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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4.4.3'.2.1.4'.2'3. Paradichlorobenzene) 1.4.cdc.2'.4'-Tetrabromodiphenyl ether (BDE 66) 2.4.2'4.gov/exposurereport/chemical_selection.4'-Tetrabromodiphenyl ether (BDE 47) 2.6-Heptabromodiphenyl ether (BDE 183) 2. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.3-Dichlorobenzene (m-Dichlorobenzene) 1.5’.2-Dichloropropane 2.What’s New in this Report What’s New in this Report In this Fourth Report.2'.2'. The process for selection is described at http://www.2'.2’. Table 1.1.5.1-Dichloroethene (Vinylidene chloride) cis-1.4. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4'.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4'.4.4'.4.4-Tribromodiphenyl ether (BDE 17) 2.2'.1-Dichloroethane 1.5'-Hexabromodiphenyl ether (BDE 153) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.5'-Tetrachlorobiphenyl (PCB 44) 2.3-Tetramethylbutyl] phenol) Triclosan (2.3.4-Dichlorobenzene (p-Dichlorobenzene. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4.4.1-Trichloroethane (Methyl chloroform) 1.3’.4'-Tribromodiphenyl ether (BDE 28) 2.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .5.5-Pentabromodiphenyl ether (BDE 99) 2.html.4’.3.4'.2'.5.4.2-Dichloroethane (Ethylene dichloride) 1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6.5.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.6'-Hexabromodiphenyl ether (BDE 154) 2.3.2-Dichloroethene trans-1.6-Pentabromodiphenyl ether (BDE 100) 2.1.5'.4.1.2-Dichlorobenzene (o-Dichlorobenzene) 1.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.4’.2'.3.5'-Tetrachlorobiphenyl (PCB 49) 2.2'.

2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Details of this procedure are provided in Appendix A. Percentiles for all three NHANES survey periods (1999-2000. 2001-2002. the presence of an interference) that produced results of inadequate quality.. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods.1). urinary 2. Fourth National Report on Human Exposure to Environmental Chemicals 3 .. Explanations for each change are provided in Appendix B. Data for other pesticides are included only for 1999-2000 and 2001-2002.5-dichlorophenol for the 1999-2002 survey periods. 2003-2004) have been re-computed by use of this improved procedure. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.4-dichlorophenol and 2. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.g. five results that all have the value 90. and these data will be included in the next release of the Report.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.g.

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

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

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

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

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

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

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

7) 75th 79.7 (55.7-64.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61.0-58.3) 86.2-93.6 (56.9-61.4-60. 2004.5) 66. as an absorbent in disposable diapers.5-80. smoking.8 (81.4-76.3 (53.3-71.4) 100 (89. 1994). acrylamide has produced upper airway irritation following inhalation of high levels.6) 90.0 (57.0 μg/kg for adults (FAO/ WHO.2 (58.3 (55.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6 (51.S.6-104) 82. Acrylamide is not thought to accumulate in the body at environmental doses. see Data Analysis section) for Survey year 03-04 is 3. FAO/WHO.8 (52.1-57.8 (57.6) 71. drinking water.2 (75.4 (54.6-61.1 (52.7 (63.1) 62. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. glycidamide. in some sealing grouts.6-75.5 (74. 2005).6-108) 61.2-77. These estimated intakes are hundreds of times lower than occupational exposures.1-64. are heated at temperatures used for frying and baking. 1990. and is either metabolized to the reactive epoxide. 2005). Elimination occurs mainly in the urine as mercapturic acid conjugates.5) 58.1 (88. Natural substances in the food are converted to acrylamide.1 (73. Estimated intakes in children are about twice that of adults (DiNovi and Howard.4-60.9) 63. and binding agents.S. Animal studies indicate that acrylamide is well absorbed.8 (91.1-61. pulp and paper production.0) 57.2-91.0-66.7 (65. Survey Geometric mean (95% conf.2-118) 98.7) 96. 2005.4 (59. In the general population. Fourth National Report on Human Exposure to Environmental Chemicals 11 . it was discovered that acrylamide is formed when starch-rich foods.7 (58.8-57. 2006). population from the National Health and Nutrition Examination Survey. Since acrylamide has limited volatility and high water solubility. mineral processing.7) 73. soil conditioners. In 1997.1 (83.0-49.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.4) 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. People may be exposed to acrylamide from foods.4) 57.6-65. in permanent press fabrics.9) 58. or to glutathione conjugates (Calleman et al. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.9) 75.5 (52.1) 101 (95. FDA.1) 53.. and in some cosmetics.6-66.1) 55.9 (54.5 (79. Recently. gels.6) 73.8-55.4-89. and from dermal contact with products that contain residual acrylamide.5 (44.4 (54.2-70.3) 70.4 (51.7) 54. interval) 61. Fennell et al.Acrylamide Acrylamide CAS No.S.2) 57. but can covalently bind to form adducts with proteins.0 (53. the main source of exposure is from the diet.9-105) 86.4-83.0 (67. and in the synthesis or compounding of dye materials. 2002).9) 57.9 (60. EPA. but are generally above the U.2-67. Tareke et al. such as potatoes and some grains. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.2) 57.0 (69.0) 85..2 μg/kg/day (U. widely distributed in tissues. and well below doses known to cause nerve damage or carcinogenicity in animals. (NTP-CERHR. 2006. 2005). 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.2 (62.5-85.4) 57.3-2. In humans.7-60.4 (53.9 (69.1-64.9-52.0-108) 152 (139-175) 126 (111-142) 108 (86. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.3) 63.7) 58.S. Commercially.1 (47.2-59.7-64. and cosmetics (NTP-CERHR.S. ocular and dermal irritation from direct contact with acrylamide containing materials.6) 50. Polyacrylamides are useful water-compatible polymers used in water treatment. 2005).0.. and an average daily intake is estimated as 0.6 (81. EPA reference dose of 0.2-114) 163 (147-191) 96. 217 million pounds of acrylamide were produced commercially in the U. 2005). and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2004). acrylamide is synthesized and used in the production of polyacrylamide polymer.1) 46. EPA.

4-98. AHA levels have been shown to increase with dietary intake (Hagmar et al.5 (59. uterine. EPA. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.2) 55.3 (56. and neuronal DNA reactivity (Doerge et al.1) 56. 2001).S.Acrylamide occupational exposures..5 (56.. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.7) 74.. 2004.1) 60. Hagmar et al. male germinal cell injury. scrotal.2-68.1-60.4 (56. thyroid.4 (51. Klaunig et al.6 (66.0) 94.. Rice.5 (42.2) 87.3) 59. population from the National Health and Nutrition Examination Survey..who. 2005. reproductive effects (reduced litter size.. EPA at: http://www. 2006). 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..3-101) 95.3) 85. altered gene expression in testicular tissues (Yang et al.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 59.8) 60..0-62.0) 118 (103-126) 121 (112-134) 113 (94. 2005. 2005) have been demonstrated in animals.9 (57. and cancer (mammary. NTP-CERHR.2) 65. although different analytic methods can affect results. IARC classifies acrylamide as probably carcinogenic to humans. and other sites) (FAO/WHO.3) 59. 2005. Vesper 2005) and smoking (Bergmark.8) 45.6-62. Additional information is available from U.7 (61.7 (84.0 (52.1-56. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.0 (70.5-92.5-66.9) 59.4) 46.2 (56.8-48.1 (57.0-93. fetal death.4-59.4 (57.2-90.0 (75. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.. respectively) are markers of integrated acrylamide exposure over the preceding few months. Maniere et al.4 (81. 2006) have been demonstrated after acrylamide dosing. Acrylamide is clastogenic and can produce dominant lethal mutations. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.5) 118 (110-129) 121 (108-140) 136 (124-149) 152 (135-170) 159 (129-204) 172 (157-194) 1841 1954 3044 Limit of detection (LOD..4-65.9-62.5 (83. 2005). Puppel et al.7-86. 2005) and sperm DNA adducts (Xie et al. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. 2002..7 (57. 2005.7-62.7 (87. 2005. 2005. 2006.. Axonal degeneration.S. 2003. 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) 62. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).9-76. Schettgen et al.5-64. Glycidamide has been shown to react with DNA (Doerge et al.4 (61.9-78. 2005. 12 Fourth National Report on Human Exposure to Environmental Chemicals ..8-49.6-64..1-70..pdf.7) 60. U. Mucci et al. 1997..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. Survey Geometric mean (95% conf.7) 61. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.5-94.1 (56.9) 65.4) 53. 2004). 2005). 2009). presynaptic nerve terminal binding (LoPachin. 2005. 2008). 2002.9 (81. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 2005..0. dominant lethality). 2005). After exposure ceases.9 (58.6-90...8-61.5) 87.1 (66.5) 75th 85.epa. interval) 59.9-64.1 (82.8 (44.3) 59.7-64.9) 87. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 1997. EPA. see Data Analysis section) for Survey year 03-04 is 4. 2005. Puppel et al. glycidamide (NTP-CERHR.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.2 (63.int/ ipcs/food/jecfa/summaries/summary_report_64_final. adrenal. U.. 2006).8 (51.1 (70.4) 83. Vesper et al.9-138) 143 (130-159) 96.1-62. Schettgen et al.4-103) 79. 2005. 2008).2 (72. In addition.4 (90. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.3-78.S.2-91. probably through its epoxide metabolite.S.5) 71.7) 90.9) 75.6 (90.0 (80. 2005).9-77.

LoPachin RM. Bergmark E. Bruze M. Doerge DR. Malmberg B. References Bergmark E. 2006. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Magnusson AL. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. et al. Zhang S. gov/~dms/acrydata.3:406-412. Wirfalt E. Chem Res Toxicol 1990. Toxicol 2005. Laurentie M. Calleman CJ. 2009 Jan 8. Haugen M. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Kamendulis LM.561:49-62. Chem Res Toxicol 1997 Jan. Tornqvist M.. smoking habits and gender. Andersen M. Mutat Res 2005. 8-17 February 2005. February. Acrylamide neurotoxicity: neurological.580(1-2):131-141. Mutat Res 2005. Fennell TR.. Mucci LA. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Bergmark E. 2004.Acrylamide In occupational settings. Wu Y.85:447-459. 2001. 64th Meeting: Summary and Conclusions (FAO/WHO).. Summer SCJ. Chicago. morphological and molecular endpoints in animal models. Maniere I. Uncertainties.html#u1004. Beland FA. Alexander J. Bergmark E. Costa LG. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Cheong HK. Twaddle NC.561:21-37.pdf. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Churchwell MI. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Scand J Work Environ Health 2001. Survey data on acrylamide in food: individual food products. Nordander C. Calleman CJ. He F. smokers and nonsmokers. Toxicol Sci 2005. Rosen I. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Doerge DR.580(1-2):157-165.cfsan. 2/3/09 Klaunig JE. Yang JS.10(1):78-84. Becher G. Bjellaas T. Churchwell MI. He F. Bridson WE. Available at URL: http://www. 1994). Determination of hemoglobin adducts in humans occupationally exposed to acrylamide.43:365–410. Fennell TR. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR).pdf. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Available at URL: http://cerhr. July.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. [Epub ahead of print] Dybing E. Food Chem. Kautiainen A. The Updated Exposure Assessment for Acrylamide. 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. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Hagmar L. In another study. NIH Publication No. 1993. et al. Osterman-Golkar S. Rome. et al. Paulsson B. April 13-15. Toxicol Sci. 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. Tornqvist M. Calleman CJ. da Costa GG. J Agric Food Chem 2008. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.27(4):219-226. Food and Drug Administration (FDA). 054472. Toxicol Appl Pharmacol 1993. Spicer R. Italy. et al. CFSAN/Office of Plant and Dairy Foods. Available at URL: http://www.126(2):361-371. National Toxicology Program. McDaniel LP. 2005. et al. Tian G. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Mutat Res 2005. Costa LG. Granath F.niehs.who. Metabolism and hemoglobin adduct formation of acrylamide in humans. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Adv Exp Med Biol 2005. Guffroy M. Mechanisms of acrylamide induced rodent carcinogenesis. 2001). Joint FAO/WHO Expert Committee on Food Additives..fda. Adv Exp Med Biol 2005. Duale N. Illinois. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Snyder RW. Paulsen JE. Acrylamide intake through diet and human cancer risk. 6013-6019. 2/3/09 Perez HL.580(1-2):119-129. Human exposure and internal dose assessments of acrylamide in food.Toxicol Appl Pharmacol 1994. 2/3/09 Hagmar L. Burgess J.gov/chemicals/ acrylamide/Acrylamide_Monograph. Axmon A. Farmer PB. DiNovi M and Howard D. Wilson KM.120(1):45-54. 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.56.nih. Hagmar et al. and Research Strategies. Aprea P. Perez et al. 1999). Godard T.

Drexler H. Office of Pollution Prevention and Toxics. The carcinogenicity of acrylamide. Agudo A. Jin Y. September. Angerer J. Letzel S. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Licea-Perez H. Hallmans G. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.txt.epa. Vesper HW.epa. revised 1/3/06. propylene oxide. Liu Y. Tjønneland A. Myers GL. Ingham L.20(6):959-64. U. et al. Drexler H. 14 Fourth National Report on Human Exposure to Environmental Chemicals . U. Smith A. Available at URL: http://www. Int J Hyg Environ Health 2003. Broding HC. Karlsson P.134(1-3):65-70. Mutat Res 2005 Feb 7. Rossbach B. Lee SH.50(17):4998-5006. Chemical Summary for Acrylamide. Environmental Protection Agency (U. et al. Toxicological effects of acrylamide on rat testicular gene expression profile. EPA). Available at URL: http://www. Toxicol Lett 2002. Adv Exp Med Biol 2005.580(1-2):71-80. Marko D. Schettgen T.207(6):531-9. Integrated Risk Information System (IRIS). Meyers T. Kutting B. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. a carcinogen formed in heated foodstuffs. Chae C. Eriksson S.gov/chemfact/s_acryla. Liu K. Hemoglobin adducts of ethylene oxide. Fueller F.S. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.Acrylamide glycidamide by gas chromatography-mass spectrometry. Rapid Commun Mass Spectrom 2006. Vesper HW. Puppel N. Meyers T. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. 2/3/09. Yang HJ.S. J Agric Food Chem 2008. Xie Q.S. Int J Hyg Environ Health 2004. Angerer J. Rydberg P. Angerer J.163(2):101-8. Ospina M. Benetou V. Reprod Toxicol 2005. Schettgen T. Choi JH. Han DU. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Tornqvist M. Weiss T.274(1):59-68. Ding X.561:89-96.56(15):6046-53. EPA).S.19(4):527-34. Tjaden Z.htm. Acrylamide. Tareke E. 1994. Washington (DC). Mutat Res 2005. J Agric Food Chem 2002.gov/iris/subst/0286. Gray JG. Sun H. 2/3/09 Vesper HW. Anal Biochem 1999. Toxicol Lett 2006. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Schettgen T. Han CH.580(1-2):3-20.206(1):9-14. Slimani N. Drexler H. Fu D. Lee MH. Ospina M. Rice JM. Analysis of acrylamide. Environmental Protection Agency (U.

071) .060) .077) .100-.080-.76 (1.087-.990) . 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.131 (.580) .061) < LOD .88 (1.95) 1. and 0.580-1.860 (.350 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.050) .20 (1.175 (.63 (2.920 (.Cotinine Cotinine CAS No.110) . < LOD means less than the limit of detection.670) .015 ng/mL.19-2.660) .99) 2.14) .68) 2.42 (1.09-2.068) .150) .188) .570 (.900-1.44) 2.310) 90th 1.740-1.050 (<LOD-. Cigarettes contain about 1.110-.050-.070 (<LOD-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.050) .15 (2.70-2.05.163 (.96) 2.164 (.190-.077) . and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.180 (.059-.076-.108) * . Children exposed to ETS are at increased risk for sudden infant death syndrome.990 (. and 03-04 are 0.710 (.44) 2.062 (.910-1.120 (.180) .428-.93) .140-.520 (.020-.187) .12-4.01 (1.120-.198) * . 2004).01) 3.030-.600-1.05) 1.140-.5% nicotine by weight (Kozlowski et al.09-3.11) .23 (1. respectively.310) .26-1. 2006).21 (.S. cardiovascular disease.533-.066) .110 (.080 (. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.260-1.32-2.063) .50-4.66-3.052 (<LOD-.630 (.625) .17 (1.216 (.00) 1.43 (1.040-.44 (2.14) .047-.68 (1.130) .450-.120 (.12 (1.300) .213) .120 (.77 (1.20 (.430-1.00) .197) .630 (.30) 2.410) .160) .02) 1.770-1. population from the National Health and Nutrition Examination Survey.047-.075 (. 1998).180) .48-3.820) . Fourth National Report on Human Exposure to Environmental Chemicals 15 .137 (.050 (<LOD-.500 (.96 (1.230 (.071 (.110 (.75) 1.60-2.39 (1.350-.70) 2.57) 2.770) . which may vary for some chemicals by year and by individual sample.230) .84-3.800 (.55-2.150) .110 (.066-.200) 1.20) .060-.23-2. acute respiratory illness.840) 3.050 (.480-.88 (.690 (.34 (1.19) 1.50 (1.052 (<LOD-.580 (.960-1.32) 1.05 ng/mL.997-3.160) .260) 1. 2004).080-.99) 2.20-2.S.030-.015.089) Age group 3-11 years 99-00 01-02** 03-04 .12) 1.92 (1.28-1.070) . producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.730 (.14-1.621-1.190-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .120 (.68) .32-2.55 (1.02) 1. see Data Analysis section) for Survey years 99-00.77 (1.030-.81-2.15) 2.160 (.33-2.164 (. stroke.124 (.620 (.950-1.140 (.070) .850 (.060-.570-1.54 (1.120-.080) < LOD < LOD .080) < LOD .23 (2.87-3.163) .220) . and various other disorders (U.50) 3.060 (<LOD-.66) 1. maternal exposure during pregnancy can result in lower birth weight.47-3.308 (.280 (.950 (.160-.087) < LOD < LOD .620-1.059-.350-.505 (.45) 1.77 (2.060 (.42-4.068) .220-.154-.120) .12 (2.148-. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.54) 1.770) .210 (.480-1.78) 2. 83% of measurements had an LOD of 0. emphysema.110) .126) .040-.17) .190-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .030 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.930 (.160 (.234) .17 (.130 (.540 (.180) .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 .070-.65 (1.066 (.310-1. DHHS.087 (.360) .054 (.28) .106-.110 (.144 (.18-3.086 (.20) 1.040 (.080-.070) 75th .94) 1.060 (<LOD-.85 (1.49) 1.09-3.66 (1.53 (1.104-.043-.050-.058 (.30) 2.073) < LOD .62 (2.050 (<LOD-.400-.142-.137-.S.370-.44 (1.145) . and exacerbated asthma (U.110-.320) .090-.23 (.89) 1.180 (.62) 2.310-1.110-.080-.38-2.040 (.312) .79) 3.726) .48-2.153-.740-1.39) 3.094) .02 (.30) * .193) . 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.160 (.140 (.83-2.180) .96-4.470-.088-. ** In the 2001-2002 survey period.057-.19) .040 (.16) .060 (.22) 2.35 (2.630 (.54 (1. Survey Geometric mean (95% conf.53-4.302) .49) 1.540-.084) .053 (<LOD-.220) .510 (.050 (<LOD-.40) .120 (.201) .04 (1.060-.506 (.167 (. and 17% had an LOD of 0.139) * .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.111-.790) .63-2.21-1.090-. DHHS.50-1.110 (. ear problems. acute respiratory infections.21-1.115-..090-.180) .240 (.080 (.

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

Warner K. Jacob P III. Herrera B. 4/13/09 National Cancer Institute (NCI). Racial/ethnic differences in serum cotinine levels among adult U. Coordinating Center for Health Promotion. Atlanta (GA): 2005.iarc. 4/13/09 Centers for Disease Control and Prevention (CDC).4:313-316. Schwartz SS. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Turner DM. Etzel RA. Third National Report on Human Exposure to Environmental Chemicals.cancer. Respiratory nicotine absorption in non-smoking females during passive smoking. Houseman TH. JAMA 1996. Sweeney CT. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Int Arch Occup Environ Health 1991. Available at URL: http://monographs. Exposure of the U. Absorption and metabolism of nicotine from cigarettes. Jacob P III. Schober SE. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Office on Smoking and Health [online] 2006.gov/ntp/roc/eleventh/profiles/ s176toba. Available at URL: http://ntp. Kira S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Pirkle JL. Pharmacol Rev 2005. et al. J Pharmacol Exp Ther 1999. Tob Control 1998. Flegal KM.94(2):314-320. Benowitz NL.56:483-493. Mowery PD. the United Kingdom. BMJ 1975. Benowitz NL.php. Ethnic differences in N-glucuronidation of nicotine and cotinine.fr/ENG/Monographs/allmonos90. Department of Heath and Human Services. 11th ed. Kozlowski LT. 1999. Brody DJ. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. In Report on Carcinogens. Lewis PJ. Environ Health Perspect 2006. Pechacek TF. Jacob III P. Perez-Stable EJ. Benowitz NL. Tobacco related exposures.S Department of Health and Human Services (U. Jarvis MJ.S.pdf.niosh.fr/ENG/Monographs/ allmonos90. 4/13/09 International Agency for Research on Cancer. DHHS).63:139-43. Metabolism and disposition kinetics of nicotine.7:369-375. Pickett MA. Soliman S. Pollack HA. Vol 83. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. National Institute for Occupational Safety and Hygiene (NIOSH). Centers for Disease Control and Prevention.S. and the United States.18:188-204. Hukkanen J. Summary of Data Reported and Evaluation [online] 1986.15:302-307. Dollery CT. [online]. Tobacco Smoke. 1999-2002.cdc. Vogler GP.S Department of Health and Human Services (U.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Curtin LR. Benowitz NL. Bernert JT.nih. Brody DJ. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. U. Available at URL: http:// cancercontrol. 1988-1991. population to secondhand smoke: 1988-2002. U.275:1233-1240.gov/tcrb/monographs/10/. Tob Control 2006. 4/13/09 Perez-Stable EJ. Pechacek TF. June. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.S. Richter PA. Herrera B. JAMA 1998. Nicotine metabolism and intake in black and white smokers. References Armitage AK. Benowitz NL. Clin Pharmacol Ther 1994. Epidemiol Rev 1996. Tobacco Smoke and Involuntary Smoking. Maurer KR.gov/library/ secondhandsmoke/. Caraballo R. National Toxicology Program (NTP). 4/13/09 Iwase A. U. Am J Public Health 2004. Summary of Data Reported and Evaluation [online] 2004.S. Bernert JT. Caudill SP. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. et al.114(6):853-858. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.291(3):1196-1203. 4/13/09 U. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.gov/eid/rmca/critdocs/ criteriadoc/33. IARC Monogr Eval Carcinog Risks Hum. Available at URL: http://monographs. Aiba M.php. JAMA 1998.280:135-140. Department of Heath and Human Services. Strauss WJ.surgeongeneral. DHHS). IARC Monogr Eval Carcinog Risks Hum. Giovino GA. Giovino G. Modin G. available at URL: http://mtn. Sosnoff CS. Centers for Disease Control. Pirkle JL. Coordinating Center for Health Promotion. 1988-1991. Fong I. Centers for Disease Control and Prevention.niehs. cigarette smokers: the Third National Health and Nutrition Examination Survey. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.S.280:152-156. iarc. 1991. Jacob P. International Agency for Research on Cancer. Cotinine as a biomarker of environmental tobacco smoke exposure. Vol 38. Available at URL: http://www.57(1):79115. George CF. Mehta NY. National Center for Chronic Disease Prevention and Health Promotion. 2004.S.pdf. Trends in the exposure of nonsmokers in the U. Smoking and Tobacco Control Monograph 10 [online].S.

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

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .120-.100 (<LOD-.EPA.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110-.epa.270) 688 678 518 700 598 956 Limit of detection (LOD.130 (.110 (. One survey detected DEET in 74% of sampled streams in the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190) < LOD .520) < LOD ..120-.100-. (Kolpin et al.140) < LOD . About 3-8% of dermally applied DEET is absorbed.S. and it has not been rated by IARC or NTP with respect to human carcinogenicity.170 (.140-. 2003).560) < LOD .N-Diethyl-meta-toluamide (DEET) N. 1995. DEET has low acute toxicity.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 .100-.110 (. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. Fourth National Report on Human Exposure to Environmental Chemicals 19 .1.220 (.gov/pesticides/. DEET is also used in combination with dermal sun screens (U.S.150) < LOD .EPA. DEET is not a developmental or reproductive toxicant in animals (U.S. DEET is not genotoxic. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.100-.130-.210 (. Survey Geometric mean (95% conf. EPA. and they range in concentration from 4% to 100%.100-. including seizures and encephalopathy. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.N-Diethyl-meta-toluamide (DEET) CAS No.170 (. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.250) < LOD .110-.130 (.100-.130) < LOD . There are over 225 insect repellents brands containing DEET.180 (.130-.140) < LOD .N.140 (.110 (. After absorption.110 (.449 and 0.180) < LOD . Its use is recommended for prevention of several vector-borne diseases.S.130) < LOD .240) < LOD .140) < LOD . 2002).110 (<LOD-. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. 2005).180 (. have been reported as result of self-poisoning by ingestion or excessive dermal application. 134-62-3 General Information N.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 .130-..180 (.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 . 1998). DEET is not registered for use on agricultural commodities. 2002).S.EPA at: http://www. (U. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.130-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2003). DEET can be applied to clothing and the skin to repel biting insects.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample. Sudakin and Trevathan. population from the National Health and Nutrition Examination Survey. Neurological effects in humans. Urinary N.110 (<LOD-. < LOD means less than the limit of detection. Additional information is available from U.100-. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.130 (.. 1998).S.160) < LOD .

500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.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 .190-.150) < LOD .250) < LOD . Urinary DEET levels as high as 5.270 (.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.270 (<LOD-.390-.240) < LOD .490) < LOD .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2005).270-. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.300 (.330 (.230-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .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 .350) < LOD .350) < LOD ..280-1.300) * * 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 .330 (.320 (.630) < LOD .150-..640 (.200 (.93) < LOD . Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect. 2007).250 (.410 (.250-.170-. Survey Geometric mean (95% conf.240-. 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.190 (.280 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.270) < LOD . representative subsamples from NHANES 2001-2002.290-.320) < LOD . the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500 (.S. population from the National Health and Nutrition Examination Survey.190 (<LOD-. Urinary N.N.410-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410 (. 20 Fourth National Report on Human Exposure to Environmental Chemicals .350-.130 (<LOD-.480 (. In this survey period.S.440) < LOD .190 (.370-. 1992).230) < LOD .140-.230-.370) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.

Fundam Appl Toxicol 1995.16(1):10-13. J Anal Toxicol 1992. Washington (DC): U.gov/oppsrrd1/REDs/0002red. Furlong ET. and other organic wastewater contaminants in U.EPA. Chemical Summary. Available at URL: http://www. Barr DB. Environ Health Perspect 2007.N.S. Veltri JC. Zaugg SD. 1993-1997. Toxicity and Exposure Assessment in Children’s Health. 1999-2000: a national reconnaissance. EPA 738-R98-010.2:341352. Tapia J. Thurman EM. Smallwood AW. 2005 Kolpin DW. pp. September 1998. et al. Quandt SA.41(6):831-839. Selim S.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Trevathan WR. N. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Osimitz TG.N-diethyl-mtoluamide following dermal application to human volunteers. hormones. Environmental Protection Agency (U. 4/9/09 U. U. Schoenig GP. Atlanta (GA). Int J Toxicol 2002. streams. Environmental Protection Agency (U.25:95-100. Available at URL: http://www. Lowry LK. and excretion of N. 2005.epa.S. Bell JW. Centers for Disease Control and Prevention (CDC). Pharmaceuticals.S. U.EPA).N-Diethyl-meta-toluamide (DEET) References Arcury TA. EPA. Grzywacz JG.S.S. Gabriel KL.gov/teach/chem_summ/ DEET_summary. DeBord KE.36(6):1202-1211. Sudakin DL. pdf. Chen H. Page BC. Hartnagel RE Jr.S. Barber LB.epa. Diethyltoluamide (DEET). J Toxicol Clin Toxicol 2003. Environ Sci Technol 2002. Third National Report on Human Exposure to Environmental Chemicals. Human exposures to N.pdf. metabolism.EPA). 1-118. DEET: a review and update of safety and risk in the general population.115(8):1254-1260. Reregistration Eligibility Decision (RED): DEET.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography.S. Absorption. Meyer MT.

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

Bisphenol A.14(2):149-157.jrc. Zacharewski TR.59(4):403-408. Needham LL. Serizawa S. Wong LY. vom Saal FS.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt.145:592-603. MacLusky. Joint Research Centre Institute of Health and Consumer Protection. Human Health.116(1):39-44. Italy. Occup Environ Med 2002. Munro IC. Endocrinology 2008. Department of Health and Human Services. Rhomberg et al. Yang M. J Am Dent Assoc 2006.149:988-994.S. Hughes C.pdf. Ekong J. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Rubin C. Kolpin DW. Park S. Kroes R. Environ Health Perspect 2005.36(6):1202-1211.pdf . Sottas CM. Nippon Eiseigaku Zasshi 2004. DirectorateGeneral Health and Consumer Protection.pdf. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Arakawa C. Chem Res Toxicol 2001. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Belgium.europa. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. and other organic wastewater contaminants in U. Chung MK.eu/ health/ph_risk/committees/sct/documents/out156_en. Ye X.113(4):391-395. bisphenol A glucuronide.68(1):121-146. Available at URL: http://cerhr.. 2003.nih. Calafat AM. Hum Ecol Risk Assess 2004. Thurman EM. et al. Needham LL. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Kiguchi M. NC. Fujii S. Koulova AI. Calafat AM. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Shin HC. Thomas BF. C. National Toxicology Program. Ecotoxicity and the Environment (CSTEE). Tyl RW. Klinefelter GR.J. Doull J. 2002. 2008. Exposure of the U.pdf. Kuklenyik Z. Ikka T. Howdeshell KL. Zaugg SD. Furukawa M. Han SS. 2/4/09 Fujimaki K. Gender differences in the levels of bisphenol A metabolites in urine. Cunha G. J Chromatogr B Analyt Technol Biomed Life Sci 2002. and Hardy MP. Kim YH. Szigeti-Buck. September. Pyo MY. Ispra. Barber LB. Hanaoka T. Barr JR. August 2001. Harazono A. Marr MC.69(22):2611-2625.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. 4. hormones. Brine DR. European Commission. niehs. Bradley S. et al. Haighton LA.10:875-921. In vitro and in vivo interactions of bisphenol A and its metabolite. 5: 505-523. Lynch BS. National Institute of Environmental Health Sciences. Matthews JB.nih. 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. An evaluation of the possible carcinogenicity of bisphenol A to humans. National Institutes of Health. Reidy JA. Keimowitz AR. niehs. Cha SW. 2/4/09 European Commission.780(2):365-370. Myers CB.gov/chemicals/bisphenol/bisphenol. Koh WS. Gray GM. Leranth. Twomey K. Life Sci 2001.. Available at URL: http://cerhr.S. Environ Health Perspect 2008. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Environ Sci Technol 2002. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Available at URL: http://ecb. U. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Watanabe S. Tsugane S. 1999-2000: a national reconnaissance.137(3):353-362. Meyer MT.35(2 Pt 1):238-254. Proc Natl Acad Sci USA 2005. Barr DB. Brussels. Cohen JT.312(2):441-448.Scientific Committee on Toxicity. Hara K. May 22.. streams. with estrogen receptors alpha and beta. Toxicol Sci 2002. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.gov/chemicals/bisphenol/BPAFinalEPVF112607. Timms BG. K. Furlong ET. Kim CS.pdf . 2/4/09 Ouchi K. November 26. 2007. Reidy JA. Ema M.Environmental Phenols References Akingbemi BT. Imai H. Joskow R. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats.nih. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents.niehs. Needham LL. Kawamura N. Han SY. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Richter CA. McConnell EE. Caudill SP. Reprod Toxicol 2001. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population.S. Watanabe C. Regul Toxicol Pharmacol 2002. Yoshinaga J. Kim JC. Research Triangle Park. et al.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Endocrinology 2004. T. Available at URL: http://ntp. N. Calafat AM.102(19):7014-7019. Biochem Biophys Res Commun 2003. Available at URL: http://ec. Barton L. Pharmaceuticals. Hlywka JJ. and Hajszan. Rat two-generation reproductive toxicity study of bisphenol A.59(9):625-628. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy.

Chem Res Toxicol 2002. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Biological monitoring of bisphenol a in a Korean population. Witorsch RJ. bisphenol-A. Hughes C. vom Saal FS.44(4):546-51. Chuang JC. Food Chem Toxicol 2002. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Dekant W. Environ Res 2007. et al.113(8):926-33. Vom Saal FS. Jang JY.Environmental Phenols Volkel W. Kim SY. Chang SS. Lordo RA. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Arch Environ Contam Toxicol 2003. and nonylphenol at home and daycare. Filser JG. Yang M. Nagel SC. Csanady GA. Large effects from small exposures. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Welshons WV.103(1):9-20.40(7):905-12. An observational study of the potential exposures of preschool children to pentachlorophenol. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Sheldon LS. Kawamoto T. Morgan MK. Colnot T. Lee SM. Wilson NK. III.15:12811287. Endocrinology 2006. Environ Health Perspect 2005.147(6 Suppl):S56-69.

3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.500) . Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.Environmental Phenols 4-tert-Octylphenol CAS No..500-1.600-1. is used to manufacture alkylphenol ethoxylates.300 (<LOD-.20 (1.60-3.30 (..60) 1.299-.50-2.S.600) .600) 1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression..50) .30 (1..200-. 1997.50-3. During the 1980s and 1990s. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.600-1.20-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.50 (1.300 (<LOD-.400 (. 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.900 (. 2002).30 (1.50) . and to alkylphenoxycarboxylates.80 (1.500) .5% of 139 U.900 (.10) 1.g. textiles. < LOD means less than the limit of detection.70 (1. testicular atrophy.90) 2.497) * .400 (. industrial cleaners. and was quickly eliminated from the blood (Certa et al.600-1.40) 1.. see Data Analysis section) for Survey year 03-04 is 0.00) 1229 1288 03-04 03-04 03-04 * .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 . Saito et al. through sewage.60) 613 652 1092 Limit of detection (LOD. Katsuda et al.400) 1.357 (.80 (1. In rats..200-.900 (.300-. altered estrus cycles and reproductive outcomes.30) 2.500) 75th .40) 2.300 (<LOD-. orally administered 4-tert-octylphenol was well absorbed.90) 2.10 (1. The alkylphenol ethoxylates enter the environment through human use of products containing them.60) . 2002). leading to inhalation as another potential exposure route (Rudel et al.30 (1.20-2. In the 1990s.900 (. Several alkylphenols. 2000.507) * < LOD . the various alkylphenols have also been used as emulsifiers and modifiers in paints. Ying et al. streams in 30 states (Kolpin et al.274-. and through manufacturing waste streams (Warhurst. 34 Fourth National Report on Human Exposure to Environmental Chemicals . They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). to shorter chain alkylphenol ethoxylates. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. and emulsifiers.000 tons of alkylphenol ethoxylates were produced annually worldwide. Less frequently. and impaired spermatogenesis (e.50) 1.700-1. 1995.20) 1.800-1.. 2004). altered neonatal sexual development. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.300-.60-3.70 (1.20-2.00 (.40) 2. and some of their degradation products are toxic to aquatic life. Disposition in humans has not been studied sufficiently.30 (1. Bian et al.. 140-66-9 General Information 4-tert-Octyphenol. did not bioaccumulate.60-3. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.60-3.60-3. which may vary for some chemicals by year and by individual sample. and some personal care products. The alkylphenols can bioaccumulate in some fish.70 (1. 1996).40) * 03-04 03-04 03-04 . Indoor and to a lesser extent.10 (.600) .1. pesticides. including 4-tert-octylphenol.10 (.600) .20-2.50) 1. impaired steroidogenesis.50) 1. Urinary 4-tert-Octylphenol (4-[1.369 (. an alkylphenol.477) . 2000.00 (.40 (1.600-1.30) 1.g.00 (1. which are anionic surfactants used in detergents.300 (<LOD-. Laws et al. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.500) . Blake and Boockfor. have demonstrated estrogenic effects particularly when injected at high doses in animals. 2003.30-2.40) 1.S.500 (.70 (1. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.80 (1.2. In 1999-2000. 2006.80) 2..20-2.300 (<LOD-.20-2.600-1.30) 90th 1.389 (. Survey Geometric mean (95% conf.600-1.. fish) and drinking water. and from contact with some personal care products and detergents. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 2.500-1.3. 4-octylphenol monoethoxylate was detected in 43.400 (.900 (. and the polyethoxy chain may consist of up to 50 ethoxy units.268-. population from the National Health and Nutrition Examination Survey.60-3.10) 2.10-2.20) 314 715 1488 03-04 03-04 * * . over 500.

770 (. In a small number of adult Japanese volunteers.410 (.54) * 03-04 03-04 03-04 . the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.890-2.25) 2.269 (.320 (<LOD-.00 (.349) * < LOD .33 (2.03 (1.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.64 (.300 (<LOD-.40 (1.00) 2.470-1.59 (1.400) .S.170-.450) .450) 1.71) 2.60 (1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. representative subsample of NHANES 2003-2004..67-2.740 (.06 (2.530) .640-1.11) 2.25) 90th 1. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.36-3.11) 1. at lower or environmentally relevant doses (Blake et al. 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.81 (1.31-2.620) .33) 3..160-.43) 1. Nagao et al.15) 1..14) 314 713 1487 03-04 03-04 * * .570) .384) * . Sweeney et al. 1999).43) 1.96-4.62) .40-4.3.62 (1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.85 (1. 4-tert-Octylphenol is not considered directly genotoxic.435 (.630-1. Survey Geometric mean (95% conf.610) .910 (. 2004.276 (.53-3.29) 2.470-1.31 (1.207-.10-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.470) 75th .41) .22) .420) .78) 1228 1286 03-04 03-04 03-04 * . Yoshida et al.620-1.850 (. 2001. 2000. or their corresponding ethoxylates with respect to human carcinogenicity. population from the National Health and Nutrition Examination Survey.59) 1.370 (<LOD-.270-.199-.260 (<LOD-.860 (.560) .. 2005.337-.68-2.00) 2. Kawaguchi et al.18-4.65-3.43-3.730-1.550-1. It is unclear if estrogenic or other effects occur in animals through oral dosing.03-6.1.540-1. Urinary 4-tert-Octylphenol (4-[1.280-. 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. 2003.S.00 (.73) 2.05-2.740 (.68) 2.76 (2.78 (1. Fourth National Report on Human Exposure to Environmental Chemicals 35 .500-1. 2001).78) 3.02-4. 2004).08) 1.11-2.62 (1.. IARC and NTP have not rated octylphenol.03 (1.00) 1.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .20 (1.270 (.Environmental Phenols Myllymaki et al.270 (. Tyl et al. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U. nonylphenol.50 (2.25-2.460 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Calafat et al.17 (.380 (<LOD-.

Yoshida M. Makino T. pesticides. Anal Chim Acta 486:41-50. Fedtke N. Two-generation reproduction study with para-tert-octylphenol in rats. Ono H. Wiegand HJ. Nicol L. Cooper RL. Sweeney T. Bolt HM.15(6):683-692. Myers CB.foe. Biol Reprod 1997. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Laws SC. Estrogenic activity of octylphenol. Takai N. Nair-Menon JU. Horie M. polybrominated diphenyl ethers.141(7):2667-2673. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Camann DE. Marr MC. Katsuda S.14(5):325-332. Usumi K.28(3):215-226.116(1):39-44. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Paranko J. Toxicol Sci 2000. Furlong ET. Available at URL: http:// www. Rudel RA. et al.37(20):4543-53. and testosterone. Needham LL. Yoshimura Y. Exposure of the U. Toxicol Appl Pharmacol 2000. Arch Toxicol 1996. Watanabe G. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Pharmaceuticals. and sertoli cell number. et al. Blake CA. Ye X. bisphenol A and methoxychlor in rats.799(1):119-125. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. 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. Kookana R.Environmental Phenols References Bian Q. Song L. Zaugg SD. et al. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. 2003. Barber LB. Regul Toxicol Pharmacol 1999. Toxicol Lett 2001. Environ Health Perspect 2008. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Onuki A.S. Calafat AM. Brine DR. alkylphenols. Saito I. Food Chem Toxicol 2006. Ito R.121(1):21-33.44(8):1355-1361. Reprod Toxicol 2004. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Yoshimura S. Seto H.folliclestimulating hormone. Kawaguchi M. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Blake CA. Boockfor FR. et al. prolactin. 2/4/09 Ying GG. Kolpin DW. and other endocrine-disrupting compounds in indoor air and dust. Carey SA. Watanabe G. Millette CF. 1995. Bodman GJ. Kawaguchi M. Saito Y. Phthalates. Endocrinology 2000. Korn LR. Roche JF. Williams B. Qian J.uk/resource/reports/ethoxylates_alkylphenols. Xu L.30(2 Pt 1):81-95. Certa H. Wong LY.57(2):255-266. Inoue K. hormones. testis size. Maekawa A. Chen J. Sakui N. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Haavisto TE. Takenaka A.S. Nakagomi M. Tyl RW. Karjalainen M. Boockfor FR. streams. Spengler JD.co. Environ Int 2002. Reidy JA. Katsuda S. Brody JG. Toxicol Appl Pharmacol 2005.pdf. Fail PA. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. 1999-2000: a national reconnaissance. Raychoudhury SS. Seely JC. Thurman EM. Maekawa A. Environ Sci Technol 2003.207(1):59-68. Myllymaki SA. Ferrell JM. Muller AM. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Reprod Toxicol 2001.18(1):43-51. Meyer MT.71(1-2):112-122.165(3):217-226. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Inoue K. McCoy GL.36(6):1202-1211. Nagao T. nonylphenol.54(1):154-167. Izumi S. Taya K. Yoshida M. Warhurst AM. Taya K. Okada F. Wang X. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Indoor Air 2004. Toppari J. Indoor air pollution by alkylphenols in Tokyo. Brooks AN. and other organic wastewater contaminants in U. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Environ Sci Technol 2002.

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

S.9-61.7) 10.3) 47. Survey Geometric mean (95% conf.22-10.4) 25.4) 7.29-12.6-14.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.3.43-13.4) 51.6-20.1 (8.4 (11.5 (11.20-13.0-19. see Data Analysis section) for Survey year 03-04 is 2.00 (4.5-86.1) 9.20-11. population from the National Health and Nutrition Examination Survey.1) 13.4) 73.4.9 (50.8) 14.1) 14.2 (13. interval) 12.5) 13.2 (37.11-11.3-67.4 (38.0-15.0 (11.4) 317 (231-433) 144 (96.45-10.4) 357 (225-456) 203 (87.3) 10.50) 10.0-15.10) 84.S.6) 12.0-73.21 (6.45 (5.94 (7.45-13. interval) 13.6-37.1 (45.93 (7.9) 75th 47.6-14.5) 66.3 (26.6 (9.50-10.3-31.7 (9.6-65.80 (5.7 (39.6) 39.6) 31.6-111) 33. Urinary Triclosan (2.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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 9.10-9.00-8.5) 20.3 (9.3-35.4.1) 9.30-14.7 (11.40-17.2-46.9 (33.1) 11. Survey Geometric mean (95% conf.1 (15.6-15.20-10.8 (21.40-11.9 (8.4 (12.9) 7.92-12.0 (36.8) 7.4) 90th 249 (188-304) 03-04 03-04 03-04 8.7 (28.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.4-19.0 (26.89-11.Environmental Phenols Urinary Triclosan (2.0) 49.2-14.18 (5.6 (10.3-15.2) 12.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.1) 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 9.1) 9.3 (11.5-14.7 (14.1) 7.0 (8.9) 32.2 (11.0 (34.9) 8.0-213) 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 .5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.9 (11.4-18.7) 292 (151-432) 132 (78.9-236) 193 (90.6) 90th 212 (172-241) 03-04 03-04 03-04 9.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (12.8-127) 37.2-58.38-18.0) 9.82 (8.7) 123 (36. population from the National Health and Nutrition Examination Survey.2) 13.2 (10.8-63.8-112) 30.2-58.8) 9.60 (8.74 (5.0) 65.1) 9.8-60.2 (25.72-13.90-10.5) 11.2 (27.20 (7.4) 75th 43.16 (6.32-14.6 (30.70-16.48 (8.6) 10.3) 6.1-39.60 (6.3 (8.86-12.8) 116 (39.20 (7.4 (32.2) 9.8-85.48-10.55 (4.54 (8.1) 50.

Williams FM. Watanabe N. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Adolfsson-Erici M. Food Chem Toxicol 2000.28(9):1748-1751. Ye X. Windham G.80(3):217-227.83(1):84.69(20):1861-1873. et al. Veldhoen N. Chemosphere 2007. Mar Environ Res 2000.S. Gunderson MP. Osachoff H. Environ Health Perspect 2007.50(1-5):153-156.67(4):532-537. Am J Infect Control 1996. Meyer MT.115:116-121. J Toxicol Environ Health A 2006. Moss T. Triclosan: applications and safety. and phenols in girls. Arch Environ Contam Toxicol 1988. Furlong ET. et al. Bennett ER. Thurman EM. Needham LL. Hirano M. Pinney SM. Chelimo C. Wong LY. Kanetoshi A. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Environ Sci Technol 2002. Percutaneous penetration and dermal metabolism of triclosan (2. Hong HC.66:1052-1056. Fernandez-Alba AR. Wolff MS. Wigmore H. Urinary concentrations of triclosan in the U. Levy SB. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Gomez MJ. Gilbert RJ. Kolpin DW. Mezcua M. Okui T. Kaneshima H. Evidence of 2.Environmental Phenols References Aiello AE.524:241-247. Hernando MD. Biol Pharm Bull 2005. Zaugg SD. Erratum in: Aquat Toxicol 2007. Bodey GP. Teitelbaum SL.4. Photolytic degradation of triclosan in freshwater and seawater. Pharmaceuticals. Foran CM. Pharmacokinetics of triclosan following oral ingestion in humans. and other organic wastewater contaminants in U. et al. hormones. Ishibashi H. Calafat AM. Ogawa H. Leonard PA.. Ekstrand J. Skirrow RC.24(3):209-218.38(4):361370. Williams PE. streams.S. Br J Clin Pharmacol 1987. Katsura E. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.17(5):637-644.116(3):303-307. population: 2003-2004. The oral retention and antiplaque efficacy of triclosan in human volunteers. J Invest Dermatol 1976. Aguera A. IMS Ind Med Surg 1969. Howes D. Aquat Toxicol 2006. Barber LB. 1999-2000: a national reconnaissance. Larson EL. Sandborgh-Englund G. Reidy JA. et al. Furia T. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Aranami K. Toxicology of 2. 4.23(5):579-583. Lyman FL.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.4’-trichloro-2’hydroxydiphenyl ether).45 Suppl 2:S137-S147.38(2):64-71. Readman JW. Shiratsuchi H. Benson WH. Bhargava HN. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.7/2. Environ Health Perspect 2008. Odham G. Anal Chim Acta 1004. 4’-trichloro-2’-hydroxydiphenyl ether. phthalates. Britton JA. Nagao Y. Ebersole R. Clapson DJ. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Pilot study of urinary biomarkers of phytoestrogens. Matsumura N.36(6):1202-1211. Ferrer I.

water and sediments because of the large amounts that were produced and used historically. Acute.350-.30) .S.30) 1.37 (.60) 1. and possibly of lindane (IPCS.990-2.510-3. After a single dose.500-2. 2002.350 (. PCP cannot be used on wood in residential or agricultural buildings.350-.48-2.32 (. < LOD means less than the limit of detection.350-1.98 (1. PCP is distributed to most tissues and is not extensively metabolized.350-2. In the environment.350-.78) 1.47-5.10 (.890 (.350 (.350-. along with small amounts of tetrachlorohydroquinone and conjugates.30 (1.54-2.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . and dermal contact with PCP-treated products.5.350) < LOD . PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350-.350-1.350) < LOD .60) 1.350-. After absorption.00) 1. 1979).660 (. PCP use in the U.350) < LOD .. are eliminated in the urine.350 (.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350 (.480-2.91 (1.350 (. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350 (.350) < LOD ..350 (.350-. and metabolic acidosis were observed in CAS No. ingestion of contaminated food or water.850-2.25 and 0.350) < LOD . The parent compound and conjugates.90 (1. PCP is eliminated over a few days (Braun et al.83 (2.33-2.860-2. Human exposure to PCP has become less common.73 (1. Kohli et al.00) 1.350-.350 (.23 (. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350 (.67) 1. plants.350-.350 (.18 (<LOD-1. algaecide and insecticide.08-3.350 (. PCP is degraded by sunlight and metabolized rapidly by microorganisms.45-2.350-2.650 (.350 (.990 (<LOD-2. 40 Fourth National Report on Human Exposure to Environmental Chemicals .00 (.350 (.960) 1.10) 1.94 (1.350) < LOD .390 (.30 (.680-1.10) 1. air.350) < LOD < LOD 75th .70) 2.47-3.37) . has been restricted.58-2.. herbicide.350) < LOD . with repeated or chronic exposure.350-. mollusicide.350 (.65 (.350-. Effects including hyperthermia. Since 1984. and it is used primarily as a preservative for wood to be used outdoors (e.350-1.630 (.350) < LOD .350) < LOD .350-.350-2. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.10 (1.04) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.00) 2.350-.350) .590-1.70) .350) < LOD .76) .350-.650) 1.S.350) < LOD .09) .50) 1.40 (.64) 1. which may vary for some chemicals by year and by individual sample.530) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.58-2.350) 90th .350 (. the elimination half-life may be a week or more (Uhl et al.33) .51) 1.. hypertension. General population exposure to PCP may occur by inhalation of contaminated air.80) . To-Figueras et al.350-.75) 2.350) < LOD . 1986).770 (.90) 2.980 (.350-.65 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350) < LOD . and animals.350 (. population from the National Health and Nutrition Examination Survey.90) 1.350-.76) 1.390 (.350 (. utility poles and fence posts).30 (. 1997).350) < LOD .350 (.. other polychlorinated benzenes. Survey Geometric mean (95% conf.350-.30) 1.10 (<LOD-1. PCP is absorbed rapidly and well by all exposure routes.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .94 (1.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . PCP has been detected in soils.510-5.350 (.350) < LOD .350-.01 (<LOD-1.890-1.53) 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 .350-.350-2.350 (.350 (.42) 696 680 521 696 603 951 Limit of detection (LOD.350-.350-1.g. bactericide. so it is relatively non-persistent.350-2.350) < LOD .48 (.62 (.350-. 1976.

52 (<LOD-1.35) 1.700-2.40) 1.320) < LOD .00-1.25-2.300 (. children in the 1980’s.800) < LOD 1. In animals. 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.82) 1.67 (1.09 (<LOD-2.84 (1. carcinogenic.270-.290) < LOD .67-3.40) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. environmental levels) and health effects is available from the U.gov/ toxpro2.00) 1.320) < LOD .610 (.S. EPA has developed standards for PCP in drinking water and the environment.73 (1.560) < LOD . EPA at: http://www.650 (.78) 1.6 and 14. 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.92) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.html.S.40) 1.. 2003).990 (..440 (.630 (.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .260 (.510-.56) 1. respectively) (Becker et al.67-3.320 (.29-3. 1989).e.280) < LOD .35) 1.06 (. population from the National Health and Nutrition Examination Survey.470 (.30 (.330-.26 (1.500-. Fourth National Report on Human Exposure to Environmental Chemicals 41 .40) 1.360 (..850 (.10 (1.94 (1. inhalation. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.S. Survey Geometric mean (95% conf.580-.920 (.650 (.51) 1.10-2.510-.69 (1.370 (.430-.780-1. respectively) (Seifert et al.710-1.25-2.340-.epa.55) 1.800-1.300 (.730) < LOD .84-4. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.34 (.320) < LOD < LOD 75th ..52 (<LOD-1.. 2000).19) 2.500 (.300 (.19 (1. 2004. 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.420) < LOD .560-.910-1.18) .310-.220-.430) < LOD .67-2.36) .25 (1.270-.310) < LOD .18 (1.21 (. and the FDA has established a standard for bottled water.09-1.06-3.220-.290-.52) 1.13 (.760 (.25 (1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans. The U.950-1.82 (1.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th . 1989). 1991).52 (1.950-1.350) < LOD .79) 1.57 (1.Fungicides adults and children severely exposed to PCP through ingestion.19) 2.11) 2.240-. 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.250 (.30) 1.19) 2.67 (1.48-2.S.EPA.94-3.0 mg/L. In a small sample of U.950-1. 1995).380-.30-2.78) 1.67 (1.900-1.570 (.35-2.25-1. OSHA has established an occupational standard.gov/ pesticides/ and from ATSDR at: http://www.cdc.06) 1.00-1.290-. Pentachlorophenol is not mutagenic or teratogenic.830) < LOD .. or skin absorption.30) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .590-1.590) < 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.490) < LOD .16-1.83 (1.75 (<LOD-2.40) 1. Among adults in the NHANES 1999-2000 subsample.atsdr. van Raaij et al. Death can result from seizures and cardiovascular collapse.250 (..90) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.560) < LOD .40-2.25) 1.67 (1.75) 1. chronically administered high doses of PCP were hepatotoxic. and adversely affected thyroid function (U.650) 90th 1.84) 1.360-.35-2.780) < LOD .26 (1.9 mg/L.400 (. In NHANES 2001-2002 subsamples.67 (1.16 (.S.21-2.94 (1.95) 3. 2003). More information about external exposure (i.08 and 5.500-1.57 (..55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .

Environ Res 1995.4:289296. Gregg M. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats.10:552-65.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. International Programme on Chemical Safety (IPCS). Phillips DL. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Jones D. Fast DM. 4/21/09 van Raaij JA. et al. Hill RH Jr. Schlatter C. Holler JS. Arch Toxicol 1986. Needham LL. Shealy DB. drinking water and indoor air. Hill RH. Can J Biochem 1976. 4/21/09 Kohli J. To-Figueras J. r e g u l a t i o n s .org/documents/jmpr/jmpmono/2002pr08. Head SL. available at URL: http://www. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. htm. 42 Fourth National Report on Human Exposure to Environmental Chemicals . house dust. PCP: Human Risk Characterization [online]. van den Berg KJ.S. Int J Hyg Environ Health 2003. Santiago-Silva M. 206:15-24. et al. Uhl S. Lindane. Safe A. Rodamilans M.58:182-186. Baker S. Becker K. Seifert B. Arch Environ Contam Toxicol 1989. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. U. Braun WH. Pharmacokinetics of pentachlorophenol in man. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. 11/30/2004. Blau GE. Arch Environ Contam Toxicol 1989. Cline RE. Toxicology 1991: 67(1):107-16. Seiwert M. Schulz C. Schulz C. Available at URL: h t t p : / / w w w. Needham LL. The metabolism of higher chlorinated benzene isomers. Smith SJ.inchem. Kaus S. Seiwert M.105(1):78-83.S. et al. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Dev Toxicol Environ Sci 1979.71:99108. Sala M. urine. Chenoweth MB. Pesticide residues in urine of adults living in the United States: reference range concentrations.54(3):203-208. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. References Becker K. 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. Bailey SL.18:475-481. Seifert B. 2002. Helm D. Krause C. Bragt PC. Engel R. hair. Otero R. Environmental Protection Agency (U. Schmid P. EPA). Notten WR. Barrot C. To T. 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. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Hill RH Jr.18(4):469-474. J Expo Anal Environ Epidemiol 2000. Environ Health Perspect 1997.

interval) .370-.90) .580-1.590-2.490 (<LOD-.90) 1. Workers who manufacture.389-.780) < LOD . formulate.10 (1.490 (<LOD-.500-2.85) 2. however. sodium ortho-phenylphenate (SOPP). and it has limited water solubility.770 (. but OPP and SOPP are still used on pears and citrus (U.00 (1.02) 1.10) .3 and 0. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.890 (.S.470 (<LOD-.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .410-.750-2.930 (.710) 3.370-.621) * . in paints.. Estimated human intakes have been below recommended intake limits (U.17 (.624) * . 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.364-.496 (.61) 2.90) 2.389-.80 (2.490 (<LOD-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.00) < LOD .00 (1.88) 1. 1998.20-3. EPA. General population exposure can occur via dermal. Timchalk et al.76) 1.10 (1.690-1. In the past.60 (1.90 (1.820 (.60-3.638) * .90 (1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.480-1.50-3.19 (.600) < LOD 75th .50) < LOD .10) .450 (<LOD-.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .50) 1.636) * .20) < LOD 2.20) < LOD 1.40-5. population from the National Health and Nutrition Examination Survey.800-3.50 (1.770 (.466 (. which may vary for some chemicals by year and by individual sample. leaving the chemical residue OPP. or 2-phenylphenol) and its water-soluble salt. 1989).830 (.570-.836) * .420 (<LOD-.10-1.490 (<LOD-.600-1.10) 1.27 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2. OPP is volatile. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.550-1. 2006).840-1.00) .570-2.20 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . 2006).50-2. Survey Geometric mean (95% conf.40-5.349-. it was used in home sanitizers for surfaces.600-1.14 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.520 (.509 (.497 (..350-1. SOPP is applied topically to the crop and then rinsed off.760-2.600) < LOD 1.30-7.80-3.40 (.890 (.20) 2.50) < LOD .09) 2.60-2.10) . 2006).90) . or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.570-1.34) 1. OPP is still used as a disinfectant fungicide for industrial applications.80) 1.10-2.30 (1.EPA.20 (1.508 (.00-2. 90-43-7 General Information Ortho-phenylphenol (OPP.60 (1. inhalational.20 (1. Most agricultural food applications have been revoked. Both have been used in agriculture to control fungal and bacterial growth on stored crops.670) 2.50 (1.690) < LOD .970 (. Fourth National Report on Human Exposure to Environmental Chemicals 43 .23) 695 680 520 695 603 953 Limit of detection (LOD. and as a wood preservative.560-8.540-2.80) 1.600) < LOD .S.742) * . Cnubben et al.92 (.493 (.3.370-.630) < LOD .860 (. 1998).50-4. 2006).433-.30) < LOD 1. OPP is considered to be moderately toxic after acute oral doses in animal studies.450 (<LOD-.40-7.710-2.490 (<LOD-.570 (.S.498 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.00 (1.50) < LOD .640) < LOD .740 (.S.600) < LOD .890) 1.50 (1.00) .390-.30) < LOD 90th 1. Available evidence suggests that OPP does not accumulate in the body.850 (.07 (.600-1.610 (.552 (. or apply these chemicals may be more highly exposed than the general population.386-.33 (.450 (<LOD-. on ornamental plants and turfs.60 (1.28 (..30) 1.03) 1. such as fruits and vegetables.402-.880-2.22) 2. fungicides.645) * .28-3.696) * . small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.50) . 2002.22 (.30-2.790) 2.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .20-2.Fungicides ortho-Phenylphenol CAS No. whereas SOPP is not volatile and is more water soluble. < LOD means less than the limit of detection.10) 2.EPA.10) 1. and sanitizers.30) < LOD .00 (1.610-1.567 (. are antimicrobial agents used as bacteriostats.40-2. Both chemicals degrade within hours to weeks in the environment (U.950) < LOD .570 (.

08) 1.980 (. 2002.17 (.51-3.93) 1..09 (1.38) 2.11) < LOD 90th 1.301-.990) < LOD .514 (. Bomhard et al. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.96) 1. Volunteers exposed to 0. reproductive.96 (1. Murata et al.410 (<LOD-..860 (.550 (.20) < LOD 3.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .750 (.248-.61 (1.06-5. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.640-1.420 (<LOD-.600-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.320 (<LOD-. 1984.444 (.620-1.470 (<LOD-.470) < LOD .81) 1. Additional information is available from U.78 (2.650-1.43 (1.880-1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .29) 1.59) .810-1.291-.353-..93 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08-2. and it has classified OPP as not classifiable with respect to human carcinogenicity.Fungicides anemia.580) < LOD . 44 Fourth National Report on Human Exposure to Environmental Chemicals . Nakagawa et al.770-2.570) < LOD 1.74 (1.S.550) < LOD .53) 1.43) 3.455-.EPA 2006).27) < LOD .810) < LOD ..25-6.17) 2.910 (.59) 1.910-1. but no neurologic.900) < LOD .18) 2. 1998.420 (<LOD-.47) .460-.4) 3.24-2.580-1.88-4.64 (2.44 (1.21) 1. leading to production of two metabolites.750-2.04-4.40-13. Zhao et al.21-2.05-2.00 (1.13) 1.93) .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 . Detectable levels were seen in over half the U.38) 1.S.33-2. 2005).690 (.21 (..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.38-3.gov/pesticides/. interval) .270-.29) 1.380 (. Brusick.750 (.52 (.01) 1. 1999.560-2.96-4.382 (. CDC.43-2.. population from the National Health and Nutrition Examination Survey.568) * .780 (.69 (1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.32) 3.0) 1.62) .32) 1.550-. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.970) 1.410 (<LOD-.08-1. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated..epa.EPA at: http:// www. 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) * .510-.11 (.12-2.86 (1.11) 4. Kwok et al.S. U.910 (<LOD-1.329-.510 (<LOD-.46) < LOD 1.900-1. 1986).58) 2.02 (. or. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.500) < LOD .620-1.800-1.93) .440 (.11-1. 1992..791) * .00 (.940-2. by possible genotoxic mechanisms (Hagiwara et al. Ito et al.17 (.11 (.361-. less likely.EPA 2006).24-2.980 (<LOD-1.12) < LOD 1.670 (.28 (2.28 (<LOD-4. 2005.31) < LOD .S. OPP was not found to be mutagenic.26) 1. 1984. 1999.311-.07) 2. Survey Geometric mean (95% conf..508) * .496 (.61 (.360 (<LOD-.780-14.75 (1.43-2.89 (1.484) * . 2000.96 (1. Biomonitoring Information Urinary OPP levels reflect recent exposure.33) .385 (. IARC has classified SOPP as a possible human carcinogen..453 (.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2005).473) * .06-4.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . 2002.610) < LOD 1. Pathak and Roy.75 (1.97 (2.670 (.403-.S. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.343 (.61 (2.09-6.06 (1.860 (.666) * .840 (. U.950) < LOD .09-3.656) * .560) < LOD 75th . 1993.91 (1. In high dose animal studies. or developmental toxicity was observed (Bomhard et al.84 (1. 2002). Smith et al.670) < LOD .480-. 1997.

Christenson WR. Brusick D.17(8):411-417.niehs. Leser KH.286(2):309-319. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.74(2):61-71. Toxicol Appl Pharmacol 1998. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Comparative metabolism of orthophenylphenol in mouse.159(1):18-24. Shirai T. EPA-560/5-89-003. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Mutat Res 1993. Kwok ES. Bartels MJ. Environ Mol Mutagen 2005. The carcinogenicity of the biocide ortho-phenylphenol. 2005. Sangha GK.54(16):5731-5735. Smith RA. Environmental Protection Agency (U. July 28. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Eadon G. Glas K.S. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. J Agric Food Chem 2006. Bartels MJ. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Zhao S. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Bromig KH. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats.45(5):460-481. Hagiwara A.S. Cnubben NH.pdf.nih. Vogel JS. Moriya K.28(6):579594. Cano M.(56):399-407. Regul Toxicol Pharmacol 2002. et al. Kawanishi S. et al.gov/oppsrrd1/REDs/ phenylphenol_red.703(12):97-104. Food Chem Toxicol 1984. Elliott GR. Eastmond DA. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. rat and man. Tayama S. Shibata M. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No.22(10):809-814. Toxicol Appl Pharmacol 1999.50(11):3351-3358. Arnold LL.43(7):14311437. Stanley JS. Buchholz BA. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol.20(5):851-857. Coelhan M. Freyberger A. U. Meuling WJ. Richter M.gov/ntp/htdocs/LT_ rpts/tr301. Bomhard EM. Atlanta (GA). Brendler-Schwaab SY. Available at URL: http://ntp. Moore GA. EPA 739 R-06004. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Fukushima S.Fungicides References Appel KE. EPA). Arch Toxicol 2000.pdf. Nakagawa Y. Crit Rev Toxicol 2002. Moldeus P. Biochem Pharmacol 1992. Fourth National Report on Human Exposure to Environmental Chemicals 45 . 1989. March 1986. 90-43-7) in Swiss CD-1 mice (dermal studies). Timchalk C. Sangha G. 4/13/09 Onstot JD. Narang A. Ito N. Murata M. Office of Toxic Substances. Hum Exp Toxicol 1998.EPA). Pathak DN. J Chromatogr B Biomed Sci Appl 1997. Selim S. Brzak KA. van de Sandt JJ. Inoue S.35(2 Pt 1):198-208.. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Xenobiotica 1998. J Agric Food Chem 2002. Bormett GA.epa. Carcinogenesis 1999. Hakkert BC. Turteltaub KW. Mendrala AL. 2006. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Gierthy J. IARC Sci Publ 1984. Bartels MJ. National Toxicology Program (NTP). Identification of SARA compounds in adipose tissue. Fukushima S. 4/9/09. Third National Report on Human Exposure to Environmental Chemicals.S. Drugs. McNett DA. Ito N.150(2):402-413. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Timchalk C. Environmental Protection Agency (U. Centers for Disease Control and Prevention (CDC). St John MK. Herbold BA. Roy D. U. Hagiwara A. Roberts AL.S.32(6):551-625. Hirose M. Christenson WR. Available at URL: http://www. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Imaida K. Bartels MJ.

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

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

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

37(4):10881093. Lefevre PA. Available at URL: http://www. and metolachlor herbicides in rats. Furlong ET. Barr DB. Feng PCC. Environ Sci Technol 2005. Number 15. Kier L. 1998.html. Heederik D. Kolpin DW. Peter CJ. Jefferies PR. Occurrence of sulfonylurea. 2005. Wratten SJ. et al. Striley CA. Larsen GL. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.24(10):1003-1012. 5/30/06 U.248(2-3):123-133.S.Herbicides References Ashby J.cce. Davison KL. Barr DB. Chem Res Toxicol 1998.pdf. Thurman EM.17(6):559-566. Reynolds SJ. Hsiao JJ. Coleman S. Hladik ML. EPA). Sci Total Environ 2000.cornell. Andrews HF. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Kinney PL. Deddens JA. Tinwell H. Rose RL. J Agri Food Chem 1989. Wilson AG.EPA): http://pmep. EPA 738-R-00-009. Xenobiotica 1994. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Burkhardt MR. epa.S.15(9):702-735.39(17):6561-6574. Hum Exp Toxicol 1996. 2000. Available at URL(non U. Feil VJ. acetochlor. Roberts AL. U. Atlanta (GA). Green T.111(5):749-756. et al. Camann DE.S. Hein MJ. EPA). Barr DB. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Bravo R. Olsson AO. Casida JE. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Curwin BD. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.S. Comparative metabolism and elimination of acetanilide compounds by rat.248(2-3):115-122. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Sanderson WT.15(6):500-508.S. et al. Hines CJ. pages 3682-3690.108(12):1151-1157. Ward EM. reservoirs and ground water in the Midwestern United States. Volume 65.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Environ Health Perspect 2000. 5/30/06. Environmental Protection Agency (U. Whyatt RM. Barr JR. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Centers for Disease Control and Prevention (CDC). Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Battaglin WA. J Expo Sci Environ Epidemiol 2007. Environmental Protection Agency (U. Federal Register: January 24. sulfonamide. and other herbicides in rivers.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. March 2006. Environ Health Perspect 2003. Dialkylquinonimines validated as in vivo metabolites of alachlor. J Expo Anal Environ Epidemiol 2005. Acetochlor (Harness) Pesticide Petition Filing 1/00. imidazolinone. Quistad GB. Third National Report on Human Exposure to Environmental Chemicals. Alavanja MC. Linderman R. Hodgson E. Linhart SM.11(4):353359. Sci Total Environ 2000.

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

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

who.43(9):2504-2512. Kinney PL. Quistad GB. Henningsen G. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.248(2-3):115-122. Environ Sci Technol 2005. Background document for development of WHO Guidelines for Drinking-water Quality. Available at URL: http:// www. Kimmel EC. Tessier DM. Hill RH Jr. Linhart SM. Barr DB. 1996. Peter CJ. Feng PCC.S. revised February 15. Geological Survey (USGS). U. Occurrence of sulfonylurea. Martens MA. Available at URL: http://water. Kolpin DW. Feil VJ. Erratum in: Life Sci 1989. Striley CA.pdf.248(2-3):123-133. Sci Total Environ 2000. Burkhardt MR.pdf. Whyatt RM. 1999. Roberts AL. Hladik ML. Sanderson WT. Environmental Protection Agency (U. Clark JM. acetochlor. Alachlor in Drinking-water.111(5):749-756. Am Ind Hyg Assoc J 1995. Biagini R. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Comparative metabolism and elimination of acetanilide compounds by rat. Circular 1291. Quistad GB.epa. and other herbicides in rivers. and metolachlor herbicides in rats.18(6):363-391. World Health Organization (WHO). Casida JE. 1992-2001.org/documents/pds/pds/pest86_e. Hum Exp Toxicol.24(10):1003-1012. 2005. Hsiao JJ. Reregistration Eligibility Decision (RED) Alachlor. Andrews HF. Brown KK. et al. 86.11(4):353359. Driskell WJ.395(2-3):159-171.Herbicides References Battaglin WA.htm. Available at URL: http://www. 1999. sulfonamide.43(25):2087-94. Heydens WF. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Shealy DB. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . ALACHLOR.int/water_sanitation_health/dwq/chemicals/en/alachlor. Wratten SJ. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. 1997. Chem Res Toxicol 1998. Wilson AG. Geneva. Bull Environ Contam Toxicol 1996. Third National Report on Human Exposure to Environmental Chemicals. imidazolinone. 2/27/09 U.37(4):10881093. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. December 1998. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. 2/27/09 Jefferies PR. Available at URL: http://www. World Health Organization. Jefferies PR. 2007. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. reservoirs and ground water in the Midwestern United States. Environ Health Perspect 2003. Thurman EM.56(6):853-859. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. EPA 738R-98-020. Hines CJ.39(17):6561-6574. Tolos W.inchem. Xenobiotica 1994. J Agri Food Chem 1989. J Ag Food Chem 1995. Casida JE. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Camann DE.S. Atlanta (GA). Barr JR. Hines CJ.usgs. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Sci Total Environ 2000.S.php. Dialkylquinonimines validated as in vivo metabolites of alachlor. 98-4245 (by Barbash JE. Life Sci 1988.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. International Programme on Chemical Safety (IPCS). No. Kolpin DW. Hill AB. Supplemental Technical Information (available on-line only). 1998. EPA). Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Centers for Disease Control and Prevention (CDC). Gilliom RJ). 4/2/09 U. Thake DC. Lau H.56(9):883-889. 2003. WHO/ FAO Data Sheets on Pesticides. et al. Casida JE. Deddens JA. Biagini RE.gov/oppsrrd1/ REDs/0063. Larsen GL. Shoemaker DA. Davison KL.44(18):1325. Brown MA. Mutat Res. DNA adduct formation by alachlor metabolites. March 2006. Geological Survey (USGS). Furlong ET. Kier LD. Ann Occup Hyg 2003. MacKenzie B.47(6):503-517. Sacramento. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Thelin GP. Hull RD.S. California.

1993. In soils. It is also used as a non-selective herbicide. 1990). The dealkylated chloroatrazine metabolites. resulting in atrazine mercapturate and N-dealkylation products (IPCS. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al. Atrazine was first registered as an herbicide in 1958. drinking water is an infrequent source of atrazine exposure. U. Fourth National Report on Human Exposure to Environmental Chemicals 53 . Atrazine is well absorbed orally.. metabolized. < LOD means less than the limit of detection.EPA.EPA. and then eliminated in the urine over a few days (Bradway et al. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination. 2003b). and cyanazine. In regions where atrazine is used. Atrazine does not bioaccumulate. which may vary for some chemicals by year and by individual sample. 2002.S. Applicators of atrazine may be exposed dermally and by inhalation. all of which act by inhibiting plant photosynthesis. which have half-lives of several months. but it is leachable into ground and surface waters. population from the National Health and Nutrition Examination Survey. In animals and humans. 1996.and post-emergence to agricultural land for crops such as corn and sorghum. propazine. 2003a).. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. Atrazine is applied pre. As a result.. 2003b).. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. it is one of the more commonly detected pesticides in surface and ground waters (USGS.EPA. 2007). Atrazine has limited water solubility and is not tightly bound to soil. Related chlorotriazine herbicides include simazine. Hayes et al. More than 70 million pounds have been applied annually in recent years. Timchalk et al. Survey Geometric mean (95% conf.3.791 and 0..S. 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.Herbicides Atrazine CAS No. U.S. atrazine is slowly degraded to dealkylated products. with about 75% of corn cropland receiving treatment. Catenacci et al. 1982.. but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1993). 2005. glutathione conjugation appeared to be the major route of biotransformation.S. For the general population. Bacteria and plants can metabolize atrazine to hydroxyatrazine. Urinary Atrazine mercapturate Metabolite of Atrazine 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.

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

.. Breckenridge CB. 82. No. Stoker TE.atsdr. J Toxicol Environ Health 1994. Sanderson WT. Carr WC Jr. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Maroni M.58(2):366-376. Freeman NC. Hines CJ. Simpkins JW. In a study of 60 farm worker children. World Health Organization. J Agric Food Chem 1982. Pest Manag Sci 2005. Cooper RL. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. 2000). Cooper RL.cdc. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.15(6):500-508. Bradway DE. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Lioy PJ. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Catenacci G. Biological monitoring of human exposure to atrazine. 2005). Ferrell JM. Curwin BD. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 .76(1):190-200.61(4):331-355. Toxicol Lett 1993. Reynolds SJ. Wetzel LT. J Toxicol Environ Health 1994. Barr DB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Proc Natl Acad Sci USA 2002. Pfeifer KF.inchem.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Barbieri F.43(2):155-167. et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.html. Laws SC. 2005). Wetzel LT. Barr DB. Heederik D. Sanborn JR.115(8):1254-1260. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Moseman RF. Tapia J. Jones AD. Noriega N. Lucas AD. Stoker TE. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Barr DB. Toxicological profile for atrazine.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. 2007). Environ Health Perspect 2007. 2003.99(8):5476-5480. Cottica D. Gillis JH. In small studies of Maryland residents in 19951996 (MacIntosh et al. Bersani M. diamino-S-chlorotriazine and hydroxyatrazine. Biagini RE. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Toxicol Sci 2003. et al.org/documents/pds/pds/pest82_e.. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.htm. Blewett C. Stevens JT. Eldridge JC. Goodrow MH. Toxicol Sci 2000. WHO/ FAO Data Sheets on Pesticides. Available at URL: http:// www. References Adgate JL. Stuart AA. Fleenor-Heyser DG. 1996. Gillis JH. Toxicol Sci 2000. Deddens JA. In a small number of field workers. 3/11/09 Laws SC. 2001).gov/toxprofiles/tp153. Geneva. Hayes TB. Cooper RL. International Programme on Chemical Safety (IPCS). et al. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats..53(2):297-307. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Hermaphroditic. Seiber JN. Gammon DW. Environ Health Perspect 2001. 3/11/09 Arcury TA. 1993). Ferioli A. ATRAZINE. atrazine was detected in only four children (Arcury et al. Shoemaker DA. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Quandt SA. Hein MJ. J Expo Anal Environ Epidemiol 2005. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Ferrell JM. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. A risk assessment of atrazine use in California: human health and ecological aspects. Perry et al. Striley CA. Brown KK.64(9):672-678.43(2):155-167. Chen H. Collins A.30(2):244-247. Atlanta (GA). 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. Eberly LE. et al. Third National Report on Human Exposure to Environmental Chemicals. Tyrey L.69(2):217-222. Stoker TE. Steroids 1999. levels of atrazine mercapturate were generally not detectable (CDC. Goldman JM. 2005. 2001 [online]. Lee M. Vonk A. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Mendoza M. McElroy WK. et al. et al. The geometric mean of urinary atrazine mercapturate was 1.47(6):503-517. In the NHANES 2001-2002 subsample.. Saiz SG.. Available at URL: http://www. Schmid J. Grzywacz JG. Eldridge JC.109(6):583-590. Agency for Toxic Substances and Disease Registry (ATSDR). Aldous CN. Ann Occup Hyg 2003. Clayton CA. Centers for Disease Control and Prevention (CDC). Extrom PC.

Available at URL: http://www. Needham LL. Cooper RL. Fenton SE. Supplemental Technical Information (available on-line only). Environmental Protection Agency (U. Breckenridge CB.pdf. Available at URL: http://www. Sathiakumar N. Stoker TE. 2007. Toxicol Sci 2002. Urinary biomarkers of atrazine exposure among farm pesticide applicators.182(1):44-54.S. Guidici DL. A review of epidemiologic studies of triazine herbicides and cancer. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.php. Interim Reregistration Eligibility Decision For Atrazine. Environmental Protection Agency (U. Toxicology 1990. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . J Expo Anal Environ Epidemiol 1999. Office of Prevention. Singzoni B.S. Hammerstrom KA. Toxicol Sci 2000. Washington (DC). Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Ryan PB. Toxicol Appl Pharmacol 2004.gov/oppsrrd1/REDs/ atrazine_ired. Lansbergen GW. Christiani D. A longitudinal investigation of selected pesticide metabolites in urine. Pesticides and Toxic Substances. Kastl PE. March 2006. 6/1/09 U. revised February 15. 1992-2001.usgs.epa. Delzell E.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. van den Berg M.195(1):23-34. Boerma J. Tortorelli J. Available at URL: http://water. Wood C.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.9(5):494-501. Cooper RL. U. J Toxicol Environ Health A 1999. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Timchalk C. EPA). Stevens JT.Herbicides development of a biomarker of exposure. Langvardt PW. EPA). May 2003a. Rayner JL.56(2):69-109. Laws SC.67(2):198-206. MacIntosh DL. White paper on potential developmental effects of atrazine on amphibians. Pesticides in the Nation’s Streams and Ground Water. Dagenhart D.6(1):107-116. Stoker TE. Dryzga MD. Crit Rev Toxicol 1997. Sanderson JT. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Guidici DL. Osborne DW. The Quality of Our Nation’s Waters. 0062. Toxicol Appl Pharmacol 2002. Case No.S. Chem Res Toxicol 1993.58(1):50-59. A risk characterization for atrazine: oncogenicity profile. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.S.27(6):599612. 2003b. EPA Office of Pesticide Programs. Environmental Fate and Effects Division. Perry M. 3/11/09 U.epa.S.10(7):479.61(1):27-40. Circular 1291. Laws SC. Wetzel L. Geological Survey (USGS).pdf. Ann Epidemiol 2000.

260 (<LOD-.EPA.16) < LOD . although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and aquatic environments. population from the National Health and Nutrition Examination Survey.230 (<LOD-.4-D may occur during residential applications.21) 1.S. Kohli et al. these herbicides can enhance plant growth.952 and 0.4-D can be applied either as an aqueous salt or as oil-soluble esters. it acts as a plant growth hormone. dizziness.210-.370-.890 (.07 (. It is not well absorbed through the skin.4-D have been below recommended intake limits (U. Sauerhoff et al.60) 1. Recent estimates of chronic intakes of 2.490) < LOD < LOD < LOD .03) 695 659 520 668 589 892 Limit of detection (LOD.330 (.51 (1. and delayed Urinary 2.730 (.27 (.540-.08) < LOD .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . headache.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.410) < LOD . Once absorbed.930 (.690 (.560-1.13) < LOD . nausea.680-1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. As much as 62 million pounds of 2. It is rarely detected in ground waters (USGS. 2. abdominal pain. 94-75-7 General Information Widely used throughout the United States. At low levels. the chlorophenoxy herbicide 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S.S.40) 1.10 (<LOD-1.760 (.670-1. 1974.10) < LOD 1. with a half-life of several days to several weeks.4-D or exposed for prolonged periods. General population exposure to 2. Fourth National Report on Human Exposure to Environmental Chemicals 57 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.310 (.EPA.32 (1. and mecoprop).210 (<LOD-.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .66) < LOD 1. and by consuming food or drinking water contaminated with 2.930-1.320) 90th .690 (.4-D) controls broadleaf weeds in residential.30 (<LOD-2..02-1.350) < LOD < LOD < LOD .70) 1.S. It is poorly bound in soils.43) 1.EPA in 1948. 2.440-1. by direct contact with agricultural and residential areas after applications. Survey Geometric mean (95% conf.560-. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. hypotension.4-D has low acute toxicity.230-. It was first registered with U.Herbicides 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.960-1.4-dichlorophenoxyacetic acid (2.4-D is rapidly absorbed via oral and inhalation routes. 1989.400) < LOD .. but at higher levels they are herbicidal.22) < LOD .810-1. 2.740 (. 2005).550-1.660) 1. 1977).690-1.24 (. which may vary for some chemicals by year and by individual sample. myotonia. renal and hepatic injury. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.420) < LOD .27 (1.4-D were used in the U. 2007).27-2.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .4-Dichlorophenoxyacetic Acid CAS No.910) < LOD .910) 1.05-2.690 (.310) < LOD . agricultural. 2. < LOD means less than the limit of detection.20 (. in 2001 (U. 4-D.250 (<LOD-.48) < LOD 1.80) 1.55 (1.890) < LOD .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 .420-.00-2.2. MCPA.20 (<LOD-1. 2004).490 (.610 (.250 (<LOD-.10 (<LOD-1. Similar to other chlorophenoxy herbicides.. Human health effects from 2.S. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.610-.

2005)..590 (<LOD-1. population from the National Health and Nutrition Examination Survey. IPCS.270-.S.. 1989).410) 90th . IOM.810-1.740 (.920) < LOD 1. U.850) < LOD .350 (<LOD-. Post-application levels in farmers and home gardeners were dependent on Urinary 2. 1995.580-.390) < LOD < LOD < LOD .19) .410) < LOD < LOD < LOD .08 (. or teratogenic effects in chronic rodent studies (Charles et al. Survey Geometric mean (95% conf.610-.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2. 1995)..S.380 (<LOD-. It is unclear whether these associations are related to the chlorophenoxy herbicides.660 (. U.550-.13 (. 2005.32 (<LOD-2.S.17 (. thyroid..410 (<LOD-. 1996. IPCS. 2004).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 .790) < LOD .08 (. 2005).29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2005. population (Hill et al.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.780) .epa. IPCS.790) 1.720 (. eyes. adrenals and gonads (NTP..890-1. 1996. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 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.640 (.670 (.560-.4-D are eye irritants..EPA at: http://www..13 (.670 (.380 (<LOD-.380) < LOD .890) < LOD 1. Frank et al. liver. 58 Fourth National Report on Human Exposure to Environmental Chemicals . 1992).4-D does not have significant reproductive.810-1. 1985.4-D production plant workers and a few forestry workers spraying 2.780 (.4-D levels were detectable in less than a quarter of the individuals studied.340-. 2002.73) . Knopp et al. 2006. Kutz et al.3. Additional information is available from U. 2005). U.S.340 (.590 (<LOD-1. 1994). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.930-1.EPA.700 (.620-. myotonia.570) < LOD . In previous samples of the U.4-D reflect recent exposure. 1996. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.560-.41 (1.520-.35) < LOD . Average post-application urinary levels of 2. and evidence of histological injury to the kidneys.660) < LOD . or to contaminants in the herbicide formulations (specifically 2.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.16) 1.27-1.270 (<LOD-.410) < LOD 1.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.. Acute high doses administered to laboratory animals produced ataxia. Epidemiological studies have reported associations of several types of cancer.S. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 2.480 (.39) < LOD 1.24) 1. in small samples of children (Hill et al..05) .S.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2002.440 (.08 (. The acid and salt forms of 2.EPA. 2003. CDC. 2005).680) < LOD .EPA 2005). 2. Pearce and McLean.. Kolmodin-Hedman and Erne.780-1. Hill et al. urinary 2.14 (.470) < LOD . Biomonitoring Information Urinary levels of 2.610-. other exposures.S.980) < LOD 1.330-.56) . U.gov/pesticides/.670 (<LOD-1. 2005.EPA.7.Herbicides neuropathy (Bradberry et al. 2000). developmental. 2001.4-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. and of adults and children (Baker et al.380-.820-1. 2005.490 (.990-1. 1980.

Cook BT.4-D) epidemiology and toxicology. Ritter L. Environ Res 1995. and the use of protective clothing or equipment (Arbuckle et al.4-D in urine does not mean that the level of the 2. Beeson MD.4-D than levels found in the general population. Bailey SL. Updated March 7. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Hanley TR Jr.71(2):99-108. Survival and Growth Curves from NTP Toxicity Studies. TOX-63 Peroxisone Project (2. Biomonitoring of herbicides in Ontario farm applicators.edu/catalog.4-D and 2. Khanna RN. Sanderson WT. Occup Environ Med 1994. 3/17/09 Knopp D.31 Suppl 1:98-104.4-D were highest in the farmers who applied the 2. In farm families. Mandel et al.4:97-100.51(3):152-159.4-Dichlorophenoxyacetic Acid). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.4:427-435. 2006.27(1):23-38.4-dichlorophenoxyacetic acid (2.Herbicides the time since application. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.60(1):121-131.4-dichlorophenoxyacetic acid in man. Curwin BD. 1992). general population. Atlanta (GA). Gupta BN. Centers for Disease Control and Prevention (CDC).nih. Brody D. Tables. Needham LL. J Toxicol Environ Health 1992.S. Wilson RD.31(2):121-125. Reynolds SJ. Biomonitoring for farm families in the farm family exposure study. Toxicol Sci 2001. Baker BA. Bus JS. Needham LL. Vet Hum Toxicol 1989. Harris SA.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. Honeycutt R. Finding a measurable amount of 2. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Arch Environ Contam Toxicol 1989. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Baker S. Kohli JD. Washington (DC): National Academies Press. To T. Frank R. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.37(2):277-291.5-T). Shealy DB. Kutz FW. 2003.4-D will result in an adverse health effect.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Hill RH Jr. Cole DC.. Ripley BD. Dichlorophenoxyacetic acid.10(6 Pt 2):789-798. Pesticides residues in food: 1996 evaluations Part II Toxicology. Driskell WJ. Tandon JS..4.15(6):500-508.nap.4-D). Available at URL: http:// www.4 dichlorophenoxyacetic acid (2. Stephenson GR. Forestry workers involved in aerial application of 2. Available at URL: http://ntp. Estimation of occupational exposure to phenoxy acids (2. J Expo Anal Environ Epidemiol 2005 Nov.. National Toxicology Program (NTP). et al. Holler JS. Scand J Work Environ Health 2005. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . International Programme on Chemical Safety-INCHEM (IPCS). Smith SJ.4-D): exposure and urinary excretion. Solomon KR. Xenobiotica 1974. 3/17/09 Institute of Medicine (IOM).4-D. et al.18(4):469-474. Review of 2. the number of acres to which it was applied (Curwin et al. Absorption and excretion of 2. Heederik D.inchem. Crit Rev Toxicol 2002.4-. TOX-63: TOXICITY REPORT CURVES. 2.4-dichlorophenoxyacetic acid and its forms.4:318-321. Kolmodin-Hedman B. Arch Environ Contam Toxicol 1985. Veterans and Agent Orange: update 2002. Head SL. van Ravenzwaay B.htm.32(4):233-257. Philbert MA. the amount of pesticide applied. Scand J Work Environ Health 2005. Developmental toxicity studies in rats and rabbits on 2. 2005. References Arbuckle TE. Erne K.4-dichlorophenoxyacetic acid (2. J Expo Anal Environ Epidemiol 2000. Barr DB. 2005. Chapman P. Beasley VR. Garabrant DH. Carter-Pokras OD. Arnold EK. Campbell RA. Selected pesticide residues and metabolites in urine from a survey of the U. Pesticide residues in urine of adults living in the United States: reference range concentrations. 2005 Charles JM. Alexander BH. Hill RH Jr. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.org/documents/jmpr/jmpmono/v96pr04.niehs.. Available at URL: http:// www. Third National Report on Human Exposure to Environmental Chemicals. 914. Murphy RS.php?record_id=10603. 2005). J Environ Sci Health B 1992. Baker SE. Acquavella JF. Hein MJ. Sirons G J. Exposure of homeowners and bystanders to 2. Sircar KP. Arch Toxicol Suppl 1980. Harris et al. Dhar MM. Fast DM. Assessment of exposure to 2. et al. 2005). Biomonitoring studies of 2. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.31 Suppl 1:90-97. Mandel JS.gov/index. Board on Health Promotion and Disease Prevention. Gregg M. Barr DB. geometric mean urinary levels of 2.

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

Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Herbicides Metolachlor available from U.200 μg/L (CDC. 2005). and eliminated in urine and feces over two to three days (WHO. WHO. formulators. Estimated human intakes have been below recommended limits (U. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. 1989. and field workers may have significant exposures via this route.. Davison et al. 1998). 2000. EPA at: http://www.. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. The geometric mean metolachlor mercapturate was 4. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. EPA.S. 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. and convulsions were observed at lethal doses in animal studies. Metolachlor is well absorbed dermally. mercapturate conjugates were the predominant metabolites.epa. 2005. WHO. Biomonitoring Information CAS No. 2005).S. though the 95th percentile for males was 0.S. U. 1999. sorghum and other crops. in both ground and surface waters (Battaglin et al. Hines et al. 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. 51218-45-2 General Information Metolachlor is a chloroacetanilide type herbicide that is applied for preemergent control of grasses and broadleaf weeds on agricultural crop land. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. Fourth National Report on Human Exposure to Environmental Chemicals 61 . 2003). 2007.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al. including corn. metolachlor levels in water have exceeded lifetime human health advisory levels (U. 1995).EPA. Hladik et al. People exposed to metolachlor will excrete metolachlor mercapturate in their urine.gov/pesticides/. and on non-crop land for general weed control. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003). soybeans. USGS.. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. 2003). 1995. and it was not mutagenic in mammalian cells (U. 1994. lacrimation. NTP and IARC do not have ratings regarding human carcinogenicity. Feng and Wratten.S. so applicators. 2000.EPA. 2007. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. In animal studies. whereas 60% of applicators had detectable amounts. It is absorbed by plants and inhibits plant protein synthesis.. Occasionally in the past. Salivation.S. 1995).EPA. In animals..EPA considers metolachlor to be a possible human carcinogen. Gilliom. Jefferies et al.. General population exposure may occur through the consumption of contaminated food or drinking water.. metolachlor was quickly absorbed after dermal or oral doses. Kolpin et al. (2003) showed that 2. Metolachlor has low potential for acute toxicity (U. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. 1995). Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample.S.

< LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.670 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.2. which may vary for some chemicals by year and by individual sample.200 (<LOD-.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. 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 .440 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.240) 679 701 957 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0. 62 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf.200 (<LOD-. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

Sanderson WT. March 2006. usgs. Linhart SM. California. Environ Health Perspect 2000. Hladik ML. World Health Organization (WHO). Sci Total Environ 2000. EPA 738R-95-006. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.S. Striley CA. Gillion.S. Roberts AL. Available at URL: http://www. Geological Survey (USGS).who. Ann Occup Hyg 2003.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Thelin GP.S. Circular 1291.111(5):749-756. and metolachlor herbicides in rats. Casida JE. 1998. U. revised February 15.gov/nawqa/ pnsp/pubs/wrir984245/text. Pesticides in U. Dialkylquinonimines validated as in vivo metabolites of alachlor. Burkhardt MR. 6/1/09 Whyatt RM. R.47(6):503-517. Jefferies PR. Biagini RE. Brown KK. Environmental Protection Agency (U. Occurrence of sulfonylurea. Available at URL: http://water. 4/2/09 U. et al. Camann DE.37(4):10881093.usgs. Ward EM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Centers for Disease Control and Prevention (CDC). Barr DB. Barr DB. EPA). imidazolinone. Background document for development of WHO Guidelines for Drinking-water Quality. acetochlor.108(12):1151-1157. 3/26/09 U. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. et al.11(4):353359. Xenobiotica 1994. sulfonamide. Third National Report on Human Exposure to Environmental Chemicals.248(2-3):115-122. Larsen GL. Peter CJ. Chem Res Toxicol 1998.html. Quistad GB. Environ Health Perspect 2003. Thurman EM. Deddens JA. 2007. Available at URL: http://water. Furlong ET. Sacramento. Kolpin DW. 2003. Wratten SJ. Heederik D. 2005.gov/oppsrrd1/ REDs/0001. Alavanja MC.pdf.usgs. reservoirs and ground water in the Midwestern United States. Davison KL. and other herbicides in rivers. Hein MJ. Gilliom RJ). 1992-2001.S.ESTfeature_gilliom. Linderman R. Sci Total Environ 2000. Kinney PL. Hsiao JJ.gov/nawqa/pnsp/pubs/files/051507.41:3409-3414. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.epa. streams and groundwater.24(10):1003-1012. April 1995. J Agri Food Chem 1989. Curwin BD. Metolachlor in Drinkingwater. Kolpin DW. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Atlanta (GA). 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Reregistration Eligibility Decision (RED) Metolachlor.S. Andrews HF.pdf. J Expo Anal Environ Epidemiol 2005. Shoemaker DA. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://water.int/water_sanitation_health/dwq/chemicals/ metolachlor.php.pdf 3/30/09 Hines CJ. 1999. Environ Sci Technol 2005. Geological Survey (USGS). Available at URL: http://www. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Feil VJ. 98-4245 (by Barbash JE. Environ Sci Technol 2007. Barr JR. Hodgson E.39(17):6561-6574. Comparative metabolism and elimination of acetanilide compounds by rat. Feng PCC. Reynolds SJ. Rose RL.248(2-3):123-133.15(6):500-508. Coleman S.Herbicides References Battaglin WA. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Supplemental Technical Information (available on-line only).

Omer. population from the National Health and Nutrition Examination Survey. abdominal pain.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1974).4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..4. 2. and delayed neuropathy (Bradberry et al.5-T use as a herbicide in 1985. headache.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Although 2.5-T was once applied as either an aqueous salt or as an oil-soluble ester.7.. Given the commercial unavailability of 2.4. Survey Geometric mean (95% conf. 2. At low levels. 2. The half-life of 2. 2.g. Mohammad and St. 93-76-5 General Information 2. Epidemiological studies have reported associations of several types of cancer.4. renal and hepatic injury.5-T degrades to 2. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. which may vary for some chemicals by year and by individual sample.4. 1989.2 and 0. Kohli et al.S.4.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4. 1986.4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. 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. the general population is unlikely to be exposed to it. < LOD means less than the limit of detection. nausea.5-T in soil varies with conditions.4.4. 1992).1. Chlorophenoxy herbicides act as plant growth hormones.4. and concern about contamination with 2.5-T (Holson et al.Herbicides 2. myotonia.5-Trichlorophenoxyacetic acid (2.3..4. 1992.5-T and 2. ranging from several weeks to many months. Ester forms of 2.5-T has been rarely detected in ground waters (USGS. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.5-T is eliminated mostly unchanged in the urine.5-trichlorophenol and other degradates.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Once absorbed into the body. Nelson et al. these herbicides can enhance plant growth. 2007)..4.4.5-Trichlorophenoxyacetic Acid CAS No.. Agent Orange).4. but higher levels are herbicidal. dizziness. it is not well absorbed through the skin. with an elimination half-life of approximately 19 hours (Arnold et al.4.4-D were used as defoliants in the Vietnam War (e. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. 2004). 64 Fourth National Report on Human Exposure to Environmental Chemicals .5-T.. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.5T is rapidly absorbed via oral and inhalation routes. hypotension. Human health effects from 2.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-T than levels found in the general population. Mean urinary levels of 2. or to contaminants in the herbicide formulations (specifically 2. in which urinary levels of 2.S. It is unclear whether these associations are related to the chlorophenoxy herbicides. 2005. Fourth National Report on Human Exposure to Environmental Chemicals 65 . Urinary 2.4.4.S.7.5-T itself is not mutagenic. 2003.5-T also were below the limit of detection (Kutz et al.4. Biomonitoring studies on 2. 1992).. 1996.5-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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-T does not mean that the level will result in an adverse health effect.4.3. other exposures. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. similar to results of NHANES II (19761980). IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.5-T were generally below the limit of detection.gov/pesticides/.4. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. 2005).5-T reflect recent exposure. IOM.4. U.Herbicides or contaminated herbicides. Biomonitoring Information Urinary levels of 2. urinary levels of 2.4. Additional information is available from U. 2.S. 2004). 2002. Finding a measurable amount of 2. Pearce and McLean.4.EPA.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.EPA at: http://www. 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.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.epa. IPCS. 1980).

Vet Hum Toxicol 1989.Herbicides References Arnold EK. Proudfoot AT. Gaylor DW. Brody D. Pearce N.EPA). Sheehan DM. Office of Prevention Pesticides and Toxic Substances. Vale JA. Kutz FW.19(2):298-306. Philbert MA. Developmental toxicity of 2. Available at URL: http:// www. Gaines TB. Scand J Work Environ Health 2005. LaBorde JB.5-trichlorophenoxyacetic acid (2.php?record_id=10603.S. Murphy RS.4. Sircar KP. Neurobehav Toxicol Teratol 1986.epa. Centers for Disease Control and Prevention (CDC). St Omer VE.4-D and 2. Mohammad FK. gov/oppbead1/pestsales/01pestsales/market_estimates2001.5-trichlorophenoxyacetic acid (2.31(2):121-125.5-t mixture.4-dichlorophenoxyacetic acid (2. Arch Toxicol Suppl 1980. 2003. Holson JF.4-D) epidemiology and toxicology. International Programme on Chemical Safety-INCHEM (IPCS). II. Selected pesticide residues and metabolites in urine from a survey of the U.31 Suppl 1:1825. 3/17/09 Kohli JD. Board on Health Promotion and Disease Prevention. Cook BT. I.inchem.4. Agricultural exposures and non-Hodgkin’s lymphoma. May.edu/catalog. Multireplicated dose-response studies with technical and analytical grades of 2. 2004. Developmental toxicity of 2. Beasley VR. LaBorde JB.4. 914. Atlanta (GA). J Toxicol Environ Health 1992.4.EPA. Gupta BN. Washington (DC): U. Nelson CJ. Toxicol Rev 2004. Available at URL: http://www. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Arch Int Pharmacodyn Ther 1974. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .5-T). 2.4.19(2):286-297. Holson JF.4. Gaines TB. Bradberry SM. Garabrant DH. 2005. Kolmodin-Hedman B. Pesticides residues in food: 1996 evaluations Part II Toxicology.23(2):65-73. U.5-T). Khanna RN. 210:250-255.37(2):277-91. Dhar MM. Pesticide industry sales and usage .pdf. Fundam Appl Toxicol 1992.8(5):551-60. 3/17/09 Institute of Medicine (IOM). Nelson CJ. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Poisoning due to chlorophenoxy herbicides.S. Wolff GL.S. Third National Report on Human Exposure to Environmental Chemicals. Behavioral and developmental effects in rats following in utero exposure to 2. S.4-. Tandon JS.5-trichlorophenoxy acetic acid in man. Available at URL: http:// www.4-D/2. Review of 2. Estimation of occupational exposure to phenoxy acids (2.5-T in four-way outcross mice. Erne K. McCallum WF. Crit Rev Toxicol 2002. et al. Carter-Pokras OD.nap. Dichlorophenoxyacetic acid. et al. Fundam Appl Toxicol 1992.4. Environmental Protection Agency (U.32(4):233-257. McLean D. Veterans and Agent Orange: update 2002.2000 and 2001 market estimates. general population.5-T). Washington (DC): National Academies Press.4:318-21. discussion 5-7.htm. Absorption and excretion of 2.org/documents/jmpr/jmpmono/v96pr04.4.

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

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

Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. EPA has established environmental standards for aldrin and dieldrin. OSHA has established workplace exposure standards for aldrin and dieldrin.S. 1991). Kanthasamy et al. 2000). 1998). 78 Fourth National Report on Human Exposure to Environmental Chemicals . but no estrogenic effect was noted in a study that used cultured cells (Tully et al. When dieldrin was fed to pregnant rodents. 2000). Survey Geometric mean (95% conf.S. 2005..gov/toxpro2. In a study of pesticide applicators with occupational exposure to aldrin.. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. environmental levels) and health effects is available from ATSDR at: http://www.atsdr. 1989). the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al. When fed to experimental animals. and seizures.cdc. similar to results in a subsample of NHANES II (19761980) (Stehr-Green. 1998) and behavioral changes (Carlson and Rosellini.Organochlorine Pesticides twitching. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al... 2000. Information about external exposure (i. tremors. nausea. population from the National Health and Nutrition Examination Survey. 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. 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. In samples obtained between 1973 and 1991 from Norwegian women. 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.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). 2005). and the FDA monitors foods for pesticide residues. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 2275 1946 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 756 588 1519 1358 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1057 946 1218 1000 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 559 456 512 485 1045 881 < LOD means less than the limit of detection for the lipid adjusted serum level.. in which only 10.e. serum aldrin levels were below the limit of detection. Li et al. 1995). IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. dieldrin at higher doses caused irritability... 2004). 1987). both aldrin and dieldrin caused liver enlargement and liver tumors. seizures (Smith. and occasionally. 2004). vomiting. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al.html.. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al.. The U.. Serum dieldrin levels at the 95th percentile in NHANES 2001-2002 and 2003-2004 subsamples were approximately ten times lower than the corresponding percentile measured in NHANES II (1976-1980).. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

160 (. population from the National Health and Nutrition Examination Survey.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.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.8) 15.8-25.120 (.4) 95th 20.9 (13.069) < LOD < LOD . 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 .1) 15. 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.242) .9-38.059 (.109-.8-17.110 (.100 (.130-.8 (9.5-17.7-22. Survey years 01-02 03-04 Geometric mean (95% conf.190) .1-24.1 (18.6-24.093) .6-24.2) 15.103 (.113 (.080 (.064) 90th .4 (12.00-14.060) .1 (13.0-21.4-18.149) .50) 15. which may vary for some chemicals by year and by individual sample.138) .5) 15.00 (8.054-.8) 14.190) .80-10.056-.4) 21.077 (.120) .140 (.8.5-17.8-19.4) < LOD < LOD 16.4) 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 8.3 (18.50 (8.147 (.8 (11.0) 21.100-.1) 13.30 (8.054-. Survey years 01-02 03-04 Geometric mean (95% conf.103 (.6 (15.109-.0) 19.130) .086-.150 (.9-22.070) .112-.3 (14.101) .1) 14.098 (.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 .5-15.102 (.2) 12.6) 16.S.048 (<LOD-.110-.1-16.062 (.9 (13.130-.0 (10.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.1) < LOD 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130) .10 (<LOD-16.070-.6) 9.1) 10.1) 15. < LOD means less than the limit of detection.4-17. Fourth National Report on Human Exposure to Environmental Chemicals 79 .130) .100-.8 (18.5 (<LOD-11.124) .160 (.100-.7 (14.9 (12.180) .5 (16.080) .7-19. 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 9.180) .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .3 (19.062-.120-.5) 19. which may vary for some chemicals by year and by individual sample.60-10.110) .8-17.40-9.090 (.30 (8.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .2-15.077-.4 (12.9 (12.2) 14.170) .80-9.117) < LOD .130 (.140-.6 (15.7 (15.5 and 7.100) .0 (10.110) .4) 14.138 (.112) 95th .6-33.116) .8-24.90) 90th 15.3 (13.2) 11.150 (.1-19.70 (7.7) 15.080-.063-. 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.110 (.7 (<LOD-15.6 (14.096-.055 (.110 (.S.090-.160) .8) < LOD 8.120 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.062 (.088-.090 (<LOD-.139 (.120 (.064 (.054-.158) .4) 539 456 484 487 980 885 Limits of detection (LOD.140) .075) < LOD .40-10.0 (11.109 (.9 (14.6) 19.089 (.0-25.4) 20.090-.130-.084-.80 (<LOD-10.4) 19.108-.1-18.049-.3 (18.058) < LOD .053 (<LOD-.9-23.1) 20.3-21.090-.070 (<LOD-.139 (.0 (15.073-.0) < LOD 9.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.083-.5) 21.100) .

Chlorinated Hydrocarbon Insecticides. References Agency for Toxic Substances and Disease Registry (ATSDR). Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Kanthasamy A. Aldrin and Dieldrin [online]. Corrigan FM. August 2008. Turner W. J Toxicol Environ Health 1989. PA. Organochlorine insecticides in substantia nigra in Parkinson’s disease. VT. Sonnenschein C. Six high-priority organochlorine pesticides. Cox. David VL.inchem.atsdr. Food and Drug Administration (FDA). Chemosphere 2004. Priestly BG. Available at URL: http://www. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.fda. J Toxicol Environ Health. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 15. Ginsburg KS. Exp Neurol 1998.150:263-271. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.91(1):122-126. bioaccumulation. 4/21/09 Jorgenson JL. Song S. Patterson DG Jr. Garrett N.66(4):229-234. Kanthasamy AG.109(Supp1):113-139. Chung KL. No:429-436.27:405-421. Andersen A. Available at URL: http://pubs. McIntosh LJ. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease.352:1816-1820. Neurotoxicol 2005. Jr and Laws ER. Environ Health Perspect 2001. Ellis H. 4/21/09 Bates MN. Jorgensen T. Roy ML. toxicology. 1991. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Grajewski B. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Smith AG.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Tully DB. Stehr-Green.gov/toxprofiles/ tp1. September 2002. 2 Classes of Pesticides.gov/ circ/2005/1291/. Academic Press. Part A 2000. pp. Edwards JW. plasma dieldrin. Toxicol Lett 1992. and lymphocyte sister chromatid exchange.9:1357-1367. Frey JM. Sanchez-Ramos J. Mumtaz MM. Facca A. 4/21/09 Hoyer AP. Kitzazwa M. Inc. Olea N. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Mann D. Finley B. Shore RF. Jr. Li AA. are nonestrogenic in transfected HeLa cells. Brock JW. Toxicological profile for aldrin/dieldrin [online]. In Hayes WJ. Available at URL: http://www. 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. Organochlorine exposure and risk of breast cancer. Lancet 1998.html. Aldrin and dieldrin: A review of research on their production environmental deposition and fate.54:1431-1443. Environmental Health Criteria 91. Teta MJ. Vol. United States Geological Survey (USGS). Environ Health Perspect 1995. et al. Rosellini RA. Grandjean P. Cancer Epidemiol Biomarkers Prev 2000. Serrano FO. Mink PJ. either singly or in combination. Available at URL: http://www. Soto AM. Anantharam V. and epidemiology in the United States.26:701-719. Int Arch Occup Environ Health 1994. Chapin RE. Psychopharmacology (Berl) 1987. J Occup Environ Med 2005.103(Suppl 7):113-122. Needham LL.64-65 Spec. Revised Feb. International Programme on Chemical Safety (IPCS).org/documents/ehc/ ehc/ehc91. Pesticides in the Nation’s Stream and Ground Water. Buckland SJ.cdc. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. 6/1/09 Ward EM. Patterson DG Jr. 1989. Hartvig HB. et al. Carlson JN. 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.cfsan. 731-915. Eds. Daniel SE. Schulte P.gov/~dms/ pesrpts.14:95-102. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Fernandez MG.usgs. Handbook of Pesticide Toxicology. Narahashi T. 1992-2001. Wienburg CL. Reprod Toxicol 2000.html. Basit A.47:1059-1087. New York.59:229-234. Demographic and seasonal influences on human serum pesticide residue levels. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.htm. 2007 [online].

7 (19.2 (41.3-45.Organochlorine Pesticides Chlordane CAS No.0) 27.8.6-12. fish. 2007).4 (35.8 (42.8-20.2) 46.5-38.9 (36. 10.1-19.5) 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 * * * * 11.0 (20. 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.6) 48.7-70.7 (<LOD-32.2 (39.1) * 11.9) 31. and 7.3) 18.1) * 11.4-40. in addition to trace amounts of numerous other related compounds (ATSDR.8) 52.6-18. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.5-43. 1994).9 (15.5) < LOD < LOD < LOD < LOD 13.2) < LOD 11. chlordane was used to kill termites and other insects on agricultural crops.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.S.6) 11.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.9 (29.3 (25.8) 44.7) 42.5) 10.5 (<LOD-12.5-32.2 (9.89-10.8) 18.9 (15.9) 11.9 (26.0-25.5-42.9) 17.6-53.0) 21. see Data Analysis section) for Survey years 99-00.9) 23.63 (8.4 (31.1-51.6) 9.4 (30.3 (20.9-38.90 (8.3) 37. lawns. 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.0 (32.8 (10.7-39.5-44.6-24.3-45.5) 21.8-73.5 (34. < LOD means less than the limit of detection.70 (<LOD-10.2-49. foods high in fat such as meat. buildings.6-45.6) 39.9 (26.7-56.6) 20. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.4-45.4) 37.3 (9. Consequently. and in soil.5) 38.5-41.5) < LOD < LOD 9.10 (8.0) 37.1 (<LOD-12.5) 44.1 (<LOD-12.82-11.0 (26.1 (27.3) 10.8) 27.1-25. population from the National Health and Nutrition Examination Survey. the technical grade product of each chemical contains 10%-20% of the other chemical.1) < LOD < LOD < LOD < LOD < LOD 8.4 (22.20-10.1) 30.9-21.4) 12.S.37 (8.1 (16.6) 9.8 (40.3 (28.5.1-65.8-23.9-21.20 (<LOD-11.8-33.2) 22.2 (10. Fourth National Report on Human Exposure to Environmental Chemicals 81 .1) 22.4) 18.3-32.8 (10.5.9) 37.1 (40.1 (25.9 (21.4) < LOD < LOD < LOD 23.10-18.2-56.2) < LOD 11.1) 30.9 (11.0 (<LOD-12.2 (36.7) 31. 57-74-9 Heptachlor CAS No.1-50. 2007).1) 90th 34.8) 52.7) 28.2) 37. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.5 (41.8 (17.7 (34.9) 13.3 (21.2) * 12. Technical grade chlordane had contained 7% trans-nonachlor.4) 22.1) 16.9) 23.3) 10.5-40.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3-49. respectively.9-40.2 (37.69-10.2-26.1 (<LOD-12.7-14. As a result of the manufacturing process.5) 56.7 (43.6) 23.9-42. which may vary for some chemicals by year and by individual sample.0-61.30-11.6 (9.36-11.0-67.9 (11.2) 34.9 (31.9 (18.0) 75th 20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 41.6 (43.8-61. 01-02.0-18.8-32.5) 37.2-28.9) 36.9 (17.0 (37.7) 35.6) 49.7) 9.7 (<LOD-13.6) 36.5 (31.2) 33.6) < LOD 11.5 (33.9) 11.5-47.7 (17.0-13.7 (42.7-12.0-33.4 (<LOD-12.7) 19.4-14.S.6) 48.1-25.20-11.0) 31.6 (25.1 (20. Since 1992.5-65. Survey Geometric mean (95% conf.4-21. and 03-04 are 14.8-33.8) 53.2-21.3 (11.8 (18.9) 10.3-24.4 (30. from the early 1950’s until the mid-1980’s.3 (<LOD-19.9) 39.4) 39.0 (16.3-43.3 (27.8-31.74 (<LOD-10.7) 19.1 (44. and dairy products are the usual sources of exposure to these chemicals in the general population.1-15.6) 8.2 (21.1 (15.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.5-13.7 (10.2-49.0) 20.1 (17.7 (32. Until 1988.4 (10.8 (17.8-43.6 (9.1 (11.. 1994.3 (26. Chlordane is not currently produced or used in the U.4) < LOD 11.0) 41.6-24.4-51.2) 36. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.10-11. heptachlor use has been limited to treatment of fire ants near power transformers.2 (28.5 (8.5) 9.4) 29.3) 18.7-25.6 (16.8-42.7 (34.9) 47.0-12.

373) .115-.079) .260 (.068-.290) .190-. 82 Fourth National Report on Human Exposure to Environmental Chemicals .240-.126 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.400) .170) .063) .350 (.070 (<LOD-.060 (<LOD-. 1991). OSHA has established occupational exposure criteria.062) < LOD .246-..270 (.270 (.077) . Survey Geometric mean (95% conf.180-.065-.286 (.140 (.140 (.120 (.223) .280-.057) * .450) .190-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .063-.149 (.160) .100-.310-.057-.067 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .280-. and inhalation exposure.104) .100 (<LOD-.320 (. 2007).270 (.230) . Le Marchand et al. The major metabolite of heptachlor is heptachlor epoxide.110 (<LOD-.090) .063 (.112 (.146) < LOD < LOD .240-.119 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. dermal.140 (.080) .200 (. and breast milk is a major excretion route in lactating women.348) .258 (.070 (<LOD-.170) . which may vary for some chemicals by year and by individual sample. Rogan.048-.370 (.058-.133) 90th .090-. to heptachlor.380) .208 (.130-.199-.110-. 1991. 1986).077) .130 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130-.204 (.315 (.070-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.230-.053-.104-.300) . 1977a.340) .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.074-.063 (.079) < LOD < LOD < LOD .063 (.350 (.092) .050-.150 (.203-.230-.047 (<LOD-.300) .290-.077) .071 (. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.300) .055-.242-.120-.128 (.430) .064) < LOD .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * . 1981).370 (.Organochlorine Pesticides (Dallaire et al.082 (.150-. 1996.150 (.269 (. The U.077) .140) . Chlordane and heptachlor are absorbed after oral.170-.063) * .302) . chronic doses of heptachlor have produced liver enlargement and injury. population from the National Health and Nutrition Examination Survey.200-.150 (. Shindell and Ulrich. FDA established allowable residues of chlordane.271 (.290) .106-.450) .140 (.170) ..207 (.068) 75th .130-.290 (.400) . neonatal mortality. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.160 (.180) .220-.075 (.260 (.410) .320 (.070) < LOD < LOD < LOD < LOD < LOD .258-.049 (<LOD-.130) .510) .S.160) .140-.286 (.320 (. characterized by seizures and paralysis.073 (. 1986). Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS. 2001. and the U.108-.056 (.130-.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 * * * * .340) .210 (. 2007.250 (.066-.S.320 (.066-.130-.170) .230 (.070 (<LOD-.080) .280 (.050 (<LOD-.200-.165-.210 (.180-.120-.057 (.213) * .070 (.240 (.253-.207) .245-.310) .069 (<LOD-.300 (.148-.280) . and heptachlor epoxide in foods and bottled water.063 (.168-.370 (.260-.170) .070-.280 (.250 (. 2006).287) .430) . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.240) .136) .070-.220-..291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .560) .S.227) < LOD .066 (<LOD-.091) .216-.148) .115 (.290-.190-. Takahashi et al.225 (.058 (.100-.070) . 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.440) . IARC.230 (.076) < LOD .061-. Acute.189 (. 2002. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.360) .146) . which is also persistent in the body (ATSDR.250-.310) .087-.200-.130) .310 (.320) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.068) .073) < LOD < LOD < LOD < LOD .300-.310) .058-.126) .230-.090) .320) .080 (. and alterations in immune function of offspring. 1977b.080 (. heptachlor.330 (.120-.231) . EPA has established environmental criteria for chlordane and heptachlor.210-.066 (.080) . and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide. In laboratory animal studies. Elimination of all these chemicals from the body occurs over months to years.083) . Smith.300) .260 (.130 (.220 (..100 (.150) .070 (<LOD-.130 (.189-.290-.083 (.280-.053-.180) .350) .160) .140-.

than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. 2001-2002. In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries.html. 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. transnonachlor.htm#ref. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000..org/documents/cicads/cicads/cicad70. than the 90th percentile values of NHANES 1999-2000 (Baker. Finding a measurable amount of oxychlordane. A recent assessment of heptachlor is available at: http://www. 1988). environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects. 1993).atsdr. respectively. transnonachlor. the reported oxychlordane and trans-nonachlor geometric mean levels from Canada and Greenland groups were about threefold to fivefold higher than among females in this Report (van Oostdam et al. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher... 2004). resulting in human exposure to heptachlor epoxide that was excreted into the milk.. 2006). respectively. Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 .. A small sample of Polish women had mean levels of oxychlordane and trans-nonachlor that were about fivefold lower than in females in the NHANES 20012002 subsample (Jaraczweska et al. Biomonitoring studies on levels of oxychlordane.gov/toxpro2. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn 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. 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. or heptachlor epoxide causes an adverse health effect.Organochlorine Pesticides about external exposure (i. inchem. In the Hawaii episode.e. trans-nonachlor. from ATSDR at: http://www. or heptachlor epoxide in serum does not mean that the level of oxychlordane.cdc. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high. 2000)... For the exposed persons drinking milk in the Arkansas episode. 2003). 2002).

1) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1-38.6 (16.3) 18.3) 23.7-25. Survey Geometric mean (95% conf.2-27.7-19.10-13.2 (<LOD-25.5 (18. and 03-04 are 14.6 (16.6) 14.8 (<LOD-23.4 (11.6 (<LOD-27.0 (15.9-25.3) 27.1-16.0) 13.6 (12.5 (11.5 (<LOD-21.3) 10.8) 19.2 (18.4) 18.8) 20.6) 13.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8 (13.0-17.8) 13.4 (<LOD-19.8) 21.6 (8.6.3) 22.2-16.6-17.5) 19.6) 22. 84 Fourth National Report on Human Exposure to Environmental Chemicals .S.3 (13.8 (15.7 (10.2) 15.5) < LOD 14.2-17.8 (18. which may vary for some chemicals by year and by individual sample.90 (<LOD-9.6-21.8) 14.5) 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 7.1) 20.2-27.4) 21.0-54.8 (13.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (11.50) < LOD < LOD < LOD 17. 01-02.0) 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 13.9 (15. respectively.1-15.5 (10.5.9-29.9-23.0 (11.9 (12.9) * * * 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) 26.4 (11. see Data Analysis section) for Survey years 99-00.0-16. 10.3-18.2) 20.8-46.6 (14.40) 15.6) < LOD < LOD < LOD 27.20 (<LOD-9.7 (13.7 (16. < LOD means less than the limit of detection.1) 23.8-24.1 (19.8-24.2 (<LOD-16.8) 14.8) 16.9) 15.3) 18.4 (<LOD-54.4 (15.9-16.2) 13. population from the National Health and Nutrition Examination Survey.5 (<LOD-32.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8.3) 16.7-18.3 (<LOD-25.0-17.8) 15.1-29.6 (11.2 (<LOD-62.8-23.8-24.8 (18.8) 13. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.3) 18.9-29.0-19.8) 19. and 7.1 (16.6 (13.

110 (.063) .170 (.117) .130) .100 (.190) .113) .180 (<LOD-.130) .077-.120 (<LOD-.074-.110 (.135 (.097) < LOD . which may vary for some chemicals by year and by individual sample.180) .270) .170 (<LOD-.130-.170) .116) < LOD < LOD < LOD .135 (.130 (<LOD-.200 (.100-.090-.140) .150 (.120 (.180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.100-.071-.190) .128 (.149) .380) .090-.087 (.094 (.053-.094 (.157) .140-. population from the National Health and Nutrition Examination Survey.180) .082-.200) .100 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.111) .240) .063) < LOD < LOD < LOD .130-. Survey Geometric mean (95% conf.110 (<LOD-.110-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .150 (<LOD-.077-.170) .100 (.110) .110-.120-.180) . Fourth National Report on Human Exposure to Environmental Chemicals 85 .150 (.055 (<LOD-.133 (.S.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 .120) .110 (<LOD-.220) .140) .180) .070-.069 (.090 (<LOD-.120 (<LOD-.101 (.110) .310) .170 (.310) .108-.090-.130-.113-.090 (.170) .106-.107-.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 .096 (.190 (.100 (<LOD-.098 (.100 (.120) .200) .111-.057 (<LOD-.090-.170 (.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 .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .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.101 (.130 (.104) .180 (.090-.076-.190) .130-.090-.067-.108) .126 (.

9-65.1-34.9-20.9-22.8 (28.9 (28.5) 9.0-23.4-52.2 (27.3) 30.5-111) 68.0-23.8-90.8-90.5 (15.3 (14.1) 17.8 (28.6 (52.3) 15.5) 36.1-55.86-13.4 (30.9 (<LOD-14.1-28.1 (17.3) 36.0 (60.0 (29.0) 40.8 (16.5.9 (47.2-23.5 (15.7 (35.8 (28.1) 17.3) 18.8 (17.2 (15.2) 20.0 (13.1) 32.2-21.0) 49.3) 25.2) 34.5) 48.5) 20.9 (15.9 (36.1-51.9-64.6) 13.2 (14.5.4-23.2) 39.6-88.0-123) 74. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 13.3-32.9) 14.5) 78.2 (59.8-67.6) 84.7) 59.1) 78.5-19.3 (49.0 (16.1 (10.7 (59.2 (19.5) 22.5) 77.1) 17.6) 34.0-113) 68.1 (65.4 (67.1) 30.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.7 (28.4 (28.5-17.9) 51.8 (11.7-35.8-41.5) 19.8-79.0 (48.1 (47.1-34.3-58.10 (<LOD-11.0) 19. 01-02.0-93.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. Survey Geometric mean (95% conf.1-22.7) 15.3 (45.6-19.3) 32.4 (11.7) 73.4) 55.7) 17.3) 18. 86 Fourth National Report on Human Exposure to Environmental Chemicals .9) 14.0 (14.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.6 (57.8 (13.8-110) 59.5-95.8-16.7 (59.1 (22.8-21.1) 31.3) 16.9-40.3-86.7-18.8 (13.6-20.3 (17.9-65.4-35.2-88.5-20.2 (7.0 (15.2 (64.1) 17.1) 18. and 03-04 are 14.7-77.0) 18.6 (<LOD-14.6) 56.5) 14.0 (19.6) 82.7-34.7-160) 86.7 (74.9-35.6-22.0-20.2 (36.7) 78.3-39.8-19.7 (30.5 (25.7-29.6 (56.6) 54.2) 30.2-18.2 (26.9) < LOD < LOD < LOD 20.7-113) 68.9) 51.7-22.2-18.4) 19.0-24.3) 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.8) 47.5) 90th 55.8) 19.4-18.1) 17.1) 78.S.7-17.7-20.3-21. and 7.1) 14.7-23.0) < LOD < LOD 8.3) 32.4 (16.8 (26.7 (13.6-54.6) 10.0) 75th 31.8-19.4 (45.2) 59.1-16.0-93.0 (42.6 (15.3-50.2 (25.9 (29.8) 51.6 (50. < LOD means less than the limit of detection.8-16.0-68.1) 18.2 (14.7) 56.70 (<LOD-12.5-36.4) 20.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.1-126) 67.8 (12.1-16.8.7-21.3-30.5) 14.2-17.5-87.6 (56. population from the National Health and Nutrition Examination Survey.5) 35.6) 60.4) 16.3) 19.1 (48.8 (<LOD-20.8 (42.4-67.7) 52.7) 35.6 (12.8 (71.9 (16.0-37.0 (62.6-82.7) 78.8) 80.0-22.7 (16.9 (51.4-62.1) 17.7-38.9 (15.2) < LOD 10.2) 19.0 (13.9 (66.3 (56.4) 59.7) 28.5) 26.0 (16.2 (60.8-129) 74.5 (45.9 (51.8 (15.7 (11. respectively. interval) 18.1) 62.5 (13.8 (26.2) 17. see Data Analysis section) for Survey years 99-00.1-20.1 (41.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.0) 33.0-143) 112 (68.4-36.6 (32.7 (18.8 (30.8 (49.4-22.5-69.1-18.9-89.7) 14.3) 30.0 (42.4) 107 (84. which may vary for some chemicals by year and by individual sample.7-32.6 (16.8 (19.6) 25.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.5) 30.1) 16.3-57. 10.9-58.6) 56.9-69.3 (58.4 (12.0-59.2-37.3-74.9-36.8 (45.5 (44.9 (19.3 (16.9-45.4) 48.3 (14.1) 17.2-16.6-66.0-38.8 (26.8-77.0 (15.

450) .280) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .180-.092 (.130) .080-.220 (.190-.205 (.370 (.079-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .126) .760 (.069-.470 (.173-.440-.116-.651) .085-.180-.190-.119) < LOD < LOD < LOD .840) .327 (.041 (<LOD-.125 (.130 (.093-.310-.830) .310-.097) .096-.285-.490 (.160-.340) .220 (.317 (.390 (.099-.400-.150) .400-.105 (.111 (.116) .071 (<LOD-.125) .680) .171-.113) .490 (.090) .480) .100-.069) .113) < LOD .047-.091) .112 (.106 (.220 (.110 (.122) .161) .100 (.470-.080-.060) .120-.288-.117) .220 (.240) .590) .460-.320-.240) .080-.210) .080-.090 (.310 (.161-.220 (.060 (<LOD-.210) .124) .130) .081-.520 (.420 (.630) .250) .082) .430-.108) .202 (.055 (<LOD-.270-.070 (.400) .580 (.186-.120 (.360-.310-.430-.120) .390 (.409-.120 (.300) .110 (.084-.290-.355 (.131) .081 (.108) 75th .220) .405) .093) .410-.230 (.090-.395-.120-.087 (.080) .301-.116 (.160 (.106 (.520 (.420) .098 (.111-.109 (.272-.090 (<LOD-.141) .440) .497-.380 (.630) .186 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .128 (.288 (. interval) .135 (.112 (.400 (.104-.310-.110 (.390) .120 (.580 (.210-.470-.395) .140) .095-.190-. Survey Geometric mean (95% conf.109 (.330-.110 (.210) .330 (.096) .120) .550 (.370 (.100-.490) .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.250) .108 (.093-.130) .170 (.110 (.098) .324 (.260) .130) .250) .565) .237) .371) .279-.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.390 (.100-.340-.930) .600 (.180-.684) .350 (.210 (.286-.330-.210 (.122) .090-.460) .061-.S.090-.510 (.390 (.054-.190-.119) Selected percentiles ( 95% confidence interval) Sample 95th .414 (.100-.510-.120) .830) .400 (.190-.343 (.100 (.470 (.134) .085-.800) .103 (.090-.260) .129) .240 (.068-.390) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.430-.210 (.500) .190-.098 (.110 (.594) .573 (.600) .580 (.062 (.310) .078-.177-.098-.090-.240) .20) .410-1.320-.079-.460) .340-.240-.120) .103 (.237) .130) .094 (.130) .127) < LOD < LOD .520) .470 (.211) 90th .141) .104 (.590 (.490-.960) .220 (.093-.078 (.080 (.158-.559) .089 (.099-.690) .360-.090-.210-.367) .397-.220 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .085-.640 (.110) .096-.220 (. which may vary for some chemicals by year and by individual sample.300-.106 (.232) .461 (.191 (.145-.458 (.242) .092 (.630) .130) .150) .417 (.110-.091-.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 .540) .120-.690) .060-.114) .130 (.183 (.350-.590 (. population from the National Health and Nutrition Examination Survey.680 (.234) .390-.

Gilman A. Charles MJ.330:55-70. 2001.Summaries & Evaluations. Available at URL: http://ntp. Stehr-Green P. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. et al.htm. Takahashi W. Environ Health Perspect 2003. National Toxicology Program (NTP). Eds. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). 1993. Dewailly E. 4/21/09 James RA. Organochlorine exposures and breast cancer risk in New York City women. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Sci Total Environ 2004.50(3):108-118. A Report to the Hawaii Heptachlor Research and Education Foundation.niehs. Bjerselius R. Chashchin V. Pollutants in breast milk. et al. 1991 pp. Available at URL: http://www.nih.html. Vol. 4/21/09 Dallaire F. Arch Environ Health. Jaraczewska K. 88 Fourth National Report on Human Exposure to Environmental Chemicals .atsdr. Inc. Odland JO. Senie R. Wolff MS. Berkowitz GS.niehs. International Agency for Research on Cancer (IARC). Wong L. Vol. Voorspoels S.cdc.html.heptachlor. Distribution of polychlorinated biphenyls.8:1-123. Tartter P. 79.28:497501. Jr and Laws ER. 731-915. Wohlleb JC. In Hayes WJ. et al. Drews K. Circumpolar maternal blood contaminant survey. Jr. Organochloride pesticide residues in human milk in Hawaii. Available at URL: http://www. International Agency for Research on Cancer (IARC) .pdf. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.gov/toxprofiles/tp31. Arch Pediatr Adolesc Med 1996. Academic Press. J Occup Med 1986. August 2007. Dewailly E. Bioassay of heptachlor for possible carcinogenicity. Brower S. Covaci A. Lawrence River (Quebec.nih. Granath F. Available at URL: http://www. May 1994. Smith AG.259(3):374-377. Glynn AW.org/documents/iarc/ vol79/79-12.41:145–148. et al.org/ documents/cicads/cicads/cicad70. Hansen JC. Laliberte C.111:349355. 1963-1967. Ayotte P. Bull Environ Contam Toxicol 1981:27:506-511.110:617-624. Bleiweiss IJ. Baker DB.inchem. Saidein D. Willman E. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.cdc.pdf.gov/ntp/ htdocs/LT_rpts/tr009. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.150:981-990. 2 Classes of Pesticides. 1979-1980. Hawaii Med J 1991. Lulek J. Barker J. 1986. Atuma S. Mortality of workers employed in the manufacture of chlordane: an update. Organochlorines in Swedish women: determinants of serum concentrations.372:20-31.html. Siegel BZ. Loo S. Environ Health Perspect 2002.84:151-161. Dendle WH. Van Oostdam JC. Canada). Sci Tot Environ 2006. Available at URL: http://www. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Shindell S and Ulrich S. Hertz-Picciotto I. Natl Cancer Inst Carcinog Tech Rep Ser 1977b.110(8):835-838. Available at URL: http://ntp. gov/toxprofiles/tp12. Toxicological profile for chlordane [online].inchem. LeMarchand L.htm. Keller JA. 6/1/09 Rogan WJ.org/site/foundation/ research/projects2. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Bioassay of chlordane for possible carcinogenicity. New York. 4/21/09 Baker DB. Handbook of Pesticide Toxicology. 6/1/09 National Toxicology Program (NTP).9:1-109. Head SL. Chlordane and heptachlor [online]. maternal serum and milk from Wielkopolska region. 1994-1997 organochlorine compounds. Environ Health Perspect 2002. Muckle G. Concise International Chemical Assessment Document 70 Heptachlor [online]. Environ Res 2000. Kolonel LN. Royce W. KalubaSkotarczak A. 2006. 9/25/07 International Programme in Chemical Safety (IPCS). Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Chlorinated Hydrocarbon Insecticides. Darnerud PO. Takei G.atsdr.gov/ntp/ htdocs/LT_rpts/tr008. JAMA 1988. Poland. Available at URL: http://www.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Aune M. Toxicological profile for heptachlor and heptachlor epoxide [online].

continues to be the primary source of DDT exposure.0) 19. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. DDT is converted in the environment to other more stable chemical forms.0-155) 83. population from the National Health and Nutrition Examination Survey.0) 40. 17. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.90 (<LOD-12.8) 15.5-36.8-39.0 (10. DDT and DDE can cross the placenta.9 (21.5) 23.1 (<LOD-39.7 (15. Smith.3) 22. and 03-04 are 20. population.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.S. fish. or dermal exposure.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. resulting in fetal exposure.9 (10.9) 14.1 (33.9) < LOD < LOD 9.50-11. Both Serum p.0) 20.4) < LOD 17. Only a small proportion of DDT is metabolized and excreted (Smith. o.p’-DDD (4% or less). Food imported from countries that still use DDT may contain the chemical or its residues.8-17. Gunderson. 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. DDT is converted to DDE and several other metabolites.3-590) 293 (104-541) 48. as well as in plant and animal tissues. 2002.0 (18.3) 21.5) 25.7 (19.2 (<LOD-40. 2008.8-23. particularly for endemic vector and malaria control.0-15.7-16.9 (<LOD-20. The biodegradation half-life of DDT in soil varies from 2 to 15 years.0-35. although DDT and DDE intakes have decreased over time (FDA.7.9-34.0 (18.S.3-16.2-bis(p-chlorophenyl) ethane (DDD). 01-02.9-28.1-71.10-13. 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.8.9) 29. after World War II until 1972. including 1.3 (<LOD-31.2-65.5 (14.5 (23. respectively. and water.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 8.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. food. Fourth National Report on Human Exposure to Environmental Chemicals 89 . which is a mixture containing p. sediments.3 (<LOD-21.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. p.0) 26.4) < LOD < LOD < LOD 61.5 (15.4. It was produced and used in the U.00 (<LOD-10.S.1-27.6 (22.7) < LOD 18. DDT was used at one time as a treatment for head and body lice.5-54.8) 30.3-236) 24. DDT can be absorbed after ingestion.1’-(2. and dairy products.0-27.2) < LOD < LOD 9.1 (23.9) 17. particularly meat. It is still used in some countries. see Data Analysis section) for Survey years 99-00. and 7.1) 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 12.2 (11.6 (<LOD-25.3) 28. DDT usually refers to the technical product.1’-dichloro-(2. < LOD means less than the limit of detection.0-37.6 (25.p’-DDT (15%-21%).p’-DDT (65%-80%). 1988).6 (31.9 (10.8-26.1) 31.7) 12.3) 21.5 (23.10 (<LOD-12.3 (27. These chemicals are highly persistent in soil. depending on conditions.5) < LOD < LOD 9.4 (23. inhalation.0-53.9 (10.0 (21. and trace amounts of several related compounds.8) 36. 1991).2) 30.2) 155 (59. when virtually all use of it was banned.6-33.70 (8. In the body.6 (9. In the general U.2-95. air. 1991).

240 (.061) < LOD < LOD < LOD .068-. lung cancer.230) .530 (.086 (.400 (. accidental exposures.112 (.054-.. Longnecker et al.071 (.087 (. 2006). 2000.26) 1. resulting in exposure to nursing infants (Rogan. which may vary for some chemicals by year and by individual sample.00) . and o. Snedeker.140) .. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190-1.078 (. Jusko et al. 2006.074-. have not been consistently demonstrated (Beard.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 .34) .330-4.220) . 2006. 2006. Gladen and Rogan.230) .201 (. 1956).530) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .400) .071-..150) .106) .p’-DDD and p. Hayes et al. Beard.059-. polychlorinated biphenyls. 2001).069) . 2001).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 .078-.107) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.065-.. 2002. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.142 (. premature delivery.00 (.. A workplace standard for DDT has been established by Serum p. 90 Fourth National Report on Human Exposure to Environmental Chemicals .048 (<LOD-. Gray et al.120 (<LOD-. DDT may bind to estrogen receptors (Chen et al.075) 1. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR.203) . 2002.130 (<LOD-.. population from the National Health and Nutrition Examination Survey.S.313 (.170 (. tremor.120-.128 (.290) .150-.. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.200 (..150-.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. Survey Geometric mean (95% conf.190 (.220) . 1996).260) .189-.063 (<LOD-. 1995. Reproductive effects in humans affecting birth weight.. 1997). 2002.343) < LOD . fertility.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .01) . other organochlorines. Calle et al. overt signs of acute human toxicity include vomiting.079) < LOD < LOD .180 (.143) < LOD < LOD . Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.180) . Studies of DDT exposure and pancreatic cancer.108 (. 1998). 2004.570-4..114-. and altered behavior after neonatal exposure (Eriksson and Talts.180-.080-. and duration of lactation.130 (<LOD-. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.627) .084 (.240) .250-1.190 (.180 (. 2006).150 (<LOD-. In laboratory animals.105-. and leukemia have also been inconclusive (ADSDR. dioxins and furans).150 (<LOD-.180) .p’-DDE can produce anti-androgenic effects (Gray et al..064 (..170-.106) < LOD < LOD .Organochlorine Pesticides chemicals are excreted in breast milk.132-.146 (.160-.g. 2001). It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.420) . Jusko et al. In high dose. and seizures. 2006).095) < LOD . 2002. reproductive organ abnormalities. Animal studies reported reduced fertility.250 (. Mariussen and Fonnum.051 (<LOD-.130-.140-.106-.170) . 2001).146 (.098-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.130 (<LOD-.189) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .62 (.

levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. population declined by about fivefold to tenfold.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.0-114) 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. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 91 . 2003). see Data Analysis section) for Survey years 99-00. respectively. and 7. 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. 1991). 1989). so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Compared to females in the NHANES 1999-2000 subsample.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. for males and females in the NHANES 19992000 subsample (Pavuk 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. 2005).gov/ pestcides/ and from ATSDR at: http://www. IARC classifies DDT (p.Organochlorine Pesticides OSHA and a guidance established by ACGIH. Stehr-Green. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p..gov/ toxpro2.. Smith.S.epa..7-119) 113 (100-140) 93.. More information about external exposure (i. 8. 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..6.. In a population-based sample of men and women from eastern Slovakia. Biomonitoring Information DDE persists in the body longer than DDT. 1998. compared to levels observed in this Report (Anderson et al.atsdr. 2003. environmental levels) and health effects is available from the U.cdc. 2004). mean serum levels of DDT and DDE in the U. 2002. Survey Geometric mean (95% conf. Heudorf et al.html.. 2002.6 (81.S. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.8. population from the National Health and Nutrition Examination Survey..p’-DDT) as a possible human carcinogen. Link et al. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. respectively. Declining DDE levels over time have also been observed in the German population.3. and 03-04 are 18.e. In general. EPA at: http://www. Since the 1970’s. NTP considers DDT as being reasonably anticipated to be a human carcinogen.S. 01-02.

63 (1.43-4.8-90.28) 1.820-1.40 (3.32 (1.6 (9.65) 1.53) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. considerably higher than levels in this Report (Smith.56-3.45 (1.77 (1.53 (2.55-9.20 (.59) 3.70) 1.01-15.53) 7.13-2.10-1.96) .19-14.52 (3.92 (3.8) 15.10) 2.2) 26. 2005).36) 3. 1991).85 (1.00-1.05) 1.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .37-4.18) 1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.635) 1.33-1.80) 1.2 (19.09-1.8 (13.38 (1.7 (8.72) 1.6) 8.30 (1.25) 1. or p.04-1.91) 3.87 (5.46 (1.59 (1.57-13.05 (3.18-3.4 (12.66) 1.0 (9.5) 10.2-32.58) 75th 3. In a subsample of NHANES II (19761980) participants.37-1.66-4.80) 3.29 (1.22-1.6) 9.62-6.60-13.4) 9. less than one percent had detectable serum levels of o.76) 1.71 (6. 309 versus 268 ng/g lipid.02 (2.9) 7.860 ng/L) and DDE (about 14.48 (6.97 (3.80) 1.24-17.78 (4.5) 16.11 (2.54-7.70-3.71) 32.69 (1. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.51-49.34) 6.49 (1.6) 12.14) 2.32-1.75) 6.34) 2.557) 1.01) 1.18-1.68) 2.385-.79) 4.88 (2.99) 1.64-2.680-1.590 (.34-11.1) 40.35) 1.5) 22.52-6.26-10.22 (7.14 (1.5) 5.61-2.43-4.6) 9.3-43.36-1.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.58) 1.965-1.59) 6.31-2.4-19.59 (4.00 (.66-17..15-4.4 (8.72) 1.9-17.36-2. 1989).7-20.22) .57-3.726) .8 (9.64) 3.0 (12..6 (8. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.57) 2.75) 2.520 (.87-16.534-.51-8.10-5.32-9.43-8.7) 13.11-1.56-2.07) 1.51) 1.69 (.04 (6.30-1.06) 1.34 (7.47 (1.96) 1.13 (1.92 (3.37-10. In the NHANES 1999-2000.25-16.68 (2.6) 13.75 (8.01-5.66) 1.57 (3.56-6.02-8.3) 10.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.870 (.16-1.8 (14.43 (5.2 (9.92) 1.00) 7.19) 4.59 (1.12 (.6) 9.2 (9.07) 1.75 (4. 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.69 (2.p’-DDT.88-35.01-1.76 (2.12-1.76-3.p’-DDT were below the limits of detection. 2004).25) 8.55 (2.31 (1.85-10.03-1.40-8.66) 3.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.1 (9.47) 3.18 (6. Finding a measurable amount of p. o.85-4.Organochlorine Pesticides nearby agriculture (Botella et al.01-1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.796 (.54 (1. 2001-2002 and 2003-2004 subsamples.17 (3.63 (6.40-4.39-2.2) 19..41-12.14-1.430-.890-1.4) 14.81-5.57 (1.77 (1.66-2. 2004).6) 11.38 (1.76) 1.51 (1.39 (3.S.39-1.93 (7.26 (1.23 (7.8 (13.00 (6.53-15.63-15.46 (1.500-.45 (1.730) .30-1.37-16.80 (2.91 (6.44) 1.27-1.61 (1.2 (6.39) 1.17-3.516 (.0) 2.66) 4.50-17.69) 8.37 (1.1 (8.7) 16.57-2.01-11.14-9..90) 22.3) 13.25 (.41 (1.3) 16.27) 3.963-1.49 (6.71) 12.6 (7.600) .68-4.18-1.16 (2.1) 12.611-1.623 (.32-1.9 (26.3 (9.30 (1.40-4.01) 1.456 (.52 (1.81-18.82) 1.75) 1.82 (1.83 (1. serum levels of o.58) 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 . Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.91-2.12 (6.51-15.48-4.646) .97-4.18-4.50 (2.31-12.1) 7.7-48. population from the National Health and Nutrition Examination Survey.81 (1.46-2. 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.419-.6) 9.54) 8.06) 3.3 (8.24 (1.32 (1.26) 3.7) 9.49) 8.81 (7.36 (3.49 (1.26-2.91-3.13) 4.10) .25 (1.488-.5) 7.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.561 (.81) 11.p’-DDT (Stehr-Green. Survey Geometric mean (95% conf.994-2.9) 5.84-3.21) 3.71 (5.63 (1.57 (1.51) 3. 1971).7-19.36-11.4) 13.14) 2.01-11.03-4.84 (3.9-38. High mean levels of whole blood DDT (about 3.6 (17.07 (5.32) 1. Serum p.24) 1.p’-DDT.65 (1.56) 2.90-8.21) 90th 7.9 (15.02) 1.69) 4.34-3. interval) 1.25-14.

8.4. Fourth National Report on Human Exposure to Environmental Chemicals 93 .Organochlorine Pesticides Serum o. Survey Geometric mean (95% conf.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 01-02. see Data Analysis section) for Survey years 99-00.S.7. respectively. * 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. and 7. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 17. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. and 03-04 are 20.

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

Longnecker MP. Ellis H. Sci Tot Environ 2006. Furr J. et al. Calle EE. Olson J. Bates MN.205:297-308. Hanrahan L. Herrman T. August 2008. Moysich KB.53(8):1161-1172. and other chemicals. Organochlorines in Swedish women: determinants of serum concentrations. Glynn AW. DDE and shortened duration of lactation in a northern Mexican town. Am J Public Health 1995. Crespo J. Bloom MS.1-dichloro2. Environ Health Perspect 2003. Willman EJ. Brock JW. Hum Reprod Updat 2001. Chen CW. Bull Environ Contam Toxicol 2004. Jr. Savitz DA. Bjerselius R. April 1982 to 1984. Gladen BC. et al. Maternal serum level of 1. and dichloro(diphenyl)ethylene (DDE). Zaidi SS.. Wolf CJ. India. Levels of DDT.355:7889.html. Paepke O. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Patterson DG Jr.21(1-2)37-48. Katz SH. Olea-Serrano MF. Arnold SF. Needham LL.52:301-309. Frumkin H. Cerrillo I.206:485-491. Biomonitoring of persistent organochlorine pesticides. Kulkarni PK. CA Cancer J Clin 2002. Gray KA. hypospadias. Environ Health Perspect 2004. lindane (g-HCH).72:261265. Gunderson EL. et al. Barr DB.cdc. Granath F. Krause C. Am J Epidemiol 2002. Thun MJ.58:1185-1201. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. DDE. dietary intakes of pesticides. The Great Lakes Consortium. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Kashyap R. Cueto C. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Effects of environmental antiandrogens on reproductive development in experimental animals. Environ Res 2004. Vorojeikina DP.155(4):313-322. Gray LE Jr. Kaus S. Baker RJ. Davis MD. Durham WF. Ostby J. Vena JE. Bhatnagar VK. Neurotoxicol 2000. Epidemiology 2006. Link B. Gabrio T. Greenfield TA. FDA total diet study. Lepom P. Garrett N.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Beard J. dichlorodiphenyldichloroethylene. Food and Drug Administration (FDA). The effect of known repeated oral doses of chlorophenothane (DDT) in man.111:349355. Jusko TA. Saiyed HN. Fourth National Report on Human Exposure to Environmental Chemicals 95 . et al. Buckland SJ. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Jr. Henley SJ. Rivas A. Brock JW. J Assoc Off Anal Chem 1988.gov/~dms/ pesrpts. Needham LL. Available at URL: http://www.17(6):692-700. Lancet 2001. et al.96:34-40.97(2):178192. Environ Health Perspect 1998. JAMA 1956. hexachlorobenzene. Heudorf U. Hediger ML.71(6):1200-1209. and HCB residues in human blood in Ahmedabad. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.106(5):279-289. Burse VW. Falk C. Zhou H. Notides AC. September 2002. Atuma S. et al. Int J Hyg Environ Health 2003. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.gov/ toxprofiles/tp35. Darnerud PO. Angerer J. Olea N. Koepsell TD.112(17):1761-1767. Zhou H. Parks L.atsdr. Biochem Pharmacol 1997. Hurd C. Piechotowski I. Available at URL: http://www. Talts U. Chemosphere 2005.54:1431-1443. 4/21/09 Anderson HA. DDT and human health.fda. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Olson JR. and DDD [online]. Needham LL. Seiwert M. 4/21/09 Gladen BC.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Organochlorines and breast cancer risk. Eriksson P. and polythelia among male offspring. Environ Res 2005. Chemosphere 2004. Toxicological profile for DDT. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Aune M. Longnecker MP. HCH. Drexler H.85:504508. Swanson MK.7(3):248-264. Klebanoff MA. et al. Rogan WJ. Hayes WJ. Klebanoff MA.html. Profiles of ortho-polychlorinated biphenyl congeners. Maternal DDT exposures in relation to fetal and 5-year growth. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Botella B. Klebanoff MA.162:890-897. et al. Exposure of women to organochlorine pesticides in Southern Spain. et al. Lambright C. Charles MJ.cfsan. Int J Hyg Environ Health 2002. selected elements. Zoellner I.358:110-114. Schulz C. Becker K. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings.

Demographic and seasonal influences on human serum pesticide residue levels.54:1509-520. Jones CR. Arch Pediatr Adolesc Med 1996. Crit Rev Toxicol 2006. Thomas PE. Astolfi E.53:455-477. Inc. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Pesticides and breast cancer risk: a review of DDT. 731-915. Comparative pharmacodynamics of CYP2B induction by DDT. and DDD in male rat liver and cultured rat hepatocytes. Rogan WJ. Neurochemical targets and behavioral effects of organohalogen compounds: an update. et al. Lubet R.Organochlorine Pesticides Mariussen E. DDE. Chovancova J. 1991 pp. Rey AA.150:981-990. Deichmann WB. Stehr-Green. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Environ Health Perspect 2001. Chlorinated Hydrocarbon Insecticides.27:405-421. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. 2 Classes of Pesticides. J Toxicol Environ Health 1989. children and newborn infants. Pavuk M. Lynch CF. Handbook of Pesticide Toxicology. Jr and Laws ER. Fonnum F. New York.20(2):186-193. Schecter A. Eds. Vol. In Hayes WJ. PA. Toxicol Appl Pharmacol 1971. Radomski JL. Pollutants in breast milk. Nims R.109:35-47. Cerhan JR. Petrik J. and dieldrin. Reddy AB. Jr. Academic Press.36:253-589. Snedeker SM. Fox S. J Toxicol Environ Health Part A 1998. DDE. et al. Smith AG. Chemosphere 2004.

Hepatic effects of endrin exposure have included necrosis. < LOD means less than the limit of detection.. Smith. Endrin does not accumulate in body tissues (IPCS.10 (<LOD-5. unlike aldrin and dieldrin. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. a stereoisomer of dieldrin.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.S.S.50) < LOD 5. IPCS.. 1991). 1992). endrin is converted rapidly to its major metabolite. total diet surveys (FDA. 1996. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and inflammation (Smith. manufactured. Kavlock et al.40-5. 1992.S.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..40 (<LOD-6. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. In the body.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 5.8.S. Ketoendrin is a major photodegradation product (IPCS. 1992).60 (5. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Survey Geometric mean (95% conf. is no longer manufactured in the U. 1991). 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. endrin can persist for years. 1981). fatty infiltration. EPA. or discarded. 1992). All uses of the pesticide in the U. or from contact with contaminated soils and sediments in areas where endrin was applied. which may vary for some chemicals by year and by individual sample. rodenticide and avicide.S. anti-12hydroxyendrin. Because it is metabolized so rapidly. Over time.30 (<LOD-6. 72-20-8 General Information Endrin. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. Endrin was not widely used as a termiticide.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.20 (<LOD-5.50) < LOD < LOD < LOD 5.30) < LOD 5. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Depending on soil conditions. At high doses. 2008). inhalation or dermal exposure routes. Endrin is absorbed rapidly after ingestion.. and occasionally at low levels in sediment and surface waters. 1987). Fourth National Report on Human Exposure to Environmental Chemicals 97 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. have been cancelled by the U. 1979.Organochlorine Pesticides Endrin CAS No. unless the dose is high and the exposure is very recent. Endrin was used as an insecticide. endrin has been detected with declining frequency in U.20 (<LOD-5. population from the National Health and Nutrition Examination Survey. endrin usually is not detected in serum of exposed individuals.09 and 7.10 (<LOD-5. An epidemic of acute endrin poisoning. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Endrin has been detected in soils.

IARC has determined that endrin is not classifiable with regard to human carcinogenicity.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 .atsdr. interval) Selected percentiles ( 95% confidence interval) Sample 95th . and the FDA monitors foods for pesticide residues.cdc..020 (<LOD-.S. 2004).020 (<LOD-.020-. In a small study of Spanish women hospitalized for elective surgery. serum levels of endrin were below the limit of detection. Information about external exposure (i. This finding is consistent with other general population studies (Bates et al.020 (<LOD-.24 ng/mL (about 6. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.020) < LOD < LOD < LOD . EPA has established environmental standards for endrin. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.020 (<LOD-. 2004.020) < LOD . Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. which may vary for some chemicals by year and by individual sample.020 (.html.24 ng/g of serum) (Botella et al. 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. endrin was detected in 9% of serum samples. with the highest value 6..020 (<LOD-. 2000). Ward et al.Organochlorine Pesticides The U.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 . Workplace exposure standards for endrin have been established by OSHA. 98 Fourth National Report on Human Exposure to Environmental Chemicals .gov/toxpro2. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.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 . Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. environmental levels) and health effects of endrin is available from ATSDR at: http://www..e. population from the National Health and Nutrition Examination Survey.020 (<LOD-.020) < LOD ..

Gray J. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 4/21/09 Kavlock RJ. Garrett N. Turner W. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. 4/21/09 Bates MN. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Patterson DG Jr. Narahashi T. Burse VW. Gray LE.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).cfsan. Exposure of women to organochlorine pesticides in Southern Spain. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Environmental Health Criteria 130. Rowley DL. Chlorinated Hydrocarbon Insecticides.gov/~dms/ pesrpts. Ward EM.html. et al. Hanisch RC. Fetotoxic effects of prenatal exposure in rats and mice.org/documents/ehc/ehc/ ehc130.96:34-40. et al. Buckland SJ. Perinatal toxicity of endrin in rodents. Frey JM.html. Chemosphere 2004. Chernoff H.21:141-150. Cancer Epidemiol Biomarkers Prev 2000. et al. Gray JA. Pediatrics 1987. Grajewski B. Schulte P. Inc. Smith AG. In Hayes WJ. Convulsions caused by endrin poisoning in Pakistan. Patterson DG Jr. Ginsburg KS. Eds. 731-915. Rogers E. Chernoff N. No:429-436. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Endrin [online]. Environ Res 2004. Saleem M. Botella B. Academic Press. Olea-Serrano MF. Available at URL: http://www. 1992. II. 1991. Cerrillo I. Jr. Ellis H. Food and Drug Administration (FDA). 2 Classes of Pesticides. Toxicology 1981. Jr and Laws ER. Needham LL. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.9:1357-136. Crespo J. Kavlock RJ. Whitehouse DA. 4/21/09 International Programme on Chemical Safety (IPCS).htm. Andersen A.inchem.64-65 Spec. Handbook of Pesticide Toxicology. et al. pp. Liddle J. Hardjotanojo W. Sokal D.13:155-165.54:1431-1443. Fetotoxic effects of prenatal exposure in hamsters. Rab MA.gov/toxprofiles/tp89.fda. Available at URL: http://www. Roy ML. Toxicol Lett 1992. New York. I. Hanisch RC. Perinatal toxicity of endrin in rodents.79(6):928-934. Gray LE. August 1996.atsdr. Rivas A. Toxicological profile for endrin [online]. Vol. August 2008.cdc. Olea N. Available at URL: http://www. Toxicology 1979.

2) < LOD < LOD 13. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.9) < LOD < LOD 15.4) < LOD < LOD 22.0 (14.5-14. < LOD means less than the limit of detection.8 (22.1 (14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7 (15.5 (14.9) < LOD < LOD 20. 2005). air.3 (12.4-16.5-15.5-TCP) and 2. Gunderson.0) < LOD < LOD 15.7-29. 2002).S. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.6 (21.9) < LOD < LOD 28. EPA cancelled its use in 1984.6-19.4-15. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. water.7) * * 14. or game taken from areas with HCB contamination.4) < LOD < LOD 18. particularly by consuming fish.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 * * 16.8-15.3) < LOD < LOD 20. Although it is not manufactured as an end-product in the U.9) < LOD < LOD 16.2-15. and elimination occurs by renal and fecal routes.2 (13..4.0) < LOD < LOD 24.3 (16. see Data Analysis section) for Survey years 99-00. wildfowl.5) < LOD < LOD 18.0-16. Survey Geometric mean (95% conf.7-22. 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.2-31.3-26.7-30.0) < LOD < LOD 15.0 (18. and 7.8 (15.4 (22.5-15.6) < LOD < LOD 24.2-15.7-21.3 (22.5-33.0 (25.4) < LOD < LOD 14.3-20.6 (23.9-20.5-18.3) * * 15. 1988). primarily as a fungicide and seed treatment until the U.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.8.9 (25.4 (18. 1976).9) 19. and sediment (Barber et al.1) * * 15.5 (13.4) < LOD < LOD 23.6-TCP) (To-Figueras et al.0-19.9-15.2 (14.1 (13.9 (14.Organochlorine Pesticides Hexachlorobenzene CAS No..7 (15.9) < LOD < LOD 19. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways..6) < LOD < LOD 25.7) < LOD < LOD 24.7-15.6-33.7-16. and foods with a high fat content.S.3) < LOD < LOD 29.1 (14.7-16.4) < LOD < LOD 19. 31. 100 Fourth National Report on Human Exposure to Environmental Chemicals .9-30.4.2 (17.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.9) < LOD < LOD 20.4 (11.3-22.8 (26.. The general population may be exposed to HCB through diet.3 (20. and accumulates in fatty tissues where it persists for years.2 (24.1-20. HCB is well absorbed after oral administration.4. distributes widely throughout the body. HCB is slowly metabolized.0-25.2 (14.S. population from the National Health and Nutrition Examination Survey. 2008.4) < LOD < LOD 33. 01-02.4.2) < LOD < LOD 29. Urinary metabolites include pentachlorophenol (PCP).0-28.6) < LOD < LOD 26.0) * * 15.5-trichlorophenol (2.9-24.6-44. Therefore.5 (13.3 (14.S.7 (27.1-16.3) 24.4.9-32. respectively.6 (24.9-17.7 (19.1 (17. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.7-26. breast milk is an additional route of elimination in nursing women.9 (25.6) 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. 2.5-14. The FDA dietary surveys have shown that over time.9 (23.6) < LOD < LOD 26. and has been detected in soil.4 (18.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. 1997).8) < LOD < LOD 27.6-32.3 (22.6) < LOD < LOD 14.1) < LOD < LOD 15. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. which may vary for some chemicals by year and by individual sample.0 (18.6-trichlorophenol (2. and 03-04 are 118. HCB has been detected in fewer foods since the 1980s (FDA.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0.6-26.

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

1986. As a result of the lower limit of detection in NHANES 2003-2004. Link et al. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. FDA total diet study.44 mg/L.. Lackmann.77:173182. Piechotowski I. Santiago-Silva M.81(2):82-85. Bryan GT. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 4/21/09 Barber JL. HCB levels were directly related to age. September 2002.fda. J Exp Sci Environ Epidemiol 2007. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. In Spain. more HCB levels were quantified.349:144. Aune M. Fenster L. 1999). Kohli J. Dallaire F. Sala M. Schulz C. 2006). Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Lawrence River (Quebec. Granath F.. Chemosphere 2005. 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. Available at URL: http://www. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Int J Hyg Environ Health 2002. HCB detection in serum also was proportional to age. Arch Dermatol 1999. Herrman T. Canada). Becker K. Gunderson EL.71(6):1200-1209. Environ Health Perspect 2002.. Ayotte P. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al.. In the 1976-1980 NHANES subsample. April 1982 to 1984. The metabolism of higher chlorinated benzene isomers.135(4):400404. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.9% of participants had quantifiable levels (Stehr-Green. Can J Biochem 1976. Jones KC.cfsan. Herrero C. Environ Health Perspect 2003. Krause C. 2002). Muller C. Kemper FH. et al. selected elements. Peters HA.. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. et al. In a representative sample of the 1998 German adult population. 2005). Ozalla D.gov/~dms/ pesrpts. Bradman A... J Assoc Off Anal Chem 1988. et al.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Over the past two decades. van Wijk D. Biomonitoring of persistent organochlorine pesticides. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.cdc. trends and processes. 2002. Hexachlorobenzene in the global environment: emissions. Otero R. Arch Neurol 1982. Jones D. Schwartz JM. Organochlorines in Swedish women: determinants of serum concentrations.. Dewailly E. Laliberte C. respectively. Darnerud PO.58:1185-1201. Gocmen A.atsdr. August 2008.17:388–399. Holland NT. Lackman.54(3):203-208. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 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. only 4. Lepom P. Kaus S. levels. 2002) and among children (Link et al.39(12):744-749. Cripps DJ.gov/ toxprofiles/tp90. Glynn et al. Sweetman AJ. Bjerselius R.205:297-308. but overall.... 102 Fourth National Report on Human Exposure to Environmental Chemicals . et al.110(8):835-838. 4/21/09 Glynn AW. 2002. Link B. Seiwert M. and other chemicals. Bradman et al. Dogramaci I. dietary intakes of pesticides. Safe A. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.111:349355. 2003). Biol Neonate 2002. 2002. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Available at URL: http://www. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Muckle G.html. Sci Tot Environ 2005. Lecha M. Toxicological profile for hexachlorobenzene update [online]. Gabrio T. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Bertram et al. Barr DB. distribution. however. Eskenazi B. Food and Drug Administration (FDA). Bertram HP. Lackmann GM. 2005).html. Paepke O. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. 2005. Atuma S. 2002. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. and the geometric mean concentration of HCB in whole blood was 0. References Agency for Toxic Substances and Disease Registry (ATSDR). IARC Sci Publ 1986. Zoellner I. Reference values updated. 1989).

Barrot C. Stehr-Green. Cutaneous porphyria in Turkey.Organochlorine Pesticides Schmid R. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Sala M. Rodamilans M. Fourth National Report on Human Exposure to Environmental Chemicals 103 . J Toxicol Environ Health 1989. et al. To-Figueras J.27:405-421. Demographic and seasonal influences on human serum pesticide residue levels. Environ Health Perspect 1997. Santiago-Silva M. N Engl J Med 1960.263:397-398. PA. Otero R.105(1):78-83.

4) 901 1067 952 992 1224 1007 Females 11.9 (62.8) 52. The gamma isomer.S.0-21.5 (8.4 (8.4-73.0 (35.68 (<LOD-10.4-50.6) 35. Lindane has a half-life of about two weeks in soils and water. water. and delta.8) 95th 68.7 (62.9) 17.3 (42.8 (10.61-12.8 (9.S.7 (<LOD-16.S.2 (29. HCH isomers. see Data Analysis section) for survey years 99-00.6-62.5 (43.6) 36.90-8.5528.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.5-123) 49.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.3) 14.66-12.56-12.60-13.6-89.9-21. 58-89-9 General Information Hexachlorocyclohexane (HCH).8) 7.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16. soil. Technical grade HCH is a mixture of all four isomers.0 (33.7-20.2-55.8) * * * * * * 15.0-23.8 (21.6 (17. and 7.20-16.9-81.1 (9.89 (<LOD-9.1-32.7) 73.5 (16.8 (23.90) 7. and 03-04 are 9.1-49.9 (11.6) 18.7-96.4 (12.0-70.5) 14.5) 16.7) 32.50) 8. 6. formerly referred to as benzene hexachloride.0) 8.0) 71. EPA cancelled agricultural uses of lindane (ATSDR.8. population from the National Health and Nutrition Examination Survey.7-69. 01-02.7) 18.4) 11.6-37. respectively.8) 39.2 (50.5 (14. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.3 (42.1-16.46-11.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.9-14.8-199) 134 (85.7 (30.6) 16.5) 29. the U. 319-85-7 gamma-Hexachlorocyclohexane CAS No. interval) 9.0) 41.9 (32.1) 12.9 (50.2-20.6 (33.7-26. gamma.70-12.2) 9.7 (25.80 (6. However.6) 50.2-67.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.0 (14.0) 17.3) 51.2-42. containing about 64% alpha and 10%-15% gamma isomers.9 (26.7) 27.9 (9.5 (37. environmental levels declined.6) 653 758 589 1240 1533 1370 20 years and older 10.2-46.4 (50.4) 44.0-20. and have been used either as fungicides or to synthesize other chemicals.9-51.0 (8.7 (29.9 (40.2) 13.6-42.8) 27.4) 21.9-56.4) < LOD < LOD < LOD 46.1 (18.76.1-37.0) 7. each result has been multiplied by 1. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.1) 12. beta.1 (27.5 (11.0-111) 70.6-47.7 (35.8 (17. particularly alpha and gamma have been detected widely in air.5 (24.5) 11.6 (22. **In survey period 2001-2002.3) 25.4 (11.3) 37.0 (19. 608-73-1 beta-Hexachlorocyclohexane CAS No. In 2006. and sediment as a result of historic production and use.9-178) 48.1) 31.9) 15.1-27. See the section “What’s New” at the beginning of this Report for details. 104 Fourth National Report on Human Exposure to Environmental Chemicals .1-32.8 (32.9 (30.8-54.9) 45.1 (9.70 (6.2) 36.4) 10.8-87.0-34.6-18.7) 56.1 (16.36. which may vary for some chemicals by year and by individual sample.6-14. HCH isomers are lipophilic.0 (37.4) 51. so they can accumulate in fatty tissues of animals.3 (13.4) 27.1 (12. It is no longer produced or sold in the U. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.70-19. * 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.7) 10.7 (53. including alpha.1 (11.9-24.2) 62.3-56.2-98.3) 34.6) 47.04-10.90-8.2-22. 2005).7) 97. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.7-69.2) 142 (99.70 (8.6 (40.43 (<LOD-9.1) 71.0 (<LOD-12.5) 40.3 (26.Organochlorine Pesticides Hexachlorocyclohexane CAS No.1-15.1) 13.3 (62.8-16.5) 67.2 (18.7-166) 70.3-38.87 (9.1-36.4-111) 84.30-11.0) 35.8 (64.8-19. exists in several isomeric forms.5) 22.8-68.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.2-52.4-45.2 (9. commonly known as lindane.6 (10. 2005).0-70. The other isomers can be formed during the synthesis of lindane.8) 12.1 (30. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.2 (34.1 (21.7) 10.9) 81.5) 90th 42.80 (<LOD-14.8 (33.6-20.7-96.2-87.4 (52.8) < LOD 10.2 (48.6 (16.3-85.2-17.7 (13.4) < LOD 9.6-135) 69.2 (31.4 (16. As pesticide applications of HCH were increasingly restricted or eliminated.5-29.7) 23.

080 (.090 (.370-. 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. Rogan.37) 1.294-.250 (.078 (. enlarged livers.110) .290 (.120 (.056-.S.S.560 (.089) .222 (.150-.210) .090 (.372 (.560) .270 (. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.050 (<LOD-.050-.050 (.120) .072 (.580 (.450) . paresthesias.32) .200-.260) .450-.103-.260-.310 (.120) .460) .412 (.150) . Gunderson 1988).057 (<LOD-.661) 901 1067 952 992 1224 1007 Females .290 (..250) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .067) .190-.297-. hepatic enzyme induction.281 (.240-.170-.216 (.290) .070 (.090-.290 (.100) .210 (.100-.048 (<LOD-. HCH isomers are absorbed after inhalation.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .080 (.580-1. 2002).380 (.100 (.056-. and nephropathy developed (IPCS.058 (<LOD-.350 (.250 (.360 (.065 (. The beta isomer accumulates in fatty tissues and is metabolized more slowly.050 (<LOD-..521 (.470 (.057-.300-.070-.840) .690) . Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.083) .390 (. U.100-.103 (. ingestion.310) .050) . 1977).. 1986). probably by blocking inhibitory neurotransmitters in the central nervous system.510) .350) .070) .180-. which may vary for some chemicals by year and by individual sample.191-.210 (.620-1. or dermal exposure.305) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.070 (.700) .118-.460 (.067 (.410 (.050 (.214) .140 (.120 (.910 (.360-. ataxia.077) < LOD .089-. The U.050-.167 (.710) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .080-.040-.091) .587) 653 758 589 1240 1533 1370 20 years and older .390-.501) .240 (.139 (.070-. and seizures.146-.400) .210-.110) .442 (. Saxena et al.234 (. tremors. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.103) 90th .160) .130-. the serum half-life was about 20 hours among children (Ginsburg et al.404) .Organochlorine Pesticides exposure to HCH is through the diet.065 (. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.130) .077) < LOD .051 (<LOD-.220-.069) .081-.308-.140) .190) .150 (.410) .221-. each result has been multiplied by 1.244-.570 (.220-. OSHA and ACGIH have established workplace standards and guidelines.090 (. for lindane. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.254) 95th .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-. After dermal application of lindane 1% lotion.086) < LOD < LOD < LOD < LOD < LOD < LOD .250 (.814) .410-. and memory loss (Nigam et al.190) .410) .110-.118 (.057-.140) .098 (.340-.160 (.287 (. Workers who directly handled HCH have complained of headache.420-.092 (.331 (.170-.080-.400) .120-..175 (.130 (.080) * * * * * * .068-.680) .450 (.120-. respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.620) .200 (.01 (.050-.080-.5528.051-.200-.050-.330-.100) .330 (.190-1. 2008. EPA has established a drinking water standard.150) .120-.480) .070-.064 (.047-.05) .144 (. and FDA has established a bottled water standard and food residue tolerances for lindane. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al. When animals were chronically fed lindane at high doses. 1971.083 (.191-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .250-.140) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.060) . Distribution is mainly to fatty tissues.480 (.124-.173-.319) .280-.470) .290) .059-.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 .096) .110) .064) .220 (.230-. interval) .174) ..310) .250-. resulting in a half-life of about seven years.160-.073-.119) .120 (.100 (. 1996.260) .125) < LOD < LOD < LOD .600) .220) . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. 1983).080) .S.280-. **In survey period 2001-2002.360) . 1981). See the section “What’s New” at the beginning of this Report for details.131-. population from the National Health and Nutrition Examination Survey.480 (.382-.320 (.340) .062 (.062 (.

which may vary for some chemicals by year and by individual sample. 1971. 1998. aged 9-11 years. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Stehr-Green.e.S. 2004) and India (Bhatnagar et al. and a diet that includes meat (Becker et al. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. In recent years. Additional factors associated with higher beta-HCH levels include rural residence. 10. 106 Fourth National Report on Human Exposure to Environmental Chemicals . environmental levels) and health effects is available from the U.atsdr. 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.5.cdc. 2004). Becker et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004. the maximum and 95th percentile beta-HCH values.epa. Sturgeon et al. Kutz et al. respectively.. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. 1998).S. 2002. older age. population from the National Health and Nutrition Examination Survey.. 1989). Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR.gov/pesticides/ and from ATSDR at: http:// www.. < LOD means less than the limit of detection. 1991... Biomonitoring Information Because of its longer half-life. In NHANES 1999-2000.. see Data Analysis section) for Survey years 99-00.8.5. More information about external exposure (i. 1991. were similar to the 95th percentiles in this Report.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 01-02. Stehr-Green. 2005. Survey Geometric mean (95% conf... 2001-2002. and 2003-2004.. respectively. serum levels of lindane were generally below the limits of detection. 2005. In an earlier (1996-1997) sample of German children. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers.. Bates et al. Kutz et al. male sex. and 03-04 are 14. Radomski et al..html. In populationbased studies of New Zealand adults and German adults and children. and 7. Link et al. 1989. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens.. 2002).gov/toxpro2. EPA at: http://www.

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

Siddiqui MKJ.inchem.57(4):315-320. et al. Olson J. Karnik AB. The Great Lakes Consortium. Metabolism of gammahexachlorocyclohexane in man. Rivas A. Raju GS. et al. Biomonitoring of persistent organochlorine pesticides.91:998-1000. Botella B. Brinton LA. Available at URL: http://www. Visweswariah K. Int J Hyg Environ Health 2002. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. J Assoc Off Anal Chem 1988. Angerer J. Absorption of lindane (g benzene hexachloride) in infants and children. Cancer Causes and Control 1998. Bjerselius R. Kutty D. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). 2002. Stehr-Green.cfsan. Crespo J. Pollutants in breast milk. Zaidi SS. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rey AA. Becker K. et al. Majumder SK. Link B. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. selected elements. Gabrio T. Saiyed HN. Astolfi E. Bhatnagar VK. Bull Environ Contam Toxicol 2004. August 2005. Placental transfer of pesticides in humans. International Programme on Chemical Safety (IPCS). Piechotowski I. J Toxicol Environ Health 1989. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Zoellner I. and other chemicals. Int Arch Occup Environ Health 1983. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Rothman N. and HCB residues in human blood in Ahmedabad.27:405-421.71(6):1200-1209.atsdr. Levels of DDT.205:297-308.gov/~dms/pesrpts. HCH. Glynn AW.htm.52(1):59-67. August 2008. Toxicol Appl Pharmacol 1971.20(2):186-193. Needham LL. Available at URL: http://www.48:127-134. Wood PH. Maass R. Lindane.111:349355.150:981-990. Sturgeon SR. Krause C. Bai KM. Lepom P.96:34-4Food and Drug Administration (FDA). Herrman T. Demographic and seasonal influences on human serum pesticide residue levels. Arch Toxicol 1981.58:1185-1201.106(5):279-289. Atuma S. 4/21/09 Anderson HA. Toxicological profile for hexachlorocyclohexanes update [online].54:1431-1443. India. Darnerud PO. Bates MN. available at URL: http://www. Brock JW. Hanrahan L. 4/21/09 Ginsburg CM. et al. Int Arch Occup Environ Health 1986.72:261265. Reisch JS. Kashyap R.120:1-82.html. Ellis H. Environ Health Perspect 1998. Seiwert M. et al. Patterson DG Jr. Radomski JL. Chemosphere 2004. J Pediatr 1977. Kaus S. Kulkarni PK. April 1982 to 1984. et al. Schulz C. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Saxena MC. Potischman N. Garrett N. et al. Olea-Serrano MF. PA. Needham LL. Rev Environ Contam Toxicol 1991. Granath F. Burse VW. Needham LL. Krishna Murti CR. Rogan WJ. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Buckland SJ. org/documents/jmpr/jmpmono/2002pr08. Cerrillo I. Exposure of women to organochlorine pesticides in Southern Spain. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Nigam SK.9(4):417-424. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Aune M. Environ Health Perspect 2003. Heinrich R. Chemosphere 2005. Arch Pediatr Adolesc Med 1996. Bottimore DP. Environ Res 2004. Falk C. dietary intakes of pesticides. children and newborn infants. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Organochlorines in Swedish women: determinants of serum concentrations. 4/21/09 Kutz FW. Paepke O. gov/toxprofiles/tp43. Gunderson EL.fda. Bhargava AK. Deichmann WB. FDA total diet study.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). VI. Olea N.cdc. Lowry W. Occupational exposure to hexachlorocyclohexane.html.

Occupational exposure is limited to workers at sites where mirex contamination is present. aquatic organisms. where it was applied directly to soil and by aerial spraying. 1985.0 (<LOD-108) < LOD < LOD 50. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.0-374) 11.0 (14. or pesticide application. Formerly. 2385-85-5 General Information Mirex has not been produced or used in the U.6 (<LOD-31.0) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 19.8 (<LOD-73.5-82. Mirex has been detected in air.6 (<LOD-108) 9.10-37.1 (8.S.7) < LOD 66. (Kutz et al.5-425) 40. see Data Analysis section) for Survey years 99-00. Fourth National Report on Human Exposure to Environmental Chemicals 109 . Mirex is absorbed through the skin and from the gastrointestinal tract. 1995). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.6.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. In studies conducted in the 1970’s and 1980’s.8) < LOD 15.5 (<LOD-42.6) < LOD < LOD < LOD < LOD 71.6-305) 15. Mirex binds strongly to soil.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 13.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3 (15.2 (7.S.2-230) 13.8 (12. 1991).70-24.4) < LOD 15.5-291) 11. 10.8. 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. disposal. < LOD means less than the limit of detection.4 (8. sediments. Some states and the U.1 (<LOD-65.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. which may vary for some chemicals by year and by individual sample.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. after which it is widely distributed in the body and stored in fat. population from the National Health and Nutrition Examination Survey. Mirex is not metabolized in the body. 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.4) < LOD 63.5 (<LOD-115) 153 (30.10 (<LOD-15. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.2) 51. animals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and foods.70-40.6 (<LOD-23. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. 01-02.7 (12. especially those from persons living in the southeastern U. mirex was detected in human adipose samples.4-230) 18.S. and 03-04 are 14. respectively.7 (<LOD-47.40 (<LOD-13.3 (15. water. soil.5 (9.6) 9. since 1977. it is a highly persistent chemical in the environment.Organochlorine Pesticides Mirex CAS No.S.5..3-225) 15. resulting in exposure to newborns and nursing infants. where it has a half-life of 12 years. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. Mirex can cross the placenta and be excreted in breast milk.S. Survey Geometric mean (95% conf.90-29.1 (13.7) 8..70 (<LOD-15. and 7.0 (12.

73) .310 (. 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.8.112 (.450) 1. as well as in a subsample of NHANES II (1976-1980) participants.92) .02) .170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . IARC classifies mirex as possibly carcinogenic to humans.106) < LOD . population from the National Health and Nutrition Examination Survey.220 (<LOD-..055-.110 (<LOD-.170) < LOD .093 (. 110 Fourth National Report on Human Exposure to Environmental Chemicals .080-1.610) < LOD < LOD < LOD < LOD . 1991). Laboratory animals fed high doses developed liver enlargement and liver tumors.100 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .268) < LOD .635) < LOD .090-1.174) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.370 (.090-1.gov/toxpro2.064 (<LOD-. 1989).077 (<LOD-. 1995.510) < LOD < LOD .470) .090 (<LOD-.080-1.450 (.. 2004). environmental levels) and health effects is available from the ATSDR at: http://www.108 (.090-1.7 ng/g of lipid. 7. 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.256 (. 2001-2002. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.41) .070-1.102) < LOD < LOD < LOD < LOD .S.079 (<LOD-. Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions.. In samples obtained between 1994 and 1997. serum mirex levels were generally below the limits of detection (Stehr-Green.090 (<LOD-. In addition.052-.79) .690) .37) .410 (. reproductive toxicity included decreased fertility and testicular damage.79) . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.cdc.220) .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 . 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.140 (<LOD-.106 (.atsdr. and 2003-2004 subsamples.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 .089-. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.053-.470 (.Organochlorine Pesticides exposures are unknown.html. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .430 (. Survey Geometric mean (95% conf.170-3. The U. Biomonitoring Information In the NHANES 1999-2000.100 (<LOD-. which may vary for some chemicals by year and by individual sample.054 (<LOD-.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Smith. EPA has established environmental standards for mirex.e.062-. The geometric mean mirex levels of the Inuit mothers were 8.470) .059 (<LOD-.S.090 (<LOD-.08 (. and 4. 2005). More information about external exposure (i.

References Agency for Toxic Substances and Disease Registry (ATSDR). Academic Press. Carra JS. dichlorodiphenyldichloroethylene. Olson JR. Available at URL: http://www. Leininger CC. J Toxicol Environ Health 1985. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.html. Strassman SC. Jr and Laws ER. 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. Sci Total Environ 2004. Bottimore DP. Kutz FW. Inc. Smith AG.330:55-70. Hansen JC. Handbook of Pesticide Toxicology. 731-915. et al. Environ Res 2005.15:385-394. Stroup CR. Rev Environ Contam Toxicol 1991. Stehr-Green. 1991 pp. Moysich KB. 4/21/09 Bloom MS. Toxicological profile for mirex and chlordecone [online]. Chlorinated Hydrocarbon Insecticides. Profiles of ortho-polychlorinated biphenyl congeners. Demographic and seasonal influences on human serum pesticide residue levels. Circumpolar maternal blood contaminant survey. Eds.27:405-421. Chashchin V. Vena JE. 1994-1997 organochlorine compounds. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. New York.97(2):178192. Vol. Kutz FW. Dewailly E. Gilman A. Odland JO. 2 Classes of Pesticides.gov/toxprofiles/ tp66.Organochlorine Pesticides effect. Swanson MK. hexachlorobenzene. In Hayes WJ. J Toxicol Environ Health 1989. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Watts DL.atsdr. PA. The human body burden of mirex in the southeastern United States.cdc. August 1995. et al. Wood PH. Van Oostdam JC. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Jr.120:1-82.

40-11. and polychlorinated benzenes (Kohil et al.40 (2.50 (2.0) 14.0) 2.940-3.72) < LOD 1.6-Trichlorophenol CAS No..0) 5.50) < LOD 1.20-36.50 (1.8) 21.0 (4.00 (2.9 (<LOD-121) 9.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.980-3. 1999).4.00-8.50-16. public drinking water systems did not detect 2.20) < LOD 90th 5.0 (5. Trichlorophenols are no longer manufactured commercially.40 (1. are metabolites of several organochlorine chemicals. Both chemicals have been detected in air.40 (2.6-trichlorophenol (2.0) < LOD 5.30) < LOD 4. Exposure to trichlorophenols also may result from metabolism of lindane.40 (.30-40.40) < LOD 4.20) < LOD 1.9.63) 18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. however. other organochlorines.6-TCP in any of the samples (U.9 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.7) 24.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Formation of 2.4.4.60 (4.4. 2.30-27.71 (<LOD-8.60 (2.4.30-44. soils. may occur by inhalation or dermal routes. < LOD means less than the limit of detection. Such workers would probably Urinary 2.40) < LOD 6.0 (4.0 (8. 2.4.4.00-3.40 (1. 2.42 (<LOD-8.20-71.5TCP and 2.4. usually at herbicide production or waste incineration facilities.0) < LOD 11.20) < LOD 5. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.03) 9.27) 696 661 521 696 603 939 Limit of detection (LOD.0) 2.30-27.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.50-25.27) 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 1.30-27.90-33.4.0) < LOD 21. including hexachlorobenzene and hexachlorocyclohexanes.980-3.0 (4.40-18.60 (.19 (<LOD-6.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. Occupational exposures.60-8.0 (3.60-18.80) < LOD 1.00 (3. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.0 (3.80-41. 1976).4. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.0) 2. and sediments. 112 Fourth National Report on Human Exposure to Environmental Chemicals .80 (2. 2006). Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.0) < LOD 5.6-TCP were used as intermediates in the production of certain pesticides. which may vary for some chemicals by year and by individual sample. recent sampling of U.5-Trichlorophenol CAS No.57 (<LOD-15.71 (<LOD-8.42 (<LOD-12.6-TCP).50-63. hexachlorobenzene.40 (.30-11.3.50 (.40) < LOD 1.60) < LOD 8.0) 2.40 (2. population from the National Health and Nutrition Examination Survey.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. surface water.30-3.4.0) 2.0) < LOD 11.5-trichlorophenol (2.0) 2.00-3.S.5-TCP) and 2.900-2.920-3. Historically.7. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) < LOD 5. 1999).30) < LOD < LOD < LOD < LOD < LOD 1.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .31 (<LOD-9. 95-95-4 2.5-trichlorophenol. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80 (1.950 (<LOD-1.20 (4.10-3.S. Survey Geometric mean (95% conf. EPA.30 (.4.40 (2.Organochlorine Pesticides 2.S.

13-13.67 (1.75 (3.78) < LOD 1.html.atsdr.820-2.4 (6. Neither 2.78-19.9) 12.00) < LOD 4.8) 4.57 (<LOD-7.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Laboratory animals chronically fed high doses of 2.4.20-6.6) 4. Urinary 2.53-3.67 (1. 1989).44 (1.4.02-3.4) < LOD 3.74) 11.24) < LOD 6.17) 9.4.31) < LOD 2.83-12. Fourth National Report on Human Exposure to Environmental Chemicals 113 .69 (2. 2003..29 (1. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.68 (<LOD-8.2) 2.5-TCP nor 2.93-11.75 (<LOD-6. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.5) < LOD 12.81 (<LOD-9.4) 5.1) 2.24 (3.53-3.46 (1.43) < LOD 12.95 (3.19-12. NTP classifies 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.27-17.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). 2004). 2003).37) 16. Survey Geometric mean (95% conf..11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.33) < LOD < LOD < LOD < LOD < LOD 2. 1995) and up to 19 times higher than the 95th percentile value of 1.49 (1.1 (<LOD-58.Organochlorine Pesticides be exposed to mixtures of chlorophenols..69-18.920-2.2) < LOD 5.4.24) < LOD 1.57 (<LOD-7.05-17.6-TCP levels at the 95th percentile were up to eight times higher than 3.9 (5.00-29.5-TCP or 2. At lower doses.cdc.82 (<LOD-32.2 (2.05-8.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 mg/L reported in German adults aged 18-69 years (Becker et al. urinary 2.57 (3.4.44 (.0) 7.88-16.5) 11.gov/toxpro2. and lymphomas.6-TCP as reasonably anticipated to be a human carcinogen. IARC classifies combined exposures to polychlorophenols.55 (4.4.90 (4. The 95th percentiles for 2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.60-3. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.6-TCP.79-4.47-8.78 (3. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.50) < LOD 2.37-11.68-4.15) < LOD 2.7 (4.64 (4. In the same 2-6 year old children. population from the National Health and Nutrition Examination Survey.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. and other chlorinated compounds.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. in addition to dioxins. 7.86 (3.6) 4.S.5-TCP and limited for 2. 1989). as being possibly carcinogenic to humans.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995) were similar.4..36 (1. which includes trichlorophenols.8) < LOD 9..4.3 mg/L in a nonrandom subsample from NHANES III (Hill et al..5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.4.24-11.43 (2.8 (5. animals showed hepatocellular abnormalities.80 (1.0 mg/L.980 (<LOD-1.19-4.4.. However. Among 6-11 year old children in NHANES 1999-2000.6-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. furans. 2003).73 (<LOD-8.4.6-TCP had increased rates of hepatic tumors.. Human health effects from 2.16 (. environmental levels) and health effects is available from ATSDR at: http://www. More information about external exposure (i.5-TCP. leukemias.24) < LOD 5. the 95th percentile urinary 2. Radon et al.e.4.00-19.6) 4.28-25.. the 95th percentile urinary 2.4) < LOD 3.16) < LOD 90th 5.32) < LOD 4.62-20.02) < LOD 7.4.3 (5.

0) 7.87-14.3-26.0) 12.40-2.36 mg/g creatinine.56 (3.65 (5.67) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-3.4. Finding a measurable amount of 2.9) 694 677 519 696 602 931 Limit of detection (LOD.52-3.78 (2.28) * 2.50-5.40 (2. In harbor workers exposed to chlorophenol-contaminated river silt.40) 2.67-12.06) * 2.0 (15.5-TCP level of 0.3-17.91-4.28) 24.2) 25.0 (6.40-4.4.0) 17.9 (11.0) 13.3) 23.20) 4.70) 5.20-6.10) 6.4.0) 14.66 (8.18-3.44) 75th 4.58-3.84) 2.30-11. Urinary 2.60-37. which may vary for some chemicals by year and by individual sample. the median urinary 2.47 (3.0-44.02) 2.1-25.7 (9.0) 19.7 (13.4.1) 16.0 (14.10 (5..4.0 (4. Biomonitoring studies on levels of 2.60-21.76) 3.0) 9.2) 12.40) 4.70-6.79 (5. Biomonitoring data will also help scientists plan and conduct research about 2.33-4.60) < LOD 5.80-6.4.73-9.4 (8.8 (9.0 (20.32) * 3.6-19.23-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.98-11.0 (16.0) 15.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.6 (11.3) 20.0) 11.36-5.00 (1.99) 6.4 (17.74 (2.0) 17.49 (6.80 (3.00 (2.35-3.40-2.90 (3.5-46.20-3.70 (2.0 (6.4 (9.0) 13.1 (10.60 (3.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.7) 21.0) 10.30-2.0 (11.78 (2. was about six times lower than the median urinary levels for males in this Report (Radon et al.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.0 (6. 114 Fourth National Report on Human Exposure to Environmental Chemicals .6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.4-17.0) 11.31 (3.60-3.60) 6.0 (14.70) 3.6) 26.36 (1.14 (2.4.23) 3.80 (2.8-24.5-TCP and 2.0-68.80-20.5-TCP or 2.6TCP values.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.10-2.2-0.57 (<LOD-2.31) * 2.63) 90th 15.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.4.7 mg/L.40) 2.40-32.0 (7. Mean values of 2.53) 2.0-41..80-7.72-10.10) 2.2 (14..4.52 (2.6 mg/g creatinine) and 2.90 (4.54) 6.7-3.90-8.23) 2.8-13.75 (8.20 (3.01-6.69 (3.3 (11.0) 6.1 (8.0-54.0 (9.70) 5.5 mg/g creatinine) were similar to the limit of detection for 2.89-6. 2003).32) 3.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.0) 9.32-4.26 (2.8) 32.00-21.4.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.48-26.0-43.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.09) 15.8) 18.20 (3.92 (2.65) 15.4.10-3. 1991). for males in NHANES 19992002 (Agramunt et al. Urinary 2.0 (15.6 (12.4.9 (13.45 (5.0-37.7-16. 2004).85 (2.24 (2.5-TCP (0.7) 33.4.40 (2.08 (2.04) 2.6-TCP level.6-17.95 (4.80 (2.95) 3.6-TCP in urine does not mean that the level of 2.6TCP causes an adverse health effect. 0.5-TCP or 2.6-TCP than are found in the general population.4.0) 13.00-4. population from the National Health and Nutrition Examination Survey.4.40-7.S.55-3.5-TCP and 2.58 (1.89 (3.09-7.59) 4.70-6.4 (10.9) 13.4.50 (2.40-14.70 (2.0 (8. interval) 2.74-3.85) * 3.0) 13.25-11.46-3.6-22. 1998).53) 4.0) 7.07 (<LOD-3.95-6.4.59-6.3 (11.98-7.5-TCP or 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.0) 19.0 (12. < LOD means less than the limit of detection.40) 3.12) 2.0 (14.80-25.70) 1.30-2.0-50.0 (8. Survey Geometric mean (95% conf.3.0) 14.0-38.45-9.51-12.0 (20. respectively.0) 10.45 (2.6-TCP exposure and health effects.30) 4.0-38.68 (<LOD-2.30-33.6-TCP (0.0 (13.60 (2.20-23.6) 21. similar to the limit of detection for this Report (Anderson et al.60 (3.4.5-TCP and to the median 2.4.0 and 1.0-18.10-3..00 (4.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.80) 1.90) 2.8-15.45) < LOD 11.4.3) 37.5-TCP or 2.

5) 12.68) 2.2 (12.6) 13.53 (3.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 12.7-36.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.52 (5.98) 10.28-4.72-16.83-6.16-10.4 (12.5) 9.60 (4.38) 22.83-5.33 (7.81-9.13 (1.06-2.90) 2.41 (3.5) 11.14-2.76-8.17) 2.00 (2.59 (2.58 (4.66-4.76) 2.29-4.33 (1.02 (1.88-7.95-2.3 (9.88) * 2.01 (3.22-9.6 (12.56-5.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.25 (3.55-2.8) 21.00) 4.8 (8.75) 75th 4.83-6.40 (2.51) 18.44 (3.02) 3.67-17.7) 6.4.9) 8.05 (3.6-31.18-2.5) 11.43 (<LOD-2.43-7.98 (1.15 (6.4 (11.38 (2.1-32.10-9.52) 2.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.1) 11. Survey Geometric mean (95% conf.90 (1.9 (9.73-22.1 (8.73) 5.06) 11.3-23.4) 4.11) 10.78) 90th 12.2) 19.6 (9.6 (6.65) 2.78 (2.2 (8.0 (9.5-28.17) 13.68) 2.76) 4.96) < LOD 4.92) 4.7 (14.06) 4.87-6.82 (8.3-37.6 (5.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.65) 18.9 (9.5 (8.87 (3.82-2.88) 1.4) 8. interval) 2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .0) 8.6) 8.00) 4.30-2.62-15.87) 2.91-2.53) * 2.72) 32.2 (13.0 (6.22 (1.0) 10.9-64.21-11.50 (2.6 (22.22-2.15 (1.4) 9.88 (2.25-15.63 (2.14-13.52 (3.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.77) 2.71 (3.10) 4.54 (2.35 (3.32 (2.09-3.53-11.20-2.53) 4.63-15.17-4.9-29.10 (6.5 (10.52) 2.24 (1.88) 5.46-14.42 (2.0 (11.27-9.49) 4.3) 8.8) 19.77-4.51 (2.88) 4.8 (7.29-4.63) * 4.38-5.5) 8.42) 2.25 (3.2 (7.23) 4.9) 7.04-2.94-13.1) 14.82 (3.04-16.63 (<LOD-2.91 (3.05 (6.1-21.88) 4.41-6.43 (2.87) * 2.33-2.40 (7.08-2.78) 2.6 (10.1 (13.70-9.9-32.49-3.50-8.25-17.65-21.00 (3.89-2. population from the National Health and Nutrition Examination Survey.23 (1.63) 4.51-21.7) 25.65-2.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.63-13.6 (9.26-13.22 (3.33) * 2.56) < LOD 11.26 (6.48-2.38 (4.9-34.87-7.99-2.9) 8.76) 1.47-5.56 (7.60-2.89) 10.S.29 (6.18-4.8) 12.79-17.13-6.91 (7.Organochlorine Pesticides Urinary 2.8) 11.19-5.83 (3.5 (7.32-19.25-2.82) 2.81) 2.22 (<LOD-2.9) 19.

Schulz C. Holler JS.EPA). Smith SJ. Seifert B. Lindroos L. Poschadel B. Domingo A. Pesticide residues in urine of adults living in the United States: reference range concentrations. Available at URL: http://www. The Great Lakes Consortium. Jones D. 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]. Anderson HA. Hill RH Jr. Bailey SL.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Wegner R. Kohli J.S. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Jarvisalo J. 4/21/09 Agramunt MC. Toxicological profile for chlorophenols [online]. Pekari K. Luotamo M.45:440-445. Baur X. Burse VW. Needham LL.63:57-62. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. The metabolism of higher chlorinated benzene isomers. Aitio A. Safe A. Szadkowski D. Shealy DB. Int J Hyg Environ Health 2003. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . html. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. et al. et al.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.gov/toxprofiles/tp107. Kaus S. Falk C.cdc. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Fast DM. Toxicol Lett 2003. Environ Res 1995. 206:15-24. Needham LL. To T. Heinrich-Ramm R.71:99108. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.atsdr. Int Arch Occup Environ Health 1991. December 2006 Draft. Urinary excretion of chlorinated phenols in saw-mill workers. Am J Ind Med 2004. Baker S. Domingo JL. Can J Biochem 1976. Seiwert M. et al. Hanrahan L. Gregg M. Head SL. Corbella J. Available at URL: http://www. Hill RH Jr. Radon K. Becker K.54(3):203-208. Environ Health Perspect 1998. Olson J.146:83-91.18(4):469-474. Arch Environ Contam Toxicol 1989.106(5):279-289.epa. Environmental Protection Agency (U. July 1999. S.pdf. U.

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

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

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

01-02.0 (8.94) * * .40-19.36-4.4 (9.0 (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.16 (2.8) 7.02-5.2-20.20-7. < LOD means less than the limit of detection.40-5.717-1.08-2.44-38.2 (14.20 (.55-6.85 (3.80-22.86 (1.63) 1.60-18.55-8.00-12.0) 6.98-5.9-18.70-14.58 (2.52) * * 1.82-12.623-1.2) 14.3) 14.00-27.04) < LOD 1.90) 3. which may vary for some chemicals by year and by individual sample.80-24.0) 5.44-3.830 (<LOD-3.0) 7.1) 10.81) 11.670-1.93 (4.00 (4.30-4.40-14.80) 11.98-12.70) < LOD < LOD 1.981 (.80) 3.0) 15.0 (6.530 (<LOD-2.66) * * 1.99 (5.00-7.490-2.890 (<LOD-2.37 (3.83 (5.5 (11.50 (.30 (2.57-7.15-12.2 (14.79-7.0-27.17-3.21 (.0-28.76 (2.2 (9.56 (4.20-30.90-5.56-13.50 (2.2) 16.2 (11.840-1.33 (5.0) 9.0) 6.80-4.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 5.14) * * .50-5.08 (<LOD-2.1) 95th 13.S.30-6.70-19.2 (7.70) .0 (7.52) 6.93-24.2.02) 4.97) 90th 7.80) 2.00) 3.60) .4) 18.60) < LOD < LOD 4.80) .0 (9.34-3.79 (5.0) 10.0) 10.12) 4.5 (8.4 (7.2 (7.80) 4.80 (2.21) 9.95) 5. 120 Fourth National Report on Human Exposure to Environmental Chemicals .0 (7.71 (2.35-12.9) 14.70 (2.10) < LOD < LOD 4.68-7.70) < LOD < LOD 75th 3.03 (.10 (2.90 (1.42-3.954 (.740-2.1 (10.40 (.0 (8.30 (2.1.81) 1.26 (5.72) 5.1-17.47) * * 1.70-11.20 (.80 (4.40-11.810-1.20-4.290 (<LOD-.0) 5.86-15.0 (8.60 (5.48-7.0) 11.94) 3.600 (<LOD-1.13 (2.5) 20.34-7.0) 10.11 (.2 (9.0 (5.27-15.27-3.46) 10.8 (8.58 (3.26-8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.67) 3.30 (4.3) 17.52-11.10 (.80) 2.758-1.955 (.47) 5.13 (2.5-17.07-10.90) 2.4 (7.0) 11.05-7.71-9. and 03-04 are 0.70 (4.0) 11.61) 4.5-16.12-19.00 (1.50) 2.70-23.8) 11.16) 4.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.9 (8. 0.0) 20.7) 11.6) 7. see Data Analysis section) for Survey years 99-00.750-1.2) 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 1.26-6.15) 14.89) 9.74 (8.700-1.0 (7.2.4) 17.42) .0) 10.2 (7.8-32. respectively.51) 2.50-36.35-16.8) 19.73) * * .28) 1.7 (14.5) 15.579-1.43-12. interval) 1.1 (9.96-3.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.38-5.56 (6.60-11.80) 2.4 (9.970-2.8) 7.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.1-23.01) * * 1.29) * * 1.3-15.8 (9.00-19.50 (4. population from the National Health and Nutrition Examination Survey.0) 6.0 (6.2) 16.00 (5.00) 3.3) 16.620-1.00-27. and 0.60-25.54 (3.10 (.290 (<LOD-1.81) 11.8 (14.0) 10.20 (.40-1.00-12.08-15.33-18.13-2.32 (.74 (8.22 (.0) 11.56 (1.60 (1.780) < LOD 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.91) 4.6) 18.757-2.0) 12.0 (4.40-16.4) 20.45 (2.35-11.0 (7.97) 8.20 (2.10 (2.10-7.80) .58 (5.39 (8.44 (2.860-2.82) 10.39 (3.0 (12.20 (.61 (3.23-5.53) 4.599-1.7 (12.10) < LOD .9) 8.19) 9.90-4.1) 13.8 (12.32) 1.

80 (2. interval) .10 (3.3) 952 1187 927 997 1332 1001 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.74) 4.4) 4.9 (9.61-13.35 (1.64-5.39 (2.924 (.6) 13.633-1.710 (<LOD-1.09 (.02 (2.82-6.53) 9.620-1.05 (.960 (<LOD-2.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.94-23.28 (5.85 (6.30) 2.42) 12.90-8.996 (.80 (7.07 (.40-5.88-15.53-11.00-17.830-1.58) * * 1.56-13.37-5.73 (1.45-11.540-1.8 (10.5) 11.76) < LOD .83) 8.2) 8.10-13.3) 16.62-5.88 (5.77 (6.84) 7.5-16.5-13.7 (9.61-29.61 (1.855 (.41) .1 (8.20-8.90-5.06-2.62) .52) 4.28-9.03 (7.31-14.8) 6.2) 5.574-1.960 (.60-9.0) 7.6 (9.56) .2) 13.54-4.60) * * .67) 4.51-5.69) 2.66 (2.71-2.18 (.7 (10.6 (10.1-15.2 (10.68) < LOD < LOD 3.05) .790 (.5) 7.26) * * .89) * * 1.9) 11.28) 10.75-7.75 (7.01-2.95 (3.34 (6.40-3.46) 2.60) 2.40-14.00 (4.27) < LOD 2.88-10.71) 10.69) 4.40 (3.47 (3.38 (1.56) 7.5-20.93-9.03) 2.41) Selected percentiles ( 95% confidence interval) Total * * 50th .29 (2.41-12.3) 5.75) 2.98) .98 (3.3) 15.94 (2.1) 4.69-10.40-28.98-5.30 (1.510-1.47 (1.94-22.40-12.04 (1.34 (6.93) 9.6) 8.82-14.47) * * .28 (4.87-5.500-1.57-10.24-3.4) 13.37 (5. Fourth National Report on Human Exposure to Environmental Chemicals 121 .7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .05 (1.8) 8.440 (<LOD-2.09) 2.85) 2.773-1.43 (.84 (5.870-2.2) 9.45-5.40) < LOD < LOD 75th 2.0 (8.1 (7.66-34.549-1.1 (10.900 (.80) 9.15-10.9) 12.00-13.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.38) .98-22.650-1.7) 18.00-19.54-15.37 (4.19 (4.46-5.2 (8.80 (6.55-20.54-11.98) 9.57) 4.430-1.45-5.2) 5.47) 2.1) 4.890 (<LOD-1.9 (9.570-1.9) 16.57 (6.5 (4.34) < LOD < LOD .54) .35) < LOD < LOD 3.78 (2.780 (<LOD-1.04-6.79-3.7 (8.67-19.66-15.608-1.7) 5.2) 95th 12.94-10.76-4.560-1.02-2.87 (3.72) 11.94 (4.02-14.75) 14.25) 6.13) 4.92-5.1 (6.36) * * 1.820 (.44 (2.750 (<LOD-1.50) 7.8) 16.66 (5.34) * * .25) < LOD .66 (1.57 (4.88) 2.533-1.82-26.4 (4.566-1.8) 12.03 (2.14 (3.1 (11.7) 12.00 (4.29) * * .932 (.40) 4.42 (3.79-9.98) .94-9.21-23.6) 11.11-6.37) 9.00) 8.43) 2.2) 7.02 (7.28 (2.1) 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 1.53 (6.23) 4.03-6.0) 6.87 (1.5) 7.6) 9.67) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.883 (.23 (4. population from the National Health and Nutrition Examination Survey.82-14.47 (3.S.920 (.2 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 12.5) 8.818 (.68-4.89-3.09-11.1 (9.890 (<LOD-1.9-28.32-12.75 (3.81-5.54-2.37-3.5-32.03) 2.43 (3.4 (9.61 (1.56) 4.860 (.5) 12.95) 2.69 (4.92-2.4) 4.31 (3.81 (1.74) 90th 7.8) 7.83 (7.93-5.9 (5.

20) 3.35-3.15-6.80 (5. 0.53 (3.80-4.28 (7.90) 8.80 (2.8 (12.75 (2.20 (<LOD-2.10 (<LOD-1.00-4.84-4.50-5.0 (5.33-11.90-15.1-23.5-26.52 (6.11-6.0 (15.2 (9.8-20.0) 7. and 03-04 are 0.99 (3.40 (2.30) 8.96) 90th 7.37) 2.64) 10.90 (1.0-24. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .80 (2.06 (2.4) 7.67) 3.6-41. respectively.1) 11.3 (9.0) 11.78) 5.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.04 (3.34-10.86-10.45 (3. see Data Analysis section) for Survey years 99-00.62-17.27) .5 (8.35 (6.8 (12.61 (3.49-4.0) 12.51) < LOD 1.8-17.18) * * * * * * * * 1. 122 Fourth National Report on Human Exposure to Environmental Chemicals .20-4.0 (7.46-4.70-5.95 (5.00 (.67-10.5) 21. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6) 14.39 (5.00) 8.90) 4.80) .7 (10.75 (3.8) 9.14 (6.90 (2.670 (<LOD-1.24-5.0-19.40) < LOD < LOD 75th 2.7-19.67) 4.00) 3. 01-02.30) < LOD < LOD 4.2 (7.0) 12.90 (6.50) 5.95 (2.30) < LOD < LOD .98-9.6 (10.81-6.0) 6.29) < LOD < LOD < LOD < LOD 3.4-17.18 (3.58 (1.9-15.97-4.74) * * * * * 1.7 (11.00) < LOD .5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .39-13.0) 14.70 (1.70 (8.24 (2.3 (7.5.34 (6.0 (9.12 (4.0-29.9-14.27 (3.22 (6.9) 9.5 (9.4 (14.00-16.740 (<LOD-1.96) 3.66) 4.650-1.61-32.16-1.40 (2.92-17.72) 2.0 (10.0-24. < LOD means less than the limit of detection.80-6.0 (13.22-12.9-17.3 (12.31) 1.89 (2.88) 10.20-18.00-4.3) 8. which may vary for some chemicals by year and by individual sample.3) 20.670 (<LOD-1.970 (<LOD-2.8-20.00-18.60) < LOD < LOD 2.80-14.6) 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 * * * 1.00-18.34-5.90 (6.70-8.3 (11.01 (2.0) 19.34-3.3 (6.47-6.5. and 0.00) 3.70-9.60 (2.22) 8.73) 7.20-8.3) 14.88) 3.4 (10.80) 5.6-19.90 (6.22 (6.00) 7.S.50) .58.2) 14.10 (.80-12.0) 13.50-4.0) 18.8-21.80-8.0) 14.90 (2.6) 11.70-9.10-4.9 (12.30) 3.680 (<LOD-1.90-9.3) 22.17 (7.0 (10.0 (14.90-15.27) 4.7) 15.90 (2.41-5.27 (7.3 (9.20) 3.20) .7) 16.10-10.0 (9.59-3.5 (8.8) 8.0) 9.70) 2.6 (10.1 (10.15-2.82) 8.35) 4.670 (<LOD-1.31-7.0) 12.30) 3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80-3.6) 18.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.910 (<LOD-2.50) 3.92) 9.0) 23.0-33.60 (6.9) 10.37 (3.63-14.4 (10.46-28.00-9.27) 9.9) 16. population from the National Health and Nutrition Examination Survey.0) 11.1 (10.80) .29-4.9) 95th 14.6) 14.77-14.89) 2.7-21.670 (<LOD-1.60 (5.95-9.3) 10.77-3.90-31.42 (1.790 (<LOD-1.7) 22.9 (7.0) 13.41) 3.90 (5.66-13.10-15.4) 11.7) 10.7) 14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.580-2.25 (2.0) 9.90 (6.10) 6.80-21.0 (8.31-12.

6) 6.79-9.8 (8.71) < LOD < LOD 2.83 (6.2) 12.05-3.99) 2.36 (2.8) 11.54 (7.0 (10.37-5.12) < LOD < LOD 4.50 (6.2) 12.78-10.85-8.58 (4.34-18.3) 6.54) 9.5 (15.9) 19.29) 3.9) 16.03) 3.93-10.4) 15.97-4.68) .6) 7.9 (9.38 (2.59-3.89 (2.760 (<LOD-1.1) 13.00 (2.27-13.8) 16.89-13.29 (5.1 (19.11-3.03 (6.06 (<LOD-1.16 (3.7) 14.95) 3.5) 13.690 (.73 (5.6 (10.63 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4-16.48 (2.51-10.2) 12.88-7.28) 6.0 (8.93 (<LOD-2.86-3.15 (1.2) 8.32-8.27) 5.25-9.51-7.33) 3.8) 14.99 (4.38) 1.30) 2.3-21.4) 7.00 (<LOD-1.86) 9.2) 16.3-15.1 (8.4 (11.69-11.6) 13.4) 9.2 (9.38-13.71 (1.07-3.6) 95th 16.5-17.0 (11.44-6.96-10.75-3.940) < LOD < LOD 1.7 (10.34) < LOD < LOD < LOD < LOD 3.02-4.920 (<LOD-1.6 (11.7 (10.5) 22.89) 5.47-9.72-4.82-11.0 (13.2) 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.0-21.78 (4.12 (7.67 (7.53-8.00) 2.5 (8.63 (6.42-19.850 (<LOD-1.16-14.25 (4.97) < LOD .7) 9.91-9.21) * * * * * 1.7) 14.7) 12.4) 7.43 (2.00) 8.9-25.83 (7.30-5.29 (2.89 (3.82-8.39-17.68-19.3) 8.79-6.64-11.2-30.973 (.5 (9.88 (1.6 (13.4-15.590 (<LOD-.03 (2.19) 3.23-3.S.86 (3.70-2.80) 3.810 (<LOD-1.89-3.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.61 (2.00 (<LOD-1.15) < LOD < LOD 75th 2.85-17.20-3.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.3-17.30) 8.3) 9.28 (1.6) 14.92) 3.3) 12.1 (13.42) 8.00 (7.6) 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 * * * .29-2.74-4.910 (<LOD-1.27) * * * * * * * * 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09-11.2-15.28-12.55) .5 (10.07) 2.87 (3.6 (12.9 (9.07) 2.7) 15.18) 2.0-19.1) 20. population from the National Health and Nutrition Examination Survey.11 (5.4) 16.7 (11.27) < LOD .38 (.0) 14.32) 2.54-5.95) 90th 8.4-18.2) 10.7-23.6 (11.42) 7.1) 10.04) 9.75-3.30) 7.50-17.01-5. Fourth National Report on Human Exposure to Environmental Chemicals 123 .8 (10.9-17.3-34.6) 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 * * * * * * .70-35.6 (13.7-19.3 (7.06) .81 (7.93 (2.78 (6.2) 19.4) 6.72) 4.55 (2.5) 8.41 (7.94-14.6) 12.7 (8.14 (2.5) 10.33-10.89-3.4-16.77 (2.620 (<LOD-.3-17.890-2.2) 15.45) 3.45) 6.38 (1.92 (5.74-19.27) 1.530-1.52-3.96-11.68-4.09-11.93 (6.9 (9.67 (1.00 (5.2 (9.00 (3.55) 16.5 (11.6-19.94 (5.77) 3.95 (2.78) 4.91) 3.77 (2.780-1.89-10.4) 7.68-10.950) .07 (5.21-21. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .37) 3.

01-02.49) .303-.657) * * .80) 3.550 (.16) 1.86) 3.11-3.450 (<LOD-.09 (.22-2.20-3.960) .449 (.50 (1.20) 2.46 (1.592) * 50th .79) .22-3.690 (.32-1.31-3.83 (2.46 (2.930-1.36-4.40 (1.20 (1.30) 4.61 (1.650-.810) .31) 2.50 (1.89) 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 * .08 (2.04) 1.990-1.16) 2.33-2.570) * .80 (1.700) .11-3.80) 3.70 (1.759) * .980) 1.68-5.23-3.03) 1.54) .201-.17) 1.75 (2.20 (1.42-2.60) 2.750-1.510 (.382-.820 (.08 (2.50-2.850) < LOD .83 (2.760 (.960) 1.80) 2.390-.80) 3.380) .600 (<LOD-.336-.96-5.570 (.950) 90th 1.22-3.730) .83) 2.592) * .00-2.30-3.1.710) .510 (<LOD-.01-1.949) .457 (.79) .930) 1.70 (1.505 (.930) < LOD .670) .35) 1.710 (.S.10) 3.90) 3.69-4.50-2.18 (.425 (.98) .910) 1.560-.58 (1.240 (<LOD-.30-1.64 (1.57 (1.98 (2.690-1. and 0.48 (1.34) 2.749 (.343 (.10) 1.47 (1.960) .89-6.45 (1.20 (1.580-.700) .500 (<LOD-.86 (1.01-3.880) < LOD 75th .20-2.790 (.70-2. < LOD means less than the limit of detection.710 (.98-3.50 (1.77 (1.840 (.720 (.95) 2.17) 1.800 (.05-3.60-4.380-.570 (.90 (1.10-1.570-1.22-8.57 (2.467 (.91) 2.600-.780) . respectively.90-4.455 (.41 (2.74) 3.440-.930 (.540 (.94 (2.453 (.80) 2.910 (.00) 1.48 (2.34) 2.25-1.590-.380-.830 (.597) * .90) 2.600-1.490 (<LOD-.690-.970) .340-.63 (1.09.15) 2.90) 2.10-1.549 (.55 (3.37-2.780 (.30 (. which may vary for some chemicals by year and by individual sample.580-1.27 (2.30 (1.750) 1.32 (1.20-1.820 (.45 (2.15) 2.89) .45 (1. interval) Selected percentiles ( 95% confidence interval) Total * .160 (<LOD-.910-1.780 (.95 (2.280-.20) 3.585) * * .77-2.17-4.73-5.01) .740 (.30 (.73 (1.550 (.30 (.31) 95th 2.26 (2.14 (1.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.54 (2.459 (.398-.29-2.30) 1.18 (1. 0.2.88) 1.19-1.46-3.10) 1.353-.620-1.350-.31-3.29) 1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .880) < LOD .20) 1.970) 1.38) 1.30) 4.96-3.390-.400) .22 (1.460-. see Data Analysis section) for Survey years 99-00.690) .570 (<LOD-.13) 2.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.860) < LOD < LOD .388-.260 (<LOD-.54-2.00) 2.618) * .94) .592-.14-1.960-1.26) .74-5.210 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.720-1.70 (1.49) 2.39) 2.04) . and 03-04 are 0.87-3.59-2.20 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.32) 3.60) 3.584) .89) 1.83) . population from the National Health and Nutrition Examination Survey.20-2.16-3.76 (1.65 (2.10) 1.940) < LOD .00-4.50) 1.80) 5.680-1.21) 3.740-.50 (1.680-1.45-4.94 (3.570 (<LOD-.59-6.350-.740-1.20) 3.880 (.20) 1.78) .27 (3.95-5.40 (1.00 (1.740 (.720-1.960 (.70-7.13) .46) 1.587) * * .47) 2.73 (2.30-3.76-6.78) 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 * .05-2.75-2.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .30) 2.60 (2.97 (2.41-5.83) 1.80 (2.359-.50 (1.20) 2.

560-.380) .57-4.76) 1.509 (.742) * * .06) 4.38-3.840) 1.403) .33) .535 (.920) .81) 2.97) 2.80) 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 * .72 (1.23) 1.560-.82 (2.07-3.69 (1.97 (1.800) < LOD .70 (3.07) 1.10) 2.580-.05) < LOD .22-3.900) 1.700 (.67) .09) .43) 2.16-1.53) .840) .45 (2.22) .460 (.32-1.300-.08-2.330 (<LOD-.97) 1.19 (1.318-.43) 1.80) 2.760) .597) * .64 (2.05-4.136-.550-1.79) 1.42-8.97) 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.750 (.70 (2.350) .07-2.32) 5.49-4.870) .71) .69 (3.830) 90th 1.580 (.36) 3.930-1.250 (<LOD-.740) < LOD 1.72) 1.730) .03-1.98) 1.444-.380-1.645) .08-3.45 (1.470) .66 (2.88) .63 (1.05-2.11-2.29-4.471-.71) 2.552 (.310-.04) 95th 2.73 (2.470 (<LOD-.94) .S.480-1.82) 2.20-7.08-3.02-6.00-1.99) 1.830 (.18-2.08-3.700 (.253-. population from the National Health and Nutrition Examination Survey.310 (<LOD-.61 (3.390) .380-.79 (1.25-3.739) * .57 (3.73-3.58 (1.285-.61-3.77-3.84-6.310 (<LOD-.710 (.790) .448 (.67 (1.550-.640 (.00 (3.22-2.58) 3.61) 2.47 (1.335-.320-.72-4.91 (1.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.23) 2.77 (3.92) 3.95) 1.17-2.17) 2.89 (1.43 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.515) * * .250 (<LOD-.60 (2.24) 4.55-3.590-1.30-2.850) 1.510 (.08) 1.700 (.07) 1.64 (2.20-2.300 (<LOD-.720-1.550) .07) 1.820) .840) 1.75 (2.13 (1.32) 1.92 (1.447 (.38 (2.99) 2.50 (1.78) 3.30) 3.08 (.55 (1.42) .04-1.31-1.820) 1.49 (1.60 (1.88 (1.453 (.280 (<LOD-.16) 1.270 (<LOD-.90) 2.11 (.07 (.510 (.393 (.460-1.75-3.688) * .22) 4.22-3.372 (.630) * .03-2.28 (1.710 (.22) 1.590 (.62 (1.330-.72 (2.690) < LOD < LOD .660-.670 (.92-8.400-1.08-2.62 (2.44) 2.52 (1.305 (.89-3.940-1.550-.38 (1.17) 2.42-6.180 (<LOD-.67-3.270-.84 (2.32 (.08-3.990-1.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .23) 3.412-.39) 2. interval) Selected percentiles ( 95% confidence interval) Total * .43) 2.368) * .760) < LOD 75th .390-1.485) * * . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.08 (2.39 (1.790 (.348-.870 (.02-3.42 (.640 (.71 (1.710 (.58-6.680 (.60) 1.520-.23 (.75) 6.980-1.320-.20) 1.00-3.41 (.44-2.57-2.61-3.34 (1.590) * 50th .540-.22 (2.67) 1.16-2.52) 3.07) 5.370-.270-.08-2.591 (.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .50) 1.520 (.57 (1.750 (.880) 1.230 (<LOD-.950-2.460) .65) 2.234 (.910) < LOD .580) .640 (. Fourth National Report on Human Exposure to Environmental Chemicals 125 .32) 2.47 (1.11) 1.377-.23) 2.440-1.08) 2.510-.05 (1.66) .480) .05) 1.14 (2.67 (1.500-.77-4.800-1.60) .530 (.97 (1.04-5.75 (1.02-3.47-4.560 (.720 (.490 (.06-2.740) .400) .87 (2.33 (1.

0) 4.64-3.88) 3.8) 41.0 (32.0) 18.S.29) 2.40-4.0 (20.71-2.11 (4.50-2.1-47.9 (10.2-26.0) 4.26 (.0) 5.78 (1.8) 62.19-2.3 (23.6 (15.4) 19.0 (7.2-47.10 (7.50-20.23-2.0-41.0) 45.530-4. interval) 1.3) 31.0) 3.02 (2.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.53 (1.0) 28.8-21.1 (11.0 (6.6-22.0) 6.81-2.1-25.0-52.76 (2.23) 9.0-39.5) 69.0-230) 35.6 (11.8) 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 1.06 (1.13 (1.10 (1.0) 20.4-22.18) 20.66-5.0) 16.2-62.95 (5.10-13.1) 38.0-110) 34.9 (19.78) 9.21 (1.59 (1.69) 2.0 (40.64-8.29-9.10 (1.5-74.0) 8.44) 3.86 (1.0-43.53) * 2.41 (1.6) 52.57-2.54 (1.83-2.79 (1.0-29.54 (3.0 (8.60 (2.80-2.9 (23.00 (.70-17.20-4.4-76.8 (12.70 (1. which may vary for some chemicals by year and by individual sample.2-27.1 (22.0 (38.0) 13.88) 1.41) 1.30) 4.63-6.94 (1.74-2.5.05) * 2.05) 1.65 (4.43-7.0 (26.0 (38.0) 20.3) 38.1) 95th 48.0) 15.2 (12.1) 18.59 (1.20 (2.0 (37.0 (38.0) 32.0 (21.83 (3.1 (25.85 (1.09 (4.9) 17.6 (26.9-21.3 (24.50-5.10-4.3 (14.7-41.0 (38.0-49.41) 5.3 (12.97) 6.90 (1.0 (20.13 (1.0) 17.20) 1.0 (13.4 (10.0 (17.52 (4.0) 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 2.7-22.76 (2.5-20.92-5.8-24.80) 1.86-3.0) 3.6 (9.9) 48.12) 1.7) 20.5-27.0-31.93-3.9) 18.44-7.48-2.0-110) 42. 0.0 (33.3) 28.70) 1.40) 50th 2.0) 15.57-2.61-2.470 (<LOD-1.53) 1.8) 39.90-8.80) < LOD 1.60) < LOD 1.40-16.80) .80-18. see Data Analysis section) for Survey years 99-00.30 (.30) 11.16) 2.3) 33.33 (5.0 (8.77) 38.00 (.90) 11.70 (7.7 (12.6-45.0-69.0-39.40) < LOD 1.0 (19.42) 1.8 (12.9-51.0 (38.41-4.10) 39.0) 33.1 (26.17-2.18) 6.11) 2.2-80.0 (24.12 (3.0-53.79-2.99 (2.46 (.10) .61 (1.45) 2.10 (1.91 (4.0-92.04) 3.05-3.0) 17.1-46.0-58.2 (19.29-4.2-27.16) * 1.70) 1.40) < LOD 2.600-2.00-24.9 (19.0) 42.8) 32.70 (.1 (25.1-19.7) 47.14) 5.0-53. population from the National Health and Nutrition Examination Survey.46-2.70-6.0 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-50.75-14.21 (3.2) 31.26) 75th 11. and 0.0) 30.0) 3.830-3.72 (1.49-2.41) 1. < LOD means less than the limit of detection.1-20.83-2.0-41.13) 12.48-2.6-27.6-54.2) 16.85) * 2.1) 38.4) 38.0 (25.30-14.18) 14.19) 2.50-17.0) 3.0) 16.10 (1.0) 4.2-39. 01-02.27-6.3) 26.18.5 (24.50-7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.21 (4.77 (1.830-4.0-62.4 (19.0 (11.5-40.0-260) 34.3 (12.0-47.07-5.23-2.83 (1. 126 Fourth National Report on Human Exposure to Environmental Chemicals .81-3.46-6.90 (1.80) 90th 38. respectively.4.06) * 2.04-8.96) 5.44) Selected percentiles ( 95% confidence interval) Total * 2.690-3.1 (10.2-33.0) 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. and 03-04 are 0.0-58.79 (2.70 (1.610 (<LOD-1.44) 2.71 (4.50 (2.92) * 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.0-41.35-6.71) 5.0) 31.5) 30.98 (1.53) 40.0) 28.9 (27.7 (12.36-2.98) * 2.48) 5.58-2.5-45.4 (15.9) 38.1) 140 (46.0 (38.1-40.0-62.67 (1.04 (<LOD-2.8 (26.7 (28.31-6.58) 16.82 (1.25-3.87-7.0 (38.660-2.8 (22.3 (10.32 (2.70) 5.45) 2.0) 19.

50 (2.95) 90th 32.9) 12.46-22.0-40.15 (.36-13.2 (9.68) 47. Fourth National Report on Human Exposure to Environmental Chemicals 127 .60) 4.0-71.1) 27.60 (.19-6.870-3.94-20.2 (8.72) 2.1 (34.1) 15.95 (2.88 (1.52-4.6-38.680-4.6 (24.35) 1.3-22.0 (14.91 (6.19) 5.12) 3.4-71.06-1.27) 50th 2.9) 3.47 (3.23-1.4 (11.7-20.54-15.58-2.99-4.17-3.18-1.0 (25.45-1.8-43.2 (21.88 (1.2-34.7-43.93) 5.6) 19.03-2.48 (4.1 (39.64 (1.0 (19.1) 17.07-2.3-19.62) 4.4) 12.88 (4.11-2.43-12.9) 24.8) 32.2) 4.09 (5.47-17.7-38.28 (1.1-22.7-47.19-14.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.38-5.6) 3.5-190) 30.27-3.35 (2.51) .2) 41.7) 34.66 (1.7) 66.32-3.3) 28.76-2.66 (1.7 (11.3-27.75) * 1.83 (.9) 24.70-4.8) 31.9 (39.16-2.7) 30.0) 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 1.06) 1.4 (25.44) 9.67 (1.4) 3.00-16.86) * 2.38-1.57 (6.61 (1.31) 2.08) 1.33-5.8-37.888-1.750 (<LOD-1.5 (17.48) 1.75-6.63-5.4 (9.22-2.5 (41.860 (<LOD-1.6-51.9 (13.07-2.20-5.3) 13.899-2.82 (2.5) 27.6) 3.3 (8.5-36.38) 5.6) 11.7 (18.1 (25.17) 2.27) 10.23) 37.9-18.2) 13.1-63.890-4.2 (16.5-43.91-2.7 (18.2-47.38 (3.79 (2.80-8.88 (4.9-36.06) 75th 9.2) 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.52 (1.40-7.12 (1.0) 13.37-2.2 (22.71 (1.45 (1.36 (4.1-60.7) 26.870-3.4) 12.7-109) 22.62 (2.5 (8.58-17. interval) 1.21 (4.14 (.4 (5.1) 25.9 (7.4-34.6 (27.1) 36.1) 27.6) 23.33) < LOD 1.1) 52.2) 33.9-37.37 (1.9-41.4 (25.06) 1.80 (1.71-2.55 (2.23) < LOD 2.22 (2.16 (1.9 (10.4-39.90 (.33) 2.0) 48.16 (1.71) 8.68 (1.1) 13.34) * 1.14-8.6) 112 (40.S.5 (15.67-3.00) 6.18) 3.6-49. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-45.5-97.3 (10.84-13.25-3.96) 2.0 (39.43) * 2.67 (1.46) 1.95-16.02) 1.3 (20.9) 3.29-5.1 (50.41 (2.1) 13.5 (6.33) 1.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.4 (12.8) 23.95-16.8-34.97 (1.0) 47.2-38.86) * 3.5 (13.07) 9.8) 15.3 (9.26-4.19) 5.51) < LOD 1.18) * 2.40 (2.5) 70.56) 1.4-21.4-67.8) 11.0 (32.8 (7.0) 30.7) 23.26-2.7) 95th 51.56 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.59-15.22-3.36) 10.2-28.4 (21.5 (34.3 (10.16 (1.67-16.7) 15.94) 19.08 (1.83) .53) 1.27 (6.1 (33.870-3.5 (15.1) 25.59-2.24 (1.69-18.0 (23.2) 13.47 (1.9) 54.7 (10.7-37.6) 7.69-5.4 (19.0 (17.28) 1.79-17.2-70.20) Selected percentiles ( 95% confidence interval) Total * 1.46-6.0) 3. population from the National Health and Nutrition Examination Survey.40-4.9 (19.0 (23.0) 25.54-2.61-22.8-26.670-1.35) .66) 8.70 (1.9-95.2 (15.7-19.82) 1.8) 3.75 (1.32 (3.94) 1.6 (11.9 (26.1 (12.7 (24.46-5.2) 36.9-52.0 (6.6-32.30) 28.19 (1.75 (1.930 (<LOD-1.39 (1.0) 10.59-2.22 (.02 (.96-16.40 (5.57) 4.03) 1.3-42.61-2.0-118) 29.01 (.4) 14.2) 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 1.50-5.43-2.00 (4.7) 61.6 (7.11) < LOD 1.00) 1.02) * 1.0-70.

10) . and 0.60) 1.090 (<LOD-.050-.090 (<LOD-.450 (.360-.30) .220 (.190 (.410-1.36) .560 (.650 (.440-1.850) < LOD .400-.10) .310-.150) .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 * * * * * * * * * .160-.850 (.080 (<LOD-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .130) .550) .380-.830) .1.610-.360-.099-.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 * * * * * * .770) < LOD 95th .310 (.470-1.620 (.1.730-. see Data Analysis section) for Survey years 99-00.990) .740) < LOD .310) < LOD < LOD < LOD < LOD .084-.310) < LOD < LOD < LOD < LOD .990 (.200) < LOD < LOD .650-1.390) < LOD < LOD .290) < LOD < LOD < LOD < LOD .640) .090 (<LOD-.940 (.640) .830) < LOD .870) < LOD .410) < LOD < LOD < LOD < LOD .410-.270 (.210 (.610 (.15) .10 (.090 (<LOD-.190 (.160) .700-1.300-1.230) .S.210 (.680 (.170-.30) .680-1. population from the National Health and Nutrition Examination Survey.120 (<LOD-.350) .162) * * * * * .830 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals . 01-02.720) .58) .650-1.700-1.03) .140-. respectively.900 (.860) .650) .930 (.720 (.540) .05.370-.690-1.120-.140-.20) .780) < LOD 1.700-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .370-.760) < LOD .310 (.870 (.320 (. and 03-04 are 0.570) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (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) .640 (.650) .190 (.40) .110-.12 (.820 (.380-.530-.860-1.220 (<LOD-.080 (<LOD-.770 (. which may vary for some chemicals by year and by individual sample.460-.290 (<LOD-.090 (<LOD-.600 (.130 (.840) .171) * * .640-1.350) < LOD < LOD < LOD < LOD .42) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130-.730) .320-.830 (.150 (<LOD-.460 (.280) < LOD < LOD < LOD < LOD .450 (.990) .840) .540 (<LOD-.090 (<LOD-.870 (.100 (.42) .117 (.390 (.630 (.610-1.470 (.30) .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 .430-.120-.330-.680) .870 (.630 (.850 (.560 (.720-1.180) .430 (.450 (.540) .490 (.380-.820 (.00) .300-.130-.260 (.290) < LOD < LOD < LOD < LOD 90th . < LOD means less than the limit of detection.130-.32) .700-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10) .610 (.660 (.680-1.870 (.140) . 0.140-.510-1.240 (<LOD-.870 (.130) .230-.410-.13) .420-.

450) .200 (.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.140-.290) < LOD < LOD < LOD < LOD 90th .36 (1.S.86) .43) .800-1.38) 1.360 (.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .140-.720 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .00) < LOD .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 .540 (.380 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300-.500-1.170 (.700 (.700 (.270) < LOD < LOD < LOD < LOD .084-.340-.190-.510-.230 (<LOD-.120) .29 (.070 (<LOD-.580 (.58) 1.380-1.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.01 (.970) . Fourth National Report on Human Exposure to Environmental Chemicals 129 .560 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.310) < LOD < LOD < LOD < LOD .880 (.220 (.070 (<LOD-.270 (.440-1.500 (<LOD-.600) .810 (.280) < LOD < LOD < LOD < LOD .120) .220) < LOD < LOD < LOD < LOD .670 (.410 (.570-.570-1.140-.860 (.740 (.410) < LOD < LOD .660-1.670 (.140-.02) .260) .600-1.410) .780 (.19 (.12) < LOD .170) < LOD < LOD .24 (.580) .670-1.550 (. population from the National Health and Nutrition Examination Survey.390-.150-.080 (.740) < LOD 1.540) 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 * * * * * * .940) .870) .057-.330 (.080 (<LOD-.20) 1.780) < LOD 1.720 (.760) .330-.03) .161) * * .140-.370 (<LOD-.260-.890 (.140) .730 (.700) .24) .240-.650) < LOD .610-1.111) * * * * * .500) .330-.700-1.850 (.540 (.300 (.320 (<LOD-.450 (.116 (.440 (.400 (<LOD-.410 (.190 (.360-.880-1.67) .230-.14) 1.490-1.330 (.070 (<LOD-.860 (.110) .78) .410-.03 (.09) .380-.730) .960) .66) 1.300-.03 (.860-2.080) .070 (<LOD-.400) .190 (.170 (.410-.360-.360) < LOD < LOD < LOD < LOD .750) < LOD 95th .200 (.650-1.550 (.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 * * * * * * * * * .100-.570 (.580) < LOD .990) .940) .110) .580 (.330-.86) .100 (<LOD-.730) .990) .640-1.470 (<LOD-.710-1.460 (.110-.540) .380-.250-.02-1.390-.090 (.580-1.520-.03 (.230) < LOD < LOD < LOD < LOD .60) .62) 1.380-.060-.110) .050 (<LOD-.730) .180-.090 (<LOD-.210 (.110) .

< LOD means less than the limit of detection.00) .510-.18) 1.07-3.45 (2.0) 7.24-7.6) 5.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .0) 2.97) 20.080-1.62-8.52) 5.38-3.62) 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 * * * * * * .68) 2.0-40.800) 90th 13.370-.640 (.400-1.90) .110 (<LOD-.0 (4.83) 2.52 (1.67) .770 (<LOD-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (3.30-6.0) 2.01) 5.90-37. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 4. and 03-04 are 0.21) 3.90 (1.67 (1. population from the National Health and Nutrition Examination Survey.07 (1.0 (7.00-17.580 (.350-.610 (.90-20.0 (5.76 (1.28) .210-1.40 (1.31-10. see Data Analysis section) for Survey years 99-00.S.0) 4.0 (17.910) 2.53-7.0) 4.425-1.70) 2.620-1.49 (1.0) 2.830 (.65) 1.90-28.360-1.87) 12.32 (1. which may vary for some chemicals by year and by individual sample.890 (.70-50.07 (3.90-9.350-.59-5.480-.0) 2.0 (17.82-4.32-9.08.83-3.40-8.12-1.0) 4.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.0 (17.94-3.600 (.00) .330 (<LOD-1.61 (1.900 (.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 .00 (.87) 5.96 (1.35-10.770) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.99) 19.0 (17.0) 5.0-38.26 (2.0) 2.0) 5.14) .250 (<LOD-.30) .39 (2.0 (6.840 (<LOD-1.74) 5.10-3.97) 20.880) 5.88-3.40) 2.610) < LOD < LOD < LOD < LOD < LOD 2.42) 2.0) 3.1.90) .00 (1.30 (1.840-3.37) .94-8.20-4. 0.05 (3.83-3.52 (1.48) 13.750-2.50) 2.720) 2.55-4.21-3.20-17.30 (.99) 11.90 (2.0 (13.690 (.80 (4.10-3.53 (2.67 (2.15) 14.63 (3.30-7.35) 5.43-4.03 (.36-3.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.870) < LOD < LOD .39) .70-17.36-3.53) 20.20 (1.50) .590 (.0-40.0-38.07) 1. 130 Fourth National Report on Human Exposure to Environmental Chemicals .85-3.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.74 (3.30 (2.40-7.190-1.33 (4.20 (1.20-4.14) 2.49 (1.20) < LOD < LOD < LOD < LOD < LOD 1.29-10.800-4.40-4.0-38.70-7.28) 1.11) .0 (5.13 (3.750-1.30) 95th 19.15) 19.28-9.0) 5.90) .51-8.40-20.260-.94 (1.35) 11.23-6.00) 1.170-1.31) .10-9.55-8.47 (3.0 (5.86) 4.48 (2.691 (.66) 4.99 (1.46 (1.0 (3.70-30.0) 2.640 (.12) * * * * * * * * .0 (17.10 (.30 (1.960 (<LOD-1.00-17.60) .30 (1.10 (3.0-39.850) 16. and 0.40 (1.0) 5.800) 17.07 (3.05 (2.0 (16.14-5. respectively.730 (.11) 13.0 (5.05-3.380-. 01-02.0 (5.30-3.740 (.40) 1.51 (2.0-44.960 (.0 (4.63) 32.1.60) 1.07-3.11 (1.840 (.70-3.42) .49) 17.0) 2.

450 (. population from the National Health and Nutrition Examination Survey.48-42.62-17.56) 2.9) 6.0 (9.474-1.2-38.36 (.21-3.860-2.67 (2.39) 20.43) .470 (.18) * * * * * * * * .02-4.4-34.850-3.7) 4.57-40.50) .540 (.370-1.50) 11.840-3.2 (8.53) 27.09-3.33 (3.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.55) 21.29 (4.150 (<LOD-.1) 2.51-44.11) .65 (2.07-21.370) < LOD < LOD < LOD < LOD < LOD 1.60 (1.10 (2.83-11.45 (1.32-6.77 (.40) 1.5) 2.55 (3.800-2.310-.92 (2.67) 2.8) 2.64-4.1 (7.61) 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 .86) .00-19.88 (2.88-3.40 (.600 (<LOD-1.28-6.90-6.88 (.48 (4.830-3.47-10.740-1.07 (2.69) 2.40-2.37) 4.940-4.630-1.17 (1.31) .64) 30.96-25.430) 1.11-5.820) .25-38. Fourth National Report on Human Exposure to Environmental Chemicals 131 .51-4.4) 2.55) 21.3) 3.790) 11.330-1.56 (1.660) < LOD < LOD .40-12.85 (1.23-7.14 (1.33-3.02 (.14-6.56) .50 (4.650 (.590) 2.83 (4.12 (4.8-33. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.7) 5.0) 4.340-.33-5.6) 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 * * * * * * * * * .22-27.260-.670 (.770) .30 (4.69-7.10) 2.580 (.340-.00) .97) .49-2.190-1.18) 95th 21.15) 9.01 (1.730-3.8) 2.5 (9.9 (11.8) 7.53) .500 (.75) 5.560 (.12-4.270-.8 (20.7 (6.960 (.270 (<LOD-.22) 2.18) 1.08) .970-3.79 (.650) 90th 10.84) 9.57) 1.7 (12.790 (.02 (1.80 (.59 (1.67-6.3) 2.57) 8.430 (<LOD-.06 (.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.930) .700) 6.5 (11.24) 3.340-.33-4.02) .50 (2.67) 1.17) 5.580-1.390-.240-.33 (1.03) 2.96) 2.5) 7.81-17.74 (2.700) < LOD < LOD < LOD < LOD < LOD 1.830 (.9) 5.47) .748 (.5) 2.44) .360 (.890 (.7) 6.57 (.73 (4.5 (8.29-4.66-47.8) 7.41 (4.03) 16.04-16.580) 16.04 (1.780-4.62 (1.13 (2.80) 3.96-8.1) 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 * * * * * * .S.52 (.38 (2.250 (<LOD-.320-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.91) 2.05) .370 (.8) 4.47) 5.25 (1.41) 18.82-11.35 (.340 (.89 (2.5-40.1 (5.86 (3.540-1.10-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25-9.31-7.88) 17.32) 9.580) 1.85-3.0 (4.820 (.7) 3.27 (2.31-18.48-7.260-.31) .690-5.710 (<LOD-1.4 (4.620-3.98 (4.8) 1.1) 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.44-11.71 (2.47-10.71 (.91-4.

Pilkington A. Mathieu L. Orsi D. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. 132 Fourth National Report on Human Exposure to Environmental Chemicals .49(9):751-760. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. A clinical neurological. Davis SW. Blanchard O. The relationship between maternal and fetal effects following maternal organophosphate exposure during gestation in the rat. Fiedler N. Heudorf U. Sartorelli E. accidental. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina.16(5):417-426. Ann NY Acad Sci 1997. Eaton DL. Fenske RA. Environ Res 2001. Neurophysiological function in farm workers exposed to organophosphate pesticides. J Expo Sci Environ Epidemiol 2006.12(6):619-645. Chevrier J.111(3):377382.177:37-41. Curl CL. Lu C. Hansen S.15(2):164-171. Koch D. Quandt SA. J Toxicol Environ Health 1981. Environ Health Perspect 2005. Toxicol Ind Health 1998b. Davies JE. Peterson JC. Castorina R. Farahat FM. Barr DB. Fenske RA. Aprea C. Fenske RA. 2005. J Occup Environ Med 2004. Farahat TM. Richardson RJ. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Sci Total Environ 1996. Urinary excretion of alkylphosphates in the general population (Italy). and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides.60(4):279-286. et al. Hawk R. Neuropsychological performance among agricultural pesticide applicators. Chen W. Fenske RA. Keifer MC. Organophosphate urinary metabolite levels during pregnancy and after delivery in women living in an agricultural community. Engel LS. Gillham RA. Kedan G. Anger WK. Arcury TA. Charnley G. Shebl MM.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW. Chukwudebe A. Centers for Disease Control and Prevention (CDC). Environ Res 1992.108:521-525. Environ Health Perspect 2003. Amr MM. Jolley L. Arch Environ Health 1998.53(1):714.113(12):1802-1807. Aprea C. Garabrant DH. Robinson LR. Neurobehavioural effects among workers occupationally exposed to organophosphorous pesticides. Barr DB. Grzywacz JG. Griffith W. Jamal GA. Greenhalgh R. Kipen H.7(5):715-731. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Checkoway H. Castorina R. et al. Environ Health Perspect 2000. et al.59(1):217-228. Vaughan TL. Bradman A. Bozzi N. Boccalon P. Kissel JC. Momas I. Strambi M. Environ Health Perspect 2003. Daniell W. Eskenazi B. Abdel-Azis M. Bouvier G. Krieger RI. Angerer J.837:257-268. Sartorelli P. Elgethun K. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort. Giordani B. J Expo Anal Environ Epidemiol 2005. Barnhart S. Am J Ind Med 1997. 86:80-87. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Lunghini L. Buchanan D. Barr DB. Leffingwell JT. Environ Health Perspect 2002. Bradman A. Abdelrasoul GM. Franklin CA. Seta N. Astroff AB. Regul Toxicol Pharmacol 2003. Lu C.38(1):91-97. Berent S. Kissel JC. Barr DB. Eigenberg DA. et al. Eskenazi B. Reprod Toxicol 1998a. Freshwater KJ. Novelli MT. Sciarra G. Kelly-McNeil K. Duggan A. Denley HV. Astroff AB.111(13):1640-1648.37(3):382-395. Regul Toxicol Pharmacol 2003. Surveillance of occupational. Fisker-Andersen J. Occup Environ Med 2002. neurophysiological. Demers P.59(7):434-441. Schweitzer SJ. Long-term use of organophosphates and neuropsychological performance. et al.46(4):367-378. McKone TE. Curl CL. Garrison RP. Miller M.32(5):487-496. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Costa LG. Bravo R. Am J Ind Med 2006. Fenske R. Curl CL. Occup Environ Med 2003. et al.110(8):829-833. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. Harnly ME.14(6):869-889. Young AD.

Rothlein J. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Chronic central nervous system effects of acute organophosphate pesticide intoxication. Calvert IA. Scand J Work Environ Health 1998. Bradman A. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Office of Prevention Pesticides and Toxic Substances. Wickremasinghe AR.52(2):190-195. et al.12(2):153-172. Rohlman D. Washington (DC). Chronic neurological sequelae of acute organophosphate pesticide poisoning. Environmental Protection Agency (U. Neurotoxicology 2005. Jamal GA. Buccafusco JJ. Jenkins B.52(10):648-653. metabolite clearance. Kidd M. Salvini S. Robson MG. Aprea C. Seiber J. Muniz J. Available at URL: http://www. Neurotoxicity among pesticide applicators exposed to organophosphates. Schenker M. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. low-level organophosphate exposure on delayed recall. Arch Environ Health 1988. Lambert WE. McConnell R. Rodnitzky RL. Available at URL: http://books. Bravo R. Ames RG. Phillips J.338(8761):223-227. National Research Council (NRC).30(2):98-103. The Pesticide Health Effects Study Group.epa. Dinoff TM. Neurotoxicol Teratol 1998. Lancet. Arch Environ Contam Toxicol 2000. Samuels S. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.68(3):209-227 Maizlish N. Spurgeon A. Am J Public Health 1994. Stark A. Pesticide industry sales and usage . Lasarev M. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 4/7/09 Young JG. van der Hoek W. Tumino R. Washington (DC): U. Rothlein J. Ruberu DK.S. Gillham R. Lancet 1995.43(1):38-45. S. Narang A. Beach J.44(4):352-357.12(2):134-141.24(1):18-29.nap. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. London L.edu/ openbook. Weisskopf C. Terry AV Jr. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Savage EP. Chrislip D. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Sci Total Environ 2004. et al.58(11):702710.84(5):731-736. Nell V. McCauley L. Effects of long-term organophosphate exposures on neurological symptoms. Prendergast MA. Malathion deposition. Lu C. Stokes L. Russo J. Berry H. Occupational exposure to organophosphate pesticides: a neurobehavioral study. vibration sense and tremor among South African farm workers. Rosenstock L. EPA). Occup Environ Med 2001. Petchuay C. EPA. A behavioral evaluation of pest control workers with short-term. Pesticides in the Diets of Infants and Children. Lewis JA. Thompson ML. J Occup Environ Med 2002. Keefe TJ.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Effects of chronic. Heaton RK. and cholinesterase status of date dusters and harvesters in California. Chronic neurological sequelae to organophosphate pesticide poisoning. et al. Caltabiano LM. National Academy of Sciences. Mounce LM.pdf. 1/12/09 Peiris-John RJ. Pilkington A.2000 and 2001 market estimates. Claypoole K. Visuthismajarn P. U. Int J Occup Environ Health 2006. Bull Environ Contam Toxicol 1994.20(2):115-22. Saieva C. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Marshall E. Pedersen L. Lasarev M. Masala G. Keifer M. low-level exposure to the organophosphate diazinon. Daniell WE. 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. Arch Environ Health 1975. Muniz J. et al. Environ Health Perspect 2005.S. Steenland K. Myers JE. Burcar PJ. Weerasekera G.php?record_id=2126&page=1. Vitayavirasak B. 2004. et al. Hore P. and spatial learning in monkeys and rats. Irish RM. Buchanan D. Santana J. 1991. J Toxicol Environ Health A 2005. May. Eskenazi B. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Smit LA. Barr DB.38(4):546-563. Levy LS. Environ Health Perspect 2006.26(2):199-209.345(8958):11351139. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. O’Malley M. Scherer J. 1993 [online]. Johnson C. discrimination.114(5):691-696. Frasca G.113(4):504-508. Takamiya K. Am J Ind Med 1987. Gladstone EA.332(1-3):71-80. Occup Environ Med 1995. Stephens R. Hansen S.

The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. For example.5.6-Trichloro-2-pyridinol (6515-38-4) 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol 2-Isopropyl-4-methyl-6-hydroxypyrimidine (2814-20-2) Malathion dicarboxylic acid (1190-28-9) para-Nitrophenol (100-02-7) 2-(Diethylamino)-6-methylpyrimidin-4-ol/one 134 Fourth National Report on Human Exposure to Environmental Chemicals . These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. parathion and methyl parathion are metabolized to para-nitrophenol. malathion is metabolized to malathion dicarboxylic acid. In addition to reflecting exposure to the parent insecticide. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3.Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies. For general information about the organophosphorus class of insecticides. the level may reflect exposure to the environmental degradation products of these pesticides.

60) 5.40) 9.80-10.40-13.09 (3.000 pounds are used per year.50 (2. 5598-13-0 General Information The chemical 3.10 (3.63 (1.70-16.80) 12.43-2.9) 697 660 521 701 602 947 Limit of detection (LOD.39) 4. Fourth National Report on Human Exposure to Environmental Chemicals 135 .00) 3.66-15.90) 7.30-11.7) 8.0 (7.4 (10.61 (1.30-12.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.10) 2.10) 6. Estimated intakes from diet and water have not exceeded recommended intake limits.0) 11.61-7.70 (1.and post-construction structural applications for termite control were to be phased out by 2005 (U.95 (4.77-6.74-9.5.52-12.9 (9. 2002).1-16. chlorpyrifos was no longer registered for indoor residential uses in the United States.0-28.3 (11.20 (4.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.72) 2.40) 2.0) 12.98-15.34) 1.20-16.37 (1.47-9.10-17.30-5.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.55-5. dermal.47) 1.9-18.02 (7.76 (1.50-5.50-8.5 (8.97) 2.35) 2.90 (1.60 (5.20-2.00-24.70-17.04-10.47-11.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60-4. It has low leachability.83) 1.13 (1.53 (1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.37) 5.68 (7.0) 9.86) 4.20-11.50-2.00) 1.5) 7.16) 2.02) 1.8) 9.7-23.88 (1.40 (6. population from the National Health and Nutrition Examination Survey.80) 1.90-2.0) 10.S.0 (7.97) 2. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators..30-9.4. and inhalation routes.95) 7.62-2.3 (8.3) 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. but can be detected in streams receiving runoff from application sites.0) 12.29) 90th 7.91) 16.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.40 (5.19-3.20) 10.50-4.20) 4.20) 2.0) 10.21) 3.67 (2.7) 13. interval) 1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.25) 3.26) 7.84) 1.24-1.63 (8.89-2.70) 1.8-15.28) 2.30 (2.0) 10.32) 2.74 (1. Survey Geometric mean (95% conf.46-2.50-14.27 (7.60 (2.EPA.96) 3.30) 4.36 (4.97) 7. 2007).47-13. applied to structures to kill termites.40-26.57 (2.5-24.90 (6.10 (1.40-2. in 142 urban homes and preschools in North Carolina.79-2.02 (1.31-2.35) 1.01) 1.25) 1.0) 8.71 (1.7) 9. The general population may be exposed to chlorpyrifos via oral.90-4.76 (1. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al. staying bound to soil particles.71 (2. Chlorpyrifos is degraded in agricultural soils with a half-life of several months. 2921-88-2 Chlorpyrifos-methyl CAS No.24-3.22 (1. For instance.92 (1.15 (1. Approximately 80.78 (7. 1999.0) 7.30-2. air.0 (7.50-2.70-11.22) 2. and sprayed to kill mosquitoes. Chlorpyrifos is Urinary 3.28-3.50 (1.10 (5.9) 11.59) 2.90-7.90) 3.60-3.0) 6.2 (10.EPA.30) 4.13-3. 2002).04-10.63 (2. and is infrequently detected in ground water (IPCS.9 (10.87-6.99-4.64) 3.S.45 (1.60-3.68-2.70-5.0) 12.31-2.6) 7.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.1) 5.0) 15.61) 75th 3.51) 1.60-2.80-8.59-2.43-2.4 (9.0 (10.77 (1.0 (9.50 (2.77) 1.80 (1.80 (7.67 (2.30 (4.39-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10 (4.30 (2.20-4.05-5. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.19 (1. and dust.70 (1.0 (7.51 (1.90 (2.4 and 0.67 (1.0 (7.20 (2.20-3.77-15.97-7.37 (4.09 (2.50 (1.40-10. 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.90 (1.5.60 (4.90 (3.72-4.50 (2.4-15.50-4.0 (13.91 (1.20) 2.29-1.70-15.66-4.20-14.40 (5.03) 1.89 (2.44-2.97) 4.90-8.4 (8. 2005).44-5.00-8. USGS. and on plants for days to several weeks.32-1.44 (3.S. Exposure can also result from contact with contaminated surfaces. Approximately 21-24 million pounds per year were used domestically from 1987-1998.81-2.17 (1.47 (4. pre.0) 12. After 2001.52-2.38 (3.05) 1.80) 2.3) 8. It also has been applied directly on animals to kill mites.0) 8.00) 2.9 (7.71 (6.30-1.0) 18.94 (4. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.3 (10.0) 14.80) 4.8) 10.51-2.0) 12.30) 5.

interval) 1.21-6.91-4. Urinary 3.46 (1.60 (1.91 (4. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.0) 10.80) 3.88-8.24) 75th 2.07) 1.1-21.58-5.6-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.5) 5.85 (2.06 (5.63 (4.93 (1. Howard et al.62-7.86 (1.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.97) 3.86 (1.05-3.65-15.24-24.46 (2.02 (5.68) 1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Ricceri et al.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.68) 6.27-1.69 (1.97 (3. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.22) 1.91-13..39) 6.41 (1.1 (7.75) 6.39 (4.82-4.48 (2.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.95 (3.0) 6.3 (7.28) 2.55 (4.91) 10.44 (5. 2000).0) 16.60-3.91) 1.98 (7.94-12.43 (4.58 (4.4) 4.11) 7.25-11.11 (2.94-14.55 (1. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.47 (5.00) 1.1 (10.72) 1.37 (1.16 (4.05-4.33 (5.90-9.19-2. Roy et al.24-4. Based on animal data and human cholinesterase monitoring during occupational exposure.05) 3. Survey Geometric mean (95% conf. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).S.53 (2.43-10.33 (1.91 (3.80-6.85-4.09 (1.05-8.20-1.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.76 (3. In pesticide applicators. Once absorbed.75 (1.50 (4.5 (6.58 (1.17-4.82) 8.25-1. 2002).42-2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.33-7.65-11.80-4.17-4.99-8.47-2.44 (5.19) 3. TCPy can also occur in the environment from the breakdown of the parent compounds.00-8.0) 12.55) 1. Slotkin et al. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.39-1.29 (3. vomiting. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.77) 1.97-3.11 (2.93) 2.00 (7. resulting in excess acetylcholine at nerve terminals.79-13.56 (1.63-2.21-1.93) 5.64-2. Metabolic hydrolysis leads to the formation of TCPy.S.57-2. Betancourt et al.49 (1.24) 5.64-7.88-8. paralysis.5.14-8.88-9.30-4.84-6..45-1. 2006a.27-7. and producing acute symptoms such as nausea.06-4.45 (1..23-1.82 (3.22-6.81 (3. neurotransmission. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.39 (2. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.940-1.22 (4.64 (1.23) 14.47 (1.51 (1.81) 2.14) 1.85 (3.52 (5. 2006.59) 3.20 (2. 2006b).09-2.44 (1.71 (1.82 (2.00-13.56-2.7) 7.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .40) 1.49-2.35-1. cholinergic effects.47 (1.19-1.85) 4.07) 5.83-11.78 (1..16) 6. weakness. 2005.99) 1.88 (1.72-2.31-1.EPA.1-38.93 (4.56) 5.58) 5.24 (1.34-1.05-1.31-4.19) 6.3) 9. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.86 (3.88 (1.44-6.12-1.92 (1.96) 3. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.62) 1.66) 1.97) 3.12) 1.87-3.44 (6.36) 1.6) 9.22 (6.33 (.24-5.56 (4.8) 9.57) 9.92) 3.70-4.48 (1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.66 (1.58 (1.57) 2.74) 1.73 (1.06 (1.76 (2.63 (5.9 (12.38) 3.91) 2.42 (5..31) 1.66-11.15 (4.95 (1.89) 4.58) 1.09-1. 1984). 2006.91) 1. 2005.01) 3.25-12.35) 2.3) 8..11-9.72) 2.6) 10.71) 3.49-2.88-10.08) 6.93 (2.54 (2.32) 1.56) 2.57-2.83-2..12-3.80-11.97 (2.59-2.03) 1.2 (7.3) 8.49-2. and seizures.09-3.24-1.85) 1. 2005.42 (6.01) 3.53-5.44 (1.26-14. TCPy is more persistent in the environment than chlorpyrifos itself (U.83) 1.28) 2..2) 6.01) 1.98 (6..33) 2.88) 6.30-1.92-2.62) 90th 5.35) 1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.54) 5.02) 7. and other metabolites. Thus. population from the National Health and Nutrition Examination Survey.

S. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. 2005).. Slotkin TA.. Lioy PJ. 2007).. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. et al. Burns CJ.S. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. 2005). Seidler FJ. 2003. Barr DB. Chlorpyrifos exposure and biological monitoring among manufacturing workers. 2000). Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. U.atsdr.Organophosphorus Insecticides: Specific Metabolites 2004. Clayton CA.. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Toxicol Sci 2006. Following crack-and-crevice application of chlorpyrifos in their homes..92(2):500-506. MacIntosh et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005).EPA. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Betancourt AM. 2001) and Italy (Aprea et al. Levels of TCPy in the U.113(8):1027-1031. Barisano A.S. Freeman NC.. Of 482 pregnant women living in an agricultural community.Reference values of urinary 3.cdc. Meyer A. Environ Health Perspect 2001.82(2):305-312. 2005. environmental levels) and health effects is available from ATSDR at: http://www. Aprea C..S. Haidar S. 2006).109(6):583-590. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Occup Environ Med 2006. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al.S. but levels were roughly four to six times higher than the geometric means in the U. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. CDC. In Iowa farm families using several different pesticides. 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. Garabrant D. EPA at: http://www. 2005).6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). 2004). 2005). Eberly LE.63(3):218220. urinary TCPy levels in children were reported not to have increased (Hore et al. Additional information about external exposure (i. In Minnesota and South Carolina farmers who used chlorpyrifos. Aldridge JE. Whyatt et al... but not chlorpyrifos. Albers JW.. Perera et al. Koch et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Carr RL. Giordani B. Environ Health Perspect 2005. Curwin et al. 2005). 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. 2005. Betta A. 2004).. Berent S. Magnaghi S. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Biomonitoring Information Urinary TCPy levels reflect recent exposure. 2002). References Adgate JL. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.. 2005. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. et al. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.gov/pesticides/. population (CDC. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections.e.5. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. the geometric mean urinary TCPy levels were similar in parents and children.epa. 1992. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.. Burgess SC. representative subsample of NHANES 19992000 (CDC.. J AOAC Int 1999.gov/toxpro2.. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Catenacci G. 2001).. Lotti A. Fourth National Report on Human Exposure to Environmental Chemicals 137 .html and from U. In a probability-based sample of 102 Minnesota children aged 3-13 years. 1999).

Slotkin TA.93(1):105-113. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Kinney P. Environmental Health Criteria 198. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.htm. Seidler FJ.niehs. Chrislip DW. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Howell RJ. et al. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Heederik D. Mandel JS. Ann Occup Hyg 2007. J Expo Anal Environ Epidemiol 1999. Rauh V. et al. Shealy DB. Ryan L. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Available at URL: http://www. Chlorpyrifos: pharmacokinetics in human volunteers. Kromhout H. Environ Health Perspect 2006. Barr DB. Hammerstrom KA. 2005. chlorpyrifos. Striley C. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Third National Report on Human Exposure to Environmental Chemicals. Pellizzari E.71:99108.inchem. Sanderson WT. Wartenberg D. Saunders JH. Environ Health Perspect 2004. 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. Baker S.5. Needham LL. Nolan RJ. Scand J Work Environ Health 2005.nih. Robson M. Pesticide residues in urine of adults living in the United States: reference range concentrations.113(2):211-219.S. Honeycutt R. Freshour NL. Weltzien E.114(10):1542-1546. J Expo Anal Environ Epidemiol 2005. J Expo Anal Environ Epidemiol 2000. mothers and fathers living in farm and non-farm households in Iowa. Sharma V. Dick RB.207(2):112-124. Interim registration eligibility decision for chlorpyrifos. Baker BA. Irish R.73:8-15.108(4):293-300. Hines CJ.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC).111(2):201-205. Lorenzini P. Acquavella JF. U. Meeker JD. Bailey SL. Environ Health Perspect 2006a. Seidler FJ. Slotkin TA. Harley K. 1999. Hardt J. Bradman A. et al. Levin ED. Sheldon LS. Croghan CW. et al. A longitudinal investigation of selected pesticide metabolites in urine. MacIntosh DL. Hein MJ. Reid TM. et al.15(4):297-309. Adgate JL. 2921-882.204(2-3):175-180. Barr DB. Slotkin TA. Hore P. Howard AS. et al. Jewell NP. Urinary pesticide concentrations among children. Bruun D. National Toxicology Program (NTP).51(1):53-65. Exposures of preschool children to chlorpyrifos and its degradation product 3. International Programme on Chemical Safety-INCHEM (IPCS). Seidler FJ. Environmental Protection Agency (U.10(4):327-340. Edwards RD. Lioy PJ. Bucelli R. et al. gov/ntpweb/index.114(5):746-751. Biomonitoring for farm families in the farm family exposure study. Environ Health Perspect 2005. Chlorpyrifos.114(2):260-263. Roy TS. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Gurunathan S. Jones PA.S. 4/7/09 Perera FP. Tsai WY. February 5. Environ Health Perspect 2006b. Head SL. et al. EPA).6-trichloro-2-pyridinol. Ricceri L. Steenland K. Bennett DH.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Environ Health Perspect 2000. Atlanta (GA). Rick DL. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Neurologic function among termiticide applicators exposed to chlorpyrifos. J Expo Anal Environ Epidemiol 2005. Angerer J. et al. Ozkaynak H.31 Suppl 1:98-104. Freeman N. Levin ED. Yang D. Int J Hyg Environ Health 2001. Fenske RA. Capone F. Hill RH Jr. Lein PJ.155(1):71-80. Eskenazi B.15(3):271-281. Chuang JC. Robertson GL. Ryde IT. Jett DA. Bravo R. 1992. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Cometa MF. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity.5. Venerosi A. Environ Health Perspect 2003. Chapman P. Brain Res Dev Brain Res 2005. Bravo R.org/documents/jmpr/jmpmono/ v99pr03. Toxicol Sci 2006.9(5):494-501. Camann D. Zhang J. Curwin BD. Morgan MK. Ryan PB. Executive summary of safety and toxicity information. Gregg M. 4/7/09 Koch HM. Fortuna S.6-trichloro 2-pyridinol in their everyday environments. Toxicol Appl Pharmacol 2005. Toxicol Appl Pharmacol 1984. Tate CA. Alexander BH. Barr DB. Available at URL: http://ntp.112(10):1116-1124. Lu C. Barr D. Herrick RF. Freeman N. Environ Res 1995. Toepel K. et al.

Environ Health Perspect 2003.usgs. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Barr JR.gov/circ/2005/1291/.Organophosphorus Insecticides: Specific Metabolites 01-007. et al. 6/1/09 Whyatt RM. February 2002.S. Available at URL: http://pubs.epa.pdf. Camann DE. revised February 15. Geological Survey (USGS). Fourth National Report on Human Exposure to Environmental Chemicals 139 .gov/ oppsrrd1/REDs/chlorpyrifos_ired. Pesticides in the Nation’s Streams and Ground Water. Barr DB. 2007 [online]. March 2006.111(5):749-56. 1/14/09 U. 1992-2001. Andrews HF. Kinney PL. The Quality of Our Nation’s Waters. Available at URL: http://www.

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

S. see Data Analysis section) for Survey year 01-02 is 0.380 (<LOD-. population from the National Health and Nutrition Examination Survey.670 (<LOD-1.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. 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. 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-.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 .S.200 (<LOD-. population from the National Health and Nutrition Examination Survey.270) < LOD 659 701 920 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 141 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2. Survey Geometric mean (95% conf. 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 . < LOD means less than the limit of detection. 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 .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 .

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

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

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

Third National Report on Human Exposure to Environmental Chemicals. May 2004. Centers for Disease Control and Prevention (CDC). Banister EW. U.114(2):260-263. Mason HJ. Jones K. International Programme on Chemical Safety-INCHEM (IPCS). Environ Health Perspect 2006. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Drug Chem Toxicol 1986. Swan SH. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Biochem Pharmacol 1992. Bravo R. In 23 children. Seifert J. Barr DB. Redmon JB. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .44(11):2243-2250.111(12):1478-1484. Sadowski MA. Beeson MD.gov/circ/2005/1291/. Fenske RA. Drobnis EZ. Garfitt SJ. Oloffs PC. Needham LL. Dumas P.50(5):505-515. Pewnim T. Bouchard M. Baker SE.37(4):501-507. Liu F.S. Driskell WJ. Pesticides in the Nation’s Streams and Ground Water.S. Interim reregistration eligibility decision (IRED.9(2):117-131. Carrier G. Barr DB. Oloffs PC.Organophosphorus Insecticides: Specific Metabolites 2005). March 2006. In a small number of men visiting fertility clinics in Missouri and Minnesota. Noisel N. Brunet RC.epa. Cocker J. 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. Olsson AO. Environmental Protection Agency (U. Environmental Health Criteria 198. Ann Occup Hyg 2006. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. Nguyen JV. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Available at URL: http://www. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Swan et al. Semen quality in relation to biomarkers of pesticide exposure. References Anthony J. 1992-2001.htm. 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. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Geological Survey (USGS).. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Irish R.. Environ Health Perspect 2003. J Expo Anal Environ Epidemiol 2000. Barr DB. et al. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.376(6):808-815. 1/14/09 U. In 54 Canadian greenhouse workers. Kruse RL. Barr DB. 2006). 2007 [online]. Toepel K. Rajendra W.gov/ oppsrrd1/REDs/diazinon_ired.org/documents/ehc/ehc/ehc198.S. 4/7/09 Lu C. revised February 15. Bull Environ Contam Toxicol 1986. EPA). Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Atlanta (GA).inchem. Diazinon. 2006). A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Anal Bioanal Chem 2003. 1998.10(6 Pt 2):789-798.pdf. Effect of sublethal levels of diazinon: histopathology of liver. Diazinon. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. The Quality of Our Nation’s Waters. Banister E. 2005. Toxicol Lett 2002. Study for Future Families Research Group.usgs.134(1-3):105-113. EPA 738-R-04-006. Available at URL: http://pubs.

2007). < LOD means less than the limit of detection.80 (<LOD-5. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5%) to kill body lice. malathion dicarboxylic acid. inhalational. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound.. vomiting. malathion has low acute toxicity. Malathion is slowly absorbed through the skin. 146 Fourth National Report on Human Exposure to Environmental Chemicals . the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate. Estimated intakes for the general population have not exceeded recommended intake limits. It is moderately to highly toxic to fish. Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Thus. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff. 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. and seizures. in fruit fly control. and other metabolites. gardens. Malathion is infrequently detected in groundwater sampling (USGS. as well as lawns. Malathion is also used medically in lotion form (0.S.50) < LOD < LOD 453 660 807 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 937 983 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 680 498 580 Limit of detection (LOD. see Data Analysis section) for Survey year 99-00 is 2. In addition to being a metabolite of malathion. Survey Geometric mean (95% conf.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. ornamental trees. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006).S. Metabolism of malathion leads to the formation of malathion monocarboxylic acid.64. Once they are absorbed. population from the National Health and Nutrition Examination Survey. and producing acute symptoms such as nausea. 2000). which is an organophosphorus insecticide that is used on a wide variety of agricultural crops. shrubs. It has a short halflife in soils and water and is not considered persistent in the environment. or oral routes (U. but is more rapidly and efficiently absorbed via ingestion. paralysis. When malathion is used on food or feed crops. Limited general population exposure occurs through the diet. and plants. resulting in excess acetylcholine at nerve terminals. Severe toxicity or deaths have been reported from Urinary Malathion dicarboxylic acid Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. cholinergic effects. Compared with other organophosphorus insecticides. It is registered for use in public health mosquito control. 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion.EPA. depending on the species. which may vary for some chemicals by year and by individual sample. usually only a small fraction of the crop is treated. weakness.S. and in government programs such as the USDA’s Boll Weevil Eradication Program. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al. At high doses. 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. Pesticide applicators and agricultural workers can have higher exposures via dermal. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 2003). 2006).EPA.

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

htm. Blasiak J. Malathion deposition.114(2):260-263.S. metabolite clearance. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. EPA). Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.73(1):182-94. Krieger RI. Environ Health Perspect 2006.S. Mutat Res 1999. Lioy PJ. Reregistration eligibility decision (RED) Malathion. Hertz-Picciotto I. Nicklas JA. Am J Epidemiol 1990. Bravo R.77:1009-1010. U. revised February 15. et al. Clayton CA. 2005. Pesticides in the Nation’s Streams and Ground Water. The Quality of Our Nation’s Waters. Hooper K.pdf. Irish R. Prasad SB. Lu C. Available at URL: http://www. et al. Environ Mol Mutagen 1993. 2007 [online]. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. J Expo Anal Environ Epidemiol 1999. 6/1/09 U. Harley K. Dumoulin MJ. Barr DB. Available at URL: http://www. Available at URL: http://pubs.22(1):7-17.org/documents/jmpr/jmpmono/v2003pr06. EPA 738-R06-030. Giri A.S. Grether JK.514(1-2):223231. A longitudinal investigation of selected pesticide metabolites in urine. Jewell NP. Eberly LE. Geological Survey (USGS). Petitti D. Samuel O.9(5):494-501. Eskenazi B. Pluth JM. et al. Barr DB.usgs. Malathion (addendum).15(2):164-171. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.56(10):2393-2399. Atlanta (GA). Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Toxicol Sci 2003 May. Barr DB. Trzeciak A.109(6):583-590. Environ Health Perspect 2001. Neutra R.112(10):1116-1124. Barr DB. Cancer Res 1996.38(4):546-553. Weltzien E.epa.gov/circ/2005/1291/.132(4):794-795. Reproductive outcome in women exposed to malathion. Hammerstrom KA. Ryan PB. J Expo Anal Environ Epidemiol 2005. Brunet RC.74(2):following table of contents. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. July 2006. Griffith W. Dinoff TM. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Lu C. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .445(2):275-283. 1992-2001. March 2006. Am J Public Health 1987. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Flessel P. and cholinesterase status of date dusters and harvesters in California. Szyfter K. Arch Environ Contam Toxicol 2000. Albertini RJ. Toepel K. Curl CL.inchem. 4/7/09 Kissel JC. Third National Report on Human Exposure to Environmental Chemicals. Jaloszynski P. Erratum in: Toxicol Sci 2003 Aug. Swan SH. Centers for Disease Control and Prevention (CDC). O’Neill JP. Rappaport E. Harris JA. Giri S. Fenske RA. Mutat Res 2002. Kedan G. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Goldhaber M. Needham LL. Freeman NC. Sharma GD. International Programme on Chemical Safety-INCHEM (IPCS). Quintana PJ. Genetic toxicity of malathion: a review. Carrier G. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.gov/oppsrrd1/REDs/ malathion_red. Bradman A. Gosselin NH. Environmental Protection Agency (U. MacIntosh DL. Environ Health Perspect 2004. Bouchard M. Thomas D.

15-3. and has a short half-life in soils and on plants. < LOD means less than the limit of detection.21 (2.32 (1. Methyl parathion has low water solubility..26 (1. and of the chemical nitrobenzene.60 (4.50) 3.57-4. pulmonary. binds tightly to soils resulting in low leachability. was once a restricted-use insecticide with limited applications on certain agricultural crops.10 (3. Once absorbed.45) 5.70 (<LOD-3..32-1. Methyl parathion is not registered for residential use in the United States.50 (1. Increased risk of exposure via dermal. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides. Morgan et al.13-1.19 (.0) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.27) 2.01) 695 660 518 679 603 941 Limit of detection (LOD.20 (<LOD-2.40-4.40-4.00) 3.70) 2.50 (2.12) < LOD < LOD 1. on cereal grains.61) < LOD 1.11) 2.60-24.91-3.33) 2.8 and 0.18-3.40) 2.28 (1.10 (3.28-4.28 (1.30-16.850) < LOD .70) 2.22-3. Estimated intakes from diet and drinking water have been below recommended limits.80) 2.30-3.34 (3..70-6.90 (1.0) 3.58) 3.50) 3. peak domestic use was as high as 5-6 million pounds per year. 2007).48) 90th 2.90-9.01) 4.30 (2.66 (2. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.50 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.36-1.300-.20 (2. Ethyl parathion.00 (2.10) 4.50-9.70 (2. first registered in 1948.05) 4.50) 1. Survey Geometric mean (95% conf.90-11.0) 3. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.62 (1.910) < LOD .910) < LOD < LOD < LOD 1.70-3.EPA.00) size 1989 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.10) 22. and oral routes can occur in pesticide and agricultural workers (Muttray et al.10 (<LOD-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.57) 1.45 (1.0 (3.72 (3.49 (1. 2006).70-6.790 (<LOD-.50 (2.30-5.0) 4.37-4.32-1.46 (3.33 (1. with limited applications in agriculture.S.71 (3.10-1. In the 1990s. population from the National Health and Nutrition Examination Survey.50 (1.69 (2.20) 5.60-19.40) 4. Methyl parathion use is highly restricted.70 (2.85 (2. ethyl parathion.92-2.50 (1.80 (1.1.70-6.80 (2.21-1.S.70 (3.16) < LOD 1.0) 3.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .50-14.01-4.20-5.0) 2.940 (<LOD-2.67 (1. Methyl Parathion.92) 5. In animal studies.910) < LOD < LOD .44) 2.60-36. 2000).30 (1. but by 2003.40) 1. and eliminated rapidly from the body after absorption (Kramer et al. and aquatic invertebrates. more slowly absorbed through the skin.60-5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.11-4.40 (1.32-3.70) 2.0) 3. It had been applied to cotton. Both are toxic to birds. Given its limited use.74) 5.770 (. fish.70-3.60) 1.40-3.50) 2. 2002.41-4.S. methyl parathion was rapidly absorbed after ingestion.80 (2.69) 4. and to a lesser extent.02-6. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.67) < LOD 1.298-00-0 Ethyl Parathion CAS No.79) 4. 1977). the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Many previous registered agricultural uses of methyl parathion have been cancelled (U.700 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.09-1.990-1.10-11. which may vary for some chemicals by year and by individual sample.860 (<LOD-1. all registered uses were voluntarily cancelled (U.37) 2.730 (<LOD-. 2003).89 (2.61) < LOD 1. Fourth National Report on Human Exposure to Environmental Chemicals 149 .70 (2.37-4.47) 2.71 (2. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.EPA.00 (2.37-2.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .

940 (<LOD-1.57-7.970 (. gov/pesticides/.13-12. Methyl Parathion.970 (. In large doses. 2004).. resulting in excess acetylcholine at nerve terminals.72-2. 1991).EPA considers methyl parathion unlikely to be carcinogenic to humans.16-4.86 (2.79 (1.73 (1..29 (2.26) 17.33-6.720 (<LOD-.400 (<LOD-.98-7.26 (1.97 (2.. weakness.78-2.35-3. Parathion and methyl parathion have high acute toxicity in animal testing.92 (2.05) 4.html and from U.20) .10 (1. population from the National Health and Nutrition Examination Survey.4 (3.2) 2.. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.67-2. methyl parathion. 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.90 (1.540) < LOD .80 (1. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. 1995).23) 1.30-1.79) 1.08-3.S.67 (3. paralysis.38-3.89 (2.60-2.15-10.800-1.430 (.71) 1.950) < LOD . 2006.370 (<LOD-.epa. paranitrophenol.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 .7) 3.13) 4.60 (1.00 (1.82) < LOD .55) 2.07 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4..94-4. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion. but lists ethyl parathion as a possible human carcinogen.790-. 1978.44-3. vomiting. 1995. WHO. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.76-14.e.41-2.15) 3.88) 1. accidental exposure. gov/toxpro2. Karanth and Pope et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.61) 4. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.87 (1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.21-21.3) 2. teratogenic.29) 1.930 (. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.830-1.730-1.cdc. EPA at: http://www.29) 2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 2006.96 (1. cholinergic effects.43) 4.80 (1. Orsorio et al. 2003.35-3.94-47.25 (2. 2004).07) 2. ethyl parathion. environmental levels) and health effects is available from ATSDR at: http://www.60) 2.08) < LOD .00 (1.S. and seizures.20 (3. At high animal doses of methyl parathion.01-3.17) .39) 1..57) 6.08 (1.850-1. 150 Fourth National Report on Human Exposure to Environmental Chemicals . para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. Slotkin et al.39 (1.17-4.Organophosphorus Insecticides: Specific Metabolites Metabolites”).31-3.2) 2.44-3.33-3. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. Survey Geometric mean (95% conf.57-2.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .10) 90th 2.720-1.840 (.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.870) < LOD .14-3.88 (1.20) 3. 2005.95) 1.93 (2.04) 1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .640) < LOD < LOD 1.56-2.59 (1. Thus.S.11) 1.680 (<LOD-1.37-1.70) 3.21) 1.25) 1.82 (2.91) 1. Zurich et al..1) 2.01 (.89 (2.790-1.440 (<LOD-.71 (1.83 (1.310-.500) < LOD < LOD .33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .97 (<LOD-4.78-2. and unintentional acute or chronic high-level occupational exposure (Hill et al.33-3.97-10.01 (2. 1990.11-4. Methyl parathion is not considered genotoxic.91 (1.930 (.530) < LOD < LOD < LOD .9) 1.atsdr.690-1.31) < LOD . and producing acute symptoms such as nausea.78 (2.48-4. and other metabolites. Jaga and Dharmani.00) 2.30) 3.55 (<LOD-3.04 (2.96 (1. Additional information about external exposure (i..980 (.09) 2.880 (. Lores et al.78) 2. The metabolite.84) 3. does not inhibit acetylcholinesterase enzymes.77-7. U. In addition to being a metabolite of methyl and ethyl parathion.

Lewalter J. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Karanth S. 1999). Pesticide workers may have much higher levels following pesticide applications. Neurotoxicol Teratol 2003. 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. Harley K. Role of individual susceptibility in risk assessment of pesticides. Hill RH Jr. 1995. Laboratory investigation of a poisoning epidemic in Sierra Leone. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Moseman RF. 2005). J Expo Anal Environ Epidemiol 2005. Ashley DL. 2005). 2002). Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 2005.. and levels were similar or slightly lower that those in a small convenience sample of the U.110 Suppl 6:1075-1078.. 2005. Lu C.. Hill RH Jr. Pharmacokinetics of methyl parathion: a comparison following single intravenous.. Moomey CM.6(2-3):159-173. Turner WE. Rev Environ Health 2006. Hill et al. Baker SE. Barr JR.inchem..215(3):182-190. Jewell NP. Lin LI. 2004). 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. Pathak S. Gregg M. Shealy DB. In a study of workers who handle parathion. Environ Health Perspect 2002. Head SL.. McClure PC.71:99108. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. oral or dermal administration. J Biomed Sci 2002. 2005. Needham LL. Baker S.org/documents/jmpr/jmpmono/v95pr14. Bradway DE. Guizzetti M. et al. et al. Baker RC. Occup Environ Med 1999. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Environ Health Perspect 2002. Head SL. ACGIH recommends a BEI of 0. Environ Res 1995.25(5):599-606. Kedan G. Giordano G.9:311-320.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. McCann et al. Parathion-Methyl (addendum). 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. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. DiPietro E.S. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Atlanta (GA). Bailey SL. Methyl parathion: an organophosphate insecticide not quite forgotten. Arch Environ Contam Toxicol 1977. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicology 2005. Clark JM.21(1):5767. Costa LG.5 mg (500 µg)/g creatinine for workers at the end of shift. References Barr DB. Hryhorczuk DO.14(4):213-216. Runkle KD. general population (CDC.110 Suppl 6:1085-1091.15(2):164-171. Kissel JC. Curl CL. Cline RE. Slach EF.htm. Rubin et al. a range of values several hundred times higher than levels found in the U. et al. Kramer RE. Bradman A.33(5):270-276. Available at URL: http:// www. Alley CC. Centers for Disease Control and Prevention (CDC). et al. 2002. Environ Health Perspect 2004. McCann KG. Fourth National Report on Human Exposure to Environmental Chemicals 151 . et al. Barr DB. Weltzien E. J Anal Toxicol 1990. Chicago area methyl parathion response. International Programme on Chemical Safety-INCHEM (IPCS). CDC. Dharmani C. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Lores EM. 4/7/09 Jaga K. Pesticide residues in urine of adults living in the United States: reference range concentrations. Griffith W. Rockhold RW. Arch Environ Health 1978. population (Olsson et al. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. Morgan DP. Wellman SE. Hetzler HL.S. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Eskenazi B.112(10):1116-1124.56(7):449553. and many residents were symptomatic (Barr et al. 1995).. 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. Barr DB. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Leng G. 2002. Pope C.

EPA). 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. Methyl parathion in drinking water. WHO/SDE/WSH/03.D. Hill RH Jr. et al. Rubin C.20(4):533-546.S. 152 Fourth National Report on Human Exposure to Environmental Chemicals . 1992-2001. Environ Health Perspect 2002.162(2-3):219-224. U. Pesticides in the Nation’s Streams and Ground Water. Tate CA. Case No. 6/1/09 World Health Organization (WHO). 1995-1996. Dunlop B.epa. External and internal exposure of wine growers spraying methyl parathion.201(2):97-104. Letzel S. Levin ED.int/water_sanitation_health/dwq/chemicals/ methylparathion. revised February 15. May 2003.S. 2004. Honegger P. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Facts. Mengle DC.who. Geological Survey (USGS). 5/19/09 Zurich MG. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. 1/14/09 U. 0153.376(6):808-815. Costa LG. Olsson AO. Available at URL: http://www. Nguyen JV.E. Ohio. Kieszak S. Seidler FJ. gov/oppsrrd1/REDs/methylparathion_ired.S. 2007 [online]. The Quality of Our Nation’s Waters.114(10):1542-1546. Backer G.S. Esteban E. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Ethyl parathion. Toxicol Lett 2006. EPA).04/106. EPA-738-FOO-009. Monnet-Tschudi F. Hill G.Organophosphorus Insecticides: Specific Metabolites Muttray A.gov/oppsrrd1/REDs/factsheets/0155fct. Environmental Protection Agency (U. 1/12/07 U.gov/circ/2005/1291/. Environmental Protection Agency (U. Yacovac R. Slotkin TA. pdf.S. Sadowski MA. Am J Ind Med 1991. September 2000. Investigation of a fatality among parathion applicators in California.pdf. Rosenberg J. Available at URL: http://www. Available at URL: http://pubs. Available at URL: http://www. R. Environ Health Perspect 2006.110 Suppl 6:1047-1051. Osorio AM. Jung D. Anal Bioanal Chem 2003. Ames RG. Schilter B. Barr DB. March 2006.pdf.epa. Ryde IT.usgs. Toxicol Appl Pharmacol 2004. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.

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

S.780 (.760 (<LOD-.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .31) .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2. population from the National Health and Nutrition Examination Survey.S.780 (<LOD-1. Survey Geometric mean (95% conf.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 .430 (<LOD-.780 (.840) 669 687 929 Limit of detection (LOD.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 .07) .820) < LOD < LOD .15) < LOD .740-1. < LOD means less than the limit of detection.470 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700-1.94) .17 (.780 (<LOD-1.210 (<LOD-.850 (.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .500 (.64) .55) .21) < LOD .210-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .950) < LOD < LOD 1.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.27) .700-. see Data Analysis section) for Survey year 01-02 is 0. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th .680 (<LOD-.210-.200-. population from the National Health and Nutrition Examination Survey.840 (.740 (.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .610 (<LOD-1.250 (<LOD-.300-1. Survey Geometric mean (95% conf. 154 Fourth National Report on Human Exposure to Environmental Chemicals .580-1.670 (<LOD-1.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.410 (<LOD-1.

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

In agriculture.. organophosphorus. warehouses. and sumithrin) are also registered for use in mosquito-control programs in the United States.2-Dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. EPA. This class of pesticides has low toxicity in birds and mammals. They are ranked as having moderate acute oral toxicity. The table shows the urinary pyrethroid metabolites measured in this Report. Estimated intakes from diet and drinking water are below recommended limits. agricultural fields. and then eliminated over several days in urine and bile (Kuhn et al. cyfluthrin.. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. cypermethrin. 2005. Compared with other classes of insecticides such as organochlorines. animal facilities. After absorption from inhalation or ingestion. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. or carbamate pesticides.. pyrethroid pesticides have less acute toxicity in animals and people. and are rarely detected in ground waters (USGS.S. 2003. 2003. Pyrethroids are not well absorbed through the skin (ATSDR. and greenhouses.. Woollen et al.EPA. followed by conjugation. Soderlund et al. bind to soils. 1992). Certain pyrethroid insecticides (such as permethrin.. and deltamethrin have been used frequently on cotton. 2002). About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. which are natural chemicals found in chrysanthemum flowers. They are also applied on livestock to control insects.S. they are not persistent in the environment due to their rapid degradation within days to several months.. such as piperonyl butoxide. 2006a. There are about 30 different pyrethroid pesticides in use. in some situations replacing the use of DDT. 1999. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. Soderlund et al. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. pyrethroids are rapidly metabolized. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Possible other additional actions on neuroreceptors Pyrethroid Insecticides Metabolites in this Report Pyrethroid (CAS number) Cyfluthrin (68359-37-5) Cypermethrin (52315-07-8) Cyfluthrin (68359-37-5) and Permethrin (52645-53-1) Deltamethrin (52918-63-5) Cyhalothrin (68359-37-5) Cypermethrin (52315-07-8) Deltamethrin (52918-63-5) Fenpropathrin (39515-41-8) Permethrin (52645-53-1) Tralomethrin (66841-25-6) Urinary metabolite (CAS number) 4-Fluoro-3-phenoxybenzoic acid (77279-89-1) cis-3-(2.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. Pyrethroid pesticides have low volatility. 2002.2-Dibromovinyl)-2.. Unmetabolized pyrethroids have been measured in breast milk. so usage is restricted near water (U. 2007). Generally. Leng et al. Outside the U. 2006b). solvent oils. 2005). The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use.S. WHO. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. by either ester hydrolysis or hydroxylation.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. and synergists. 1992). 2002).. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. but pyrethroids are highly toxic to fish and some aquatic invertebrates.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichlorovinyl)-2. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. but may be poorly transferred across the placenta (ATSDR. resmethrin. Woollen et al. 1997.

et al.27(4):609-614. Go et al. Hu JY.gov/toxprofiles/ tp155. Kim HS. 1991. Neurotoxic effects of two different pyrethroids. Biochem Biophys Res Commun 1998..300(3):161-165. Wieseler B.62:101-108. Kim TS. epa. Bernardi MM. Elwan MA. fenvalerate.. Moniz AC. Shafer. 2003.50(2):245-255. 2003. Seth PK. J Reprod Dev 2004. 2003. Fourth National Report on Human Exposure to Environmental Chemicals 157 .35(2 Pt 1):227-237. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Adhami VM. Levsen K. Regul Toxicol Pharmacol 2002. Salzgeber SA. Eriksson and Fredriksson.8(1):18-21. Hu et al.23(6):665-673. Cruz-Casallas PE.. 2002. Kunimatsu et al. Berger-Preiss E. Moniz et al. Neurotoxicol Teratol 2001. Soderlund et al. Chen JH. Go V. 2001.atsdr. Estrogenic and antiprogestagenic activities of pyrethroid insecticides.. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Bull Environ Contam Toxicol 1999. Pogo BG. Ranft U. Xenobiotica 1997. 1998. Garey J. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. 2002). Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Neurotoxicol Teratol 2005. and striatal dopamine levels in male and female rats. Lazarini CA. Kang IH. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.. 2006).27(12):1273-1283. Environ Health Perspect 1999. Garey J. et al. Abell AD. Neurosci Lett 2001.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. WHO. choreoathetosis. Song L. In developing rodents. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. dopaminergic. References Agency for Toxic Substances and Disease Registry (ATSDR). In California. hypersensitivity.211(3):188-197. Fredriksson A. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.. Estrogenicity of pyrethroid insecticide metabolites. Ray et al. Thomson BM. Bernardi MM. 2006. Florio JC.8(1):197-202. Varoli FM.. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Lee SJ. and permethrin) in the Hershberger and uterotrophic assays. Generally. Agrawal AK.cdc. Leng A. cdc.. McCarthy et al.205(6):459-472. Available from URL: http://www. bioallethrin and deltamethrin. 2005). 1999. Shukla Y. Effects of prenatal exposure to deltamethrin on forced swimming behavior. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Int J Hyg Environ Health 2002. Kuhn K. Shin JH. J Environ Monit 2006. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity.107(3):173-177. Lemonica IP. tremor. Lewalter J. Okuno Y. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.108(1):78-85. Zhao RC. motor activity. 2005). Toxicol Appl Pharmacol 1991. Indoor pyrethroid exposure in homes with woollen textile floor coverings..gov/pesticides/ and from ATSDR at: http://www. Leng G. Pauluhn J. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Toxicological profile for pyrethrins and pyrethroids. Idel H.251(3):855-859. Spinosa HS. 2005). Guillot TS. McCarthy AR. Sunami O. Wolff MS. Garey and Wolff. 2004. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. 2000. Shaw IC. Eriksson P. 2001. Richardson JR. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. September 2003. et al. and seizures (ATSDR. Idel H. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Leng G. 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. Leng G.gov/toxpro2. salivation. Yang J. Elwan et al. Additional information about pesticides is available from U.S. Caudle WM. 2003. Ose K.1/15/09 Aziz MH. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Kim et al.html. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Wang SL. Pyrethroid pesticide-induced alterations in dopamine transporter function.. Kamita Y. et al. Wolff MS. Kim IY. neurochemical changes in cholinergic.html... Lazarini et al.. Yamada T. Toxicol Appl Pharmacol 2006. Kunimatsu T. Miller GW.atsdr. EPA at: http://www. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 2005). Sugiri D. 2006. 2002). Kuhn KH.

Environ Health Perspect 2005. pdf. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.who.10.epa.171:3-59. 5/26/09 Woollen BH. Marsh JR. Available at URL: http://www. et al. Lesser JE.epa.Pyrethroid Pesticides Ray DE. Pyrethroid illnesses in California. and therapy. Rev Environ Contam Toxicol 2006. Pyrethroid insecticides: poisoning syndromes. Clark JM.pdf. 1992–2001. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Reregistration Eligibility Decision for Cypermethrin.S.epa. Revised February 25.gov/ circ/2005/1291/. Available at URL: http://www. sumithrin synthetic pyrethroids for mosquito control. Environmental Protection Agency (U. U. Geological Survey (USGS).S. Available at URL: http://pubs. EPA).gov/oppsrrd1/REDs/cypermethrin_red.22(8):983-991. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.usgs. March 2006. April 2002.S. Environmental Protection Agency (U. June 2006b.S. 5/26/09 U. 2005. synergies. Pesticide and Evaluation Scheme. 5/26/09 U.38:95-101. Mullin LS.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Environmental Protection Agency (U. 2007.186:57-72. resmethrin. O’Malley M. Sargent D. EPA). 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Permethrin.htm. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www.113(2):123-136. Sheets LP.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.S. EPA). Safety of pyrethroids for public health use.S. World Health Organization (WHO). Forshaw PJ. Toxicology 2002. Laird WJ. Crofton KM.S. Spencer J. Xenobiotica 1992. Meyer DA. Soderlund DM. Available at URL: http://whqlibdoc. 5/26/09 U. Piccirillo VJ. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. 19962002. J Toxicol Clin Toxicol 2000.htm. June 2006a.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Shafer TJ.

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

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

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

109(3):213-217. Heudorf U. Williams RL. 19962002. Krieger RI. et al. Int J Hyg Environ Health 2003. Rev Environ Contam Toxicol 2006. Angerer J. Schulz C. J Expo Anal Environ Epidemiol 2003. Drexler H.206(2):85-92. Leng G. Centers for Disease Control and Prevention (CDC). Ball M. Olsson AO. Heudorf U. Pyrethroid illnesses in California. 2005. Atlanta (GA). Angerer J.46(3):281-288. Barr DB. Arch Environ Contam Toxicol 2004.209(3):293-299. Kolossa-Gehring M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Hadnagy W. Angerer J. Butte W. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. O’Malley M. 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. Seiwert M. Heudorf U.186:57-72. Int J Hyg Environ Health 2006.Pyrethroid Pesticides References Baker SE. Third National Report on Human Exposure to Environmental Chemicals. Int Arch Occup Environ Health 2004. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Ranft U. 162 Fourth National Report on Human Exposure to Environmental Chemicals .209(3):221-233. Hoppe HW. Bernard CE. Environ Health Perspect 2001. Berger-Preiss E. Int J Hyg Environ Health 2006. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Becker K. Sugiri D. Spencer J. Angerer J.13(2):112-119. Idel H.77(1):67-72.

420-. Generally. Biomonitoring Information Urinary levels of cis. Cyfluthrin.110-. In the body.180) .400-.250 (. more of the trans-metabolite than Urinary cis-3-(2.120-.68) .630-.960 (.110 (<LOD-.270-.460-1.460-.160 (<LOD-.550) .790 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.240) . and trans-cyfluthrin.410) .740-1.140 (.900 (.880 (.510 (.35) 1.650-1. cis-permethrin.262) * * * < LOD < LOD .210-.600) .230) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.820 (.50) .77 (.580) 1.220-.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .200) . which may vary for some chemicals by year and by individual sample.68) .460 (.270 (. ciscypermethrin and cis-cyfluthrin.200-.S. 1985. Survey Geometric mean (95% conf. 1985.10) 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 .680 (.600-1.640 (.08) . but it can also reflect exposure to cis-3-(2.2-Dichlorovinyl)-2.11) .32) .580-1.670 (.160 (.54) .380-.220) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.490-.780) .155-.770-1. cis-cypermethrin.220-.200 (. The chemical trans-3(2.890 (.24) 1.200-. < LOD means less than the limit of detection.470 (.28) 671 680 518 701 591 957 Limit of detection (LOD.120-.2-dichlorovinyl)-2.200) < LOD < LOD < LOD .740) 1.470-1.430-.890 (.160 (.44 (.53) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (. and ciscyfluthrin.2dichlorovinyl)-2.490-1.2-dichlorovinyl)- CAS No.370 (.120-.730 (.21) .200) .200-.510 (.270 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .35) . The presence of cis-3-(2. Kuhn et al.790-1.270 (.240) .570 (.610) . 1999). the presence of trans-3-(2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.520) .280 (. trans-permethrin.280-.202 (.300 (.2dichlorovinyl)-2.300-.15) ..500 (.110-.300-. cis-3-(2.380-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.490-1.47 (.700) .630) .250-.180 (.340-.410) .920) 1.330) .690) .2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.110-.210) .80) .740 (.2-dichlorovinyl)-2. Fourth National Report on Human Exposure to Environmental Chemicals 163 .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.740-2.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .790-1.610) .260 (.710) .950-2.140 (<LOD-. trans-cypermethrin.570-.510 (.or trans-3-(2. Kuhn et al. transcypermethrin and trans-cyfluthrin.710-1.220-.380) .310) .68359-37-5 Cypermethrin Permethrin CAS No.630 (. but can also reflect exposure to trans-3(2.770) .2-dichlorovinyl)2.43) .330 (.500 (.340) .870) 1.670-1.910-5.350) .600 (. population from the National Health and Nutrition Examination Survey.730 (.380-. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.150 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.12 (.1 and 0.440 (.and trans-isomers.680-3.490-.530 (.370-.210) 90th . 52315-07-8 CAS No. Similarly.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.790) .1. 1999).68 (.340) .630) .2-dichlorovinyl)-2.670-1.380 (.670-2.220-.850 (.120-.170 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.13 (.730 (.07 (..

S.260 (.150-. 2004.220 (.190) .350) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.400 (. 2002).2-dimethylcyclopropane carboxylic acid did not increase.140-.260 (.540) .300-. In a study of urban residents in Germany (Berger-Preiss et al. 2005).2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.510-1.2-dichlorovinyl)-2. Other studies have provided evidence that urinary levels of cis.370-.. 2006).59 (1. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.710-3. urinary levels of cis-3-(2.440 (.540 (. Schettgen et al.24) . 2003).11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .780) 1.640 (.200) .170) < LOD < LOD < LOD .500 (.120 (.200-.320) .250-.182) * * * < LOD < LOD .290) .2-Dichlorovinyl)-2.270 (.440-.580) .710 (. 2005).280-.270-.03) 1.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.680-1.410) .430-.260) ...470-1.12 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al..270) .570) .340) .340) .550) . 2001) showed urinary levels of cis.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .440 (.230-.350 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.450 (.430 (.12-2.250-.340-.180-. Studies in Germany of 396 children and adolescents (Becker et al.11) . post- Urinary cis-3-(2.810 (.680-1.300 (.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 .320-. In these volunteers.370-.2dichlorovinyl)-2.550) ..520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .640-1.250) 90th .300) .700) .80) .590 (.67 (. 2006).250) . 2006.260-.59) ..170 (.380-. 164 Fourth National Report on Human Exposure to Environmental Chemicals .550-1.210-.S.and trans-3(2.290 (.890 (.230-.2-dichlorovinyl)-2.540 (.250 (<LOD-.780 (.59) .880) .250-.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.180 (.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.Pyrethroid Pesticides 2.200 (.420 (.33) . population from the National Health and Nutrition Examination Survey.640-1.11) .37) . 2001.550-1.530 (.390-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al. 2005).580-1.600 (.260 (.890) . median urinary levels of trans-3-(2.800 (. 2005) In a small group of indoor pest-control operators.160 (<LOD-. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.560) .440-. urinary trans-3-(2.900 (.250) ..080-.49) .680 (. Survey Geometric mean (95% conf.590) . 2006) and 1177 urban adults and children (Heudorf et al. 2003). the median and 95th percentile of urinary levels of cis-3-(2.170 (..190) .750 (. Cyfluthrin.700-2.750-1.560) 1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. 2006. In a study of volunteers. representative NHANES 2001-2002 subsample (CDC. 2002). 2005).240 (<LOD-.2dichlorovinyl)-2.300 (.360-1.33 (.and trans-3-(2.67) .370-.150-.230-.840 (.550 (.300) .450-1.640-.640) 1.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.290-.380 (.920 (.840 (.104-.31) .380) .230 (.280 (.290) .21) .11 (.130-.400-1..150-. Lu et al.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.700) .220) .11) 1.690-1.220 (.450-.. In the same residents.138 (.530 (.830) .270) .190 (.29 (.2-dichlorovinyl)-2. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.430-1..390-.390 (.2-dichlorovinyl)-2.

14) 1.62 (1.66) 691 680 518 690 595 954 Limit of detection (LOD.4.10) 2.2dichlorovinyl)-2.12-6.11-2.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.55-5.27 (1.89 (2. Survey Geometric mean (95% conf.60-4. 2005).2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.20 (.17 (.95) 2.81) 2.420 (<LOD-.60) .2-dichlorovinyl)-2.28 (1. 2005). Urinary trans-3-(2.410-.580 (.750) .66) .48) 4.11-1.830-1.68-3.5) 2.620) < LOD 2.2-dichlorovinyl)-2.820) .55-3.490 (<LOD-.40 (1.41-14.4 and 0.56 (1.17-1.68) 1.810-1.400-.76-4.680-1.520-.610) 1.01 (1.410 (<LOD-.700) .940 (.35) 1.910-1.22 (1.14-2.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.42 (2.69) 1.49-5. however.63) 1.60) 1.56 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .850-1. < LOD means less than the limit of detection.39-5. Fourth National Report on Human Exposure to Environmental Chemicals 165 .26 (.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . trans-Cypermethrin.09 (.570) 90th 1.25 (1.95) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.860) . Finding a measurable amount of cis.43) 2.460-.410 (<LOD-.530) . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.920-1.550 (.470 (.710 (.64-4.77) 2.91 (1.41 (1. population from the National Health and Nutrition Examination Survey.560 (.55-4.25-3.500-.19 (2.480-.840-1.39 (1.560 (.54 (1.400 (<LOD-.760) .14-6.03-1. The maximum post-application urinary levels.77) 1.28 (2. Biomonitoring studies on urinary levels of cisor trans-3-(2.49-3.68) 2.20 (.7) 2.13) .910-1.07-3.780 (.08-4.490-1.76-3. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.670) .77 (1.19) 1.08-6.59 (1.730) .23 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07 (1.20 (.470 (<LOD-.670) .23) 2.01) 4.16) 1.56) 2.69 (1.660) 1.and 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 .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.2-Dichlorovinyl)-2.68) 1.94 (1.56) 2.37 (1.or trans-3-(2.410-.08) 1.S.520) .68-2.50 (1.19 (3.560 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.700-1.63) 1.500 (. which may vary for some chemicals by year and by individual sample. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.49-3.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.17 (.800-1.440 (<LOD-.03-1.85) 4.970 (.90) 1.460-.87 (1.54) 4.500) .Pyrethroid Pesticides application median urinary levels of summed cis.84 (1.42) 1.97-11.

15-3.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .610-.31) 1.470-.930-1.770) < LOD 2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.12-1.57) 3.89) 2.48-2.880 (<LOD-1.15) 3.560 (.3) 2.740) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660) .07-2.780) 90th 1.11) .760 (.57 (1.91-11.530 (.60 (1.S.570 (<LOD-.27-2. 166 Fourth National Report on Human Exposure to Environmental Chemicals .87) 1.08 (.27-2.56-5.55 (2.80) 1.91) 1.70 (.520 (<LOD-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2-Dichlorovinyl)-2.20 (1.55 (2.75 (1.880 (.440-.15-3.08 (.31 (.02-1.60) 2.880-1.22-1.470 (.22-2.00-5.570 (. population from the National Health and Nutrition Examination Survey.42) 1.40-2.16 (1.33-2.47-2.900 (<LOD-1.800-1.86 (2.00) 5.64 (1.74) 2.00) 1.640) .91 (1.36 (1.540) .33-1.500-.570-.56-2.81 (2.44) 2.35 (1.820-2.850) 1.15 (1.670) .11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .39) 1.19 (1.87-8. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.74) .61) 1.48 (1.98 (1.47-2.700 (.87-3.730) .65) 1.56 (1.87) 1.720 (<LOD-.15-3.00 (1.34-4.65 (2.700 (.720-1.07) 2.55 (2.850-3.31 (2.68) 3.750) .47 (1.87 (1.22) 1.00) 1.30-6.20-2.13) .60) 2.530 (<LOD-.480-.34-3.07-3.07-1.850) .33 (1.28) 2.67 (2.19) .41) 1.780 (<LOD-.Pyrethroid Pesticides Urinary trans-3-(2.15) 2.30-3.42 (.700-.39 (1.36) 2.35) 1.970 (.29) 1.780) .26 (1.720-1.580 (.13) 1.580) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.12 (.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 . trans-Cypermethrin.410-.800-1.07) 2.45 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.45-2.37 (1. Survey Geometric mean (95% conf.

Sugiri D. Hadnagy W. Bartell S. Schulz C. Bravo R. Int Arch Occup Environ Health 2003. Atlanta (GA).206(2):85-92.134(1-3):141-145.209(3):293-299. Angerer J. Leng G. et al. Levsen K. Int J Hyg Environ Health 2002.209(3):221-233. Leng G.77(1):67-72. J AOAC 1985. Kuhn K. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Idel H. Bull Environ Contam Toxicol 1999. Int J Hyg Environ Health 2006. Ball M. Int J Hyg Environ Health 2006. George DA. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J.62:101-108.114(9):14191423. Permethrin and its two metabolite residues in seven agricultural crops. Butte W. Angerer J. Berger-Preiss E. Drexler H. Ranft U. Biological monitoring of workers after the application of insecticidal pyrethroids.109(3):213-217. Environ Health Perspect 2001. Kolossa-Gehring M.68(6):1160-1163. Centers for Disease Control and Prevention (CDC).205(6):459-472. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Drexler H. Angerer J. Hoppe HW. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Leng G. Heudorf U. Heudorf U. Ranft U. Pearson M. Idel H. Third National Report on Human Exposure to Environmental Chemicals. Schettgen T.Pyrethroid Pesticides References Becker K. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Barr DB. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Sugiri D. Hardt J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Lu C. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Int Arch Occup Environ Health 2004. Berger-Preiss E. 2005.76(7):492-498. Int J Hyg Environ Health 2003. Wieseler B. Angerer J. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Heudorf U. Environ Health Perspect 2006. Idel H. Seiwert M.

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

< LOD means less than the limit of detection.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1.1 and 0. Survey Geometric mean (95% conf.S. which may vary for some chemicals by year and by individual sample.Pyrethroid Pesticides Urinary cis-3-(2.2-Dibromovinyl)-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

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

2003.52315-07-8 CAS No. Becker et al. Thus. In a small group of indoor pest-control operators. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. 52645-53-1 Tralomethrin CAS No.. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 2003. A study of 396 German children (Becker et al.. 2005. 2005)... The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. Urinary 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 . In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 2005). In one study of 145 urban residents in 80 private homes in Germany. 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. 2006). Following residential spraying with deltamethrin for malaria protection in Mexico. In the New York City study. 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. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. 2005).Pyrethroid Pesticides Cyhalothrin CAS No. 2003). 2005). Baker et al. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. CDC. 2005). 39515-41-8 CAS No. 52918-63-5 use and house dust levels (Lu et al. CDC. 2006.S.. Saieva et al. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al.. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2005). 2004). the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al.. 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. Fenpropathrin Permethrin CAS No. 2005). 2002. Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. 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. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 68359-37-5 Cypermethrin Deltamethrin CAS No. Hardt and Angerer. 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. representative NHANES 2001-2002 subsample (CDC. 2005.

270) .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.05) 1.233-.300 (.340) 75th .321 (.364) .360) .428-.227-.04-5.250 (.29-1.325 (.190-.586) .362) .220-.273 (.427) .830-2.300 (.510-.387) .35 (1.02-6.92-3.60) .190-.30) 3.33) .940) 1.240 (.25-4.507 (.03 (3.69) 3.640 (.350-.35) 2.800 (.26) 2.288 (.253-.730 (.32 (1.81 (1.417 (.292-.780) 4.560-.300 (.210-.246-.320) .710 (.13 (.601) .26) 2.710 (.160-.440) .34 (2.320) . Survey Geometric mean (95% conf.960 (.600 (.190-.850) .250-.288-.230-.71 (1.328 (.430-.850) .740 (.670 (.250 (.72 (1.226-.25 (2.93 (1.620-1.990) .295) .280 (.454 (.238-.18 (2.34-6.46) 2.76 (1.320) . interval) .260 (.200-.160-.810) 1.56-5.292 (.52-4.41 (1.36) 1.69 (1. population from the National Health and Nutrition Examination Survey.260 (.750) .78) 1.550-.369) .180-.1) 3.1) 3.16-1.49-2.12) .265-.28) 1.73) 1.260-.21 (2.610) .370) .79) 3.32-21.374) 99-00 01-02 99-00 01-02 99-00 01-02 . Fourth National Report on Human Exposure to Environmental Chemicals 173 .53) 1.700-1.240 (.210-.530-.90) 1.406) .560-.62-8.48-2.33 (2.271-.840-1.530-.13) .51-6.420) .820) .277-.314) .51-3.820) .45-5.384) .55 (1.30 (.750) .260 (.330) .340) 1.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .630) .315 (.230 (.78) 1.27-2.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.23 (2.12) 4.450 (.740 (.35 (2.300) .65-2.27-2.27-11.18 (1.314 (.352-.230-.595) .63 (3.470-.230 (.750-1.250 (.590-.320) .30 (1.78 (1.390) .355) .34) 8.46) .41-2.35) 1.16) 1.1.64) 697 680 524 701 603 957 Limit of detection (LOD.353 (.200-.650 (.04) .760 (.42-2.266-.434) .83-11.41) 3.590 (.48-2.200-.43) 3.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .290 (.05) .65 (1.33 (1.8) 3.311 (.830) 90th 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 .570-.430-.510-.570-1.870 (.25-1.297 (.49-2.330) .62-6.490-.340) .75 (1.247-.86 (1.45 (2.14-6.1) 3.S.49 (1.276-.267 (.53-3.520 (.26-2.230-.38 (2.560-1.700 (.12 (.800) 1.32 (2.680 (.54) 1.44) 5.336 (.190-.373) .50 (2.38 (2.41-3.78) 6.270 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Deltamethrin.320 (.1 and 0.298 (.49 (1.01 (1.52-5.25 (2.62) 5.490) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.39) 2.35) 2.25-7.89-71.63-3.

490-.490 (.52) 2. interval) .224-.264 (.09-2.446) .261-.09 (.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .75-8.27) 1.225-.362 (.37) 1.44) 2.401) .226-.200-.670) .240 (.450 (.311 (.246 (.350) .216-.94 (1.13 (.530-.312 (.300-.229-.09-2.370-.278) .240-.437) .240-.309 (.560 (.480 (.19 (2.590) .860 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.550 (.55 (1.62) .270 (.328) .280 (.810) 1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .44 (1.380-.10 (2.238-.83 (1.480-.410) .590) .S.700-1.210 (.570) .357) .64-5.37 (1.400-.178-.510 (.200-.330) 75th .300-.05-3.88-5.04 (.41-4. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.272) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.60-4.440-.35) 1.91 (2.40 (1.86 (1.25-2.290-.378 (.309) .270) .03 (.390-.372) .07-5.53 (1.534) .580 (.610 (.150-.290) .270) .43 (2.590-1.720 (.730) .13-1.48 (1.67 (1.490 (.21-4.329) .380 (.274 (.00) 1.253) .272 (.280) .13-1.41) 1.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .06-3.274-.540 (.275 (.677) .330 (. Deltamethrin.210 (.49) 3.220-.400-.80) 4.840-1.400) .81 (1.730) .35) .67 (1.530-.299-.190-.261 (.329) .19-6.330) 1.190 (.200-.290) .21 (1.49 (1.0) 3.330) .960-1.22 (1.510 (.330) .650) .88) size 1998 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .240-.190-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .280 (.49-2.500) .323 (.930) 1.234 (.240 (.310) .02 (2.60) 1.43-64.160-.860-1.640 (.630) .49) 1.230) .62) 1.74) 3.36-6.35 (1.510 (.40) 2.09) 3.52 (1.250 (.230-.590) .04 (3.91) .73-4.550 (.860-1.210-.410-.43 (1.670) 3.51-7.43) 1.36 (1.220 (.200-.271-.321-.00) 5.640 (.280-.270 (.72 (1.55) 3.35-3.11 (.387) .90) 3.61-2.930) .17 (.03-1.25-5.96 (1.227 (.280 (.240-. population from the National Health and Nutrition Examination Survey.73) 1.202-.420-.750-1.240 (.730-1.280) .250) .00) 1.83) 1.550 (.19) 2.07) 2.316 (.250 (.335-.460-.740) .32 (2.173-.370 (.320) .440-.760) .67) 1.580) .84 (1.39) 1.16-4.720) 90th 1.423 (.440-.270-.17-1.11 (.240 (.15-2.350 (.91) 9.25) 2.63) 1.63-3.95) 1. Survey Geometric mean (95% conf.54 (1.91-4.460-.02-1.230-.

Sugiri D. Leng G. Lopez-Guzman OD. Int J Hyg Environ Health 2006. Pearson M. Godbold J. Biological monitoring of workers after the application of insecticidal pyrethroids. Hadnagy W. Lu C. Seiwert M. Ball M. Deych E.113(6):782-786. Idel H. Barr DB. Grimaldo M.46(3):281-288. Berger-Preiss E. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. et al. Angerer J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Arch Environ Contam Toxicol 2004. Obel J. Environ Health Perspect 2006. Fourth National Report on Human Exposure to Environmental Chemicals 175 . 2005. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Bravo R. Leng G. Int J Hyg Environ Health 2003. Ranft U.206(2):85-92.114(9):14191423. Environ Health Perspect 2005. Becker K. toxicokinetics. and genotoxicity in exposed children. Ranft U. Third National Report on Human Exposure to Environmental Chemicals. Kolossa-Gehring M. Angerer J. et al. Liu Z. Atlanta (GA). Ortiz-Perez MD. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Hoppe HW. Barr DB. Batres LE.209(3):221-233. Lapinski R. Olsson AO. Exposure to indoor pesticides during pregnancy in a multiethnic. Environ Health Perspect 2003. Carranza C. Berger-Preiss E. Sugiri D. Int J Hyg Environ Health 2002. urban cohort. Berkowitz GS. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Levsen K.205(6):459-472.Pyrethroid Pesticides References Baker SE. Bartell S. Centers for Disease Control and Prevention (CDC). Hardt J.76(7):492-498. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Idel H. et al.111(1):79-84. Int Arch Occup Environ Health 2003. Torres-Dosal A.

see Data Analysis section) for Survey years 99-00.440) .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 .300-. and refuse incinerators that process or release antimony.200-.190-.160) .330 (.220) 95th .330) .300) .410) .130 (.460 (.360) .130) .108 (.280) .230) .600) .220-.136-.410-.070 (<LOD-.260-.100 (. and +5.119) . 01-02.360) .230-.140 (.310) . 7440-36-0 General Information Antimony is found in ores or other minerals. 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.130) .110-.390-.200 (.350 (.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 .400) .460 (.300-. from air and drinking water.400) .120-.130-.310 (.132 (.098-.230) .510) .095-.175 (.220 (.Metals Antimony CAS No.115-.240 (.117-.190) .150-.310 (. castings. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite. and excretion of antimony vary depending on its oxidation state.07. 0.178) .190) .220-.144) .070 (<LOD-.160) . It is used in metal alloys.143 (. coal-fired plants.120) .180-.190-. and glass.190-.150 (.200 (.103) .200-.270-.090 (<LOD-.250-.120-.146 (.150) .320-.120-.240 (.197) .280-.200-.430 (. interval) .310-.210) .460) .207) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.330) .125 (.108-.109-.120-.080) .112-.330-.150-.350) .140) .115) . People are exposed to antimony primarily through food and.260) .117-.160-. Dermal contact with soil.170-.230-.122 (.120 (.210) .120) .137) .200) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.145) Selected percentiles ( 95% confidence interval) 50th .130 (.200) .135) * .410) .04.710) .200) .350-. and 0.350 (.S.330 (.190 (.260 (.210 (.100) . It is also used in paints.134-.200 (.136) * .154) .140) .330-.220) .180 (.130 (.470) .130 (.270) .170-.130-.330 (.280) .260 (.350) .180-.120-.160 (. < LOD means less than the limit of detection.176 (.240 (.145 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .180 (. respectively. or other substances containing antimony is another means of exposure.090-.180 (.240) .180 (.210) .140) .320 (. metal bearings.140) .128 (. enamels. fireworks.400 (.140 (.370) .120) .150) .142 (.170 (.200 (.158 (.250 (.390-.370-.430 (.300 (.250-.190) .160 (.390 (.350-.350 (.260) .110-.250 (.150-.110 (.150 (.460 (.100 (.170-.220) .530) . which may vary for some chemicals by year and by individual sample.390) .280-.390) .120 (. +3.130 (.141-. to a lesser extent. 0.290-.320 (.500) .300-.130 (.160) .190) .400) .130-.400 (.240-.340 (.470) .280 (.105 (.150-.090) 75th .270 (.340) .080 (<LOD-.390) . and as a fire-retardant in textiles and plastics.310-.160-.119-.220) .220-.210) . distribution.430 (.250-.170) .300) .120 (.350) .330) .240 (.300 (.131-.190) .290-.230 (.180) .184) .148-. Stibine is a metal hydride form of antimony used in the semiconductor industry.240 (.210) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140) .130-.154-.210-.280-.140 (.400-.220-.200 (.220 (.230 (.190 (.137) .440) .150) 90th .220-. water.350 (.140) .320-. solder.200-.150 (.470 (.190-.090 (. and pewter. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140-.161) .350) .134 (.126 (. ceramics.169 (.230 (. and 03-04 are 0.310 (.300) .200) .180-.110-.095 (.130-.570) .110) .280-. Workplace exposures can occur at smelters.120 (. ammunition.390-.360-.150) .230-.500) .260 (.180 (.130-.210 (.250 (.320) .180-.120-.280 (.180) .260-.270) .280-.110-.310 (.093 (.440 (.160) .130 (.157) .087-.079-.080) .230-.100-.360 (.100-.160) .210-.080-.120-.150-.270 (.120-.280) .132 (.350 (.400 (.130) < LOD .123 (.340 (. Antimony enters the environment from natural sources and from its use in industry.320-.240-.180 (.190-.120) .170-.390) . Antimony can exist in one of four valences in its various chemical and physical forms: -3. sheet and pipe metal.190 (.250) .260) .280) .130 (.130-.190 (.190 (.164-.330) .090-.220-.490 (.360 (.200 (.180-.320) 316 368 290 663 762 725 1297 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .270 (.140 (.160-.230-.120 (.290 (.160-. storage batteries.088-.490) .126-. The absorption.154) .230) .320) Total .160 (.099 (.120-.128 (.270 (.560) .170-.320-.250-.156-.070-.04.133) * .420) . population from the National Health and Nutrition Examination Survey.170 (.350-.160) .114) .130) .310) .

267 (.136) .185 (.135 (. and route of exposure (Elinder and Friberg.200-.248) .233-.265 (.132) .120 (.133) .357) .069-.125 (.429) . species.199-.485) .148) * .139 (.417) .195-.107-. 1973).183) .148-.148-.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 .500) .480) .357-.200-.209) .213 (.113-.277 (.280 (.250-.153-.228-.134) .082) .135 (.159-.194-.120 (.076-.308-.170 (.352 (.211) .161) .250 (.071-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.079 (<LOD-.137 (.310) .253-.278) .160 (.300) .414) . 1988.152) .147-.086) 75th .208-.108 (.225 (.S. and kidney have been demonstrated in high dose animal studies depending on the dose. Acute antimony poisoning may cause a metallic taste.333 (.310) .081) . liver.176 (.182 (.178-.111 (.256 (.118 (.116-.438) .364 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140) .741) .238 (.228 (.267) .153 (.185 (.321) .123) .198) .159-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .173) .129) .109-.308) .077) .121 (.143) . 1986). resulting in hemolysis with abdominal and back pain (Dernehl et al.113-.117-.068 (.120 (.298 (.152) .229-.167-.143) Selected percentiles ( 95% confidence interval) 50th .086 (.288 (.225) .098-.126 (.111-.128-.226 (.417) .115) .107-.192 (.080 (<LOD-.087) .121 (.061-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.163 (.109 (.167 (.300) .114 (.099-.135) .123 (.102-. skin.082 (<LOD-.317) . Ming-Hsin et al.727) .Metals than for trivalent compounds (Elinder and Friberg.092-.185-. population from the National Health and Nutrition Examination Survey.245) .317) .253 (.124) .176-.238) .178 (.192) .144-.250 (.164) .471 (.119-.217 (.352) .333) .125-.205-.112 (.106-.280-.150-.333-.209 (.114 (.405) .130) .121) .173-.278 (.085) .143) .196 (.135) .233) .115 (.238) .230) 95th .103-.425) .193 (.104-.108-.187) .250-.320 (.138-.224 (.164 (.192-.235-.257) .074 (.206-.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 .117-.188-.317) ..364 (.175 (.131) .250) .227-. 1954).119-.098) .127) .259 (.315) .373) . Inorganic antimony salts irritate the mucous membranes.105-.333-1.081 (<LOD-.310 (.127) .320-.191 (.200) . 1962).195-.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 .122 (.444) .080 (.250-.151) .132 (.241-.391) .076-.114 (.124 (. interval) .263-.208 (.138 (.255-.150-.333-.124-.447 (.126) .107-.181) .112 (.272) .179-. 1944).113) .154-.122 (.209-.161) .267-.163 (.320-.200-.207) .127 (.075 (.131 (.222 (.471) .343 (.156-.186) .103-.146-.127) .444) .391) .078 (.333 (.167 (.173 (.380 (.115 (.209) .171) . 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.139 (.286 (..126-.138-.263 (.092) .181) .189 (.146) .269 (..214) . 1958) and occupational exposures (Briegner et al.102-.242-.167 (.333 (.320) .421) .115-.100 (.318-.129 (.244-.143) 90th .145) .429 (.228 (. Histopathologic inflammatory and degenerative changes in the lung.084) .162-.108-.112-.268) .096-.30) .236 (.195 (.135) .281-.097-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.138) * .318-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and ulcers (Werrin. myocardium.266 (.082) .203) .130) .265-.430) .146-.109 (.271-.233 (.250-.313-.295 (.248-.203) .176 (.261) .146-.338 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.149) ..204-..119 (.106-.131-.333-. 1986).220) .140) < LOD .276 (.143 (.149-.181) .247) . diarrhea.099-.069-.230-.172-.188) .400 (.300 (.120 (.127) .385 (. abdominal pain.108-.117-.193) .294) Total . and eyes.124-.075 (.338) .115 (.338 (.156 (.095-. 1995).118 (.147) .095-.241-.129) * .371 (.129 (.116 (.255) .239-. 1953).115-.098-.104-.068-.164-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and gastrointestinal symptoms such as vomiting.130 (.159-.320 (.130) .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.741 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.089) .173 (.

Alimonti A. Luedersdorf R. 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. Shao-Chi C.. Fuchs A. Minoia C. Yang C-Y. Handbook on the toxicology of metals.. Chest 1973. Vouk VB.76(2):103-115. Elinder CG. Mayne P. 2002. indium. 1986. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Skulsukai G..48:93-97. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Arsine. Cheng-Wei L. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Industrial antimony poisoning. Apostoli P. gallium. 26-42. or exposure differences.atsdr.. Biological monitoring of exposures to aluminum. J Clin Pathol 1998. 2nd ed. Stocks J. Centers for Disease Control and Prevention (CDC). Suchenwirth R. Stone FD. clinical efficacy. Atlanta (GA). Dunkelberg.. Stead FM.. Mayer P. environmental levels) and health effects is available from ATSDR at: http://www.158:165-190. which may be due to methodologic. Trace element reference values in tissues from inhabitants of the European community I. Chemotherapy for leishmaniasis: Biochemical mechanisms. Kentner et al. Third National Report on Human Exposure to Environmental Chemicals. Friberg L. Liao Y-H. Rev Infect Dis 1988. Biomonitoring Information Levels of urinary antimony reflect recent exposure.51:238-240. pp.html. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. et al. Review of elements in blood. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Element reference values in tissues from inhabitants of the European community.. Schaller KH. Industrial Medicine and Surgery (Dec. Bolten C. Wade A. Briegner H. Dezateux et al. Kentner M. Kiberd B. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Gallorini M. Pulmonary edema of environmental origin. Pilgrim L.S. Biomonitoring of a worker population exposed to low antimony trioxide levels. Pietra R. Van der Venne MT.Metals to antimony have been established by OSHA and ACGIH. 1997). Konings J. 20012002. Industrial Medicine 1944. Sabbioni E.59:469-474. Wu M-T. Chia-Yu H. Ming-Hsin H. Antimony trioxide is rated by IARC as a possible human carcinogen. Cullen A. Leinemann M. Arch Dis Child 1997. et al. Gebel TW. Kuo-Juie Y.. EPA.. 2004. 1990. Paschal et al. and hydrogen sulfide. Semisch CW. and 2003-2004. Delves HT. Br J Ind Med 1991. External and internal antimony exposure in starter battery production. 1995.67:119-123.10(3):560-586. Cordasco EM. Nordberg GF. Chen J-R. et al..64(2):182-185. 1991. Int Arch Occup Environ Health 1995. New York: Elsevier. Carelli G. Information about external exposure (i. Sci Total Environ 1994.. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Mahieu P. Iavicoli et al.46:931-936. gov/toxpro2. Nau CA. Pozzoli L. In: Friberg L. respectively. even when exposure levels were below workplace air standards (Bailly et al. Ju-Sun P. Matthews T. Antimony. Earlier measurements in general populations (Minoia et al. Buchet JP. 1998) or compiled reference ranges (Hamilton et al. Ho C-K. eds. Hamilton EI. Costeloe K.106:33-39. HH. Chin Med J 1958. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Environ Health Perspect 1998. Biological assessment of exposure to antimony and lead in the glass-producing industry. Roland H. Delves HT. Dezateux C. References Berman JD. and antimony in optoelectronic industry workers. VI. Weltle D. Iavicoli I. Liao Y-H et al.76:432436. Sabbioni E.16: 33-39. J Trace Elem Med Biol 2002. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. population. 2005.e. 1994) have reported values slightly higher than those in this Report. stibine. 1998. Urinary antimony in infancy. Petrucci F.521-523. Caroli S.. J Occup Environ Med 2004. Lenert G.)1954. Int Arch Occup Environ Health 1987. arsenic. Stasney J. Dernehl CU.cdc. Yu H-S. 1998). 1987). Piatnek DA. and a drinking water standard has been established by the U. Schacke G. Bailly R.13:361-362. Ludersdorf et al. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. O’Regan M. Antimony in blood and urine of infants. Lauwerys R. and future strategies.

Trace metals in urine of United States residents: reference range concentrations.95:89-105.76(1):53-59. and serum of Italian subjects. Chemical food poisoning. blood. Morrow JC. Ting BG. Antimony poisoning in industry. Sampson EJ. Environ Res 1998. 27:38-45. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Paschal DC. Werrin M. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Renes LE.Metals in urine. et al. Industrial Hygiene and Occupational Medicine 1953. Sci Total Environ 1990. Pirkle JL. Jackson RJ.99-108.

2-20.9 (8. arsenic as elemental metalloids may be used in some ammunition.2 (12. In nature.12-10. Arsenic is measurable in most soils. such as arsenopyrite (FeAsS) and realgar (As4S4). arsenites.25-9.4) 40. and in lead-acid storage battery grids. mental disorders.00-9.0 (43.90-8.9) 21.5-178) 46. lead.90-14.30) 17. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.6-43.30 (7. and as a cosmetic to lighten complexion. and gray forms).1-40. and as homicidal poisons.5-52.90-8.41 (7.1 (32.9-46.1) 7.6 (9.8) 7.1) 1281 1276 03-04 03-04 03-04 9. Gallium. Also.8) 34.27) 9. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.7) 65.2 (41.10) 10.90 (5. though in some locations arsenite may be prevalent (WHO.6) 618 722 1074 Limit of detection (LOD.8) 30.3-15. from coal burning.10-10.1-18. Arsenic and its compounds have had many uses in the past and present as medicines.3-19.84) 8. ocean and fresh waters.3) 10. the smelting of copper. The United States no longer produces arsenic from mining but imports about 22. see Data Analysis section) for Survey year 03-04 is 0.0-19. 2005).66-8. meats. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. aluminum. 2001). In the last century. were used as treatments for syphilis.8) 33. Since the 1940s.74. Various arsenic compounds were used in paint pigments and for tanning animal hides.5 (40. referred to as inorganic arsenic compounds. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.6 (32.5-41.7) 24. Arsine (AsH3) is a reactive. copper arsenates.9-62.34-10.80-9.8-77.55 (7.90) 16. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.0 (14.00 (6. sodium arsenite. arsenocholine.8) 29.8-61.34-9. and arsenosugars.70 (6. and other metals. pesticides.9) 68.7 (11.20 (8.5) 41.02-8.4) 60.70-9. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.08 (5. Survey years 03-04 Geometric mean (95% conf. arsenic compounds.000 metric tons annually.10-7.90 (7.0-60.3) 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 7.7-95.29 (8. to a lesser extent.8) 17. and. semiconductors. trimethylarsine oxide.50-14.30 (6.90 (7. Before the 20th century.0 (15.5 (36.4) 13. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. +3 and +5). retaining walls.5) 43.80) 6.8) 7. Arsenic trioxide (As2O3. Arsenic trioxide is approved to treat acute promyelocytic leukemia.4 (26.2 (51.90-7.3-111) 78. Although it is still widely used in the United States. alloys. interval) 8. and produce.19-9. General population exposure to inorganic arsenic can occur through consumption of drinking water and.2-61.0 (11.2-17. psoriasis.9 (17.1 (38.2) 46.4 (31. 180 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.2) 15.4 (7.80 (5.5-19.90) 75th 16.97) 8. and foods. black.6 (15.6-35.5) 95th 65. it is found in over 200 crystalline or mineral forms.4 (48.5 (14.7) 90th 37.40) 7. lead hydrogen arsenate. gaseous hydride manufactured in small quantities for use in the semiconductor industry.1) 290 725 1542 03-04 03-04 9.9-34.10 (6.5 (34.7-83.4-65. cacodylic acid.50 (8.4 (24. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.6 (13. and arsenates (oxidation states of -3.13-8. particularly arsenic trioxide.12 (6.S.Metals Arsenic CAS No. grain.2-93.5 (23.5) 66.77) 6. and indium arsenides are used in the semiconductor industry.57) Selected percentiles ( 95% confidence interval) 50th 7. to a lesser extent. cancers.0 (22. as alloy in metal bearings. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.70) 8. Water sources contain mostly inorganic arsenate. solders. and play sets.6) 11. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.90-11.1) 15.2 (13.8 (48.6-141) 53.84) 8. mostly for use in wood preservation (ATSDR. or rarely as elemental metalloids (yellow.

S.35) 7. Smoking tobacco is also a source of inorganic arsenic.07-9. 2001).6 (10.9) 53.10-16. Arsenate is reduced in the body to arsenite (oxidation state +3). Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.75) 13. WHO.76 (6.2 (12. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.01) 7. WHO. NRC.33-10.8) 22.00 (6.6 (35. 2007.3) 9. kelp.47-6. have caused clinical arsenic poisoning.1) 58.32 (5.24 (7.7 (11.. Children may have additional exposures from ingestion of contaminated soils (e.6-17.0) 12.3-53. selenium. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. trimethylarsine oxide (TMAO).44-11.3-41. 2007.8 (12.10-8.S.8 (21. 2001). 2001. cacodylic acid and monosodium methyl arsenate.40) 8. After absorption.8 (20. 2001).4) 54. and some other seafood can contain organic forms of arsenic including arsenobetaine.20-9. and arsenosugars. Chowdhury et al.3-62.1 (11.13) 8. population from the National Health and Nutrition Examination Survey.1) 8.75 (5.66-8.96) 12.7) 95th 50.9) 13.86-17.3-64.59) Selected percentiles ( 95% confidence interval) 50th 7.5 (9.5) 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. dose level.8-75.7-35. gallium arsenide and indium arsenide. In aquatic organisms.01) 11.7 (9.0-18.93-8.4 (11. 2001). arsenic does not show biomagnification in the food chain (WHO.6 (17.4 (40.88 (5.41) 6. 2001).04) 7.47 (6. In aquatic sediments.0) 33. interval) 8. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.47 (7.8 (11.0) 14. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. are used in enclosed ultraclean operations within the semiconductor industry.88) 7. 2003.61 (7.7-17.1) 24.4-64.33 (6.7-34. arsenocholine. Extremely high groundwater arsenic levels.38-10.1 (14.7-18.44) 6.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.64 (7.4 (42. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.31 (6. 2001). 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.25-9.0-69.0) 42. EPA.. as observed in Bangladesh where millions of people have been exposed.3 (24. Gamble et al..93-9. and contact with CCA-preserved wood structures.4 (24.23-7.2) 90th 30.3 (27. Tseng.8-32..28-7.8) 27.12-10. mine tailings). 2007.2-46. and folate status (Chen et al. 2001).06 (4.25 (6.4 (12.50 (6. Steinmaus et al. 2006.04 (5.9-56.5) 290 725 1542 03-04 03-04 8.45) 5. U. dust.0-26. organic arsenic can be converted back to methylated and inorganic arsenic. 2001).3) 6. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.6) 45.0-38.5) 17. so exposure to the general population is extremely limited.8-62.2) 40. 2001. but is poorly absorbed dermally (WHO.18 (5.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .2) 15. 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. EPA’s maximum contaminant level (Hughes.1-36.8 (27.66-8. Survey years 03-04 Geometric mean (95% conf.S. age.0) 26.1) 6.9 (45.99-9. 1988).g.0 (31. inorganic arsenic is widely distributed within the body.0 (17. Fish.7-188) 27. Though modest bioconcentration occurs in some aquatic life. 2006.66 (7..51) 75th 14.2-15. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.11 (5.7) 28.5-120) 40. The semiconductor dopants. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. Direct exposure to DMA and MMA may result from use of the two pesticides.7 (25. Inorganic forms of arsenic demonstrate high acute toxicity..30-9. shellfish.1) 7.81-9. though some reduction may occur in the gut prior to absorption.4 (26.4) 32.0) 1281 1276 03-04 03-04 03-04 8.5-17.58-10.

arsenic trioxide) includes hemorrhagic gastritis with nausea. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. NRC. Chronic arsenic exposure in humans is considered to be a cause of skin. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.10 (<LOD-1. 2001). 2004. The U. 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. and DNA repair inhibition (Cohen et al. substitution in phosphate metabolism. and endothelial injury (Kumagai and Sumi. gluconeogenesis. Survey years 03-04 Geometric mean (95% conf. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. 2004). it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1. food residue. leading to a decrease in adenosine triphosphate energy production. Although arsenate is reduced in the body to arsenite. The organic forms of arsenic occurring in seafood have little known toxicity. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.. peripheral vascular disease.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. can cause peripheral sensorimotor neuropathies. WHO. Chile). some of these effects may take years to develop.g. increased oxidative stress. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. With chronic exposure. Chronic human intake of arsenic at less than acutely toxic doses.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. and by uncoupling oxidative phosphorylation (NRC. and altered gene expression. 2001. but additional or confirmatory research is needed (Kapaj et al. 2001.g. hematocytopenias. 2001).20 (<LOD-1. apoptosis. Taiwan. population from the National Health and Nutrition Examination Survey. hepatotoxicity. Chronic elevated arsenic intakes have been associated with diabetes. Cardiac arrhythmias.10 (<LOD-1. 2001). U. and it also will inhibit succinate dehydrogenase. respectively.10 (<LOD-1.50) 621 725 1078 Limit of detection (LOD..10 (<LOD-1. 1998. WHO. 2007. Cohen et al. 2001). 182 Fourth National Report on Human Exposure to Environmental Chemicals . renal failure.S. 2006. Cellular glucose uptake. and hyperpigmentation of the skin (NRC.S. WHO.. fatty acid oxidation. 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. 2006. including inhibition of numerous enzymes..S.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1... 2007).10 (<LOD-1. and diarrhea.20 (<LOD-1.EPA. interference in signal transduction pathways. and production of glutathione may be affected as well. hypertension.S.. NRC. 2000.0. Raml et al. drinking water have not been associated with increased cancer rates (Schoen et al. 2004). Such actions may lead to decreased energy production. cytotoxicity. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. hyperkeratosis. Arsenic has many actions demonstrated in cellular studies. WHO. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. Studies of arsenic at levels typical of U. 2006.50) 1. < LOD means less than the limit of detection.EPA has established drinking water.. Bredfeldt et al. including drinking water sources with elevated arsenic levels (e. lung.20 (<LOD-1.. which may vary for some chemicals by year and by individual sample. vomiting. cell transformations. and childhood neurodevelopmental effects in observational human studies. 2001). and bladder cancer (IARC. Acutely. noncirrhotic portal hypertension.20 (<LOD-1. 2001).. Bangladesh. 2007. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. see Data Analysis section) for Survey year 03-04 is 1.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.60) 1.30) 1. 2006) or when exposure occurs in smokers (Chen et al.60) 1. which can lead to dehydration and shock...

89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006).S.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2007.. population from the National Health and Nutrition Examination Survey... 1999. Calderon et al. and were about two-fold lower than those for the U. Offergelt et al. 2000). In animal studies. 1999). 2006....41) 3. Levels of total urinary arsenic in the U. Pellizzari and Clayton 2006). In a Nevada town where groundwater levels were naturally elevated.S.S. 2008).Metals compounds. 2004. median urinary total arsenic levels in 4052 adults varied with seafood intake. 2006.. gov/toxpro2. 1998.html.. Consequently.18) 3.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.04 (<LOD-3. 2001). 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.18 (<LOD-3.. Vahter et al..80 (<LOD-4.. although urinary arsenic levels were not associated with CCA contact (Shalat et al. population in NHANES 2003–2004 (Schulz et al. Shalat et al.. 1986). 2007. 2003. population (Rubin et al. Caldwell et al. Caldwell et al. and the FDA has established a bottled drinking water standard. 2000.50) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. In the German Environmental Survey III of 1998. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.00) 1. arsenic has been fetotoxic and teratogenic.. Fourth National Report on Human Exposure to Environmental Chemicals 183 .cdc. 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... environmental levels) and health effects is available from ATSDR at: http://www. Survey years 03-04 Geometric mean (95% conf. 2006. had decreased since the prior 1990– 1992 survey. 2008. Josyula et al. Meza et al.75 (<LOD-2.19) 3.. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 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. Pellizzari and Clayton. 2004.69 (<LOD-3.. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.. Pellizzari and Clayton. WHO.atsdr. Additional information about external exposure (i. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. 2001). but generally only at maternally toxic doses (WHO. 2001).33 (<LOD-3.S. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. Compared with this Report. 2006). 2006)..e.. 2006). Valenzuela et al. 1992. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 1999.75 (<LOD-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. DMA produced bladder cancer in some chronic rat studies (Cohen et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. 2008)...61 (<LOD-3. Shalat et al. 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.33 (<LOD-3.

6 (11.S.80) 1. population in the NHANES 2003–2004 subsample.00-4.6-44. population (Sun et al.68) .3) 95th 35.1-94.80 (.7) 15.60-3.400-.40) 5.3) 1284 1284 03-04 03-04 03-04 1.20) 18.1) 45.45 (1.50) .e. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. with DMA. arsenobetaine. These associations are stronger at higher urinary levels. 1990.0 (27. 2005.800 (.4) 31.6. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.6) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1. 2008).. and TMAO.6.20 (.05) < LOD . Measurable organic arsenic species in this Report are three biologically generated environmental forms.10) 4. Blom et al. Caldwell et al.00-12.28) 1.29 (1. population (Ahsan et al.S. 2000.6 (13.9 (7.20 (4.5) 292 728 1548 03-04 03-04 1. Sun et al. arsenocholine.4 (16. geometric mean levels were about 70-fold higher than for the U. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. 2008). when seafood organic arsenic is subtracted).5 (26. and TMAO were detected in only 7.4) 23.8-40.90-29.00 (. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.1-25.3 (9. 2005.5) 29.7-22.600 (.900 (.20) 3.55 (1. After recent seafood ingestion. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.70-21. and other factors such as nutrition.0 (26. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.40-6.5) 621 725 1078 Limit of detection (LOD.800-4. population from the National Health and Nutrition Examination Survey. arsenocholine.0-23. In most human studies.00 (1.70 (3.17-1.62) 2..20-3.00-1.80 (3.4. 2003). see Data Analysis section) for Survey year 03-04 is 0. 2007) with higher levels of arsenic in the drinking water. vasospasm.20) 7..20-25. and 0.11-1.60) 1. 4. < LOD means less than the limit of detection. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-38.70-21.37 (1.3-39.3% of a representative sample of the U.50-6..19 (.. arsenite. China.80 (4. MMA.. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.74 (1.700-1. 2001). Survey years 03-04 Geometric mean (95% conf. DMA and MMA.. Caldwell et al. For residents of Inner Mongolia. Caldwell et al. 2008. Aposhian et al. arsenite.40-7.10 (4. population showed a higher contribution of arsenobetaine (Caldwell et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70) 6..93) 1.8-50.. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.3) 35.800 (.50) ..500-1.66 (1. 2008. Individually measurable species resulting from inorganic arsenic exposure are arsenate. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.5) 32.. which may vary for some chemicals by year and by individual sample.. 1985.00) 3. in NHEXAS 1995–1996.30) 10. Tseng et al.10) 8.Metals other areas of the world (Ahsan et al.1-51.2 (6. 2005. Arsenate. In the residents of a Chilean town who consumed water with high levels of arsenic. methylation capacity.8) 35. WHO.7) 13.9) 13.. Valenzuela et al.800-1.. Some noncancer effects of arsenic (e.900-1.S.30) 2.8.43-1. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.4-35.40) 75th 5.7 (13.S.30 (2. When seafood intake is avoided.9-23.871-1.30 (1. 2008).700-1. Caceres et al.83) Selected percentiles ( 95% confidence interval) 50th 1.20 (2. and duration of exposure are also considered important. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.00-6. Pellizzari and Clayton. 2000. 2008).. interval) 1. 1..0) 4.. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.70 (5.31-1..800) 1.20-190) 31. Also. The higher percentiles of total urinary arsenic levels in the U.0) 29.g.20 (1. dermal keratosis... 2000. 1996. 2006). 184 Fourth National Report on Human Exposure to Environmental Chemicals .2-35.80-5. and two methylated metabolic products. respectively. 2001.5 (14.7 (21. In the late 1980s.9 (6. 2007).90-7. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.48-2.6 (25.8 (17.3 (21.8 (12. Chowdhury et al.1) 18.S.50) 90th 16.

The 95th percentile of the U.47 (2.400-.36) 2.29 (4. 2008).531 (.612-1.30) 1.938-1.1 (26.S. Vahter et al.833-1.0-36.2 (4. 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. 2007).3) 95th 29.79 (1.15-4.47 (1.67) 1. interval) 1.2 (12.83) 8. 2006.10 (.00 (1.16 (.9 (13. which is below the ACGIH BEI (Caldwell et al. 2001)..65 (1. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.1) 26.68 (1.91) 90th 16.50-15.58 (3.4) 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 * * 1.21) 5. 1998.18-1.93 (1.3-24.9-18. 1992.901-2..76-27.7) 9.Metals as with DMA.7) 30. Caldwell et al. 1986. 2003.88 (5.15-1.9 (25.6 (9... 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.3 (10.37-2.82) 4..67) 4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.62-6.00 (3.7) 17.877 (. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.4) 32.80-153) 17. Fourth National Report on Human Exposure to Environmental Chemicals 185 .638) 1.4-21.15-1. Information about the biological exposure indices is provided here for comparison.55) 1.88) 2.30-1.4-82.61-6. Survey years 03-04 Geometric mean (95% conf.11 (.25 (.51-2.959-1.50-7.45) 1.1-18.4) 13. population from the National Health and Nutrition Examination Survey. 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.5 (18.28) 1.4) 292 728 1548 03-04 03-04 1.64-29.29-14.6-29.32-7.3) 1284 1284 03-04 03-04 03-04 1.14 (1. 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.786-1.72) 12.0 (9..3 (10.25-7.5 (18.91 (4.S.39-3.82) Selected percentiles ( 95% confidence interval) 50th 1. 2008).43) 75th 5.13-39.05) 1.4-28.70) 5.54 (1.4 (24. Offergelt et al.5) 26. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.40) 1. In recent years.78-5. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9) 14. not to imply a safety level for general population exposure.1-36.44 (1.51) 5.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.43) 14.5-20.19-2.78 (3. population for the sum of inorganic related species was 18.80) . 2001).4 (11.2 (12.909-1.9 μg/L.81 (4.8) 29.12) < LOD .05 (. Sun et al.5) 17.53 (..6-32. WHO..6 (6.6) 19.40 (1.2 (13.83) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-46.9) 32.73-6.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 2.40 (<LOD-1. population from the National Health and Nutrition Examination Survey.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.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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 1.20 (<LOD-1. < LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.00 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1.95 (<LOD-2.00 (<LOD-2. which may vary for some chemicals by year and by individual sample.S.44) 2. Fourth National Report on Human Exposure to Environmental Chemicals 187 . population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2.80) < LOD 621 725 1078 Limit of detection (LOD.S.

0) 9.00 (4. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.70 (3.1-15.17-6.00) 7.00 (7.09 (7.20-12.45) 8.37 (3.7.00-4.0 (14.77 (3.34-4.00-11.50-5.33-4.00 (3.34 (3.48 (2.S.00-12.S.80-3.45) 3.82-5.49-4.30) 3.65-8.37 (2.61-16.00-4.00-4.0 (8.52) 3.7) 12.0) 16.0 (13.31-4.3 (8.32-10.86-21.27-2.0) 9.0) 11.8) 7.3 (7.0 (10.00) 12.16 (4.57-5.0 (9.00-4.98) 4.82) 3.0-18.71 (4.0) 16.6) 292 728 1548 03-04 03-04 3.70-3.0) 13.71 (3.69 (3.44 (2.69 (3.44) 5.00 (3.00 (5.1-18. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 3.00-8.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.24) 3.0 (12.5) 12.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.0) 17.00) 5.78 (4.50-15.95-3.90) 2.9 (11.70) 5.48 (3.61-11.71) 3.1-22.2) 10.0-17.57 (3.00) 6.80) 7.0) 12.11) 4.0 (9.70-4.29-4.84-8.15) 4.95-6.00-7.0) 9.7-16.17-4.0) 10.90) 5.00-4.05) 5.97-3.0-16. interval) 3.60-3.74 (2.14) Selected percentiles ( 95% confidence interval) 50th 3.18 (6.00-11.0 (10.25 (4.03-6.17 (2.00 (3.60-4.0 (8.00) 4.86-7.24-4.0) 621 725 1078 Limit of detection (LOD.00) 75th 6.42) 3.0) 95th 16.00-5.27 (3.34-4.33) 3.91) 75th 5.65-6.8) 7.59 (6.6) 1284 1284 03-04 03-04 03-04 4.0) 14.7) 13.95 (4.27 (2.10) 6.00 (7.0) 11.00-15.00-22.00 (5.20-4. population from the National Health and Nutrition Examination Survey.28) 2. see Data Analysis section) for Survey year 03-04 is 1.00-10.00-7.67) 9.90 (3.0 (9.00 (3.46 (4.00 (5.89 (3.9) 11.6 (9.0) 13.0-12.0-19.6-18.73 (3.94-3.5) 95th 13.0 (10.80-6.0) 17.00-3.86 (2.32 (4.19) Selected percentiles ( 95% confidence interval) 50th 3.9 (7.69-3.27-5.84-18.00) 6.60-6.7) 1284 1284 03-04 03-04 03-04 4.0-17.9) 13.74) 90th 9.88 (4.82-9.0-16.7 (10.67) 8.34) 3.78) 4.80 (4.55 (2.00-7.12 (3.38 (3.4 (7.05) 10.70-12.0 (10. Survey years 03-04 Geometric mean (95% conf.05) 3.60-7.00-3.00 (3.80-5.16-11.00) 90th 11.10) 3.00 (6.32 (8.94) 3.00-12.79 (3.50 (4.16 (2.30 (7.20) 11.92) 3.00 (6.71-4.06) 5. interval) 3.00-15.31) 4.9) 5.39-3.80) 2.00) 3.00-4.49) 10.69-6.9) 12.95-4.11 (3.62) 4.00-7.00-9.03 (3.85 (3.00 (5.00-13.00) 6.22) 4.00 (6.00 (3.00) 6.00) 9.1 (8.00-15.12-4.0) 292 728 1548 03-04 03-04 4.0 (13.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .08 (2.34 (3.0 (12.0-25.00-11.0 (11.81 (5.14) 3.3 (8.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.5 (11.45 (8.73) 6.00 (5.13-4.00) 4.72 (4.92-12.

30 (1.40-3.900-1.00) 2. population from the National Health and Nutrition Examination Survey.9.54) 90th 2.57) 95th 2.45) 3.00 (1.90) 2.60) 1. which may vary for some chemicals by year and by individual sample.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.20) 2.82-2.33 (1.80) 1.10-1.70-2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (2.34) 2.00 (<LOD-1.20 (1.70-2.36 (1.70-2.46 (1.30-2.31 (1.S.10 (.00-1.17) 2.70) 2.30-1.96-2.10 (<LOD-1.30) 1.28 (1. population from the National Health and Nutrition Examination Survey.61) 2.853-1.10 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.40) 1.80 (1.31-3. < LOD means less than the limit of detection.84-3.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.30 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.50) 1.60) 2.15-1.00-1.11-1.86) 3.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.77) 1.88-2.90) 1.60-2.10-1.82-2.00) 1.22 (1.80-2.37 (1.52 (2. Survey years 03-04 Geometric mean (95% conf. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80 (2.20 (1.23) 1.81) 1.61-3.00-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.85) 2.10) 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-2.86 (2.20-3.00) 1.40 (1.07 (1.00-4.60 (2.80 (1.86) 2.30) 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.93) .14-1.30) 2.20-1.90 (1.816 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 03-04 Geometric mean (95% conf.22) 3.80 (1.40) 1.10-3.00 (<LOD-1.50 (<LOD-1.10) 95th 2.58) 2.18-1.79) 2.07) 2.40-3.90) 2.20 (1.16 (2.50) 621 725 1077 Limit of detection (LOD.73-2.00) 2.60) 2.86 (2.80) 1.07-3.70-2. see Data Analysis section) for Survey year 03-04 is 0.30) 90th 1.20 (1.30-1.53-2.40-2.60 (1.30 (2.50 (2.30 (1.20 (1.53 (1.50 (1.62) 2.46-2.28 (1.43-3.33 (1.90 (2.18-1.S.20 (1.05-1.80 (1.40) 2.71-2.985) 1.36) 1.40 (2.00) 1.00 (2.35-3.85) 1.88 (1.10 (.10 (1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .40-2.70-3.63 (<LOD-1.80-2.50-2.88 (1.

Metals Urinary Trimethylarsine oxide Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. Urinary Trimethylarsine oxide (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. Survey years 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 1. 190 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.0. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.

Beck BD. Environ Health Perspect 1996. Gurzau A. House dust and inorganic urinary arsenic in two Arizona mining towns. Chowdhury UK. Updated September 2004 [online]. et al. MMA(V).89:145-151. Environ Res 2005. Lu X. Matczak W.216(1):69-79.fr/ENG/Monographs/vol84/ volume84. placebocontrolled folic acid-supplementation trial in Bangladesh.107(8):663-667. Kurzius-Spencer M.pdf. Fourth National Report on Human Exposure to Environmental Chemicals 191 . 2001. Arsenic methylation patterns before and after changing from high to lower concentrations of arsenic in drinking water. 8/7/08 Ahsan H. Sturup S. Clinical and neurophysiological studies. Excretion of arsenic in urine as a function of exposure to arsenic in drinking water. McClellen H. Crit Rev Toxicol 2006.42(12):1195-1201. Kalman DA.104(11):1200-1207. Chen SY. Jakubowski M. Le XC. Calderon RL. Kapaj S. Reduction in urinary arsenic with bottled-water intervention.html. Hsu LI. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Hall M.38(1):87-113. Gurzau ES. Parvez F. J Expo Anal Environ Epidemiol 2003. J Appl Toxicol 1988. Int Arch Occup Environ Health 1998. Norin H. Moldeus P. Gamble MV. Trzcinka-Ochocka M. et al. Slavkovich V. et al. Rahman A. Scand J Work Environ Health 1985. Eldan M. et al.98(2):151-159. Healy SM.iarc.11(4):265-269. Liu X. Coble K. Pilsner JR. Folate and arsenic metabolism: a double-blind. Ahsan H. Lewis AS. J Environ Sci Health A Tox Hazard Subst Environ Eng 2006. Chem Res Toxicol 2000. Environ Health Perspect 1990. Amigo H. Zheng Y.292(24):2984-2990. Biological monitoring of occupational exposure to arsenic by determining urinary content of inorganic arsenic and its methylated metabolites. Poplin GS. Hughes J. Arsenic exposure to smelter workers. Am J Clin Nutr 2006.114(11):1790-1796.13(8):693697. Eblin KE.atsdr. Ilievski V. Needham LL. Wu MM. J Health Popul Nutr 2006. Loomis D. Gandolfi AJ.13(3):211-218. O’Rourke MK. September 2005 [online]. Lodh D. Atalah E. Bhattacharya P. Kumagai Y. Biomarkers of exposure: a case study with inorganic arsenic. Biggs ML. Jagadish B. Aposhian HV. Thor H. Hudgens E. Environ Health Perspect 1999. Perrin M. Lagerkvist B. J Occup Environ Med 2000. Environ Health Perspect 2006.8(2):119-127. and lung cancer risk: a follow-up study in arseniasis-endemic areas in Taiwan. Ryhage R. Ingested arsenic. cigarette smoking. Hysong TA. Exposure to inorganic arsenic in drinking water and total urinary arsenic concentration in a Chilean population. Pino P. Hysong TA. Ye X. Methylated arsenicals: the implications of metabolism and carcinogenicity studies in rodents to human risk assessment. Sengupta MK. Cebrian Garcia ME. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. American Conference of Government Industrial Hygienists (ACGIH). Hopenhayn-Rich C. Bredfeldt TG. Linderholm H. International Agency for Research on Cancer (IARC).Metals References Agency for Toxic Substances and Disease Registry (ATSDR).71 Suppl:S29-32. and biotransformation involved in cellular response and toxicity. Summary of Data Reported and Evaluation. Montesinos N. Parvez F. Stute M. J Environ Sci Health A Tox Hazard Subst Environ Eng 2003. Available at URL: http://monographs. including Arsenic. Chiou HY.84(5):1093-1101. A prospective study of blood selenium levels and the risk of arsenic-related premalignant skin lesions. Cellular metabolism of arsenocholine. et al. van Belle G. Hughes MF.16(2):207-213. Smith AH. Available at: http://www.cdc. Burgess JL. Bolgiano D. 7th edition.116(7):893-897.41(10):2399-2428. 8/7/07.gov/toxpro2. Moore LE. Arnold LL. Blom S. Hsueh YM. Pattern of excretion of arsenic compounds [arsenite. Sumi D. Reidy JA. Rahman MM. Schreinemachers D. Cincinnati (OH): ACGIH Worldwide. Arsenic: signal transduction. Volume 84. Chen CL. DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh. Human health effects from chronic arsenic poisoning--a review. Christakopoulos A. Some Drinking-water Disinfectants and Contaminants. Documentation of biological exposure indices. Monomethylarsonous acid induces transformation of human bladder cells. Toxicological profile for arsenic.24(3):298304. et al. Razniewska G. Cancer Epidemiol Biomarkers Prev 2007. Environ Health Perspect 2008. Associations between drinking water and urinary arsenic levels and skin lesions in Bangladesh. Liber K. et al. Slavkovich V. Roy S. transcription factor. Caceres DD. van Geen A. Calafat AM.36(2):99-133. Chanda CR. arsenate. Le XC. Graziano JH. Mash EA. et al. Annu Rev Pharmacol Toxicol 2007. Burbacher T. Sandstrom M. Wong LY. JAMA 2004.47:243-262. Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Thomas DJ. Peterson H. Kalman DA. Cohen SM. Josyula AB. Chen Y. Toxicol Appl Pharmacol 2006. The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species.

20(8):1120-1125. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Sci Total Environ 2006. Jones RL. Liaw J. Tseng CH. urinary arsenic metabolites and human diseases: current perspective. 8/7/07. Ibata K. Guidelines for Biological Monitoring. Rumpler A. Chem Res Toxicol 2007. Arsenic in Drinking Water. Environmental Protection Agency (U. Clayton CA. Belson MG. J Toxicol Environ Health A 2007. Available at URL: http://www. Int Arch Occup Environ Health 1986. Solo-Gabriele HM. Lauwerys R.70(2):159-170. Geneva 2001. CruzGonzalez MB. Ochi T. Arsenic exposure. Nevada. Garcia-Montalvo EA. et al.367(1):80-88. Schulz C.org/documents/ehc/ ehc/ehc224. Gandolfi AJ. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Chen CJ.htm. Environ Health Perspect 2005. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley.36-37. Yang MH. Ferreccio C.49(6):387-393. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. Kolossa-Gehring M. Goessler W. Suzuki KT. Vahter M. Boeckx M. et al. Rahnster B. National Research Council (NRC). Toxicol Appl Pharmacol 2005. U. China. Marshall G. pp. Seiwert M. Sonora. Black K.115(4):648-652. 8/7/07 U.210(3-4):271-297. Environ Health Perspect 2007. Available at URL: http://www. von Ehrenstein O. Lewis Publishers. using a routine LC-ICP-MS method. J Anal Toxicol 2006. Francesconi KA. Buchet JP.114(2):220-227.S. Hoet P. Vahter M. Jimenez M. Flanders WD. Burgess JL. Investigating childhood leukemia in Churchill County. Available at URL: http://www. Meza MM.57(2):79-91. Mexico. Arsenic methylation.222(3):374-380. Fact Sheet: Drinking Water Standard for Arsenic.30(5):293-301. Shipp M. 1998 [online]. Becker K.inchem. Wang Z. World Health Organization (WHO). Nygren A.gov/safewater/arsenic/regulations_factsheet. Br J Ind Med 1992.96(2):119126. Arsenic.gov/iris/subst/0278. Environmental Protection Agency (U. Jhangri GS. Environ Health Perspect 2006.206(3):299-308. January 2001 [online]. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells. 2001. In:Industrial Chemical Exposure. EPA 815-F-00-015. Kieszak SM. Li X.S. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Holmes AK. Environ Res 2004. Roels H. Boca Raton (FL). and metabolism of arsenic. Morton J.Metals Kwon E. 3rd Ed. Moore LE. Kopplin MJ. Raml R. Smith AH. et al. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. Jin Y.211(2):175.S.epa. Toxicol Appl Pharmacol 2007. Huang YL. 2001. Huang YK. Friberg L. Lu X. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Arsenic and Arsenic Compounds. html. Pellizzari ED. Genetic polymorphisms in MTHFR 677 and 1298. Offergelt JA. 2nd ed. Fok N. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Garcia-Vargas GG. Naranmandura H. Calderon-Aranda ES. Arsenic in drinking water-2001 update. Rey OA. Borja-Aburto VH. A pilot study of children’s exposure to CCAtreated wood from playground equipment.112(14):1375-1380. Environmental Health Criteria 224. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS). Rubin CS. Int J Hyg Environ Health 2007.113(3):250-254. Li L. Steinmaus C. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. Environ Health Perspect 2007. et al. Washington (DC) National Academy Press. Li B. Nolinder P. Buckley BT. EPA). Environ Health Perspect 2004. Arsenic on the hands of children after playing in playgrounds.htm. inorganic.25(1):1-22.S. et al. Biggs ML. Lauwerys RR. Valenzuela OL.114(8):1293-1296. Integrated Risk Information System. EPA). et al. Kalman D. Sun X. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Seifert B.K. Conrad A. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals .115(1):151-157. GSTM1 and T1. et al. Xu Y. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. Sun G. Mason H. Tseng CH. Environ Health Perspect 2006. urinary arsenic speciation.epa. Arsenic. Erratum in: Toxicol Appl Pharmacol 2006. Shalat SL. Zhang H. Yuan Y. Fleming LE. Chung CJ.

91) 6.24-1.49) 11.67) 6.65) 1.10) 3.30 (3.15 (6.14 (6.93-2.80-3.07 (2.60-2.15-1.28) 90th 5.49) 2.63 (1.65-5.35) 5.87 (6. Certain foods.54-8.70 (5.34) 2.47-1.72) 1.91) 2.93-8.73-5.73) 1.Metals Barium CAS No.50 (2.08 (6.35 (3.59-11.30) 5.18) 3.20-8.00) 1.20-1.00) 6.09 (2.21-8.90) 1.8 (6.85) 1.16 (1. In nature.37-8.21-2.90) 2.50 (1.40 (5. soluble forms of barium.29-5.00 (2. 2001).4) 6.50) 2.61 (1.1) 9.56) 1.60-6.44-5. and food.60) 1.12-1. 0.53) 2. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.86 (4.50 (1.99 (4.30-5.63 (5.80 (1.99-5.57-7.70-2.81-3.17-1.70 (1.80 (1.71) 1.78-3.40 (5.50-6.50) 4.19-1. such as barium chloride.20-1.00) 1. whereas others are practically insoluble (e.62) 1.06-2.00-76.S.04-6.50) 1.31.20 (1.47) 4.90-9.15 (2.45) 7.40) 7.86-4.90) 4.65) 1.05% of the earth’s crust.54) 1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10) 5. and 03-04 are 0.30) 8.37) 1.86-5.50-6.36 (1.34 (2.00-3.46) 1.30-1. and ceramics.68 (1.52 (4. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).71 (2.39) 1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.15 (1.92) 2.97 (1.40) 7.34 (1.20-8.66) Selected percentiles ( 95% confidence interval) 50th 1.40-13.39-1.60-3.70-6.10 (3.50-1.50 (1.12 (2.80 (1.78) 1.70-3.32) 8.12 (2.08-8.27 (1.30-2.30-2.51 (1. Workers employed by industries that make or use barium compounds can be exposed to barium dust.77 (3.54 (6.88 (5.9) 5.50 (1.39) 4.55-7. Barium compounds are used by the oil and gas industries to make drilling muds.36-1.95 (4.64-3.90 (4.62 (1.62 (1.86) 6.87 (5.48) 1.28-1.30) 2. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0..50 (4.72) 4.61 (2.14-6.20-1.65-1.43) 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 1.40) 3.43) 6.76 (3.21 (1.95-6.76-3.26-7.82) 1.54-1.30) 4.98) 1.37-1.42 (1.20 (3.70) 1.70) 7.50-1. see Data Analysis section) for Survey years 99-00.49-9.80-7.10-4.71-9.87-3.46) 1.12) 6.48 (6.40 (1.87-14.20) 2.63 (2.81-2.g.41-3. such as brazil nuts.56 (2.80 (5.39 (1. tiles.52 (1.73 (5.65) 3.35-1.11 (2.40 (1.60) 4.00 (1.63) 1.48) 1.11-1.38 (1.50 (5.90-13. interval) 1.90 (6.02 (7.65-8.70-2.31 (2.30 (5.65 (5.04-2.22-1.71) 2.76-2.61 (3.50 (6.41-1.82-6.01-7.25-11.30 (1.70-5.51) 7.05-2.4) 9.91 (2.00-8.30) 3.69 (1.43 (5.12.80 (2.64 (1.57) 3.86 (4.62) 1.8) 5.49-1.56 (6.55-3.30 (5.10) 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 1.24-1.27 (1.77-3. Barium compounds are also used commercially in paint.30 (2.60-6.26) 2.49) 4.38 (1.61-8.25 (1.57 (5.60) 3.38) 8.87-9.19) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.93 (4.66 (4.56 (1.29-1.10-5.2) 6.44-2. 01-02.78) 1.40 (4.70) 3.10 (4.30-1. The general population can be exposed to low amounts of barium in air.60 (2.8) 9.11 (3.76) 1.18-1.43 (1.43 (1.00) 4. and 0.72) 75th 3.30) 5.33 (1.14-1.81-2.61 (1.50 (4.39 (1.16) 5.88) 7.06-1.54) 2.74) 3.11 (3.70) 1.30-3.63) Total 1.25-1.60-10. rubber.87) 7.56) 4.01 (4.43) 2.46-1. respectively.94-6. fireworks.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 2.34 (1.37 (4.80) 7. barium sulfate and barium carbonate).18 (6.54) 1.60 (1.53) 1. Some barium salts are freely soluble in water.70) 4.73 (6.22-1.80) 6. Fourth National Report on Human Exposure to Environmental Chemicals 193 .70) 5.21 (1.50) 2.51) 1.80-5.80) 1.45 (1.20-6.32-1.75-3.87-7. it combines with other chemicals such as sulfur or carbon and oxygen.4) 7.50 (4.22) 6.24 (4. glass.49 (1.26-1.09 (1.74-2.15-11.88) 4.36) 5.70-8.15-1. water.75) 2.12.35-4. bricks.27) 2.77) 1.78-2.36-1.59) 3. Small amounts of barium can be released into the air during mining and other industrial processes.90) 2.63 (8. depilatories.40 (5.35-1.10 (2.20-1.90-2.71) 95th 6.80 (2.61 (5.48-4.53-5. population from the National Health and Nutrition Examination Survey.41) 1.26) 5.20 (4.20-5.96-2.85 (2.32-7.35 (1. Barium salts have also been available as rodenticides.82) 2.48-4.84) 5. In single dose animal studies.49) 8.50 (1.31-2. are high in barium (Genter.37) 5.90 (1.51) 2.47-1.29) 5.15) 5.76-7.85) 1. 7440-39-3 Medically.35 (2.40 (1.50 (3.74-3.54-1.63) 1.88) 1.30) 5.12) 7.20-8.36 (4.60) 1.38) 2.54 (2.56 (1.73) 3.44 (1.80-2.03 (1.

52-10. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.4 (5.26-1. Following intravenous injection in animals.46) 3..74) 1.35-3.78 (2. Toxicity from soluble barium salts is rare.91 (3.11) .30 (1.66 (1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.45 (3.777-1. Perry et al.55-5.20 (1.44-2.29 (1.57-10.2) 6. weakness.84 (3.48 (1.52) 2.36 (3.15-4.26-4.52) 7.29-1.37) 2.60 (5.37-2.28) 5.754-1.29-4.35-1.38-1.88 (6..43) 1.64) 7. such as those used in medical radiographic procedures.81-6. Barium is not rated for human carcinogenicity.710-1. in urine.62 (2.00-7.28-6.16-1. 2001). NTP. 1985.65 (5.19-2.60 (2.97-3.38-5. 1986).82) 1.76 (3.65 (2.50) 1.31 (1.00 (3.29-7.71 (5.26-1.22-1.73-4.36 (3. hypertension.58) 75th 2.97 (5.54) 2.75) 1.52 (3.00 (3.06) 2.39-5.38) 1.4) 5.97-4.96) 4.51 (1.10) 6. Wones et al.26-1.29-3. vomiting.25 (1.00-1.56-3.12) 2.13-3.92) 2.55-6.39-1.59-7.32) 2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.98 (2.58-6.19-1.85-5.32 (1.18 (1.3 (6.60 (2.41) 4.01) 1.96) 7.76 (4.72) 6.68-3.06) .59 (1.44 (1.2) 5.33 (1.41 (1.46-22.03-1.76) 2.25) 4.31) 5.55 (1.51 (1. and cardiac dysrhythmias.55) .41 (1.81-6.30) 2.40-1.63) 1.42) 1.54 (2.91) 2.20) 4.34-3.47 (5.72 (2.40 (1.36 (5.61 (4.45) 1.47) 1.68 (3.24-1.S. paralysis. interval) 1.53-21.50) 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 1.77) 1.2 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.86-7.75-22.00 (5.39 (3.49-1.28-7.49-1. and route of exposure.02-5.33 (5.49-1.24-6.09) 6.81-7.48-1.57-7.39-10.43-6.45-1.34 (1. a benign condition that may occur among barite ore miners.48-3.83) 2.52) 1.76 (2.10) 3.04) 1.77) 1.84) 2.00) 4.36-2.89 (2.83) 3.73) 2.10 (6.99 (4.14-2.55 (1.47-8.31-1.38-7.44-2.27-1.38 (1.51 (3.20-2.55 (4.68) 1.59) 2.24) 3.963 (.47) 10.33 (1.10-1.62 (1.53 (2.27-3.49 (1.53) .42) 1.03) 2.46 (2..11-2.97 (4.24-11. Symptoms following acute high dose include perioral paresthesias.45 (1.84-2.01 (5.38) 4.26-1.18 (1.51) 4.00 (2.891 (. chemical form.0) 5.22-2.37-1.99) 1.33-1.832-1.87) 1.29-4.25-11.00) 1.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.64 (1.36 (1. diarrhea.21 (1.58) 4.80) 4.04 (2.11) .64 (1.86 (2.88 (2. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.89) 90th 4.905 (.28-1.56 (1.96 (4.57) 2. 1990).41) 5.45-1.68-3.05-1.72) 4.02) 4.37 (1.02) .77-5.31-1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.19-1.34-1.22-1.56 (1.48-5.0) 7.39 (2.30 (1.38) 1.8) 4.22-4.04) 5.86) 5.80-6.56) Selected percentiles ( 95% confidence interval) 50th 1.57-5.84-5.32) 2.45) 95th 6.35-1.58) 1.08-1. are not absorbed when administered. 1989).48 (1.39 (2.00) 6.24 (3.27) 7.96 (4.96) 4. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.48 (1.90-2.19-1.99 (2.52-4.54 (1.33) 1.91-2.921 (.64) 7.49 (1.23-1.36 (1.00) 4.24-3.37 (1.64 (1.73-2. Insoluble barium salts.03) 1.57 (6.39 (2.64 (1.77) 5.31-1.68) 3.46) 2.47) 1.50 (4.38 (4.27) 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 .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.Metals was eliminated primarily in feces and to a lesser extent.74 (5.51-3.76-3.26) 4.23-5.54) 1.01 (4.0) 6.77) 1.42 (4.32 (1.33-4.82) 1.50) 1.39) 4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.60 (1.51) 4.69 (5. water solubility.91 (3.45-6.20-1.96) 4.47) 4.40 (1.34) 1.75) 2.28-11.32 (2.20-8.38 (1.24 (5.79) 1.10-2.59 (1.915 (.51) 6.39-1.34-5.703-1.59) 1.67-6.62 (4.97) 1.28 (1.80) 3.41 (2.69-9.68 (2.58 (2.75) 2.881 (.31 (4.38 (4.77) Total 1.29) 1.08-2.58 (4.16) 11.75) 1.23-2.70) 10.16 (1.56) 4. 1994.03-1.02 (3.60 (1.92 (4.70) 1.3) 6.27 (2.47 (2.45-8.76) 1.36-1.29 (3.63-4.03) 3. The health effects of exposure to barium compounds depend on the dose.75-3.13-2.46) 1.76) 2. Chronic high doses in animals resulted in kidney damage (McCauley et al. population from the National Health and Nutrition Examination Survey.50) 2.24-1.59) 1.96-6.79-5.33) 6.61) 2.880-1.68 (3.70) 4.24-6.40 (1.55 (5. 1984.36-1.48) 2.74) 1.62) 2.

Epidemiological study of barium in Illinois drinking water supplies. Princeton (NJ): Princeton Scientific Publications. Paschal et al. ed. Genter MB. 1984. LA. In: Calabrese EJ. 84-94.. Available at URL: http://ntp.S. Wones RG. Exposure to soluble barium compounds: an interventional study in arc welders. Patty’s toxicology.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Biomonitoring Information Levels of urinary barium reflect recent exposure.gov/toxpro2.28(3):373-388.S. Apostoli P. J Toxicol Environ Health. Schaller KH. et al. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect.niehs. p. In: Inorganics in drinking water and cardiovascular disease. p. et al. 1986.64(1):13-23. Costa R. Calabrese EJ. Stadler BL. Advances in modern toxicology. Frohman. Jr. ed. Ash KO. Perry EF. 1994. [online]. 1990. Centers for Disease Control and Prevention (CDC). pp. Ting BG. 2000) to levels in NHANES 1999-2000 and 2001-2002. Atlanta (GA). Minoia C. 231-249. Minoia et al. Pirkle JL. 1998). New York: John Wiley & Sons. environmental levels) and health effects is available from ATSDR at: http://www. Trace element reference values in tissues from inhabitants of the European community I. and a drinking water standard has been established by U.. Levy. 4/8/09 Paschal DC. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding.nih. Gallorini M. EPA. p. calcium. A study of 46 elements in urine. and radium In: Bingham A. et al. Kopp SJ. Int Arch Occup Environ Health 1992. Environ Res 1998. Princeton NJ: Princeton Scientific Publications. blood..296(1-2):71-90. PS. barium. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Vol 2: Specific Metals.cdc.. Cohressen B. Handbook on the Toxicology of Metals.e. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. 1985.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. New York: Elsevier. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Environ Health Perspect 1990.85:355-359. and serum of Italian subjects. 2001. In Friberg L. Laurie RD. Douglas BH. Trace metals in urine of United States residents: reference range concentrations.76(1):53-59. and 2003-2004 (CDC.atsdr. Barium. Zschiesche W. patient population and literature reference intervals for urinary trace elements. Sci Total Environ 1990. Powell C. McCauley PT. Pozzoli L.gov/ntp/htdocs/LT_rpts/tr432. 2001-2002. Clin Chim Acta 2000. Jackson RJ.197210. Third National Report on Human Exposure to Environmental Chemicals. Morrow JC. 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. Comparison of representative ranges based on U. strontium. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Magnesium. Reeves AL.gov:8080/cs. Vouk VB.. Howerton K. 221-252 Komaromy-Hiller G.95:89-105. 2005. et al. 5th ed. National Toxicology Program (NTP).html?charset=iso-88591&url=http%3A//ntp. eds. Sabbioni E. 2005. 1992). Weltle D.html. eds. the welders had no obvious adverse clinical effects (Zschiesche et al. Investigations into the effect of drinking water barium on rats.. Inc. Lack of effect of drinking water barium on cardiovascular risk factor. Perry HM.niehs. Information about external exposure (i.nih.. References Brenniman GR.. Pietra R. Sampson EJ.. 1989. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Nordberg GF. 2nd Ed. NTP.

beryllium is used in instruments. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 03-04 are 0. and volcanic dust. Two types of minerals. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and refined beryllium is used in mirrors and special metal alloys for the automobile. and from breathing tobacco smoke. 7440-41-7 General Information Pure beryllium is a hard gray metal. In studies of laboratory animals. are mined for commercial recovery of beryllium. soil. or drinking water containing the metal. computer.13.13. 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 .Metals Beryllium CAS No. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. x-ray machines.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 . Low-level beryllium exposure in the general population can occur through breathing air. electrical.130 (<LOD-.130 (<LOD-. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.13. 196 Fourth National Report on Human Exposure to Environmental Chemicals .160) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. eating food. and dental bridges. nuclear. In medicine. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. 0. and machine-parts industries. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample. 01-02. and can be found in mineral rocks. aircraft. near some hazardous waste sites. see Data Analysis section) for Survey years 99-00. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. Exposure to beryllium occurs mostly in the workplace. bertrandite and beryl.S. and 0.140 (<LOD-. < LOD means less than the limit of detection. coal. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. respectively. Beryllium compounds are commercially mined. 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.231 (<LOD-. based upon excess lung and central nervous system cancers in studies of workers. and drinking water and environmental standards have been established by U.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. EPA. NTP considers beryllium to be a known human carcinogen. Maier.391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. respectively. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 . 1990). IARC has classified beryllium as a human carcinogen. Chronic beryllium disease. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa.346 (<LOD-. or berylliosis. 2003. 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 .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 .281 (<LOD-. S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. which produces pneumonitis. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. including contact dermatitis and subcutaneous nodules. population from the National Health and Nutrition Examination Survey. Skin exposure can result in delayed hypersensitivity reactions.. 2002). Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. 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. Fourth National Report on Human Exposure to Environmental Chemicals 197 .S.

Paschal et al. Paschal DC. blood. it is likely that urinary beryllium levels in the U. and the fact that most NHANES participant levels were undetectable. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998). urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Pietra R. Howerton K.gov/toxpro2. Hamilton EI. Gallorini M.12 to 0. et al. Kriess K.html.S. VI. Environmental Health Criteria. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Clin Chim Acta 2000. Trace metals in urine of United States residents: reference range concentrations. International Programme on Chemical Safety (IPCS).158:165-190. Sampson EJ. HLA-DPB1 and chronic beryllium disease: a HuGE review. patient population and literature reference intervals for urinary trace elements.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. 1990.13 μg/L. 198 Fourth National Report on Human Exposure to Environmental Chemicals . and the 95th percentile for males in NHANES 2001-2002. Jackson RJ. population are lower than levels in workers.23:827-839. 2001).org/documents/ehc/ehc/ ehc106. Hamilton et al. et al. Apostoli P.e. Trace element reference values in tissues from inhabitants of the European community I. Am J Epidemiol 2003. 0.e. Beryllium [online]. In other studies. Sabbioni E..157:388-398. Review of elements in blood. Pirkle JL. References Apostoli P.. 3/27/08 Komaromy-Hiller G. They reported urinary beryllium levels ranging from 0. Int Arch Occup Environ Health 2001. Given these results. Sci Total Environ 1990.Metals (i. Weston A. less than 0. Schaller KH.S. Atlanta (GA) 2005. Costa R. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. 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.74:162-166. Levels of beryllium in urine for the U.296(1-2):71-90. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure.. 1990.95:89-105.S. Ash KO. Sabbioni E.inchem.. Ting BG. Andrew M. environmental levels) and health effects is available from ATSDR at: http://www. Minoia C. 20012002. Minoia et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. 2000. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. A study of 46 elements in urine. Third National Report on Human Exposure to Environmental Chemicals. 106. Sci Total Environ 1994.. Available at URL: http://www.htm.cdc.atsdr. which approximate this Report’s limit of detection. population were generally undetectable in NHANES 1999-2000. Clin Chest Med 2002. McCanlies EC.76(1):53-59. and serum of Italian subjects. Pozzoli L. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Genetic and exposure risks for chronic beryllium disease. Element reference values in tissues from inhabitants of the European community. Van der Venne MT. Centers for Disease Control and Prevention (CDC). and 2003-2004. Maier L. Comparison of representative ranges based on U.1 μg/L). Morrow JC. Environ Res 1998.

386-.366) * * .30) 1.10) 1.3.60) 1.500 (.400-.452) .40 (1.400 (.600 (.400-.400 (.300) .378 (.700) .300-.400) .300 (.50 (1.300 (<LOD-.600-.400 (.20) 1.500) .600) .300-.00 (.900 (.60 (1. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.400 (.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 .70) 1.300-.400) .500 (.283 (.10 (.700) .300 (.400 (.400 (.10 (1.900-1.700) .300 (.400 (.200 (.500) .40 (1.400 (.400) < LOD .403 (.500) .403) .00 (.600 (.200-.368-.449) Selected percentiles ( 95% confidence interval) 50th .10) 1.300-.60) Total * .60) 1.400-.700) .500-.200-.300-.300) .900-1.424) * .300 (.00 (.20) 1.420 (. which may vary for some chemicals by year and by individual sample.400) .300 (<LOD-.00 (.289-.00-1.00) .400-. EPA.344) .30) 1.300) .90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .20-1.400 (.700-1.50 (1.10 (1.500-.40) 1.500 (.00-1.500-.40 (1.300 (. coatings and plating.200) .500-.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 * * * * * * .700 (.700) .600 (.700) .400 (.50) 1.600 (.20-1.427) * . 01-02.359-. during refining of lead and copper from sulfide ore.393 (.333 (.gov/minerals/pubs/commodity/cadmium).500-.50) 1.700) .400-.500-.500-.20) 95th 1.300) .400-.300 (. and 0.400) .500-.30) 1.10) 1.400-.500-.20) 1.40 (1.900-1.20) 1.600 (.200 (<LOD-.700) 1.400 (.400 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .300) .00 (.300-. and incineration of municipal waste materials.600) .300) .200 (.80) 1.900-1.20-1. Cadmium also may be emitted into the air from zinc.500 (.20) .400-.300-.300 (<LOD-.400 (.300-.80 (1.300-.400-.10) 1.300-.00 (.460) .80) 1.500-.900-1.600) .255) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300) 1.300-.200-.40 (1.10) 1.00 (.20 (1.400) .400) < LOD .500-.00 (1.300-.900-1.300 (.400) .421 (.500 (.900-1.14.235 (.500) .600-.20-1.30-1.300-.500-. as zinc sulfide) and to a lesser extent.20) 1.600 (.00-1.400-.500 (.200 (<LOD-.412 (.300 (<LOD-.441) * .40-1.300) 75th .40) 1.60) 1.216-. cadmium use has declined in response to environmental concerns (http:// minerals.700-1. and 03-04 are 0.Metals Cadmium CAS No.10 (1.70) 1.300-.800-1.10) 1.900-1.470) * .300-.600 (.30-1.60 (1.600 (.337) .S.500-.10 (1. The predominant commercial use of cadmium is in battery manufacturing.00-1.376-.300-.20-1.30-1.500) . Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Since 2001.00 (.400-.usgs. respectively.40-1.300) .500-.200-.398) < LOD < LOD < LOD < LOD < LOD < LOD .00-1.400) < LOD .800) .361-.600) . plastic stabilizers.60 (1.331) .10 (1.40 (1.800) .200) .400) .600-1.00-1.600) .60-1.362-.367-.600) . or copper smelters (U.400 (.50-1.300 (.90) 1.600 (.400) .309-. and nonferrous alloys.600 (. malleable.60 (1.500 (.304 (. < LOD means less than the limit of detection. interval) .30) .50-1.10 (1.266-.500-.300) .20) 1.500 (.300-.S.800 (.20) 1.600) 1.300) .70) 1.300 (.400) .395 (.300) .400) < LOD < LOD < LOD .00-1.20 (.300 (.300 (.425 (.300) .600) . 0. 7440-43-9 General Information Cadmium is a soft.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800 (.600) .60 (1.400) .300-.296-.S.900-1.304 (.600 (.378-. see Data Analysis section) for Survey years 99-00.600 (.00-1.300-.900-1.10) 1.600) 90th 1.10) 1.20) 1.40 (1.400) .300-.300) .275-.304-. lead.30-1.20-1.300-. Other uses include pigment production.426-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300 (.500 (.313 (.20) .200 (.382 (.300) . U. population from the National Health and Nutrition Examination Survey.326 (.700) .50-1.50-1.00-1.900 (.500-.600 (.3.00 (1.30-1.500) .500) .00) .400 (.400) .00 (.50 (1.200-.500-.600-.50 (1.400) .400) .400 (.00 (.400 (.300 (.50) 1.600 (.30 (1.800) 1.513) .500-.600) .300 (.10 (1.468 (.700-1.20-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.800-1.70) 1.

843-1.126) .680 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein. For nonsmokers who are not exposed to cadmium in the workplace.400-.426 (.530) .440-.203) .390-.919) .198) .817 (.733-.151-.281 (.316 (.150) .310 (.109 (.229-.255) .270 (.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 .482) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.157-.191-.390 (.257) .06-1.290-.230 (.222) .806) .233) . however.255) .190-.214-. calcium.980-1.28-1.067-. Horiguchi et al.366-.360) .189-.193-.265) .336) .114-.322 (.179-.610) .372) .717-.490) 1.74) 1.440 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.559 (.092 (.170-.10 (1.19) 1. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.177-.466 (.06.989-1.135 (.633-1.810-1.940-1.17 (.237-.302 (.210 (.886-1.249) .284) .748-1.065-.623) .38) .890-1.820 (.232 (.36) 1.607) ..493-.230) .200 (.169-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .210) .980) .790 (.350 (.308) .230) 75th .260-. 2001).980-1.713) . The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.092) .47) 1.20 (1.265 (.090) .890 (.277 (.270 (.633 (.436-.210 (.700-.918-1.081) .191 (. 2003).858 (.229) .229) .180 (.753-.191-.475 (.087-.219 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.202-.231) .388-.211-.04 (.354) .120 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.366) .101) .440 (.203 (.479) .06.09-1.148) . interval) .875 (.38) .199 (. population from the National Health and Nutrition Examination Survey.183-.875) .210 (.977) .S.28) 1.283 (.714-1.28 (1.329 (.110-. Kikuchi et al.800-.490) .500) 90th .157) .227 (.209 (.640) .160) .181 (.170-. 2003).820) 1.51 (1.189) .193 (.239 (..310) .150-. 1994).445 (.226) .170 (.730-.189-.211 (.430) .077 (.763-.15) 1.20 (1.300 (.194-.433-.06) .221 (.320) .519) .165-.20-1. drinking water is a source for cadmium intake. rice.03) .892-1.253-.498-. 2003).160 (.733) .077 (.766 (.067-.255) .210) .112-.456-.190-.251) .160-.240-.272-. To a lesser extent.232) .22 (1.200 (.551 (.412) . 01-02.351-.387) .57) 1.963-1.173) .306 (. 1999.836-1.381-.060-.263) . respectively.24) 1. Renal tubular and glomerular damage.20 (1. Cadmium absorption may be increased with iron deficiency (Berglund et al.892 (.450 (.238) .330-.960 (.210 (.480) .282 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .700-.22 (.196-.200-.430-.204 (.100-.34) 1.249-.83) 1.817 (.366-.700-.210 (.200-.860) 1.72) 1.820-1. Cadmium in soil is absorbed by plants.790 (.32 (1.235) .530 (.01) .52 (1.20) 1.295) .246) .261-.362) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.01-1.220) .192-. and 03-04 are 0.Metals 2000). copper) and protein..190-.167-.219 (.447 (..741-1.247) .13 (.43) 1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.15 (. including many food crops such as cereal grains. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.38) 1. 2003.455 (..300) .818 (.02-1.37) 1121 1335 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 .061-.01 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.216 (.130 (.206 (.980 (. With chronic exposure.540) .327 (.848 (.148-.128 (.220-.178-.078 (.262) .510) .192-.539) .30-1.25 (1.233) .390-. 200 Fourth National Report on Human Exposure to Environmental Chemicals . and 0. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.234 (.476-.134) .135-. ingestion through food is the largest source of exposure.510-.423-.140 (.25) 1.12-1.813 (.972 (.107-.870) .12 (.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.260 (.141 (.492 (. wheat. 0.06-1.705-.394-.686-.121 (.160) .82) 1.221) .175 (.175 (.280 (.238-.400-. potatoes.115-.153-.240) .04 (.299) .285-. zinc.452 (.458 (.223 (.208-.109-.06.187 (.241) .184-.462 (.261-.41 (.090) .339) .201 (.171-.061 (<LOD-.220 (.080 (.15) .257-.800 (. Cadmium is absorbed via inhalation and ingestion.519) .839 (.393-.886) .195-.545 (.960) 1. and various seeds.880) .500) . see Data Analysis section) for Survey years 99-00.507) .980) .450 (. an inducible metal binding protein.13) .17) .202 (.596) .13-1. 2004a.313) .990) .279 (.481) .855-1.580) .17 (.219 (.38) 1.243-.48 (1. Diamond et al.17 (.207-.445 (.470-.520-.136) .551) .326) .289-.589 (.220-.260-.07-1.273 (.206) .** Survey Geometric mean (95% conf.550 (..

143) .148 (.159 (. 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.094) .197-.123-.438) 90th .173 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .304-.783) .830-1.491-.833-1.232) ..412 (.210) .183) .158-.536 (.063-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .208-.830) .10) 1.085-.767) .166 (.856) .490 (.757) ..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 .470) .157-.170-.335 (.210 (.173-.207-.303) .218) .189-.086 (.382) .340) .927-1. 2004).131-.147-. Olsson et al.161-.191 (..198) .241) .826-1.479 (.404 (. 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.200 (.308 (.06 (.08) .382-.191-.850) .085 (..091) .909-1.247-.00 (.311) .176 (.729 (.329 (.414 (.434 (.067-.07 (.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.051-.261-.391-.700) .171-.194-.181-.783 (.686 (.865 (.096) .293-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.289) .338 (.818) .236-. 2003.078-.135) .268 (.216-.757 (.224 (.418) .418-.917 (. Staessen et al. 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.162 (.343-.300-.240) .210 (.209) .667) .647-.446) .727-.693 (.182) .107) .280 (.184) .211 (.826-1.206-.278) .266) .175-.691-.423-.941 (.113-.126 (.106) .207) . 2002.247-.112) .828) .140-.075 (<LOD-. However.288-. Horiguchi et al.281) .813-.423 (.163 (.541) .143-.163) .136-. 2000.090 (..350) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.998) .318 (.157-.263 (.146-.795) 1.253 (.856 (. Jarup et al.267 (.545) .484 (.444-.09 (.140-.093 (.674-1.263-.228-.325 (. 2002.700 (.784) .091 (.719 (. 2004b).101) .225) .130-.551) .192) .185) .221-.591 (.156 (.473 (.187) .929) .678 (.225) .650-.336-.631) .387 (.084-.438-.075-.321) .414-.196 (.266-..168-.223) .940 (.289) .297) .740 (.288) .767 (.487 (.077-.12) 1.250) .449) . During the 1950’s and 1960’s.769 (.190 (.229) .387-.653) .292) .876-1.331 (.398-.204-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.440) .184-.174-.091 (.537-.663 (.282 (.273 (.308) .185 (.170 (.267 (.253) .156) .181) .219 (.607) .725-1.187-.084 (.111-.238) .754) .716) .208 (.235) .917) .219 (.083-.255-.191) .261 (.316 (.261) .071 (.16) .562-.144-.940-1.690 (. 1999).175 (.476) .209) Selected percentiles ( 95% confidence interval) Sample 95th ..242) .199 (.690-.806-1.252 (.122 (.222-.296 (.150-.270 (..687 (. 1999).614) .789 (.441-..440) .202 (. 1996.183 (.181 (.143-.950) .500-.792 (.316) .421 (.256-. can result from high dose chronic exposure. most often a result of occupational exposure (Roels et al.432 (.240) .136-. 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.381-.** Survey Geometric mean (95% conf.712 (.123-.097) .708-1.215 (.470) .17) .874-1.233 (.239-.02 (.531 (.176 (.220 (.154-.472) .074-.617 (.05) 1.979 (.212 (.190 (.304) .533) .827) .182) .104) .696-.274) 1. Noonan et al.283 (.839) .154 (.873 (.507-.687-.137 (.666-.630-.178-.156-.288 (.364) .234-.431) .559-.182) .245 (.433-.159 (.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 .07) .147 (.404) .352) .00 (. 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.234 (.098) .538) .184-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .168 (.716-. population from the National Health and Nutrition Examination Survey.104) .690-. interval) .232) .227-.078 (.199-.377-.688-. 1999).560-.906) .884) .678-.668-.645-.221 (.205 (..931 (.501 (.516-. 2002.722-.147-.919 (.S.818) . At lower environmental exposures.226) 75th .178) .622 (.802 (.281) .238-.247-.100 (.481 (.175 (.962) .718 (.177) .518) .234) .137-.779 (.985 (.168-.13) .38) .850) .16) 1. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.201-.181 (.415) .426-.813-1.388-.

. 2005. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. Staessen et al. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. maternal blood or maternal urine and birth weight (Nishijo et al. Olsson et al. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. 2003.... 2000...46 mg/gram of creatinine) (Ezaki et al. Acute and heavy exposure to airborne dusts and fumes. 2004. as may occur from welding cadmium-alloyed metals.. 2002. 2003. 2002).. 2003. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Mannino et al.. 2002). potentially fatal pneumonitis (Fernandez et al.gov/ toxpro2. 2003). 2004. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine).26 and 3. 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. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. 2002). 1999). Both IARC and NTP consider cadmium a human carcinogen. 2002. 2000. However. Jarup et al. data (CDC. Jin et al. Ezaki et al. has resulted in severe.S.. 2004. with peak values observed in the fifth to sixth decades (CDC. 2006). not to imply a safety level for general population exposure. 1999). respectively. In the typical environmental exposure.... 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.. approached these values associated with subclinical changes in renal function and bone mineral density. Becker et al.. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. 2003. 1999. Olsson et al.. Cadmium can produce lung. 2002.. Creatinine-corrected urine cadmium values in U. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity.html. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.e. 2006. 2005). 2005. In postmenopausal women..cdc.. 2002). Staessen et al. 2004b). 2005. 2002. EPA.. 1996).S. and drinking water and environmental standards have been established by U.. Suwazono et al. environmental levels) and health effects is available from ATSDR at: http://www. 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. Wennberg et al.. 2004... Staessen et al. Friedman et al. Noonan et al... Salpietro et al.. Ezaki et al.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. Occupational standards are provided here for comparison only. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.atsdr. Becker et al. Olsson et al.. CDC. 2004b. 2002) and length at birth (Nishijo et al. 1988).. 2004). Women had higher blood and urine cadmium levels compared to men of similar ages. intermediate in former smokers and lower in never-smokers (Becker et al.. 2006). 2006.... 2002. 2002... Jarup et al.S. Wennberg et al. 2000).. Horiguchi et al. Animal studies have demonstrated reproductive and teratogenic effects. Information about external exposure (i. 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. In adults aged 60 years and older. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. Wilhelm et al. Komaromy-Hiller et al... Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al... For NHANES 19992000. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.1 mg/L (Alfven et al. 1996. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. 2005. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. 2003.. 2002). respectively. Further research is needed to address the public health consequences of such exposure in the United States. Zhang et al. 2003. Becker et al. 2000. Moriguchi et al. Horiguchi et al.

110:699-702. Alfven T. Environ Res 2006. Howerton K. Taylor AJ.148(1-2):11-20. Dekio F. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Elinder CG.46:372-374. Akesson A. Oguma E. Lepom P. Int Arch Occup Environ Health 2003.95:20–31. Comparison of representative ranges based on U. Buchet JP. Environ Health Perspect 1994. Hellstrom L. 206:15-24. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Furuki K. Ikeda Y. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. environmental. Kumagai N. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Consonni D. Ikeda Y. Bo M. Lancet 1988. Lauwerys R.html. Fernandez MA. Neurotoxicology 2003.45:43-52. J Toxicol Environ Health 2003. Davison AG. 4/8/09 Alfven T. Fukui Y. Moriguchi J. Seiwert M. 102:10581066. Mascagni P.59:194-8. et al. Comprehensive study of the effects of age. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Sanz P. Thorax 2004. Schulz C. Becker K. Bregante G. Tsukahara T. Occup Environ Med 2000. Jarup L. Grubb A. Chislovska NV. Becker K. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Olfactory function in workers exposed to moderate airborne cadmium levels.atsdr. Lison D. Chiappino G. Horiguchi H.24:717-724. Environ Health Perspect 2002. Ye T. Lundh T.96:353-359.13(11):1627-1631. Sasaki S. Lidfeldt J. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Mucha A. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Ezaki T. Pickering CA. Vahter M.296(1-2):71-90. Wang H. Available at URL: http://www. diabetes mellitus. Furuki K. Diamond GL. Palomar M. et al.gov/toxprofiles/tp5. Kaus S. Toxicol Lett 2004. References Akesson A. Jin T. Seiwert M. Centers for Disease Control and Prevention (CDC). Berglund M. Nordberg G. Machida M. Bellerup P. ShkiryakNizhnyk AZ. 1999 [online]. Friedman LS.102:83-89. Sasaki S. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Holguin F. Seifert B. Kaus S. Choudhury H. et al. Greves HM. possibly better than b2microglobulin. et al. Environ Res 2004. Thayer WC. 196:114-123.66(Pt A):2141-2164. Anthropometric. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Hotz P. Nermell B.cdc. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Gadea E.000 women in the Japanese general population: a nationwide large-scale survey. Moriguchi J. Ash KO.57:668-672. Horiguchi H. Bernard A. Miyamoto K. Fayers PM. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Costa R.1(8587):663-667. Cadmium fume inhalation and emphysema. Fukui Y. et al. et al. Mannino DM. Persson B. Uemura T. Lukyanova EM. Agency for Toxic Substances and Disease Registry (ATSDR). Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Vahter M. Lancet 1999. Zhu G. Environ Res 2004b. Krause C. Savage-Brown A. et al. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2002. Toxicological profile for cadmium update. Atlanta (GA).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. Darbyshire J. Jones RL. Occup Med 1996. Toxicol Appl Pharmacol 2004a. et al.59:497]. Okamoto S. Fatal chemical pneumonitis due to cadmium fumes. Jarup L. Clin Chim Acta 2000. Ukai H. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Nomiyama T.S. Takebayashi T. Oguma E.76:186-196. Miyamoto K. Nerbrand C.S. Venables KM. Stock AL. population. et al. Kikuchi Y. Serra J. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Environ Health Perspect 2005. Carlsson MD. Komaromy-Hiller G. et al. Tsukahara T. iron deficiency.205:297-308. Machida M. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Int J Hyg Environ Health 2003. J Occup Health 2003. Kundiev YT. 2005.354:1508– 1513. Schulz C. patient population and literature reference intervals for urinary trace elements. Ezaki T. Toffoletto F.

Roels HA. Cadmium carcinogenesis. J Environ Sci Health B 2004. iron status. lead. Lybarger JA. Lison D. and mercury in the population of northern Sweden. EPA). Merlino MV.Metals Nishijo M. Jansson J-H. eds.100:330-338. Sarasua SM.S.110:1185-1190. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. and former smoking – association of renal effects. Gangemi S. et al. Environ Res 2006. Nogawa K. Tanebe K. Environmental exposure to cadmium. 151-168. Wilhelm M.30(5):395-399.59:394-397. Fan YG. et al.59(1):22-25. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Minciullo PL. Vangronsveld J.21(3-4):251-262. Nordberg M. Toyama. Kuznetsova T. Emelianov D.209:301305. Schultz C. Stegmayr B. Saito S. Relationship between newborn size and mother’s blood cadmium levels. Nakagawa H. Gallmans G. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Bensryd I. Olsson IM. forearm bone density. Ren Fail 1999. Nakagawa H. et al. Lauwerys R. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Occup Environ Med 2002. United States Environmental Protection Agency (U. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Zhu HD.353:1140-1144.html. cadmium. Environ Res 2000. Environ Health Perspect 2002. Okubo Y. New York: Plenum Press. and risk of fractures: prospective population study. pp.110:151-155. Honda R. Japan. Friberg L. 4/8/09 Waalkes MP. age. 2004. Revised and new reference values for arsenic. J Cardiovasc Risk 1996. created 1992. Revised 2000 [online]. Tawara K. J Perinat Med 2002. dietary intake. lead. Salpietro CD. Mutat Res 2003. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Usefulness of biomarkers of exposure to inorganic mercury. Skerfving S. Kido T. Wang JX. Kathman SJ. Time trends in burdens of cadmium. et al. Suwazono Y. Schwenk M. Nishijo M. Nordberg GF. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Zhao YC. Noonan CW. Available at URL: www. Thijs L. Cadmium compounds. Stelitano A. Cadmium in blood and urine – impact of sex. Tanebe K. Int J Hyg Environ Health 2006. Staessen JA. Staessen J. 2001. Kobayashi E. Honda R.gov/ttn/atw/ hlthef/cadmium. Nakagawa H. lead. Zhang YL. Roels HA. Lijnen P. Oskarsson A. Campagna D.84 (Section A):4455. Environ Health Perspect 2002. Lancet 1999.epa. Bergdahl IA. Hazard Summary. Wennberg M. Liu QF. 2000. Mueller PW. Ginucchio G. Lundh T. In: Clarkson TW.533(12):107-120. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Nordberg GF. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Bruiglia S. et al. Hoet P. Ottosson H. Lundh T. Buchet JP.39:2507-2515. Sager PR. Roels H. Arch Environ Health. Biological monitoring of cadmium. et al. Biological monitoring of toxic metals.3:26-41.

10 (8.01) 7.70 (6.82) 5.26-11.87-7.1-12.9 (11.0) 11. and cardiac arrhythmia (ATSDR.90) 5.8 (11.9) 12.83-4.54-11.89) 4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.90-12.87 (4.09) 5. 0.20-5.22 (4.38) 5.12-5.4) 10.9 (11.16-6.45-5.71-5.14. population from the National Health and Nutrition Examination Survey.2-13.7 (8.80-10.12) 5.49) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80) 7. and 03-04 are 0.73-5. 01-02.71-8.80 (4.26) 4.33-5.60) 7.1 (10. the body half-life is estimated to be 70-109 days based on 137Cs exposures.55 (4.8-13.47-8.80-11.20) 5.55-11.4 (9.3 (8.50 (4.8) 11.3-13.60-6.01-8.09-5.86 (7.64) 4.50) 5.30-10.6 (9. and clay.3-15.39) 7.56) 5. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.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 4.20) 4.80-6.68) 9. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.05-5.4) 12.32-5.6 (11. scintillation counters.54) 4.42) 6.4) 12.1) 11.35 (4.5) 9.10 (6.3) 9.80-10.96 (6.99) 7.27) 4.59-5.1) 9.08) 7. photographic emulsions.62 (5.Metals Cesium CAS No.60) 7.1 (9.70) 5.63 (4.7) 11. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.70) 7.6 (9.90) 7.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4. However.71 (8.82-4.40-5.4 (10.0) 10.99-11.50 (4.2.20-8.84) 5.77 (9.67 (4.7 (9.90) 4.5 (10. Whether cesium compounds are carcinogenic is unknown.2-13.21) 90th 9.86-12.91-8.80-10.99) 9.08-5.94 (4.6 (9.6) 11.03 (4.53 (6.50 (7.02 (4.20-7.7-14.50-7.5 (8. although cesium was generally of low toxicity when given to animals.87 (4. For absorbed cesium salts.9 (11.17) 4.8) 9.42) 7.52) 7.61-6.9 (10.1) 10.0) 9.60 (8.63) 6.94-4.7 (10.10-8.3) 12.72) 4.40-5.50 (6. Fourth National Report on Human Exposure to Environmental Chemicals 205 .40-7.2-13.5-16.90 (6.59) 7.7 (10.45-8.64 (4.70-8.90-10.70 (6.43 (5.1) 11.7 (11.80 (8.0-13.0) 12.20 (6.4 (9.60-7.21 (4.63-4.7) 10.14 (4.30) 5.29) 4. Most human exposure to cesium occurs through the diet.31-8.5-14.9) 11.89-5.74 (4.95) 5. Little is known about the health effects of this metal.3-13.84-9.8 (10.3 (8.8) 9.34) 9.20 (4.53-11. diarrhea.34 (4.99-6.40-11.1-12.69-6.71 (4.35 (4.29 (4.27 (7.1 (11.64-5.2 (9.74) Selected percentiles ( 95% confidence interval) 50th 4.05) 5.60-12.57-5.30 (6.0) 12. 2004).36 (6.13 (7.72-7.90 (4.2 (9.10-7.12-11.60-7.98 (7.70 (9.10 (8.81) 4.4-13.3) 10.44 (8.81 (4.74-5.4) 95th 11.50) 9.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00-8.2-14.56-11.81) 4. Radioactive 137Cs has been used medically to treat cancer.33 (5.40) 5.55 (7.36) 3.84 (4.80 (4.80 (8.94 (4.5-13.6 (11.95 (3.7) 11.68 (7.00) 4.25 (3.40-11.71) 4.24) 4.40-5.42-7.88 (8.0-15.87 (4.2) 11.13 (8.1-13.33 (6. soil.8) 11.15-8.0 (9.0) 11.23-4.08 (6.2) 12.1) 9.4) 9.60 (7.32) 4.66 (7.97 (7.13-8.95-4.90-8.81-14.17-6.23) 9.37) 5. and as polymerization catalysts. nausea.71-9.83) 6.77 (4. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.80 (8.52-9.00) 6.30) 7.00-4.8 (10.10-9.62) 4.73-11. interval) 4.14.08-5.84-5.76-6.87) 5.90-12.27-5.30 (6.89) 5.5) 12.8) 12.64) 5.7 (9.04) 7.9) 8.49 (4.00-10.40) 5. and 0. and high-power gas-ion devices.79 (4.98 (7.8) 12.40-5.9 (10.8) 12.20) 8.50 (4.40) 7.00 (7.64-10.10 (6.40 (4.05-5. cesium hydroxide is corrosive and irritating at high concentrations.07) 4.3) 10.6 (9.49) 75th 7.59 (5.70 (4.00) 7.5-14.49 (5.26) 7.90) 9.37) 7.90-10.30-5.70-5.90) 5.7 (9.92-13.9) Total 4.3) 10.47-4.12 (4.46) 7.56 (4.86-11.05) 5.0 (10.39-4.77-8.97-7.25) 4.01-6.56 (4.60-6.03-4.59-5.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.4) 10.61) 7. infrared lamps.32 (3.6) 10.03 (4.70 (8.81) 9.3) 10. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.35-5.94) 4.60-5.07-11.99-11.22-4.17 (6.08 (7.7) 10.97) 4.7 (10.13 (5.93 (4.80-13.5) 10.64) 5.9 (11.20) 7.84) 8. respectively.26 (3.77 (9.S.91 (7.4) 11.62 (5.59-5.10-5.60) 5.43-8. see Data Analysis section) for Survey years 99-00.36 (3.25-5.00-8.00-9.70 (5.20-4.2-12.04 (4.80 (4. semiconductors.16-6.0) 12.90-10.70) 5.70 (8.

17) 9.18-6.89-4.04-5.17-4.60) 3.85) 5.20-4.54 (5.51 (7.3 (9.43 (4.30 (7.98) 5.35 (3.01-8.7) 10.78 (3.43 (3.07 (5.56-10.24-4.88-10.38-7.31 (4.30) 10.51) 4.79) 4.0) Total 4.66 (5.88-4.83-7.40) 6.74 (4.94 (5.97) 8.27 (8.34 (5.15 (7.61 (7.74) 3.06 (5.58) 3.43-11.95) 10.9 (10.96-4.08 (6.27 (6.48) 90th 7.98 (7.53 (6.95) 4.29) 4.50 (5.03-6.22) 6.53 (4.74-11.68) 6.21-3.23 (7.58) 8.09 (4.30-4.71 (7. Using clinically submitted specimens.64) 9.14) 4.33-8.19-6.71) 6.64) 4.06 (3.55 (3.44-9.29-3.97-4.58 (4.51 (3.00-9.41-7.63 (7. Komaromy-Hiller et al.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.22 (3.78) 4.77 (6.18) 8.07) 8.79-5.47) 6.75 (7.65-4.63) 6.06) 4.20-4.05) 3.40) 7.91) 4.16-8.27-6.91-9.84-7. and were also roughly similar to those in this Report.56) 3.4) 10.75-11.96 (4.64 (4.60 (3.81 (4. population from the National Health and Nutrition Examination Survey.86 (4.84-7.13 (3.S.25) Selected percentiles ( 95% confidence interval) 50th 4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.96) 4.83-6.33-3.03) 5.20) 5.05-4.28) 8.35-7.43-6.03) 6.38 (3.37) 4.90 (7..92) 3.8 (9.0 (7.63 (6.08 (3.47) 4.3 (8.50 (7.74 (5.1) 11.21-4.7-12.04-11.38-12.50 (6.61-3.84-9.12 (3.16-5.42 (5.27) 4.95) 8.36-10.04) 5.76-6.77-5.70) 7.18-7.70) 6.79) 9.20-8.26 (3.96) 4.36-6.79 (5.63-6.45 (4.00 (8.60-20.64) 5.30-4.41 (8.03-5.09) 4.41) 9.05-3.80) 6.12) 3.S.16) 5.62-8. 2004).91) 5.93-9.50-5.29) 5.10 (3.56 (4.28 (4.67) 5.33 (5.29-3.67 (5.76-9.13-9.87-4.77 (7.35) 3.46) 6.72 (4.55-5.04) 6.91 (5.95 (5.11 (5.50) 4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.17 (6.30 (3.91 (5.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .8) 6.37-3.18 (7.28 (5.7) 10.24 (3.20-4.3-15.31-4.46 (8.66 (6.08) 3.85) 4.92 (5.53) 6.96-4. Minoia et al.65 (6.06) 5.14-7.91) 5.72) 4.91-6.83) 8. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.10 (5.39) 8.59-8.00-8.38) 10.90-3.97-5.5) 9.51 (3.14 (6.54 (3.43 (4.46-4.08 (5.19-3.33 (5.07-4.14-4.49) 3.70 (7.00-4.24-10.87 (5.27 (6.93-7.27-4.13) 7. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.21 (2.47) 6.47 (7.02 (5.00-5.08) 4.2 (8.99 (3.9 (9.67 (6.11 (5.26-6.90-8. Two small studies of European populations reported urinary cesium levels similar to U.40-5. 1990).44 (8.42-4.74) 75th 5.8) 10.16-8.08) 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.08-7.56) 4.84-9.26 (4.28) 7.6 (9.68) 4.62) 5.48-6.42-6.95-6.82) 7.39) 5.2) 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 3.72-5.51 (4.81 (4.15-4.68) 3.39 (5.30 (4.13-9.29) 4.36-3.6 (9..05) 6.10 (3.44) 3.52-5.78 (3.17) 4.77) 4..22-11.91-7.42-4.82-4.99-4.64 (8.98 (6.45-6.66-6.31-6.S.25) 4.95-12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.99) 4.73 (3.0) 7.8) 5.02-4.68 (4.63-6.59) 4.58 (6.98) 5.07) 8.54 (4.48) 7.09) 8.3) 9.38 (3.35 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.41 (4.41-4.3) 11. population.10) 7. population results shown in this Report (Alimonti et al.90-8.43) 8.56) 4.64-6.14) 4.00) 6.08-3.95 (3.53) 3.55) 4.60 (5.10-4.46-8.21-5.05 (4.84-11.41 (5. (2000) found urinary cesium levels that were slightly lower than those reported for the U.51 (4.57) 3.35-11.46 (7.12-6.54 (4. 2005.58-5.44-5.3 (10.73-4.47 (4.05-3.66 (5.99-9.47) 7.44 (4.2 (8.75 (6.9) 10.15) 95th 8.65-3.30) 10.41) 4.77 (4.00-10.94) 7.14-6.87) 5.99-9.2) 11.60-10.5) 7.50) 4.50) 8.42 (4.85-4.50) 4.43 (8. interval) 4.63 (4.00-5.78) 4.5 (9.15-11.6) 6.79) 6.68-11.31 (4.5) 9.

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

16 (1.28 (1. and 0.900) .750 (.13) 1. hard metal (alloys of cobalt and tungsten carbide).370) .270-.960-1.369 (.450) .490-.750 (.390 (.05 (.68 (1.16 (.305-.291-.850) .21) 1.930) . Usual human exposure is from food sources. diamond-polishing wheels.08) .880-1.890) .320 (.450) .64) 1.380-.03) .487) .390-.364-.810-.350-.430) .830-1.33-1.515 (.08-1. It is also a component of porcelain enamel applied to steel bathroom fixtures.520) .380 (.17 (1.431) .690-.388-.930-1.600) .410-.900) .81) 1.340-.338-.530-.390 (.32 (1.26-2.09 (.81) 1.920) 1.360-.570) .350) 75th .610 (.313) .47) 1.373-.710) 1.03) 1.259-.398) .15-1.700) .950 (.434 (.03) 1. 01-02.04-1.620-.890) 95th 1.07-1.99) 1.870 (.48) 1.416) .46 (1.450-.371 (. and fertilizers.45 (1. and soil. 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.16) 1.330-.452 (.340 (.550 (.560 (.790-.870 (.680 (.760 (.600 (.520 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.29 (1.660) .333-.399) .820 (.05) 1.23) . shiny.650 (.359 (.410 (. seawater.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.419) Selected percentiles ( 95% confidence interval) 50th .09) . population from the National Health and Nutrition Examination Survey.465) .07.28-2.940-1.570-.370-.67) 1.520-.374 (.418 (.350-.319) .398 (.390 (.333-.890-1.930 (.740-.480 (.590) .790 (.520-.820 (.350 (.428-.17 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals . Cobalt is used as a drying agent in paints.860 (.05 (.520 (.640) .400-.32) 1.04) 1.386) .02-1.S.570-.340) .540-. Cobalt compounds are also used in manufacturing battery electrodes.520 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.01-2.47) 1.37-1.499 (.379 (.380 (. automobile airbags.424) . see Data Analysis section) for Survey years 99-00.377-.950 (.850-1.S.431) .00) .340-.33 (1.750 (.26) Total .47 (1.290-.427-.680) .348-.900-1.380 (.24 (.410) .570) .940-1. respectively.367 (.410 (.26-1.50) 1.750-.620-.24 (1.435 (.900-1.950-1.710 (.530) .461 (.500 (.470) .310-.16) 1.420 (.420) .04 (.22) 1.610) .410-.06 (.410 (.53) 1.800-.352 (.373) .496) .840) .Metals Cobalt CAS No.04-1.670 (.44) 1.890-1.880 (.469-.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 . It is emitted into the environment from burning coal and oil and car and truck exhaust.12) 1.372) .450) .405-.950) .502) .393-.660-.47 (1.370-.59 (1.39) 1. and in synthesizing polyester and other materials.630 (.900) .581) .850) 1.770) .670 (.564) .350-.23-2. Cobalt occurs naturally in airborne dust.48) 1.390) .540-.370 (.520) .410 (.680) . 0.520 (.360-.580 (. and kitchenware.300-.950-1.92) 1.28 (1.75 (1.07-1.800) .07 (.610) .640) .650 (.26) 1.440-.32-2.09 (.460-.550-.550) 90th .540-. industry is imported or obtained by recycling scrap metal that contains cobalt.07.327-.375 (.450) .670-.330) .25-1.460 (.22-1.20 (1.16-1.523) .650-.543) .360-.380-.460 (.01 (.430 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.03-1.01 (.420) . and inks.316-.285 (.16-1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.04-1.463-.790) . hard metal or in combination with other elements.740-.17-1.56) 1.580 (.820 (.15 (1.520-.03 (.430 (.414) .570 (.800-.270-.600-.710) .940 (.308-.590-.06 (.740 (.06-1.355-.730) 1.16 (1.690-. and magnetic recording media.08.690 (.330 (.14-1.370-.590 (.336-.17 (1.519 (.42) 1. interval) .340) .343 (.640) .60 (1.379 (.810) . and 03-04 are 0.980-1. Cobalt compounds are used as catalysts in producing oil and gas.620) .460) .460) .540-. large appliances.410 (.620-.430 (.700) .316 (.850-1.03 (.810) .510) 1.36) 1.300 (.580 (.301 (.280-.32) 1. The cobalt used in U.410-.590-.920-1.480 (. blue-colored pigments.680 (.19) .32 (1.890-1.22 (1.331-.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 .870-1.450-.394) . varnishes.630-.430-.670-.630 (.460) .530 (.670 (.334) .410) .540) 1.65) 1.310 (.348-.470 (.660) .73) 1. steel-belted radial tires.12) 1.583) .52 (1.760) .404) .339 (.454 (.28 (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 .50 (1.500) .490-.910-1.14) .520-.01-1.294 (.270-.610-.480-.980) .430) .417) .

844 (.361-.561) .12 (.275-.513-.319-.804) 1.534 (.435 (.433) .738 (.393-.733-1.15) 1.344-.278 (.25 (.362-.513) . 2003).938) .60) 1.829-1. interval) .861-1.669) .279) .960 (.268 (.10-1.326-.313-.461) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.33) .781) 95th 1.434-.595) .421) .750-..467-.368 (. 1972).388 (.391) Selected percentiles ( 95% confidence interval) 50th .408 (.301) .630-.975 (.50 (1.27) 1.362 (.282 (.963-1.259 (.36) 1.349) .324-.35) 1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.317 (.09) 1.879-1.522) .740-1.599) .662) .756 (.331-.667-1.83) 1. cobalt is excreted predominantly in the urine.55) .487-.757-1.611) .278-.12-1.585) .234 (.402 (.630-.378-.372) .400 (.581) .361-.29 (1.281) . and to a lesser extent.842) .753-.. Cobalt is absorbed by oral and pulmonary routes.660-.691 (.563-.990) .533 (.594) .346 (.33) 1.361 (.358 (.529 (.468) .515 (.27) 1.327-..606 (.02 (.14 (.280-.593) .248-.247 (.689 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.29 (1.543) .215-.00) .387) .333-.829) .10 (.313-.36) 1.723 (.298 (.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 .297-.275-.339-.547 (.537 (.04 (.291 (.313 (.00 (.703-.381) .30 (1. population from the National Health and Nutrition Examination Survey.932-1.857-1.361 (.505) .328 (. A portion of cobalt retained for long periods is concentrated in the liver.15 (.673-.396) . 1979).598 (.542 (.786-.49) 1.736-.983) .439) .251-.391 (.17) .303-.333-.290 (.850 (.495 (.760-1.382-.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 .28) 1.302-.316 (.644 (.378 (.861 (.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 .475 (. 1972).392 (.963) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.360) ..384) .329 (.S.562) .417 (.425-.73) 1.429) 1.781-1.310) .750) .352 (.50) 1.259-.368) . Exposure in the workplace may come from electroplating. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.600-.409) .337) . or using diamond-polishing wheels that contain cobalt metal. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).376 (.792 (.632-.388 (.301-.272-.273 (. 1994). 1994.404-.838 (.304-.647) .744) 1.419) .534-.737 (.300) .683-.314 (.274-. Smith et al.963) .271 (.237-..353 (.257-.851 (.560-.462) .435-.396) .824 (.777-.25 (.365) .313-.488) .428-.333-.471 (.353-.785) .704-.328 (.826-1.728 (.952 (.727 (.554 (.29 (1.905) .334) .426 (.00 (.00 (.11-1.591 (.16 (.16 (1.562) .289) .304) .425) .394) .455 (.Metals fabricated from cobalt alloys (Lhotka et al.355) .35) .50) 1. an essential human nutrient.239-.983-1.243-.728) .821-3. respectively.469-.407 (.328) .29) .753) 1.16) .457 (.19) .955) .57) 1.694) .481) 90th ..898 (.282-.323) .449) .11-1.508-.833-1.830 (.248-.279 (.313-.380-.500 (.872 (.333 (.365-.917) .608 (.457) .487-.638-1.297) .700 (.500-.635 (.503-.16 (.990-1.60) 1.471-.976 (. refining or processing alloys.393 (.256-.03-1.900-1.250) .309) .327 (.343 (.609) .54) 1.938-1.444 (.296-.10) Total .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 .963-1.324) .476-.471-.640) .293 (.00 (.634-.06 (.335 (.438) .257 (.29) 1.378-.949) .457-.582-.378-.821 (.44 (.615) . using hard metal cutting tools.286) .513 (.294-.342-.00) .850-1.847) .554 (.895-1.352) .259) .848 (.362) .552 (.479) .616-.449-.479-.574-.550-.626-.937 (.290 (.352 (.296) .523 (.03 (.277-.337 (.00-1.708) . in the feces.895-1.738 (.452-.792-1.290 (.24) .667-1.774 (. Once absorbed and distributed in the body.929) .386 (.368) .313-.707) .329-.548 (.363) .955) .306 (.417) . with pulmonary clearance half-lives of from one to two years (Hedge et al.407) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.964 (.679-.348) .10) .523 (.700 (.04-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.369 (.442-.911-1.463-. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.343-.500-.23 (1.611) .306) 75th .

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

Mosconi G. Dunstan E. Schramel P.22:359367. Hoet P. Vitali MT. Respiratory health of cobalt production workers. Lison D. Moulin JJ. Weber A. Zobelein P. Gross RT. Pradhan C.87(5):628-631. Sabbioni E. and hard metal dust. Stanescu D. 1985. Radulescu M. Sanghrajka AP. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. J Trace Elem Med Biol 2006. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Iavicoli I.Metals effects of cobalt. MacDonald SJ. Romazini S. Linnainmaa M.” Contact Dermatitis 2001. Angerer J. Shirakawa T. HoffmannB. X. et al. Zweymuller K. Lison D. Szekeres T. McCalden RW. Kraus T. Oksa P.69(3):193-200. Hedge AG. Kuska Y. Clin Orthop Relat Res 2003. Salama A. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Lison D. Meier R. Cobalt and antimony: genotoxicity and carcinogenicity. DeSantis V. Wild P. Bozec C.150. salt. Sci Total Environ 1994. Meyer zum Buschenfelde K-H. Lhotka C.406:282-296. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Contact Dermatitis 2003. Linna A.36:732-734. Sabbioni E. Smith T. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Am J Ind Med 2003. Goto S. Salvatori S. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. et al. Lung cancer risk in hard-metal workers. Fujimura N. Kato M.157:117121. Ghat IS.204:147-160.21(2):189-195. The release of metals from metal-onmetal surface arthroplasty of the hip. White MA.533:135-152. Cresti R. Unwin P. McMinn DJ. Chest 1989. Christensen JM. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.20(1):25-31. Kristiansen J. 2001. Blunn G. Long-term clearance of inhaled 60Co. Sci Total Environ 1994. Mutat Res 2003. Edmonds CJ. Sabbioni E. a study of 13 elements in blood and urine of a United Kingdom population. Health Phys 1972.48:172-173. Int Arch Occup Environ Health 1997. Leghissa P. J Bone Joint Surg Br 2006. et al. Kiilunen M. Barnaby CF. Thomassen H. J Occup Med 1992. Occup Environ Med 2001. Kusaka Y. Robinson C. Epidemiological survey of workers exposed to cobalt oxides. et al. J Bone Joint Surg Br 2005.95:29-37. Arch Intern Med 1990. J Orthop Res 2003.150(1-3):167-171. Rorabeck CH. Boca Raton (FL): Lewis Publishers. Uitti J. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Dunning SP. 3rd ed. Roto P. Tilley S.44:124-132. Kriss JP. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Goldberg MA. Heki S. Am J Epidemiol 1998. Trace element reference values in tissues from inhabitants of the European Union. J Rheumatol 2001. Goto S. cobalt salts.58(10):631-634. et al.216:253-270. Science 1988. Occup Environ Med 1994. A report of two cases from mineral assay laboratories and a review of the literature. Zedda S. Bunn HF. De Boeck M. Pisati G. Steffan I. Co-sensitivity between cobalt and other transition metals. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Bourne RB. Occupationallyinduced “isolated cobalt sensitization. Thakker DM. Alessandrelli M.51(7):447450.242:1412-1415. Br J Ind Med 1993. Schaller KH. Swennen B. Outcome of occupational asthma due to cobalt hypersensitivity. Diepgen TL. Lauwerys R. Sci Total Environ 1998. Absorption and retention of cobalt in man by whole-body counting. et al. Zhuber K. Daniel J. Buchet JP.45:246-247. Falcone G. Schank M. and cobalt metals. Jarvis JQ. Iversen BS. Lisi P. Fourth National Report on Human Exposure to Environmental Chemicals 211 .150:177-183. Hoher T.50(9):835-842. Lauwerys R.28(5):1121-1128. Peltier A. Lauwerys RB. Bacis M. oxides. Laippala P. Hammon E.34:620-626. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Palmroos P.55(4):269-276. Cleland D. Sci Total Environ 1997. Lasfargues G. Thabe H. Chess DG. Int Arch Occup Environ Health. Health Phys 1979. Ziaee H. Weyher I. Ichikawa Y. Carnes WH. Dickel H. Cannon SR. Cobalt cardiomyopathy. Molders J.(1-3):133-139. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Kirsch-Volders M. Biological monitoring of workers exposed to cobalt metal.148:241-248. Swennen B. Buchet JP.88(4):443448.

942 (.40) 1.30 (2.90) 1.00) 4.Metals Lead CAS No.90) 2.80) 2.20 (3.51 (1. Lead has a variety of uses in manufacturing: storage batteries.60) 5.93-2.60 (1.49-1.20-3.00-5. plastics.66 (1.70) 3.30 (2.10) 1.09) 1.89) 1.60) 2.14-1.80 (1.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.946 (.20-1.60 (2.00-4.40-1.60-1.10 (2.10-8.70) 2.62-1.10) 3.70) 1.10-2.69 (1.25 (1.90) 2.20-6.20) 3.30 (2.90 (3.60 (2.45-1.30-1.80 (2.10-1.60) 4.60-4.50-3.39-1.80 (1.80 (2.40-4.60-2.00-1.65 (1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 0.75-1.40 (1.30-2.40-2.30 (1.70-2.60) 2.60-4.80) 2.3.00) 1.70) 4.80 (1.80) 1.04-1.30 (2.70 (3. population was aerosolized lead emitted from combustion engines that used leaded gasoline.80-4.899-.80) 1.50 (1. malleable.g.80-3.40-5.17) . such as lead phosphate and tetraethyl lead.40 (5.69) 1.60) 3.40-3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.70 (2.80) 1.40-2.00-6.80 (5. brass.70) 1.60) 5.80-3.40) 3.39) 1.02) 1.83 (1.55 (1.30-4.10-1.60) 4.60) 1.75 (1.22 (1.62 (1.10) 3.10-6. bronze).900 (.30) 5.68-1.90-3.60 (1.60) 3.80-3.70) 3.20) 4.80) 2.45 (1.80 (5.800-1.71-1.50 (3.70 (1. Lead was used in plumbing for centuries and may still be present.50-1.50 (2.10-2.20 (2.12-1.75) 1.50-5.50-1.10 (1.60) 2.69) 1.20 (4.S.60 (1.10) 1.10-3.52 (1.70) 4.10-3.90-4.50) 1.43-1.36-1.30) 2.10) 2. Since lead has been eliminated from gasoline. interval) 1.50) 1.60-1.87) 1.40 (4.60) 2.20) 3.70 (5.00) 2.50) 4.50) 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 (3.50 (1.40) 2.00 (5.90) 2.30 (2.40-6.50-2.19 (1.00) 3.90-2.20 (1.90) 1.90) 3. see Data Analysis section) for Survey years 99-00.60 (4.40) 1.37-1.30-2.20 (3.87 (1.50) 5.50 (2.70) 1.20 (1.90 (1.30-1.50 (2.S.50) 1. 01-02.20) .96-2.30) 1.50-2.40-1.20) 5.60) 1.90 (3.10-2.95) 1.32-1.878-1.40-1.50) 1.40 (1.10-2.80 (1.30 (1.80 (1.50) 5.90-4.00-1.43) 1.48) 1.90) 1.81) 1.72) Selected percentiles ( 95% confidence interval) 50th 1.60 (3.51) 1.53) 1.50-3.30-1.40-2.50 (1.60) 3.80-4.40 (1.10) 1.14-1. blue-gray metal that occurs naturally in soils and rocks.70-2.60 (1.40) Total 1.90-2.60) 1.20) 3.60-6.20) 90th 3. and 0.43) 1.50-1.40) 2.40) 4.20) 2.30-6.40) 5. Lead is most often mined from ores or recycled from scrap metal or batteries.90-6. metal alloys (e.20-3.00) 2.80 (1.60) 3.30 (4.75-2.50 (2.50-2.56 (1. and for radiation shielding.80) 1.80) 3.00 (1.10 (2.50) 3.30) 2. the main source of lead exposure for the general U.60 (2.55-1.70-5.37 (1.70 (3.80-4.20) 4.70-6.70) 4.28.40 (3.62) 1.40) 2.25) 1.70-1.60) 2.60 (3.80) 1.20 (3.30-2.50 (4.10) 3.00) .00) 6.91) 1.10-6.60 (2. solders.900-1.40) 2.77 (1.10) 2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .00 (4.20 (3.00 (3.30-1.40-1.30) 2.30 (2.70 (2.60 (2.00 (6.20 (3.10-4.80-2.00) 1.30 (2.20) 3.10-3.37 (1. antique-molded or cast ornaments.50-1.50-4. In the past.40-1.10 (4.60 (2.70 (2.90 (3.00) 1.00) 1.00) 5.40 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20) 1.70) 1.10-1.46 (1.30 (1.90 (4.90) 2. ammunition.70-1.90-2.01 (1.30) 95th 5.00) 1.40-1.60) 1.30-5.50) 4.36) 1.90 (2.30-1.80 (3.900 (.40) 1.50-1.60-2.20 (1.43 (1.00-4.20-2.00) 4. population from the National Health and Nutrition Examination Survey.50 (2.70 (1.60 (3.00 (1.90) 2.00 (4.20-3.90) 3.50) 2. Elemental lead can be combined with other elements to form inorganic and organic compounds.25 (1.90 (1.70-1.50 (3.30 (4.60) 4. ceramic glazes.10) 5.55-1.70-4.70 (1.90-2.50) 7.80) 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. dense.10 (1.30 (1.52-1.986) .80 (4.60-3.66) 1.60-1.30 (4.23 (1.10-3.20 (1.50 (1.30-2.00-4.50-4.00 (2.20 (2.40 (2.60) 4.34-1.60 (1.52-1.78 (1.70-3.20-4.14-1.80-3.70) 4.50-2.43 (1.60-1.50) 2.50-6.60 (1.90 (2.20 (1.80) 2.50-5.70) 1.31) 1.50) 75th 2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.60 (3.40-3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.80-5. 7439-92-1 General Information Elemental lead is a soft.10-4.36-1.70) 3.70-2.00) 2.70 (1. and 03-04 are 0.90) 5.32-1. leaded glass.30 (3.00) 3.10 (1.20-3.90-4.40-3.10 (2.10-2.00-2.20-2.90-4.90 (3.90 (3.10-2.10) 4. Before the 1980’s.3.00) 2. respectively.20 (3.20-1.80 (2.30-1.40-6.60) 1.50 (4.86) 1.60 (1.69 (1.20 (3.40 (1.80 (4.

40 (1.810-1.40) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.620 (.90 (2.30 (3.40-1.564 (.610 (.506-.70-2.40 (2.660) .828) Selected percentiles ( 95% confidence interval) 50th .70 (1.659 (.60-3. or water contaminated by mining or smelting operations.60 (1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .790 (.00 (1.800) . 1991).00-2.90) 2.11 (1.920 (.923 (.09) 1.90 (1.40 (1.90-4.20-1.75) 3.80) 2.40 (2.00 (2.86 (1.27) 1.558 (.600) .613) .30-1.10 (.700 (.00) .556-.30) 2.30) 2.900) .20) .20) 1.773) .20 (1.86-2.589-.17 (1.23) .20 (1.600 (.579-. and 0.13) .800 (.820-1.21 (2.00) 1.580-.80) 1.10) .20-1. and contact with soil.800) .64) 2.24-1.49 (1.82 (1.900-1.800 (.62) Total .80) 3.800 (.80) 1.800 (.20) .40 (1.10-5.857) .986) . older plumbing systems with leaded pipes or lead soldered connections.900-1.30) 1.695 (.700-.900) .535-.990) 2.90) 1.920 (.22) 1.674) 1. imported children’s trinkets and toys.680-. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.20 (1.20) .600-.10) 2.60-2.10-1. Approximately half of the absorbed lead may be incorporated into bone.70) 1.50 (2.680) 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 1.80-3.70) 2.625-.70 (2.10-1.10-3.00-1.20) .70 (2.700-1.818) . However.19 (1. bullet fragments retained in human tissue.32 (1.60 (2. or after soluble lead compounds are ingested.89) 2.00-2.931) .600-.500-.729-.625 (.80) 2.S.900) .72) 1.14-1. and 03-04 are 0.960-1.20) 1.30-5.66 (2.604 (.03-2.90-3.690) 75th 1.10 (1.900-1. 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.90-2.50-2.605) .86) 1.10-1.60-3.540-.90-2.20-1.688 (.50-2.20 (1.30-1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.40-3.671-.553-.766 (.691-.14 (1.40 (1.31-3.44-2.10-1.50 (2. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.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 1.80 (2.50) 3.620) 1.73 (1.30-1.04 (.641-.70) 3. In the blood.70) 1.833-1.600-.90) 2. 0.785) .710-1.50 (1.70-3. stained glass framing.00) .579-.40) 1. 01-02.661-.900 (.795 (. Lead is absorbed into the body after fine lead particulates or fumes are inhaled. respectively.30-1.50 (1.60-2.570-.30) .90 (2.710-.862) .50) 1.640-.30-3.40) 1.718) . 2007.700-.60-1.50) 1.78-2.40) 1.642 (.590 (. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.30) 1.30 (2.850 (.23-4.00-2.00 (1.59-2.13-3.745-.90) 2.29) 2.00-1.40) 2. interval) .10) 2.708-.955-1.10 (1.700 (.10-3.80) 2.800-1.50) 2.11) 2.40) 3.50-3.10 (. CDC. population from the National Health and Nutrition Examination Survey.30) 1.10) .700) .51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.540 (.616) .40-1.90-2.680-.637-. Fourth National Report on Human Exposure to Environmental Chemicals 213 .40-5.00 (1.600 (.1. lead-contaminated dust in indoor firing ranges.600) .90 (2.591 (.731 (.07-1.50) 2.595-.970-1.940 (.40-1.06) .80) 3.35 (.52 (1.480-.840 (.04-2.20-2.40) 1.66 (2.10 (1.700-. lead-containing folk remedies and cosmetics.800-.40-2.40-1.10-3.20 (2.62-4.900) .82 (2.78-2.70 (2.78-2.960-1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.560-.800-1.14 (1.02) 1.80) 2.900) .700) 1.800) .20 (3.33.20) 1.10-1.80-2.27 (1.738) .90 (1.30) 1.701) .808 (.651) .20 (2.91) 2.40) 1.60) 2. 2000).630 (.60 (1.04 (.910-.75) 4.822-1.800-.753 (.848 (.900-1.07 (.20 (2.700-.00) 2.40 (1.60 (1. lead-based painted surfaces undergoing renovation or demolition..40) 2.815 (.700 (.90-2.80) 1.80 (1.12) 90th 2.677 (.700 (.900 (.935) 1. pewter utensils and drinking vessels.628) 1.29 (2.20 (1.50) 1.59) 1.572-..80 (1.833 (.700 (. see Data Analysis section) for Survey years 99-00.526-.30 (1. battery and radiator manufacturing) and recreational sources.00) .749) .80-2.680) .960 (.800) .Metals occupational (e.50 (2.00 (.40 (2.80) 2.915-1.573 (.04) .650) 1.990) 1.730 (.04) 2.40 (2.10) 1.10 (.03 (1. dust.20-2.00) .600-.00 (1.70) 3.70 (2.86) 95th 2.1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.40) 2.20 (1.636 (.900) .600-.41) 2.00-1.00) 2.52-1.90 (1.33 (2.31 (1.18-1.60 (1.900 (.700-.757-.800) .50-1.97) 4.02 (.941) .70) 1.50-2.52-1.90-3.700 (.640 (.752 (.30-2.g.30) 2.30) 1.33-2.10 (1.

763) .375 (.62-2.92) 2.44 (1.758) .94-2.61) 1.17-1.96 (1.56-3.710) .03) .992-1.25-1.679-. seizures.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 . Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.86 (1.01 (.25-1.718) 1.38 (2.975-1.618 (.03 (.492-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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.725) .755 (.887 (.609 (.617-.89-2. Schwartz.997-1.05 (. 2003.37-1.753) .20-3.404 (.918-1.701) .75 (2.469 (. and nails (Leggett.Metals 90% of the body lead burden in most adults.702) .06 (.639) .46 (1.53) 1.66 (1.78 (2.731-.981-1.510-.667-.971 (.657) 1. For instance.812-1.639 (.85-2. 1993).655) .408-.11 (1.667-. zinc.97-18.31 (1.703) . Lead can cross the placenta and enter the developing fetal brain.05-1.28) 2.607-.75-2.654) .918 (.622 (.10) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites 214 Fourth National Report on Human Exposure to Environmental Chemicals . kidney injury.61) 1.677) .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 1.22-1.632 (.97) 1.693 (.882-1.652 (.658 (.900 (.963-1.61) 3.686) .962 (. with a half-life of years to decades.742) Selected percentiles ( 95% confidence interval) 50th .52 (1.43) 1.33) 2. O’Flaherty.707 (.55 (1.51) 1.61) 1.588-.698) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.601-.10) 1.15-2.853-1.87) 1..667) .14 (1.05-1.67-4.957-1.50) 1.S.569 (.508) .655) 75th 1.742) .19) 1.698) .50-2.38 (2.20) .53-1.88) 1.00 (.28) .623 (.496 (. Approximately 70% of lead excretion occurs via the urine.933-1.27 (1.781-1.838) .696 (.793-1.612-.03) 90th 1.679) 1.03 (.579-. 2004.47) 1.50-2.644) .62-3.33 (1.720 (.988 (.06) .31 (1.64 (1. and through binding to ion channels and regulatory proteins.938 (.635 (.18) 1.07) .720 (.03) 2.03) 1.26) Total .721 (.33-1.644 (.633 (.72-2.00 (1.841-1.18 (1.828) .460-.01) .708 (.676) . 1991.72-2.342-.98-2.898) .535) .18) 1.08-2.06 (1.66) 2.88) 2.41 (1.22-2.31) 1.734) .04) 2.08) .18) 2.09) 1.605-.22) 1. 1993.64-2.85) 1.541-.0) 3.608 (.603-.583-.79) 2.56) 3.58) 1. Nash et al.46 (2.72) .11-1.990 (.639 (.14) 1.15-2.07 (.00) .38 (2.559-.688) .11 (.64) 95th 2.722 (.09-1.63) 1. with lesser amounts eliminated via the feces.701 (.739) . CDC.938-1.71 (1.04-3. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.988-1.34-1.43-1.88 (1.65-2.682) .645-.800-.725) .78-4.51 (1.876-1.615 (.29 (1.11 (.870 (.55 (1.05 (1. and paralysis.765) .98) 2.587-.07-1.82) 1.623 (.69 (1.940 (.992-1.603-.683-.59-3.83 (2.670) 1.77) 2.718) .41) .606-.702) .43 (2..649 (.23 (1.709 (.22) .24 (1.594-.593 (. scant amounts are lost through sweat. and iron. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.746) .62-1. abdominal pain.56-2.432 (.17 (.12-1.648 (.62) 2.22) 1.33) 1.06) 1.11) 1. The skeleton acts as a storage depot.893) .88-2.09-1. encephalopathy.09-1.796-1.08) .20) .10 (.436) .44 (1.19-5.79 (1.638 (. 1995.97) 1.677 (.774 (. 2007).10 (1.03 (1.94 (1.671 (.828-1.40-1. In 1991.428) .44) 1.11 (1.673) .639 (. Large amounts of lead in the body can cause anemia.43) 2.43 (1.63) 4.621 (.85-2.98 (1.790) .383-.404 (. 1996).551-. BLLs and associated toxic effects differ in children and adults.02) 1.36-2. 1995).26) 2.74 (1.49 (1. The toxic effects of lead result from its interference with the physiologic actions of calcium.66 (1.15-3.700-.810 (. Staessen et al.681-.461) .641 (.722 (.914-1.79) 1.31 (2.594-.15) 1.571-.592-.85 (1.712 (.615 (.39-1.677-.88) 2.02-1.03-2.588-.914 (.529-. through the inhibition of certain enzymes. population from the National Health and Nutrition Examination Survey.03) .702-.668-.604-.15) 1.561-.917-1.68 (1.655-.18) .862-. interval) .97 (1.47 (2.47 (1.03) 1.45 (1.50-1.64) 2.35) 2.380-.31) 1.03) 2.50-2.645-.. based on prospective population studies.70 (1.400) .89-5.83) 1.851) .625 (.00 (1.571-.56 (1.52) 1.926 (.608-.586-.03 (.41-1.65 (1.933) .979 (.48 (1.730) 1.404-. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.603 (.37-1.73) 2.681-.61) 1.28-1.00 (1. hair.50 (1.73-2.11) .659-.920-1.914 (.977) 1.946-1.20) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .71-2.

gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. Pirkle et al. 1984.2 µg/dL in males and 3. 1999). NTP considers lead and its compounds reasonably anticipated to be human carcinogens.. usually with BLLs greater than 40 mg/dL. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. Urine levels may reflect recently absorbed lead. 2003. 1995. IARC considers inorganic lead compounds probable human carcinogens. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.. including minority race or ethnicity. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 1996.07 µg/dL (Becker et al.. 2005a).. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.. Schwartz et al.xls). 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. the geometric mean BLL was 3.. which is an 84% decline.. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Data submitted through state public health programs from 2006 showed that 1.Metals µg/dL or higher as the level of concern in children. 2003. 2006). Schwartz. lead in women may be associated with hypertension during pregnancy. 2005b). 2000). 2006). 2005b. Muntner et al. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR..4% in NHANES 1999-2004. Borja-Aburto et al. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. 1991.cdc.e. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. premature delivery. 1996. almost double the geometric mean of 1.S.000 adults. Fourth National Report on Human Exposure to Environmental Chemicals 215 . 1999).6%) were lower than those from NHANES 1991-1994. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. residing in housing built before the 1950’s.6% in NHANES 1988-1991 to 1. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.0 µg/dL in females (Soldin et al. the prevalence rate has declined annually since 1994 (CDC.. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Both drinking water and ambient air standards for lead have been established by the U. and spontaneous abortion (Baghurst et al. when the geometric mean BLL was 2..S. Lanphear et al. and peripheral neuropathy generally occurring at much higher levels (e.. higher than 100-200 µg/dL)... 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. 2009). However. 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.atsdr. 1998). and low family income (CDC.3 million children tested had BLLs of 10 mg/dL or higher (http://www.. and organic lead compounds not classifiable with respect to human carcinogenicity. Korrick et al.5 per 100. Payton et al. both the geometric mean (1. Information about external exposure (i. with overt encephalopathy..gov/toxpro2. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH.html.S. Staessen et al. 2002. reduce sperm count.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 1987. environmental levels) and health effects is available from ATSDR at: http://www. seizures.. 1994).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. 2003.. In occupationally exposed adults. EPA. 1996. adults in the 1999-2000 NHANES sample. The U. 2002a).S.. In NHANES 1999-2002 in children 1-5 years old... Overall.cdc. particularly in the skeleton. adults in the 19992000 NHANES sample (Apostoli et al. and decrease fertility (Alexander et al. may alter sperm morphology. 2007). Bellinger 2005.g. Jones et al. At low environmental exposures. 2002). urban residence. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.4% of children had BLLs of 10µg/dL or higher (CDC.75 µg/dL in U. adult residents. 2003). For example. Surveillance data reported by U... Telisman et al. More recently. respectively. 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. 2001).S. approximately 11.S. CDC. High dose occupational lead exposure. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.21% of approximately 3..7 µg/dL and 4. 2000).

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. Hu H. Pediatrics 2004. Speizer FE. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Manton WI. Baghurst PA.54(20):513-516. Rios C. 4/14/09 Centers for Disease Control and Prevention (CDC). 4/14/09 Centers for Disease Control and Prevention (CDC). McMichael AJ.htm. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Brody DJ. et al.55(32):876-879. Luukkonen R. Payton M. Atlanta (GA). Coresh J.10:43-50. 1991 [online]. Rotnitzky A.275:1177-1181. 2005. Sparrow D. Bellinger D. Auinger P. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Caldwell KL. et al. Muntner P. Aro A. Hu H. Birth Defects Research (Part A). Ronchi L. Blanco J. van Netten C. Rotnitzky A. Available at URL: http://www. Chiodo LM. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Meyer PA. Lead and hypertension in a sample of middle-aged women. Batuman V. Vupputyuri S. Teratogen update: lead and pregnancy. MMWR Morb Mortal Wkly Rep 2006. Atlanta.205:297-308. Korrick S. Sci Total Environ 2002. 4/14/09 Alexander BH. Int J Hyg Environ Health 2002. Schulz C. Inorganic and Organic Lead Compounds. Lead. Hertz-Picciotto I. Checkoway H.89:330-335.gov/nceh/lead/ CaseManagement/caseManage_main.cdc.htm. Kim R. Available at URL: http://www. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Bellinger D. Jones RL. JAMA 1996. Blood lead levels measured prospectively and risk of spontaneous abortion.275(15):1171-1176. Baj A. Cox C.150(6):590-597. Environ Res 2000.348:15171526.26:359-371. Hu H. Neurotoxicol 1987. 2002 [online]. Ewers TG. Dietrich K.82:60-80.cdc. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . doi:10.gov/nceh/lead/publications/ books/plpyc/contents. Jacobson JL.cdc. Available from URL: http://www. Public Health Rep 2000. Hernberg S. Apostoli P.htm. Environ Health Perspect 1993. 4/14/09 Centers for Disease Control and Prevention (CDC). Preventing Lead Poisoning in Young Children. 4/14/09 Centers for Disease Control and Prevention (CDC). N Engl J Med 2003. Blood lead levels—United States. References Agency for Toxic Substances and Disease Registry (ATSDR). Jacobson SW. et al.8(3):395-401. Atlanta (GA). 1988-2004. Stanek KL. Jusko TA. Neri A. Am J Epidemiol 1999. Wager C.atsdr.287:1-11. Cory-Slechta DA. Available at URL: http://www. Lanphear BP.html. Wigg NR. Ga. Leggett RW. Pirkle JL. Canfield RL. Scand J Work Environ Health 1984. The relationship of bone and blood lead to hypertension.cdc. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Pediatrics 2009. gov/mmwr/preview/mmwrhtml/mm5420a5. CDC. Weiss ST. JAMA 1996. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Rojas LM. Hunter DJ. Neurotoxicol Teratol 2004. Blood lead reference values: the results of an Italian polycentric study. Adult blood lead epidemiology and surveillance—United States.101(7):598-616. Acquisition and retention of lead by young children. Seiwert M. 1999-2002. Muller CH. Lanphear BP. MMWR Morb Mortal Wkly Rep 2005a. Bavazzano P. Ganzi A. et al. Homa DM. Weiss ST. Kaufman JD.53:411-416. Aug 2007 [online]. Farias P. Mantere P. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Available at URL: http://www. Reese YR. Robertson EF. Semen quality of men employed at a lead smelter.87:1-471. Angle CR. Roberts RR. Sparrow D. Lepom P.73:409-420.115:521-529. Korrick SA. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. IARC Monogr Eval Carcinog Risks Hum 2006.gov/mmwr/preview/mmwrhtml/ mm5532a2. 2005b. Managing Elevated Blood Lead Levels Among Young Children. Kaus S. 2003-2004.gov/toxprofiles/tp13. Occup Environ Med 1996. Henderson CR. Becker K. Toxicological profile for lead. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Am J Public Health 1999.123:e376-e385.113(4):1016-1022. Kuehnemann TJ. Cox C.1542/peds:2007-3608. Hänninen H. Neurodevelopmental effects of postnatal lead exposure at very low levels. Age-specific kinetic model of lead metal in humans.htm.cdc. Borja-Aburto VH. Vimpani FB. Krause C.

Use of endogenous. J Hum Hypertens 1995. Smith DR. Am J Epidemiol 1994. Semen quality and reproductive endocrine function in relation to biomarkers of lead. and copper in men. Soldin SJ. et al. Sparrow D.209:301305.9:303-327.Metals results from NHANES III. Gunter EW. and tibia lead with neurobehavioral test scores in South Korean lead workers. Staessen JA. Lee SS. Low-level lead exposure and renal function in the Normative Aging Study. Soldin OP. Clin Chim Acta 2003. IV. Jurasovic J.153(5):453464. et al. Weiss ST.140:821-829.104(1):60-66. 50:31-37. Hickman T. Rubin R. Nash D. Schwartz BS. Lustberg M. blood pressure. Gavella M. Brody DJ. Environ Health Perspect 1996. Revised and new reference values for arsenic. Payton M.327:109-113. Lead.S. O’Flaherty EJ. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Roels H. Kaufmann RB.108(1):45-53. Pizent A. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Kaufmann R. Environ Health Perspect 1998. Telisman S. zinc. Hu H. Blood lead. Kidney Int 2003. Sherwin R.106:745-750. Physiologically based models for bone-seeking elements. Toxicol Appl Pharmacol 1993.63:1044-1050. Stewar WF. lead. JAMA 2003. Lee BK. Schwartz J. Wilhelm M. Osterloh JD. Rocic B. Hwang KY. Flegal AR. Paschal DC. Pirkle JL. Am J Epidemiol 2001. Hanak B. Schwenk M. Amery A. Environ Health Perspect 2000. Schulz D. cadmium. Low-level lead exposure and blood pressure. population to lead: 1991-1994. stable lead isotopes to determine release of lead from the skeleton. cadmium. Blood lead concentrations in children: new ranges. dimercaptosuccinic acidchelatable lead. Lauwerys RR. Kinetics of lead disposition in humans. Arch Environ Health 1995. and hypertension in perimenopausal and postmenopausal women. Lee GS. Magder L. blood pressure and cardiovascular disease in men. Cvitkovic P. Exposure of the U.289(12):1523-1531. Int J Hyg Environ Health 2006. Association of blood lead.118:16-29.

00 (.700-. thermostats and switches).900 (. Survey years 03-04 Geometric mean (95% conf.30) 1.80 (3.40 (4.30-2.70 (1.979 (..500 (.800-1.60 (2.500) .30-6.. Some cosmetic skin creams from countries other than the U.60) 1. may contain inorganic mercury.672) .900) .50) 5.500-.700) . 1994.50) 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 . thimerosal. Woods et al.. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.60 (1.00 (1..800 (.50) 1.00) 4. Apart from methyl mercury.60) 2085 2293 3478 Limit of detection (LOD. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.500-.900) 1. mercuric chloride). interval) . constitutes the main source of dietary mercury exposure in the general population.00 (2.40) 3.800-1. or oxygen. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.00) 1. 2007).927) .90) 3.70-2.70) 911 856 2081 4525 03-04 03-04 . The ingestion of methyl mercury.418-. and organic forms.689-.419 (. Elemental mercury is a shiny.753-1.Metals Mercury CAS No.700 (.30-4. Accidental spills of elemental mercury.80) 3.781 (.S. merbromin). sulfur. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.300 (.2.50-2.90) 90th 3.02) .400-.00 (.20) 2.80) 1. an organic form of mercury. and is distributed to most tissues..860-1.90) 95th 4.500 (.60-6.00 (2. electrical lamps.30) 3. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).12) . The kinetics of the different forms of mercury vary considerably.60) 1.. Hursh et al. and dental amalgam.700-. 1999 .80 (1. 2002).20-4.40-2.400 (.285-.30) 3.30 (2.70 (4.776 (.600) 1.g. and mining and smelting.g.40-1. In addition.900) 75th 1.60-3.40-3.90 (1.700-.700-.10-3.300-.50) 4.90 (4.919) . see Data Analysis section) for Survey year 03-04 is 0. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.700) .40-1.80 (1.326 (. 1993).30 (1.30-5.40) 1.60 (1.10) . have often required public health intervention (Zeitz et al.50-1.484) .00 (..30) 4132 4241 03-04 03-04 03-04 . water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges. 218 Fourth National Report on Human Exposure to Environmental Chemicals .00 (2. Atmospheric elemental mercury can be deposited on land and water. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.70 (3.655-.900) 1.g. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).30) 1.00) .00-1.90 (1.20 (2.800 (.70 (1.90-3. synthetic organomercury compounds were once used in pharmaceutical applications.00) 1.877 (. to form inorganic mercury compounds or salts.80 (1.80) 4.700-. which create an episodic potential for volatization and inhalation of mercury vapor. Also. 1998.40 (4.490 (.886) .800-1. Other major uses include electrical equipment (e.903) Selected percentiles ( 95% confidence interval) 50th . Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.20-3.703-. solid-waste incineration. Kingman et al.S.600 (.797 (.714-.00) 3.400-.50-3. Poorly absorbed from the gastrointestinal tract.00 (.g.60-6.574) . with the highest concentrations occurring in the kidneys (Barregard et al. such as chlorine (e.300) .30) 5. IARC. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. phenylmercuric acetate) or topical antiseptics (e. population from the National Health and Nutrition Examination Survey.900) 1.00-5. inorganic. and mercury compounds are still used as preservatives (e.814 (.800 (.800-1.800-1.800 (. sphygmomanometers and barometers.563 (. After elemental mercury is absorbed.. predominantly from fish and other seafood. 1980.472-. which can bioaccumulate in aquatic and terrestrial food chains. thermometers.40 (3.372) .363-.40 (3.40-2. elemental mercury is absorbed mainly by inhaling volatilized vapor.50) 2.60-2..20-4.60-5.

299-. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.90) 5.10-3.40-2.73) 1.. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.10 (1.374) .30) 3.20) 1.40) 2. 2005).300 (.00) 1.10 (5.50-12. 2003).944 (.20-11. 1998).700 (.40-1.30 (1.80-3. 1995.20-3.700 (.40 (1. 1984.700 (.800) .200-.20-3.700-.70-5.50-3.800 (.500-.40 (1.00 (2. 1996.70-3.10) .20 (.. Miettinen et al.317 (.60) 2.300) .80 (1...80) 579 527 370 436 588 806 Limit of detection (LOD.0) 4.50) 2..300) . Smith and Farris.377) .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 .00 (1.300) .90) 3. 1992 and 1999.20) .00) . Sandborgh-Englund et al.20-2.268-.3) 4.20 (2.300 (.60) 1. 1993). 1999-2002. Methyl mercury enters the brain and other tissues (Vahter et al.7) 4.00-2. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . and the newborn’s levels decline gradually over several weeks (Bjornberg et al. a measure of accumulated dose (Cernichiari et al.900-1.200 (..14 and 0.400-.27) .29) .395) ..256-.10 (.738-.30) 1.00-1.200 (. Methyl mercury is incorporated into growing hair.50-2.820 (..Metals the tissues to mercurous and mercuric inorganic forms.30-3.700 (.. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.377 (.940) Race/ethnicity (females.50) 3..700-1.70) 4..300 (. Vahter et al.60 (1.200-.800-1.269-. National Health and Nutrition Examination Survey.00) 6.. 2004. Vimy et al. 1991.90 (4. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations..407) .825-1. 1998). 1975. 1994).10-1.10 (1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.919) .90 (1.900-1..90) 90th 1.30 (. 1994. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al. 1999).60 (3.00 (3.14.30 (1.800) 1.30) 1..06-1.300) .70) 4.30-6.200-.70 (1.90) 2. 2003).70-6. McDowell et al.697-.20) .500-1.500-..800 (.369) 1.800) 75th .S.23) .833 (.900 (.10 (3.00-2.900 (. population.50) 1.10) 1.00 (2.700-1.30-4.30-2. Fourth National Report on Human Exposure to Environmental Chemicals 219 . Smith et al.800-1..30 (1. 1990). Geometric mean Survey years (95% conf.80) 1. 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.00) 1.70-3.700) 2.06 (.50 (2.300) . 1973).00 (2.90 (4.800 (.30-5. Suzuki et al.10 (.329 (. interval) Selected percentiles (95% confidence interval) 50th .343 (..824) 1.871-1.500-.500 (.800) 1.. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.60 (1. 1971). 1992). with most elimination occurring through in the feces (Sherlock et al.70 (1.300 (.70) 1.667 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1993).307 (.30-6.600) .80 (3. 1992.01) .10) .40) 1.70 (1..200-.90 (3.200-.60 (1.500 (.20-3. and a useful marker of exposure in epidemiologic studies (Grandjean et al.265-. 1996).10 (1.700-.60 (3. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.60 (2.297-.00) 2.726-1.600 (.30-11. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.475) .00) 4.300) .664-1.00-2.90 (1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.800-1.60) 1. 1969. 1994) and then undergoes slow dealkylation to inorganic mercury.30-6.90) 2.40-2.318 (. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.50) 95th 2.541-.70-5.. 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. Myers et al.00-3.200-.00) 7.800) . thereafter.50) 1.600) . After exposure to elemental mercury.40) 5. for both acute and chronic exposures.900 (. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.50 (1.60) 3.02 (.500-..35 (1.30-4.00-6. Excretion occurs by renal and fecal routes.500-. Jonsson et al.

600) . 1998. Overt poisoning from methyl mercury primarily affects the central nervous system.500 (. pain in the extremities.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 . limb deformities. Oskarsson et al.600 (. gingivitis. Drexler and Schaller. Acute.500-. hearing impairment.. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.700 (.500-. dysarthria. fatigue. Vupputuri et al.. 2005.600 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . maculopapular rash. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.500-. 1995.500-. In recent epidemiologic studies. and pinkish discoloration of the hands and feet (Tunnessen et al. 1951. depression.500-. short-term memory loss.600 (. see Data Analysis section) for Survey year 03-04 is 0. sensory impairments. 1987).700-. Factor-Litvak et al. and neurocognitive and behavioral disturbances. Survey Geometric mean (95% conf. The constellation of findings may include anorexia.600) .600 (. 2000. 1996). 2004. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.. lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC.500-. Stern 2005.700 (. 2000). DeRouen et al. 1963).. and progressive constriction of the visual fields. the existence of a causal relation is unresolved (Chan and Egeland..42. population from the National Health and Nutrition Examination Survey. Smith et al. 2004). At levels below those that cause acute lung injury.600 (. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al..500-. dysarthria.700 (.500) .. Inorganic mercury exposure usually occurs by ingestion. 2004). 2003). 2004. 2005). 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. and sleep disturbance (Bidstrup et al. hypertension.600-. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.500-. Rice.500 (<LOD-.800) .700 (.600 (.500 (<LOD-. 2006. Sakamoto et al.600-.Metals may be more efficient for inorganic mercury (Grandjean et al. 2000.700) 2007 2240 3406 Limit of detection (LOD.. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. cerebellar ataxia. Bellinger et al.700 (. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis... 2002.700-. typically after a latent period of weeks to months.800) . Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. Rissanen et al.. which may vary for some chemicals by year and by individual sample. Sakamoto et al. < 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.. irritability. 1993). Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.. insomnia. altered physical growth. anorexia. Smith et al.600) .500 (. ataxia. Salonen et al.. and cerebral palsy (NRC.. particularly irritability.. overt signs and symptoms of chronic inhalation may include tremor.700-.600 (.500-. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.600) .. 1970.S. Once absorbed.600) . 1995. 1983).600) .600) . 220 Fourth National Report on Human Exposure to Environmental Chemicals .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600) .600 (.. 2006.600-.600-.600) .700) .700 (. causing parasthesias.

total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.330 (.63-2.78-2.30) 3.890 (.250) . see Data Analysis section) for Survey year 03-04 is 0.88) 287 722 1529 03-04 03-04 . These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.460 (. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 221 .77-2. 1997. particularly methyl mercury. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.520) .700-1.14-2.28) 1. slightly higher total blood mercury levels were found in U. Benes et al.480) 75th 1..14) 90th 2. 2003).433 (.08 (1.16 (1.76-3. 2001. EPA at: http://www.495 (.99-6. In NHANES 19992002. total blood mercury increased with age.gov/toxprofiles.304) .23) 2.700 (.330-. Grandjean et al.360-.213-. population from the National Health and Nutrition Examination Survey.34-3. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.870-1.509) .400 (.340-.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 .447 (.200 (.405-.26 (1.66) 3.33 (2.54 (2.160-.420 (.420 (. 2009).60) 619 713 1066 Limit of detection (LOD.08 (1.. range 40 years to 78 years) had an average total blood mercury concentration of 2.530) .05) 3. the total blood mercury concentration is due mostly to the dietary intake of organic forms.413-. During the same survey periods. Mahaffey et al.89) 3.55 µg/L. 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.07 (. Survey years 03-04 Geometric mean (95% conf. average age 33 years.530) .360 (... adult women in several ethnic subgroups (Hightower et al.65) 1. 2003). aged 18 to 69 years.350-. 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.58 µg/L for 4645 adults.770-1. Schober et al.18) 2.60 (1. 2006).416 (. EPA.52) 2.19 (1. total blood mercury geometric mean levels in females aged 16-49 years did not change.03-4.463) .46 µg/L for children.840-1..840-1...530-.76-3.280-. 1998).S..cdc.96 (1.408) .00) 1.31) 2.492) Selected percentiles ( 95% confidence interval) 50th .67-2.870-1.60-2.12 (. 1998).382-. 2001. 758 children.480 (.24) 1..S.Metals standard for inorganic mercury has been established by U.441 (.313-.330-.406-.epa.19 (2.358 (.430 (.549) . et al.290-.410-. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.93 (1.610-1.476 (.S.61) 1.8 years.88 (1.430 (. interval) ..534) .20 (1.. Information about external exposure (i.90) 2.430) .16 (..00 (.. Over the NHANES 1999-2006 survey periods. However. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.46) 3.23) .9 years). These distinctions can help interpret mercury blood levels in people.05) 1. Biomonitoring Information In the general population.67-3.14.96 (1. In Germany the geometric mean for blood mercury was 0. Total blood mercury levels increase with greater fish consumption (Dewailly et al.39-3.509) .85-2. the median concentration of blood mercury was 0.330-.940 (.930-1.S.42) 95th 3.. 1995.13-2.555) .254 (.S.e. A cohort of 1127 U. From 1996 through 1998. Kingman et al.840) 1.370) .440 (. 2002).68 (2.78 µg/L for adults and 0. who participated in a 1998 representative population survey (Becker et al.570) .gov/mercury and from ATSDR at: http:// www. environmental levels) and health effects is available from the U.01 (.24 (2. military veterans (mean age 52.29) 1.396-. 2004. average age 9.360-.460) . and the age-related changes differed across the groups (Caldwell et al.580) . Among the three racial/ethnic groups.442-.960 (. 2000). Sanzo et al.31) 1266 1272 03-04 03-04 03-04 .76-4.09 (2.atsdr. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.88-3. 2009).97) 2.

599) . not to imply a safety level for general population exposure.384 (.486) Selected percentiles ( 95% confidence interval) 50th . ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.. 2002) adult population surveys were similar to those in a U.00) 286 722 1529 03-04 03-04 . Survey years 03-04 Geometric mean (95% conf. reversible increase in urinary N-acetyl-glucosaminidase.30) 2.365 (.65 (1.28 (.472-.447-.969-1.309-.32 (1. Levels in U.16) 1. interval) .1 µg/L for each surface with a dental amalgam (Kingman et al. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.09) 1.07) 1.275) . et al.40-1.522-.537) .. the urine mercury increased by approximately 0.25 (.545 (. In the study of U.696 (.400-. and Italian (Apostoli et al. An expert-panel report recently prepared for the U.12-3.208-.21) 1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.385-. women of childbearing age have generally been much lower than these levels (CDC.652) .255 (.35 (1..785-1.498) 75th .616) ..289) .23-2.246-..909 (.619-.280-.31 (1.S. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.485 (. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. et al.06 (.62 (1.00 (.417) . Urinary mercury levels in recent German (Becker et al..88 (1.443 (.88-2. 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.404-. Czech (Benes et al.01) 2.41-2.67 (1.970 (.376-.400) .217 (.32-2.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals . 2006).620-.358) .77 (2.86) 95th 2.13 (1.67 (1.392-. 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.301-. 2005).875-1.Metals 2000).964-1.800-1..56) 1266 1271 03-04 03-04 03-04 .276 (.06 (.51-2.1 µg/L.11) 2. population from the National Health and Nutrition Examination Survey.455) . Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.391) .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 .78-4.00) 90th 1. 1988. 2006.343 (.76 (1.. Langworth et al.347) .306 (.463 (.225-.784) 1. 2003).44) 1.297 (.S. and on average.196-..46-2.667-1.04-3.265-.03) 2.18-1.508 (.333-.40 (1.687) . mean urinary mercury was 3. DeRouen et al.587 (.64-2. 2009)..307-.532 (.54 (2.525 (. Department of Health and Human Services noted that several studies have observed a modest.11-2.79 (1.365 (.588) . 2009).464 (. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.30) 1.391-.714-1.87) 2.79) 1. military veterans with dental amalgams.566) .11) 1.990) .535) 1.368) .447 (.480) .S. 2002).88-2.13-2.630) . 1992). 1998).63) 1.39) 1. Information about the biological exposure indices is provided here for comparison.455-.61) 1. Urine mercury and the number of dental amalgams were correlated. a biomarker of perturbation in renal tubular function.768 (.362 (.455-.S.476 (.S.87 (1.

42) 90th 2.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .658 (.10-2.686) .45-2.98 (5.3) 5.39-3.790) .54) 595 531 381 442 594 826 Limit of detection (LOD.59-5.560-.41 (2.910) .582-.53-3.565 (.81 (3.600 (.526-.56 (1.710 (.76-5.03) 1.68) 3.850-1.744) 1. 1999-2002.97 (1.592 (.516 (.00 (2.615 (.410-.50 (1.09-1.97) 2.540 (.772 (.S.710 (.62 (3.91 (2.31-1.632 (.810) .99-2.42) 2.28 (1.699) 1.95 (2.930) .966) .79) 3.83-3.15-1.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . National Health and Nutrition Examination Survey.16-5.664) .624-.94) 1.560 (.14.846) .30-2. Geometric mean Survey years (95% conf.522 (. interval) Selected percentiles (95% confidence interval) 50th .35) .46 (1. 1999-2002.806) .655 (. Geometric mean (95% conf.22-3.81-6.16) 5.47) 1.46) 3.03-2. 16-49 years) 99-00 01-02 .799) .502-.540-.06 (.553-.45 (1.99) 1.450-.25) 2.622-.69 (1.30 (1.18) 3.32-3.31 (1.520-.13 (2.685 (.57-4.620 (.520-.639 (.04-10.65-4.41 (1.51 (3.833) .637) .23-1.79) 1.870) .41 (1.15 (2.742-1.52) 3.824) .45-3.85-3.580-.657 (.22 (.03 (.62 (4.426-.578-.892) .501-.17) 95th 5.92) 3.650) 1.77) 2.500-.76) 2.30 (2.42-3.45) 95th 3.03 (.774) .68-3.27 (2.87-4.84 (2.420-.740 (.61-6.650 (.610-.665) .07-5.508-. population.656-.605-.38) 4.09-1.84 (2.650 (. population.616-.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.55) 90th 3.21 (2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .670) 75th 1.636-.05 (2.709) .37) 1.21-3.27-1.23-1.596 (.724 (.909-1.709) 75th 1.91-7.97) 2.45) 2.61) 1.14) 3.50-4.77) 1.45) 2.43-1.07) 1.27 (1.92) 4.475-.S.14-1.05 (3.Metals Urinary Mercury−Females Aged 16-49 Years Old.809) .69-3.92) 2.99 (2.68 (3.24) 6.85) 4.387-.24-1.89 (2.97) 2.723 (.65) 1.46-4.831) .760 (.50 (2.56) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.21 (1.721 (.10-4.13-4. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.62 (1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.04-1.41-6.631-.35 (1.569-.56) 4. 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.606 (. National Health and Nutrition Examination Survey.00) 2.37 (1.32) 2.99 (3.832-1.51) .557-.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.831) .579-. 16-49 years) 99-00 01-02 .710) 1.691) .30 (2.47) 1.48 (2. interval) Selected percentiles (95% confidence interval) Survey years 50th .14-2.55-3.44) 3.580 (.76 (1.07-2.70 (2.14 and 0.706 (.32 (1.18 (3.719 (.72) 1.00 (3.

205:297-308. Kaus S. Gagliardi T. Greitz U. Bonnell JA. Cu. et al. Grandjean P. Caldwell KL.Metals References Aberg B. Cerna M. Pb. Barregard L.47(3):185-195. Cejchanova M. Cortesi I. Berglund B. Fish consumption. Barregard L. Hasselgren G. Martins IP. Becker K. Kinetics of mercury in blood and urine after brief occupational exposure. Environ Health Perspect 2003. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Enzymuria in workers exposed to inorganic mercury. Jorgensen PJ. Myers GJ. Jorgensen PJ. I. mercury exposure. Smid J.16(4):705-710. Total blood mercury concentrations in the U. Atlanta (GA). Fawcett J.289:1324. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Lebel G. Weihe P. Egeland FM. Jarvholm B. Zn. Seifert B. Cent Eur J Public Health 2000. Locket S. Cincinnati (OH): Signature Publications. Cox C. Lancet 1951. Bellinger DC. Mercury derived from dental amalgams and neuropsychologic function. Levallois P. Lapham LW. Environ Health Perspect 2005. Ekman L. Lepom P. Apostoli P. Barregard L.61:65-69.295(15):17841792. Sandborgh-englund B. Marsh DO. Markers of early renal changes induced by industrial pollutants. Schuzt A. and Se in blood of the population in the Czech Republic. Centers for Disease Control and Prevention (CDC). White RF. Biennow M. JAMA 2006.72:169-173. Kaus S. Videro T. Arch Environ Health 2001. JAMA 2006. Osterloh JD. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Int Arch Occup Environ Health 1988.149:301-305. DeRouen TA. Drexler H. The concentration levels of Cd. Budtz-Jorgensen E. Bidstrup PL. Hg. et al. Skerfving S.77(2):124-129. Nutr Rev 2004. Falk R.212:588-598. Bjornberg KA. Sallsten G. Martin MD.2:856-861. Benes B. Cardenas A. Leitão J. Metabolism of methyl mercury (203Hg) compounds in man. Townes BD.. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Application to workers exposed to mercury vapour. Seiwert M. 52:19-33.19:478-484. Barregard L. et al. Elia G. Factor-Litvak P. Daniel D. Int J Hyg Environ Health 2003. Jacobs D. Martin MD. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices.8(2):117-119. ACGIH. Cutress T. Sallsten G. Br J Ind Med 1993. Cernichiari E. Vahter M. Tissue levels of mercury determined in a deceased worker after occupational exposure.50:17-27. Leroux BG. Clarkson T. Brewer R. Int JHyg Environ Health 2002. Debes F. Grandjean P. Chan JM. Garrett N. Trachtenberg F. Woods JS. population: 19992006. Bernard AM. Luis H. 2007 TLVs and BEIs. Cernichiari E. et al. Weihe P. Subrt P. Int J Epidemiol 2004. Persson G. Ayotte P.62(2):68-72. Begg M. selenium. Roels H. Caudill SP. Harvey DG. Int Arch Occup Environ Health 1999. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Mortensen ME. Tavares M. Cianciola ME. Schulz C. Arch Environ Health 1969. Chronic mercury poisoning in men repairing direct-current meters. Conradi N. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. et al.33:1-9. Buchet JP. Third National Report on Human Exposure to Environmental Chemicals. Woods JS. Environ Res 1998. 206:15-24. Lauwerys RR. Health effects of dental amalgam exposure: a retrospective cohort study. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Kline J. Arch Environ Health 1992. Barbon R. et al. and lead. Attewell R. Weber JP. Int J Hyg Environ Health 2009. Impact of maternal seafood diet on fetal exposure to mercury. et al. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Rosenbaum G. Bates MN. Krause C. Neurotoxicology 1995. Echeverria D. Geier J. Schutz A. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. J Toxicol Environ Health 1997. McKinlay S. Cernichiari E. 2005. and heart diseases.295(15):1775-1783.56(4):350-357. Sci Total Environ 2002. Niklasson B. Jones RL. Schaller KH. Sallsten G. Seiwert M. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Mangili A. Aposian HV. Drago I.111:719-723. Castro-Caldas A. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Becker K. Hultberg B. Bruneau S. Arch Environ Health 1992. Kjellstrom T. Snihs JO. Spevackova V.S.113(10):1381-1385. Schulz C. Bernardo M. Am J Epidemiol 1999. Dewailly E.7(3):176-184.

Salonen JT.3dimercaptosuccinic acid (DMSA). Nakano A. Renal and immunological effects of occupational exposure to inorganic mercury. Environ Sci Technol 2004. Demuth S. Vesterberg O. Ann Clin Res 1973. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. Acute mercurial intoxication treated by hemodialysis. National Research Council (NRC). Ohlin B. Barregard L. Mercury in biological fluids after amalgam removal.51(3):234-241. Langworth S. Murata K. Arch Toxicol 1996.361:1686-1692. O’Hare A. Rice DC. Miettinen JK. et al. Seppanen K. The distribution and biological half-time of 203 Hg in the human body according to a modified whole-body counting technique. Skerfving S. Langworth S. Environ Res 1995. Hattula T. Schultz A. and Exposures in the Glass Manufacturing industry. Needham LL. Clickner RP. Davidson PW. McDowell MA. Kantola M. docosahexenoic acid and docosapentaenoic acid.S. Elinder CG. Elinder CG. Environ Res 2004. Ann Clin Res 1971. The US EPA reference dose for methyl mercury: sources of uncertainty. and the risk of myocardial infarction and coronary. Hirayama K. Rahola T. Patterson DG Jr. Br J Ind Med 1991. Ekstrand J. Pacific Islander. Schutz A. Osterloh J. Environ Physiol Biochem 1975. Amalgam tooth fillings and man’s mercury burden. et al. Kingman A. Schutz A.3(2):116-122. Toxicological effects of methylmercury. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population. Blood mercury reporting in NHANES: Identifying Asian. Kubota M.48:247-53. and any death in eastern Finnish men. J Pharmacol Exp Ther 1980. Burse VW. Hattula T. Greenwood MR. Tillander M.fr/ENG/Monographs/vol58/index. Washington (DC). Lakka TA. 2000. methylmercury transport across the placenta via neutral amino acid carrier. Circulation 1995. Bodurow CC. Hair mercury levels in U. Lagerkvist BJ. Shamlaye CF.103:2766-2679. Myers GJ. Liu XJ. Environ Res 2002. Elimination of free and protein-bound ionic mercury (203Hg2+) in man. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Adachi T. Urinary excretion of mercury after occupational exposure to mercury vapor and influence of the chelating agent meso-2. et al. IARC Monographs on the Evaluation of Risks to Humans. Bolger PM. Arch Environ Health 1996. Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey. 1999 and 2000. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers.13:496-501. Nyyssonen K.38:3860-3863. Sanchez-Sicilia L. Intake of mercury from fish. 7/15/09 Jonsson F. Cernichari. 1993. Cadmium. Sandborgh-Englund G.59(5):692-706. Kauhanen J.5:214-219. Miettinen JK. Nyyssonen K. Korolainen A.95:406-13. Beryllium. Available at URL: http:// monographs. Mehaffey KR. Oskarsson A. Satoh H. Halbach S.112(11):1165-1171. and the risk of acute coronary events— The Kuopio Ischaemic Heart Disease Risk Factor Study. J Dent Res 1998. Relation of a seafood diet to mercury. Nakamoto S. Sakamoto M. Sallsten G. Lancet 2003. Environ Health Perspect 2006. Sampson EJ. Sakamoto M.50(9):814-821. Boeckx M. Native American. Cox C. Roels HA.155(2):161-168. Brown LJ. lipid peroxidation.77(4):615-624. Br J Ind Med 1992. Environ Health Perspect 2004. Mercury. Yasutake A. Allen J.php. Declining risk of methylmercury exposure to infants during lactation. Elimination of 203Hg-methyl mercury in man. Pellizzari E. Weihe P. Dillon CF. Fourth National Report on Human Exposure to Environmental Chemicals 225 .70(5):310-314. Matsumoto S. Korpela H. Rahola T. Clarkson TW. Toxicol Appl Pharmacol 1999. The effect of ethanol on the fate of mercury vapor inhaled by man. Salonen JT. Rissanen T. Br J Ind Med 1993.214(3):520-527. cardiovascular. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. Lauwerys RR. A compartmental model for the kinetics of mercury vapor in humans. Johanson G. KajiwaraY. Kolff WJ. Ceulemans E.Metals Grandjean P. et al. Ann Intern Med 1963. International Agency for Research on Cancer (IARC). Hursh JB.91:645655. and polychlorinated biphenyl and other organochlorine concentrations in human milk. Sundquist KG.71(1):29-38. Hernandez GT.5:252-257. Hattula T. Hum Exp Toxicol 1994.iarc.114(2):173-175. Fernando R. Albertini T. Circulation 2000. Palumbo D. Seto DS. Environ Health Perspect 2004. Rahola T.77(3):461-467. Hightower JM. National Academy Press.112(5):562-570.90:185-189. Kubota M. Sandborgh-Englund G. selenium. Volume 58. Akagi H. Nakai K. Hallen IP. Voutilainen S. children and women of childbearing age: reference range data from NHANES 1999-2000. Rissanen K. arsenic.49(6):394-401. J Dent Res 1998. Fish oil-derived fatty acids. and multiracial groups.

Toxicol Appl Pharmacol 1996. Environ Health Perspect 2007. Environ Health Perspect 2002. Toxicol Appl Pharmacol 1994. Toxicol Appl Pharmacol 1994. et al. The contribution of dental amalgam to urinary mercury excretion in children. Kaye WE. Hongo T. Stern AH.Metals Sanzo JM. Jones RL. Whittle K.98(1):133-142. Turner MD. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Fisher HL. Guo S. JAMA 2003. Tunnessen WW. Goldberg J. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Stern AH. The kinetics of intravenously administered methyl mercury in man.115(10):1527-1531. Langolf GD. Matsuo N. Martin MD. Osterloh J. Orr MF. Blood mercury levels in US children and women of childbearing age. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Smith JC. Dorronsoro M. Shen DD. Methyl mercury pharmacokinetics in man: a reevaluation. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Nakazawa M.79:786789. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Acrodynia: exposure to mercury from fluorescent light bulbs. Baser M. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Mottet NK. Woods JS. McMahon KJ.128(2):25125-25126. Lind B. Allen PV. Newton G. Am Ind Hyg Assoc J 1970. Br J Ind Med 1983. Lorscheider FL. DeRouen TA. Bernardo MF. Vupputuri S. Mooney TF.48(4):221229. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Leroux BG. Friberg L. Environ Res 2005. Daniels JL. Vorwald AJ. Yoshinaga J. Hall LL. Patil LS. Hum Toxicol 1984. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Amiano P. Smith RG. Zeitz P. Imai H. Vahter M.110:129-132.40:413-419. 1993-1998. Am J Physiol 1990. Leitao JG. Arch Environ Health 1993. Sinks TH. Suzuki T. Longnecker MP. Environ Health Perspect 2003. et al. Takahashi Y. Smith AE. Aguinagalde FX. Azpiri MA.4(5):981-988. McDowell M.258(4 Pt 2):R939-945.2:117-131. Effects of exposure to mercury in the manufacture of chlorine. Public Health Nutr 2001. Amurrio A. Smith JC. Sandler DP. Topping G.37:245-252. 1999-2000. Bolger PM.31:687-700. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Schober SE. Pediatrics 1987. Hislop D.124:221-229. Sherlock J.289(13):1667-1674. Vimy MJ. Environ Res 2005. Effects of occupational exposure to elemental mercury on short term memory. et al. Smith PJ. Most B. Burbacher T.111(12):1465-1470.97(2):195-200. Farris FF. The hair-organ relationship in mercury concentration in contemporary Japanese.

2-79.8) 44.7-105) 69.5-66.7 (73.2-53.4-52.7 (71.8 (42.9-55.6) 93.7-50.0-38. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 62.4) 76.5) 60.6-46.5) 47.7 (50.3-115) 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.0 (43. semiconductor and battery industries have begun to use molybdenum. At a daily oral molybdenum dose of 24 µg.1 (91. interval) 45.5 (48.7) 78.8) 40.4-82.3 (79.2) 48.1) 60.7) 86.9 (44.2 (83.1 (71.7 (44.7 (58.4) 45.1-55.0-65.0-100) 63.7) 45.9) 34.4) 49.8 (85.0-53.8) 48.7) 77.3) 65.0) 84.3-91.5-52.6 (55.6-72.2 (55.2-59.2) 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 (98.8.0) 54.6 (40.1-51.0-56.8 (82. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.5 (41.6-58.3 (38.1 (34.7-51.6-55. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources. and in pigments for ceramics.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.2) 79.9-56.5-46.7) 46.7 (37.7 (45.6) 51.2 (61.6 (52. 01-02.7-96.1) 46.0 (76.7-41. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. 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.4-61.7) 75th 84.0) 55.7) 78.2) 40.4) 41. hydrogenation catalysts. population from the National Health and Nutrition Examination survey. urinary excretion over six days CAS No.9) 62.0) 60.6 (55.8-49.5-41.1-88.3 (64. Fourth National Report on Human Exposure to Environmental Chemicals 227 .3 (47.4 (72.0 (42.3) 54.3 (55.5. WHO.1-63.5) 80.7-84.7-122) 93.7 (36. see Data Analysis section) for survey years 99-00.0-85.2 (56.6-111) 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 52.1) 35. 1996).9-85.5-68.0-71.1) 57.8) 75. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.0-77. More recently.7-91.2) 41. and 03-04 are 0.9 (32..5) 44.6) Selected percentiles ( 95% confidence interval) 50th 50.4 (80.6-82.2-42.5) 85.5 (41.0) 45.7-73.1 (38.2-91.9 (78. Compounds of molybdenum are also used as corrosion inhibitors.7) 51.8-94.0-62.Metals Molybdenum or ore deposits.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 47.1-52.9-83.3 (71.7) 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 78.8 (67.3 (46.3) 47.6 (73. chemical reagents in hospital laboratories. and 1.S. lubricants.6 (40. 1997).1-48.5-124) 108 (92.2) 52.0 (48.0) 97.9 (40.3-47. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.9-109) 97.3) 41. respectively.8-46. aldehyde dehydrogenase. 2001).8.6) 71.8-90.5 (81.2-37.0) 39.4 (48.9 (73.3) 37.3 (73.3) 83.8) 46.2 (38.5 (43.1-59.1) 82. inks.9 (37.7) 57.6) 53.6-96. and xanthine oxidase (Kisker et al.9 (34.7-39.4) 56.9) 67.5) 80.0 (42.5 (37.2 (49.2) 53.6) 71.2-70.4 (79.3 (55.7-60.0 (41.1-52.3-44.7-47. 0.2 (40.3-75.2 (69.9-55.4 (48.1) 59. Excretion occurs predominantly via the kidneys.3 (37.8-108) 87.1) 126 (106-147) 109 (94.7-68. which exert homeostatic regulation over molybdenum balance.7 (51.4-75.4) 52.4) 42.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.1-44. The recommended dietary allowance for adult men and women is 45 µg/day (IOM. and paints.2) 37.2-59.8-106) 88.3 (84.5-91.3) 85.9 (52.5-65.5 (49.0 (81. 7439-98-7 General Information Elemental molybdenum is a silver-white.5 (67. 2001.2 (63.9-82.5-52.2 (49.6-42. In humans.0-101) 82.6-62.5 (74.9 (33.7-92.8) 39.6 (43.0 (46.0-110) 90.3 (53.4 (34.

U.9-68. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6 (36.7-40.2-40.1-109) 89.1-81.6 (57.3-141) 109 (81.4-42.0-46.2) 39.3-56. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.4-185) 106 (94.1 (42.4) 122 (107-133) 109 (99.3) 37.5 (38.6-63.2) 38.6) 43.8 (57.2) 42.7 (66.3-115) 98.3) 64.7) 75th 63. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0. at daily oral doses of 95 µg and 428 µg.1) 101 (83.5 (37.9-45.5 (41. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.7 (77.3) 44.3) 40.5-35.9 (39.0) 39.7) 45.9-45.3 (71.6-78.8) 38.6) 39.8) 79.0 (35..8) 38.7) 41.5) 71.1) 40.3-43.8 (36.9 (35.4) 116 (101-126) 104 (88.0) 88.0-46.3) 41.7) 112 (95. and urinary levels reflect intake from all sources.1-100) 86.2 (40.Metals was 18% of the ingested dose.5 (80.1) 56. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.2 (43.4 (78. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown..1-41.9 (39.5-45.5 (37. of the ingested dose (Turnlund et al.4 (59.5 (40. and clinical or epidemiologic evidence of adverse effects is limited.6) 48. interval) 43.4) 60.2-65.7-52. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-47.0 (80..5-62.1-39.1) 37.5 (78.2) 58.4-76.3) 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 85.8-67.1-39.5-46.4 (37.5-50.2) 37.3 (36.1 (37.4-66.1-45.8-47. 1993).0) 33.2 (36.3 (58.5 (79.2-103) 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 42.8-46.5-119) 90.1) 43.5) 73.9 (79.4) 89.8) 61.3 (36.9) 44.3 (37. In industry.7-100) 77.0 (58.9-71.7 (30.4 (53.5) 63.5 (35.2) 43.7-93.5-69.4-118) 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 .5 (54.5) 72.3) 57.2-121) 107 (92.6 (42.7-43.0 (74.1-40.6 (71.5-92.6) 36.1-127) 90.4) 77.0-120) 85.1-112) 78.1) 65.9 (73.0-133) 119 (88.S.7) 62.1-43.2 (52.9 (40.1 (44.1 (30.6-63.3-46.8-65.7) 42.0-38.8) 39. but available epidemiologic data are scant. 1999).2 (37.6 (59.7 (75.3 (53.8-52.4) 48.1 (38.0-41.7-62.0) 36.9 (36.9-96. population from the National Health and Nutrition Examination survey.7) 57.1 (54.4) 40.8-118) 81.9 (49.4-106) 85.2) 55.4-107) 85.9-61.3-45.6-61.8 (37.0) 62. 1995).0) 72.8-66.7) 115 (93.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.9-117) 57.0-103) 103 (90.5 (83.9) 79.3) 56.5 (34.0) 44.1-67. 1961.5-99. urinary excretion over six days rose to 50% and 67%.0) 39.3 (71.6) Selected percentiles ( 95% confidence interval) 50th 41.1) 37.9-118) 91.5 (59.1-34.6-41.3 (51.5 (39.3) 61.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.6 (38.2 (40.2 (73.8 (75.5 (41.2-80.5 (65.4) 44.S.3 (55.2 (40.3 (37. respectively.5-60.5-44.5 (36.9-42.2) 42. 2001).4 (55. 1997).2 (57.5 (40.7-38. Based on studies finding adverse reproductive effects in rats and mice.2-96.3 (83.1 (82.5 (39.2) 39.3-44.5-48.2 (69.8) 45.6-88.2-49.5) 60.9 mg/kg/day and established a tolerable upper intake level of 0.1 (39.03 mg/kg/day in humans (IOM.3-59.8-42. EPA.9) 31.5 (35.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.4) 47.8) 71.9) 92.7-44. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.4-39.6 (36.6-76.4 (44.7-137) 129 (109-155) 112 (97.9 (64.9 (64.5) 90th 108 (97.2-41.7-120) 87.1 (33. Molybdenum is generally considered to be of low human toxicity.4 (56.1-43.9) 40.8) 62.1 (40.9-40.4) 61.1 (49. Biomonitoring Information Molybdenum is an essential element for health. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.1-38.0) 38.4 (67.5 (65.5-70.6) 39.8-47.8 (90.2 (50.9-87.9) 41.9-41.6-61.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.5 (50.4-120) 101 (84.0) 53.5-97.8 (56.6-45.4) 58.3-68.2) 37.4 (40.0-56.2-46.3-52.4-41.3) 43.1 (38.8-84.2 (33.7) 53.2-96.1-79.8) 37.

gov/index. National Toxicology Program (NTP). Geneva: WHO. References Centers for Disease Control and Prevention (CDC). population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Vermeire PA.. pp. U. Biomonitoring studies on levels of molybdenum can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of molybdenum than are found in the general population.nap.15(2-3):149-154. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. et al. molybdenum. 4/14/09 Sievers E. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. copper. vitamin K. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Droste JHJ. Kristiansen J. 4/14/09 White MA. 2001. World Health Organization (WHO).62(4):790-796. boron. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. iron. 1996.gov/iris/ subst/0425. Third National Report on Human Exposure to Environmental Chemicals. Schaub J. chromium. Am J Clin Nutr 1995.123(1):81-85. silicon.Metals in urine for the U. Schindelin H.S.htm. Trace element reference values in tissues from inhabitants of the European Union. Environmental Protection Agency (U. 1998. 1998). Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. arsenic. White MA. Sci Total Environ 1998. A study of 13 elements in blood and urine of a United Kingdom population. J Trace Elem Med Biol 2001. Occup Environ Med 1999. Van Meerbeeck JP. Turnlund JR. Shmavonyan DM. Schleyerbach U.php?record_id=10026&page=420. TR-462. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. excretion. 16:1313-1319. Ronchi A. Molybdenum-cofactorcontaining enzymes: structure and mechanism. nickel. Atlanta (GA). EPA). vanadium. 2002. 4/14/09 Iversen BS. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Fourth National Report on Human Exposure to Environmental Chemicals 229 .66:233-267. Kisker C. Sciarra G.S. (DC): National Academy Press. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Rees DC. Ann Rev Biochem 1997. 2005). Molybdenum 1993 [online]. Occupational risk factors of lung cancer: a hospital based case-control study. 144-154. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Minoia C. 56:322-327.niehs. Available at URL: http://ntp. Sabbioni E. van Sprundel MP. and zinc: a report of the Panel on Micronutrients. manganese. Aprea C. 2001). Molybdenum. Molybdenum absorption. Turci R.S. Washington. X. Dietary reference intakes for vitamin A. Sabbioni E. Peiffer GL.epa. 420-441. White and Sabbioni. Weyler JJ. iodine. Christensen JM. Zhurnal Obshchey Biologii 1961. edu/openbook. In: Trace elements in human nutrition and health..216:253-270.nih. Menne C. Available at URL: http://books. Minoia et al. Analyst 1998.22(3):179-191. Available at URL: http://www. Molybdenum in infancy: methodical investigation of urinary excretion. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Gatti A. pp. Koval’skiy GA.. Yarovaya GA. 2005. Keyes WR. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Food and Nutrition Board. Institute of Medicine (IOM). Rapid Comm Mass Spectrom 2002.

Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. population from the National Health and Nutrition Examination Survey. 0. and as drugs (e. < LOD means less than the limit of detection. cisplatin. thick-film circuits printed on ceramic substrates. 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 03-04 are 0.g. 230 Fourth National Report on Human Exposure to Environmental Chemicals .Metals Platinum CAS No. and iron. which may vary for some chemicals by year and by individual sample. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. copper. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. and 0. jewelry. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Platinum compounds are used in electrodes. however. Important properties of platinum are resistance to corrosion.. 1998). carboplatin) in the treatment of cancer. see Data Analysis section) for Survey years 99-00. respectively. strength at high temperatures. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. 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. 7440-06-4 General Information Platinum is a silver-gray. 01-02. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. as oxidation catalysts in chemical manufacturing.07. dental alloys.04. and high catalytic activity..S.04. * 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 231 . whereas soluble platinum compounds (e. 1969).. Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf...g.g. or recommended for the metal form by NIOSH (Czerczak and Gromiec. Platinum metal and insoluble salts can produce eye irritation..g. route of exposure (e.. inhalational. Information about external exposure (i.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. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. The carcinogenicity of other platinum compounds remains uncertain.. population from the National Health and Nutrition Examination Survey. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP. or organometallic). 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. platinum metal and insoluble salts are very poorly absorbed (<1% of a dose) and cleared from the body within a week after a single dose. 1969. inorganic salt. oral). 1975a.Metals doses or at biomonitored levels from low environmental exposures are unknown. metallic. and duration of exposure. cutaneous. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Platinum metal is biologically inert. 2000).S. environmental levels) and health effects is available from Urinary Platinum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1975b). Saindelle et al. Toxicity is determined by the type of compound (e.. Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH. When ingested or inhaled. intravenous medicinal use.

55(2):138-140. Wilhelm et al.. Urinary excretion of platinum from platinum-industry workers. Farago ME. Hysell D. rhodium. Levels of platinum in urine for the U. and in blood and urine in the United Kingdom. Moore W Jr.56(3):283-286. Hauff K. 2003). Environ Health Perspect 1975b.207(1):69-73. Stilianakis NI. 1998). Pethran A. ruthenium. J Expo Anal Environ Epidemiol 2003. 2003. International Journal of Hygiene and Environmental Health 2003. Environ Res 1975a. Iavicoli I. 1997.org/documents/ehc/ehc/ ehc125. Herr et al. Czerczak S. 1991 [online]. Part 1: monitoring of urinary concentrations. Urinary platinum levels associated with dental gold alloys. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004). Influences on human internal exposure to environmental platinum. Jankofsky M. Turfeld M. Platinum. Patty’s Toxicology. Arch Environ Health:1969. 2004. 5th ed. Schierl R. Schierl. Ruff F: Histamine release by sodium cholorplatinate. Neuendorf J. Pethran A... Kelly J. 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.org/documents/ehc/ehc/ehc125. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Kuster W. Int J Hyg Environ Health 2004. osmium. Biomonitoring of traffic police officers exposed to airborne platinum..005 µg/L (Iavicoli et al. Nowak D. pp. Int Arch Occup Environ Health 1997. palladium. Several studies have shown that background concentrations in general populations were usually less than 0. Occup Environ Med 2004. Platinum concentrations in urban road dust and soil. et al. 2000. 289-380.. 2001).inchem. New York: John Wiley & Sons. Environmental Health Criteria 125. Herr CE. Bocca B. Seifert B..123(3):451-454. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Thornton I.35:313-321. Gromiec JP. Ewers U.9:152-158. Int Arch Occup Environ Health 2003. and gold excretion of patients after insertion of noble-metal dental alloys. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Saindelle A. which elevate urinary platinum by five to twelve-fold (Begerow et al. Schierl R. Begerow J. Schulz C. Blanks R. Schierl et al.13(1):24-30. Schierl R. Petrucci F. Ensslin AS.. palladium. eds. et al.01 µg/L (Becker et al. Saindelle A. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. van de Weyer C. Gieler U. Boos KS. Kavanagh P. Grimm CH. Available at URL: http://www. Allergy and histamine release due to some platinum salts. Br J Pharmacol 1969. 206:15-24. Biomarkers 1999. In: Bingham E.4(1):27-36. Kaus S. Parrot JL. 2004) or less than 0. Schierl R. Hall L. population were below the limit of detection (0. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Analyst 1998. Senofonte O. 1999. Wilhelm M. and platinum. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.. Angerer J. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Hebert R. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. 3/31/08 Moore W Jr. 1998). References Becker K. Arch Environ Health 2001. Powell CH. Occup Environ Med 1998.. Kazantzis G.70(3):205-208. Uptake of antineoplastic agents in pharmacy and hospital personnel. Fruhmann G.S.04 µg/L) in this Report. Pethran et al.. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Fries HG. Nickel. 2003. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Alimonti A.10:63-71. et al. Seiwert M. Raab W. 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.76(1):5-10. 2003. et al.. Rommelt H.Metals the International Programme on Chemical Safety at http:// www.htm. Duneman L:Long-term urinary platinum. Hysell D.htm. Ruff F: Platinum and platinosis. Campbell K.inchem. Cohrssen B. Schulz C. Kulka U. Huber R. International Programme on Chemical Safety (IPCS). Crocker W.19:685-691.61(7):636-9. Carelli G. Biomonitoring Information Urinary platinum levels reflect recent exposure. Herr et al.

290-.200 (.173) .196) .147-.360-.175) .310 (.480) .230-.170-.350) .420) .180-.300 (.260-.290) .390-.310 (.400) . and 0.160-.200-.690) .340-.160 (.420) .160-.180-.190 (.220) .240) .220) .370 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.260 (.215) .340-.430 (.200) .320) .380 (.430 (.220 (.280 (.167-.230) .172 (.350-.220) .450) .240-.290) .370 (.400-.200) .240-.147-.310) .370) .167-.480) .280-.170 (.340) .270 (.200-.390-.360 (.290 (.200) .220-.400 (.206) .410-.340) .500) .210 (.370-.300) .470) .150-.450 (.260 (.440 (.400) .520) .340 (.171 (.170-.177) .280 (.02.202 (.440-.470 (.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 .159 (.250-.410 (.290) 90th .200 (.160-.172 (.185-.280) .218) .220) .230) .410) .350 (. From these and other sources.390) .450 (.400 (.360 (.270 (.390) .490) .420) . thallium has been restricted from use in rodenticides and Urinary Thallium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.230) . the latter being the current major industrial consumer of thallium in this country.260-. thallium was obtained as a by-product of smelting other metals.300) .200 (.240-.250-.230) .180-.170 (.420) .520) .360-.380 (.243) . 01-02.146 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.250-.360) .510 (.190 (.360-.270-.153-.420-. In addition.330-.470 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.250-.170-.300-.250 (.290 (.420 (.280-.250-.260 (.200 (.320 (.220) .217) .150-.400-.380) .179-.200 (.290) .370-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.280) .480) .400 (.360-.590) .160-.180 (.270 (.Metals Thallium depilatory cosmetics.184 (.410-. interval) .460-.170-.230 (.157-.330-.500) .239) .270) .510) .270 (. 0.260-.470) .S.390) .280) .218) .360 (.188) .310-.490 (..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 . representing distribution into other tissues.181-.440 (.350 (.400) .135-.217 (.240) .280 (.370 (.202 (.350-.250 (. In the past.400 (.160-.410 (.150-.230-.173) .450 (.370-.158) . see Data Analysis section) for Survey years 99-00.410-.156) .400) 95th .330-.440) .170) .330-.440 (.220 (.170) .350) .330-.176 (.156) .490) Total .450 (. thallium readily crosses the placenta and also distributes into breast milk.410-.640) .200) .160 (. population from the National Health and Nutrition Examination Survey.290 (. respectively.260-.170 (.520 (.240) .159 (.197-.220 (.350-.02.300 (. and 03-04 are 0.180) 75th .220 (.170-.550 (.150-.490) .165 (.290 (.500 (.196) .162-.178) .410 (.390-.190 (.370 (.400-.155 (.430 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .430 (.290) .173-.380-.320) .134-.250-.197 (.450 (.149 (.400 (.300) .159 (.201 (.201 (.250) . it has not been specifically mined or refined in the United States since 1984.200-.410 (.170) . Thallium disappears from the blood with a half-life of several days.420) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.420-.192) Selected percentiles ( 95% confidence interval) 50th .520) .380-.185 (.172) .160 (.490) .200 (.630) .150-.183) .167 (.133-.190-.170-.590) .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 .450 (.183) .220) .390-.147-.270-.350-.290 (.480) .370-.270) .440 (.145-.190 (.410-.400) .180 (.156-.430) .350-.420-.360 (.430-.220 (.191 (.145 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting. 2005).450 (.140-.370 (.470) .330) . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.410 (. Human health effects from thallium at low environmental CAS No.290-.370 (.170-.200) .148-. In the United States.450 (.160 (.400-.400-.230-.300) .430-.420) .187-.260-. however.210) .330) .150-.144 (.202) .390 (.420) .210 (.370 (.160 (.300 (.180) .460) .200) .360-.290 (.320-.390) .340-.02.154-.260) .250-.200-.330) .500) .430-.190 (.330-.440) .180 (.420-.370) .250-.163) .210-.270-.320) .180-.410 (.440) .350-.340-.390 (.460 (.190 (.480) .430) .270 (.310 (.330-.330) .145-.450 (.560) .137-.225) .182-.410-.

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

Schaller et al.76(1):53-59. Atlanta (GA). Sabbioni E. Radiat Prot Dosim. Apostoli P. Trace element reference values in tissues from inhabitants of the European Union. 1998. (1981) studied 1. 1990.113(1):47-53.html. and serum of Italian subjects. Trace metals in urine of United States residents: reference range concentrations. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Environ Res 1998. Celier D..cdc. 1981. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Boisson P. Kramer U. Int Arch Occup Environ Health 1980. Trace element reference values in tissues from inhabitants of the European community I.216:253-270. Minoia et al. Gallorini M. A study of 13 elements in blood and urine of a United Kingdom population. Dolger R.. Pirkle JL. Martin J-C. Valentin H. Challeton-de Vathaire C. 7/15/09 Blanchardon E.S. Sampson EJ. Schmidt M. A study of 46 elements in urine. 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. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Cassot G. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. blood. Wiegand H. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Morrow JC. et al.gov/toxprofiles/tp54.. Manke G.atsdr. Available at URL: http://www. 2005) and are shown with results from NHANES 2003-2004 in this Report. Sci Total Environ 1998. 1985). 1992 [online].95:89-105. Ting BG. with concentrations ranging up to 76. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. 2005.. Marcus RL. Sci Total Environ 1990. Paschal et al. J Soc Occup Med 1985. Brockhaus A. White and Sabbioni. 2005. Int Arch Occup Environ Health 1981. 1998). et al. 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. Jackson RJ.Metals (CDC. Investigations of thallium-exposed workers in cement factories. Schaller KH. Soddemann H. References Agency for Toxic Substances and Disease Registry (ATSDR). Paschal DC.1 mg/m3 (Marcus. Pietra R. Ewers U. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Brockhaus et al. Buhlmeyer G. Centers for Disease Control and Prevention.48(4):375-389. Minoia C. Pozzoli L. Third National Report on Human Exposure to Environmental Chemicals.47(3):223-231. Sabbioni E. et al. Raithel HJ.5 μg/L. X. 1980. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Toxicological profile for thallium.35(1):4-9. White MA. Investigation of a working population exposed to thallium.265 people living near a thallium-emitting cement plant in Germany. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

170) .082-.070 (.095-.105 (.04.210 (.500 (.080 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.310-.110) .330-.090 (. and 0.104) .070) .090) .100 (.230-. and as catalysts in the petroleum industry.180) .400) .120-.53) .050-.530 (.113 (.120) .100-.093-.800) .340) .160 (.460 (.810) .086 (.350) .101-.300 (.088 (.370 (.130) .560) .076 (.130) .630) .150) .110 (.180 (.111-.077-.070-.160 (.210 (.280-.470 (.270 (.160-.080 (.120-.097-.100) .100 (.120-.090 (.400 (.120) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.230-.200 (.130-.090-.160-.400 (.071 (.123-.060 (.800) .135) .140-.140) 90th .220 (.058-.360-.090 (.340-.180) .04.090-.310) .510 (.260-.100) .300) 95th .060-.095-.380 (.420-.120) .081 (.260) .360 (.480) Total .690) .073-.410-.151) .410 (.090-.150 (.310-.150 (.056-.500 (.080 (.400 (.160) .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 .300 (.084) .520) .100 (. Evidence is lacking for the carcinogenicity of tungsten. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.069-.133) .170-.110 (.230 (.087) .290) . see Data Analysis section) for Survey years 99-00.770 (.073-.069) .107 (.570 (.280 (.090) .440) .350-1.350 (.180 (.190-.650) . bronzes in pigments.130 (.450-.260 (.065 (.100) Selected percentiles ( 95% confidence interval) 50th .200) .140-.060-.210 (.070) .087-.110 (.100) .270-.320-.370-.320 (.101 (.290) .090-.530 (.510-.070 (.070) .04.088) .082 (.180) .093) .380) .160-.350) .260-.056-.260-.200-.080 (.270 (.560 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.360 (.096 (.210 (.064-.370 (.113 (.092 (.460 (.062 (.250) .520) .670) .190-.620 (.062 (.370) .370-.080) . which is used in the steel industry.122) .076 (.620) .290-.310-.120-.150-.470-.080 (.100-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).120) .580) .100) .360-.190-.120-.550) .830) .073 (.00) .070-.230-.500) .220) .560) .550) .570 (.450 (.550) .078-. 0.490) .120) .470) .120 (.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 .250) .060-.310 (.370 (.080) .092) .060 (.Metals Tungsten CAS No.290 (.280 (.340-.390 (.510-1.640 (.240 (.096-.310-.490 (.090-.360 (. Tungsten compounds are used as lubricating agents.120-.060-.430-.090) . Tungsten is used mainly for producing hard metals.080-.080) 75th .320) .380 (.460) .430) .360) . interval) .210) .180) .190-.110 (.250-.060 (.140 (.250) .330-.093 (.090-.380-.300-.530 (.130-.070-.250-.084-.113 (.S.110-.230-.110-.180-.100) .065-.340-.060 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.070-.150 (.070) .190 (.132) .170) .130) .140 (.300) .250) . which are used in rock drills and metal-cutting tools.430 (. 01-02.110 (.460 (.240-.170) .270-.430 (.590) .170) .204) .620) . population from the National Health and Nutrition Examination Survey.109) . mainly as scheelite (CaWO4).790) .380-.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.470 (.230) .290-. respectively.230) .116) .160 (.170 (.091) .270 (.070-.060-.060 (.330) . 236 Fourth National Report on Human Exposure to Environmental Chemicals .050-.082) .090-.130 (.320-.210-.190 (.050-.080) . and it has not been classified with respect to its carcinogenicity by either IARC or NTP. filaments for incandescent lamps.100 (.073) .071-. and 03-04 are 0.060 (.068) .130-.420-.090-.220) .130) .250) .050-.550 (.300 (.180-.137 (.130-.170 (.380-.310-.220-.290-.520) .180-.120) .090) .380-.110) .140 (.320 (.430-.160-.190) .084 (.066-.220) .250) . and for producing ferrotungsten.950) .470) .092 (.560) .160) .430 (.074-.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 . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone. Little information is available on the toxicity of tungsten. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.110-.560) .330 (.160 (.070 (.060-.270-.400-.126) .160 (.210 (.180-.100-.260 (.080-.270-.082 (.350) .390) .460) .158 (.105) .330) .130) .140 (.080-.113 (.400 (.

161) .167) .300-.214-.283) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.089 (.317 (.158) . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.143-.116-.079) .214) .069 (.086) .364 (.317) .105 (.880) .203-.083-.107-. or exposure that a control group of non-metal workers had mean levels differences.065-.287) .250 (.S.224) .294 (.176-.201) .197) .205-.078 (.078 (.538) .095-.082) .074) 75th . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.084) .341 (.074-.145 (.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 .211 (.360 (.071 (.105 (.065 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure. population.087) .151 (.071) .085 (.453) .071 (.098-.071) .347 (.186 (.315-.072-.168 (.078-.061-.119 (.059-.108-.148 (.071) .353 (.482 (.090-.231-.120) .091) . interval) .064-.439 (.215 (.180-.133) .381) .096) .233-.091 (.329-.063-.152-.386) .065 (.333) .158) .094) .080 (.065-.068-. 2005).727) .075-.484 (. 1997).340 (.049-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.155-.301) .188-.414) .109-.073 (.385 (.063-.216-.069-.075) .452-.088) .077-.209-.079) .136-.088) .054-.070 (.329 (.154) .106 (.255 (.216 (.582) .136-.158) .099-.066 (.258-.158 (. 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.299 (.080-.634 (.300) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.090-..253) 95th .222-.098-.326) .465) .215) .091 (.250 (.333) .116 (.060-.216-.060 (.095) Selected percentiles ( 95% confidence interval) 50th .108) .131-. and 2003-2004 (Paschal et al.086) .237-.217-.554) .094-.436-1.245-.064-.153-.122-.201 (.284) .085) .059-.333 (.293 (..333 (.100 (.198) .279 (.176-.139) .28) .179-.354-.061-.133) .074-.439) 1160 1306 1281 1178 1345 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .136-.067 (.055-.086-.(Kraus et al.667 (.240-. 1998).130-.333 (.302-.091) .121-.250-.084 (.436) .222) .285) .143 (.117) .056-.157) .153) .267-.174 (.169 (.253 (.797) .190) .079) .124-.208-.059-.075 (.S.067 (.164 (.200-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.084 (. population from the National Health and Nutrition Examination Survey.054-.081 (.082 (.216-. Patients with medically-inserted tungsten found at increased levels in drinking water.169) .093-.124 (.138 (.144 (.187) .667) .167-.333-.078) .358) .383 (.077) .270 (.200-.085-.139-.117 (.331-.080-.079 (.181 (.077-.555 (.497 (.063-.081 (.359 (.093) .104-.439 (.306) .122 (.333-.261-.412 (. (1987) found possibly due to methodologic.216 (.462) .072 (.086) .184 (.092) .302-.077) .075 (.074 (.439) Total .231 (.279 (.138 (.278-.431) . Using neutron activation analysis to 2000.255 (.098) .091) .279 (.165) .126-.081-.094) .253-.237) .217-.087 (. similar to those in this Report (Schramel et al.410-.065) .079) .146 (.300 (.068 (.091) .065-.081) .073 (. measure urinary tungsten.071 (.058-.154) .823) .150-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.062 (. 2001).206-.465) .063 (. Nicolaou et al.083 (.057-.500) .073 (.199 (.136 (.059 (.060-.170-..057-. 2001-2002.089) .339 (.056-.082) .100) .150 (.237) .339 (.125) .354) .459) .120) .392) .359 (.301) .080 (.139 (.071-.375) .053-.431) .130 (.353 (.116) .146 (.144-.S.197) .150-.301) .197-. population (CDC.111 (.121 (.344-.063 (.072-.061-.605) .174) .133) 90th .317-.426) .167) .070 (.074) .148) .075) .179-.098-.272-.098 (.431) .426) .379 (.146) .267) .075-. 2003.138) .084) .484) .103-.069 (.066 (.199 (.083) .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 .083) .198-.078) .125 (.136-.258 (.073 (.275 (.109 (.255-.167-.100) .067-.218 (.079 (.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 .083 (.308) .333 (.119-.197 (.739) .286-.308) .063-.265 (.122-.300-.

Catheter Cardiovasc Interv 2004. Kraus T. Angerer J. Sampson EJ. et al. Morrow JC. Weber A. Occup Environ Med 2001. The determination of metals (antimony. Centers for Disease Control and Prevention. Seghizzi P. Schramel P. Wendler I. Cassina G. Sabioni E. mercury. and hair (Bachthaler et al. palladium. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load.69(3):219-223. Schaller KH. tellurium. Paschal DC. Manke C. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Angerer J. Pietra R.cdc. Jackson RJ. Feuerbach S. Cancer Clusters. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Res 1998. Paetzel C. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Pirkle JL. Trace metals in urine of United States residents: reference range concentrations. J Trace Elem Electrolytes Health Dis 1987. cadmium. Schramel P.gov/nceh/clusters/Fallon/study. platinum. Available at URL: http://www. Mosconi G. lead. Nicolaou G. Link J. Lenhart M. thallium. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report.76(1):53-59. Int Arch Occup Environ Health 1997.58(10):631-634. [online] 2003. Atlanta (GA).htm.(2):73-77. 4/15/09 Centers for Disease Control and Prevention. Churchill County (Fallon). bismuth. 2005.62:380-384. urine. Nevada Exposure Asssessment. Third National Report on Human Exposure to Environmental Chemicals. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. National Center for Environmental Health. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect.Metals blood. Ting BG. 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. Zobelein P. References Bachthaler M..

016) .030 (.007) .063) .017 (.016) .016-.023 (.007-.007-.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .008-.006-.012-.012-.018) .049) .069) .009-.033-.060 (. Variable concentrations of uranium occur naturally in drinking water sources.012 (.026 (.158) .025-.020-.008 (.009 (.017-.008) .054) .014 (. Thus.015 (.008 (.067) .008 (.040 (.009 (.035) .037) .017) .010 (.008-.013-.040 (.035-. milling.010) .005-.008 (.027 (.027 (.015 (.047 (.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .027-.030 (.062) .027) .011) .014 (.031 (.054) .011 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.027) .007 (.008) .010-.017 (.021) .033 (.010-.114 (.036) .007 (.010-.007 (.021-. and 0.016) .016) .007-.021 (.065) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).008 (.024-.048) .036) .024-.009 (.020-.006 (.017) .017-.012) .030 (.056) .042 (.007-. including nuclear weapons.007 (.007) .041 (.012 (.020) .073) .011-.007-.009 (.039) .037) Total .010) .016-.012-.72%).016 (.016) . 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.006-.027-.021-.008 (.017) .008 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.020-.072) .008 (.014 (.015) .009) .038) .046 (.012-.031 (.010) * .009-.034-.023-.023) .017-.009) .023-.006-.010) * .026 (.024 (.009) .017-.010 (.008 (.009-.010) .027 (.012) .017-.013 (.010 (.026) .009) .009) .016) .012 (.007) 75th .064 (. see Data Analysis section) for Survey years 99-00.045) .045) .015 (.013) .014 (.023) .026) .028 (. respectively.011-.009-.010 (.026 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.009-.007-.017) . Since the 1990’s.010-.034-.011) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.007 (.004.042) .017) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.018-.007-.022 (.006-.009) . 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.009) * .005-.028 (.009-.007-.007-.018) .011) .006-.008-.054-.008 (.007-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .052 (.037) .046 (.009-.013-.055 (.006-.030-.007-.088) .046 (.022-.026) 95th .031 (.032 (.026-.012 (.005-.043) .006-.006 (.050) .027) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium. In workplaces that involve uranium mining. interval) .007-.009) .009-.046) .029-.007-.053) .034) .014 (.012-.018) .007) .038 (.006-.008 (.022-.011) .017-.021 (.007 (.011) .009) Selected percentiles ( 95% confidence interval) 50th .008 (. and 03-04 are 0.009) .029 (.028-.039) .004.009) .007) .039-.036 (.013 (.021) .023 (.007 (.037-.033) .015) .023) .019-.013) 90th . 235U (about 0.009) .031 (.043 (.027 (.013 (.011-.020 (.030) .040-.008 (.009 (.279) .007 (.023-.023-.010) .028-.027-.046 (.006-.018) .005-.019 (.009) .007-.009 (. Uranium has many commercial uses.035) .031-.051) .012 (.007 (.036-.005-.050) .008-.008-.028 (.012) .011 (.006-.022-.010) .021) .024-. population from the National Health and Nutrition Examination Survey.008) .009 (.008-.013-. and as an aid in electron microscopy and photography. 0.006 (.067) .007) .033 (.015-.010) .018 (.010) . human exposure occurs primarily by inhaling dust and other small particles.006 (.046-.011-.S.019-.008 (.037 (.007-.040) .008-.013 (.Metals Uranium CAS No.011-.008) .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 .007-.027) . or processing.044 (.011-.026-.065) .008 (.048 (.020) .040) .012) .037) .006-.008 (.008) .011) .021 (.066) .015 (.013 (.049) .029-. in some ceramics.007-.007 (.020-.031 (.016-.013 (.010) .023 (. and 234U. 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.012-.010 (.009) .010-. 01-02.005.127) .020-.011-.009) .010-.009 (.006-.011) .007-.009 (.019-.018 (.006-.009-.036 (.022) .041 (.012 (.009-.007 (.008-.009 (.040-.056) .053 (.019-.014 (.013 (. nuclear fuel.036-.008 (.

008) .006-.040 (.014-.028) .013) .026 (.014) .007 (. Radiation risks from exposure to natural uranium are very low.010-.048) .048) .011) .017 (.009) .022-.005-.006 (.006-. In cases of retained DU shrapnel.020) .009 (.006-.006 (.008) .022 (.008-.010 (. 2005).011-.011-.029) .027-.022 (.022) .018 (.013 (.017) . After inhalation.007 (.019-.007-.034 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.034 (.016-.059 (.012 (.012 (.008-.015) .020 (.017) .100 (.042-.019-.005 (.006-.010 (.007-.027) .005-.008 (.025-.011) * . Inhaled uranium-containing particles are retained in the lungs.015-.270) .006 (.015) .010) .010-.019 (.007 (.007-.017-.019-.008 (.008 (.018-.022 (.006-.024 (.019 (.011-.008-.015 (.009) * .146) .027-.006-.Metals impact. 2003).039) .016) . Uranium is eliminated in feces and urine..016) .010) .019 (.007 (.029) .051) .018-.026) .015 (.027) . where limited absorption occurs (less than 5%).058) .006-.018-.011-.033 (.009-.024-.007 (.027 (.028) .010-.014) .007 (.005-. kidneys.019) .007) .047) .027-.067) ..008-.011) .009-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.005-.042) .027 (.013 (.012 (.006-.005-.029) .032) .007 (.011-.006) . Health effects from uranium exposure result from chemical toxicity to the kidney.045 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.030 (.042) .011-.007-.010 (.006-.005 (.021) .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 .041) .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 .006-.006-.006-.012 (.061) . which represents distribution and excretion.006) .012) .007) .035 (.033 (.028) .015-.009) .018-.006-. Depending upon the specific compound and solubility.012-.006-.007 (.027-.012) .019) .010-.007 (. which can occur occasionally from high occupational exposure.006 (.007 (.014-.013 (.008) 75th .005 (.010 (.010) .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 . After long term or repeated exposure.024) .026 (.026-.032) .014 (.034 (.007 (.008) .008) .043 (.034-.015 (.010-.008-.008) .009-.010-.009 (.030 (.080) .030-.012 (.006-. with much slower elimination from bone.034 (.050) .007 (.010-.026 (.010) .011 (.009) .016-. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.008 (.017-.016) .022-.008) .010 (.005 (.007 (.008) .021 (.012) .016) .016) .051) .010-.011-.009) .033 (.013 (.012 (.007-.006 (.006 (.024) .028 (.007 (.008 (.010-.008 (. 0.009-.050) .023-.013 (.S.006-. population from the National Health and Nutrition Examination Survey.030 (.024) .031 (.009) .025 (.020 (.035 (.012 (.025-.016 (..015-.033 (.015-.020-.028-.009) .053) .021-.009) .009 (.053) .028) .013 (.016-.011-.009) .022-.010-.020 (.007 (.030) .019-.031-.037 (.013 (.006-.033) .020-.054) .058) .008 (.025) 95th .007-.009) .020-.013 (.029 (.006) .050 (.013) .007-.007 (.029 (.009-.040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result.007 (.010) .006-.014) .021 (.011) .021 (.013 (.008 (.024-.015 (.007 (.006-. low level exposure.016) .012-.051) .011 (.008) . After exposure to soluble uranium salts.039) .027 (.034-.017 (.007 (. 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.034) .017-.020-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.008-.039) .014 (.007) .017-.006) . interval) .013 (.008) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .015) .016) .010-.010) .006) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.009) .009) .016) .009-.074) .034 (.029 (.024 (.051 (.063) . liver.011-.007 (.016-.025-.024) .013-.008) .030-. the shrapnel acts as a source of chronic.007 (.007-.024 (.030) .008 (.014-.018) .044) .015-. 1992).039) Total .005-.014) 90th .007-.009) Selected percentiles ( 95% confidence interval) 50th .009 (.024-.007-.056) .005-.017) .015) .029) .024) .021 (.013) .006-.025-.006-.1%-6% of an ingested dose may be absorbed.019-.004-.004-.010) * .025 (.009 (.006-.008) .077) .008 (.018-.006-.006-.028 (.

. Benedik L. 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. respectively. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 2004). 2003. Six workers in a depleted uranium program showed concentrations of 0.55 μg/L (median 0.. Hamilton et al. Volf V. Karpas et al. 2004). Boyd P.cdc.. the median urinary concentration was 0. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure.html. 2000). environmental levels) and health effects is available from ATSDR at: http://www. 28 soldiers who may have been exposed to DU by inhalation.. Information about external exposure (i. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. 2006). Metivier H.62:562-566. References Bhattacharyya MH. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. 2006).. 1991. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.78:143-146.gov/ toxpro2.S. 2001-2002. but in whom no shrapnel was embedded. In the same study. Dietz LA. Ejnik JW.S. Stradling GN.. Zimmerman I.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Thomas RG.. 1994. 2004). A cohort of 46 U. soldiers evaluated before. Muggenburg BA. 2006). Galletti. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2002. ingestion. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.. 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. (May et al. 41 (1).. Third National Report on Human Exposure to Environmental Chemicals. although slightly increased during and after deployment.S. EPA. had a mean urinary uranium concentration of 0. McDiarmid et al..066 μg/g creatinine (Gwiazda et al. Atlanta (GA). or wound contamination. 2004). Byrne AR. et al. Komaromy-Hiller et al. Squibb K. Dang HS. 2000). population. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Vol. Tolmachev et al. Pullat VR. Centers for Disease Control and Prevention (CDC). Drinking water and other environmental standards have been established by U. In two studies of a Finnish population with high natural uranium concentrations in their drinking water... Sci Total Environ 1991.. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. the geometric mean urinary uranium concentration was 0.e. and no consistent effects on multiple endpoints of kidney function were found. pp.107:143-157.1996. 2002). In a study of 105 persons exposed to natural uranium in well water. Horan P. in that the levels were below their respective detection limits (Byrne et al. Durakovic A. Hamilton MM.S.078 μg/L (ranging up to 5. with emphasis on quality control. Guidebook for the treatment of accidental internal radionuclide contamination of workers.. (Kurttio et al. Pillai KC.. 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.168(8):600-605. the median urinary uranium concentration was 2...011 μg/L (McDiarmid et al. Health Phys 1992. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.. Uranium content of blood. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. In 17 U. and 2003-2004 (Dang et al. urinary levels of uranium were as high as 9.162 μg/L) (Orloff et al.65 μg/L).S. In: Gerber GB. 1978). 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. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 1992. Mil Med 2003. IARC and NTP have no ratings for uranium human carcinogenicity. Kent (England): Nuclear Technology Publishing. The U. 2005. Radiation protection dosimetry. 2006. Fourth National Report on Human Exposure to Environmental Chemicals 241 . 1-49.atsdr. Breitenstein BD.1992. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.110 to 45 μg/L (Ejnik et al.S. 2006). NRC. Carmichael AJ. eds. during. McDiarmid M. Health Phys 2000.61 μg/g creatinine.

Cremisini C. Sampson EJ. U. Kuwabara J. Renal effects of uranium in drinking water. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Paretzke HG.86:12-18. Karpas Z. patient population and literature reference intervals for urinary trace elements. Kane R. Environ Health Perspect 2002. Review of elements in blood. Environ Res 1999.82(4): 527-532. Howerton K. Karpas Z. Noguchi H.79(1):11-21. Human exposure to uranium in groundwater. Oberbroekling KJ. Cordero S. Health Phys 2004. Halicz L. Gwiazda RH. Kidney toxicity of ingested uranium from drinking water. Health Phys 2003. Costa R. et al. Hancock RG. Washington (DC): NRC. concentration and daily excretion of uranium in urine of Japanese. Health Phys 2006. et al. Charp P. Mistry K. Kalinsky V. D’Annibale L. May LM.71(6):879-85. J Toxicol Environ Health A 2004. Harmionen A. Scott K. Metcalf S. NRC). July 1978. Shelly T. Tolmachev S. Squibb K. Oliver M. Sci Total Environ 1994.22–Bioassay at uranium mills. Pekkanen J. Pinto V. Inductively coupled plasma mass spectrometry as a simple. rapid. Radiat Environ Biophys 2005.85:228-235. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Am J Kidney Dis 2006. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Saha H. et al. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.S. Auvinen A. Health Phys 2004. Li WB. Marko R. Katorza E. Nuclear Regulatory Commission (NRC) Guide 8. Bennett LG. Salonen L.44:29-40. et al. Hollriegl V. Marino R.S. Ash KO. Element reference values in tissues from inhabitants of the European community. Squibb K. Komaromy-Hiller G. Oeh U. Auvinen A. Andrews WS. Hamilton EI. Saha H. VI.47(6):972-982.94:319-326. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Roiz J. Biologic monitoring for urinary uranium in Gulf War I veterans. Wahl W. Int Arch Occup Environ Health 2006. Kurttio P. Salonen L. Jackson RJ. Kurttio P.S. Wilson PD. Komulainen H. Engelhardt SM. McDiarmid M. McDiarmid MA.296(1-2):71-90. et al. Gucer P.158:165-190. Clin Chim Acta 2000. Pirkle JL.87:51-56. Smith D. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium.S. Ting BG. McDiarmid MA. Health Phys 2002. Ejnik J. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Nuclear Regulatory Commission (U. U.Metals Galletti M. Comparison of representative ranges based on U. Health Phys 1996. Uranium daily intake and urinary excretion: a preliminary study in Italy.91(2):144-153. Lewis BM. Heller J. Makelainen I. Orloff KG.67(8-10):697-714. Paschal DC. Roth P. Jarrett JM. Sabbioni E.81:45-51. Environ Res 2004. et al. Biokinetic modeling of uranium in man after injection and ingestion. Ough EA.110(4):337-342. Lorber A. Uranium and thorium in urine of United States residents: reference range concentrations. Englehardt SA. Van der Venne MT.

90-12.0 (9.20) 7. and limited applications in pharmaceutics.20) 4.35 (3.0-14.S.80-4.20-12.0-23.0 (8.0 (11.10 (5.0) 12.40 (5.0 (10.51 (3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.g. It is normally found and produced as the anion of a sodium.49-3.90-9. and reducing agents.80) 3.50) 5. see Data Analysis section) for Survey years 01-02 and 03-04 are 0. 1998).31) 2.40-13.20 (5.80 (6.40 (4.88) 3.90 (3.30) 6.01 (2.03) 3.0) 10. certain catalytic metals.90-6. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0 (9.20 (4.40 (5.0 (11.29-3.30-6.50-11. 2002). lettuce) can be the main sources of intake for humans (FDA.70-3.40 (8.05.70 (3.50) 3.60 (7.0) 14.80-6.70-7.30-7. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.84) 14.90-9.0-17.90-3.40-6.81) Selected percentiles ( 95% confidence interval) 50th 3.80 (3. leather tanning.0 (12. but has strong oxidant properties in the presence of concentrated acids.0-17.90 (4. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant. 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. Drinking water.20 (8. Perchlorate was added to the U.80-15.30) 6.12) 3.20-4.0) 13.05 and 0.79 (2.0 (11.0 (8..10-11. potassium.20 (4.93-4.67-5.74-3.0-18.60) 8. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.10) 3.87-3.20 (2. milk.10-7.96 (3.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.20 (7.66) 3.20 (6.00-5.0) 9.0) 11.0 (12.0) 13.50 (5.0) 13.40 (3.EPA.0-17. 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.19-4.90 (5.0 (12.0) 13.80-12.60 (4.0) 9.0) 8.50 (3.70 (3.50-4.70-5.51 (3.10) 5.0) 11. 2005).10) 12.0-17.80 (3.30 (5.10-11..75-3.39-4. Perchlorate is stable under most environmental and physiological conditions.0 (8.80) 75th 6.70-11.0) 13.0-15.89-3.0) 13.0 (8.0) 14.10-4.90 (5.0 (12.40 (5.0) 95th 14.19 (3.10) 3.38) 5.40-5.0) 10. interval) 3.00) 3.75 (3.0 (13.0) 19.0) 15.45-4.40) 4.0 (8.90) 6.54 (3.93-3.40) 2.0) 10.00-6.40-11.70) 3.0) 13.90-3.70-12.00) 7.50) 6.09) 3.0-29. matches.10 (2.02 (3.0 (11.0) 9.0 (9. laboratory analysis.0 (11.90-11. fabric dyeing.30-19.0) 16.10 (6.22 (2.40-4.0-18.0) 15.0) 9.S.11) 3.80-8.0) 9.32 (3.40 (4.40) 6.20-4. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .60-6.50-4. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0 (11.50 (8.93 (4.00) 5. In addition.08-3.60-7.0) 9. 2007).0) 14.46) 3.Perchlorate Perchlorate (Urbansky.56) 3.10) 5.07-4.76) 4.90-11. and electroplating.50) 11.40-4.0-19.40 (3.00-6. 2005).10 (7.11) 4.0 (9.0 (9.30 (2.60 (4.65) 3.80 (7.47-4.0 (9.30-17.60) 5.05 (2. 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.20-11.40) 3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.0) 8.0-18.10-12.S.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0 (9.30-7.60) 3. Other manufactured uses include fireworks.22-5.40) 3.40) 90th 10.0-20.50-7.90) 5.21 (2.80-4.0 (11.00) 3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.20) 3.0-17.76 (3.00) 4.90 (5.26 (2.70-6.62 (3.90 (2. population from the National Health and Nutrition Examination Survey.0 (11. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al. Survey years 01-02 03-04 Geometric mean (95% conf.0 (11.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0) 13.40) 3. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.18-3.0) 11.30 (2.50) 5.0-17.0 (11.30 (5.80) 12. and certain plants with high water content (e.44-4.80) 7.70 (3.70-3.50-3.20 (2.70-9. or ammonium salt.10 (6.16) 3.0-15.90-10.20-3.81-16.68) 4.40-7.

42 (3.20-10.0) 11..91) 4.1-14. 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.40 (3.35) 3. age. Steinmaus et al.35 (4.29-6.90 (4.87-3. 2005.07 (2.41-9.51-4.0 (10. 2000).61-5.4) 8.20 (7.S.1-13.76 (3.S...43) 6.15-12.10) 3.1) 8.20 (2.98) 3.7 (11.02-4.19-6.60) 8.24-2.95 (2.30) 90th 9.20-3.14 (2.0 (11.80-3.00 (6.99-3.52-9. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.39-4.45) 3..60) 3.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.10-3.44-6.00-3.0) 7.08) 3.58) 2.30) 3.54 (3.60-5.25) 5.22-4.. population from the National Health and Nutrition Examination Survey.35 (2.60-8.90-15.10) 6.51 (3.70-3.34-3. 2006.52 (8..89-3.1-16.36 (8. Also.46 (3.10 (2.16-3. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005).66) 3.09) 3.80-3.08 (3.0) 4.60-11.87 (5.80) Selected percentiles ( 95% confidence interval) 50th 3.50) 95th 12.90) 5.10 (4.2) 8. and the presence of other substances known to affect thyroid function (e. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition. although iodine intake was higher than U.30 (6.89 (2.77 (3.61 (5.00 (4.4 (11.S.70-5. thiocyanate. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.3 (10.76-3.3) 11.4) 13.0 (8.0) 13.05 (4. 2003.50-5..80 (7.3) 8.90-3.0 (11.0) 12. U.87 (7.12 (6.10-7.0) 12..40) 17.6-17.0) 9. 2002.30-5. However.0-14. 2002.32) 5.60-3.25) 5.86) 4. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.20 (4.33 (7.50-9.60-5.40-10.90 (2.09 (7.20) 3. 2005.21 (2.00) 4.0) 6.97-5.1 (11.56 (3.90-20.03 (2.93-7.60-8.87) 2.70) 2. 2007).20 (3.2) 8.30 (5.. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses. dietary iodine intake.44) 3.40 (4. Many factors may be important in consideration of perchlorate action on the thyroid: dose. Survey years 01-02 03-04 Geometric mean (95% conf.S.90-11.5 (13.50) 9.50 (3.4 (10.30) 75th 5. nitrate.61-10.S. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.90 (7.10) 13.93-5. 1999.02) 3.70 (2.25) 5. 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.75) 3.40) 3.EPA.00 (2.93) 3.00-11.4 (8.70 (4.0-19.00) 9.S.90-2.24 (4. Lamm and Doemland.50) 2.20-4. in a representative sample of U.g. interval) 3.20 (6.80 (4.96) 2.0) 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 3.18-3.90-9.10 (4.1-22.53 (2.60-11.87) 7.22 (2.84) 2.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals . levels.80 (7.8 (11.0 (9. chronicity of exposure.0 (8.22-4.S.26) 4.46-13.72 (3.00-2. medications). 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. up to 68% RUI has been demonstrated.54 (2.0-14.0) 10. 2005).67) 5. 2001.00) 3.EPA.20-9.70) 10.0) 13.5) 8. Lawrence et al.Perchlorate inhibition (RUI). women with urinary levels of iodine less than 100 micrograms per day.73) 3.50) 5.45-2.4-16.30-5.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.6) 20.33-12.50 (6.0) 12.0) 14.26 (3.0 (11.64) 5. perchlorate is negative in most genotoxic assays (U.70-15.12-2.10 (6.40 (7.30 (3..25 (3.70 (2.10) 4.3-14.50-3.37-13.83 (5.3) 12.19-10.30-10.56-3.90 (2.64-3.37 (4.50) 2.6) 12. NAS.99 (5.74) 7. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.20-3.81-3.0-17. 2002).04-3. During gestation and infancy. 2005).0-44.47) 2.40 (3.40) 5.4 (11.0) 12. menopausal status.50) 6.60) 10. Li et al.29) 2.59) 3.60-15.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.82 (5.60 (3.20) 8.30) 5.0 (9.93-5.33-6.22-6.39 (3.0) 9.70-4. levels and sufficient in most participants (Tellez et al.1 (8.10 (1. gender.71 (5.60-6. In the U.93-8.39) 2.04-3. Greer et al.0 (9.46-4.

42(2):200-205. epa.cdc..45(10):1116-1127. Kirk AB. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Daaboul JJ. Caldwell KL. J Expo Sci Environ Epidemiol 2007. Perchlorate in the United States.40(21):6608-6614. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Erratum in: Environ Health Perspect 2005. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Crump KS. Blount BC. Lamm SH. et al. Li Z. CFSAN/Office of Plant & Dairy Foods. Blount et al. National Academy of Sciences (NAS). Kelsh MA. Lawrence JE. Rutherford GW. most of the population is considered to be below the U.htm. and nitrate on thyroid function in workers exposed to perchlorate long-term. Deyhle GM. Perchlorate Exposure of the US Population. 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. Environ Sci Technol 2006.fda. Additional information about exposure and health effects is available from the U. 2005). Steinmaus C. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect..113(11):A732. May 2007. Thyroid 2001. Lamm SH. Lamm SH.113(8):10011008. Washington (DC): National Academy Press. EPA reference dose (Blount et al. Braverman LE. Primary congenital hypothyroidism. 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.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. J Occup Environ Med 2000. Valentin-Blasini L. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Low dose perchlorate (3 mg daily) and thyroid function. Jackson WA.115(9):1333-1338. Braverman LE.S. Dyke JV. He X. Landingham CB.11(3):295. Howd R. Lau EC. Pleus RC. References Blount BC.110(9):927-937. Analysis of relative source contributions to the food chain.html and from ATSDR at: http://www. J Clin Endocrinol Metab 2005. J Occup Environ Med 2003. Abarca CR. Benchmark calculations for perchlorate from three human cohorts. thiocyanate. Food and Drug Administration (FDA). Doemland M. et al. Goodman G. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Available at URL: http://www. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis.gov/safewater/ccl/perchlorate/perchlorate. Lawrence J. Barnard JC. Pirkle JL. 2007). Also. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Tellez RT. 2001-2002. The effect of perchlorate. population.atsdr. Buffler PA. Environ Health Perspect 2005. Osterloh JD. Braverman LE. Skeels MR. 2005. Byrd D. et al. Page Last Updated: 05/28/2009. newborn thyroid function. Sesser DE. Cross M. Pino S.S.46(5):509. Gibbs JP.S. Health Implications of Perchlorate Ingestion.90(2):700-706.10(8):659-663. Environ Health Perspect 2007. Blount BC. 6/2/09 Greer MA. 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. Thyroid 2000. (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.gov/toxpro2. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. et al.html. and environmental perchlorate exposure among residents of a Southern California community. Erratum in: J Occup Environ Med 2004. National Research Council of the National Academies. Crump KS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.17(4):400-407. Dasgupta PK.EPA at: http://www. Richman K. Greer SE. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Magnani B. Mauldin JP. Li FX. Lamm S. Neonatal thyroxine level and perchlorate in drinking water.41(5):409-411. Osterloh JD. 2005). Environ Health Perspect 2002. Miller MD. Valentin-Blasini L..114(12):1865-1871. Pirkle JL. Pino S. Environ Health Perspect 2006. Chacon PM.

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

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

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) . 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.500-1. 2003).500-1.50) .. At doses causing maternal toxicity.900 (.40) .10) * 03-04 03-04 * * < LOD < LOD < LOD . animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 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. Cook et al..700) . 2003..600 (.400-.400-. population. and humans..S. reproductive.00 (..800) 1. 2007a.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 2007b)...500) . 2004.900 (. In such studies. 2003a). 2007.80) 485 538 962 Limit of detection (LOD.900 (.800 (. perfluorohexanesulfonate (PFHxS). Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. the potential to estimate risks to humans from animal doses is uncertain. 2003). development in offspring was stunted and hypothyroxinemia was observed. possibly related to lung immaturity (Lau et al. monkeys.400 (<LOD-.400) .3.600-2.400-1.10 (. Lau et al. hepatotoxicity. 1992. However. 2001.600 (.80) 640 1454 03-04 03-04 * * < LOD < LOD . 2005). 2003a. Olsen et al.500) . U. PFOS. which may vary for some chemicals by year and by individual sample.500-... the median PFCs values tend to be roughly similar in these age categories (Olsen et al.400-1. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. 2003. At high but non-toxic maternal doses of PFOS.. population from the National Health and Nutrition Examination Survey. PFOA.400 (<LOD-..500) 90th .. 2004).700 (.500-1. In comparing three separate reports on adults.20) . thyroidal). 2004a. Harada et al. 2003a). Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years... Fei et al. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. Olsen et al. U.. 2005).S.800 (.500-1.00) . and changes in thyroid hormone concentrations (Grasty et al. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2007a.400-1. see Data Analysis section) for Survey year 03-04 is 0. Olsen et al.500) . 2003a. 2007b.300 (<LOD-.500) .300 (<LOD-..S. EPA.. < LOD means less than the limit of detection.108 times higher than background serum levels in humans (Butenoff et al. 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. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP...500-3.80) 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 . elderly and children. 2007). Thibodeaux et al.600 (. 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. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.500 (.800 (. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.800) 1.S. 2003. 2004).400-1. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.300-1. PFOS.00) .400 (<LOD-. 2003). Survey Geometric mean (95% conf. developmental and teratogenic effects were demonstrated in offspring. Animal studies of PFOS have demonstrated weight loss. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. 2003a.500 (<LOD-1.10) . EPA.800 (.. PFOA.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.500 (. 2004b).400-1. 2004.. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1999.300 (<LOD-. Kennedy et al.10) . Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. and there was no clear evidence of excess all-cause or diseasespecific mortality.

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

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.S.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) 485 538 962 Limit of detection (LOD.0.400 (. see Data Analysis section) for Survey year 03-04 is 0.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample.300 (<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.300 (<LOD-. see Data Analysis section) for Survey year 03-04 is 1. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 251 . Survey Geometric mean (95% conf.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 . < LOD means less than the limit of detection.500 (<LOD-.300-.600) < LOD . population from the National Health and Nutrition Examination Survey.900) < LOD .400) .500-.600 (. < LOD means less than the limit of detection.3. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (<LOD-. population from the National Health and Nutrition Examination Survey.400 (<LOD-.S.

20 (6.60 (1.30 (7.20) 1.900-1.42 (1.900-1.30) 3.697-1.30-9.30 (6.800-1.900 (.50 (4.80 (4.700-1.90 (2.10-9.17 (1.40) 1.20-1.80-8.27) 1.10) 6.40-1.10 (.30-2.6) 7.20 (1.00-7.50 (1.70-6.80) 3.80-2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.30 (2.90) 1.40) 2.40-1.00-1.80-7.09 (.10) 75th 1.00 (.40) 1.01 (1.10 (.80) 4.S.92 (1.40 (1.60-3.689 (.20 (1.20-1.72 (1.1) 485 538 962 Limit of detection (LOD.5) 5.10) 4.20-2.50 (4.30 (1.60-7.20-1.70) 1.80-8.20) 485 538 962 Limit of detection (LOD.00 (. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. interval) .70 (2.60-2.72) 1.50 (1.852 (.73-2.70) 3.816-1.62-2.60-2.70) 1.77-2.809) 1.80-3.30 (3.50 (6.00 (1.04) .10-9.60 (1.00) 1.70) 13.10) 1.900 (.51) 1.90) 1.50-3.50 (2.80-12.80 (1.90 (4. see Data Analysis section) for Survey year 03-04 is 0.800 (.3.90 (1.40 (1.00) 2.30-6.90-2.00-1.90 (4. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60-8.40 (1.600-.90-10.08) 2.00-8.50 (1.586-.30 (1.50) 6.20 (6.20) 2.900-1.30 (1.10 (.10) 8.3 (9.40) .60) 9.70) 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 1.721-1.50 (6.60 (6.26) 2.50-10.963 (.05-2.00) 3.50-6.03) 1.10) 4.90-19.1.10) 75th 3.10) 1.10) 6.40 (1.900) 1.984 (.90) 1.60) 1.80-3. Survey Geometric mean (95% conf.80-6.10 (4.40) 4.700 (.50 (1.14 (.835-1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.54) .93 (1.10-5.90 (1.90 (1.20) .60) 2.0) 8.80 (1. Survey Geometric mean (95% conf.00 (1.10 (1.12) .0) 1053 1041 03-04 03-04 03-04 1.60 (1.56-1.20) 03-04 03-04 2.30) 3.S.80) 1.5) 8.10) 1053 1041 03-04 03-04 03-04 .44 (2.67-2.90) 8.91) 2.912-1. population from the National Health and Nutrition Examination Survey.70-5.10) 5.80-4.80) 5.90) 3.70-2.900-1.50-6.00 (2.900-1.16) .60-3.40-3.00 (1.60-4.861 (.60-2.10 (4.70) 2.900-1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.80-4.966 (.826-1.90) 90th 5.80-7.834-1.70) 2.70-2. population from the National Health and Nutrition Examination Survey.50) 2.70-7.30) 3.20 (1.86 (1.20-3.20-1.00) 1. interval) 1.80-4.87-2.00-6.50) 2.90 (1.00 (1.30-12.40) 640 1454 03-04 03-04 2.60) 3.80) 90th 2.30 (1.20) 1.00 (5.70 (1.60-4.40 (2. see Data Analysis section) for Survey year 03-04 is 0.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.30 (2.30) 03-04 03-04 .20 (1.30) .17-1.70-10.40) 640 1454 03-04 03-04 1.

40) 3.4) 640 1454 03-04 03-04 23.90-4.5 (28.7 (35.40-6.8-81.5) 19.20) 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 21.2-22.50-13.7-53.50) 7. see Data Analysis section) for Survey year 03-04 is 0.96 (3.20) 5.7-30.6 (19.40) 90th 7. population from the National Health and Nutrition Examination Survey.37 (2.3) 42.50-6.8) 32.50) 4. Survey Geometric mean (95% conf.80-4.4 (23.60-14.4) 21.7 (43.10 (3.47 (4.30-5.10 (3.8-78.2 (21.89 (3.1-33.1 (19.0-66.6) 18.2 (18.1.6) 62.0 (27.5) 8.2) 640 1454 03-04 03-04 4.5-33.50-4.S.00 (5.20-9.6) 21.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.9-23.10 (6.6 (42.3-61.60 (5.80) 8.5) 7.3 (28.85-4.6) 1053 1041 03-04 03-04 03-04 3.7 (35.30-11.7-69.2 (27.5 (28.0) 90th 41.8) 27.40-14.1) 15.0) 03-04 03-04 19.9-38.3 (35.7-49.40) 75th 5.21-3.2) 30.1-35. interval) 3.1 (23.20) 10.1) 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) 6.2) 45.60 (4.35) 3.5) 18.70-7.7 (7.70-5.70-9.40 (4.2) 30.79) 4.99-3.8 (34.5) 32.60 (3.6) 42.9 (13. population from the National Health and Nutrition Examination Survey.80 (6. Fourth National Report on Human Exposure to Environmental Chemicals 253 .5) 57.27) 4.3-22.1 (24.70 (5.2 (16.7 (19.1-24.8-22.0) 21.95 (3.4 (28.6) 35. interval) 20.9-19.60) 03-04 03-04 3.6-24.0 (20.80-12.9 (22.80-9.7) 39.53) 3.20-4.1-52.6-50.0) 23.0) 21.5) 9.30) 6.4) 20.2 (19.70) 4.20) 5.4) 75th 30.60-13.90 (7.0-20.40) 5.60 (7. see Data Analysis section) for Survey year 03-04 is 0.11 (2.8-22.47-4.8-30.67-4.3 (35.3 (17.4-42.91) 3.60 (6.4) 56.5-62.30 (3.84-3.60 (6.4 (19.70-7.40-10.0) 43.3) 28.70 (3.70) 3.3 (44.S.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.8-22.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.82) 4.3) 41.8) 46.50 (4.5-23.9) 22.40-6.30 (5.3) 485 538 962 Limit of detection (LOD.10) 5. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.6) 7.0) 36.0-16.65-4.90-12.90 (7.20-5.6 (44.7-33.4-25.6-45. Survey Geometric mean (95% conf.40 (6.7-23.90) 6.1) 57.20) 7.18 (3.70-10.4 (17.7 (43.90 (5.8 (37.9 (19.8-35.1-25.60) 8.30-6.80 (5.4-17.50 (3.0) 485 538 962 Limit of detection (LOD.2 (28.30-8.10-3.00 (3.30) 7.20) 7.1-36.9 (17.20 (4.40-17.6) 9.70 (5.9) 9.5) 1053 1041 03-04 03-04 03-04 14.4.9) 22.90-4.7 (13.80 (6.00 (5.30-3.20 (4.60-9.80 (7.4 (19.9) 27.00) 3.60-6.90 (7.6 (35.0-70.2-57.07-4.30 (3.5-21.8 (45.

interval) Selected percentiles ( 95% confidence interval) Sample 95th .500) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.200-.300) .300) .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.4.300) .400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .300) .200-. see Data Analysis section) for Survey year 03-04 is 0.200-.500) .500) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) < LOD 485 538 962 Limit of detection (LOD.300 (. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.400 (<LOD-.300 (.300-.200-.200 (<LOD-.300 (.300 (.300-.300 (.200-.200-.2. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.300-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection. 254 Fourth National Report on Human Exposure to Environmental Chemicals .500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.300 (.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .S.300 (. population from the National Health and Nutrition Examination Survey.300) .500) 485 538 962 Limit of detection (LOD.300 (. see Data Analysis section) for Survey year 03-04 is 0.200-. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.300) . population from the National Health and Nutrition Examination Survey.300-.300 (.300) .200-.300 (.

80) 1.00 (.700 (<LOD-. population from the National Health and Nutrition Examination Survey.10-1.90) .50 (1.30 (1.80) 1.10 (.30 (1.30) .10) 1.70) 1.10) * 03-04 03-04 * * < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 1.900 (<LOD-1.S. see Data Analysis section) for Survey year 03-04 is 0.600) .60) 485 538 962 Limit of detection (LOD.00 (.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .800 (<LOD-.400 (<LOD-.300 (<LOD-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .10 (1.10 (.900-1.900-1.600 (<LOD-1. which may vary for some chemicals by year and by individual sample.700) 90th 1.40) < LOD < LOD .300-2.900 (. population from the National Health and Nutrition Examination Survey.00) < LOD .700) .10-1.10) 1.20) 1. Fourth National Report on Human Exposure to Environmental Chemicals 255 . < LOD means less than the limit of detection.3.900) .900-1.800) .700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700) 1.900-1.10 (.600 (<LOD-.700 (<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 .40) 1. see Data Analysis section) for Survey year 03-04 is 0.30) 1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (<LOD-.400 (<LOD-1.10-1.10-1.50 (1.10-1.900-1.300 (<LOD-.10) .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.900-1.700) 1.30 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. which may vary for some chemicals by year and by individual sample.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.700 (<LOD-.900-1.600 (<LOD-1.60) 640 1454 03-04 03-04 * * < LOD < LOD .00 (.20 (1.600 (<LOD-1.800) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .900) 485 538 962 Limit of detection (LOD. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500 (<LOD-.00-1.700 (<LOD-.20-1.700 (<LOD-.10) . Survey Geometric mean (95% conf.900) 1.6.700 (<LOD-2.00 (. < LOD means less than the limit of detection.

179:99-121. Keller JM. Rev Environ Contam Toxicol 2003. Wong LY.S. Needham LL. Aguilar-Villalobos M. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Suzuki E. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Olsen J. Grasty RC. Environ Sci Technol 2005. Arendt MD. Inoue K. Kannan K. Halden RU. Koizumi A. Cook JC. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Characterization of risk for general population exposure to perfluorooctanoate. et al. Edwards EA. Needham LL. Butenhoff JL. Harada K. Kamiyama S.Koizumi A. Kuklenyik Z. Kuklenyik Z. and ex vivo studies. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Needham LL. et al. Chlorinated. Moore JA. O’Connor JC. Chem Biol Interact 2000. Apelberg BJ. Mandel JH. Peterson RE. Hurtt ME. Murray SM. McLaughlin JK. Wijeratna S. Kennedy GL Jr. Loganathan BG.104(2):322-333. 2007b. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Moore RW. Falandysz J. Bookstaff RC. Dinglasan MJ. Guruge KS. Kannan K. et al. Environ Health Perspect.38(17):4489-4495. Toxicol Appl Pharmacol 1990. Environ Sci Technol 2004. Katakura M. Calafat AM. Environ Sci Technol 2005. Kawashima Y.7(4):371-377.39(23):9057-9063. Herbstman JB. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Environmental and toxicity effects of perfluoroalkylated substances.60(1):44-55. Gaylor DW.S. Yoshinaga T. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Day RD.134(1):18-25. Mohotti KM.41:2237-2242. Butenhoff JL. The influence of time. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Caudill SP. et al. et al. Liu RC. Grey BE. Harada K. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Holmstrom KE. Jarnberg U. Hurtt ME. Biegel LB. Cook JC. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Biegel LB. Bignert A. Mandel JS.and perfluorinated acids. Cook JC. Chemosphere 2006b. Seneviratne HR. Lau CS. Polyfluoroalkyl chemicals in the U. and perfluorinated contaminants in livers of polar bears from Alaska. Environ Sci Technol 2005. Tarone RE. Reidy JA. Corsolini S. brominated. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Evans TJ. Taniyasu S. Taniyasu S. Olsen GW. Crit Rev Toxicol 2004. Environ Res 2005. Fillmann G.38(10):2857-2864. Hekster FM. Sasaki S. Yun SH. Olsen GW. de Voogt P.60(10):722729. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Yoshinaga T. Kuklenyik Z.1968--2003.39(3):363-380. J Occup Health 2004. Occup Environ Med 2003. Kuklenyik Z.39(1):80-84. Kumar KS. The toxicology of perfluorooctanoate.115(11):1596-1602.46(2):141-147.39(23):9101-9108. Morikawa A.115(11):1670-1676. Toxicol Appl Pharmacol 1995. Saito N.113(2):209-217. Olsen GW. Calafat AM. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism.99(2):253-261.40:21282134. Birth Defects Res B Dev Reprod Toxicol 2003. Calafat AM. Ingall GB. Tully JS. Witter FR.115(11):1677-1682. Bandai N. et al.34(4):351-384. Frame SR. Fluorotelomer alcohol biodegradation yields poly. Hurtt ME. Rogers JM. Fei C. Environ Sci Technol 2007a. Seacat AM. Laane RW.68(6):465-471.63:490496. Tully JS. Watanabe T. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Environ Sci Technol 2004. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Needham LL. Regul Toxicol Pharmacol 2004. Reidy JA.Perfluorochemicals References Alexander BH. Environ Health Perspect 2007. Androgenic deficiency in male rats treated with perfluorodecanoic acid. O’Connor JC. Environ Health Perspect 2007. Mandel JH. Kudo N. Yamashita N. Toxicol Sci 2001. Rodricks J. Kannan K. Frame SR. Caudill SP. Mabury SA. Burris JM.124(2):119-132. in vivo. Ye Y. Reidy JA. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Environ Sci Technol 2006a. et al. Perfluorinated chemicals in selected residents of the American continent. Yamashita N. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Calafat AM. Perkins RG. Toxicol Appl Pharmacol 1992. J Environ Monit 2005. Calafat AM. Inoue K. Reidy JA. Saito N.

fate and transport of perfluorocarboxylates. Ehresman DJ. Environ Health Perspect 2005. birds. Thibodeaux JR. fish. U. Available from URL: http://www. Butenhoff JL. Grey BE. Seacat AM. Burris JM. Biochim Biophys Acta 1993. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. 2003a. Toxicol Sci 2003. Buck RC. Stanton ME. Chemosphere 2007b. Toxicol Sci 2002. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Olsen GW. Burris JM.198(2):231-241. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat.68:105–111. and food items prepared in their packaging.113(5):539-545. Huang HY.26(1):47-51. Mandel JH. Pepper K. Peterson RE. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Bronson R. Half-life of serum elimination of perfluoroo ctanesulfonate. Gamo T. Thomford PJ. Korzeniowski SH. J Ag Food Chem 2007. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Helzlsouer KJ. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.82(1):359. Moisey J. Historical comparison of perfluorooctanesulfonate. EPA). Butenhoff JL.Perfluorochemicals Kudo N. II: postnatal evaluation. Seymour C. Nesbit DJ. Lau C. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Burris JM. Sources. Mandel JH. Lundberg JK.41(9):799-806. J Occup Environ Med 1999. Richards JH. 2007a. Butenhoff JL. 1/15/06 Vanden Heuvel JP. Yamashita N. Church TR. Toxicol Sci 2003. Environ Sci Technol 2003.45(3):260-270. Kannan K. Hanson RG. Taniyasu S. Olsen GW.55:3203-3210. Thibodeaux JR. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Olsen GW. Kannan K.2(1):53-76. Hansen KJ. van Belle G. et al.perfluorohexanesulfonate. Chemosphere 2004a. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. A global survey of perfluorinated acids in oceans. Burlew MM. Church TR. Prevedouros K.115(9):1298-1305.) Tittlemier SA. Barbee BD. Taniyasu S. Rogers JM. Ellefson ME. The developmental toxicity of perfluoroalkyl acids and their derivatives. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. htm. Zobel LR. perfluorooctanoate andother fluorochemicals in human blood.40(1):32-44. Butenhoff JL.68(1):249-264. Butenhoff JL. 2003. Ehresman DJ. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Sterchele PF. Larson EB.S. and perfluorooctanoate in retired fluorochemical production workers. Church TR. Petrick G. Rogers JM. Grey BE.gov/opptintr/pfoa/pfoara.epa. Lundberg JK.74(2):369-381. et al. Mandel JH. Cousins IT. Hansen KJ. Hanson RG. Burris JM. fish. Olsen GW. Horii Y.74(2):382-392.111(16):1900) Olsen GW. Hansen KJ. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Olsen GW. J Children’s Health 2004b.1177(2):183-190. Biol Pharm Bull 2003. Mair DC. fast foods. Coordinate induction of acyl-CoA binding protein. and humans from Japan. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. I: maternal and prenatal evaluations.54(11):1599-1611. Hansen KJ. Rogers JM. Washington.111(16):1892-1901. Hansen KJ. Froehlich JW. Olsen GW.S. Cao XL et al. Burris JM. Reagen WK. et al. Olsen GW. Seacat AM. Olsen GW. Environ Sci Technol 2006. Hanari N. Butenhoff JL.37(12):2634-2639. Yamashita N. J Occup Environ Med 2003b. et al. et al. Case MT.. Horii Y. Kawashima Y. Miller JP. (Erratum in: Environ Health Perspect. Mar Pollut Bull 2005. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. et al. Environmental Protection Agency (U. Toxicol Appl Pharmacol 2004. (Erratum in: Toxicol Sci 2004. Mandel JH.51(8-12):658-668. Environ Health Perspect 2003a. Environ Health Perspect. Lau C.

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

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

Richthoff J. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. 2000a [online]. Boehmer S. Stringer WT. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets.html.25(2):293-302. et al. Dalgaard M.niehs. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Environ Health Perspect 2002. Jonsson BAG. Research Triangle Park (NC). Fromme H. Davis BJ. Suzuki T. Calafat AM. Hauser R. Grote K. Tsukino H.195:142-153. Environ Health Perspect 2003. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Park S. et al. Leffers H. Singh NP.11(5):381-387. Borch J.html. Balasubramanian AV.64(8):555-560.46(11):643-647. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Int J Hyg Environ Health 2007. David RM.112(17):1740]. Meeker JD. Lovekamp-Swan T. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. White R. Environ Health Perspect 1995. Hartle RW. consumer milk. Csanády G. Wang P. Zhang S. Reprod Toxicol 2005. 2000c [online]. Skakkebaek NE. Giwercman A. 2006 [online].gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Liss GM.26(8):1219-24. Kalita JC. Gans G. Nielsen J. Henttu P. Available at URL: http://cerhr. Kessler W. Reynolds T.18(1):122. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. gov/chemicals/dehp/dehp-eval. Research Triangle Park (NC). Harris CA. 6/2/09 Okubo T. et al.103:582-587. Hum Reprod 2007. Kano I.382:10841092.niehs. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Baird DD. Butala JH. Available at URL: http://cerhr. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. The estrogenic activity of phthalate esters in vitro. Determination of phthalate monoesters in human milk. Am Ind Hyg Assoc J 1985. Available at URL: http://cerhr. Hoppin JA. 6/2/09 NTP-CERHR. NTP-CERHR. Brock JW. Pan G. Ladefoged O.html. Biol Pharm Bull 2003.gov/chemicals/ phthalates/dbp/dbp-eval. Reprod Toxicol 2004. Skerfving S. Silva MJ. Jobling S.112(17):1734-1740. Research Triangle Park (NC). Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Brock JW. Environ Health Perspect 1998.nih. Calafat AM. McKee RH. Chen Z. Jacobsen H.nih. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. and infant formula by tandem mass spectrometry (LC-MS-MS). Silva MJ. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.gov/chemicals/dehp/dehp-eval. Hass U.niehs. Kano K. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).nih.22(3):688-695.Phthalates in human urine samples. Chahoud I.html. Davis BJ. Park MG. Sumpter JP. Available at URL: http://cerhr. Filser J. Mortensen GK. Yokoyama Y. Environ Health Perspect 1997. Hauser R.106(1):23-26.nih.105:802-811. Main KM. 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 . Scand J Work Environ Health 1985. Toxicol Appl Pharmacol 2004. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int Arch Occup Environ Health 1993.210:21-33. Epidemiol 2005. Duty SM. J Androl 2004. 6/2/09 NTP-CERHR. Hagmar L.niehs. 6/2/09 NTP-CERHR. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 2004. Parker MG. Albro PW. Bolte G. et al.110(5):515-518. Hanaoka T. Numtip W. Ryan L. Jarfelt K. Meeker JD. Drexler H. Reproducibility of urinary phthalate metabolites in first morning urine samples. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Milligan SR. Duty S. Angerer J.16(4):487-493. Andersson A-M. Ryan L. Rylander L.19(4):505-515. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Yoshimura M. Research Triangle Park (NC). Akesson B. Anal Bioanal Chem 2005. Sumpter JP. Silva MJ.111(2):139-145. Koch HM. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Mechanisms of phthalate ester toxicity in the female reproductive system. 2000b [online].

Jackson SJ. Malek NA. et al. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Peters JM. Urinary levels of seven phthalate metabolites in the U. Lambright CR.114(11):1643-1648. Bratt H. Clemons JH. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Rhodes C. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.65:299-308. Pratt IA.36:459-479. Orton TC. Caudill SP. Klinefelter GR. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Barr DB. Cunningham ML. Albro PW. Abbott BD. Environ Health Perspect 2004. Hodge CC.112(3):331-338. Fielden MR. Silva MJ. Toxicol Sci 1998. Parks LG. Zacharewski TR. Matthews JB. Wu ZF.46:282-293.S.Phthalates phthalate (DEHP): a cross-sectional study in China. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Reidy JA. Ostby JS. Crit Rev Toxicol 2006. Peck CC. Environ Health Perspect 1986.58:339349. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Environ Health Perspect 1982. Batten PL. Toxicol Sci 2000. Environ Health Perspect 2006. et al. Meek MD. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. 112(5):A270]. et al.45:11-17. Rusyn I. Barlow NJ.

2) 15.1-16.0-55. 01-02.5 (13. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.9 (39.3-88.6) 15.9) 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. because it is not bound to products in which it is incorporated.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3-27. 2000).4) 75th 35.8-48.6-39.3 (54.0) 24. High dose BzBP and its monoester metabolites.1) 13.5-41.4-15.3-18.8 (38.2-116) 122 (102-143) 101 (84. vinyl tile.5-84.4 (32.6 (13.8-64.3-43.1.9 (28.4 (59.7) 40.0 (55.3-21.5 (27.8-76.4) 12.4 (10.4 (48.6-72.7 (15.9 (21.6) 24. interval) 15.0 (15.S.3-18. 2001-2002.1 (14.6) 37.4 (32.0 (33.4) 81.1-39.3) 13.1-35.8) 14.4) 14..8 (21.3-75.6) 63.3) 13.0 (12.9-190) 86.8-121) 79. residents (Blount et al.3) 37.4-16.3-91.9) 12.8) 28.7-58.9 (13. it can be released into the ambient air during use or disposal of the products.0 (30.0) 23.0 (23.9-87.3) 15.5) 65.4 (27.5) 16.0) 90th 67.5) 27.6 (66.8-98.6) 50.1-120) 52.5-33.2-33.7 (82.2) 66.2-115) 113 (91. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.2) 14.3 (12.5) 15.1) 14.9) 14.0-106) 58.6 (13.4) 129 (98.6 (13.5-36.1) 31.5 (26.8 (71.4) 80.9 (70.1-15.7-172) 103 (74.9-47.2) 33.4-127) 80.2 (25.2-20.8-17.1 (32.3 (33.2) 13.2 (10. respectively.8 (10.7 (51.2-183) 101 (78.2-155) 91.1) 29.4-62. some personal care products.9 (11.6) 29.4 (68.5 (67.5-145) 138 (106-241) 143 (127-179) 120 (99.9) 49.2-19.9-27.5-36.0-26. particularly male animals (McKee et al.5-35.8 (53.4 (63. see Data Analysis section) for Survey years 99-00.9) 13.6) 14.4 (53..1 (19.1 (58.6) 67.8 (12.6-132) 103 (84.3-130) 122 (88.5 (61.4 (10.3-12.7-35.1) Selected percentiles ( 95% confidence interval) 50th 17.7) 38. and 0.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16. and 03-04 are 0.0 (34.5 (57.3) 63.3-82.7-16.7-119) 99. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.7-15. including MBzP.8 (86.7-13. 2004.6 (21.5) 30.9 (12.7-170) 169 (134-198) 152 (99.4) 71.1-116) 122 (93.8 (14.8 (80.6-17.0 (43. 2000).7 (53.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.4) 33.0 (20.7 (11.2-38.7 (80.5 (76.9 (12.5 (66. and diet is the major source for general population exposure.3) 54.2) 12.5) 82.6 (53.3.9 (16.5 (47.S.9-14.4) 38.1-214) 166 (116-191) 145 (110-213) 88.8-18.3 (12.Phthalates Benzylbutyl Phthalate CAS No.2 (19.3 (13.1) 67.2) 17. 0.2-31.3 (30.4 (13.5-40.4-24.6) 25.6-92. 262 Fourth National Report on Human Exposure to Environmental Chemicals .6 (13.3 (22.9-28.4) 51.7 (12.3 (44.8 (50.2) 32.6) 95th 103 (94.1) 68. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1-90.2-40.5 (55.0-85.6) 13.6-92.8-16.6 (12.8-72.5-18.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.5-94.9) 43.6) 13.8-16.7-17.4) 98.1-15.1 (13.0 (15.8-17.0 (26.7-14.6) 35.2 (19.3 (29.9) 11.7 (70.4-25.6) 35.9-49.1-43.5-97.8-35. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (30.0) 33.1) 12.0 (27.6-43. BzBP can be released into the environment during its production and.3 (12.1 (10.6 (32.8-133) 89.9-62.9) 15.2-17.8) 33.1-16.1) 32.8 (30.1-38.2 (11.8-14.2 (47.7-82.0 (11.8-41. sealants.9 (22.6) 16.1 (13.5) 55.3-34. population from the National Health and Nutrition Examination Survey.2 (43.6-18.6) 14.8) 24.3-125) Total 15. Food crops take up BzBP.7) 23.2) 22. car care products.9) 14.9-16.7 (13. can produce developmental and reproductive toxicity in rodents.6-116) 122 (102-142) 101 (85.3 (29.3) 23.6-29.3-74.8.2) 78.4) 65.4 (31.2) 14.4) 35.9) 18.5-62.7-25.4) 35.7-16.5-14.1) 76.6-38.1-61.1 (55.9-30.5-25.2 (14.3) 94.0) 70.8) 63. and 2003-2004 were generally similar those reported in U. IARC considers BzBP not classifiable with respect to human carcinogenicity.5) 15.2-39. and to a lesser extent.7-16.2-16. NTPCERHR.6-79.8-14.1-18.6 (41.4) 108 (96.1 (14.4 (29.0) 34.0) 20.8-13.4 (53.0-130) 101 (86.5) 23.2) 69.1 (20.6-150) 94.4-92.8 (71.0) 32.3-161) 99.4) 49.2-16.0 (14.8 (28.0) 16.

4-23. 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. In an annual sample of German university students.8) 16.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.2) 15.0 (49.0 (12.8 (10. 2005).1-125) 86.1 (53.9 (9.2-21.3 (39.3 (12.3) 29.8-42.8) 11.7-90.3) 13.2-26.3) 90.8) 54.5-58.1 (21.1 (11.7) 38.9) 12.9) 42.6-20.6 (19.9 (29.4-93.8-39. 2007).6) 25.3-34.9 (24.6-86.1) 27.5 (48.9-62.7-12.7 (11.4 (10.2-117) 95.1) 24.2-13.5-23.9) Total 14.5-26.1 (21.7) 25.3) 12.8 (30. 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.2-57.0 (10.6) 12.7) 56.9) 52.1-12.7-14.1 (18.4-142) 134 (116-176) 136 (85.8-64.7-123) 77.5) 95th 77.7 (14.2) 11.5-61.8 (46.1) 17.8) 24. Weuve et al.1 (13.7-56.95-14.S.1 (25.5) 13.6) 53.9-13.6) 38.9-13.8-60.1-35.8-14.4-18.0 (11.9 (43.9) 11. and females compared to males (Silva et al.9-14.6) 58.4 (25. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.5) 23.1 (46.8) 33.3 (23.0 (12.8-48.9-83.6 (30.1) 23.2) 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. Hauser et al.3) 14.7 (13.5 (10.9 (22. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.5 (35.7 (19.7-31.8) 26.7 (11.9 (10.5-42.3) 18.9) 64.4) 50. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults. 2004).4) 28.1-79.4-19.8-13.3 (13.9-16.8 (50.0) 12.1) 12.9 (15.3-38.9-104) 62.8 (49.7 (18.6-47.8-34.5) 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 . in young Swedish men (Jonsson et al.8-13.4 (34.3) 36.7-29.4 (74.7-19.5-38.2-17.0) 11.8) 34.7 (23.3) 21.8) 53.8) 46.4 (69.5-76.. interval) 14.8) 71.4) 21.3) 55.1 (15.1-27.4-14. and in a small sample of German residents (Koch et al.0 (41.4 (21.4-60.1 (41.4 (63.6-15.5) 46.1-120) 77.9 (12.6-99. In NHANES 1999-2000.2 (40... 2002.5-99.4-17.4 (13.Phthalates York City (Adibi et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 104 (89... 2002).6) 13.8-69.4 (11.0 (41.7 (12.8 (69.3 (15.5-31.7-69.2-51.6 (11.4-79.2) 67.4-116) 73.9) 12.4) 90th 50.2-15.4-27.0) 13.5 (12.6-26.5) 41. 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.4) 17.9) 24..9-23.2) 12.5) 78.5-79.9) 11.5 (9.2) 26..6-40.7 (54. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. adolescents compared with adults.3 (60.8 (57.0-27.0) Selected percentiles ( 95% confidence interval) 50th 13.4 (11.1 (13.1) 142 (99.8-15.6-12.73-12.3) 67.3 (38.4-42.6 (36.6-116) 74.6) 73.7-15.1 (14.4 (26.3) 14.3) 89.3-16..7 (59.4 (60.2 (27.9-115) 57.1 (21.6) 75th 25.9) 12.1) 80.9 (24.9 (55.4) 44.9 (10.6 (30.4) 60.5) 10.8-16. in men attending a Boston infertility clinic (Duty et al.6 (11.4-99.8) 13.0-51.5 (56.3 (35.8 (11.5-58.5) 17.8 (64.4) 12.1 (23.7 (55.4) 14.1) 35.0 (62.9) 100 (80.0-109) 65.5-26.7 (38.1 (19.5 (11.7 (21.4 (33.3-11.1-14.4-14.5 (49.1-12.0-48.69-11.3-73.2-49.0) 24.8) 53.1-58.3) 13.1 (43.1) 24.6 (57.8) 108 (75.5-16.7) 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 40.0 (33.6 (14.5 (42..9-40.6-81.7-397) 70.7) 19.8-85.8-173) 195 (121-305) 229 (99.1-29.2 (41.0) 49.6) 12.8 (12.0 (38.7 (13.4-15.1 (34.5-213) 49.2-13.5) 20.5-13.2 (56.4 (11. 2005.8) 68.2) 32.4-102) 70.5) 14.9 (51. A small study of African-American women in Washington.9-69.9 (15.1) 39.0 (67.3) 13.4 (12. population from the National Health and Nutrition Examination Survey.7-20.4) 13.0-15.0 (13. 2007).7) 11.2-15.0) 15.6 (24.4) 13.3) 73.7-15.8-15.7 (11.4) 25.6-13.5-57. Hoppin et al.4 (46.7-19.5) 16.0-90.3) 37.8 (13.9-28.1 (9.7-20.7-61.0) 24.4-90.3-64.2-12.6 (15.0) 60.6 (11. 2003). 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.2-78.4) 15.8) 80.9 (12.8-80..7) 46.3 (24.8-27.5-29. 2003).9 (54.6 (22.8) 56.3) 16.6 (51.8-14. 2004.6 (34.8-13.1 (21.8) 15.8) 33.2 (69.5 (10.2) 11.0-26. 2006).6) 30.9 (39.4) 51.7-14.0-53.2) 11.

Barr DB. Silva MJ. Wiesmuller GA. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Hagmar L. 112(5):A270]. Environ Health Perspect 2004. Caudill SP. Duty SM. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Silva MJ.nih.22(3):688-695. McKee RH. Silva MJ. Singh NP. Meeker JD. Environ Health Perspect 2000. et al. Available at URL: http://cerhr. et al. Malek NA. Bull Environ Contam Toxicol 2002. Giwercman A. Prenatal exposures to phthalates among women in New York City and Krakow.110(5):515-518. 2000 [online]. Davis BJ. Reprod Toxicol 2004. J Androl 2004.114(9):1424-1431. et al. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Butala JH. Hilborn ED. Reproducibility of urinary phthalate metabolites in first morning urine samples. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Richthoff J. Wittassek M. Brock JW. Environ Health Perspect 2006. et al. Camann DE.210(3-4):319-333. et al. et al.68:309-314. Reidy JA. Jedrychowski W. Koch HM. Jonsson BAG. Helm D. Needham LL. Hum Reprod 2007. Drexler H. Sampson EJ. Baird DD. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Poland. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Hauser R. Rossbach B. Brock JW. Green RA. Ryan L. Koch HM. Gans G. Int J Hyg Environ Health 2007. Calafat AM. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Schettler T. Centers for Disease Control and Prevention (CDC). Perera FP. David RM. Needham LL.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Third National Report on Human Exposure to Environmental Chemicals.html. Hoppin JA. Caudill SP.93:177-185.Phthalates References Adibi JJ.112(3):331-338. Rylander L. Angerer J. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Sanchez GN.108(10):979-982. Brock JW. Urinary levels of seven phthalate metabolites in the U.111(14):1719-1722. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Blount BC. 2005. Hu H. Environ Res 2003.25(2):293-302. Pirkle JL. Calafat AM. Chen Z. Research Triangle Park (NC). et al. Environ Health Perspect 2002. Levels of seven urinary phthalate metabolites in a human reference population. NTP-CERHR. Duty S.16(4):487-493. Ryan L. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Caudill SP.niehs. 4/20/09 Silva MJ. Dobler L. Epidemiol 2005. Weuve J. Jacek R. Hodge CC. Barr D. Environ Health Perspect 2003.18(1):122. Atlanta (GA).S. Silva MJ. Phthalate monoesters levels in the urine of young children. Eckard R.

46) 2.7 (18.80 (5.0) 24.8) 677 652 703 699 1216 1088 Limit of detection (LOD.0-38.70-4.3 (18.3-43.7) 7.97-7. and insecticides.5-29. residents (Blount et al.30) 10.20-12.8) 40.5) 25..1) 25.0) 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 2.44-2.20-9.90-4.80 (2.63) 3. and also in some printing inks. 2007)..30 (4.0) 13.6) 10.00-9.7) 14.1-20. and in a small sample of Japanese adults (Itoh et al.17) 4.90 (4.9-23.30-2.6) 17.7) 18.5) 18.49-2.7) 4.1) 22.40-9. Koch et al. they have been referred to as monobutyl phthalate (MBP).20-6.56) 3.1 (8.0 and 0. Fourth National Report on Human Exposure to Environmental Chemicals 265 .02) 4.4) 12.3) 33.3 (11.3 (13. 2004..20) 7.46 (3.6 (10. in men attending a Boston infertility clinic (Duty et al.0-18.6-14.5) 12. 2005). 2005.9-14.82-3.5) 22.30-6.30 (3.00) 7.84) 4.6) 26. Following oral administration of DBP to humans.3-48. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.66) 2. in a small sample of pregnant women in New York City (Adibi et al.50-4.20 (3. NTP-CERHR.56 (3.5) 14.11-3.3-24.40 (7.30) 6.46 (2.22 (3.. interval) 2.5 (20.00) 6.2 (11.33 (2. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.5-16.2-14.3-20.70) 5.80 (2. 2005).10) 11.00-6.73-5.10-9.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.30) 5.6) 16.20) 4.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.7 (17.40-4. 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.80-5.28-5.91) 4.00 (5. When total DBP metabolites have been measured. 2005).1-12.90-2.3-30.5-16.10-9.0-25..40 (6.50) 90th 12.40 (3.20 (6.3 (16. CDC. 2004.96) 3.48 (2.4 (14. 2000).59) 3. 2001). Survey Geometric mean (95% conf.Phthalates Di-n-butyl Phthalate CAS No.7-18.40-5.70) 3.7 (9.4 (20.10 (4.5 (27.6 (10.3 (16.50 (3.50) 5.. 84-74-2 Di-isobutyl Phthalate CAS No.5 (10.6 (11.43) 6.60 (4.50-2.8 (9.10) 9.20-2.3 (19.55) 2.40-12.40-3.90) 12.50-6. 2003).30-7.60 (5.1-17.90-4. 2003).0 (11.6 (9.71 (2.6-26. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.60 (8.2 (8.2 (12.17 (2. pharmaceutical coatings.6) 12.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.1-25.6 (14. Biomonitoring Information Median concentrations reported in the NHANES 19992000.90 (3.70-8.97) 4. Hauser et al.40-17.90-7.30-6.40 (2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.7 (16.6) 16.68 (2.81 (3.00) 10.7 (17. population from the National Health and Nutrition Examination Survey.50) 7. OSHA has established a workplace air standard for external exposure to DBP.3) 3. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.40-3.. In addition. 2000.4-27.80 (3.5) 19. Studies of children found age-related differences in urine MBP levels.4) 22. mostly as MnBP (Anderson et al.70 (5.10 (4.00-6.70 (2.40 (2.50-10.85-6.8) 21.20 (7.S.1 (13.6-34.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.4) 5.5 (11.22) 3.0) 12.60) 3.90 (4.5) 18.5-24.3 (13.70-4.9) 15.6 (13.40) 5.10) 2.30) 10. about 65% to 80% of a dose is eliminated in urine within 24 hours.5 (17.56 (5.7 (7.7-31.2-22.3) 18.26 (2.60-6.30 (1.73 (2.9 (16.0 (13.0 (13.00-4.97) 2.50 (6.50) 8.7-31. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.80 (5.80-5.S.9 (16.7-20.72-3.46-5.0 (19.37) 6. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates..9) 10.10) 8..24-8.30-3.19-3.6 (14. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.07 (3.67 (5.5) 23.3-19.10-2.3.00 (7.56-4.6-18. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.30-13.4-12.0-14.2) 5.55 (3.00-11.50) 2.00) 4.10) 3.6 (13.90 (6.1) 16.2-33.7) 15.50) 18.6) 17.00) 4. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.60 (2.80) 75th 5.10 (3.0) 9.20-12. DBP can produce reproductive toxicity in male rodents (McKee et al.30-11.30) 2.40-4.3-18.6-20.6 (29.0) 20. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.

7 (13.43) 3.68) 3.37) 3.1-24.20-3.8 (10.09-2.8) 10.3 (13.3) 18.81 (3.32 (3.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .62-12. than adults in NHANES subsamples during the same time period.1) 13.75 (4.01-2.79-6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9 (15. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.0) 15.39-3.29-3.28-13.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.17-12.4) 15.34 (3.4) 23.6-19.82) 4.66) 10.46) 3.33 (2. Survey Geometric mean (95% conf.56) 5. 2007).07 (2.08) 75th 4.0) 11.1) 11. 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.00-3.88 (2..64-7..08-2.9-40.95-3.6) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.32 (7.18 (4.52 (2.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.89 (3.55-6.8-36.31 (7.7) 3.53-3.51) 2.58-4.80) 7.57 (3.1) 4.98 (2.24) 3. population from the National Health and Nutrition Examination Survey.9-26.78) 9.03 (5.9 (11.13 (2. In an analysis of NHANES 1999-2000.84 (8.2-13.0 (12.65 (4.95) 2.57 (3.78-8.84 (4.18-10.1) 7.0 (10.10-5.52-20.32) 7.03-11..99-4.20 (7.6-19.3) 16.1-25.04) 3.72-7.86-4.76 (3.68) 5.7 (11.25) 5.91-6. up to four and 13 fold.59 (4.and gender.53-5.4-16.44 (3.17 (2.33-9.56) 2.2 (11.68 (2. the students’ median values for MiBP levels remained relatively unchanged.69) 4.47-12.35) 3.45) 3.31) 2.3) 13.61-3. An analysis of NHANES 2001-2002 showed similar age.11 (5.74-3.11) 5.S.17) 90th 8.46 (2.6 (10.38 (6.46-11.8-18.33 (3.7) 11.0-18.2) 24.2) 9.3) 13.5-19. respectively.0 (8.11-2.7 (21.58-3.7) 19.64-7. samples from German university students had consistently higher median urine levels of MnBP and MiBP. 2004)..78) 8.89) 6.82 (4.21 (5. 2005). 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.29-8.69 (2. Weuve et al.6 (12.2 (10. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30) 2.6 (15.39) 5.1 (11.74 (4..85 (2. interval) 2. Over this time. ranging from more than one-tenth the NHANES median (Itoh et al. 2005).79 (4.7) 10.3 (17.20 (2.92 (7.8-13.86) 6.02-10.54) 2.43) 3.94 (5. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples. Between 1998 and 2003.94) 6. 2004).66 (8.28 (4.18) 3.5 (11.95) 10.76-15. 2006).2) 8..72) 5.20-4.18) 4.43) 3.19 (2.75 (6. 2002.93-6.1-15.94-12.66) 4.89-5.76-3.33) 3.2-15.0) 7.3) 28.73 (5.5) 13.02 (7.69-7.80-3.30 (6.81 (6.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.51) 5.00-7.1) 10.20 (2.65-4.0) 3.97-2.14 (4.99) 7.9-16.52) 3.47-5.52-3.05) 2.7 (9.15) 3.8 (8. 2007). 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.64-10.26 (2.22 (2.81) 9.8 (9.00-3.53-4.7-28.65-11.54 (4.00 (3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.57-4.36-7.79-8.6) 13.9) 12.07-5.56-15.6 (8. while MnBP declined (Wittassek et al.66) 2.47 (3.03-7.31) 2.51) 15.80 (3.1) 15.6 (9.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.04-5.1-12..67-5.69) 6.20-2.4 (12.54 (2.18 (1.21) 10.56-4.42) 2.5) 15.62 (6.36-2.15-4.27-12.8-18.83 (2.6) 11.41 (2.13-6.81) 4.38-10.1 (10.04) 7.9 (9.6 (8. to about two to fourfold higher (Fromme et al.76-3.26-2.96 (3.31 (2.4) 7.18-4.5 (9.

6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7) 124 (98.3) 21.3-67.0) 84.7-24.7 (43.2-93.7-117) 118 (108-143) 93.7 (18.7-34.7 (18.5-43.7-124) 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.1.7 (70.6 (61.4-60.6 (44.7 (28.7) 28.6-24.7-26.2-49.4 (71.7) 74.9) 75.5) 40. 01-02.6) 71.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.2-24.7-53.5) 20.8) 62.6) 80.0 (36.3) 26.6-143) 127 (99.3) 18.3 (37.4) 64.9-42.6-29.7 (24.5-117) 95.0 (23.0) 120 (98.3 (60.1-80.1 (62.4 (35.1) 25.7-121) 97.6) 21.0 (20. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3) 40.4-42. Fourth National Report on Human Exposure to Environmental Chemicals 267 .3 (23.5 (59.2) 26. population from the National Health and Nutrition Examination Survey.4 (38.1) 19.1 (18. interval) 24.9) 29.1-51.6 (16.4) 22.1) 17.4-31.5 (59.1 (17.7-42.2 (20.7-91.0) 20.0-21.7) 42.6) 35.0-24.0 (17.8-29.4 (36.1-27.1 (19.6) 20.6-113) 108 (90.8) 23. Survey Geometric mean (95% conf.0 (15.3-85.3 (23.9-114) 116 (97.3-96.9-28.3-60.1) 31.2 (58.6 (32.0-51.3) 24.2 (17.6 (90.3-21.0 (18.7-116) 95.9) 18.6-31.3 (36.1) 23.2-56.9) 26.3 (17.5) 21.1 (19.8) 48. referred to as monobutyl phthalate (MBP).3-79.1) 20.7 (51.6-37.1-29.4.5) 36.9-22.7-106) 69.9 (20.6 (65. 1.1 (51.7 (16.9.0) 117 (104-131) 112 (84.3-145) 85.8-132) 95.4) 59.4-18.8-123) 101 (90.1-24.2-114) 73.5-27. and 03-04 are 0.9-101) 77.4-26.6-33.6-48.0 (25.5-44.0 (72.6 (55.7 (33.7-111) 64.S.1) 36.9) 46.0) 21.9-87.5) 47.7-92.8) 58.6) 17. respectively.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.2-33.4 (19.1-92.0 (31.7-127) 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 22.8-42.4-20.3-40.5) 85.2) 32.4 (23.6-49.7 (19.6 (19.1-20.5) 36.6-69.7-42.0-58.5) 24.1 (16.1 (19.9 (79.5 (29.4 (35.9) 71.4-159) 107 (84.7) 52.2 (21.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.1-82. and 0.4 (84.1) 23.2 (75.5-47.2-21.5-47.0) 30.6-44.8) 43.9 (79.1 (19.5) 95.3-136) 137 (107-162) 119 (90.1) 23.9-33.1) 47.9) 36.3-24.2) 90th 98.2) 20.5 (30.5-42.4 (72.9) 21.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8 (57.2) 42.2-63.1) 46.6) 46.2) 62.5) 65.8-119) 90.4) 52.8 (19.6 (26.1 (36.7 (38.1-75.3 (30.5) 34.2-22.5) 37.6-29.6) 38.3 (56.2-23.4 (35.2 (74.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.4 (35.0-24.0-19.2) 38.2 (21.2 (79.1) 30.0) 31.7) 92.3) 19.6-36.0 (45.9 (17.1 (21.6-40.5 (28.0-32.2 (25.7-34.2 (18.1 (41.2-159) 92.5-53.0) 38.4-25.8-25.3 (42.7 (22.3-76.0) 27.2 (19.3 (51.4-44.4 (21.2 (59.5-121) 106 (94.1 (58.8) 75th 51.1 (26.2-87. *In the 1999-2000 survey period.9-92.2) 68.6 (22.9-22.6 (48.6) 39.5) 17.5) 31.2 (78.5) 26.0-26.5-60.8-22.6-20.5) 19.3) 36.0-73.0-19.3) 23.4 (25.5) 78.1 (28.9 (17.9-79.7 (64.8) 19.5 (74.7-20.9-53.0 (30.0 (78. see Data Analysis section) for survey years 99-00.4) 20.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1 (54.1-22.1 (34.3 (30.2-32.1 (31.

5-22.9) 28.6-119) 63.6-128) 96.7 (20.4) 15.7-51.9-14.4 (31.1) 20.8 (16.5 (18.9) 62.0) 41.8) 34.8-24.2-18.5) 90th 68.3) 52.9 (58.4 (16.8-235) 137 (108-198) 88.9 (35.8) 13.4-47.3-20.5 (81.6 (25.8) 35.5-76.2-108) 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.4) 15.5-21.8) 63.5-37. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1-99.6-43.6 (72.3 (21.6 (19.6) 83.1) 42.9) 14. 268 Fourth National Report on Human Exposure to Environmental Chemicals .2-179) 84.6-27.9 (30.0 (71.3 (48.5 (18.0) 108 (71.4 (37.4) 62.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.9) 30.0-19.1) 61.2-73.0) 70.8 (25.5) 17.8) 75th 38.2) 21.1 (56.8) 22.1-18.4-164) 96.3 (24.4-65.5) 91.7 (12.9 (35.2 (19.8) 20.9) 39.9 (19.6) 65.8-24.2-22.2 (35.9) 91.5-41.3-106) 74.5) 60. interval) 22.4 (50.0) 55.0 (20.2) 65.3-114) 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) 94.4 (23.0) 28.7 (81.5) 39.2) 159 (102-263) 147 (93.3) 17.7-26.1) 44.9 (30.0) 53.8 (13.4) 21.4 (18.3) 20.7) 36.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.8) 30.1 (15.3 (46.3 (60.1) 53.7-20.5-15.7 (27.2 (38.5) 134 (93.1-62.5-142) 81.0-113) 104 (83.6-44.6) 39.9 (20.9-105) 85.2-106) 64.6-24.9 (16.1 (61.4-131) 81.3-71.6-92.1) 17.0-38.7 (54.3) 19.8) 17.6 (61.3-39.7 (57.8) 20.8 (18.6) 23.2-22.0 (69.9-68.3-17.4) 19.6 (25.0) 19.3-32.8) 19.6) 38.5-16.3 (42.0 (18.4-72.1) 37.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-18.6-16.3) 33.8-23.8-43.6-28.4 (47.8 (50.9 (39.4 (45.3) 67.4 (17.6) 25.7-80. Survey Geometric mean (95% conf.0-41.S.7-21.7 (28.3 (17.8 (17.0 (70.1) 21.8) 28.9-38.7-19.6 (29.9) 49.3) 21.8) 40.6) 24.7-78.0) 26.4 (50.6-74.2-22.6-23.3-26.0 (16.1-21.4 (31.2) 59.7 (60.6-44.1-99.2) 16.6 (17.9 (73.4) 51.5) 82.6-155) 91.1) 20.8) 17.3 (71.4 (16.2-16.9-26.5 (64.6) 31.7 (43.7) 42.5-70.4-24.9-49.8 (22.4 (17.6 (74.3) 35.6-42.9) 24.6-53.3-81.0) 25.8) 34.4 (33.7-37.1 (21.8-32.2) 74. population from the National Health and Nutrition Examination Survey.0-17.2-85.3-78.4-61.4 (53.9-100) 86.2-28.0-92.2-86.0 (27.4 (13.4 (31.9) 19.5-23.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.5) 84.9-68.6 (31.6-24.4 (19.6 (57.2 (83.2-61.4 (20.3) 33.7) 20.6) 34.7 (14.4 (68.0 (18.0 (52.3) 59.3-21.7 (16.0) 35.8 (18.6-26.2-48.1 (32.0-90.3 (28.7-19.1) 50.6) 24.6) 18.4) 20.3-38.3-21.6) 64.7 (73.9-84.5 (30.1) 22.0 (50.3 (76.1-32.1-23.6-50.3-40.0) 59.8) 17.0) 29.8 (33.9-36.4) 16.4) 53.6-19.5-30.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.6-32.6 (41.2 (16.9) 20.7-42.0-47.7-23.3 (69.0 (34.6 (27.4-34.0) 81.6) 14.9 (21.3 (17.0 (19.7-39.4-103) 117 (83.1-83.9 (37.0) 75.4 (56.3 (17.9 (56.0-75.6) 37.9 (30.8 (65.5-142) 89.3) 19.7-28.3-18.7 (19.9) 52.2) 31.2 (19.3 (52.0-60.5-64.3 (19.9 (64.3 (52.9-70.8 (18.8) 23.1 (34.3 (16.1 (46.3 (55.2-21.1) 35.6-22.7) 19.5) 21.3) 18.0 (61.3-23.2-27.4-76.9-34.7 (60.5 (14.9-56.4-135) 71.5 (15.1 (29.0 (43.6-23.0 (15.3-49.1-128) 97.0 (26.

Calafat AM. Springall C. Castle L. Itoh H. Butala JH.111(14):1719-1722. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Pirkle JL.114(9):1424-1431. Sampson EJ. Yoshida K. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Reprod Toxicol 2004. Eckard R. Environ Health Perspect 2006. J Androl 2004. NTP-CERHR.18(1):122. Hauser R. Weuve J. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Levels of seven urinary phthalate metabolites in a human reference population. Duty S. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Angerer J. Research Triangle Park (NC). Environ Health Perspect 2003. Rylander L. Reidy JA. Wiesmuller GA. Hu H.S. Scotter MJ.16(4):487-493.html. Environ Health Perspect 2004. Drexler H. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://cerhr. Massey RC.22(3):688-695. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Barr DB. Schettler T.210:21-33. Needham LL. et al. Needham LL. Sanchez GN. Brock JW.niehs. Caudill SP. Jonsson BAG.93:177-185.210(3-4):319-33. Caudill SP. et al.nih. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Poland. Jacek R. Hodge CC.68:309-314. Dobler L. 4/20/09 Silva MJ. 2000 [online]. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Giwercman A. Camann DE. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Fromme H. Atlanta (GA). David RM. McKee RH. Barr D. 2005.18(12):10681074. Wittassek M. Green RA. Ryan L. Environ Health Perspect 2000. et al. Brock JW.gov/chemicals/ phthalates/dbp/dbp-eval. Chen Z. Duty SM. Phthalate monoesters levels in the urine of young children. 112(5):A270]. Hum Reprod 2007.208:237-245. Caudill SP. Int J Hyg Environ Health 2005. Urinary levels of seven phthalate metabolites in the U.112(3):331-338. Drexler H. Int J Hyg Environ Health 2007. Masunaga S. et al. Prenatal exposures to phthalates among women in New York City and Krakow. Int J Hyg Environ Health 2007. Rossbach B.108(10)979-982. Silva MJ. Koch HM. Angerer J. Silva MJ. Gans G. Perera FP. Koch HM. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Koch HM. Bull Environ Contam Toxicol 2002. Jedrychowski W. Silva MJ. Helm D. Centers for Disease Control and Prevention (CDC). Ryan L. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Epidemiol 2005. Environ Res 2003. Hagmar L. et al. Calafat AM.25(2):293-302. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Food Addit Contam 2001. Bolte G. Richthoff J. et al. Anderson WA. Singh NP. Malek NA. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Meeker JD. Blount BC.Phthalates References Adibi JJ. Boehmer S. Silva MJ. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Hilborn ED. et al. et al.

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 (.20) .500 (. which may vary for some chemicals by year and by individual sample.400 (<LOD-.300 (. see Data Analysis section) for Survey years 99-00.00) .400 (.200-.200-.50) .300 (<LOD-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. 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.400 (.300-.600 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.80) .200-.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 1.200-. polyvinyl acetate.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 .500) < LOD < LOD . population from the National Health and Nutrition Examination Survey.500 (.50) .400 (.300 (.400-.400-.600) < LOD .500 (. and 03-04 are 0.00 (<LOD-1.700) .500 (.400 (.400-.500) < LOD < LOD . including nitrocellulose. In this Report. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.200 (<LOD-. and polymers.600) .S.500) .500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.400 (<LOD-.500) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.500-.200-.400) 1.500) .10 (<LOD-2.200-.300-.500 (. 0.300) < LOD .300-.300-.500) .600) .300 (.3.900-1.400 (.300-.400) < LOD 1.400 (<LOD-.500) 1. 01-02.70 (1.500 (.9.400) < LOD < LOD .400 (.300 (.500 (.300-. resins.300) < LOD .500) .70 (1.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300-.600) .00-3.300-.300 (.500) 1. and 0.00 (<LOD-1.600) .Phthalates Dicyclohexyl Phthalate CAS No.10 (<LOD-1. only levels at or above the 90th percentile could be characterized. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.10 (<LOD-1.70) .70) .2.400 (<LOD-.700) .00 (<LOD-1.500) < LOD 1.90) .700) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and polyvinyl chloride.400-. respectively.400-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. 270 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.10 (.00-2.600) .400-.500 (. 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.10) .400) 1. < LOD means less than the limit of detection.300-.400 (.300-. Survey Geometric mean (95% conf.

450 (.690-1.16 (<LOD-3.06) .360-.54-6.470 (.500 (.740) < LOD < LOD .33 (<LOD-3.500-.82 (1.770) < LOD 2.310-.00 (<LOD-3.05) .S.18) .910 (.910 (.370 (<LOD-.530-1.250 (.690 (.400-.660) .410 (.12-1.800-1.420-.260-.690) < LOD 2.560) 1.690) < LOD < LOD .16) .590 (<LOD-.770 (.530 (.630 (<LOD-. Survey Geometric mean (95% conf.82) .910 (.380 (.940 (.830) 1.220 (<LOD-.17) .67 (1.880 (.34) .470) 3.670 (<LOD-.310) < LOD .14 (<LOD-3.950 (.330 (.610 (.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.390 (.44) .530) 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 1.420-.290-.240-.43 (1.74) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.770-1.530-.36-1.490) .790-1.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .620) < LOD .510-.33) .480 (.770-1.54 (<LOD-2.630 (<LOD-.740) .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 .400-.670-1.590 (.450 (.710) .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.420-.660) < LOD < LOD .770-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170-.500) 3.330 (. Fourth National Report on Human Exposure to Environmental Chemicals 271 .53) .00) .54) .510 (.10) .06) .22 (<LOD-1. population from the National Health and Nutrition Examination Survey.11) .270) < LOD .350-.910 (.380-.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 .53) .

particularly those containing fragrances. DC (Hoppin et al. 2002).. shampoos. 01-02.7 (70. respectively.2-102) 95.9 (61.1 (71. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2001-2002. and 03-04 are 1. 0. and also in men attending a Boston infertility clinic (Hauser et al. population from the National Health and Nutrition Examination Survey.2. 272 Fourth National Report on Human Exposure to Environmental Chemicals . colognes.1-93. soaps. and hand lotions.8-111) 85.9-92.9.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.3 (82. In contrast.S.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. Products that may contain DEP include perfumes. interval) 179 (156-204) Selected percentiles ( 95% confidence interval) 50th 164 (136-201) 169 (141-194) 174 (151-208) 75th 454 (370-538) 465 (415-527) 502 (457-555) 90th 1260 (1010-1480) 1230 (1040-1440) 1380 (1170-1750) Total 178 (159-199) 193 (169-220) Sample size 2840 (2150-3770) 2536 2500 (1860-3220) 2782 2700 (2160-3310) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 91. and 0.3-103) 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.7) 71. 2007).4 (62. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. 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. 2003) and African-American women in Washington. 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.Phthalates Diethyl Phthalate CAS No. see Data Analysis section) for Survey years 99-00.5) 81. Biomonitoring Information MEP levels in the NHANES 1999-2000.. deodorants.4.3 (74.

.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 .5-113) 122 (93.6 (65. Biomonitoring studies on levels of MEP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEP than are found in the general population. In an analysis of NHANES 1999-2000. 2003) were slightly lower than levels found in NHANES 2001-2002. 2005). population from the National Health and Nutrition Examination Survey. 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.Phthalates 2002 (Brock et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Analysis of NHANES 2001-2002 showed similar findings. 2004).7-110) 81. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.6 (77.0 (66. Median MEP levels found in a small sample of German residents (Koch et al. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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.9-110) 96.S.3-105) 87. Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect. Other population estimates also differed by sex and race ethnicity (Silva et al.2 (66. 2002).. This age-related trend is opposite the direction seen for other phthalates.5-114) 101 (87.9 (82. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.

Barr D. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Reidy JA. Hauser R. Brock JW. Silva MJ. Koch HM.68:309-314. Hoppin JA. Caudill SP. Reproducibility of urinary phthalate metabolites in first morning urine samples. Caudill SP. Silva MJ. Prenatal exposures to phthalates among women in New York City and Krakow. Silva MJ. 112(5):A270]. Environ Health Perspect 2004. Malek NA. Singh NP. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.93:177-185. Ryan L.S. Hodge CC. Davis BJ. Drexler H. Perera FP. Jacek R. Angerer J.22(3):688-695. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Hilborn ED.Phthalates References Adibi JJ. Environ Res 2003. Camann DE. Environ Health Perspect 2003. Hum Reprod 2007.110(5):515-518. Jedrychowski W. Brock JW. Poland. Urinary levels of seven phthalate metabolites in the U. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.111(14):1719-1722. Third National Report on Human Exposure to Environmental Chemicals. et al. Bull Environ Contam Toxicol 2002. et al. Atlanta (GA).112(3):331-338. et al. Duty S. 2005. Barr DB. Environ Health Perspect 2002. Rossbach B. Baird DD. Centers for Disease Control and Prevention (CDC). Meeker JD. Phthalate monoesters levels in the urine of young children. Needham LL.

3) 13.67-4.2 (7.70-3.20 (3.10-3.5 (24.40 (2.1) 19.9) 5.60) 9.60 (5.7) 22.30 (6.4) 22.00) 1. 1982.60) 4.7 (14.44) 4.40) 8.50-16.2) 6.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.7-58.15 (1.0 (19.57-7.21 (2.70-5.60) 8.5) 31.2) 42.8 (19. 1.00) 5.9-55. and 0.80 (4.4-20. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).00) 2.35 (1.14 (1.00 (2.0 (19.2 (31.5) 37.90 (1. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.50-6.10 (3.70 (1.2 (29.30-11.5-36.57 (3.00 (5.4) 13.0) 23.0 (9.5 (18.30 (3.70-8.24-4.00-3.70 (5.21 (2.40 (6. and 03-04 are 1.9-48.4) 23.23) 3. which is used for many consumer products.20 (1.0 (13.50 (7.3-25.10 (6.5-28.9 (7.10-5.54) 4.7) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60) 90th 14. and blood product storage and intravenous delivery systems.6 (41.70 (1.4 (13.90-8.90) 4.63-4.90-3.3 (15.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.30) 2.5 (12.0 (21.5 (11. mainly polyvinyl chloride.96) 4.10 (2.50-14.30-8.9 (13.7) 37.5-17. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.80) 9.9-26.96-5.50 (3.4) 22.00) 11.03-2.4-42.92-2.90 (4.0-18.6-130) 31.10) 3.2-39.2) 4.10-2..50) 4.9) 15.0 (16.91-3.85) 4.41 (3.70) 16.82) 3.1 (8.90) 1. packaging film.6) 95th 23.40-9.70 (3.50-6.98) 2.51) 4.9 (15.10-5.5) 19.0-18.1 (8.60) 4.10-5.5) 21.3-26.92-5.60 (6. Albro and Lavenhar.30 (7.39) 3.10) 4.4-20.84 (2.30-13.5 (30. and in humans.6-23.3) 52.7) 35.50-20.1 (11.90-11.90) 7.27) 2.4) 15.40-11.5 (12.6-28.80-5.80-3.40 (4.80) 13.40-1.4 (16.84) 3.6 (11.10 (5.40-12.50-5.6 (10.1-17.00 (7.8 (17.3-49.5-27.5) 43.1) 25.10) 2.60) 10.20 (1.31 (3.2 (10.6 (20.50-11.9-19.5-41.75 (3.70) 7.50 (3.1-29.46) 3.80-9. 2002.60) 3.3 (11. 01-02.90) 3. see Data Analysis section) for Survey years 99-00.50-5.86) 2.6) 5.8-50. Fourth National Report on Human Exposure to Environmental Chemicals 275 .23 (2.5 (18.80-4.9 (17.40) 2.0 (17. as glucuronide conjugates (Albro et al.16 (2.40-8.42) 3.1-48.2 (11.S.4-40.9 (29. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).00-5.50-3.3) 28. respectively.2) 29.1) 29.34 (2.93) 6.61 (3.6-60.50 (3.00) 3.40) 4.9.5 (25.90-4.42-5.60) 7.8) 17.70 (1.35) 4.9 (16.50-8.9 (26.50 (7.00) 9.5) 23. Following ingestion.40) 11.10) 3. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).0) 39.82 (3.41) 3.3 (24.40) 75th 7.40-8.70 (7.9) 18.80-8.10-4.23 (3.0-19.5 (31.70-6.90-5