10) .0) 45.9 (19.830-3.8-21.5-27.0) 31.92-5.50-20.6-22.0) 5.7) 20.4) 19.57-2.0-49.83 (3.31-6.54 (3.0) 13.07-5.81-3.1 (25.0 (32.82 (1.11 (4.2-39.18.0-52.20-4.98 (1.8) 39.33 (5.57-2.95 (5.86-3.1) 18.2-27.90) 11.45) 2.8 (22.44) Selected percentiles ( 95% confidence interval) Total * 2.40-4.99 (2.2) 16.0 (8.20 (2.0 (25.10 (1.83-2.76 (2.13) 12.610 (<LOD-1.91 (4.0 (20.71 (4.8-24.6-27.2-33.53) 40.1-46.0-43.30 (.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.70) 1.3) 38.09 (4.6 (11.10) 39.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 19.0 (19.64-8.1 (25.530-4.80) 90th 38.23-2.29-4. 0.80) 1.29-9.53 (1.6 (15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30-14.0-230) 35.3 (23.16) 2.5) 69.58) 16.36-2.0) 28.16) * 1.0) 15.0-41. see Data Analysis section) for Survey years 99-00.40-16.78 (1.0) 3. interval) 1.9-51.44-7.3) 26.0 (26.21 (3.6-45.21 (4.76 (2.85 (1.0-41.3) 28.5-40.50-2.78) 9.48-2.2 (12.10 (1.0) 17.77 (1.7 (12.60) < LOD 1.30) 4.

1) 27.06) 75th 9.95-16.16-2.33) 1.1) 17.19) 5.47-17.30) 28.1) 36.6) 3.1) 13.24 (1.00-16.9) 3.1) 13.5 (17.4 (11.2) 13.4) 12.52 (1.33) < LOD 1.0-118) 29.2 (8.45-1.4 (21.7) 23.7-43.3-42.36) 10.46-6.20) Selected percentiles ( 95% confidence interval) Total * 1.0 (25.3-27.3 (20.930 (<LOD-1.37-2.70 (1.6) 3.95-16.870-3.4-39.5 (6.2) 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 1.50-5.2-70.16 (1.8-34.1 (33.4-67.02) 1.88 (4.38) 5.62 (2.29-5.750 (<LOD-1.00) 6.62) 4.48 (4.71) 8.36-13.45 (1.22 (.1 (34.75-6.7-109) 22.5 (8.1) 25.27) 50th 2.870-3.7) 30.0-70.9-41.33-5.19-14.44) 9.14-8.7-47.7) 15.0) 13.0 (39.95) 90th 32.67 (1.4 (12.93) 5.3 (10.2) 41.97 (1.S.99-4.1) 52.8) 11.22-2.1) 27.46-22.35) 1. interval) 1.41 (2.39 (1.06) 1.26-4.0-40.71 (1.72) 2.4) 3.7 (24.67-16.80 (1.1 (39.94) 1.6) 23.3) 28.40 (5.37 (1.1 (50.28) 1.55 (2.00) 1.71-2.9-52.91-2.19 (1.79-17.48) 1.47 (3.1-63.82 (2.22 (2.0) 10.5) 70.2 (15.54-15.6-49.5 (15.0 (23.6-51.8) 32.6) 19.2) 33.03-2.9 (13.5) 27.5-36.96) 2.8) 31.7 (18.03) 1.59-15.1 (12.9) 3.7) 34.0) 25.2) 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.86) * 2.23) < LOD 2.12 (1.23) 37.54-2.9 (39.1) 15.2-34.23-1.68) 47.07-2.8-37.11) < LOD 1.40-7.88 (4.75) * 1.9) 54.0-71.68 (1.9) 24.17-3.6) 11.07-2.0) 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 1.4 (25.96-16.5-97.4-21. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-47.28 (1.5 (15.1) 25.60 (.7-38.75 (1.18) * 2.7 (11.91 (6.84-13. Fourth National Report on Human Exposure to Environmental Chemicals 127 .15 (.6 (11.5-190) 30.88 (1.46) 1.40-4.9 (19.64 (1.46-5.76-2.61-2.3-19.6-32.3) 13.67-3.9-37.31) 2.70-4.7-37.95 (2.0) 47.890-4.8) 15.51) < LOD 1.61-22.2 (21.21 (4.860 (<LOD-1.08) 1.38 (3.2-28.83) .47 (1.17) 2.36 (4.0 (14.67 (1.8) 23.0) 48.670-1.8-45.66 (1.80-8.69-18.4 (19.43) * 2.9 (26.60) 4.680-4.0 (17.7-20.27-3.50 (2.2-38.1-60.56 (2.79 (2.38-5.3-22.61 (1.9 (7.2) 4.26-2.59-2.0 (19.35) .5 (13.2 (9.02) * 1.75 (1.58-2.66) 8.25-3.94) 19.0) 30.9-36.38-1.9-95.4 (25.7) 26.1 (25.20-5.00 (4.4 (5.32 (3.8-26.02 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (7.4) 12.5 (34.8-43.56) 1.43-12.07) 9.59-2.6) 7.5-43.86) * 3.1-22.53) 1.4 (9.08 (1.8 (7.12) 3.4-71.06) 1.06-1.43-2.7) 61.4) 14.0 (6.7-19.58-17.27 (6.9-18.5 (41.09 (5.7) 66. population from the National Health and Nutrition Examination Survey.2 (16.11-2.18-1.0 (23.34) * 1.2) 13.57 (6.6) 112 (40.2) 36.9) 24.52-4.16 (1.888-1.51) .14 (.7 (18.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.94-20.18) 3.6 (24.9 (10.7) 95th 51.66 (1.7 (10.6-38.0 (32.83 (.899-2.82) 1.40 (2.27) 10.33) 2.3 (10.3 (9.32-3.9) 12.16 (1.6 (27.2) 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 2.870-3.69-5.19) 5.88 (1.19-6.4-34.3 (8.22-3.57) 4.0) 3.01 (.35 (2.2 (22.63-5.8) 3.90 (.

interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .430-.720-1.130-.100 (.820 (.12 (.080 (<LOD-.700-1.850) < LOD .050-.080 (<LOD-.730-.680 (.410-.1.32) .610 (.870 (.310) < LOD < LOD < LOD < LOD .S.171) * * .300-.570) . which may vary for some chemicals by year and by individual sample.700-1.990) .510-1.900 (.090 (<LOD-.650-1.15) .320-.60) 1.10 (.140-.760) < LOD .650) .090 (<LOD-.930 (.630 (.680-1.00) .650 (.410-1.770) < LOD 95th .640) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700-1.460 (.450 (. population from the National Health and Nutrition Examination Survey.540) .870 (. 0.090 (<LOD-.310 (.099-.560 (.990) .320 (.190 (.850 (.720) .10) .390) < LOD < LOD .58) .190 (.170-.460-.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 * * * * * * .730) . and 03-04 are 0.20) .130-.390 (.40) .380-.430 (.310-.280) < LOD < LOD < LOD < LOD .640-1.600 (.350) < LOD < LOD < LOD < LOD .820 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks . respectively.860) .290 (<LOD-.140) .110-.30) .870 (.220 (<LOD-.162) * * * * * .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 .550) .300-1.540 (<LOD-. 01-02.160-.330-.120-.310) < LOD < LOD < LOD < LOD .130) .230-.840) .640) .05. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.560 (.470-1.870 (.160) .130-.380-.360-. and 0.610-1.690-1.03) .120-.830) < LOD .410-.36) .470 (.990 (.180) .610-. 128 Fourth National Report on Human Exposure to Environmental Chemicals .940 (.117 (.830) .30) .640 (.1.090 (<LOD-.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.160) .360-.210 (.230) .210 (.270 (.42) .290) < LOD < LOD < LOD < LOD 90th .10) .770 (.870 (.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 * * * * * * * * * .150) .450 (.620 (.290) < LOD < LOD < LOD < LOD .140-.700-1.450 (.30) .150 (<LOD-.220 (.660 (.680) .140-.830 (.540) .420-.870) < LOD .130 (.240 (<LOD-.090 (<LOD-.130) .850 (.200) < LOD < LOD .440-1.10) .610 (. < LOD means less than the limit of detection.120 (<LOD-.380-.42) .530-.490 (.830 (.630 (.084-.350) . see Data Analysis section) for Survey years 99-00.13) .090 (<LOD-.260 (.370-.650) .400-.680-1.740) < LOD .780) < LOD 1.410) < LOD < LOD < LOD < LOD .190 (.860-1.840) .310 (.650-1.370-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.

66) 1.060-.450 (.070 (<LOD-.400) .580 (.870) .650) < LOD .230 (<LOD-.270) < LOD < LOD < LOD < LOD .140-.400 (<LOD-.12) < LOD .670 (.880-1.300-.161) * * .080 (<LOD-.14) 1.140) .03 (.62) 1.070 (<LOD-.110-.650-1.260-.880 (.20) 1.670-1.410-.510-.540 (.730 (.860-2.01 (.940) .110) .720 (.260) .810 (.300-.850 (.100 (<LOD-.610-1.570-.640-1.330 (.580-1.057-.500 (<LOD-.200 (.220) < LOD < LOD < LOD < LOD .240-.700) .800-1.170 (.280) < LOD < LOD < LOD < LOD .410) .540) .390-.19 (.00) < LOD .580 (.490-1.730) .86) .730) .380-.720 (.110) .410) < LOD < LOD .340-.230) < LOD < LOD < LOD < LOD .410-.570-1.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .111) * * * * * .080) .580) .24) .050 (<LOD-.120) .700 (.230-.290) < LOD < LOD < LOD < LOD 90th .520-.320 (<LOD-.460 (.080 (.540 (.960) .760) .410 (.03) .170) < LOD < LOD .60) .380-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .370 (<LOD-.440 (.780) < LOD 1.640) 952 1187 945 997 1328 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .300 (.710-1.170 (.090 (.190 (.78) .500) .67) .310) < LOD < LOD < LOD < LOD .190-.330-.140-.550 (.700-1.860 (.660-1.200 (.360-.140-.110) .100-.570 (.24 (.560 (.070 (<LOD-. population from the National Health and Nutrition Examination Survey.990) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.116 (.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .890 (.780 (.110) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220 (.150-.03 (.090 (<LOD-.190 (.330-.730) .38) 1.740) < LOD 1.360) < LOD < LOD < LOD < LOD .970) .86) .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 * * * * * * .250-.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.410 (.600-1.670 (.02) .43) .390-. Fourth National Report on Human Exposure to Environmental Chemicals 129 .210 (.440-1.070 (<LOD-.700 (.990) .140-.270 (.360-.380-.58) 1.380-.330 (.29 (.S.380 (.120) .360 (.740 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.500-1.860 (.450) .03 (.330-.550 (.084-.600) .36 (1.470 (<LOD-.140-.750) < LOD 95th .940) .180-.02-1.580) < LOD .09) .

99 (1.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0) 5.38-3.750-1.00-17.46 (1.12-1.70-3.30 (1.0) 2.48 (2.47 (3.960 (<LOD-1.20-4.32 (1.36-3.1.88-3.360-1.67) .0) 2.0 (17.20-4.890 (.31-10.03 (.0-39.76 (1.11) .20 (1.110 (<LOD-. which may vary for some chemicals by year and by individual sample.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.87) 12.0 (3.880) 5.70-50.580 (.840 (<LOD-1.1.49 (1.07-3.42) 2.05 (2.0-44.08.70-17.0) 2.94-8.30-3.080-1.39) .60) .35) 5.0) 4.40) 1.68) 2.13 (3.20) < LOD < LOD < LOD < LOD < LOD 1.37) .16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .0 (7.0 (5.610 (.40-7.640 (. 130 Fourth National Report on Human Exposure to Environmental Chemicals .70) 2.0) 3.90 (1. and 0.30) 95th 19.90-20.0) 5.900 (.690 (.510-.770 (<LOD-1.610) < LOD < LOD < LOD < LOD < LOD 2.30 (1.0) 2.840 (.11 (1.94-3.18) 1.53-7.0) 2.07 (3.00-17.0 (17. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2. 0.425-1.0) 7.35) 11.90-37.740 (.40 (1.30 (2.07-3.0-38.99) 11.53) 20.05 (3.20-17.28) 1.74 (3.0 (4.0 (17.24-7.250 (<LOD-.67 (2.15) 19.14) 2. see Data Analysis section) for Survey years 99-00.40-20. respectively.910) 2.0) 2.210-1.0 (17.31) .50) .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 * * * * * * * * * .640 (.400-1.62-8.480-.90-28.28) .170-1.0-38.97) 20.10 (3.830 (. 01-02.49) 17.0) 2.10-3.70-7.14) .52) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.99) 19.0 (5.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.55-8.00) 1.07 (3.90-9.90) .33 (4.380-. < LOD means less than the limit of detection.20 (1.82-4.190-1.0) 4. population from the National Health and Nutrition Examination Survey.01) 5.83) 2.63 (3.60) 1.55-4.86) 4.63) 32.59-5.330 (<LOD-1.36-3.30 (.800) 17.67 (1.260-.23-6.51-8.0 (6.51 (2.370-.87) 5.0) 5.90) .40 (1.52 (1.0) 5.10 (.0 (5.0 (5.74) 5.0-40.590 (.97) 20.0-40.S.12) * * * * * * * * .52 (1.840-3.07 (1.11) 13.960 (.65) 1.750-2.32-9.05-3.800) 90th 13.83-3.720) 2.14-5.870) < LOD < LOD .85-3.48) 13.15) 14.00) .50) 2.850) 16.21) 3.90) .350-.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.90 (2.0 (17.800-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.96 (1.30-7.00 (1.00 (. and 03-04 are 0.26 (2.30-6.21-3.42) .0 (5.691 (.6) 5.0 (4.0) 4.53 (2.0-38.07) 1.40-8.45 (2.00) .30) .10-3.30 (1.40) 2.94 (1.0 (13.10-9.43-4.10 (3.39 (2.61 (1.29-10.730 (.40-4.0 (16.600 (.770) 2.83-3.0) 4.66) 4.49 (1.80 (4.28-9.350-.70-30.620-1.35-10.

02 (.44) .53) .51-4.37) 4.4 (4.730-3.5 (8.890 (.88) 17.75) 5.340-.7 (6.40 (.3) 3.370) < LOD < LOD < LOD < LOD < LOD 1.9 (11.260-.10) 2.50) 11.1) 2.8) 7.14-6.430) 1.64) 30.850-3.48-42.32-6.90-6.02) .770) .740-1.1) 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 * * * * * * .700) < LOD < LOD < LOD < LOD < LOD 1.30 (4.33 (3.4-34.86 (3.85 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.03) 16.5-40.96-25.31) .47) 5.700) 6.8-33.66-47.04-16.74 (2.73 (4.07 (2.69-7.430 (<LOD-.17) 5.150 (<LOD-.80) 3.240-.40-2.57-40.96) 2.50) .0 (9.790 (.0 (4.09-3.270-.92 (2.12-4.00-19.330-1.710 (<LOD-1.02 (1.56) .17 (1.04 (1.840-3.6) 952 1187 934 997 1330 993 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .S.590) 2.580) 16.2-38.56) 2.12 (4.41 (4.67 (2.620-3.7 (12.55 (3.57) 1.28-6.1) 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.190-1.10-3.36 (.474-1.01 (1.41) 18.970-3.8) 7.940-4.88 (2.69) 2.83-11.33-3.5 (11.47-10.98 (4.47) .64-4.59 (1.97) .9) 5.31-18.62 (1. population from the National Health and Nutrition Examination Survey.5) 2.340 (.40-12.89 (2.7) 5.62-17.7) 6.51-44.91) 2.270 (<LOD-.670 (.25 (1.18) 95th 21.33-5.88 (.91-4.07-21.800-2.0) 4.55) 21.31) .23-7.40) 1.32) 9.38 (2.18) 1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .250 (<LOD-.50 (4.310-.31-7.57 (.52 (.27 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.340-.580 (.930) .29-4.86) .8) 2.830 (.50 (2.2 (8.370 (.470 (.22-27.500 (.340-.03) 2.450 (.830-3.650 (.11) .11-5.53) 27.60 (1.1 (5.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.600 (<LOD-1.55) 21.96-8.1 (7.5) 7.7) 4.81-17.8) 4.24) 3.15) 9.13 (2.5) 2.8) 1.39) 20.47-10.560 (.48-7.79 (.360 (.650) 90th 10.960 (.08) .25-38.5 (9.660) < LOD < LOD .44-11.67) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.71 (2.67) 2.33 (1.88-3.580-1.10 (2.77 (.540 (.02-4.748 (.56 (1.320-1.80 (.35 (.390-.260-.71 (.06 (.14 (1.57) 8.48 (4.7) 3.43) .820 (.22) 2.780-4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.3) 2.61) 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 .790) 11.540-1.580) 1.370-1.85-3.00) .25-9.84) 9.67-6.05) .820) .82-11.4) 2.49-2.690-5.630-1.8 (20.83 (4.33-4.860-2.8) 2.45 (1.18) * * * * * * * * .9) 6.29 (4.65 (2.21-3.

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Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Hansen S. Lu C. Caltabiano LM. National Academy of Sciences. Weisskopf C. McConnell R. Keefe TJ. Thompson ML. Lancet. The Pesticide Health Effects Study Group.24(1):18-29.52(10):648-653. Pesticide industry sales and usage . EPA.43(1):38-45. 1991. Scand J Work Environ Health 1998. Vitayavirasak B. Bull Environ Contam Toxicol 1994. Pedersen L. Irish RM. Spurgeon A.12(2):134-141. Hore P. Eskenazi B. Neurotoxicity among pesticide applicators exposed to organophosphates. A behavioral evaluation of pest control workers with short-term.12(2):153-172. van der Hoek W. Stephens R. discrimination. Smit LA. low-level organophosphate exposure on delayed recall. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Seiber J.2000 and 2001 market estimates. Environ Health Perspect 2006. S. Rosenstock L. Ames RG. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Schenker M. Russo J. Washington (DC). Rohlman D. Mounce LM.S. Am J Ind Med 1987. Visuthismajarn P. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Aprea C. Rothlein J. Malathion deposition. Buccafusco JJ. J Toxicol Environ Health A 2005. Neurotoxicol Teratol 1998. Wickremasinghe AR. et al. Environmental Protection Agency (U. Muniz J.epa. et al.nap. Stark A. Masala G. Am J Public Health 1994. Neurotoxicology 2005. metabolite clearance. low-level exposure to the organophosphate diazinon.84(5):731-736.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. et al. Int J Occup Environ Health 2006. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Savage EP. EPA). Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Stokes L. et al. Steenland K. Pilkington A.php?record_id=2126&page=1. Salvini S. Marshall E. and spatial learning in monkeys and rats.58(11):702710. Gladstone EA. Nell V. Gillham R.345(8958):11351139. Phillips J. Environ Health Perspect 2005. Arch Environ Contam Toxicol 2000. 2004. Prendergast MA. Kidd M. Lancet 1995. Lasarev M. Effects of chronic. Robson MG. Effects of long-term organophosphate exposures on neurological symptoms. Berry H. Washington (DC): U. Available at URL: http://www. Lewis JA. Available at URL: http://books. Burcar PJ. U.26(2):199-209. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Bravo R. and cholinesterase status of date dusters and harvesters in California. Claypoole K. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Chrislip D. 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. Occup Environ Med 2001. Narang A.113(4):504-508. Weerasekera G. Rothlein J. Myers JE. Office of Prevention Pesticides and Toxic Substances.38(4):546-563. Arch Environ Health 1988. 4/7/09 Young JG. Takamiya K.332(1-3):71-80. vibration sense and tremor among South African farm workers. 1993 [online].20(2):115-22.114(5):691-696. Jenkins B. Tumino R. Dinoff TM.pdf. Buchanan D.68(3):209-227 Maizlish N. Petchuay C. Calvert IA. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. et al. Rodnitzky RL. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Lasarev M.edu/ openbook. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Daniell WE. J Occup Environ Med 2002. Terry AV Jr. Saieva C. Levy LS. Arch Environ Health 1975. Johnson C. Scherer J. May. Occup Environ Med 1995. O’Malley M. Santana J. Pesticides in the Diets of Infants and Children. Heaton RK. Frasca G. Jamal GA. Chronic neurological sequelae to organophosphate pesticide poisoning. Beach J. Sci Total Environ 2004. Bradman A.338(8761):223-227. National Research Council (NRC).44(4):352-357. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Samuels S. McCauley L.S. Keifer M.30(2):98-103. London L. Muniz J. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. 1/12/09 Peiris-John RJ. Ruberu DK. Lambert WE. Barr DB.52(2):190-195.

These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. For general information about the organophosphorus class of insecticides. For example.Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report.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 . the level may reflect exposure to the environmental degradation products of these pesticides.” 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) 3.5. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. In addition to reflecting exposure to the parent insecticide. parathion and methyl parathion are metabolized to para-nitrophenol. malathion is metabolized to malathion dicarboxylic acid.

10 (1. staying bound to soil particles.20-16.60 (5.50 (2. 1999.90-7.10-17.32) 2.02 (7.25) 1.76 (1.8-15.90 (2.94 (4. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.37) 5.0) 7.83) 1.70-16.77-15. Chlorpyrifos is Urinary 3. Approximately 80.97) 2.45 (1.24-3.S.0 (7.80) 4.77 (1. Approximately 21-24 million pounds per year were used domestically from 1987-1998.3) 8.04-10.4-15.30 (2.38 (3.80) 2.5) 7.5 (8.70-11.70-17.13 (1.00) 3.95 (4.35) 1. chlorpyrifos was no longer registered for indoor residential uses in the United States.43-2.3) 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 1.74-9.66-15.72) 2.50-2.3 (11.8) 9.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.04-10.6) 7.0) 12.60-3.0) 9.EPA.0) 12.50-2.60 (2.20-4. population from the National Health and Nutrition Examination Survey.50 (1.30-5.90 (3.2 (10.47) 1.63 (1. 2005).29-1.0 (10.53 (1.32-1.20 (2.90 (1.92 (1.35) 2.00) 2.29) 90th 7.28) 2.64) 3.40-26.40 (6.50 (1.20) 2.20 (4. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.31-2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.0) 15. Survey Geometric mean (95% conf.30-2. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.5.68 (7.70 (1.37 (4.39-2. For instance.20) 10.70 (1.7) 8.52-2.30) 5. and on plants for days to several weeks.36 (4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.87-6.40 (5.and post-construction structural applications for termite control were to be phased out by 2005 (U. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.80-8.59-2.3 (10.5-24.89 (2.90-8.9 (9.0 (7.15 (1. After 2001. dermal.90 (6.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.77-6.88 (1. Estimated intakes from diet and water have not exceeded recommended intake limits.77) 1.09 (2.44-5.00) 1.7-23.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. 2002).50-14.52-12. 2921-88-2 Chlorpyrifos-methyl CAS No.20-3.19 (1.20-14.30) 4.90 (1.02 (1.30-12.19-3.91 (1.0 (13. Fourth National Report on Human Exposure to Environmental Chemicals 135 .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) 18.50-4.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.30-11.39) 4.89-2. interval) 1. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.4.80-10.40-13.0) 10. Exposure can also result from contact with contaminated surfaces. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.16) 2.7) 9.05-5. and is infrequently detected in ground water (IPCS.10) 2.0) 14. 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.80 (7. The general population may be exposed to chlorpyrifos via oral.55-5.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.47 (4. in 142 urban homes and preschools in North Carolina.90) 7.84) 1.50 (2. USGS.000 pounds are used per year.86) 4.44 (3.60-3.68-2.28-3.26) 7.61-7.27 (7.80) 12.40 (5.96) 3.8) 10.9 (7.74 (1.9-18.0) 11.9) 11. air. applied to structures to kill termites.17 (1.40) 9.02) 1.0) 12. and dust.97-7.44-2.51 (1.10 (5.47-9. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.4 (8.61 (1.43-2.30 (4.09 (3.79-2.0) 10.76 (1.98-15.0 (7.57 (2.90-2.10 (3.50-5.70-15.22 (1.50 (2.71 (6.90) 3. It also has been applied directly on animals to kill mites.67 (2.70-5.31-2.63 (8.70) 1.71 (2.00-8.51) 1.67 (2.60 (4.78 (7.EPA.71 (1.67 (1.03) 1.60-4.20) 2.20-11.S.0) 6.1) 5. 5598-13-0 General Information The chemical 3.66-4.0 (7. and inhalation routes.7) 13.05) 1.0 (7.47-11.61) 75th 3.1-16.0) 10.25) 3.4 and 0.30 (2.0 (9.40) 2.97) 2.62-2.0) 12.60-2.10 (4..10) 6. It has low leachability.63 (2.97) 7.4 (9.13-3.22) 2. 2002).40-2.00-24.90-4.99-4.50-4.0) 12.46-2.5.59) 2.21) 3.20-2.37 (1.80 (1. 2007).0-28.30-1.34) 1.S.80) 1.91) 16.4 (10.95) 7.97) 4.81-2.40-10.0) 8.9 (10.20) 4.30) 4.3 (8. and sprayed to kill mosquitoes.01) 1.47-13.30-9.60) 5.72-4. but can be detected in streams receiving runoff from application sites.9) 697 660 521 701 602 947 Limit of detection (LOD.50-8. pre.0) 8.51-2.24-1.

89) 4.7) 7.83) 1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis. TCPy can also occur in the environment from the breakdown of the parent compounds.14) 1.34-1.24-1.63 (4.12-1.33 (1.79-13. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.05-8.58) 1.65-11.36) 1.91-13.97-3.76 (2.72) 2.6) 10.24-5.66) 1.41 (1.85-4.1 (7. 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.39 (4.940-1.66-11.83-11.81 (3.00 (7.57-2.44 (6. vomiting.54 (2.58-5.22-6.11 (2.92) 3.63-2.86 (3.39-1.39) 6.26-14. Metabolic hydrolysis leads to the formation of TCPy.1-21.08) 6.00-8. and other metabolites..88-8. Betancourt et al.91) 1.25-11.24-4. Once absorbed.94-12.3 (7.19) 6. resulting in excess acetylcholine at nerve terminals.17-4.88-8.16 (4.06-4.44 (5. 2006.80-4.65-15.8) 9.49-2. neurotransmission.33) 2.17-4.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.82) 8.60-3.5 (6. Howard et al.5) 5.58 (4.46 (2.53 (2.51 (1. Thus.37 (1.56 (4.58 (1.31) 1.82 (3. TCPy is more persistent in the environment than chlorpyrifos itself (U. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity. and seizures. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.35) 2.05-4.96) 3.92-2..01) 1.62-7.09-1.72) 1.58) 5.05-3.24) 75th 2.24-24. paralysis. Slotkin et al. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.71 (1.25-12.31-4.31-1.0) 6.06 (1.12-3..06 (5. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.9 (12.02 (5.27-7.42 (6.09-2.99-8..21-1.47 (5.69 (1.28) 2.85 (2.14-8. interval) 1.82-4.64-2.38) 3.42 (5.01) 3.93 (4.05-1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.40) 1.2 (7.32) 1.55 (1.62) 90th 5.22 (4.75) 6.. 2006b).52 (5.55 (4. and producing acute symptoms such as nausea.09-3.93) 2.02) 7.91-4.64 (1.21-6.58 (1. population from the National Health and Nutrition Examination Survey..97 (2.S.07) 5.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .97) 3.90-9..49-2.0) 10.56 (1.42-2. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.86 (1.98 (6.30-4.86 (1.77) 1. Ricceri et al. 1984).11-9.94-14.44 (5. In pesticide applicators.30-1.71) 3.75 (1.85) 1.88-9.5.46 (1.57) 9.3) 8.54) 5.48 (1.. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.49-2.59) 3. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).20 (2.44 (1.66 (1.09 (1.56) 2. 2002).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 1.91) 1.85 (3. 2005.25-1.0) 16.03) 1.44 (1.88 (1.27-1.88-10.59-2.56) 5.91 (3.63 (5.3) 8.S.22) 1.39 (2.73 (1.74) 1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.19-2.33-7.24 (1.07) 1.11 (2.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.28) 2.EPA.64-7.80) 3.1-38.57) 2.3) 9.4) 4.55) 1.29 (3.91) 10.93) 5.88 (1.11) 7.82 (2.78 (1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.2) 6.80-6.24) 5. cholinergic effects.01) 3. 2005.70-4.83-2.23-1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.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. weakness.19-1.99) 1.49 (1.56-2.. 2006. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.76 (3.84-6.33 (5.00-13.97 (3.47-2. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.15 (4.85) 4.1 (10.45-1.95 (1.93 (1.35) 1.12) 1.19) 3.68) 6.88) 6.22 (6.43 (4.48 (2.00) 1.43-10.47 (1.6) 9.60 (1. Survey Geometric mean (95% conf.80-11.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.68) 1. 2000).98 (7.92 (1.05) 3.23) 14.93 (2.35-1.0) 12. 2006a.62) 1.45 (1.20-1.50 (4. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.87-3. Urinary 3.91) 2.47 (1. Roy et al.81) 2.33 (.16) 6.53-5.44-6. Based on animal data and human cholinesterase monitoring during occupational exposure.91 (4.97) 3.57-2.72-2. 2005.95 (3.

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

S.204(2-3):175-180. Hein MJ. National Toxicology Program (NTP). et al. Bucelli R. Barr DB. EPA). Striley C. Neurologic function among termiticide applicators exposed to chlorpyrifos. Rauh V. Chapman P. 4/7/09 Perera FP. Robson M.112(10):1116-1124. Yang D. Freshour NL. U. Bravo R. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. gov/ntpweb/index.114(10):1542-1546. Bravo R.114(2):260-263. Hore P. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Levin ED. et al. et al. Chlorpyrifos: pharmacokinetics in human volunteers. Robertson GL. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Pesticide residues in urine of adults living in the United States: reference range concentrations. Honeycutt R. J Expo Anal Environ Epidemiol 2000. MacIntosh DL. Ryan PB. Tsai WY. Jett DA. Environ Health Perspect 2006b. Biomonitoring for farm families in the farm family exposure study. Bradman A.15(4):297-309.9(5):494-501. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. et al. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Howard AS. Bailey SL. Chrislip DW. Third National Report on Human Exposure to Environmental Chemicals. Howell RJ. Ozkaynak H. Shealy DB. Tate CA. Lorenzini P. et al.6-trichloro-2-pyridinol. Baker BA. Bruun D. Toxicol Appl Pharmacol 2005. Ryde IT. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Freeman N. mothers and fathers living in farm and non-farm households in Iowa. Harley K. Zhang J. Steenland K. Jewell NP. Toxicol Appl Pharmacol 1984.htm. Hardt J.inchem. Toepel K.5. Curwin BD. Angerer J. Alexander BH. Fenske RA. Chuang JC. Sharma V. et al. Freeman N. Hines CJ. Pellizzari E. Hammerstrom KA. 1992. Environ Health Perspect 2005. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Chlorpyrifos. Seidler FJ. et al. Dick RB. Executive summary of safety and toxicity information. Saunders JH. Environ Health Perspect 2006a. Environ Health Perspect 2004. Slotkin TA. A longitudinal investigation of selected pesticide metabolites in urine. Ricceri L.6-trichloro 2-pyridinol in their everyday environments.5. J Expo Anal Environ Epidemiol 2005. Kromhout H. Seidler FJ.114(5):746-751. Capone F.niehs. Barr DB. Environmental Health Criteria 198. Interim registration eligibility decision for chlorpyrifos.71:99108. Gregg M. Levin ED. Baker S. Barr DB. et al.S. Adgate JL.10(4):327-340. Meeker JD. Mandel JS. Weltzien E.31 Suppl 1:98-104. Sheldon LS. Scand J Work Environ Health 2005.111(2):201-205. Herrick RF. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures.15(3):271-281. Bennett DH.93(1):105-113. Heederik D. 2921-882. Eskenazi B. Head SL. Kinney P. Environ Health Perspect 2003.51(1):53-65.207(2):112-124. Morgan MK. Seidler FJ. Environ Res 1995.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Acquavella JF. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . J Expo Anal Environ Epidemiol 1999. Urinary pesticide concentrations among children. Barr D. Camann D. Jones PA. Brain Res Dev Brain Res 2005. Reid TM. et al. et al. Cometa MF.73:8-15. Needham LL. Temporal variability of urinary levels of nonpersistent insecticides in adult men.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Venerosi A. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Lioy PJ. Slotkin TA. International Programme on Chemical Safety-INCHEM (IPCS). Exposures of preschool children to chlorpyrifos and its degradation product 3. Available at URL: http://ntp.org/documents/jmpr/jmpmono/ v99pr03. Environ Health Perspect 2000. Slotkin TA. Int J Hyg Environ Health 2001. Hill RH Jr. Ann Occup Hyg 2007. Edwards RD. Environmental Protection Agency (U. chlorpyrifos. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 1999. Fortuna S. Environ Health Perspect 2006. Lu C. 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. February 5.155(1):71-80. Ryan L. Available at URL: http://www.113(2):211-219. Croghan CW. Lein PJ. Wartenberg D.nih. Atlanta (GA). 4/7/09 Koch HM. Sanderson WT. Roy TS. Rick DL. Toxicol Sci 2006.108(4):293-300. J Expo Anal Environ Epidemiol 2005. 2005. Nolan RJ. Gurunathan S. Irish R.

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

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

270) < LOD 659 701 920 Limit of detection (LOD.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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection. 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 .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey.S. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.200 (<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. Fourth National Report on Human Exposure to Environmental Chemicals 141 .380 (<LOD-. which may vary for some chemicals by year and by individual sample. 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 .S.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 .670 (<LOD-1.200 (<LOD-.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.

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

and particularly when it was ingested in granular form. Once absorbed. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. but is rapidly absorbed orally (IPCS.7. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS.S. 1998). < LOD means less than the limit of detection. Diazinon is not well-absorbed through the skin. Survey Geometric mean (95% conf. 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. Inhalational and dermal routes of exposure can be significant for pesticide applicators.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. since 2004. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. 1998. in the past.2 and 0.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.49 (<LOD-2. population from the National Health and Nutrition Examination Survey. Estimated intakes from diet and water do not exceed recommended intake limits (U. and forage crops. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.S. diazinon produced wild bird kills before use restrictions were in place. seed and foliar applications are planned to be phased out (U. diazinon cannot be sold for residential use. Prior to 2000. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). It is also used for cattle ear tag applications to control flies and ticks and. and other metabolites. fruits. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. diazinon was widely used in residential and garden application. USGS. 2004). an organophosphorus insecticide that is used to control insects on nuts.EPA. about 13 million pounds of diazinon were used annually on agricultural sites in the United States.EPA.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. vegetable. Fourth National Report on Human Exposure to Environmental Chemicals 143 . Most granular formulations. 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. 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. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Before these restrictions.45 (<LOD-3.S. 2007). It is toxic to birds. in some pest strips. aerial. which may vary for some chemicals by year and by individual sample. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. but these uses have been phased out. 2004).

2003). 1998). vomiting. resulting in excess acetylcholine at nerve terminals.76 (<LOD-3. 2000.EPA considers diazinon unlikely to be carcinogenic in humans. subsamples of NHANES 1999-2000 and 20012002. Intoxications in humans from intentional overdose. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. population from the National Health and Nutrition Examination Survey. weakness. EPA at: http://www..45 and 1. In two nonrandom samples of United States adults and children. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. or reproductive toxicant (IPCS.S. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.atsdr.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.49 μg/L. 1986 Rajendra et al. agricultural. animal carcinogen.gov/pesticides/..Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. 1992). respectively (Baker et al. In animals.S. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. and producing acute symptoms such as nausea.html and from U. paralysis. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. Thus.. Diazinon is not considered to be a mutagen. 1986. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. in the 2001-2002 subsample (CDC. 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. teratogen. At high doses.gov/toxpro2.72 (<LOD-4. Seifert and Pewnim. In the U. Additional information about external exposure (i. respectively. environmental levels) and health effects is available from ATSDR at: http://www.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. and indoor applications have been documented. Olsson et al.e. 2002).. 1998). In addition to being a human metabolite of diazinon.S. diazinon does not accumulate in tissues (IPCS. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. Diazinon has moderate acute toxicity in animal studies. and seizures. The U.cdc. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure.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. 144 Fourth National Report on Human Exposure to Environmental Chemicals .epa. cholinergic effects..

. Bull Environ Contam Toxicol 1986. Barr DB. Swan et al. 2006). Study for Future Families Research Group. Garfitt SJ. Liu F. Anal Bioanal Chem 2003. Drobnis EZ. March 2006. Redmon JB. Beeson MD. Dumas P. Biochem Pharmacol 1992. Available at URL: http://pubs. In 23 children. Barr DB. Cocker J.inchem. J Expo Anal Environ Epidemiol 2000. Ann Occup Hyg 2006. In a small number of men visiting fertility clinics in Missouri and Minnesota. Environmental Protection Agency (U.44(11):2243-2250.gov/ oppsrrd1/REDs/diazinon_ired. Interim reregistration eligibility decision (IRED. Available at URL: http://www. Sadowski MA. Swan SH.. Barr DB. Jones K.376(6):808-815. 1992-2001. Oloffs PC. Diazinon. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Third National Report on Human Exposure to Environmental Chemicals.S. Available at URL: http://www.gov/circ/2005/1291/. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Environ Health Perspect 2006. Banister E. 2007 [online]. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Brunet RC. In 54 Canadian greenhouse workers. Drug Chem Toxicol 1986. 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. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Bouchard M. Toepel K.9(2):117-131. Semen quality in relation to biomarkers of pesticide exposure. May 2004. Geological Survey (USGS). Barr DB. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Centers for Disease Control and Prevention (CDC).htm.S. Carrier G. et al.Organophosphorus Insecticides: Specific Metabolites 2005). Seifert J. 1/14/09 U. Toxicol Lett 2002. Diazinon. Fenske RA.111(12):1478-1484. Bravo R.usgs.org/documents/ehc/ehc/ehc198. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Atlanta (GA). Driskell WJ. Oloffs PC. revised February 15. 2006).37(4):501-507. Rajendra W.epa. Effect of sublethal levels of diazinon: histopathology of liver.114(2):260-263. Baker SE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Mason HJ. Kruse RL.pdf. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Irish R. 4/7/09 Lu C. International Programme on Chemical Safety-INCHEM (IPCS). Environmental Health Criteria 198.134(1-3):105-113.50(5):505-515. Olsson AO. Noisel N. 2005. Pewnim T.10(6 Pt 2):789-798. Environ Health Perspect 2003. EPA). (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Pesticides in the Nation’s Streams and Ground Water. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Nguyen JV. 1998. References Anthony J. Needham LL. EPA 738-R-04-006. U. Banister EW. 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. The Quality of Our Nation’s Waters.

It has a short halflife in soils and water and is not considered persistent in the environment. inhalational.S. Most of the estimated 15 million pounds used annually are applied to cotton (U. phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide. weakness. shrubs. 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. the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate.S. usually only a small fraction of the crop is treated. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. It is moderately to highly toxic to fish.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).64. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Malathion is slowly absorbed through the skin. 2007).EPA. and producing acute symptoms such as nausea. < LOD means less than the limit of detection. see Data Analysis section) for Survey year 99-00 is 2. and seizures. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al. and plants. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Survey Geometric mean (95% conf. ornamental trees. malathion dicarboxylic acid. in fruit fly control. which may vary for some chemicals by year and by individual sample. 2003). Once they are absorbed. Compared with other organophosphorus insecticides. 146 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey. When malathion is used on food or feed crops. Pesticide applicators and agricultural workers can have higher exposures via dermal. 2006). which is an organophosphorus insecticide that is used on a wide variety of agricultural crops. Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and in government programs such as the USDA’s Boll Weevil Eradication Program. malathion has low acute toxicity. Metabolism of malathion leads to the formation of malathion monocarboxylic acid.S. paralysis. Thus. Estimated intakes for the general population have not exceeded recommended intake limits.EPA.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff. Malathion is infrequently detected in groundwater sampling (USGS. Malathion is also used medically in lotion form (0. Limited general population exposure occurs through the diet. gardens. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion. It is registered for use in public health mosquito control. In addition to being a metabolite of malathion. 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. or oral routes (U. 2000). depending on the species.80 (<LOD-5.5%) to kill body lice. At high doses. as well as lawns. cholinergic effects.. but is more rapidly and efficiently absorbed via ingestion. vomiting. and other metabolites. resulting in excess acetylcholine at nerve terminals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Human studies of single oral doses between 0.e. 2005. 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. 2006).S. 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. environmental levels) and health effects is available from ATSDR at: http://www. Malathion itself has not been considered genotoxic (U. Lu et al... CDC.. 2004). Toxicity from unprotected bystander exposure during applications is rare (U.EPA.74 (<LOD-5.. 1999).. 2005).gov/toxpro2..html and from U.epa.S. and it is not considered an animal teratogen or a reproductive toxicant. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh 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. 1990). 1996. 2006).atsdr. 2002. Of 382 pregnant women living in an agricultural community. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 147 .. Additional information about external exposure (i. but cholinesterase activity was not affected. Flessel et al. 1993. EPA at: http://www.EPA. 1987. Thomas et al.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 2000). Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. Pluth et al..S. 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. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. 2001.. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 2005). but isomalathion. 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.S. Giri et al. 2003). representative subsample from NHANES 19992000 (Adgate.gov/pesticides/.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. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. IARC considers malathion not classifiable as a human carcinogen.5 and 5. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. Survey Geometric mean (95% conf. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 1999. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..S. 2006). some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample..cdc. Biomonitoring studies of malathion dicarboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of malathion than are found in the general population.

2007 [online]. Goldhaber M. Barr DB. Krieger RI. 2005. A longitudinal investigation of selected pesticide metabolites in urine. Nicklas JA. Reregistration eligibility decision (RED) Malathion.56(10):2393-2399. Barr DB. EPA). Kedan G. Albertini RJ. Blasiak J. Available at URL: http://pubs.org/documents/jmpr/jmpmono/v2003pr06. Swan SH. Environ Health Perspect 2006. Eberly LE. revised February 15.114(2):260-263.74(2):following table of contents.epa. Neutra R. Harris JA. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Jewell NP. Fenske RA.S. Carrier G. Environmental Protection Agency (U. Gosselin NH. Eskenazi B. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.132(4):794-795. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Harley K. Bravo R. Rappaport E. 6/1/09 U.445(2):275-283. Bradman A. Irish R. Toxicol Sci 2003 May. Pesticides in the Nation’s Streams and Ground Water. Lioy PJ. Dinoff TM.9(5):494-501. Toepel K. Available at URL: http://www. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.gov/oppsrrd1/REDs/ malathion_red.inchem.109(6):583-590. Curl CL. 1992-2001. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Mutat Res 2002. Sharma GD.15(2):164-171. Barr DB. Cancer Res 1996. Reproductive outcome in women exposed to malathion. U. Trzeciak A. metabolite clearance. Environ Health Perspect 2004.38(4):546-553. Lu C.73(1):182-94. Petitti D.pdf.usgs. O’Neill JP.S. Griffith W. Freeman NC.S.112(10):1116-1124. Environ Health Perspect 2001. Giri S.22(1):7-17. Hammerstrom KA. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.gov/circ/2005/1291/. Atlanta (GA). Ryan PB. Barr DB. Weltzien E. htm. Malathion (addendum). Am J Public Health 1987. Erratum in: Toxicol Sci 2003 Aug.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Lu C.514(1-2):223231. Malathion deposition. Geological Survey (USGS). EPA 738-R06-030. Clayton CA. and cholinesterase status of date dusters and harvesters in California. Hooper K. Prasad SB. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure.77:1009-1010. Arch Environ Contam Toxicol 2000. et al. Thomas D. Flessel P. Genetic toxicity of malathion: a review. Szyfter K. International Programme on Chemical Safety-INCHEM (IPCS). July 2006. Samuel O. et al. Pluth JM. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. March 2006. MacIntosh DL. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 4/7/09 Kissel JC. J Expo Anal Environ Epidemiol 2005. Dumoulin MJ. The Quality of Our Nation’s Waters. Bouchard M. Brunet RC. Hertz-Picciotto I. Quintana PJ. J Expo Anal Environ Epidemiol 1999. Giri A. Needham LL. Am J Epidemiol 1990. Available at URL: http://www. Environ Mol Mutagen 1993. Jaloszynski P. Grether JK. et al. Mutat Res 1999.

28-4.71 (2. 2000).11-4.80 (2.30-5.79) 4.20) 5. all registered uses were voluntarily cancelled (U.10 (3. Fourth National Report on Human Exposure to Environmental Chemicals 149 .0 (3. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. and has a short half-life in soils and on plants.50) 1.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . 2002.37-2.910) < LOD < LOD . Ethyl parathion.32-1.37-4.18-3.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .67 (1.19 (.S.70) 2.12) < LOD < LOD 1.0) 3. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.44) 2.50-9.298-00-0 Ethyl Parathion CAS No.50) 3.50) 2.50 (2. 2007). with limited applications in agriculture. 2006).300-.36-1.10-1.00 (2.69 (2.70) 2.05) 4.01) 695 660 518 679 603 941 Limit of detection (LOD.70-6.50) 3.46 (3. Survey Geometric mean (95% conf.70 (<LOD-3.20 (2. < LOD means less than the limit of detection.22-3.21-1.37-4.0) 3. peak domestic use was as high as 5-6 million pounds per year. binds tightly to soils resulting in low leachability.10-11.47) 2.70 (3. more slowly absorbed through the skin.790 (<LOD-.80) 2.60-36.28 (1.50 (1.50 (1. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.57-4.58) 3.69) 4.40) 4.40) 2.00) 3.910) < LOD . Increased risk of exposure via dermal.EPA.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .61) < LOD 1.90-9.02-6.990-1.74) 5.EPA.01) 4.09-1.10) 4.S.21 (2. Once absorbed.90 (1. fish.41-4.00 (2..0) 2.34 (3.10 (<LOD-6. Methyl Parathion.850) < LOD .91-3.57) 1.1.20 (<LOD-2.30 (1.30-3.32 (1. population from the National Health and Nutrition Examination Survey. Many previous registered agricultural uses of methyl parathion have been cancelled (U.10 (3. It had been applied to cotton. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. but by 2003. which may vary for some chemicals by year and by individual sample.. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. pulmonary.60 (4. Methyl parathion is not registered for residential use in the United States. Morgan et al. and eliminated rapidly from the body after absorption (Kramer et al.15-3.71 (3. Estimated intakes from diet and drinking water have been below recommended limits.70 (2.33 (1.70 (2.32-1.700 (<LOD-.730 (<LOD-.37) 2.50 (1.40 (1. and of the chemical nitrobenzene. 2003).28 (1. 1977).48) 90th 2.60-5. ethyl parathion.16) < LOD 1.40-3.70-6. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.70) 2.8 and 0.45) 5.13-1. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.32-3.860 (<LOD-1.60-24. methyl parathion was rapidly absorbed after ingestion.01-4. and aquatic invertebrates.50 (1.60) 1.910) < LOD < LOD < LOD 1.S.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.60-19.70-3.0) 3.10) 22.30 (2. and oral routes can occur in pesticide and agricultural workers (Muttray et al. In the 1990s.45 (1.89 (2.61) < LOD 1.80 (2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40) 1.67) < LOD 1.50-14.80 (1. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.62 (1. Methyl parathion has low water solubility. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-3.66 (2.26 (1.92) 5. was once a restricted-use insecticide with limited applications on certain agricultural crops. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.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. and to a lesser extent.40-4.0) 3.85 (2.20-5.40-4.33) 2..27) 2.30-16. Both are toxic to birds.50 (2.70 (2.92-2. Given its limited use.72 (3.90-11.70-6.49 (1. In animal studies. first registered in 1948.0) 3. on cereal grains. Methyl parathion use is highly restricted.940 (<LOD-2.770 (.11) 2.0) 4.

.89 (2.2) 2. 2005.950) < LOD .720-1. Orsorio et al. 1990. paralysis. Zurich et al.88) 1. gov/pesticides/. 1995). WHO.790-.30) 3.98-7.680 (<LOD-1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.29 (2.73 (1.95) 1.57) 6.. The metabolite.540) < LOD .08 (1.atsdr. paranitrophenol.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 150 Fourth National Report on Human Exposure to Environmental Chemicals .59 (1.440 (<LOD-.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 .78) 2. 2006.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .31) < LOD .77-7.71 (1.2) 2.29) 2.96 (1.01 (2.88 (1.3) 2.11-4..830-1.38-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.23) 1.79 (1.15) 3. Lores et al. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.720 (<LOD-.01-3. Parathion and methyl parathion have high acute toxicity in animal testing.04) 1.33-3. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.44-3.4 (3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.16-4.09) 2. 2003. Jaga and Dharmani. 2004).17-4.310-.93 (2.60 (1.78-2.13) 4. vomiting.370 (<LOD-.10) 90th 2.92 (2.44-3.17) .14-3.39) 1.78 (2.00) 2.94-4.00 (1.7) 3.26 (1.48-4.96 (1.25 (2.84) 3.800-1.83 (1.30-1.11) 1.37-1.html and from U.840 (.430 (. At high animal doses of methyl parathion.97-10.08-3. U. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown..04 (2. resulting in excess acetylcholine at nerve terminals.10 (1.08) < LOD .56-2.790-1.Organophosphorus Insecticides: Specific Metabolites Metabolites”).940 (<LOD-1. 1991).epa. In addition to being a metabolite of methyl and ethyl parathion. teratogenic.31-3.9) 1.57-2.20) 3.91) 1.76-14.70) 3.970 (.55) 2.82 (2.39 (1. In large doses.21-21.S..97 (2.78-2. and unintentional acute or chronic high-level occupational exposure (Hill et al. 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.e. methyl parathion.850-1.55 (<LOD-3. but lists ethyl parathion as a possible human carcinogen. population from the National Health and Nutrition Examination Survey. Methyl Parathion.67 (3.67-2.00 (1. 2006.87 (1. and other metabolites.. Thus.500) < LOD < LOD .01 (.57-7.930 (.cdc. cholinergic effects.61) 4. and seizures. environmental levels) and health effects is available from ATSDR at: http://www.07) 2.41-2. EPA at: http://www. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.60-2. weakness.20 (3. 1978.72-2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.870) < LOD . 1995.33-6. gov/toxpro2.29) 1.35-3.530) < LOD < LOD < LOD . Methyl parathion is not considered genotoxic. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. does not inhibit acetylcholinesterase enzymes.79) 1. Karanth and Pope et al. and producing acute symptoms such as nausea.86 (2.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD ..930 (.20) .80 (1.35-3.S.60) 2.13-12.97 (<LOD-4.26) 17.970 (.80 (1.43) 4.07 (1.71) 1.94-47.89 (2. Slotkin et al. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.25) 1. ethyl parathion. Additional information about external exposure (i.880 (..21) 1.33-3.980 (.690-1.15-10.400 (<LOD-. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. 2004). Survey Geometric mean (95% conf.EPA considers methyl parathion unlikely to be carcinogenic to humans.91 (1.640) < LOD < LOD 1.1) 2.90 (1.730-1. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.05) 4. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.S.82) < LOD . accidental exposure.

Griffith W. Available at URL: http:// www. and many residents were symptomatic (Barr et al. Pope C.21(1):5767. Lewalter J.org/documents/jmpr/jmpmono/v95pr14. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect..inchem. Rubin et al. Costa LG. Barr JR. Dharmani C. Moomey CM.. 2005). end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Runkle KD.110 Suppl 6:1075-1078. et al. Eskenazi B. and levels were similar or slightly lower that those in a small convenience sample of the U. Moseman RF. 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. 2005. Environ Health Perspect 2004. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.25(5):599-606. Baker SE. Baker S.htm. Alley CC. Shealy DB. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Barr DB. Turner WE. 2005). Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. population (Olsson et al. References Barr DB. Arch Environ Contam Toxicol 1977. 2005. Methyl parathion: an organophosphate insecticide not quite forgotten.S.. Guizzetti M. Pathak S. Slach EF. 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. CDC. Karanth S.112(10):1116-1124. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lin LI. Head SL. Hetzler HL.215(3):182-190. McCann et al. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Baker RC. Neurotoxicol Teratol 2003. Role of individual susceptibility in risk assessment of pesticides. J Expo Anal Environ Epidemiol 2005. Morgan DP. Kedan G. Giordano G. Gregg M. Environ Health Perspect 2002. Rockhold RW.14(4):213-216. Environ Res 1995. Clark JM. Hill RH Jr.5 mg (500 µg)/g creatinine for workers at the end of shift.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. et al.33(5):270-276. International Programme on Chemical Safety-INCHEM (IPCS). Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. 2002. In a study of workers who handle parathion.S. J Biomed Sci 2002. Fourth National Report on Human Exposure to Environmental Chemicals 151 . et al. 2004). oral or dermal administration. Occup Environ Med 1999. Ashley DL. ACGIH recommends a BEI of 0.. Third National Report on Human Exposure to Environmental Chemicals. Wellman SE.. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Hill RH Jr. Barr DB. 1995. Needham LL. 1999).110 Suppl 6:1085-1091.9:311-320. McCann KG. a range of values several hundred times higher than levels found in the U..56(7):449553. Jewell NP. Environ Health Perspect 2002. Cline RE. Leng G. 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. Pesticide workers may have much higher levels following pesticide applications. Curl CL. Chicago area methyl parathion response. Arch Environ Health 1978. 2005. 2002). Toxicology 2005. McClure PC. Rev Environ Health 2006. et al. Lores EM. DiPietro E. Atlanta (GA). Bradman A.6(2-3):159-173. et al. Bradway DE. Pharmacokinetics of methyl parathion: a comparison following single intravenous. J Anal Toxicol 1990. general population (CDC. Weltzien E. 1995). Harley K. Hill et al. 2002.. Hryhorczuk DO. Parathion-Methyl (addendum). Bailey SL.71:99108.15(2):164-171. Laboratory investigation of a poisoning epidemic in Sierra Leone. Kissel JC. Barr DB. 4/7/09 Jaga K. Head SL. Lu C. Centers for Disease Control and Prevention (CDC). Pesticide residues in urine of adults living in the United States: reference range concentrations. 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. Kramer RE.

Facts. Nguyen JV. 2007 [online]. Ames RG. Available at URL: http://www. Barr DB.Organophosphorus Insecticides: Specific Metabolites Muttray A. Environ Health Perspect 2006. Schilter B. Pesticides in the Nation’s Streams and Ground Water.pdf. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Slotkin TA. Am J Ind Med 1991. Osorio AM.201(2):97-104. pdf.D. Backer G. Sadowski MA. Hill G.20(4):533-546. Geological Survey (USGS).S. Costa LG. EPA). Yacovac R. Hill RH Jr. 1995-1996. Ethyl parathion. 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. 2004. Investigation of a fatality among parathion applicators in California. Anal Bioanal Chem 2003. EPA-738-FOO-009. Honegger P. The Quality of Our Nation’s Waters. gov/oppsrrd1/REDs/methylparathion_ired. Interim reregistration eligibility decision (IRED) for Methyl Parathion.114(10):1542-1546. R. March 2006. Environ Health Perspect 2002. 6/1/09 World Health Organization (WHO). Methyl parathion in drinking water. Levin ED. Mengle DC. U. Letzel S. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Olsson AO. September 2000. External and internal exposure of wine growers spraying methyl parathion. Kieszak S.S.110 Suppl 6:1047-1051.S. Toxicol Lett 2006.who. Environmental Protection Agency (U. Dunlop B.376(6):808-815.04/106.E. Esteban E. 1992-2001.usgs. 0153. 5/19/09 Zurich MG.S. May 2003. Rubin C. et al. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Seidler FJ. Ryde IT. Available at URL: http://www.S. Ohio.epa. EPA). Available at URL: http://pubs. Case No. Available at URL: http://www. Rosenberg J.int/water_sanitation_health/dwq/chemicals/ methylparathion.pdf. Monnet-Tschudi F.162(2-3):219-224. revised February 15.epa. 1/14/09 U. Environmental Protection Agency (U. WHO/SDE/WSH/03.gov/circ/2005/1291/.gov/oppsrrd1/REDs/factsheets/0155fct. Jung D. Toxicol Appl Pharmacol 2004. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Tate CA. 1/12/07 U.

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

840 (. 154 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.680 (<LOD-.700-1.840) 669 687 929 Limit of detection (LOD.200-. see Data Analysis section) for Survey year 01-02 is 0.07) .780 (.250 (<LOD-.94) .27) .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .15) < 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.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .760 (<LOD-.700-.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .210-1.780 (. which may vary for some chemicals by year and by individual sample.17 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670 (<LOD-1.430 (<LOD-.410 (<LOD-1.780 (<LOD-1.31) . * 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 .S.300-1.950) < LOD < LOD 1.740 (.S. Survey Geometric mean (95% conf.210 (<LOD-.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. < LOD means less than the limit of detection.780 (<LOD-1.580-1.470 (. Survey Geometric mean (95% conf.610 (<LOD-1.210-.820) < LOD < LOD .770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .740-1.21) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .2.55) .850 (.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . 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.64) .500 (. 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.

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

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

Salzgeber SA. Additional information about pesticides is available from U. Environ Health Perspect 1999. Toxicol Appl Pharmacol 1991. Neurotoxicol Teratol 2001. 2005). Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Thomson BM. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. 2001. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR.. Agrawal AK. Effects of prenatal exposure to deltamethrin on forced swimming behavior.. Biochem Biophys Res Commun 1998. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Kim HS. Wang SL. Kunimatsu et al. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. McCarthy et al. Zhao RC. Kuhn KH.. Shin JH. and seizures (ATSDR. 2005). Pogo BG.cdc. 2003. Shaw IC.50(2):245-255. Wolff MS. 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.. hypersensitivity. salivation.8(1):197-202.27(12):1273-1283. epa. Wieseler B.. Xenobiotica 1997. Moniz et al.atsdr. Caudle WM. Yamada T. Ray et al. 2002. Neurosci Lett 2001. September 2003. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Lee SJ. Pyrethroid pesticide-induced alterations in dopamine transporter function. 1999. Sugiri D. and striatal dopamine levels in male and female rats. EPA at: http://www. Eriksson P. Guillot TS. Spinosa HS..1/15/09 Aziz MH. bioallethrin and deltamethrin. et al. 2003. Kamita Y.27(4):609-614. J Reprod Dev 2004.35(2 Pt 1):227-237. In developing rodents. Kim TS. Shukla Y. WHO. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. 2006). Shafer. J Environ Monit 2006.gov/toxpro2. Yang J. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley.251(3):855-859. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Kunimatsu T. Song L. 1998. 2006. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.300(3):161-165. Available from URL: http://www. 2003. et al. Lewalter J.. Garey J. Idel H.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Lazarini CA. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides.html. Regul Toxicol Pharmacol 2002. Go et al. Wolff MS.. 2003. Lazarini et al. Leng G. Varoli FM. Leng A. Soderlund et al. McCarthy AR. Bull Environ Contam Toxicol 1999. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Chen JH. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Elwan et al. 2005). Richardson JR. Kuhn K. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. 1991. Garey and Wolff. choreoathetosis. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Florio JC. Go V. Abell AD. Leng G.atsdr. Toxicol Appl Pharmacol 2006. Bernardi MM.gov/toxprofiles/ tp155. References Agency for Toxic Substances and Disease Registry (ATSDR). neurochemical changes in cholinergic. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al..html. Idel H. Kim et al.. 2004. In California. tremor. Estrogenicity of pyrethroid insecticide metabolites. Toxicological profile for pyrethrins and pyrethroids. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Garey J. et al. 2002). Sunami O. Neurotoxicol Teratol 2005. Kim IY. Lemonica IP. dopaminergic. Hu JY. Generally.S. Neurotoxic effects of two different pyrethroids. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Fredriksson A. Seth PK.62:101-108. Int J Hyg Environ Health 2002. Berger-Preiss E. Okuno Y. Adhami VM.107(3):173-177. Elwan MA. 2000. Hu et al. Ose K. 2002).23(6):665-673. et al. Moniz AC.. Indoor pyrethroid exposure in homes with woollen textile floor coverings. 2001. Levsen K. Leng G. and permethrin) in the Hershberger and uterotrophic assays. Ranft U. Miller GW.205(6):459-472.gov/pesticides/ and from ATSDR at: http://www. Cruz-Casallas PE. Kang IH.211(3):188-197.108(1):78-85. Eriksson and Fredriksson.. Bernardi MM. motor activity. cdc. 2006. Pauluhn J.. fenvalerate. 2005).8(1):18-21. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides.

Shafer TJ. 5/26/09 U. pdf.S. Permethrin. synergies. Rev Environ Contam Toxicol 2006. Available at URL: http://whqlibdoc. Environmental Protection Agency (U.S. Environmental Protection Agency (U. Laird WJ.htm. EPA). Available at URL: http://pubs. June 2006a. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .38:95-101. J Toxicol Clin Toxicol 2000.gov/oppsrrd1/REDs/cypermethrin_red. March 2006. Piccirillo VJ. et al. Mullin LS. Pyrethroid illnesses in California. 19962002.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.epa. Environ Health Perspect 2005. O’Malley M. resmethrin. Pyrethroid insecticides: poisoning syndromes.171:3-59. Lesser JE. 5/26/09 U.who. Marsh JR. 2007. Available at URL: http://www. Toxicology 2002.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. and therapy.186:57-72.S.S. Geological Survey (USGS). 1992–2001. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Soderlund DM. Crofton KM. 2005. Pesticides in the Nation’s Streams and Ground Water. Revised February 25.10. sumithrin synthetic pyrethroids for mosquito control. Xenobiotica 1992.Pyrethroid Pesticides Ray DE.htm.usgs.gov/ circ/2005/1291/. Spencer J. Forshaw PJ.113(2):123-136. EPA). Available at URL: http://www. EPA). Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Safety of pyrethroids for public health use. Sheets LP. Clark JM. 5/26/09 U. World Health Organization (WHO).pdf. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Meyer DA. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.epa. Available at URL: http://www. Environmental Protection Agency (U.epa. April 2002. 5/26/09 Woollen BH. U.S.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Pesticide and Evaluation Scheme. Reregistration Eligibility Decision for Cypermethrin. Sargent D. June 2006b.22(8):983-991.S.S.

Baker et al. 2005). Leng et al.S. Studies in Germany of 396 children and adolescents (Becker et al.. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002...68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. 2005). 2005. 2003). most of which were dermal and respiratory irritations (Spencer and O’Malley. Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al.. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. 2006). representative 2001-2002 NHANES subsample (CDC. Fourth National Report on Human Exposure to Environmental Chemicals 159 . Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). 2003). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. 2006) and 1177 urban adults and children (Heudorf et al. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.S. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate.95 µg/L. Cyfluthrin is rapidly metabolized and eliminated from the body. 2003).. Thus. Finding a measurable amount of 4-fluoro-3-phenoxybenzoic acid in urine does not mean that the level will result in an adverse health effect. 2001.. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.2 μg/L) in the U. Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population.. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0.Pyrethroid Pesticides Cyfluthrin CAS No. representative subsample in NHANES 2001-2002 (CDC. Urinary levels for adults and children in these studies were similar (Heudorf et al. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. 2004). 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. Following an indoor application exposure.

160 Fourth National Report on Human Exposure to Environmental Chemicals .2 and 0.S. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 831 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 701 594 957 Limit of detection (LOD. 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. < LOD means less than the limit of detection.2.

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

Int J Hyg Environ Health 2006. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. Angerer J. 2005. Seiwert M. Bernard CE. Ball M. Drexler H. Heudorf U. et al. Berger-Preiss E. Ranft U.Pyrethroid Pesticides References Baker SE. Pyrethroid illnesses in California.109(3):213-217.13(2):112-119. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.46(3):281-288. Williams RL.209(3):293-299. Butte W. Atlanta (GA). Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Centers for Disease Control and Prevention (CDC). Heudorf U. Krieger RI. Rev Environ Contam Toxicol 2006. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Leng G. Schulz C. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Int Arch Occup Environ Health 2004. 19962002. O’Malley M.206(2):85-92. Angerer J.209(3):221-233. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Spencer J. Angerer J. Environ Health Perspect 2001.186:57-72. Becker K.77(1):67-72. Hadnagy W. Int J Hyg Environ Health 2003. Idel H. Olsson AO. Int J Hyg Environ Health 2006. Kolossa-Gehring M. J Expo Anal Environ Epidemiol 2003. Heudorf U. Arch Environ Contam Toxicol 2004. Hoppe HW. Sugiri D. Third National Report on Human Exposure to Environmental Chemicals.

370 (. ciscypermethrin and cis-cyfluthrin.2-dichlorovinyl)- CAS No.270 (.202 (.2dichlorovinyl)-2.790-1.910-5.300-.53) .220-.160 (.710-1.680-3.160 (.200-. population from the National Health and Nutrition Examination Survey.280-.510 (.110-.740-2. In the body.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.260 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. the presence of trans-3-(2.670-1.870) 1. < LOD means less than the limit of detection.120-.670-1.690) .220-. but it can also reflect exposure to cis-3-(2.270-. 52315-07-8 CAS No. Survey Geometric mean (95% conf..120-.460-1.220-.12 (.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 .S.13 (.210) 90th .730 (.600) . Fourth National Report on Human Exposure to Environmental Chemicals 163 .77 (.200) .80) . cis-permethrin. Generally.400-.35) .160 (<LOD-.2-dichlorovinyl)2.900 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.490-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.120-.44 (.610) .920) 1. trans-cypermethrin.140 (.2-dichlorovinyl)-2.11) .740) 1.250-. more of the trans-metabolite than Urinary cis-3-(2.270 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1 and 0.670 (.and trans-isomers.54) .200-.880 (. transcypermethrin and trans-cyfluthrin. Cyfluthrin.420-.460 (. cis-cypermethrin. 1999).580) 1.150 (.2-Dichlorovinyl)-2.340-.890 (.510 (.270 (.470-1.960 (.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.490-1.790-1. The presence of cis-3-(2.490-.740 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .600 (.200) < LOD < LOD < LOD .28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .300 (.630-. which may vary for some chemicals by year and by individual sample.280 (.790) .530 (.330 (.50) .68) .68) .07 (.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.600-1.180) .340) .500 (. 1985.110-.730 (. 1985.850 (.570 (.200 (.410) .43) . 1999).200-.490-1.820 (. The chemical trans-3(2.330) . Kuhn et al.770-1.230) .740-1. Biomonitoring Information Urinary levels of cis.700) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.410) .200) .262) * * * < LOD < LOD .630) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.110-.440 (.220-.680 (.570-.350) .610) .68359-37-5 Cypermethrin Permethrin CAS No. and trans-cyfluthrin.21) .890 (.140 (<LOD-. Kuhn et al.24) 1.2-dichlorovinyl)-2.470 (.730 (.32) .550) .790 (.510 (.580-1.650-1.310) . trans-permethrin.2dichlorovinyl)-2.300-.380-. but can also reflect exposure to trans-3(2.370-.1.950-2.210) .640 (.2-dichlorovinyl)-2.460-.28) 671 680 518 701 591 957 Limit of detection (LOD.15) .220) .180 (. cis-3-(2.380-.520) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.630) .340) .630 (.170 (.670-2. and ciscyfluthrin.380) .68 (.47 (.210-.780) ..430-.or trans-3-(2.380 (.300 (.120-.240) .380-.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.710) .155-.500 (.250 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.35) 1.240) . Similarly.770) .110 (<LOD-.

population from the National Health and Nutrition Examination Survey.640-1.370-.Pyrethroid Pesticides 2.550) .590 (.33) .300-.104-. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.140-.33 (.450-1.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.2-dichlorovinyl)-2. 2003).67 (.130-.830) .138 (..49) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.150-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.440 (.270) .11) 1..14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.220) .370-.260 (.250 (<LOD-.380 (.390-.640-1.500 (. 2004. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.440 (.340-.900 (. Lu et al.380-. In these volunteers.230-.200-.320-.560) .350 (. 2005).260 (.150-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .320) . Other studies have provided evidence that urinary levels of cis..810 (.880) .03) size 1951 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th . 2006.230 (.59 (1.250) 90th .640) 1. urinary levels of cis-3-(2.290-.690-1.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.440-.450-.340) .59) .11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.260 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.550) .250-.2-dimethylcyclopropane carboxylic acid did not increase.450 (. 2006) and 1177 urban adults and children (Heudorf et al. 2006).800 (. 2005) In a small group of indoor pest-control operators.550-1. 164 Fourth National Report on Human Exposure to Environmental Chemicals .550 (. 2004).24) .580) .and trans-3-(2.440-.21) .380) .2dichlorovinyl)-2.780) 1.160 (<LOD-..390-.37) .570) .680 (.580-1.S.S.250) .590) .31) .290) .920 (.400 (.280-. the median and 95th percentile of urinary levels of cis-3-(2.710 (.200 (.700) .700-2. 2003). 2001) showed urinary levels of cis.840 (.2-dichlorovinyl)-2.180-. In the same residents.220 (.540 (.190) . 2006).29 (..300 (. 2005).2dichlorovinyl)-2.. Cyfluthrin.700) . representative NHANES 2001-2002 subsample (CDC. Survey Geometric mean (95% conf.270) .2-dichlorovinyl)-2. In a study of urban residents in Germany (Berger-Preiss et al.430-.360-1.510-1.540 (.390 (. 2001.410) .530 (.170 (. 2005).300 (.220 (.300) .400-1.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.430 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. 2006.80) .03) 1.230-.290 (. In a study of volunteers.and trans-3(2. 2002).260-.270 (.11 (.370-.420 (.67) .190 (.190) . Schettgen et al..840 (.240 (<LOD-.540) .640 (.680-1.170) < LOD < LOD < LOD .230-. 2002).300) .550-1. median urinary levels of trans-3-(2..250) . 2005).260) .890) .12-2.750 (.200) .430-1..350) .280 (.340) .890 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.150-.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.080-.680-1.2-dichlorovinyl)-2.710-3..2-Dichlorovinyl)-2.640-.59) .12 (.750-1. urinary trans-3-(2.210-. Studies in Germany of 396 children and adolescents (Becker et al.290) ..520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.11) .180 (.182) * * * < LOD < LOD .170 (.120 (.250-. post- Urinary cis-3-(2.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.600 (.270-.780 (.250-.200-.11) .560) 1.530 (.470-1.

49-5.60-4.2dichlorovinyl)-2.85) 4.550 (.95) 3.11-1.69 (1.480-.S.08) 1.39 (1.19 (2.68-3.76-4.700-1.07-3.12-6.4.750) .Pyrethroid Pesticides application median urinary levels of summed cis.94 (1.660) 1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.64-4.16) 1.500 (.500-.23 (.22 (1.43) 2.95) 2.830-1.620) < LOD 2.68) 1.35) 1.and trans-3-(2.42) 1.60) 1.800-1.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.25 (1.69) 1.68) 1.49-3.970 (.11-2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (. Fourth National Report on Human Exposure to Environmental Chemicals 165 . 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.76-3.63) 1.17 (.560 (.460-.55-5.700) .670) .77) 1.2-dichlorovinyl)-2.89 (2.26 (.940 (.730) .84 (1.81) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.780 (.17-1.5) 2.13) . 2005).610) 1.66) .08-6.55-4.41-14. Urinary trans-3-(2.70) 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 .820) .850-1.420 (<LOD-.860) .90) 1.920-1.14-6.01) 4.530) .28 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20 (.680-1.19) 1.840-1. Survey Geometric mean (95% conf.520) .40 (1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .17 (.07 (1.55-3.20 (.500) .7) 2.77 (1.09 (.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.560 (. however.01 (1.37 (1.28 (1. which may vary for some chemicals by year and by individual sample.56) 2.14) 1.470 (.810-1.56 (1.91 (1.03-1.54) 4.710 (.910-1.03-1.59 (1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .580 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.570) 90th 1.460-.410-.42 (2.2-dichlorovinyl)-2.77) 2.54 (1. 2005).520-.910-1.08-4. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.410 (<LOD-. Biomonitoring studies on urinary levels of cisor trans-3-(2.66) 691 680 518 690 595 954 Limit of detection (LOD.10) 2.62 (1.39-5.56) 2.27 (1.760) .60) .or trans-3-(2.48) 4.41 (1.410-.560 (.400-.23) 2.2-Dichlorovinyl)-2.490 (<LOD-.63) 1. < LOD means less than the limit of detection. Finding a measurable amount of cis.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.14-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. The maximum post-application urinary levels.49-3.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.19 (3.4 and 0.50 (1.440 (<LOD-.68-2.97-11.56 (1.400 (<LOD-. trans-Cypermethrin.470 (<LOD-.670) .490-1.410 (<LOD-.25-3.68) 2.87 (1.

850-3.31 (.28) 2.700-.33 (1.34-3.41) 1.30-3.720-1.00-5.16 (1.08 (.87 (1.820-2.64 (1.44) 2.34-4.56-2.47-2.20 (1.39) 1.91-11.470-.75 (1.570-.930-1.470 (.13) 1.56-5.57 (1.87-8.42) 1.87) 1.11) .07-2.33-2.580) .57) 3.81 (2.07-1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .580 (.880 (<LOD-1.56 (1.27-2.440-.48-2.45 (1.410-.720-1.570 (<LOD-.30-6.36) 2.20-2.22-1.27-2.480-.00) 5.42 (.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.86 (2.780 (<LOD-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.91) 1. population from the National Health and Nutrition Examination Survey. 166 Fourth National Report on Human Exposure to Environmental Chemicals .S.500-.07-3.880-1.640) .48 (1.19) .15) 3.47-2.55 (2.Pyrethroid Pesticides Urinary trans-3-(2.22) 1.570 (. Survey Geometric mean (95% conf.12 (.2-Dichlorovinyl)-2.13) .60) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.65 (2.31 (2.520 (<LOD-.610-.00 (1.74) 2.00) 1.750) .15-3. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.700 (.15 (1.87-3.55 (2.91 (1.730) .31) 1.780) 90th 1.530 (<LOD-.07) 2.60 (1.15) 2.530 (.89) 2.850) 1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .560 (.68) 3.15-3.15-3.3) 2.98 (1.800-1.36 (1.08 (.87) 1.60) 2.12-1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.70 (.00) 1.720 (<LOD-.37 (1.35 (1.780) .770) < LOD 2.700 (.55 (2. trans-Cypermethrin. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.22-2.540) .10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .45-2.33-1.970 (.67 (2.800-1.670) .850) .39 (1.660) .19 (1.29) 1.02-1.35) 1.740) .80) 1.61) 1.900 (<LOD-1.65) 1.760 (.47 (1.74) .26 (1.880 (.07) 2.40-2.

Heudorf U. Environ Health Perspect 2001.205(6):459-472. Angerer J. Berger-Preiss E.68(6):1160-1163. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Butte W.114(9):14191423. Barr DB. Leng G. Angerer J. Idel H. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Wieseler B. Hardt J. Int J Hyg Environ Health 2003. Sugiri D. Seiwert M. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Levsen K. Angerer J. Int J Hyg Environ Health 2006.76(7):492-498. J AOAC 1985. Permethrin and its two metabolite residues in seven agricultural crops. et al.209(3):221-233. Bravo R.206(2):85-92. Environ Health Perspect 2006. Heudorf U. Ball M. Heudorf U. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2006. Indoor pyrethroid exposure in homes with woollen textile floor coverings.Pyrethroid Pesticides References Becker K.209(3):293-299. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Drexler H. Leng G. Bartell S. Int J Hyg Environ Health 2002. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Ranft U. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ranft U. Int Arch Occup Environ Health 2004. Lu C. Int Arch Occup Environ Health 2003. Third National Report on Human Exposure to Environmental Chemicals.134(1-3):141-145. Idel H. Pearson M. Sugiri D. Hadnagy W. Biological monitoring of workers after the application of insecticidal pyrethroids.77(1):67-72. Schulz C. Idel H. Schettgen T. Leng G. Heudorf U. Hoppe HW. Kuhn K. Bull Environ Contam Toxicol 1999. Kolossa-Gehring M.109(3):213-217.62:101-108. George DA. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Atlanta (GA). Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Drexler H. Berger-Preiss E. 2005. Angerer J.

2006) and 1177 urban adults and children (Heudorf et al. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.. Biomonitoring Information Urinary levels of cis-3-(2. Outside the U. Thus. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 52918-63-5 General Information 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-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.2dimethylcyclopropane carboxylic acid formed in the environment. Studies in Germany of 396 children and adolescents (Becker et al.Pyrethroid Pesticides Deltamethrin CAS No. In the NHANES 2001-2002 subsample.2-dibromovinyl)-2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.. (2004) reported a geometric mean concentration of cis-3(2. 2001) showed that urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dibromovinyl)-2..2-dibromovinyl)-2. urinary levels of cis-3-(2. 168 Fourth National Report on Human Exposure to Environmental Chemicals . 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.3-0.5 μg/L) than the detection limit (0. deltamethrin has been used against mosquitoes that carry malaria.2-dibromovinyl)-2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 2005).1 μg/L) for the NHANES 2001-2002 subsample (CDC. Finding a measurable amount of cis-3-(2.. 1990).39 µg/L.2-dibromovinyl)-2.2-dibromovinyl)-2. mean peak urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. 2001.S.2-dimethylcyclopropane carboxylic acid of 0. Baker et al. 2005). in detection of cis-3-(2.2-dibromovinyl)-2..2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dibromovinyl)-2.2-dibromovinyl)2.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. Deltamethrin can degrade to cis-3(2. Urinary levels for adults and children in these studies were similar (Heudorf et al. in some situations replacing the use of DDT. 2004). Following residential spraying with deltamethrin for malaria protection in Mexico.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.. 2005).2-dibromovinyl)-2.

S. population from the National Health and Nutrition Examination Survey.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin 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. 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.Pyrethroid Pesticides Urinary cis-3-(2. Fourth National Report on Human Exposure to Environmental Chemicals 169 . * 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.2-Dibromovinyl)-2.1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.1 and 0.

Survey Geometric mean (95% conf.S. 170 Fourth National Report on Human Exposure to Environmental Chemicals .Pyrethroid Pesticides Urinary cis-3-(2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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.2-Dibromovinyl)-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 830 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 700 527 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

Angerer J. Third National Report on Human Exposure to Environmental Chemicals.109(3):213-217. Available at URL: http://www. Heudorf U. Deltamethrin.Pyrethroid Pesticides References Becker K. Schulz C. Batres LE.209(3):293-299. Angerer J. toxicokinetics.htm. Heudorf U. Seiwert M.org/documents/ehc/ehc/ ehc97. Angerer J. Carranza C. et al. Angerer J. and genotoxicity in exposed children. International Programme On Chemical Safety (IPCS). Fourth National Report on Human Exposure to Environmental Chemicals 171 . Butte W. Heudorf U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Ball M. Environ Health Perspect 2001. [online] 1990. Hoppe HW. Centers for Disease Control and Prevention (CDC). Kolossa-Gehring M. Grimaldo M. Drexler H. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Lopez-Guzman OD. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.113(6):782-786. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.inchem. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Int Arch Occup Environ Health 2004. Int J Hyg Environ Health 2006. 5/26/09 Ortiz-Perez MD. Atlanta (GA). Environ Health Perspect 2005. et al. 2005.77(1):67-72. Torres-Dosal A. Environmental Health Criteria 97.209(3):221-233. Int J Hyg Environ Health 2006.

CDC. CDC. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 2003. 2005). Saieva et al. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. A study of 396 German children (Becker et al. Following residential spraying with deltamethrin for malaria protection in Mexico. 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. 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. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2005.Pyrethroid Pesticides Cyhalothrin CAS No. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. In a small group of indoor pest-control operators. In one study of 145 urban residents in 80 private homes in Germany. 68359-37-5 Cypermethrin Deltamethrin CAS No. 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. 2002.. Fenpropathrin Permethrin CAS No. 2006. representative NHANES 2001-2002 subsample (CDC.52315-07-8 CAS No. Hardt and Angerer. 2003. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above.. CDC. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. 2005). median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al... Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2006). 52645-53-1 Tralomethrin CAS No. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC.. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 2005). 2003).. 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. 2005). 39515-41-8 CAS No. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 2005).S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Thus.. 2005). Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. In the New York City study. 52918-63-5 use and house dust levels (Lu et al. Baker et al. Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals .. 2005). Becker et al. 2004).

650 (.280 (.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.300) .750-1.45 (2.86 (1.384) .250-.570-.190-.800) 1.69) 3.36) 1.560-.01 (1.210-.63 (3.750) .330) .750) .200-.23 (2.670 (.295) .586) .314) .238-.54) 1.30 (.710 (.51-3.41 (1.300 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .35) 1.369) .620-1.35 (2.190-. Deltamethrin.62-6.210-.430-.51-6.360) .601) .27-2.300 (.33 (1.250 (.530-.1) 3.340) 1. interval) .320) .240 (.52-5.740 (.71 (1.350-.04) .260-.29-1.30) 3.72 (1.25-1.35) 2.470-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .247-.78) 1.65 (1.311 (.1) 3.89-71.8) 3.49-2.600 (.560-1.490-.230-.13 (.190-.25 (2.560-.64) 697 680 524 701 603 957 Limit of detection (LOD.298 (.520 (.590 (.292-.700 (.50 (2.850) .800 (.48-2.265-.450 (.63-3.25 (2.190-.69 (1.434) .730 (.04-5.270 (.340) .530-.510-.420) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.570-1.160-.79) 3. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32 (1.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .44) 5.740 (.90) 1.440) .55 (1.45-5.760 (.03 (3.49 (1.260 (.34-6.200-.49 (1.26) 2.640 (.276-.246-.277-.550-.230-.05) .336 (.355) .12) .27-11.940) 1.30 (1.200-.680 (.35 (1.960 (.78) 1.62) 5.53) 1.S.595) .427) .1) 3.41-2.270) .60) .292 (.630) .352-.78) 6.288-.34) 8.48-2.253-.321 (. Survey Geometric mean (95% conf.315 (.271-.16-1.330) .12 (.250 (.870 (.320 (.227-.1 and 0.314 (.510-.14-6.1.230 (.820) .92-3.288 (.93 (1.53-3.364) .83-11.810) 1.52-4.34 (2.250 (.373) .38 (2.25-7.230 (.42-2.26) 2.18 (1.43) 3.18 (2.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.490) .370) .820) .76 (1.353 (.590-.430-.390) .990) .700-1.387) .220-.16) 1.49-2. Fourth National Report on Human Exposure to Environmental Chemicals 173 .260 (.290 (.328 (.340) 75th .362) .41) 3.35) 2.840-1.325 (.46) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .226-.38 (2.428-.266-.65-2.180-.62-8.25-4.32-21.273 (.320) . population from the National Health and Nutrition Examination Survey.830) 90th 1.12) 4.28) 1.267 (.78 (1.73) 1.830-2.233-.260 (.320) .33) .27-2.230-.02-6.710 (.05) 1.406) .300 (.320) .41-3.46) 2.81 (1.26-2.417 (.297 (.56-5.39) 2.21 (2.160-.33 (2.13) .240 (.454 (.507 (.610) .75 (1.780) 4.850) .32 (2.

160-.09-2.272) .730) .200-.362 (.290) .670) 3.39) 1.15-2.240-.321-.280-.440-.225-.13-1. Survey Geometric mean (95% conf.200-.290-.264 (.670) .300-.04 (.00) 5.67 (1.67) 1.73-4.230-.240 (.253) .311 (.06-3.400-.43 (1.580) .229-.740) .240-.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 .92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .480-.35) 1.350 (.500) .329) .49) 3.335-.330) .94 (1.380 (. Deltamethrin.91) 9.40 (1.178-.309 (.25) 2.370-.09) 3.07) 2.03-1.420-.460-.720 (.43 (2.63) 1.440-.240-.446) .372) .02 (2.13-1.227 (.35 (1.330 (.03 (.25-2.43) 1.550 (.860-1.570) .44 (1.90) 3.720) 90th 1.17 (.440-.230-.72 (1.480 (.640 (.27) 1.274-.410-.19 (2.43-64.52) 2.74) 3.550 (.63-3.272 (.40) 2.730-1.02-1.400) .36-6.246 (.290) .216-.278) .270) .590) .275 (.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .0) 3.510 (.630) .49-2.300-.250 (.44) 2.67 (1.10 (2.96 (1.280) .21 (1.173-.62) 1.860 (.270) .250) .17-1.490 (.91) .36 (1.S.930) 1.16-4.274 (.224-.540 (.37 (1.190-. population from the National Health and Nutrition Examination Survey.450 (.200-.61-2.04 (3.365) 99-00 01-02 99-00 01-02 99-00 01-02 .11 (.220 (.320) .09-2.750-1.400-.52 (1.35) .49 (1.510 (.610 (.810) 1.299-.270 (.530-.310) .860-1.270-.271-.370 (.150-.280) .55) 3.07-5.09 (.329) .88-5.650) .62) .316 (.86 (1.91 (2.54 (1.261 (.83 (1.330) 75th .41-4.590) .48 (1.590-1.240-.13 (.550 (.840-1.21-4.640 (.35-3.280 (.323 (.510 (.190-.390-.730) .41) 1.73) 1.95) 1.437) .240 (.490-.930) .210 (.250 (.378 (.190 (. interval) .226-.25-5.960-1.330) 1.55 (1.423 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .240 (.80) 4.677) .580 (.19-6.238-.280 (.22 (1.700-1.410) .75-8.83) 1.280 (.00) 1.51-7.210 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.387) .19) 2.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.261-.210-.11 (.200-.84 (1.37) 1.530-.309) .590) .230) .05-3.53 (1.560 (.760) .49) 1.534) .240 (.220-.32 (2.350) .270 (.312 (.328) .00) 1.60-4.202-.380-.357) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.490 (.64-5.330) .81 (1.91-4.60) 1.460-.234 (.401) .

Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Angerer J. et al. Carranza C. Idel H. Godbold J. Barr DB. Ball M. Seiwert M. Torres-Dosal A. Angerer J. Atlanta (GA). Leng G. Berger-Preiss E. Becker K. Barr DB. Int J Hyg Environ Health 2003. and genotoxicity in exposed children.111(1):79-84. Lapinski R. Ranft U. Kolossa-Gehring M.76(7):492-498. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. toxicokinetics.114(9):14191423. urban cohort. Idel H.113(6):782-786.206(2):85-92.46(3):281-288. Lu C. Levsen K. Batres LE. Bravo R. Obel J. et al. Biological monitoring of workers after the application of insecticidal pyrethroids. Hardt J. et al. Sugiri D. Bartell S. Environ Health Perspect 2006. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2002. Deych E. Berkowitz GS. Sugiri D. Environ Health Perspect 2005. Arch Environ Contam Toxicol 2004. Olsson AO. 2005. Grimaldo M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Ortiz-Perez MD. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Hadnagy W. Ranft U. Hoppe HW. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Pearson M.Pyrethroid Pesticides References Baker SE. Int Arch Occup Environ Health 2003. Exposure to indoor pesticides during pregnancy in a multiethnic. Leng G. Int J Hyg Environ Health 2006. Berger-Preiss E. Centers for Disease Control and Prevention (CDC). Lopez-Guzman OD.209(3):221-233.205(6):459-472. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Environ Health Perspect 2003. Liu Z.

080-. The absorption.141-.400 (.200 (. distribution.070 (<LOD-.Metals Antimony CAS No.140 (.320 (.190 (.133) * .340) .120-.230) .280-.250 (.460 (. Dermal contact with soil.210 (. and +5.270 (. ammunition.300 (.120-.250-.190) .137) .220) 95th .390-.500) .220-.156-.280) .270 (.180) .130-.110 (. storage batteries.140 (.150 (.230) .230-.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 .130-.210) . It is used in metal alloys.128 (.098-.130 (.170-.370-.490 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite. respectively.190-.270) .100 (.150-.132 (.400) .120) .117-.330) .250-.160-.200 (.250 (.120-. sheet and pipe metal.180-.210) .154) .370) .S.390) .510) . It is also used in paints.143 (.390) .087-.200 (.310-. metal bearings.220 (.080 (<LOD-.132 (.120-.130-.180-.400-.470 (.360) .200 (.350 (.130) < LOD .330 (.090 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300) .125 (.250) .310) . and refuse incinerators that process or release antimony.150) .130 (.190) .190 (.131-. castings.390 (.135) * .137) .330 (.120 (.170-.440) .320 (.320) Total .080) .200-.184) .220) .260-.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 .126-.100-. 01-02.120-. Antimony can exist in one of four valences in its various chemical and physical forms: -3.290-.390-.260) .230-.360 (.093 (. 7440-36-0 General Information Antimony is found in ores or other minerals.180 (.200 (.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 .160) .280-.280-.164-.430 (.140) .350 (.120) .120-.100) .230-.140 (.220) .103) .460) .119-.710) .160) .250-.330-.240 (. +3.140) .500) .095-.150-.128 (.200-.250-.130) .170 (.120 (.440 (.190) . People are exposed to antimony primarily through food and.160 (.300-.230-.230) .150 (.190) .115-.170-.350-. interval) .330 (.230 (.140) .108-.090-.146 (.120-.088-.160-. see Data Analysis section) for Survey years 99-00.150 (.310 (.200-.350) .180) .207) .300) .410) .112-.410) .220 (.110-.260-.130) .161) .240-.360) .150) .100-.110-.350) .290 (.220-.130) .154-.145) Selected percentiles ( 95% confidence interval) 50th .350 (.400) . fireworks.190 (.154) .120 (.158 (.079-.105 (.180 (.220-.210-. 0.120 (.180 (.190) .170-.360-.600) .140) .260) . and as a fire-retardant in textiles and plastics.280-.160 (.200) .144) .160 (.350-.100 (.136) * .390) . ceramics. Stibine is a metal hydride form of antimony used in the semiconductor industry.169 (. and glass.180-. water.350 (.220-.109-. Workplace exposures can occur at smelters. and 03-04 are 0.200) .170 (.570) .134-.260 (.123 (.180 (. enamels.115) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .470) .200) .210) .280 (.07.390-.200) .117-.470) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.178) .440) .120) .530) .300-.290-.130 (.280) .130 (.157) .410-.460 (. 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.260) .160) .310) .210) .150-.210 (. Antimony enters the environment from natural sources and from its use in industry.320-.270) .140) .130-.190-.310 (.122 (.280 (.114) .230 (.190-.280-.340 (.110-.120-.099 (.350) .130 (. 0.126 (.300) .200-.320-.210-.400 (.160-.120 (.300 (. and excretion of antimony vary depending on its oxidation state.190 (.136-.330) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.090 (.460 (.230-.130-.150) .160-.230 (.150-.108 (.120-.310 (.240 (.080) .220-.280) .120) .350-.220-.142 (.240) .190-.197) .150) 90th .095 (.190 (.110) .160) .270 (.170) .280) .350 (. to a lesser extent.360 (.176 (.260 (.350) .270 (. < LOD means less than the limit of detection. coal-fired plants.310-.140-.210) .145 (.119) .148-.130-.340 (.270-.260 (. population from the National Health and Nutrition Examination Survey.330-.150-.200 (.04.090-. from air and drinking water.180-. which may vary for some chemicals by year and by individual sample.130 (. solder.160) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180 (.180-.090) 75th .330) .490) .190-.240 (.134 (.160) .220) . and 0.170-.070-.240 (.070 (<LOD-.320-.130 (.04.130 (.400) .390) .430 (.250 (.300-.140 (. and pewter.240-.320-. or other substances containing antimony is another means of exposure.320) .560) .175 (.400 (.310 (.240 (.180 (.140) .430 (.420) .130-.330) .110-.

076-.113-.173 (.127) . interval) .417) .195-.111 (.250-.150-.082) .318-.S. skin.124) .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.143 (.238) .209) .113) .152) .124-.188) .146-.075 (.152) .075 (.120 (.109 (.148) * .256 (.127) .192-.198) .147-.318-.146) .139 (.163 (.471 (.086) 75th .170 (.230-.265 (.084) .294) Total .267 (..112 (.156 (.130) .068-. species.263 (.108-.444) .125-.417) .228 (.225) .194-.135) .298 (.438) .160 (.105-.124-. 1988.135) .178-.192) .320-.118 (.208-.421) . 1973).087) .250 (.250) .220) .115 (. liver.074 (.727) .241-.195 (.149-.085) .352) .320 (.255-.485) .115 (.183) .148-.276 (.255) .227-.136) .272) .320-.107-. myocardium.200-.278) .120 (.224 (.741 (.176 (.131) .153-. 1962).146-.257) .095-.143) .207) .333-1. and route of exposure (Elinder and Friberg.098-. and gastrointestinal symptoms such as vomiting.108 (.108-..113-.171) .138) * .371 (.076-.310) .213 (.150-.172-.300) .127 (.099-.200-.444) .129) * .116 (..199-.211) .181) .131-.200) .250-.245) .400 (.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 .338) .286 (.159-.185 (.108-.310 (.098) .078 (.162-.102-.391) .126) .385 (.107-.130) .193 (.156-.321) .242-.173) . resulting in hemolysis with abdominal and back pain (Dernehl et al.117-.092-.080 (.373) .261) .300 (.191 (.122 (.131 (.115-.205-.425) .176-.238 (.115) .109 (.241-.364 (.082 (<LOD-.109-. 1995).140) ..135) .430) .235-.149) .071-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.206-.173-.114 (.217 (.114 (.429) .117-.317) .133) .114 (.164 (.320 (.143) Selected percentiles ( 95% confidence interval) 50th .123 (.099-.277 (.138-.119 (.061-.313-.333-.181) .079 (<LOD-.266 (.429 (.263-.159-.137 (.333-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.112 (.204-.203) .229-.089) .280 (.159-.250 (.333-.069-.193) .119-.343 (.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 .315) ..239-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.185 (.128-.116-.080 (<LOD-.233-.129 (.126 (.068 (.233) .082) .271-.500) . 1986).086 (. population from the National Health and Nutrition Examination Survey.138-.226 (.129 (.317) .069-.178 (.115 (.236 (.253 (.447 (.333 (.130) .167 (.140) < LOD .391) .096-.222 (.267-.280-.300) .104-. Inorganic antimony salts irritate the mucous membranes.181) .196 (.208 (.265-.127) .187) .30) .154-.480) .097-. Ming-Hsin et al.267) .111-.188-.182 (.124 (.320) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.132) . and eyes.269 (.173 (.175 (.120 (.308-.268) .143) 90th .248-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.214) .134) .153 (.230) 95th . The toxicity of stibine after acute inhalational exposure is similar to that of arsine. Fourth National Report on Human Exposure to Environmental Chemicals 177 .077) .121) .192 (.176 (.189 (.195-.127) .144-.081) .244-.333 (.253-.185-.135 (.333 (.098-.103-.250-. 1958) and occupational exposures (Briegner et al.120 (.338 (.209) .209-.138 (. and ulcers (Werrin.135 (.228 (.233 (. 1986).106-. 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.471) .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 . and kidney have been demonstrated in high dose animal studies depending on the dose.121 (.148-. 1944).308) .126-.129) .146-.247) .333) .081 (<LOD-.163 (.203) . abdominal pain.186) .295 (.103-.104-.164) .248) .288 (.338 (.102-.167-.167 (.139 (.357-.281-.250-.352 (.414) .130 (.380 (. 1954).147) .106-.123) .161) . diarrhea. Histopathologic inflammatory and degenerative changes in the lung.115-.278 (.119-.117-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.357) .132 (.145) .100 (.118 (.228-.364 (.741) .200-.259 (. 1953).405) .209 (.112-. Acute antimony poisoning may cause a metallic taste.107-.167 (.125 (.095-.238) .121 (.122 (.161) .310) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.164-.092) .317) .179-.Metals than for trivalent compounds (Elinder and Friberg.143) .225 (.151) .

atsdr. Chen J-R. Biomonitoring of a worker population exposed to low antimony trioxide levels. Dunkelberg. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Element reference values in tissues from inhabitants of the European community. Alimonti A.13:361-362. VI. Bolten C. Van der Venne MT.16: 33-39. Piatnek DA. Pulmonary edema of environmental origin. Int Arch Occup Environ Health 1987. environmental levels) and health effects is available from ATSDR at: http://www. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.521-523. 2004. 26-42. 2nd ed.. or exposure differences. Sabbioni E. Kiberd B. Paschal et al. Dezateux et al. Briegner H.48:93-97. Minoia C. Int Arch Occup Environ Health 1995. Centers for Disease Control and Prevention (CDC). Yang C-Y. Ming-Hsin H. New York: Elsevier. Earlier measurements in general populations (Minoia et al. Urinary antimony in infancy.S. et al. Ju-Sun P. 1995. indium. Gallorini M..html. Dernehl CU. Caroli S. Stone FD.. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication.67:119-123. J Trace Elem Med Biol 2002.. Petrucci F. Shao-Chi C. Review of elements in blood. Dezateux C. Rev Infect Dis 1988.. et al. Mayne P. Environ Health Perspect 1998. Lenert G. Yu H-S.. Stead FM. clinical efficacy. Lauwerys R. Schaller KH. Kentner et al. 1998. O’Regan M.64(2):182-185.. Biological monitoring of exposures to aluminum. Stasney J. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Schacke G. stibine. and 2003-2004. even when exposure levels were below workplace air standards (Bailly et al. 20012002.10(3):560-586. Arch Dis Child 1997. 2002. Trace element reference values in tissues from inhabitants of the European community I. Wu M-T. which may be due to methodologic. Third National Report on Human Exposure to Environmental Chemicals.. Nau CA.. Information about external exposure (i.)1954.46:931-936. arsenic. gov/toxpro2. Vouk VB.51:238-240. Biological assessment of exposure to antimony and lead in the glass-producing industry.. Industrial antimony poisoning. and antimony in optoelectronic industry workers. Liao Y-H. Pietra R. 1998). Buchet JP. Stocks J. Kuo-Juie Y. Antimony.76:432436.e.. Carelli G. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Industrial Medicine and Surgery (Dec. Cordasco EM. 1997). Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. 1990. Delves HT. 1987). Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. gallium.Metals to antimony have been established by OSHA and ACGIH. External and internal antimony exposure in starter battery production. Antimony trioxide is rated by IARC as a possible human carcinogen. 1986. Luedersdorf R. Pilgrim L. Kentner M. Br J Ind Med 1991. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Sabbioni E. Mahieu P. Elinder CG. Pozzoli L. Skulsukai G. References Berman JD. Antimony in blood and urine of infants. Matthews T. Chin Med J 1958. Ludersdorf et al.. J Occup Environ Med 2004. 1991.106:33-39. Cullen A. and a drinking water standard has been established by the U.76(2):103-115. Konings J. Liao Y-H et al. 2005. Weltle D. Fuchs A. Arsine. EPA. Iavicoli I. Atlanta (GA).59:469-474. Mayer P. 1994) have reported values slightly higher than those in this Report. Chia-Yu H. Bailly R. Friberg L. 1998) or compiled reference ranges (Hamilton et al. pp. Gebel TW. Industrial Medicine 1944. HH. Nordberg GF. J Clin Pathol 1998. Wade A. population. Delves HT. eds. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Cheng-Wei L. 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. Chest 1973. and future strategies. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.cdc. and hydrogen sulfide. Ho C-K. Chemotherapy for leishmaniasis: Biochemical mechanisms.158:165-190. Sci Total Environ 1994. Iavicoli et al. Hamilton EI. Costeloe K. et al. Leinemann M. Handbook on the toxicology of metals. Semisch CW. In: Friberg L. Suchenwirth R. respectively. Roland H. Apostoli P.

Industrial Hygiene and Occupational Medicine 1953.95:89-105. blood.76(1):53-59. Renes LE. Sci Total Environ 1990. Chemical food poisoning. Paschal DC. Antimony poisoning in industry. Werrin M. Morrow JC.Metals in urine. Environ Res 1998. Jackson RJ. and serum of Italian subjects. Trace metals in urine of United States residents: reference range concentrations. Quarterly Bulletin of the Association of Food and Drug Officials 1962.99-108. Sampson EJ. et al. Pirkle JL. Ting BG. Fourth National Report on Human Exposure to Environmental Chemicals 179 . 27:38-45.

5) 43. The United States no longer produces arsenic from mining but imports about 22.84) 8. population from the National Health and Nutrition Examination Survey.12 (6.0-19.1 (32. though in some locations arsenite may be prevalent (WHO.2 (12.13-8.0 (43. grain. and in lead-acid storage battery grids.S. psoriasis. Although it is still widely used in the United States. and arsenates (oxidation states of -3.2-61. and other metals.6-141) 53.4) 13. to a lesser extent.70) 8.90-8.7) 90th 37.2 (41.8) 7.90) 75th 16. Gallium. 2005).8) 17. mental disorders.80 (5.4 (26.7-95. arsenites.1-40. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.4 (24. Also. and indium arsenides are used in the semiconductor industry.2 (51.97) 8. from coal burning. and as a cosmetic to lighten complexion.57) Selected percentiles ( 95% confidence interval) 50th 7. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.5 (23. it is found in over 200 crystalline or mineral forms. as alloy in metal bearings.5 (34.6 (32.4) 60. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. alloys. such as arsenopyrite (FeAsS) and realgar (As4S4).34-9.4 (48. and as homicidal poisons. Arsenic trioxide (As2O3.19-9.8 (48.00 (6.5 (40. Various arsenic compounds were used in paint pigments and for tanning animal hides.41 (7. and arsenosugars.5 (14.1-18.5 (36. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.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. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.84) 8.90-11. Arsenic is measurable in most soils.50 (8.9-34.90-8. black. Before the 20th century.2-93.5) 41. and gray forms).10) 10. gaseous hydride manufactured in small quantities for use in the semiconductor industry. cacodylic acid.5-19.66-8.80-9.8) 29.0 (11.6 (13. trimethylarsine oxide.20 (8.3) 10. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.8-61. Arsenic trioxide is approved to treat acute promyelocytic leukemia.0-60. and.80) 6. meats.02-8.1) 7. +3 and +5).8-77.9-46. interval) 8. 2001). solders.1 (38.2) 46. copper arsenates.77) 6.9 (8. Arsine (AsH3) is a reactive. arsenic compounds.4 (31.4-65.4) 40. and foods. referred to as inorganic arsenic compounds.2-20. lead hydrogen arsenate.0 (14. arsenic as elemental metalloids may be used in some ammunition.5) 95th 65.30) 17.6 (9. Since the 1940s.3-111) 78. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.70 (6.2-17.90-7.90-14.90 (7.6-43.7-83. lead. aluminum.6-35.6) 618 722 1074 Limit of detection (LOD.12-10. particularly arsenic trioxide.8) 33.29 (8.6 (15.2 (13.90 (7.6) 11.0 (15.Metals Arsenic CAS No.7) 65.5-52.00-9.25-9. the smelting of copper. 180 Fourth National Report on Human Exposure to Environmental Chemicals .40) 7. see Data Analysis section) for Survey year 03-04 is 0.90 (5.9) 68.70-9.50-14. arsenocholine.7) 24. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. Arsenic and its compounds have had many uses in the past and present as medicines. cancers. In the last century.34-10.74. mostly for use in wood preservation (ATSDR. semiconductors. sodium arsenite. Water sources contain mostly inorganic arsenate.27) 9.7 (11.8) 30. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.10 (6.10-7.3-19. to a lesser extent.5-41.8) 7. ocean and fresh waters.8) 34.0 (22.5-178) 46. or rarely as elemental metalloids (yellow.1) 1281 1276 03-04 03-04 03-04 9.10-10.55 (7.3-15.08 (5.2) 15.000 metric tons annually. General population exposure to inorganic arsenic can occur through consumption of drinking water and.9 (17.30 (6. Survey years 03-04 Geometric mean (95% conf.1) 15. retaining walls.9) 21. and play sets.5) 66.4 (7.9-62. pesticides. were used as treatments for syphilis.90) 16. and produce.30 (7. In nature.1) 290 725 1542 03-04 03-04 9.

7 (11.7-35.3 (27.7) 28. 2001.8) 22.8 (11. population from the National Health and Nutrition Examination Survey.33-10.04 (5.5) 290 725 1542 03-04 03-04 8. and some other seafood can contain organic forms of arsenic including arsenobetaine.2) 40. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.75 (5. 2001). age.01) 11. 2007.S.93-8.0) 42. In aquatic organisms.5-17.6 (35.1) 24. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.2 (12.25-9. gallium arsenide and indium arsenide.7-188) 27.0 (17. Extremely high groundwater arsenic levels. arsenic does not show biomagnification in the food chain (WHO.06 (4.7 (9.5 (9. though some reduction may occur in the gut prior to absorption.8 (12.75) 13.99-9.88 (5.13) 8.7 (25. 2001).32 (5.9 (45. 2006.4 (26.33 (6.30-9.4 (42. Survey years 03-04 Geometric mean (95% conf.93-9..10-16. WHO. have caused clinical arsenic poisoning. 2001).00 (6.40) 8.0-26. Arsenate is reduced in the body to arsenite (oxidation state +3). arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.0 (31. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. 2006. 2001). EPA.24 (7.66 (7. 1988). shellfish.04) 7.4) 54. so exposure to the general population is extremely limited. as observed in Bangladesh where millions of people have been exposed. Gamble et al.0) 14..9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .50 (6.8) 27. Inorganic forms of arsenic demonstrate high acute toxicity.10-8.47-6. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.51) 75th 14. 2001).0) 26. inorganic arsenic is widely distributed within the body. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.86-17.61 (7.3) 6.S. kelp.6) 45.3) 9. The semiconductor dopants.44-11. 2007.81-9.1 (14.66-8.4 (12.3-53. Chowdhury et al.2-46. U.58-10..1 (11. interval) 8.2) 15.6 (10.01) 7. dust.11 (5. NRC.35) 7. dose level.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.8 (20. mine tailings).0) 33. 2001.9) 13.2-15.5) 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 8.0-69. 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.3-64. 2003. Smoking tobacco is also a source of inorganic arsenic. and folate status (Chen et al.59) Selected percentiles ( 95% confidence interval) 50th 7.. trimethylarsine oxide (TMAO).5) 17. 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.20-9. 2001).47 (6. EPA’s maximum contaminant level (Hughes.41) 6. In aquatic sediments. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.4-64.7-17.64 (7.8 (21.88) 7.38-10.8-62.0) 1281 1276 03-04 03-04 03-04 8. Steinmaus et al.1) 8.12-10.45) 5. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. are used in enclosed ultraclean operations within the semiconductor industry. WHO.7) 95th 50. cacodylic acid and monosodium methyl arsenate. Direct exposure to DMA and MMA may result from use of the two pesticides. Though modest bioconcentration occurs in some aquatic life.9) 53.1-36. selenium.7-34.6-17.1) 58.25 (6. After absorption.1) 7.47 (7. organic arsenic can be converted back to methylated and inorganic arsenic.7-18.4) 32.96) 12.66-8.g. 2001).6 (17.3 (24.0) 12..07-9.9-56.2) 90th 30.3-62..0-38.44) 6.8-75.18 (5.23-7. Tseng. but is poorly absorbed dermally (WHO.4 (24. arsenocholine.S. Fish. and arsenosugars.76 (6.5-120) 40.31 (6. 2007.3-41. Children may have additional exposures from ingestion of contaminated soils (e. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.28-7.8-32.0-18.4 (11.1) 6. 2001).4 (40. and contact with CCA-preserved wood structures.8 (27.

and by uncoupling oxidative phosphorylation (NRC... 2001). Such actions may lead to decreased energy production. see Data Analysis section) for Survey year 03-04 is 1. 2000.20 (<LOD-1. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. WHO. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 2001). and childhood neurodevelopmental effects in observational human studies. hyperkeratosis. but additional or confirmatory research is needed (Kapaj et al.0.. gluconeogenesis. and altered gene expression.. Cohen et al. 2006. Chronic elevated arsenic intakes have been associated with diabetes. 2004). increased oxidative stress.20 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. WHO. WHO. Cellular glucose uptake. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 2006. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.10 (<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 Sample size 1.60) 1.20 (<LOD-1. Taiwan.. Raml et al. lung. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. drinking water have not been associated with increased cancer rates (Schoen et al. 2001). 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. 2004). some of these effects may take years to develop.S. which can lead to dehydration and shock. 2007). 2006) or when exposure occurs in smokers (Chen et al. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. Arsenic has many actions demonstrated in cellular studies.S. and diarrhea. Chile).. Chronic arsenic exposure in humans is considered to be a cause of skin. and endothelial injury (Kumagai and Sumi. including inhibition of numerous enzymes. including drinking water sources with elevated arsenic levels (e.30) 1. < LOD means less than the limit of detection. apoptosis. hepatotoxicity. interference in signal transduction pathways. Survey years 03-04 Geometric mean (95% conf. leading to a decrease in adenosine triphosphate energy production. vomiting. food residue..g. 2001.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. substitution in phosphate metabolism. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.EPA. 2007. noncirrhotic portal hypertension. 2007.10 (<LOD-1. 2001. and DNA repair inhibition (Cohen et al.. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. The organic forms of arsenic occurring in seafood have little known toxicity.. 2006. fatty acid oxidation. Chronic human intake of arsenic at less than acutely toxic doses. respectively. cell transformations.80) 1.S. NRC.. 2001).EPA has established drinking water. Acutely. and it also will inhibit succinate dehydrogenase. renal failure. and production of glutathione may be affected as well..60) 1. With chronic exposure. Studies of arsenic at levels typical of U.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. U.10 (<LOD-1. arsenic trioxide) includes hemorrhagic gastritis with nausea. 182 Fourth National Report on Human Exposure to Environmental Chemicals . and bladder cancer (IARC. Cardiac arrhythmias.10 (<LOD-1..10 (<LOD-1. 1998.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. Bangladesh. can cause peripheral sensorimotor neuropathies.50) 1. and hyperpigmentation of the skin (NRC. peripheral vascular disease. hematocytopenias. Bredfeldt et al. which may vary for some chemicals by year and by individual sample.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. cytotoxicity. 2001). 2004. population from the National Health and Nutrition Examination Survey.g. hypertension. NRC. The U.20 (<LOD-1.50) 621 725 1078 Limit of detection (LOD. 2001). WHO. Although arsenate is reduced in the body to arsenite.

89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 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...S. 1998. Meza et al. Shalat et al. 2006.. and the FDA has established a bottled drinking water standard.69 (<LOD-3. population (Rubin et al. Offergelt et al. 2000).. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2004. environmental levels) and health effects is available from ATSDR at: http://www. Calderon et al. Survey years 03-04 Geometric mean (95% conf.. population from the National Health and Nutrition Examination Survey. In the German Environmental Survey III of 1998. 1999.e.75 (<LOD-2. although urinary arsenic levels were not associated with CCA contact (Shalat et al. 1992. Shalat et al. Fourth National Report on Human Exposure to Environmental Chemicals 183 .18 (<LOD-3..cdc.atsdr. 2006). 2008.75 (<LOD-2..18) 3. 2008). median urinary total arsenic levels in 4052 adults varied with seafood intake. arsenic has been fetotoxic and teratogenic. 2006). 2001). Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon 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. In animal studies... 2000. Valenzuela et al. gov/toxpro2..S. Compared with this Report. 1986). 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. Pellizzari and Clayton. Caldwell et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result...04 (<LOD-3.. DMA produced bladder cancer in some chronic rat studies (Cohen et al.00) 1.41) 3. 1999... 2007. population in NHANES 2003–2004 (Schulz et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. but generally only at maternally toxic doses (WHO.80 (<LOD-4. Vahter et al.61 (<LOD-3. Additional information about external exposure (i. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.. 2007.. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. 2006.19) 3. In a Nevada town where groundwater levels were naturally elevated. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. and were about two-fold lower than those for the U. Pellizzari and Clayton 2006).50) 1.S.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Josyula et al. 2006). 1999)..50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.S. Pellizzari and Clayton. had decreased since the prior 1990– 1992 survey..33 (<LOD-3.html... Levels of total urinary arsenic in the U. 2006).Metals compounds.. 2004.. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. 2008). WHO. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 2003.33 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. 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. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Consequently. 2006. Caldwell et al. 2001). 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).

19 (.5) 32.7 (21.10) 8.800) 1.900 (.70) 6. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.S. dermal keratosis.74 (1. In most human studies. Caldwell et al.. arsenocholine. 1985. respectively.43-1.05) < LOD . DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.40) 5.. 1996. population (Ahsan et al.5 (26. and TMAO. Chowdhury et al.6. 2001. When seafood intake is avoided.20-3. In the late 1980s..80 (. 2003).2 (6.6 (11. 2007).5) 621 725 1078 Limit of detection (LOD. population (Sun et al. 2005. vasospasm. and duration of exposure are also considered important.50) 90th 16.. 2008.S.00-12.80 (3. China. in NHEXAS 1995–1996.50-6.5 (14. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.80) 1.6) 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 * * 1.00 (.30 (1.30) 2..8-50.400-.. and TMAO were detected in only 7. interval) 1.. Aposhian et al.20 (1.S. Tseng et al..40) 75th 5.. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. Measurable organic arsenic species in this Report are three biologically generated environmental forms.1) 45.4) 31.5) 29. Arsenate.80-5.3 (9. and 0.3-39. Pellizzari and Clayton. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. when seafood organic arsenic is subtracted).83) Selected percentiles ( 95% confidence interval) 50th 1.1-51.871-1.1-94..30) 10.2-35. 2008. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3) 35.700-1. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. 2005.9) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..55 (1. with DMA. arsenobetaine.50) ..e.70 (3.30 (2.28) 1. MMA.. Also.31-1.20) 7.00-4.800-1.2-38.6.S.4.Metals other areas of the world (Ahsan et al. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.93) 1.0 (26..20 (2.. Caldwell et al. and other factors such as nutrition. 2005. Individually measurable species resulting from inorganic arsenic exposure are arsenate.8-40.20 (. which may vary for some chemicals by year and by individual sample. 2007) with higher levels of arsenic in the drinking water.g. population from the National Health and Nutrition Examination Survey. 2008).10) 4.500-1.900-1.00 (1. 4. 2008).S. population in the NHANES 2003–2004 subsample.70-21.90-7.3) 1284 1284 03-04 03-04 03-04 1. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.5) 292 728 1548 03-04 03-04 1.3) 95th 35.20 (4.20) 18.60-3.60) 1. DMA and MMA. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.20-25.600 (.7) 13.17-1.800-4.20-190) 31. These associations are stronger at higher urinary levels. see Data Analysis section) for Survey year 03-04 is 0.40-6. 2006). 2000.1-25.90-29.6 (25.48-2.20) 3.00-1.10 (4..11-1.800 (. In the residents of a Chilean town who consumed water with high levels of arsenic.37 (1. The higher percentiles of total urinary arsenic levels in the U. 1990..0) 4.00) 3. Some noncancer effects of arsenic (e.9-23.. Caceres et al. 184 Fourth National Report on Human Exposure to Environmental Chemicals . Blom et al. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. arsenite. Sun et al.0) 29.4) 23. arsenocholine. Valenzuela et al.7) 15. For residents of Inner Mongolia.9 (6.8 (17. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.62) 2. < LOD means less than the limit of detection.700-1. 1.9 (7.40-7. arsenite.70-21. geometric mean levels were about 70-fold higher than for the U.0-23. 2000.6-44. 2000.6 (13.4-35.800 (. WHO. 2001).8) 35.45 (1.8 (12. methylation capacity. and two methylated metabolic products. After recent seafood ingestion.7 (13.7-22.0 (27.29 (1.3 (21.3% of a representative sample of the U.8. Survey years 03-04 Geometric mean (95% conf. population showed a higher contribution of arsenobetaine (Caldwell et al. Caldwell et al.00-6.. 2008). 2008). Total arsenic measured in the urine includes all species of inorganic and organic arsenic.50) .80 (4.66 (1..68) . and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.4 (16.70 (5.1) 18.

4-21.65 (1.13-39.40) 1.6) 19.76-27.4 (24. population from the National Health and Nutrition Examination Survey.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.79 (1.2 (12.53 (.6-32.5) 26.10 (.64-29.51) 5.6-29.11 (.15-1. Studies of small groups of metal and sulfuric acid smelter workers with varying industrial hygiene conditions have reported urinary inorganic arsenic levels (arsenate + arsenite + DMA + MMA) ranging as high as several hundreds of μg/L during or after work exposure (Jakubowski et al. which is below the ACGIH BEI (Caldwell et al.30) 1.2 (4.4) 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 * * 1.25-7. 1986. 2003.82) Selected percentiles ( 95% confidence interval) 50th 1.S.00 (3.05 (.15-1.88 (5.7) 9.14 (1... Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.3) 1284 1284 03-04 03-04 03-04 1.959-1.6-46.. Survey years 03-04 Geometric mean (95% conf.05) 1.4) 13.9) 32. population for the sum of inorganic related species was 18.4) 32.638) 1.36) 2.47 (2. 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.877 (.54 (1.83) 8.68 (1.6 (6.00 (1.58 (3. 1998.4) 292 728 1548 03-04 03-04 1.7) 30.50-15.43) 14.72) 12.5-20.Metals as with DMA.786-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4-28.29-14. Vahter et al.43) 75th 5.. interval) 1.S. 2008). The 95th percentile of the U.4 (11.1) 26. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.91) 90th 16. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Caldwell et al. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (26. 2001).67) 1.16 (.531 (.15-4.5 (18.12) < LOD .93 (1.9) 14.9 (25. 2008).39-3.2 (13.612-1.32-7. In recent years. 2001).40 (1.83) 2.45) 1. 2006.3 (10.78-5.78 (3.30-1.28) 1.8) 29.44 (1.2 (12. Information about the biological exposure indices is provided here for comparison.9-18.3-24.51-2.50-7.1-36.9 μg/L... WHO.3) 95th 29.29 (4. 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.73-6.901-2. Fourth National Report on Human Exposure to Environmental Chemicals 185 .400-. Sun et al.91 (4.61-6.47 (1.9 (13.21) 5.3 (10.55) 1. 1992.6 (9.0 (9.37-2.88) 2.62-6.833-1..7) 17. not to imply a safety level for general population exposure.0-36.80-153) 17.70) 5.80) .18-1.5 (18.909-1.81 (4.5) 17.25 (. 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. Offergelt et al. 2007).19-2..1-18.67) 4.82) 4.4-82.938-1.

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

which may vary for some chemicals by year and by individual sample.08 (<LOD-4. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey years 03-04 Geometric mean (95% conf.40 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95 (<LOD-2.80) < LOD 621 725 1078 Limit of detection (LOD.00 (<LOD-2.76) < 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. 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.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. Survey years 03-04 Geometric mean (95% conf.44) 2. Fourth National Report on Human Exposure to Environmental Chemicals 187 . population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00 (<LOD-3.S. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.00) 1.20 (<LOD-1.

09 (7.S.7 (10.86-21.37 (2.00-9.0) 13.00) 12.00) 3.00) 75th 6.00 (5.69-6.45 (8.0 (11.1-22.18 (6.0 (12.48 (3.16-11.00 (5.1-18.34-4.0 (9.69 (3.73 (3.00-7.20-4.33-4.34) 3.12 (3. Survey years 03-04 Geometric mean (95% conf.1-15.80-6.00) 6.0 (12.74) 90th 9.86 (2.82) 3.14) Selected percentiles ( 95% confidence interval) 50th 3.62) 4.34 (3.6) 292 728 1548 03-04 03-04 3.95 (4.0) 17.0) 9.00-5.8) 7.00) 90th 11.7) 12.7.11 (3.5) 12.17-6.00 (6.0) 16.5) 95th 13.0-18.11) 4.S.0 (13.70) 5.00-11.00 (3.00) 6.28) 2.00 (3.50-5.00-4.84-18.9) 5.6 (9.0 (10.4 (7.0-12.7-16.0) 13.13-4.7) 1284 1284 03-04 03-04 03-04 4.00) 4.80 (4.94) 3.03-6.33) 3.24) 3.69-3.44 (2.00 (6.70-3.98) 4.0-16.5 (11.45) 3.27-5.57-5.0-19.48 (2.6) 1284 1284 03-04 03-04 03-04 4.94-3.60-7.3 (8.50 (4.29-4.06) 5.3 (8.24-4.90) 2.44) 5.0) 16.2) 10.32-10.03 (3.82-5.69 (3.9) 13.9 (7.05) 10.78 (4.49) 10.86-7.89 (3.30) 3.00 (3.60-6.60-3.00 (6.95-4.78) 4.0 (8.84-8.00-11.7) 13.3 (7.0-17.0-16.32 (4.71) 3.70-4.16 (2.39-3.88 (4.00-4.00-3.80-3.97-3.31-4.00-4.00 (5.27 (2.77 (3.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .10) 6.0) 9. population from the National Health and Nutrition Examination Survey.30 (7.61-11.71 (4.00-10.00) 4.27 (3. interval) 3. see Data Analysis section) for Survey year 03-04 is 1.00) 3.12-4.15) 4.05) 3.17 (2.0) 14.00-7.61-16.0) 11.00 (5.20) 11.71-4.95-3.19) Selected percentiles ( 95% confidence interval) 50th 3.00 (7.0 (14.34-4.00-8.1 (8.32 (8.67) 8.00-15.57 (3.25 (4.31) 4.71 (3.0-25.00-22.82-9.37 (3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.92) 3.59 (6.49-4.10) 3.0) 292 728 1548 03-04 03-04 4.00) 5.00-4. population from the National Health and Nutrition Examination Survey.95-6.00 (5.00 (7.00) 6.0 (10.00-7.92-12.0) 95th 16.6-18.00-15.27-2.73) 6. interval) 3.00) 7.0 (10.0 (9.00-12.22) 4.00) 9.91) 75th 5.0) 11.0 (10.20-12.0) 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 4.65-6. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.42) 3.00-13.70 (3.00) 6.81 (5. Survey years 03-04 Geometric mean (95% conf.85 (3.0) 621 725 1078 Limit of detection (LOD.8) 7.8) 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 3.00-12.00-15.65-8.9) 11.60-4.0) 17.0) 10.0 (13.0-17.67) 9.34 (3.00 (4.17-4.00 (3.00-4.14) 3.70-12.0 (8.08 (2.80) 2.55 (2.90 (3.00-11.9 (11.16 (4.80) 7.9) 12.46 (4.0) 9.90) 5.52) 3.00-7.74 (2.00-3.00 (3.0 (9.38 (3.05) 5.72 (4.79 (3.00 (3.0) 12.45) 8.00-4.50-15.80-5.

30-1.28 (1.46-2.34) 2.30-1.10 (<LOD-1.90 (1.10 (.30-2.80) 1.50) 621 725 1077 Limit of detection (LOD.86 (2.80 (1.80-2.14-1.40) 1.81) 1.00 (<LOD-1.50 (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 1.80 (1.90) 2. which may vary for some chemicals by year and by individual sample.05-1.30 (1.50 (2.00-4.70-2.52 (2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .82-2.20 (1.70) 2.60) 2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.61) 2.20-1.18-1.33 (1.60 (2.62) 2.37 (1.96-2.00-1.36) 1.10-1.80 (2.20 (1.30) 1.33 (1.30) 2.73-2.88 (1.50 (1.70-2.40) 2.10-1.61-3.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.40 (1.80-2.985) 1.80) 1.30 (2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00) 2.816 (<LOD-.54) 90th 2.22 (1.60) 2.15-1.86 (2.23) 1.40-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 1.00 (<LOD-1.35-3.10 (1.79) 2.28 (1.88 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.84-3.88-2.57) 95th 2.00) 2.60-2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.31-3.10) 95th 2.77) 1.58) 2. population from the National Health and Nutrition Examination Survey.10 (.85) 1.40-3. Survey years 03-04 Geometric mean (95% conf.10) 2.07-3.16 (2.00-2.00) 1.20-3.90) 2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.70-3.17) 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30 (1.53-2.90) 1.71-2.45) 3.70-2.853-1.80 (1.S.07 (1.50-2.53 (1.18-1.31 (1.20 (1.S.20 (1.11-1.00-1.85) 2.50 (<LOD-1.10-3. Survey years 03-04 Geometric mean (95% conf.40) 1.60 (1.82-2.86) 3.63 (<LOD-1.00-2.10 (1.43-3.00) 1.00 (2. population from the National Health and Nutrition Examination Survey.07) 2.30 (1.40-2.00 (2.00) 1.9.30) 90th 1.00 (1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.20 (1.50) 1. see Data Analysis section) for Survey year 03-04 is 0.40-2.40 (2. < LOD means less than the limit of detection.20 (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.93) .70-2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.60) 1.86) 2.22) 3.20) 2.36 (1.80 (1.46 (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 1.900-1.90 (2.

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

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15 (2.73) 1.90) 2.39 (1.14-1.10) 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 1.37) 1.61 (3.76 (3.30-1.00-76.43 (1.08-8.60 (1.12 (2.57-7.61 (1.80 (2.60-6.52 (1.63) 1.38 (1. 0.59) 3.63 (5.20-6.56 (2.12) 7.10-4.33 (1.35-1.50) 2.85) 1.Metals Barium CAS No.90-13. Workers employed by industries that make or use barium compounds can be exposed to barium dust.48-4.30 (5.50 (5.85 (2.70 (5.77-3.54) 1.88 (5.63) Total 1.75) 2.18 (6.30 (5.82) 2.40-13.4) 6.64-3.25-1.63) 1.16 (1.20-5.00) 1.28-1.70-2.74-3.88) 7.70-5.20-8.63 (8.31.21 (1.30-2.36) 5.94-6.60-6.84) 5.34) 2.47-1.8 (6.50-1. 01-02.32-7. whereas others are practically insoluble (e.60-2.47) 4.31-2.70-2.19) 2.1) 9.81-2.30-1.21-8.05% of the earth’s crust.30) 8.54-1.43) 2.37-1.39-1. depilatories.30) 2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20-1.62) 1.65-8.8) 9.40 (5.70) 4.86 (4.50-6.87-14.55-7.60) 1.40 (4.80 (2.74) 3.86-4.50 (1.19-1.87-7.35) 5.20-1.54-8.S.81-3. Barium salts have also been available as rodenticides.80 (1.29-1.64) 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 2.49-9. Certain foods.93-2.54) 1.29-5.49) 2. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).70) 7.20-8.10) 5.51) 7.27 (1. The general population can be exposed to low amounts of barium in air.93 (4.97 (1. are high in barium (Genter. In nature.26) 2.54 (2.62) 1.05-2. bricks.78-3.01-7.68 (1. respectively.00) 1.15 (1.50 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.12.61 (1. Some barium salts are freely soluble in water.70-3.40) 7. such as brazil nuts.38 (1.03 (1.20-8.35 (2.73) 3. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.02 (7.56 (1.46) 1.32-1.10 (4.12 (2.15-11.10) 3.73-5.54 (6.80-5.17-1. water.25-11.60-3.65) 3.71) 1.26-7.10 (2.65) 1.95-6.90 (1.20 (1.31 (2.30-3.76-2.82) 1.56 (1.48) 1.62 (1.36 (1.42 (1.12) 6.99-5.85) 1.78) 1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.8) 5.90 (4.12.50) 1.40) 7.86-5.08 (6.87 (6.g.99 (4.61 (2.91 (2.50 (2.41) 1.26-1. Small amounts of barium can be released into the air during mining and other industrial processes.49) 11.60) 1.00) 6.93-8.87 (5. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract. Barium compounds are also used commercially in paint.52 (4.73 (6.65 (5.50) 2.06-1.37 (4.76-7.24-1.62 (1.70) 5.70 (1.15-1.57) 3.80) 1. it combines with other chemicals such as sulfur or carbon and oxygen.00) 4.90) 2.11 (3.30-2.27 (1.60 (2.30) 5.30) 4.35 (3. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0. soluble forms of barium.70) 1.75-3.54) 2.70-8.56) 1.53) 2.39) 1.86 (4.71) 95th 6.24 (4.04-2.30 (2.01 (4.30-5. In single dose animal studies.00 (1.90 (6.48-4. 7440-39-3 Medically.51) 1.49) 8.65-1.4) 9.44-2.80-7.24-1.20) 2.40) 3.06-2.55-3. see Data Analysis section) for Survey years 99-00. rubber.56) 4.71) 2.10-5.51) 2.48) 1.35-1.30) 5.90-9.21 (1.91) 6.80 (1.11-1.72) 75th 3.45 (1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .16) 5.69 (1.27) 2.81-2.07 (2.30 (1.87) 7.73 (5. and food.25 (1. such as barium chloride.63 (1.41-1.20-1.45) 7.44 (1.48 (6.90-2. barium sulfate and barium carbonate).72) 4.59-11.71 (2.86) 6.47-1.50 (6.30) 5.50 (1.49 (1.20-1.43) 6.20 (4.50-1.65) 1.87-9.77) 1.54-1.76-3.82-6.46) 1.53) 1.32) 8.50 (1. 2001).56 (6.50 (1.40 (1.34 (1.41-3.80) 7.36 (4.34 (1.30 (3.11 (3.57 (5. fireworks.49) 4.09 (2.44-5.80-3.26) 5. Barium compounds are used by the oil and gas industries to make drilling muds.09 (1.22-1.40 (5.60) 3.90) 4.61-8.78) 1.71-9.50 (4.60-10.90) 1.10 (3.66) Selected percentiles ( 95% confidence interval) 50th 1.70) 1.9) 5.28) 90th 5.38) 2.00-3.80 (1.35-4.30) 3.53-5.76) 1.80-2.18-1.43 (1.92) 2.36-1.78-2.4) 7. interval) 1.46-1.87-3.60) 4.29) 5.15-1.77 (3.74-2.35 (1.88) 1.22) 6.49-1.70) 3.15 (6.80 (5.88) 4.50 (4.20 (3.39) 4.51 (1. population from the National Health and Nutrition Examination Survey.39 (1.50 (1.37-8.22-1.00 (2.96-2.91) 2.65-5.21-2.04-6.63 (2.12-1. and 03-04 are 0.40 (1.98) 1.61 (5..50-6. tiles.64 (1.40 (1. and 0.14 (6.36-1.15) 5.67) 6.34 (2.95 (4.40 (5.50 (3.72) 1. and ceramics.11 (2.38) 8.70-6.43 (5.66 (4.80) 6.18) 3.50) 4.2) 6.37) 5. glass.14-6.00-8.

33 (1.99) 1.36 (1.27 (2.27-3.57) 2.09) 6.48 (1.75) 2.41 (2.11) .18 (1.63) 1.64) 7. NTP.38 (4.53-21.20 (1.91-2.0) 7.73) 2.49-1. 1994.85-5.86-7.46) 2.55 (1.47) 1. 1989).32) 2.03) 1.46-22. in urine.963 (.33) 1.49 (1.67-6.832-1.26) 4.29-1.10 (6.96 (4.20-1.29 (1.89 (2.50 (4. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.56 (1.63-4.91 (3.80) 3.38) 1.29 (3.47) 4.22-1.37-1. water solubility.49-1.27) 7.35-1.41) 5.73-2.20) 4. and route of exposure.51) 6.92) 2.72) 4.50) 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 1.76 (3.42) 1.84-5.96) 4.83) 2.52-4.78 (2.87) 1.55-5.88 (6.08-1.49-1.52) 1.91 (3.58) 75th 2. Following intravenous injection in animals.68 (2.29-7.00) 1.60 (1.48-1.880-1.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .59 (1.51) 4.23-5.37) 2.59) 1.45) 1.74) 1.39 (3.710-1.33-1.75) 2. such as those used in medical radiographic procedures.36 (3. Barium is not rated for human carcinogenicity.46 (2.97) 1.44 (1.83) 3.70) 4.52) 2.61 (4.43-6.74) 1.02) 4.24-3.73-4.47) 10.24-11.31-1.26-1.31) 5.51) 4.46) 1.77) 1.76 (2. 1984. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.69 (5.54) 1. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.88 (2.75-22.24 (5.39-10.16) 11.30 (1.32 (1.68) 3. paralysis.76) 2.703-1.76-3.02) .34-3.64 (1.38 (4.75) 1.96) 4.48-3.24-1.51 (1.00) 6.59) 2.34) 1.52 (3.15-4.68 (3.24-6.22-1.81-7.65 (5.79) 1.79-5.56) 4.77) 1.915 (.26-1.00 (2.16-1.19-1.47 (2.8) 4.55 (4.13-2.76 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.41) 4.0) 6.84 (3.2 (3.921 (.96) 7.43) 1.36 (5.81-6.00) 4.16 (1.48 (1.56) Selected percentiles ( 95% confidence interval) 50th 1.54 (2.80) 4.96 (4.70) 10.58 (2.881 (.51 (3.98 (2.24-1.59 (1.55 (5..03) 3.92 (4.38-1.57-7.60 (1.57 (6.72) 6.06) 2.36-1.47) 1.26-1.10) 6.10-2.48-5.19-2.81-6.45-1.60 (2.03-1.01 (5.45) 95th 6.86) 5.23-1.54 (1.41 (1.32) 2.38) 1.24) 3.38 (1.04 (2.68 (3.5) 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 1.21 (1.66 (1. 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. Insoluble barium salts.18 (1.33 (1.33 (5.77-5.56-3.40 (1.13-3.36-1.25-11.60 (5.99 (4.41 (1.20-2.39-5.84) 2.39 (2. Symptoms following acute high dose include perioral paresthesias.38-7. are not absorbed when administered. vomiting.39-1.80-6.2) 5. Perry et al.14-2.45 (3. 1985.22-2.39 (2.77) 1.64) 7.72 (2.68-3.38) 4..27-1.75-3.53) .Metals was eliminated primarily in feces and to a lesser extent.55 (1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.69-9.55) .64 (1.77) 5.68-3.74 (5.08-2.51-3.48 (1.71 (5.37 (1.57-5.2) 6.40 (1. population from the National Health and Nutrition Examination Survey.28) 5.97 (4.64 (1.35-3.45-1.76) 2.28-1.4 (5.55-6.84-2.40-1.51 (1.34-1.45-8. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.34 (1.28 (1.29) 1.42 (4.82) 1.59-7.3 (6.04) 5.77) Total 1.34-5.22-4.38 (1.58-6.89) 90th 4.96-6.24-6.25 (1.29-4.57-10.20-8.48) 2.46) 3.25) 4.36-2. Toxicity from soluble barium salts is rare.61) 2.96) 4.29-3.19-1.91) 2.39-1. chemical form.54) 2.75) 1.4) 5.33) 6.891 (.0) 5.24 (3.58) 1.45-6.01 (4.28-7. The health effects of exposure to barium compounds depend on the dose.70) 1.59) 1.00-1.10-1.50) 2.26-4.31 (1.64 (1.47 (5.42) 1.37-2.58 (4.32 (1.33-4.44-2. 1986).00) 4.05-1.02 (3.56 (1.00 (5.11-2. 2001). Wones et al.905 (. 1990).777-1.23-2.99 (2.68) 1.00 (3.47-8.62 (4.97-4. weakness.58) 4.45 (1.30 (1.01) 1.30) 2..52) 7.36 (1.50) 1.62) 2.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.31-1.36 (3. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis. a benign condition that may occur among barite ore miners.76) 1.39 (2. diarrhea.12) 2.02-5.52-10. hypertension.35-1.10) 3.38-5. Chronic high doses in animals resulted in kidney damage (McCauley et al.26-1.03-1.65 (2.97-3.62 (1.40 (1.29-4.28-6.3) 6.S.04) 1.06) .03) 2.00-7.31-1.39) 4.97 (5. and cardiac dysrhythmias.32 (2.44-2.28-11.31 (4. interval) 1.00 (3.11) .86 (2.49 (1.62 (2.60 (2.50) 1.19-1.53 (2.82) 1.754-1.37 (1.90-2.

Ting BG. Laurie RD. p. Atlanta (GA).e. p. environmental levels) and health effects is available from ATSDR at: http://www.. and serum of Italian subjects.. 2nd Ed.. pp. et al. Morrow JC. Information about external exposure (i. Vouk VB. Kopp SJ. 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. Epidemiological study of barium in Illinois drinking water supplies. Magnesium.197210. eds. and 2003-2004 (CDC.S. 2005.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Trace element reference values in tissues from inhabitants of the European community I. Costa R. PS. J Toxicol Environ Health. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.nih. and a drinking water standard has been established by U. EPA. Sci Total Environ 1990. Weltle D.gov:8080/cs. 1989.. 1986. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Paschal et al. Apostoli P. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. et al. Wones RG. 221-252 Komaromy-Hiller G.html?charset=iso-88591&url=http%3A//ntp.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. 1992). Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. NTP.gov/ntp/htdocs/LT_rpts/tr432. Douglas BH. 5th ed.. Vol 2: Specific Metals.niehs.28(3):373-388. et al. 1990. ed.. and radium In: Bingham A. Trace metals in urine of United States residents: reference range concentrations. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Inc. 1998)..85:355-359. Minoia C. 2000) to levels in NHANES 1999-2000 and 2001-2002. Comparison of representative ranges based on U.S. blood. In: Calabrese EJ. National Toxicology Program (NTP). Perry EF. 231-249. Princeton (NJ): Princeton Scientific Publications. Environ Res 1998.. 1984. barium. the welders had no obvious adverse clinical effects (Zschiesche et al. 1994. et al. [online]. Clin Chim Acta 2000. Pirkle JL. Cohressen B. 84-94. New York: Elsevier. Int Arch Occup Environ Health 1992.76(1):53-59. Gallorini M. calcium. Lack of effect of drinking water barium on cardiovascular risk factor. Centers for Disease Control and Prevention (CDC). In Friberg L. Available at URL: http://ntp. patient population and literature reference intervals for urinary trace elements. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Zschiesche W.95:89-105. Genter MB.nih. Howerton K. Reeves AL.html.atsdr. Stadler BL. Patty’s toxicology..gov/toxpro2. Advances in modern toxicology. 2005. Jr.296(1-2):71-90. Investigations into the effect of drinking water barium on rats.64(1):13-23. eds. Sabbioni E. Princeton NJ: Princeton Scientific Publications. Jackson RJ. Pozzoli L. Minoia et al. Levy. Nordberg GF. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Frohman. 2001. Perry HM. 1985. Ash KO. p. Barium. Exposure to soluble barium compounds: an interventional study in arc welders. Third National Report on Human Exposure to Environmental Chemicals. Powell C.cdc. 2001-2002. ed. Sampson EJ. Handbook on the Toxicology of Metals. A study of 46 elements in urine. Biomonitoring Information Levels of urinary barium reflect recent exposure. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. New York: John Wiley & Sons. 4/8/09 Paschal DC. McCauley PT. strontium. Calabrese EJ. Schaller KH. LA. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Fourth National Report on Human Exposure to Environmental Chemicals 195 . Environ Health Perspect 1990. References Brenniman GR. In: Inorganics in drinking water and cardiovascular disease.niehs. Pietra R.

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 . bertrandite and beryl. and machine-parts industries. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and can be found in mineral rocks.13. population from the National Health and Nutrition Examination Survey. beryllium is used in instruments. Low-level beryllium exposure in the general population can occur through breathing air. Exposure to beryllium occurs mostly in the workplace. the lightest of all metals.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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and volcanic dust.13. < LOD means less than the limit of detection. aircraft.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 . soil. computer.130 (<LOD-. Two types of minerals. Beryllium compounds are commercially mined. electrical. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. see Data Analysis section) for Survey years 99-00. x-ray machines. respectively. or drinking water containing the metal. and from breathing tobacco smoke. and 03-04 are 0. and refined beryllium is used in mirrors and special metal alloys for the automobile.Metals Beryllium CAS No. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. near some hazardous waste sites. eating food. nuclear.S. 01-02. are mined for commercial recovery of beryllium.140 (<LOD-. and 0. and dental bridges. 7440-41-7 General Information Pure beryllium is a hard gray metal. 196 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.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. 0. In studies of laboratory animals.13.130 (<LOD-. In medicine. coal.

based upon excess lung and central nervous system cancers in studies of workers. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. or berylliosis. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al.281 (<LOD-.273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . IARC has classified beryllium as a human carcinogen. Chronic beryllium disease. 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). population from the National Health and Nutrition Examination Survey. 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 . Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. respectively. EPA. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response..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 . which produces pneumonitis. 2003.346 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and drinking water and environmental standards have been established by U.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. NTP considers beryllium to be a known human carcinogen.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.S. 1990). S.231 (<LOD-. Skin exposure can result in delayed hypersensitivity reactions. Maier. Fourth National Report on Human Exposure to Environmental Chemicals 197 . The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.

Environ Res 1998. and serum of Italian subjects. Sampson EJ. Levels of beryllium in urine for the U. Element reference values in tissues from inhabitants of the European community. Paschal DC. Apostoli P. Morrow JC. Howerton K.S. Ash KO.13 μg/L. Costa R.. 1990.. which approximate this Report’s limit of detection. less than 0.org/documents/ehc/ehc/ ehc106. VI. Paschal et al. Comparison of representative ranges based on U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. et al. McCanlies EC. Schaller KH. 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. and the 95th percentile for males in NHANES 2001-2002.inchem. Given these results.12 to 0. Pirkle JL. Ting BG.html. Clin Chim Acta 2000. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. 1998). Environmental Health Criteria.e.htm. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. it is likely that urinary beryllium levels in the U. population were generally undetectable in NHANES 1999-2000. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures.S.1 μg/L).e. patient population and literature reference intervals for urinary trace elements. Am J Epidemiol 2003. 3/27/08 Komaromy-Hiller G. population are lower than levels in workers. Jackson RJ. Van der Venne MT. Centers for Disease Control and Prevention (CDC). et al.74:162-166. Hamilton et al. Trace metals in urine of United States residents: reference range concentrations. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect..158:165-190. HLA-DPB1 and chronic beryllium disease: a HuGE review.76(1):53-59. Clin Chest Med 2002. 198 Fourth National Report on Human Exposure to Environmental Chemicals .S.atsdr. In other studies.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Pietra R.. and 2003-2004. Kriess K. They reported urinary beryllium levels ranging from 0. 0.Metals (i.23:827-839.95:89-105.gov/toxpro2. 106. Minoia et al. 2000..296(1-2):71-90. Sci Total Environ 1994. Gallorini M. 1990. Sabbioni E. blood. and the fact that most NHANES participant levels were undetectable. Andrew M. Maier L. Sabbioni E. 20012002. 2001). Minoia C. Genetic and exposure risks for chronic beryllium disease. Sci Total Environ 1990. Beryllium [online]. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Atlanta (GA) 2005.157:388-398. Weston A. Hamilton EI. International Programme on Chemical Safety (IPCS). Available at URL: http://www. Trace element reference values in tissues from inhabitants of the European community I. Review of elements in blood. environmental levels) and health effects is available from ATSDR at: http://www. Pozzoli L.cdc. Third National Report on Human Exposure to Environmental Chemicals. References Apostoli P. Int Arch Occup Environ Health 2001. A study of 46 elements in urine. plasma and urine and a critical evaluation of reference values for the United Kingdom population.

00-1.600) .50-1.00 (1.304 (.700) .40 (1.60 (1.60) 1.200 (.283 (.500) .300) .300 (.500) .20) 1.600-1.300 (.20-1.500 (.400 (.441) * .20) 1.400-.10 (1.40) 1.900 (. coatings and plating.300) .300 (<LOD-.600) .300 (.200) .500-.60 (1.400) < LOD .300 (. Cadmium also may be emitted into the air from zinc.00 (.300-.70) 1.400-.300-.300) .300-. and 03-04 are 0.gov/minerals/pubs/commodity/cadmium).00 (.300 (. U.300) .700) .600 (.600) .600 (.216-. plastic stabilizers.500-.361-.00-1. Other uses include pigment production.386-.300-.300 (.20) .40 (1.900-1.200 (.500-.400) < LOD .20 (.300-.412 (.300-.304-.300-.10 (1.40 (1.20) 95th 1.400 (.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .300) . which may vary for some chemicals by year and by individual sample.400-.403 (.30) 1.400-.344) .600-.200-.30 (1.700) .20-1.10 (1. Since 2001.600-.300) .500-.393 (.266-.600 (.366) * * .400) .900-1.600) 1.00-1.40) 1.600 (.10) 1.400) .40 (1.300) 1.60) 1.421 (.800) 1.30-1.900-1.300 (<LOD-.300) .00 (.400) .30) 1. and nonferrous alloys. 0.400) .10) 1. malleable.400 (.500 (.400-.200-.20-1.300) .700) .00) .10) 1.500 (.50 (1.400) . Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.300-.900-1.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .00-1.600 (.50 (1.378 (.700) 1. see Data Analysis section) for Survey years 99-00.500-.200 (<LOD-.400 (.400) < LOD < LOD < LOD .3.800) .500-.20) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .700) . bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.500-.40-1.00-1.900-1.275-.700-1.398) < LOD < LOD < LOD < LOD < LOD < LOD .400-. The predominant commercial use of cadmium is in battery manufacturing.20) 1.452) .00 (.300-.359-.300 (.420 (.700 (.30) 1.500) .20-1.300 (<LOD-.00-1.235 (.300 (.400 (.20) 1.425 (.395 (.30-1.600) .80) 1.300-.300) 75th . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 1.70) 1.378-.400 (.50) 1.300-.449) Selected percentiles ( 95% confidence interval) 50th .326 (.300 (.200-.600) .300-. respectively.10 (1.367-.20 (1.10) 1.900-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) .400-.289-.10) 1. and incineration of municipal waste materials.800 (.40-1.300-.S.900-1.200) .10 (1.400) .313 (.400) < LOD .600 (.40 (1. lead.403) .60-1.300) .600) .30-1.600 (.50 (1.700-1.40 (1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60 (1.200 (.800 (.500-.500 (.400 (.80 (1.600 (. cadmium use has declined in response to environmental concerns (http:// minerals.376-.400 (.500 (.500 (.3.300) . and 0.424) * .368-. as zinc sulfide) and to a lesser extent.500 (.600) .14.00 (.600 (.80) 1.200-.00 (.00 (.400-.300 (.60 (1.700-1.400) .500-.20-1.40 (1.10) 1.500-.300 (.500) .300-.400 (.460) .600) .900 (.400 (.00 (1.20) 1.300-. or copper smelters (U.400) .400 (.300-.470) * .S.300-.500) .10) 1.S.400) .900-1.426-.337) .200-.60) 1.20-1.400) .500-.300 (.200 (<LOD-.500) .20) 1.500-.600) 90th 1.300-.300 (.50-1.500-.309-.382 (.400) .300-.600 (.10 (1.400 (.300-.400 (.600) .00-1.400 (.300) .50-1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.400-.800-1.400) .400-.500) . 01-02.400 (.Metals Cadmium CAS No.500-.300-.600-.304 (.60 (1. interval) .00-1.320) 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 * * * * * * .600 (.255) .900-1.30) . < LOD means less than the limit of detection.800-1.300) .500-.300-.300) .00 (.30-1.90) 1. population from the National Health and Nutrition Examination Survey.500-.usgs.300 (<LOD-.400) .00) .50) 1.70) 1.900-1.50-1.800) .600 (.500-.296-.300 (. during refining of lead and copper from sulfide ore.362-.468 (.10) 1.513) .70) 1.60) Total * .400 (.00 (.00-1.400-.20) 1.427) * .333 (.600 (.00 (.500 (.500 (. 7440-43-9 General Information Cadmium is a soft.10 (.500-. EPA.400 (.20-1.400) .20) 1.700) .10 (1.50 (1.331) .600 (.700) .30-1.

240-.171-.860) 1.277 (.237-.219 (.440 (.265 (..960) 1.820) 1.372) .160 (..279 (.191-.919) .714-1.272-.201 (.490) 1. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.06-1.447 (.308) . The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.800 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.892 (.249) .302 (.17 (.490) .160-.300 (.741-1.179-.452 (.362) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.261-.141 (. an inducible metal binding protein.17 (..482) .077 (.232) .092) .28) 1. ingestion through food is the largest source of exposure.226) . 1994).607) .234 (.492 (.22 (.210 (.733-.733) .52 (1.180 (.20 (1.38) .426 (.121 (.150-.193-.717-.450 (.980 (.202 (.243-.100-.187 (. 2003).196-.229-. Inhalation of cigarette smoke is a predominant source of exposure in smokers.455 (.067-.115-.366-.128 (.36) 1.01) .284) .090) .220 (.400-.817 (.219 (.360) .466 (.239 (.282 (.12 (.980-1.25 (1. 2004a.980) .265) .20-1.200 (.140 (.32 (1.41 (.387) .193 (.189) .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..51 (1.316 (.07-1.450 (.892-1.886-1.195-.230) 75th . 2003).388-.875 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.061-.393-..01 (.078 (.25) 1. respectively.220) .72) 1.394-.17) .067-.886) .238-.235) .222) .12-1.700-.194-. Kikuchi et al.806) .74) 1.077 (.255) .04 (.200-.240) .545 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.890-1.192-.640) .285-.381-.223 (.229) .160) .763-.390 (.15) .980-1.170 (.206 (.157) .114-.551 (.153-.940-1.257-.109 (.43) 1. population from the National Health and Nutrition Examination Survey.320) .S.766 (.20 (1.351-.507) .160) .633 (.500) 90th .540) .03) .423-.170-.326) .680 (. To a lesser extent.313) .13-1. 1999.366-.210 (.192-..220-. wheat.47) 1.295) .963-1.270 (.257) .190-.090) .232 (.813 (.848 (. 0.686-.700-.350 (.445 (.972 (. copper) and protein.20) 1. whose body burdens of cadmium can be approximately twice that of nonsmokers.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .177-.456-.858 (.204 (.48 (1.289-.262) .227 (.15) 1. rice.200-.610) .28-1. 200 Fourth National Report on Human Exposure to Environmental Chemicals .191 (.13) .470-. potatoes.977) .169-.210 (.705-.510-.700-.230 (.458 (.730-.189-.520-.06-1.281 (.10 (1. 2001).135-.412) .339) .890 (.184-.880) .181 (.107-.445 (.221 (.354) .510) .109-.206) .34) 1.82) 1.136) .238) .191-.57) 1.253-. and various seeds.790 (.241) .** Survey Geometric mean (95% conf.820 (.530) .843-1. however.210) .475 (.270 (.255) .060-.493-.216 (.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 . see Data Analysis section) for Survey years 99-00.306 (.150) .02-1. calcium.130 (.190-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.148-.210 (.135 (.04 (.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 .173) .519) .261-.38) 1.17 (. Cadmium is absorbed via inhalation and ingestion.870) .247) . Renal tubular and glomerular damage.151-.989-1.233) .918-1.550 (.189-.820-1.260-. 2003).203) .551) .110-.06.208-.280 (.28 (1.221) .210 (.480) .06) .790 (. including many food crops such as cereal grains.300) .251) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .178-.330-.817 (.210) .198) .092 (.120 (.299) .24) 1.183-.214-.13 (.175 (.748-1.500) .233) .112-.081) .498-.273 (.390-.818 (.462 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.190-.080 (.065-.260-. Horiguchi et al.589 (.960 (.713) .329 (.165-. interval) .263) .20 (1.440-.167-.310 (.479) .231) .322 (.430) .134) .01-1.436-.633-1. 01-02.230) . 2003.440 (.19) 1.980) .170-.481) . For nonsmokers who are not exposed to cadmium in the workplace.219 (.530 (.290-.260 (.09-1.061 (<LOD-.203 (.836-1.211 (.101) .175 (.559 (.06.476-. With chronic exposure.202-.390-.433-.283 (.810-1.38) 1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.310) .875) . Cadmium in soil is absorbed by plants.211-.839 (.209 (.990) .087-.855-1.753-. drinking water is a source for cadmium intake.148) .200 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.207-.336) .229) . Diamond et al.83) 1.519) . and 03-04 are 0.800-.580) .327 (.430-.596) .06.199 (.30-1.22 (1.157-.539) . and 0.126) .623) .Metals 2000).255) .366) .400-. zinc.220-.38) .15 (.246) .249-.

304-.387 (.343-.071 (.472) .140-. Horiguchi et al.850) .940 (.827) .07 (.170 (.104) .162 (. population from the National Health and Nutrition Examination Survey.622 (.293-.321) .826-1.247-.828) .135) .288 (.16) 1.440) .178-.** Survey Geometric mean (95% conf.783 (.216-.181 (.123-.418-.917 (.06 (.434 (.181-.261) .191 (.156 (.283 (.500-.650-.716) .767) .404) .38) .113-.335 (.242) .240) .234-.691-.297) .02 (.157-. 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.130-.112) .906) . 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.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.979 (. most often a result of occupational exposure (Roels et al.207) .232) .224 (.13) .194-.075 (<LOD-.985 (.779 (.158-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate. 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.541) .712 (.210 (.077-.190 (.239-.250) ..247-.205 (.444-.143-.282 (.150-.537-.678-.090 (.850) .126 (. 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.308 (.078-.238-.329 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.12) 1.187-.174-.263-.238) .690 (.252 (.197-.674-1.07) .718 (.161-.441-. Noonan et al.438-.086 (.559-.255-.067-.267 (.176 (.178) .364) .168 (.232) .719 (.168-.241) .206-.387-.199-.263 (.507-.107) .229) .156) .331 (.336-.490 (.722-. During the 1950’s and 1960’s.091) .078 (.382) .221-.219 (.106) .874-1.789 (. 2002.491-.382-.136-.051-..813-1.281) .876-1.097) .204-.085 (.767 (.123-.666-.175 (.192) .201-..740 (.104) .226) 75th .388-..631) .940-1.617 (.962) .784) .184) .176 (.182) .418) .833-1.318 (.311) .826-1.136-.865 (.830) .101) .998) .431) .338 (.131-.727-.813-..433-.212 (.09 (. At lower environmental exposures.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 . 1996.414-.154-.802 (.220 (.352) .209) Selected percentiles ( 95% confidence interval) Sample 95th .190 (.199 (.184-.173 (.156-. 2003.686 (.614) .234) .170-.300-. Staessen et al.690-.225) .501 (. 2002.219 (.308) .292) .607) .261 (.143-.189-.325 (.479 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.856) .536 (.919 (.182) .094) .516-.218) .806-1.207-.288) .159 (.729 (.538) .412 (.091 (.391-.316) .667) .185) .591 (.074-.792 (.063-..173-.075-.531 (.221 (.100 (.191-.533) .208 (.560-.280 (.414 (.228-.233 (.222-.927-1.340) .16) .647-.261-.432 (.700) .470) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .645-.235) .05) 1.148 (.00 (.122 (.147-.690-.182) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .144-.191) . 2000.08) .415) .175 (.111-.208-.187) .098) .440) .757) .795) 1.274) 1.266) .929) .083-.278) .253 (.856 (.518) .227-.423 (.931 (.084 (.146-.215 (.154 (.183 (.084-.091 (.783) .181 (. 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.754) .S.288-.175-.687 (.210 (.209) .426-.223) .00 (.678 (.270 (.421 (. 1999).304) ..185 (.171-. Olsson et al.143) .668-.268 (.267 (.708-1..398-.716-.839) .481 (.159 (.350) . can result from high dose chronic exposure.487 (..184-.085-.830-1.236-.177) .316 (.917) .183) .289) .196 (. Jarup et al.147-.700 (.818) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .273 (.909-1.296 (.663 (.253) .163) .941 (.256-.202 (.688-.950) .210) .234 (. 1999).147 (.725-1.404 (.17) .181) . 2004b). 1999).470) .873 (.211 (.166 (.093 (.266-.446) .449) .245 (.630-.096) .545) .289) .377-.757 (.818) .438) 90th .168-.240) .476) .157-.484 (.423-. interval) .163 (.551) . 2002.653) . 2004).137 (.225) .473 (.10) 1.696-..247-.687-.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 .140-. However.198) .693 (.884) .381-.303) .281) .137-.200 (.562-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.769 (.

. 2003. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 2003.46 mg/gram of creatinine) (Ezaki et al. 2000... CDC.S.. Cadmium can produce lung. 2006). Jarup et al. 2002. 2002. Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. Noonan et al. EPA. Both IARC and NTP consider cadmium a human carcinogen.cdc. Horiguchi et al. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. respectively. Zhang et al.. 2000.. Occupational standards are provided here for comparison only. Further research is needed to address the public health consequences of such exposure in the United States. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.. 2002).. 2005. with peak values observed in the fifth to sixth decades (CDC. 1988). 2006.. Horiguchi et al.. study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. Wilhelm et al.. environmental levels) and health effects is available from ATSDR at: http://www. Becker et al.. 2000)... Staessen et al.. and drinking water and environmental standards have been established by U. 2004b. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. 2003. intermediate in former smokers and lower in never-smokers (Becker et al. Olsson et al..... 1996).. as may occur from welding cadmium-alloyed metals. Becker et al. Komaromy-Hiller et al. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U. In the typical environmental exposure. 2002. 2005.. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. 2004. 1999). Creatinine-corrected urine cadmium values in U.html. Salpietro et al. Animal studies have demonstrated reproductive and teratogenic effects. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. Staessen et al. 2002.. Olsson et al.. data (CDC. 2002). 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). 1996.26 and 3.1 mg/L (Alfven et al.gov/ toxpro2.. 2004. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.. 2006.. 1999. Friedman et al. 2003.. However. Wennberg et al. Women had higher blood and urine cadmium levels compared to men of similar ages. 2005). Jin et al.e. has resulted in severe. In postmenopausal women. Suwazono et al... not to imply a safety level for general population exposure. 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. Ezaki et al.. approached these values associated with subclinical changes in renal function and bone mineral density. Wennberg et al.S. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. respectively. 2002. 1999). Becker et al.. maternal blood or maternal urine and birth weight (Nishijo et al. Information about external exposure (i.. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. Mannino et al.atsdr. 2005... Staessen et al. Olsson et al.. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2002). 2006). 2000. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. 2004. 2003. 2003. Jarup et al. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity.. Ezaki et al. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al.. 2004). 2003). 2002). In adults aged 60 years and older.. For NHANES 19992000. 2002). Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. 2002) and length at birth (Nishijo et al. 2004b). 2005. 2002. Acute and heavy exposure to airborne dusts and fumes.. 2004...S. potentially fatal pneumonitis (Fernandez et al..

Becker K. Atlanta (GA). and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Hellstrom L. Lundh T. References Akesson A. Ikeda Y. Costa R. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Seiwert M. Environ Health Perspect 2002. et al. Tsukahara T.66(Pt A):2141-2164. Ukai H. Vahter M. environmental. Horiguchi H. Third National Report on Human Exposure to Environmental Chemicals. et al. Venables KM.76:186-196. Serra J. 206:15-24. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Thayer WC.110:699-702. et al. possibly better than b2microglobulin. Alfven T.95:20–31. Oguma E.354:1508– 1513. Holguin F. Kundiev YT. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Vahter M. Schulz C. population. Mascagni P. Sasaki S.205:297-308.S. et al. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Chiappino G. Kaus S. Schulz C. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Clin Chim Acta 2000. Nermell B. Environ Health Perspect 2005. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Toxicological profile for cadmium update. Chislovska NV. Int J Hyg Environ Health 2003. Occup Environ Med 2000. Furuki K. Consonni D. 196:114-123. Greves HM. Davison AG. Zhu G. Machida M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Miyamoto K. Krause C. Environ Res 2004. 1999 [online]. Fatal chemical pneumonitis due to cadmium fumes. Stock AL. Fernandez MA. Horiguchi H. et al.24:717-724. et al.102:83-89. Hotz P. Ezaki T. iron deficiency. J Toxicol Environ Health 2003. Kikuchi Y.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.148(1-2):11-20. et al. Oguma E. Nordberg G. Akesson A. Bernard A. et al.96:353-359. Palomar M. Comparison of representative ranges based on U.57:668-672. Fukui Y. Lison D. Occup Med 1996. Komaromy-Hiller G. Jones RL. Diamond GL.atsdr. patient population and literature reference intervals for urinary trace elements. Mannino DM. Wang H.S. Thorax 2004. Toffoletto F. Sasaki S. Taylor AJ. Berglund M. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U.gov/toxprofiles/tp5. Environ Res 2004b. Furuki K. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Machida M. Anthropometric. Comprehensive study of the effects of age.45:43-52. 2005.1(8587):663-667. Becker K. Nerbrand C. Miyamoto K. Choudhury H. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Olfactory function in workers exposed to moderate airborne cadmium levels. Environ Health Perspect 1994. Uemura T.13(11):1627-1631. Agency for Toxic Substances and Disease Registry (ATSDR). Lukyanova EM. Howerton K. Friedman LS. Buchet JP. Ikeda Y. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Dekio F. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Mucha A. Bellerup P. Cadmium fume inhalation and emphysema. Ye T. Int Arch Occup Environ Health 2003. Toxicol Appl Pharmacol 2004a. Grubb A. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Pickering CA. Lancet 1988. J Occup Health 2003. Lancet 1999. Jarup L. Carlsson MD. Lauwerys R. Bregante G. Moriguchi J. Jin T. Ezaki T. Environ Res 2006.000 women in the Japanese general population: a nationwide large-scale survey. et al.59:497]. Okamoto S. Sanz P.html. Tsukahara T. diabetes mellitus. Savage-Brown A.296(1-2):71-90. 4/8/09 Alfven T.cdc. et al. Lepom P. Seifert B. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Available at URL: http://www. Persson B. Ash KO. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Takebayashi T. et al. Gadea E. Elinder CG. Seiwert M.59:194-8. Kumagai N.46:372-374. Toxicol Lett 2004. Fukui Y. Neurotoxicology 2003. Int J Hyg Environ Health 2002. Kaus S. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Fayers PM. Darbyshire J. Nomiyama T. Bo M. Centers for Disease Control and Prevention (CDC). Moriguchi J. ShkiryakNizhnyk AZ. 102:10581066. Jarup L. Lidfeldt J.

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66 (7.3-13.08 (6.01-8.13-8.4) 10.84) 5.01) 7.00) 7.16-6.3) 12.2) 12. However.4 (10.14.55 (7.6) 11.7) 11.43 (5.72-7.50) 5.60-7.2.79 (4.92-13.04) 7.7 (10.10-5.20) 7.03 (4.94-4.53 (6.40 (4.0) 10.87 (4.25-5.1 (10.20-8.20-7.39) 7.00) 4.00-4.70 (9. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.73-11.26 (3.77 (4.40-5.82) 5.63-4.71-9.10 (8.38) 5.97 (7.20 (6.99) 7.57-5.29 (4.8 (10.35 (4. interval) 4. soil.89-5.7) 11.05) 5.45-8.5) 10.59-5.7 (9.33 (5. cesium hydroxide is corrosive and irritating at high concentrations. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock. and 03-04 are 0.90) 9.91 (7.4 (9.89) 4.3) 9.60) 5.26-11.7 (9.25 (3.67 (4.80 (8.80 (4.9 (11.0-15.6 (9.04 (4.4 (9.40) 7.56-11.4-13.Metals Cesium CAS No.90) 4.14.50 (4.49) 4.0) 11.6 (9.3) 10.2-14.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and cardiac arrhythmia (ATSDR.6 (11.50) 9.0 (9.21 (4.2-13.80-10.70 (6.13 (7.49) 75th 7.00 (7.80-6.97) 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 4.1) 10.9) 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 4.77 (9.5-13.42) 6.8) 9.1-13. population from the National Health and Nutrition Examination Survey.9 (10.8 (11.99-6.10 (6.86-11.94) 4.98 (7.34 (4.90) 5. Most human exposure to cesium occurs through the diet.50 (4.07-11.7 (10.20-4.76-6.15-8.52-9.81 (4. Inorganic cesium compounds are used in photomultiplier and vacuum tubes. the body half-life is estimated to be 70-109 days based on 137Cs exposures.86-12.3 (8.9) 11.70 (8.5-14.1) 9.07) 4.7 (8.6 (9.1 (9.52) 7.90 (6.95-4.86 (7.70) 7.99) 9.1) 11.00) 6.17-6.13 (8. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.83-4. and 0.9 (11.7-14.00-8.80 (4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.3) 10.84-5.9) 8.5 (8.08 (7.S.14 (4.9 (11.10-7.70) 5.02 (4.43-8.60 (7.42) 7.9) 12.56 (4.33 (6.70-8.95) 5.08) 7. and high-power gas-ion devices.40-11.4) 10.4) 12.30 (6.0) 12.90 (4. scintillation counters.47-4.56 (4.60) 7.27) 4.5-14.40-7.63 (4.37) 5.10-8.59) 7.0) 12.70 (6.97-7.45-5.20) 8.64) 5.7 (9.0 (10. and clay.2-13.1) 11.27-5.81) 4.29) 4.90) 5.10-9.8 (10.90-12.90) 7.87-7.6 (9.99-11.80 (8.2 (9.4) 11.37) 7.97) 4.0) 12.62 (5.9 (11.60-12.12-5.3) 10.60-5.17 (6.2-12.5) 9.3-15.81) 9.98 (7.90-8. 01-02.35 (4. respectively.1-12.64-5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .60-6.05-5.3) 10.53-11.80 (8.34) 9.70-5.71) 4.8) 9.60) 7.20) 5.74 (4.84-9. 0.93 (4.74-5. 2004).54) 4.0) 11.30-10.32) 4.50 (4.62 (5. Radioactive 137Cs has been used medically to treat cancer.90-12.71 (8.63) 6. see Data Analysis section) for Survey years 99-00.62) 4.7) 10.44 (8.68 (7. semiconductors.80-13.59-5.49 (5.70) 5.6) 10.87 (4.5-16.77-8.2-13.70 (8. although cesium was generally of low toxicity when given to animals.36 (3.95 (3.00-10.27 (7.81) 4.91-8.30-5.72) 4.30) 5.40-5.20-5.8) 11.4) 9.36 (6.9) Total 4.59 (5.82-4.36) 3.64) 4.90-10.23-4.6 (11.12) 5.89) 5. infrared lamps.0-13. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.94 (4.81-14.32-5.17) 4.00-9.71 (4.69-6.73-5.5 (10.12 (4.7) 10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40-5.10 (8.70 (4. nausea.4) 95th 11.16-6.3-13.61) 7.77 (9.08-5.88 (8.61-6.80-10.4) 12.08-5.80-10.90-10.30) 7.40) 5.60-6.59-5.32 (3.87 (4.60 (8.50 (6.90-10.7 (10.40) 5.54-11.26) 4.26) 7.1) 9.8-13.22-4. Little is known about the health effects of this metal.56) 5. photographic emulsions.00-8.25) 4.8) 12.40-5.47-8.40-11.23) 9.03 (4.1-12.71-5.12-11.2) 11.8) 12.31-8.7 (11.71-8.84 (4. Whether cesium compounds are carcinogenic is unknown.0) 9.2 (9.60-7.55-11.87) 5.24) 4.46) 7.80-11.5) 12.50-7.8) 12.80) 7.49 (4.64-10.13 (5. diarrhea.21) 90th 9.30 (6.99-11.9 (10.09-5.50 (7.09) 5.80 (4.83) 6. and as polymerization catalysts. For absorbed cesium salts.20 (4.8) 11.33-5.70 (5.1 (11.3 (8.01-6.64) 5.64 (4.05-5.39-4.68) 9.05) 5.20) 4.03-4.84) 8.42-7.35-5.74) Selected percentiles ( 95% confidence interval) 50th 4.22 (4.94 (4.96 (6.10 (6.55 (4.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.

96 (4. 1990).5 (9.44-5.54 (3.45 (4.99-9.64) 4.7) 10.4) 10.07 (5.S.41 (4.74 (4.29-3.28 (4.16-8.3-15.30 (3.12) 3.93-7.47) 6.95 (5.43 (3.3 (8.8) 10.91-9.82-4.07) 8.21 (2.83-6.76-6.3 (10.65 (6.64 (8.56) 4.90-3.96) 4.20-4.06) 5.40) 6.07) 8.92 (5.85) 5.97) 8.72 (4.83) 8.91) 5.50) 8.10) 7.04) 6.50 (5.04) 5.2 (8.60) 3.08-3.68 (4.40) 7.62) 5.30 (4.70 (7.85) 4.60 (5. (2000) found urinary cesium levels that were slightly lower than those reported for the U.81 (4.50 (6.63 (6.13-9. Komaromy-Hiller et al.61 (7.29) 5.78 (3.56 (4.93-9.58 (4.78) 4.36-6.75 (6.50 (7.27-4.82) 7.95) 4.38-12.18-7.35 (3.51 (4.05) 3.44-9.91 (5.7-12.72-5.51 (3.91 (5.73-4.42-6.29) 4.53) 3.42 (5.87 (5.67 (6.68-11.18 (7.0) 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 .90 (7.41-7. Two small studies of European populations reported urinary cesium levels similar to U.95) 8.87-4.94 (5.04-11. and were also roughly similar to those in this Report.97-5.00-5.19-6.14 (6.64) 9.71 (7.0 (7.66 (5.22-11.91-7.04-5.73 (3. population results shown in this Report (Alimonti et al.27 (6.21-4.84-7.14) 4.24-10.6 (9.15 (7.41 (5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.91) 5. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.55-5.74) 75th 5.98 (7.08) 4.27) 4.08 (5.17-4.84-11.60-10.78) 4. interval) 4.25) 4.33-8.18-6.41 (8.14-4.05-3. population from the National Health and Nutrition Examination Survey.06 (5.20) 5.47) 6.74) 3.16) 5.42-4.03-6.28) 7.48) 7.39) 8.47) 4.08 (6.89-4.10 (3.9) 10.46) 6.3) 11.33 (5.52-5.53) 6.41) 4.66 (5.09) 8.59-8.11 (5.06) 4.1) 11.66 (6.35-7.38 (3.91) 4.44 (8.75-11.60 (3.26 (3.47) 7.86 (4.80) 6.77 (7.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.20-4.00-9.78 (3.37) 4.77 (4.29) 4.15-11.22 (3.63-6.68) 6.98) 5.99-9.03-5.20-4.79) 4.31 (4.37-3.44 (4.10 (3.79) 6.26 (4.90-8.87) 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 5.02-4.77-5.30-4.58-5.90-8.35-11.6 (9.16-8.12 (3.14-7.74 (5.67 (5.47 (4.96) 4.46 (8.67) 5.26-6.40-5.57) 3.15) 95th 8.71) 6.79-5.58) 3.05-3.42 (4.28) 8.61-3.00) 6.65-3.5) 9.51) 4.47 (7.36-10.48) 90th 7.8) 5. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.05 (4.31-4.54 (4.30) 10.36-3.30-4.75 (7.06 (3.5) 7.41-4.56) 4.13-9.53 (6.27 (6.77 (6.79 (5.09 (4.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.09) 4.42-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.38 (3.43) 8.08 (3.43-11.38) 10.68) 3.59) 4.84-9.81 (4.99) 4.8) 6.51 (3.97-4.44) 3.74-11.30 (7.0) 7. 2004).24 (3.22) 6.8 (9.45-6.S.70) 7.15-4.95-12.51 (7.6) 6.18) 8.58) 8.5) 9..41) 9.11 (5.12-6.00-10.63 (4.16-5.31-6.65-4. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.96-4.60-20.94) 7.9 (9.29-3.87) 5.50-5.35) 3.9 (10.91-6.43 (8.50) 4.77) 4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.88-10.95 (3.51 (4.17) 4.64) 5.17 (6.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.21-3.13) 7.46-8.99-4.79) 9.10 (5.27-6.00-5.98) 5.55 (3.34 (5.83-7.10-4.08) 3.08-7.25) Selected percentiles ( 95% confidence interval) 50th 4. Using clinically submitted specimens.33 (5.00 (8.17) 9.64-6.56) 3.05) 6.53 (4.63-6.99 (3.08) 4.68) 4.05-4.43 (4.48-6.39) 5.02 (5.55) 4.96-4.03) 5.14-6.38-7.49) 3.21-5.28 (5.85-4.24-4.95) 10.84-7.72) 4.33-3.43 (4.64 (4..2 (8.03) 6.30) 10.58 (6.50) 4.00-4.46-4.54 (4.7) 10.92) 3. Minoia et al.19-3.3) 9.98 (6.84-9.46 (7.13 (3.63 (7.0) Total 4.63) 6.66-6.27 (8.54 (5.3 (9.50) 4..00-8.14) 4.23 (7.56-10.62-8. population.88-4.70) 6.07-4.31 (4.39 (5.35 (4.95-6.43-6.01-8.20-8.2) 11.76-9.

patient population and literature reference intervals for urinary trace elements. Sewell CM.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).14:120-128. Sci Total Environ 1990. New Mexico. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Pozzoli L. J Expo Anal Environ Epidemiol 2004.html.19:3131-3138.95:89-105. Centers for Disease Control and Prevention (CDC). Paschal D. et al. blood. Apostoli P.296(1-2):71-90. Gallorini M. Sabbioni E. et al. Assessment of urinary metals following exposure to a large vegetative fire. Howerton K. Atlanta (GA) 2005. Gatti A. 2000. et al. Wolfe MI. cesium. Trace element reference values in tissues from inhabitants of the European community I. Mott JA. Pietra R. A study of 46 elements in urine. antimony and tungsten. Ash KO.atsdr. Mincione G. Comparison of representative ranges based on U. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Voorhees RE. Minoia C. Clin Chim Acta 2000. Forte G. Available at URL: http://www. and serum of Italian subjects.cdc. Third National Report on Human Exposure to Environmental Chemicals. Costa R.S. Rapid Commun Mass Spectrom 2005. Spezia S.2004 [online].gov/toxprofiles/tp157. 4/8/09 Alimonti A. Ronchi P. Toxicological profile for cesium. Wood CM. Komaromy-Hiller G.

950) .09) .640) . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.285 (.760 (.75 (1.259-.960-1.740-.465) .270-.580 (.360-.390 (.710) 1.930) .800) .08) .850-1.870 (.850-1.08-1.590-.01 (.502) .760) .14-1.540-.630-.380-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.880 (.319) . and inks.583) . hard metal (alloys of cobalt and tungsten carbide).300 (.370-.520 (.430 (.416) . shiny.47 (1.400-.461 (.520) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .680) .410 (. and kitchenware.32 (1.350 (.435 (.S.06-1.308-.980) .540-.470) .820 (.940 (.26-2.26) 1.390 (.850) .375 (.07 (.410 (.81) 1.301 (.880-1.290-.670-.520-.333-. Cobalt occurs naturally in airborne dust.340 (. and 0.890) .910-1.47) 1.48) 1. diamond-polishing wheels.16) 1.09 (.452 (.355-.430 (.S.56) 1. large appliances.32 (1.21) 1.570) .07-1.07.32-2.32) 1.390-.590 (.530-.336-.25-1.520 (.550 (.46 (1.540-.940-1.480 (.600) .373) .580 (.53) 1.16) 1.690 (.16-1.81) 1.23-2.47) 1.750 (.600 (.04-1. seawater.630 (.790 (.420) .450) .410-.670 (.680 (. hard metal or in combination with other elements. and in synthesizing polyester and other materials.04) 1.05 (. and soil.28 (1. respectively.460 (.496) .900) .16-1.950-1.543) .500) .740-.73) 1.371 (.660-.800-.850) 1. steel-belted radial tires.520-.316 (.419) Selected percentiles ( 95% confidence interval) 50th . see Data Analysis section) for Survey years 99-00.540-.590-.710 (.660) .310-.410) .560 (.520-.460) .930-1.06 (.370-.380 (.388-.870-1.515 (.350) 75th .430) .360-.487) .59 (1.60 (1.450-. population from the National Health and Nutrition Examination Survey.45 (1.431) .379 (.950 (.510) 1.490-.950 (.470 (.820 (.350-.427-.370-.490-.338-.750 (.519 (.499 (.14) .07. Cobalt compounds are also used in manufacturing battery electrodes.24 (.420) .820 (.348-.424) . varnishes.369 (.650 (.04 (.570-.520) .99) 1.530) .12) 1.26-1.600-.39) 1.19) .294 (.01 (.364-.890-1. Cobalt compounds are used as catalysts in producing oil and gas.690-.650-.480-.42) 1.47 (1.05) 1.04-1.520 (.410) .28-2.770) .01-2.790-.920) 1.469-.450-.900-1.28 (1.367 (.359 (.67) 1.270-.610) . industry is imported or obtained by recycling scrap metal that contains cobalt.690-.399) .800-. The cobalt used in U.17 (. Usual human exposure is from food sources.890-1.00) .360-.890-1.68 (1.33 (1.980-1.05 (. Cobalt is used as a drying agent in paints.790) .372) .20 (1. automobile airbags. blue-colored pigments.300-.430) .64) 1.03-1.830-1.530 (.620-.840) .860 (.08. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.418 (.750-.330-.334) .348-.380 (.700) .430-. and magnetic recording media.460) .410-.333-.01-1.36) 1.428-. 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.450) .270-.32) 1.15-1.73) 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 .940-1.44) 1.680) .590) .52 (1.16 (1.581) .410 (.440-.390) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.340-.02-1.03) .340) .410-.660) .950-1.377-.900-1.390 (.07-1.730) 1.710) .460 (.09 (.17 (1.414) .06 (.373-.04-1.750 (.398 (.523) .17-1.930 (.310 (.564) .03 (.630 (.374 (.670-.316-.22) 1.331-.405-.580 (.50) 1.870 (.480 (.380-.740 (.500 (.550-.460) . It is also a component of porcelain enamel applied to steel bathroom fixtures.33-1.03) 1.14) 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 .810-.343 (.920-1.48) 1.330 (.520-.380 (.350-. interval) .900) .410 (.340) .431) .450) .350-.450) . and fertilizers.570-.330) .700) .320 (. 01-02.430 (.339 (.680 (.810) .Metals Cobalt CAS No.640) .17 (1.386) .640) .890) 95th 1.327-.13) 1.620) .03 (.352 (.570 (.92) 1.23) .22-1.434 (. 0.15 (1.313) .610) .410 (.65) 1.305-.393-.22 (1.398) .520 (.900) .340-.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 . and 03-04 are 0.550) 90th .29 (1.670 (.620-.16 (.670 (.280-.03) 1.460-.24 (1.404) .420 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.12) 1.28 (1.610 (.610-.417) .291-.50 (1.16 (1.370) . It is emitted into the environment from burning coal and oil and car and truck exhaust.463-.394) .810) .379 (.620-.650 (.454 (.370 (.26) Total .540) 1.570) .37-1.

337) .550-.35) .280-.635 (.581) .703-.274-.495 (.487-.900-1.301) .844 (.313-.12-1.513 (.291 (.829) .964 (. in the feces.439) .792-1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.679-.409) .976 (.333-.380-.313 (.417 (.360) .60) 1.33) 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 .04 (.911-1.378-.10 (.463-.282 (.329 (. an essential human nutrient.833-1.259-.381) .983-1.378-.392 (.384) .27) 1.369 (.50) 1.309) .781-1.290 (.503-.319-.14 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.304-.963-1.16 (1.396) .54) 1. 1972).523 (.949) .365) .938) .408 (.740-1.563-.259) .598 (.50) 1.694) .10) . A portion of cobalt retained for long periods is concentrated in the liver.700 (.591 (. Smith et al.983) .523 (. cobalt is excreted predominantly in the urine.293 (.404-.372) .616-.461) .297) . with pulmonary clearance half-lives of from one to two years (Hedge et al.736-.452-.25 (.417) .932-1.468) .. or using diamond-polishing wheels that contain cobalt metal.606 (.57) 1.462) .73) 1.257 (.00) .313-.297-.786-.963) .781) 95th 1.333-.03 (.756 (.723 (.348) .03-1.727 (.400 (.16 (.286) .294-.426 (.16 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.634-.963) .407) .352 (.296-.425-.19) .362 (.361-.683-.738 (.00 (.343-.700 (.15 (.402 (. 1994).29) 1.282-.851 (.433) .667-1.425) .467-.505) .632-.215-.290 (.861 (.537 (.975 (.554 (.513-..599) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.323) .917) .301-.Metals fabricated from cobalt alloys (Lhotka et al.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 .960 (.355) .334) .303-.11-1.S.449-.481) 90th .00) .06 (.708) .50 (1.333-.393-.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 .689 (.362) .277-.963-1.11-1.438) .00 (. respectively.500-.313-.479-.29) .239-.298 (.952 (.396) .850 (. 2003).391) Selected percentiles ( 95% confidence interval) 50th .826-1.272-.29 (1.393 (.750) .444 (.850-1.09) 1. 1994.449) .428-.626-.251-.00 (.314 (.313-.331-.310) .744) 1.368 (.662) .990) .10-1.582-. refining or processing alloys.394) .317 (.16) .15) 1.387) .343 (.281) .44 (.479) .17) .344-.560-.257-.328) .898 (.595) .600-.737 (.667-1.300) .760-1.476-.28) 1..937 (.457) .278 (.361-. Once absorbed and distributed in the body.25 (.327 (.376 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).353 (.552 (.329-.469-.02 (.955) .279 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.337 (.728) .857-1.335 (.821-3.821 (.339-.00-1.313-.673-.660-.457-.785) .306) 75th .733-1.326-.237-.29 (1.306 (.585) .275-. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.562) . population from the National Health and Nutrition Examination Survey.611) .248-.349) .49) 1.386 (.419) .488) .750-.838 (.500 (.328 (.30 (1.534 (.333 (.990-1.861-1.27) 1.273 (.561) .275-.316 (.435-.824 (.777-.548 (.352) .362-. Exposure in the workplace may come from electroplating. 1972).304) .247 (.738 (.248-.12 (.435 (.421) .753-.611) .554 (.471-.368) .543) ..346 (..358 (.382-.388 (. interval) .04-1.594) .368) .938-1.429) 1.842) .475 (.33) .24) .327-. Cobalt is absorbed by oral and pulmonary routes.640) .872 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.10) Total .522) .905) .328 (.753) 1.804) 1.83) 1.471 (.830 (.268 (.757-1.574-.353-.647) .542 (.547 (.471-.290 (.508-.33) 1.457 (.513) .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 .278-.256-.378 (.774 (.324) .792 (.895-1.352 (.704-.847) .728 (. using hard metal cutting tools.388 (.500-.562) .279) .848 (.609) .691 (.302-.35) 1.243-.593) .895-1.638-1.250) .361 (.487-.234 (.407 (.271 (.296) .608 (.378-.529 (.955) .707) .533 (.23 (1. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.669) . and to a lesser extent.455 (.442-. 1979).60) 1.829-1.434-.630-.534-.36) 1.630-.363) .55) .361 (.644 (.929) .00 (.391 (.342-.289) .259 (.365-..879-1.36) 1.324-.515 (.615) .29 (1.

population (CDC. Lauwerys and Hoet. White and Sabbioni.. Centers for Disease Control and Prevention (CDC).e. A 1982-1992 surveillance programme on Danish pottery painters. 1955).. 1993). IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. Dunstan et al. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. Bucher JR.. Morgan WKC. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. 2003. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Sills RC. References Alexander CS. Daniel et al..Metals Toxic effects of cobalt have been encountered in workplace settings. has been associated with exposure to dusts that contain cobalt. 1997). Am J Med 1972. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. Toxicol Sci 1999. 1998).. 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. For workers exposed to cobalt in the air. 1994. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al.S.. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al.atsdr.gov/ exposurereport/.. although substantial occupational exposures have produced elevated urinary levels for many weeks. 2001.. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. Roycroft JR.. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. Arch Environ Health 1988.. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Available at URL: http://www. usually in combination with tungsten carbide (Cugell et al. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. Sci Total Environ 1994. Poulsen OM. Cobalt was once added as a foaming agent to beer. 1998). 1997. Cobalt-beer cardiomyopathy.. environmental levels) and health effects is available from ATSDR at: http://www. Swennen et al. 1992). 2005..43(4):299-303.cdc..cdc.. Iavicoli et al.. Linnainmaa and Kiilunen. 1988). 1988). Grumbein SL. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. with mean levels that were about 15-20 times higher than in the general U. 2005 [online]. 1994. 2005. 1999). Rubin A. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. et al. Thomassen et al. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Shirakawa et al. Haseman JK. 1990). A clinical and pathological study of twenty-eight cases.. 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. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. Cugell DW. 2001. Perkins DG. Krause et al.. Atlanta (GA). The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . Information about external exposure (i.. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Third National Report on Human Exposure to Environmental Chemicals. 210 2006. 2003). 1993). Alexandersson R.. Urinary measurements mainly reflect recent exposure.gov/toxpro2. Lisi.S. Hailey JR..50(13):95-104. 1972). 1994). and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. “Hard metal” disease. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better... Lison et al.49:56-67.53:395417. 2006. 2003. 1989).html. 2001. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. population results in this Report (Kristiansen et al. MacDonald et al... Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Blood and urinary concentrations as estimators of cobalt exposure. Information about the BEI is provided here for comparison.. 1985. 2001). Inhalation toxicity and carcinogenicity studies of cobalt sulfate. 4/3/08 Christensen JM.

Unwin P. Sci Total Environ 1994. Sabbioni E. Long-term clearance of inhaled 60Co. Buchet JP. 1985. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Schank M. Cobalt cardiomyopathy. Chess DG.242:1412-1415. Bozec C. Kriss JP. Zobelein P. Salvatori S. et al. Goto S. Wild P.22:359367.150:177-183. et al. Stanescu D. Am J Epidemiol 1998. Sci Total Environ 1994. Kuska Y. Lauwerys RB. Mosconi G. Thabe H. Arch Intern Med 1990. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Outcome of occupational asthma due to cobalt hypersensitivity. Daniel J. The release of metals from metal-onmetal surface arthroplasty of the hip.87(5):628-631. Peltier A.216:253-270. Shirakawa T. Cresti R. Goto S. Sabbioni E. salt. Science 1988. McCalden RW. Lauwerys R. Biological monitoring of workers exposed to cobalt metal. Vitali MT. et al. Lison D. Kristiansen J. Weyher I. Rorabeck CH. Diepgen TL. Kirsch-Volders M. Meier R. Barnaby CF. Kusaka Y. Lasfargues G. Kato M. Angerer J. Leghissa P. et al. Fujimura N. Schaller KH.150. a study of 13 elements in blood and urine of a United Kingdom population. Dunstan E. HoffmannB. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Boca Raton (FL): Lewis Publishers. Cleland D. Ziaee H. Kraus T. Int Arch Occup Environ Health 1997. Zhuber K. Radulescu M.55(4):269-276. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Carnes WH. Health Phys 1979.51(7):447450. Cobalt and antimony: genotoxicity and carcinogenicity. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Thakker DM.150(1-3):167-171. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group.157:117121. Molders J.88(4):443448. Salama A. Chest 1989. Steffan I. Pradhan C. Respiratory health of cobalt production workers. Christensen JM. Meyer zum Buschenfelde K-H. Uitti J. Dunning SP. DeSantis V. Roto P. Epidemiological survey of workers exposed to cobalt oxides. Occup Environ Med 1994. Health Phys 1972. Lison D. 2001. Alessandrelli M. Zedda S.95:29-37. Palmroos P. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.50(9):835-842. Thomassen H.48:172-173.45:246-247. Moulin JJ. J Trace Elem Med Biol 2006. White MA. Bourne RB. oxides. Am J Ind Med 2003.” Contact Dermatitis 2001. J Orthop Res 2003.21(2):189-195. Goldberg MA. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. et al. Heki S. Swennen B. Schramel P. Absorption and retention of cobalt in man by whole-body counting. Swennen B. Zweymuller K. 3rd ed. et al. Lison D. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Trace element reference values in tissues from inhabitants of the European Union. Iversen BS. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.58(10):631-634. Smith T. De Boeck M. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Sci Total Environ 1998. Sabbioni E. Oksa P. Dickel H.Metals effects of cobalt. and hard metal dust. Pisati G. Jarvis JQ. MacDonald SJ. Blunn G. J Bone Joint Surg Br 2005. Robinson C. Edmonds CJ. Sci Total Environ 1997. Ghat IS. Br J Ind Med 1993.(1-3):133-139. Lhotka C. Mutat Res 2003.204:147-160.34:620-626.44:124-132. Buchet JP. Int Arch Occup Environ Health. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Cannon SR. McMinn DJ. J Bone Joint Surg Br 2006. Sanghrajka AP. Tilley S.406:282-296. X. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Iavicoli I. Falcone G. Bunn HF. Co-sensitivity between cobalt and other transition metals. Linna A. Romazini S. Weber A. Ichikawa Y. Gross RT. Lung cancer risk in hard-metal workers. Occup Environ Med 2001. J Rheumatol 2001. Linnainmaa M.148:241-248. Lisi P. Laippala P. Hammon E. Contact Dermatitis 2003.533:135-152. Bacis M. J Occup Med 1992. A report of two cases from mineral assay laboratories and a review of the literature. Occupationallyinduced “isolated cobalt sensitization. cobalt salts. Hedge AG. and cobalt metals. Hoher T. Kiilunen M. Hoet P. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Clin Orthop Relat Res 2003.20(1):25-31. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors.36:732-734. Szekeres T.69(3):193-200. Lauwerys R.28(5):1121-1128.

40 (2.90 (1.50) 5. In the past.60) 5.70-2. bronze). see Data Analysis section) for Survey years 99-00.70 (2.43 (1. interval) 1.20 (3.30 (4.50) 75th 2.00 (5.50 (2.00 (2. 01-02.60) 1.60 (1.878-1.00-4. blue-gray metal that occurs naturally in soils and rocks.78 (1.10-3.50-4.40 (1.900 (.87 (1.34-1.39-1.00) 2.40 (1.40-3.60 (3.60) 5.40 (4.71-1. malleable.10 (4.50-2.40-2.43 (1.40) 2.09) 1.50) 1.80 (1.20) 3.30) 2.70) 2.70) 4.90-2.43-1.02) 1.50 (2.10-3.20 (2.50-1.10 (2.75 (1. Lead has a variety of uses in manufacturing: storage batteries. respectively.60 (1.30-1.90-6.20) 5.60) 3.60) 3.89) 1.80 (5.14-1.25 (1.60-4.30-5.40) 5.50-1.40 (5.31) 1. leaded glass.60) 4.10) 3.60 (1.60) 2.80 (5.00 (1.80) 1.70) 1.70) 1.60-4.90) 2.10 (2.20) 3.30 (2.10 (1.10-8.20) 4.70) 4.43) 1.45 (1.17) . lead was added to gasoline and residential paints and used in soldering the seams of food cans.00 (4.20 (1.10 (1.40) 2.70-4.10) 1.90 (2.90) 3.70 (2.50-4. Before the 1980’s.75) 1.00) 6.80) 1.30 (3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.50) 4.90) 2. 0.00) 4.20 (3.30 (1.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.40) 2.68-1.70 (1.00) 1.30) 2.87) 1.50 (1. and 0.14-1.80-3.37-1.80-2.10-1.40-1.00-4.50) 2.80 (4.83 (1.50 (3.70-3.80-4.80 (1.30-2.80 (2.60 (1.90 (3.30-4.10 (3.66 (1.30) 95th 5.00) 5.946 (.10-2.40 (1.20-3.90 (3.70 (1.70 (1. brass.30 (2.60 (3.60) 2.60 (2.70-2.80 (3.40 (3.20) 3.90 (3.40-4.900-1.80-5. 7439-92-1 General Information Elemental lead is a soft.46 (1.40-1.60 (1.01 (1.00-1.36) 1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.70-5.50-3.40 (2.22 (1.50) 2.30) 2.40-3.30 (1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.40-1. the main source of lead exposure for the general U.30-1.10) 2.60-1.60) 1.50-1.60 (1.20 (1.55 (1.800-1.20 (3.69) 1.60) 1.77 (1.60) 4.00) 2.30-2.20-4.30-6.55-1.20-2.96-2.40-6.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.10) 3.40) Total 1.70) 3.50) 1.90-2.00 (1.40-3.80) 2.40) 3.70-1. Lead was used in plumbing for centuries and may still be present.30 (2.60) 3.10-3.70-1.66) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 3.90-2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .04-1.30) 5.90 (3.00) .80) 1.30-2.10-2.40-1.20 (3.30 (2.75-2.10-3.40 (1.3.S.00) 1.80) 1. ammunition.10) 5.00-1.00 (6.80-3.30 (4.70 (2.37 (1.30 (1.70) 3.80) 2.30 (4.70) 3.80-3.10-1.30-1.20 (3.50 (3.55-1.80) 3.10 (2.48) 1.10) 1.70) 4.50-1.25) 1.90-4.20 (2.00-5.51) 1.00) 2. dense. Lead is most often mined from ores or recycled from scrap metal or batteries.65 (1.50-5.53) 1.10) 2.52 (1.90-3.19 (1.20-1.986) .90-4.50) 5.10 (1.10-6. and 03-04 are 0.10-4.50 (4.80) 2.40-6.30 (2.50) 7.80) 2.50) 1.20 (3.40) 2.S.80 (2.20) 4.70-6.00) 1.80-4.60) 2.40-1.20) .69 (1.30-1.30-1.80 (4.25 (1.60) 4.60-6.70 (3.45-1.37 (1.70 (5.69) 1.20 (1.50 (1.00-6.70) 1.60) 2.39) 1.50 (2.70 (1.86) 1.40-2. antique-molded or cast ornaments.60-2.30-2.70-2.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.20-1.40) 4.80 (2.50-2. plastics.50 (1.90-4.14-1.62 (1.50) 4.60 (4.90) 1.942 (.70 (3.23 (1.90 (4.3.60) 3.80-3.60 (2.60 (3.51 (1.60) 4.50-5.20) 3.80 (1.80-4.90) 1.80 (1.00) 2.10) 1.10-1.00) 4.70-1.60 (2. ceramic glazes.91) 1.00) 3.00-2.50 (1.90) 2.69 (1.60 (2.62-1.30 (2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50-3.20 (3.60) 2.50) 1.56 (1.90 (2.20) 90th 3.10-2.40) 1.60-1.20) 1. Since lead has been eliminated from gasoline.36-1.20-3.30) 1.75-1.52-1.49-1.60-1.50 (4.10-2.36-1. such as lead phosphate and tetraethyl lead.80 (1.90 (1.30 (1.899-.20 (4.Metals Lead CAS No. population from the National Health and Nutrition Examination Survey.40-5.60-1.90-2.90) 3.90 (3.60 (2.60-3.80 (1.12-1.70) 1.50-2.50-6.60-2.40-1.00-4.g.90) 2.20 (1.70) 4.20 (1.60) 1.95) 1.52-1.50 (2.40) 1.81) 1.00) 1.20-3.90-4.32-1. Elemental lead can be combined with other elements to form inorganic and organic compounds.60) 1. and for radiation shielding.60 (1.20-3. solders.00) 3.10-6.93-2.40) 1.72) Selected percentiles ( 95% confidence interval) 50th 1.900 (.28.90) 5.80) 1. metal alloys (e.00 (3.20-2.60 (3.10) 3.50-1.50-2.40-2.90) 2.00) 1.10-2.50 (2.20-6.10-4.20) 2.70) 1.43) 1.30 (2.62) 1.10) 4.10-2.30-1.90) 1.00 (4.60 (2.32-1.

50 (1. bullet fragments retained in human tissue.80) 2.09) 1.700-.50 (1.30) 1.800 (.810-1.540 (.600-.800-1.97) 4.710-1.820-1.00) 1.815 (.640-.02 (.833 (. However.773) .708-.70 (1.20 (1.27) 1.613) . interval) .62-4.00 (1. battery and radiator manufacturing) and recreational sources.636 (.535-.915-1.640 (.579-.30) 2.S.808 (.540-.70 (2.920 (.40-3. respectively.40 (1.80 (2.44-2.66 (2.595-.630 (.40 (2.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.941) .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 .10 (1.89) 2.558 (.Metals occupational (e.10-1.33-2.680-.40) 1.00-1.59-2. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.900) . dust.766 (.90) 2.600-.710-.29) 2.10-3.60-1.78-2.75) 3.10-3.20 (1.701) .60 (1.553-.04 (.20-2.90-2.560-.526-.04) . 0.20) .556-.931) .637-. population from the National Health and Nutrition Examination Survey.20-1.50) 2.800) .840 (.659 (.12) 90th 2.833-1.20) 1.20 (3.10 (.70) 1.30) 1.02) 1.10-5.570-. CDC.90) 2.40-5.82 (1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.600-.20) .900-1.40) 1.729-.10 (1.600-. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.23-4.41) 2.82 (2.78-2.10) 1.850 (.70 (2.70-2.10) 2.500-.680) .59) 1.33. lead-based painted surfaces undergoing renovation or demolition.600) .20-1.40) 3.04) 2.80) 2.40 (2.20 (1.17 (1.18-1.1.50) 2.40-2. see Data Analysis section) for Survey years 99-00.40-1.900) .700 (.24-1.900-1.21 (2. In the blood. 01-02.80) 1.80 (1.800 (.628) 1.00 (2.90) 2.00 (.52-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.10-1.795 (. or water contaminated by mining or smelting operations.900) .70) 3.671-.40-1.10 (.50) 1.600 (.00 (1.40) 1.688 (.86) 1.00-1.64) 2.10) .20 (2.700 (.674) 1.620 (.80-3.900 (.752 (.862) .40 (2.. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.14 (1..920 (.749) .40 (1.800-1.30 (1.60-3.20) .40 (2.960-1.00) .90-2.650) 1.00) 2.50-2.80) 1.757-. 2000).80-2.86-2.70 (2.700-.80-2.642 (.90-2.50) 1.822-1.30) 1.60 (1.506-. 2007.80) 1.49 (1.30-1.07-1.00-2.30) .625 (.700-.00-2.00 (1.10-3.800) .700 (. 1991).40) 2.70) 2.857) .800-.60 (2.591 (.480-.90 (2.848 (.03-2.30-2.70) 1.900-1.20 (1.677 (.86) 95th 2.40) 2.60-2.00-1.32 (1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .40) 1.60-2.20) 1.10 (1.753 (.07 (.10-1.80) 2.573 (. lead-contaminated dust in indoor firing ranges.600 (.910-.30) 2.52 (1.06) .589-.80) 2.800) .20) 1.78-2.10-1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.90-3.990) 1.30) 1. and contact with soil.30) 2.680-.600-.20 (1.90) 1.11) 2.900-1.818) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00) .800 (.00 (1.900 (.70-3.50) 1.04 (.13-3.700-.50 (2.10) 2.738) .27 (1.800-.604 (.90-3.790 (.731 (.31 (1.620) 1.700) .22) 1.10 (. imported children’s trinkets and toys.691-.20-1.616) .00) . stained glass framing.40) 2.50-2.660) .564 (.20-2.935) 1.30-1.70) 3.66 (2.580-.75) 4.30-3.30) 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 1.90-2.970-1.50) 3.30 (3. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.00) 2. Approximately half of the absorbed lead may be incorporated into bone. or after soluble lead compounds are ingested.70) 1.80) 3.40-1.900 (.800 (.40-1.730 (.10-1. pewter utensils and drinking vessels. lead-containing folk remedies and cosmetics.11 (1.90 (2.800) .990) 2.718) .651) .90 (1.50-2.572-.10 (1.30) 1.30-1.900) .605) .625-.40 (1.14 (1.13) .60 (1.91) 2.900) .40 (1.700 (.745-.690) 75th 1.86 (1.700 (.60-3.30-1.600) .00-2.23) .641-.80) 2.20 (2.20 (1.960 (.20 (2.940 (.700-1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.960-1.955-1.52-1.700-.30-5.785) .90 (1.590 (.90 (2.04-2.33 (2.10) .579-.70 (2.19 (1.30 (2.60 (1.50 (2. and 03-04 are 0.900) .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 1.72) 1.35 (.90 (1.1.661-.800) .695 (.50 (2.00) .40) 2.50-3.40) 1.828) Selected percentiles ( 95% confidence interval) 50th . and 0.03 (1.73 (1. older plumbing systems with leaded pipes or lead soldered connections.986) .62) Total .700 (.923 (.20) .g.610 (.31-3.14-1.40 (1.700) 1.80 (1.90-4.50-1.60) 2.29 (2.80) 3.

05 (1.50-2.01) .641 (.61) 3.918 (.914 (.604-.72-2. through the inhibition of certain enzymes.88) 2.648 (.621 (. and through binding to ion channels and regulatory proteins.586-.36-2.72-2.645-.03 (.10 (1.755 (.92) 2.72) .22) 1.700-.658 (.720 (.79 (1.06) .0) 3. encephalopathy.97 (1.50-2.461) .35) 2.85 (1.529-.61) 1.22-1.98 (1.43 (2. BLLs and associated toxic effects differ in children and adults.04-3.53-1.946-1.720 (.03) .588-.838) .828-1. scant amounts are lost through sweat.03) 2. 2004.603-.47 (2.88 (1.19) 1.70 (1.622 (.870 (.66 (1.796-1.790) .603-.28) .677 (.14) 1.17-1..709 (.31 (1.18) .86 (1. kidney injury.594-.933) .979 (. Lead can cross the placenta and enter the developing fetal brain.682) .00) .11) 1. 1996).652 (.43) 1.05-1.64-2.98-2.41 (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.758) .963-1.97) 1.997-1.37-1.841-1.78-4.605-.400) . The toxic effects of lead result from its interference with the physiologic actions of calcium.645-.41) .43-1.45 (1.33) 2.44) 1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.50-1.10) 1.03) .615 (.06 (1. 2007). Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR. population from the National Health and Nutrition Examination Survey.68 (1.11 (.61) 1.460-.615 (.810 (.561-.918-1.03) 1.33 (1.914 (.40-1.55 (1.679-. Nash et al.404 (.09-1.08) . hair.977) 1.63) 1.33-1.64) 95th 2.66 (1.436) .342-.75-2.625 (. 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.654) .83 (2.725) .05-1. 1995).29 (1.46 (1.781-1.62-3.551-.15) 1.657) 1.34-1.63) 4.774 (.59-3.971 (.746) .10 (.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 .50 (1.739) .659-.67-4.606-. 1993).85-2.683-.07 (.812-1.07) . 1995.639 (.47) 1.696 (.623 (.17 (.38 (2.88-2.01 (.725) .65 (1.992-1.11 (1.20-3.721 (.375 (.603 (.09-1.608-.686) .853-1.765) .47 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.701 (.03 (.88) 1.702) .97) 1.03) 1.33) 1.938 (.98) 2.27 (1.583-.18) 1.56) 3.632 (.85) 1.09) 1.66) 2.Metals 90% of the body lead burden in most adults.383-.41-1.990 (.43 (1. and paralysis.882-1.71 (1.938-1.731-.639) . zinc.670) 1.432 (.15-2.940 (.609 (.89-2.571-.559-.53) 1.594-.688) .639 (.763) .718) .85-2.31 (1.79) 2.08-2.701) .698) .635 (.900 (.37-1.28-1.893) .03 (.50) 1.55 (1.11-1.25-1.587-.708 (.988-1.77) 2.31) 1.52) 1.703) .508) .00 (1.828) .25-1.56-3.492-.730) 1.962 (.702) .03) 90th 1.681-.22-2.975-1.681-.623 (..06 (.742) Selected percentiles ( 95% confidence interval) 50th . For instance.82) 1.677-.08) .15-2.667-.11) .78 (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 1.18) 1.03-2.64 (1.920-1.31) 1. 2003. with a half-life of years to decades.988 (.20) .981-1.617-.712 (.655) .633 (. Schwartz.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 .408-.44 (1.612-.15-3.87) 1.38 (2.718) 1.09-1.722 (.61) 1.51) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.12-1. based on prospective population studies.644 (. interval) .917-1.62-2.74 (1.48 (1.39-1.22) .571-.496 (.601-.03 (1.51 (1. In 1991.44 (1.677) .428) .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 .11 (1.579-.43) 2.15) 1.722 (.62) 2.02) 1.83) 1.06) 1.992-1.79) 1.89-5.94 (1.11 (.64) 2.710) .97-18.655) 75th 1.851) .73-2.639 (. 1993. Staessen et al.05 (.38 (2..469 (.73) 2.702-.898) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger. Approximately 70% of lead excretion occurs via the urine.914-1.00 (.04) 2.742) .404-.75 (2.56-2.00 (1. and iron. Large amounts of lead in the body can cause anemia.56 (1.88) 2.593 (.541-.679) 1. The skeleton acts as a storage depot.638 (.S.18 (1.535) .569 (.887 (.22) 1.644) .26) 2. O’Flaherty.31 (2.876-1.50-2.07-1.588-. abdominal pain.03) 2.698) .667-.707 (.734) . seizures.753) . with lesser amounts eliminated via the feces.19-5.14 (1.668-.933-1.862-.71-2.00 (1.18) 2.667) .23 (1.26) Total .673) .65-2.607-.58) 1.46 (2.793-1.96 (1.693 (.61) 1.52 (1.28) 2. 1991.800-.380-.94-2.592-.671 (.957-1.69 (1.24 (1.655-.62-1.20) .618 (. and nails (Leggett.404 (.676) .649 (.926 (.02-1.510-. CDC.49 (1.608 (.

Fourth National Report on Human Exposure to Environmental Chemicals 215 . 1999). Both drinking water and ambient air standards for lead have been established by the U. and decrease fertility (Alexander et al. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.S. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. For example. Overall.. almost double the geometric mean of 1.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1...6%) were lower than those from NHANES 1991-1994. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 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.cdc. residing in housing built before the 1950’s.4% in NHANES 1999-2004. 2007). which is an 84% decline. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.. and organic lead compounds not classifiable with respect to human carcinogenicity. environmental levels) and health effects is available from ATSDR at: http://www. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC... Jones et al. higher than 100-200 µg/dL). 1996. 2003. Schwartz. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 2006). 1999). Urine levels may reflect recently absorbed lead. 2002a).5 per 100. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 2002.cdc. Borja-Aburto et al. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.2 µg/dL in males and 3. CDC.. 1984.gov/toxpro2.S. BLLs reflect both recent intake and equilibration with stored lead in other tissues. 2001).g. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. However. Payton et al.21% of approximately 3. premature delivery. usually with BLLs greater than 40 mg/dL. Information about external exposure (i.. the prevalence rate has declined annually since 1994 (CDC. and low family income (CDC.. adult residents.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. when the geometric mean BLL was 2. adults in the 19992000 NHANES sample (Apostoli et al. the geometric mean BLL was 3. respectively.. 2000).000 adults. Pirkle et al. and spontaneous abortion (Baghurst et al.S. More recently. reduce sperm count. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. 2005b). may alter sperm morphology. with overt encephalopathy. 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.e. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al.6% in NHANES 1988-1991 to 1.atsdr.. 1991. approximately 11. Lanphear et al. seizures.. lead in women may be associated with hypertension during pregnancy. both the geometric mean (1.3 million children tested had BLLs of 10 mg/dL or higher (http://www.4% of children had BLLs of 10µg/dL or higher (CDC. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. Schwartz et al. 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. 2000). At low environmental exposures.. Korrick 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...html.07 µg/dL (Becker et al.S. urban residence.xls). Telisman et al. The U. IARC considers inorganic lead compounds probable human carcinogens. Surveillance data reported by U..75 µg/dL in U. 1987. 1998). Muntner et al. 1996. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.. Staessen et al. 2003. 1996. 2005a). 1994).. including minority race or ethnicity.. 2002). particularly in the skeleton. 2009). 2005b.0 µg/dL in females (Soldin et al. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. Data submitted through state public health programs from 2006 showed that 1. 2006). In NHANES 1999-2002 in children 1-5 years old.7 µg/dL and 4. 1995.Metals µg/dL or higher as the level of concern in children.. Bellinger 2005. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. In occupationally exposed adults. and peripheral neuropathy generally occurring at much higher levels (e. adults in the 1999-2000 NHANES sample.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. High dose occupational lead exposure... 2003). EPA..S.S. 2003.

Bellinger D. van Netten C. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Neurotoxicol Teratol 2004. Blood lead levels measured prospectively and risk of spontaneous abortion.gov/mmwr/preview/mmwrhtml/ mm5532a2. Available at URL: http://www. Adult blood lead epidemiology and surveillance—United States.htm. Am J Epidemiol 1999.html.115:521-529.cdc. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.348:15171526. Inorganic and Organic Lead Compounds. Sparrow D. 2003-2004. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Chiodo LM. Jusko TA.cdc. Batuman V. 4/14/09 Alexander BH. Weiss ST. Cox C. 2005. 1999-2002. Available at URL: http://www. Muller CH. et al.73:409-420. Lanphear BP. Lead and hypertension in a sample of middle-aged women. Pirkle JL. Ronchi L.cdc.53:411-416. Ewers TG. Hu H. 4/14/09 Centers for Disease Control and Prevention (CDC). Hernberg S. Meyer PA. Robertson EF.275:1177-1181. Age-specific kinetic model of lead metal in humans. Baghurst PA. et al. Luukkonen R.113(4):1016-1022. Muntner P. Environ Res 2000. Teratogen update: lead and pregnancy. Coresh J.287:1-11. Seiwert M. Dietrich K. JAMA 1996. Lanphear BP. MMWR Morb Mortal Wkly Rep 2006.8(3):395-401. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.atsdr. Preventing Lead Poisoning in Young Children. Rotnitzky A. Henderson CR. Atlanta (GA). Cox C. Birth Defects Research (Part A). Pediatrics 2009. Roberts RR. Rotnitzky A. Manton WI. Scand J Work Environ Health 1984. Becker K. Angle CR. 2005b. Blood lead levels—United States. Atlanta (GA). Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Public Health Rep 2000. Environ Health Perspect 1993. 2002 [online]. References Agency for Toxic Substances and Disease Registry (ATSDR). Available from URL: http://www. Ga. Jacobson SW. Hänninen H. Korrick S. Blanco J. Bavazzano P.150(6):590-597. Checkoway H. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Kaufman JD. Sci Total Environ 2002. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Korrick SA. Kim R. Auinger P. Third National Report on Human Exposure to Environmental Chemicals. Managing Elevated Blood Lead Levels Among Young Children. Wager C. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. The relationship of bone and blood lead to hypertension.55(32):876-879. Sparrow D. Cory-Slechta DA. MMWR Morb Mortal Wkly Rep 2005a. Krause C.101(7):598-616. Neurodevelopmental effects of postnatal lead exposure at very low levels. Blood lead reference values: the results of an Italian polycentric study. Lepom P. Lead. Vimpani FB. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Acquisition and retention of lead by young children. Hu H. JAMA 1996.82:60-80. Speizer FE.123:e376-e385. 4/14/09 Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Neri A. Schulz C.htm. Ganzi A. et al.205:297-308. McMichael AJ. Jones RL.89:330-335. Caldwell KL. 1991 [online]. Occup Environ Med 1996. Int J Hyg Environ Health 2002.gov/toxprofiles/tp13. Kaus S.87:1-471. et al. Brody DJ. Vupputyuri S. 1988-2004. Payton M. doi:10. Weiss ST.htm.htm. Wigg NR. et al.cdc.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.gov/nceh/lead/publications/ books/plpyc/contents. Apostoli P. Mantere P. Hertz-Picciotto I.10:43-50. Atlanta. Centers for Disease Control and Prevention (CDC). Available at URL: http://www. Aug 2007 [online].54(20):513-516. Toxicological profile for lead. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Neurotoxicol 1987. Am J Public Health 1999. 4/14/09 Centers for Disease Control and Prevention (CDC). Bellinger D. N Engl J Med 2003. IARC Monogr Eval Carcinog Risks Hum 2006. Baj A. Available at URL: http://www.cdc. Borja-Aburto VH. Leggett RW. Pediatrics 2004. Farias P.1542/peds:2007-3608. Hunter DJ. Canfield RL.275(15):1171-1176. Hu H. Reese YR. CDC. 4/14/09 Centers for Disease Control and Prevention (CDC). Kuehnemann TJ. Stanek KL.gov/nceh/lead/ CaseManagement/caseManage_main. Jacobson JL. Rojas LM. Rios C. Semen quality of men employed at a lead smelter. gov/mmwr/preview/mmwrhtml/mm5420a5. Homa DM. Aro A.26:359-371.

J Hum Hypertens 1995. Schulz D. zinc. Schwartz BS. Gunter EW. blood pressure and cardiovascular disease in men. Blood lead.153(5):453464. Nash D. Soldin SJ. Cvitkovic P. Pirkle JL. blood pressure. Wilhelm M. et al. Hanak B. Sparrow D. Hickman T. 50:31-37. Weiss ST. Clin Chim Acta 2003. Sherwin R. Arch Environ Health 1995.9:303-327. Payton M. Amery A. Gavella M. Pizent A. Kinetics of lead disposition in humans. Jurasovic J. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Kaufmann RB. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine.63:1044-1050. Osterloh JD. and copper in men. Stewar WF. Low-level lead exposure and renal function in the Normative Aging Study.289(12):1523-1531. Lee SS. O’Flaherty EJ. Hwang KY. Roels H. Use of endogenous. Staessen JA. Toxicol Appl Pharmacol 1993. Environ Health Perspect 1998. Lauwerys RR. stable lead isotopes to determine release of lead from the skeleton. Flegal AR. JAMA 2003. Rocic B. Environ Health Perspect 1996. Telisman S. Low-level lead exposure and blood pressure. IV. Am J Epidemiol 1994.Metals results from NHANES III. Int J Hyg Environ Health 2006. Brody DJ. Am J Epidemiol 2001. cadmium. et al.327:109-113. Lee BK.209:301305. Lee GS. Smith DR. Rubin R. Schwenk M. Paschal DC. Kidney Int 2003.104(1):60-66. and tibia lead with neurobehavioral test scores in South Korean lead workers. Environ Health Perspect 2000. Kaufmann R. Blood lead concentrations in children: new ranges. dimercaptosuccinic acidchelatable lead.118:16-29. and hypertension in perimenopausal and postmenopausal women. Schwartz J. Lead. Lustberg M. Revised and new reference values for arsenic.106:745-750. Physiologically based models for bone-seeking elements.S. cadmium. Exposure of the U.108(1):45-53. Soldin OP. Association of blood lead. lead. Magder L.140:821-829. Hu H. population to lead: 1991-1994.

500 (. and organic forms.50) 4.300) .30) 4132 4241 03-04 03-04 03-04 .30 (2. 1994.900) 1.30) 3. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.00) .00) 1. Atmospheric elemental mercury can be deposited on land and water.40) 1. 1999 . 218 Fourth National Report on Human Exposure to Environmental Chemicals .g.80 (1. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.700-.800-1.703-. and is distributed to most tissues. which create an episodic potential for volatization and inhalation of mercury vapor. synthetic organomercury compounds were once used in pharmaceutical applications.. merbromin).800 (.00 (. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.40 (4.50) 1.00-1.700) . elemental mercury is absorbed mainly by inhaling volatilized vapor.419 (.689-.30) 1.80) 1..800-1.500-. and mercury compounds are still used as preservatives (e.90-3. or oxygen. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).372) .672) .800-1.70) 911 856 2081 4525 03-04 03-04 .60 (1.20) 2.800-1.80 (1. Some cosmetic skin creams from countries other than the U.40 (3.90 (4.70-2.40 (3. 1980.70 (3. thermostats and switches). thermometers.00 (2. Poorly absorbed from the gastrointestinal tract.60) 1. 2002).700-.30-2.S.500) .40) 3.60-5.00) 3. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. an organic form of mercury.472-. 1993).900) . 1998.285-.g.60 (2.979 (.g. The ingestion of methyl mercury.00 (2.12) .326 (.927) .20-3.80) 4.80 (1.02) . mercuric chloride).500-.20-4.900 (.700-. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). phenylmercuric acetate) or topical antiseptics (e. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.814 (. 2007). to form inorganic mercury compounds or salts. interval) .30-4.30 (1.50-2.70 (1.714-.600 (.Metals Mercury CAS No. After elemental mercury is absorbed.40-3. Elemental mercury is a shiny.574) . with the highest concentrations occurring in the kidneys (Barregard et al.700 (. IARC.700-.50-3..40-1.60-6.00-5.50) 5.400-.60 (1. have often required public health intervention (Zeitz et al.877 (. solid-waste incineration. predominantly from fish and other seafood.20 (2.. Kingman et al.30) 1.80 (3.60-3.903) Selected percentiles ( 95% confidence interval) 50th . electrical lamps.900) 75th 1. Accidental spills of elemental mercury. In addition.781 (.800 (.600) 1. Hursh et al.50-1.860-1. sulfur.60) 2085 2293 3478 Limit of detection (LOD.90 (1.00) 4. 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.. The kinetics of the different forms of mercury vary considerably. Also.50) 2.20-4.363-.S.400 (. Other major uses include electrical equipment (e.753-1. inorganic.40 (4.797 (.90) 95th 4.490 (.300-. such as chlorine (e.886) . and mining and smelting. thimerosal.500 (.70 (1. Survey years 03-04 Geometric mean (95% conf.40-1. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. which can bioaccumulate in aquatic and terrestrial food chains..00 (.30-6. Apart from methyl mercury. constitutes the main source of dietary mercury exposure in the general population. sphygmomanometers and barometers...900) 1.800-1. Woods et al.80) 3.60-6.60-2.90) 3. may contain inorganic mercury.300 (.60) 1.2.418-. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.484) . population from the National Health and Nutrition Examination Survey.90 (1. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.776 (.700-.563 (.30) 3.40-2.70 (4.10) .919) .800 (.655-.800 (.40-2.900) 1.g.10-3.00 (2.00 (1.00 (.00 (.30-5.00) 1.700) .90) 90th 3. and dental amalgam.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 .400-..30) 5.

00) 4.01) .00) 6.395) .30 (1..871-1.300) .60) 2.400-.10 (.700 (.600) .825-1.269-.600) . 1994.200-.20-11.20 (..700-1.40) 2.. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.60 (1.S.00 (2. 1991. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. Fourth National Report on Human Exposure to Environmental Chemicals 219 .23) .30 (.900-1.50) 1.30) 1. 1998).20-3.00) 1.90) 2.697-.800-1.738-.90 (4.Metals the tissues to mercurous and mercuric inorganic forms.00) 2.297-..800 (.200 (.50-12.. 1992). 2004. 1994).200-.800) 1..10-3.700 (. 1990).940) Race/ethnicity (females.60 (1.60 (2. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations. Geometric mean Survey years (95% conf.820 (.90) 5.29) .70-5.30) 1.70) 4.800-1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.50 (1.70-6.300) .30-2.10 (1.30-4.377 (. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola..200-.80) 1..90 (1.900 (.667 (.14.40) 5.50-2.500 (.200 (..30) 3.300 (. 1993). Excretion occurs by renal and fecal routes.20 (2.. Miettinen et al.10-1.800) 75th .90 (1.00-2.299-.700-. Vimy et al. for both acute and chronic exposures.10) . The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.800) . 2003).200-.20-3. 1993).60 (1..06-1.500 (.20) 1.00) 1.40-2.374) .90) 90th 1..40-1. Vahter et al.10 (3.00) . 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. with most elimination occurring through in the feces (Sherlock et al.20) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.70) 1.00-6. 1996).00 (2. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.900 (.90 (3. 1971).10) 1.70-5.70-3.14 and 0.70-3.70 (1.50) 95th 2.20) .600 (.27) .90) 2.40 (1.824) 1.50) 1.90) 3.00 (2.200-.475) .60) 1.700 (.407) .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 .10 (. 1999-2002.300 (..00-2.500-1.700-. 2005).50 (2.329 (.70 (1.265-..800-1. 1984. thereafter.80 (3.10 (5.369) 1. 1999). 1992 and 1999.. Suzuki et al.200-.268-.50) 2.7) 4. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.30 (1.20-2.300) .10) . population.800 (..700 (..60) 1. After exposure to elemental mercury.90 (4.300 (.726-1.60) 3.500-.300 (. 1995.317 (.50) 3.00) 7.900-1.70) 4. 1998). Sandborgh-Englund et al. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.00 (3.377) .307 (.3) 4. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.80-3.300) . Methyl mercury enters the brain and other tissues (Vahter et al. 1992.919) .73) 1.256-.500-.0) 4.30-6.30-5. National Health and Nutrition Examination Survey... and a useful marker of exposure in epidemiologic studies (Grandjean et al.500-. 1969.700-1.833 (.900 (.800) 1.500-. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al. 1975. a measure of accumulated dose (Cernichiari et al..500-.02 (.10 (1.800) . 2003).35 (1.40 (1.30-4. interval) Selected percentiles (95% confidence interval) 50th .50-3.30-11. Jonsson et al. Smith and Farris.30-3..00-1.80) 579 527 370 436 588 806 Limit of detection (LOD. Methyl mercury is incorporated into growing hair.541-.30-6.10 (1.664-1.80 (1.300) .06 (.700) 2. 1973). 1994) and then undergoes slow dealkylation to inorganic mercury.20-3. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al..40) 1.00 (1.30-6.40-2.30 (1. Smith et al.00-2.00-3.318 (.60 (3. McDowell et al.944 (.343 (.60 (3.70 (1.300) . The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al. Myers et al.800 (. 1996.

ataxia. short-term memory loss..600 (. causing parasthesias..600) . high-dose exposure to elemental mercury vapor may cause severe pneumonitis.500 (<LOD-. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 2004). see Data Analysis section) for Survey year 03-04 is 0. 1963).600 (. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. typically after a latent period of weeks to months.600) . population from the National Health and Nutrition Examination Survey. 1970..800) . and cerebral palsy (NRC.600) .600) . cerebellar ataxia. Smith et al. 2004.S.500 (... Overt poisoning from methyl mercury primarily affects the central nervous system.600-. Factor-Litvak et al. 2000. 2004. 2005. Drexler and Schaller. 1951. fatigue.800) .. insomnia. < LOD means less than the limit of detection. Acute.700 (.600 (. Survey Geometric mean (95% conf. 2004). interval) Selected percentiles ( 95% confidence interval) Sample 95th . dysarthria. Once absorbed. 2003).600) .600) .500) .600 (. 1995. gingivitis. Inorganic mercury exposure usually occurs by ingestion. Sakamoto et al. 1993).700-..600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . DeRouen et al. 2000.500-. Salonen et al. 1996). 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. 1987). Stern 2005. 220 Fourth National Report on Human Exposure to Environmental Chemicals . 1995. Rissanen et al. limb deformities. Oskarsson et al.. the existence of a causal relation is unresolved (Chan and Egeland.700) .500 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (. 2005).600 (.700 (. anorexia.500-. 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. Sakamoto et al...800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD ... and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.. The constellation of findings may include anorexia.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .. 2006.. and sleep disturbance (Bidstrup et al. 1983). depression. 1998. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. 2006. Smith et al.600 (. dysarthria. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.700-.500-. irritability.700) 2007 2240 3406 Limit of detection (LOD. 2000). Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. In recent epidemiologic studies.700 (.600) .500 (. pain in the extremities. overt signs and symptoms of chronic inhalation may include tremor. and neurocognitive and behavioral disturbances.600-. altered physical growth.600-.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 .Metals may be more efficient for inorganic mercury (Grandjean et al. particularly irritability.500-.600) .700-.500-.700 (.. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. Rice..700 (. and pinkish discoloration of the hands and feet (Tunnessen et al.. which may vary for some chemicals by year and by individual sample. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.600-.600) . sensory impairments.500-.500-.42. Bellinger et al.600 (.500-. At levels below those that cause acute lung injury. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.600 (.500-. 2002. maculopapular rash. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. hypertension. hearing impairment. Vupputuri et al. and progressive constriction of the visual fields.

03-4.509) . Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. total blood mercury increased with age.. the median concentration of blood mercury was 0. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. and increased slightly in non-Hispanic white children (Caldwell.26 (1.01 (. EPA at: http://www.330 (.420 (.76-4.08 (1.770-1. During the same survey periods.200 (.31) 1266 1272 03-04 03-04 03-04 .360 (..S.cdc.413-.S.46) 3.610-1.23) .39-3.530-.67-3. Schober et al..20 (1.78 µg/L for adults and 0. population from the National Health and Nutrition Examination Survey.313-.Metals standard for inorganic mercury has been established by U..18) 2.534) .54 (2.440 (.31) 2.358 (. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. Survey years 03-04 Geometric mean (95% conf.290-.14-2.530) .480) 75th 1.330-.42) 95th 3.570) . 2000). Biomonitoring Information In the general population.13-2. A cohort of 1127 U. the total blood mercury concentration is due mostly to the dietary intake of organic forms.16 (.90) 2. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.280-..08 (1.408) . These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC. particularly methyl mercury.495 (. Sanzo et al.406-.360-.530) .55 µg/L.... Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.840-1.00) 1.atsdr. who participated in a 1998 representative population survey (Becker et al.07 (.19 (2. 2001.480 (. 2009).28) 1..960 (.85-2. Over the NHANES 1999-2006 survey periods. Kingman et al.420 (.250) .870-1.89) 3.96 (1. 2003).840) 1.460) .340-.8 years.78-2. EPA.430 (. et al.23) 2..09 (2. In NHANES 19992002.14. military veterans (mean age 52.940 (.430 (. From 1996 through 1998.430) .382-. Mahaffey et al.76-3.60) 619 713 1066 Limit of detection (LOD. 2004.460 (.19 (1.476 (.05) 1. see Data Analysis section) for Survey year 03-04 is 0.60-2.97) 2.410-. Fourth National Report on Human Exposure to Environmental Chemicals 221 .77-2.360-. 2001.. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.304) . In Germany the geometric mean for blood mercury was 0.66) 3. Total blood mercury levels increase with greater fish consumption (Dewailly et al.34-3.447 (. 2006).24) 1.88 (1. environmental levels) and health effects is available from the U.63-2.99-6.700 (.68 (2.52) 2. slightly higher total blood mercury levels were found in U. and the age-related changes differed across the groups (Caldwell et al. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.S. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. 1998).254 (.330-.433 (.65) 1.370) .463) .88) 287 722 1529 03-04 03-04 .96 (1.e.509) .88-3.67-2. range 40 years to 78 years) had an average total blood mercury concentration of 2.330-..492) Selected percentiles ( 95% confidence interval) 50th .00 (.520) . average age 33 years. Grandjean et al.gov/mercury and from ATSDR at: http:// www.549) .400 (.14) 90th 2.350-.442-.epa. 1995.213-. interval) . Information about external exposure (i. 1998). (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.46 µg/L for children.S.29) 1. These distinctions can help interpret mercury blood levels in people.93 (1.33 (2..930-1..60 (1.396-.840-1. 758 children.700-1.870-1.555) . Benes et al.58 µg/L for 4645 adults.12 (.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 . 1997. aged 18 to 69 years.160-.05) 3.441 (.580) .16 (1. Among the three racial/ethnic groups. 2009).416 (.76-3.30) 3.S.9 years). 2002).gov/toxprofiles.24 (2. total blood mercury geometric mean levels in females aged 16-49 years did not change. However.405-. adult women in several ethnic subgroups (Hightower et al. average age 9. 2003).890 (.61) 1.

Urine mercury and the number of dental amalgams were correlated.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 .1 µg/L. In the study of U.376-.301-.307-.S. An expert-panel report recently prepared for the U.32-2.875-1.652) .289) .31 (1. Department of Health and Human Services noted that several studies have observed a modest. Survey years 03-04 Geometric mean (95% conf.333-..225-.347) . Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Urinary mercury levels in recent German (Becker et al.447-.358) .07) 1. 2002).276 (.S.599) .88-2. Levels in U.463 (.522-..485 (.784) 1.09) 1.. 1998).714-1.11) 2.63) 1. 2009).417) . DeRouen et al.588) .472-.87) 2.62 (1.498) 75th .208-.362 (.696 (.25 (.619-.16) 1.365 (.28 (..21) 1. et al. 2006.1 µg/L for each surface with a dental amalgam (Kingman et al..909 (.87 (1.78-4.11-2. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. the urine mercury increased by approximately 0..32 (1.06 (.88 (1.616) .297 (.391-.18-1. et al.30) 1.39) 1. 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.620-.S.964-1. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.667-1.12-3.23-2.476 (. 2003).537) .00) 90th 1.969-1.587 (.00) 286 722 1529 03-04 03-04 . Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.03) 2.196-. 2002) adult population surveys were similar to those in a U.343 (.11) 1.65 (1.00 (.532 (.443 (.280-.77 (2..365 (.56) 1266 1271 03-04 03-04 03-04 .384 (.970 (.480) .S.S. 2005).61) 1. population from the National Health and Nutrition Examination Survey.525 (.40-1.392-.35 (1. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.64-2.06 (.768 (..79 (1.76 (1. mean urinary mercury was 3.Metals 2000).. military veterans with dental amalgams.687) .79) 1.785-1.88-2.385-. 1988.368) .464 (. interval) .455-.800-1.990) . and Italian (Apostoli et al. 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.30) 2. Information about the biological exposure indices is provided here for comparison. reversible increase in urinary N-acetyl-glucosaminidase.46-2..86) 95th 2.309-. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.54 (2. Czech (Benes et al.566) .275) . a biomarker of perturbation in renal tubular function.400-.455-.04-3.535) 1. and on average.01) 2. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.13-2. Langworth et al.51-2.630) .404-.455) .40 (1.400) .255 (.306 (.265-.13 (1.41-2.508 (. not to imply a safety level for general population exposure. women of childbearing age have generally been much lower than these levels (CDC. 1992).67 (1. 2009).447 (.545 (.486) Selected percentiles ( 95% confidence interval) 50th .90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .217 (.67 (1. 2006).246-.391) .44) 1.

636-.91 (2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.99 (2. population.685 (.37) 1.774) .17) 95th 5.665) .410-.831) .14-2.706 (. 16-49 years) 99-00 01-02 . 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.47) 1.56) 3.07-5.615 (.76) 2.13-4.69 (1.38) 4.45-2.50 (1.616-.24-1.99 (3.03 (.05 (3.89 (2.721 (.501-.56) 4.50 (2.742-1.27 (1.46 (1.00) 2.27-1.47) 1.97) 2.650) 1.85) 4.03) 1.710 (.580 (.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .09-1.582-.97 (1.622-. interval) Selected percentiles (95% confidence interval) Survey years 50th .426-.45) 2.16) 5.475-. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U. 16-49 years) 99-00 01-02 .709) 75th 1.809) .25) 2.658 (.540 (.65) 1.06 (. National Health and Nutrition Examination Survey.99-2.27 (2.72) 1.31-1.32-3.48 (2.68) 3.655 (.18 (3.670) 75th 1.65-4.10-2.30 (2.850-1.95 (2. 1999-2002.03 (.37 (1.00 (3.740 (.14 and 0.910) .98 (5.35) .84 (2.631-.624-.892) .41 (1.806) .31 (1.14-1.719 (.69-3.83-3.799) .30 (1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.24) 6.42) 90th 2.21 (1.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .639 (.650 (.520-.07) 1.45-3.68 (3.52) 3.S.54) 595 531 381 442 594 826 Limit of detection (LOD.23-1.Metals Urinary Mercury−Females Aged 16-49 Years Old.522 (.97) 2.15 (2.723 (.14.32) 2.42) 2.560 (.41 (2.553-.79) 3.46) 3.53-3.51) .21 (2.691) .22-3.710) 1.61-6.580-.76-5.569-.699) 1.81 (3.45 (1.620 (.516 (.68-3.44) 3.41 (1.686) .92) 2.557-.70 (2.520-.610-.637) .578-.59-5.22 (.650 (.23-1.99) 1.81-6.00 (2.92) 4.42-3.97) 2.772 (.S.21-3.77) 1.57-4.560-.833) .04-10.91-7.05 (2.04-1.09-1.92) 3.760 (.565 (.43-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.596 (.966) .45) 95th 3.710 (.387-.709) .87-4. population.508-.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.62 (3.664) .450-.824) . National Health and Nutrition Examination Survey.30 (2.870) . 1999-2002.600 (.14) 3.50-4.420-.810) .39-3.3) 5.526-.500-.41-6.657 (.909-1.61) 1.10-4.94) 1.606 (.28 (1.55-3.46-4.07-2.56 (1.45) 2.85-3.656-.930) .13 (2.846) .55) 90th 3.84 (2.832-1. Geometric mean Survey years (95% conf.16-5.579-.744) 1.15-1.03-2.79) 1.62 (1.62 (4.32 (1. Geometric mean (95% conf.790) .30-2.18) 3.724 (.76 (1.632 (. interval) Selected percentiles (95% confidence interval) 50th .51 (3.540-.592 (.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .831) .77) 2.605-.502-.35 (1.

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Amurrio A. Sinks TH. Topping G.2:117-131. Allen PV. Osterloh J. Leroux BG. Mooney TF. Blood mercury levels in US children and women of childbearing age. Patil LS. Langolf GD. Smith AE. Leitao JG. Goldberg J.128(2):25125-25126.98(1):133-142. Toxicol Appl Pharmacol 1996. McMahon KJ. Sandler DP. Smith JC. et al. Most B.110:129-132.4(5):981-988. Pediatrics 1987.124:221-229. Hum Toxicol 1984. et al. Vimy MJ. Newton G. Guo S. Hall LL. Vupputuri S. Azpiri MA. Takahashi Y.48(4):221229. Am J Physiol 1990. Amiano P. 1999-2000. Stern AH.115(10):1527-1531. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment.289(13):1667-1674. Toxicol Appl Pharmacol 1994. Nakazawa M. Environ Health Perspect 2002. Br J Ind Med 1983. Sherlock J. The contribution of dental amalgam to urinary mercury excretion in children. Vahter M. Shen DD. Vorwald AJ. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Tunnessen WW.40:413-419. McDowell M. et al. Martin MD. Lorscheider FL. Stern AH. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Environ Res 2005. Friberg L. Schober SE. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Lind B. Orr MF. Aguinagalde FX. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Hongo T. Smith RG. Environ Health Perspect 2003. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings.Metals Sanzo JM. Woods JS. Bernardo MF. Longnecker MP. Toxicol Appl Pharmacol 1994. Hislop D. 1993-1998. Environ Res 2005. Am Ind Hyg Assoc J 1970. Jones RL. Fisher HL. JAMA 2003.79:786789. Turner MD. Smith JC. Environ Health Perspect 2007. Effects of occupational exposure to elemental mercury on short term memory. Acrodynia: exposure to mercury from fluorescent light bulbs. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Suzuki T.111(12):1465-1470.97(2):195-200. Methyl mercury pharmacokinetics in man: a reevaluation. Imai H. The kinetics of intravenously administered methyl mercury in man. Effects of exposure to mercury in the manufacture of chlorine. Arch Environ Health 1993. Farris FF. Bolger PM. Matsuo N. Smith PJ.37:245-252. The hair-organ relationship in mercury concentration in contemporary Japanese. Mottet NK. Zeitz P. 226 Fourth National Report on Human Exposure to Environmental Chemicals . DeRouen TA. Kaye WE. Burbacher T. Yoshinaga J.258(4 Pt 2):R939-945. Whittle K. Daniels JL. Public Health Nutr 2001. Dorronsoro M.31:687-700. Baser M.

7) 78. WHO.5-52.0) 84.1) 60.7 (51.7-92.6-62. 2001.5-68.2 (63.1 (34.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.4-61. At a daily oral molybdenum dose of 24 µg.7-68.2) 40.6-46.8 (67. 1996).3 (84.5-52.2-91.0) 39.5) 80. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.3) 65.5 (41.8.3) 41.6 (73. 2001). population from the National Health and Nutrition Examination survey.5 (49.1-48.0-100) 63.0) 45. 01-02. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.3 (71.0-62.5-91.0 (76.5-66.0-38.4) 52. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.7) 86.0-101) 82.7-122) 93.7-41.9 (44. 1997).0-77.5-124) 108 (92.3 (47.0) 54.3) 47. interval) 45.1-59.2-59.3 (64.7 (45.9-85.6-82.3-115) 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.6) Selected percentiles ( 95% confidence interval) 50th 50.6-42.6) 71.2-70.3) 83. aldehyde dehydrogenase..4) 76.9 (32.9-55.7) 77.3 (38.1-52.7 (71.2 (49.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.3 (79. Excretion occurs predominantly via the kidneys.2 (56.7) 51.4) 42.7 (44.5-65.0-53.1-88.0) 97.7-51.2-42.1-52.6 (55.4 (48.S.4 (72. see Data Analysis section) for survey years 99-00. and xanthine oxidase (Kisker et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 39.3) 85.2) 53.7) 57.0-85.3) 54. chemical reagents in hospital laboratories.2 (49.Metals Molybdenum or ore deposits.8) 48.4 (79.9 (33. 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.0-56.6) 53.4) 49.4) 45.7 (58.8) 75.3) 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 78.1) 46.8) 40.6 (40.8 (82.7-39.6 (40. respectively.8 (85.9-83.8) 46.5 (43. and in pigments for ceramics.2) 52. Fourth National Report on Human Exposure to Environmental Chemicals 227 .9) 62.6-96.1) 59.8-108) 87.7-50.6-72.7) 45.7) 46. More recently.0 (48. lubricants.1-44. which exert homeostatic regulation over molybdenum balance.4-82.7-105) 69.7-91.1-55.2-53.0-65.3-108) 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. and 1.7 (73.0) 60.5 (37.6) 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 (99.2) 41.5) 44.6) 93.7 (50.6 (55.8-90.5) 85.5) 60. 7439-98-7 General Information Elemental molybdenum is a silver-white.4 (80.1) 126 (106-147) 109 (94.3 (46.1-63.9-109) 97.9 (52.0 (46.0 (42.2 (38.4 (34.2) 48. hydrogenation catalysts.9-56.1-51.1 (91.9) 67.2-59.6-58.5) 80.7 (37.3 (37.0 (81.3-75.0) 62.2-79.7-73.5 (74.5.6-111) 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 (48.5 (81.1 (71.0 (41. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.9 (78.9 (40.2 (61.2 (83.1) 57.2) 37.7) 75th 84.7-47.3-91.8.4) 41.0-71.9) 34. and 03-04 are 0. Compounds of molybdenum are also used as corrosion inhibitors.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. In humans.5-46.3 (73.8-106) 88.2 (40.8-49.3-44. and paints. semiconductor and battery industries have begun to use molybdenum.6 (43.9-82.3 (55.7-60.8-46.9-55.9 (73.0 (42.5 (41.1) 82.5 (48.6) 51.2) 79.3-47.5 (67.6) 71. inks. urinary excretion over six days CAS No.2 (55.7) 78.2-37.5-41.2 (69.1 (38.0) 55.7-96.8 (42.4-52.0 (43.3 (55.6-55.6 (52.4-75.9 (34. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.7-84.5) 47.1) 35.3 (53. 0.9 (37.8) 44.0-110) 90.8-94.7 (36. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.4) 56.

4 (37. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.9-42.8-118) 81. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.1 (82.0) 39.5) 60.2) 42.2) 55.3) 44.8) 38.9-40.7) 62.3) 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 85.0) 88.8 (36.0) 53.6-88. Biomonitoring Information Molybdenum is an essential element for health.0) 72.5 (38. population from the National Health and Nutrition Examination survey.8-47.1 (33.8) 37.4-42.6) 48.5 (36. respectively. and urinary levels reflect intake from all sources.2) 39.3 (36.4 (55.4-66.1 (30.9 (39.1 (38.1-67.2 (73. interval) 43.8-67.7 (30.0-133) 119 (88.5-46.2-40..9-45.1 (49.3 (37. EPA.1 (42.6 (38.4) 122 (107-133) 109 (99.4 (44.7 (77. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3-43.6-61.5 (35.3-102) 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 40.6 (36.4 (67. and clinical or epidemiologic evidence of adverse effects is limited.5 (80.5-50.6 (42.8-52.7-137) 129 (109-155) 112 (97.2 (52.3-56.1-45. 1995).5-48.2 (50.5 (83.7-43.2) 39.4) 60..8) 45.1-79.1) 40.6-63.3) 40.8-66.9) 92.6-78.0 (80.1 (44.1-38.5 (40.2) 58..9-118) 91.4) 44.4-185) 106 (94.9-87.9-68.2) 43.5-44. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure. of the ingested dose (Turnlund et al.2-46.5 (34.9 (73. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-117) 57.5 (50.5 (79.9-45.3-68.9 (64.6 (71.5 (41.S.2-96.0-56.1) 56.3 (36.3) 43.4 (40.6-61.9 mg/kg/day and established a tolerable upper intake level of 0.5 (35.0 (58.5-35.2 (40.0-38.5 (39.4-106) 85.2-80.1) 101 (83.9-71.1-81.7-93.2-65.9-41.1-43.3 (51.4-118) 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 .8) 62. In industry.2-41.1) 43.6 (59.4) 116 (101-126) 104 (88.9 (64.4) 89.0-120) 85.2 (37.8) 38.5-70.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.4) 77.3-141) 109 (81.0-41.4) 47.3 (58. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.6-45.6) 36.2 (40.9-61.8) 39.9) 79.0-103) 103 (90.6-63.6 (57. 1997).8-42.3-115) 98.2 (43.5 (37.5-62.03 mg/kg/day in humans (IOM.7-44. U.3-45.9) 31.6-41.5) 72.4) 58. 1999). and molybdenum has not been systematically evaluated for carcinogenicity by IARC. 1961.8 (56.5-99.7-38.1 (37.2) 42.5 (40.8-84.9) 41.3 (71.1-112) 78. urinary excretion over six days rose to 50% and 67%.5-97.1 (38.2-121) 107 (92. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.8 (75.1) 65.9 (40.6) 39.Metals was 18% of the ingested dose.1-43.1-127) 90.4 (53.0) 38.5 (39.2-96.0) 36.8 (90.5 (59.1 (39.7) 115 (93.0-46.5-92.7) 57.2-49.1) 37.0) 44.5) 63.0) 33.7) 112 (95.5 (65.6) 43.3 (37.7) 41.2 (69.1-39.0 (74.4) 40.1 (40.3) 56.2 (33.3) 64.5 (37.8) 71. 2001).5) 71.1-40.4-41.S.0) 62.7) 45.7) 75th 63. Based on studies finding adverse reproductive effects in rats and mice. Molybdenum is generally considered to be of low human toxicity.2 (40.4-76.3-59.1-39.5) 73.8) 79.0-46.9) 40.2) 37.3 (71.7-100) 77.5-45.8-47.1-109) 89.8 (57. at daily oral doses of 95 µg and 428 µg.2) 37.3-44.5 (41.5 (78.3) 61.4) 48.8-65.3 (83.2 (57.9-96.1-41.4-120) 101 (84.9 (36.1-100) 86.4) 61.4-39.7) 42.3-46.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.9 (35.3 (55.8) 61.3-52.1) 37.4 (59.1 (54.9) 44.2-47.3) 37. 1993).0) 39. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3) 57.7-40.7-120) 87.3) 41.5-69.7) 53.5) 90th 108 (97.3 (53.5-60.9 (49.5 (54.6-76.8 (37.6 (36.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.7-62.4 (56.5-119) 90.7-52.0 (35.1-34.6) Selected percentiles ( 95% confidence interval) 50th 41.2) 38.8-46.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.7 (66.2 (36. but available epidemiologic data are scant.4-107) 85.7 (75.4 (78.5 (65.9 (79.9 (39.6) 39.

Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Shmavonyan DM. 144-154.Metals in urine for the U. Am J Clin Nutr 1995.. Kisker C. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Molybdenum absorption. Analyst 1998. edu/openbook. 4/14/09 White MA. Molybdenum in infancy: methodical investigation of urinary excretion.epa. White MA.gov/iris/ subst/0425. Peiffer GL. 2001. Available at URL: http://books. Schleyerbach U. Sciarra G. Available at URL: http://ntp. Food and Nutrition Board. iron. 1998. chromium. Trace element reference values in tissues from inhabitants of the European Union.S. Minoia C. Turnlund JR. 4/14/09 Iversen BS. Sci Total Environ 1998. Vermeire PA. EPA). A study of 13 elements in blood and urine of a United Kingdom population. Aprea C. and zinc: a report of the Panel on Micronutrients. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Occup Environ Med 1999. Third National Report on Human Exposure to Environmental Chemicals. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. vanadium.htm. U. Institute of Medicine (IOM). 1996. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 420-441. 2005. Ronchi A. et al. Turci R.nap. 1998). Schaub J. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Molybdenum. Zhurnal Obshchey Biologii 1961. iodine. Occupational risk factors of lung cancer: a hospital based case-control study.62(4):790-796. nickel. excretion. Sabbioni E. 4/14/09 Sievers E. J Trace Elem Med Biol 2001. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect.nih. Schindelin H. arsenic. Christensen JM. Van Meerbeeck JP. References Centers for Disease Control and Prevention (CDC). Geneva: WHO. Available at URL: http://www. Sabbioni E. 2002. Keyes WR. Rapid Comm Mass Spectrom 2002. Gatti A. van Sprundel MP. (DC): National Academy Press. In: Trace elements in human nutrition and health. Molybdenum 1993 [online]. manganese. 56:322-327.S. pp.php?record_id=10026&page=420. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes.15(2-3):149-154.66:233-267. Atlanta (GA). Rees DC. Menne C. Droste JHJ. Minoia et al. molybdenum. Dietary reference intakes for vitamin A. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. pp. boron.216:253-270. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Washington. Ann Rev Biochem 1997. White and Sabbioni. 16:1313-1319. Kristiansen J.22(3):179-191. Yarovaya GA. TR-462. Koval’skiy GA. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. World Health Organization (WHO). silicon.. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. 2005).S.123(1):81-85. Environmental Protection Agency (U. 2001). X.gov/index. vitamin K. copper. 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. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Weyler JJ.. National Toxicology Program (NTP).niehs.

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

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

.. Schierl R.61(7):636-9. Blanks R. Patty’s Toxicology. Urinary excretion of platinum from platinum-industry workers. Occup Environ Med 1998. Environ Health Perspect 1975b. 2004. Turfeld M. Thornton I. 2003. 1998). et al. 2004). 5th ed. Angerer J. Petrucci F. Crocker W. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Part 1: monitoring of urinary concentrations. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Kavanagh P. References Becker K. Nowak D. 3/31/08 Moore W Jr... Herr CE. Kuster W. Seiwert M. International Programme on Chemical Safety (IPCS). Herr et al. 206:15-24. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.org/documents/ehc/ehc/ ehc125.. Urinary platinum levels associated with dental gold alloys. New York: John Wiley & Sons. Neuendorf J.org/documents/ehc/ehc/ehc125. Analyst 1998.207(1):69-73. Herr et al. Schierl et al. Cohrssen B.005 µg/L (Iavicoli et al. Biomarkers 1999. and in blood and urine in the United Kingdom. palladium. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. In: Bingham E. Influences on human internal exposure to environmental platinum. Czerczak S. Hauff K.01 µg/L (Becker et al.76(1):5-10. Schulz C. Fruhmann G. 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.. 2003).19:685-691. Wilhelm M. et al.9:152-158. Pethran A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hysell D. Kulka U. 289-380. Huber R. Schierl R.htm. 2003. et al. Ewers U. Fries HG. Hysell D. which elevate urinary platinum by five to twelve-fold (Begerow et al. rhodium. Int J Hyg Environ Health 2004.123(3):451-454. Environmental Health Criteria 125.inchem. Jankofsky M.. Allergy and histamine release due to some platinum salts. Saindelle A. Nickel.13(1):24-30. Several studies have shown that background concentrations in general populations were usually less than 0. J Expo Anal Environ Epidemiol 2003. Br J Pharmacol 1969.Metals the International Programme on Chemical Safety at http:// www. Moore W Jr.35:313-321.04 µg/L) in this Report. Platinum concentrations in urban road dust and soil. ruthenium. Arch Environ Health 2001. 2001). Campbell K. Begerow J. Platinum. Iavicoli I. Ruff F: Histamine release by sodium cholorplatinate. Wilhelm et al. 1997. Levels of platinum in urine for the U.. Ruff F: Platinum and platinosis. Biomonitoring of traffic police officers exposed to airborne platinum. Raab W. Grimm CH. Kelly J. Int Arch Occup Environ Health 1997.56(3):283-286. Uptake of antineoplastic agents in pharmacy and hospital personnel. Farago ME. Arch Environ Health:1969. Kazantzis G. 1998). Saindelle A. Schulz C. 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. Carelli G. Alimonti A. Int Arch Occup Environ Health 2003. 1999. 2000.inchem.. Bocca B. Environ Res 1975a. Rommelt H. Gromiec JP.55(2):138-140. International Journal of Hygiene and Environmental Health 2003.. Ensslin AS.10:63-71. 1991 [online]. Hebert R. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. van de Weyer C.S. Schierl R. eds. Parrot JL.htm. Occup Environ Med 2004. Duneman L:Long-term urinary platinum. Schierl. Biomonitoring Information Urinary platinum levels reflect recent exposure. Boos KS. Seifert B. Stilianakis NI. Pethran et al. Hall L. Senofonte O. pp. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Gieler U. Pethran A. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine.. palladium. 2003. et al. Schierl R. Available at URL: http://www. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Kaus S. and platinum. and gold excretion of patients after insertion of noble-metal dental alloys. Powell CH. 2004) or less than 0.70(3):205-208. population were below the limit of detection (0. osmium.4(1):27-36.

400-.410-.260-.147-.380 (.290-.200 (.160 (.590) .172 (.202 (.156-.300 (.360-.450 (.460-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.410-.160-.350-.240) .480) .170-.230 (.270 (.390-.440) .450 (.196) . and 03-04 are 0.420) .360-.183) .420 (.400-.350-.370 (.170-.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 .177) .300) . Human health effects from thallium at low environmental CAS No.380-.145 (.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 .410-.159 (.170-.197-.360 (.510) .250-.490) .180) 75th .156) .300 (.330-.450) .165 (.200-.290) .200) .370) .390-.183) .370 (.220 (.340) .180-.430 (.390) .240) .280 (.146 (.470) .172) .350 (.140-.410 (.350 (.350-.210-.280) .290 (.167-.300-.200 (. From these and other sources.490) .410-.185 (.220-.150-.340) .250-.340 (. population from the National Health and Nutrition Examination Survey.420) .450 (.370 (.370-.206) .520 (.330) .420-.172 (.370-.370) .340-.450 (.410) .243) .217) .200) .137-.260-.180) .150-.400 (.290-.220) .197 (.156) .500) .250-.220) .230) .250-.440) .270) .Metals Thallium depilatory cosmetics.220) .200 (.270-.250-.500 (.370-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.440 (.290 (.310) .390) .370 (.181-.160-.300) .400 (.320) .330-.270) .260 (.420) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.440 (.310 (.410-.330) .350) .149 (.190-.154-.173-.158) .144 (.400-.190 (.440 (.550 (.310-. In the past.330-.163) . 0.430 (.430) .380-.260) .450 (.370 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.500) .218) .290) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.220) .160 (.190 (.260-.480) .185-.200 (.200) .220 (.180 (.450 (.320) .170) .210 (.200-.157-.360) .330) .280 (.170) .218) .430-.480) .153-. 2005).350-.470) .430 (.330-.230) .220 (.170) .380 (. representing distribution into other tissues.460 (.220) .390 (.420-.470) .320 (.400) .145-.180 (.500) .400 (.400 (.450 (.170-.300 (.220) .160 (.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 .250-. Thallium disappears from the blood with a half-life of several days.179-.160-.167 (.200-.380) .360-.170-.320-.134-.360-.180 (.239) .184 (.420) . however.280 (.340-.430-.400) . and 0.225) .370 (.260 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.S. respectively.400) .360 (.191 (.360 (.300) .178) .690) .310 (.217 (. 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.192) Selected percentiles ( 95% confidence interval) 50th .230) .220 (.170 (. see Data Analysis section) for Survey years 99-00.630) .480) .490 (.330-.360 (.260 (.470 (.410 (.520) .170 (. it has not been specifically mined or refined in the United States since 1984.420-. thallium readily crosses the placenta and also distributes into breast milk.147-. In the United States.200) ..170-.560) .520) .190 (.210) .350) .200-.02.250 (.145-.200) .290) .290) .400-.270 (.410 (.410-.02.510 (.290 (.202) .215) .160-.170-.160 (.190 (.187-.220 (.390-.170 (.135-.250 (.280) .430-.640) . thallium was obtained as a by-product of smelting other metals.270-.270 (.330-.420) .173) .240-.150-.270 (.200) .280-.150-.490) Total .150-.202 (.260-.02.150-.420-.440 (.400 (.330) .210 (.410 (.420) .201 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.180-.200 (.133-.147-.250-.350-.175) . the latter being the current major industrial consumer of thallium in this country.400) 95th .250-. 01-02.410 (.160 (. In addition.196) .440) .182-.390 (.400-.270 (.490) .450 (.230-.340-.390) .190 (.155 (.200 (.330-.390-.188) .180-.460) .160-.176 (.240) .350-.340-.167-.300) .320) .360-.390) .159 (.420) .520) . interval) .230-.250) .480) .159 (.148-.173) .280) .290) 90th .260-.290 (.290 (.280-.370 (.400) .230-.590) .240-.440-.450 (.370-.290 (.171 (.430) .470 (.430 (.162-.310 (.240-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .190 (.270-.180-.410 (.230) .201 (.

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

Ewers U.. Apostoli P. 1998.47(3):223-231. (1981) studied 1. et al. Investigations of thallium-exposed workers in cement factories. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect.35(1):4-9. Raithel HJ. 1992 [online]. X.113(1):47-53. Sampson EJ. A study of 46 elements in urine. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Sci Total Environ 1990. 7/15/09 Blanchardon E.265 people living near a thallium-emitting cement plant in Germany. Investigation of a working population exposed to thallium. 2005.216:253-270. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Environ Res 1998. 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. blood. Sabbioni E. Int Arch Occup Environ Health 1981.. Int Arch Occup Environ Health 1980. Manke G. Boisson P. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. and serum of Italian subjects. Trace element reference values in tissues from inhabitants of the European Union. Trace element reference values in tissues from inhabitants of the European community I. Schaller et al. Pirkle JL. Ting BG. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Soddemann H. Wiegand H. Kramer U. 2005) and are shown with results from NHANES 2003-2004 in this Report. Fourth National Report on Human Exposure to Environmental Chemicals 235 . et al. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Available at URL: http://www. Centers for Disease Control and Prevention. Celier D. Minoia et al. Brockhaus et al. Sabbioni E. Schaller KH. Trace metals in urine of United States residents: reference range concentrations. Pozzoli L.48(4):375-389. 1981. 1990. Paschal DC.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Soc Occup Med 1985. Paschal et al. Valentin H. Marcus RL. Third National Report on Human Exposure to Environmental Chemicals. Buhlmeyer G. Minoia C. population) are thought to correspond to workplace exposures at the threshold limit value of 0.Metals (CDC. Sci Total Environ 1998. Toxicological profile for thallium.html. with concentrations ranging up to 76. Dolger R.. White MA. Pietra R.1 mg/m3 (Marcus. Gallorini M. 1980. 1985).gov/toxprofiles/tp54. White and Sabbioni.76(1):53-59. et al. Cassot G. Schmidt M.S. Atlanta (GA).5 μg/L. Challeton-de Vathaire C.95:89-105. A study of 13 elements in blood and urine of a United Kingdom population. References Agency for Toxic Substances and Disease Registry (ATSDR). Brockhaus A. Martin J-C. 1998).cdc. Radiat Prot Dosim. Morrow JC. Jackson RJ. 2005.atsdr. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. 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.

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 .340) .082 (.380) .073) .074-.360 (.109) .110 (.080 (.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 .490) .100) . filaments for incandescent lamps.130) .400 (.160 (.250) .330-.093-.530 (.120) .058-.070 (.130 (.180-.510 (.290 (.120) .090-.500) .350) .560 (.320) .090-.090) .132) .087) .077-.120-.070) .100) .076 (.110-.380-.210-.260) .097-.400 (.570 (.370-.400 (.100) .133) .620) .160) .090-.180) .470-.210) .230-.310-.105 (.260 (.140) 90th .082-.370 (.570 (.060 (.180) .260-.53) .770 (.220) .210 (.240 (.204) .230-.270 (.650) .120-.140 (.400) .160-. see Data Analysis section) for Survey years 99-00.069-.090 (.160-.200) .180-.093) . Occupational exposure is from dusts released during grinding or drilling of hard metals.340-.370 (.230-.088) .113 (.084-.113 (.130-.810) .170) .330-.430 (.095-.062 (. respectively.116) .250) .120) .350-1.101-.430-.120-.080 (.070-. which are used in rock drills and metal-cutting tools.310-.380-.070 (.100) Selected percentiles ( 95% confidence interval) 50th .180) .300 (.340-.056-.580) .065 (.350) .470) .430-.090-.290-.830) .140 (.080 (.160 (.080-.130) .350) .450-.800) .070) .250) .180) .220-.080 (.100-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).071-.520) .330 (.071 (.380-.092) .160-. interval) .530 (.084) .130-.084 (.060-.093 (.320 (.110 (. and for producing ferrotungsten.340-.113 (.950) .090) .060-.520) .530 (. and 03-04 are 0.150 (. population from the National Health and Nutrition Examination Survey.120-.190) .240-.280-.120) .137 (. 0.095-.00) .510-1. mainly as scheelite (CaWO4).090-.080 (.420-.400 (.065-.073-.170 (.060-.230) .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 .090) .190-.380-.060 (.630) .270 (.060 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.190-.510-.160 (.370 (.158 (.080) .068) .790) .130-.550) .056-.210 (.151) .480) Total .270-.110) .120) .220) .Metals Tungsten CAS No.105) .130) .250) .280 (. and as catalysts in the petroleum industry.080-.370-.120-.270 (.100 (.160 (.070) .190 (.120 (.100 (.082 (. Evidence is lacking for the carcinogenicity of tungsten.088 (.290) . which is used in the steel industry.140 (.410 (.460 (.070-.120) .150 (.101 (.090 (.04.520) .430 (.620) .140 (.080) .064-.270-.320-.400-.300) .550 (.560) .050-.100) .090 (.110) .092 (.670) .126) .230-.060-.150-.180-.060-.260 (.100) .190-.440) .060 (.210 (.550) .220) .090-.330) .250-.060 (.250) . 01-02.150 (.370) .270-.170) .073 (.090-.04.190 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .320 (.080) .210 (.230 (.096 (.104) .070-.180 (.090-.107 (.110 (.460) .130) .096-.140-.410-.390) .390 (.290-.330) .140-.070 (.210 (.490 (.460) .060-.081 (.640 (.110-.04.100-.180 (.470) .170 (.100 (.220 (. Little information is available on the toxicity of tungsten.130) .135) .086 (.350 (.360-.470 (.170-.050-.310-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.360-.230) .190-.270-.062 (.150) .300-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.078-.430 (.560) .430) .260-.800) .130-.360) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.160 (.092 (. Tungsten is used mainly for producing hard metals.050-.200-.500 (.122) .310 (.420-.450 (.300) 95th .620 (.066-.170) . and 0.360 (.300 (.200 (.100-. bronzes in pigments.460 (.070-.069) .082) .310-.250-.S. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.290-.180-.160-.080) 75th .113 (.073-.130 (. Tungsten compounds are used as lubricating agents.250) .500 (.111-.260-. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.560) .300 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.080-.310) .110-.123-.460 (.070-.550) .380 (.280 (.160) .170) .590) .380 (.360 (.690) .310-.060 (.100 (.110 (.087-.560) .090) .320-.091) .050-.076 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.070) .290) .470 (.120-.110 (.

130 (.088) .823) .339 (.133) .344-.317 (.100) .083 (.060-.109 (.359 (.067 (.068 (.301) . Using neutron activation analysis to 2000.059 (.094) .079 (.131-.136-.302-.061-.085-.105 (.198) .085 (.082) .197-.452-.079 (.075) .080 (.174) .341 (.148) .075) .203-.096) .073 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.090-.084) . population (CDC.198-. similar to those in this Report (Schramel et al.091) .217-.253 (.465) .061-.071 (.148 (.176-.074-.116-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.201 (.098 (.245-.211 (.078-.199 (.125 (.090-.201) .063-.071 (.283) .333-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.S.122-.098-.146) .063-.233-.080 (.265 (. 1998).098-.136-..255 (.093-.133) .071-.065-.122 (.077) .279 (.121 (. interval) .317-.426) .094-.167) .089) .074) 75th .070 (.120) .381) .222-.169 (..216 (.144 (.205-.083 (.111 (.067-.333) . 2003.436-1. population from the National Health and Nutrition Examination Survey.107-.383 (.184 (.354) . 2005).500) .S.326) . or exposure that a control group of non-metal workers had mean levels differences.136 (.267) .066 (.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 .060-.453) .208-.286-.062 (.484) .426) .279 (.093) .270 (.360 (.299 (.079) .065) .117 (.086) .253) 95th .231 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.105 (.119-.064-.057-.124 (.084 (.070 (.267-.333) .053-.083) .300) .077) .190) .069 (.080-.294 (.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 .482 (. population.100 (.063-.153-. 2001).739) .215) .081) .153) .216 (.126-.154) .333 (.079) .054-.167-.216-.079) .081 (.278-. Nicolaou et al.095-.215 (.364 (.188-.078) .073 (.116 (.065-.167) .083) .284) .087) .315-.439) Total .439 (.138 (.109-.258-.072-.146 (.067 (.081 (.089 (. and 2003-2004 (Paschal et al.116) .082) .250-.143-.054-.099-.412 (.331-.386) .554) .459) .179-.150-.462) .077-.084 (.231-.066 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.100) .555 (.329 (.333 (.075-.237) .119 (.083-.060 (.347 (.098) .333-.059-.117) .250 (.308) .880) .080-.165) .122-.293 (.098-.155-.095) Selected percentiles ( 95% confidence interval) 50th .214-.068-.465) .S.069-.431) .086) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.081-.414) .108-.074-.130-.065 (.154) .092) ..28) .057-.091 (.359 (.065 (.237-.077-.329-.214) .797) .200-.136-.353 (.158) .169) .075 (.197) .158) .063 (.308) .186 (.088) .151 (.079) .300-.174 (.255 (.087 (.072-.091) .158) .139) .258 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.375) .074) .354-.065-.104-. measure urinary tungsten.237) .121-.075-.353 (.339 (.255-. (1987) found possibly due to methodologic.061-.059-.158 (. Patients with medically-inserted tungsten found at increased levels in drinking water.049-.333 (.333 (.058-.150 (.(Kraus et al.392) .209-.145 (.091) .071) .300 (.084) .056-.410-.431) .144-.069 (.300-.106 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.133) 90th .071 (.075 (.436) .206-.176-.484 (.078 (.059-.138 (.064-.071) .634 (.108) .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 .250 (.197) .167-.275 (.078) .071) .222) .094) .340 (.063-.120) .667 (.301) .287) .152-.253-.218 (.072 (.379 (.073 (.224) .216-.385 (. 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.091) .181 (.125) .285) .086) .279 (.216-.055-.157) .272-.727) .667) .439 (.168 (.164 (.199 (.170-.150-.085) .217-.078 (.538) .187) .056-.605) .161) .180-.358) .301) .136-.582) .240-.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 . 1997).431) .497 (.146 (. 2001-2002.179-.139-.074 (.302-.139 (.317) .073 (.091 (.200-.197 (.063 (.143 (.138) .103-.124-.086-.306) .261-.082 (.

Pirkle JL. Kraus T. Available at URL: http://www. Angerer J. Paschal DC. Nevada Exposure Asssessment. Catheter Cardiovasc Interv 2004.htm. lead. Schaller KH. and hair (Bachthaler et al. National Center for Environmental Health. The determination of metals (antimony.58(10):631-634.69(3):219-223.gov/nceh/clusters/Fallon/study. platinum. Paetzel C. References Bachthaler M. Angerer J. bismuth. 4/15/09 Centers for Disease Control and Prevention. Mosconi G. J Trace Elem Electrolytes Health Dis 1987. Churchill County (Fallon). cadmium. Manke C. 2005. Zobelein P. Trace metals in urine of United States residents: reference range concentrations. urine. Nicolaou G. Cancer Clusters. Jackson RJ. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Sampson EJ. mercury. Third National Report on Human Exposure to Environmental Chemicals. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Schramel P.62:380-384. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Atlanta (GA). Seghizzi P. Morrow JC. Int Arch Occup Environ Health 1997.Metals blood. Sabioni E. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis.. Link J. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. [online] 2003. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.(2):73-77. Schramel P. Ting BG. palladium.cdc. Pietra R. Weber A. Centers for Disease Control and Prevention. Feuerbach S. et al. Occup Environ Med 2001. Lenhart M. 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.76(1):53-59. thallium. tellurium. Environ Res 1998. Wendler I. Cassina G.

036) .017) .008) .016 (.053 (.020-.030-. and 03-04 are 0.008 (.006-.009) .010) .013 (.008-.017) .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 .005-.006-.010-.034) .008 (.065) .006-.016) .037-.009) .046-.007 (.027) .016) .016-.021) .011) .069) . 235U (about 0.007) .040) .031 (.007-.040-. and as an aid in electron microscopy and photography.035-.007-.027) .013 (.010) * .009-.011) .030 (.009) .049) .010-.037) .017) .006 (.015 (. in some ceramics.009-.037) Total .008 (.008 (.007-.009 (.056) .008 (.020-.026) 95th .009 (.036-.027-.019-.010-.009) .017-.028-.011 (.049) .011-.011-.023) .010) .037 (.013-.006 (.021-.023-.008) .047 (.015) .046 (.054) .007) .014 (.027) .72%).028 (.007-.016) .007-.010 (.005-.008 (.021 (.023-.065) .019 (.038 (.036) .073) .012 (.031 (.024-.013 (. interval) .006-.010-.031 (.012 (.016-.043) .009 (.007-.013-. including nuclear weapons.008-.033-.040 (.008) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.006-.012) .011) .022) .022-.055 (.007-. Thus.018-.009) .009) .018 (.008) .022-.015-.013) 90th .013 (.017-.012-.027 (.007-.031-.011-.006-.021) .040-.026 (.017 (.029 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.158) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%). nuclear fuel.021 (.010) * .012 (.009 (.008-.008) .018) .012-.013) . 01-02.016) .042) .010-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.026 (.009) .007-.009-.012) .007 (.010-.021 (.008 (.008 (. 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.008-.017-.008-.014 (.007 (. 0.006-.027 (.013 (.041 (.016-.028 (.033) .056) .007) .007 (.020-.009) .008-.027-.017 (.011) .046 (.030) .027 (.025-.054-.007 (.060 (.015 (.012-.279) .007-.008-.006-.051) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 .009-.013 (.010) .012) .008 (.007-. milling.006-.007-.013 (.007-.036-.043 (.022 (.039-.011-.023 (.015 (.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .063) .009 (.005-. and 0.018) .017) .006-.052 (. and 234U.011) .009-.038) .033 (.035) .023) .009) .029-.046 (.006-. respectively.010) .040) .039) .042 (.050) .020-.014 (.Metals Uranium CAS No.021-.023-.010 (.026) .029-.036 (.067) .039) .009 (.019-.006 (.053) .011 (.020) .062) .040 (.020-.011) .009-.008 (.030 (.006-.006 (.005-.064 (. 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.054) .066) .024-.009) .004.024 (.012-.007) .017-.020 (.027) .010 (.009 (. or processing.007 (.009) .045) .006-.012-.005-.004.127) .016) .009) * .009 (.009) .005.020) .019-.026-.009 (.015) .013-.015 (.044 (.067) .011-.034-.017-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .012-.008 (.011-.007 (.014 (.008 (.034-.048) .018) .046) .009) Selected percentiles ( 95% confidence interval) 50th .011-.026-.023) .033 (. Variable concentrations of uranium occur naturally in drinking water sources.009 (.072) . In workplaces that involve uranium mining.023 (.012 (.017-.010) .007-. Since the 1990’s.028 (.009-.030 (.S.008 (. human exposure occurs primarily by inhaling dust and other small particles.018 (.023 (.021) .012 (.008 (.007) .023-.008-.027 (.019-.032 (.007 (.012 (.088) .041 (.007 (.011) .007-.014 (.007 (.010 (.010) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.010) .014 (.009-. see Data Analysis section) for Survey years 99-00.008 (.026 (.024-.031 (.018) .007 (.022-.012) .035) .007) 75th . population from the National Health and Nutrition Examination Survey.010 (.114 (.031 (.017) .008 (. Uranium has many commercial uses.036 (.009-.027-.037) .007-.009) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.048 (.050) .045) .007-.009-.010) .037) .007-.008 (.016) .028-.046 (.026) .

027 (.S.006 (.012 (. which can occur occasionally from high occupational exposure.015 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.005-.018-.007 (.010-.010) . the shrapnel acts as a source of chronic.058) .016) .011) .007-.005-.034) .006-.021 (.004-.007 (.045 (.039) .053) .013 (. which represents distribution and excretion.020 (.008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .007 (.010-.010-.026 (.033 (.013 (. where limited absorption occurs (less than 5%).033 (.006) .025-.009) * .014) .009-. low level exposure.014) .017-.008 (.007 (.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 .074) .025-.009 (.018) .051) .020-.006-.016 (.008) .013 (.008) .010) .015 (.006-.020-.007-.020-.100 (.033) .050) .007) .010 (.026 (. with much slower elimination from bone. the initial half-life of uranium is about 15 days (Bhattacharyya et al.035 (.019-.026-.009 (.010) .017) .024 (. 1992).037 (.022-.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.033 (.058) .016-.024-. liver.011 (.027) .034 (.027-.011-.024) .005-. After exposure to soluble uranium salts.008) .020-.040 (.012) .010) .008 (.024-.009) .015) .270) .011) * .031 (.010) * .059 (.014 (.025-.039) Total .006-.015 (.025-.024) .013-.077) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .006-.007-.044) .007-.016-.024) .011-.051 (.022 (.013 (.016) .028-.010 (.014) 90th .022 (.008) .034-.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 .027 (.030 (.008 (. In cases of retained DU shrapnel.010-.027 (.009-.009) .012) .028) .011-.005-.015-.042) .030 (.006-.053) .009-.035 (.146) .1%-6% of an ingested dose may be absorbed.012) .025) 95th .016) .018-.007 (.013 (.019 (.009) .007) .008 (.023-.007 (.034 (.007 (.009) .006 (.009) .014-.007 (.005-.005 (.009) . interval) .028 (.017-.013 (. Uranium is eliminated in feces and urine.041) .016) .018-.008) .027-.027-.027) .008 (.028) .013 (.034 (.009) .006-.022) .015) .011) .009 (.030) .007-. kidneys.010-.067) .005 (.017) .008-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006-.018 (.012-.019-.007-.008) .009-.028 (.013) .016) .008 (.007 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.021 (.005-.011-.008) .024 (.030-.008) .012-.021 (.010 (.006-.008-.024) .015-.022 (.029 (.012 (.008 (.006-.033 (.020) .006-.012 (.007 (. 2003).050) .011-.017-.028) .011-.024) .007 (. After inhalation.007 (.008-.016) .013) .006-.007 (.007-.005 (.019) .061) .048) .051) .017 (.008) .019 (.043 (.015) .011 (.020 (.080) .007-.006) .024 (.006-.010-.006-.016) .020 (.050 (.006) .019 (.009 (.006-.029) .030-.039) .006-.007 (. After long term or repeated exposure.008) 75th .011-.014-.016-.009) .030 (.042-.006 (.007 (.029) .009 (.019) .039) .031-.017) .008) .007 (.010 (.010) .006-.011) .015-.048) .014-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.009) .006-.014) .021-.006) . Depending upon the specific compound and solubility. Radiation risks from exposure to natural uranium are very low.008 (.014 (.056) .006-.011-.028) .006 (.029 (.006 (.025 (.007 (.047) .012 (.012 (.022-.010-..063) .019-.007) .007-.010-.034-.013 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.006-.029) .004-.005-.027-.Metals impact..019-. Health effects from uranium exposure result from chemical toxicity to the kidney.010-.015-.007 (.006-.022-.015-.034 (.016-.029) .007 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.017 (.018-.018-. 2005).010) .006-.021) .007 (.029 (.009) Selected percentiles ( 95% confidence interval) 50th .006-.013) .009-.025 (.005 (.008) .012 (.012 (.026) .017-. 0.009) .008 (.007-.016) . 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.042) .015 (.007 (.008 (.032) .054) .034 (.008-..030) . population from the National Health and Nutrition Examination Survey. Inhaled uranium-containing particles are retained in the lungs.026 (.010 (.006-.009-.021 (.010-.008-.011-.010-.013 (.006 (.032) .013 (.051) .015) .019-.009) .006) .024-.008-.

2000). Information about external exposure (i. 1991. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.gov/ toxpro2. NRC. and no consistent effects on multiple endpoints of kidney function were found. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. The U. In a study of 105 persons exposed to natural uranium in well water.011 μg/L (McDiarmid et al. pp. environmental levels) and health effects is available from ATSDR at: http://www. 2005. Pillai KC. Durakovic A. Drinking water and other environmental standards have been established by U. et al. 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.62:562-566. Health Phys 1992. 2003. but in whom no shrapnel was embedded.65 μg/L).110 to 45 μg/L (Ejnik et al.Metals injury associated with elevated urinary uranium levels (Kurttio et al. urinary levels of uranium were as high as 9.168(8):600-605. during. population. the median urinary uranium concentration was 2. 1978).. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Muggenburg BA. Squibb K.. Guidebook for the treatment of accidental internal radionuclide contamination of workers. References Bhattacharyya MH. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.1992.. respectively. 2004). Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 41 (1). in that the levels were below their respective detection limits (Byrne et al. A cohort of 46 U. eds.. Byrne AR. Boyd P. although slightly increased during and after deployment. with emphasis on quality control. Volf V. 2006). Third National Report on Human Exposure to Environmental Chemicals. Stradling GN.1996.html.. 28 soldiers who may have been exposed to DU by inhalation.S. Mil Med 2003. 2002. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.S..atsdr. Ejnik JW. had a mean urinary uranium concentration of 0. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.066 μg/g creatinine (Gwiazda et al.. 2006).S. McDiarmid et al. Carmichael AJ. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Centers for Disease Control and Prevention (CDC). Komaromy-Hiller et al. Dietz LA.55 μg/L (median 0. Kent (England): Nuclear Technology Publishing. 2004). Pullat VR. In the same study. 1994. In: Gerber GB.107:143-157. Atlanta (GA). 1-49. Sci Total Environ 1991.. soldiers evaluated before.e. Health Phys 2000..S. Horan P. and 2003-2004 (Dang et al. Breitenstein BD. or wound contamination... IARC and NTP have no ratings for uranium human carcinogenicity.. Dang HS. the geometric mean urinary uranium concentration was 0. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. ingestion. Hamilton et al. Metivier H. 2004). In 17 U. 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.. EPA. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.S. (Kurttio et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.078 μg/L (ranging up to 5. 2006. Uranium content of blood. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 2006). Zimmerman I. 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.162 μg/L) (Orloff et al.. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 2004). Benedik L. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Six workers in a depleted uranium program showed concentrations of 0.. Tolmachev et al.61 μg/g creatinine. 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. 2000). Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Radiation protection dosimetry.. Karpas et al. 2002).S.cdc.78:143-146. 2006)... Vol. Hamilton MM. Galletti. Thomas RG. 1992. McDiarmid M. the median urinary concentration was 0. (May et al. 2001-2002.

Nuclear Regulatory Commission (NRC) Guide 8.94:319-326.Metals Galletti M. Health Phys 2002.86:12-18. Kalinsky V. Gwiazda RH. Lewis BM.44:29-40. Engelhardt SM. Paretzke HG. U. Health Phys 1996.85:228-235. Environ Res 2004. Salonen L. Oeh U. July 1978. et al. Salonen L. D’Annibale L. Clin Chim Acta 2000. Pirkle JL.79(1):11-21. Inductively coupled plasma mass spectrometry as a simple. Biologic monitoring for urinary uranium in Gulf War I veterans. Renal effects of uranium in drinking water.91(2):144-153. May LM. NRC). 242 Fourth National Report on Human Exposure to Environmental Chemicals . Bennett LG. Biokinetic modeling of uranium in man after injection and ingestion. Komaromy-Hiller G. Katorza E. Kuwabara J. Sampson EJ. Kurttio P. patient population and literature reference intervals for urinary trace elements. McDiarmid MA. Karpas Z. Environ Health Perspect 2002. Orloff KG. Ash KO.71(6):879-85.87:51-56. Health Phys 2004. J Toxicol Environ Health A 2004. Cremisini C.22–Bioassay at uranium mills. Oberbroekling KJ.158:165-190. Am J Kidney Dis 2006.S. Scott K. Heller J. Sci Total Environ 1994. Komulainen H. Squibb K. Auvinen A. Karpas Z. rapid. et al. Wilson PD. et al. et al. Halicz L. Kane R. Harmionen A. Int Arch Occup Environ Health 2006. Washington (DC): NRC. Radiat Environ Biophys 2005. Lorber A. Element reference values in tissues from inhabitants of the European community.S. Jackson RJ.110(4):337-342. Smith D. Shelly T.81:45-51. Costa R. Health Phys 2006. Cordero S. Hollriegl V. Ting BG. Ough EA. Kurttio P. Pinto V.47(6):972-982. et al. Health Phys 2004. Englehardt SA. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Nuclear Regulatory Commission (U. Noguchi H. Metcalf S. Roth P. Human exposure to uranium in groundwater. Comparison of representative ranges based on U. Jarrett JM. concentration and daily excretion of uranium in urine of Japanese. Saha H. Hancock RG. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Environ Res 1999. Charp P. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Roiz J. Wahl W. McDiarmid M. Marino R. Review of elements in blood.67(8-10):697-714. Van der Venne MT. McDiarmid MA. Uranium and thorium in urine of United States residents: reference range concentrations. Sabbioni E. Howerton K. U. Ejnik J.S.296(1-2):71-90. Andrews WS. Saha H. Li WB.82(4): 527-532. Mistry K. Uranium daily intake and urinary excretion: a preliminary study in Italy. Kidney toxicity of ingested uranium from drinking water. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Tolmachev S.S. Auvinen A. Makelainen I. et al. Pekkanen J. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Paschal DC. Squibb K. Oliver M. Gucer P. VI. Marko R. Hamilton EI. Health Phys 2003.

S.10-4.70-9.67-5.30 (5.0) 15.60) 5.84) 14.0 (9. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms. and electroplating.20) 7.62 (3. certain catalytic metals.05.20 (4.80 (6.40 (5.0-14. In addition.0) 95th 14.0) 19. 1998).0) 14.10-11.40 (8..50) 6.20-4.05 and 0.30 (2.0) 8.60 (7.32 (3.10) 3.40-6. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.66) 3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.22 (2.80) 7.40 (5.40 (4.0 (10.20 (5.0 (12.29-3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.0 (8.90) 6.50-7.0) 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. but has strong oxidant properties in the presence of concentrated acids.90-6.88) 3.0-19.0-17.44-4.10) 5.0 (12.0-18.40-7.70-3.0 (9.10-11.60) 3.00-5.50 (8.81-16.00-6.90-3. leather tanning.00-6.0-17.0) 13.05 (2. potassium.80-12.0) 13.0) 11.40) 3.0 (11. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0) 13.19-4.47-4.0-17. 2002).02 (3.20) 3.80) 12.90 (3.0 (13.50 (5.EPA.S. matches.80-4.30-17.0) 11.0 (11.0) 11.50) 3. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.70-6. It is normally found and produced as the anion of a sodium.0 (11.0) 14.60-6. milk.40 (4. Drinking water.51 (3.20-4.21 (2. 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.50-4.19 (3.60) 8.0) 9.70 (3. population from the National Health and Nutrition Examination Survey.90-11.79 (2.0-23.40) 4.40) 90th 10.54 (3.0 (11.0) 16.20 (2.0 (12.80) 75th 6.39-4.30-7. or ammonium salt.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0 (11.80 (3.09) 3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4. Perchlorate was added to the U.90-12.0 (12.03) 3.70 (3.50) 5.0-18.90 (2.96 (3. and reducing agents.50-11.60-7.0-17.11) 4.00) 3.93 (4.10 (7.70) 3.0 (8.60 (4.0) 14.16) 3.22-5.40 (5.0 (8..20-11.90-9.0) 9.0 (9.00) 7. Survey years 01-02 03-04 Geometric mean (95% conf. interval) 3.0-20.90-3.10) 3.90 (5.0 (11. lettuce) can be the main sources of intake for humans (FDA.40) 2.20 (2.40-4.40) 3.10-7.10-12.70-12.90-10.51 (3.0) 13.0 (8. laboratory analysis.87-3.70-7. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.0) 10.0-18.76) 4.93-3.30-6.50) 11.0 (9.20 (7.68) 4.50 (3.0 (9.0 (11.40 (3. and limited applications in pharmaceutics.00) 5.10 (6.30-19.80 (3.89-3.40-5.26 (2. 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.80) 3.0) 15.49-3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 . Other manufactured uses include fireworks.90-11.0-17.50-3.0-15.0) 9.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.20 (4. fabric dyeing.0) 13.0) 10.18-3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.40-11. 2005).20-3.20) 4.40-13.0) 8. 2007).g. 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.35 (3.46) 3.0) 9.70-3.30) 6.30 (5.10 (5.40-4.38) 5.S. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.70-5.50-4.0 (11.00) 3.74-3.0 (11.12) 3.80-6.0) 9.0) 10.0-15.07-4.0 (9.20-12.Perchlorate Perchlorate (Urbansky.80-15.0) 13.90 (5.0) 13.0 (11.0) 708 617 681 652 1228 1092 Limit of detection (LOD.45-4.0) 13.60 (4.10 (2.90) 5.40 (3.75-3.30) 6.0-29.10) 12.40) 3.31) 2.90 (5.70 (3.76 (3.00) 4.0 (8.50) 5.80-8.0-17.75 (3.08-3.30 (2.30-7.90-9.0) 12. and certain plants with high water content (e.0 (9.10 (6.80-4.11) 3.40) 6.90 (4.20 (6.93-4.10) 5.20 (8.81) Selected percentiles ( 95% confidence interval) 50th 3.56) 3.0) 9. 2005).01 (2.80 (7. Perchlorate is stable under most environmental and physiological conditions.65) 3.70-11.

70-3.00-11.05 (4.24-2.S.70) 10.90-11.76 (3.1-13.50-3.10 (2.04-3.g.45) 3.51 (3.50 (6.32) 5.75) 3.90-9.70-4. Steinmaus et al.37-13.64) 5.21 (2.80) Selected percentiles ( 95% confidence interval) 50th 3..30 (6.98) 3.S.40-10.95 (2.4 (11.12-2. levels. NAS.07 (2.60-5.90) 5.54 (3.46-4. women with urinary levels of iodine less than 100 micrograms per day.30 (3.1 (11.56-3.0-44.0) 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 .60-5.00 (2. 2005. U.0) 4.0-14.Perchlorate inhibition (RUI).60-8.09) 3. perchlorate is negative in most genotoxic assays (U.43) 6. Also. 2005).25) 5.93-7.20 (2.0) 9.0 (11.1 (8.EPA.16-3.60) 3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.6) 20.10 (4. Li et al.41-9.50) 6.80 (4.39 (3. although iodine intake was higher than U.81-3.3-14.61-10.60) 10.58) 2.10 (6.6-17.1-16.25) 5.35) 3. age..33 (7. 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. 2000).3) 11.60-3. population from the National Health and Nutrition Examination Survey. 2005.00 (6.4) 8.93) 3.12 (6. Lamm and Doemland. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.80 (7.61 (5.99 (5. 2006.87) 7.0 (11. menopausal status. levels and sufficient in most participants (Tellez et al..25 (3.39-4.89-3.08 (3.10-7.0 (9. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.18-3.29-6.26 (3.20-4..90 (2.66) 3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.50) 9.20 (7.82 (5.40 (3.80-3..10) 13.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.50-9.4-16.3 (10.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.61-5.0 (9. chronicity of exposure.30-10.02) 3. However.52 (8.20 (4.30-5.70-15.22 (2.0) 12.20) 8.29) 2.70 (4.60-11.33-6. 2005).50) 2.0) 6.60-6.51-4..90 (4.0) 13.0 (8.0-19.20-3. dietary iodine intake.8 (11. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.2) 8.10-3.EPA.0) 12..59) 3. Lawrence et al.74) 7.S.87 (5.6) 12.25) 5..03 (2.77 (3.00-2..09 (7.87) 2.60-8. 2005).1-22.52-9.4 (10.20-9.7 (11.99-3.20) 3.80-3.36 (8.0 (9.00-3.40) 17. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.87-3.33-12.90-3.5 (13.64-3.20 (3.73) 3.0) 11.0) 14. 2002.19-10.0) 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 3.67) 5. Survey years 01-02 03-04 Geometric mean (95% conf.0) 9..10 (1.22-6.60) 8.0 (11. 2001.37 (4.89 (2. 1999.08) 3.24 (4. gender.60 (3.15-12.40) 3.30) 5. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.20-10.70 (2.30-5.90-2.39) 2.93-8. thiocyanate.30) 75th 5.4) 13.3) 12.02-4.70) 2. In the U. up to 68% RUI has been demonstrated. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.56 (3. interval) 3.90-20. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.22-4. 2007).40 (7. Many factors may be important in consideration of perchlorate action on the thyroid: dose.0) 7.35 (2.84) 2. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.20 (6.44-6.10) 6.91) 4. and the presence of other substances known to affect thyroid function (e.50-5.S.34-3.04-3.0) 13.93-5.2) 8.35 (4.5) 8.4 (8.4 (11.72 (3. 2002).1-14.90 (2.20-3. Greer et al.0) 12.19-6. 2003.00) 3.00) 9.S.47) 2. nitrate. During gestation and infancy.10) 4.70 (2.71 (5.46-13.22-4.S.10) 3.42 (3.50) 95th 12.50 (3.0 (8.90 (7. in a representative sample of U.54 (2.30) 3.26) 4.0) 12.40 (3.45-2.60-11.0) 10.60-15.0-17.90-15.3) 8.0-14. medications).96) 2.40 (4.46 (3.87 (7.93-5.83 (5.30) 90th 9. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.00 (4.00) 4.86) 4.10 (4. 2002.50) 5.76-3.14 (2.30 (5.40) 5.97-5.50) 2.70-5.0 (10.1) 8.44) 3.53 (2.80 (7.S.

. Magnani B. J Occup Environ Med 2003. EPA reference dose (Blount et al. 2005). Kirk AB.45(10):1116-1127. epa. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Lamm S. 6/2/09 Greer MA.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. most of the population is considered to be below the U. Erratum in: Environ Health Perspect 2005.114(12):1865-1871. Lamm SH. Lamm SH. Environ Sci Technol 2006. Thyroid 2001.17(4):400-407. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Braverman LE. and nitrate on thyroid function in workers exposed to perchlorate long-term. 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. 2001-2002. National Academy of Sciences (NAS). Deyhle GM. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Perchlorate Exposure of the US Population. Pleus RC. Perchlorate in the United States.41(5):409-411. et al. The effect of perchlorate.EPA at: http://www. population. Pino S. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Daaboul JJ. Neonatal thyroxine level and perchlorate in drinking water. Crump KS. Food and Drug Administration (FDA). Primary congenital hypothyroidism. Skeels MR. Thyroid 2000.40(21):6608-6614. Braverman LE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.html. Li Z. Braverman LE. Crump KS. Blount et al. J Clin Endocrinol Metab 2005. Cross M. Valentin-Blasini L. Landingham CB. et al. Greer SE. Environ Health Perspect 2007. Jackson WA. et al. Benchmark calculations for perchlorate from three human cohorts. 2005). CFSAN/Office of Plant & Dairy Foods.113(11):A732. Gibbs JP. Health Implications of Perchlorate Ingestion. The effect of short-term low-dose perchlorate on various aspects of thyroid function. (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. Mauldin JP.. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. 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. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.46(5):509. Osterloh JD. Analysis of relative source contributions to the food chain.htm. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. References Blount BC. Erratum in: J Occup Environ Med 2004. Lawrence J. Lawrence JE.atsdr. Pino S. Environ Health Perspect 2006. and environmental perchlorate exposure among residents of a Southern California community. Chacon PM. Buffler PA. Abarca CR. Valentin-Blasini L.11(3):295. Tellez RT. Additional information about exposure and health effects is available from the U.110(9):927-937.fda. Howd R. Rutherford GW. Blount BC. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Low dose perchlorate (3 mg daily) and thyroid function.S.gov/safewater/ccl/perchlorate/perchlorate. Sesser DE. He X.10(8):659-663. Miller MD. Caldwell KL. Pirkle JL. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Also. Goodman G.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Osterloh JD.90(2):700-706. Available at URL: http://www. 2005.gov/toxpro2. Richman K. Steinmaus C. Pirkle JL.. Blount BC. et al.S. J Occup Environ Med 2000. Washington (DC): National Academy Press. Li FX. Environ Health Perspect 2005. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.cdc. 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. Byrd D. Page Last Updated: 05/28/2009. J Expo Sci Environ Epidemiol 2007. Lamm SH. Lau EC. 2007).html and from ATSDR at: http://www.42(2):200-205. Dasgupta PK. National Research Council of the National Academies. Environ Health Perspect 2002.S. newborn thyroid function. May 2007. thiocyanate.115(9):1333-1338. Kelsh MA. Doemland M. Biomonitoring Information Urinary perchlorate levels reflect recent exposure.113(8):10011008. Dyke JV. Barnard JC.

U. Perchlorate as an environmental contaminant. EPA). 246 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Sci Pollut Res Int 2002.Perchlorate pregnancy and the neonatal period. Available from URL: http://cfpub. Revised 2/11/05. Perchlorate.S.9(3):187-192. Environmental Protection Agency (U. Drinking Water Contaminant Candidate List. Doc. Integrated Risk Information System (IRIS).S.gov/iris/quickview. EPA).epa. No. Urbansky TF. cfm?substance_nmbr=1007. Thyroid 2005. EPA/600/F-98/002 Washington (DC).S. Environmental Protection Agency (U. 1988.15(9):963-975.1/15/06 U.S.

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

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

00) ..500) .40) .900 (.600 (.108 times higher than background serum levels in humans (Butenoff et al.400 (<LOD-.400-1. Animal studies of PFOS have demonstrated weight loss. Survey Geometric mean (95% conf. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.500 (. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.10) . developmental and teratogenic effects were demonstrated in offspring.00) . Olsen et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 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.500) .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 .Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. < LOD means less than the limit of detection.. PFOS. or increased cancer rates (Alexander et al. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 2007a.800 (.. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. 2003. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. Thibodeaux et al.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 2003a. 2007. 2004). Fei et al.800 (. At doses causing maternal toxicity.600-2.400-1. 2004). hepatotoxicity.800 (.300 (<LOD-.S. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. PFOS.500-1. 2007b.300 (<LOD-. In comparing three separate reports on adults. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. Olsen et al. 1992. Kennedy et al.10) .. 2003). population from the National Health and Nutrition Examination Survey. thyroidal). U. 2007). 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.400) . perfluorohexanesulfonate (PFHxS). PFOA. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. At high but non-toxic maternal doses of PFOS.20) .700 (.500 (<LOD-1.10) * 03-04 03-04 * * < LOD < LOD < LOD .S. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. Olsen et al.400 (<LOD-. In such studies.600 (.600 (. and humans.. and changes in thyroid hormone concentrations (Grasty et al..500-. PFOA. However. 2003. 2003.400 (<LOD-. reproductive.500-1. 2004b).800) 1..500-1.80) 485 538 962 Limit of detection (LOD.80) 640 1454 03-04 03-04 * * < LOD < LOD ..S.. 2004.800 (.700) .00 (.S. 2004a.400-. elderly and children. 2003a). which may vary for some chemicals by year and by individual sample. Harada et al. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.300 (<LOD-.. 1999.900 (. 2003a. 2003).00) . monkeys.800) 1. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. EPA...3..500 (. 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. possibly related to lung immaturity (Lau et al. 2007b).300-1. the potential to estimate risks to humans from animal doses is uncertain. 2005).500) . population.900 (..400-1. 2001.10 (.. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 2003a).. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003a. 2004. Lau et al. 2003).500-1.500) 90th ... Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Fourth National Report on Human Exposure to Environmental Chemicals 249 .400-1.400-. EPA.500) . see Data Analysis section) for Survey year 03-04 is 0..50) .500-3. U. 2007a.. development in offspring was stunted and hypothyroxinemia was observed. Cook et al.400-1. and there was no clear evidence of excess all-cause or diseasespecific mortality..

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

300 (<LOD-.400 (<LOD-. which may vary for some chemicals by year and by individual sample.S.600 (.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.900) < LOD . 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 .400 (<LOD-.400 (.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.600) < LOD . which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 251 . population from the National Health and Nutrition Examination Survey.500) 485 538 962 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400) .0.3. see Data Analysis section) for Survey year 03-04 is 1.500 (<LOD-.300-.500-. population from the National Health and Nutrition Examination Survey.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. < LOD means less than the limit of detection.

90 (1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.54) .60 (1.51) 1.5) 8.900-1.72 (1.10 (. interval) 1.80-3.50 (4.70-2.00 (2.809) 1.50 (1.90) 3.60-2.20) 485 538 962 Limit of detection (LOD.900 (.10 (.10) 4.20) 2.26) 2.40) 4.966 (.80 (1.77-2.27) 1.30-9.30) 3. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-2.600-.00 (1.50) 2.50 (1.67-2.90 (1.1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.912-1.70-10.87-2.700 (.900 (.60-8.10) 6.20) 03-04 03-04 2.60-4.70-5.20-1.60 (1.50 (6.60-2.90) 1.10 (4.60) 9.10) 75th 3.S.60 (1.800-1.20 (1.00-8.05-2.50-3.70-6.20) 1.09 (.90) 1.50) 2.689 (.10 (1.900-1.30) 3.963 (.80-6.20 (1.60-2.20-2.70) 13.90 (4.700-1.90 (1.30 (7.80-4.70 (1.91) 2.92 (1.50 (6.00) 1.73-2.10) 1.90 (4.30) 03-04 03-04 .40 (1.70) 2.6) 7. population from the National Health and Nutrition Examination Survey.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.90-2. see Data Analysis section) for Survey year 03-04 is 0.00) 2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.835-1.30) 3.20 (1.90-19.30 (1.93 (1.60-7.20-3.80-7.10) 4.70 (2.70) 1. population from the National Health and Nutrition Examination Survey.90) 8.900-1.14 (.50-10.30 (2.40) 640 1454 03-04 03-04 1.40 (2.20) 1.80-12.70) 3.1) 485 538 962 Limit of detection (LOD.852 (.80) 1.01 (1.50 (2.70) 2.00 (1.10) 5.50 (1.50) 6.00 (5.10) 8.5) 5.10-9.50-6.90 (2. 252 Fourth National Report on Human Exposure to Environmental Chemicals .3. interval) .62-2.00) 1.80) 5.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.80 (4.900-1.80-4.17-1.00 (.80-8.40 (1.30 (1.90 (1.80 (1.800 (.816-1.30-12.20) .00-7.721-1.20 (6.900-1.40) 1.40) .20-1.984 (.80) 3.30 (6.44 (2.586-.20 (1.10 (4.20-1.90) 90th 5.30) . Survey Geometric mean (95% conf.12) .40 (1.03) 1.0) 1053 1041 03-04 03-04 03-04 1.70-2.826-1.60) 2. Survey Geometric mean (95% conf.60-3.10 (.10-9.30 (3.16) .17 (1.60 (6.50 (4.72) 1.40 (1.60) 1.40-3.40) 640 1454 03-04 03-04 2.70) 1. see Data Analysis section) for Survey year 03-04 is 0.697-1.10) 1.00-6.80-8.80-3.30 (1.70-7.30 (1.00-1.80-4.60) 3.80) 4.90) 1.S.04) .00) 3.861 (.834-1.90-10.50 (1.50-6.30-2.00 (1.30 (2.08) 2.900) 1.40-1.10) 75th 1.86 (1.56-1.30-6.00 (.20 (6.00-1.40) 1.60-4.10) 6.40) 2.42 (1.3 (9.40-1.00 (1.80) 90th 2.0) 8.10-5.80-7.10) 1053 1041 03-04 03-04 03-04 .60-3.900-1.20-1.

30-5.80 (6.7-49.3) 485 538 962 Limit of detection (LOD.5-23.4-17.40-17.80-12.4-25.5) 32. interval) 20.85-4.8 (37.7-23.90 (7.9) 9.60-14.40-14. see Data Analysis section) for Survey year 03-04 is 0.6) 42.9-38.20-4.0-16.3 (17.20) 5.90 (7.9 (13.89 (3.80-4.10 (6.2) 640 1454 03-04 03-04 4.95 (3.47 (4.40-10.20 (4.4) 640 1454 03-04 03-04 23.8) 46. Fourth National Report on Human Exposure to Environmental Chemicals 253 .0 (20.65-4.3 (35.7 (7.30 (5.4.5) 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 21.20) 4.5) 9.00) 3.70-5.00 (3.07-4.1-52.0) 23.60 (3.4 (17.7) 39. Survey Geometric mean (95% conf. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) 7.90 (5.2) 30.70) 6.60-9.20) 5.40) 90th 7.3) 42.8-22.50 (3.84-3.7-69.5) 19.40) 3.7-33.5) 8.8) 32.40-6.30 (3.8-30.70 (5.60 (6.4 (23.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.40 (6.21-3.20) 7.90-4.7 (13.3 (44.37 (2.0-20.0) 21.3) 28.5-21.30-3.30) 6.30-6.3-22.40-6.1) 57.1-33.0) 03-04 03-04 19.6) 35.70-9.4 (19.4 (28.4) 20.10) 5.40) 75th 5.96 (3.6 (35.6) 18. Survey Geometric mean (95% conf.10-3.20-9.6) 62.9-19.S.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20 (4.90) 6.2 (27.8-81.40 (4.80 (6.50-6.6) 7.2) 30.4) 75th 30.3 (35.5 (28.80) 8.5) 1053 1041 03-04 03-04 03-04 14.7 (35.0) 21.9 (19.91) 3.7-30.5) 7.90-4. interval) 3.6 (19.90 (7.0 (27.5-62.2 (28.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.7 (35.7 (19.1 (23.6) 21.3-61.2 (16.1) 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 4.70-10.0-70.70) 3. see Data Analysis section) for Survey year 03-04 is 0.70-7.50-4.11 (2.70 (3.9) 22.8 (34.60-6.60 (5.30-8.67-4.00 (5.6) 9.2 (19.60 (4.5-33.5) 18.2 (21.30 (3.1-36.2) 45.6 (44.0) 485 538 962 Limit of detection (LOD.8 (45.47-4.8-22.3) 41. population from the National Health and Nutrition Examination Survey.80 (5.99-3.80-9.5 (28.4-42.1 (19.79) 4.0-66.60 (6.7 (43.1-24.0) 36.20) 10.4) 56.50) 7.7-53.50) 4.1.8) 27.82) 4.6-50.6) 1053 1041 03-04 03-04 03-04 3.2-22.00 (5.10 (3.4 (19.2-57.40) 5.50 (4.60 (7.35) 3.70 (5.5) 57.18 (3.9) 22.70) 4.9) 27.7 (43.6-45.2 (18.1) 15.60-13.1-25.4) 21.30) 7.S.10 (3.70-7.50-13.60) 03-04 03-04 3.6 (42. population from the National Health and Nutrition Examination Survey.8-22.9-23.0) 43.90-12.0) 90th 41.80 (7.9 (17.53) 3.30-11.27) 4.8-78.6-24.1 (24.20-5.9 (22.8-35.3 (28.1-35.60) 8.

300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . 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) .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300) .400 (<LOD-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .200-.300 (.300-. population from the National Health and Nutrition Examination Survey.300-.200-.200-.300 (. Survey Geometric mean (95% conf.300) .300 (.200-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.300 (. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.300 (.300 (.4.300-.200-.500) .500) .200-.300 (. which may vary for some chemicals by year and by individual sample.300 (.S.300 (.300) . Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0.200-.200 (<LOD-.500) < LOD 485 538 962 Limit of detection (LOD.200-.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.200-.200-.300) .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. which may vary for some chemicals by year and by individual sample.300 (.300 (. Survey Geometric mean (95% conf.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .2.400) 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-.500) .300) . * 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. < LOD means less than the limit of detection.10) 1.300-2.10) .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.400 (<LOD-1. population from the National Health and Nutrition Examination Survey.700) 90th 1. Survey Geometric mean (95% conf.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 .10 (1.10) .10 (.700) .00 (.600 (<LOD-1.80) 1.20) 1. which may vary for some chemicals by year and by individual sample.70) 1.20 (1.700) 1.30 (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.S.300 (<LOD-. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700) 1.300 (<LOD-1.30) .900 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700 (<LOD-.900) 1. see Data Analysis section) for Survey year 03-04 is 0.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-.6.10-1.30 (1.800) .00 (. Fourth National Report on Human Exposure to Environmental Chemicals 255 . Survey Geometric mean (95% conf.3.900-1.600 (<LOD-1.600 (<LOD-1.10) 1.S.600 (<LOD-.10-1.900-1.700 (<LOD-.40) 1.10-1.10) * 03-04 03-04 * * < LOD < LOD .900 (.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) < LOD .900-1. population from the National Health and Nutrition Examination Survey.700 (<LOD-.700 (<LOD-.30) 1.800 (<LOD-.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .10 (.30) 1.00 (.700 (<LOD-.900) .80) 1.900-1.500 (<LOD-.50 (1.30 (1.00 (.00-1.40) < LOD < LOD .60) 640 1454 03-04 03-04 * * < LOD < LOD .10 (.600) .60) 485 538 962 Limit of detection (LOD.90) .700 (<LOD-.50 (1. which may vary for some chemicals by year and by individual sample.700 (<LOD-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10-1.900-1. < LOD means less than the limit of detection.900-1.10-1.900) 485 538 962 Limit of detection (LOD.800) .20-1.900-1.

Bookstaff RC. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Biegel LB. The toxicology of perfluorooctanoate. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Olsen GW. Kudo N.39(23):9057-9063. Cook JC. Witter FR. Apelberg BJ.179:99-121. Olsen J. Arendt MD. Inoue K. Mabury SA. Peterson RE. Seacat AM.41:2237-2242. Tully JS. Environ Res 2005. Rodricks J. Taniyasu S. Environ Sci Technol 2005. Hurtt ME. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Cook JC. Saito N. Calafat AM. Kuklenyik Z. and perfluorinated contaminants in livers of polar bears from Alaska. Reidy JA. Harada K. Occup Environ Med 2003.104(2):322-333. Environ Sci Technol 2004. Grey BE. Dinglasan MJ. Yoshinaga T. Frame SR. Toxicol Appl Pharmacol 1995. Toxicol Sci 2001. Mohotti KM. Aguilar-Villalobos M. Calafat AM. et al. Environ Health Perspect. Needham LL. Needham LL.115(11):1677-1682. Fluorotelomer alcohol biodegradation yields poly. Needham LL.1968--2003. Hurtt ME. Cook JC. Grasty RC. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.115(11):1596-1602. Calafat AM.68(6):465-471. Burris JM. Halden RU. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Mandel JH.and perfluorinated acids. Suzuki E. Environmental and toxicity effects of perfluoroalkylated substances. et al.60(10):722729. Saito N.39(23):9101-9108. Needham LL. Mandel JH. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Liu RC. Regul Toxicol Pharmacol 2004. Frame SR.38(10):2857-2864.7(4):371-377. Environ Sci Technol 2004. Evans TJ. Kawashima Y. Ye Y. Kannan K.39(3):363-380. Reidy JA. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years.46(2):141-147. Rogers JM. Butenhoff JL. Morikawa A. Moore RW. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Toxicol Appl Pharmacol 1990.115(11):1670-1676. et al.Koizumi A.S. Yamashita N. in vivo. et al. Falandysz J. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ Health Perspect 2007. Yamashita N. Calafat AM. et al. Laane RW.124(2):119-132. Environ Sci Technol 2006a. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism.113(2):209-217. Watanabe T. Kuklenyik Z. 2007b. Characterization of risk for general population exposure to perfluorooctanoate. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats.134(1):18-25. Perfluorinated chemicals in selected residents of the American continent. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Caudill SP. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Perkins RG. Katakura M. Kumar KS.Perfluorochemicals References Alexander BH. Butenhoff JL. McLaughlin JK.40:21282134.63:490496. Inoue K. Crit Rev Toxicol 2004. Guruge KS. Bignert A. Rev Environ Contam Toxicol 2003. Day RD. de Voogt P. Koizumi A.39(1):80-84. Environ Sci Technol 2005. Yun SH. Loganathan BG.S. Yoshinaga T. Murray SM. Edwards EA. Birth Defects Res B Dev Reprod Toxicol 2003. Ingall GB. Moore JA. and ex vivo studies. Hurtt ME. J Occup Health 2004. Chemosphere 2006b. J Environ Monit 2005. Olsen GW.34(4):351-384. Wijeratna S. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.99(2):253-261. Fillmann G.60(1):44-55. Kamiyama S. et al. Tully JS. Holmstrom KE. Environ Sci Technol 2007a. Corsolini S. Herbstman JB. Calafat AM. Keller JM. Fei C. brominated. O’Connor JC. Chem Biol Interact 2000. Kuklenyik Z. Environ Sci Technol 2005. Kannan K. Tarone RE. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Biegel LB. Chlorinated. Olsen GW. Polyfluoroalkyl chemicals in the U. Mandel JS. et al. Kuklenyik Z. Environ Health Perspect 2007. Harada K. Bandai N. Reidy JA. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Seneviratne HR. Gaylor DW. Toxicol Appl Pharmacol 1992. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Jarnberg U. Lau CS. O’Connor JC. Kennedy GL Jr. Hekster FM. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Taniyasu S. Wong LY. Reidy JA. The influence of time. Caudill SP. Sasaki S.38(17):4489-4495. Kannan K.

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

but there are known species-related differences in the hydrolysis of diester phthalates. 2004. at very high levels. 2002). efficiency of intestinal absorption. Calafat AM. NTP-CERHR. 1982).atsdr.. Food Addit Contam 2001. 2001. 2002). 1986). 2004. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. Springer. reducing estrogen production.. and extent of metabolite conjugation to glucuronide (Albro et al. 2006). 2001. Albro PW and Lavenhar SR. 2000c. Environ Health Perspect 1997. Kessler et al. Environ Health Perspect 1982. Sauer MJ..gov/ toxprofiles/tp9.html.html). Rhodes et al. Silva MJ. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al.niehs. Anderson WA. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. However.nih. 2003.. phthalates have been shown to induce peroxisomal proliferation in rodents.3. Dave M. Connor C. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. 2005. 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. ovarian abnormalities in the female animals (Jarfelt et al. 1982. Jongeneelen FJ. Mackay D. Springall C. McDonnell DP. testicular atrophy. Cousins IT. variation also occurs in the same person during repetitive monitoring (Fromme et al. J Chromatogr B 2004. Also.gov/toxprofiles/ tp135. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . Part Q: Phthalate Esters.gov/toxpro2. Clark K. Metabolism of di(2-ethylhexyl) phthalate. 2000b. van der Broek PH.cdc. Evaluation of a recombinant yeast cell estrogen screening assay. Information about external exposure (i.html. 227-262. Hoppin et al. The Handbook of Environmental Chemistry. Dirven HA.. Castle L. Peck and Albro. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Herbert AR. 2000a. Available at URL: http://www. Vol. Assessment of critical exposure pathways.805:49-56. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. 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. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Toxicological profile for di(2-ethylhexyl)phthalate update [online].. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). phthalates produced anti-androgenic effects by reducing testosterone production and. In Staples CA (ed). interactions with macromolecules and species differences in metabolism of DEHP. Toxicological profile for di-n-butyl phthalate update [online]. References Agency for Toxic Substances and Disease Registry (ATSDR). Corbett JT.Phthalates and metabolites have been tested.. Jordan S.. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. Slakman AR. 2005).. and race/ethnicity (Silva et al. at higher doses. dibutyl phthalate (DBP). Matthews HB.cdc. Scotter MJ. 2004. pp. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Massey RC. Pharmacokinetics. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.gov/ reports/index. 2004). 2006).. gender. 105:734-742. which may be a pathway to the development of liver toxicity and cancers in these animals..New York. Lovekamp-Swan and Davis..e.21:13-34.45:19-25. Schroeder JL. 2001). atsdr. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. 2007. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels.. 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. Coldham NG. 2007). Population estimates of concentrations of specific phthalate metabolites may differ by age. Hauser et al. In animals. 4/20/09 Albro PW. 1985... and Sertoli cell abnormalities in the male animals and. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester.18(12):10681074. High doses of di2-ethylhexyl phthalate (DEHP).. Drug Metab Rev 1989. 2002. These differences may contribute to species-specific differences in toxicity (ATSDR. Needham LL. McKee et al. 2004.atsdr. 2003. Hauser et al.html.cdc. Available at URL: http://www. Silvapathasundaram S.

Suzuki T. Yoshimura M. Hass U. Chahoud I.112(17):1740]. consumer milk. Bolte G. Nielsen J. Pan G. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Sumpter JP. Jacobsen H.niehs. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Reynolds T. Dalgaard M. Zhang S. Filser J. Duty SM. 2006 [online]. Stringer WT. Boehmer S. Meeker JD. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Baird DD. Hagmar L. Hauser R. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.112(17):1734-1740.gov/chemicals/dehp/dehp-eval. Environ Health Perspect 1997. Rylander L. Research Triangle Park (NC). Lovekamp-Swan T. Singh NP. Leffers H.103:582-587. Fromme H. Davis BJ. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).110(5):515-518. Hanaoka T. Available at URL: http://cerhr. Silva MJ. Determination of phthalate monoesters in human milk. Akesson B. Yokoyama Y. Jonsson BAG. White R. Kano I.25(2):293-302.64(8):555-560. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. McKee RH. Kalita JC. 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 . Occurrence and daily variation of phthalate metabolites in the urine of an adult population. 2000a [online]. Butala JH. Drexler H.nih. Environ Health Perspect 2003. 6/2/09 NTP-CERHR. Silva MJ. Research Triangle Park (NC).105:802-811. Available at URL: http://cerhr. 6/2/09 NTP-CERHR. NTP-CERHR. Research Triangle Park (NC). Environ Health Perspect 2004. David RM. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. J Androl 2004. Available at URL: http://cerhr. Kessler W. Hum Reprod 2007. Am Ind Hyg Assoc J 1985. Park MG. Richthoff J.16(4):487-493. Hauser R. Environ Health Perspect 1995. Henttu P.Phthalates in human urine samples. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).html. Brock JW. Hoppin JA. et al.22(3):688-695. Main KM. Environ Health Perspect 1998. Reprod Toxicol 2005. Mortensen GK. Available at URL: http://cerhr.26(8):1219-24.niehs. Brock JW.html. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.nih. Grote K. Gans G.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Skerfving S. Silva MJ. Numtip W. Ryan L. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Ryan L. et al. Hartle RW. 2000b [online]. 2000c [online]. Csanády G. Duty S. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Scand J Work Environ Health 1985. et al. Skakkebaek NE. gov/chemicals/dehp/dehp-eval. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Epidemiol 2005. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).html. Environ Health Perspect 2002.niehs. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Ladefoged O.19(4):505-515.11(5):381-387.195:142-153. Anal Bioanal Chem 2005. Calafat AM.html.111(2):139-145. Calafat AM. and infant formula by tandem mass spectrometry (LC-MS-MS). 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. Albro PW. Davis BJ. The estrogenic activity of phthalate esters in vitro. Jarfelt K.210:21-33. Balasubramanian AV. Toxicol Appl Pharmacol 2004. Int J Hyg Environ Health 2007. Angerer J. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Int Arch Occup Environ Health 1993. Biol Pharm Bull 2003.nih. Reprod Toxicol 2004.46(11):643-647. Giwercman A. Sumpter JP. Kano K. Mechanisms of phthalate ester toxicity in the female reproductive system. Andersson A-M. 6/2/09 Okubo T.niehs. Wang P. Jobling S.nih.gov/chemicals/ phthalates/dbp/dbp-eval. Milligan SR.106(1):23-26. Research Triangle Park (NC). DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Koch HM. Reproducibility of urinary phthalate metabolites in first morning urine samples. Meeker JD. Parker MG. Borch J. 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Rusyn I. et al. Hodge CC. et al.S. Orton TC. Reidy JA. Lambright CR. Toxicol Sci 2000. Parks LG. Malek NA. Jackson SJ. Ostby JS. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Fourth National Report on Human Exposure to Environmental Chemicals 261 .46:282-293. 112(5):A270]. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Pratt IA. Clemons JH. Environ Health Perspect 2004.112(3):331-338. Cunningham ML. Peck CC. Bratt H. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 1986. Silva MJ.114(11):1643-1648. Wu ZF.58:339349. Barr DB. Rhodes C. Zacharewski TR. Peters JM. Caudill SP. Barlow NJ. Fielden MR. Batten PL. Crit Rev Toxicol 2006.36:459-479. Environ Health Perspect 1982. Meek MD. Klinefelter GR. et al.45:11-17. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Matthews JB. Albro PW. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Abbott BD.Phthalates phthalate (DEHP): a cross-sectional study in China. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Environ Health Perspect 2006.65:299-308. Toxicol Sci 1998. Urinary levels of seven phthalate metabolites in the U.

0-130) 101 (86.2-31.9-27.6) 50.4 (53.6) 13.6) 95th 103 (94.6 (41.9) 43.2-155) 91..0 (14. 2004.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3 (12.4 (31.7 (13.7-82. car care products.2 (25.6) 14.5) 82.5-25.1-16.9 (12.9) 14.8) 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 16.0) 33.4) 98.3 (22.3-125) Total 15.9-14.3-18.4 (29.5-94. because it is not bound to products in which it is incorporated.1) Selected percentiles ( 95% confidence interval) 50th 17.4-92.9 (22.4) 71. 262 Fourth National Report on Human Exposure to Environmental Chemicals .7-25. and 2003-2004 were generally similar those reported in U.7-172) 103 (74.3-43.2) 17.1) 76.4 (13.7-16.5 (47. and 03-04 are 0.6 (13.1 (10.5) 23.9-49.5) 65.4) 108 (96.5 (55.5 (26.0 (20.0 (15.1-90.7-14.3 (30.4-16.2 (43.1 (20.3) 54.6 (13.2 (47.6 (12.4) 33. it can be released into the ambient air during use or disposal of the products.8 (86.0-106) 58.8-14.1-39.5) 30.8-72.0) 34.6) 37.5-14.0) 16.6-132) 103 (84.5 (67.3) 15.1) 68.2 (19.4) 75th 35.2 (14.8-41.4 (59.1 (55. some personal care products.8 (12.9 (21.4) 14.8 (28.1) 12.2) 14.0 (43.2-40.8 (14. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.3 (12.2) 66.2-19.0 (30. sealants.1-116) 122 (93.9) 49.2 (11.6) 29.0 (26. see Data Analysis section) for Survey years 99-00.4) 81. respectively.5-36.7-17.5 (66.8-48.6 (53. NTPCERHR. interval) 15.4-24. IARC considers BzBP not classifiable with respect to human carcinogenicity.1-120) 52.3 (33.2-16.7-119) 99.8 (30. BzBP can be released into the environment during its production and. and to a lesser extent.8-35.6-72.3-21.9 (13.1 (32.6) 24.8) 63.6-116) 122 (102-142) 101 (85.1-18.3) 13.7 (82. population from the National Health and Nutrition Examination Survey.5 (13.6-92.8-76.6) 35.8 (50.4) 35.2) 32.0 (23.8 (10.4) 80. particularly male animals (McKee et al.8 (71.6-43.0-55.8-17.8-14. 2000).0) 23.5-97.1 (14.4 (10.4-62.5-18.9) 12. can produce developmental and reproductive toxicity in rodents.4 (10.2 (10.5) 27.6) 35. 2001-2002. Food crops take up BzBP..4-15.1) 13.8-64.9 (28.8-17.5) 15.5 (76.4 (27.0 (15.6 (13.7) 23.2) 69.4) 65.6-17.3-74.6 (21. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.6-150) 94.8-18.3) 63.3 (13.9) 18.3-91. High dose BzBP and its monoester metabolites.8-133) 89.1) 14. including MBzP.5) 16.9-28.5) 15.7 (12.0 (12.3-161) 99. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9) 11.7 (51.4) 38.3 (29.S.0-85.4) 35.8 (71.2) 15.3-88.7-58.5-84.6) 14.7-16.9-62.2) 22.1-15.7) 38.2-183) 101 (78.1 (58.7 (15.9-30.4 (48.2-17. and diet is the major source for general population exposure.4) 49.4-25.5 (61.0) 24.4) 129 (98.6) 16.3-82.3-18.7-16.6-79.6) 63.0 (27. vinyl tile.7 (11.0 (11.6-92.8) 14.9) 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 39.6) 15.3.8 (53.9) 14.8.4 (53.3) 94.8-121) 79.9-87. 2000).3 (44.3-27.5) 55.3 (12.5-40.2-20.5-41.2-16.5-33.2-115) 113 (91.3-12.0 (34. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.4) 12.3) 37. and 0.1-43.1 (19.8-13.1 (13.2) 14.9-47.4 (63.2) 33.7-15.1) 29.6-39. 0. residents (Blount et al.2 (19.9) 15.2-33.3-130) 122 (88.Phthalates Benzylbutyl Phthalate CAS No.8-16.8-16.0) 90th 67.7-35.8) 28.7-13.1-38.S.5-36.4) 51.6) 25.2-38.2) 12.5 (57.1) 32.0 (33.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-39.1.7 (70.1-214) 166 (116-191) 145 (110-213) 88.4 (32.7 (53.6-38.6) 13.2) 78.1-61.0-26.4 (68.2) 13.9 (11.0 (55.8 (80.5-62.8) 33.5-145) 138 (106-241) 143 (127-179) 120 (99.9) 13. 01-02.3) 13.7) 40.6) 67.6 (13.1 (14.7 (80.9 (70.3) 23.8 (21.9-16.6-18.3 (29.0) 32.6 (66.8-98.8 (38.9 (16.2-116) 122 (102-143) 101 (84.3-34.3-75.9 (12.1) 31.3 (54.5 (27.1 (13.1-16.6-29.0) 70.7-170) 169 (134-198) 152 (99.5-35.4-127) 80.4-120) 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 (32.8) 24.1-15.9 (39.4 (32.0) 20.9-190) 86.1) 67.1-35.0 (30.

7) 19. interval) 14.4) 104 (89.5-213) 49.7 (14.8) 53.0) 49.4) 13.6-99.4 (74.9) 11.3-73.5-99. 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..0 (12.5) 41.8 (30.2) 26.1) 12.5-26.6) 30.4 (12.2) 15.4 (63.8) 53.4 (26.4 (60.2) 12.0) 13.3) 14.3) 55.7-20.4) 14.4 (11.3 (15.2) 32.4-15.4) 50.7-123) 77.4 (11.0 (11.8-14..3) 90.5-61.1 (21.2-13..5-29.6) 12.4 (34.6 (51.9-13.3 (24.1 (11.3) 21.6 (24.9 (10.6 (11.4) 51.7-61.8 (69.5 (11.3 (38.4-142) 134 (116-176) 136 (85.4-19.9 (9.7 (13.7-14.8-42.7) 46.7 (38.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.1 (46.7-90.9-115) 57.4) 21.5 (42.4-42.3) 37.7 (55.7-20.8) 46.8-80.3-34.9-28.6-20.1 (23.7) 25.6) 25. 2007).0-15.6) 58.2) 11.9) 11. adolescents compared with adults.5) 23.7) 11.4-17.8 (50.5-42.4 (11.4 (13.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .S.7 (18.0-90.8-69.8-13.5) 10.2-15.8 (57.6-81.7-397) 70.6) 73.7 (59.1-58.5-58. 2005.2) 11.8) 71.1) 39. 2003).8) 15.0-48. 2003).0 (10.69-11.1 (21.5-16. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al.7) 56.9) 12.9 (29.2-15.8) 24.4-93.3) 89.8-16.2-49.9) 100 (80.7 (19.1 (34.8 (13.8-48.6-40..0) 12. population from the National Health and Nutrition Examination Survey.0-51.6 (57.8) 33.3) 67.5) 17.7-56.9 (24.0) 60.6-26.8) 68.7 (13.1 (53.1) 24.73-12. 2002).0) 15.1-120) 77.1-12.8 (10.7) 38.0) 24.2 (27.7 (21.6-15.2) 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 12.8) 108 (75.3) 29.2-57.9-14.7 (54.4-99.4 (25.9) 24.9) 42.0) Selected percentiles ( 95% confidence interval) 50th 13.7-31.1 (21.7 (12.0 (33.8 (11.3 (13.3 (60.8-27.6-12.3 (35.8) 16.3) 13.0 (12.5) 20.2 (40.8-15.9-23.9 (12.2-51.4) 28.1 (43. In NHANES 1999-2000.5 (49.3) 18.1-12.3) 12.4-90. In an annual sample of German university students.6-47.3) 14.9) Total 14.9-16..6 (19.4-18.1) 17.3-11.4) 13.2) 11.7 (11.5 (10.6 (11.4) 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 12.6 (30. Weuve et al.8-64.7-12.9-13.Phthalates York City (Adibi et al.5) 13.4 (10.9 (15.9) 12.0) 11.5) 95th 77.8 (49.4-27.3 (12.3) 13.8-14.2 (56.9 (10.3) 36.5-31.5-13.4) 60.4-14.6-116) 74.0 (38. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.9 (24.1) 23.8) 33.7-19.5 (56.7 (23. A small study of African-American women in Washington.3 (23. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.1 (21.3 (39..5 (12.0 (41.5-79.1 (15.7-29.9-62.9) 52.0 (49.95-14.5) 78.0-53.2) 67.8 (46.9-69.2 (41.8-85.1) 24.2 (69.4) 90th 50.3) 16.4 (46.5) 14.1 (25.4-23.3) 73.4 (21.4) 17.7-69.7-14.0-26. 2006).9 (12. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.6-86.4-102) 70.5-23.9-40. 2007).5 (10.1) 80.9 (15.5-57.6) 53.1 (18..9 (22. in men attending a Boston infertility clinic (Duty et al.4-116) 73.4-60.6 (36.8-13. and in a small sample of German residents (Koch et al.4-14.9-83.2-13. 2004. 2004).8) 54. in young Swedish men (Jonsson et al.0 (67.8-60.6 (11.1-125) 86.9 (51.1-35.2-17.1 (41.4) 44.7 (11.5 (9.8-15.2-78.7-19.7-15.1 (14.. Hoppin et al.. Hauser et al.8) 26.5-58.5) 46. and females compared to males (Silva et al.6-13.8) 11.8) 80.8-13. 2002.8-173) 195 (121-305) 229 (99.5-38.4 (69.4) 25.4 (33. 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.6) 12.3) 13.1 (13.1-14.1 (13.5) 16.0 (41.8-39.7 (11.9 (55.3-64.8) 56.9 (54.9 (39.0 (13.6 (30.4) 15.1) 27.8 (64. 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.2-117) 95.1) 142 (99.2-21.6 (15..9 (43.4) 12.3-16.0-27.1 (19.1-27.5 (48.2-26.8) 34.7-15.3-38. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-26.1 (9.0-109) 65.1-29.5 (35.1-79.6) 75th 25.1) 35.9) 64.6 (22.0 (62.8) 13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6) 38.4-79.6 (14.8 (12.9) 12.8-34.0) 24. 2005).5-76.9-104) 62.6) 13.6 (34.2-12.

et al. Hauser R. Baird DD. Rossbach B. Duty SM.Phthalates References Adibi JJ. Environ Res 2003. Calafat AM. et al. Barr D.108(10):979-982. Centers for Disease Control and Prevention (CDC). NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Barr DB. Koch HM. Wiesmuller GA. Perera FP. et al. David RM. Schettler T. Sanchez GN. Davis BJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Ryan L. Hoppin JA. Environ Health Perspect 2000. Epidemiol 2005. Giwercman A. Bull Environ Contam Toxicol 2002. Poland. Drexler H.110(5):515-518. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Environ Health Perspect 2006. Available at URL: http://cerhr. Environ Health Perspect 2004.25(2):293-302. Wittassek M. Rylander L. Angerer J. Richthoff J. Research Triangle Park (NC). Camann DE. et al. Silva MJ.93:177-185. Sampson EJ. Ryan L. Jedrychowski W. Meeker JD. Environ Health Perspect 2003. Chen Z. Needham LL. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.S.gov/ chemicals/phthalates/bb-phthalate/bbp-eval.210(3-4):319-333. McKee RH. Reproducibility of urinary phthalate metabolites in first morning urine samples. Int J Hyg Environ Health 2007. Silva MJ. Hodge CC. Levels of seven urinary phthalate metabolites in a human reference population. Silva MJ. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. NTP-CERHR. Singh NP. Third National Report on Human Exposure to Environmental Chemicals.18(1):122. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Hagmar L. et al. Environ Health Perspect 2002. Eckard R. Gans G. Helm D. Atlanta (GA). Hum Reprod 2007. et al. Brock JW. Jacek R.68:309-314. 2000 [online]. Prenatal exposures to phthalates among women in New York City and Krakow. J Androl 2004.nih. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.22(3):688-695. Calafat AM. 264 Fourth National Report on Human Exposure to Environmental Chemicals .16(4):487-493. Butala JH. Koch HM.112(3):331-338. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Brock JW. Caudill SP. Reidy JA.niehs. Urinary levels of seven phthalate metabolites in the U. Jonsson BAG. 112(5):A270]. Hilborn ED. Phthalate monoesters levels in the urine of young children. Blount BC. Hu H. Green RA. Brock JW. Caudill SP. Malek NA. 2005.111(14):1719-1722. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Duty S. et al. 4/20/09 Silva MJ. Pirkle JL.114(9):1424-1431.html. Reprod Toxicol 2004. Weuve J. Needham LL. Silva MJ. Caudill SP. Dobler L.

When total DBP metabolites have been measured.60 (2.5) 23. 2000. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.59) 3.07 (3.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.9-23.30 (1.3-48.90 (4.5) 19.97) 2.6) 26.6-14.20-12.00-6.5) 12.7 (7. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine. Biomonitoring Information Median concentrations reported in the NHANES 19992000. and in a small sample of Japanese adults (Itoh et al..50 (3. 2005).6) 16.4-27.44-2.40 (3.5-24. 2003).9) 10.22) 3.6 (13.50-2.20-2.26 (2.. 2007).6) 16. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.00) 10.00) 6.7) 18.3) 3.5 (11.40-5.60 (5.2-22. In addition.5) 25.17 (2. 2000). and insecticides.5 (20.10-9.40-9.1-25.82-3.S.3 (18.5) 18.30-13.49-2.67 (5.80) 75th 5.9 (16.50) 18.24-8.30-11.00 (5.3-20.20 (6.40-4.17) 4.56 (3.20) 4.1-17.20-9.7 (16.20-6.28-5.70) 3.50-10.5) 14. they have been referred to as monobutyl phthalate (MBP).25) 01-02 03-04 01-02 03-04 01-02 03-04 4.90-2.00-6.7-18.3 (11.1 (8.0 (11. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.72-3.70-4. about 65% to 80% of a dose is eliminated in urine within 24 hours.46 (2.30 (4.0-38.40-3.5) 18.30 (3.50) 8.73-5. and also in some printing inks. Survey Geometric mean (95% conf.5-16.3-24. mostly as MnBP (Anderson et al.S.50-4.0 (13.84) 4.0 and 0.00 (7.40-4.3. 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..46) 2. in a small sample of pregnant women in New York City (Adibi et al.60 (8.00-4.6-26.10 (4.1) 25. 2005.3-30. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.50-6.6 (13. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.43) 6.63) 3.3-43. residents (Blount et al.56-4.10) 8.85-6.6) 12.8) 40.80 (5.40-12.2) 5.55 (3.40 (6.90 (6. 2005).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 2.3 (13.0-25.56) 3.40-17.9) 15.97) 4.10) 2.11-3.10-9.30) 10.6 (14.66) 2.0 (13.56 (5. DBP can produce reproductive toxicity in male rodents (McKee et al.3-19.30-7.2-14.50) 2.2 (12.60-6.80-5.7-31.0) 13.0) 24.0) 12. Studies of children found age-related differences in urine MBP levels.80-5.40 (2.6 (10. 2003).8) 677 652 703 699 1216 1088 Limit of detection (LOD.5 (10.30) 2.50) 7.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.9-14.7 (17.1-12.90) 12.6) 17.40 (7..6 (9.5 (27.7 (18.7 (17.0-18.80 (5.97-7.55) 2. OSHA has established a workplace air standard for external exposure to DBP.10) 11.70-4.1) 16.90-4.00) 7..20 (7. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.3 (19.6-20. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.30) 5.5-29.0-14.80 (3.91) 4.3 (16. Fourth National Report on Human Exposure to Environmental Chemicals 265 .10 (4.6) 17.90 (3.30-6.96) 3.73 (2.00-9..70 (2.4) 22.3) 18.60) 3.7 (9. CDC.40 (2..4-12. Koch et al.6 (10.19-3.80 (2.70 (5.70-8.50 (6.90-4.10) 9. 2004.9 (16.02) 4. pharmaceutical coatings. Following oral administration of DBP to humans.6-18.4) 5.2 (8. 2005).30-2.3 (13.Phthalates Di-n-butyl Phthalate CAS No.50) 90th 12.8) 21.10) 3.20 (3.40) 5.0 (19. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.6 (14.00) 4..30-3.71 (2.4 (14.5 (17.33 (2.7) 15.6-34.1-20.30-6.7) 14.10-2.30) 6.4 (20.60 (4.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.37) 6.00-11.2 (11..1) 22.7-20.3-18.7-31.4) 12.5) 22.00) 4.6 (29.8 (9.20) 7.10 (3.0) 20.7) 4.90-7.70) 5.0) 9. population from the National Health and Nutrition Examination Survey.6) 10. interval) 2. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.40-3.81 (3. in men attending a Boston infertility clinic (Duty et al.5-16. Hauser et al.80 (2.50) 5. 2001).22 (3.30) 10.7) 7.2-33.3 (16.48 (2. 2004.46-5.3) 33. 84-74-2 Di-isobutyl Phthalate CAS No.68 (2.90 (4.20-12.6 (11. NTP-CERHR.46 (3.1 (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.91-6.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.5 (9.33 (3.2) 24.53-5.78) 9.26 (2.95) 10.64-7.21 (5.1) 15.83 (2.55-6.3 (13.22 (2.08) 75th 4.84 (8. than adults in NHANES subsamples during the same time period.31 (7.25) 5.30 (6.42) 2.6 (15.7) 10.1-15.28-13. respectively.32 (3.7) 3.1 (11.9-16.69) 4. 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.1) 11.8-18.76-3.66) 4.35) 3.20-4.72-7.31) 2.15) 3.56-4.7-28.0 (8. 2005).17) 90th 8.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.8 (10.7) 19. Weuve et al.04-5.6) 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 2.18-10. 2007)..38-10.73 (5. 2006).79-8.6 (10.75 (6.05) 2.1 (10.76-15.47-12.11) 5. 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.51) 5.09-2.8-36.6) 13.47-5.81 (6.52 (2.61-3.20-2.99-4.33) 3.56) 2.3) 18.S.79-6.9 (11.13-6.4) 15.3) 16. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.7 (11.1-24.62 (6.0) 11.51) 15.6 (8.51) 2.5) 13.75 (4. 2002.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.0) 3.94-12.02 (7.20 (2.7 (13.95-3. 2007).37) 3.11-2.24) 3. 2004).68 (2.1) 4.20-3.30) 2. samples from German university students had consistently higher median urine levels of MnBP and MiBP.5) 15.18) 3.28 (4.9 (9.8 (9.76 (3.2-13.03 (5.53-4.66) 2.99) 7.98 (2.47 (3.81) 9.8) 10.46 (2.79 (4.80) 7.10-5.33 (2.7 (9. ranging from more than one-tenth the NHANES median (Itoh et al.17 (2.59 (4.52-20.94 (5.78) 8.1-25.54 (2.94) 6.15-4.86-4.9) 12.20 (2.68) 5.. 2004).67-5.81) 4.03-7.36-7.9-26..81 (3.9-40.89-5.54 (4.69-7.84 (4.96 (3.32) 7.45) 3.1-12.0 (12.65 (4.44 (3.00-3.7 (21.88 (2.29-8.26-2.34 (3.38 (6.46) 3.33-9.32 (7. An analysis of NHANES 2001-2002 showed similar age.1) 10.43) 3.53-3.76-3.52-3.18 (1.6 (9.74 (4.89) 6.00) 01-02 03-04 01-02 03-04 01-02 03-04 4..85 (2.66 (8.56-15. 2005). Over this time.18) 4.02-10.72) 5.46-11.6-19.29-3.95) 2.57 (3.69) 6.39-3.54) 2.03-11.68) 3.6) 11.00-3.4 (12.56) 5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.8-18.2-15.20 (7. Survey Geometric mean (95% conf.04) 3.3) 28.3) 13.58-4.78-8.93-6..73) Selected percentiles ( 95% confidence interval) Sample 95th 12.80 (3.00 (3. the students’ median values for MiBP levels remained relatively unchanged.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.6 (12.6 (8.21) 10.62-12..66) 10.01-2.18 (4.07-5.82 (4.2 (10.97-2.64-7.14 (4.82) 4.7) 11.31) 2.27-12.13 (2.92 (7.2) 9.0 (10.74-3.0) 15.65-4.1) 7.36-2.6-19.0-18.80-3.08-2.04) 7.1) 13.86) 6.3) 13.43) 3. In an analysis of NHANES 1999-2000.4) 7.and gender.9 (15.8-13.64-10.65-11. 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) 8.19 (2.00-7.41 (2. up to four and 13 fold. to about two to fourfold higher (Fromme et al.43) 3.52) 3. interval) 2.57 (3.57-4.18-4.58-3. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples..17-12.8 (8.11 (5.0) 7.69 (2.39) 5.3 (17.07 (2.31 (2.4) 23. population from the National Health and Nutrition Examination Survey.2 (11. Between 1998 and 2003. while MnBP declined (Wittassek et al.5 (11.5-19.4-16.89 (3.

1 (36. Survey Geometric mean (95% conf.7-42.7-106) 69.3) 18.1 (16.4-26.4 (23.1 (19.2 (18.6-31.2 (21. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.9-114) 116 (97.1-80.0-51.0-73.6-40.8-132) 95.2) 42.7-20.5) 47.7-34.5 (74.2) 32.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.8 (19.5) 36.7-117) 118 (108-143) 93.4) 59.0-24.7 (28.2-114) 73.2 (58.7-26.6-33.5-60.7-121) 97.3 (17.0) 27.7-92.1 (54.0) 84.3 (30.4 (36.5-121) 106 (94.8-123) 101 (90.9) 71.2) 20.3-40.1 (31.S.2-32.8) 48. Fourth National Report on Human Exposure to Environmental Chemicals 267 .6-48.2 (17.2-159) 92.1) 17.7-111) 64.0 (78.7 (70.2-49.1-24. *In the 1999-2000 survey period.2-63.6) 21.0-24.6 (65.6) 20.3-145) 85.4 (84.5) 17.0 (23.1-27.0) 38.6 (19.6 (48.7 (18.7) 28.9 (79.2) 90th 98.7 (22.2-93.1 (62.1-51.4) 22.6-29.6 (44.6-49.4-31.9-101) 77.9 (20.2-33.2) 26.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.5) 65.9) 36.9) 21.5) 26.2 (74.6 (55.7 (24.4-20.7-34.7 (38.0 (45.9-28.0 (18.2) 68.6-37.0) 120 (98.1-82.9) 29. and 03-04 are 0.4-159) 107 (84.2-21.5-47.0 (31.3) 24.3) 40.5-43. see Data Analysis section) for survey years 99-00.8) 19.6) 35.0) 31.6-143) 127 (99.6-20.6) 80.1 (41.3-85.6 (26.6 (16.0-32.0) 117 (104-131) 112 (84.0 (30.2-22.0) 30.7-124) 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.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.3-76.2 (59.7) 74.1) 31.5) 95.1) 20.6) 17.6-29.5-47.5) 78.0 (15.5-53.1) 47.7-24.6-113) 108 (90.1 (18.8-111) 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 23.0 (25.6-69.5 (29.3 (36.6 (61.1) 23.0 (36.3-21.1-92.5 (30.2 (20.4 (19.1-29.4) 20.7 (19.1 (28.0 (20.2 (79.5) 85. interval) 24.8 (57.7-53.8-29.4 (21.8) 62.5) 40.8-22.5) 37.2 (25.4 (71.4 (35.9) 26.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.8) 43.3) 19.9-42.1 (58.4-25.4.3 (51.1-75.7-116) 95.1 (19.1 (34.4-44.2) 38.6-24.5-117) 95.2-56.3) 26.5) 19.7 (18.4 (25.2 (21.5) 31. referred to as monobutyl phthalate (MBP).6-44.1) 23.4 (35.6) 46.1 (51.1 (19.3-67.1-22.2-24.6 (32.6) 71.5-44.9-87.1) 30.3) 23. population from the National Health and Nutrition Examination Survey.4) 64.4) 52.1 (19.5 (59.0) 21.7 (33.7) 92.0-21.9) 75.3) 36.4-42.4 (35.5) 34.6 (90.2 (75.9-53.3 (23.2) 62.6) 39.5 (28.7) 124 (98.4 (38.9 (17.7 (64.3 (42.1 (26.0-26.4 (72.7-127) 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 22.8) 75th 51.2 (19. respectively.8-42.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.7 (51.2-87.1) 46.6) 38.8-25.1) 25.1) 23.7-42.7) 52.9 (79.7 (43.7 (16.5) 24.0 (72. 01-02.6 (22.5) 21.8) 23.3-136) 137 (107-162) 119 (90.9 (17.7) 42.8-119) 90.6-36.3 (30.0-19.4-60.1 (21.2 (78.3-96.9-33.3-24.5-27.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. 1.4 (35.5 (59.9-22.3-60.0-19.2-23.0 (17.4-18.3 (23. and 0.1) 36.5) 36.9-79.3) 21.1-20.8) 58.0) 20.9) 18.0-58.9) 46.3 (37.9.9-22.9-92.5-42.3 (60.1.1 (17.3 (56.1) 19.5) 20.7-91.3-79.

6) 24.2-86.6-44.6-50.6-24.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9-100) 86.4-24.4 (16.6-23.1) 20.3) 20.8) 23.4 (31.3 (55.5 (14.7-20.8) 35.8) 20.4-61.5-41.2 (38.6-53.7 (60.7-39.5 (30.4) 51.3-21.2 (19.6-32.9 (19.5) 134 (93.6 (17.8 (17.7 (14.8) 13.9) 14.3) 17.9) 28.2) 65.5) 84.7-42.4-47.0-17.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.6-128) 96.9 (21.4) 62.2-22.3 (17.4-76.7 (57.4) 16.7) 20.9) 39. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1-99.8) 19.3-20. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0) 35.3-23.1 (32.9-34.7 (16.6-24.0) 59.7) 42.8 (18.1) 53.0 (52.3) 18.8-24.8 (18.6) 34.0 (61.3) 52.4) 19.6-43.2-21.6) 24.1-83.3 (60.0-19.4-131) 81.2-22.6-74.9 (73.9) 24.4 (23.0 (20.1) 20.0 (18.5-64.0 (69.4) 15.7-37.6-22.8-43.5-21.3-26.9 (30.3 (21.2-18.8-235) 137 (108-198) 88.3 (48.0 (71.2 (35.2) 31.5 (18.8) 28.4 (31.6 (25.4 (17.9-105) 85.7-23.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.9) 20.4-65.5-23.7 (73.3-78.3 (52.7 (28.6-23.9 (30.5) 90th 68.7 (20.7-26.2) 16.1-128) 97.2-179) 84.3 (17.4-164) 96.7 (60.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.9-68.6 (41.3) 67.0-41.9 (35.0) 28.8) 34.7) 19.3) 19.6-119) 63.2-27.2) 74.4 (16.2-85.0 (15.6-44.7-51.6) 65.9-49.6) 31.0-90.4 (45.6) 18.2-61.3 (69.7 (54.7-19.0 (43.0 (70.2-16.9) 49.4 (53.6-92.8 (22.9) 62.3 (24.9 (56.4 (33.5) 82.3-71.5) 60.7-19.3-40.0 (26.9-84.9 (64.1) 22.3-106) 74.4 (68.9-56.6-26.3-21.3-17. Survey Geometric mean (95% conf.7 (27.5-37.9-70.1) 50.6 (74.1) 37.5 (64.1) 44.7-78.9) 91.7 (81.8) 34.1-62.2-22.2) 21. population from the National Health and Nutrition Examination Survey.4 (17.9-68.6 (25.8) 17.1) 35.6) 38.1 (61.5-16.2) 59.0) 26.3-38.9 (35.5) 17.8) 20.8-32.3) 21.8) 75th 38.4 (47.0) 70.4 (50.9) 30.8 (25.0-92.2 (19.3) 19.6) 14.8) 40.3-18.5) 21.S.3 (16.4-103) 117 (83.0) 53.6-16.0-47.7 (19.5-15.4) 15.4-72.2 (16.9 (16.6-27.8) 17.6-19.0) 19.7) 36.4) 20.0 (18.1) 17.9) 52.6 (72.9 (20.8 (33.1) 61.0-38.6) 83.8 (50.3) 33.9 (39.4 (20.6) 23.4 (31.1) 21.6) 37.3 (52.0-113) 104 (83.7 (43.1-99.9-38.6 (61.8 (65.3 (46.8-24.0 (16.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.1) 42.7 (12.0) 81.6 (31.0 (34.2-48.8 (16.7-80.4) 21.6 (57.1-23.4-34.8-23.1 (56.1-21.4 (18.3-32.2-28.2 (83.3-114) 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 17.0 (50.7-21.2-106) 64.6) 25.0) 108 (71.5 (81.6) 64.5-18.0) 41.5-76.4 (56.8) 17.6-42.4 (13.4) 53.1-32.9 (58.5-30.8) 22.5) 39.3 (17.1 (15.0) 75.0-75.1 (29.9 (37.6-155) 91.6 (27.3-81.3) 35.6 (19.2) 159 (102-263) 147 (93.9) 19.4 (37.5 (15.0) 55.0) 94.3 (19.0-60.8) 63.1 (21.2-73.6 (29.8 (13.3 (76.1-18.3) 59.9-14.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.8 (18.0 (19.9 (30.3 (28.1 (46. interval) 22.6) 39.5) 91.3 (42.3-49.4-135) 71.3) 33.5-142) 89.0) 25.0 (27.5-22.4 (50.5 (18.3-39.1 (34.4 (19.6-28.9-26.5-142) 81.9-36.7-28.3 (71.8) 30.0) 29.5-70.

Environ Health Perspect 2000. Koch HM. Prenatal exposures to phthalates among women in New York City and Krakow.114(9):1424-1431. Jacek R. Caudill SP.111(14):1719-1722. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Jedrychowski W. Silva MJ. Rossbach B. Barr D. Angerer J.108(10)979-982. Wiesmuller GA. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Angerer J. Atlanta (GA). Int J Hyg Environ Health 2007. Massey RC.Phthalates References Adibi JJ. Third National Report on Human Exposure to Environmental Chemicals.18(1):122.93:177-185. Urinary levels of seven phthalate metabolites in the U.niehs. Masunaga S. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Brock JW. Environ Health Perspect 2004. Weuve J. Duty SM. Anderson WA.210(3-4):319-33. McKee RH. Needham LL.68:309-314. et al.18(12):10681074. Silva MJ. Duty S. J Androl 2004. Hum Reprod 2007. Singh NP. Chen Z. Hauser R. et al. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Calafat AM. Boehmer S. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Giwercman A. Hagmar L. David RM. Pirkle JL. Wittassek M. Koch HM. Research Triangle Park (NC). Sanchez GN. Scotter MJ. Drexler H. et al. Bolte G. Caudill SP. Calafat AM. 2000 [online]. Drexler H. Meeker JD. Helm D. Hu H. Centers for Disease Control and Prevention (CDC). Jonsson BAG. Levels of seven urinary phthalate metabolites in a human reference population. Sampson EJ. Hilborn ED. Perera FP. Poland. Springall C. Environ Health Perspect 2006. Green RA. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Gans G. et al. Reprod Toxicol 2004. Camann DE. et al.S. NTP-CERHR. Castle L. Needham LL.html.nih. Int J Hyg Environ Health 2005. 2005. Reidy JA. Richthoff J.gov/chemicals/ phthalates/dbp/dbp-eval.210:21-33. Int J Hyg Environ Health 2007. Hodge CC. Rylander L. Silva MJ. Butala JH. Itoh H. Blount BC. Eckard R. Caudill SP.208:237-245. et al. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Ryan L.16(4):487-493. Fromme H. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Koch HM. Environ Res 2003. Food Addit Contam 2001. Available at URL: http://cerhr.22(3):688-695. Epidemiol 2005.25(2):293-302. Silva MJ. Malek NA.112(3):331-338. Barr DB. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Yoshida K. 112(5):A270]. 4/20/09 Silva MJ. Dobler L. Phthalate monoesters levels in the urine of young children. Environ Health Perspect 2003. et al. Bull Environ Contam Toxicol 2002. Ryan L. Schettler T. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Brock JW.

Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. 0.700) . only levels at or above the 90th percentile could be characterized.300-.500) 1.400) 1.300) < LOD .500 (.300 (.400 (.300-.500 (. see Data Analysis section) for Survey years 99-00.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (.600) .300-.400 (.10 (.500) .500) . and polyvinyl chloride.400 (<LOD-. and 03-04 are 0.500 (.600) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.500) < LOD < LOD . respectively.500-. In this Report.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.400 (<LOD-.400-.20) .400-.500 (.200 (<LOD-.200-.300 (.300 (.300-.300-.50) .70) .400 (.500 (. 01-02.400) < LOD < LOD .400 (.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.500 (.00-2.400-. and polymers.2.80) . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500 (.400-.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300-. 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.700) .200-.500) < LOD 1.300-.70) .00) . 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.500) 1.400 (.00 (<LOD-1.10) . and 0.900-1.200-.10 (<LOD-2.500) < LOD < LOD .600 (.300 (<LOD-.600) < LOD .300-.Phthalates Dicyclohexyl Phthalate CAS No.3.00 (<LOD-1.400 (.S.500) .300 (. resins. including nitrocellulose.10 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-3.300 (.400) 1.400) < LOD 1. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.600) . which may vary for some chemicals by year and by individual sample.9.500 (.70 (1. Survey Geometric mean (95% conf.70 (1.300 (.500 (.200-.600) .400 (<LOD-.200-.90) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00 (<LOD-1. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.300-.600) . < LOD means less than the limit of detection. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.50) .200-.400 (<LOD-.400-.500) 1.10 (<LOD-1.300) < LOD .400-. 270 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.700) .400-.500) . polyvinyl acetate.300-.

420-.54) .16 (<LOD-3.S.590 (<LOD-.950 (.36-1.690) < LOD 2.770 (.790-1.830) 1.260-.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.400-.910 (.33 (<LOD-3.330 (.18) .490) .330 (.54 (<LOD-2.880 (.470) 3.530-1.590) 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 .11) . Fourth National Report on Human Exposure to Environmental Chemicals 271 .350-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.690-1.630 (<LOD-.910 (.420-.530) 1.06) .530-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.660) < LOD < LOD .00 (<LOD-3.690) < LOD < LOD .420-.22 (<LOD-1.310-.16) .170-.670 (<LOD-.450 (.770-1.82) .500-.670-1.560) 1.310) < LOD .910 (.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 .240-.33) .710) .380-.480 (.630 (<LOD-.290-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .12-1.53) .470 (.05) .690 (.770-1.620) < LOD .17) .74) .360-.770) < LOD 2.250 (.380 (.740) < LOD < LOD .44) .530 (.34) .800-1.690) < 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 1.500) 3.910 (.220 (<LOD-.400-.67 (1.410 (. population from the National Health and Nutrition Examination Survey.450 (.740) .06) .43 (1.940 (.660) .53) .14 (<LOD-3.10) .54-6.510 (.510-.00) .590 (.500 (.610 (.270) < LOD .82 (1.770-1.370 (<LOD-.390 (.

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. particularly those containing fragrances. Biomonitoring Information MEP levels in the NHANES 1999-2000.1-93. deodorants. 2001-2002.8-111) 85.. and hand lotions.5) 81.3-103) 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.4.7 (70. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. and also in men attending a Boston infertility clinic (Hauser et al. 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. population from the National Health and Nutrition Examination Survey. and 03-04 are 1.3 (82. soaps. Products that may contain DEP include perfumes.2. In contrast. 01-02.2-102) 95. 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 91.4 (62.9-92. 2007). Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.3 (74.9 (61. see Data Analysis section) for Survey years 99-00. colognes.. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.S. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.7) 71. shampoos.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. and 0.9. respectively. DC (Hoppin et al. 0. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples..Phthalates Diethyl Phthalate CAS No. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (71. 2002). 272 Fourth National Report on Human Exposure to Environmental Chemicals . 2003) and African-American women in Washington.

This age-related trend is opposite the direction seen for other phthalates.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7-110) 81. Median MEP levels found in a small sample of German residents (Koch et al.6 (77. 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. population from the National Health and Nutrition Examination Survey. Analysis of NHANES 2001-2002 showed similar findings..0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.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 . 2003) were slightly lower than levels found in NHANES 2001-2002.. In an analysis of NHANES 1999-2000.9 (82.5-114) 101 (87. 2002). Finding a measurable amount of MEP in urine does not mean that