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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4.3-Tetramethylbutyl] phenol) Triclosan (2.2'. Paradichlorobenzene) 1.5’.4.1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2’.2-Dichloroethane (Ethylene dichloride) 1.2'3.4’.4'. Table 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. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.1-Dichloroethene (Vinylidene chloride) cis-1.4.4'.4-Dichlorobenzene (p-Dichlorobenzene. The process for selection is described at http://www.5'-Tetrachlorobiphenyl (PCB 44) 2.5.4’.4'.1.1-Dichloroethane 1.2'.1.4'-Tetrabromodiphenyl ether (BDE 47) 2.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'.2'.4.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.3'.4'-Tribromodiphenyl ether (BDE 28) 2.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2-Dichloropropane 2.4'.4.6-Heptabromodiphenyl ether (BDE 183) 2.2'.2'4.5'-Hexabromodiphenyl ether (BDE 153) 2.6-Pentabromodiphenyl ether (BDE 100) 2.5.4.gov/exposurereport/chemical_selection.3-Dichlorobenzene (m-Dichlorobenzene) 1.4-Tribromodiphenyl ether (BDE 17) 2.4.5.2'.2'.cdc.2-Dichlorobenzene (o-Dichlorobenzene) 1.5.2-Trichloroethane Trichloroethene (Trichloroethylene) m.What’s New in this Report What’s New in this Report In this Fourth Report.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.3.4.2'.1-Trichloroethane (Methyl chloroform) 1.5-Pentabromodiphenyl ether (BDE 99) 2.4.5'-Tetrachlorobiphenyl (PCB 49) 2.6'-Hexabromodiphenyl ether (BDE 154) 2.4.1.3.3. 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'-Tetrabromodiphenyl ether (BDE 66) 2.html.2-Dichloroethene trans-1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.6.3’.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.5'.2'. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4.3.4.

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

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

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

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

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

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

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

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

Acrylamide is not thought to accumulate in the body at environmental doses.1) 55. and is either metabolized to the reactive epoxide..2-118) 98. EPA. as an absorbent in disposable diapers.4 (59.2 (58. mineral processing.S.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.0 (67. 2005). Animal studies indicate that acrylamide is well absorbed.S.5) 66. soil conditioners. These estimated intakes are hundreds of times lower than occupational exposures.3) 70.1 (73. 2006).1-57. 2005.3 (53.0 (69. 2005).5 (79.3-2. In 1997. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 11 .7-64.8 (91. EPA.4 (51. and an average daily intake is estimated as 0.0-49. such as potatoes and some grains.S.0-108) 152 (139-175) 126 (111-142) 108 (86. EPA reference dose of 0.7) 58. 2002). 2005). but can covalently bind to form adducts with proteins.9 (54.4) 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. pulp and paper production.4 (53.3-71. (NTP-CERHR.7) 75th 79.7 (63.. Natural substances in the food are converted to acrylamide. population from the National Health and Nutrition Examination Survey.S.1 (83.7-64.4) 57. or to glutathione conjugates (Calleman et al..4-76. and cosmetics (NTP-CERHR.0 (57. FAO/WHO.2-59.2 μg/kg/day (U. ocular and dermal irritation from direct contact with acrylamide containing materials. Recently.7 (55.6) 90.9-61. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.6) 50.0 μg/kg for adults (FAO/ WHO.4-60.8-57.0) 57.0) 85.4 (54.2-114) 163 (147-191) 96.6) 71.8 (81.7) 54. 1990.0-58.2 (75.6 (51.4-83. 2004). and in the synthesis or compounding of dye materials.1-64. 1994).9) 57.1 (47.0-104) 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 61.6 (56. 217 million pounds of acrylamide were produced commercially in the U. Tareke et al. and binding agents. gels. and well below doses known to cause nerve damage or carcinogenicity in animals. Elimination occurs mainly in the urine as mercapturic acid conjugates.4 (54. acrylamide has produced upper airway irritation following inhalation of high levels.6-104) 82. and from dermal contact with products that contain residual acrylamide.8 (52.5 (44.2-67. 2005).1) 101 (95.1-64.2-93. Survey Geometric mean (95% conf.3) 86. and in some cosmetics.9) 75.6-61.2 (62.4) 57.5 (52. interval) 61.2) 57.6-65.Acrylamide Acrylamide CAS No.2-70. Estimated intakes in children are about twice that of adults (DiNovi and Howard.8 (57. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.1 (88. In the general population.5-85.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. People may be exposed to acrylamide from foods.6 (81.9 (60.1) 53.4-89.1 (52. are heated at temperatures used for frying and baking.0 (53. Fennell et al.9) 58.4) 100 (89.7) 96.9-52.5) 58. Since acrylamide has limited volatility and high water solubility.5 (74.2-77.5-80. smoking. FDA. 2005). Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. the main source of exposure is from the diet. In humans.7 (65.2-91.3 (55.0.8-55.6-66. it was discovered that acrylamide is formed when starch-rich foods. Commercially.6) 73. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.0-66.9 (69. but are generally above the U. drinking water. acrylamide is synthesized and used in the production of polyacrylamide polymer.9-105) 86.1-61. in some sealing grouts. glycidamide. Polyacrylamides are useful water-compatible polymers used in water treatment. 2004.9) 63.7 (58.S. in permanent press fabrics.2) 57.1) 46.7-60. 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.1) 62.7) 73. see Data Analysis section) for Survey year 03-04 is 3.4-60.3) 63.6-75. widely distributed in tissues. 2006.6-108) 61.

12 Fourth National Report on Human Exposure to Environmental Chemicals .6 (90. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.5-94. 2005.7) 74. AHA levels have been shown to increase with dietary intake (Hagmar et al. glycidamide (NTP-CERHR. Survey Geometric mean (95% conf.1) 56.0) 118 (103-126) 121 (112-134) 113 (94.0 (75. EPA. 2005.4-65.0 (80.3) 59. 2005).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.. and neuronal DNA reactivity (Doerge et al.9) 87.4-59. 2005.7-62.7-64.8-48..7) 61.4 (81.3-101) 95.epa.1-62.6 (66.2-91.9) 65. Rice. 2004).2) 65. Glycidamide has been shown to react with DNA (Doerge et al.9-78.2-90. respectively) are markers of integrated acrylamide exposure over the preceding few months.5 (59.2) 87.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.0 (70..4-103) 79. Klaunig et al. 2005) have been demonstrated in animals.4-98. 2002.2 (56.. Hagmar et al. 2005. Maniere et al. 2005. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.. In addition. Schettgen et al..5) 87. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. Mucci et al..9-62. Puppel et al.0-62.pdf. scrotal. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).4) 83.1 (57.3) 59.0-93.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.S. 2005.5-92.. 2006).5 (56. IARC classifies acrylamide as probably carcinogenic to humans.6-90. After exposure ceases. 2006).S. presynaptic nerve terminal binding (LoPachin.7 (87. interval) 59.int/ ipcs/food/jecfa/summaries/summary_report_64_final.9) 59. 2008).9-76. 2005..3-78. fetal death. 1997. population from the National Health and Nutrition Examination Survey. 2006.who.6-62. Vesper et al.1) 60. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.4 (90.1 (66. 2006) have been demonstrated after acrylamide dosing.8) 60.. 2005)..4 (57.7 (61.4) 53.1-60.2) 55.2-68. thyroid. U.8-49. 2005.Acrylamide occupational exposures.8 (51. 2005.7) 60.2 (72. see Data Analysis section) for Survey year 03-04 is 4.1 (70.5-64. Puppel et al.2 (63. and cancer (mammary. male germinal cell injury. EPA.5-66. U. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.3) 59. uterine.0 (52.S. most non-smokers had levels less than about 100 pmol/gram hemoglobin. EPA at: http://www. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. although different analytic methods can affect results. NTP-CERHR. 2005)..9-64.9 (57.5) 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.. 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.. 1997. 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. 2005) and sperm DNA adducts (Xie et al. and other sites) (FAO/WHO. 2005.6-64. altered gene expression in testicular tissues (Yang et al. dominant lethality).9-77.1 (56.5) 75th 85.0) 94.7 (84.. 2001).4 (51.. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.7) 90.4 (56.1 (82.1) 62.S.7-86. 2002.3) 85.. reproductive effects (reduced litter size.1-56. adrenal.0.9 (58. Axonal degeneration.9) 75.8) 45. Vesper 2005) and smoking (Bergmark.9 (81. 2003.7 (57.8 (44. 2008).3 (56.9-138) 143 (130-159) 96. Acrylamide is clastogenic and can produce dominant lethal mutations. 2009).5 (42. 2004. Additional information is available from U. 2005. Schettgen et al..5) 71..4 (61. 2005).4) 46.5 (83.1-70. probably through its epoxide metabolite.8-61.

Chem Res Toxicol 1997 Jan. Available at URL: http://cerhr.56. 2/3/09 Klaunig JE. Paulsen JE. Godard T. National Toxicology Program. Mucci LA. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Aprea P. Malmberg B. et al. CFSAN/Office of Plant and Dairy Foods. smoking habits and gender. J Agric Food Chem 2008. Available at URL: http://www. Bergmark E. Bridson WE. Snyder RW. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose.html#u1004. Magnusson AL.120(1):45-54. Churchwell MI. Tian G.pdf. 2/3/09 Hagmar L. LoPachin RM.Toxicol Appl Pharmacol 1994.85:447-459. Cheong HK. 8-17 February 2005. Perez et al. Bergmark E. Mechanisms of acrylamide induced rodent carcinogenesis.pdf. Haugen M. et al. Kamendulis LM. He F. Chicago. February. Food and Drug Administration (FDA). Farmer PB. [Epub ahead of print] Dybing E. Calleman CJ. smokers and nonsmokers. and Research Strategies. Rome. Toxicol Sci 2005. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. McDaniel LP. Granath F. Guffroy M. Mutat Res 2005.nih. Beland FA. Bergmark E. Biomonitoring studies of acrylamide or glycidamide hemoglobin adducts provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acrylamide than are found in the general population.580(1-2):119-129. He F. Toxicol 2005. 1993.580(1-2):131-141. 2001. NIH Publication No. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.43:365–410. April 13-15. Tornqvist M. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.. References Bergmark E. Rosen I.. Twaddle NC.niehs.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Mutat Res 2005. Alexander J.27(4):219-226. Doerge DR. Illinois. 2/3/09 Perez HL. Chem Res Toxicol 1990. 2009 Jan 8. gov/~dms/acrydata. Laurentie M. Hagmar L. Acrylamide neurotoxicity: neurological. Italy. Toxicol Sci.Acrylamide In occupational settings. Bjellaas T. 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. Adv Exp Med Biol 2005. Human exposure and internal dose assessments of acrylamide in food.580(1-2):157-165. 2004.fda.who. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Costa LG. Andersen M. Nordander C. Axmon A.561:49-62. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Paulsson B. Summer SCJ. Zhang S. Tornqvist M. 2006.. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Bruze M. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 2005.126(2):361-371. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. 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. Costa LG. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. 6013-6019.. Maniere I. 1999). Calleman CJ. Survey data on acrylamide in food: individual food products. da Costa GG. Burgess J. Scand J Work Environ Health 2001. et al. Osterman-Golkar S. Available at URL: http://www. In another study. Joint FAO/WHO Expert Committee on Food Additives. 64th Meeting: Summary and Conclusions (FAO/WHO). morphological and molecular endpoints in animal models. Wirfalt E. Fennell TR. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. DiNovi M and Howard D. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Acrylamide intake through diet and human cancer risk. Becher G. Calleman CJ. Wu Y. Kautiainen A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. July. Food Chem. Wilson KM. et al. Toxicol Appl Pharmacol 1993. Hagmar et al. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Churchwell MI. 054472.10(1):78-84. 1994). Uncertainties. The Updated Exposure Assessment for Acrylamide.561:21-37. et al. 2001). Fennell TR. Adv Exp Med Biol 2005.3:406-412. Yang JS.cfsan.. Doerge DR. Mutat Res 2005. Duale N. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Spicer R. Metabolism and hemoglobin adduct formation of acrylamide in humans.gov/chemicals/ acrylamide/Acrylamide_Monograph.

Chemical Summary for Acrylamide. Schettgen T. 1994. Environmental Protection Agency (U. Hallmans G.561:89-96. Eriksson S. Rossbach B. J Agric Food Chem 2002.gov/chemfact/s_acryla.S. Angerer J. Washington (DC).txt. Yang HJ. propylene oxide. 2/3/09.50(17):4998-5006. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Rapid Commun Mass Spectrom 2006. Ospina M. Vesper HW. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.htm. Drexler H. Adv Exp Med Biol 2005. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Meyers T. Mutat Res 2005 Feb 7. Puppel N.epa. Myers GL.S. Agudo A. Han CH. Reprod Toxicol 2005. Available at URL: http://www. Toxicol Lett 2002.163(2):101-8. Liu Y. Lee MH.19(4):527-34. Letzel S. Rice JM. Broding HC. Kutting B. Chae C. Anal Biochem 1999. Ingham L.580(1-2):71-80. Vesper HW. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.56(15):6046-53. J Agric Food Chem 2008. Drexler H. 2/3/09 Vesper HW.274(1):59-68. et al.207(6):531-9. Schettgen T. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Lee SH. Analysis of acrylamide. Toxicological effects of acrylamide on rat testicular gene expression profile. Weiss T. Han DU. Int J Hyg Environ Health 2003. Acrylamide. Int J Hyg Environ Health 2004. Karlsson P. Hemoglobin adducts of ethylene oxide.134(1-3):65-70. Drexler H. Liu K. Toxicol Lett 2006.Acrylamide glycidamide by gas chromatography-mass spectrometry. Ospina M.206(1):9-14. Marko D. September. Fueller F. Fu D. Tjønneland A.20(6):959-64. et al. U. Sun H. Tareke E. revised 1/3/06. EPA). Choi JH. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells.epa. U. Gray JG. Smith A.S. Tjaden Z. Schettgen T. Jin Y. Rydberg P. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. a carcinogen formed in heated foodstuffs. Benetou V. Xie Q. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Environmental Protection Agency (U.gov/iris/subst/0286. Mutat Res 2005. Office of Pollution Prevention and Toxics. The carcinogenicity of acrylamide.S.580(1-2):3-20. Licea-Perez H. Tornqvist M. Angerer J. Meyers T. Available at URL: http://www. Angerer J. Integrated Risk Information System (IRIS). EPA). Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Slimani N. Ding X.

080-.19) .070) .163) .089) Age group 3-11 years 99-00 01-02** 03-04 .93) .160) .058 (.48-2.520 (. ear problems.09-3.05.180) . acute respiratory infections.68) .070) .88 (1.21-1.840) 3. and 17% had an LOD of 0.740-1.68) 2.730 (.53-4.080) < LOD < LOD .050-.153-.44 (2.175 (.073) < LOD .137-..234) . population from the National Health and Nutrition Examination Survey.164 (.621-1.950-1.860 (.21-1.23 (.00) .850 (.77 (2.148-. < LOD means less than the limit of detection.450-.42 (1.050-.480-.770) .108) * .057-. and various other disorders (U.18-3.32-2.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .068) .110) .066-.142-. Children exposed to ETS are at increased risk for sudden infant death syndrome.620-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.620 (.310-1.131 (.052 (<LOD-. 83% of measurements had an LOD of 0.110) .120) .040 (.180) .01 (1. 2004).S.500 (.160) .44) 2.080-.04 (1.110-.198) * .070-.540-.42-4.300) .570 (.30) * .110 (.040 (.086 (.540 (. ** In the 2001-2002 survey period.144 (.120-.690 (.140-.63 (2.54 (1.015 ng/mL.070 (<LOD-. DHHS.320) .45) 1.197) .09-3.080 (.167 (.11) .997-3.670) .62) 2.066 (.080-.20-2.110-.015.310-1.120 (.580 (.19) 1.120 (.087-.99) 2.350-.92 (1. 1998).12-4.910-1. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.32) 1.900-1.50-4.110 (.77 (1.19-2.12) 1.193) .20) 1.570-1.053 (<LOD-.120 (.180) .95) 1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.34 (1.350-. DHHS. stroke.40) .60-2.78) 2.071) .090-. 2004).820) .140-.060 (.030-.726) .66) 1.110 (.02) 1.126) .87-3.060 (<LOD-.145) . and 0.084) .625) .050 (.50-1.087) < LOD < LOD .370-.140 (.059-.160 (. Cigarettes contain about 1.55 (1.20 (.17 (.088-. emphysema.104-.430-1.110 (.066) .220) .49) 1.040-.070) 75th .28-1. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.44 (1.180 (.Cotinine Cotinine CAS No.506 (.30) 2.770-1.790) .040 (.060-.533-.15 (2.216 (.020-.02 (.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 .510 (.50 (1.050 (<LOD-.068) . acute respiratory illness.35 (2.410) .080-.110-.137 (. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00.30) 2.030-.38-2.190-.050 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 15 .39 (1.187) .950 (.052 (<LOD-.20) .17 (1.060-.33-2.77 (1.213) .66 (1.043-.350 (.220) .115-.076-.190-.47-3.060-.20 (1.061) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.54 (1.48-3.139) * .120 (.54) 1.83-2.110 (.85 (1.79) 3.308 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.077) .160-.930 (.75) 1.05) 1.063) .94) 1.5% nicotine by weight (Kozlowski et al.84-3.230) .047-.28) .400-. 2006).96 (1.120-.32-2.23 (1.050) .76 (1.02) 1.580) .050 (<LOD-.150) .01) 3.43 (1.470-.190-.077) .05 ng/mL.57) 2.990 (.89) 1.800 (.63-2.53 (1.580-1.201) .480-1.100-.200) 1.09-2.230 (.88 (.040-.180) .23-2.050) .060 (.160 (.106-.17) .16) .260) 1.23 (2.062 (. respectively.920 (.44) 2.55-2.059-.060 (<LOD-. which may vary for some chemicals by year and by individual sample.111-.090-.710 (.080) < LOD .094) .220-.740-1.70-2.060) .164 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.22) 2.630 (.160 (.080 (.39) 3.050 (<LOD-.50) 3.00) 1.96-4.S.12 (1.047-.210 (.12 (2.428-.65 (1.071 (.030 (. maternal exposure during pregnancy can result in lower birth weight.81-2.990) .087 (.505 (.120 (.14) .15) 2.150) .124 (. and 03-04 are 0.14) .630 (.49) 1.600-1. 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.310) 90th 1.660) .180) .70) 2.770) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.280 (. cardiovascular disease.302) .26-1.62 (2.360) .240 (.154-.66-3.260-1.130) .310) .030-.21 (.130 (. and exacerbated asthma (U.075 (.090-.188) .14-1.99) 2.163 (.68 (1.630 (.054 (.312) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .S.180 (.96) 2.49) 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.140 (.960-1.

Iwase et al. Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff.. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans. 2006).. Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. salivation. Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al.. 2004). Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. More information about the effects of smoking and nicotine can be found at: http://www. 1975.3 to 30 µg/m3. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al. Hukkanen et al. eggplants. In homes with one or more smokers. seizures. Acute tobacco or nicotine intoxication can produce dizziness. saliva. nausea. 2005). craving. contains nicotine in larger amounts than other nicotine-containing plants. 2005. Nicotiana tabacum. and hair. Perez-Stable et al. nicotine has a half-life in blood plasma of several hours (Benowitz. html. 1999. 1991). 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. variable changes in blood pressure and heart rate. 1996). 2005). Over the previous decade... Children are primarily exposed to ETS by parents and caregivers who smoke. Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. 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. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL.. Cotinine. 2006. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS... nasal sprays. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration.. 1999. (CDC. 2005. urine. or chewing gum. and death.nida. a process involved in the development of addiction. During each previous NHANES survey.. Symptoms of 16 nicotine withdrawal include irritability.. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. Soliman et al. chewing tobacco. 2006). 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. which include potatoes. 1999). For an adult. Wilson et al. NCI. Cotinine can be measured in serum. 1998). The serum cotinine levels seen in the NHANES 20032004 appear approximately similar to levels seen in the previous survey period (NHANES 2001-2002) for the total population estimates. or skin patches that contain nicotine.gov/researchreports/nicotine/nicotine. However. 1996). The IARC and the NTP consider tobacco smoke to be a human carcinogen. with higher levels measured in restaurants and bars. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke.. diarrhea. Pirkle et al. 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. diaphoresis. Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. tomatoes. cognitive and sleep disturbances. 2004). with heavy exposure to ETS producing levels in the 1–10 ng/mL range. and peppers. Once absorbed. 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. vomiting.. mean air concentrations typically range from 2 to 14 µg/m3 (NTP.Cotinine 1994. the primary metabolite of nicotine. Hukkanen et al..nih. and increased appetite. 2005). Serum cotinine has been measured in many studies of nonsmoking populations. The tobacco plant. 1994). Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al. 1998).. 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. Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al.

Tobacco related exposures. National Toxicology Program (NTP). References Armitage AK. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Benowitz NL. Environ Health Perspect 2006. 11th ed. Pechacek TF. Aiba M. J Pharmacol Exp Ther 1999. Pirkle JL. U. Jacob P III.114(6):853-858. 4/13/09 National Cancer Institute (NCI). [online]. Herrera B.291(3):1196-1203. Racial/ethnic differences in serum cotinine levels among adult U. 1991. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Vogler GP. Epidemiol Rev 1996. Benowitz NL. Lewis PJ. Kira S. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.nih. Curtin LR. Benowitz NL. Benowitz NL. JAMA 1996. Clin Pharmacol Ther 1994.cancer. et al. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Smoking and Tobacco Control Monograph 10 [online].gov/ntp/roc/eleventh/profiles/ s176toba.63:139-43. Benowitz NL.18:188-204. Schober SE. Office on Smoking and Health [online] 2006. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Coordinating Center for Health Promotion. Richter PA. the United Kingdom. International Agency for Research on Cancer. 1999.S Department of Health and Human Services (U.4:313-316. Tob Control 2006.php. Respiratory nicotine absorption in non-smoking females during passive smoking. population to secondhand smoke: 1988-2002.iarc.cdc.gov/eid/rmca/critdocs/ criteriadoc/33. Vol 83. Atlanta (GA): 2005.94(2):314-320.fr/ENG/Monographs/allmonos90. National Institute for Occupational Safety and Hygiene (NIOSH). Dollery CT. 4/13/09 Perez-Stable EJ.56:483-493. Tobacco Smoke and Involuntary Smoking. DHHS). Vol 38. Herrera B. Absorption and metabolism of nicotine from cigarettes. National Center for Chronic Disease Prevention and Health Promotion.S. June. Jacob P. Centers for Disease Control and Prevention. Pechacek TF. 1988-1991. Etzel RA. and the United States. DHHS). et al. 4/13/09 Iwase A. JAMA 1998. Available at URL: http://ntp.S. Trends in the exposure of nonsmokers in the U. Third National Report on Human Exposure to Environmental Chemicals.S Department of Health and Human Services (U.S. Summary of Data Reported and Evaluation [online] 2004. Pirkle JL. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Modin G. Cotinine as a biomarker of environmental tobacco smoke exposure. George CF. Summary of Data Reported and Evaluation [online] 1986. 4/13/09 Centers for Disease Control and Prevention (CDC).gov/tcrb/monographs/10/. Brody DJ. Bernert JT. 2004. U. Centers for Disease Control.php. Houseman TH. Department of Heath and Human Services. iarc.7:369-375. Soliman S. 1999-2002. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.280:135-140. Perez-Stable EJ. Giovino GA.gov/library/ secondhandsmoke/. Ethnic differences in N-glucuronidation of nicotine and cotinine. Jacob III P. Caudill SP. IARC Monogr Eval Carcinog Risks Hum. Caraballo R. Hukkanen J. Kozlowski LT.pdf. cigarette smokers: the Third National Health and Nutrition Examination Survey.pdf. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Jacob P III. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. U. Mehta NY. Metabolism and disposition kinetics of nicotine.57(1):79115.niehs. 4/13/09 International Agency for Research on Cancer. Maurer KR. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Available at URL: http:// cancercontrol.S.275:1233-1240. Pollack HA. 1988-1991. Schwartz SS.surgeongeneral. Coordinating Center for Health Promotion. Strauss WJ. Exposure of the U. In Report on Carcinogens. Flegal KM. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. BMJ 1975. Warner K. Sweeney CT.S.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Sosnoff CS. Available at URL: http://monographs. Pharmacol Rev 2005.fr/ENG/Monographs/ allmonos90. Turner DM. Mowery PD. Brody DJ. Bernert JT. Int Arch Occup Environ Health 1991. Giovino G. Jarvis MJ.280:152-156. 4/13/09 U. Tobacco Smoke.niosh. Available at URL: http://www. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.S. JAMA 1998. Centers for Disease Control and Prevention.S. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Department of Heath and Human Services. Pickett MA. Available at URL: http://monographs. Nicotine metabolism and intake in black and white smokers. Am J Public Health 2004.15:302-307. Tob Control 1998. IARC Monogr Eval Carcinog Risks Hum. Fong I. available at URL: http://mtn.

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

140-.130 (.180 (.epa.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 .140) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.240) < LOD .S.100 (<LOD-.110 (.S.170 (.130) < LOD .160) < LOD .130 (.N. 134-62-3 General Information N. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.560) < LOD .110 (. 2002).220 (.. 2002).170 (..1.140 (. 2003).140) < LOD . DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .EPA. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1998). Survey Geometric mean (95% conf.100-. DEET can be applied to clothing and the skin to repel biting insects.100-. DEET is not a developmental or reproductive toxicant in animals (U.110 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.130-.449 and 0.130 (.110 (<LOD-.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 . 2005).270) 688 678 518 700 598 956 Limit of detection (LOD. After absorption.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . EPA.100-.S. DEET has low acute toxicity. DEET is not registered for use on agricultural commodities.190) < LOD .N-Diethyl-meta-toluamide (DEET) CAS No. have been reported as result of self-poisoning by ingestion or excessive dermal application.180 (. Additional information is available from U. There are over 225 insect repellents brands containing DEET.110-. (U. and it has not been rated by IARC or NTP with respect to human carcinogenicity. 2003).EPA. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.110-. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.130-. which may vary for some chemicals by year and by individual sample.120-. < LOD means less than the limit of detection. including seizures and encephalopathy. DEET is also used in combination with dermal sun screens (U.130-..150) < LOD . One survey detected DEET in 74% of sampled streams in the U. population from the National Health and Nutrition Examination Survey.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. 1998). About 3-8% of dermally applied DEET is absorbed. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/pesticides/. Sudakin and Trevathan.140) < LOD . Neurological effects in humans.110 (.180 (.N-Diethyl-meta-toluamide (DEET) N. Urinary N.S. 1995.120-.S.S.130-. and they range in concentration from 4% to 100%. (Kolpin et al.210 (.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 . DEET is not genotoxic.EPA at: http://www.130) < LOD .110 (<LOD-.100-.100-.100-.180) < LOD . Its use is recommended for prevention of several vector-borne diseases.520) < LOD . Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.250) < LOD .

Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.330 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410 (.250 (.250-.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.410 (.130 (<LOD-.370-.270-.240-.500 (.350) < LOD . Urinary N.190 (<LOD-.190-.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 .230-. 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. Survey Geometric mean (95% conf.350-.500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.480 (.190 (. 2005).440) < LOD .290-..140-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . population from the National Health and Nutrition Examination Survey. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.350) < LOD .270) < LOD .280-1.250) < LOD .390-.150) < LOD .300 (.170-. In this survey period. representative subsamples from NHANES 2001-2002.320 (.270 (.93) < LOD .640 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.330 (.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2007).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 . 20 Fourth National Report on Human Exposure to Environmental Chemicals ..490) < LOD .230-. Urinary DEET levels as high as 5.150-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.630) < LOD .230) < LOD .410-.190 (.370) < LOD .S.270 (<LOD-.280 (.240) < LOD .200 (.N. 1992).320) < LOD .

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

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

Yoshinaga J. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Hum Ecol Risk Assess 2004. Calafat AM. Pharmaceuticals. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Koulova AI. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. 2/4/09 European Commission. Endocrinology 2008. Timms BG. Bisphenol A. Wong LY. Needham LL. August 2001. 4. Reprod Toxicol 2001..Environmental Phenols References Akingbemi BT. Research Triangle Park. Arakawa C. Calafat AM. Zaugg SD.59(4):403-408. Thurman EM. Han SY. niehs. Ispra. Bradley S. Kolpin DW. Haighton LA. European Commission. bisphenol A glucuronide.35(2 Pt 1):238-254.69(22):2611-2625.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Ekong J. Needham LL. National Institutes of Health. Available at URL: http://ntp.nih. Chung MK. C.145:592-603. Thomas BF. Hanaoka T. Fujii S. Harazono A. Cohen JT.. N. Kim CS. 5: 505-523. Hara K. Imai H. Hughes C.gov/chemicals/bisphenol/BPAFinalEPVF112607. Cunha G. Meyer MT. Kawamura N. Matthews JB. Twomey K. Ecotoxicity and the Environment (CSTEE). Gender differences in the levels of bisphenol A metabolites in urine.pdf. Proc Natl Acad Sci USA 2005. Leranth. Barber LB. and Hajszan. Joint Research Centre Institute of Health and Consumer Protection. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Ema M. Kim YH.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt.pdf .nih. T.102(19):7014-7019. Howdeshell KL. Kroes R. and other organic wastewater contaminants in U. Environ Health Perspect 2005. Environ Sci Technol 2002.europa.S. Available at URL: http://cerhr. with estrogen receptors alpha and beta. Doull J. Yang M. National Toxicology Program. streams. Watanabe S.pdf. Human Health. Available at URL: http://cerhr. Calafat AM. In vitro and in vivo interactions of bisphenol A and its metabolite. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Italy. Tsugane S. Furukawa M. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite.pdf. Rubin C. Munro IC. Brine DR. et al. Myers CB. Reidy JA. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Barr JR.780(2):365-370. NC. Barton L. Needham LL. Belgium.312(2):441-448. Tyl RW.Scientific Committee on Toxicity. Kiguchi M. Caudill SP. Han SS. Szigeti-Buck. Shin HC.S.pdf . et al. Occup Environ Med 2002.59(9):625-628. McConnell EE. National Institute of Environmental Health Sciences. Marr MC. Available at URL: http://ecb. Ye X. Environ Health Perspect 2008. Pyo MY. Rhomberg et al.113(4):391-395. Park S. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).. Exposure of the U. Joskow R.S. MacLusky.J. Endocrinology 2004. Reidy JA. 1999-2000: a national reconnaissance. 2002. Furlong ET. Rat two-generation reproductive toxicity study of bisphenol A. 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. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. and Hardy MP. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy.eu/ health/ph_risk/committees/sct/documents/out156_en. DirectorateGeneral Health and Consumer Protection. Department of Health and Human Services.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Kuklenyik Z. J Chromatogr B Analyt Technol Biomed Life Sci 2002.gov/chemicals/bisphenol/bisphenol. November 26. niehs. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Watanabe C. Richter CA. Gray GM. Nippon Eiseigaku Zasshi 2004. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).149:988-994. Zacharewski TR.137(3):353-362. Brussels. Barr DB. An evaluation of the possible carcinogenicity of bisphenol A to humans.10:875-921. U. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. 2003. Cha SW. J Am Dent Assoc 2006.68(1):121-146.14(2):149-157. 2/4/09 Fujimaki K. September. Serizawa S.36(6):1202-1211.niehs.nih. 2008. hormones. K. Chem Res Toxicol 2001. Life Sci 2001. Keimowitz AR. Hlywka JJ. et al. 2007.116(1):39-44. Available at URL: http://ec. Klinefelter GR. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Ikka T.jrc. Lynch BS. Sottas CM. 2/4/09 Ouchi K. Toxicol Sci 2002. vom Saal FS. Regul Toxicol Pharmacol 2002. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Kim JC. Biochem Biophys Res Commun 2003. Koh WS. May 22.

Environ Res 2007. Lordo RA. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Witorsch RJ. Chuang JC. Sheldon LS. Kawamoto T. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure.40(7):905-12. Kim SY. et al. Morgan MK. An observational study of the potential exposures of preschool children to pentachlorophenol. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration.113(8):926-33. Large effects from small exposures. Environ Health Perspect 2005. Jang JY. Csanady GA. Yang M. Filser JG. and nonylphenol at home and daycare. Endocrinology 2006. Vom Saal FS. Food Chem Toxicol 2002. Hughes C. Arch Environ Contam Toxicol 2003. Biological monitoring of bisphenol a in a Korean population.15:12811287. Wilson NK.147(6 Suppl):S56-69.44(4):546-51. Welshons WV. Lee SM. Chang SS.Environmental Phenols Volkel W. Nagel SC. vom Saal FS. Chem Res Toxicol 2002. III. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. bisphenol-A. Dekant W. Colnot T. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.103(1):9-20.

500-1.600-1.400 (.10) 1.389 (.507) * < LOD .1.30) 2. leading to inhalation as another potential exposure route (Rudel et al. textiles.200-..00 (.600-1.300-. altered estrus cycles and reproductive outcomes. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.60-3. 2002).3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Laws et al.10 (.900 (.20 (1.600-1.80) 2.900 (. 34 Fourth National Report on Human Exposure to Environmental Chemicals . streams in 30 states (Kolpin et al.300 (<LOD-.600) . pesticides. is used to manufacture alkylphenol ethoxylates.50) 1.20) 314 715 1488 03-04 03-04 * * .20-2. 140-66-9 General Information 4-tert-Octyphenol. population from the National Health and Nutrition Examination Survey. 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.800-1.S..20-2.600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Indoor and to a lesser extent. Less frequently. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.5% of 139 U.50) ..500) . Bian et al. During the 1980s and 1990s.600) .50) .60-3. the various alkylphenols have also been used as emulsifiers and modifiers in paints.. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.80 (1.900 (. and through manufacturing waste streams (Warhurst. Ying et al.10-2.500) . In the 1990s.50) 1. 1995.50 (1.30) 90th 1. The alkylphenol ethoxylates enter the environment through human use of products containing them.60-3.20-2.20) 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 . 2000.357 (.50) 1.80 (1.S. an alkylphenol.40) 2.274-.20-2.40) 1. industrial cleaners. 2006. 1996). and to alkylphenoxycarboxylates. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.30 (.30 (1. which may vary for some chemicals by year and by individual sample. Katsuda et al. fish) and drinking water.600) 1.700-1.40) 2. orally administered 4-tert-octylphenol was well absorbed.900 (. In 1999-2000.00) 1229 1288 03-04 03-04 03-04 * . and emulsifiers.40) 1. and the polyethoxy chain may consist of up to 50 ethoxy units.300 (<LOD-. and was quickly eliminated from the blood (Certa et al.10 (1.60) 1.20-2. did not bioaccumulate.30 (1.50-2. and from contact with some personal care products and detergents. In rats. altered neonatal sexual development.20) 2. Several alkylphenols. over 500.600-1.. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.477) . Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. 2000..30-2.60-3.60) 613 652 1092 Limit of detection (LOD.00 (1. which are anionic surfactants used in detergents. testicular atrophy.500-1.. and impaired spermatogenesis (e.20) 1..500 (.10 (.70 (1.3.30 (1.70 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.299-. Survey Geometric mean (95% conf. 2003.60-3.g.20-2. including 4-tert-octylphenol. < LOD means less than the limit of detection.90) 2.00 (.600-1.70 (1.600-1. 4-octylphenol monoethoxylate was detected in 43.60-3.500) .900 (.000 tons of alkylphenol ethoxylates were produced annually worldwide.10) 2. The alkylphenols can bioaccumulate in some fish.80 (1. Urinary 4-tert-Octylphenol (4-[1.300-. to shorter chain alkylphenol ethoxylates.30 (1. 2002).60) . 2004).400) 1. and some of their degradation products are toxic to aquatic life.50-3.2.40) * 03-04 03-04 03-04 .300 (<LOD-.400 (.300 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.Environmental Phenols 4-tert-Octylphenol CAS No. impaired steroidogenesis.. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. and some personal care products.70 (1. Disposition in humans has not been studied sufficiently. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).369 (.30) 1. Blake and Boockfor. have demonstrated estrogenic effects particularly when injected at high doses in animals. Saito et al.40 (1.497) * .400 (.90) 2. 1997.200-..500) 75th .268-. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.300 (<LOD-.g. through sewage.

540-1.62 (1.40 (1.31-2. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.1.170-. Survey Geometric mean (95% conf.730-1. IARC and NTP have not rated octylphenol.78) 1228 1286 03-04 03-04 03-04 * .740 (. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect. 2001).570) .17 (.67-2.64 (.260 (<LOD-. Sweeney et al. 1999).160-.10-2.15) 1.400) .. at lower or environmentally relevant doses (Blake et al.50 (2.620-1.Environmental Phenols Myllymaki et al.41) . Calafat et al.36-3.500-1.460 (. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.03-6.349) * < LOD . population from the National Health and Nutrition Examination Survey.33 (2.270 (.05-2.68-2. representative subsample of NHANES 2003-2004.300 (<LOD-.59) 1. or their corresponding ethoxylates with respect to human carcinogenicity.384) * . 2005.860 (.270-. It is unclear if estrogenic or other effects occur in animals through oral dosing.20 (1. 2001. 4-tert-Octylphenol is not considered directly genotoxic.560) .59 (1.00) 1.76 (2.02-4.08) 1.470-1.910 (. 2003. Yoshida et al.640-1. nonylphenol.33) 3.276 (.610) .630-1.00 (..450) .00 (.22) .54) * 03-04 03-04 03-04 . Fourth National Report on Human Exposure to Environmental Chemicals 35 .380 (<LOD-.53-3.470-1.370 (<LOD-.890-2..550-1. Urinary 4-tert-Octylphenol (4-[1.25) 90th 1.207-.73) 2.270 (. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.81 (1.530) . 2004).450) 1.03 (1.280-.850 (.29) 2.85 (1.43-3. In a small number of adult Japanese volunteers.00) 2.11-2.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.68) 2.06 (2.00) 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 .96-4.14) 314 713 1487 03-04 03-04 * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.25-2.620) .31 (1.3..03 (1.269 (.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.320 (<LOD-.60 (1.00) 2.435 (. Kawaguchi et al.740 (.337-.410 (.11) 1.770 (.62 (1.78) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000.. 2004. Tyl et al.71) 2.43) 1.43) 1.420) .S..18-4.62) .65-3.11) 2. 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.78 (1. Nagao et al.470) 75th .40-4.25) 2.199-.S.

Phthalates. Inoue K.37(20):4543-53.pdf.S. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Zaugg SD. Katsuda S. 1995. et al. Nicol L. Thurman EM. J Chromatogr B Analyt Technol Biomed Life Sci 2004. nonylphenol. Nakagomi M. Chen J. Takenaka A. Maekawa A. prolactin. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Boockfor FR. Anal Chim Acta 486:41-50. et al.71(1-2):112-122. Muller AM. Saito I. alkylphenols. Maekawa A.co. Katsuda S. Wang X. Saito Y. Song L. Nair-Menon JU. Brody JG. pesticides. Environ Health Perspect 2008. 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. et al.Environmental Phenols References Bian Q.36(6):1202-1211.165(3):217-226. Millette CF. Environ Int 2002. Onuki A. Indoor Air 2004. Food Chem Toxicol 2006.141(7):2667-2673. Needham LL. bisphenol A and methoxychlor in rats. Toxicol Sci 2000. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Ye X. Pharmaceuticals. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.15(6):683-692.14(5):325-332. Environ Sci Technol 2002. Endocrinology 2000. Taya K. Roche JF. and testosterone.207(1):59-68. Qian J. Tyl RW. Karjalainen M. An environmental assessment of alkylphenol ethoxylates and alkylphenols.799(1):119-125. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Furlong ET. Korn LR. Raychoudhury SS. Available at URL: http:// www. Xu L. Exposure of the U. Horie M.116(1):39-44. Spengler JD. Ferrell JM.44(8):1355-1361. Seely JC.uk/resource/reports/ethoxylates_alkylphenols. Blake CA. Taya K. Watanabe G. Regul Toxicol Pharmacol 1999. hormones. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Fedtke N. Haavisto TE. Two-generation reproduction study with para-tert-octylphenol in rats. Yoshida M. Williams B.folliclestimulating hormone. 1999-2000: a national reconnaissance. Watanabe G. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry.S. et al. Wiegand HJ. Sakui N. Usumi K. Okada F.28(3):215-226. Sweeney T. Kolpin DW. Yoshida M. Ito R. 2003.foe. Warhurst AM. Certa H. and other endocrine-disrupting compounds in indoor air and dust. Meyer MT. Toxicol Lett 2001. streams. Biol Reprod 1997. Boockfor FR. and other organic wastewater contaminants in U. Seto H. McCoy GL. Brooks AN. Kookana R. Fail PA. Makino T.54(1):154-167. Brine DR. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Rudel RA. Izumi S. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Barber LB. Calafat AM. Myllymaki SA. Estrogenic activity of octylphenol. Reprod Toxicol 2004.30(2 Pt 1):81-95. 2/4/09 Ying GG. Nagao T. Reidy JA. Kawaguchi M. Indoor air pollution by alkylphenols in Tokyo. Kawaguchi M. Toppari J. Reprod Toxicol 2001.121(1):21-33. Bolt HM. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Blake CA. Takai N. Ono H. Marr MC. Camann DE. polybrominated diphenyl ethers. Inoue K. Bodman GJ. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.18(1):43-51. Environ Sci Technol 2003.57(2):255-266. Toxicol Appl Pharmacol 2000. Yoshimura Y. Laws SC. Toxicol Appl Pharmacol 2005. Yoshimura S. Wong LY. Paranko J. Cooper RL. Carey SA. and sertoli cell number. testis size. Myers CB. Arch Toxicol 1996.

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

7 (14.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.54 (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 .3-67.8-63.9 (8.10) 84.9-236) 193 (90.1) 9.7) 10.22-10.5-86.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.18 (5.1) 9.45-13.2 (25.6-20.48-10.1 (15.0-15.3 (8.55 (4.9 (50.5) 20.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) 12.3) 10.50-10.00-8.93 (7.2) 13.9) 32.1 (45. Survey Geometric mean (95% conf.40-11.6 (12.Environmental Phenols Urinary Triclosan (2.S.45 (5.0 (36.6-37.3 (9.4 (38.80 (5.1-39.9 (11. population from the National Health and Nutrition Examination Survey.1) 14.8) 7.8-112) 30.6-111) 33.16 (6.3-35.2 (13.9-61.38-18.6) 31.1) 11.2-58.86-12.40-17.9 (33.11-11.00 (4.5) 66.3) 47.4 (12.92-12.1) 9.S.4.4) 357 (225-456) 203 (87.48 (8.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.6 (9.6) 12.6-14.89-11.4-18.9) 8.82 (8.1) 13.0 (34.8 (21.72-13.6) 10.1) 7.8) 9.10-9.0) 9. see Data Analysis section) for Survey year 03-04 is 2. population from the National Health and Nutrition Examination Survey.0 (11.6-15.8-127) 37.2-58.0-19.4-19.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.3 (11.29-12.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.32-14.60 (8.4) 317 (231-433) 144 (96. Survey Geometric mean (95% conf.7 (11.6-65.20-10.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.1) 50.4) 73.7 (28.20-11.5) 11.7 (39. interval) 13.4) 25.0-15.9) 75th 47.7) 292 (151-432) 132 (78.74 (5.6) 90th 212 (172-241) 03-04 03-04 03-04 9.3.60 (6.8-85.0 (8.90-10.7) 123 (36. Urinary Triclosan (2.0 (26.2 (27.0-73.5-14.0) 49.70-16.20 (7.4) 7.4) 90th 249 (188-304) 03-04 03-04 03-04 8.50) 10.2-46.2 (37.6 (10.3) 6.2) 9.45-10.8) 116 (39.2) 12.7 (9.4) 51.6 (30.8) 14.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.20 (7.2-14.30-14.8-60.21 (6.3-31.4.4 (32.20-13.9) 7.2 (10.3 (26.2 (11.5) 13.0) 65.43-13.1) 9.5 (11.3-15.1 (8.4) 75th 43.6) 39.6-14.94 (7.4 (11.

Environ Health Perspect 2008. Lyman FL. Triclosan: applications and safety. Fernandez-Alba AR. Foran CM. Teitelbaum SL. streams. Calafat AM.S. Urinary concentrations of triclosan in the U. Shiratsuchi H. J Invest Dermatol 1976. The oral retention and antiplaque efficacy of triclosan in human volunteers. Chemosphere 2007. Williams PE. Arch Environ Contam Toxicol 1988. Environ Health Perspect 2007. Ye X.115:116-121. Anal Chim Acta 1004.38(4):361370. Ferrer I. Veldhoen N. Nagao Y. et al. J Toxicol Environ Health A 2006. 4. Mar Environ Res 2000. Food Chem Toxicol 2000. Chelimo C. Gilbert RJ. Thurman EM.67(4):532-537. Aguera A. Furlong ET. Br J Clin Pharmacol 1987.4.24(3):209-218. Matsumura N.116(3):303-307.7/2.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Wolff MS. Williams FM. Osachoff H. Ogawa H. Gomez MJ. Pharmacokinetics of triclosan following oral ingestion in humans. phthalates. Erratum in: Aquat Toxicol 2007. Kolpin DW.45 Suppl 2:S137-S147. Percutaneous penetration and dermal metabolism of triclosan (2. Photolytic degradation of triclosan in freshwater and seawater.17(5):637-644.83(1):84. Aquat Toxicol 2006. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. and other organic wastewater contaminants in U. Leonard PA. and phenols in girls. Howes D. Meyer MT. population: 2003-2004. Ebersole R. Ishibashi H. Katsura E. Skirrow RC. Odham G. Clapson DJ.524:241-247.S. 4’-trichloro-2’-hydroxydiphenyl ether. Wong LY. Toxicology of 2. Barber LB. Sandborgh-Englund G. Hirano M. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Kanetoshi A. Developmental evaluation of a potential non-steroidal estrogen: triclosan.38(2):64-71. Windham G. 1999-2000: a national reconnaissance. Am J Infect Control 1996. Gunderson MP. Mezcua M. Evidence of 2. Bodey GP.50(1-5):153-156. Levy SB. Needham LL. Okui T.23(5):579-583. Ekstrand J. Benson WH. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Environ Sci Technol 2002.28(9):1748-1751. Pinney SM. hormones. Larson EL.80(3):217-227. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis).. et al. Kaneshima H. Wigmore H. Pilot study of urinary biomarkers of phytoestrogens. et al. Watanabe N. Aranami K.66:1052-1056. Hernando MD. IMS Ind Med Surg 1969. Zaugg SD.36(6):1202-1211. Furia T.4’-trichloro-2’hydroxydiphenyl ether). Britton JA. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Bennett ER. Moss T. Biol Pharm Bull 2005.69(20):1861-1873. Readman JW. Hong HC. Pharmaceuticals. Fourth National Report on Human Exposure to Environmental Chemicals 39 .Environmental Phenols References Aiello AE. et al. Reidy JA. Adolfsson-Erici M. Bhargava HN.

350 (.90 (1.54-2. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.58-2.350 (. and possibly of lindane (IPCS. To-Figueras et al.76) .350) < LOD .390 (.350) < LOD .42) 696 680 521 696 603 951 Limit of detection (LOD.10 (<LOD-1.350) < LOD . which may vary for some chemicals by year and by individual sample.32 (.350 (. so it is relatively non-persistent.350-.45-2.30 (.350 (.48 (.70) 2. The parent compound and conjugates.33-2.00) 1.350) < LOD < LOD 75th .30 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .10 (1.850-2.08-3.350-.30 (1.960) 1.350-.94 (1.00) 1. Since 1984.350 (.510-3.350-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350 (.350-2.350 (. plants.350) 90th .50) 1.500-2.00) 2.350) < LOD .350 (.350-.g. bactericide. Effects including hyperthermia. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. 1979).990-2.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. After absorption.47-5.350) < LOD .350-.350) < LOD .350-.350) < LOD .350) < LOD .660 (.S.350-2. 1997)..350-.62 (.390 (.83 (2.350) < LOD .75) 2.890 (.350-1.350 (. utility poles and fence posts).350-.980 (.480-2.350) < LOD .350) < LOD .350-. hypertension. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene. population from the National Health and Nutrition Examination Survey.350) < LOD .40 (.860-2. has been restricted. with repeated or chronic exposure.350) < LOD .90) 1.350-1.350) < LOD .64) 1. and it is used primarily as a preservative for wood to be used outdoors (e. Kohli et al. are eliminated in the urine. PCP is degraded by sunlight and metabolized rapidly by microorganisms.48-2. PCP is eliminated over a few days (Braun et al.10) 1.350-.350) < LOD .73 (1. Survey Geometric mean (95% conf. Acute.00 (.S.350-.590-1.67) 1.350-2.350-1.650 (.47-3. and dermal contact with PCP-treated products. PCP cannot be used on wood in residential or agricultural buildings. 1986). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. the elimination half-life may be a week or more (Uhl et al.5.58-2.53) 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 . other polychlorinated benzenes.350 (.350-1. After a single dose.37 (.350) .350-. and animals. herbicide. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.65 (. algaecide and insecticide. and metabolic acidosis were observed in CAS No.350 (..23 (.890-1.350 (.990 (<LOD-2.09) . General population exposure to PCP may occur by inhalation of contaminated air. water and sediments because of the large amounts that were produced and used historically. In the environment.350-. < LOD means less than the limit of detection.350-2.10) 1. along with small amounts of tetrachlorohydroquinone and conjugates.80) .350 (.91 (1. 2002.350 (.94 (1.04) 1.530) 1.18 (<LOD-1.350 (. 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.510-5.30) 1.33) . PCP is absorbed rapidly and well by all exposure routes.350 (.350-.30) 1.350-.01 (<LOD-1.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Human exposure to PCP has become less common.680-1.350 (.70) .350 (.65 (. 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.25 and 0.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .650) 1.51) 1..630 (.98 (1.30) . ingestion of contaminated food or water. PCP use in the U.350-.350-2..350-.770 (. PCP has been detected in soils.10 (..60) 1.350-.350-.350-. PCP is distributed to most tissues and is not extensively metabolized. air. mollusicide. 1976.90) 2.350-.78) 1.60) 1.350 (.37) .350) < LOD .350 (.76) 1.

29-3.67 (1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .21-2.Fungicides adults and children severely exposed to PCP through ingestion. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.75 (<LOD-2.290-.10-2.420) < LOD . EPA has developed standards for PCP in drinking water and the environment..35) 1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .94-3. 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 (4.25 (1.830) < LOD .EPA.atsdr. and adversely affected thyroid function (U.730) < LOD .52 (<LOD-1. population from the National Health and Nutrition Examination Survey.67-2.400 (.910-1.67-3.00-1.780) < LOD .340-.79) 1.09-1.19) 2.430) < LOD .S.25) 1.epa.800-1.06-3. 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.250 (.cdc. More information about external exposure (i.950-1.330-.S.25 (1.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.52 (<LOD-1.06 (. children in the 1980’s. respectively) (Becker et al.26 (1.67-3.06) 1.69 (1.300 (.52) 1.320 (.e. 2003).800) < LOD 1.13 (. respectively) (Seifert et al.94 (1.900-1.560) < LOD . In animals.84-4.84) 1.19) 2.360 (.18 (1.94 (1..290) < LOD ..67 (1. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al.16 (.320) < LOD . Pentachlorophenol is not mutagenic or teratogenic.30) 1.48-2.35-2.240-.310-.370 (. chronically administered high doses of PCP were hepatotoxic. In a small sample of U.700-2.430-. and the FDA has established a standard for bottled water.470 (. The U.650) 90th 1. Death can result from seizures and cardiovascular collapse.40-2.590-1.84 (1..220-.610 (.82 (1.30) 1.570 (.67 (1. carcinogenic.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .220-.82) 1.35) 1.78) 1.10 (1.25-2.650 (.S.67 (1.590) < LOD .320) < LOD < LOD 75th .40) 1.320) < LOD .6 and 14.19 (1.650 (.gov/ pesticides/ and from ATSDR at: http://www.500 (. 2004.950-1.280) < LOD .html.0 mg/L. 1991).850 (.300 (.57 (.16-1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al. 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. van Raaij et al.25-1.52 (1.36) . 1989).78) 1.26 (1.760 (.990 (.90) 1.35-2.83 (1.270-.40) 1. EPA at: http://www.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 . 2003).380-. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.00) 1.21 (.34 (.S.11) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.75) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . or skin absorption.67 (1.350) < LOD .500-1. Survey Geometric mean (95% conf.290-. 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.56) 1.18) . Among adults in the NHANES 1999-2000 subsample.92) 1.710-1.30 (.310) < LOD ..580-.300 (. 2000).780-1.360-.510-.57 (1.510-.9 mg/L.630 (.08 and 5..40) 1. In NHANES 2001-2002 subsamples.09 (<LOD-2.440 (.260 (.920 (.73 (1.500-.950-1.95) 3..250 (.00-1.55) 1.30-2.40) 1. 1989). environmental levels) and health effects is available from the U. OSHA has established an occupational standard.S.270-.40) 1.560-.51) 1. 1995).25-2.560) < LOD .08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.gov/ toxpro2. inhalation.490) < LOD .19) 2.

4/21/09 van Raaij JA.S. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Blau GE. References Becker K. Engel R. Can J Biochem 1976. house dust. Smith SJ.105(1):78-83. et al.S. International Programme on Chemical Safety (IPCS). Needham LL. Phillips DL. Becker K. Hill RH. 206:15-24. Schmid P. Seifert B. available at URL: http://www.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Barrot C. Toxicology 1991: 67(1):107-16. Otero R. Fast DM. Jones D. et al. Rodamilans M. PCP: Human Risk Characterization [online]. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. U. 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. Pesticide residues in urine of adults living in the United States: reference range concentrations. To T. Chenoweth MB. Hill RH Jr. hair. Pharmacokinetics of pentachlorophenol in man. 11/30/2004. Safe A. 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. Lindane. Arch Toxicol 1986. Gregg M. Hill RH Jr. htm. Kaus S. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects.18(4):469-474. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. van den Berg KJ. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Krause C. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Arch Environ Contam Toxicol 1989. Baker S. 4/21/09 Kohli J.58:182-186. Bragt PC. The metabolism of higher chlorinated benzene isomers. Sala M. Shealy DB. Schlatter C. et al. Holler JS. Dev Toxicol Environ Sci 1979. Int J Hyg Environ Health 2003. 2002. Arch Environ Contam Toxicol 1989. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.4:289296. r e g u l a t i o n s . Uhl S. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Helm D. Environmental Protection Agency (U. Needham LL. To-Figueras J.54(3):203-208. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Bailey SL. Cline RE. Schulz C. Seifert B. J Expo Anal Environ Epidemiol 2000. EPA). Available at URL: h t t p : / / w w w.inchem.org/documents/jmpr/jmpmono/2002pr08. urine. Santiago-Silva M. Head SL. Schulz C.18:475-481.10:552-65. Seiwert M. Environ Res 1995. Notten WR. Seiwert M. Environ Health Perspect 1997. Braun WH. 42 Fourth National Report on Human Exposure to Environmental Chemicals . drinking water and indoor air.71:99108.

520 (.61) 2. < LOD means less than the limit of detection.00) .03) 1.00 (1. Fourth National Report on Human Exposure to Environmental Chemicals 43 .570-1.20 (.10-2. it was used in home sanitizers for surfaces.950) < LOD .50) < LOD . formulate.640) < LOD .40-7.760-2. Cnubben et al.567 (.496 (. 1989).00-2.600-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 2.450 (<LOD-.600) < LOD .690) < LOD . In the past.20 (1.80-3. 2006).570-2. sodium ortho-phenylphenate (SOPP).466 (.490 (<LOD-.610 (. 1998).493 (.780) < LOD .60 (1.740 (.90) 2.3 and 0.85) 2. in paints.Fungicides ortho-Phenylphenol CAS No.S.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 .930 (.645) * . OPP is efficiently absorbed from the gastrointestinal tract and through the skin.600) < LOD 1.10 (1.30-2.10) .750-2.402-.23) 695 680 520 695 603 953 Limit of detection (LOD.600) < LOD .433-.07 (.621) * .60-3. Most agricultural food applications have been revoked. which may vary for some chemicals by year and by individual sample. inhalational. Estimated human intakes have been below recommended intake limits (U.10) .630) < LOD .800-3.552 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .50-2.836) * .30) 1.890 (.490 (<LOD-. General population exposure can occur via dermal.S.970 (.480-1.370-.600) < LOD 75th . Available evidence suggests that OPP does not accumulate in the body. 2002.600-1.50) < LOD .60 (1.638) * .508 (.20-3.22) 2.696) * .40-2.50) .EPA.389-.60-2.33 (.20) < LOD 2.820 (.40-5.17 (.390-.00) < LOD . but OPP and SOPP are still used on pears and citrus (U. Both chemicals degrade within hours to weeks in the environment (U.624) * .860 (.498 (.00) .50-4.S.410-. or apply these chemicals may be more highly exposed than the general population.349-.690-1. 90-43-7 General Information Ortho-phenylphenol (OPP.80 (2. on ornamental plants and turfs. are antimicrobial agents used as bacteriostats.76) 1.742) * .10) 1.00 (1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.580-1.50 (1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.09) 2. OPP is volatile.890) 1.10) 1.560-8. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. or 2-phenylphenol) and its water-soluble salt.90) .20 (1.10) 2.30) < LOD .420 (<LOD-.90) . SOPP is applied topically to the crop and then rinsed off.30) < LOD 90th 1.710) 3. Survey Geometric mean (95% conf.770 (.890 (.364-.570 (.850 (.30-7.450 (<LOD-. 1998. Both have been used in agriculture to control fungal and bacterial growth on stored crops. and sanitizers.50 (1.80) 1.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . EPA.90 (1. OPP is still used as a disinfectant fungicide for industrial applications.S. whereas SOPP is not volatile and is more water soluble. fungicides.50 (1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.. interval) .90 (1. Timchalk et al.570 (.350-1.30) < LOD 1.27 (.490 (<LOD-.490 (<LOD-.92 (. and as a wood preservative.509 (.22 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20) < LOD 1.790) 2.14 (<LOD-3.670) 2.550-1..389-.34) 1. leaving the chemical residue OPP.610-1.636) * .50) < LOD .02) 1.590-2.490 (<LOD-.20-2. Workers who manufacture. and it has limited water solubility.. 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.28-3.497 (.40-5.50-3.470 (<LOD-.90) 1.370-.19 (. however.830 (. 2006).540-2.600-1.500-2.370-. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.10) . population from the National Health and Nutrition Examination Survey.710-2.840-1.450 (<LOD-. OPP is considered to be moderately toxic after acute oral doses in animal studies.570-.28 (.386-. such as fruits and vegetables. 2006).770 (.3.60 (1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. 2006).50) 1.880-2.40 (.10-1.30 (1.00 (1.10 (1.88) 1.80) 1.00 (1.EPA.

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.750 (. 1992.33-2. Nakagawa et al.950) < LOD .09-3.13) 1.93) . In high dose animal studies.810-1.51-3.17 (. Zhao et al.910 (. Brusick.93) .06 (1. leading to production of two metabolites.EPA 2006).32) 1. 2002).380 (.43-2.09 (1.43) 3.. 1984. 1999.550) < LOD .69 (1.361-.00 (1.S. Murata et al.28 (<LOD-4.600-1.61 (2. 1986)..04-4.59) .38-3. Kwok et al.93 (1. OPP was not found to be mutagenic. Survey Geometric mean (95% conf.81) 1..329-.510 (<LOD-.780 (.248-.00 (.470) < LOD .08) 1.550-.382 (.38) 2.440 (.4) 3. but no neurologic.96 (1.58) 2.. population from the National Health and Nutrition Examination Survey. U.59) 1.62) .08-2.gov/pesticides/.385 (.840 (.96 (1. 1984.620-1.44 (1. less likely. Volunteers exposed to 0.17 (. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.970) 1. 2005).53) 1.420 (<LOD-.910-1. 2000.910 (<LOD-1.64 (2. Bomhard et al.S.620-1.484) * .74 (1.29) 1.980 (<LOD-1.670 (.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . U. Biomonitoring Information Urinary OPP levels reflect recent exposure.91 (1.78 (2.96-4.17) 2.780-14..06-4.06-5.610) < LOD 1.980 (.860 (.43 (1.18) 2.291-.353-.656) * .46) < LOD 1.508) * .570) < LOD 1.860 (. 1999. 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. 2005).26) 1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.25-6.500) < LOD .43-2.690 (. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.epa.. reproductive.09-6.11) < LOD 90th 1.01) 1.21) 1.301-.666) * .EPA at: http:// www.20) < LOD 3.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .12-2.900-1.Fungicides anemia. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.320 (<LOD-.S. 2002. 2005. or developmental toxicity was observed (Bomhard et al.96) 1.670) < LOD .21-2.770-2.580) < LOD .460-.360 (<LOD-. CDC.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.11) 4.453 (.343 (.0) 1.580-1.. Ito et al. or.550 (. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.97 (2..670 (.473) * .21 (. Detectable levels were seen in over half the U.510-.07) 2.568) * .61 (1. interval) .420 (<LOD-. Additional information is available from U.800-1. 44 Fourth National Report on Human Exposure to Environmental Chemicals .470 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.75 (1.24-2.900) < LOD .640-1.12) < LOD 1. IARC has classified SOPP as a possible human carcinogen.40-13.750-2.560-2.29) 1.410 (<LOD-.93) 1. Smith et al.89 (1.38) 1.590) * . 1997.444 (.52 (.791) * ..311-.11 (.560) < LOD 75th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.750 (.88-4.11-1.810) < LOD . and it has classified OPP as not classifiable with respect to human carcinogenicity.05-2.61 (.270-.480-. 1998.496 (. 2002.28 (2..514 (.990) < LOD .410 (<LOD-.86 (1.32) 3. 1993.880-1.EPA 2006).33) .47) .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 .31) < LOD . Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.455-. by possible genotoxic mechanisms (Hagiwara et al.24-2.84 (1.11 (. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.02 (.S.27) < LOD .75 (1.650-1.S.403-.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .08-1. Pathak and Roy.940-2.

Shirai T. Christenson WR. Ito N. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes.43(7):14311437. Bormett GA.(56):399-407. 4/13/09 Onstot JD. Atlanta (GA). Freyberger A. Toxicol Appl Pharmacol 1999. Moldeus P. Hagiwara A. Richter M. Herbold BA. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Murata M. Bartels MJ. Bromig KH. National Toxicology Program (NTP). Moriya K. Fukushima S. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Timchalk C. St John MK. 4/9/09. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. March 1986.150(2):402-413. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Mutat Res 1993.niehs. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Pathak DN.EPA). 90-43-7) in Swiss CD-1 mice (dermal studies).S. Bomhard EM. Meuling WJ. Cano M. U. Elliott GR. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Leser KH. Eastmond DA. Hagiwara A.22(10):809-814. 2005. EPA-560/5-89-003. rat and man.Fungicides References Appel KE.20(5):851-857.703(12):97-104. Identification of SARA compounds in adipose tissue. Available at URL: http://www.pdf. Toxicol Appl Pharmacol 1998. Moore GA. Kwok ES. Food Chem Toxicol 1984. Carcinogenesis 1999. Environmental Protection Agency (U. EPA). Sangha GK. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. J Agric Food Chem 2006. Brendler-Schwaab SY. Tayama S. Gierthy J. Zhao S.45(5):460-481. Brusick D. Kawanishi S. 2006. Sangha G. Drugs. Narang A. Xenobiotica 1998. Bartels MJ.S. Arnold LL. Selim S. 1989. Roy D. Fukushima S.pdf. Crit Rev Toxicol 2002. Third National Report on Human Exposure to Environmental Chemicals. Buchholz BA. Biochem Pharmacol 1992. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Coelhan M. et al.50(11):3351-3358. Timchalk C.54(16):5731-5735. J Chromatogr B Biomed Sci Appl 1997.17(8):411-417. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Arch Toxicol 2000. Mendrala AL.epa. Available at URL: http://ntp.28(6):579594. U.nih.32(6):551-625. Office of Toxic Substances. Hirose M. McNett DA.S. Shibata M. Regul Toxicol Pharmacol 2002. Roberts AL. Eadon G. EPA 739 R-06004. Stanley JS. J Agric Food Chem 2002. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Centers for Disease Control and Prevention (CDC). Nakagawa Y..35(2 Pt 1):198-208. van de Sandt JJ. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). July 28. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Imaida K.74(2):61-71. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol.gov/oppsrrd1/REDs/ phenylphenol_red. Comparative metabolism of orthophenylphenol in mouse. Smith RA. Turteltaub KW.286(2):309-319. Bartels MJ. Environmental Protection Agency (U. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. IARC Sci Publ 1984. Inoue S. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Cnubben NH. Ito N.gov/ntp/htdocs/LT_ rpts/tr301. et al.159(1):18-24.S. Hum Exp Toxicol 1998. Glas K. The carcinogenicity of the biocide ortho-phenylphenol. Hakkert BC. Bartels MJ. Brzak KA. Vogel JS. Christenson WR. Environ Mol Mutagen 2005.

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

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

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

Roberts AL. Bravo R. Kier L. Environmental Protection Agency (U. Hein MJ. Camann DE. Tinwell H.37(4):10881093. Hines CJ. Wratten SJ. Quistad GB. Coleman S. Furlong ET. Hodgson E. et al. March 2006. Alavanja MC. and metolachlor herbicides in rats. EPA). Environ Health Perspect 2003. Feil VJ. Chem Res Toxicol 1998. 2000. Linderman R.11(4):353359. Burkhardt MR. J Agri Food Chem 1989. reservoirs and ground water in the Midwestern United States.Herbicides References Ashby J. Heederik D.pdf.17(6):559-566. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Centers for Disease Control and Prevention (CDC). Comparative metabolism and elimination of acetanilide compounds by rat. Barr DB. Environ Sci Technol 2005. Sci Total Environ 2000. Davison KL. Kolpin DW.248(2-3):123-133.24(10):1003-1012. Acetochlor (Harness) Pesticide Petition Filing 1/00. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Linhart SM. Jefferies PR. acetochlor.cce. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Xenobiotica 1994. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Larsen GL. Barr JR. Wilson AG. et al. J Expo Anal Environ Epidemiol 2005. pages 3682-3690. 1998. Andrews HF. Barr DB. Lefevre PA.html. Feng PCC. Volume 65. Environmental Protection Agency (U. Available at URL(non U. 5/30/06 U.cornell. Atlanta (GA). Hsiao JJ. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Sci Total Environ 2000. Battaglin WA. 5/30/06. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Hladik ML. Ward EM.39(17):6561-6574.15(6):500-508. sulfonamide.S. epa. Deddens JA. Kinney PL. and other herbicides in rivers.S. Thurman EM.111(5):749-756. 2005. Environ Health Perspect 2000. Occurrence of sulfonylurea. Peter CJ. Federal Register: January 24. Striley CA. Rose RL. J Expo Sci Environ Epidemiol 2007. Green T. EPA 738-R-00-009. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. et al. U. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. EPA).edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Reynolds SJ.S.248(2-3):115-122. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.S.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Curwin BD. imidazolinone. Number 15. Hum Exp Toxicol 1996.108(12):1151-1157. Olsson AO. Whyatt RM. Sanderson WT. Available at URL: http://www.S. Casida JE.15(9):702-735.EPA): http://pmep. Dialkylquinonimines validated as in vivo metabolites of alachlor. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.

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

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

248(2-3):115-122. Andrews HF. Camann DE.pdf. reservoirs and ground water in the Midwestern United States. Barr JR. Hill RH Jr.S. EPA 738R-98-020.11(4):353359. Mutat Res. Available at URL: http://www.usgs. World Health Organization. Hull RD. Sacramento. Alachlor in Drinking-water. Environmental Protection Agency (U.Herbicides References Battaglin WA. December 1998. Am Ind Hyg Assoc J 1995. International Programme on Chemical Safety (IPCS). 1999. Chem Res Toxicol 1998. Hladik ML. Available at URL: http://water. U.56(6):853-859. and metolachlor herbicides in rats. EPA). MacKenzie B. et al. Available at URL: http://www. Kolpin DW. Gilliom RJ). 98-4245 (by Barbash JE.39(17):6561-6574. Atlanta (GA). 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Bull Environ Contam Toxicol 1996. Driskell WJ. Martens MA. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Hum Exp Toxicol. Circular 1291.56(9):883-889.18(6):363-391.43(9):2504-2512. 1999. 2/27/09 U. revised February 15. Barr DB. Dialkylquinonimines validated as in vivo metabolites of alachlor. Feil VJ. Casida JE. Thurman EM.S.44(18):1325. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. 1992-2001.37(4):10881093.pdf. Henningsen G. Geological Survey (USGS).gov/oppsrrd1/ REDs/0063. DNA adduct formation by alachlor metabolites. Biagini R. Supplemental Technical Information (available on-line only). Shealy DB. Striley CA. J Agri Food Chem 1989. Hines CJ. 1996. 2007.htm. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Environ Health Perspect 2003. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Sci Total Environ 2000.org/documents/pds/pds/pest86_e. Casida JE. Quistad GB. Whyatt RM. 1998. Hines CJ.php. California. Casida JE.43(25):2087-94. Burkhardt MR. Brown MA. Davison KL.47(6):503-517. Reregistration Eligibility Decision (RED) Alachlor. and other herbicides in rivers.111(5):749-756. Thelin GP. Biagini RE. Quistad GB. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Lau H. Erratum in: Life Sci 1989. Tolos W.S. Shoemaker DA. Wratten SJ. who. Life Sci 1988.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Feng PCC. Brown KK. Kier LD. Linhart SM. 86. March 2006. Jefferies PR.int/water_sanitation_health/dwq/chemicals/en/alachlor. Heydens WF. Kimmel EC.epa. Environ Sci Technol 2005. Kinney PL. Peter CJ. 2003. Roberts AL. ALACHLOR. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. imidazolinone. Clark JM. 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). Kolpin DW. acetochlor. Larsen GL. Tessier DM. Geological Survey (USGS). 1997. Geneva. Hill AB. Hsiao JJ. Xenobiotica 1994. Comparative metabolism and elimination of acetanilide compounds by rat. Wilson AG. Background document for development of WHO Guidelines for Drinking-water Quality.inchem. Deddens JA. No. Sci Total Environ 2000. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Third National Report on Human Exposure to Environmental Chemicals. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.S. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. 2/27/09 Jefferies PR.395(2-3):159-171. Available at URL: http:// www. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Sanderson WT. Occurrence of sulfonylurea. Thake DC. sulfonamide. 4/2/09 U. 2005. J Ag Food Chem 1995. Ann Occup Hyg 2003. et al. WHO/ FAO Data Sheets on Pesticides. Furlong ET.248(2-3):123-133.24(10):1003-1012. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. World Health Organization (WHO).

which may vary for some chemicals by year and by individual sample. 2003b).EPA. Related chlorotriazine herbicides include simazine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. U. 2003a). More than 70 million pounds have been applied annually in recent years. Survey Geometric mean (95% conf.and post-emergence to agricultural land for crops such as corn and sorghum. In soils.. In animals and humans. For the general population. Atrazine has limited water solubility and is not tightly bound to soil. In regions where atrazine is used.. and then eliminated in the urine over a few days (Bradway et al. resulting in atrazine mercapturate and N-dealkylation products (IPCS. but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. 1990). As a result. Timchalk et al.Herbicides Atrazine CAS No. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. 1982. 2003b). Applicators of atrazine may be exposed dermally and by inhalation. drinking water is an infrequent source of atrazine exposure.. 1993. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al. propazine. Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2007). Bacteria and plants can metabolize atrazine to hydroxyatrazine. 1996. population from the National Health and Nutrition Examination Survey. with about 75% of corn cropland receiving treatment.S. metabolized. U.3.EPA. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. atrazine is slowly degraded to dealkylated products. all of which act by inhibiting plant photosynthesis. It is also used as a non-selective herbicide. The dealkylated chloroatrazine metabolites. and cyanazine.. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. Catenacci et al. Atrazine does not bioaccumulate.. Atrazine is well absorbed orally.S.EPA. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination. 2002.791 and 0. 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. it is one of the more commonly detected pesticides in surface and ground waters (USGS. but it is leachable into ground and surface waters. which have half-lives of several months.. glutathione conjugation appeared to be the major route of biotransformation. Hayes et al.S. Atrazine is applied pre. 1993). 2005. Fourth National Report on Human Exposure to Environmental Chemicals 53 . < LOD means less than the limit of detection. Atrazine was first registered as an herbicide in 1958.S.

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

et al. McElroy WK. Toxicological profile for atrazine. Quandt SA. et al. 2005. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.. Lee M.. 3/11/09 Arcury TA. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Eldridge JC. Extrom PC. Blewett C. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.99(8):5476-5480. Toxicol Sci 2000. In small studies of Maryland residents in 19951996 (MacIntosh et al. Striley CA. Tyrey L. 2005). Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.gov/toxprofiles/tp153. et al. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Breckenridge CB. Eldridge JC. Goldman JM. 3/11/09 Laws SC. Aldous CN. Proc Natl Acad Sci USA 2002. Seiber JN. Noriega N. J Toxicol Environ Health 1994. J Toxicol Environ Health 1994.43(2):155-167.69(2):217-222. atrazine was detected in only four children (Arcury et al. Schmid J. 2001 [online]. References Adgate JL. 2000).. In a study of 60 farm worker children. Mendoza M. World Health Organization. Cooper RL. Lucas AD. Moseman RF.. Gillis JH. Ferrell JM. Third National Report on Human Exposure to Environmental Chemicals. Grzywacz JG. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.76(1):190-200.html. Simpkins JW. 2005). Pfeifer KF. Cooper RL. Toxicol Lett 1993. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Biological monitoring of human exposure to atrazine. Stevens JT. et al.53(2):297-307. Environ Health Perspect 2007. Ann Occup Hyg 2003. Cooper RL. Stoker TE. levels of atrazine mercapturate were generally not detectable (CDC. Stoker TE. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Sanborn JR. In the NHANES 2001-2002 subsample.43(2):155-167.109(6):583-590. Deddens JA. J Expo Anal Environ Epidemiol 2005. 2007). International Programme on Chemical Safety (IPCS).. A risk assessment of atrazine use in California: human health and ecological aspects. Brown KK.. Eberly LE. Geneva. Maroni M. Chen H. Reynolds SJ. In a small number of field workers. Stuart AA. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.30(2):244-247. Toxicol Sci 2000. Sanderson WT.. Hines CJ. Pest Manag Sci 2005. Environ Health Perspect 2001. Bradway DE. Bersani M. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.cdc. Available at URL: http:// www. Centers for Disease Control and Prevention (CDC). Atlanta (GA). Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Cottica D. Hayes TB.64(9):672-678. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Ferrell JM.58(2):366-376.61(4):331-355. Gammon DW. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. et al. Barr DB. Wetzel LT. Ferioli A. No. Hein MJ. Shoemaker DA. Stoker TE.15(6):500-508. Toxicol Sci 2003.47(6):503-517. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Wetzel LT. 1996. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. WHO/ FAO Data Sheets on Pesticides. Available at URL: http://www. diamino-S-chlorotriazine and hydroxyatrazine.org/documents/pds/pds/pest82_e. Steroids 1999. The geometric mean of urinary atrazine mercapturate was 1. 2001). Laws SC. Agency for Toxic Substances and Disease Registry (ATSDR). Lioy PJ. Gillis JH. Carr WC Jr. Heederik D. Hermaphroditic. Clayton CA. Curwin BD. Vonk A. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Perry et al. Saiz SG. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. ATRAZINE. 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. Barbieri F. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Catenacci G. Goodrow MH. 1993).atsdr. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. 2003. Jones AD. et al. Collins A. Barr DB.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Freeman NC. Barr DB.115(8):1254-1260. Tapia J. Fleenor-Heyser DG. Biagini RE. 82.inchem.htm. J Agric Food Chem 1982.

Needham LL. Office of Prevention.58(1):50-59. Toxicol Appl Pharmacol 2004. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Ryan PB. Rayner JL. Supplemental Technical Information (available on-line only). Perry M. Toxicol Sci 2002. Chem Res Toxicol 1993. Sanderson JT. Sathiakumar N. Environmental Protection Agency (U. Environmental Fate and Effects Division. Hammerstrom KA.S.S.27(6):599612.61(1):27-40. Osborne DW. Circular 1291.10(7):479.67(2):198-206. Tortorelli J. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Stevens JT. Environmental Protection Agency (U. Guidici DL. Toxicol Sci 2000. 3/11/09 U. EPA).pdf. Available at URL: http://water.6(1):107-116. Washington (DC). Timchalk C. Ann Epidemiol 2000. Cooper RL. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. U. Geological Survey (USGS).S. 0062.usgs.195(1):23-34.pdf. Guidici DL. Toxicol Appl Pharmacol 2002. Breckenridge CB. 6/1/09 U. Lansbergen GW. van den Berg M. Langvardt PW.epa. revised February 15. 2003b. J Toxicol Environ Health A 1999. Wood C. March 2006. Dagenhart D.9(5):494-501.S. Available at URL: http://www. Wetzel L. Pesticides in the Nation’s Streams and Ground Water. Kastl PE. Stoker TE. Cooper RL. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. A review of epidemiologic studies of triazine herbicides and cancer. Stoker TE.epa. Crit Rev Toxicol 1997.182(1):44-54.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. The Quality of Our Nation’s Waters. 2007. EPA). Dryzga MD. Laws SC. Available at URL: http://www. MacIntosh DL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Interim Reregistration Eligibility Decision For Atrazine. Laws SC. EPA Office of Pesticide Programs.Herbicides development of a biomarker of exposure. Singzoni B. J Expo Anal Environ Epidemiol 1999. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Christiani D. White paper on potential developmental effects of atrazine on amphibians. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. 1992-2001. A longitudinal investigation of selected pesticide metabolites in urine.php.gov/oppsrrd1/REDs/ atrazine_ired.56(2):69-109. Toxicology 1990. May 2003a. Case No. Delzell E. Pesticides and Toxic Substances. Boerma J. Fenton SE.S. A risk characterization for atrazine: oncogenicity profile.

810-1.16) < LOD . dizziness.680-1. 2.22) < LOD .660) 1.230 (<LOD-. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.S. 2. Similar to other chlorophenoxy herbicides.210-. < LOD means less than the limit of detection. Kohli et al.730 (.4-D may occur during residential applications..27-2.4-D) controls broadleaf weeds in residential. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.Herbicides 2.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.400) < LOD . and mecoprop).210 (<LOD-. Sauerhoff et al. It is poorly bound in soils.4-D has low acute toxicity. it acts as a plant growth hormone.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .66) < LOD 1. and delayed Urinary 2. with a half-life of several days to several weeks.60) 1.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . Human health effects from 2.890 (. 2007). 2004). 1989.560-1.30 (<LOD-2.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.4-D can be applied either as an aqueous salt or as oil-soluble esters.310) < LOD .S.00-2.10) < LOD 1.670-1.24 (.40) 1. 94-75-7 General Information Widely used throughout the United States.. 2. which may vary for some chemicals by year and by individual sample. 4-D. nausea. Once absorbed.EPA.55 (1.03) 695 659 520 668 589 892 Limit of detection (LOD. Recent estimates of chronic intakes of 2.690-1. 1977).930 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.490) < LOD < LOD < LOD .550-1. hypotension.EPA.490 (. headache. MCPA. these herbicides can enhance plant growth. but at higher levels they are herbicidal. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. It is not well absorbed through the skin.560-.250 (<LOD-. abdominal pain.760 (. myotonia.690 (. Survey Geometric mean (95% conf.910) < LOD .70) 1.4-D is rapidly absorbed via oral and inhalation routes. General population exposure to 2.80) 1.690 (.51 (1. 2005).02-1. 1974.4-dichlorophenoxyacetic acid (2. renal and hepatic injury. agricultural.08) < LOD .S.370-.48) < LOD 1.EPA in 1948.740 (. by direct contact with agricultural and residential areas after applications.4-Dichlorophenoxyacetic Acid CAS No.690 (.4-D were used in the U.27 (.27 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.420) < LOD .440-1.230-.350) < LOD < LOD < LOD .540-. and by consuming food or drinking water contaminated with 2.320) 90th . the chlorophenoxy herbicide 2.10 (<LOD-1.43) 1.10 (<LOD-1.32 (1.410) < LOD .21) 1.S.310 (.S. 2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.930-1.260 (<LOD-.250 (<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 .20 (. As much as 62 million pounds of 2.4-D or exposed for prolonged periods.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.610 (.2.960-1.4-D have been below recommended intake limits (U. At low levels.05-2.. population from the National Health and Nutrition Examination Survey.952 and 0.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . It was first registered with U.07 (. and aquatic environments. Fourth National Report on Human Exposure to Environmental Chemicals 57 .13) < LOD .610-.890) < LOD .910) 1. in 2001 (U.20 (<LOD-1.420-. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. It is rarely detected in ground waters (USGS.330 (.

670 (.990-1.16) 1. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.S.08 (. eyes.610-.35) < LOD . 1995).380-. 2005).S.05) . other exposures.S.700 (.gov/pesticides/.740 (.EPA. Epidemiological studies have reported associations of several types of cancer. In previous samples of the U. 2. Kolmodin-Hedman and Erne.850) < LOD .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 .720 (.580-. 2000).890-1.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.480 (. Survey Geometric mean (95% conf.570) < LOD .560-.EPA. Post-application levels in farmers and home gardeners were dependent on Urinary 2.440 (. CDC.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. developmental. 2005. in small samples of children (Hill et al..660 (. U. 2.550-..930-1. 1989).380 (<LOD-. or to contaminants in the herbicide formulations (specifically 2.340 (.680) < LOD .13 (. Hill et al.640 (. adrenals and gonads (NTP.810-1. U.14 (. The acid and salt forms of 2.590 (<LOD-1.32 (<LOD-2.340-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .810-1.820-1.470) < LOD . IPCS.4-D levels were detectable in less than a quarter of the individuals studied.EPA at: http://www.660) < LOD . Frank et al.980) < LOD 1.73) .. Biomonitoring Information Urinary levels of 2.Herbicides neuropathy (Bradberry et al. or teratogenic effects in chronic rodent studies (Charles et al.17 (. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S... 2. Knopp et al. 1996.410) < LOD < LOD < LOD . U.920) < LOD 1. liver.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.24) 1. 58 Fourth National Report on Human Exposure to Environmental Chemicals . 1980. 2005).670 (<LOD-1. 2003. 2001.4-D production plant workers and a few forestry workers spraying 2..330-.56) . It is unclear whether these associations are related to the chlorophenoxy herbicides.7.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.380 (<LOD-. IOM. 2005). Pearce and McLean. urinary 2. 2005.620-. 1996.41 (1.410 (<LOD-.39) < LOD 1.19) . IPCS.520-. 1995. thyroid. population (Hill et al.590 (<LOD-1.EPA 2005). population from the National Health and Nutrition Examination Survey.780-1. Average post-application urinary levels of 2.890) < LOD 1.490 (. and of adults and children (Baker et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1..4-D reflect recent exposure.08 (. U. 2005.. Acute high doses administered to laboratory animals produced ataxia.270-.13 (..790) 1. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.610-.270 (<LOD-. IPCS.27-1.08 (. 2002.4-D does not have significant reproductive.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. Kutz et al.4-D are eye irritants.780 (.380) < LOD . 2004).EPA.780) . 2002. and evidence of histological injury to the kidneys.390) < LOD < LOD < LOD .S. 1996.410) < LOD 1.4-D in farmers were more than 25-fold higher than the 95th percentiles in the NHANES 1999-2000 and 2001-2002 subsamples (Arbuckle et al.S. 2006.410) 90th .790) < LOD . 1992). 2005. Additional information is available from U. 2005).560-.S.350 (<LOD-. 1985.670 (.3.. 1994).epa. 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. myotonia.

Driskell WJ. Kutz FW.4-D and 2. Veterans and Agent Orange: update 2002.. Chapman P. Tandon JS.4-dichlorophenoxyacetic acid (2.4 dichlorophenoxyacetic acid (2. Sanderson WT.4-D were highest in the farmers who applied the 2. Ripley BD. Review of 2. 2005. Alexander BH. Barr DB. 3/17/09 Knopp D.. National Toxicology Program (NTP). Assessment of exposure to 2.4. J Environ Sci Health B 1992. Wilson RD. Philbert MA.4-.4-dichlorophenoxyacetic acid and its forms.4-D) epidemiology and toxicology. Sirons G J. In farm families. 1992). Mandel et al. Finding a measurable amount of 2. et al.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 2.5-T). Crit Rev Toxicol 2002. Hill RH Jr. Developmental toxicity studies in rats and rabbits on 2. Murphy RS. Honeycutt R.php?record_id=10603. Needham LL. Vet Hum Toxicol 1989.nih. Bus JS.4-D. Needham LL. Arnold EK. Forestry workers involved in aerial application of 2. 914. Barr DB. Baker S.niehs. Scand J Work Environ Health 2005.51(3):152-159.gov/index. Dichlorophenoxyacetic acid. Mandel JS. Estimation of occupational exposure to phenoxy acids (2.inchem.32(4):233-257.4-Dichlorophenoxyacetic Acid).4-D): exposure and urinary excretion. Hein MJ.4:97-100.18(4):469-474. Absorption and excretion of 2. Harris et al. Biomonitoring for farm families in the farm family exposure study. Carter-Pokras OD.4:318-321. Hanley TR Jr. Centers for Disease Control and Prevention (CDC). Pesticide residues in urine of adults living in the United States: reference range concentrations. Harris SA. Erne K. Available at URL: http:// www. Kolmodin-Hedman B. TOX-63: TOXICITY REPORT CURVES. Solomon KR. Bailey SL.4-dichlorophenoxyacetic acid in man. Biomonitoring of herbicides in Ontario farm applicators. Hill RH Jr. 3/17/09 Institute of Medicine (IOM). 2005 Charles JM. Khanna RN. Fast DM. Shealy DB.31 Suppl 1:98-104.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Atlanta (GA). the amount of pesticide applied. Sircar KP. Kohli JD. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Brody D. J Expo Anal Environ Epidemiol 2005 Nov. Curwin BD. Biomonitoring studies of 2. et al.15(6):500-508. J Expo Anal Environ Epidemiol 2000. Environ Res 1995. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Arch Toxicol Suppl 1980.4-D than levels found in the general population. 2. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Cole DC. 2005). and the use of protective clothing or equipment (Arbuckle et al. Tables. Smith SJ.4-D in urine does not mean that the level of the 2.S. Frank R.10(6 Pt 2):789-798. Head SL. References Arbuckle TE. the number of acres to which it was applied (Curwin et al. Available at URL: http:// www.. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Arch Environ Contam Toxicol 1985. Heederik D. International Programme on Chemical Safety-INCHEM (IPCS). Available at URL: http://ntp. Washington (DC): National Academies Press. Selected pesticide residues and metabolites in urine from a survey of the U. Stephenson GR. 2003. Beasley VR. Pesticides residues in food: 1996 evaluations Part II Toxicology. Garabrant DH. Board on Health Promotion and Disease Prevention. Survival and Growth Curves from NTP Toxicity Studies.org/documents/jmpr/jmpmono/v96pr04.Herbicides the time since application.4-dichlorophenoxyacetic acid (2.37(2):277-291. Baker SE. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Reynolds SJ. Campbell RA. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Ritter L. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4-D will result in an adverse health effect. TOX-63 Peroxisone Project (2. Baker BA. Updated March 7. Toxicol Sci 2001. Dhar MM.31(2):121-125. 2005.60(1):121-131. Beeson MD. general population. Cook BT. Arch Environ Contam Toxicol 1989. Xenobiotica 1974.27(1):23-38. geometric mean urinary levels of 2.4:427-435.71(2):99-108. Exposure of homeowners and bystanders to 2. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Third National Report on Human Exposure to Environmental Chemicals. Acquavella JF. Holler JS. Occup Environ Med 1994.31 Suppl 1:90-97.nap. To T.edu/catalog. 2005). Gupta BN. van Ravenzwaay B.4-D). J Toxicol Environ Health 1992. Scand J Work Environ Health 2005. et al.. Gregg M. 2006.htm.

The Quality of Our Nation’s Waters. March 2006. June 2005.S. 2007.usgs. The fate of 2. 2004. 60 Fourth National Report on Human Exposure to Environmental Chemicals .htm.S.4-dichlorophenoxyacetic acid (2. 4/2/09 U. Environmental Protection Agency (U.8:3-1U.epa. Environmental Protection Agency (U. Available at URL: http://www. Circular 1291.2000 and 2001 market estimates.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.S.EPA). 3/17/09 U.4-D RED Facts. 3/17/09. Supplemental Technical Information (available on-line only). Pesticides in the Nation’s Streams and Ground Water.epa. revised February 15.pdf.4-D) following oral administration to man. Pesticide industry sales and usage .php. Available at URL: http://www.EPA. May. Gehring PJ.S. 2.gov/oppsrrd1/ REDs/factsheets/24d_fs. 1992-2001. EPA 738 F-05-002. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Office of Prevention Pesticides and Toxic Substances. Available at URL: http://water. Blau GE.Herbicides Sauerhoff MW.S. Washington (DC): U.EPA). Geological Survey (USGS). S. Toxicology 1977. Braun WH.

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

population from the National Health and Nutrition Examination Survey.2. Survey Geometric mean (95% conf. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.S.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th < 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 .440 (<LOD-.S.670 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 01-02 is 0.240) 679 701 957 Limit of detection (LOD.200 (<LOD-.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 . 62 Fourth National Report on Human Exposure to Environmental Chemicals .Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor 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.200 (<LOD-. which may vary for some chemicals by year and by individual sample.

Background document for development of WHO Guidelines for Drinking-water Quality. Andrews HF. Sanderson WT.47(6):503-517. revised February 15. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Quistad GB. Gilliom RJ). 6/1/09 Whyatt RM. Pesticides in U. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Alavanja MC. Ward EM. acetochlor. Barr DB.usgs. Linhart SM. Geological Survey (USGS).pdf. Reregistration Eligibility Decision (RED) Metolachlor.pdf.usgs. EPA 738R-95-006. Coleman S. Available at URL: http://water.248(2-3):115-122. U.24(10):1003-1012. 2003. Camann DE. Sci Total Environ 2000. J Expo Anal Environ Epidemiol 2005. 4/2/09 U.S. Centers for Disease Control and Prevention (CDC).php.39(17):6561-6574.248(2-3):123-133. Heederik D. Davison KL. 3/26/09 U.pdf 3/30/09 Hines CJ. Rose RL.111(5):749-756. 1998. usgs. Sacramento. Kinney PL. Environ Sci Technol 2005.ESTfeature_gilliom. April 1995. Chem Res Toxicol 1998. EPA). Environ Sci Technol 2007.S. R.108(12):1151-1157. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Atlanta (GA). sulfonamide. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . World Health Organization (WHO). 1999. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Curwin BD. Hsiao JJ. Wratten SJ. Environ Health Perspect 2003. Available at URL: http://water. Feng PCC. Kolpin DW. Jefferies PR. Reynolds SJ. 98-4245 (by Barbash JE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Hodgson E. Linderman R. Available at URL: http://water. Environ Health Perspect 2000. Comparative metabolism and elimination of acetanilide compounds by rat. Available at URL: http://www. Hladik ML. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.int/water_sanitation_health/dwq/chemicals/ metolachlor. Deddens JA. J Agri Food Chem 1989. Shoemaker DA. Burkhardt MR. and metolachlor herbicides in rats. Barr DB. Third National Report on Human Exposure to Environmental Chemicals.15(6):500-508. Biagini RE. Peter CJ. California. Larsen GL. Hein MJ.S. Occurrence of sulfonylurea. Available at URL: http://www.gov/nawqa/ pnsp/pubs/wrir984245/text. and other herbicides in rivers. Environmental Protection Agency (U. Casida JE. March 2006. Supplemental Technical Information (available on-line only).37(4):10881093. Circular 1291. Dialkylquinonimines validated as in vivo metabolites of alachlor.who. Sci Total Environ 2000. Thelin GP. Furlong ET.html. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. 2005. streams and groundwater. Striley CA. et al. Gillion.41:3409-3414.S.gov/nawqa/pnsp/pubs/files/051507. Barr JR. Ann Occup Hyg 2003. 2007. 1992-2001. reservoirs and ground water in the Midwestern United States. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.epa.S. Kolpin DW. Brown KK. et al. Xenobiotica 1994. Metolachlor in Drinkingwater. imidazolinone. Geological Survey (USGS). Feil VJ.gov/oppsrrd1/ REDs/0001. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.11(4):353359. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.Herbicides References Battaglin WA. Thurman EM. Roberts AL.

4-D were used as defoliants in the Vietnam War (e.5-T (Holson et al.. Once absorbed into the body.4.5-T and 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. 1989.. 64 Fourth National Report on Human Exposure to Environmental Chemicals .5-T.g. 1992). Human health effects from 2.4... headache. < LOD means less than the limit of detection. abdominal pain. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 2. myotonia.5-trichlorophenol and other degradates. the general population is unlikely to be exposed to it. Ester forms of 2.4. 2007). 2.4.5-T has been rarely detected in ground waters (USGS.4.5T is rapidly absorbed via oral and inhalation routes. Chlorophenoxy herbicides act as plant growth hormones.5-T was once applied as either an aqueous salt or as an oil-soluble ester. 1974).4.4. 2004). Kohli et al. 2.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. Nelson et al. 1986. Agent Orange).4. Given the commercial unavailability of 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. At low levels. and delayed neuropathy (Bradberry et al. ranging from several weeks to many months. it is not well absorbed through the skin.4.4.3. which may vary for some chemicals by year and by individual sample. The half-life of 2. but higher levels are herbicidal. Mohammad and St.Herbicides 2.4.1. nausea. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. hypotension.4. with an elimination half-life of approximately 19 hours (Arnold et al. these herbicides can enhance plant growth.4. 93-76-5 General Information 2.2 and 0. 1992.7.5-Trichlorophenoxyacetic Acid CAS No.. population from the National Health and Nutrition Examination Survey.4. Omer. 2. renal and hepatic injury..S.5-T is eliminated mostly unchanged in the urine.5-Trichlorophenoxyacetic acid (2.5-T in soil varies with conditions. and concern about contamination with 2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Although 2. Survey Geometric mean (95% conf.5-T degrades to 2.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.4. dizziness. Epidemiological studies have reported associations of several types of cancer.5-T use as a herbicide in 1985.

2005.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2. U.4. Finding a measurable amount of 2. IOM.S. 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.5-T reflect recent exposure. 1980). Urinary 2. IPCS. urinary levels of 2.gov/pesticides/. population from the National Health and Nutrition Examination Survey.EPA.7. Mean urinary levels of 2.4.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. Biomonitoring studies on 2. 2. 1992). 2003.S.4.epa.4. similar to results of NHANES II (19761980). Biomonitoring Information Urinary levels of 2.5-T itself is not mutagenic.3..5-T were generally below the limit of detection. or to contaminants in the herbicide formulations (specifically 2. 1996.5-T does not mean that the level will result in an adverse health effect.Herbicides or contaminated herbicides. Survey Geometric mean (95% conf.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. in which urinary levels of 2.EPA at: http://www. 2002. 2005). In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.4. Pearce and McLean. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 65 . IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.5-T also were below the limit of detection (Kutz et al. other exposures. It is unclear whether these associations are related to the chlorophenoxy herbicides. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4.S.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.4. Additional information is available from U.5-T than levels found in the general population.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

Nelson CJ. Toxicol Rev 2004. Holson JF. Holson JF. Selected pesticide residues and metabolites in urine from a survey of the U. Environmental Protection Agency (U. May. Estimation of occupational exposure to phenoxy acids (2. St Omer VE.EPA. Vale JA. Agricultural exposures and non-Hodgkin’s lymphoma. Washington (DC): National Academies Press.32(4):233-257. Proudfoot AT.S.org/documents/jmpr/jmpmono/v96pr04.EPA). Gaines TB.4. Khanna RN. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Gaines TB. Pesticides residues in food: 1996 evaluations Part II Toxicology.4. Centers for Disease Control and Prevention (CDC). Fundam Appl Toxicol 1992.5-T). Board on Health Promotion and Disease Prevention. 2005.4.19(2):298-306.5-trichlorophenoxyacetic acid (2.5-T in four-way outcross mice. Sheehan DM.4-D/2.htm. Scand J Work Environ Health 2005. 210:250-255. Murphy RS. Available at URL: http:// www. Brody D. S.pdf. Veterans and Agent Orange: update 2002. discussion 5-7. general population. Neurobehav Toxicol Teratol 1986. Sircar KP. Atlanta (GA). Review of 2.4:318-21. Washington (DC): U.epa. Pesticide industry sales and usage .5-trichlorophenoxy acetic acid in man.4-.4. Vet Hum Toxicol 1989. Beasley VR. Nelson CJ. II. 2. 2004. 3/17/09 Institute of Medicine (IOM).5-T).4-D and 2.23(2):65-73.4.S.4. Crit Rev Toxicol 2002. Gaylor DW.5-trichlorophenoxyacetic acid (2. 914. Mohammad FK. Dichlorophenoxyacetic acid. et al.php?record_id=10603. Kolmodin-Hedman B. J Toxicol Environ Health 1992. Poisoning due to chlorophenoxy herbicides.4-D) epidemiology and toxicology. 2003. 3/17/09 Kohli JD. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4.edu/catalog. Office of Prevention Pesticides and Toxic Substances. Cook BT. Arch Int Pharmacodyn Ther 1974.5-T). Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. McCallum WF. Kutz FW. U.4. Gupta BN. Tandon JS. Developmental toxicity of 2. Available at URL: http://www. Arch Toxicol Suppl 1980.inchem. Behavioral and developmental effects in rats following in utero exposure to 2.Herbicides References Arnold EK. Garabrant DH.19(2):286-297. LaBorde JB.5-t mixture.31(2):121-125. Available at URL: http:// www. et al. I. Absorption and excretion of 2.S.37(2):277-91. Bradberry SM. Developmental toxicity of 2. LaBorde JB.2000 and 2001 market estimates. Wolff GL. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. gov/oppbead1/pestsales/01pestsales/market_estimates2001. McLean D. Third National Report on Human Exposure to Environmental Chemicals. Pearce N. Philbert MA.31 Suppl 1:1825. Carter-Pokras OD. Fundam Appl Toxicol 1992.nap. Multireplicated dose-response studies with technical and analytical grades of 2.8(5):551-60. International Programme on Chemical Safety-INCHEM (IPCS). Dhar MM.4-dichlorophenoxyacetic acid (2. Erne K.

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

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

Organochlorine Pesticides twitching. vomiting. 2005.atsdr.cdc. 2004). and occasionally. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity.S. EPA has established environmental standards for aldrin and dieldrin.. Kanthasamy et al.. environmental levels) and health effects is available from ATSDR at: http://www. When dieldrin was fed to pregnant rodents.. Survey Geometric mean (95% conf. and the FDA monitors foods for pesticide residues. population from the National Health and Nutrition Examination Survey.gov/toxpro2. 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. Li et al. In a study of pesticide applicators with occupational exposure to aldrin.e. OSHA has established workplace exposure standards for aldrin and dieldrin. similar to results in a subsample of NHANES II (19761980) (Stehr-Green.. 1991). 1987). Danish women whose serum was collected in 1976 had a median dieldrin level near the 95th percentile for females in this Report (Hoyer et al. median levels of dieldrin were more than thirtyfold higher than the 95th percentile Serum Aldrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. 78 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al.. which may vary for some chemicals by year and by individual sample. When fed to experimental animals... Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al. 1995). nausea. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 2275 1946 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 756 588 1519 1358 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1057 946 1218 1000 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 559 456 512 485 1045 881 < LOD means less than the limit of detection for the lipid adjusted serum level. 2004). 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). and seizures. 1998) and behavioral changes (Carlson and Rosellini.. 2000). 2000). both aldrin and dieldrin caused liver enlargement and liver tumors. in which only 10. seizures (Smith. The U. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. dieldrin at higher doses caused irritability. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. 1998).. 1989).. 2000.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). serum aldrin levels were below the limit of detection..html. but no estrogenic effect was noted in a study that used cultured cells (Tully et al. tremors. 2005). In samples obtained between 1973 and 1991 from Norwegian women.S. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al. Information about external exposure (i.

4) 21.062 (.070-.1) < LOD 9.1) 14.40-10.8 (9.112) 95th .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .100-.8-19.053 (<LOD-.8 (11.190) .8-25.8) < LOD 8.054-.8 (18.0) 21.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .100-. Survey years 01-02 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.7) 15.3 (13.8-24.090 (.062 (.4-18.0) < LOD 9.2) 12.138 (.101) .160) .7 (<LOD-15.1) 10.6) 16.0 (15.60-10.090-.073-.4) 95th 20.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.102 (. which may vary for some chemicals by year and by individual sample.5-15.S.080 (.8) 14.098 (.1-16.103 (.096-.048 (<LOD-.140) .139 (.093) .5 (<LOD-11.055 (.140-.40-9.075) < LOD .158) .084-.5 and 7.100-.50) 15.4) 14.5) 19.9-38.077-.138) .120 (.1) 15.8) 15.7-22.5-17. 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 .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.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.90) 90th 15.7 (14.0 (10.9 (12.6-24.7 (15.6 (14.80-9.160 (.8-17.4 (12.180) .069) < LOD < LOD .160 (.9-22.1) 20.110) .058) < LOD .30 (8.4) 539 456 484 487 980 885 Limits of detection (LOD.1 (18.054-.3 (14.4) 20.080-.070 (<LOD-.130 (.108-.80 (<LOD-10.3-21.1-18.070) .090-.130) .049-.083-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4 (12.120 (.6) 9. see Data Analysis section) for survey years 01-02 and 03-04 are 10.00-14.1) 13. Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.117) < LOD .9 (12.0 (11.147) 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 . which may vary for some chemicals by year and by individual sample.50 (8.70 (7.109 (.5) 21. Survey years 01-02 03-04 Geometric mean (95% conf.112-.1-19.110 (.2) 11.060) .30 (8.9 (13.6) 19.120 (.089 (.147 (.150 (.116) .103 (.9 (13.110 (.109-.9-23.6 (15.10 (<LOD-16.120) .063-.1 (13.110 (.4) 19.6-24.110) .3 (18.086-.110-.9 (14.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.100) . population from the National Health and Nutrition Examination Survey.0) 19.139 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-25.130-.064) 90th .100) .7-19.170) .8.130-.113 (.080) .088-.4) < LOD < LOD 16.064 (.1) 15.054-.056-.149) .120-.8-17.80-10.190) .124) .S.090-.090 (<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 9.100 (.3 (19.130) .150 (.130) . < LOD means less than the limit of detection.00 (8.6-33.2) 15.130-.0-21.5-17.4) 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 8.6 (15.059 (.3 (18. Fourth National Report on Human Exposure to Environmental Chemicals 79 .109-.0 (10.242) .140 (.5 (16.1-24.062-.2-15.077 (.180) .2) 14.4-17.5) 15.

htm. bioaccumulation. Narahashi T. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Fernandez MG. September 2002. Patterson DG Jr. Toxicol Lett 1992. Jr. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Available at URL: http://www. Ellis H. Teta MJ. Turner W. 2 Classes of Pesticides. In Hayes WJ.59:229-234. Mumtaz MM. Rosellini RA. Neurotoxicol 2005. Effect of occupational exposure to aldrin on urinary D-glucaric acid. et al. McIntosh LJ. 4/21/09 Hoyer AP. 1989.inchem. 4/21/09 Jorgenson JL. 80 Fourth National Report on Human Exposure to Environmental Chemicals . J Toxicol Environ Health 1989.cfsan. Reprod Toxicol 2000. pp. and lymphocyte sister chromatid exchange. Revised Feb. 4/21/09 Bates MN. Smith AG. Mink PJ. J Occup Environ Med 2005. Corrigan FM. 6/1/09 Ward EM. Jr and Laws ER. Academic Press.gov/~dms/ pesrpts.9:1357-1367. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Shore RF. et al. Exp Neurol 1998. 731-915. Sanchez-Ramos J. 15. United States Geological Survey (USGS).Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Hartvig HB. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Lancet 1998. Olea N. Brock JW. Pesticides in the Nation’s Stream and Ground Water. Part A 2000.gov/toxprofiles/ tp1. Kanthasamy A. David VL.64-65 Spec. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Available at URL: http://pubs. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 2007 [online]. Mann D. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. New York. Jorgensen T. Environ Health Perspect 1995. Roy ML. Chlorinated Hydrocarbon Insecticides.html. Basit A. Edwards JW.cdc. Available at URL: http://www. References Agency for Toxic Substances and Disease Registry (ATSDR). Wienburg CL. Chung KL. and epidemiology in the United States. August 2008.91(1):122-126. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Sonnenschein C. Environmental Health Criteria 91. Chemosphere 2004. Environ Health Perspect 2001.109(Supp1):113-139. Buckland SJ. Ginsburg KS. toxicology.gov/ circ/2005/1291/. Inc. 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. J Toxicol Environ Health.26:701-719. VT. Priestly BG. Grajewski B. Stehr-Green.47:1059-1087. Soto AM. Cancer Epidemiol Biomarkers Prev 2000.14:95-102.150:263-271. Garrett N. Toxicological profile for aldrin/dieldrin [online]. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.org/documents/ehc/ ehc/ehc91. Finley B. 1992-2001. Handbook of Pesticide Toxicology. Daniel SE. plasma dieldrin. Frey JM. Tully DB. Kitzazwa M. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Kanthasamy AG. Int Arch Occup Environ Health 1994.103(Suppl 7):113-122. Psychopharmacology (Berl) 1987.66(4):229-234. Schulte P.usgs. Aldrin and Dieldrin [online]. Grandjean P. Li AA. Carlson JN.atsdr. Serrano FO. Cox. 1991. Needham LL.fda. Vol. Available at URL: http://www. International Programme on Chemical Safety (IPCS). Song S.html. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Six high-priority organochlorine pesticides.54:1431-1443. PA. Patterson DG Jr. Demographic and seasonal influences on human serum pesticide residue levels. either singly or in combination.352:1816-1820. No:429-436. Anantharam V. are nonestrogenic in transfected HeLa cells. Organochlorine exposure and risk of breast cancer. 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. Eds. Facca A. Food and Drug Administration (FDA). Andersen A.27:405-421. Chapin RE.

3) 41.3) 37.7 (17.9 (26.30-11.6 (9. 10.7 (19.4 (22. Until 1988.2 (21. 2007).69-10. 1994).4-45.1-15.7 (34.8 (10.7 (<LOD-32.2 (37.3 (28.2 (10.9) 47. and dairy products are the usual sources of exposure to these chemicals in the general population.7) 19.4) 12.9 (31.6-45. foods high in fat such as meat. 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.7) 19.5) 10.4-40.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.8-33.1 (25.9) 31.5.7) 35.3 (11.9) 17.0) 75th 20.20-10.0) 27.7-14.7-70.6) 20.3-45.2 (9.7 (43.9 (36.8-33.5-40.5 (8.0) 31.6) < LOD 11.3) 18.0 (20. 01-02.5 (41.0) 41.3) 18.7-39.3 (27.8-31.1) 30.3-24.S.2 (41.9-40.2-49.9) 37.9 (15.89-10.2) 33.8 (40.0-67.9 (17. 57-74-9 Heptachlor CAS No. in addition to trace amounts of numerous other related compounds (ATSDR.8) 27.5) 9.82-11. chlordane was used to kill termites and other insects on agricultural crops.3 (<LOD-19.0 (<LOD-12.8) 18.5-43.8 (10.6-53. Consequently.1) 16.8-73.9-42.1) 90th 34.2 (28.Organochlorine Pesticides Chlordane CAS No.8.9 (29.5 (<LOD-12.7) 28.2-26.8-20.1-50.1) * 11. 1994.5) < LOD < LOD < LOD < LOD 13. Chlordane is not currently produced or used in the U.2) * 12.10 (8.2) 46. heptachlor use has been limited to treatment of fire ants near power transformers.4) 39.8) 52.7-12.7) 9.6) 9.7-25.3 (26.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.8-42.20 (<LOD-11.1-51.5-38.5 (33.1) 30.1 (15.9 (15.6) 49.1 (<LOD-12.4) 37.7 (32.7 (<LOD-13.6) 9.6) 8.4) 22.1 (27.1 (20.0 (16. and 7.9-21.8 (18.4-21. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.6-24.1 (16.1 (<LOD-12.10-11.2-49.9-38.4 (<LOD-12.8) 44.5) 56. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.8-32.1 (11.4 (30.9) 13.2-21.7) 31.5) 38.9 (26.6-24.0) 20.3-49.90 (8. lawns. from the early 1950’s until the mid-1980’s.. buildings.5-32. Survey Geometric mean (95% conf.8-23.2) 22.4) < LOD < LOD < LOD 23.5) 44.9 (11.5-65.4-51.0-25.4 (35.36-11.5. see Data Analysis section) for Survey years 99-00.6 (16.1) * 11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-18.5) < LOD < LOD 9.2) < LOD 11.9) 10.4 (10.9) 23.1 (<LOD-12.1-25.8 (17. 2007).1 (17.20-11.3) 10. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.8) 53.70 (<LOD-10.7) 42.9) 23.4 (31. and in soil.3 (25.6) 23.6 (43.37 (8.S.6 (25. Fourth National Report on Human Exposure to Environmental Chemicals 81 .9 (11. the technical grade product of each chemical contains 10%-20% of the other chemical.0-61.4 (30.7-56.5-42.0 (37.9) 36.2) < LOD 11.6) 39.1 (44.0-13.5-44.5-41.0 (26.9) 11.3 (21. Technical grade chlordane had contained 7% trans-nonachlor.9-21.4) < LOD 11.1) 22. 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. respectively.4) 29.6) 11. population from the National Health and Nutrition Examination Survey.9 (21.1-19.0-12.5 (34.5-13. fish. Since 1992.3-43. which may vary for some chemicals by year and by individual sample.6) 48.7 (34.5) 37.4-14.5) 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 * * * * 11.7 (10.2 (36.0) 37. and 03-04 are 14.8 (17.5 (31. 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.2-28.6-12.3-32.2) 34.2-56.9 (18.9) 11. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.1) < LOD < LOD < LOD < LOD < LOD 8.8-43. < LOD means less than the limit of detection. As a result of the manufacturing process.2) 37.1-25.8-61.63 (8.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1-65.7 (42.0-33.1 (40.4) 18.S.8) 52.5) 21.6-18.6) 36.5-47.0) 21.3 (20.0-18.3-45.74 (<LOD-10.3) 10.3 (9.6 (9.9) 39.2 (39.0 (32.6) 48.8 (42.2) 36.

130 (. Shindell and Ulrich.207 (.190-.216-.290) .083 (.280-.430) .062) < LOD .165-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1977b.092) .330 (. 1996.070 (<LOD-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.310 (.510) . chronic doses of heptachlor have produced liver enlargement and injury.290-. 1981). population from the National Health and Nutrition Examination Survey.240 (.213) * . dermal.286 (.370 (.063 (.130-.280) .260 (.203-.300) .220-.170) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.066 (.057-.130 (.348) .315 (.253-.370 (.320) .168-.079) < LOD < LOD < LOD .300) .350 (.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 * * * * .057) * .290-.260 (. Acute.170) .310) .148-.199-.170-. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.190-.115 (.180) .146) < LOD < LOD .242-.230-.250 (.280 (.082 (.150) .106-.180) .250-.280 (..140 (.053-.210-.070 (<LOD-.290-.231) .160) .056 (. 1986).077) .060 (<LOD-.150 (.070) < LOD < LOD < LOD < LOD < LOD .220 (.080) .410) .048-.066 (<LOD-.080 (. neonatal mortality.170) .115-.071 (.320 (.104) .140) .286 (. and alterations in immune function of offspring.064) < LOD .240-.073) < LOD < LOD < LOD < LOD . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.058-.108-.200-.258 (. 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.149 (.080) .100-.070-.300) . 2006).140 (.310-.Organochlorine Pesticides (Dallaire et al. 82 Fourth National Report on Human Exposure to Environmental Chemicals .340) .S.230 (.400) .110 (<LOD-.210 (.302) . 1986).063-. Rogan.230-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .320 (.049 (<LOD-.269 (.091) . OSHA has established occupational exposure criteria. which may vary for some chemicals by year and by individual sample.223) .320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .140-. 2001.110-.136) .373) .260-.150-.270 (.450) .119 (.170) . EPA has established environmental criteria for chlordane and heptachlor.258-.230 (.065-.083) .100 (. and inhalation exposure.057 (.S.340) .053-.058 (.300) .560) .380) .400) .S. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.140 (.350 (.050 (<LOD-.077) .240-.047 (<LOD-.074-.066-.146) .170) .200 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.058-.070-. 2002..204 (. 1991.270 (.077) .063) . Takahashi et al.246-.130 (.208 (..075 (.271 (.430) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.200-.070 (<LOD-.320 (.050-. and breast milk is a major excretion route in lactating women.063) * . Le Marchand et al.080) .090) . Smith.061-.100 (<LOD-.160) .310) .140-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .290) .130-.068) .067 (.300-.073 (.210 (.190-.250 (.077) .130) .270 (.128 (.130-. The major metabolite of heptachlor is heptachlor epoxide.150 (.350) .260 (.240) . which is also persistent in the body (ATSDR.180-.079) .133) 90th . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.245-. The U. 1991).189-.320) .063 (.130-. 1977a.310) .227) < LOD .120 (. 2007).320 (.063 (.225 (.070 (<LOD-.063 (.189 (. 2007.126) .120-.120-. Elimination of all these chemicals from the body occurs over months to years.280-. IARC.100-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.440) .150 (. FDA established allowable residues of chlordane.126 (.300 (.076) < LOD .070) . In laboratory animal studies. to heptachlor.104-.055-.. Chlordane and heptachlor are absorbed after oral.140 (.090-.087-. and heptachlor epoxide in foods and bottled water.450) .080 (.230) .066-.120-.130) . and the U.207) .370 (. Survey Geometric mean (95% conf.287) .360) .070-.160) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.148) .068-.280-. heptachlor.220-.068) 75th .180-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility. characterized by seizures and paralysis.070 (.290 (.160 (.200-.112 (.090) .130-.230-.069 (<LOD-.

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

7-19.50) < LOD < LOD < LOD 17.6) < LOD < LOD < LOD 27.8-46.8-24.1-15.5) < LOD 14.5 (11. 01-02.5 (11.2 (<LOD-62.3) 23.9) * * * 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 8.9) 15.3) 27.8 (15.8) 21.4 (<LOD-19.0-17. respectively.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8-23.6 (<LOD-27.10-13.40) 15.9 (15.9 (12.3 (<LOD-25.3) 18.3 (13.3) 22.2) 20.1 (19.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8) 14.4 (<LOD-54.90 (<LOD-9.8) 15.8 (13.1 (16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.6 (8.0-16.8 (<LOD-23.6. which may vary for some chemicals by year and by individual sample.2) 26.1) 13.8.4 (11. see Data Analysis section) for Survey years 99-00.9-29.4 (11.9-29.7-18.6) 22.8) 20.2-27.0 (15.3) 18.5 (<LOD-21.5.4) 18.20 (<LOD-9.2-27. Survey Geometric mean (95% conf.2-17.9-23.1) 23.2-16.0) 13.8) 13.8) 19.1-16.8 (18. 84 Fourth National Report on Human Exposure to Environmental Chemicals .0-17.0-19.6 (16.3) 18.7-25. and 03-04 are 14. population from the National Health and Nutrition Examination Survey.6 (12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-24.6 (16.5 (<LOD-32.2) 15.3) 10.5 (10.0 (11.8) 19.1) 20.7 (10.6 (13.6) 13.2 (18.6 (14.8) 16.5) 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 7.2) 13.8) 14.9-16. 10.3) 16.1-38.2 (<LOD-16.6-17.5 (18.5) 19.S.4 (15.8 (13.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.6 (11.7 (16.4) 21.2 (<LOD-25.8-24.6-21.9-25.8) 13.0-54. and 7.8 (18.3-18.7 (13. < LOD means less than the limit of detection.6) 14.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1-29.

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

1) 17.2 (60.3-30.9 (51.9) 51.5) 48.9 (51.8-21.0 (60.8 (42. 86 Fourth National Report on Human Exposure to Environmental Chemicals .6 (50.5-17.4) 19.1) 18.0) < LOD < LOD 8.7-160) 86.5) 22.6 (15.3) 18.1-55.1) 17.6) 60.9 (15.2) 19.0 (13.9) < LOD < LOD < LOD 20.7 (74.2 (25.7-21.3 (14.6) 34.8-79.6-66.0-23.5) 14.7) 15.1) 17. 01-02.7-32.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.6) 13.0 (42.9 (36.8) 19.1-20.3 (14.2 (64.5) 35.6 (57.9-22.1) 16.5) 78.1-51.5) 14.4) 20.1) 30.1-34.4-62.3) 16.4) 16.7-113) 68.0) 33.5.2) 59.4) 48.8) 51.9-40.0 (19.8 (17.6 (56.2 (59.1 (65. which may vary for some chemicals by year and by individual sample.7) 59.9-65.7-34.8-90.0-24.1) 17.2 (26.8-19.7 (30.9 (47.6-54.0 (13.7 (18.9-58.6 (32. < LOD means less than the limit of detection.7) 52.3 (56.7) 78.2-18.9-20.3) 19.8 (71.4-35.2-37.3) 25.1-16.5-95. population from the National Health and Nutrition Examination Survey.4-22.0-93.7-17.1 (17.5.1 (22.1 (47.4) 107 (84.2) 17.5 (13.9 (29.9-35.5) 20.4 (45.5 (45.0 (15.1) 17.8 (13.7) 14.2-23.4-23.7 (59.6 (12.4) 55.0-59.5-20.7 (59.6 (<LOD-14.7-29.0-93.3-32.6-19.9-65.2) 30.0) 75th 31.9-64.8.4-18. 10.8 (12.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.8-41.9) 14.8-19.6 (56.0) 18.8 (19.9) 14.2-17.8-67.2) 20.8 (15.1-126) 67.8-16.0 (14.2-16.6-82.2 (15.0-38. see Data Analysis section) for Survey years 99-00.2-21.1-28.6) 54.9) 51.1) 14.0 (62.8 (49.7) 17.3 (17.8) 80.1) 32.0 (48.1 (48.4-52.3 (16.3) 15.5) 90th 55.7-22.8-77.0) 19.2 (27.6) 10. Survey Geometric mean (95% conf.2-88.0-22.5) 77. and 7.5-69.7-20.9-36.8 (28.5 (15.7-18.9 (15.4 (28.5) 9.9 (16.8 (26.5 (44.6) 84.0-113) 68.10 (<LOD-11.3-21.3) 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.8-129) 74.3-57.1) 17.8-110) 59.8 (45.9 (28.7) 35.2) 39.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.70 (<LOD-12.6) 82.1) 78.0-37.2) < LOD 10.3 (45.5 (15.0 (16.7) 78.7 (11.1-34.4 (12.9 (19.3 (58.8 (26.7 (13.4-67.1-18.1-16.8 (30.8 (28.5) 19.5) 30.9-45.3-39.0 (29.8-16.8 (11.0 (15.6) 56.3-58.0-68.0-123) 74.5-111) 68.9 (<LOD-14.2 (14.1-22.8 (26.3 (49.4-36.8 (16.3) 18.4 (30.9 (66.8) 47.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.6) 25.8 (28.5-87.7 (35.1 (10.4 (11.6-20.7 (16.5) 26.8 (13.7-35.6 (52. respectively.0-143) 112 (68.1) 31.S.2-18.3) 32.3-74.2) 34.3-86.1 (41.9-89.5-36. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 30.7 (28.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.0-23.1) 78.7) 56.6-88.4 (16.7-77.7) 28.0 (42.7-38.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.8 (<LOD-20.2 (7.6-22.1) 62. and 03-04 are 14.2 (36.6) 56.3-50.3) 30.0-20.3) 36.9-69.6 (16.8-90.0) 13.2 (14.86-13.5 (25.5) 36.7) 73. interval) 18.0) 49.0) 40.1) 17.5-19.3) 32.4 (67.0 (16.7-23.2 (19.1) 18.4) 59.

041 (<LOD-.116 (.190-.106 (.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .180-.150) .558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .210 (.310-.220 (.125 (.120-.330-.240-.600) .190-.069-.288-.360-.099-.380 (.085-.220 (.111-.350-.092 (.250) .079-.161) .099-.145-.420 (.430-.497-.109 (.460) .171-.460) .128 (.270-.594) .085-.830) .120 (.210) .242) .260) .130) .420) .120 (.960) .093-.110 (.400 (.400) .071 (<LOD-.205 (.080) .100 (.409-.122) .830) .430-.390 (.390 (.240 (.054-.220 (.390 (.300-.080-.173-.540) .120-.160 (.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.580 (.161-.395-.760 (.110 (.220 (.320-.078-.400-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .108) 75th .20) .240) .310-.470 (.550 (.078 (.090 (<LOD-.090-.130 (.127) < LOD < LOD .470 (.400-.210-.129) .100-.490 (.177-.430-.084-.117) .651) .081-.100-.080 (.390 (.108 (.310-.630) .090-.220 (.098 (.279-.559) .390-.119) Selected percentiles ( 95% confidence interval) Sample 95th .141) .460-.470-.340) .090-.300) .202 (.330 (.089 (.272-.130) .108) .520 (.100-.116-. interval) .090-.093-.320-.630) .310) .327 (.330-.110 (.080-.290-.110 (.210-.250) .680 (.240) .082) .180-.600 (.355 (.119) < LOD < LOD < LOD .360-.112 (.095-. population from the National Health and Nutrition Examination Survey.150) .565) .087 (.210) .440-.055 (<LOD-.234) .310 (.134) .098 (.390) .130) .110-.410-1.690) .190-.340-. which may vary for some chemicals by year and by individual sample.104 (.160-.122) .417 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470 (.458 (.371) .630) .186 (.183 (.096-.180-.100 (.684) .405) .060) .080-.343 (.141) .097) .120 (.096-.092 (.116) .093) .085-.047-.367) .800) .100-.124) .232) .131) .190-.060-.130) .310-.120) .120-.400 (.094 (.091-.130) .114) .324 (.191 (.230 (.370 (.069) .490) .640 (.286-.317 (.280) .340-.370 (.110) .109 (.350 (.126) .930) .690) .S.061-.397-.113) .288 (.081 (.440) .210 (.680) .070 (.186-.490-.301-.106 (.098-.079-.470-.580 (.060 (<LOD-.500) .112 (.260) .098) .170 (.510 (.125) .190-.590) .080-.285-.120) .211) 90th .096) .110 (.510-.410-.135 (.220 (.220 (.068-.090-.237) .113) < LOD .130) .580 (.450) .461 (.105 (.130 (.520) .103 (.140) .220) .093-.240) .190-.395) .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.090 (. Survey Geometric mean (95% conf.120) .103 (.091) .158-.390) .210) .120) .490 (.480) .210 (.840) .414 (.110 (.111 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .250) .062 (.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 .520 (.104-.590 (.220 (.590 (.237) .090-.573 (.130) .106 (.090) .

html. Keller JA. et al. 1986. Bioassay of heptachlor for possible carcinogenicity. Hawaii Med J 1991. Available at URL: http://ntp. et al. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. A Report to the Hawaii Heptachlor Research and Education Foundation. May 1994. Loo S.inchem. Available at URL: http://www.atsdr.cdc.330:55-70. Available at URL: http://www.372:20-31. Aune M. Head SL.8:1-123. Concise International Chemical Assessment Document 70 Heptachlor [online]. 6/1/09 Rogan WJ.9:1-109. LeMarchand L. Baker DB. Siegel BZ. Inc. Kolonel LN. 79. Environ Res 2000. 1994-1997 organochlorine compounds. Willman E.259(3):374-377.html.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Dendle WH. Dewailly E. 2001. Toxicological profile for heptachlor and heptachlor epoxide [online]. Laliberte C. Eds. Royce W. Available at URL: http://www. Drews K. Shindell S and Ulrich S.niehs. Atuma S. Odland JO. Glynn AW. Dewailly E. Chashchin V. Wohlleb JC. 9/25/07 International Programme in Chemical Safety (IPCS). International Agency for Research on Cancer (IARC) . 88 Fourth National Report on Human Exposure to Environmental Chemicals . Sci Total Environ 2004. Sci Tot Environ 2006. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.110(8):835-838. Jr and Laws ER. Barker J. Handbook of Pesticide Toxicology. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor.org/site/foundation/ research/projects2. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 James RA. Bull Environ Contam Toxicol 1981:27:506-511.84:151-161. In Hayes WJ. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Bjerselius R.gov/ntp/ htdocs/LT_rpts/tr008. 1963-1967.28:497501. Darnerud PO. Jr. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. 2 Classes of Pesticides. 2006.nih. 1991 pp.heptachlor. et al.org/ documents/cicads/cicads/cicad70.pdf. Chlorinated Hydrocarbon Insecticides. JAMA 1988. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Arch Pediatr Adolesc Med 1996. Toxicological profile for chlordane [online]. International Agency for Research on Cancer (IARC). Canada). Hansen JC.110:617-624. Hertz-Picciotto I. Available at URL: http://www. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Vol.htm.niehs. Environ Health Perspect 2002. Smith AG. maternal serum and milk from Wielkopolska region.41:145–148. Environ Health Perspect 2002. Covaci A. Charles MJ. 4/21/09 Dallaire F. Organochlorines in Swedish women: determinants of serum concentrations. Organochloride pesticide residues in human milk in Hawaii.pdf. Lawrence River (Quebec. Berkowitz GS. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Environ Health Perspect 2003. Available at URL: http://www. Jaraczewska K. Saidein D. Granath F. KalubaSkotarczak A. Available at URL: http://ntp. Academic Press.50(3):108-118.inchem. Pollutants in breast milk.150:981-990. 1993. Wolff MS. Bioassay of chlordane for possible carcinogenicity. Vol.htm. Ayotte P. New York. Wong L. Chlordane and heptachlor [online].nih. Takei G. 1979-1980. Distribution of polychlorinated biphenyls. Poland. Organochlorine exposures and breast cancer risk in New York City women. Tartter P. Mortality of workers employed in the manufacture of chlordane: an update. National Toxicology Program (NTP). 731-915. Bleiweiss IJ. Brower S.atsdr. 4/21/09 Baker DB. Senie R. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort.Summaries & Evaluations. Lulek J. Van Oostdam JC. Gilman A. Arch Environ Health. et al.gov/toxprofiles/tp31. J Occup Med 1986. 6/1/09 National Toxicology Program (NTP).org/documents/iarc/ vol79/79-12. Circumpolar maternal blood contaminant survey. gov/toxprofiles/tp12. Takahashi W.html. Muckle G.gov/ntp/ htdocs/LT_rpts/tr009. Stehr-Green P. August 2007.cdc.111:349355. Voorspoels S.

4) < LOD 17.2 (<LOD-40.2) 155 (59.5) < LOD < LOD 9.1) 31. which is a mixture containing p. DDT and DDE can cross the placenta.0-155) 83.7.7) < LOD 18. and dairy products. depending on conditions.3 (27. DDT is converted in the environment to other more stable chemical forms.0) 20.2-65.2) < LOD < LOD 9. o. continues to be the primary source of DDT exposure.3 (<LOD-31.6 (9.7 (19.8-26.9 (<LOD-20. DDT is converted to DDE and several other metabolites. Only a small proportion of DDT is metabolized and excreted (Smith.4.5-36. and water.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 12.4 (23.3 (<LOD-21. 1988).1’-(2.1-71. particularly for endemic vector and malaria control.0-35. food.3) 21. Food imported from countries that still use DDT may contain the chemical or its residues.5 (14. 50-29-3 General Information Dichlorodiphenyltrichloroethane (DDT) has been used widely as a broad spectrum insecticide in agriculture and for control of vector-borne diseases.9 (10.1’-dichloro-(2. 17. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.2) 30. DDT usually refers to the technical product.9) 29.9-28.p’-DDT (15%-21%). Smith.10-13.0) 19.9 (21. inhalation. which may vary for some chemicals by year and by individual sample. DDT was used at one time as a treatment for head and body lice.8.0 (18.1-27.8-23. 1991).3-16.9) 14.8-39.1 (33. Fourth National Report on Human Exposure to Environmental Chemicals 89 . It was produced and used in the U. 2008. although DDT and DDE intakes have decreased over time (FDA.5) 25.1 (23.10 (<LOD-12. 01-02.2-95. In the body. population from the National Health and Nutrition Examination Survey. when virtually all use of it was banned.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. or dermal exposure.3) 21.p’-DDD (4% or less).0 (18.S. as well as in plant and animal tissues.9) 17.8-17. < LOD means less than the limit of detection. p.9-34.2 (11.0-53.5 (15.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1 (<LOD-39.5 (23.50-11.0) 26.6 (<LOD-25.6-33.3-236) 24.0-27.9) < LOD < LOD 9. 2002.5-54.3) 22. Gunderson. including 1.9 (10.70 (8.90 (<LOD-12.0 (10.8) 30.8) 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. respectively.6 (31.7-16. particularly meat. fish.7 (15. after World War II until 1972. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. see Data Analysis section) for Survey years 99-00. In the general U. The biodegradation half-life of DDT in soil varies from 2 to 15 years.3) 28.3-590) 293 (104-541) 48. Survey Geometric mean (95% conf. and trace amounts of several related compounds.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.00 (<LOD-10.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. resulting in fetal exposure. These chemicals are highly persistent in soil. population.8) 15. sediments.0 (21.S.4) < LOD < LOD < LOD 61.7) 12.7) 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 10.5) 23. DDT can be absorbed after ingestion.S.0-37.8) 36. air.p’-DDT (65%-80%).0) 40.0-15.5 (23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1991). and 03-04 are 20.6 (25. and 7.2-bis(p-chlorophenyl) ethane (DDD).6 (22.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. It is still used in some countries.9 (10. Both Serum p.

both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. lung cancer.095) < LOD .063 (<LOD-.146 (.061) < LOD < LOD < LOD .150 (<LOD-.250 (..084 (.170 (. and seizures.160-. have not been consistently demonstrated (Beard.130 (<LOD-.220) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.260) . Jusko et al. 2002.130 (<LOD-.051 (<LOD-. 2006).Organochlorine Pesticides chemicals are excreted in breast milk.190 (..106-.114-. A workplace standard for DDT has been established by Serum p.343) < LOD .180-.190-1. and leukemia have also been inconclusive (ADSDR. Beard.140) .150-. Gladen and Rogan.059-.201 (.00) . 2002. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.071 (.313 (. Studies of DDT exposure and pancreatic cancer. 2000. and o.150-. DDT may bind to estrogen receptors (Chen et al. which may vary for some chemicals by year and by individual sample. Hayes et al..069) . other organochlorines.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. Animal studies reported reduced fertility. Gray et al.130 (<LOD-.106) < LOD < LOD . Snedeker. 2001).62 (.230) . 2006).112 (.150) . 2002.143) < LOD < LOD .p’-DDE can produce anti-androgenic effects (Gray et al.098-.120 (<LOD-.230) .071-.140-.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. 1995.106) . overt signs of acute human toxicity include vomiting..570-4. Reproductive effects in humans affecting birth weight.203) .054-.146 (. 2004..075) 1.086 (.074-.627) . 2002. 2001). 2001).132-.240 (.530 (.420) .. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. 2006). and duration of lactation.p’-DDD and p. premature delivery. 2001). tremor.. In high dose.170-.180 (. Calle et al.048 (<LOD-..290) . 1997).189-. 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. fertility.34) . accidental exposures. 2006. In laboratory animals. 2006. 90 Fourth National Report on Human Exposure to Environmental Chemicals ..078 (.105-.400) .240) .250-1. polychlorinated biphenyls.108 (.180 (. Survey Geometric mean (95% conf.00 (. 1956). population from the National Health and Nutrition Examination Survey.330-4.530) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (.. 2006.g.079) < LOD < LOD .078-.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 .120-.064 (. and altered behavior after neonatal exposure (Eriksson and Talts.180) .065-.150 (<LOD-. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.170) . 1996).167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .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 .130-.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 .068-.. Jusko et al. Mariussen and Fonnum. reproductive organ abnormalities..220) . dioxins and furans).200 (.180) . resulting in exposure to nursing infants (Rogan. Longnecker et al.190 (.142 (. 1998).080-.26) 1. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.128 (.01) .087 (.

environmental levels) and health effects is available from the U. 1991). and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. respectively. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.. 1989).7-119) 113 (100-140) 93. 2004). 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.. 1998. Survey Geometric mean (95% conf.p’-DDT) as a possible human carcinogen. IARC classifies DDT (p.6. 2002.gov/ toxpro2. 2003). and 03-04 are 18. 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.cdc. EPA at: http://www. Compared to females in the NHANES 1999-2000 subsample.. 2004). levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.. Since the 1970’s.. see Data Analysis section) for Survey years 99-00.epa.gov/ pestcides/ and from ATSDR at: http://www. population from the National Health and Nutrition Examination Survey. 2005). Fourth National Report on Human Exposure to Environmental Chemicals 91 . Declining DDE levels over time have also been observed in the German population. 01-02.html. In a population-based sample of men and women from eastern Slovakia. 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. Smith. compared to levels observed in this Report (Anderson et al.S.6 (81. 2002.S.atsdr.e. mean serum levels of DDT and DDE in the U. 2003. In general. Heudorf et al. Biomonitoring Information DDE persists in the body longer than DDT..8.. Link et al.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. Stehr-Green. and 7.Organochlorine Pesticides OSHA and a guidance established by ACGIH. More information about external exposure (i. population declined by about fivefold to tenfold.p'-Dichlorodiphenyldichloroethene (DDE) (lipid adjusted) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 8. NTP considers DDT as being reasonably anticipated to be a human carcinogen..S. for males and females in the NHANES 19992000 subsample (Pavuk et al. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.3. respectively.

00 (.71) 32.7-48.06) 1.730) .25) 1.p’-DDT were below the limits of detection.57) 2.82) 1. interval) 1.69) 8.76 (2.07 (5.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.2 (6.69 (2.01) 1.36-1.34-11.430-. 2001-2002 and 2003-2004 subsamples.49 (1. Survey Geometric mean (95% conf.09-1.456 (.820-1.8 (9.90-8..48-4.1 (9.76-3.68-4.8 (13.57 (1.90) 22.8-90.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.14-9.39-1. o.63 (1.30-1.40-8. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.17 (3.31 (1.5) 16.61 (1.4-19.6) 9.45 (1.39) 1. In a subsample of NHANES II (19761980) participants.590 (.37 (1.54) 8.534-.7) 16. 2004).3 (9.2 (9.37-1.4) 14.63 (1.26-10.9 (26.4) 13.2 (9.1 (8.52 (1.32-9.34) 2.18-4.51) 3.12 (6.75 (4.646) .60-13.04-1.00) 7.796 (.7) 9.963-1.1) 40.38 (1.69 (.3-43.65) 1.27-1.19-14.12 (. or p.6 (17.66-17.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.18-1.57 (3.51 (1.19) 4.77 (1.6 (7.52-6.500-.46 (1.75) 1.01-11.96) 1.81-5.516 (.40-4.46 (1.41-12.10) 2.9 (15. High mean levels of whole blood DDT (about 3.55-9.385-.30-1.54-7.635) 1.9-38.25 (1.49) 8.10) .6) 9.84 (3.26-2.22-1.80) 1.83 (1.47 (1.14-1.8 (14.59 (1.91-3.71) 12. 1991).16-1.33-1.36-2.51) 1.92 (3.25-16.55 (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3 (8.419-.78 (4.14) 2..994-2.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.56-2.58) 75th 3.52 (3.18) 1.66-4.51-49. Finding a measurable amount of p.1) 12.43-4. serum levels of o.965-1.30 (1.13 (1. In the NHANES 1999-2000.34 (7.69 (1.88 (2.87 (5.13) 4.8 (13.11-1.32) 1.17-3.01-15.5) 7.75) 2.6) 13.0) 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 .34) 6.31-12.81) 11.70-3.7-19.01-1.37-16.9-17.80 (2.5) 22.92) 1.611-1.2 (19.64) 3.93 (7.85-4.57-13.61-2.6 (8. less than one percent had detectable serum levels of o.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .38 (1.66) 1.53 (2.4 (12.22 (7.2-32.9) 7.96) .726) .59) 6.46-2.03-1.72) 1.49 (1.54 (1.50-17.05) 1.21) 90th 7.p’-DDT. population from the National Health and Nutrition Examination Survey.24) 1.97 (3.4) 9.85 (1.6) 12.91-2.75) 6..5) 5.06) 3.87-16.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3. 1971).p’-DDT.8) 15.81 (1.p’-DDT (Stehr-Green.7 (8.84-3.80) 3.68 (2.91 (6.48 (6.00 (6.81 (7.890-1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.24-17.66-2.43 (5.14) 2.57-3.32-1.69) 4.S. 1989).37-10.14 (1.3) 10.860 ng/L) and DDE (about 14.36 (3.6) 9.07) 1.44) 1.56) 2.32 (1.25) 8.24 (1.45 (1.18-3.63-15.32 (1. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.02 (2.57 (1.66) 3.51-8.31-2.66) 1.39 (3.01-5.85-10.59 (4.600) .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.07) 1.47) 3.2) 19.40 (3..75 (8.25 (.77 (1.520 (.35) 1.4 (8.32-1.10-1.557) 1.58) 1.15-4.51-15.40-4.6 (9.66) 4.28) 1. considerably higher than levels in this Report (Smith.870 (.9) 5.41 (1.488-.6) 9.623 (.7) 13. 2004).680-1.02-8. 2005).29 (1.72) 1. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.26 (1.21) 3.18-1.6) 8.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.63 (6.13-2.23 (7.30 (1.56-3.2) 26. Serum p.3) 16.25-14.71 (6.80) 1.71 (5.0) 2.68) 2.62-6.04 (6.20 (.36-11.11 (2.27) 3.22) .10-5.7-20.59 (1.6) 11.01) 1.03-4.5) 10.79) 4.01-1.43-8.64-2.37-4.56-6.82 (1.00-1.34-3.70) 1.1) 7.39-2.91) 3.50 (2.18 (6.26) 3.01-11.76) 1.16 (2. 309 versus 268 ng/g lipid.53) 1.81-18.49 (6.88-35.92 (3.02) 1.561 (.43-4.05 (3.76) 1.0 (12.0 (9.53) 7.57-2.97-4.58) 1.99) 1.36) 3.53-15.59) 3. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.3) 13.Organochlorine Pesticides nearby agriculture (Botella et al.65 (1.12-1.

and 7. population from the National Health and Nutrition Examination Survey. 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.S.7. respectively. Survey Geometric mean (95% conf.8.Organochlorine Pesticides Serum o. < 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.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. which may vary for some chemicals by year and by individual sample. 01-02.4. see Data Analysis section) for Survey years 99-00. Fourth National Report on Human Exposure to Environmental Chemicals 93 . and 03-04 are 20. 17.

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

Patterson DG Jr. Jusko TA. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Zhou H. Zaidi SS. Ellis H.cdc.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). et al. August 2008. Food and Drug Administration (FDA). et al.162:890-897. Longnecker MP.53(8):1161-1172. Gladen BC.gov/~dms/ pesrpts. Baker RJ. et al. September 2002. Furr J. Ostby J.85:504508. Heudorf U.112(17):1761-1767. Profiles of ortho-polychlorinated biphenyl congeners. Chemosphere 2004. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Olea-Serrano MF. Olea N. Glynn AW.7(3):248-264. Vorojeikina DP. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.106(5):279-289. Beard J. Henley SJ. Herrman T.72:261265. Jr. Am J Epidemiol 2002.96:34-40. Sci Tot Environ 2006.358:110-114. Cerrillo I. Swanson MK. CA Cancer J Clin 2002. Environ Health Perspect 1998.71(6):1200-1209. Piechotowski I. and other chemicals. Zhou H. Wolf CJ. 4/21/09 Anderson HA.58:1185-1201. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.54:1431-1443. Barr DB. Exposure of women to organochlorine pesticides in Southern Spain. Jr. Granath F.111:349355. Gray KA. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Gabrio T. Maternal serum level of 1. Neurotoxicol 2000. et al. DDT and human health. Greenfield TA. Chemosphere 2005. Biomonitoring of persistent organochlorine pesticides.206:485-491. Lancet 2001. HCH. Charles MJ. Hanrahan L. Falk C.atsdr. Olson JR. FDA total diet study. Link B. Willman EJ. JAMA 1956. et al. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Lambright C.html. Brock JW. Eriksson P. Organochlorines in Swedish women: determinants of serum concentrations. Am J Public Health 1995. Effects of environmental antiandrogens on reproductive development in experimental animals. Klebanoff MA.21(1-2)37-48. dietary intakes of pesticides. Hum Reprod Updat 2001. Notides AC. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Brock JW. Saiyed HN. hypospadias. Durham WF. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Paepke O. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. April 1982 to 1984. Rivas A. et al. Savitz DA. Seiwert M. Drexler H. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Burse VW. Maternal DDT exposures in relation to fetal and 5-year growth. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Kulkarni PK. J Assoc Off Anal Chem 1988. Epidemiology 2006. hexachlorobenzene. Levels of DDT. Biochem Pharmacol 1997. Longnecker MP. Chen CW. Kaus S. Bjerselius R. DDE. Hediger ML.97(2):178192. Bull Environ Contam Toxicol 2004. Hurd C. Atuma S. Environ Health Perspect 2004. Davis MD. Toxicological profile for DDT.355:7889. and dichloro(diphenyl)ethylene (DDE). Klebanoff MA.52:301-309. Rogan WJ.. Calle EE. Krause C. Bhatnagar VK. Botella B. Environ Res 2004. Katz SH. lindane (g-HCH). and polythelia among male offspring. Gunderson EL. Moysich KB. Bloom MS. Cueto C.html. Becker K. Aune M. and HCB residues in human blood in Ahmedabad. Kashyap R. Darnerud PO. Buckland SJ. and DDD [online]. Arnold SF. Environ Res 2005. Klebanoff MA. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. 4/21/09 Gladen BC.17(6):692-700. Int J Hyg Environ Health 2002. Parks L. Angerer J. Gray LE Jr. Lepom P. Talts U.205:297-308. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Hayes WJ. Organochlorines and breast cancer risk. Zoellner I.fda. Crespo J. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Garrett N. Environ Health Perspect 2003. Koepsell TD. Available at URL: http://www. selected elements.155(4):313-322. Int J Hyg Environ Health 2003. India. Needham LL. Needham LL. Vena JE. Olson J. Thun MJ. The Great Lakes Consortium. et al.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. DDE and shortened duration of lactation in a northern Mexican town.gov/ toxprofiles/tp35. Needham LL.1-dichloro2. dichlorodiphenyldichloroethylene. Frumkin H. Available at URL: http://www. et al.cfsan. Bates MN. Schulz C.

Astolfi E. Stehr-Green. Jr.20(2):186-193. Pollutants in breast milk. Inc. Academic Press. children and newborn infants.150:981-990.27:405-421.36:253-589. J Toxicol Environ Health Part A 1998. Crit Rev Toxicol 2006. Snedeker SM. and DDD in male rat liver and cultured rat hepatocytes. Schecter A. Vol. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. 96 Fourth National Report on Human Exposure to Environmental Chemicals .54:1509-520. et al. Jones CR. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. and dieldrin. Reddy AB. Petrik J. Demographic and seasonal influences on human serum pesticide residue levels. Chemosphere 2004. Arch Pediatr Adolesc Med 1996. Cerhan JR. et al. 1991 pp. Rey AA. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Eds. Smith AG. Rogan WJ. Radomski JL. 731-915. Fox S. Handbook of Pesticide Toxicology. Toxicol Appl Pharmacol 1971. J Toxicol Environ Health 1989. Jr and Laws ER. In Hayes WJ. Deichmann WB. DDE.Organochlorine Pesticides Mariussen E. DDE.53:455-477. Nims R. Environ Health Perspect 2001. Fonnum F. Pesticides and breast cancer risk: a review of DDT. Lynch CF. 2 Classes of Pesticides. Pavuk M. PA. Thomas PE. Chovancova J. New York. Chlorinated Hydrocarbon Insecticides.109:35-47. Comparative pharmacodynamics of CYP2B induction by DDT. Lubet R.

. EPA..S. manufactured. unless the dose is high and the exposure is very recent. Endrin has been detected in soils. 1981). High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Because it is metabolized so rapidly. is no longer manufactured in the U. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. unlike aldrin and dieldrin.S. rodenticide and avicide. IPCS. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. endrin usually is not detected in serum of exposed individuals. Kavlock et al. An epidemic of acute endrin poisoning. 1992). or discarded.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 5.50) < LOD < LOD < LOD 5.Organochlorine Pesticides Endrin CAS No. Endrin is absorbed rapidly after ingestion. population from the National Health and Nutrition Examination Survey.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. Survey Geometric mean (95% conf. inhalation or dermal exposure routes. 1991).60 (5. a stereoisomer of dieldrin.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. Ketoendrin is a major photodegradation product (IPCS. 1992). which may vary for some chemicals by year and by individual sample.10 (<LOD-5.40 (<LOD-6.20 (<LOD-5. < LOD means less than the limit of detection. 1996. endrin can persist for years. Hepatic effects of endrin exposure have included necrosis. anti-12hydroxyendrin.50) < LOD 5. Endrin was used as an insecticide.S. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 72-20-8 General Information Endrin. Smith..40-5. or from contact with contaminated soils and sediments in areas where endrin was applied. At high doses. Endrin does not accumulate in body tissues (IPCS. 1991).S. endrin is converted rapidly to its major metabolite. have been cancelled by the U. 1979. Endrin was not widely used as a termiticide. 1987). interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. Depending on soil conditions. 2008). fatty infiltration.10 (<LOD-5. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. and occasionally at low levels in sediment and surface waters. 1992.09 and 7.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.S. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1992).30) < LOD 5. and inflammation (Smith. endrin has been detected with declining frequency in U.30 (<LOD-6.8. All uses of the pesticide in the U. total diet surveys (FDA. Over time. In the body. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al..20 (<LOD-5. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.

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

cfsan. Exposure of women to organochlorine pesticides in Southern Spain. 1991. Ellis H.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 2 Classes of Pesticides. Endrin [online]. Chemosphere 2004.atsdr.79(6):928-934. Rogers E.inchem. Handbook of Pesticide Toxicology. Vol. Hardjotanojo W. Convulsions caused by endrin poisoning in Pakistan. Cerrillo I.gov/toxprofiles/tp89. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Whitehouse DA. Chlorinated Hydrocarbon Insecticides. Schulte P. Needham LL.cdc. Toxicology 1981. August 2008. Hanisch RC. Saleem M. 4/21/09 Kavlock RJ. Olea-Serrano MF. Hanisch RC. Sokal D. Liddle J. Kavlock RJ. Fetotoxic effects of prenatal exposure in hamsters. Garrett N. Jr. Turner W. Jr and Laws ER. Roy ML. et al. Eds. pp. Olea N. Burse VW. Rivas A.org/documents/ehc/ehc/ ehc130. Ward EM. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Gray J. Frey JM. Environmental Health Criteria 130. Rowley DL. Perinatal toxicity of endrin in rodents. Grajewski B. Toxicological profile for endrin [online].54:1431-1443. Gray LE. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Patterson DG Jr.13:155-165. Perinatal toxicity of endrin in rodents. et al. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. No:429-436.fda. Available at URL: http://www. Academic Press. Botella B. Cancer Epidemiol Biomarkers Prev 2000. 4/21/09 International Programme on Chemical Safety (IPCS). 1992.htm. et al.96:34-40. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Available at URL: http://www.21:141-150.gov/~dms/ pesrpts. Food and Drug Administration (FDA). August 1996. Toxicol Lett 1992.9:1357-136. 4/21/09 Bates MN. Chernoff H. Patterson DG Jr. Gray JA. Inc.html. Pediatrics 1987. In Hayes WJ. Rab MA. Andersen A. Gray LE. Toxicology 1979. II.html. Smith AG. 731-915. Ginsburg KS. Narahashi T. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.64-65 Spec. New York. Crespo J. Chernoff N. Environ Res 2004. Available at URL: http://www. I. et al. Fetotoxic effects of prenatal exposure in rats and mice. Buckland SJ.

0 (18.9-15.1 (13.4.2-15.9-24. particularly by consuming fish..0 (25.8.7) < LOD < LOD 24. and has been detected in soil.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-16.7-21.9) < LOD < LOD 20. The general population may be exposed to HCB through diet.1) * * 15..Organochlorine Pesticides Hexachlorobenzene CAS No.2-31.3 (22.2) < LOD < LOD 29.3) < LOD < LOD 29. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.5 (13.6-TCP) (To-Figueras et al.5-33.1 (17.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. and elimination occurs by renal and fecal routes.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.6-trichlorophenol (2.9 (25.0 (18.0-28.0-25.9) < LOD < LOD 28.8 (26. breast milk is an additional route of elimination in nursing women. EPA cancelled its use in 1984.2 (14. or game taken from areas with HCB contamination. 01-02. The FDA dietary surveys have shown that over time. 100 Fourth National Report on Human Exposure to Environmental Chemicals . 1997). primarily as a fungicide and seed treatment until the U. 31.4 (18.6) < LOD < LOD 25.5-14. and 03-04 are 118.4 (11.5-14.3 (22.9-32. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.6 (24. 2002).8 (22.3) * * 15.2 (13.7 (27.6) < LOD < LOD 24.4) < LOD < LOD 33.2) < LOD < LOD 13.3) 24.4-16.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.4) < LOD < LOD 22.0-19.5-TCP) and 2..3-20.7-22.7 (15.S.6) < LOD < LOD 26.7 (15. Urinary metabolites include pentachlorophenol (PCP).4) < LOD < LOD 23.S.9) < LOD < LOD 16.9 (25.7-30.4) < LOD < LOD 19. see Data Analysis section) for Survey years 99-00.3 (16.6-26.7-26. and foods with a high fat content.S. 1976). distributes widely throughout the body.4) < LOD < LOD 14.8 (15. and 7.6-19.9) < LOD < LOD 20.6) < LOD < LOD 14. 2.5-18.3) < LOD < LOD 20.9-17.1 (14.0) * * 15.4. Although it is not manufactured as an end-product in the U.6) < LOD < LOD 26.1) < LOD < LOD 15.6-44. HCB is well absorbed after oral administration.6-32.3 (12.3-26. air. and sediment (Barber et al.7-16. Gunderson.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 * * 16.5 (14.4-15. respectively.7-16. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.1-16..5-15.6 (23.0) < LOD < LOD 24.9) < LOD < LOD 19.1-20.2 (17. wildfowl. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (13.8-15.5-trichlorophenol (2. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.5) < LOD < LOD 18. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.5-15. 2005).7-29.0.9 (23. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.4. and accumulates in fatty tissues where it persists for years.7 (19.2 (24.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. HCB has been detected in fewer foods since the 1980s (FDA. water.4.0) < LOD < LOD 15.9) 19. which may vary for some chemicals by year and by individual sample.9-30.3-22.3 (20. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. Survey Geometric mean (95% conf.2-15.4. HCB is slowly metabolized.2 (14.3 (14. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.0) < LOD < LOD 15.9 (14.S.6-33. 1988). 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.7-15.9) < LOD < LOD 15.6 (21.4 (22.4 (18. 2008.8) < LOD < LOD 27.9-20.1 (14.4) < LOD < LOD 18.0 (14. Therefore.7) * * 14.

environmental levels) and health effects is available from the U.107-.083) < LOD < LOD .091-.113-.163 (. reproductive and developmental toxicities.174-.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.097) .186 (.099) < LOD < LOD .125 (.123 (.094) < LOD < LOD .145-..077-.095) * * .156 (. anorexia.127-.095-.S.118-.095) < LOD < LOD 75th < LOD < LOD 90th * * . 1960). Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.118-.121 (. as well as hypertrichosis. and weakness.102) < LOD < LOD .089-.148-.094 (.098 (.epa. Schmid. and many died before 2 years of age (Peters et al. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.160 (.078 (.203) < LOD < LOD .178-.111) < LOD < LOD .092 (.090 (.225 (..175) < LOD < LOD .176) < LOD < LOD .081 (.Organochlorine Pesticides chemical.097) < LOD < LOD . Biomonitoring Information Serum concentrations reflect the body burden of HCB.157-.S. 2002). More information about external exposure (i. This condition.111-.079 (.203) < LOD < LOD .114-.176-.196) < LOD < LOD .100) < LOD < LOD .115 (.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 * * . which may vary for some chemicals by year and by individual sample.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . population from the National Health and Nutrition Examination Survey.073-. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.109) * * .089-.086-. In humans.060-.130) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .167 (.107) < LOD < LOD . IARC classifies hexachlorobenzene as possibly carcinogenic to humans.065 (. and the FDA has established a bottled water standard for HCB. ACGIH has developed workplace exposure limits for HCB.e. and liver and thyroid cancers (ATSDR.090 (.097 (. HCB interferes with normal heme synthesis.123 (. EPA has established a drinking water standard. EPA at: http://www.atsdr.088-.062-.085) * * .163) < LOD < LOD .191 (.072-.087 (.155) < LOD < LOD .082-.143-. 1982.223) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * . very high.182 (.123 (.104 (. Chronic feeding studies in animals have demonstrated kidney injury.132) < LOD < LOD .085-.173) < LOD < LOD .141) < LOD < LOD .145-.064 (.088-.092-.126) .102 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 . Survey Geometric mean (95% conf.092 (. HCB levels were generally below the limits of detection Serum Hexachlorobenzene (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.S.gov/pesticides/ and from ATSDR at: http://www.088-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .135-.html.190 (.129) < LOD < LOD .152) < LOD < LOD .gov/toxpro2.090-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.095 (.069) * * . With chronic exposure.140 (.122) < LOD < LOD . acute doses produce central nervous system depression and seizures.095 (. The U.179 (.cdc. Infants were exposed transplacentally and through breast milk.099) < LOD < LOD .120 (.099) < LOD < LOD .159-.081-.086) < LOD < LOD .157 (. arthritis.258) < LOD < LOD . immunologic abnormalities.092 (.090 (.147 (.171 (.118) < LOD < LOD . thyromegaly.169-.147-.163-.086-.114-. 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.069) < LOD < LOD .

349:144. Bertram et al.77:173182. Lepom P. 2005). HCB detection in serum also was proportional to age. Lackmann GM.17:388–399.. only 4..gov/~dms/ pesrpts. Safe A. Reference values updated. Becker K. Toxicological profile for hexachlorobenzene update [online].39(12):744-749. Lecha M. distribution. et al. Biomonitoring of persistent organochlorine pesticides. Schulz C. Paepke O.. Gabrio T. Eskenazi B.135(4):400404. Granath F. In a representative sample of the 1998 German adult population. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. In the 1976-1980 NHANES subsample.58:1185-1201. 2002. Sci Tot Environ 2005.html. Available at URL: http://www. Otero R. 1986. Sala M. Holland NT.fda.9% of participants had quantifiable levels (Stehr-Green. Barr DB. Bryan GT. Peters HA. but overall. Int J Hyg Environ Health 2002. Available at URL: http://www. Gocmen A. Herrman T. Bjerselius R. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Over the past two decades. et al. Aune M. levels. Bradman et al. Arch Neurol 1982. 2002. Ozalla D. Environ Health Perspect 2003. Lackmann.111:349355. J Exp Sci Environ Epidemiol 2007. more HCB levels were quantified.44 mg/L. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. 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. 2003). Dallaire F. trends and processes. Hexachlorobenzene in the global environment: emissions. HCB levels were directly related to age. FDA total diet study. References Agency for Toxic Substances and Disease Registry (ATSDR). German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Seiwert M. Sweetman AJ. Zoellner I. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Bertram HP. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lawrence River (Quebec.gov/ toxprofiles/tp90.. 2005). Dogramaci I. Link et al. Ayotte P. and other chemicals. however. September 2002. August 2008. As a result of the lower limit of detection in NHANES 2003-2004. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Fenster L. Kaus S. Gunderson EL.cdc. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 2002. Chemosphere 2005. Kemper FH.110(8):835-838. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.. Muller C. and the geometric mean concentration of HCB in whole blood was 0. Piechotowski I..71(6):1200-1209. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.54(3):203-208. 2002) and among children (Link et al. Lackman. Food and Drug Administration (FDA). van Wijk D. 2006).81(2):82-85. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Muckle G. IARC Sci Publ 1986. Arch Dermatol 1999. 4/21/09 Barber JL.. 2005. dietary intakes of pesticides...atsdr. 2002). Cripps DJ. Jones D. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.html.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. 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. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. et al. Dewailly E. 2002. 1999). In Spain. Organochlorines in Swedish women: determinants of serum concentrations. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. respectively. Link B. Herrero C. 1989). Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Schwartz JM. Santiago-Silva M.. Krause C. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Jones KC.cfsan.205:297-308. Darnerud PO. J Assoc Off Anal Chem 1988. selected elements. Canada). Can J Biochem 1976.. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. The metabolism of higher chlorinated benzene isomers. Atuma S. Biol Neonate 2002. 4/21/09 Glynn AW. Laliberte C. April 1982 to 1984. Glynn et al. Environ Health Perspect 2002. Bradman A. et al. Kohli J.

Rodamilans M. Cutaneous porphyria in Turkey. Otero R. Barrot C. J Toxicol Environ Health 1989. To-Figueras J. et al. Environ Health Perspect 1997. Stehr-Green. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Demographic and seasonal influences on human serum pesticide residue levels. Santiago-Silva M. Fourth National Report on Human Exposure to Environmental Chemicals 103 . N Engl J Med 1960.27:405-421.Organochlorine Pesticides Schmid R.105(1):78-83. PA.263:397-398. Sala M.

water.7 (53.8) 7.1 (16.S. so they can accumulate in fatty tissues of animals.6-14.0 (14. and have been used either as fungicides or to synthesize other chemicals.S.1 (27.6 (17.7 (30.6 (10.2 (31. beta.8 (21.5) 90th 42.9 (11.0 (35.6) 35.3 (26. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-46.89 (<LOD-9.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.8-68. The other isomers can be formed during the synthesis of lindane. < LOD means less than the limit of detection. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. see Data Analysis section) for survey years 99-00.8) < LOD 10.7-69.9 (30.8) 39. and delta.2-87. Technical grade HCH is a mixture of all four isomers.3) 14. 58-89-9 General Information Hexachlorocyclohexane (HCH).5) 40.7) 97. HCH isomers.8 (33. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice. It is no longer produced or sold in the U.4-73.6) 47. However.6-42.8-54. 2005).8) 12.4 (50.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14. 6.7) 27.4) 901 1067 952 992 1224 1007 Females 11.5 (43.70-12.7 (29.3) 37.2-22.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.1-49.2 (29.4 (12.9 (9.1 (21.5-123) 49.70 (6.90-8.3 (62.60-13.5) 29.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.8) 52.80 (6.2) 36.9 (40.3-85. commonly known as lindane.1) 13.0-70.70 (8. formerly referred to as benzene hexachloride.2 (9.2) 13.7 (25.5) 16.20-16.S.7 (13.8) 27.8-199) 134 (85.7-96.8-87.1-32. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.2) 9.1-37.2-67.8 (9. containing about 64% alpha and 10%-15% gamma isomers.1-36.6) 18.4) 21.46-11. In 2006.4-50.9) 45.87 (9.1) 31.0-23. interval) 9.0-111) 70.1 (9. 608-73-1 beta-Hexachlorocyclohexane CAS No.4-111) 84.0) 8.5 (11.0-34.1) 12.1) 12. 01-02.43 (<LOD-9.1-16.3) 51.50) 8.6-20.66-12. including alpha.8 (23.2-52.9) 17. and sediment as a result of historic production and use.1-27. soil.0-20.9) 81.6-89.4) 27.1 (11.3-38.9 (50.6 (16.3) 34. Lindane has a half-life of about two weeks in soils and water.70-19.6-37. population from the National Health and Nutrition Examination Survey. See the section “What’s New” at the beginning of this Report for details.2-55.8 (64.1) 71.3-56. respectively.0 (19.0) 7.6 (40.5) 11.5-29.8) * * * * * * 15.7) 18.5 (16.9 (62. particularly alpha and gamma have been detected widely in air.0 (<LOD-12. gamma.6-47.0 (8. environmental levels declined.9-24.8-19.7-26.7) 23. the U.6 (22.7) 32. EPA cancelled agricultural uses of lindane (ATSDR.0 (37.9 (32.7) 73.0) 41.6) 653 758 589 1240 1533 1370 20 years and older 10.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.5) 14.5 (37.7 (35.0 (33.0) 17.9-178) 48.7) 10.5 (14.6-62.4) 44.7 (<LOD-16.76.7-69.1-32.1 (9. **In survey period 2001-2002.6) 36.1 (18.2-20.90) 7.2 (18. The gamma isomer.7-96.5528.6-135) 69.61-12.2 (48.4 (11. 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.2-42. and 7.4 (8.Organochlorine Pesticides Hexachlorocyclohexane CAS No.7) 10.8) 95th 68.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.9 (26.5 (24.9-51.0) 35.2-98. each result has been multiplied by 1.90-8.6 (33.3 (42.4) 11.7-166) 70.4-45.4) 51.4 (52.3 (13. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.4) < LOD 9.5) 22.8 (10.5 (8.8 (32.04-10.1 (12. 104 Fourth National Report on Human Exposure to Environmental Chemicals .30-11.9) 15.0-70.2 (34.8 (17.4) < LOD < LOD < LOD 46.4 (16.4) 10. which may vary for some chemicals by year and by individual sample.3 (42.0) 71. exists in several isomeric forms.7) 56. HCH isomers are lipophilic.6) 50.9-56.68 (<LOD-10.0-21.36.9-21.2 (50.80 (<LOD-14.3) 25.9-14.1-15.2-17. 2005).6) 16.2) 62.56-12.7 (62.2) 142 (99. As pesticide applications of HCH were increasingly restricted or eliminated.1 (30.8-16.5) 67.8.9-81.7-20. and 03-04 are 9.6-18. 319-85-7 gamma-Hexachlorocyclohexane CAS No.

Organochlorine Pesticides exposure to HCH is through the diet.310) .120) .064) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.560) .270 (.144 (.580-1.064 (.086) < LOD < LOD < LOD < LOD < LOD < LOD .070 (. Distribution is mainly to fatty tissues.360 (.560 (.119) .190) .330 (.680) .S.222 (.080 (.090 (.090-.083) .150 (.460 (.340) .092 (.062 (.080-.190) .065 (.100-. U.234 (.080-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .089-.081-.070-.065 (.167 (.281 (.131-.150-.310 (.310) .160-.480 (.380 (.480 (. and nephropathy developed (IPCS. Rogan.091) .290 (.280-. respectively.060) . or dermal exposure.661) 901 1067 952 992 1224 1007 Females .160 (. When animals were chronically fed lindane at high doses.073-.175 (.350 (.130 (.100) .047-.S.118-.216 (.191-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.840) .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.140) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al.059-.450 (.078 (.120 (.170-.221-.150) . hepatic enzyme induction.083 (.050-.360) .050 (<LOD-.124-.372 (.057 (<LOD-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . resulting in a half-life of about seven years.501) .319) .300-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.174) . 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.230-.100 (.5528.240 (.244-. and seizures.048 (<LOD-.062 (.058 (<LOD-.400) .160) .250 (.118 (.120 (.080-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .410 (.814) .420-.297-.210 (.090 (. the serum half-life was about 20 hours among children (Ginsburg et al.620) .587) 653 758 589 1240 1533 1370 20 years and older .410-. Saxena et al.290) .080) * * * * * * . HCH isomers are absorbed after inhalation.350) .250 (..050-.260-. EPA has established a drinking water standard. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.120-.120 (.210 (.510) .382-. 1996.01 (.570 (.050 (<LOD-.130) . probably by blocking inhibitory neurotransmitters in the central nervous system. from 6% of samples in 1982-1984 to 2% in 1994 (FDA. 1971.37) 1.140) .067 (. OSHA and ACGIH have established workplace standards and guidelines.390-.690) .100-.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. ataxia. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.050 (. which may vary for some chemicals by year and by individual sample.32) .370-.068-. Workers who directly handled HCH have complained of headache.057-.. The U.700) .200 (.070-.110-. and FDA has established a bottled water standard and food residue tolerances for lindane.140 (.040-. See the section “What’s New” at the beginning of this Report for details.103-. 1981).070-.287 (. enlarged livers.070 (.05) . population from the National Health and Nutrition Examination Survey.103 (. The beta isomer accumulates in fatty tissues and is metabolized more slowly. 1986).180-.077) < LOD .056-.290 (.139 (.580 (. interval) .100 (.250) .280-.480) .220-.100) .130-.120-.200-.146-.410) .450-.600) .190-. paresthesias. After dermal application of lindane 1% lotion. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. each result has been multiplied by 1.210) .250-.470) .067) .S.331 (.080) .330-.254) 95th .110) .080 (.290 (.190-1.442 (. Gunderson 1988).110) .521 (. ingestion. 1983).710) . Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.170-.072 (.050-.103) 90th .910 (.096) .210-.051 (<LOD-.077) < LOD .125) < LOD < LOD < LOD .120) .260) .340-. tremors.308-.412 (. 2008.220-.098 (.050-.050) .305) .057-. 2002).150) .050 (. **In survey period 2001-2002.090 (.470 (.400) .220) .100-.220 (.051-.056-.320 (.450) .120-. and memory loss (Nigam et al. 1977).191-.260) .214) .294-.. for lindane.173-..069) .404) .410) .140) .620-1.460) .240-.070) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .290) .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 .360-.110) .390 (.200-.089) .250 (.250-.

2002). Kutz et al. 10. Survey Geometric mean (95% conf. Becker et al.. and 03-04 are 14. aged 9-11 years. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. < LOD means less than the limit of detection. Stehr-Green. Stehr-Green. respectively. the maximum and 95th percentile beta-HCH values. 01-02... 2004) and India (Bhatnagar et al. 2005. male sex. respectively. In NHANES 1999-2000. Link et al. 2001-2002.html.e. serum levels of lindane were generally below the limits of detection. and 7.8. In populationbased studies of New Zealand adults and German adults and children. 2004). older age. 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.. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers.cdc. 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. and a diet that includes meat (Becker et al.gov/toxpro2. Sturgeon et al.epa. Biomonitoring Information Because of its longer half-life. 106 Fourth National Report on Human Exposure to Environmental Chemicals . 1998). In recent years. 2002... were similar to the 95th percentiles in this Report..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans.. Bates et al. In an earlier (1996-1997) sample of German children. see Data Analysis section) for Survey years 99-00.gov/pesticides/ and from ATSDR at: http:// www. Radomski et al. 1991.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. More information about external exposure (i.atsdr. 1989. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR... population from the National Health and Nutrition Examination Survey. 1998. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. EPA at: http://www.5.. 1989). 1971. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. 2004. which may vary for some chemicals by year and by individual sample. Additional factors associated with higher beta-HCH levels include rural residence. and 2003-2004.S. environmental levels) and health effects is available from the U.5. 2005. Kutz et al.S. 1991.

Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect.. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. 1986.. Beta-HCH and lindane levels in workers involved in HCH production have been more than 1000-fold higher than the 95th percentile and limit of detection (lipid adjusted).. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. population from the National Health and Nutrition Examination Survey. in this Report (Nigam et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Survey Geometric mean (95% conf. respectively. Radomski et al. 1998).. 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.Organochlorine Pesticides 2001-2002 survey period (Link et al.S.. In a small study of adults who consumed sport fish from the Great Lakes. 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. 1971). which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 107 .

Piechotowski I. Brinton LA.html. Int J Hyg Environ Health 2002. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. HCH. Zaidi SS.fda. Bull Environ Contam Toxicol 2004. Potischman N. Schulz C. Aune M. Brock JW. Rivas A. Siddiqui MKJ. Olson J. Bottimore DP.111:349355.atsdr. Angerer J.150:981-990. The Great Lakes Consortium. Stehr-Green. gov/toxprofiles/tp43. J Pediatr 1977. 4/21/09 Anderson HA. Bjerselius R. Rogan WJ.58:1185-1201. Olea-Serrano MF. Exposure of women to organochlorine pesticides in Southern Spain. PA.71(6):1200-1209. Arch Toxicol 1981. Pollutants in breast milk. Kutty D. Becker K. and HCB residues in human blood in Ahmedabad. Burse VW.cdc. Seiwert M. et al. VI.inchem. Needham LL. J Assoc Off Anal Chem 1988. Glynn AW. Crespo J. 2002. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. children and newborn infants. Toxicol Appl Pharmacol 1971. August 2005.57(4):315-320. Falk C. Cancer Causes and Control 1998. Garrett N. Reisch JS. Zoellner I. Available at URL: http://www. Botella B. Lindane. et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Darnerud PO. Absorption of lindane (g benzene hexachloride) in infants and children. Krishna Murti CR. Bates MN. April 1982 to 1984. FDA total diet study. Biomonitoring of persistent organochlorine pesticides.html.gov/~dms/pesrpts. Karnik AB. et al. Levels of DDT.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Demographic and seasonal influences on human serum pesticide residue levels. Needham LL. Metabolism of gammahexachlorocyclohexane in man. Int Arch Occup Environ Health 1986. Gabrio T. et al. Cerrillo I.96:34-4Food and Drug Administration (FDA). Int Arch Occup Environ Health 1983.cfsan. Hanrahan L. et al. International Programme on Chemical Safety (IPCS).27:405-421. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. et al. available at URL: http://www.20(2):186-193. Needham LL. 4/21/09 Ginsburg CM. et al. Raju GS. selected elements. 4/21/09 Kutz FW. Rey AA. Environ Res 2004. Heinrich R. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). org/documents/jmpr/jmpmono/2002pr08. Environ Health Perspect 1998. Ellis H. August 2008. Kaus S. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Maass R. Lepom P. Toxicological profile for hexachlorocyclohexanes update [online]. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Lowry W. Kashyap R. Granath F. Radomski JL. Saxena MC. Herrman T. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Astolfi E. Arch Pediatr Adolesc Med 1996. Buckland SJ.52(1):59-67.9(4):417-424. Visweswariah K.72:261265.htm. Occupational exposure to hexachlorocyclohexane. Patterson DG Jr. J Toxicol Environ Health 1989. Olea N. Chemosphere 2005. Gunderson EL. Saiyed HN. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Placental transfer of pesticides in humans. Rothman N. Deichmann WB.91:998-1000. Bai KM. Bhargava AK. Sturgeon SR. and other chemicals.106(5):279-289. Bhatnagar VK.48:127-134. Organochlorines in Swedish women: determinants of serum concentrations. Krause C. Majumder SK. Kulkarni PK. Chemosphere 2004. Nigam SK. Environ Health Perspect 2003.54:1431-1443. Rev Environ Contam Toxicol 1991.120:1-82. Available at URL: http://www. 108 Fourth National Report on Human Exposure to Environmental Chemicals . India. Atuma S. dietary intakes of pesticides.205:297-308. Paepke O. Link B. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Wood PH. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.

soil. since 1977.3 (15.8 (12.10-37. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.8. water. sediments.4) < LOD 15..4-230) 18. Mirex binds strongly to soil.90-29.8) < LOD 15. or pesticide application.5-291) 11.7 (12. where it has a half-life of 12 years. where it was applied directly to soil and by aerial spraying.2 (7.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. resulting in exposure to newborns and nursing infants.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 16.5 (<LOD-115) 153 (30. 01-02. aquatic organisms. 2385-85-5 General Information Mirex has not been produced or used in the U. disposal.5-425) 40.S.5 (<LOD-42. 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. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. 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.0-374) 11.5 (9. 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. Mirex can cross the placenta and be excreted in breast milk.0 (12.3 (15. Occupational exposure is limited to workers at sites where mirex contamination is present. Some states and the U.6 (<LOD-23.1 (8.8 (<LOD-73.0) * * * 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. mirex was detected in human adipose samples. population from the National Health and Nutrition Examination Survey. Mirex is not metabolized in the body.10 (<LOD-15. and 03-04 are 14.S.6) < LOD < LOD < LOD < LOD 71.3-225) 15.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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 (13. 1991). respectively.Organochlorine Pesticides Mirex CAS No. 10.5-82.4) < LOD 63. Formerly. Mirex is absorbed through the skin and from the gastrointestinal tract.1 (<LOD-65.2) 51.70 (<LOD-15.. Fourth National Report on Human Exposure to Environmental Chemicals 109 . 1985.4 (8.6-305) 15.S.70-24. In studies conducted in the 1970’s and 1980’s. and 7.7 (<LOD-47.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. it is a highly persistent chemical in the environment.S. (Kutz et al.S.40 (<LOD-13.6.6) 9.70-40.7) 8. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. animals.5. after which it is widely distributed in the body and stored in fat.2-230) 13.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.6 (<LOD-31.7) < LOD 66. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.6 (<LOD-108) 9.0 (14. Mirex has been detected in air. and foods. see Data Analysis section) for Survey years 99-00. 1995). especially those from persons living in the southeastern U.0 (<LOD-108) < LOD < LOD 50. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.

450 (.052-.690) . In addition. 2001-2002.79) .470) .090 (<LOD-. More information about external exposure (i. population from the National Health and Nutrition Examination Survey. 7.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .062-.106) < LOD .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.268) < LOD .170-3.470) . The geometric mean mirex levels of the Inuit mothers were 8. 110 Fourth National Report on Human Exposure to Environmental Chemicals .08 (.110 (<LOD-.e.8.635) < LOD .S...256 (.090-1.079 (<LOD-.79) .610) < LOD < LOD < LOD < LOD .102) < LOD < LOD < LOD < LOD .090-1.html. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100 (<LOD-.510) < LOD < LOD .054 (<LOD-.7 ng/g of lipid. 1989).S.370 (. Laboratory animals fed high doses developed liver enlargement and liver tumors.41) . 1991).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 .73) .112 (.450) 1. 2005). 2004). 1995. reproductive toxicity included decreased fertility and testicular damage.Organochlorine Pesticides exposures are unknown.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 .atsdr.37) . 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. IARC classifies mirex as possibly carcinogenic to humans.080-1. serum mirex levels were generally below the limits of detection (Stehr-Green. 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.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 . environmental levels) and health effects is available from the ATSDR at: http://www.059 (<LOD-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . Smith.92) .410 (.gov/toxpro2. 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. Biomonitoring Information In the NHANES 1999-2000.cdc.470 (. which may vary for some chemicals by year and by individual sample.093 (. and 4.070-1.090 (<LOD-. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.140 (<LOD-. Survey Geometric mean (95% conf.. as well as in a subsample of NHANES II (1976-1980) participants.090 (<LOD-. and 2003-2004 subsamples. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .310 (.055-.064 (<LOD-.106 (.108 (. EPA has established environmental standards for mirex.089-.100 (<LOD-.02) .220) .090-1.077 (<LOD-.220 (<LOD-.080-1. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.053-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. The U.170) < LOD .430 (. In samples obtained between 1994 and 1997. 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.

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

20-71.30-27.4.42 (<LOD-8.4. 2.30) < LOD 4.0 (5.20) < LOD 1.40 (2.0) < LOD 11.00 (3. 2006).5-Trichlorophenol CAS No. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Formation of 2.5-TCP) and 2.30-11.S.3. recent sampling of U.900-2.0) < LOD 11. 1999).60-18.71 (<LOD-8.50) < LOD 1.Organochlorine Pesticides 2.30-44.0) 14.950 (<LOD-1.03) 9.7.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.4.S. and polychlorinated benzenes (Kohil et al. 1999).31 (<LOD-9. including hexachlorobenzene and hexachlorocyclohexanes. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.5-trichlorophenol (2. Trichlorophenols are no longer manufactured commercially.6-trichlorophenol (2.4.50-25.30-27. 2.72) < LOD 1.0) 2.4. 2. soils.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.6-TCP).0 (3. EPA.50 (.940-3.7) 24.50-16.42 (<LOD-12.8) 21. however.6-TCP in any of the samples (U.40 (. Such workers would probably Urinary 2.40 (2.9 and 0.60 (. are metabolites of several organochlorine chemicals.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .40) < LOD 4.30-40..5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (1.0 (3. Occupational exposures.6-TCP were used as intermediates in the production of certain pesticides.40 (.4.80-41.4.0) 2. Both chemicals have been detected in air. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-3.40-18. may occur by inhalation or dermal routes. surface water.0 (4.40) < LOD 1.4. Exposure to trichlorophenols also may result from metabolism of lindane.S.980-3.30 (.60) < LOD 8.980-3.60 (2. 95-95-4 2.4.40 (1.40 (1.00-3.80 (2.0) 2. usually at herbicide production or waste incineration facilities. and sediments.5-trichlorophenol.4. hexachlorobenzene. 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.4. 1976).9 (<LOD-121) 9.57 (<LOD-15. Survey Geometric mean (95% conf.0 (4.9.6-Trichlorophenol CAS No.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. Historically.5TCP and 2. which may vary for some chemicals by year and by individual sample.90-33.30-3.63) 18.19 (<LOD-6.0 (4. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.10-3.20-36.50 (2.60-8.0) < LOD 5.50-63.40 (2. 112 Fourth National Report on Human Exposure to Environmental Chemicals .0) 2.00 (2.60 (4.30-27.0) 5.27) 696 661 521 696 603 939 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.20 (4.0) 2.40) < LOD 6. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.40-11.0 (8.20) < LOD 5.00-8.920-3.0) < LOD 5.0) < LOD 5.80) < LOD 1. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. public drinking water systems did not detect 2.0) < LOD 21.71 (<LOD-8.20) < LOD 90th 5.4.80 (1.30) < LOD < LOD < LOD < LOD < LOD 1. < LOD means less than the limit of detection.40 (2. population from the National Health and Nutrition Examination Survey.0) 2.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1. other organochlorines.

0) 7. Urinary 2.4..4.33) < LOD < LOD < LOD < LOD < LOD 2. as being possibly carcinogenic to humans.5) 11.53-3.5-TCP or 2..43) < LOD 12.95 (3.28-25. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.6) 4.86 (3.4.6-TCP.9) 12. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. which includes trichlorophenols.4. in addition to dioxins.02) < LOD 7.24) < LOD 1.75 (3. population from the National Health and Nutrition Examination Survey.44 (. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.46 (1.2) 2. the 95th percentile urinary 2.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .2 (2. 2003).37) 16. IARC classifies combined exposures to polychlorophenols.78-19.83-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.73 (<LOD-8.4. and other chlorinated compounds. 7. Human health effects from 2. Among 6-11 year old children in NHANES 1999-2000.4.57 (<LOD-7.5-TCP nor 2.24) < LOD 5.17) 9.90 (4..37-11. Neither 2.43 (2.e. However.4) < LOD 3.29 (1.Organochlorine Pesticides be exposed to mixtures of chlorophenols.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).32) < LOD 4.36 (1.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.16) < LOD 90th 5.6) 4. NTP classifies 2..4. The 95th percentiles for 2. 2004).74) 11.02-3. At lower doses. environmental levels) and health effects is available from ATSDR at: http://www.5-TCP and limited for 2.88-16. and lymphomas.69 (2.6-TCP had increased rates of hepatic tumors.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. leukemias.7 (4.4 (6.6-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.3 mg/L reported in German adults aged 18-69 years (Becker et al. furans. Laboratory animals chronically fed high doses of 2.64 (4.cdc.4.05-17... Radon et al.82 (<LOD-32.80 (1.4.6) 4.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.5-TCP.html.820-2.19-12.62-20.68-4.9 (5. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. Survey Geometric mean (95% conf.4) < LOD 3.78 (3.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.6-TCP levels at the 95th percentile were up to eight times higher than 3.gov/toxpro2..75 (<LOD-6.4.31) < LOD 2..15) < LOD 2.69-18. 2003.67 (1.4.19-4.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.55 (4.8 (5.27-17.78) < LOD 1. animals showed hepatocellular abnormalities.2) < LOD 5.47-8.1 (<LOD-58. Fourth National Report on Human Exposure to Environmental Chemicals 113 .13-13.44 (1.57 (<LOD-7. urinary 2.S.79-4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.60-3.20-6. 1989). More information about external exposure (i. 1989).24-11..0 mg/L.1) 2.24 (3.11) 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 2.920-2.00-29.4.49 (1. the 95th percentile urinary 2.24) < LOD 6.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00-19.6-TCP as reasonably anticipated to be a human carcinogen.4) 5.93-11.68 (<LOD-8.8) < LOD 9.4.05-8.81 (<LOD-9.16 (. In the same 2-6 year old children.00) < LOD 4.980 (<LOD-1. 2003).6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.57 (3.atsdr.8) 4.50) < LOD 2. 1995) were similar.67 (1.3 (5.5) < LOD 12. 1995) and up to 19 times higher than the 95th percentile value of 1.53-3.

80-7.70) 3.3) 20.0 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40-4.10) 6.58-3.78 (2.2 (14.85 (2.8) 32.32) 3.12) 2.45-9.54) 6.80-20.5-TCP (0.9 (11.36 mg/g creatinine.31) * 2.8-13.35-3. Finding a measurable amount of 2.0) 10.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2. 2004).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 2.01-6.0-68.20) 4.4.6-22.55-3.0) 9.20-23.0 (20.9 (13.04) 2.60 (2.0) 19.0 (15. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.95-6.5-46.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2. which may vary for some chemicals by year and by individual sample.0) 13.09) 15.30-33.90 (3.0 (12.5-TCP and 2.80 (2.4.28) * 2.0 (7.60) 6..5-TCP or 2. < LOD means less than the limit of detection.0) 13.65) 15.10-3.0-43.73-9.98-7.30-2.00 (4.6-TCP (0.10-2.60 (3.33-4.4 (9. population from the National Health and Nutrition Examination Survey.0) 17. 1998).85) * 3.48-26.74 (2.69 (3.60 (3.60-37.0 (11.72-10.5-TCP and 2.47 (3.0 (15.3.7-3.74-3.70) 5.80-25.52 (2.0 (20.31 (3.7 (13.0) 19.84) 2..36-5.0 (8.3 (11.80 (3.4 (17.30) 4.14 (2.52-3.32) * 3.40-32.0 (6.4.49 (6.2) 12.20-3.70-3. Urinary 2.6) 21.0-18.9) 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 2.09-7.1 (8.0) 14.56 (3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1 (10.7-16.6-TCP exposure and health effects.0 (6.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002. Survey Geometric mean (95% conf.80 (2.66 (8.87-14.46-3.67) 4.40 (2.0 (8. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 13.2-0.57 (<LOD-2..4.02) 2. Mean values of 2.4.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.30-2.80) 1.70-6.1-25.5 mg/g creatinine) were similar to the limit of detection for 2.6) 26. 2003).89-6.68 (<LOD-2. was about six times lower than the median urinary levels for males in this Report (Radon et al.7 (9.95) 3.40-2.40-7.26 (2.00-4.20 (3.8 (9.S.70) 1.59-6.40) 2. 1991).0-37.6TCP values.4.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2. respectively. Biomonitoring studies on levels of 2.40) 3.8-24.00 (2.3) 37.4.95 (4.0 and 1.0) 12.5-TCP level of 0.40-14.5-TCP or 2.0 (13.25-11.80-6.20-6.92 (2.4.0 (14.18-3.3-17.4.0-41.6-TCP than are found in the general population.6 (11.10-3.0) 7.7) 21.60) < LOD 5.4.0-38.0 (14.0-38.5-TCP or 2.5-TCP and to the median 2.30-11.4.63) 90th 15.20 (3.90-8.0) 15..7) 33.67-12.50-5. the median urinary 2.10 (5.45 (5.00-21.0 (9.0) 9. 0.23-2.70 (2.4-17.45 (2.90 (4.1) 16.0-44.0 (16.4.0) 10. 114 Fourth National Report on Human Exposure to Environmental Chemicals .0 (6.7 mg/L.0) 13.0) 17.6-TCP level.4.6 mg/g creatinine) and 2.2) 25.0) 6.40) 4.6-TCP in urine does not mean that the level of 2.6-17.3) 23.6TCP causes an adverse health effect.0) 11.6-19.0) 11.0 (14.70) 5.28) 24.8) 18.60-3.23) 2.90) 2.4. interval) 2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.5-TCP or 2. Biomonitoring data will also help scientists plan and conduct research about 2.0-50.58 (1.4 (8. for males in NHANES 19992002 (Agramunt et al.59) 4.0) 14.08 (2.4.51-12.8-15. In harbor workers exposed to chlorophenol-contaminated river silt. Urinary 2.65 (5.40 (2.4.40-2.78 (2.07 (<LOD-3.6 (12.0-54.3 (11.32-4.4.23) 3.53) 2.06) * 2.4.76) 3.70-6.10) 2.00 (1. similar to the limit of detection for this Report (Anderson et al.0) 7.60-21.75 (8.4 (10.99) 6.40) 2.98-11.45) < LOD 11.91-4.50 (2.9) 694 677 519 696 602 931 Limit of detection (LOD.89 (3.4.70 (2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.3-26.53) 4.9) 13.24 (2.44) 75th 4.36 (1.4.79 (5.

6 (6.87-7.87) 2.89) 10.49) 4.9-29.02 (1.00 (3.54 (2.18-2.76) 4.63-13.43-7.59 (2.33 (1.5) 11.52) 2.8 (7.60-2. interval) 2.3) 8.7 (14.00) 4.05 (6.2 (7.20-2.51) 18.4) 9.66-4.71 (3.5) 8.43 (2.40 (2.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.56-5.17) 13.68) 2.9) 7.1) 11.06) 4.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.96) < LOD 4.77) 2.51 (2.63-15.1-32.4) 4.01 (3.77-4.5) 12.Organochlorine Pesticides Urinary 2.23) 4.13 (1.4 (11.88 (2.98 (1.02) 3.76-8.6 (9.21-11.10) 4.33 (7.76) 2. population from the National Health and Nutrition Examination Survey.05 (3.18-4.29-4.25-17.1) 14.67-17.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.88) * 2.78) 2.65) 18.11) 10.9-34.10-9.50 (2.1-21.44 (3.87) * 2.58 (4.S.06-2.25 (3.17) 2.7-36.88) 5.81-9.63) * 4.9-64.72) 32.3-23.38 (4.52 (3.87 (3.06) 11.88-7.4) 8.33-2.13-6.6 (22.17-4.8) 21.24 (1.3-37.62-15.28-4.83-6.32 (2.19-5.98) 10.6 (5.2 (13.3 (9.29 (6.91-2.56 (7.9) 8.65) 2.92) 4.00) 4.08-2.0) 8.88) 1.90 (1.16-10.14-13. Survey Geometric mean (95% conf.65-2.30-2.83-5.38) 22.56) < LOD 11.63 (<LOD-2.65-21.6) 13.55-2.22-2.2 (12.9 (9.88) 4.0 (6.2 (8.6) 12.68) 2.0 (9.8) 11.82 (3.23 (1.5 (7.6-31.6 (9.5 (10.94-13.8 (8.22-9.04-2.53) 4.42 (2.1 (13.73-22.4.43 (<LOD-2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.9 (9.22 (<LOD-2.35 (3.73) 5.00 (2.60 (4.9) 19.89-2.0) 10.26 (6.10 (6.26-13.5) 11.5 (8.81) 2.47-5.25-15.52 (5.88) 4.33) * 2.83 (3.6) 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 2.63) 4.5) 9.78) 90th 12.7) 25.51-21.9) 8.22 (1.8) 19.04-16.6) 8.75) 75th 4.2) 19. Fourth National Report on Human Exposure to Environmental Chemicals 115 .25 (3.83-6.27-9.50-8.25-2.76) 1.38 (2.70-9.32-19.49-3.79-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (7.29-4.95-2.38-5.82 (8.72-16.78 (2.5-28.1 (8.90) 2.82) 2.14-2.0 (11.6 (12.6 (10.09-3.87-6.7) 6.91 (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.22 (3.91 (7.53-11.41-6.8) 12.41 (3.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.48-2.99-2.15 (1.52) 2.82-2.4 (12.9-32.53) * 2.46-14.63 (2.53 (3.15 (6.42) 2.

html. Domingo A. Environ Res 1995. Shealy DB.45:440-445. Becker K. et al. Hill RH Jr. Int Arch Occup Environ Health 1991. Szadkowski D.gov/toxprofiles/tp107. Fast DM. Kohli J. Seifert B.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Smith SJ. Corbella J. Seiwert M. Holler JS.atsdr. 4/21/09 Agramunt MC. Kaus S. To T. Am J Ind Med 2004. Pekari K. Safe A. The Great Lakes Consortium.63:57-62. Chlorophenol exposure in harbor workers exposed to river silt aerosols. U. Head SL.pdf. et al. Jones D.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Baur X. Int J Hyg Environ Health 2003.18(4):469-474. Aitio A. Schulz C. Wegner R. 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]. Toxicological profile for chlorophenols [online]. Jarvisalo J. Bailey SL. Needham LL. Hanrahan L. Luotamo M. Available at URL: http://www.106(5):279-289. July 1999. Toxicol Lett 2003. Needham LL. Hill RH Jr.146:83-91. S. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .S. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.epa. Baker S. Arch Environ Contam Toxicol 1989.EPA). Can J Biochem 1976. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Gregg M. Lindroos L. 206:15-24. Burse VW. Radon K. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. et al. December 2006 Draft. The metabolism of higher chlorinated benzene isomers. Olson J.cdc. Heinrich-Ramm R. Available at URL: http://www. Environ Health Perspect 1998. Poschadel B.71:99108. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Falk C. Anderson HA.54(3):203-208. Urinary excretion of chlorinated phenols in saw-mill workers. Environmental Protection Agency (U. Pesticide residues in urine of adults living in the United States: reference range concentrations. Domingo JL.

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

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

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

00-12.8 (8.12-19.4 (9.74 (8.0 (8.32 (.1.8) 19.0) 12.0) 6.70-11. 0. and 0.35-11.2 (11.8 (12.40-5.00 (1.490-2.82) 10.0) 15.08-2.5 (11.0) 6.599-1.55-8.4) 17.72) 5.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.86 (1.30 (4. 01-02.90) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-20. see Data Analysis section) for Survey years 99-00.80-22.30-6.1 (9.80) .4) 20.80) .0) 10.758-1.56 (6.26-6.954 (.33-18.94) 3.30 (2.0) 7.97) 8.26 (5.757-2.47) * * 1.70) .20-30.0) 20.53) 4.71-9.1) 95th 13.0) 5.0) 6.1) 13.28) 1.10 (.9 (8.2 (9.80) 11.44-3.00-12.11 (.0) 10.0 (6.13 (2.860-2.80) 2.45 (2.13-2.0-28.50-5.00) 3.4 (7.60) < LOD < LOD 4.2 (14.0 (7.27-15.2) 16.58 (5.0) 10.970-2.89) 9.20 (2.0 (9.50) 2.40 (.03 (.0) 10.30 (2.81) 1.00) 3. and 03-04 are 0.0) 11.43-12.9-18.33 (5.1-17.60) .80-24.2.04) < LOD 1.2 (14.80) 4.0 (8.20-4.981 (.46) 10.290 (<LOD-.56 (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 1.7 (14.42-3.00 (4.810-1.2.2 (7.16) 4.15) 14.70-23.67) 3.02) 4.14) * * .0) 10.58 (3.27-3.56 (4.61) 4.0 (12.40-14.00-27.80 (2.290 (<LOD-1.10) < LOD .13 (2.90-5.30-4.07-10.97) 90th 7.600 (<LOD-1.76 (2.0) 11.29) * * 1.5) 20.840-1.60 (1.10 (2.750-1.8) 11.530 (<LOD-2.0-27.579-1.35-16.44-38. interval) 1.50 (2.10) < LOD < LOD 4.98-5.4) 18.8) 7.39 (8.20 (.0 (7.00-19.70) < LOD < LOD 1.68-7.0 (7.0 (5.73) * * .74 (8.39 (3.80) 2.95) 5.21 (.47) 5.82-12.2) 14.93-24.3) 16.0) 9.19) 9.99 (5.52) * * 1. population from the National Health and Nutrition Examination Survey.37 (3.90) 2.6) 7.2 (9.9) 8.57-7.7) 11.60-25.16 (2.3-15.0 (9.55-6.5) 15.44 (2.3) 17.96-3.34-3.1 (10. 120 Fourth National Report on Human Exposure to Environmental Chemicals .9) 14.8 (9.7 (12.83 (5.79 (5.90 (1.2 (7.60-11.5-16.08 (<LOD-2.80) 3.70-14.10-7.60 (5.2) 16.830 (<LOD-3.10 (2.40-16.05-7.56-13.890 (<LOD-2.32) 1.80-4.61 (3.20-7.8-32.22 (.66) * * 1.54 (3.620-1.20 (.0 (6.3) 14.36-4.70-19.0) 11.0) 5.80 (4.48-7.34-7.00-27.5-17.5 (8.40-1.40-11.15-12.6) 18. which may vary for some chemicals by year and by individual sample.93 (4.1) 10.4 (7.23-5.21) 9.38-5.91) 4.26-8.52-11.8 (14.52) 6.94) * * .51) 2.70 (4.00 (5.70 (2.1-23.08-15. respectively.0 (7.63) 1.80) 2.S.0 (4.02-5.81) 11.955 (.0) 11.700-1.70) < LOD < LOD 75th 3.81) 11.10 (.780) < LOD 3.4 (9.60-18.2) 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 1.17-3.740-2.58 (2. < 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.0 (8.40-19.717-1.623-1.71 (2.670-1.50 (.35-12.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (.00-7.90-4.0) 5.79-7.85 (3.2 (7.98-12.42) .8) 7.20 (.50-36.01) * * 1.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.86-15.50 (4.12) 4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

25) 6.2) 13.74) 4.43 (.89) * * 1.608-1.80 (7.40-3.02 (2.41) .5-16.40 (3.1 (7.5-32.1) 4.932 (.62-5.39 (2.24-3.25) < LOD .9) 16.81 (1.1 (6.53 (6.75-7.8) 12.98) 9.23) 4.53) 9.98) .28) 10.5) 12.37 (4.34) < LOD < LOD .71) 10.46) 2.42) 12.900 (.510-1.2) 5.01-2.47) 2.3) 5.95 (3.92-2.7 (8.98-5.2) 95th 12.93) 9.7) 18.7 (9.02-14.710 (<LOD-1.88 (5.73 (1.31 (3.19 (4.85 (6.8) 8.35) < LOD < LOD 3.81-5.98) .94-9.1 (9.4) 4.47 (3.54) .54-15.89-3.3) 16.6) 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.440 (<LOD-2.61-13.75 (3.67-19.10 (3.76-4.620-1.430-1.03 (2.37-5.56) 4.66 (5.S.40-5.60) 2.45-5.533-1.30) 2.7) 12.7) 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 .95) 2.90-8.32-12.75) 2.960 (.69) 2.94 (4.6) 13.57-10.37 (5.2 (8.94-10.03) 2.52) 4.54-4.790 (.40-12.82-6.1 (8.7) 5.82-14.890 (<LOD-1.40-14.818 (.67) 1.37-3.20-8.76) < LOD .47 (3.1) 4.03) 2.2) 5.93-5.883 (.88) 2.750 (<LOD-1.69 (4.72) 11.55-20.40) < LOD < LOD 75th 2.40) 4.40-28.5) 8.2 (6.549-1. population from the National Health and Nutrition Examination Survey.00 (4.9 (9.34 (6.9) 12.43 (3.8) 7.560-1.21-23.04 (1.4) 4.80) 9.57 (6.00 (4.6 (9.960 (<LOD-2.00-19.38 (1.54-11.62) .890 (<LOD-1.56) .15-10.60) * * .5-20.5) 7.34 (6.50) 7.90-5.54-2.66-34.31-14.540-1.28 (4.633-1.45-11.0 (8.9 (9.996 (.38) .5) 7.69-10.02 (7.75) 14.820 (.860 (.47) * * .28 (5.64-5.98-22.8) 6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.41) Selected percentiles ( 95% confidence interval) Total * * 50th .574-1.29) * * .87 (1.82-14.07 (.05 (1.05) .43) 2.6 (10. interval) .0) 6.88-10.09 (.79-3.10-13.94 (2.00-17.830-1.66 (1.61 (1.3) 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 1.26) * * .56-13.570-1.75 (7.94-23.57 (4.0) 7.2) 9.93-9.1 (10.2 (10.88-15.11-6.80 (2.1-15.5 (4.28 (2.14 (3.80 (6.60-9.44 (2.1 (11.46-5.51-5.9) 11.28-9.74) 90th 7.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.68) < LOD < LOD 3.8 (10.1) 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 1.84 (5.500-1.6) 11.18 (.87-5.04-6.69) 4.87 (3.61-29.7 (10.00) 8.71-2.9 (5.29 (2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .9-28.00-13.09) 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.650-1.13) 4.58) * * 1.82-26.85) 2.05 (.53-11.66-15.66 (2.8) 16.4 (9.3) 12.5-13.4 (4.23 (4.47 (1.4) 13.870-2.27) < LOD 2.84) 7.37) 9.2) 7.566-1.79-9.855 (.42 (3.3) 15.45-5.94-22.56) 7.61 (1.773-1.09-11.36) * * 1.78 (2.77 (6.06-2.6) 9.92-5.67) 4.98 (3.03-6.780 (<LOD-1.2) 8.83 (7.5) 11.34) * * .57) 4.03 (7.30 (1.68-4.83) 8.41-12.924 (.920 (.35 (1.02-2.

670 (<LOD-1.27) 4.67) 3.00) < LOD .8-17.6) 18.24-5.8-21.30) < LOD < LOD .4) 11.0-33.0) 12.70) 2.33-11.4 (10.0) 13.46-28.0 (14.58 (1.1) 11.60 (2.6) 14.0 (9.82) 8.61-32.90-31.34-5.60 (6.28 (7.80) .22 (6.0-24.90 (2.80 (2.00-4.59-3.670 (<LOD-1.11-6.53 (3. 122 Fourth National Report on Human Exposure to Environmental Chemicals .90) 8.7) 22.25 (2.92-17.27 (3.7) 16.0) 6. population from the National Health and Nutrition Examination Survey.70-9.45 (3.90 (6.20 (<LOD-2.10-15.34-10.3 (11. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .34-3.27) .00) 3.580-2.0-24.16-1.9-15.9-14.50-5.20) 3.80-4.88) 3.10 (<LOD-1.74) * * * * * 1.4-17.75 (3.790 (<LOD-1.80-6.80-14.27 (7.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 (5.90-9.0) 9.9) 10.0) 23.00) 7.30) 8.910 (<LOD-2.1-23.63-14.9 (7.9-17.80-3.80 (2.15-6.70 (8.61 (3.40 (2.80) .7-21.6-41.4 (10. and 03-04 are 0.42 (1.37) 2.89 (2.00 (.7 (11.0) 7.90 (6.650-1.04 (3.20-4.3) 10.6) 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 * * * 1.00-16.4 (14.64) 10.0-29.78) 5.81-6.73) 7.20-18.5-26.00) 3.0) 14.77-14.31-7.96) 90th 7.90 (5.0 (7.0 (13.670 (<LOD-1.00-9.3) 22.22) 8.92) 9.95 (2.5.14 (6.35 (6.3 (9.0 (5.670 (<LOD-1.2 (9.24 (2.12 (4.0) 11.6) 11.47-6.50-4.31) 1.66-13.98-9.70 (1.8 (12.6 (10.10 (.9) 95th 14.34 (6.3 (9.90 (2.97-4. which may vary for some chemicals by year and by individual sample.40) < LOD < LOD 75th 2.52 (6.3 (7.0) 12.67-10.96) 3.06 (2.70-5.8) 9.00) 8.18) * * * * * * * * 1.75 (2.0) 12.67) 4.84-4.60) < LOD < LOD 2.15-2.3 (12.50) .7) 15. respectively.80-8.0-19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 3.60 (5.90 (2.37 (3.70-9.88) 10.99 (3.0 (15.39 (5.7) 10.0 (10.5 (8.89) 2.70-8.90-15.40 (2.S.41-5.17 (7.0 (9.46-4.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.7) 14.86-10.10-4.00-18.66) 4.5 (8.680 (<LOD-1.0) 13.01 (2. < LOD means less than the limit of detection.9) 16.5.8) 8.6) 14.90) 4.62-17.8 (12. 01-02.58.30) 3.970 (<LOD-2.90 (6.27) 9.39-13.3) 8.0) 18. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 0.3) 14.95-9.22-12.00-18.80-12.41) 3.0 (8.20-8.77-3.31-12.7 (10.0) 19.20) .72) 2.18 (3.8-20.51) < LOD 1.8-20.3 (6.6-19.00-4.49-4.7-19.0 (10.0) 9.1 (10.3) 20.22 (6.10-10.35-3.0) 14.1 (10.30) 3.29) < LOD < LOD < LOD < LOD 3. see Data Analysis section) for Survey years 99-00.0) 11.90 (1.6 (10.95 (5.35) 4.80-21.9 (12.30) < LOD < LOD 4.5) 21.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.740 (<LOD-1.50) 5.4) 7. 0.5) 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 * * * * * * .5 (9.2 (7.50) 3.29-4.9) 9.80) 5.90 (6.10) 6.2) 14.90-15.

55) 16.15) < LOD < LOD 75th 2.42-19.06) .67 (1.30) 2.63 (6.32-8.890-2.3) 8.93 (<LOD-2.34-18.3) 6.43 (2.00) 2.54-5.68) .07) 2.7) 9.12) < LOD < LOD 4.4-16.61 (2.18) 2.03 (2.28-12.620 (<LOD-.07-3.21) * * * * * 1.50 (6.09-11.0 (8.06 (<LOD-1.99 (4.19) 3.5-17.78) 4.47-9.29 (5.68-4.69-11.2) 16.11-3.03 (6.29) 3.7 (11.03) 3.6 (11.79-9.940) < LOD < LOD 1.16 (3.58 (4.00 (5.7 (10.96-10.7 (10.9 (9.2) 10.52-3.850 (<LOD-1.29 (2.15 (1.30) 7.72-4.1) 13.77 (2.38) 1.4 (11.6) 95th 16.5) 13.38 (1.7 (8. population from the National Health and Nutrition Examination Survey.3-34.83 (6.6 (13.95) 90th 8.8) 14.6) 12.3-17.71 (1.28) 6.6 (11.89) 5.86-3.8) 16.86 (3.2 (9.5) 10.00 (3.5 (15.760 (<LOD-1.9) 16.7-23.690 (.44-6.3 (7.910 (<LOD-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2) 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.780-1.8 (10.95 (2.5 (9.02-4.38 (2.92 (5.37) 3.29-2.1 (8.36 (2.0) 14.4) 15.0 (11.530-1.48 (2.07) 2.00 (7.2) 12.4) 16.33-10.85-17.67 (7.S.59-3.45) 6.3-15.8) 11.38-13.1) 20.16-14.6 (10.5) 8.74-19.3-21.73 (5.6 (13.7) 12.01-5.88-7.04) 9.89-10.8 (8.09-11.950) .53-8.97-4.86) 9.3) 9.30-5.28 (1.89-13.2-30.0-21.83 (7.00 (<LOD-1.87 (3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .72) 4.5 (10.23-3.2) 19.91) 3.51-10.88 (1.85-8.78-10.68-10.94 (5.32) 2.30) 8.1 (13.4) 7.3-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 12.4) 9.51-7.70-2.6) 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 * * * * * * .7) 15.99) 2.0 (10.9 (9.27) 5.5) 22.6) 14.4-16.75-3.20-3.590 (<LOD-.82-11.34) < LOD < LOD < LOD < LOD 3.74-4.2) 15.45) 3.79-6.93-10.89 (3.27) < LOD .4-18.920 (<LOD-1.2) 12.25-9.37-5.77 (2.6) 13.82-8.38 (.05-3.54) 9.89 (2.71) < LOD < LOD 2.4) 7.5 (11.2) 8.54 (7.2 (9.27) * * * * * * * * 1.6) 6.63 (2.93 (6.11 (5.75-3.5 (8.55) .4) 7.9-17.42) 8.6) 7.1 (19.6 (12.6) 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 1.00) 8.25 (4.70-35.3) 12.9 (9.6-19.7-19.41 (7.42) 7.94-14.39-17.91-9.93 (2.81 (7.810 (<LOD-1.80) 3.78 (6.33) 3. Fourth National Report on Human Exposure to Environmental Chemicals 123 .77) 3.0 (13.0-19.92) 3.4-15.27) 1.7) 14.12 (7.97) < LOD .64-11.14 (2.50-17.95) 3.89-3.55 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-15.21-21.1) 10.973 (.9) 19.78 (4.27-13.96-11.7) 14.9-25.07 (5.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .89-3.00 (2.68-19.00 (<LOD-1.4) 6.

710 (.618) * .960 (.910) 1.98 (2.720-1.80) 2.210 (<LOD-.680-1.700) .690 (.930) 1.30) 4.22-3.20-2.83 (2.77-2.453 (.930 (.31) 2.880) < LOD 75th .400) .18 (1.22-8.73 (1.970) .01-3.20) 1.42-2.940) < LOD .820 (.749 (.20) 2.549 (.960-1.30 (.16) 1.20) 2.00 (1.00) 2.50 (1.50-2.490 (<LOD-.59-2.64 (1.46-3.840 (.26 (2.94) .75 (2.760 (.30) 2.540 (.90) 2.97 (2.54) .810) .70-2.30 (.68-5.560-.910 (. 124 Fourth National Report on Human Exposure to Environmental Chemicals .34) 2.78) .380-.60) 3.00-4.570) * .S.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 * .73 (2.60-4.32-1.950) 90th 1.10-1.95 (2.14 (1.20) 3.04) 1.86 (1.83) .13) 2.96-5.87-3.17) 1.45-4.500 (<LOD-.47 (1.41 (2.359-.20 (1.45 (2.650-.710) .09 (. and 03-04 are 0.49) .280-.1.570 (.880 (.20 (1.04) .949) .15) 2.95-5. interval) Selected percentiles ( 95% confidence interval) Total * .22-3.74-5.657) * * .05-3.980) 1.79) .457 (.01-1.76 (1.759) * .570 (<LOD-.750) 1.98-3.39) 2.41-5.57 (1.46) 1.440-.59-6.510 (<LOD-.780) .75-2.60) 2.31-3.600-1.79) .17-4.700) .570-1.95) 2.720 (.31) 95th 2.455 (.590-.83 (2.710 (.88) 1.670) .80 (1.50) 1.16) 2.592) * .70 (1.08 (2.201-.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 * . see Data Analysis section) for Survey years 99-00.10) 1.46 (2.336-.730) .27 (3.29) 1.32 (1.48 (2.61 (1.45 (1.505 (.930-1.74) 3.11-3.690-1.27 (2.780 (.160 (<LOD-.91) 2. and 0.600 (<LOD-.40 (1.76-6.398-.50 (1.89) 1.34) 2.49) 2.50-2.33-2.94 (2.80) 3.600-.10) 1.592-.08 (2.46 (1.20-1.20 (2.303-.570 (.32) 3.550 (.90-4.340-.05-2.47) 2.910-1.40 (1.90) 3.380-.260 (<LOD-.382-.50 (1.460-.63 (1.30 (.35) 1.584) .70-7. which may vary for some chemicals by year and by individual sample. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.800 (.23-3.750-1.30 (1.592) * 50th .30-1.69-4.990-1.820 (.90) 2.30) 4.09.570 (<LOD-.11-3.77 (1.65 (2.960) . respectively.10) 3.54 (2.960) 1. 0.450 (<LOD-.690) .58 (1.25-1.86) 3.80) 3.80) 5. < LOD means less than the limit of detection.510 (.00-2. 01-02.780 (.13) .22-2.37-2.80) 3.20-2.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.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2.740 (.15) 2.350-.580-1.20) 1.50 (1.880) < LOD .350-.449 (.83) 2.89-6.850) < LOD .467 (.14-1.720-1.680-1.50 (1.03) 1.26) .740-.22 (1.18 (.353-.31-3.19-1.01) .00) 1.94 (3.17) 1.343 (.240 (<LOD-.36-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740-1.960) .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 * .57 (2.10) 1.60 (2.55 (3.38) 1.80) 2.70 (1.970) 1.29-2.80 (2.388-.790 (.390-.930) < LOD .597) * .70 (1.830 (.587) * * .620-1. population from the National Health and Nutrition Examination Survey.380) .10-1.20) 3.390-.30) 1.98) .459 (.20 (1.30-3.96-3.580-.30-3.54-2.550 (.45 (1.425 (.20-3.83) 1.73-5.860) < LOD < LOD .21) 3.16-3.89) .90 (1.48 (1.690-.585) * * .740 (.

22-2.08 (2.480) .23) 2.11-2.39 (1.71 (1.43) 2.08-3.720 (.07-3.47-4.710 (.580-.67 (1.330-.22 (2.62 (1.509 (.33 (1.20-2.29-4.80) 2.70 (3.99) 2.82) 2.70 (2.36) 3.740) < LOD 1.44) 2.471-.760) .57 (1.75) 6.45 (2.52) 3.980-1.250 (<LOD-.50) 1.34 (1.590 (.08 (.22-3.80) 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 * .61 (3.412-.790 (.535 (.28 (1.92-8.400-1.32 (.560-.305 (.453 (.640 (.43 (1.42 (.02-6.90) 2.99) 1.04-5.05) 1.04-1.08) 1.310 (<LOD-.89-3.480-1.57-2.84-6.550-.53) .42) .66 (2.830) 90th 1.30-2.67-3.60) .89 (1.380-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .07) 1.510 (.33) .60 (2.32) 2.04) 95th 2.310 (<LOD-.490 (.335-.680 (.760) < LOD 75th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800) < LOD .08-2.67) 1.23) 3.950-2.45 (1.92) 3.550) .591 (.403) .23) 1.270-.830 (.67 (1.16) 1.06) 4.58 (1.07) 1.990-1.09) .390-1.75 (2.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .07) 5.180 (<LOD-.444-.270-.47 (1.61-3.460 (.253-.20-7.460-1.71) 2.67) .14 (2.730) .688) * .08) 2.76) 1.390) .50 (1.590) * 50th .234 (.24) 4.500-.550-1.310-.550-.448 (.470 (<LOD-.60) 1.750 (.710 (.32-1.07-2.460) .520 (.285-.08-2.92 (1.44-2.400) .11) 1.88 (1.23 (.72 (1.60 (1.377-.510 (.700 (.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.69 (1.630) * .17-2.640 (.20) 1.900) 1.95) 1.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .55 (1.38-3.368) * .22) .790) .32) 1.350) .03-1.25-3.00-3.870) .05) < LOD .380) .05-4.700 (.393 (.710 (.66) .22-3.41 (.11 (.348-.88) .13 (1.91 (1.280 (<LOD-.330 (<LOD-.61) 2. population from the National Health and Nutrition Examination Survey.03-2.39) 2.530 (.19 (1.43) 2.740) .16-2.920) .515) * * .62 (2.08-3.38 (2.17) 2.97 (1.380-.690) < LOD < LOD .71) .08-2.18-2.300-.42-6.10) 2.560-.06-2.580) .136-.580 (.540-. interval) Selected percentiles ( 95% confidence interval) Total * .910) < LOD .742) * * .820) .08-3.700 (.30) 3.77 (3.590-1.58-6.22) 1.02-3.57 (3.739) * .850) 1.320-.560 (.61-3.230 (<LOD-.81) 2.78) 3.72) 1.07) 1.73-3.42-8.870 (.670 (.97) 2.31-1.79) 1.75-3.17) 2.64 (2.72 (2.23) 2.79 (1.64 (2.320-.97 (1.510-.318-.84 (2.97) 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.372 (.485) * * .58) 3.00 (3.660-.720-1.840) 1.05 (1.552 (.77-3.470) .300 (<LOD-.370-.820) 1.98) 1.49 (1.32) 5.940-1.02-3.16-1.840) 1.00-1.77-4.69 (3.645) .97) 1.47 (1.S.94) .63 (1.05-2.270 (<LOD-.440-1.38 (1.447 (.08-3.72-4.840) .640 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.930-1.49-4.800-1.82 (2.597) * .73 (2.880) 1.87 (2.43) 1.250 (<LOD-.55-3.22) 4.07 (.57-4.75 (1.750 (.52 (1.65) 2.520-.

2-47.92) * 2.87-7.40-4.10 (1.0-62.71 (4.16) * 1.0-41.57-2.80-2.2 (19.04-8.0-92.70 (1.70 (.5-20.59 (1.77 (1.7 (12.64-8.0-53.0) 3.0-62.00 (.0-110) 34.90 (1.13 (1.0) 30.98 (1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.2-33.06) * 2.12) 1.26 (.80) 90th 38. population from the National Health and Nutrition Examination Survey.0) 3.0-110) 42.74-2.0 (26.0) 17.0-39.54 (3.0-50.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (38.48) 5.81-3.00 (.18) 14.600-2.S.2-39.0 (33.72 (1.1 (22.43-7.13) 12.29-9.05) 1.9 (19.0-58.5) 69.78) 9.92-5.65 (4.830-4.5 (24.16) 2.5-45.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 20.8) 32.13 (1.83 (1.6-22.0-58.0 (38.4) 19.9) 18.20-4.50-7.0-41.20 (2.05-3.10 (1. and 03-04 are 0.63-6.8 (12.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.7 (12.8 (22.0-53.83-2.90 (1.3) 38.95 (5.0 (40.46-6.14) 5.23-2.0 (24.46 (.48-2.0) 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 2.61 (1.44) 2.9-21.690-3. interval) 1.8-24.61-2.0) 4.67 (1.0) 6.40-16.7) 20.0-41.45) 2.2) 16. 0.830-3.98) * 2.33 (5.0 (25.58-2.0) 20.42) 1.36-2.26) 75th 11.4 (10.6 (11.90) 11.530-4.0-31.50 (2.32 (2.8-21.0) 33.83 (3.0-29.7-22.79 (2.3) 31.53) 40.0) 28.50-5.86 (1.0-260) 34.1) 140 (46.0 (38.27-6.80) 1.10 (1.3 (12. which may vary for some chemicals by year and by individual sample.4 (19.45) 2.48-2.0) 16.69) 2.0-230) 35.0) 5.8) 39.76 (2.3 (14.1) 18.5) 30.3) 26.94 (1.88) 1.70) 5.85 (1.49-2.30-14.20) 1.52 (4.2-62.76 (2.3) 33.40) < LOD 1.70) 1.2-80.86-3.9 (23.19) 2.40) < LOD 2.50-17.0 (8.11) 2.53) * 2.60) < LOD 1.0) 4.59 (1. 01-02.9-51.0 (11.25-3.79-2.70) 1.0) 45.57-2.1-47.0 (38.41) 1.23-2.1 (10.0 (8.41) 5.83-2.0) 4.0 (19.0) 18.610 (<LOD-1.8) 62.0 (38.6 (9.0 (17.4-22.1-19.31-6.58) 16.88) 3.60 (2.23) 9.66-5.71) 5.0) 42.1) 38.18.93-3.54 (1.9 (27.5-40. and 0.9) 17.75-14.10 (1.41-4.0 (7.0 (38.82 (1.1 (25.3 (10.0-47.53 (1.7-41.10) 39.0 (37.18) 6.6 (15.64-3.06 (1.91 (4.2-26.99 (2.6-27.1-40.0) 28.0-39.0-43.0 (20.44) 3.29) 2.44) Selected percentiles ( 95% confidence interval) Total * 2.8 (26.21 (4.70-6.04 (<LOD-2.0-52.10 (7.5-27. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 (23.10-4.0 (6.0) 8.17-2.660-2.80) .0) 3.0 (20.1 (25.0-49.2 (12.90-8.00-24.5-74.79 (1.1-46.470 (<LOD-1.21 (1.6-45.77) 38.9) 38.9 (10.70 (7.44-7.18) 20.0-69.6) 52.70-17.9 (19.0 (38.1-20.1 (26.81-2.80) < LOD 1.4-76.2) 31.80-18.71-2.50-2.0) 32.6 (26.4.04) 3.3 (24.50-20.0 (8.7) 47.0 (21.30 (.11 (4.21 (3.09 (4.12 (3.10) .41) 1.0) 19. < LOD means less than the limit of detection. 126 Fourth National Report on Human Exposure to Environmental Chemicals .30) 11.0) 13.4 (15.1) 95th 48. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 17. respectively.8) 41.35-6.3 (12. see Data Analysis section) for Survey years 99-00.0) 31.19-2.46-2.85) * 2.2-27.40) 50th 2.0 (13.2-27.1-25.97) 6.70 (1.6-54.7 (28.96) 5.0) 15.9) 48.4) 38.30) 4.41 (1.0) 3.29-4.1 (11.07-5.3) 28.1) 38.0 (32.53) 1.02 (2.0) 15.0) 16.8 (12.5.78 (1.05) * 2.10-13.

28) 1.43) * 2.51) < LOD 1.3-42.4 (25.3 (8.67 (1.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.899-2.06-1.3 (20.7-43.88 (1.02) 1.3 (10.7-47.06) 75th 9.3) 13.9) 3.1) 27.00) 1.7 (18.66 (1.0 (25.6) 11.0) 30.9-41.86) * 3.69-18.40 (2.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.03-2.88 (4.20) Selected percentiles ( 95% confidence interval) Total * 1.75-6.12) 3.2 (22.1 (39.14 (.6 (27.7) 66.26-4.08 (1.670-1.7) 95th 51.4 (12.0-70.6) 7.6 (24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.22-3.27) 10.8) 32.0-40.48 (4.4-67.52 (1.4-21.02) * 1.82) 1.26-2.9) 24.19-14.2) 33.67-16.59-2.69-5.7-37.43-2.4 (11.7) 15.1) 15.52-4.1 (12.0) 3.36 (4.95) 90th 32.4-71.S.16 (1.9 (19.8) 31.70-4.870-3.07) 9.0) 10.1) 52.6) 112 (40.16 (1.00-16.07-2.5 (15.9) 24.2-38.6-38.88 (1.9 (26.7-38.32-3.63-5.35) .47-17.23) < LOD 2.1) 13.19-6.5) 27.36) 10.50 (2.3) 28.2 (8.2 (16.4 (5.18) * 2.09 (5.41 (2.44) 9.58-2.8-43.57 (6.2 (15.2-34.9-37.7) 30.80-8.5-190) 30.46-6.0 (23.94-20.0) 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 1.9-36.5-97.62 (2.46) 1.29-5.2 (21.9-95.9-52.27-3.33-5.680-4.40 (5.68) 47.94) 1.0 (17.0 (39.27 (6.0) 13.4 (21.0 (19.14-8.90 (.91 (6.24 (1.0 (32.45-1.11) < LOD 1.8-45.37 (1.860 (<LOD-1.83) .8 (7.56 (2.55 (2.37-2.7 (24.930 (<LOD-1.7 (10.96) 2.2-47.4-39.9 (39.31) 2.23-1.9) 3.75) * 1.51) .2-70.36-13.8) 3.9-18.6) 23.47 (1.1-63.58-17.1-22.1 (25.3-22.11-2.64 (1.2) 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 1.40-7.2) 36.06) 1.71-2.95-16.59-15.18-1.33) 1.88 (4.19) 5.48) 1.7) 26.6-51.0) 47.08) 1.6 (11.17) 2.5 (15.70 (1.2) 4.0 (23.46-5.2) 13.56) 1.4) 12.4-34.9) 12.6-32.27) 50th 2.0-71.3-19.5 (8.5-43.66 (1.67 (1.0 (14.9 (7.6-49.0) 48.5 (41.68 (1.7-20.5-36.57) 4.00 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 13.8) 11.19) 5.3 (10.46-22.62) 4.35 (2.4 (9.890-4.7-109) 22.8-37.5 (17.1) 36.12 (1.07-2.35) 1.01 (.4 (19.5) 70.6) 3.54-2.5 (6.99-4.1 (34.60 (.4) 3.16 (1.72) 2.7) 34.6) 3.9) 54.38 (3.43-12.33) < LOD 1.0) 25.7-19.22 (2.1) 27.02 (.3 (9.60) 4.76-2.22-2.61-22.3-27.9 (10.23) 37.6) 19.95-16.79-17.4) 12.5 (34.40-4.19 (1.61 (1. interval) 1.96-16.8-26.94) 19.1) 25.1 (50.2) 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.45 (1.21 (4.83 (.22 (.750 (<LOD-1.47 (3.79 (2.1) 25.03) 1.0-118) 29.97 (1.870-3.80 (1.870-3.33) 2.18) 3.59-2.38) 5.38-5.1) 13.30) 28.8) 15.75 (1.17-3.34) * 1.54-15.28 (1.53) 1.61-2.7 (11.20-5. Fourth National Report on Human Exposure to Environmental Chemicals 127 .888-1.75 (1.2-28.38-1.16-2.82 (2.06) 1.86) * 2.15 (.9 (13. population from the National Health and Nutrition Examination Survey.1) 17.71 (1.1 (33.32 (3.00) 6.4) 14.0 (6.2) 41.95 (2.1-60.6 (7.71) 8.67-3.5 (13.84-13.7) 23.2 (9.7 (18.91-2.7) 61.93) 5.39 (1.50-5.66) 8.8) 23.8-34.25-3.4 (25.

450 (.540 (<LOD-.610 (.540) .940 (.099-.610-.370-.30) .550) .560 (.420-.640 (.160) .510-1.700-1.490 (.840) .200) < LOD < LOD .770 (.460-.090 (<LOD-.160-.1. 01-02.220 (<LOD-.410-.380-.00) .830) .400-.100 (.690-1.220 (.640) .42) .12 (.730-.300-.050-.410-1.290) < LOD < LOD < LOD < LOD .360-.280) < LOD < LOD < LOD < LOD .560 (.190 (.130-.350) < LOD < LOD < LOD < LOD .600 (.130 (.990) . 0.080 (<LOD-.650-1.610 (.740) < LOD .370-.190 (.160) .120-.860-1.990) .260 (.150) .084-.300-1.03) .830) < LOD .05.10) .870 (.270 (.S.290) < LOD < LOD < LOD < LOD 90th .090 (<LOD-.13) .42) .820 (.240 (<LOD-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .290 (<LOD-.30) .310) < LOD < LOD < LOD < LOD .830 (.10) .130-.430 (.630 (.650-1.310-.760) < LOD .630 (.15) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.850 (.162) * * * * * .310 (.140) .32) .360-.770) < LOD 95th . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .130) .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 * * * * * * * * * .130-.130) .60) 1.140-.820 (.1.700-1.430-.870 (.780) < LOD 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.117 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .210 (.390) < LOD < LOD .120 (<LOD-.380-.210 (.171) * * .680-1.20) . < LOD means less than the limit of detection.660 (.720-1.450 (.840) . see Data Analysis section) for Survey years 99-00.310 (.900 (.610-1.120-.320 (.650 (.570) .080 (<LOD-.990 (.540) .870) < LOD .110-.730) .700-1.640-1.830 (.090 (<LOD-.140-.530-.30) .180) .440-1.40) . and 0.470 (.850 (.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 * * * * * * .450 (.170-.680 (.870 (.720 (. which may vary for some chemicals by year and by individual sample.190 (.720) .10) .410-.230-.230) .310) < LOD < LOD < LOD < LOD .090 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.930 (.850) < LOD .680) .090 (<LOD-.350) . population from the National Health and Nutrition Examination Survey.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 .320-. and 03-04 are 0.700-1.140-.640) .330-.10 (.470-1.36) .650) .410) < LOD < LOD < LOD < LOD .460 (.860) .390 (.380-.870 (.090 (<LOD-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD. respectively.620 (.58) .870 (.650) .150 (<LOD-.680-1.

720 (.730) .580 (.230 (<LOD-.580) .370 (<LOD-.03 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.940) .390-.660-1.330-.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.29 (.380 (.670-1.260) .140-.710-1.100-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.700 (.640-1.140-.120) .360-.230-.380-1.670 (.12) < LOD .050 (<LOD-.860 (.38) 1.500 (<LOD-.060-.490-1.970) .410) .410-.66) 1.230) < LOD < LOD < LOD < LOD .43) .390-.170 (.110) .300-.161) * * .500) .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 * * * * * * * * * .09) .990) .360 (. population from the National Health and Nutrition Examination Survey.730) .110) .610-1.450 (.400) .170) < LOD < LOD .860-2.070 (<LOD-.02) .700-1.740 (.520-.080 (<LOD-.140) .410) < LOD < LOD .057-.62) 1.220 (.650-1.670 (.550 (.380-.116 (.940) .310) < LOD < LOD < LOD < LOD .150-.540) .290) < LOD < LOD < LOD < LOD 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.440 (.410 (.650) < LOD .140-.100 (<LOD-.280) < LOD < LOD < LOD < LOD .400 (<LOD-.780 (.86) .780) < LOD 1.60) .850 (.730) .110) .080) .01 (.410 (.330-.86) .58) 1.570 (.330 (.570-.270 (.120) .03 (.070 (<LOD-.560 (.730 (.090 (<LOD-.140-.070 (<LOD-.960) .760) .700 (.880 (.03 (.320 (<LOD-.180-.380-.190 (.02-1.860 (.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 .450) .20) 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 * * * * * * .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .S.340-.170 (.600-1.084-. Fourth National Report on Human Exposure to Environmental Chemicals 129 .260-.36 (1.78) .740) < LOD 1.00) < LOD .470 (<LOD-.800-1.700) .440-1.111) * * * * * .540 (.460 (.330 (.250-.24) .200 (.090 (.110-.300 (.240-.190-.500-1.200 (.540 (.140-.510-.550 (.580-1.220) < LOD < LOD < LOD < LOD .080 (.14) 1.270) < LOD < LOD < LOD < LOD .03) .880-1.330-.67) .580 (.110) .600) .210 (.890 (.870) .720 (.580) < LOD .190 (.990) .070 (<LOD-.300-.380-.360) < LOD < LOD < LOD < LOD .19 (.810 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .360-.750) < LOD 95th .410-.570-1.24 (.

14-5.0) 4.40-20.35) 11.260-.67 (1.400-1.10 (3.18) 1.080-1.1.380-.86) 4. which may vary for some chemicals by year and by individual sample.70-50.0-40.800-4.32 (1.38-3. and 0.691 (.750-1.350-.00) .30 (1.90-9.76 (1.0-40.00-17.90) .87) 5.720) 2.90) .600 (.690 (.39 (2.36-3.210-1.40) 2.11) 13.60) 1.52 (1.99) 11.83-3.40-8.74) 5.0) 2.70-17.0) 5.31) .20-4.0 (17.51-8.37) .94-3.840-3.49 (1.40-7.52 (1.08.40 (1.0 (5.425-1.33 (4.23-6.770 (<LOD-1.90 (1.14) 2.99) 19.29-10.49) 17.70-30.20 (1.30 (1.83) 2.61 (1.51 (2.94-8.10 (.0 (17.53-7.590 (.83-3.580 (.480-.15) 19.14) .30-6.90 (2.360-1. 0.28-9.0 (4.0-38.30-7.0 (16.730 (.0 (17.35) 5.30) 95th 19.42) 2. and 03-04 are 0.47 (3.63 (3.12-1.840 (.80 (4.640 (.40-4.24-7.610 (.870) < LOD < LOD .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 * * * * * * .05 (3.97) 20.250 (<LOD-.87) 12.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.05-3.110 (<LOD-.0 (6.50) .43-4.960 (.90-20.0-38.32-9. population from the National Health and Nutrition Examination Survey.890 (.0 (5.53) 20.0-38.07-3.59-5.40 (1.90) .900 (.0) 2.90-28.10-3.0-39.70) 2.21-3.28) 1.55-8.770) 2.0 (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 * * * * * * * * * .20-17.20) < LOD < LOD < LOD < LOD < LOD 1.50) 2.96 (1.13 (3.10-9.0) 5.28) .03 (.880) 5.62-8. respectively.20-4.S.10 (3.00) .00) 1.6) 5.60) .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.00 (1.39) .07) 1.66) 4.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.26 (2.21) 3.850) 16.0) 5.88-3.48) 13.42) .82-4.00 (.52) 5.1.830 (.67) .0 (17.0) 2.30-3.0 (17.97) 20.90-37.0) 3.0) 5.11 (1.35-10.46 (1.70-7.67 (2.07 (3.99 (1.370-.65) 1. see Data Analysis section) for Survey years 99-00.510-.640 (.63) 32.20 (1.07 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15) 14.0 (5.750-2.0) 2.0-44.740 (.53 (2.07 (3.00-17.31-10.10-3.620-1.0) 2. 130 Fourth National Report on Human Exposure to Environmental Chemicals .610) < LOD < LOD < LOD < LOD < LOD 2.0) 4.74 (3.800) 90th 13.12) * * * * * * * * .190-1.07-3.85-3.45 (2.40) 1.350-.30) .0) 2.0) 4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0 (4.0 (7. < LOD means less than the limit of detection.30 (.36-3.800) 17.0 (5.01) 5.05 (2.0 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 01-02.30 (1.48 (2.0) 2.330 (<LOD-1.30 (2.49 (1.840 (<LOD-1.70-3.16) 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 .55-4.170-1.94 (1.0) 4.68) 2.11) .0 (13.0) 7.910) 2.960 (<LOD-1.

88 (.43) .9) 5.75) 5.8) 2.02 (1.800-2.17) 5.32) 9.1 (7.S.650) 90th 10.580) 16.57) 8.84) 9.09-3.67-6.56 (1.540 (.51-44.330-1.4 (4.340-.4-34.04 (1.630-1.60 (1.85-3.474-1.0 (9.91) 2.11-5.580-1.7) 3.89 (2.97) .370) < LOD < LOD < LOD < LOD < LOD 1.55) 21.41) 18.08) .64) 30.18) 1.850-3.29-4.3) 2.33-5.840-3.12 (4.50) .39) 20.9) 6.53) 27.780-4.05) .660) < LOD < LOD .890 (.24) 3.0 (4.33-4.960 (.580 (.40) 1.00-19.340 (.69) 2.56) 2.62 (1.430) 1. population from the National Health and Nutrition Examination Survey.340-.69-7.8 (20.310-.7) 5.07 (2.370-1.44-11.690-5.66-47.390-.18) 95th 21.57 (.96) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.830-3.860-2.5-40.90-6.150 (<LOD-.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 * * * * * * * * * .77 (.80 (.700) 6.96-8.23-7.260-.03) 16.710 (<LOD-1.31-18.8) 1.33 (3.86) .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.370 (.35 (.2 (8.98 (4.01 (1.65 (2.30 (4.700) < LOD < LOD < LOD < LOD < LOD 1.03) 2.53) .270-.80) 3.790 (.92 (2.40 (.67) 2.670 (.57) 1.240-.36 (.85 (1.47) .28-6.82-11.33-3.56) .430 (<LOD-.13 (2.44) .37) 4.4) 2.47-10.59 (1.55) 21.450 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.770) .15) 9.1 (5.67) 1.790) 11.2-38.33 (1.7 (12.8) 4.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.8) 2.41 (4.45 (1.55 (3.07-21.38 (2.8) 7.40-2.22-27.18) * * * * * * * * .50 (4.830 (.930) .79 (.22) 2.10) 2.580) 1.7) 4.25-9.740-1.81-17.27 (2.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.540-1.250 (<LOD-.31-7.25-38.14 (1.3) 3.730-3.31) .11) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.560 (.12-4.02) .21-3.04-16.17 (1.31) .5 (9.10-3.14-6.470 (.83 (4.67 (2.71 (2.91-4.40-12.57-40.7) 6.71 (.86 (3.5 (8.5) 2.500 (.590) 2.5) 7.29 (4.340-.8) 7. Fourth National Report on Human Exposure to Environmental Chemicals 131 .32-6.748 (.47) 5.51-4.88-3.320-1.48-42.970-3.06 (.25 (1.5) 2.600 (<LOD-1.73 (4.7 (6.620-3.02-4.8-33.260-.88 (2.270 (<LOD-.48-7.00) .62-17.88) 17.50) 11.49-2.74 (2.940-4.48 (4.02 (.820) .1) 2.820 (.10 (2.650 (.360 (.0) 4.61) 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 .83-11.190-1.52 (.47-10.5 (11.64-4.1) 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 * * * * * * .9 (11.50 (2.96-25.

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Levy LS.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Chronic neurological sequelae of acute organophosphate pesticide poisoning.332(1-3):71-80. Chronic neurological sequelae to organophosphate pesticide poisoning. and spatial learning in monkeys and rats. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Buchanan D. Stokes L. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Effects of long-term organophosphate exposures on neurological symptoms. Environ Health Perspect 2005. Keifer M. Ruberu DK. Salvini S. Pedersen L.113(4):504-508. Available at URL: http://books. Santana J. Lancet 1995.epa. McCauley L. May. Neurotoxicology 2005. Scand J Work Environ Health 1998. Weerasekera G. Sci Total Environ 2004. et al. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Available at URL: http://www.nap. Malathion deposition. Office of Prevention Pesticides and Toxic Substances. Am J Ind Med 1987.26(2):199-209.S. vibration sense and tremor among South African farm workers. Arch Environ Contam Toxicol 2000. Jenkins B. Barr DB. Bravo R. low-level organophosphate exposure on delayed recall. Lewis JA. Daniell WE. Masala G. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Weisskopf C. Frasca G.43(1):38-45. Johnson C. Vitayavirasak B. Spurgeon A. low-level exposure to the organophosphate diazinon.12(2):153-172. Hore P. Rodnitzky RL. London L. Pilkington A. Nell V. van der Hoek W. Bull Environ Contam Toxicol 1994.52(2):190-195. Samuels S. Mounce LM. Muniz J. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates.edu/ openbook. Rothlein J. Takamiya K. et al. Environmental Protection Agency (U. EPA. et al. Petchuay C. Chrislip D. McConnell R. S. Calvert IA. National Academy of Sciences. U. Robson MG. A behavioral evaluation of pest control workers with short-term. 1/12/09 Peiris-John RJ.52(10):648-653. Russo J. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Occup Environ Med 2001. O’Malley M. Narang A.2000 and 2001 market estimates. Steenland K. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Lambert WE. Bradman A. Schenker M. Rothlein J. The Pesticide Health Effects Study Group. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Stephens R. J Toxicol Environ Health A 2005. Prendergast MA. metabolite clearance.pdf. Tumino R. Myers JE. Wickremasinghe AR. Buccafusco JJ. Berry H.20(2):115-22. Lasarev M.84(5):731-736. Heaton RK. Beach J. Washington (DC): U. Savage EP. 4/7/09 Young JG. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Hansen S. Seiber J. Gladstone EA. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Neurotoxicity among pesticide applicators exposed to organophosphates.58(11):702710. 1993 [online].38(4):546-563. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Muniz J. Effects of chronic. Stark A. Eskenazi B. Pesticides in the Diets of Infants and Children. Am J Public Health 1994. Lancet. discrimination.44(4):352-357.24(1):18-29. Phillips J. Washington (DC). 1991. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. J Occup Environ Med 2002. Arch Environ Health 1975. Caltabiano LM.345(8958):11351139.30(2):98-103. Smit LA. EPA). Environ Health Perspect 2006. Arch Environ Health 1988. Ames RG. Marshall E. Aprea C.114(5):691-696.338(8761):223-227. 2004. Thompson ML. Saieva C. Burcar PJ. Kidd M. Rohlman D. Neurotoxicol Teratol 1998. Gillham R.12(2):134-141. and cholinesterase status of date dusters and harvesters in California.php?record_id=2126&page=1. Visuthismajarn P. Lu C. Pesticide industry sales and usage .S. et al. National Research Council (NRC). 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. Jamal GA. Rosenstock L. Claypoole K. Dinoff TM. et al. Occup Environ Med 1995.68(3):209-227 Maizlish N. Irish RM. Terry AV Jr. Keefe TJ. Int J Occup Environ Health 2006. Lasarev M. Scherer J.

parathion and methyl parathion are metabolized to para-nitrophenol. the level may reflect exposure to the environmental degradation products of these pesticides.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.” 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. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. malathion is metabolized to malathion dicarboxylic acid. For general information about the organophosphorus class of insecticides.5. For example. In addition to reflecting exposure to the parent insecticide. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.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 .

2005).77-6.2 (10.25) 3.70 (1.0) 12.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.70 (1. The general population may be exposed to chlorpyrifos via oral.0) 10.90) 3.22 (1.44 (3.90-4.10-17.70-15.60 (2.5.37 (4. Exposure can also result from contact with contaminated surfaces.71 (6.0) 11.66-4.1) 5.22) 2. Chlorpyrifos is Urinary 3.61) 75th 3.9 (9.50-14.0) 10.32-1.83) 1.40-2.99-4.30-12.77 (1.68-2.20-16.19-3.8-15. pre.20 (4.09 (2.5) 7.91) 16.70-5.47-13.20-14. 5598-13-0 General Information The chemical 3.62-2.0) 8.95 (4.3) 8.50 (2.47-11.77-15.50 (1. dermal.40 (5.20) 2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.0 (7.30-5.0) 12.13-3.72) 2.30 (2.59) 2.80 (1.8) 9.4 (9.0 (13.16) 2.72-4.50-4.50-5.3 (11. For instance.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.97-7.97) 2.51) 1.4 and 0.10 (3.. 2002).20 (2.97) 4.02 (1.7) 13. It also has been applied directly on animals to kill mites.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.96) 3.0 (7.70-17. 2921-88-2 Chlorpyrifos-methyl CAS No.90-7.90 (1.05) 1.35) 2.89-2.53 (1. and inhalation routes.55-5.47-9.24-1.40-26.95) 7.00) 3.66-15. population from the National Health and Nutrition Examination Survey.0-28.30 (2.80) 2.80) 4. but can be detected in streams receiving runoff from application sites.0) 10.39) 4.20) 2.04-10.00) 1. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.50 (2.0) 18.80-8.91 (1.30-2.9-18.79-2.10) 2.02 (7.81-2.86) 4.50 (2.90 (1.78 (7.70-16.00-8.37 (1.20) 10.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.S.43-2.13 (1.40 (5. air.94 (4. After 2001. Approximately 80.30) 4.35) 1.24-3.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.0) 9.9 (7.63 (1.10) 6.30-11.S. Estimated intakes from diet and water have not exceeded recommended intake limits.50-2. applied to structures to kill termites.39-2.30-1.21) 3.20-4.46-2.60 (4.S. interval) 1.31-2.38 (3.04-10. 2007).52-12.29-1.40-13.40) 2.01) 1.60-2.5-24.0 (7.80-10.03) 1.4.9) 11.15 (1.50 (1.0) 6.0 (9.71 (2.27 (7.76 (1.00-24.8) 10.9 (10.30) 4.17 (1.47) 1.00) 2.0) 15.92 (1.50-2.51-2.40) 9.44-5.0) 14.51 (1.EPA.5 (8. and on plants for days to several weeks.32) 2.25) 1.28-3.71 (1.80 (7. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.87-6.45 (1.9) 697 660 521 701 602 947 Limit of detection (LOD.6) 7.4-15. USGS.7) 8.10 (1.20-2.20-11.44-2.EPA.63 (8.90 (2. Approximately 21-24 million pounds per year were used domestically from 1987-1998.89 (2.7-23. Survey Geometric mean (95% conf.0 (10.05-5.50-4. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.74 (1.74-9.19 (1. 2002).and post-construction structural applications for termite control were to be phased out by 2005 (U.43-2. in 142 urban homes and preschools in North Carolina.63 (2.97) 2.80) 12.97) 7.88 (1.77) 1.10 (5. and is infrequently detected in ground water (IPCS.52-2.90-8.20) 4.61 (1.70) 1.90 (3.59-2.0 (7.0) 12.20-3.10 (4.30) 5.34) 1.0) 12.68 (7.90-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.98-15.37) 5. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.57 (2.28) 2. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.40-10.3 (10. staying bound to soil particles.4 (8.60) 5.67 (2.0) 8. Fourth National Report on Human Exposure to Environmental Chemicals 135 .61-7.0 (7. 1999.64) 3.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.5.4 (10.3 (8. 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. and sprayed to kill mosquitoes.76 (1.30-9.02) 1.47 (4.29) 90th 7.50-8.40 (6.000 pounds are used per year.0) 12.90 (6.84) 1.1-16.67 (1.60-3.70-11. and dust. chlorpyrifos was no longer registered for indoor residential uses in the United States.80) 1.09 (3.90) 7.36 (4.67 (2.30 (4.7) 9.0) 7.60-3.60 (5.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.60-4.26) 7. It has low leachability.31-2.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.

54 (2.. Metabolic hydrolysis leads to the formation of TCPy.85 (3.05-4.3) 8.55 (4.05-3.95 (3.73 (1.42-2.49-2.S. cholinergic effects. 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.57) 9.92-2.14-8.80) 3.07) 5.60 (1. 2005. neurotransmission.2) 6.7) 7.39 (4.0) 12. weakness.16 (4.33) 2.65-11. In pesticide applicators.31-4.82 (2.32) 1.81 (3.81) 2.33 (.97 (2.24-1.85-4.63 (4.46 (1.41 (1.09-1.94-12.88 (1.97 (3.34-1.14) 1.23) 14.64-2.39-1.06 (5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.09-2.1 (7.93 (4.12) 1.86 (3. TCPy can also occur in the environment from the breakdown of the parent compounds.05) 3. Thus.86 (1.37 (1. 2006. 2002).77) 1. Slotkin et al.86 (1.93) 2.56) 2.78 (1.31) 1.31-1.66) 1.2 (7.17-4.01) 99-00 01-02 99-00 01-02 99-00 01-02 3. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.90-9. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.01) 3.91) 2.56 (4. 2000).55) 1.93 (1.65-15.52 (5.19-2.63 (5.6) 9.93) 5..85) Selected percentiles ( 95% confidence interval) Sample 95th 8. Based on animal data and human cholinesterase monitoring during occupational exposure. 2006.58-5.6-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.70-4.5.49 (1.16) 6.05-8.71 (1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.88-8.44 (6.49-2.99) 1.91-13.19) 6.80-6.5 (6.58 (1.64-7. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body. Betancourt et al.3) 8.35) 2.40) 1.56-2.01) 3.75 (1.00 (7.84-6.94-14.51 (1.75) 6.24) 5.46 (2.33 (5.44-6.4) 4.11-9.44 (1.44 (1.63-2.80-4.62) 90th 5.0) 10.93 (2.00) 1. 1984).62) 1.07) 1.9 (12. and other metabolites.58) 1.95 (1. paralysis.24-4.85) 1. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.30-4.76 (2..28) 2.88-9.72-2.59-2.11) 7.91) 10. vomiting.88 (1.48 (2.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .57-2.38) 3. Roy et al.66-11..43 (4.68) 1.56 (1.11 (2.6) 10.53 (2.26-14.68) 6.27-1.0) 6. and producing acute symptoms such as nausea.08) 6.3) 9.24 (1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.06-4.69 (1.00-8.25-1.82) 8.64 (1.19-1.35) 1.1-21. 2006b).Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.23-1.83-2.88-10.03) 1.91) 1.92 (1. population from the National Health and Nutrition Examination Survey.05-1.50 (4.39) 6.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.91) 1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.42 (5.97) 3.88-8.15 (4.82 (3..00-13.82-4.87-3.60-3.S. and seizures..76 (3.91-4.36) 1.98 (7.72) 1.17-4.22 (4.35-1.44 (5.940-1.55 (1.91 (3.09 (1.96) 3.33-7.21-1.72) 2.0) 16.97) 3.21-6.83) 1.58 (4.53-5.58) 5.09-3.20-1. 2006a.91 (4.48 (1.98 (6.02 (5.22-6.45-1.47 (1.49-2.99-8.11 (2.1 (10.43-10.02) 7..01) 1.27-7. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.06 (1.30-1.56) 5. 2005.24-24.85 (2.47-2.19) 3.20 (2.24-5.74) 1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.29 (3.66 (1.54) 5.28) 2.97-3. Urinary 3.8) 9.22) 1.47 (5.88) 6. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.57) 2. Once absorbed.EPA. interval) 1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.39 (2.12-1.45 (1.58 (1. Survey Geometric mean (95% conf.80-11.24) 75th 2.. Ricceri et al.71) 3.79-13.83-11.62-7.3 (7.25-12. Howard et al.33 (1.5) 5.57-2.1-38. resulting in excess acetylcholine at nerve terminals.85) 4.92) 3.. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.25-11.59) 3.42 (6.89) 4.47 (1. 2005.3) 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 1.12-3.44 (5. TCPy is more persistent in the environment than chlorpyrifos itself (U.22 (6.

Catenacci G. 2005). et al.cdc. 2001). 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. 2005.63(3):218220..6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study).atsdr.S. Environ Health Perspect 2005. the geometric mean urinary TCPy levels were similar in parents and children. J AOAC Int 1999. In Minnesota and South Carolina farmers who used chlorpyrifos.92(2):500-506. Garabrant D.epa. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Haidar S. Burns CJ. urinary TCPy levels in children were reported not to have increased (Hore et al.S. Perera et al. Chlorpyrifos exposure and biological monitoring among manufacturing workers.. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. 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 about a fourfold decrease in urinary levels of chlorpyrifos. et al.. representative subsample of NHANES 19992000 (CDC. population (CDC. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.S. 2003. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. 2005). Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Barisano A.109(6):583-590. Following crack-and-crevice application of chlorpyrifos in their homes. Toxicol Sci 2006. Betta A. In a probability-based sample of 102 Minnesota children aged 3-13 years. Whyatt et al. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U.Reference values of urinary 3.. 2005).. Berent S. 2006). 2005.Organophosphorus Insecticides: Specific Metabolites 2004. 2005. Lotti A....S.S. Betancourt AM. Clayton CA. CDC. Aldridge JE... Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Magnaghi S. References Adgate JL. 1999). Giordani B. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Meyer A. Eberly LE. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. 1992. Environ Health Perspect 2001. Aprea C. Additional information about external exposure (i. 2007). Fourth National Report on Human Exposure to Environmental Chemicals 137 . 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.. Occup Environ Med 2006. Carr RL. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Freeman NC. et al. In Iowa farm families using several different pesticides. Albers JW.EPA. 2002). MacIntosh et al. 2005).e.5. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. 2000). Seidler FJ.gov/pesticides/. U. Burgess SC.. 2005). but levels were roughly four to six times higher than the geometric means in the U. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. but not chlorpyrifos. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.gov/toxpro2. Koch et al. 2005). Curwin et al. 2001) and Italy (Aprea et al. EPA at: http://www.113(8):1027-1031. Levels of TCPy in the U. 2004).html and from U.. Barr DB. environmental levels) and health effects is available from ATSDR at: http://www. Lioy PJ. Of 482 pregnant women living in an agricultural community.. 2004).82(2):305-312.. Slotkin TA..

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Needham LL. Freshour NL. 4/7/09 Koch HM. Kromhout H. Urinary pesticide concentrations among children. Bruun D. U. Int J Hyg Environ Health 2001. Morgan MK.31 Suppl 1:98-104.73:8-15.niehs. Honeycutt R. Levin ED. Environ Health Perspect 2006b. Saunders JH.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F.111(2):201-205. Baker S. Environ Health Perspect 2005. Exposures of preschool children to chlorpyrifos and its degradation product 3.S. Hill RH Jr. Barr D. et al. Weltzien E.114(5):746-751. Camann D.114(10):1542-1546. International Programme on Chemical Safety-INCHEM (IPCS). Bravo R. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Fortuna S. Environ Health Perspect 2006. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Fenske RA. A longitudinal investigation of selected pesticide metabolites in urine. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Executive summary of safety and toxicity information. et al.5. Slotkin TA. Wartenberg D.

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

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

380 (<LOD-.S.200 (<LOD-.S. population from the National Health and Nutrition Examination Survey.2. < LOD means less than the limit of detection.200 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 141 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270) < LOD 659 701 920 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 01-02 is 0.670 (<LOD-1. 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.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 .Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.

Freshwater KJ. Barr DB. Environmental Protection Agency (U. Olsson AO.S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. U. Available at URL: http://www. Third National Report on Human Exposure to Environmental Chemicals.gov/oppsrrd1/ REDs/0018tred. Sadowski MA.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Nguyen JV. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Reprod Toxicol 1998.12(6):619-645. Eigenberg DA. Anal Bioanal Chem 2003. Atlanta (GA).S.epa.376(6):808-815. Centers for Disease Control and Prevention (CDC). September 2000. 2005. EPA).pdf. EPA 738-R-00-010. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals .

and particularly when it was ingested in granular form. and forage crops. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Prior to 2000. 2004). vegetable. It is also used for cattle ear tag applications to control flies and ticks and. population from the National Health and Nutrition Examination Survey.S.EPA. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. but these uses have been phased out. Most granular formulations. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. diazinon was widely used in residential and garden application. diazinon produced wild bird kills before use restrictions were in place.45 (<LOD-3. 1998. 2004). 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. Once absorbed. and other metabolites.S.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. since 2004. diazinon cannot be sold for residential use. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. 2007). in some pest strips. Before these restrictions. Diazinon is not well-absorbed through the skin.7. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). It is toxic to birds.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. which may vary for some chemicals by year and by individual sample.EPA.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. 1998). in the past. 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. but is rapidly absorbed orally (IPCS. fruits. Fourth National Report on Human Exposure to Environmental Chemicals 143 . aerial. seed and foliar applications are planned to be phased out (U. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Inhalational and dermal routes of exposure can be significant for pesticide applicators. an organophosphorus insecticide that is used to control insects on nuts. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks.49 (<LOD-2.S. Estimated intakes from diet and water do not exceed recommended intake limits (U. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.2 and 0. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. USGS.

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

Barr DB. 2006). urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al.S. Environ Health Perspect 2006. Brunet RC. Cocker J. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Sadowski MA. Available at URL: http://www. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. EPA 738-R-04-006. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Baker SE. Ann Occup Hyg 2006. Drug Chem Toxicol 1986. Pesticides in the Nation’s Streams and Ground Water. In 23 children. Drobnis EZ. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Anal Bioanal Chem 2003.S. Banister EW. Semen quality in relation to biomarkers of pesticide exposure. References Anthony J. Biomonitoring studies of 2-isopropyl-4-methyl-6-hydroxypyrimidine provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of diazinon than are found in the general population. Liu F. 2005. Carrier G.inchem. Environ Health Perspect 2003. Fenske RA. 1/14/09 U.44(11):2243-2250. Jones K. revised February 15.. International Programme on Chemical Safety-INCHEM (IPCS). Study for Future Families Research Group. 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. Barr DB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.epa. Pewnim T. 2006). 4/7/09 Lu C.org/documents/ehc/ehc/ehc198. In a small number of men visiting fertility clinics in Missouri and Minnesota. 2007 [online]. Beeson MD. May 2004. The Quality of Our Nation’s Waters. Seifert J. Redmon JB.114(2):260-263. Toepel K. Swan et al. Bull Environ Contam Toxicol 1986. Atlanta (GA). Kruse RL. et al. Centers for Disease Control and Prevention (CDC).134(1-3):105-113. J Expo Anal Environ Epidemiol 2000. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Nguyen JV.htm. Toxicol Lett 2002. Interim reregistration eligibility decision (IRED. Available at URL: http://www. Banister E. Effect of sublethal levels of diazinon: histopathology of liver. Environmental Health Criteria 198. Environmental Protection Agency (U. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Rajendra W.111(12):1478-1484.37(4):501-507.376(6):808-815. Oloffs PC. Noisel N. Biochem Pharmacol 1992. Mason HJ.S. Available at URL: http://pubs. Dumas P. Barr DB. Garfitt SJ.Organophosphorus Insecticides: Specific Metabolites 2005). Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. EPA). U.. Swan SH.gov/circ/2005/1291/. 1992-2001. Third National Report on Human Exposure to Environmental Chemicals. 1998. Diazinon. Geological Survey (USGS). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Diazinon. Bouchard M.10(6 Pt 2):789-798. Olsson AO.50(5):505-515.gov/ oppsrrd1/REDs/diazinon_ired. Irish R. Oloffs PC.pdf. Needham LL. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Driskell WJ. March 2006.9(2):117-131. Barr DB.usgs. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. In 54 Canadian greenhouse workers. Bravo R.

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

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

Hooper K. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Quintana PJ. Ryan PB. A longitudinal investigation of selected pesticide metabolites in urine. metabolite clearance. Flessel P. Bravo R. Toxicol Sci 2003 May. htm. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. and cholinesterase status of date dusters and harvesters in California. Eberly LE.gov/circ/2005/1291/.56(10):2393-2399. Environmental Protection Agency (U.gov/oppsrrd1/REDs/ malathion_red. Neutra R.S. Malathion (addendum). Griffith W. Available at URL: http://www. Am J Public Health 1987. 2007 [online]. Sharma GD. Kedan G. 4/7/09 Kissel JC. Environ Health Perspect 2006. Brunet RC. Gosselin NH.132(4):794-795.9(5):494-501. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. Reproductive outcome in women exposed to malathion.114(2):260-263. Hammerstrom KA. Lioy PJ. Szyfter K. Samuel O. Giri S.usgs. Arch Environ Contam Toxicol 2000. Pluth JM. Blasiak J. International Programme on Chemical Safety-INCHEM (IPCS). Clayton CA.S. Barr DB. Atlanta (GA). revised February 15. Available at URL: http://www. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Weltzien E. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Reregistration eligibility decision (RED) Malathion. Geological Survey (USGS). Harley K.77:1009-1010. et al. Rappaport E. 1992-2001. Environ Health Perspect 2001. Fenske RA. The Quality of Our Nation’s Waters. Malathion deposition.15(2):164-171. Toepel K. Eskenazi B. Environ Mol Mutagen 1993. Carrier G.74(2):following table of contents.38(4):546-553. Available at URL: http://pubs. Curl CL. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. 6/1/09 U. Jewell NP. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.514(1-2):223231. Erratum in: Toxicol Sci 2003 Aug. Lu C.org/documents/jmpr/jmpmono/v2003pr06. J Expo Anal Environ Epidemiol 2005. Centers for Disease Control and Prevention (CDC). Genetic toxicity of malathion: a review. Prasad SB. Needham LL.pdf. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Hertz-Picciotto I. Irish R. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. et al. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. J Expo Anal Environ Epidemiol 1999. EPA 738-R06-030. Environ Health Perspect 2004. O’Neill JP. Petitti D. Bouchard M.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Barr DB. Swan SH. March 2006. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. MacIntosh DL.445(2):275-283. Goldhaber M. Thomas D.112(10):1116-1124. Dumoulin MJ. Trzeciak A. EPA). Nicklas JA.22(1):7-17.epa. Lu C. Harris JA. Freeman NC. Jaloszynski P. Albertini RJ. U. Krieger RI.109(6):583-590. Bradman A. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Giri A. Mutat Res 1999. Barr DB. Pesticides in the Nation’s Streams and Ground Water. et al. July 2006.inchem. Cancer Res 1996. Grether JK.S. Mutat Res 2002. Am J Epidemiol 1990.73(1):182-94. Dinoff TM.

80 (2.92) 5.40) 4. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (2.11-4.20 (2.940 (<LOD-2. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. Increased risk of exposure via dermal.21 (2.0) 3.S. binds tightly to soils resulting in low leachability.44) 2.770 (.40-4.80 (1.50-9.33) 2.10) 22.37-2.67) < LOD 1.10 (<LOD-6.00 (2.50) 2.EPA.26 (1.70 (2.66 (2.92-2. more slowly absorbed through the skin. see Data Analysis section) for Survey years 99-00 and 01-02 are 0..74) 5.70) 2.0) 3.89 (2. Ethyl parathion.33 (1.60) 1.0 (3.70-6. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. 2003).09-1.S.48) 90th 2.730 (<LOD-.41-4.32-3.50) 3. pulmonary.50 (2. was once a restricted-use insecticide with limited applications on certain agricultural crops.58) 3.70-3.30-16.28-4. first registered in 1948.00) 3. fish.62 (1.10) 4.10 (3.61) < LOD 1.28 (1.45) 5.910) < LOD .70 (<LOD-3.90-11. Once absorbed. 2006). which may vary for some chemicals by year and by individual sample.32 (1.300-.40-3.71 (2.10-11.67 (1.20 (<LOD-2.16) < LOD 1..69 (2.S.700 (<LOD-.90 (1. 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 .01) 4.80 (2.47) 2.37-4.36-1.61) < LOD 1.70-6.20-5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.850) < LOD .790 (<LOD-. In animal studies.27) 2. ethyl parathion.85 (2.01-4. with limited applications in agriculture.12) < LOD < LOD 1. all registered uses were voluntarily cancelled (U.860 (<LOD-1.18-3. and aquatic invertebrates. Methyl Parathion.02-6.0) 2.40-4.80) 2.70-6.72 (3.1.00 (2.70) 2. 2000).50 (1.32-1.70) 2.57) 1.46 (3. and has a short half-life in soils and on plants.70 (2.40 (1.69) 4.298-00-0 Ethyl Parathion CAS No.70-3. Many previous registered agricultural uses of methyl parathion have been cancelled (U.22-3. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.19 (.30 (1.21-1.15-3. but by 2003.60 (4.50 (1.01) 695 660 518 679 603 941 Limit of detection (LOD. and eliminated rapidly from the body after absorption (Kramer et al.40) 1.50) 1. and oral routes can occur in pesticide and agricultural workers (Muttray et al.05) 4.0) 3. and to a lesser extent.32-1.50) 3.30-5. Estimated intakes from diet and drinking water have been below recommended limits.60-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.91-3.910) < LOD < LOD < LOD 1. Methyl parathion has low water solubility. Both are toxic to birds.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .0) 3.10 (3. peak domestic use was as high as 5-6 million pounds per year.79) 4.90-9. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 149 . Methyl parathion use is highly restricted.60-19.40) 2.990-1.34 (3.13-1.71 (3. methyl parathion was rapidly absorbed after ingestion.28 (1.37) 2. 2007).50 (1.70 (2.45 (1. 2002.. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.910) < LOD < LOD .37-4.EPA.20) 5. Given its limited use.57-4.10-1. Methyl parathion is not registered for residential use in the United States. on cereal grains.11) 2.60-24.8 and 0. In the 1990s. 1977).0) 4.70 (3. < LOD means less than the limit of detection.50 (1. and of the chemical nitrobenzene.0) 3. Morgan et al.50-14.30-3. population from the National Health and Nutrition Examination Survey.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . It had been applied to cotton.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 1.30 (2.49 (1.60-36.

04) 1. Methyl parathion is not considered genotoxic.840 (.01-3. 1991).00) 2.680 (<LOD-1. Slotkin et al.78-2.690-1.33-3.940 (<LOD-1.95) 1.23) 1.09) 2.01 (2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.870) < LOD . 2004).55) 2..93 (2. 2005.67 (3. gov/pesticides/.79) 1. Lores et al.89 (2. WHO.44-3.90 (1. Orsorio et al.83 (1.13) 4.43) 4. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. 1995).00 (1. Additional information about external exposure (i.11-4.00 (1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.61) 4.930 (.430 (.830-1. does not inhibit acetylcholinesterase enzymes. paralysis.55 (<LOD-3.33-6. and other metabolites.10) 90th 2. paranitrophenol.35-3.86 (2.310-.21-21.78 (2.04 (2. At high animal doses of methyl parathion.EPA considers methyl parathion unlikely to be carcinogenic to humans. accidental exposure. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.56-2.44-3.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 1995. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.07 (1. Karanth and Pope et al.60 (1.2) 2.88) 1.17) . and unintentional acute or chronic high-level occupational exposure (Hill et al..1) 2. methyl parathion. 1990.94-4.70) 3.72-2. Zurich et al.S.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .500) < LOD < LOD .97 (2. vomiting.17-4. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.67-2.39 (1.60-2.92 (2.S.80 (1.2) 2..79 (1. weakness.76-14. Parathion and methyl parathion have high acute toxicity in animal testing.e. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. ethyl parathion.25 (2.89 (2.71 (1..60) 2.26) 17.9) 1. and seizures. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. U.80 (1.10 (1.21) 1.08) < LOD .15-10.41-2.980 (..html and from U.20) 3.57-2. gov/toxpro2.78-2.31) < LOD . teratogenic.82) < LOD .30-1.37-1.08-3.epa.Organophosphorus Insecticides: Specific Metabolites Metabolites”).11) 1. 2006. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.91 (1.14-3..440 (<LOD-.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th .91) 1.370 (<LOD-. 2003.05) 4.30) 3.16-4.atsdr.01 (. EPA at: http://www. resulting in excess acetylcholine at nerve terminals. cholinergic effects.57) 6.7) 3.640) < LOD < LOD 1.33-3.880 (.530) < LOD < LOD < LOD . but lists ethyl parathion as a possible human carcinogen.800-1.790-1.970 (. In addition to being a metabolite of methyl and ethyl parathion.850-1. Methyl Parathion.57-7..29) 1.3) 2.35-3.S. population from the National Health and Nutrition Examination Survey.cdc.08 (1.38-3.73 (1. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.20) .15) 3.930 (.87 (1.71) 1.. 2004).96 (1.720 (<LOD-.48-4. Thus.07) 2.13-12. 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.94-47.720-1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.96 (1.77-7.25) 1.4 (3.78) 2.97 (<LOD-4.970 (.59 (1.88 (1. 150 Fourth National Report on Human Exposure to Environmental Chemicals .950) < LOD . 2006.540) < LOD . 1978.39) 1.730-1. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.84) 3.400 (<LOD-. Survey Geometric mean (95% conf.29) 2.97-10. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.82 (2. environmental levels) and health effects is available from ATSDR at: http://www.98-7.20 (3. Jaga and Dharmani.26 (1. The metabolite. and producing acute symptoms such as nausea.29 (2.31-3. In large doses.790-.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .

1999). 2005.71:99108. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S..215(3):182-190. ACGIH recommends a BEI of 0. Lores EM. Pesticide workers may have much higher levels following pesticide applications. Costa LG.. Environ Health Perspect 2002. Available at URL: http:// www. 2002. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Environ Health Perspect 2004.. 2005). et al. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention (CDC). Methyl parathion: an organophosphate insecticide not quite forgotten.inchem.9:311-320. and many residents were symptomatic (Barr et al. Karanth S. Lin LI. Hetzler HL. 1995. Hryhorczuk DO. Barr DB. CDC. Pathak S. Slach EF. Lu C.. Rev Environ Health 2006. McCann et al. Runkle KD. In a study of workers who handle parathion.. 2005. Arch Environ Health 1978. et al. Ashley DL. Baker RC. et al. Morgan DP. Clark JM. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Griffith W. Gregg M.. Needham LL. Alley CC. Pope C. Role of individual susceptibility in risk assessment of pesticides.5 mg (500 µg)/g creatinine for workers at the end of shift.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. References Barr DB.33(5):270-276. Cline RE. Parathion-Methyl (addendum). Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Shealy DB. 2005.56(7):449553. International Programme on Chemical Safety-INCHEM (IPCS). 2005).21(1):5767.htm. Rockhold RW. 4/7/09 Jaga K. Occup Environ Med 1999. 1995). 2004). Turner WE.15(2):164-171. Head SL. 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. Hill RH Jr. Laboratory investigation of a poisoning epidemic in Sierra Leone. J Expo Anal Environ Epidemiol 2005. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. a range of values several hundred times higher than levels found in the U. McClure PC.25(5):599-606. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. 2002). Jewell NP. Moseman RF. Neurotoxicol Teratol 2003. 2002.14(4):213-216.. Pesticide residues in urine of adults living in the United States: reference range concentrations. Leng G. Rubin et al. Barr DB. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. McCann KG. 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. Dharmani C.110 Suppl 6:1075-1078. Weltzien E. Baker SE. Baker S. Bradman A.112(10):1116-1124.org/documents/jmpr/jmpmono/v95pr14. Hill et al. J Biomed Sci 2002. Kedan G. Bailey SL. 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. Lewalter J. Bradway DE. et al. Kissel JC. Giordano G. Hill RH Jr. Head SL. population (Olsson et al. Arch Environ Contam Toxicol 1977.110 Suppl 6:1085-1091. Chicago area methyl parathion response. Atlanta (GA). Harley K. and levels were similar or slightly lower that those in a small convenience sample of the U. Barr JR. general population (CDC. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Environ Res 1995. Eskenazi B. Toxicology 2005. 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. oral or dermal administration.S. DiPietro E. Barr DB. Moomey CM. Wellman SE. Curl CL. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. et al. J Anal Toxicol 1990. Guizzetti M. Kramer RE.6(2-3):159-173. Environ Health Perspect 2002.

1/12/07 U.162(2-3):219-224. Environmental Protection Agency (U. Available at URL: http://www. Am J Ind Med 1991. Olsson AO. Monnet-Tschudi F. 1995-1996.S.110 Suppl 6:1047-1051. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. R. Environ Health Perspect 2006. EPA-738-FOO-009. 1992-2001. Methyl parathion in drinking water. 0153.20(4):533-546. Honegger P. EPA). Tate CA. Ames RG. Ethyl parathion. Investigation of a fatality among parathion applicators in California. May 2003. Available at URL: http://pubs. Rosenberg J. Nguyen JV. Mengle DC. Toxicol Lett 2006. The Quality of Our Nation’s Waters. Sadowski MA.who.epa. Facts.gov/oppsrrd1/REDs/factsheets/0155fct.376(6):808-815.gov/circ/2005/1291/. Pesticides in the Nation’s Streams and Ground Water. WHO/SDE/WSH/03. 1/14/09 U. revised February 15. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.int/water_sanitation_health/dwq/chemicals/ methylparathion.114(10):1542-1546. Case No. Backer G. Yacovac R. Hill RH Jr.S. Anal Bioanal Chem 2003.E. U. Geological Survey (USGS).pdf. 6/1/09 World Health Organization (WHO). March 2006.04/106. Levin ED. September 2000. Available at URL: http://www. Environ Health Perspect 2002. Esteban E. Hill G. Rubin C. Osorio AM. Toxicol Appl Pharmacol 2004. et al. EPA).S.201(2):97-104.epa.S. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Ryde IT. 5/19/09 Zurich MG. 152 Fourth National Report on Human Exposure to Environmental Chemicals . pdf. gov/oppsrrd1/REDs/methylparathion_ired.S. 2004. Available at URL: http://www.usgs. Dunlop B. 2007 [online]. Environmental Protection Agency (U. Slotkin TA. Kieszak S. 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.D.pdf. Jung D. Barr DB. Ohio. Costa LG. Schilter B. External and internal exposure of wine growers spraying methyl parathion. Seidler FJ. Letzel S.Organophosphorus Insecticides: Specific Metabolites Muttray A.

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

55) .210-1.840 (.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.210-.780 (<LOD-1.07) .410 (<LOD-1.17 (. population from the National Health and Nutrition Examination Survey. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey.580-1.21) < LOD .27) .700-.780 (<LOD-1.760 (<LOD-. Survey Geometric mean (95% conf.840) 669 687 929 Limit of detection (LOD. < LOD means less than the limit of detection.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.680 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 01-02 is 0.S.820) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.670 (<LOD-1.15) < LOD .200-.2.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700-1.S.950) < LOD < LOD 1.31) .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 . interval) Selected percentiles ( 95% confidence interval) Sample 95th .740 (.470 (.430 (<LOD-.780 (.300-1. which may vary for some chemicals by year and by individual sample.850 (.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .780 (.500 (.250 (<LOD-.94) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .740-1.610 (<LOD-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .64) .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .210 (<LOD-.

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

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

. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al.atsdr. Elwan et al. Hu JY.gov/toxpro2. 2003.S.. 1991. Lee SJ. et al. Sugiri D. Environ Health Perspect 1999. Kim TS..107(3):173-177. epa. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. 2002. Kuhn K. J Reprod Dev 2004. Elwan MA. salivation...300(3):161-165. and permethrin) in the Hershberger and uterotrophic assays. and seizures (ATSDR.html. EPA at: http://www. Fredriksson A. Neurotoxicol Teratol 2005. 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. Ranft U. Neurosci Lett 2001.205(6):459-472.html. Leng G. Available from URL: http://www.251(3):855-859. Moniz et al. Eriksson P. 1999. Go V. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats..atsdr. Kunimatsu et al.27(12):1273-1283. Lazarini et al. 2005). Kunimatsu T. Toxicol Appl Pharmacol 2006. et al. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Additional information about pesticides is available from U. hypersensitivity.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Lazarini CA. Wolff MS. Kim et al. Sunami O. 2003. tremor. 2005). Kamita Y.8(1):197-202. bioallethrin and deltamethrin. Estrogenicity of pyrethroid insecticide metabolites. Richardson JR. Kim HS. cdc. Salzgeber SA.1/15/09 Aziz MH.23(6):665-673. Lewalter J. 2002). IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Idel H. Bull Environ Contam Toxicol 1999. Adhami VM. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Soderlund et al. Levsen K. 2005). 2003. Florio JC. Pogo BG. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Shaw IC.. Kang IH. Bernardi MM. Song L. Toxicological profile for pyrethrins and pyrethroids. Xenobiotica 1997.gov/pesticides/ and from ATSDR at: http://www. Leng G.. Leng A. Int J Hyg Environ Health 2002. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Kim IY. Go et al.8(1):18-21. 2004. Garey J. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Zhao RC. Pauluhn J. Abell AD. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Shin JH. Garey and Wolff. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Shafer..cdc. McCarthy AR. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. 2001.gov/toxprofiles/ tp155. Idel H. 2002). Moniz AC. Kuhn KH. fenvalerate. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Caudle WM. Pyrethroid pesticide-induced alterations in dopamine transporter function.. Neurotoxicol Teratol 2001.. neurochemical changes in cholinergic.27(4):609-614. Wolff MS. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicol Appl Pharmacol 1991. In California. Bernardi MM. and striatal dopamine levels in male and female rats.50(2):245-255. Spinosa HS. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. 2005). Ose K. Guillot TS. Regul Toxicol Pharmacol 2002. Berger-Preiss E. WHO. motor activity. Chen JH. Lemonica IP. J Environ Monit 2006. September 2003. Miller GW. Varoli FM. Okuno Y. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Neurotoxic effects of two different pyrethroids. McCarthy et al. Yamada T. Eriksson and Fredriksson. Yang J.211(3):188-197. choreoathetosis. Ray et al. Hu et al.. Thomson BM. Seth PK. et al. Generally. 2006). Wieseler B. In developing rodents. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002.. et al.62:101-108. 2006.108(1):78-85. 2000. 2001. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Biochem Biophys Res Commun 1998. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Agrawal AK. Leng G. 2003. 2006.35(2 Pt 1):227-237. Shukla Y. Cruz-Casallas PE. Garey J. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. dopaminergic. Wang SL. 1998. Effects of prenatal exposure to deltamethrin on forced swimming behavior.

Spencer J. Shafer TJ. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Environmental Protection Agency (U.who.usgs. 5/26/09 U. Environmental Protection Agency (U. Forshaw PJ. Meyer DA. Soderlund DM. O’Malley M. Environmental Protection Agency (U.38:95-101. 5/26/09 U. et al. Available at URL: http://www.S.gov/oppsrrd1/REDs/cypermethrin_red. U. Sheets LP. Available at URL: http://whqlibdoc. J Toxicol Clin Toxicol 2000. 2005.10. Pyrethroid insecticides: poisoning syndromes.gov/ circ/2005/1291/.htm.S. World Health Organization (WHO). EPA).epa. Lesser JE. EPA).S. March 2006. Available at URL: http://www. Crofton KM.113(2):123-136.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.S. Revised February 25.pdf. Sargent D. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).S. Available at URL: http://www. Reregistration Eligibility Decision for Cypermethrin. synergies. Pyrethroid illnesses in California. sumithrin synthetic pyrethroids for mosquito control.186:57-72. June 2006b. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. June 2006a. April 2002.22(8):983-991. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . 1992–2001.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. pdf.epa. Geological Survey (USGS). Mullin LS. Available at URL: http://pubs.epa. 5/26/09 U. Piccirillo VJ. EPA).171:3-59. resmethrin.S. Marsh JR.S. Clark JM. 5/26/09 Woollen BH. Pesticide and Evaluation Scheme.Pyrethroid Pesticides Ray DE. Xenobiotica 1992. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Pesticides in the Nation’s Streams and Ground Water. 2007. and therapy.htm.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Toxicology 2002. Laird WJ. Environ Health Perspect 2005. 19962002. Safety of pyrethroids for public health use. Rev Environ Contam Toxicol 2006. Permethrin.

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

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 831 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 701 594 957 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.2 and 0. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.2. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 160 Fourth National Report on Human Exposure to Environmental Chemicals .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

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

Hoppe HW. Idel H.46(3):281-288. Drexler H. Heudorf U. Becker K. Barr DB.186:57-72. Int J Hyg Environ Health 2003. et al. Kolossa-Gehring M. Int Arch Occup Environ Health 2004. Third National Report on Human Exposure to Environmental Chemicals. Hadnagy W. Rev Environ Contam Toxicol 2006. Krieger RI. Seiwert M. Butte W. Ranft U. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. 2005. Atlanta (GA). Ball M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Arch Environ Contam Toxicol 2004. Int J Hyg Environ Health 2006. Environ Health Perspect 2001.209(3):221-233. Spencer J. Int J Hyg Environ Health 2006. Pyrethroid illnesses in California. 19962002. Williams RL. Centers for Disease Control and Prevention (CDC).Pyrethroid Pesticides References Baker SE.209(3):293-299. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Angerer J. Bernard CE. Angerer J. Leng G. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Schulz C. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.206(2):85-92. Angerer J. O’Malley M. Olsson AO. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Heudorf U. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Berger-Preiss E. J Expo Anal Environ Epidemiol 2003.13(2):112-119.109(3):213-217. Sugiri D.77(1):67-72.

340) .270 (.180) .28) 671 680 518 701 591 957 Limit of detection (LOD.890 (. 1985.710-1.740-2.570 (.110-.780) .220) .790) .500 (.270 (.200) < LOD < LOD < LOD .250 (. and trans-cyfluthrin.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. Survey Geometric mean (95% conf.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .790-1.220-.960 (.43) . but can also reflect exposure to trans-3(2.630 (. Similarly.240) .120-.330) .54) .910-5.610) .210) .280-.77 (.900 (.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 .140 (<LOD-. cis-permethrin.740 (.380 (.47 (.630) .640 (. but it can also reflect exposure to cis-3-(2.580) 1.340-.350) .13 (.430-.80) .690) .35) 1.120-.730 (.730 (.630-.150 (..110-.160 (<LOD-.270 (.330 (.220-.2-Dichlorovinyl)-2.. ciscypermethrin and cis-cyfluthrin.220-.230) .262) * * * < LOD < LOD .2-dichlorovinyl)- CAS No.120-.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .08) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.490-.380) .410) .50) .680 (.200 (.490-1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.600-1.15) .202 (.2-dichlorovinyl)2.460-.68) .870) 1. population from the National Health and Nutrition Examination Survey.24) 1.300-. and ciscyfluthrin. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.370 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.300 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.160 (.200-.740) 1. In the body.310) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.510 (.700) .140 (.670-1.630) .770-1. Biomonitoring Information Urinary levels of cis.510 (.240) .or trans-3-(2.340) . The presence of cis-3-(2.and trans-isomers.730 (.110-.300 (.11) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George. trans-cypermethrin.680-3.580-1.820 (.200-.710) . Fourth National Report on Human Exposure to Environmental Chemicals 163 .370-.460-1.200) .1 and 0.600 (.07 (.12 (.68359-37-5 Cypermethrin Permethrin CAS No. 1985.180 (.200) .790 (.890 (. 1999).650-1.170 (.2-dichlorovinyl)-2.880 (.490-. Generally.68) . the presence of trans-3-(2.260 (.220-.2-dichlorovinyl)-2.550) .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.110 (<LOD-.53) .300-. Kuhn et al. transcypermethrin and trans-cyfluthrin.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.770) .670 (.740-1. 1999). cis-3-(2.380-.610) .210-.2dichlorovinyl)-2.520) .470 (.35) .270-. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.920) 1.68 (.950-2.490-1.21) .600) . Kuhn et al.380-.380-.470-1.850 (. The chemical trans-3(2. trans-permethrin. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. cis-cypermethrin.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin. more of the trans-metabolite than Urinary cis-3-(2. < LOD means less than the limit of detection.2-dichlorovinyl)-2.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .44 (.420-.200-.210) 90th .570-. 52315-07-8 CAS No.400-.510 (.2dichlorovinyl)-2.32) .530 (. which may vary for some chemicals by year and by individual sample.670-2.670-1.460 (.120-.440 (.790-1.250-.500 (. Cyfluthrin. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.1.155-.410) .280 (.160 (.

In the same residents.59) .300-. 2003).280-.59) .190) . 2006).840 (.410) .260-.290) .120 (.170 (.170) < LOD < LOD < LOD .2-Dichlorovinyl)-2. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al..400-1.and trans-3-(2.890 (.230-.S.450-1.550 (.11 (.350 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. In a study of volunteers.250) . Studies in Germany of 396 children and adolescents (Becker et al.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin. In a study of urban residents in Germany (Berger-Preiss et al. 2003). population from the National Health and Nutrition Examination Survey.2dichlorovinyl)-2.390 (.170 (. 2004).550) .. median urinary levels of trans-3-(2.430-1. urinary levels of cis-3-(2.31) . Schettgen et al. 2002).160 (<LOD-.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.2-dichlorovinyl)-2..11) . 2005).780) 1.250-. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.138 (.390-.240 (<LOD-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .290-.320-.37) .80) .370-.220 (.260 (.350) .560) 1.290) .200) .. 2005) In a small group of indoor pest-control operators.810 (. 2005).700-2.690-1.080-.29 (. 2001) showed urinary levels of cis. representative NHANES 2001-2002 subsample (CDC.300 (. Lu et al. Other studies have provided evidence that urinary levels of cis.24) .12 (.680-1.640) 1.580-1..210-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .370-.21) . Survey Geometric mean (95% conf...700) .. 2001. urinary trans-3-(2.270 (. post- Urinary cis-3-(2.550-1.190) .49) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.600 (.250) 90th . Cyfluthrin..750 (.710-3.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.430 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.380 (.260 (. the median and 95th percentile of urinary levels of cis-3-(2.270) . 2006).14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.560) .550) .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 .400 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.420 (.540 (.200-.12-2. 2002).180-.180 (. 2006.380-.150-.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.680-1. 164 Fourth National Report on Human Exposure to Environmental Chemicals .S.700) .67 (. 2006) and 1177 urban adults and children (Heudorf et al.200 (.880) .640-.590 (.300) .250 (<LOD-.530 (.750-1.33 (.510-1. 2005).390-.59 (1.440-.440 (.2dichlorovinyl)-2.190 (.250-.500 (.182) * * * < LOD < LOD .Pyrethroid Pesticides 2.260 (.150-.03) 1.67) .2-dichlorovinyl)-2.11) 1.270) .780 (.340-.830) .290 (.300) . 2006.470-1..370-.230 (.640-1.340) . 2005).580) . In these volunteers.360-1.260) .890) .540) .900 (.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.640 (.11) .800 (.440 (.570) .540 (.220 (.440-.250-.104-.640-1.590) .550-1.680 (.920 (.340) .2-dimethylcyclopropane carboxylic acid did not increase.220) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.250) .130-.230-..270-.380) .320) .2-dichlorovinyl)-2.450-. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.840 (.200-.280 (.710 (.530 (.430-.450 (.140-.and trans-3(2. 2004.230-.150-.33) .300 (.

35) 1.410 (<LOD-.500-.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.07 (1.28 (1.25 (1.37 (1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.420 (<LOD-.12-6.970 (.520) .49-3.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .41-14.63) 1.68) 2.39-5.670) .480-.97-11.20 (.23 (.54) 4.23) 2.820) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.49-3.95) 2.520-.85) 4.77) 2.and trans-3-(2.2-dichlorovinyl)-2.55-4.60) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.01 (1.730) .2dichlorovinyl)-2.90) 1.830-1.560 (.66) .59 (1.69 (1.14-2.60-4.26 (.Pyrethroid Pesticides application median urinary levels of summed cis. Fourth National Report on Human Exposure to Environmental Chemicals 165 .17-1.40 (1.64-4. The maximum post-application urinary levels. 2005).860) .63) 1.S. which may vary for some chemicals by year and by individual sample. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.55-5.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.43) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.09 (.16) 1.39 (1.670) .660) 1.08) 1.500) .56 (1.410-.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 .710 (. Urinary trans-3-(2.560 (.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.41 (1.910-1.08-4.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.780 (.62 (1.50 (1.4 and 0.680-1.5) 2.77 (1.87 (1.610) 1.76-4.42) 1.17 (. population from the National Health and Nutrition Examination Survey.700) .89 (2.08-6. Survey Geometric mean (95% conf.460-.14) 1.19) 1.470 (<LOD-.81) 2.560 (.55-3.7) 2.760) . were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .550 (.2-dichlorovinyl)-2.11-1.810-1.400 (<LOD-.42 (2. Finding a measurable amount of cis.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .17 (. < LOD means less than the limit of detection.01) 4.460-.800-1.49-5.570) 90th 1.84 (1.13) .95) 3. trans-Cypermethrin.68) 1.22 (1. 2005).48) 4.620) < LOD 2.54 (1.68-2.2-Dichlorovinyl)-2.920-1.940 (.68-3.28 (2.490 (<LOD-.76-3.440 (<LOD-.91 (1.56) 2.20 (.580 (.03-1.77) 1.500 (.or trans-3-(2.850-1. Biomonitoring studies on urinary levels of cisor trans-3-(2.910-1.68) 1.840-1.410 (<LOD-.400-.700-1.56 (1.750) .19 (2.66) 691 680 518 690 595 954 Limit of detection (LOD.10) 2.94 (1. however.14-6.470 (.20 (.530) .69) 1.11-2.4.03-1.60) 1.07-3.56) 2.19 (3.25-3.410-.27 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.490-1.

64 (1.20-2.07-1.750) .850-3.470 (.880 (.00) 1.15-3.19) .11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.570-. trans-Cypermethrin.670) .800-1.30-3.68) 3.42) 1.45-2.11) .520 (<LOD-.07-3.S.640) .700 (.57 (1.570 (<LOD-.720-1.47-2.28) 2.07) 2.55 (2.2-Dichlorovinyl)-2.61) 1.720-1.850) 1.930-1.35) 1.47-2.34-3.410-.26 (1.75 (1.36 (1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .74) .02-1.700-.12 (.880-1.15) 2.500-.48-2.12-1.880 (<LOD-1.56 (1.3) 2.660) .60) 2.89) 2.31 (.65) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.39) 1.530 (<LOD-.16 (1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.480-.900 (<LOD-1.00) 5.15) 3.780) .81 (2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.720 (<LOD-.08 (.87) 1.13) 1.29) 1.98 (1.40-2.56-2.22-2.13) .45 (1.07) 2.35 (1.55 (2.970 (.60 (1.33 (1.91-11.87-8.560 (.27-2.70 (.44) 2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.91) 1.07-2.780) 90th 1.15 (1.580) .87-3.700 (.740) .33-2.730) .19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .850) .80) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.91 (1.37 (1.41) 1.440-.87) 1.34-4.530 (.33-1.87 (1.760 (.56-5.57) 3.820-2.00-5.780 (<LOD-.19 (1.800-1.Pyrethroid Pesticides Urinary trans-3-(2.36) 2.42 (.470-.15-3. population from the National Health and Nutrition Examination Survey.65 (2.31 (2.00) 1.60) 2.540) .48 (1.30-6.22-1.55 (2.67 (2.00 (1.15-3.20 (1.27-2.74) 2.770) < LOD 2.08 (.47 (1.570 (.610-. Survey Geometric mean (95% conf.31) 1.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .86 (2.580 (.39 (1.22) 1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .

Ranft U.68(6):1160-1163. Berger-Preiss E.62:101-108. Hardt J.76(7):492-498. Idel H. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Berger-Preiss E.109(3):213-217.77(1):67-72. Pearson M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Int Arch Occup Environ Health 2003. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Bartell S. Leng G. Kolossa-Gehring M.205(6):459-472.Pyrethroid Pesticides References Becker K. Angerer J. Int J Hyg Environ Health 2006. Wieseler B. George DA. Int Arch Occup Environ Health 2004. Angerer J. Lu C.209(3):293-299. Angerer J. Permethrin and its two metabolite residues in seven agricultural crops. Schulz C. Sugiri D. Biological monitoring of workers after the application of insecticidal pyrethroids. Heudorf U. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Schettgen T. Seiwert M. Atlanta (GA). Environ Health Perspect 2001.134(1-3):141-145. Angerer J.114(9):14191423. Bravo R. Sugiri D. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. J AOAC 1985. Bull Environ Contam Toxicol 1999. Angerer J. Hoppe HW. 2005. Butte W.206(2):85-92. Heudorf U. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2006. Kuhn K. Int J Hyg Environ Health 2003. Barr DB. Leng G. Environ Health Perspect 2006.209(3):221-233. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Ball M. Ranft U. Drexler H. Idel H. Leng G. Hadnagy W. Heudorf U. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2002. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Heudorf U. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Drexler H. Idel H. Levsen K. et al.

2-dibromovinyl)-2..2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dibromovinyl)2. 2005). In an analysis of 217 urine specimens from a nonrandom sample of United States residents..2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dibromovinyl)-2.2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2. deltamethrin has been used against mosquitoes that carry malaria.2-dimethylcyclopropane carboxylic acid in the environment (IPCS..1 μg/L) for the NHANES 2001-2002 subsample (CDC. 1990).2-dibromovinyl)-2.. Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2. 2001.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.. Baker et al.S.2-dibromovinyl)-2. 2005). Finding a measurable amount of cis-3-(2. 2004). Urinary levels for adults and children in these studies were similar (Heudorf et al. 168 Fourth National Report on Human Exposure to Environmental Chemicals .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. Following residential spraying with deltamethrin for malaria protection in Mexico. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. 2006) and 1177 urban adults and children (Heudorf et al.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2dimethylcyclopropane carboxylic acid formed in the environment..2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. 2001) showed that urinary levels of cis-3-(2. in detection of cis-3-(2.2-dibromovinyl)-2. Deltamethrin can degrade to cis-3(2.Pyrethroid Pesticides Deltamethrin CAS No.5 μg/L) than the detection limit (0. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dibromovinyl)-2. Thus. Studies in Germany of 396 children and adolescents (Becker et al.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. mean peak urinary levels of cis-3-(2. Outside the U. in some situations replacing the use of DDT. (2004) reported a geometric mean concentration of cis-3(2. In the NHANES 2001-2002 subsample.3-0. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.39 µg/L.2-dibromovinyl)-2. 2005).2-dimethylcyclopropane carboxylic acid of 0. urinary levels of cis-3-(2.

< LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD.1 and 0.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 . Survey Geometric mean (95% conf.1. population from the National Health and Nutrition Examination Survey.2-Dibromovinyl)-2.S.Pyrethroid Pesticides Urinary cis-3-(2.

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

Angerer J. Heudorf U. Heudorf U.Pyrethroid Pesticides References Becker K. Angerer J. Seiwert M.77(1):67-72. Environ Health Perspect 2005. Int J Hyg Environ Health 2006. Batres LE. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www. toxicokinetics. Grimaldo M.htm.109(3):213-217. Schulz C. Int J Hyg Environ Health 2006. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int Arch Occup Environ Health 2004. Angerer J. 2005. Ball M. Torres-Dosal A.209(3):221-233. International Programme On Chemical Safety (IPCS). Lopez-Guzman OD. [online] 1990. Environ Health Perspect 2001. Angerer J.113(6):782-786. Deltamethrin. et al. Butte W.inchem. Environmental Health Criteria 97.209(3):293-299. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Drexler H. Centers for Disease Control and Prevention (CDC). 5/26/09 Ortiz-Perez MD. et al. Kolossa-Gehring M. Carranza C. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.org/documents/ehc/ehc/ ehc97. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Hoppe HW. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Heudorf U. Atlanta (GA). and genotoxicity in exposed children.

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

28) 1.34) 8.26-2.26) 2.34 (2.73) 1.260 (.18 (1.362) .940) 1.51-3.35) 2.610) .25-1.560-1.64) 697 680 524 701 603 957 Limit of detection (LOD.292-.190-.590-.45 (2.990) .300 (.16-1.05) .12) .04-5.23 (2.55 (1.250 (.36) 1.1) 3.8) 3.14-6.295) .238-.52-4.800) 1.32 (2.41-2.51-6.550-.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.250 (. interval) .12 (.50 (2.640 (.700-1.27-2.35 (2.1.29-1.49 (1.740 (.590 (.65 (1.240 (.200-.25-7.04) .406) .490-. population from the National Health and Nutrition Examination Survey.33 (1.290 (.03 (3.355) .350-.325 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .297 (.298 (.520 (.311 (.830) 90th 1.200-.750-1.430-.27-11.454 (.570-.38 (2.260 (.45-5.44) 5.840-1.276-.700 (.92-3.270) .05) 1.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .680 (.69 (1.26) 2.230 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .586) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .330) .427) .30 (.315 (.340) 75th .41 (1.75 (1.32 (1.820) .292 (.830-2.1) 3.288 (.273 (.41-3.60) .63 (3.267 (.230 (.340) 1.390) .336 (.277-.320) .320) .507 (.240 (.260 (.314) .246-.265-.190-.420) .54) 1.227-.16) 1.48-2.364) .48-2.32-21.430-.62) 5.38 (2.470-.750) .190-.27-2.373) .21 (2.417 (.210-.260-.730 (.850) .450 (.266-.210-.750) .49-2.30) 3.434) .53) 1.18 (2.S.52-5.78) 1.780) 4.560-.300 (.63-3.820) .230-.226-.960 (.01 (1.800 (.870 (.33) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.46) 2.72 (1.510-.271-.90) 1.65-2.220-.49-2.600 (.510-.25-4.83-11.49 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.78 (1.81 (1.39) 2.530-.25 (2. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.34-6.43) 3.86 (1.314 (.384) .1) 3.89-71.35 (1.71 (1.740 (.200-.247-.340) .352-.233-.490) .320 (.78) 1.330) .710 (.180-. Survey Geometric mean (95% conf.670 (.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 .250 (.320) .33 (2.76 (1.93 (1.25 (2.570-1.370) .328 (.35) 2.530-.69) 3.650 (.360) .42-2.160-.13) .1 and 0.288-.53-3.630) .190-.369) .300 (.710 (.79) 3.280 (.560-.387) .253-.760 (.850) .02-6. Deltamethrin.78) 6.428-.250-.230-.13 (.601) .620-1.353 (.56-5.41) 3.230-.62-8.160-.12) 4.595) .270 (.440) .30 (1.320) .35) 1.300) .62-6.810) 1.321 (.46) .

00) 1.00) 1.91) 9.750-1.300-.530-.216-.280 (.270) .250) .190-.720) 90th 1.370-. Survey Geometric mean (95% conf.590) .420-.88-5.250 (.510 (.44) 2.274 (.55 (1.00) 5.240 (.41-4.328) .270-.278) .63) 1.13 (.730) .580) .91) .63-3.510 (.320) .810) 1.640 (.S.81 (1.73-4.202-.264 (.480-.446) .21-4.930) 1.550 (.378 (.07) 2.43-64.250 (.06-3.240-.460-.90) 3.17-1.372) .60-4.272 (.590-1.311 (.19-6.02-1.534) .36-6.240-.261 (.19) 2.280 (.40 (1.67) 1.440-.401) .03-1.51-7.350 (.350) .510 (.640 (.02 (2.238-.730-1.225-.860 (.48 (1.04 (.35-3.60) 1.94 (1.95) 1.677) .590) .17 (.62) .43) 1.490-.09 (.09) 3.229-.280 (.67 (1.240 (.270) .270 (.44 (1.335-.80) 4.550 (.365) 99-00 01-02 99-00 01-02 99-00 01-02 .190 (.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 .22 (1.150-.740) .370 (.220 (.35 (1.560 (.13-1.43 (1.423 (.200-.49 (1.960-1.730) .210 (.380 (.540 (.329) .329) .650) .35) 1.500) .173-.400-.330) 1.67 (1.05-3.550 (.72 (1.290) .49-2.210 (.490 (.760) .96 (1.11 (.73) 1.200-.246 (.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .450 (.309) .21 (1.09-2.10 (2.670) 3.840-1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.330 (.61-2.91 (2.210-.227 (.580 (.570) .36 (1.27) 1.670) .410) .860-1.52) 2.610 (.460-.74) 3.83 (1.440-.234 (.83) 1.200-.04 (3.330) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.930) .330) .270 (.362 (.280-.178-.224-.15-2.25-2.261-.700-1.55) 3.16-4.300-.271-.53 (1.253) .03 (.54 (1. population from the National Health and Nutrition Examination Survey.290) .410-.440-.230-.330) 75th .32 (2.91-4.49) 3.240 (.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .321-.630) .530-.437) .25) 2.357) .37 (1.25-5.310) .240 (.0) 3.62) 1.720 (.299-.275 (.390-.52 (1.309 (.387) .280) .400-.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .240-.272) .75-8.09-2.323 (.39) 1.312 (.274-.200-.490 (.07-5.13-1.64-5.230) .220-.230-.84 (1.590) .380-. Deltamethrin.400) .240-.226-.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.11 (.316 (.280) .190-.35) .480 (.860-1.160-.19 (2.40) 2.43 (2.49) 1. interval) .41) 1.290-.37) 1.86 (1.

urban cohort. Environ Health Perspect 2005. Idel H. and genotoxicity in exposed children. Environ Health Perspect 2003. Angerer J. Sugiri D. Angerer J. Becker K.114(9):14191423.206(2):85-92. Biological monitoring of workers after the application of insecticidal pyrethroids. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Hoppe HW. Liu Z. et al.113(6):782-786.205(6):459-472. Hadnagy W. Obel J. Sugiri D. Lapinski R.209(3):221-233. Atlanta (GA). Environ Health Perspect 2006. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Berkowitz GS. Indoor pyrethroid exposure in homes with woollen textile floor coverings. 2005. Torres-Dosal A.Pyrethroid Pesticides References Baker SE. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. et al. Olsson AO. Grimaldo M.76(7):492-498. Idel H. Exposure to indoor pesticides during pregnancy in a multiethnic. Int J Hyg Environ Health 2006. et al. Seiwert M. Godbold J. Ortiz-Perez MD. Third National Report on Human Exposure to Environmental Chemicals. Ball M. Int J Hyg Environ Health 2003. Kolossa-Gehring M. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Arch Environ Contam Toxicol 2004. Ranft U. Int Arch Occup Environ Health 2003. Batres LE.111(1):79-84. Lopez-Guzman OD. Bravo R. Pearson M.46(3):281-288. Ranft U. Deych E. Int J Hyg Environ Health 2002. Levsen K. toxicokinetics. Leng G. Centers for Disease Control and Prevention (CDC). Carranza C. Hardt J. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Bartell S. Lu C. Barr DB. Berger-Preiss E. Leng G. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Barr DB. Berger-Preiss E.

126 (.390-.220-.280) .170 (.170-.154) .560) .230 (.440 (.400) .169 (.190) .230 (.330-.145 (. see Data Analysis section) for Survey years 99-00.120) .180-.110-.180) .140 (.137) .250 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and as a fire-retardant in textiles and plastics.160) .390-.310) .170-.180-.180 (.140) .190-.130 (.190-. ceramics.04.150) .280-.440) .230-.230-.130-.470) . Workplace exposures can occur at smelters.250 (.131-.190 (.460) .370-.260) .190 (.130-.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 .400) .260) .320) .260) .140) .099 (.310 (.150-.158 (.250) .110) .270 (.100 (.088-.160) . and 0.170-.180 (.240-.120) .220-. < LOD means less than the limit of detection. 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.150-.330) .156-.160) .350-.130-.154-.430 (.200 (.120-.330) .190-.330) .126-.160 (.270) .510) .240 (.130) < LOD .140) .190-.120 (.210) .210) .180 (.150 (.125 (.120 (.240 (.176 (.070 (<LOD-.080 (<LOD-.500) .280-.120-.350 (.170) . enamels.400-.210-.Metals Antimony CAS No.470 (.490 (.200 (. 0. or other substances containing antimony is another means of exposure.132 (.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 .105 (.150 (.260 (.310) .410) .180-.220) .160) .350) . 01-02.070 (<LOD-.250-.148-.260-.320 (.310 (.115-.330 (.130 (.220 (.240-.250-.164-.130 (.157) .178) .130) .140) .120-.180 (.180 (. ammunition.S.220-.280-.260 (.108 (.170 (.230 (. +3.120-.070-.220) .260-.710) .250 (. and pewter.340 (. interval) .470) .390-.180 (. from air and drinking water.170-.230) .090-. Dermal contact with soil.310 (.570) .200-.360) .130 (. and excretion of antimony vary depending on its oxidation state.145) Selected percentiles ( 95% confidence interval) 50th .350) .300) .090 (<LOD-. Antimony enters the environment from natural sources and from its use in industry.350) .130 (.146 (. population from the National Health and Nutrition Examination Survey.190 (.117-.190) .108-. 0.135) * .150-.340 (.320-.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 .119-.230-.230) .190 (.270-.200 (. It is also used in paints.280 (.130-.090) 75th .120 (.200) .141-.460 (.100-.350 (.140) .300-.137) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.220) 95th . water.500) .120) .220 (.200 (.410) .260 (.200) .360) .280) .120-.330 (.300) .440) .150-.310-.110-.240 (.400) .130-.190) . 7440-36-0 General Information Antimony is found in ores or other minerals.400 (.130) .390) . and glass. It is used in metal alloys.270 (. coal-fired plants.270) . People are exposed to antimony primarily through food and. The absorption.490) .190 (.390) .144) .340) .114) .197) .134-.190) .280) .220-.430 (.122 (.350 (.230-.117-.115) .090-. Antimony can exist in one of four valences in its various chemical and physical forms: -3. 176 Fourth National Report on Human Exposure to Environmental Chemicals .207) . distribution.220-.180-. sheet and pipe metal.150) .600) .330 (.133) * .320-.095 (. metal bearings. and +5.210) .310 (.150 (.200-.320-.093 (.130) .140 (.175 (.112-.100-.460 (.154) .120-.250-.220) .280-.161) .210 (.320-.080-. which may vary for some chemicals by year and by individual sample.098-.120 (.130-.320 (.07.130 (.170-.350 (.200 (.180) .110-.134 (.160 (.120) .200) .300 (.140 (.390) .150-.150) 90th .095-.230-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.103) .200 (. castings.142 (.530) .120-.290-.160 (.400 (.132 (.300-.160-.300-.270 (.110 (.200-.140-.280-.119) .080) .240 (.160) . to a lesser extent.270 (.220-.143 (.160-.109-.330-.120-.460 (.190) .136-.090 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. storage batteries.280 (.04.290 (.160-.079-.300) . and refuse incinerators that process or release antimony. solder.180-.200) .410-.320) Total .210) .280) .250-.123 (.230) . fireworks.210 (.290-.160) .360-.136) * .130-.190-.390 (.128 (.087-.430 (.240) .130 (.210-.400 (.184) .160-.100) .350) . respectively.120 (.420) .390) .370) . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.120-.150) .110-.080) .240 (.310-.210) . and 03-04 are 0.350-.140 (.140) .360 (. Stibine is a metal hydride form of antimony used in the semiconductor industry.300 (.200-.360 (.330) .130 (.350-.128 (.350 (.100 (.

.164 (.265-.149-.298 (.118 (. 1944).152) .263-.308-.253 (.074 (.129 (.102-.146) .115-.196 (.318-.089) .320 (.081 (<LOD-.086 (.225 (.136) .176 (.159-.250 (.163 (.120 (.310) .071-. Inorganic antimony salts irritate the mucous membranes.130) .471) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.146-.176-.400 (.267) .241-.267 (. 1954).256 (.097-.143) 90th .125 (.278) .081) .245) .248) .226 (.135 (.255) .154-.447 (.272) .178-.261) .148-.135 (.265 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.113-.109-.143) .429 (.181) .061-.130) .338) .124-.170 (.112 (.167-.310 (.320) .121 (.124-..425) .115) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.135) .126-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995).255-.103-.257) .228 (.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. diarrhea.500) . and kidney have been demonstrated in high dose animal studies depending on the dose.082) .444) .132 (.183) .373) .137 (.233) .263 (.207) .300 (.111-.206-.267-.317) .250) .075 (.333 (. Ming-Hsin et al.123 (. population from the National Health and Nutrition Examination Survey.129) * .209-.179-.069-.250 (.069-.233 (.151) .108-.139 (.417) .173) .308) .129 (.120 (.300) .098) . abdominal pain. Acute antimony poisoning may cause a metallic taste.185-.259 (.242-.130) .115 (. liver.192-.171) .352) .149) .310) .250-.121) .172-.320-.485) .122 (.300) .146-.333 (. and gastrointestinal symptoms such as vomiting.286 (.229-.086) 75th .195 (.188) .145) .084) .159-.195-.115-.198) .126) .161) ..235-.121 (.128-.138-.333-.318-.123) .241-.195-.371 (.317) .143) .321) .333-1.113-.200-.117-.385 (.430) .200) .107-.167 (.127) .208-.230) 95th .127) .247) .085) .213 (.120 (.175 (. 1962). resulting in hemolysis with abdominal and back pain (Dernehl et al.333 (.082) .096-. 1986).116-.133) .098-.391) .224 (.115 (.181) .119-.153-.271-.163 (.480) .444) .333-.138) * .209 (.244-.099-.278 (.078 (.120 (.214) .253-.125-.320-.103-.107-.727) .189 (.227-.320 (.117-.209) .104-.106-.095-.217 (.193 (.364 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.277 (.100 (. 1958) and occupational exposures (Briegner et al.104-.194-.159-.109 (.130 (. 1953).139 (.092-.156 (.150-.115 (.112-. skin.147-.185 (. 1973).281-.239-. and eyes.280 (.188-.421) .233-.200-.294) Total .077) .114 (. and ulcers (Werrin.167 (.131) .199-.114 (.178 (.079 (<LOD-..269 (.107-.191 (.238) .138 (.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 .140) .338 (.187) .076-.208 (.391) .143 (.405) .429) .080 (.080 (<LOD-.099-.205-.153 (. species.109 (.238) .228-.148) * .182 (. Histopathologic inflammatory and degenerative changes in the lung.108-.203) .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 .Metals than for trivalent compounds (Elinder and Friberg.156-.230-. 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.116 (.140) < LOD .209) .250-. myocardium.126 (.203) .106-.192) .317) .164-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.343 (.124 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .225) .167 (.173 (.160 (.092) .132) .741 (.352 (. interval) .417) .288 (.075 (.236 (.280-.068 (. 1988.134) .192 (.741) .193) .162-.131-.333-.144-.146-.117-.228 (.238 (.250-.222 (.414) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.357) .119-.095-.248-.127 (.161) .30) .181) .438) .268) .135) .185 (.220) .164) .127) .200-.082 (<LOD-. and route of exposure (Elinder and Friberg.313-.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 .102-..266 (.357-.176 (.113) .098-. 1986).152) .105-.148-.143) Selected percentiles ( 95% confidence interval) 50th .068-.119 (.131 (.111 (.076-.108-.186) .135) .211) .S.333) .338 (.295 (.471 (.364 (.250-.124) .118 (.315) .114 (.276 (.204-.108 (.147) .138-.173-.127) .150-.112 (.380 (.122 (.173 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.129) .087) .

Nordberg GF. Friberg L. Iavicoli I. indium. External and internal antimony exposure in starter battery production. 2002. Biological monitoring of exposures to aluminum..cdc.. Weltle D. Element reference values in tissues from inhabitants of the European community. Delves HT. clinical efficacy. Caroli S. Br J Ind Med 1991. Atlanta (GA). respectively. Dezateux et al. In: Friberg L. Ming-Hsin H. and antimony in optoelectronic industry workers. J Trace Elem Med Biol 2002. Cheng-Wei L. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.76(2):103-115. Konings J. 1990. Van der Venne MT. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . 2nd ed. plasma and urine and a critical evaluation of reference values for the United Kingdom population.64(2):182-185. pp.Metals to antimony have been established by OSHA and ACGIH. 1987). New York: Elsevier. Shao-Chi C. 1994) have reported values slightly higher than those in this Report. even when exposure levels were below workplace air standards (Bailly et al. O’Regan M. Kiberd B. Yang C-Y. Elinder CG. Vouk VB. gallium. Chia-Yu H. Biomonitoring of a worker population exposed to low antimony trioxide levels. Stone FD. Sabbioni E. Yu H-S. Mayne P. Review of elements in blood. environmental levels) and health effects is available from ATSDR at: http://www. Stocks J. Antimony in blood and urine of infants. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. 26-42. Nau CA. Sci Total Environ 1994. Trace element reference values in tissues from inhabitants of the European community I.. population. 1998). Piatnek DA. 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.atsdr. Gallorini M. Biomonitoring Information Levels of urinary antimony reflect recent exposure.html. stibine. Stasney J.51:238-240. which may be due to methodologic. Wade A. 20012002.. Third National Report on Human Exposure to Environmental Chemicals. Petrucci F.. Chest 1973. Alimonti A. Minoia C. Mahieu P. Liao Y-H et al. Cordasco EM. Dernehl CU. J Occup Environ Med 2004. Environ Health Perspect 1998. Liao Y-H. Paschal et al. 1991.e. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Leinemann M. Hamilton EI. Delves HT. Semisch CW.59:469-474. gov/toxpro2.13:361-362..S. Handbook on the toxicology of metals. Industrial Medicine 1944. Chin Med J 1958. eds. Schaller KH. 1995. Kentner M. Kentner et al. Lauwerys R. Briegner H. EPA. Int Arch Occup Environ Health 1987. Apostoli P.76:432436. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.158:165-190. 2005. Antimony. Dunkelberg.16: 33-39. Kuo-Juie Y. Pulmonary edema of environmental origin. Skulsukai G. Arch Dis Child 1997. Lenert G.. Earlier measurements in general populations (Minoia et al. Bolten C.48:93-97. 1997). Gebel TW. and 2003-2004. Cullen A. Int Arch Occup Environ Health 1995. and future strategies. et al. Mayer P. 1998) or compiled reference ranges (Hamilton et al. Pietra R. 1986.)1954. Rev Infect Dis 1988. Arsine. Centers for Disease Control and Prevention (CDC). Wu M-T.46:931-936. Sabbioni E. and a drinking water standard has been established by the U. Fuchs A. Pozzoli L. et al.. Industrial antimony poisoning. Ju-Sun P. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. 1998. Suchenwirth R.. Chen J-R.10(3):560-586. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. References Berman JD. Buchet JP. Chemotherapy for leishmaniasis: Biochemical mechanisms.106:33-39. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Costeloe K.. Roland H. arsenic. and hydrogen sulfide.67:119-123. HH. Ludersdorf et al.. Urinary antimony in infancy. Bailly R. Matthews T.. or exposure differences. Ho C-K. Industrial Medicine and Surgery (Dec. Schacke G. Biological assessment of exposure to antimony and lead in the glass-producing industry. Iavicoli et al. Antimony trioxide is rated by IARC as a possible human carcinogen. Dezateux C. Pilgrim L. 2004. VI. Carelli G. Information about external exposure (i. J Clin Pathol 1998. et al. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Luedersdorf R. Stead FM.521-523.

blood.99-108. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Trace metals in urine of United States residents: reference range concentrations. Paschal DC. et al.Metals in urine. Morrow JC. Industrial Hygiene and Occupational Medicine 1953. Chemical food poisoning.76(1):53-59.95:89-105. Jackson RJ. Environ Res 1998. Sci Total Environ 1990. Werrin M. Antimony poisoning in industry. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Ting BG. Pirkle JL. 27:38-45. and serum of Italian subjects. Sampson EJ. Renes LE.

1) 290 725 1542 03-04 03-04 9. particularly arsenic trioxide.90 (7.9-62.90 (7.5-19. 2005).6 (32.12-10. and foods.70) 8.80-9.8) 7.3-111) 78. ocean and fresh waters.5-41. semiconductors. it is found in over 200 crystalline or mineral forms. mental disorders.7-95. Arsenic trioxide (As2O3.4 (26.3) 10.66-8.1) 7. black. from coal burning. or rarely as elemental metalloids (yellow.2-20. as alloy in metal bearings. to a lesser extent. to a lesser extent.10 (6. grain.8-77.6 (15.70-9. and produce.74.5 (34. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.8-61. referred to as inorganic arsenic compounds.12 (6.0 (11.90-11.5 (40. meats. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.5 (36. and as homicidal poisons.1 (38.19-9.2 (13. Water sources contain mostly inorganic arsenate. Various arsenic compounds were used in paint pigments and for tanning animal hides.8) 29. Arsine (AsH3) is a reactive.1) 1281 1276 03-04 03-04 03-04 9.80 (5.5-178) 46.90) 16. and in lead-acid storage battery grids.4) 40. Arsenic and its compounds have had many uses in the past and present as medicines.20 (8. mostly for use in wood preservation (ATSDR.4-65.10-7. Arsenic is measurable in most soils.7) 24. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. see Data Analysis section) for Survey year 03-04 is 0.90-8.00 (6.90) 75th 16. 2001).2-17. and.90-8. such as arsenopyrite (FeAsS) and realgar (As4S4).4) 60.70 (6. pesticides.5) 95th 65. the smelting of copper.97) 8.2) 46.2 (51. solders.84) 8.6 (13.1-40. aluminum.6-35.000 metric tons annually. psoriasis. Also.1) 15.3-15. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. interval) 8. and as a cosmetic to lighten complexion.6 (9.8) 17.34-9.2) 15.02-8. though in some locations arsenite may be prevalent (WHO. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.5) 41.50-14. Gallium.8 (48. Before the 20th century.3-19.2-61.3) 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 7.8) 30. arsenic compounds.30 (6. arsenites. sodium arsenite.77) 6. and indium arsenides are used in the semiconductor industry. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. copper arsenates. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5) 66.4 (24. In nature.1 (32.7 (11. and gray forms). arsenic as elemental metalloids may be used in some ammunition.7-83.9-34.6) 11.30) 17.30 (7. were used as treatments for syphilis. cacodylic acid. and other metals.S.6-141) 53. The United States no longer produces arsenic from mining but imports about 22.0 (43.9-46.9) 21.9 (17. retaining walls.9 (8.29 (8. lead hydrogen arsenate. Survey years 03-04 Geometric mean (95% conf.Metals Arsenic CAS No.9) 68.0-60.4) 13.2-93.8) 7. lead.5-52.40) 7.84) 8.50 (8. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.10-10.2 (12. cancers.7) 65.55 (7.00-9. and arsenosugars.8) 34. Although it is still widely used in the United States.34-10.13-8.6-43.0 (22. and play sets. alloys. Since the 1940s.8) 33.2 (41.90 (5.0-19.5) 43. arsenocholine.0 (14.57) Selected percentiles ( 95% confidence interval) 50th 7.10) 10.4 (31.0 (15. population from the National Health and Nutrition Examination Survey.4 (48.08 (5.90-7. trimethylarsine oxide.6) 618 722 1074 Limit of detection (LOD.4 (7.5 (14.80) 6.41 (7. gaseous hydride manufactured in small quantities for use in the semiconductor industry.27) 9. +3 and +5). and arsenates (oxidation states of -3.90-14. General population exposure to inorganic arsenic can occur through consumption of drinking water and.7) 90th 37.5 (23. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.25-9. Arsenic trioxide is approved to treat acute promyelocytic leukemia. 180 Fourth National Report on Human Exposure to Environmental Chemicals .1-18. In the last century.

4 (12.75) 13..6) 45.47-6.3-41. and arsenosugars.8-62.3-62. U.0) 14.35) 7.0) 42. 2001.38-10. 2001).5 (9.g. 2001).50 (6. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. 2001).76 (6.30-9. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.44-11.45) 5. shellfish.1) 6.04) 7. organic arsenic can be converted back to methylated and inorganic arsenic.2-46.28-7.5) 290 725 1542 03-04 03-04 8.9 (45.2) 15. 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.8-32.0) 33.0-26. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. as observed in Bangladesh where millions of people have been exposed.51) 75th 14.33 (6. 2001).25-9. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.0-38.00 (6. population from the National Health and Nutrition Examination Survey.2) 90th 30.S.7-35.1 (14.88) 7.8 (12. 2007.1 (11..9-56.2-15.9) 53..11 (5.9) 13. arsenic does not show biomagnification in the food chain (WHO.8 (27. 2001).8 (11.0-69.86-17. arsenocholine..64 (7. In aquatic sediments.4-64.6 (10. dose level..4) 32.8 (21.5) 17. Gamble et al.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . 2003.01) 7. 2001).88 (5. interval) 8. Extremely high groundwater arsenic levels.5-120) 40. 2006.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.32 (5.2 (12.10-8.81-9. Chowdhury et al.41) 6.4 (40.7-17.75 (5. though some reduction may occur in the gut prior to absorption.8) 22.2) 40.99-9.S.6 (35. Direct exposure to DMA and MMA may result from use of the two pesticides. WHO. Tseng.4 (11. Survey years 03-04 Geometric mean (95% conf. 2001.10-16. Inorganic forms of arsenic demonstrate high acute toxicity. age. In aquatic organisms.0 (31. selenium.0 (17.66-8. but is poorly absorbed dermally (WHO.0) 26. Arsenate is reduced in the body to arsenite (oxidation state +3).13) 8. have caused clinical arsenic poisoning. cacodylic acid and monosodium methyl arsenate.33-10.31 (6. WHO. and contact with CCA-preserved wood structures. Fish.1) 8. 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. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.18 (5. and some other seafood can contain organic forms of arsenic including arsenobetaine.47 (6. Though modest bioconcentration occurs in some aquatic life..44) 6.7) 95th 50.1) 24. Children may have additional exposures from ingestion of contaminated soils (e.1) 58.8) 27.06 (4. gallium arsenide and indium arsenide.6-17.7 (25.3-53. 2007.93-8.47 (7.7-18.5) 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. are used in enclosed ultraclean operations within the semiconductor industry.20-9.12-10.66 (7. kelp. NRC.7 (9.7-34.01) 11.3) 6.3 (24.7) 28. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.8 (20.25 (6.S. 2006. 2001).3) 9. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.7-188) 27. mine tailings). Steinmaus et al.24 (7.61 (7.66-8. The semiconductor dopants.4 (26.7 (11.1-36.5-17.58-10.4 (42. 1988). trimethylarsine oxide (TMAO).0) 12.07-9.59) Selected percentiles ( 95% confidence interval) 50th 7. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.3-64. EPA’s maximum contaminant level (Hughes.93-9.0) 1281 1276 03-04 03-04 03-04 8.3 (27.1) 7.04 (5. Smoking tobacco is also a source of inorganic arsenic. so exposure to the general population is extremely limited.0-18.4) 54. dust. inorganic arsenic is widely distributed within the body. EPA.8-75. After absorption.23-7. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.6 (17.40) 8.4 (24. 2007. and folate status (Chen et al. 2001).96) 12.

0. arsenic trioxide) includes hemorrhagic gastritis with nausea..30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. can cause peripheral sensorimotor neuropathies. 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. 2006. 2004. Cardiac arrhythmias. 2001). gluconeogenesis..EPA. 2000. 2001).20 (<LOD-1..g. The U. substitution in phosphate metabolism. apoptosis. Taiwan. population from the National Health and Nutrition Examination Survey.10 (<LOD-1.g.S. Arsenic has many actions demonstrated in cellular studies. vomiting.80) 1.60) 1.. lung.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.. and diarrhea. noncirrhotic portal hypertension. 2001. drinking water have not been associated with increased cancer rates (Schoen et al.EPA has established drinking water. cytotoxicity. Survey years 03-04 Geometric mean (95% conf. Although arsenate is reduced in the body to arsenite. see Data Analysis section) for Survey year 03-04 is 1. Such actions may lead to decreased energy production. Raml et al. food residue.20 (<LOD-1. increased oxidative stress. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.30) 1. 2004).. Chronic human intake of arsenic at less than acutely toxic doses. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. < LOD means less than the limit of detection.. including inhibition of numerous enzymes. 2001). NRC.S. Bredfeldt et al. cell transformations. 2007). Acutely. 182 Fourth National Report on Human Exposure to Environmental Chemicals . hepatotoxicity. and bladder cancer (IARC. respectively. The organic forms of arsenic occurring in seafood have little known toxicity.50) 1.S. WHO. 2001). hyperkeratosis. 2006) or when exposure occurs in smokers (Chen et al.10 (<LOD-1.10 (<LOD-1.. U. interference in signal transduction pathways. and hyperpigmentation of the skin (NRC. 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. hypertension. Cellular glucose uptake.. hematocytopenias. renal failure. 2001). 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 2001.10 (<LOD-1. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. Cohen et al. WHO. fatty acid oxidation.60) 1. 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.. and by uncoupling oxidative phosphorylation (NRC.20 (<LOD-1. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. Chronic arsenic exposure in humans is considered to be a cause of skin. NRC.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.. With chronic exposure. and childhood neurodevelopmental effects in observational human studies. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.S. Chile). Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. and DNA repair inhibition (Cohen et al. Chronic elevated arsenic intakes have been associated with diabetes. peripheral vascular disease.. WHO. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. which can lead to dehydration and shock.20 (<LOD-1. some of these effects may take years to develop. 2001).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1. and endothelial injury (Kumagai and Sumi. and it also will inhibit succinate dehydrogenase. Bangladesh. including drinking water sources with elevated arsenic levels (e. which may vary for some chemicals by year and by individual sample. and altered gene expression. 2006. leading to a decrease in adenosine triphosphate energy production. WHO. 2004). 2006. 1998. 2007. 2007. Studies of arsenic at levels typical of U.50) 621 725 1078 Limit of detection (LOD. and production of glutathione may be affected as well. but additional or confirmatory research is needed (Kapaj et al.

. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. population (Rubin et al. In a Nevada town where groundwater levels were naturally elevated. 2001)...04 (<LOD-3. WHO.atsdr.. 1998. 1999.. 2006. Shalat et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 1999). 2006. 2001). 1986).. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Fourth National Report on Human Exposure to Environmental Chemicals 183 .70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Meza et al. In animal studies. and the FDA has established a bottled drinking water standard... Calderon et al. DMA produced bladder cancer in some chronic rat studies (Cohen et al. arsenic has been fetotoxic and teratogenic...S. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. Survey years 03-04 Geometric mean (95% conf. 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. 2006. 2006).00) 1.75 (<LOD-2.. although urinary arsenic levels were not associated with CCA contact (Shalat et al. 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. 1999.33 (<LOD-3. Valenzuela et al. population from the National Health and Nutrition Examination Survey. and were about two-fold lower than those for the U.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2008). Compared with this Report. 2007. 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. population in NHANES 2003–2004 (Schulz et al.. 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. 2006). the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. but generally only at maternally toxic doses (WHO. Pellizzari and Clayton 2006). environmental levels) and health effects is available from ATSDR at: http://www..19) 3. 2007. 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. Additional information about external exposure (i. Offergelt et al. Caldwell et al. median urinary total arsenic levels in 4052 adults varied with seafood intake.. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. Pellizzari and Clayton. Josyula et al.e. Vahter et al.S.cdc.html.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.Metals compounds.50) 1.80 (<LOD-4... had decreased since the prior 1990– 1992 survey. Levels of total urinary arsenic in the U.41) 3. gov/toxpro2. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1992. 2000.. In the German Environmental Survey III of 1998. 2006).18 (<LOD-3.. Shalat et al.S..89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.75 (<LOD-2. 2004. 2006).S..18) 3. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. Caldwell et al. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. 2004. Pellizzari and Clayton. Consequently. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2000).69 (<LOD-3. 2008). 2008. 2003.61 (<LOD-3.. 2001).

0) 4.28) 1.20 (4.6.70-21.7 (21.00-4.0 (26.80 (3.70 (3.6 (25.e. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. Caldwell et al.. dermal keratosis.6-44. MMA. 2000.19 (.5) 292 728 1548 03-04 03-04 1.74 (1..5 (14. Some noncancer effects of arsenic (e. population (Ahsan et al. In the residents of a Chilean town who consumed water with high levels of arsenic. when seafood organic arsenic is subtracted).. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. Pellizzari and Clayton..S.60) 1.7-22. 4.00 (1. Tseng et al.7) 15. 2001.1) 45..00-12.00 (. 2008). 2000..45 (1.500-1. 2008). and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.800) 1.0) 29.800 (.40) 75th 5.80) 1. After recent seafood ingestion.40) 5. 2005. and duration of exposure are also considered important.2-35.70-21.50-6.4) 23.50) . Individually measurable species resulting from inorganic arsenic exposure are arsenate. geometric mean levels were about 70-fold higher than for the U. Blom et al.S. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.g. and 0. WHO..90-7.. China. The higher percentiles of total urinary arsenic levels in the U.10) 4.3 (21.80-5.0 (27. Caldwell et al. see Data Analysis section) for Survey year 03-04 is 0. and two methylated metabolic products.10) 8.10 (4. Caldwell et al. Valenzuela et al.9 (7.4) 31.20-3.8 (12.8 (17.2-38.05) < LOD . 2008).90-29.9-23.20-190) 31.80 (. population (Sun et al.700-1.3) 35. arsenocholine. vasospasm.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 * * 1.37 (1.8) 35.5 (26.30) 2.1-51.3-39.20 (2..20) 18.48-2..50) 90th 16. When seafood intake is avoided. In most human studies. 2006).6. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.1-94.800-4. which may vary for some chemicals by year and by individual sample. 2000. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.900 (.900-1.3 (9. arsenite. 1985. Also. Aposhian et al.5) 29.17-1. 1. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.20 (. Arsenate.68) . Measurable organic arsenic species in this Report are three biologically generated environmental forms.30 (2.70 (5.S.5) 621 725 1078 Limit of detection (LOD. and TMAO were detected in only 7. Chowdhury et al. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.29 (1.0-23.8. and other factors such as nutrition.600 (.4 (16. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.8-50. Caceres et al.400-. interval) 1.83) Selected percentiles ( 95% confidence interval) 50th 1.66 (1. Survey years 03-04 Geometric mean (95% conf.4.70) 6.9) 13. in NHEXAS 1995–1996.3) 1284 1284 03-04 03-04 03-04 1. < LOD means less than the limit of detection.00-1. arsenobetaine. and TMAO.80 (4.9 (6.. 1996.5) 32. DMA and MMA. 2005.7 (13.31-1. methylation capacity. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20) 3. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.6 (13.7) 13..4-35.700-1. arsenite. 2008. 2008).Metals other areas of the world (Ahsan et al. with DMA.871-1.93) 1.55 (1.40-6. population showed a higher contribution of arsenobetaine (Caldwell et al.1) 18. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. For residents of Inner Mongolia.40-7.60-3.30 (1.30) 10.3% of a representative sample of the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800 (. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.00-6. population in the NHANES 2003–2004 subsample. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.3) 95th 35.1-25.. 2005. 2007) with higher levels of arsenic in the drinking water.. 2001). 184 Fourth National Report on Human Exposure to Environmental Chemicals .00) 3. 1990. 2003). 2008. These associations are stronger at higher urinary levels.11-1.43-1. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.50) .62) 2.20 (1.S. population from the National Health and Nutrition Examination Survey.S.6 (11.. arsenocholine.. Sun et al. In the late 1980s....8-40.20-25.2 (6. respectively.20) 7. 2007).800-1..

73-6.6) 19.12) < LOD . 2006.72) 12.638) 1.65 (1.45) 1.0 (9. Survey years 03-04 Geometric mean (95% conf.400-.78 (3.43) 75th 5.6-29.80) .8) 29. 1998.9 (13.51) 5. 1992.83) 2. Caldwell et al.05 (.2 (13.47 (2.53 (.909-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In recent years.1 (26.47 (1.S. 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. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.37-2.51-2.Metals as with DMA.50-7. 2007).05) 1.612-1.6 (9. Sun et al. 2001).00 (1.43) 14. Information about the biological exposure indices is provided here for comparison.1-18.901-2. The 95th percentile of the U.4) 292 728 1548 03-04 03-04 1.58 (3. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake..4 (11.88 (5.11 (.13-39.9-18.18-1.14 (1.19-2.82) 4.55) 1. Offergelt et al. interval) 1.21) 5.62-6..10 (.50-15. which is below the ACGIH BEI (Caldwell et al.531 (. 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.29 (4.68 (1.64-29. WHO.2 (12.79 (1.15-1. 2008).29-14.1-36.4-21.3 (10..76-27.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.5) 17.6-32.91 (4.4) 13.91) 90th 16.67) 1. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. population for the sum of inorganic related species was 18.28) 1.5-20.25-7.833-1.7) 30.S.1) 26.78-5.81 (4.6-46. 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.4-28.4) 32.00 (3.80-153) 17.40 (1.2 (4.15-4.67) 4.39-3.82) Selected percentiles ( 95% confidence interval) 50th 1.44 (1. 2003.4) 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 * * 1.30) 1.2 (12.32-7. population from the National Health and Nutrition Examination Survey.54 (1.9 (25.15-1. 2008).9) 14.83) 8.70) 5. 2001).6 (6.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.88) 2.5 (18. Fourth National Report on Human Exposure to Environmental Chemicals 185 .4 (24.9 μg/L.3) 95th 29..40) 1.25 (.0-36.16 (.5) 26.36) 2.7) 17..9) 32.938-1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.959-1.4-82. 1986.3 (10. 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.786-1.3-24.7) 9.3) 1284 1284 03-04 03-04 03-04 1.. not to imply a safety level for general population exposure.30-1.. Vahter et al.5 (18.877 (.61-6.93 (1.

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

80) < LOD 621 725 1078 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.00) 1. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (<LOD-2. 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.40 (<LOD-1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.95 (<LOD-2. < 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 1.44) 2.2. population from the National Health and Nutrition Examination Survey.00 (<LOD-3.76) < 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. population from the National Health and Nutrition Examination Survey.S. Survey years 03-04 Geometric mean (95% conf.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.S.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.08 (<LOD-4.20 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 187 .

59 (6.0 (11.7) 12.00-12.98) 4.00-3.00 (7.50-15.80-6.03-6.17-4.31-4.50-5.44 (2.16 (2.12 (3.0 (12.0 (9.71 (4.9) 11.00) 4.57-5.69-6.0) 17.82-5.71-4.71) 3.27 (2.0) 13.10) 3.8) 7.42) 3.15) 4.0 (13.6 (9. interval) 3.65-6.11 (3.00 (3.00) 6.00 (3.73 (3.20-4.61-11.49) 10.92-12.77 (3.06) 5.70 (3.29-4.45 (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 4.80 (4.79 (3.00-4.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60-6.80-5.6) 292 728 1548 03-04 03-04 3.08 (2.32-10.00 (5.9) 5.13-4.73) 6.74) 90th 9.60-7.8) 7.00-11.57 (3.32 (4.00-15.0) 9.0) 16.0) 12.49-4.00) 75th 6.52) 3.69 (3.00) 6.78 (4.0) 11.18 (6.24) 3.84-18.14) 3.00-9.00 (5.89 (3.67) 9.0) 11. Survey years 03-04 Geometric mean (95% conf.74 (2.6-18.90 (3.78) 4.0 (10.80-3. population from the National Health and Nutrition Examination Survey.2) 10.8) 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) 292 728 1548 03-04 03-04 4. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00-11.82-9.00 (3.0 (10.55 (2.24-4.95-6.0-12.0-17.00 (3.5) 12.9 (7.00-15.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .85 (3.00-4.00 (4.4 (7.86 (2.0 (10.7.00-10.95-3.97-3.7-16.16 (4.00-22.82) 3.65-8.10) 6.80) 2.00) 12.12-4.46 (4.00-8.62) 4.80) 7.90) 5.00-3.00) 5.86-21.0 (12.34) 3.0) 10.31) 4.94) 3.30 (7.S.00) 7.00-4.95 (4.S.0-18.22) 4.48 (3.0 (9.34 (3.0 (10.92) 3.44) 5.48 (2.00 (6.7) 1284 1284 03-04 03-04 03-04 4.7) 13.1-22.81 (5.00) 3.28) 2.0-16.0) 13.14) Selected percentiles ( 95% confidence interval) 50th 3.11) 4.70-12.94-3.3 (7.0-16.84-8.5 (11.03 (3.0 (13.9) 13.27-2.33) 3.50 (4.95-4.05) 3.45) 8.09 (7.37 (2.00-13.69 (3.9) 12. Survey years 03-04 Geometric mean (95% conf.33-4.00 (5.00-7.0 (8.27 (3.00 (3.0-25.32 (8.1-15. population from the National Health and Nutrition Examination Survey.00) 6.0) 95th 16.30) 3.86-7.05) 5. see Data Analysis section) for Survey year 03-04 is 1.00-12.91) 75th 5.00 (5.0) 621 725 1078 Limit of detection (LOD.1 (8.34-4.0) 16.00-15.00 (5.6) 1284 1284 03-04 03-04 03-04 4.17-6.70-3.00-5.00-4.00-4.72 (4.00 (6.0) 17.00) 9.20) 11.61-16.00) 3.88 (4.0 (8.34 (3.0-17.20-12.00-11.69-3.5) 95th 13.34-4.70-4.19) Selected percentiles ( 95% confidence interval) 50th 3.3 (8.17 (2.00) 90th 11.00-7.00) 4.9 (11.0-19.16-11.45) 3. interval) 3.00) 6.71 (3.25 (4.0) 9.60-4.00-7.0) 14.90) 2.70) 5.00-7.0 (9.39-3.0 (14.38 (3.1-18.00 (3.67) 8.00 (6.00-4.05) 10.7 (10.27-5.00 (7.37 (3.3 (8.0) 9.60-3.

17) 2. population from the National Health and Nutrition Examination Survey.50 (2.00) 1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53-2.20 (1.28 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.79) 2.90) 1.70-2.86 (2. population from the National Health and Nutrition Examination Survey.70-2.88 (1.20-1.62) 2.90 (2.00 (<LOD-1.61) 2.30-1.50 (<LOD-1.10) 2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .60-2.00) 1.54) 90th 2.18-1.20 (1.9.22 (1.70-2.45) 3.88 (1.16 (2.35-3.10 (.90) 2.80) 1.40) 1.52 (2.93) .80 (2.57) 95th 2.33 (1.40-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.80-2.900-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (1.50) 1.88-2.30 (1.60 (2.00-2.30 (1. < LOD means less than the limit of detection.20) 2.73-2.96-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.80 (1.30) 1.20 (1.82-2.58) 2.30) 90th 1. see Data Analysis section) for Survey year 03-04 is 0.40-3.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (2.30-2.00-2.80 (1.86 (2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.10-3.80) 1.50-2.53 (1.37 (1.00) 1.20 (1.60) 2.20-3.10 (1.07-3.00-4.30 (2.00 (<LOD-1.30) 2.80 (1.30-1.60) 1.34) 2.70-2.10 (.00-1.10) 95th 2.10-1.10 (<LOD-1.85) 1.31 (1.00 (1.50) 621 725 1077 Limit of detection (LOD.20 (1.63 (<LOD-1.00) 2.46-2.36) 1.71-2.28 (1.82-2.07 (1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.22) 3.61-3.80 (1.46 (1.985) 1.11-1.90 (1.S.84-3.40-2.23) 1.40) 2.60) 2.43-3.86) 2.816 (<LOD-.60 (1.70) 2.31-3.50 (1.14-1.00-1.00 (2.86) 3.81) 1.30 (1. Survey years 03-04 Geometric mean (95% conf.853-1.10-1.36 (1. which may vary for some chemicals by year and by individual sample.00) 2. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.05-1.40 (1.33 (1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.90) 2. Survey years 03-04 Geometric mean (95% conf.07) 2.80-2.30) 1.85) 2.77) 1.S.18-1.70-3.50 (1.40 (2.40) 1.40-3.15-1.10 (1.

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

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80-3.78) 1. Certain foods.30) 5.71 (2.56 (6.22-1.35-4.74-2.73) 3.g.44-2.62) 1.95-6.70) 5.49) 11. In nature.21-2.80 (1.77-3.30 (2.38 (1. fireworks.74-3. and ceramics.20 (3.08-8.04-6.50 (1.87-14.41-3. Some barium salts are freely soluble in water.15 (1.76 (3.51) 2. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.80) 1.27 (1.73 (5.26-1.04-2.06-2.43 (1.70 (5.40 (1.38 (1.10-5.36-1.50) 1.51) 7.15 (6.1) 9.57-7.20-5.65-1.60-2.59) 3.00) 1.49-1.77 (3. Barium compounds are used by the oil and gas industries to make drilling muds.35 (3.37) 1.43 (1.30) 5.96-2.37-1.00) 6.60-6.00) 1.37 (4.54-8.61 (1.11 (3.25-1.30) 5.47-1.20-8.64-3.18-1. glass.80) 6.75-3.70-6.97 (1.17-1. rubber.76-3.25-11.61 (3. The general population can be exposed to low amounts of barium in air.51 (1.45) 7.60) 4.21 (1.60) 1.85) 1.87) 7.87-9.26) 5.40 (5.92) 2.19-1.8 (6.53) 2.27) 2.31 (2.54) 2.35 (2.4) 6.50 (2.90) 2.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.2) 6.88) 1.56 (1.12 (2.40 (1.30) 8.36 (4.35-1.00) 4.87 (5.90) 1.28) 90th 5. Small amounts of barium can be released into the air during mining and other industrial processes.30) 2.32) 8.50) 2.50 (1.73 (6.70-8.65) 1.31-2.70) 3.70 (1.67) 6.34) 2.33 (1.10 (2.29-5.10 (4.40 (4.63 (1.14-1.12) 6.61 (1.80-5.S.70) 1.12.06-1. Barium salts have also been available as rodenticides.60-10.78-3.48) 1.24-1.54) 1.15-11.10-4.40 (1.25 (1.49 (1.98) 1.49-9.54 (2.73-5.20-1.54-1.71) 95th 6.86) 6.54) 1.86-5..60 (1. soluble forms of barium.85 (2.12) 7.11 (3. 0.71) 2.20-6.15 (2.72) 4.55-3.18) 3.32-1.40) 3.86 (4.73) 1.75) 2.30) 3.50-1.52 (4.40 (5.88 (5.93-2.12 (2.56 (1.8) 9. 2001).57) 3.39 (1.47-1.30-1.62 (1.60-6.99 (4.4) 9.16) 5.90-2.53-5.00 (1.46-1.80 (1.52 (1.15) 5.54-1.20 (4.81-2.12.90 (6.Metals Barium CAS No.30-2.70-2.41) 1.56 (2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (1. see Data Analysis section) for Survey years 99-00.70) 7.40) 7.51) 1.10 (3.29) 5.90) 4.02 (7.50-6.27 (1.50 (3.00 (2. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.31. population from the National Health and Nutrition Examination Survey.80 (2.4) 7. In single dose animal studies.87-7. whereas others are practically insoluble (e.15-1.69 (1.80 (5.30-1.20-1.40) 7.19) 2. depilatories.91 (2. bricks. and 03-04 are 0.76) 1.50 (1.36 (1.56) 4.59-11. are high in barium (Genter.34 (1.48-4.61 (5.50-1.36) 5.37-8.05% of the earth’s crust.48 (6.20-8.50) 4.28-1.60 (2.72) 1.49) 2.80 (2. such as brazil nuts.64 (1.46) 1.20) 2.18 (6.00-8.11 (2.21 (1.70) 4.84) 5.09 (1.60) 1.26-7.71) 1.46) 1.65) 1.50 (4.38) 2.50-6.30-3.05-2.35-1.65) 3. tiles.82-6.30 (5.22) 6.99-5. water.66) Selected percentiles ( 95% confidence interval) 50th 1.20-8.20-1.39-1. 7440-39-3 Medically.82) 1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.87-3.24 (4.43 (5.87 (6.86-4.39 (1.00-76.64) 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 2.63) Total 1.35 (1. interval) 1.32-7.78-2.35) 5.55-7.80) 7.65-8.77) 1.63) 1.43) 6.88) 7.30 (3.08 (6.15-1. and food.61-8.76-2.71-9.41-1.48-4.30-5.42 (1.50) 2.93 (4.90-9.76-7.9) 5.72) 75th 3.63 (8.57 (5.80-2. and 0.62) 1.30) 4.70-3. barium sulfate and barium carbonate). were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).81-3.94-6.11-1.34 (1.22-1. 01-02.39) 4.50 (1.47) 4.44-5.50 (4.81-2.43) 2.48) 1.68 (1.29-1.63 (2.12-1.61 (2.50 (5.88) 4.01-7.66 (4. Barium compounds are also used commercially in paint.70-2.95 (4.60) 3.36-1.10) 5.63) 1.01 (4.30-2.37) 5.65 (5.16 (1.39) 1. respectively.54 (6.65-5.14 (6.38) 8.91) 2.34 (2.40 (5.93-8.86 (4. such as barium chloride.44 (1.49) 8.91) 6.26) 2.70) 1.14-6.56) 1.74) 3.40-13.82) 2.30 (1.50 (6. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.45 (1.07 (2.62 (1.60-3.30 (5.78) 1.24-1. Workers employed by industries that make or use barium compounds can be exposed to barium dust.8) 5.03 (1.50 (4.09 (2.63 (5.80-7.90) 2.00-3.85) 1.53) 1.10) 3. it combines with other chemicals such as sulfur or carbon and oxygen.21-8.90 (4.90 (1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .80 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (1.49) 4.90-13.20-1.70-5.

41 (2.32) 2.91 (3.75-22.68-3.72 (2.96) 7.54 (2. Wones et al.38 (1. Perry et al.26-1. Chronic high doses in animals resulted in kidney damage (McCauley et al.89) 90th 4. diarrhea.62) 2.52) 1.38) 1.70) 10.32) 2.00) 6.06) .61 (4.18 (1.25) 4.29-3.82) 1.83) 2.10) 3.27) 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 .58 (4.75-3.29-4.73) 2. population from the National Health and Nutrition Examination Survey.62 (2.11) .963 (.51) 6.64 (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 (1.43) 1.08-2.97 (5.33 (1.37) 2.56 (1.55 (4.39-10.25 (1.03) 1.38 (4.36 (1.40 (1.28-1. weakness.37 (1.39 (3. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) 1.44 (1.96 (4.39 (2.91) 2.00) 4.2 (3.33) 1.77-5.54) 1.10-1.88 (2.24 (3.24-6.59-7.52 (3.29 (1.60 (1.74) 1.33 (1.76 (2.20 (1.02-5.8) 4.86-7.76) 2.42 (4.31 (4.24-1.15-4. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.61) 2.84-5.53-21.20) 4.38-1.40 (1.68) 1.50) 1.84 (3.36 (5.39 (2.99) 1. The health effects of exposure to barium compounds depend on the dose.04 (2.76 (3.29) 1. paralysis.51) 4.59 (1.40-1.24-3.915 (.80) 3.32 (2.56) 4.45-1.891 (.24-11.59 (1.47) 1.21 (1.01 (4.53) .58-6.4) 5.34-1.921 (.53 (2.72) 4.00 (3.58) 75th 2. such as those used in medical radiographic procedures.36 (1.26-1.91 (3..23-2.55 (5.55-6.51 (1.57) 2.28-11.0) 7.55-5.11) .36-1.10) 6.03-1.27-1.45) 95th 6.48 (1.28) 5.64 (1.27-3.31 (1.51) 4.48-1.880-1.99 (2.00 (2. 1985.832-1.41 (1.68 (3.88 (6.54 (1.Metals was eliminated primarily in feces and to a lesser extent.03) 2.59) 1.73-4.73-2.46-22.45-6.54) 2.39-1.34) 1.49-1.60 (2.02 (3.01) 1.34 (1.65 (2.89 (2.77) Total 1.35-1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.32 (1.38) 4.52) 7.46) 1.68) 3.28-6.79-5.90-2.31-1.26) 4.32 (1.905 (. are not absorbed when administered.47 (2.97-3. 1990).80) 4.3) 6.30 (1.19-1.04) 1.S.2) 5.703-1.81-6.16-1.37-1.48 (1.47) 4.27) 7.56 (1. hypertension.00) 1.23-5.81-6.29 (3.24-6.754-1.69-9.3 (6.29-7.2) 6.02) .76 (4.09) 6.44-2.00 (5.70) 4. 2001).39-1.34-3.20-8.22-2.96) 4.63-4.00 (3.60 (1.75) 2.19-1..52-10.31-1.38 (1.59) 2.47-8. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.29-1.25-11.60 (2.35-3.62 (4.777-1.51 (3.48-3.98 (2.11-2.62 (1.00) 4.48) 2.28-7. 1984.33-4.77) 1. 1994.42) 1.50 (4. in urine.52-4.03) 3.60) 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 2.46) 3.30) 2.41) 5.38-5.881 (.39 (2. 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.83) 3.58) 1. water solubility.26-1.33-1.47 (5.12) 2.00-7.13-3.20-1.0) 5.20-2.55 (1.91-2. Toxicity from soluble barium salts is rare.47) 10.36 (3.29-4.68 (3.68-3.57-7.10 (6.22-1.30 (1.96) 4.75) 1.74) 1. NTP.76) 2.45-8.36-2.43-6. and cardiac dysrhythmias.45-1.68 (2.69 (5.96 (4.31) 5.67-6.77) 1.92) 2.28 (1.57-5.97 (4.08-1.10-2.47) 1.55 (1.86) 5.84) 2.16 (1.96-6.75) 1.02) 4.56-3.48-5.26-1.99 (4.03-1.04) 5.38 (4.57-10.37-2.13-2.06) 2.44-2.64) 7.76) 1.49-1.64) 7.74 (5.76-3.57 (6.24-1.75) 2.70) 1..18 (1.0) 6.33 (5.58 (2.72) 6.46) 2. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.27 (2.51-3.36 (3.45) 1. Following intravenous injection in animals.36-1.24) 3.66 (1.49 (1.39-5.01 (5.49-1.22-4.71 (5.35-1.38-7.52) 2.710-1.50) 2.86 (2. a benign condition that may occur among barite ore miners.97-4.49 (1.24 (5.63) 1.33) 6. chemical form.64 (1.31-1.85-5.42) 1.77) 5.34-5. vomiting.51 (1.60 (5.84-2.19-1.77) 1. 1989).56) Selected percentiles ( 95% confidence interval) 50th 1.22-1.23-1.14-2.79) 1.26-4. 1986). Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.48 (1.16) 11.50) 1.19-2.39) 4.81-7.41 (1.05-1.92 (4.45 (1.78 (2.87) 1.38) 1. Symptoms following acute high dose include perioral paresthesias.41) 4.55) .45 (3.96) 4.65 (5.97) 1.40 (1.80-6.82) 1. Insoluble barium salts.46 (2.59) 1.58) 4. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.00-1.4 (5. and route of exposure.37 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Barium is not rated for human carcinogenicity.

Trace element reference values in tissues from inhabitants of the European community I. Vouk VB. calcium. 2001. Minoia et al. 1989. Sampson EJ.. Environ Res 1998. 84-94. Jr.cdc.95:89-105. Available at URL: http://ntp. ed. J Toxicol Environ Health. Exposure to soluble barium compounds: an interventional study in arc welders. Advances in modern toxicology. 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. et al. Atlanta (GA). Princeton NJ: Princeton Scientific Publications. EPA. Inc. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. LA. eds. ed. Laurie RD. pp. Ting BG. [online].pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Fourth National Report on Human Exposure to Environmental Chemicals 195 .gov/ntp/htdocs/LT_rpts/tr432.S. Biomonitoring Information Levels of urinary barium reflect recent exposure. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect.html?charset=iso-88591&url=http%3A//ntp.. 5th ed. Perry EF.64(1):13-23. 231-249. environmental levels) and health effects is available from ATSDR at: http://www. eds. Nordberg GF. Sabbioni E. Sci Total Environ 1990. Patty’s toxicology. 221-252 Komaromy-Hiller G.gov/toxpro2. Genter MB. 2nd Ed.296(1-2):71-90. Howerton K. Schaller KH. Morrow JC.197210.niehs. 1986. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).28(3):373-388... Kopp SJ. 1994. strontium. Int Arch Occup Environ Health 1992.S. Minoia C. Levy. et al. Pietra R. Barium. In Friberg L. Information about external exposure (i. In: Inorganics in drinking water and cardiovascular disease. blood. 2005. Investigations into the effect of drinking water barium on rats. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Vol 2: Specific Metals.niehs. Apostoli P.atsdr.85:355-359. Zschiesche W. References Brenniman GR. barium.nih. 1998). Comparison of representative ranges based on U. Jackson RJ. Frohman. and radium In: Bingham A. Epidemiological study of barium in Illinois drinking water supplies. Calabrese EJ. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. p. Perry HM. Gallorini M.. Costa R. McCauley PT. p. Cohressen B. 1984. 2000) to levels in NHANES 1999-2000 and 2001-2002. 2005. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Reeves AL. Pirkle JL. Handbook on the Toxicology of Metals. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. 4/8/09 Paschal DC. Trace metals in urine of United States residents: reference range concentrations. and 2003-2004 (CDC.gov:8080/cs. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. PS. Pozzoli L.. 1992). Centers for Disease Control and Prevention (CDC). New York: Elsevier. Stadler BL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Douglas BH. et al. Third National Report on Human Exposure to Environmental Chemicals. New York: John Wiley & Sons. the welders had no obvious adverse clinical effects (Zschiesche et al. In: Calabrese EJ. Paschal et al. National Toxicology Program (NTP). NTP.html. Clin Chim Acta 2000. p. 1985. Princeton (NJ): Princeton Scientific Publications. 2001-2002. Magnesium.. et al.76(1):53-59.e. Ash KO. and serum of Italian subjects. 1990. A study of 46 elements in urine. Powell C. patient population and literature reference intervals for urinary trace elements. Lack of effect of drinking water barium on cardiovascular risk factor. Wones RG. and a drinking water standard has been established by U...Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Environ Health Perspect 1990. Weltle D.nih.

and volcanic dust. the lightest of all metals. and machine-parts industries. 7440-41-7 General Information Pure beryllium is a hard gray metal. Two types of minerals. eating food. population from the National Health and Nutrition Examination Survey. aircraft. and dental bridges.140 (<LOD-.Metals Beryllium CAS No. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. bertrandite and beryl. or drinking water containing the metal. Beryllium compounds are commercially mined. near some hazardous waste sites.13.130 (<LOD-.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 . 196 Fourth National Report on Human Exposure to Environmental Chemicals . A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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. Exposure to beryllium occurs mostly in the workplace. and 0. nuclear. and can be found in mineral rocks. respectively. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air.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 . < LOD means less than the limit of detection. 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 from breathing tobacco smoke. Low-level beryllium exposure in the general population can occur through breathing air. 01-02.13. computer. coal. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and refined beryllium is used in mirrors and special metal alloys for the automobile. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. 0. soil. In medicine. which may vary for some chemicals by year and by individual sample.130 (<LOD-. In studies of laboratory animals. beryllium is used in instruments. x-ray machines.S. electrical. and 03-04 are 0. are mined for commercial recovery of beryllium. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. see Data Analysis section) for Survey years 99-00.13.

IARC has classified beryllium as a human carcinogen.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. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.231 (<LOD-. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. and drinking water and environmental standards have been established by U. 2002). Skin exposure can result in delayed hypersensitivity reactions. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. S. or berylliosis. 1990). Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. population from the National Health and Nutrition Examination Survey.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 .S.346 (<LOD-. NTP considers beryllium to be a known human carcinogen.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.281 (<LOD-. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. 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. EPA. including contact dermatitis and subcutaneous nodules. which produces pneumonitis. respectively. based upon excess lung and central nervous system cancers in studies of workers. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .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 . Chronic beryllium disease.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Maier. 2003. Fourth National Report on Human Exposure to Environmental Chemicals 197 .

population were generally undetectable in NHANES 1999-2000.html. which approximate this Report’s limit of detection. Morrow JC. Pietra R. Given these results.95:89-105.org/documents/ehc/ehc/ ehc106. Ash KO. Kriess K. International Programme on Chemical Safety (IPCS).. Minoia C. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.S. HLA-DPB1 and chronic beryllium disease: a HuGE review. Sci Total Environ 1994.S. Genetic and exposure risks for chronic beryllium disease. population are lower than levels in workers. Element reference values in tissues from inhabitants of the European community. Atlanta (GA) 2005. Pirkle JL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jackson RJ. and the 95th percentile for males in NHANES 2001-2002.. and the fact that most NHANES participant levels were undetectable.13 μg/L.cdc. Sampson EJ. it is likely that urinary beryllium levels in the U. Hamilton et al. Clin Chest Med 2002.inchem.S.. Available at URL: http://www. They reported urinary beryllium levels ranging from 0. Clin Chim Acta 2000. References Apostoli P. 2000.296(1-2):71-90.e.Metals (i. environmental levels) and health effects is available from ATSDR at: http://www. 2001). and 2003-2004. Sci Total Environ 1990. A study of 46 elements in urine. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Gallorini M. 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. 1990. Maier L.76(1):53-59. Trace metals in urine of United States residents: reference range concentrations. patient population and literature reference intervals for urinary trace elements. 106. Sabbioni E. In other studies. 20012002. Environ Res 1998. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Am J Epidemiol 2003. Environmental Health Criteria.1 μg/L). Paschal DC. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. blood. Weston A. Costa R. Beryllium [online]. Comparison of representative ranges based on U. Review of elements in blood. et al. and serum of Italian subjects.12 to 0.158:165-190. 1990.e.htm.. et al.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.157:388-398. plasma and urine and a critical evaluation of reference values for the United Kingdom population. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Trace element reference values in tissues from inhabitants of the European community I. Ting BG. McCanlies EC. Andrew M.atsdr. Hamilton EI.23:827-839. Van der Venne MT. Sabbioni E. Int Arch Occup Environ Health 2001. Howerton K. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Schaller KH. VI. Pozzoli L. 0.74:162-166. Centers for Disease Control and Prevention (CDC).gov/toxpro2. Third National Report on Human Exposure to Environmental Chemicals.. 3/27/08 Komaromy-Hiller G. Levels of beryllium in urine for the U. Apostoli P. Minoia et al. less than 0. 1998). Paschal et al. 198 Fourth National Report on Human Exposure to Environmental Chemicals .

30-1.362-.500 (.00-1.700) .300 (.00 (1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .400) .600 (.300-.500) .200 (.300) .600-1.00 (.300-.403 (.00-1. Since 2001.300-.10) 1.300 (.800-1.60) 1.300 (<LOD-.378 (.200-.300-.300-.40) 1.20) .60 (1.60) 1.400 (.500) . Cadmium also may be emitted into the air from zinc.300) 1.20-1.500 (.800-1.00 (.50 (1.30-1.900-1.400) .400) .300-.300-.30-1.460) . malleable.300 (.10) 1.300 (.200 (<LOD-.600-.20) 1.10) 1.40) 1.00 (.50 (1.300 (.30-1.300 (<LOD-.40 (1.700) .300-.200 (<LOD-.255) .00-1.513) .425 (.300 (.400-.300) .50 (1.40-1.600 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .337) .300) .400) < LOD .304 (.426-.00-1.400-.400 (.40 (1.S.386-.70) 1.300-.10 (1.300 (.00-1.600 (.300) 75th .300-.10 (1.900-1.300) . interval) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (. as zinc sulfide) and to a lesser extent.40 (1.600) .400-.900-1.00 (.300) .400 (.403) .14.500 (.500) .300-.420 (.800) .00 (.368-.500-.378-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.30) .500-.400 (.400 (.80) 1.20) 1.300-.300 (.20) 1.700 (.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500-.400) .400) .00 (1.333 (.300) .216-. and nonferrous alloys.393 (.700) .300) .10) 1.80 (1.500 (.900-1.600) .400) .10) 1.20-1.3.600 (.50) 1.400) .326 (.10) 1.900-1.500-.20-1.700-1.400-.400) < LOD < LOD < LOD . and incineration of municipal waste materials.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 .266-.700) .300) .50-1.300) .50-1. and 03-04 are 0.800) . population from the National Health and Nutrition Examination Survey.296-.300 (.441) * .gov/minerals/pubs/commodity/cadmium). Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.600 (.500) .00 (.300 (.20) 1.304-.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 .500-.00-1.30 (1.30) 1.700) .200-.500-.600) .359-.400-.00-1.20 (1.10 (1.00) .304 (. or copper smelters (U.600 (.395 (.400-.70) 1.10) 1.400) .500) .900-1.400-.500-. and 0.80) 1.500-.40 (1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.313 (.600 (.20) 1.400 (. see Data Analysis section) for Survey years 99-00.200-.900-1.700) .412 (. The predominant commercial use of cadmium is in battery manufacturing.600-. 7440-43-9 General Information Cadmium is a soft.300-.500 (.235 (.500-.60 (1.60 (1. respectively.700) 1.500-.500-.424) * .500-. which may vary for some chemicals by year and by individual sample.300 (.50-1.400 (.3.300 (<LOD-.40 (1.300 (.40-1.331) .300-.00) .700-1.50-1.600) . during refining of lead and copper from sulfide ore.300-.900-1. 01-02.300) .20) 1.20-1.500-.500 (.500-.500-.600) 90th 1.309-.60) Total * .400) .300-.usgs.200 (.200-.20-1.700) .376-.400) .600 (.500 (.300-.400-.300) .600) .382 (. Other uses include pigment production.400) < LOD .600 (.00 (.200) .00 (. < LOD means less than the limit of detection.10) 1.90) 1.700) .900-1.600 (.60 (1.S.400 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30) 1.468 (.10 (1.300-.400-.400) .600) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .600 (.800 (.60) 1.20) .50 (1.10 (1.283 (.300-.00-1.300-.400-.400 (.400) .20-1.200) . EPA.20) 1.20) 1.400-.500-.200 (.600) .400 (.20) 95th 1.600) .361-.40 (1.600 (.289-.20 (.300 (<LOD-.800 (.10 (.70) 1.900-1.800) 1.300 (.900 (.60 (1.400) .400 (.30-1.600) .600-.366) * * . cadmium use has declined in response to environmental concerns (http:// minerals.400) . plastic stabilizers.200-.452) .00 (.449) Selected percentiles ( 95% confidence interval) 50th .500 (.421 (.400 (.400) < LOD .300) .30) 1.344) .300-.500 (.500-. lead. coatings and plating.400 (.400 (.40 (1.10 (1.10 (1.500) .470) * .900 (.427) * . U.50) 1.300) .00-1.60-1.500-.600 (.600 (.700-1.400 (.70) 1.600) 1.367-.20-1.300-.00 (.400 (.50) 1.500) .275-. 0.S.300 (.Metals Cadmium CAS No.

160 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .09-1.214-.330-.980-1.452 (.231) .285-. whose body burdens of cadmium can be approximately twice that of nonsmokers.436-.372) . calcium.180 (.170-.181 (.219 (.284) .519) .257) .208-.141 (.520-.813 (. 01-02.255) .290-.177-.279 (.730-.470-.892-1.52 (1.445 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.890-1.43) 1.109-.919) .766 (.241) .713) .120 (.47) 1.114-.28-1.490) .918-1..17) .299) .03) .240) .165-.210 (. 2001).221) .080 (.237-.148) .204 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.748-1.199 (.366-.203 (.272-.202-. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.686-.216 (. respectively.249) .705-.507) .972 (. To a lesser extent. 200 Fourth National Report on Human Exposure to Environmental Chemicals .327 (.239 (.313) .498-.700-.160) .870) . however.087-.960 (. an inducible metal binding protein.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.189-.20 (1.06.06-1.229) .107-.265 (.989-1.963-1.308) .890 (.190-.366) .51 (1.860) 1.198) .234 (.170-.280 (.061 (<LOD-.790 (.283 (.717-.550 (.623) . For nonsmokers who are not exposed to cadmium in the workplace.12-1.061-. population from the National Health and Nutrition Examination Survey.680 (.300) .090) . copper) and protein.479) .230) 75th .238-.458 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.230) .195-.171-.101) .227 (.Metals 2000). and 0.260 (..157-.530 (.818 (.191-.450 (.273 (.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 .265) . 2003).263) .240-.210) .220 (.175 (.980) .220-.169-.800-. zinc.246) .210 (.28) 1.400-.440-.306 (.980-1.466 (..06.733) .255) .173) .322 (.366-. 2003).090) .192-.848 (.551) . Diamond et al.800 (.57) 1.450 (.200 (.203) .210 (.15) .390-.817 (.447 (.858 (.790 (.184-.260-.714-1.157) .300 (.187 (.04 (.820) 1.763-.190-.610) ..462 (.412) .82) 1.192-.219 (.360) .13 (.229-.426 (.270 (. Horiguchi et al.336) .393-.232 (.19) 1.15 (.260-.130 (..251) .38) . 2003.440 (.081) .257-. 1999.839 (.490) 1.179-.700-.22 (.255) .475 (.06-1.067-.277 (.559 (.455 (.153-.078 (.12 (.065-.24) 1. and various seeds.820-1.753-.400-.220-.875) .206 (.200 (.48 (1.38) 1.351-.232) .806) .247) .210 (.06.892 (.01) .977) .430) . 2004a.476-.222) .940-1.189) .350 (.243-.221 (. interval) .140 (.249-. 2003).310) .167-.092) .354) . wheat.109 (.01-1.04 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.362) .128 (.990) .262) . With chronic exposure.456-.135 (.191-.235) .510) .433-.207-.270 (.30-1.202 (.110-.880) .74) 1.20 (1. Cadmium absorption may be increased with iron deficiency (Berglund et al.295) .633 (.112-.580) .289-.310 (.206) .211-. Cadmium in soil is absorbed by plants.390 (.423-.160-.060-.810-1.126) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.17 (.200-.482) .193-.121 (. rice.10 (1.13) ..38) 1.183-. Inhalation of cigarette smoke is a predominant source of exposure in smokers.282 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.S.339) .135-.640) .193 (.843-1.20-1.261-.160) .38) . 1994).136) .211 (.200-.530) .540) .83) 1.067-.219 (.191 (.261-.855-1. Cadmium is absorbed via inhalation and ingestion.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 .633-1.440 (.72) 1.17 (.06) .836-1.388-.596) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.326) .20) 1.190-.100-.233) .233) .820 (.733-.480) .493-. including many food crops such as cereal grains.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .500) .223 (.25 (1.01 (.196-.539) .34) 1.178-.492 (.886) .960) 1.817 (.02-1. Renal tubular and glomerular damage.875 (.387) .519) .394-.329 (.077 (.189-.13-1. see Data Analysis section) for Survey years 99-00.151-.430-.320) .316 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.302 (.148-.390-. and 03-04 are 0.17 (.32 (1.589 (.545 (.210) .741-1.28 (1.980) .22 (1. potatoes.220) . ingestion through food is the largest source of exposure.238) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.150) .253-.** Survey Geometric mean (95% conf.209 (.281 (.20 (1.25) 1.886-1.230 (.607) .381-.170 (.481) .175 (.115-. drinking water is a source for cadmium intake.510-.194-.201 (.229) .500) 90th . Kikuchi et al.15) 1. 0.445 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.150-.134) .551 (.41 (.07-1.210 (.226) .092 (.980 (.077 (.700-.36) 1.

304) .917) .560-.227-.545) .784) .171-.614) .147-.158-.415) .252 (.178-.221-.256-.421 (.224 (.199 (.100 (.154 (.826-1.067-.181 (.308 (.261) .263 (.156) .136-.140-.143-.818) .238-.839) .414-. population from the National Health and Nutrition Examination Survey.232) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .238) .078 (.247-..919 (.491-.159 (.091) .789 (.208 (.101) .209) .147-.292) .962) .104) .266) . Staessen et al.091 (.07 (.084 (.518) .423 (.318 (.146-.02 (.979 (.335 (.182) .818) .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 .219 (.078-.311) .940 (. 1999).096) .381-..418) .446) .551) .293-.856 (.077-.148 (.414 (.144-.884) .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.490 (.538) .250) .700 (.150-.207) .688-.667) .725-1.507-.222-.215 (.666-.16) .210 (.536 (.767) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .181 (.196 (.336-.218) .051-.270 (.303) .727-.687-. Horiguchi et al.438-. 1996.917 (.716) .228-.199-. Noonan et al.267 (..686 (.282 (.075-.242) . At lower environmental exposures.931 (.05) 1.263-.500-.00 (.940-1.316) .274) 1.098) .106) .207-.668-.850) .316 (.718 (.181-.830) .206-.722-. During the 1950’s and 1960’s.338 (. most often a result of occupational exposure (Roels et al..278) .541) .431) .182) .202 (.234) .184-.304-.135) . 2003.253 (.418-.198) .300-.941 (.297) .166 (.163 (.479 (.757) .216-.268 (.205 (.183) .273 (.754) .850) .189-.779 (.404 (.187-.07) . 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.487 (.190 (.161-.12) 1.783 (.343-.208-.122 (.398-.184) .391-..663 (.123-.696-.537-.484 (.211 (..183 (.247-.140-.168-.927-1.630-.423-.559-.516-.441-.220 (. 2002.261-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.757 (.690-.432 (.438) 90th .350) .** Survey Geometric mean (95% conf.280 (.162 (. 2004b)..950) . 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.184-.562-.830-1.075 (<LOD-.173 (.225) .288 (.266-.163) .071 (. can result from high dose chronic exposure.481 (.802 (.063-.873 (.434 (.708-1.693 (.209) Selected percentiles ( 95% confidence interval) Sample 95th .234 (.729 (.827) .364) .473 (.783) .700) . 1999).719 (.181) .387 (.470) .191-.182) .426-.09 (.185) .678 (.712 (.136-.856) .200 (.449) .174-. 2002.289) .645-.998) .175 (.204-.06 (.241) .111-.147 (.255-.212 (.631) .444-.331 (. 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.190 (.187) .097) .622 (.308) .191 (.104) .325 (.240) .501 (.176 (.795) 1.833-1.143-.826-1.296 (.176 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .235) .. 2000.329 (.440) .674-1.157-. 1999).909-1.591 (. Olsson et al.194-.289) .234-.607) .086 (. interval) .185 (.653) .876-1.440) .083-. 2002.126 (.210 (.38) .085-.387-.377-.687 (.154-.740 (..288) .617 (. 2004).828) .253) .177) .123-.247-.281) .531 (.321) .245 (.074-.678-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.533) .382-.085 (.388-.178) .806-1.929) .865 (.985 (.175-.233 (.650-.226) 75th .223) .792 (.690 (.267 (. However.261 (.143) .288-.874-1.156 (.340) .382) .112) .170 (.173-.137-.472) .232) .168 (.476) .236-.813-1.00 (.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 .10) 1.813-.240) .691-.168-.156-.219 (.157-.192) .210) .16) 1.197-.906) .130-.716-.201-.. 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.093 (.225) .412 (.470) .08) .229) .191) .090 (.13) .221 (.239-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.647-.352) .281) .159 (.17) .091 (. Jarup et al.170-.107) .137 (.690-.767 (.113-.433-.084-. 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.131-.175 (.094) .283 (.404) .S.769 (.

2002. intermediate in former smokers and lower in never-smokers (Becker et al. 1999.. 2004). maternal blood or maternal urine and birth weight (Nishijo et al... In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Both IARC and NTP consider cadmium a human carcinogen. 2004b. respectively. 2000. Horiguchi et al... Occupational standards are provided here for comparison only. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. 2006). 2002. 2002). Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.S. CDC. 2004. However.. Mannino et al. Staessen et al. with peak values observed in the fifth to sixth decades (CDC.46 mg/gram of creatinine) (Ezaki et al.html. 2003.. Ezaki et al. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity.atsdr.. not to imply a safety level for general population exposure... 1999). respectively. Information about external exposure (i. Olsson et al. 2004b).. 1996). In the typical environmental exposure... 2002)..e.. Horiguchi et al. Staessen et al. 2006. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Wennberg et al. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al... 1988). environmental levels) and health effects is available from ATSDR at: http://www. 2006.. 2002. Moriguchi et al. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. Acute and heavy exposure to airborne dusts and fumes. In adults aged 60 years and older. 2002). 2004. 1999).. 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. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 2004. 2002. 2003. 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.. 2005. Jarup et al. For NHANES 19992000. approached these values associated with subclinical changes in renal function and bone mineral density. and drinking water and environmental standards have been established by U. Becker et al. Wilhelm et al. 2002). 2000..cdc... study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al.. Jarup et al. as may occur from welding cadmium-alloyed metals. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.... 2005. 2003.. Wennberg et al. 2002. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. EPA. Salpietro et al.. 2002). urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. Suwazono et al... Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. 2003. Jin et al.. Becker et al.. Noonan et al. 2006). Staessen et al. 2003). Olsson et al. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al.26 and 3. 2004... Further research is needed to address the public health consequences of such exposure in the United States. 2003.1 mg/L (Alfven et al.. 2005. In postmenopausal women.. Cadmium can produce lung. Creatinine-corrected urine cadmium values in U. 1996. 2000).. Ezaki et al. Friedman et al. Becker et al. Komaromy-Hiller et al. Animal studies have demonstrated reproductive and teratogenic effects.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. 2005. 2005). Women had higher blood and urine cadmium levels compared to men of similar ages. Olsson et al.S. 2003. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al... 2000.gov/ toxpro2. data (CDC. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. 2002. Zhang et al. has resulted in severe. 2002) and length at birth (Nishijo et al. potentially fatal pneumonitis (Fernandez et al.. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine). Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al.S. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.

Ukai H. Occup Environ Med 2000. Comprehensive study of the effects of age. Elinder CG. Lundh T. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Nermell B.000 women in the Japanese general population: a nationwide large-scale survey. Lauwerys R. Venables KM. Machida M. Clin Chim Acta 2000. Occup Med 1996. Mucha A. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Hotz P.24:717-724. Persson B.66(Pt A):2141-2164. Buchet JP. Ikeda Y. Kikuchi Y. et al. Consonni D. Mascagni P. et al. Savage-Brown A. Fukui Y. Komaromy-Hiller G. J Occup Health 2003. Friedman LS. References Akesson A.95:20–31.96:353-359. ShkiryakNizhnyk AZ. Atlanta (GA). Toxicological profile for cadmium update. Berglund M. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Seiwert M. 102:10581066. Uemura T. 1999 [online]. patient population and literature reference intervals for urinary trace elements. Fayers PM. et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Horiguchi H. Okamoto S. Cadmium fume inhalation and emphysema. Oguma E. Centers for Disease Control and Prevention (CDC). Stock AL. possibly better than b2microglobulin. Agency for Toxic Substances and Disease Registry (ATSDR).148(1-2):11-20. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Costa R. Zhu G. Sanz P. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. 2005. Howerton K. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Grubb A. Holguin F. Available at URL: http://www. Mannino DM.1(8587):663-667. et al. Jarup L. Kundiev YT. Third National Report on Human Exposure to Environmental Chemicals. Miyamoto K. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. et al. Seiwert M. Bellerup P. Anthropometric. Ezaki T. Lepom P.76:186-196. Becker K. Davison AG. Lancet 1999. Int Arch Occup Environ Health 2003. Seifert B. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. population. diabetes mellitus. Oguma E.205:297-308. Machida M. Ezaki T. 196:114-123. Lukyanova EM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Carlsson MD. Nordberg G.59:497]. Kaus S. Wang H. Sasaki S. Furuki K. Int J Hyg Environ Health 2002.57:668-672.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. et al. Tsukahara T.cdc. Vahter M. Int J Hyg Environ Health 2003. et al. J Toxicol Environ Health 2003. Furuki K. Fatal chemical pneumonitis due to cadmium fumes.46:372-374. Olfactory function in workers exposed to moderate airborne cadmium levels. Toffoletto F. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Becker K. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Taylor AJ. Lison D. Dekio F. et al. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Pickering CA. Fukui Y. Neurotoxicology 2003. Schulz C. Sasaki S. Ye T. Akesson A. Takebayashi T.45:43-52. Bregante G. Schulz C. Chislovska NV. Jones RL. et al. et al. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Fernandez MA.S. Thayer WC. Greves HM. Environ Res 2004b. Nomiyama T. Darbyshire J. Kumagai N. Environ Health Perspect 2002. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. 206:15-24.atsdr. Ikeda Y. Bernard A.102:83-89.13(11):1627-1631. Choudhury H. Lidfeldt J. Lancet 1988. Gadea E. Environ Res 2004. Serra J.354:1508– 1513.S. Bo M. Moriguchi J. Miyamoto K. Toxicol Appl Pharmacol 2004a. Hellstrom L.110:699-702. Ash KO. iron deficiency. Nerbrand C. Krause C. Moriguchi J. Environ Res 2006. environmental. Kaus S. Alfven T. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Environ Health Perspect 1994. Vahter M. Palomar M. Environ Health Perspect 2005. Tsukahara T. Toxicol Lett 2004. Chiappino G. et al. Diamond GL.gov/toxprofiles/tp5. Jin T. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. 4/8/09 Alfven T.296(1-2):71-90. Thorax 2004. Jarup L. Horiguchi H.html. Comparison of representative ranges based on U.59:194-8.

84 (Section A):4455. Suwazono Y. Roels HA. Bergdahl IA. Wilhelm M. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. 151-168. Biological monitoring of cadmium. lead. Ginucchio G. Revised 2000 [online]. Lybarger JA. 4/8/09 Waalkes MP. Environ Health Perspect 2002. Merlino MV. 204 Fourth National Report on Human Exposure to Environmental Chemicals . 2001. Liu QF. Minciullo PL.Metals Nishijo M. Effects of exposure to low levels of environmental cadmium on renal biomarkers. New York: Plenum Press. Noonan CW. Environ Res 2000. Usefulness of biomarkers of exposure to inorganic mercury. United States Environmental Protection Agency (U. et al. Japan. Skerfving S.110:151-155. eds. Nogawa K.3:26-41. Nordberg GF. Lancet 1999.533(12):107-120. Lison D. EPA). Sarasua SM.30(5):395-399. Wang JX. Environmental exposure to cadmium. and mercury in the population of northern Sweden. lead. et al. Occup Environ Med 2002. 2000. Mueller PW.S. iron status. Staessen JA. Mutat Res 2003. Staessen J. Tanebe K. Wennberg M. Roels HA. Arch Environ Health. Roels H. Time trends in burdens of cadmium. created 1992. Nakagawa H. Revised and new reference values for arsenic. Cadmium in blood and urine – impact of sex. et al.353:1140-1144. Schultz C. Fan YG. J Perinat Med 2002. J Environ Sci Health B 2004. Buchet JP. 2004. J Cardiovasc Risk 1996. Friberg L. Salpietro CD. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Thijs L. Int J Hyg Environ Health 2006.209:301305. Hazard Summary. Zhang YL.110:1185-1190. Cadmium carcinogenesis. Nakagawa H. et al.html. lead. Schwenk M. Olsson IM. Gangemi S. Environ Res 2006.59:394-397. Tanebe K. Bruiglia S. Toyama. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Zhao YC. Saito S. Emelianov D. Honda R. Lundh T. Sager PR. Lauwerys R. Hoet P. In: Clarkson TW. Relationship between newborn size and mother’s blood cadmium levels. Jansson J-H. Oskarsson A. Tawara K. Nakagawa H. and former smoking – association of renal effects. Nordberg M.21(3-4):251-262. Kobayashi E. pp. et al. Kuznetsova T. Ren Fail 1999. Okubo Y. Lijnen P. Kido T.gov/ttn/atw/ hlthef/cadmium. Biological monitoring of toxic metals. Bensryd I. Kathman SJ. cadmium. Stegmayr B. Gallmans G. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Campagna D. Vangronsveld J. Zhu HD.epa. Honda R. Lundh T. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Ottosson H. age.100:330-338. dietary intake.39:2507-2515. Nishijo M. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan.59(1):22-25. Cadmium compounds. Nordberg GF. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. forearm bone density. and risk of fractures: prospective population study. et al. Environ Health Perspect 2002. Available at URL: www. Stelitano A.

40) 5.00) 4.49) 4.60-5.08 (6.1) 11. and 0.6 (9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 12.8) 12.81-14.68 (7.52) 7.42) 7.72-7.0 (10.10 (6.17) 4.90) 4.60-6.40) 5.20) 5.9 (11.60-12.64) 4.81 (4.84) 8.1 (9.20 (4.15-8.80 (4.32-5. and 03-04 are 0.97-7.80-10.5) 12.21 (4.76-6.1 (10.60) 7.89) 4.90-10.20) 4.5) 9.86-12.89-5.00-9.2-13.27) 4.60) 7.53 (6.0) 9.9) 8.16-6.0-13.63) 6. and as polymerization catalysts.13 (5.49) 75th 7.30) 7.80-13.04 (4.20) 8.34) 9.70) 5.90) 9.70 (5.59-5.50) 5.70 (8.17-6.10 (8.14.94 (4.01) 7.64-10.1) 10.60-6.69-6.8) 9.42) 6.4 (9.12 (4.40-7.37) 5.04) 7.1 (11.50 (4.84 (4.71 (4.74) Selected percentiles ( 95% confidence interval) 50th 4.92-13.93 (4.21) 90th 9.20 (6.47-4.35-5.8) 9. semiconductors. infrared lamps.01-6.80 (8.2) 11.62 (5.26-11.10 (8.80) 7.34 (4.99-6.22 (4.4) 10.33 (6.20-8.20-5.70) 5.05-5.5 (10.49 (5.8) 11.3) 12.80 (4.25) 4.1-13.08) 7.94 (4.77 (9.4) 95th 11.86-11.70 (4.84-9.63-4.6) 11.08 (7.49 (4.90) 5.26) 4.36 (6.71) 4.2) 12.59-5.0) 10.40-5.67 (4.0) 12.45-8.0) 12.00-8.95 (3.43-8.5-14.95) 5.33-5.24) 4.80-11.31-8. respectively.7 (9.42-7.9 (11.2.82-4.23-4.7 (9.7) 10.81) 4.50) 9.84) 5. scintillation counters.Metals Cesium CAS No.00-10.80-10.52-9. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.8 (10.4) 12.47-8.30 (6. 0. interval) 4.90-10.09-5.56-11.1) 9. the body half-life is estimated to be 70-109 days based on 137Cs exposures.5-14.97) 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 4.80 (8.01-8. soil.10-5.44 (8.26) 7.9 (11.50 (4.7) 11.46) 7.05) 5.71-5.91 (7.02 (4.77-8.9) 11.50 (7.94) 4.98 (7.1-12.9 (11.1-12.36) 3.2 (9.7 (8.57-5.9) 12.70 (6.87 (4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.59 (5.26 (3.17 (6.12) 5.07) 4.45-5.71-8.12-11.74 (4.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.23) 9.6 (9.71-9.99-11.90-12.98 (7.8-13. 01-02.30) 5. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.74-5.7 (11.4) 10.0) 11.70) 7.50-7.S.82) 5.55 (7.35 (4.10-9.7) 10.80 (8.37) 7.3) 9.25-5.13 (7.2-13.77 (9.8) 12.4) 9.95-4.81) 9.10-7.4 (10.3) 10.4-13.56) 5.55 (4.08-5.87) 5.9) Total 4.56 (4.64 (4.20) 7.99-11.2-14.0) 11. 2004).73-5.66 (7.59-5.16-6.10-8.86 (7.70 (6.27-5. population from the National Health and Nutrition Examination Survey.90-8.6) 10.64) 5.4) 11.5-16.40 (4.3) 10.14 (4.32 (3.80-6.40-5.60-7.0-15.53-11.81) 4.5) 10. nausea.25 (3.40-5. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH. photographic emulsions.1) 11.00-8. However.90) 5.90) 7.2-12.83-4. For absorbed cesium salts.62 (5.7) 11.72) 4.3) 10.90-12.5 (8.8 (10.60-7.70 (9.9 (10.79 (4.05) 5.8 (11.2 (9.70-8.13-8.00) 6.99) 9.6 (9.70-5.84-5.60 (7.60 (8.59) 7.70 (8.96 (6. Most human exposure to cesium occurs through the diet.35 (4.08-5.87 (4.33 (5.3-13. and cardiac arrhythmia (ATSDR.60) 5.55-11.20-7.97 (7.80-10.5-13.0 (9.05-5.32) 4.9 (10.56 (4.4) 12.91-8.3-15.27 (7.50 (6.12-5.64-5.7 (10.00 (7.03 (4.09) 5.7-14.54) 4.03 (4.7 (10.0) 12.3 (8.54-11.22-4.87 (4. and high-power gas-ion devices.77 (4.6 (11.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.90 (4.30-10.1) 9.3-13. Little is known about the health effects of this metal. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.13 (8.36 (3.00-4.63 (4. Whether cesium compounds are carcinogenic is unknown.94-4.62) 4.90 (6.6 (11. although cesium was generally of low toxicity when given to animals.2-13.50 (4.99) 7. Fourth National Report on Human Exposure to Environmental Chemicals 205 .89) 5.38) 5.30 (6.97) 4.29 (4.71 (8.7 (9. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.43 (5.40-11.3 (8. and clay.30-5.14.39-4.7 (10.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.64) 5.40) 7.20-4.68) 9.4 (9.8) 11.61) 7. see Data Analysis section) for Survey years 99-00.73-11.07-11.29) 4.90-10.10 (6.39) 7.87-7.00) 7. cesium hydroxide is corrosive and irritating at high concentrations.3) 10.83) 6.40-5.80 (4.88 (8.03-4.61-6. Radioactive 137Cs has been used medically to treat cancer.40-11. diarrhea.6 (9.

61 (7.56) 4.70) 7.05-3.8) 5...70 (7.36-10.48) 7.25) 4.51) 4.96) 4.42 (4.10) 7.77 (7.14-4. interval) 4.22) 6.62) 5.63) 6.6 (9.6) 6.4) 10.66 (6.58) 8.05-3.48) 90th 7.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.0) Total 4.22-11.98 (6.43) 8.82) 7.95-6.27-4. Using clinically submitted specimens.64) 5.50 (6.51 (3.39 (5.9 (9.00-5.12) 3.2) 11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20-8.21-5.2 (8.67 (6.54 (5.6 (9.77 (4.07 (5.06) 4.15 (7.44-9.26 (4.58 (4.43 (3.57) 3.3) 11.79 (5.86 (4.08) 4.54 (3.76-6.13 (3.03-5.35 (4.47) 7.99-9.04-11.56 (4.42-4.06) 5.95) 8.00) 6.10 (5. Komaromy-Hiller et al.78) 4.20) 5.05 (4.S.89-4.21-3.66 (5.56) 3.52-5.31 (4.84-7.97-5.34 (5.5) 9.60-20.27 (8.53) 6.24-10.13) 7.3 (9. 2005.74) 75th 5.08-3.2 (8.46) 6.33 (5.47 (7.47) 6.75 (6.46-4.50) 4.98) 5.19-6.78) 4.08 (3.50) 8.29-3.76-9.97) 8.16) 5.27) 4.17) 4.08) 4.13-9.33-3.43 (4.43 (8.29-3.95) 10.40) 7.09) 4.30 (3.00-9.9) 10.04) 5.91 (5.27 (6.28 (4.00-8.46 (8.63 (6.84-7.79) 6.15) 95th 8.27 (6.98) 5.98 (7.61-3.45-6.70) 6.28) 7.14-6.68) 6.3 (8.28) 8.55-5.53 (6.7) 10.14) 4.53) 3.63-6.11 (5.05-4.18-6.55) 4.77 (6.41 (4.08-7.35-11.07) 8.01-8. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.06 (3.87-4.47) 4.28 (5.55 (3.04) 6.85) 4.43-6.5 (9.41-4.72-5.83-6.65 (6.71 (7.0) 7.30-4.14) 4.67) 5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.99-4.92) 3. population from the National Health and Nutrition Examination Survey.75 (7.14 (6. and were also roughly similar to those in this Report.3 (10.79) 9.09 (4.51 (4.96-4.41) 9.80) 6.40-5.35-7.20-4.10 (3. population.95-12.50) 4.46-8.09) 8. population results shown in this Report (Alimonti et al.91) 5.44 (4.40) 6.30-4.30) 10.14-7.10-4.62-8.90-3.45 (4.21-4.00-5.64) 9.23 (7.50 (5.41-7. Two small studies of European populations reported urinary cesium levels similar to U.31 (4.63-6.0 (7.79) 4.51 (3.87) 5.44) 3.21 (2.1) 11.68) 3.03) 5.77-5.91-6.58) 3.41 (8.03) 6.26 (3.41) 4.56-10.90 (7.36-6.5) 9.91-7.06 (5.02 (5.65-3.20-4.65-4.90-8.43-11.50 (7.81 (4.27-6.48-6.0) 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 .58-5. (2000) found urinary cesium levels that were slightly lower than those reported for the U.90-8.72) 4.54 (4.60 (5.38-7.37-3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.08 (5.39) 5.78 (3.78 (3.30 (4.73 (3.03-6.42 (5.44-5.91) 4. 1990).16-8.37) 4.17) 9.66 (5.95) 4.63 (7.99-9.91-9.59) 4.50) 4.54 (4.99) 4.64-6.20-4.3) 9.5) 7.94) 7.53 (4.17 (6.18) 8.88-10.8) 6.87 (5.68) 4.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.39) 8.7-12.42-6.97-4.10 (3.74-11.51 (4.24-4.08) 3. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.68 (4.31-4.7) 10.12 (3.51 (7.93-7.31-6. 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.60) 3.19-3.35 (3.26-6.73-4.63 (4.07) 8.42-4.43 (4.95 (5.95 (3.11 (5.71) 6.00-4.38-12.18 (7.74 (4.85) 5. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.58 (6.00-10.47) 6.84-9.04-5.74) 3.59-8.83) 8.64) 4.17-4.56) 4.96) 4.36-3.30) 10.08 (6.22 (3.60-10.3-15.29) 5. Minoia et al.68-11.25) Selected percentiles ( 95% confidence interval) 50th 4.85-4.44 (8.13-9.66-6.00 (8.99 (3.16-8.S.8 (9.60 (3.50-5.72 (4.49) 3.02-4.29) 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 5.38 (3.84-9.84-11.29) 4.82-4.05) 6.12-6.8) 10.88-4.77) 4.91) 5.18-7.74 (5.38 (3.91 (5.07-4.94 (5.33-8.38) 10.81 (4.64 (8.83-7.64 (4.75-11..67 (5.96 (4.05) 3.47 (4.30 (7.96-4.S.15-11.9 (10.35) 3.15-4.41 (5.24 (3. 2004).46 (7.92 (5.33 (5.93-9.79-5.16-5.

Voorhees RE. A study of 46 elements in urine. Paschal D. Costa R. Sewell CM. Wolfe MI.14:120-128.cdc. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Minoia C.atsdr. Clin Chim Acta 2000. Komaromy-Hiller G. Mincione G. Apostoli P. Toxicological profile for cesium. Pozzoli L. Ronchi P.S. Sci Total Environ 1990. et al. Spezia S. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Trace element reference values in tissues from inhabitants of the European community I. Ash KO. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA) 2005. J Expo Anal Environ Epidemiol 2004. Centers for Disease Control and Prevention (CDC).Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Rapid Commun Mass Spectrom 2005. 2000.19:3131-3138. Assessment of urinary metals following exposure to a large vegetative fire. Howerton K. New Mexico. cesium. antimony and tungsten. Mott JA. et al.296(1-2):71-90. Wood CM. Comparison of representative ranges based on U. Gatti A.gov/toxprofiles/tp157. Gallorini M. 4/8/09 Alimonti A.2004 [online]. Pietra R. Available at URL: http://www. patient population and literature reference intervals for urinary trace elements.html. blood. and serum of Italian subjects.95:89-105. Sabbioni E. Forte G. et al.

Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.580 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.800-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.430) .359 (.820 (.340 (. hard metal or in combination with other elements.520-.950-1.379 (.47) 1.25-1. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.06-1.320 (. and in synthesizing polyester and other materials.334) .850-1.502) .360-.700) .660-.02-1.417) .305-.460) .68 (1.06 (.800) .09 (.65) 1.369 (.660) .270-.890) .386) .810-.390 (.650 (.16-1.50) 1.327-.850) 1.950 (.890-1.520) .730) 1.300-.496) .519 (.05 (.810) .960-1.760) .50 (1.04 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .398) .520-.340) .600) .01-1.400-.22 (1.12) 1.380 (.360-.308-.375 (.410) .17-1.590-.450) .15-1.270-. Cobalt compounds are used as catalysts in producing oil and gas.333-.490-.640) .530) .427-.416) .404) .810) .32-2.17 (.24 (. shiny.08-1.520) .300 (.520 (.285 (.44) 1.640) .380-.75 (1.870 (.740 (.330-. and soil.350-.03-1.570) .48) 1.450-.379 (.410-.16) 1.830-1.05) 1.670-. large appliances.930) .372) .900) .360-.630 (.840) .22-1.29 (1.610) .431) .880 (.620-. see Data Analysis section) for Survey years 99-00.39) 1.42) 1.820 (.01 (.380 (.310-. diamond-polishing wheels.370-.374 (.490-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.28 (1.64) 1.390 (.670 (.348-. and 0.Metals Cobalt CAS No.523) .373-. steel-belted radial tires.313) .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 .540-.19) .740-.290-.410 (. and 03-04 are 0.980) .580 (.46 (1.370 (.26) Total .15 (1.418 (.03) 1.461 (.950 (.480-.710) .750-. 0.350-.331-.23) .790) .450-.550) 90th .940 (.430 (.01 (.388-. respectively.640) .01-2.339 (.434 (.394) . and kitchenware.630 (. Cobalt occurs naturally in airborne dust. seawater.870 (.03 (.414) .364-.930-1.580 (.581) .424) . Cobalt compounds are also used in manufacturing battery electrodes.680 (.570-. Usual human exposure is from food sources.28-2.S.04-1.24 (1.343) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .980-1.570-.910-1.680) .393-.07-1.09) .32) 1.333-.470 (.99) 1.750 (.850-1.352 (.03 (. interval) .336-.60 (1.390 (.350 (.32 (1.390-.26-2.350-. industry is imported or obtained by recycling scrap metal that contains cobalt.460) .56) 1.370-.00) .600 (.500) .09 (.340-.520 (.370-.650 (.670 (.28 (1.600-.700) .520-.259-.59 (1.950) .340-.410 (.319) .450) .08.280-.530-. and magnetic recording media. hard metal (alloys of cobalt and tungsten carbide).410 (. The cobalt used in U.610 (.390) .32) 1.480 (.900-1.355-.690 (.890-1.37-1.380 (.316-.301 (.590 (.03) 1.340) .428-.540-.564) .450) .420 (.460 (. varnishes.310 (.920-1.348-.850) .21) 1.430) .660) .S.550 (.12) 1.371 (.460) .26) 1.52 (1.470) .740-.950-1.13) 1.420) .590) .465) .515 (.463-.04-1.32 (1.543) .590-.73) 1.620-.520 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.47) 1.540-.900) .450) .790 (.940-1.350) 75th .670 (.22) 1.398 (.16 (1.316 (.16-1.92) 1.380-.800-.750 (.750 (. and inks.419) Selected percentiles ( 95% confidence interval) 50th .680) .469-.26-1.670-.435 (.410 (.330) .820 (. Cobalt is used as a drying agent in paints. automobile airbags.47 (1.510) 1.430-.520 (.14-1.330 (. It is emitted into the environment from burning coal and oil and car and truck exhaust.07.710 (.650-.05 (.440-.16) 1.53) 1.04-1.07 (.790-.367 (.410-.460 (. and fertilizers.410) .338-.431) .930 (.370) .343 (.420) .550-. population from the National Health and Nutrition Examination Survey.33 (1.373) .405-.23-2.452 (.16 (1.377-.45 (1.48) 1.760 (.81) 1.890) 95th 1.890-1.620-. 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.860 (.499 (.480 (.07-1.680 (.33-1.530 (.291-.08) .67) 1.870-1.17 (1.410-.28 (1.399) .690-.630-.940-1.14) .560 (.460-.770) .36) 1.540-.880-1.570) .81) 1.690-.610-.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 .620) .900-1.487) .07.03) .920) 1.04) 1.17 (1. blue-colored pigments.430 (.294 (.520-.570 (.47 (1.270-.540) 1.410 (.430 (.06 (.16 (.610) .583) .900) . 01-02.20 (1.500 (.710) 1.454 (.

29 (1.304-.848 (.468) .15 (.708) .257 (.829) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.851 (.384) .54) 1.895-1.343 (.03-1.481) 90th .343-..361 (.361-.10-1.327-.333-.952 (.444 (.12-1.550-.821 (.362-.404-.281) .727 (.634-.513-.36) 1.824 (.563-.552 (.932-1.328 (.585) . Once absorbed and distributed in the body.949) .29 (1.25 (.644 (.425) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.00) .296-.461) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.542 (.275-.495 (.963) .60) 1.378 (.689 (.73) 1.781-1.594) .247 (.10) .469-.337) .10 (.294-.333 (.297) .306) 75th .917) .599) .29) 1.358 (.630-.515 (.291 (.19) .372) .438) .488) . in the feces.382-.611) .471 (.29 (1.861 (.33) .313-. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.16 (.348) .861-1.337 (.608 (.898 (.286) .329-.346 (.279 (.313-.316 (.543) .554 (.669) .990-1.250) .297-.271 (.703-.44 (.750) .355) .391 (.16 (1.662) .595) . using hard metal cutting tools.983) .937 (.378-.673-.27) 1.487-.04 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).616-.419) .28) 1.331-.606 (. 1972).829-1.303-. Smith et al.00-1..57) 1.380-.582-.738 (.00 (.435-.667-1.548 (.362) .523 (. or using diamond-polishing wheels that contain cobalt metal.259) .368 (.955) .609) .50) 1.736-.728 (.280-.554 (.471-.215-.391) Selected percentiles ( 95% confidence interval) 50th .S.00 (.00 (.12 (.660-.417) .35) .593) .785) .462) .753-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.353-.850-1.760-1.50) 1. refining or processing alloys.33) 1.738 (.259-.376 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.691 (.976 (.562) .455 (.396) .963-1.574-.378-.428-.632-.826-1.14 (.955) .381) .11-1.317 (.273 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.13) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 209 .00) .363) .16) .342-.733-1. Cobalt is absorbed by oral and pulmonary routes.329 (.475 (.753) 1.313-.838 (.847) .707) .278 (.756 (.324) .694) .792-1.324-.598 (. 1994).313 (.24) .737 (..757-1.301) .360) .457 (.327 (.282 (.457-.500-.561) .895-1.400 (.471-.964 (.975 (. Exposure in the workplace may come from electroplating.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 . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.429) 1.804) 1.487-.640) .500 (.349) .304) .679-.479-.700 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.326-.611) .334) .25 (.929) .529 (.425-.259 (.615) .49) 1..339-.306 (. an essential human nutrient.388 (.293 (.290 (.314 (.394) .402 (.50 (1.00 (.275-.333-.361 (.983-1.362 (.248-.234 (.256-. population from the National Health and Nutrition Examination Survey. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.23 (1.387) .523 (.313-.534-.744) 1.279) .296) .905) .792 (.03 (.344-.857-1.900-1.. 1979).388 (.426 (.328 (.750-.740-1..274-.960 (.409) .449-.581) .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 .562) .435 (.290 (.728) .328) .277-. respectively.83) 1.513) .06 (.35) 1.393-.647) .352 (.774 (.10) Total .667-1.442-.15) 1.396) .963-1.353 (. 2003).243-.392 (.467-.300) .407 (.365) .Metals fabricated from cobalt alloys (Lhotka et al.683-.513 (.27) 1.463-.439) .433) .282-.313-.723 (.60) 1.872 (.830 (.352) .879-1.547 (.04-1.938-1.600-.560-.700 (.638-1.781) 95th 1.479) .393 (.630-. and to a lesser extent. A portion of cobalt retained for long periods is concentrated in the liver.626-.503-.17) .11-1.298 (.290 (.421) .386 (.257-.505) .591 (.268 (.16 (.990) .452-.09) 1.369 (.272-.302-.704-.248-.833-1.635 (.534 (.301-.417 (. 1972).533 (.237-. cobalt is excreted predominantly in the urine.02 (.251-.842) .938) .850 (.36) 1.278-.378-.786-.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 .408 (.821-3.911-1.434-.522) .310) .289) .239-.963) .319-.844 (.476-.335 (.457) .30 (1.537 (.352 (. interval) .368) .365-.407) . 1994.29) .508-.361-.309) .449) .368) .500-.333-.323) .777-.55) .

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

Ziaee H. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Iversen BS. Cobalt and antimony: genotoxicity and carcinogenicity. Zweymuller K. Thakker DM. Biological monitoring of workers exposed to cobalt metal. et al. Boca Raton (FL): Lewis Publishers. Sabbioni E. Chess DG. Schramel P. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Fujimura N. DeSantis V.88(4):443448. Sci Total Environ 1997.34:620-626. Vitali MT. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Kiilunen M. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Cannon SR. Contact Dermatitis 2003. Thabe H. Kuska Y. Schaller KH. Peltier A. et al. Hoher T.” Contact Dermatitis 2001. Lauwerys RB. Sanghrajka AP. Sci Total Environ 1994. Occup Environ Med 1994.204:147-160.51(7):447450.406:282-296. Edmonds CJ. salt.21(2):189-195. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Falcone G. Respiratory health of cobalt production workers. Kristiansen J. Health Phys 1979. Pisati G.69(3):193-200. Schank M.28(5):1121-1128. J Occup Med 1992.44:124-132. Roto P. HoffmannB. 1985. Jarvis JQ. Br J Ind Med 1993. Ichikawa Y. Goto S. a study of 13 elements in blood and urine of a United Kingdom population. Mosconi G. Sci Total Environ 1998.533:135-152. Oksa P. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Kriss JP. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.20(1):25-31.150:177-183. A report of two cases from mineral assay laboratories and a review of the literature. Sci Total Environ 1994. Sabbioni E. Weber A. Uitti J. J Bone Joint Surg Br 2006. Iavicoli I. Leghissa P. Molders J. oxides. Clin Orthop Relat Res 2003. Radulescu M. Meier R. Long-term clearance of inhaled 60Co.148:241-248. et al. Lison D. Dunning SP. Lison D. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. J Orthop Res 2003. Zedda S. Goto S. Salama A. McMinn DJ.150.48:172-173.95:29-37. Lasfargues G. Zobelein P. Christensen JM. McCalden RW. Chest 1989. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Goldberg MA. Occup Environ Med 2001. Meyer zum Buschenfelde K-H. Gross RT.45:246-247. Hoet P. Steffan I. Lisi P. and cobalt metals. Am J Ind Med 2003. Lhotka C. Laippala P. Cobalt cardiomyopathy. Carnes WH. Zhuber K. Bozec C. J Trace Elem Med Biol 2006. Am J Epidemiol 1998. Cresti R. Lauwerys R. Cleland D. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. J Bone Joint Surg Br 2005. Buchet JP. Kraus T. 2001. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Sabbioni E. Kusaka Y. Kirsch-Volders M. Linnainmaa M. X. Palmroos P. Hammon E. Ghat IS.50(9):835-842.157:117121. Alessandrelli M. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.58(10):631-634. Moulin JJ. Co-sensitivity between cobalt and other transition metals. Tilley S. Blunn G. Szekeres T. Absorption and retention of cobalt in man by whole-body counting. Swennen B. Bacis M. Weyher I.(1-3):133-139. Occupationallyinduced “isolated cobalt sensitization. Pradhan C. et al. Romazini S. Int Arch Occup Environ Health 1997. Health Phys 1972. Unwin P. Arch Intern Med 1990. Trace element reference values in tissues from inhabitants of the European Union. Dickel H. Robinson C. Lauwerys R. Swennen B. Thomassen H. Int Arch Occup Environ Health.Metals effects of cobalt. 3rd ed. Rorabeck CH. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group.36:732-734. et al. Bourne RB. Lison D. cobalt salts.242:1412-1415. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors.55(4):269-276. Wild P.216:253-270. Outcome of occupational asthma due to cobalt hypersensitivity. Barnaby CF. Daniel J. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. and hard metal dust. Buchet JP.150(1-3):167-171. White MA. MacDonald SJ. De Boeck M. Bunn HF. Salvatori S. Shirakawa T. The release of metals from metal-onmetal surface arthroplasty of the hip. J Rheumatol 2001. Angerer J. Linna A. Lung cancer risk in hard-metal workers. Heki S. Diepgen TL. Stanescu D. et al. Mutat Res 2003. Kato M. Dunstan E.22:359367. Science 1988.87(5):628-631. Hedge AG. Smith T. Epidemiological survey of workers exposed to cobalt oxides.

02) 1.90-4.70) 3.90-4.80-4.80) 1.20 (1.30-1.80 (1.50-2.60 (1.900 (.70 (5.00 (1.00) 2.60) 2.10 (1.70) 1.50) 2.70 (3.50-5.93-2.37 (1.60) 1.30 (2.30-5.70) 4.10) 4.20 (1. such as lead phosphate and tetraethyl lead.60) 3.80 (2.20-4.10 (3.20 (3.50 (2.10-2.30 (3. population from the National Health and Nutrition Examination Survey.50) 4.50 (4.00 (1.00-4.30-1.10-2.70 (1.00-6.60) 4.50) 1.60 (2.60-1.30) 2.00) 1.90) 2.40) 1.70) 4.70) 3.40) 1.25 (1.60) 5.00-4.50-5.40-1.00-2.14-1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .71-1.50-2.87) 1.30) 2.Metals Lead CAS No.75-1.90) 3. and 03-04 are 0.09) 1.60-1.50) 2.20 (3.50) 4.60) 1.00) 2.878-1.30-1.60) 2.60) 1.50 (1.25 (1.70) 1.01 (1.90 (2.20 (1.37-1.30 (1.60 (3.20 (3. ammunition.20) 4.60 (2.30 (1.70) 1.40) 5.90) 1.00 (5.81) 1.50-1. ceramic glazes.45-1.50-6.00) 1.00) 5.80-3. 7439-92-1 General Information Elemental lead is a soft.70-1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.90 (1.20 (2.70 (1.10-6.00) 2.30 (1. dense.900-1.20) 2.60-3.80-2.60) 4.40-3.40) 4.52-1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.52-1.80) 1.36-1.22 (1. bronze). Since lead has been eliminated from gasoline.69) 1.g.10-8.80) 2.20-2.30 (2. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.90 (3.20) 3.90 (1.00) 3. Lead was used in plumbing for centuries and may still be present.70-2.12-1.10-2.30-4.00) 2.942 (.60 (3.20) 3.80 (5.04-1.70 (1.69) 1.20) 3.10-2.30 (2.66) 1.60) 4. 0.60-6.90 (4.48) 1.37 (1.60 (4.80 (4.70-5.90) 2.40) 3.60-1.60 (3.10-6.30-1.50-1.10-4.40 (2.90-6.30 (4.70 (2.60) 3. 01-02. solders.90-2.40 (1.51 (1.10-1.51) 1.30-6.20-3.30-2.30) 2.70-4.40 (5.90) 2.30 (4.10) 1.60) 2.70) 4.70 (2.60 (1.S.40-2.39) 1.30) 5.72) Selected percentiles ( 95% confidence interval) 50th 1.32-1.55-1.50-2.91) 1.40) 2. Before the 1980’s.30 (2.62-1. In the past.60 (3.80 (1.50) 75th 2.50 (1.78 (1.50) 5.62) 1.10-1. and for radiation shielding.80) 1.20) 3.30-2.90 (3.20-3.60) 4.50 (1.69 (1.77 (1.10) 1.90) 3.40) 2.30-2.90-4.00 (2.50-3.90) 2.40-3.80 (1.50-1.90) 1.10-3.31) 1.10-2.43 (1.56 (1.60 (2.10 (2.90 (3.40) 1.10 (2.70-1.90) 2. Lead has a variety of uses in manufacturing: storage batteries.70) 1.25) 1.75) 1.60 (1.00-4.50 (4.14-1.30 (1.10) 2.10-1.70-2.10) 3.30 (4.40) Total 1.70 (2.00-1.20-1. Elemental lead can be combined with other elements to form inorganic and organic compounds.80 (3.60) 5.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.50-1.30-1.75-2.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.80) 2.49-1.70-3.60) 1.55-1.60) 2.20) 1.40 (4.40-1.23 (1.90 (3.S.80 (1.90-2.80-5.10) 2. respectively.60-4.50) 5. see Data Analysis section) for Survey years 99-00.90-2.50 (3.10) 3.60) 3.70) 4.40-1.39-1.10 (2.20 (3. malleable.50) 1.60 (2.60) 3. lead was added to gasoline and residential paints and used in soldering the seams of food cans.50-3.60 (1.70 (3.55 (1.90-3.00) 4.50 (2.40 (2.00-1.00 (4.43) 1.89) 1.40) 2.986) .60-1.20) 90th 3.90 (2.60 (2.30 (2.14-1.60) 2.80 (1.28.40 (3.60 (1.900 (.40-4.80 (2.96-2.10 (4.52 (1.65 (1.40-2.40-3.20 (1.90) 5.50-2.00) 4.40-2.10) 5.50 (1.60 (1.90) 1.50) 1.3.800-1.10-3.00 (6.80 (2.20 (1. Lead is most often mined from ores or recycled from scrap metal or batteries.70) 2.80) 3.899-.80) 2.10 (1.40-1.40 (1.46 (1.20-3.20-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (2.70) 1.70 (1. interval) 1.40 (1.60) 1.80) 1.60-4.50) 7.70-2.50 (3.80) 2.60-2. brass.00-5.40 (1.86) 1.60 (1.30 (2.36) 1.80-4.10-3.53) 1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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 2.69 (1.10) 1.50-1.20-2.50 (2.946 (.30-2.20 (3.20-3.43) 1.30-1.00 (4. the main source of lead exposure for the general U.00 (3.17) .30) 95th 5.80) 1.10) 3.80-3.60-2.3.50) 3.20 (4.80 (4.00) 1.80-3.36-1.43-1.80 (1.95) 1.80-3.20 (3.90 (3.66 (1.30 (2.40-5.50-4.87 (1.60 (2. leaded glass. plastics.30) 1.10-3.00) .50) 1.20) .90-2.20-6.50 (2.70-1.70) 3. and 0.20 (2.40-1.10-4.40) 2.90-4.45 (1.00) 6.75 (1.10 (1.80-4.32-1.20) 4.80 (5.83 (1.62 (1.20) 5.00) 1.19 (1.50-4.68-1.40-6. antique-molded or cast ornaments.00) 1.40-6.70-6.34-1. metal alloys (e.00) 3. blue-gray metal that occurs naturally in soils and rocks.40-1.10-2.20 (3.43 (1.

30-2.960 (.625-.40) 1.822-1.757-.729-.10 (1.78-2.940 (.753 (.20 (2.30) 2.20) .700-.641-.808 (.857) .13-3.86) 1.86-2.62-4.50) 1.40 (2.691-.600 (.03-2.700 (.00-1.731 (.10-1.80) 3.40 (1.620) 1. or after soluble lead compounds are ingested.44-2.19 (1.900-1.677 (.80) 3.14 (1.40-5.700-.900-1.80-3.40-3.80 (2.80-2.10-3.800) .600) .20) 1.800-1.40 (2.80) 2.20 (1.90-3.600-.480-.625 (.526-.848 (.70 (1..708-.605) .00) .12) 90th 2.86 (1.72) 1.70 (2.90 (1.82 (1.00 (2.90 (2.90 (2.10 (.700) 1.1.600) . 0.636 (.73 (1.40-1.29) 2.00-1.40-1.75) 4.18-1.500-. lead-containing folk remedies and cosmetics.70) 1.50-2.40) 2. 01-02.30) 1.31-3.580-. stained glass framing.50 (2.20 (3.556-.710-1.564 (.600-.00 (1.21 (2.990) 2. Approximately half of the absorbed lead may be incorporated into bone.S.70-2.82 (2.931) .690) 75th 1.90-2.00 (. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.00) 1.80) 2.773) .700-.62) Total . dust.800 (.688 (.70 (2.661-.650) 1.579-.941) .g.680) .50) 3.20-1.00-2.40) 1. 2000).70-3.49) 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 .700 (.40 (1.680-.900) .600-.749) . Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.30) 2.10) 2.10-1.60-2.90) 1.695 (.29 (2.553-. In the blood.52 (1.50) 2.00) .50-2.90-2. lead-based painted surfaces undergoing renovation or demolition.600 (.04) .40) 1.00 (1.651) .80-2.810-1.10) .900-1. and 03-04 are 0.90) 2.700 (.50 (2.60-3.00-2.20 (2. bullet fragments retained in human tissue.920 (.10 (.833 (.800) .10-3.628) 1.41) 2.955-1.70 (2.24-1.800 (.833-1.40 (1.900-1.990) 1.70) 1.970-1.800) .90 (1.30) 2.506-.540-.04 (.90) 2.745-.40) 2.10-5.64) 2.1. imported children’s trinkets and toys.900) .960-1.91) 2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.590 (. 2007.90-4.10 (.640 (. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone. older plumbing systems with leaded pipes or lead soldered connections.795 (.10-1.10-3.80) 2.579-.862) .40-1.700 (.00) 2.40) 1.80) 1.27 (1.40 (2.710-. respectively.00) 2.10 (1.60 (1.640-.572-.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. 1991).30) 1.40) 1.613) . However.70) 2.674) 1.02) 1.680-.700) .04-2.20) 1.630 (.560-.10-1.700-1.570-.30-5.66 (2.60 (1.50-2.60 (2.59-2.900 (.700-.850 (.800-.900) .70) 3.33-2.52-1.800-.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60 (1.900) .04 (. population from the National Health and Nutrition Examination Survey.90-2.00 (1.14-1.558 (.10) 2. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.752 (.20) .800 (.80 (1.60-3.90-3.75) 3.573 (.828) Selected percentiles ( 95% confidence interval) 50th .90) 2.40) 2.90 (2.14 (1.20 (1.00 (1.815 (.10) 1.66 (2.591 (.659 (.620 (.80) 1.07-1.80) 1. lead-contaminated dust in indoor firing ranges.52-1.78-2.78-2. battery and radiator manufacturing) and recreational sources.900) .40-1.30 (2.50) 2.642 (.923 (.610 (.80) 2.07 (.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 1.660) . pewter utensils and drinking vessels.730 (.900) .30) 1.540 (.738) .27) 1.900 (.20 (1.22) 1.33 (2.30-1.800 (.40-2.40 (1. CDC.20-1.30-1.790 (.616) .30) .986) .701) .671-.40 (1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (1.35 (.20 (1.535-.700-.20 (2.595-.86) 95th 2.50 (1. interval) .20) 1.10) .820-1.785) .700 (.920 (.818) .70) 1.89) 2.17 (1.20 (1.. Fourth National Report on Human Exposure to Environmental Chemicals 213 . 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.50 (2.50 (1.00-2.23-4.900 (.70) 3.32 (1.935) 1.718) .Metals occupational (e.840 (.604 (. see Data Analysis section) for Survey years 99-00.50-1. or water contaminated by mining or smelting operations.10 (1.30 (1.637-.20) .800-1.50-3.50) 1.09) 1.90 (1.30-3.00-1.03 (1.800) .30-1.30-1.33.49 (1.11 (1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.766 (.30) 1.40 (2.589-.80 (1.50) 1.20-2.04) 2.80) 2.90-2.11) 2.10-1.13) .23) .40) 3.00) .20-1.97) 4.70 (2.600-.20) .700 (.915-1. and 0.910-.960-1.20-2. and contact with soil.30 (3.800) .60 (1.02 (.06) .59) 1.60-2.60-1.31 (1.10 (1.600-.60) 2.00) .40) 2.

63) 4.657) 1. For instance.588-.645-.559-.981-1.49 (1.37-1.66) 2.988 (.06) 1.83 (2.55 (1.15-3.97) 1.979 (.632 (.957-1. BLLs and associated toxic effects differ in children and adults.14) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.11 (.87) 1. seizures.603-.469 (.918-1. with a half-life of years to decades.26) 2.08) .962 (.22) .763) .41-1.963-1.79 (1.50 (1.933-1.10 (.89-5.828-1.977) 1.940 (.73) 2.655-.71 (1.594-.88) 2.58) 1. 1996).08) .11-1. and iron.702) .22-2.10) 1.01 (. The skeleton acts as a storage depot.988-1.35) 2.36-2.18) .900 (.753) .07-1.862-.898) .19) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.62-2.38 (2.31 (1.62-1.887 (.03 (.12-1.03) 90th 1. CDC.00 (1.85 (1.938 (.75 (2. 2004. Lead can cross the placenta and enter the developing fetal brain.22-1.709 (.838) .05 (.639 (.88-2.50-2.28) 2.604-.56) 3.698) .676) .09-1.635 (.18) 2.696 (.43 (1.608 (. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.917-1.98) 2.594-.09-1.652 (.920-1.02-1.03) .31) 1.587-.926 (.63) 1.639) .72-2.64) 2.00) .725) .53-1.61) 1.86 (1.793-1.408-.03 (.853-1. O’Flaherty.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 1.812-1.15-2.43-1.428) .712 (.50) 1.618 (.44 (1.11 (1. zinc.73-2.97 (1.702) .61) 1.681-.82) 1.617-.601-.682) .52 (1.918 (.14 (1.70 (1.677 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.11) 1.24 (1. Staessen et al.03 (.997-1.09) 1.686) .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 .461) . and nails (Leggett.50-1.61) 1.Metals 90% of the body lead burden in most adults.41 (1.85-2. and through binding to ion channels and regulatory proteins. 2007).625 (.718) ..707 (. The toxic effects of lead result from its interference with the physiologic actions of calcium.56-2.742) .68 (1.00 (. Approximately 70% of lead excretion occurs via the urine.64 (1.667-.18) 1.59-3. 1993.46 (1.20-3.62-3.31 (1.43) 2.679) 1.74 (1.607-.97) 1.11 (1.730) 1.721 (.75-2.734) .41) .702-.11) .72-2.98-2.03 (1.648 (.383-.15-2.64) 95th 2.78 (2.758) .722 (.586-.535) .701) .641 (.681-.65-2.78-4.88) 2.51) 1.52) 1.460-. Schwartz.541-.17-1.15) 1.612-.40-1.05 (1.571-.07) .774 (. based on prospective population studies.39-1.64-2.606-.380-.668-.46 (2. and paralysis.34-1. population from the National Health and Nutrition Examination Survey.583-.50-2.375 (.47 (2.20) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .621 (.31 (2.404 (.71-2.00 (1.644 (.77) 2.26) Total .742) Selected percentiles ( 95% confidence interval) 50th . with lesser amounts eliminated via the feces.0) 3.09-1.44) 1.615 (.914 (.25-1.94 (1.765) .790) .588-.673) . kidney injury.718) 1..03) 1. Large amounts of lead in the body can cause anemia.53) 1.731-.810 (. interval) .05-1.938-1.43) 1.96 (1.33 (1.18) 1.38 (2.18 (1.25-1.432 (.841-1.33-1.828) .592-.03-2. 1991.876-1.658 (. 1993).67-4.45 (1.851) .79) 1.66 (1.08-2.19-5.02) 1.623 (.31) 1.551-.47) 1. 1995).50-2.10) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites 214 Fourth National Report on Human Exposure to Environmental Chemicals .88) 1.10 (1.701 (.579-.683-.679-.710) .38 (2. Nash et al.654) .605-.609 (. In 1991.990 (.671 (.37-1.615 (.638 (.06) .633 (.404-.61) 1.28-1.722 (.639 (.28) .05-1.22) 1.89-2.496 (.85) 1. the Centers for Disease Control and Prevention (CDC) established a BLL of 10 Urinary Lead (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.51 (1. 1995.17 (.688) .23 (1.645-.893) .739) .07 (.61) 3.62) 2.992-1.698) .15) 1.97-18.593 (.44 (1.703) .708 (.83) 1.79) 2.85-2.72) .06 (.644) .88 (1.56 (1.55 (1.796-1.92) 2.781-1.700-.975-1.914-1.56-3. encephalopathy.623 (.03) 2.03) 2. scant amounts are lost through sweat.65 (1. abdominal pain.882-1.20) .870 (.01) .29 (1.933) .510-.47 (1.03) .20) .667) . 2003.03) 1.914 (.608-. through the inhibition of certain enzymes.342-.508) .992-1.436) .693 (.66 (1.677) . hair.655) .27 (1.404 (.639 (.677-.S.720 (.00 (1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.649 (.33) 2.94-2.98 (1.48 (1.33) 1.720 (.06 (1.561-.492-.946-1.655) 75th 1.755 (.725) .622 (.670) 1.04) 2.800-.04-3.43 (2.400) .603-.659-.529-.569 (.69 (1.746) .571-. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al..667-.971 (.22) 1.11 (.603 (.

..7 µg/dL and 4.. 2003. Schwartz et al. usually with BLLs greater than 40 mg/dL. 1998). 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. Borja-Aburto et al. Overall. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. Surveillance data reported by U. 2003). Information about external exposure (i. The U. 2006).g. 1996. environmental levels) and health effects is available from ATSDR at: http://www. CDC. including minority race or ethnicity. 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. when the geometric mean BLL was 2. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. 2003.2 µg/dL in males and 3. 2007). Pirkle et al. and low family income (CDC. EPA. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. 1994). 1999). Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 1991. At low environmental exposures. urban residence. which is an 84% decline. adults in the 19992000 NHANES sample (Apostoli et al.. 2002. 1987.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1.. and spontaneous abortion (Baghurst et al. approximately 11. almost double the geometric mean of 1. and decrease fertility (Alexander et al. 2001).Metals µg/dL or higher as the level of concern in children. More recently. the geometric mean BLL was 3. IARC considers inorganic lead compounds probable human carcinogens. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. adults in the 1999-2000 NHANES sample.3 million children tested had BLLs of 10 mg/dL or higher (http://www. 2006). respectively. and organic lead compounds not classifiable with respect to human carcinogenicity. 2003. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. 1995.000 adults. residing in housing built before the 1950’s... adult population has similar or slightly lower BLLs than adults in other developed nations (CDC..0 µg/dL in females (Soldin et al.S. 2005a). higher than 100-200 µg/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. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. 1984. 2002). Fourth National Report on Human Exposure to Environmental Chemicals 215 .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. Muntner et al. may alter sperm morphology.S.. 2000).6% in NHANES 1988-1991 to 1. 2009).. particularly in the skeleton.S. Both drinking water and ambient air standards for lead have been established by the U.S...html. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 1996. However. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.xls).e.5 per 100. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Korrick et al.. premature delivery. 1996.. For example. and peripheral neuropathy generally occurring at much higher levels (e.. Urine levels may reflect recently absorbed lead.atsdr. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Bellinger 2005.S. High dose occupational lead exposure.07 µg/dL (Becker et al.. adult residents. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors... 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.21% of approximately 3.. Data submitted through state public health programs from 2006 showed that 1.cdc. the prevalence rate has declined annually since 1994 (CDC. Payton et al. 2002a). Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. seizures.6%) were lower than those from NHANES 1991-1994.4% in NHANES 1999-2004. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. 2000). In NHANES 1999-2002 in children 1-5 years old.S..gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.cdc. 2005b. Jones et al. Telisman et al.75 µg/dL in U.. with overt encephalopathy. lead in women may be associated with hypertension during pregnancy. Staessen et al. Schwartz. 2005b). 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. both the geometric mean (1.gov/toxpro2. 1999). In occupationally exposed adults. Lanphear et al. reduce sperm count..4% of children had BLLs of 10µg/dL or higher (CDC.

Teratogen update: lead and pregnancy. Occup Environ Med 1996. Neri A. Meyer PA. Krause C. Semen quality of men employed at a lead smelter. Roberts RR. Preventing Lead Poisoning in Young Children.26:359-371. Auinger P. Caldwell KL. Blood lead levels—United States. Hu H. Available at URL: http://www. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Ewers TG. Inorganic and Organic Lead Compounds. Reese YR. Acquisition and retention of lead by young children. doi:10. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2002. CDC. Blood lead levels measured prospectively and risk of spontaneous abortion.gov/nceh/lead/ CaseManagement/caseManage_main.cdc. Ronchi L. Am J Epidemiol 1999. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Atlanta (GA).113(4):1016-1022. Lepom P. Kaus S. 4/14/09 Centers for Disease Control and Prevention (CDC). 2005b. Muller CH. Hertz-Picciotto I.87:1-471. Robertson EF. Batuman V. Age-specific kinetic model of lead metal in humans. Am J Public Health 1999. 2003-2004. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Mantere P. Environ Res 2000. Hernberg S. Sci Total Environ 2002. Neurodevelopmental effects of postnatal lead exposure at very low levels. Lanphear BP. Angle CR. Hunter DJ. Public Health Rep 2000.150(6):590-597. Available at URL: http://www. References Agency for Toxic Substances and Disease Registry (ATSDR).287:1-11. MMWR Morb Mortal Wkly Rep 2006. MMWR Morb Mortal Wkly Rep 2005a. et al.115:521-529. Speizer FE. Cory-Slechta DA.54(20):513-516. Atlanta.cdc. Becker K.275:1177-1181. Cox C.205:297-308. Wigg NR. Available at URL: http://www. Neurotoxicol 1987.html.gov/toxprofiles/tp13. Birth Defects Research (Part A).htm.htm. Apostoli P.89:330-335. Hu H. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.10:43-50. Wager C. Atlanta (GA). Neurotoxicol Teratol 2004. The relationship of bone and blood lead to hypertension. Jacobson JL. Lead. Luukkonen R. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 4/14/09 Centers for Disease Control and Prevention (CDC). McMichael AJ. Managing Elevated Blood Lead Levels Among Young Children. Kim R. 1999-2002. Environ Health Perspect 1993.htm. Ga. Available at URL: http://www. Schulz C. Adult blood lead epidemiology and surveillance—United States. Ganzi A. Henderson CR. Brody DJ. Blanco J. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.82:60-80. 1988-2004. 4/14/09 Centers for Disease Control and Prevention (CDC). The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Farias P.cdc.Metals Biomonitoring studies on levels of lead provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of lead than are found in the general population. Chiodo LM. Weiss ST.275(15):1171-1176. Scand J Work Environ Health 1984. Sparrow D. Sparrow D. Third National Report on Human Exposure to Environmental Chemicals. IARC Monogr Eval Carcinog Risks Hum 2006. et al. Manton WI.101(7):598-616. van Netten C. Borja-Aburto VH. Hänninen H. Cox C. 2005. Checkoway H. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.53:411-416. Jacobson SW. Korrick S. Bellinger D. Stanek KL. Rotnitzky A. Coresh J. Lanphear BP. Aug 2007 [online]. Homa DM.73:409-420. N Engl J Med 2003. Vupputyuri S.8(3):395-401. Baj A. 4/14/09 Centers for Disease Control and Prevention (CDC). Korrick SA.gov/mmwr/preview/mmwrhtml/ mm5532a2. Lead and hypertension in a sample of middle-aged women. Jones RL.gov/nceh/lead/publications/ books/plpyc/contents. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Seiwert M. 2002 [online]. Payton M. Baghurst PA. gov/mmwr/preview/mmwrhtml/mm5420a5. JAMA 1996. et al.55(32):876-879.1542/peds:2007-3608. 4/14/09 Alexander BH. 1991 [online].348:15171526. Leggett RW. Rojas LM.123:e376-e385. Rotnitzky A. Weiss ST. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Rios C. Toxicological profile for lead. Dietrich K.cdc. Available from URL: http://www.htm.cdc. Bellinger D. Bavazzano P. Pirkle JL. Canfield RL. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Jusko TA. Blood lead reference values: the results of an Italian polycentric study. JAMA 1996. Pediatrics 2004. Aro A. Hu H. Kaufman JD. Muntner P. Pediatrics 2009. Kuehnemann TJ. Vimpani FB. et al. et al.atsdr.

Hu H. Soldin SJ. Wilhelm M. Paschal DC. Brody DJ. Sparrow D. Blood lead. J Hum Hypertens 1995. Fourth National Report on Human Exposure to Environmental Chemicals 217 .118:16-29. O’Flaherty EJ. et al. JAMA 2003.9:303-327. Gunter EW. Soldin OP. IV. Arch Environ Health 1995. Jurasovic J.104(1):60-66. Schwartz J. Smith DR. Schulz D. Low-level lead exposure and renal function in the Normative Aging Study. Clin Chim Acta 2003. Hickman T. Lee SS. population to lead: 1991-1994. stable lead isotopes to determine release of lead from the skeleton. Amery A. lead. blood pressure and cardiovascular disease in men.108(1):45-53. Exposure of the U. and hypertension in perimenopausal and postmenopausal women.63:1044-1050. Am J Epidemiol 1994. Lee BK. Physiologically based models for bone-seeking elements.140:821-829. Magder L. Lustberg M. Kinetics of lead disposition in humans.209:301305. Cvitkovic P.Metals results from NHANES III. Weiss ST. Sherwin R. Pirkle JL. Am J Epidemiol 2001. Lead. Kaufmann RB. Stewar WF. Gavella M. Hanak B. dimercaptosuccinic acidchelatable lead. Lauwerys RR. Revised and new reference values for arsenic. Rocic B. cadmium. and tibia lead with neurobehavioral test scores in South Korean lead workers. Blood lead concentrations in children: new ranges. Payton M. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Environ Health Perspect 1996. Kidney Int 2003.153(5):453464. Telisman S. Schwenk M. Staessen JA. cadmium. Nash D. Hwang KY. Roels H. blood pressure. Schwartz BS. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Lee GS. Osterloh JD. 50:31-37. et al. zinc. Low-level lead exposure and blood pressure. Pizent A.327:109-113. Kaufmann R. Environ Health Perspect 2000. Flegal AR. and copper in men.106:745-750. Association of blood lead. Rubin R. Int J Hyg Environ Health 2006.S. Environ Health Perspect 1998. Use of endogenous. Toxicol Appl Pharmacol 1993.289(12):1523-1531.

700) .40 (4.60-6. The ingestion of methyl mercury.00 (2..30) 3.418-.00 (.40 (4.50-2.700-.60 (2. 1993).655-. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.00) 1.00 (. interval) .814 (.600 (.00-5.860-1.300-.500 (.700-.800-1.714-.300 (. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.30) 3.30-6.900) .40-3.30 (2..285-. and mercury compounds are still used as preservatives (e.00) .60) 1.700 (.800 (. which create an episodic potential for volatization and inhalation of mercury vapor. After elemental mercury is absorbed.2.g.90 (1. Elemental mercury is a shiny.Metals Mercury CAS No.372) . Poorly absorbed from the gastrointestinal tract.g.40-2.g.326 (.50) 1. to form inorganic mercury compounds or salts. have often required public health intervention (Zeitz et al. synthetic organomercury compounds were once used in pharmaceutical applications.472-.70 (3. merbromin).30-5.400-.300) .700) .800-1.60-6. predominantly from fish and other seafood. phenylmercuric acetate) or topical antiseptics (e.00 (. IARC. thermometers. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. 1998. 2002). or oxygen. electrical lamps.419 (.40 (3.689-.877 (.00 (2..563 (.60-5. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).30-4.60 (1. mercuric chloride).400 (. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. solid-waste incineration.20-4.00) 3.g.00 (.00 (1.50-3. 1980. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.703-.900 (. see Data Analysis section) for Survey year 03-04 is 0.50) 4. Woods et al. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.484) .80 (1..800 (. an organic form of mercury..40) 3. In addition.80) 1.50) 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 .600) 1. Survey years 03-04 Geometric mean (95% conf.02) . Other major uses include electrical equipment (e. which can bioaccumulate in aquatic and terrestrial food chains.500 (.500) .400-.90) 95th 4..781 (. and mining and smelting.60-2. such as chlorine (e.979 (.70 (1.00) 1.574) . Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.30) 1.30 (1.S. Also.672) .800-1.500-.S.70 (4.50) 5.90) 90th 3. inorganic. Accidental spills of elemental mercury.797 (. and is distributed to most tissues.90 (4. The kinetics of the different forms of mercury vary considerably.90-3.800 (.927) .776 (. thimerosal.80 (3. thermostats and switches).900) 75th 1.50-1. and dental amalgam.30) 1.363-.80 (1.700-.40-1.40-2.753-1..10-3.80) 4.30) 5.10) .800-1.490 (. Hursh et al.700-.30-2. may contain inorganic mercury.886) . population from the National Health and Nutrition Examination Survey.903) Selected percentiles ( 95% confidence interval) 50th . 2007).800 (. constitutes the main source of dietary mercury exposure in the general population. Some cosmetic skin creams from countries other than the U.60) 1.50) 2. Kingman et al..90) 3.20) 2. sulfur.700-.900) 1.90 (1.12) . Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.60-3.800-1.00 (2. Atmospheric elemental mercury can be deposited on land and water.900) 1. 218 Fourth National Report on Human Exposure to Environmental Chemicals . elemental mercury is absorbed mainly by inhaling volatilized vapor.00-1.20 (2.20-4.. 1999 . 1994.60 (1.40) 1.20-3.70-2. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. Apart from methyl mercury.40-1. with the highest concentrations occurring in the kidneys (Barregard et al.70) 911 856 2081 4525 03-04 03-04 .919) .60) 2085 2293 3478 Limit of detection (LOD.80) 3.00) 4. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).30) 4132 4241 03-04 03-04 03-04 .70 (1.900) 1. and organic forms. sphygmomanometers and barometers. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.40 (3.500-.80 (1.

1995.30-4.50) 3.70 (1...299-. 1993).0) 4.200-.70-3.800) 1.800 (.20-2.70) 1.00-3.30 (1. 1969.90 (3.70-5. Smith et al.Metals the tissues to mercurous and mercuric inorganic forms.200 (..90 (4.900-1.60 (1. Myers et al. 1999).30-5.600) .73) 1..29) .825-1..20) .30-11.00-2.90) 2.600 (.60) 3. 1994.S. a measure of accumulated dose (Cernichiari et al.900-1.10 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0..90) 90th 1.40) 5.40) 1.60) 1.20 (2..00-6.317 (.318 (.. After exposure to elemental mercury..700 (. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.300 (.30) 3.10) .256-. 1998).800-1.10 (.300) .00) 1.. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.90 (4.50-12.377 (..10-1..800 (.200 (.500-1.40-2.300 (.800) ..00-2. 1992 and 1999.60 (1.10 (1.06-1.80 (3. 1996.10) 1.329 (.300 (.50) 1.90) 2. Methyl mercury is incorporated into growing hair.600) .50-2. Jonsson et al..919) .800) 1.60 (3.06 (. Fourth National Report on Human Exposure to Environmental Chemicals 219 . Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.200-...20) 1. for both acute and chronic exposures.01) .900 (.407) . Miettinen et al.700-.475) .90 (1.500-.824) 1.30-2. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. Suzuki et al.40) 2.833 (.200-.30-4.60 (3..400-. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.10 (3.00) 2.30 (1.90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .300) . and a useful marker of exposure in epidemiologic studies (Grandjean et al.200-.35 (1.60 (1.820 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. Methyl mercury enters the brain and other tissues (Vahter et al.20 (.70-5.10) .30) 1.80 (1.300 (.00) 7... 1999-2002. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .10 (.00 (2.00-2.14.20-3.90) 5. population. 1994).00 (1.20-3. 2005).30-6.14 and 0.726-1.00-1.667 (.60 (2.343 (.70-3. Vimy et al.40 (1.00) 6.500-.70) 4.664-1.00) 1.700-1.10-3.700 (.20) .377) . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.300) . 1996).297-.. 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.40-2. 1992. thereafter.800) .307 (. 1993).70-6.30) 1.40 (1.00) .800-1.00) 4. 1973). National Health and Nutrition Examination Survey.20-11.200-. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.700 (.30-6. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.800) 75th .02 (.300) .50) 2.00 (3.900 (.20-3.800 (.300) . 1984. McDowell et al.40-1.700-.90 (1.80-3. Vahter et al.30-3.3) 4.500-.50 (1.269-. 2003). with most elimination occurring through in the feces (Sherlock et al. Geometric mean Survey years (95% conf.369) 1.50) 1.700 (.23) .738-.50) 95th 2. 2003)..265-. 1971).940) Race/ethnicity (females.90) 3.500-.70 (1.30 (1. Sandborgh-Englund et al. 1991. Smith and Farris. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.80) 579 527 370 436 588 806 Limit of detection (LOD. 2004.70) 4. Excretion occurs by renal and fecal routes.268-. 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.60) 2.30-6.200-. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.10 (5.10 (1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.395) .70 (1.700) 2.500 (.80) 1.00 (2.541-.500 (. 1992)..700-1.900 (.800-1.50 (2.7) 4. 1975. 1998).374) .871-1.00 (2.60) 1.944 (.500-.30 (. 1990).50-3.697-.27) . interval) Selected percentiles (95% confidence interval) 50th . 1994) and then undergoes slow dealkylation to inorganic mercury.300) .

2005). and neurocognitive and behavioral disturbances.42. Inorganic mercury exposure usually occurs by ingestion..700 (.600) . 2000. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.500-.700 (.600) . Stern 2005.S. 2004. altered physical growth. anorexia. 1995.. and pinkish discoloration of the hands and feet (Tunnessen et al. hearing impairment. particularly irritability. Vupputuri et al. Sakamoto et al.600-. irritability.600 (.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .600 (. limb deformities.600 (.700 (.500 (<LOD-.600) . see Data Analysis section) for Survey year 03-04 is 0. In recent epidemiologic studies.600 (.. gingivitis..600) . Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.600 (. 1993).700 (.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 . 2006..500 (. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure.600 (. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. dysarthria.500-. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 1983).. At levels below those that cause acute lung injury. 1963). high-dose exposure to elemental mercury vapor may cause severe pneumonitis. 1998. 2004. DeRouen et al. which may vary for some chemicals by year and by individual sample.600) . the existence of a causal relation is unresolved (Chan and Egeland. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.. 220 Fourth National Report on Human Exposure to Environmental Chemicals . Sakamoto et al. pain in the extremities.600 (.500-.600-. dysarthria... 2002. causing parasthesias. 1995..600) . The constellation of findings may include anorexia. hypertension. Smith et al.600) . Rice.800) . 1987). 2000.500-. short-term memory loss. insomnia.600) .600) . 2003). 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. Smith et al. overt signs and symptoms of chronic inhalation may include tremor. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) 2007 2240 3406 Limit of detection (LOD... 2006.500-. Oskarsson et al.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..700-. Rissanen et al. Once absorbed.700) . depression.. and cerebral palsy (NRC. ataxia. Overt poisoning from methyl mercury primarily affects the central nervous system.500 (. Drexler and Schaller..500-. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. fatigue. 1996). < LOD means less than the limit of detection.600 (. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. and progressive constriction of the visual fields.. Salonen et al.800) . 2004). Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.600-.Metals may be more efficient for inorganic mercury (Grandjean et al. 2000).500-.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . 1970. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Factor-Litvak et al.500 (<LOD-. Bellinger et al. typically after a latent period of weeks to months..600-.700-.500) . population from the National Health and Nutrition Examination Survey. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. sensory impairments.700 (.700 (. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. cerebellar ataxia. 1951. maculopapular rash. Survey Geometric mean (95% conf. and sleep disturbance (Bidstrup et al. Acute.500-. 2005.. 2004).500-.700-.

2009).350-.430 (.76-3.358 (.610-1. Information about external exposure (i.492) Selected percentiles ( 95% confidence interval) 50th .520) .05) 3.290-.61) 1. 2003). Benes et al.476 (..530) . Fourth National Report on Human Exposure to Environmental Chemicals 221 .93 (1.26 (1. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.30) 3.85-2.330 (.S.19 (1.840-1. particularly methyl mercury.14-2.460) . However.580) .24 (2. range 40 years to 78 years) had an average total blood mercury concentration of 2.03-4.495 (.gov/mercury and from ATSDR at: http:// www. the total blood mercury concentration is due mostly to the dietary intake of organic forms. During the same survey periods. 1995.63-2.00) 1.400 (.405-. 2006)..78 µg/L for adults and 0.14) 90th 2.S.160-. and the age-related changes differed across the groups (Caldwell et al.89) 3.433 (.463) . who participated in a 1998 representative population survey (Becker et al. Grandjean et al.33 (2.96 (1. 758 children. the median concentration of blood mercury was 0. 1998).67-2.254 (.360-.870-1.S.447 (.60 (1.05) 1.960 (..430 (..23) . 2001. Survey years 03-04 Geometric mean (95% conf.42) 95th 3.509) . From 1996 through 1998.13-2.16 (.770-1. 2001.58 µg/L for 4645 adults.23) 2.55 µg/L.330-. et al.870-1.413-.250) .396-. environmental levels) and health effects is available from the U.e.Metals standard for inorganic mercury has been established by U. average age 9.480) 75th 1.442-. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.76-3.313-.01 (. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.530-.840) 1. total blood mercury increased with age. see Data Analysis section) for Survey year 03-04 is 0.34-3.52) 2.570) .S. population from the National Health and Nutrition Examination Survey.700-1.67-3.420 (.39-3. Schober et al.08 (1. Total blood mercury levels increase with greater fish consumption (Dewailly et al. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.460 (.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 . 2004. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.07 (..430) ..65) 1.. 2003). 1998).416 (. interval) .78-2.60) 619 713 1066 Limit of detection (LOD.14.18) 2..88) 287 722 1529 03-04 03-04 .gov/toxprofiles.370) . 2002).340-.09 (2.00 (.. Biomonitoring Information In the general population.360-. total blood mercury geometric mean levels in females aged 16-49 years did not change.28) 1.441 (.700 (. Over the NHANES 1999-2006 survey periods.08 (1.840-1.66) 3.360 (..31) 2.. 2009). Among the three racial/ethnic groups. military veterans (mean age 52. These distinctions can help interpret mercury blood levels in people.68 (2.330-.930-1.46 µg/L for children.200 (.96 (1.88 (1. 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.420 (.280-.atsdr.60-2. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.530) .77-2.99-6.330-.304) . In Germany the geometric mean for blood mercury was 0. Kingman et al. average age 33 years.54 (2. aged 18 to 69 years.480 (. EPA at: http://www.410-.9 years).. EPA.509) .19 (2.97) 2.408) .8 years. Mahaffey et al..46) 3.16 (1. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.cdc.549) .29) 1.88-3.940 (. Sanzo et al.31) 1266 1272 03-04 03-04 03-04 .12 (.24) 1.534) . adult women in several ethnic subgroups (Hightower et al. slightly higher total blood mercury levels were found in U. A cohort of 1127 U. 2000).406-.20 (1.440 (.76-4. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.epa.90) 2. 1997.890 (. and increased slightly in non-Hispanic white children (Caldwell.213-. In NHANES 19992002.382-.555) .

ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.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 . not to imply a safety level for general population exposure. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. 2002) adult population surveys were similar to those in a U.12-3..S.365 (.09) 1. military veterans with dental amalgams.768 (. Levels in U.31 (1..88 (1.535) 1.44) 1.00) 286 722 1529 03-04 03-04 . 2006.1 µg/L.447 (.79) 1.61) 1. 2003).13 (1.365 (.297 (.13-2.455-.301-. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.217 (. reversible increase in urinary N-acetyl-glucosaminidase.447-. 1998). Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. 2005).667-1..384 (..566) .67 (1. 2009)..86) 95th 2. DeRouen et al.392-.486) Selected percentiles ( 95% confidence interval) 50th .964-1.196-.40-1.11) 2.62 (1..800-1.88-2.11-2.696 (.87) 2.616) . mean urinary mercury was 3.630) .545 (. In the study of U.785-1.30) 1. and Italian (Apostoli et al.455-. 2009).307-. Langworth et al.525 (.07) 1.00) 90th 1. women of childbearing age have generally been much lower than these levels (CDC.06 (.40 (1.1 µg/L for each surface with a dental amalgam (Kingman et al.376-.64-2.909 (.522-.368) .06 (.485 (. et al.54 (2. Czech (Benes et al. 1992).587 (.476 (.280-.39) 1.51-2.63) 1.78-4.11) 1. and on average.76 (1.875-1.. Department of Health and Human Services noted that several studies have observed a modest.35 (1. a biomarker of perturbation in renal tubular function. population from the National Health and Nutrition Examination Survey.309-.56) 1266 1271 03-04 03-04 03-04 .652) .498) 75th . Urinary mercury levels in recent German (Becker et al.Metals 2000).255 (.208-.532 (. Survey years 03-04 Geometric mean (95% conf.347) .400-.S..23-2.333-.18-1.588) .385-. 1988.32-2.225-. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.67 (1. 2002).537) .464 (.455) .391-. Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al.620-.87 (1.21) 1.88-2.404-.599) .01) 2.32 (1.687) . the urine mercury increased by approximately 0.265-.79 (1. Urine mercury and the number of dental amalgams were correlated.00 (.391) .306 (.65 (1.S.46-2.S. An expert-panel report recently prepared for the U.289) .714-1.30) 2. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.246-.275) .472-.417) .463 (.03) 2.16) 1. 2006).77 (2.990) . Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .970 (.S.358) . interval) . 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. Information about the biological exposure indices is provided here for comparison.04-3.276 (.362 (.480) . Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.784) 1.25 (.969-1..400) .343 (..443 (.619-.28 (.508 (.41-2. et al.

42-3.579-.501-.97) 2.10-4.615 (.16-5.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .05 (3. 1999-2002.650 (.55-3.54) 595 531 381 442 594 826 Limit of detection (LOD.522 (.650) 1.508-.46) 3.38) 4.45 (1.91 (2.42) 2.76 (1.S.22-3.410-.04-1.94) 1.516 (.719 (.69 (1.46-4.632 (.62 (3.06 (.526-.592 (.790) .56 (1.77) 1.50 (1.27 (1.65) 1.79) 3.636-.710 (. interval) Selected percentiles (95% confidence interval) Survey years 50th .721 (.686) .13-4.605-.600 (.31 (1.51 (3.83-3.44) 3.850-1.16) 5.51) .07) 1.909-1.97 (1.23-1.831) .55) 90th 3.650 (.596 (. population.557-.670) 75th 1.03 (.846) .799) .72) 1.18 (3.810) . interval) Selected percentiles (95% confidence interval) 50th . population. 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.560-.809) .639 (.656-.892) .28 (1. National Health and Nutrition Examination Survey.35 (1. National Health and Nutrition Examination Survey.61) 1.578-.53-3.81 (3.14) 3.84 (2.41-6.553-.606 (.57-4.23-1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.39-3.41 (1.32-3. 16-49 years) 99-00 01-02 .37 (1.31-1.03 (.710 (.540 (.68) 3.14 and 0.42) 90th 2.569-.565 (.30-2.76) 2.502-.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .426-.658 (.09-1.56) 4.00) 2.99 (2.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.59-5.81-6.22 (.92) 3.04-10.41 (1.05 (2.723 (.30 (2.87-4.685 (.582-.655 (.32) 2.806) .46 (1.76-5.99) 1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.45) 2.724 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.637) .620 (.85) 4.14-2. 1999-2002.45-3.03-2.910) .15-1.831) .420-. Geometric mean Survey years (95% conf.45) 2.97) 2.45-2.706 (. Geometric mean (95% conf.664) .07-5.Metals Urinary Mercury−Females Aged 16-49 Years Old.S.24-1.520-.47) 1.709) 75th 1.97) 2.37) 1.622-.740 (.560 (.35) .17) 95th 5.870) .99-2.77) 2.710) 1.450-.95 (2.3) 5.24) 6.657 (.709) .79) 1.699) 1.56) 3. 16-49 years) 99-00 01-02 .70 (2.691) .62 (4.61-6.18) 3.21 (2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.760 (.45) 95th 3.07-2.84 (2.744) 1.15 (2.27-1.92) 2.09-1.631-.772 (.43-1.32 (1.14-1.500-.69-3.616-.540-.91-7.68 (3.14.610-.13 (2.475-.27 (2.50-4.30 (1.774) .665) .624-.520-.00 (3.00 (2.824) .92) 4.387-.52) 3.85-3.89 (2.21 (1.742-1.65-4.48 (2.62 (1.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .98 (5.580 (.930) .832-1.25) 2.03) 1.833) .50 (2.41 (2.99 (3.68-3.10-2.21-3.47) 1.580-.966) .30 (2.

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Newton G. Imai H. Fisher HL. Lorscheider FL. Bolger PM.98(1):133-142. Burbacher T. Am Ind Hyg Assoc J 1970. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Langolf GD. Hongo T. Martin MD. Daniels JL. DeRouen TA.4(5):981-988. Smith JC. Topping G.111(12):1465-1470. McMahon KJ. Dorronsoro M. Aguinagalde FX. Acrodynia: exposure to mercury from fluorescent light bulbs. The kinetics of intravenously administered methyl mercury in man. Turner MD. Sherlock J. Smith PJ. Methyl mercury pharmacokinetics in man: a reevaluation. Suzuki T. Allen PV. Guo S. Matsuo N. The hair-organ relationship in mercury concentration in contemporary Japanese. Woods JS.124:221-229.289(13):1667-1674. Orr MF.48(4):221229. Stern AH. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Smith JC. Environ Res 2005. Farris FF. Public Health Nutr 2001. Vimy MJ.258(4 Pt 2):R939-945. Hall LL. et al. Environ Health Perspect 2007. Takahashi Y. Hislop D. Toxicol Appl Pharmacol 1996. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Shen DD. Yoshinaga J. Jones RL. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Stern AH. Environ Health Perspect 2003. Mottet NK. Whittle K. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Am J Physiol 1990. McDowell M. Toxicol Appl Pharmacol 1994. Friberg L. Vorwald AJ.Metals Sanzo JM.128(2):25125-25126. Public health consequences of mercury spills: hazardous substances emergency events surveillance system.2:117-131.40:413-419. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment.115(10):1527-1531. Amurrio A. Baser M. Osterloh J.31:687-700. Vahter M. et al. Mooney TF.37:245-252. Most B. Environ Health Perspect 2002. Sinks TH. Lind B. JAMA 2003. Patil LS. Blood mercury levels in US children and women of childbearing age. Arch Environ Health 1993. Leitao JG. Azpiri MA. Goldberg J. et al. Sandler DP. 1993-1998. Effects of occupational exposure to elemental mercury on short term memory. Amiano P. Effects of exposure to mercury in the manufacture of chlorine. 1999-2000. Tunnessen WW. The contribution of dental amalgam to urinary mercury excretion in children. Bernardo MF.97(2):195-200.110:129-132. Kaye WE. Nakazawa M. Smith AE. Br J Ind Med 1983. Longnecker MP. Hum Toxicol 1984. Smith RG. Pediatrics 1987. Zeitz P. Vupputuri S. Leroux BG. Toxicol Appl Pharmacol 1994. Environ Res 2005.79:786789. Schober SE.

3 (79.0) 55.2) 41.4) 41. 2001).5) 80.6 (55.2 (63.0 (42. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.1-63.5 (41. Fourth National Report on Human Exposure to Environmental Chemicals 227 .1 (38.1-88.3 (55.0-101) 82. hydrogenation catalysts.1) 46.6-55. 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.4-52.4-75.9 (33.2 (49.0) 54. which exert homeostatic regulation over molybdenum balance.2) 52. urinary excretion over six days CAS No. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.2 (55. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.9-56. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5-41.7) 77.3 (55.5 (74.8) 39.9-83.8-106) 88.0-85. 0.4 (79.7 (58.2 (40. chemical reagents in hospital laboratories.2 (69.3) 37.3-115) 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.3-75. see Data Analysis section) for survey years 99-00.6-62. inks.7-105) 69.5-46.3-91.4) 56.8.5-52.6-58.9 (78.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.2) 37.0) 84.7 (37. Compounds of molybdenum are also used as corrosion inhibitors.7-91.9 (32.7 (44.0 (46.7 (51.3) 54.2-42.5 (67.1) 60.7-39.9) 62.6) 71.6 (55.4 (48.9-82.9 (73.1) 126 (106-147) 109 (94.3) 65. 7439-98-7 General Information Elemental molybdenum is a silver-white.5-124) 108 (92.1) 35.7-60. and in pigments for ceramics.7) 57.6-46.0-53.0 (42. 1997).1-52.6-111) 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. Excretion occurs predominantly via the kidneys.3 (73.5 (41. interval) 45.6-72. 01-02.0 (48.7-47.1) 82.7) 51. population from the National Health and Nutrition Examination survey. respectively.8-94.4) 76.2-70.3 (47.6 (73.8 (42.7) 75th 84.1) 59.5-91.0) 60.Metals Molybdenum or ore deposits.2 (56.5) 47.7-92. At a daily oral molybdenum dose of 24 µg.7-41.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.6) 53.5) 85.0 (43.1-59.6 (43.7 (36.7-96.4) 49.9 (52.4 (48.7-51.2) 53.1-55. 2001.9-55.9 (44.6 (52.5-65.4 (34.3) 41.1-52.2 (61.6 (40.8-49.0) 62.8 (67.4 (72.9 (34.8-108) 87.9) 67.8-90. and 1.7 (50.1) 57.2) 79.7) 46.0) 39.2 (83..3 (38.3 (84.2-59.7) 78.0-56.1 (91.4 (80.4-82.0-110) 90.5 (37.3 (71. aldehyde dehydrogenase.5) 80.4) 42. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.5 (43.2-53.8-46.S.3) 47.0-71.0-62.7) 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 78.7 (73.1-48.2) 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 (98.7) 86.7) 78. and xanthine oxidase (Kisker et al.4-61.7-68.6 (40.8.0 (76.8 (85.4) 45.9-55.8) 40.6) 51.9 (37.7) 45.5-66. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.9 (40.2-37. WHO.7-73.3-108) 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 47.1-51. lubricants. More recently. and paints.0-100) 63.2-59.9-109) 97.3) 83.5 (81.3) 85.0-38. semiconductor and battery industries have begun to use molybdenum.8) 46.3 (64.7-122) 93.8) 75.5) 60.6-96.3 (53.3-44.5-52.2) 48.5 (48.8) 48.0 (41.5 (49.1 (71.0-65.1 (34.3 (46. In humans.5) 44.8 (82.1-44. 1996).0) 45.6) Selected percentiles ( 95% confidence interval) 50th 50.3-47.5-68.7 (45. and 03-04 are 0.4) 52.2-91.0) 97.6) 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7-84.9) 34.6-82.5.6-42.8) 44.6) 93.2-79.3 (37.0 (81.2 (49.2) 40.7 (71.0-77.9-85.6) 71.2 (38.7-50.

2-96.6 (42.8-66.2 (52. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP. 1995).5 (39.8-52.1 (39.8) 38.0-103) 103 (90.1 (33.1-43.5 (40.9-45.7-44.2) 58.9 (79.2) 55.5 (35.1-39. interval) 43.4-76.5-92.3-43.4) 44.2-41.1) 43.6-41.7-120) 87.5 (35.6 (38.5-119) 90.8 (57.2 (50.4-41.5 (59.3-141) 109 (81.0-46.3 (37.6-63.4 (53.9-41.5-50.7) 53..5) 63.1) 65.6 (57.0 (80.7-100) 77.7-93.3 (53.1) 37. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4 (78.8) 38.2-46.2 (40.3 (36.3-45.8-42.6) 39.5) 73.2) 37.1-34.8-46.6) 48.3) 43.1-41.0) 38.4) 58.9-68.6-61.4-66.8) 45.5 (37.1-127) 90.S.0) 53.7) 57. but available epidemiologic data are scant.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.6-45.9-87.6 (59.5-60.1-67.2-65. and clinical or epidemiologic evidence of adverse effects is limited.1 (40.7) 115 (93.5-46.6) 43.2-121) 107 (92.5-35.5-45.3-52.7-38. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.7-43.6-61.2 (57.S.3) 56.2 (40.1) 56.1 (37.6 (71.5 (83.8) 62.3) 37.2 (69. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.1) 37.1 (38. and urinary levels reflect intake from all sources.5 (41.8-118) 81.4) 40.8 (56.3) 40.4 (37.0-38.4) 77.3-68.8) 79..9) 92.3-44.7-62.8) 39.0 (74.5 (78.0 (58.0) 33.5 (40. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3 (71.3-102) 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 40.9 (40.0) 39.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.9-71.6-76.2 (73.2-80.8-84.9 (39.1) 40.2) 42.9) 40.9) 41.9 (73.1-79. Molybdenum is generally considered to be of low human toxicity.2-49.3) 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 85.1 (82.4-42.1 (44. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. In industry.4 (59.3 (58. respectively.2 (43.5 (79.1-81.0) 36.0-120) 85.9-117) 57.4 (55.9 (49.2 (33. EPA.2) 38.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.8) 37.6-63. 1993). and molybdenum has not been systematically evaluated for carcinogenicity by IARC.4) 48.6 (36.9 (64.3 (71.8) 61.4 (67.4-185) 106 (94.5 (50.3) 41.0-41.3) 57.1-109) 89.1-112) 78.5 (65.1 (38.9-118) 91.9 mg/kg/day and established a tolerable upper intake level of 0.3 (55.4-106) 85.2) 42. 1997).7) 112 (95.1-38.2-40.6-88.5) 72. 1999).9-45.8-65.7) 42.4) 122 (107-133) 109 (99.2) 37.7 (30.7) 41.4) 61.7-40.5 (38.1-43.3 (37. at daily oral doses of 95 µg and 428 µg.7) 45.5 (34.8 (75.5 (54.0) 88.7) 62.3 (83.0-133) 119 (88.7 (75.3) 64.1 (54.7 (66.9-40. Biomonitoring Information Molybdenum is an essential element for health.0-56.5 (36.2 (36.8 (37.03 mg/kg/day in humans (IOM.6) 36.2) 43.3) 61.1 (30.0 (35. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.4) 89.4 (40.5-97.5-99. 1961.4 (44.1-39.5 (39.3) 44. U.7) 75th 63.5 (80.6-78.4 (56.9) 31.9 (39.1-45. Based on studies finding adverse reproductive effects in rats and mice.1) 101 (83.8-67.9-61.5-69.2-96.3-115) 98.2-47.9) 79.5-44.3-46.5) 90th 108 (97.7-137) 129 (109-155) 112 (97.2) 39.9 (35.3 (36.1 (42.2-103) 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 42.4-107) 85.8-47.0) 44.0) 39.9) 44.5-62.5) 60.8-47.6) 39.4-39.5 (41.2 (37.3-59.3 (51.2) 39.7 (77.2 (40.9 (64.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .8 (36.1-100) 86. population from the National Health and Nutrition Examination survey.4) 116 (101-126) 104 (88.4) 47.4-120) 101 (84.9 (36.6 (36.5-70.1-40.0) 62. 2001).8) 71. of the ingested dose (Turnlund et al.5 (65.1 (49.9-42. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5) 71.Metals was 18% of the ingested dose.0) 72.5 (37.3-56.5-48.7-52. urinary excretion over six days rose to 50% and 67%.6) Selected percentiles ( 95% confidence interval) 50th 41..4) 60.0-46.9-96.8 (90.

16:1313-1319.gov/index. boron.Metals in urine for the U. 4/14/09 Sievers E. Sci Total Environ 1998. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Food and Nutrition Board. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. vitamin K. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Schaub J. 56:322-327. Occupational risk factors of lung cancer: a hospital based case-control study. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Van Meerbeeck JP. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Atlanta (GA). Geneva: WHO. Sciarra G.. Molybdenum in infancy: methodical investigation of urinary excretion. Minoia et al. National Toxicology Program (NTP).epa. Schleyerbach U. References Centers for Disease Control and Prevention (CDC). molybdenum. Trace element reference values in tissues from inhabitants of the European Union.S.htm. 2005). Koval’skiy GA. Schindelin H. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum.62(4):790-796.nih. Kristiansen J. 1998). 4/14/09 White MA. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Menne C. A study of 13 elements in blood and urine of a United Kingdom population. Turci R. In: Trace elements in human nutrition and health. edu/openbook. Zhurnal Obshchey Biologii 1961. Available at URL: http://books. Aprea C. 2002. Am J Clin Nutr 1995. manganese.. Gatti A. vanadium. 1998. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al.php?record_id=10026&page=420. Ann Rev Biochem 1997. EPA). Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. arsenic. Christensen JM. Available at URL: http://ntp. Dietary reference intakes for vitamin A. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population.niehs. chromium. J Trace Elem Med Biol 2001. White and Sabbioni. TR-462. World Health Organization (WHO). et al. Molybdenum 1993 [online]. Institute of Medicine (IOM).S. and zinc: a report of the Panel on Micronutrients. excretion.22(3):179-191. Vermeire PA.216:253-270..66:233-267. Yarovaya GA. nickel. Rees DC. Turnlund JR. 2005. Minoia C. Ronchi A.nap. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Sabbioni E. 420-441. Sabbioni E. pp. iodine. 2001. 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. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Third National Report on Human Exposure to Environmental Chemicals. Shmavonyan DM. 2001). Environmental Protection Agency (U. Droste JHJ. Weyler JJ. Peiffer GL. 1996. U.15(2-3):149-154.123(1):81-85. Rapid Comm Mass Spectrom 2002. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Washington.S. Molybdenum absorption. 4/14/09 Iversen BS. Keyes WR. silicon. X. Kisker C.gov/iris/ subst/0425. (DC): National Academy Press. Occup Environ Med 1999. Available at URL: http://www. Molybdenum. iron. 144-154. copper. Analyst 1998. pp. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. White MA. van Sprundel MP.

. 01-02. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. and 0. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. and high catalytic activity. 7440-06-4 General Information Platinum is a silver-gray. strength at high temperatures. and iron. carboplatin) in the treatment of cancer. cisplatin. which may vary for some chemicals by year and by individual sample. dental alloys.04. < LOD means less than the limit of detection.. copper. as oxidation catalysts in chemical manufacturing. population from the National Health and Nutrition Examination Survey. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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. 1998). lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel.Metals Platinum CAS No.07.04. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. jewelry. 0.g. and 03-04 are 0. respectively. thick-film circuits printed on ceramic substrates. and as drugs (e. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. Platinum compounds are used in electrodes. see Data Analysis section) for Survey years 99-00. 230 Fourth National Report on Human Exposure to Environmental Chemicals . however. Important properties of platinum are resistance to corrosion. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.

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

Hebert R. Petrucci F. Schierl R..61(7):636-9. Ewers U. Fruhmann G. Kazantzis G.4(1):27-36. which elevate urinary platinum by five to twelve-fold (Begerow et al. Schierl et al.10:63-71. population were below the limit of detection (0. van de Weyer C.. Saindelle A. eds. Urinary excretion of platinum from platinum-industry workers. Nowak D. Crocker W. Platinum concentrations in urban road dust and soil. J Expo Anal Environ Epidemiol 2003.Metals the International Programme on Chemical Safety at http:// www. 2003. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Grimm CH.13(1):24-30. Carelli G. New York: John Wiley & Sons. Analyst 1998. 1998). International Journal of Hygiene and Environmental Health 2003.56(3):283-286. Kelly J. Urinary platinum levels associated with dental gold alloys. Cohrssen B. Wilhelm et al. Several studies have shown that background concentrations in general populations were usually less than 0. Hauff K. Environmental Health Criteria 125. Uptake of antineoplastic agents in pharmacy and hospital personnel. Available at URL: http://www. ruthenium. Schierl R.htm.inchem.01 µg/L (Becker et al. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Levels of platinum in urine for the U. Raab W. Huber R. Kavanagh P.207(1):69-73. 2004). Occup Environ Med 1998. References Becker K. Fries HG.. Begerow J.S. Saindelle A. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. and platinum. Hall L. Campbell K. Stilianakis NI. Ruff F: Platinum and platinosis. Br J Pharmacol 1969. Herr CE. Int Arch Occup Environ Health 1997.35:313-321. Angerer J. Jankofsky M. Senofonte O. Hysell D.. 289-380. 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. Boos KS. 2004) or less than 0. Environ Res 1975a. Moore W Jr.55(2):138-140. 2004. Schulz C. 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. Int Arch Occup Environ Health 2003. Duneman L:Long-term urinary platinum. et al.76(1):5-10. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.inchem. Int J Hyg Environ Health 2004. Pethran A. Schulz C. and gold excretion of patients after insertion of noble-metal dental alloys... 2003. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Kuster W. 1997. Occup Environ Med 2004. osmium. Powell CH. 5th ed. Czerczak S. International Programme on Chemical Safety (IPCS). pp. Influences on human internal exposure to environmental platinum.19:685-691. Gieler U. et al.. 1991 [online]. Herr et al. Schierl R. palladium. Patty’s Toxicology. 1998). Schierl R. Ensslin AS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. rhodium.9:152-158. Nickel.. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. 2001). Thornton I.htm. and in blood and urine in the United Kingdom. Bocca B. Pethran A. Gromiec JP. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies.. Kaus S. palladium. 2003. Arch Environ Health 2001. Environ Health Perspect 1975b. Farago ME. Herr et al. Ruff F: Histamine release by sodium cholorplatinate. Neuendorf J. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.. 3/31/08 Moore W Jr. 2003).org/documents/ehc/ehc/ehc125. Seifert B. Allergy and histamine release due to some platinum salts. et al. Pethran et al.04 µg/L) in this Report. 2000. Parrot JL.005 µg/L (Iavicoli et al. Blanks R.. Platinum. Alimonti A. 1999. Turfeld M. Wilhelm M. Biomonitoring of traffic police officers exposed to airborne platinum.org/documents/ehc/ehc/ ehc125. 206:15-24. Kulka U. Arch Environ Health:1969. Rommelt H. Seiwert M.70(3):205-208.123(3):451-454. Hysell D. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Part 1: monitoring of urinary concentrations. Schierl. In: Bingham E. Iavicoli I. et al. Biomarkers 1999. Biomonitoring Information Urinary platinum levels reflect recent exposure.

300) .380 (.180 (.200 (.290 (.183) .250-.420-.150-.144 (.158) .500 (.420) .430 (.550 (.440 (.147-.370 (.470) .220 (.370 (.02. and 03-04 are 0.173-.520) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.218) .350-.171 (.330) .330) .280) .370) .330-.330-.02.243) .220 (.290) .240) .160 (.250-.400-.250) .360-.200) .290 (.410 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.180-.167 (.390) .280) .450 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.160 (.590) .196) .290) 90th .185 (.181-.410-.270-.470) .320 (.156-.390-.340-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.370-. In the past.690) .159 (.160-.430) .360 (.170 (.220 (.480) .320) .390) .400 (.134-.280 (.300 (.520) .440) .200) .380 (. From these and other sources.206) .520 (.184 (.201 (.170 (.159 (.420-.160 (.220) .370 (.220) .146 (.250-.330-. Thallium disappears from the blood with a half-life of several days.200 (.270-.400-.200 (.400 (.370 (.200 (.390 (.270 (.250-.201 (.191 (.400-.330-.470 (.160-.400) .150-.270) .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 .163) .310) .390-.162-.300 (.240) .180 (.450 (.167-.360-.250 (.170-.380-.330) .280 (.460) .148-.420) .260-.350-.360 (.240-.490 (.215) .560) .160 (.172 (.157-. see Data Analysis section) for Survey years 99-00.183) .330-.02.170-. 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. interval) . thallium was obtained as a by-product of smelting other metals.160-.200 (.590) .490) Total .150-.182-.290) .190 (.360 (.410-.220) .510 (.500) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.400) 95th .200-.490) .430-. however.330-.340 (.218) .200 (.480) .310 (.167-.350 (.630) .330) .330-.197-.270 (.170-.410-.370 (.147-.170) .450 (.190 (.410-.175) .300) .240) .190 (.200) .170-.410-.410-.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 .170) .260-.179-.250-.180-.400) .360 (.S.300) .260) .170-.Metals Thallium depilatory cosmetics.180) 75th .470) .410 (.370 (.320-.360-.202) .159 (.200) .390-.180) .190 (.180-.225) .176 (.240-.160-.450 (.360-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .390) .200-. the latter being the current major industrial consumer of thallium in this country.360-.220-.270) .197 (.300) .180 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.400-.500) .260 (.153-.440-.350) .480) .350-.200) .149 (.250 (.420) .430-.230 (.370-.350 (.420-.187-.430) .440 (.450 (.202 (.410 (.420-. representing distribution into other tissues.310 (.640) . Human health effects from thallium at low environmental CAS No.290 (.400) .390) .400 (.250-.230-.239) .490) .172 (.200-. it has not been specifically mined or refined in the United States since 1984.220 (.440) ..370-.300-.400-.156) .145-.340-.290) .290-.260-.220) .500) .200) .340-.420) . In the United States.150-.145 (.170-.178) .220) .440 (.430-.220) .210) .450 (.160 (.510) .430 (.450 (.470 (.210-.270 (.140-.210 (.180-.390-.210 (.190 (.260 (.202 (.380-.270 (.300 (.170 (.420) .177) .240-.420) .410 (.147-.280-.172) .200-.350-. 01-02.410 (.250-.440 (.410 (.520) .170-.290) .480) .230) .420 (.173) .290 (.460-.137-.260-.310 (.280 (. population from the National Health and Nutrition Examination Survey.280-.173) .450 (.185-.290-.340-.230-.460 (.280) .154-.420) .440) .135-.290 (.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 .430 (.230) .150-.450 (.155 (.310-. 2005).400 (.230) .480) .190 (.160-.260-.320) .192) Selected percentiles ( 95% confidence interval) 50th .217) .190-.165 (.380) .360) .430 (.270-.188) .150-.196) .230) .370) .260 (.320) . In addition.450) .370 (.217 (.390 (.270 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.350-.156) .145-.220 (. 0.350) .400) .370-. and 0.490) . respectively.170) .133-. thallium readily crosses the placenta and also distributes into breast milk.340) .340) .400 (.250-.410) .350-.290 (.230-.

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

Trace element reference values in tissues from inhabitants of the European community I. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1992 [online]. Trace metals in urine of United States residents: reference range concentrations.. Toxicological profile for thallium. et al. 2005. Brockhaus A.265 people living near a thallium-emitting cement plant in Germany.95:89-105. Environ Res 1998. blood.35(1):4-9. Pietra R. Celier D. et al. 1980. 1998. 2005. Boisson P. Sci Total Environ 1990. 1990. Sampson EJ. Paschal DC.5 μg/L. Ting BG. Trace element reference values in tissues from inhabitants of the European Union. Available at URL: http://www. X. Challeton-de Vathaire C. References Agency for Toxic Substances and Disease Registry (ATSDR). J Soc Occup Med 1985. 7/15/09 Blanchardon E. Third National Report on Human Exposure to Environmental Chemicals. Sabbioni E.atsdr.216:253-270. Kramer U.gov/toxprofiles/tp54. Manke G. White MA..47(3):223-231. Morrow JC. 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. Buhlmeyer G. Atlanta (GA). Dolger R. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Radiat Prot Dosim. Pirkle JL. A study of 46 elements in urine. Investigations of thallium-exposed workers in cement factories. Valentin H. A study of 13 elements in blood and urine of a United Kingdom population. Pozzoli L. Brockhaus et al. Cassot G. Int Arch Occup Environ Health 1981. Gallorini M. White and Sabbioni.76(1):53-59. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Int Arch Occup Environ Health 1980. There was no increase in the prevalence of symptoms at levels less than 20 μg/L and only a slight increase in nonspecific symptoms greater than 20 μg/L.Metals (CDC. et al.48(4):375-389. (1981) studied 1. Schmidt M. 1981. 1985). Paschal et al. Minoia et al.. Investigation of a working population exposed to thallium.S. Apostoli P. 2005) and are shown with results from NHANES 2003-2004 in this Report. with concentrations ranging up to 76. Schaller KH. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L.cdc. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Jackson RJ. Sci Total Environ 1998. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Raithel HJ.html. Sabbioni E. and serum of Italian subjects. Martin J-C.. Centers for Disease Control and Prevention.1 mg/m3 (Marcus. Soddemann H. Minoia C.113(1):47-53. 1998). population) are thought to correspond to workplace exposures at the threshold limit value of 0. Wiegand H. Marcus RL. Ewers U. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Schaller et al.

050-.100 (.220) .670) .Metals Tungsten CAS No.640 (.210) .290) .190-.113 (.069-.090-.066-.570 (. see Data Analysis section) for Survey years 99-00.260-.133) .560) .800) .100-.380-.120) .120) .110-.070) .122) .080) .300 (.560) .450 (.550 (.800) .510 (.190-.160 (.180) .380-.190 (.230-.370) .070-.260-.160) .260-.04.091) .087-.082) .450-.130) .093 (.360-. which is used in the steel industry.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 .086 (.200-.270-.060 (.460 (.340) .350) .510-.140 (.080 (.310-.092 (.105 (.120-.090-.100-.210 (.060-.380) .096 (.370-.360) .100 (.430-.090 (.160) .460 (.077-.060-.070-.190-.100) .210 (.080) 75th .135) .060-.350) .400-.430) .470) .050-.140-.080 (.360 (.080-.630) .530 (.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 .076 (.100) .370-.060 (.130-.380 (.080 (.070 (.180-.290-.230) .080) .300-. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.400) .180-.550) .53) .105) .160 (.071 (.310 (.151) . 01-02.400 (.080 (.320 (.420-.130-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.520) .140 (.110 (.090) .060-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.690) .110-.290-.109) .460) . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.170 (.101 (.140 (.130) . Occupational exposure is from dusts released during grinding or drilling of hard metals.00) .100 (.078-.084) .360 (.110-.080-.550) .210 (.210-.082-.150 (.620 (.130) .160-.060-.210 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.150 (.130) .082 (.320 (.460 (.300) 95th .060 (.510-1.04.090-.350) .090) .300) .190) .260 (.230-.060 (.070-.410-.070-.090 (.076 (.330) .300 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).230-.300 (.080 (.137 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 03-04 are 0.204) .140 (.250) .330) .120-.220 (.110 (.360-.126) .190-.310-.270 (.090 (.060 (.070 (.062 (.090-.056-.073 (.170 (.480) Total .500 (.180) .092 (.150-.110 (.160-.500) .210 (.123-.090) .220) .250-.270 (.101-.180-.050-.430 (.069) .470 (.400 (.140-.090) .530 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.132) .350 (.095-.330 (.260 (.250) .050-.090-.570 (.240-.116) .470-.310) .060 (. Tungsten compounds are used as lubricating agents.490 (.080) . mainly as scheelite (CaWO4).160 (.081 (.290) .370 (.093) .230-.470 (.080-.330-.470) .087) .180-.520) .370 (.560) .084-.230) .340-. 236 Fourth National Report on Human Exposure to Environmental Chemicals . which are used in rock drills and metal-cutting tools.330-.065 (.120-. population from the National Health and Nutrition Examination Survey.100) .160-.340-.270 (.120-.520) .620) .270-.350-1.092) .110) .130) .360 (.073-.390 (.068) .340-.093-.070) .130-.S.158 (.250) .270-.220) . Tungsten is used mainly for producing hard metals.380 (.280 (.110 (.250) .620) .097-.064-.170-.107 (.113 (.440) .090-.250) .120-.200 (.530 (.380-.250) .180) .320-.590) .140) 90th .830) .200) .111-. Little information is available on the toxicity of tungsten.770 (. and as catalysts in the petroleum industry.120) .100) .180) .120) .110 (.170) .410 (.250-.095-.100) Selected percentiles ( 95% confidence interval) 50th .290-.220-.104) .071-.120 (.090-.150 (.420-.060-.084 (.090-.580) .074-.310-.280-. Evidence is lacking for the carcinogenicity of tungsten.170) .490) .560 (.180 (.270-.370 (.088 (.070 (.088) . and 0.070) .460) .810) .062 (.320) .100 (. and for producing ferrotungsten.190 (.310-.04.170) .260) .430 (.065-.650) .160 (.150) .096-.430-.180 (.230 (. interval) .113 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.240 (.950) .380-.400 (.130 (.290 (.560) . filaments for incandescent lamps.550) .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 .113 (.058-. 0.130 (.070-.120) .100) .400 (.110) .082 (.073) . bronzes in pigments.500 (.170) .430 (.160-.310-.320-.056-.790) .130-.160 (.390) .073-.120-.070) .120) .280 (. respectively.100-.

067 (.198-.057-.245-..426) .082) .083 (.174) .100) .667 (.069 (.086) .074) .075 (.073 (.353 (.360 (.079 (.069 (.605) .253 (.218 (.278-.381) .199 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.080-.267-.143 (.255-.176-.124 (.167-.329 (.061-.484) . population.085) .431) .286-.075-.186 (.086) .231-.092) .138 (.063-.462) .410-.088) .074-.124-.067-.080-.071) .155-.200-.258 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.063 (.300-.119 (.168 (.497 (.216-.148 (.739) .426) .28) .072-.091 (.385 (.180-.554) .084 (.667) .414) .158 (.098 (.201) .465) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.146 (.089) .347 (.214-.083) .064-.059 (.098-.072 (.150 (.797) .167) .154) .078) .153) .065 (.084) . or exposure that a control group of non-metal workers had mean levels differences. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.116-.436-1.136-.208-.049-.079 (.300) .284) .174 (.250 (.091) .170-.094) . Nicolaou et al.121 (.306) .727) .098-.122-.086-.634 (.302-.538) .484 (.093-.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 .299 (.073 (.082) .197 (.089 (.087 (.582) . 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.066 (.315-.317) .339 (.S.279 (.431) .169) .179-.270 (.344-.083 (.279 (.217-.158) . (1987) found possibly due to methodologic.084 (. 2001).211 (.301) .091) .379 (.100 (.308) .091) .079) .250 (.146) .075-.060 (.555 (.375) .072-.339 (.088) .126-. Using neutron activation analysis to 2000.075) .063-.144 (.054-.287) .073 (.059-.116) .109-.205-.125) .144-.133) .145 (.139 (.131-.067 (.069-.120) .215 (.215) .059-.074-.216-.237) .070 (.233-.083-.071) .063-.452-.133) 90th .209-.354-.084) .237-. 2005).258-.216 (.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 .255 (.075 (.188-.300-.077) .333-.107-.065-.300 (.122 (.094) .354) .083) . 1997).091 (.154) .217-.077) .237) .255 (.198) .(Kraus et al.265 (.071) .333 (.062 (.071 (.056-.080 (.S.108) .121-. and 2003-2004 (Paschal et al.459) .317-.158) .167-.823) .086) .203-.071 (.392) .104-.061-.301) .359 (.157) .224) .090-.081) .333 (. similar to those in this Report (Schramel et al.133) .880) .250-.139-.216-.331-.412 (.087) .053-.063 (.078) . population (CDC.130 (.075) .190) .081-.056-.302-.082 (.066 (.341 (.059-.117 (.139) .176-.136 (.095-.197-.065-.436) . 1998). Patients with medically-inserted tungsten found at increased levels in drinking water.364 (.071 (.081 (.096) .200-.074 (.106 (.095) Selected percentiles ( 95% confidence interval) 50th .500) .214) .333 (.068 (.294 (.301) .279 (.060-.333) .098) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.136-.453) . interval) . measure urinary tungsten.353 (.329-.078 (. 2001-2002.439) Total .085-.080 (. 2003.439 (.136-.054-.146 (.108-.064-.077-.061-.103-.117) .152-.240-.077-.197) .161) .439 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.116 (.333-.253-.060-.079) .231 (.063-.222) .261-.150-.091) .333) .073 (.465) .098-.057-.105 (.138) .055-.317 (.222-.094-.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 .078 (.151 (.S.065-.058-.201 (.359 (.085 (.111 (.383 (.068-.253) 95th .130-.148) .138 (.125 (.197) ..119-.093) .482 (.100) .169 (.150-.071-.308) .216 (.143-.283) .158) . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.181 (.165) .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 .275 (.431) .340 (.167) .105 (.136-.120) .065 (.164 (.285) .122-.079) .099-. population from the National Health and Nutrition Examination Survey.081 (.153-.179-.070 (..272-.358) .184 (.065) .187) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.386) .293 (.078-.206-.326) .199 (.074) 75th .267) .109 (.079) .090-.333 (.

4/15/09 Centers for Disease Control and Prevention. thallium. et al. Zobelein P.. Seghizzi P. Schramel P. Cassina G.62:380-384. Environ Res 1998.69(3):219-223. Pirkle JL. Third National Report on Human Exposure to Environmental Chemicals.cdc. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Ting BG. Schaller KH. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Atlanta (GA). 2005. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Int Arch Occup Environ Health 1997. Trace metals in urine of United States residents: reference range concentrations. bismuth. tellurium. [online] 2003. Centers for Disease Control and Prevention. Nevada Exposure Asssessment. Biomonitoring studies on levels of tungsten provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of tungsten than are found in the general population. References Bachthaler M. J Trace Elem Electrolytes Health Dis 1987. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Angerer J. Churchill County (Fallon). platinum. Lenhart M.58(10):631-634. Nicolaou G. Paetzel C. lead. The determination of metals (antimony. Kraus T. Cancer Clusters. Feuerbach S. 2004). Sampson EJ. Pietra R. cadmium. Mosconi G. Wendler I. Link J.76(1):53-59. Catheter Cardiovasc Interv 2004. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Available at URL: http://www. Sabioni E.Metals blood. Angerer J. National Center for Environmental Health. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Morrow JC. palladium. Jackson RJ. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Manke C. Paschal DC.(2):73-77.gov/nceh/clusters/Fallon/study.htm. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. urine. Schramel P. mercury. and hair (Bachthaler et al. Weber A. Occup Environ Med 2001.

052 (.008-.008 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.015 (. 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.056) .005-.036-.046 (.045) .007) 75th .009) .010 (.019 (.011) .008 (.017-.027-.026) 95th .017 (.010 (.041 (.008-.023) .016-.006-.008) .013-.019-.018 (.021) .030 (.036) .005-.014 (.014 (.004.010) .008 (.026-.024-.010 (.010 (.012 (.026 (.021 (.008-.005-.037) .072) .028 (.024-. Fourth National Report on Human Exposure to Environmental Chemicals 239 . 01-02. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).028-.023 (.007-.037) Total .020-.027-.012) .030 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.013-.048 (.012-. 0.023-.010-.010) .006 (.011) .008 (.021 (.017-.046 (. Uranium has many commercial uses.007 (.069) .036 (.049) .088) .009) Selected percentiles ( 95% confidence interval) 50th .007-.012 (.013 (.040 (.026 (.062) .067) .010-.021) .006-.013 (.035-.010 (.009) .020) .044 (.054-.009) * . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.009 (.016) .015 (.014 (.022 (.009 (.008-.008 (. Variable concentrations of uranium occur naturally in drinking water sources.009 (.016 (.012 (.016) .014 (.008 (.010-.021) .032 (.066) .009 (.007-.114 (.015 (.011-.037) .020-.009 (.007-.011 (.011-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.158) .011) .009 (.018-. interval) .010-.017-.022-.012-.067) .009 (.009-.010) * .033) .053) .040-.017-.008-.037 (. and as an aid in electron microscopy and photography.012-.006-.007) .023-.007-.017) .039-.031 (.009) .008 (. and 0.048) .013) 90th .016) .009 (.007 (.011-.043) .040) .029-.006-.005.023) .020-.028 (.007-.008 (.008 (.016-.028-.009-.009-.023) .007 (.019-.010-.008-. and 234U.013 (.006-.046) .031 (.007-.007 (.009-.034-.008-.018 (.042) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.010) .007) .024-.011) .017) .025-.030 (.009) .027 (.027) .016-.063) .023-.008) . population from the National Health and Nutrition Examination Survey.007-.017) .046 (.012 (.064 (.013 (.007 (.031 (.073) .036) .007-.006-.015 (.036 (.279) .011-.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 .72%).051) .015-.012) .007-. milling.006-.010) .036-.033 (.038 (.019-.019-.050) .060 (.127) .046 (.006-.023 (.030-. or processing.009-.031 (.015) .013 (.014 (.023-.007-.014 (.009) .027-.011) .S.008) .012 (.035) .007-.007) .008 (.022-.009) .031 (.012 (.011 (.055 (. In workplaces that involve uranium mining.007-.010) .020 (.022-.013) .017 (.020-.026) .037) .043 (.009) .009 (.029-.009) .020) .054) .007-.065) .033 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.011-.027) .022) .018) .027 (.016) .008-.005-.009) .039) .011-.018) .047 (.006-.007-.029 (.065) .021-.056) .020-.034-. in some ceramics.031-.008 (.023 (. including nuclear weapons.009) .026) .007-.013 (.046-.011-.034) .007 (.011) .009-.018) .007 (.009-.012) .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 .010-. human exposure occurs primarily by inhaling dust and other small particles.013 (.007 (.037-.008 (.024 (.009) .030) .010) .010) * .008 (.042 (.017-.008 (.040-.050) .Metals Uranium CAS No.008) .016) .009-.049) .015) .007-.018) .016) .008) .035) .012-.017-.017) . and 03-04 are 0.040) .010) . see Data Analysis section) for Survey years 99-00.006 (.027 (.010) .006-.021-.007-.045) .005-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.026-.008 (.007 (.011) . 235U (about 0.008 (. Depleted uranium (DU) refers to uranium in which the proportions of 235U and 234U isotopes have been reduced compared with the proportion in natural uranium. Thus.008 (.013-.012) .041 (.053 (.054) .021 (.007 (.040 (.012-.006-.038) .027 (.007) .027) .006-.027) .017) .007) .012-.009) . Since the 1990’s.039) .009-.007 (.006 (.004.006 (. respectively. nuclear fuel.009) .039) 1227 1335 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .009-.028 (.006-.033-.009 (.026 (.

008 (.018-.043 (.008-.012 (.015) .010-.017 (.019) . After inhalation.007-.270) .027 (.053) .027) .013 (.010-. After long term or repeated exposure. 0.006-.010-.008) .011) * .011) .012 (.022-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.010) .025-.015-.011-.146) .008 (.028 (.007 (.006 (.008 (.007-.005-.005 (.020 (.006-.006-.008) .006-.015 (.020-.016) .011) .017) .007 (.028) .007) .006-.012 (.007 (.010-.031-.025) 95th .027-.020-.014-.012 (.029 (.014 (.029 (.100 (.006-.024) .009-.Metals impact.006-.007 (.028) .011-.011-.077) .008 (.030 (.022 (.009) .045 (.006 (.025 (.010) .009 (.006) .007-.008 (.010-.016) .014) 90th .007 (.012 (.007-.038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .039) .034 (.020-.018-.010) .016) .006-.010 (.030) . 2005).010-.007 (.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.024-.022) .010 (.063) ..026-.013 (.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 .028-.022-.006-.022 (.006 (.010-.024 (.024-.019-.080) .009) .009 (.005-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.006-.005-.018 (.009) .008) .013 (.016-.074) .007-.033) .024 (.013) . Radiation risks from exposure to natural uranium are very low.009) .016) .006-.050) .007-. Depending upon the specific compound and solubility. 2003).051) .015-.014-.018-.016) .050 (.039) .054) .021-.013 (.021 (.009) .033 (.013-.006) .015) .008-.024 (.047) .013) .009-.010 (.015 (.012) .051) .051 (.032) .029) .018) .011) .027-.008 (.007-.012) .030-.013 (.015 (.006-.004-.020 (.007 (.032) .015) .023-.018-.011-.018-.011-.011 (.007 (.010-.004-.029) .034-.013 (.008-.008) .039) .027 (.005 (.024) . After exposure to soluble uranium salts.014 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.035 (.006-.007 (.024) .007 (.007 (.006) .008) 75th .009) Selected percentiles ( 95% confidence interval) 50th .016) .008 (.006 (.007 (.006-. Health effects from uranium exposure result from chemical toxicity to the kidney.030 (.009) . where limited absorption occurs (less than 5%).050) .021 (. interval) .013) .034 (.009) * . population from the National Health and Nutrition Examination Survey.009-.S.013 (.007-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .009-.034) .012-.048) .017) .009 (.021) .013 (.006-.025-.025-.006-.019-.010 (.009) .034-.016) .008) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.012-.012 (.008) .042) .011-.009 (.008) .026) .008 (.008) .041) .031 (.033 (.009-.024) .013 (.035 (.008-.014-.006-. which represents distribution and excretion.017-.061) .016) .026 (.010-.034 (.029 (.007) .1%-6% of an ingested dose may be absorbed.019 (.025 (.022 (.006-.011 (.058) .011-.017-.008) .015-.007) .013 (.014) .007 (.042-.027) . Inhaled uranium-containing particles are retained in the lungs.005 (. which can occur occasionally from high occupational exposure.022-. 1992).006 (.009) .017-.030 (.033 (.017-.005 (.005-.006) .007 (.033 (.014) .007 (.005-.056) .027 (.006-. with much slower elimination from bone.007-.008-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.034 (.009 (.007 (.029) .017) .042) . In cases of retained DU shrapnel.025-.010) .015-..011-.044) .048) .007 (..028) .028 (. kidneys.005-.026 (.030-.014) .017 (.010) * .010) .007 (.067) .034 (. Uranium is eliminated in feces and urine.007 (.012) .006-.051) .015) .011-.027-.008 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.006) .024-.040 (.027-. liver.020 (.021 (.024) .039) Total .053) .037 (.019-.026 (.019 (.015-.019 (.009) .010) . 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.016 (.021 (.015 (.008 (.028) .007 (.019-.006-.030) .006-.006 (.005-.010-.019-. low level exposure.009) .008) .010-.007 (.029) .016-.009-. the shrapnel acts as a source of chronic.008-.010 (.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-.019) .016-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.059 (.009) .007-.016-.012 (.058) .006-.020-.008) .020) .

but in whom no shrapnel was embedded. 2005.Metals injury associated with elevated urinary uranium levels (Kurttio et al. EPA. (Kurttio et al. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Pillai KC.gov/ toxpro2.. Six workers in a depleted uranium program showed concentrations of 0.168(8):600-605.S.S.. urinary levels of uranium were as high as 9.. 2003. 2006). A cohort of 46 U. Biomonitoring studies on levels of uranium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of uranium than are found in the general population. Vol. 2006. Byrne AR. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Pullat VR. ingestion. Galletti..066 μg/g creatinine (Gwiazda et al.. Muggenburg BA. Information about external exposure (i. Karpas et al. Estimate of the time zero lung burden of depleted uranium in Persian Gulf War veterans by the 24-hour urinary excretion and exponential decay analysis. Health Phys 1992.1996. Kent (England): Nuclear Technology Publishing.62:562-566. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 1-49.. during. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Hamilton et al.html. although slightly increased during and after deployment.110 to 45 μg/L (Ejnik et al. In: Gerber GB. 1978). In 17 U. soldiers who had been injured and had embedded DU shrapnel for as long as eight years... 2006). environmental levels) and health effects is available from ATSDR at: http://www. respectively. 2004).. Tolmachev et al.S. Drinking water and other environmental standards have been established by U. 2004). had a mean urinary uranium concentration of 0. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.1992. soldiers evaluated before. In a study of 105 persons exposed to natural uranium in well water. Uranium content of blood. 1992.65 μg/L).. Durakovic A.. References Bhattacharyya MH. Mil Med 2003. Squibb K. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ejnik JW. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al..atsdr. Thomas RG. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. 2006).. 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. 2001-2002. Breitenstein BD. In the same study. Benedik L. 2000). IARC and NTP have no ratings for uranium human carcinogenicity. et al. 41 (1). Zimmerman I. pp. NRC. Stradling GN. Carmichael AJ. 28 soldiers who may have been exposed to DU by inhalation. McDiarmid M.107:143-157. in that the levels were below their respective detection limits (Byrne et al.. Third National Report on Human Exposure to Environmental Chemicals. eds. Health Phys 2000. or wound contamination. Guidebook for the treatment of accidental internal radionuclide contamination of workers.. 2000). and no consistent effects on multiple endpoints of kidney function were found. Horan P. Hamilton MM. 2006).78:143-146.S. Komaromy-Hiller et al. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.011 μg/L (McDiarmid et al. (May et al. The U. 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. the median urinary uranium concentration was 2. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.S. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 2002)..cdc. 1991. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. with emphasis on quality control. Radiation protection dosimetry. Centers for Disease Control and Prevention (CDC).162 μg/L) (Orloff et al. Metivier H. McDiarmid et al.61 μg/g creatinine.. Atlanta (GA). 2004). 1994.55 μg/L (median 0. the geometric mean urinary uranium concentration was 0. Dang HS..078 μg/L (ranging up to 5. Sci Total Environ 1991.S. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.e. 2004). Boyd P. Dietz LA. population. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Volf V. and 2003-2004 (Dang et al. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 2002. the median urinary concentration was 0.

S.71(6):879-85. Nuclear Regulatory Commission (U. Scott K. Health Phys 2002. U. et al. Pirkle JL. Clin Chim Acta 2000. Roth P. Mistry K.82(4): 527-532. Squibb K. Pekkanen J. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Uranium and thorium in urine of United States residents: reference range concentrations. Oeh U. July 1978. Katorza E. Health Phys 1996.44:29-40. rapid. Jarrett JM. Jackson RJ. Salonen L. Van der Venne MT. Squibb K. McDiarmid MA. Harmionen A. Charp P. Kuwabara J. Auvinen A. Am J Kidney Dis 2006. Radiat Environ Biophys 2005. Karpas Z. Marino R.79(1):11-21.91(2):144-153. Salonen L. et al. Howerton K. Komulainen H. Hancock RG. Environ Res 1999. concentration and daily excretion of uranium in urine of Japanese. Metcalf S. Sci Total Environ 1994. Kane R. Cremisini C.S. Wahl W. Hollriegl V. Andrews WS. Lewis BM. Health Phys 2003. May LM.296(1-2):71-90.158:165-190. Komaromy-Hiller G. patient population and literature reference intervals for urinary trace elements. Ejnik J. Auvinen A. Makelainen I. Military deployment human exposure assessment: urine total and isotopic uranium sampling results.86:12-18. Pinto V. Roiz J. et al.Metals Galletti M. Human exposure to uranium in groundwater. et al. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF.67(8-10):697-714. Kidney toxicity of ingested uranium from drinking water. Marko R. Washington (DC): NRC.22–Bioassay at uranium mills. Noguchi H. Orloff KG. Cordero S. Englehardt SA. Biokinetic modeling of uranium in man after injection and ingestion. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Saha H. Kalinsky V. McDiarmid M. Karpas Z. Review of elements in blood. Environ Health Perspect 2002. Costa R. Smith D. VI. Sampson EJ. McDiarmid MA. Gwiazda RH. U.94:319-326. Hamilton EI.81:45-51.87:51-56. D’Annibale L. Ash KO. Lorber A. Uranium daily intake and urinary excretion: a preliminary study in Italy. Paretzke HG. et al.85:228-235. Element reference values in tissues from inhabitants of the European community. Ting BG. Int Arch Occup Environ Health 2006. Inductively coupled plasma mass spectrometry as a simple. Sabbioni E. Comparison of representative ranges based on U. J Toxicol Environ Health A 2004. Biologic monitoring for urinary uranium in Gulf War I veterans.S. et al. Tolmachev S. Wilson PD. Engelhardt SM. Health Phys 2004. Gucer P. Health Phys 2004. NRC). Health Phys 2006. Kurttio P.110(4):337-342. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Nuclear Regulatory Commission (NRC) Guide 8. Paschal DC. Bennett LG. Kurttio P. Renal effects of uranium in drinking water. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.47(6):972-982. Shelly T. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Halicz L.S. Oliver M. Heller J. Environ Res 2004. Oberbroekling KJ. Saha H. Li WB. Ough EA.

0-17.90-6.0) 14.00) 4.87-3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4. population from the National Health and Nutrition Examination Survey.0) 9.80) 12. Survey years 01-02 03-04 Geometric mean (95% conf.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.30 (2.80-6.40-11. potassium.50 (5.05 and 0.70 (3.0 (11. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.10) 5.20-3.93 (4.60) 5.20-4.31) 2.18-3.10 (5.16) 3.00-6.20 (8.75 (3. laboratory analysis.0 (12.40 (5.0) 14.0 (11.0 (11.60 (4.0-29. matches.50 (3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0-17. but has strong oxidant properties in the presence of concentrated acids.00-5.S.0) 13.29-3.90-10.0-15.88) 3..50-4.0) 15.20 (6.0 (9.20) 7. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.20-4.0 (9.10-11.21 (2. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles. 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.45-4.80 (6. 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.19 (3.0-18.0) 14.20) 4.22 (2.00-6. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7. and limited applications in pharmaceutics.0 (11.0-19.40 (8.03) 3.80) 7.40 (3.81-16.44-4.40) 3.70-3.40-7.0 (12.00) 5.0 (11.10 (2.0-17.40-6.50) 11.0-17.10) 12.50-4.05.g. and reducing agents.0 (8.12) 3.0) 11.0-17.66) 3.50-3.90-9.90 (3.40) 3.49-3.0 (9.0 (8.56) 3.68) 4. and electroplating.70 (3.90-12.0 (11.0-18.09) 3.84) 14.0-17.40 (4. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.90 (5.26 (2.38) 5.40 (3.60) 8.54 (3.70-11.60) 3.0 (12. fabric dyeing.0 (11.30-17.80 (3.50-7.0) 9. or ammonium salt.0) 12.80 (7. 2007).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. Other manufactured uses include fireworks.62 (3.0) 9.75-3.0) 15.40 (5.60-7.90-3.20 (7.90-11.90) 6.10-7.10 (6.0 (13.00) 3.40 (5.0-18.50-11.0 (9.50) 6.19-4.Perchlorate Perchlorate (Urbansky.0 (8.0) 19. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms. 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.93-4.70-12.76 (3.0) 11.80) 3.08-3.02 (3.93-3.0 (11.0-23.20-11.70) 3.60-6.11) 3.0 (11. certain catalytic metals.50) 5. and certain plants with high water content (e.0-20.40-4.46) 3.30) 6.90-3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.70-5.40-5.10 (6. Drinking water.0) 8.90 (2.20-12.10) 3.10-11.80-8.32 (3.0 (9.40 (4.20 (5.20 (4.81) Selected percentiles ( 95% confidence interval) 50th 3. It is normally found and produced as the anion of a sodium.30-7.47-4.50 (8.S.0 (9.22-5. 2002).0) 13.35 (3.80-15.0) 13.0) 13.0) 10.30-7.80-4. Perchlorate was added to the U.0-15. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 10.80) 75th 6.67-5.00) 3. milk.89-3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.20 (2.0 (8.90) 5.0) 9. leather tanning.51 (3.0) 9.0) 9.39-4.79 (2.10) 3. 2005). Perchlorate is stable under most environmental and physiological conditions.0 (9.90-9.0 (11.40) 4.30 (5. 1998).00) 7.70-7.10) 5.20 (4.0 (10.70-3.30 (2.30-19.50) 3.70-6.0) 95th 14.10-4.0) 13.90-11.40) 6.40) 2.30-6.50) 5.01 (2.0-14.EPA.0) 13.60 (7.0) 13.74-3.40-13.76) 4.51 (3.80 (3.40-4.0) 10.0) 13.40) 90th 10.0 (12. In addition.0) 8.90 (5.07-4.05 (2.60 (4.S.30) 6. lettuce) can be the main sources of intake for humans (FDA.70-9.10-12.65) 3.80-12. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.11) 4. interval) 3.10 (7.70 (3..20 (2.40) 3. 2005).0) 708 617 681 652 1228 1092 Limit of detection (LOD.90 (5.0) 11.20) 3.0) 16.30 (5.96 (3.0 (8.90 (4.80-4.

2000).12 (6.32) 5.53 (2.20 (3.74) 7.4 (11.70 (4.40 (3.0) 11. Lamm and Doemland.24-2.36 (8.82 (5. Many factors may be important in consideration of perchlorate action on the thyroid: dose.46 (3.21 (2.39) 2.08 (3.81-3.90-2.0 (10.0-17.33 (7.0 (9.60-5. 1999.10 (1.90-9.40 (3.4-16.6-17.4) 13.40-10...10 (4.29-6. thiocyanate.3-14.04-3.0) 10.1-16.0) 12.20 (2.2) 8.0) 13.39-4.26 (3.50) 9.03 (2.30 (3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.22-4.58) 2.50-9. perchlorate is negative in most genotoxic assays (U.1-13. dietary iodine intake.22-4.10-3.0) 9.24 (4. Li et al.50) 2.80 (7.0 (9.70 (2. 2007).5) 8.0) 7.02-4.60-11.02) 3.90 (4.41-9.71 (5.70-4.10) 4.S. chronicity of exposure.09) 3.S.4 (8.0) 9.10 (6. 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.60) 10.80-3.. population from the National Health and Nutrition Examination Survey. although iodine intake was higher than U.30 (5..64-3.3) 8.83 (5.80 (4.20-3.20-10.1 (11.16-3.4 (10.80-3.0) 13. 2005.35 (2.26) 4.3 (10. Lawrence et al.80) Selected percentiles ( 95% confidence interval) 50th 3.30) 5. 2002.0 (11.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3..8 (11.0 (11.80 (7.10-7.00 (4.0) 6.0-19.10) 6.EPA.56-3.0 (11. 2006.70-3.25) 5..00) 3.90-20.33-12.0-14.40) 3..75) 3.54 (2.30) 90th 9. Greer et al. levels.89 (2.61 (5.87-3.0) 12.00 (6. Also.00) 4.6) 12.60-3.46-13.20) 3. medications).0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.50) 6.30-5. 2005).77 (3.1 (8.97-5.93-8.93-5.43) 6.g.50) 5.14 (2. In the U.99 (5.29) 2.20 (7. 2005).6) 20. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.87) 7.35) 3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.91) 4.18-3..10) 3.20) 8.0-44.20-4.20-3.08) 3.66) 3.22 (2.61-10.90 (7.60-15. interval) 3.S.95 (2.45) 3.50 (3.40 (7.45-2.67) 5.3) 11.30 (6.70) 2.44-6.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.70 (2. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.50 (6.Perchlorate inhibition (RUI).35 (4.96) 2.20-9.93) 3.86) 4.90 (2.51-4. U.64) 5.44) 3.04-3.84) 2.87 (5.87) 2.10) 13.10 (4.73) 3.. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures.0 (8.60-6.09 (7.42 (3.19-10.0) 12. 2005).50-5. 2005.30-10.40) 5.56 (3.52 (8.00-3.30) 3.07 (2.00-2.70) 10. nitrate. menopausal status.20 (4.15-12.93-5.4 (11. 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.19-6.46-4.30) 75th 5.50) 95th 12. gender. NAS.0 (8.98) 3.60-5.5 (13.90-3. levels and sufficient in most participants (Tellez et al. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.61-5.05 (4. age.S. in a representative sample of U.60-11.22-6. 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.1-14.2) 8. During gestation and infancy.47) 2.0 (9.4) 8.0) 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 .70-5.40 (4.40) 17.52-9. 2001.39 (3.93-7.90) 5.76 (3.10 (2.99-3.60-8.00 (2.3) 12. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.60 (3.33-6..00-11.12-2.0) 4.54 (3.S.50) 2.60-8.0) 14.S. However.0-14.76-3.34-3.25) 5. up to 68% RUI has been demonstrated. and the presence of other substances known to affect thyroid function (e.1-22. women with urinary levels of iodine less than 100 micrograms per day.90-15. 2002. 2003.1) 8.51 (3.70-15.87 (7.60) 3.EPA.S.30-5. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.59) 3.25 (3.37 (4.90-11.50-3. Survey years 01-02 03-04 Geometric mean (95% conf.72 (3. 2002).20 (6.90 (2.7 (11. Steinmaus et al.00) 9.0) 12.89-3.37-13.60) 8.25) 5.

gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653.113(8):10011008. Environ Health Perspect 2007. Perchlorate Exposure of the US Population.. J Clin Endocrinol Metab 2005.41(5):409-411. Pino S. newborn thyroid function.46(5):509. The effect of short-term low-dose perchlorate on various aspects of thyroid function. 2005). Lamm SH. et al.S. Dyke JV.S. J Occup Environ Med 2000. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. CFSAN/Office of Plant & Dairy Foods. Blount BC. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. population. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lau EC. Goodman G. Blount et al. 2005. Pirkle JL. J Occup Environ Med 2003. (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. Landingham CB.html. May 2007. thiocyanate.gov/safewater/ccl/perchlorate/perchlorate. Additional information about exposure and health effects is available from the U. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Mauldin JP. Environ Sci Technol 2006.gov/toxpro2. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.. Lamm S. 2001-2002. Environ Health Perspect 2002. Perchlorate in the United States.42(2):200-205. Li FX. Steinmaus C. Primary congenital hypothyroidism.cdc. Howd R.115(9):1333-1338. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Pino S. Magnani B. Cross M. Environ Health Perspect 2006. National Research Council of the National Academies. the women in the community with the highest drinking water levels had mean urinary perchlorate levels about 40 times greater than the geometric mean for participants in NHANES 2001-2002 aged 20 years and older (Tellez et al. Page Last Updated: 05/28/2009.fda.html and from ATSDR at: http://www.11(3):295. Lawrence JE.10(8):659-663. Neonatal thyroxine level and perchlorate in drinking water. Skeels MR.45(10):1116-1127. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.17(4):400-407. References Blount BC. and environmental perchlorate exposure among residents of a Southern California community. Health Implications of Perchlorate Ingestion. Braverman LE. Valentin-Blasini L. National Academy of Sciences (NAS). Food and Drug Administration (FDA). Crump KS. Greer SE. EPA reference dose (Blount et al. Li Z.90(2):700-706. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Lamm SH. Pirkle JL.atsdr. Crump KS.113(11):A732. 6/2/09 Greer MA. J Expo Sci Environ Epidemiol 2007. Thyroid 2000. 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. Available at URL: http://www. et al.. and nitrate on thyroid function in workers exposed to perchlorate long-term. Benchmark calculations for perchlorate from three human cohorts. Byrd D. Valentin-Blasini L. Kelsh MA. Sesser DE.htm. Pleus RC. Dasgupta PK. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Abarca CR. most of the population is considered to be below the U. et al.114(12):1865-1871. Osterloh JD. Deyhle GM. Tellez RT. Washington (DC): National Academy Press. He X. Analysis of relative source contributions to the food chain. Chacon PM. Also. Buffler PA.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Gibbs JP.EPA at: http://www. Osterloh JD. Kirk AB. Lamm SH. Daaboul JJ. The effect of perchlorate. Environ Health Perspect 2005. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.40(21):6608-6614. Lawrence J. Blount BC. Thyroid 2001. Doemland M. 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. Jackson WA.S.110(9):927-937. Rutherford GW. 2007). Caldwell KL. Braverman LE. Braverman LE. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Erratum in: J Occup Environ Med 2004. Low dose perchlorate (3 mg daily) and thyroid function. Miller MD. Erratum in: Environ Health Perspect 2005. Barnard JC. Richman K. 2005). epa.

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

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

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

2003). and humans.00) .20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 2004..800) 1. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. Fei et al.500) 90th . 2003a).400-. 2005).900 (.800 (. PFOA.700 (. 2007a. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.20) .. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.400) ..400-.500) . Olsen et al.500-1. development in offspring was stunted and hypothyroxinemia was observed. PFOS. * 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.10) * 03-04 03-04 * * < LOD < LOD < LOD .S. 1999.S.. 2003a).500) .700) . elderly and children.600-2. 2004b). Fourth National Report on Human Exposure to Environmental Chemicals 249 . Survey Geometric mean (95% conf. 2004)..300 (<LOD-. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP..500) .400-1.300-1.00 (... Thibodeaux et al. 2004).10 (.. 2003a. interval) Selected percentiles ( 95% confidence interval) Sample 95th . population. PFOS. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. 2003..00) .10) . Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 2003). developmental and teratogenic effects were demonstrated in offspring. hepatotoxicity. 2001. 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. At high but non-toxic maternal doses of PFOS.500-1.50) .400-1. 2007b.500) . see Data Analysis section) for Survey year 03-04 is 0.. In such studies. Olsen et al. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.500 (. Kennedy et al. 2003.800 (.S. 2007b).400 (<LOD-.10) . 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. thyroidal). U. monkeys.80) 640 1454 03-04 03-04 * * < LOD < LOD . and no substantial age trends were seen within adults ages 20-69 (Olsen et al.600 (..S. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.500-. Harada et al. 2003. 2007.900 (.400 (<LOD-. 2004a..3.800 (. Lau et al.. 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.600 (. EPA. 2005). U.400-1.600 (.500-1. reproductive.. or increased cancer rates (Alexander et al.300 (<LOD-.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 .00) . PFOA. < LOD means less than the limit of detection.80) 485 538 962 Limit of detection (LOD. In comparing three separate reports on adults. 2003a.400-1.. the potential to estimate risks to humans from animal doses is uncertain.900 (. 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. possibly related to lung immaturity (Lau et al.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 1992.500 (. Animal studies of PFOS have demonstrated weight loss.300 (<LOD-. Olsen et al.400 (<LOD-.500-3. 2003). which may vary for some chemicals by year and by individual sample.800) 1. 2007a.500-1. 2004. 2007)..500 (<LOD-1.. 2003a. At doses causing maternal toxicity. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality..108 times higher than background serum levels in humans (Butenoff et al. Cook et al. However. perfluorohexanesulfonate (PFHxS).400-1.. EPA. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. and changes in thyroid hormone concentrations (Grasty et al.800 (.40) ..

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

population from the National Health and Nutrition Examination Survey.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900) < LOD . see Data Analysis section) for Survey year 03-04 is 1.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400) . which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. Survey Geometric mean (95% conf.500) 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.300 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.400 (<LOD-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) < LOD . which may vary for some chemicals by year and by individual sample.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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3. interval) Selected percentiles ( 95% confidence interval) Sample 95th . < LOD means less than the limit of detection. Survey Geometric mean (95% conf.400 (<LOD-. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (<LOD-.600 (.500-.400 (. Fourth National Report on Human Exposure to Environmental Chemicals 251 .500 (<LOD-.0.S.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .

70 (1.00 (1.70 (2.40) 2.91) 2.80) 3.80) 5.40 (1.90 (1. Survey Geometric mean (95% conf.08) 2.00 (5.00) 3.09 (.50) 6. interval) .30 (2.30) 3.40) 640 1454 03-04 03-04 1.20 (1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1. population from the National Health and Nutrition Examination Survey.20 (1.20-3.70) 2.10 (4.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.30) .60-2.50 (4.10) 5.80) 90th 2.50 (6.20-1.80-7.90 (1.90 (2.0) 8.40) 1.90 (4.30-12.44 (2.73-2.80-2.800 (.900-1.60-4.80) 4.17 (1.900-1.966 (.0) 1053 1041 03-04 03-04 03-04 1.70-10.852 (.10 (.30 (1.90) 1.80-8.30) 03-04 03-04 .20 (1.54) .50 (2.50 (1.586-.30 (1.30 (6.80-12.50-6.80-4.20) . Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.86 (1.70-2.60 (1.60-8.20) 1.10 (1.40 (2.20-1.60) 3.80-7.900 (.10) 4.00 (.10-9.50-6.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.10-5.70-5.60) 1.70-2.90-19.50-3.62-2.56-1.20) 1.30) 3.80-3.90) 1.30 (1.90-2.60) 9.20) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.S.40) 1.30-2. population from the National Health and Nutrition Examination Survey.912-1.834-1. Survey Geometric mean (95% conf.6) 7.27) 1.70-7.5) 5.900-1.90) 8.20 (6. see Data Analysis section) for Survey year 03-04 is 0.1) 485 538 962 Limit of detection (LOD.10) 4.72 (1.00) 1.14 (.900-1.900) 1.26) 2.05-2.77-2.40) .70) 1.689 (.04) .80-3.30) 3.30-6.10) 1.03) 1.10) 1.721-1.70) 3.900-1.60 (1.40-1.30 (3.10) 6.60) 2.00-8.20-1.40) 4.70) 13.10 (.963 (.50) 2.60-3.67-2.40) 640 1454 03-04 03-04 2.90 (1.50 (6.10) 6.50 (4.20-1.42 (1.90) 90th 5.816-1.20) 03-04 03-04 2.50-10.70) 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 1.697-1.87-2.40 (1.80-4.60-4.12) .80 (1.00 (1.3.40-1.10 (.809) 1.30 (7.00-7. 252 Fourth National Report on Human Exposure to Environmental Chemicals .17-1.50) 2.00 (1.50 (1.70) 1.700 (.60-2.90 (4.16) .20-2.00) 2.984 (.10) 75th 3.900 (.60-7.30 (2.00-6.10) 1053 1041 03-04 03-04 03-04 .40 (1.20) 2.60-3.00-1.00-1.40 (1.80-8.00 (2.80 (4.10) 75th 1.80-6.51) 1.90) 1.S.900-1.861 (.72) 1.5) 8.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (.80) 1.10) 8.00 (1.01 (1.10 (4.80-4.93 (1.10-9.20 (6. interval) 1.800-1.40-3.20 (1.70-6.700-1.60-2.92 (1.90-10.600-.90 (1.50 (1.826-1.60 (6.30 (1.1.80 (1.60 (1.50 (1.835-1.30-9.70) 2.3 (9.90) 3.00) 1.

Survey Geometric mean (95% conf.7-69.7-30.5-21.9-23.5-33.80-9.80 (7.6) 18.1-33.60 (3.4) 640 1454 03-04 03-04 23.0-70.1-25.20) 5.20 (4.4-42.2 (18.9 (22.30-3.30-11.20 (4.60-9.70-9.6) 42.6 (19.21-3.9 (13.8-22.1) 57.60-13.3-61.30 (3.80 (6.10 (3.7 (35.47-4.90 (7.90-4.40) 90th 7.5-62.9 (17.8-22.2) 30.50) 4.20) 4.6) 1053 1041 03-04 03-04 03-04 3.70-7.67-4.82) 4.30-6.90-4.7 (35.30 (5.40) 75th 5.4 (19.4-17. Survey Geometric mean (95% conf.5) 18.65-4.5) 32.70 (5.1-24.30) 6.1-36.2-57.40-10.7-53.8-81.7 (43. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.8-30.0-16.2 (19.7 (43.40) 3.50-13.1 (19.6 (44.18 (3.79) 4.5) 19.3 (17.9-38.70-10.99-3.90 (7.80 (6.91) 3.2 (21.5-23.00) 3.4) 56.5) 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 21.4 (19.4) 75th 30.7) 39.2) 45.8 (37.70) 4.90-12.85-4.5 (28.0) 23.0) 485 538 962 Limit of detection (LOD.40-6.20-5. population from the National Health and Nutrition Examination Survey.10-3.70 (3.60 (7.3 (28.35) 3.S.2 (28.80) 8.80-4.00 (3.07-4.6-50.10 (6.8-78.8) 27.6) 9.50 (3.0 (20.96 (3.3 (35.3 (44.20) 7.80-12.50-6.1) 15.6-45. population from the National Health and Nutrition Examination Survey.6 (42.40-17.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.7 (19.5) 57.0) 43.7 (7.89 (3.50-4.8-22.90) 6.3-22.1.70-7.60 (5.90 (7.2) 640 1454 03-04 03-04 4.53) 3.5) 9.27) 4.7-49.30) 7.20) 10.9) 22.30-5.9) 27.9 (19.5) 1053 1041 03-04 03-04 03-04 14.0) 36.0) 21.0) 90th 41.S.4 (28.2-22.2 (16.30 (3.3) 42.50) 7.40-14.4-25.40 (6.40-6.0) 21.90 (5.70 (5.5) 7.0 (27.00 (5.1 (24.3) 485 538 962 Limit of detection (LOD.80 (5. interval) 3.4) 21. Fourth National Report on Human Exposure to Environmental Chemicals 253 .11 (2. see Data Analysis section) for Survey year 03-04 is 0.9) 22.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50 (4.3 (35.6-24.6) 62.9-19.7-33.7 (13.95 (3.8) 46.4 (17.00 (5.20-9.70) 3.60) 8.20) 5.47 (4. interval) 20.1 (23.40) 5.6 (35.6) 7.60 (6.0-66. see Data Analysis section) for Survey year 03-04 is 0.4.1-35.1-52.10) 5.6) 35.20) 7.60) 03-04 03-04 3.8-35.60-14.37 (2.3) 41.7-23.60 (4.20-4.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.5) 8.70) 6.8 (45.9) 9.60 (6.2) 30.10 (3.60-6.6) 21.4 (23.30-8.8 (34.5 (28.4) 20.40 (4.0) 03-04 03-04 19.0-20.84-3.70-5.2 (27.3) 28.1) 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 4.8) 32.

200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.200-.300-. population from the National Health and Nutrition Examination Survey.200-.200-.300) .300) .300 (.200-. population from the National Health and Nutrition Examination Survey.200-.300-.200-.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 .500) . * 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 0.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .500) < LOD 485 538 962 Limit of detection (LOD.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0.300 (.200-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.300 (.4.300 (.300 (. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 254 Fourth National Report on Human Exposure to Environmental Chemicals .300) .500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.500) 485 538 962 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.300 (.300 (.S.300 (.300 (.300 (.300) .500) .300-.300) .200-.300 (.300) . < LOD means less than the limit of detection.S. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300) .400 (<LOD-.300 (.200-.300-.500) .300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.

700 (<LOD-.900 (.30 (1.10 (.10-1.30 (1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20 (1.00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample.90) . see Data Analysis section) for Survey year 03-04 is 0.00 (.10) * 03-04 03-04 * * < LOD < LOD .50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .700 (<LOD-.50 (1.900-1.20-1.900-1.900) .10-1. population from the National Health and Nutrition Examination Survey. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.800) .30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .10-1.900-1.900-1.900 (<LOD-1.600 (<LOD-1.10-1.700) 90th 1.80) 1.00-1.30) .20) 1.400 (<LOD-1.30) 1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 255 . which may vary for some chemicals by year and by individual sample.60) 640 1454 03-04 03-04 * * < LOD < LOD .800 (<LOD-.500 (<LOD-.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.S.300 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 0.600) .300-2.10) .00 (.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .900-1.300 (<LOD-.10 (1. < LOD means less than the limit of detection.00 (.700 (<LOD-.10 (.600 (<LOD-1.700) 1.S.900) 485 538 962 Limit of detection (LOD.10 (.900-1.900-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .30) 1.80) 1.10) 1.700) 1.70) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800) . < LOD means less than the limit of detection.600 (<LOD-1.400 (<LOD-.3.40) < LOD < LOD .00) < LOD .40) 1.700) .600 (<LOD-.10) 1.30 (1.700 (<LOD-.60) 485 538 962 Limit of detection (LOD.700 (<LOD-2.50 (1.10) . Survey Geometric mean (95% conf.700 (<LOD-.10-1.900) 1.700 (<LOD-.6.

Environ Res 2005. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Chlorinated. et al. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Environ Health Perspect. Calafat AM. et al. Hekster FM. Environ Health Perspect 2007. Mandel JH. Hurtt ME. Saito N. Guruge KS. Occup Environ Med 2003. O’Connor JC. Yoshinaga T. Yoshinaga T. et al. brominated.63:490496. de Voogt P. Biegel LB.60(1):44-55. Ingall GB. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Birth Defects Res B Dev Reprod Toxicol 2003. Fillmann G. Moore JA.39(23):9101-9108. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Kennedy GL Jr. Environ Sci Technol 2007a. Cook JC. Fei C. The toxicology of perfluorooctanoate. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. O’Connor JC. Kudo N. Needham LL. Perkins RG. Apelberg BJ. Edwards EA.115(11):1596-1602. Halden RU. Needham LL. Yamashita N. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. et al. Crit Rev Toxicol 2004. Mohotti KM. Mandel JH. et al. Needham LL. Wong LY. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000.34(4):351-384.39(1):80-84. Environ Sci Technol 2004. Falandysz J. Olsen J. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Hurtt ME. et al.and perfluorinated acids. Corsolini S. Kuklenyik Z. Environmental and toxicity effects of perfluoroalkylated substances. Characterization of risk for general population exposure to perfluorooctanoate. Olsen GW. Loganathan BG. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Kumar KS. Morikawa A. Gaylor DW. Kannan K. Suzuki E.7(4):371-377. Day RD.Perfluorochemicals References Alexander BH. Frame SR. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Environ Sci Technol 2006a.60(10):722729. Laane RW.Koizumi A. Harada K.113(2):209-217.41:2237-2242. Tully JS. Moore RW. Taniyasu S. Polyfluoroalkyl chemicals in the U. Taniyasu S. Kuklenyik Z. McLaughlin JK. Arendt MD. Kamiyama S. Reidy JA. Katakura M. Ye Y. Toxicol Appl Pharmacol 1990.99(2):253-261. Butenhoff JL. Toxicol Appl Pharmacol 1992. Harada K. Calafat AM.38(10):2857-2864. Regul Toxicol Pharmacol 2004. Rodricks J. Mabury SA. Kawashima Y. in vivo. and ex vivo studies. Toxicol Appl Pharmacol 1995. Biegel LB.39(3):363-380. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Seneviratne HR. Frame SR. Herbstman JB.46(2):141-147. Rev Environ Contam Toxicol 2003. J Occup Health 2004. Koizumi A. Mandel JS. Fluorotelomer alcohol biodegradation yields poly. Saito N. Liu RC. Calafat AM. Kannan K. Bandai N. Sasaki S. Keller JM. Environ Sci Technol 2005.179:99-121. Caudill SP. Environ Sci Technol 2005. Cook JC. Inoue K.40:21282134.115(11):1670-1676. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Cook JC. Grasty RC. Evans TJ. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Caudill SP. J Environ Monit 2005. Murray SM. Aguilar-Villalobos M. Environ Sci Technol 2004. Butenhoff JL. Yun SH. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Lau CS. Wijeratna S. Environ Health Perspect 2007. Reidy JA.S.104(2):322-333. Olsen GW. Peterson RE. Perfluorinated chemicals in selected residents of the American continent. Chemosphere 2006b. Kuklenyik Z. Bookstaff RC. Rogers JM. Calafat AM. The influence of time. Inoue K.39(23):9057-9063. Hurtt ME. Jarnberg U. Reidy JA. Holmstrom KE.38(17):4489-4495. Kannan K. Olsen GW. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Watanabe T.68(6):465-471. Kuklenyik Z. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Needham LL. Seacat AM. Dinglasan MJ. et al. and perfluorinated contaminants in livers of polar bears from Alaska. Yamashita N. Toxicol Sci 2001. Grey BE. Tully JS. Bignert A.124(2):119-132. Environ Sci Technol 2005. Reidy JA. 2007b. Tarone RE.S.1968--2003.115(11):1677-1682. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Calafat AM. Burris JM.134(1):18-25. Witter FR. Chem Biol Interact 2000. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka.

Moisey J. Buck RC. J Occup Environ Med 2003b. Kannan K. birds. Toxicol Sci 2003. fish.S. et al. Olsen GW. Butenhoff JL. Larson EB. Miller JP. Olsen GW. Horii Y. Ellefson ME. Butenhoff JL.40(1):32-44.37(12):2634-2639. Prevedouros K. Lau C. Burlew MM. Mandel JH. Sources. Hanson RG. Seacat AM. Church TR. Ehresman DJ. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. et al. Zobel LR. Mandel JH. Olsen GW. htm. fate and transport of perfluorocarboxylates.74(2):369-381. Case MT.. U. Yamashita N. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children.68(1):249-264. van Belle G. Toxicol Sci 2002. Thibodeaux JR. and perfluorooctanoate in retired fluorochemical production workers. Burris JM. Burris JM. Barbee BD. Historical comparison of perfluorooctanesulfonate. Environ Health Perspect 2003a.45(3):260-270. et al. 1/15/06 Vanden Heuvel JP. Kawashima Y.113(5):539-545. Stanton ME. (Erratum in: Environ Health Perspect. Coordinate induction of acyl-CoA binding protein.74(2):382-392.perfluorohexanesulfonate. Rogers JM. Church TR.) Tittlemier SA. Washington. Seacat AM. Chemosphere 2007b. Butenhoff JL. Half-life of serum elimination of perfluoroo ctanesulfonate. Butenhoff JL. Available from URL: http://www. fish.epa. Hansen KJ. J Ag Food Chem 2007. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Chemosphere 2004a. fast foods. Mar Pollut Bull 2005.55:3203-3210. Olsen GW. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Richards JH. Biochim Biophys Acta 1993. Environ Sci Technol 2003. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Reagen WK. Lau C. Biol Pharm Bull 2003. Hansen KJ. Burris JM. Rogers JM. Hansen KJ.26(1):47-51. (Erratum in: Toxicol Sci 2004. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Mandel JH. Olsen GW. Thomford PJ. Rogers JM. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Hanari N. Toxicol Appl Pharmacol 2004. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Environ Health Perspect. Cao XL et al. Butenhoff JL.51(8-12):658-668. Peterson RE.111(16):1892-1901.198(2):231-241. EPA). Hanson RG.54(11):1599-1611. Yamashita N. et al.41(9):799-806. Thibodeaux JR. et al. Helzlsouer KJ. Olsen GW.82(1):359. Huang HY. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Pepper K. Taniyasu S. 2003a. Gamo T. Froehlich JW. Petrick G.2(1):53-76. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Environ Sci Technol 2006. Lundberg JK. A global survey of perfluorinated acids in oceans. 2007a. 2003. Sterchele PF. Horii Y. Hansen KJ. Grey BE. Ehresman DJ. Environ Health Perspect 2005. Olsen GW.111(16):1900) Olsen GW. and food items prepared in their packaging.S. Mair DC. Korzeniowski SH. Taniyasu S. II: postnatal evaluation. perfluorooctanoate andother fluorochemicals in human blood. Mandel JH. J Occup Environ Med 1999. Lundberg JK. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts.115(9):1298-1305. Hansen KJ. Butenhoff JL. Burris JM.1177(2):183-190. et al. The developmental toxicity of perfluoroalkyl acids and their derivatives. Bronson R. Nesbit DJ. Cousins IT. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Grey BE. and humans from Japan. Seymour C. Burris JM. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.gov/opptintr/pfoa/pfoara. Church TR. Toxicol Sci 2003. J Children’s Health 2004b. Environmental Protection Agency (U. Kannan K.68:105–111.Perfluorochemicals Kudo N. Olsen GW. I: maternal and prenatal evaluations.

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

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

22(3):688-695. David RM. et al. Rylander L.16(4):487-493. Mortensen GK. Environ Health Perspect 2004.26(8):1219-24. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Int J Hyg Environ Health 2007. Dalgaard M. Ladefoged O. 2000c [online]. Fromme H. The estrogenic activity of phthalate esters in vitro. Environ Health Perspect 1997. Epidemiol 2005.html. et al. Balasubramanian AV. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Brock JW. Lovekamp-Swan T.niehs. Available at URL: http://cerhr. Liss GM.19(4):505-515. White R.Phthalates in human urine samples. Davis BJ. et al. Hauser R.195:142-153. 2000a [online]. Duty SM. Silva MJ. Biol Pharm Bull 2003. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Chahoud I. Nielsen J. Csanády G. Milligan SR. Silva MJ. Yoshimura M. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.niehs. Reprod Toxicol 2004. Koch HM. Research Triangle Park (NC). Int Arch Occup Environ Health 1993. Duty S.382:10841092.105:802-811. Meeker JD. Leffers H. Zhang S.110(5):515-518. et al.nih. Meeker JD. Kano I. 6/2/09 NTP-CERHR. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Hanaoka T.64(8):555-560.112(17):1734-1740. Hoppin JA.nih. McKee RH. Stringer WT. Jonsson BAG. Kano K. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Filser J.niehs. Baird DD. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).46(11):643-647. Mechanisms of phthalate ester toxicity in the female reproductive system. Singh NP.25(2):293-302.nih. NTP-CERHR. Hum Reprod 2007. gov/chemicals/dehp/dehp-eval. Research Triangle Park (NC). Suzuki T. Grote K. Research Triangle Park (NC).nih. Jobling S. 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]. Giwercman A. Harris CA. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Henttu P.html. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Ryan L. Albro PW. Main KM. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Parker MG.gov/chemicals/dehp/dehp-eval. 2000b [online]. and infant formula by tandem mass spectrometry (LC-MS-MS). Research Triangle Park (NC).111(2):139-145. Available at URL: http://cerhr. 6/2/09 NTP-CERHR.niehs. Park MG. Bolte G. Brock JW. Am Ind Hyg Assoc J 1985. Hauser R. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Sumpter JP. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Available at URL: http://cerhr. 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 . Andersson A-M.html. Numtip W. Butala JH. consumer milk. Hartle RW. Pan G. Scand J Work Environ Health 1985. Silva MJ.18(1):122.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Kalita JC. Wang P.103:582-587. Calafat AM. 6/2/09 NTP-CERHR. Tsukino H. Angerer J. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Skerfving S.106(1):23-26. Akesson B. Environ Health Perspect 2003. Available at URL: http://cerhr. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro.html. Skakkebaek NE. Borch J. Reynolds T. Determination of phthalate monoesters in human milk. Kessler W. Environ Health Perspect 2002. 2006 [online]. Boehmer S. 6/2/09 Okubo T. Sumpter JP. Toxicol Appl Pharmacol 2004. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Davis BJ. Environ Health Perspect 1995. Hagmar L. Chen Z. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate.gov/chemicals/ phthalates/dbp/dbp-eval. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Ryan L. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Gans G. Richthoff J. Jarfelt K.112(17):1740]. Reprod Toxicol 2005. J Androl 2004. Anal Bioanal Chem 2005. Environ Health Perspect 1998. Calafat AM. Jacobsen H. 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Rusyn I.Phthalates phthalate (DEHP): a cross-sectional study in China. Wu ZF.46:282-293. Lambright CR. Pratt IA. Albro PW. Crit Rev Toxicol 2006. Meek MD. Parks LG. Reidy JA. Peck CC. Ostby JS. Malek NA. Matthews JB. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Klinefelter GR. Barlow NJ. Orton TC. Zacharewski TR. Environ Health Perspect 2004. Fielden MR. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Environ Health Perspect 1986. et al. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Cunningham ML. Toxicol Sci 2000. Environ Health Perspect 2006.S. Jackson SJ. Silva MJ. Barr DB. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters.114(11):1643-1648. Rhodes C. Urinary levels of seven phthalate metabolites in the U. Toxicol Sci 1998. Environ Health Perspect 1982. Batten PL. Peters JM. Hodge CC. Clemons JH. Caudill SP. et al.112(3):331-338.36:459-479. Bratt H. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat.45:11-17.65:299-308.58:339349. Abbott BD. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. et al. 112(5):A270].

2-38.1-15.8 (28.1 (58.2) 12.6) 50.5 (76.9-30.3) 54.8-13.2 (11.7 (80.4-92.5-97.6-43. 2000).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. interval) 15.6-18.7-58.4-24.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.6) 13.6 (12.8-16.0 (23.2-116) 122 (102-143) 101 (84.9) 15.1) 32.8-14.5) 15.3 (12.9 (70.8-72.4 (13.3-88.9-16.6) 14.7-13.4 (59. some personal care products.4) 33.1 (13. 2001-2002.6 (21.4 (32.7 (13.1) 67.5 (13.6 (66.3) 23.8 (10.5) 55.0 (20.1) 31.0-106) 58.8-133) 89.5 (26.3) 37.6) 35. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.4 (48.7-16.7-16. vinyl tile.6-39.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3 (13.1-214) 166 (116-191) 145 (110-213) 88.0 (11.3-125) Total 15.5 (55.0) 20. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-120) 52.1-15.4) 98.5-25.3-43.2) 14.2 (19.4) 75th 35.1) 12.8-16. it can be released into the ambient air during use or disposal of the products.4) 49.Phthalates Benzylbutyl Phthalate CAS No.8) 24.6 (13.S.2-16.7) 38.0 (33.8-14.4 (53.1) 14.6) 15. BzBP can be released into the environment during its production and.3-12.4-15.4 (29.2-20.1 (13.0) 70.9 (12.4 (68.8 (53.0-26.6 (13.4) 65.3) 15.0 (12.7-35.8-98.7 (12.1-61.2-17.9) 43.7 (70.4) 35. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.6-38.3 (44.4) 14.1-39.5 (66.7 (53.2) 14.8 (80.2) 22.9 (22.5) 27.0) 24. see Data Analysis section) for Survey years 99-00.1-16.2 (43.2) 78.0-55.9 (39.8 (71.6-116) 122 (102-142) 101 (85.6-132) 103 (84.9) 12.7 (51.4 (32.8 (14.5) 15.8 (21.9-28.4) 71.5) 16.9 (11.5-18.1 (20.3 (54.8-17.3 (12.8) 28. Food crops take up BzBP.5-40.1-38.6-72.3) 13.7-25.6-92. and 0.9) 14.4) 108 (96.2) 33.1) 76.5 (61.5) 65.3 (12.9 (21.5-41.2-40.5-36.4) 51.8-35.3-74.7 (11.0 (43.0) 33.5) 82.9) 14.1) 68.7-119) 99.7-14.1.5-145) 138 (106-241) 143 (127-179) 120 (99.6 (53.4) 129 (98.9) 11.3-91.6) 25. 2000).4-16.8) 14.8 (38.0 (34.6) 29.7-82.3-130) 122 (88.1-18.4) 12.2-115) 113 (91.4 (10.0) 32.8-76.5 (57. residents (Blount et al.4 (53.2) 32.2) 69.6) 37.8.9-14.8 (30.4) 38.2) 17.6) 95th 103 (94.4) 80.3) 13.6-150) 94.8) 33.2-183) 101 (78.6-17.2 (14.1) 29.S.7-16.6) 16. NTPCERHR.4-62.2 (25.2) 66.5-62.9-87.0) 23.3 (33. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.3-18.3-21.7-172) 103 (74.7) 23.0 (55. car care products.9-49.3 (22.7) 40.3-82.8) 63.9) 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 39.4) 35. 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.6 (13.2-31.0 (15.0-130) 101 (86.3.0 (26.1 (14.7 (82.7-15.0 (27.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.5-36.9 (12.4 (27.6) 67.9 (28. can produce developmental and reproductive toxicity in rodents.6 (13. High dose BzBP and its monoester metabolites.2-33.. including MBzP.6 (41. 0.1-90.1-43. IARC considers BzBP not classifiable with respect to human carcinogenicity.7 (15.6) 13.9-62.9) 49.6) 63.0) 90th 67. and to a lesser extent.9 (13.1 (14.3) 63.2-19.0-85. respectively. and diet is the major source for general population exposure.8-41.3 (29.9) 13. 2004.6-92. sealants.8-121) 79. and 2003-2004 were generally similar those reported in U.8 (86.6) 14.3-34.9) 18.2 (47.5-14.1-35. population from the National Health and Nutrition Examination Survey.5 (27.4) 81.8 (12. particularly male animals (McKee et al.8-17.5-84.6) 24.0 (30.4-127) 80.1 (55.3 (30.0) 34.7-17.2-39.5-35.2 (19.8-64. and 03-04 are 0.3 (29.2-16.1-16.1) Selected percentiles ( 95% confidence interval) 50th 17.0 (30. 01-02.9-47.7-170) 169 (134-198) 152 (99.5 (67.9-190) 86.6-29.0 (14.5) 30.9 (16.5 (47.9-27.8-18.2) 15.3-27.2-155) 91.5-94.1 (10.6 (32.0) 16.3) 94.4 (31. 262 Fourth National Report on Human Exposure to Environmental Chemicals .6) 35.5) 23.3-161) 99.4 (63.4-25.2 (10.4 (10.0 (15.8 (50.5-33.1) 13. because it is not bound to products in which it is incorporated.3-18.8 (71.6-79.8-48.1 (19.3-75.1 (32.2) 13..1-116) 122 (93.

5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .8-34. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.2) 11.9 (24.3) 67.9 (10.1 (19.1-27.8) 53.7 (21.8-13.8 (50.1 (23.9-16.5-16.1 (41.9 (51..4 (26.6 (11.9-104) 62.3 (38.5-61.4 (33.3) 21.9 (10.4-19.7 (23.9) 24.5 (35.4-14.3 (13.0) 49.7-14.8) 13.8) 33.5-42.0) 15.7-20.8-85.0 (62.6 (24.5-29. Hoppin et al.9-115) 57.2-78. 2007).4) 44.5) 17.7-69.5) 41.7-14.2) 11.6 (30.1 (18.5 (10.4) 12.0-90.3-38.1 (46.1) 12.6 (36.S.0) 11.1) 80.8-80.0 (67.0) 24.1) 17.6-99..3) 14. in men attending a Boston infertility clinic (Duty et al.6 (15.0-27.3-64.5 (12.4) 60.1 (11.1-125) 86.7 (13.3) 90.1-12.7-90.0-15.1-12.7) 56.5-99.0 (33.4) 17.4 (63.7-12.7 (14.6-15.9-23.0-51.0 (12.8-15.7 (11.2-117) 95.5-23.5 (11.6 (11.8) 16.8) 15.7 (54.3) 73.4 (21. 2006)..1-58.7-56. Hauser et al.4) 14.4) 50.6 (30.8-13.7 (13. 2002. 2003).9 (15.1 (21.5-58.0 (41. in young Swedish men (Jonsson et al.0 (12.8-60.6-47. 2004.1 (21.6) 53.5-31.7 (11.1-79.9) 12.5-38. interval) 14.5 (48.8 (30.2) 26.7-123) 77.9-62.2-26.0-48. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6) 12.8 (49. 2005.8-173) 195 (121-305) 229 (99.4) 28.6 (19.4 (69.6-12. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.9-13.8 (10.5-76. 2005).5) 16.1 (14.8-15.3) 37.1 (25.9) 12.6 (57.5 (49.4-142) 134 (116-176) 136 (85.2-13. 2002).4) 15.7 (38.4-116) 73.9 (39.6-116) 74.9-83.4 (11.1) 35.5 (42.6) 13.4-18.8-64.9) 12.7-29.4-99.8) 11.1-35.8) 46.8-69.8 (11.2-12.2-49.1) 27..8-14.3) 16. adolescents compared with adults.0 (11.2) 12.5-13.4 (11.2-13.2 (41.8) 34.4-93.5-58.6) 75th 25.8-14.7-20.1 (53.0-53.7-31. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.7-19.3 (39.9) 42.5 (10.8) 80.7) 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 40.7 (18.2-21.6) 38.9 (15.0) Selected percentiles ( 95% confidence interval) 50th 13.3) 14.9) 64.4) 13.2 (27.1) 142 (99.9) Total 14. Weuve et al.4-23.3) 12.3) 29. and in a small sample of German residents (Koch et al.3 (12.5) 95th 77.8-27.4 (74.3) 18..5) 10.5) 78. 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.6) 73.7-19.7 (55.2-57.1) 23.6 (22. and females compared to males (Silva et al.1) 39.8-39.5-26.9 (9.1 (34.7) 38.0) 24.7) 25.5-57.6-13.Phthalates York City (Adibi et al.4 (13.1 (21.8-42.2) 11.6 (34.6) 25.1 (13.4) 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 12.0 (38.0 (49.9-13.8) 56.7) 46.9-14..73-12.3-16.8) 68.4-17.8 (57.6 (11.2-17.9 (43.3) 13..9 (12.3 (24.7 (11.4-102) 70.9 (55. 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.2-15.1 (9.3) 55.9-40.3-73.3) 13.5-26.8-16.2) 15.4) 21.9) 11.4-27.0) 60.1) 24.8) 71.1 (15.3 (23.7) 19.2) 67.9 (12.9 (54. 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..8) 53.8 (64.6-86.7 (12.6 (14.5) 13. In NHANES 1999-2000..0 (41.4) 51.5) 14.0 (10.6) 12.5 (56.3 (15.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.4 (12.3) 13.8 (46.5) 46.7 (59.8 (12.0-26.0-109) 65.8) 108 (75.1-120) 77.8 (69.8) 33.4 (60.4) 104 (89.4) 13.9) 100 (80.4-60.8) 26.7-15.7-61. 2007).8 (13.6-20.7-15.4 (46.4-90.0 (13. 2004).8-48.95-14.4) 25.3) 89.1 (43.5 (9.7-397) 70.1) 24.3-11.1-14.1 (21.2-15.6) 58.5-213) 49.4-14.3-34.3 (60.9) 52.6) 30.6-81..9-28.2-51.6 (51.4 (25.1-29.7) 11. A small study of African-American women in Washington.9 (24.5) 20.9 (29.2 (56.4 (10.4) 90th 50.1 (13.4 (34.69-11.4 (11. 2003).2) 32.4-15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 24.6-40.3) 36.6-26.2 (69.7 (19. population from the National Health and Nutrition Examination Survey.2 (40.0) 13. 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.5-79.8) 54.4-79.4-42.5) 23.9) 11. In an annual sample of German university students.0) 12.9 (22.3 (35.8-13.9-69.

2000 [online]. 2005. Jacek R. Duty SM. Camann DE. Jonsson BAG. Dobler L. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Jedrychowski W. Needham LL. Malek NA.niehs. Reprod Toxicol 2004. Caudill SP. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Hum Reprod 2007. 112(5):A270]. Brock JW. Poland. et al.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Environ Res 2003.112(3):331-338. Barr DB. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Silva MJ. Sanchez GN. Barr D. Hauser R. Brock JW. Chen Z.16(4):487-493. Calafat AM.93:177-185. Ryan L. et al.Phthalates References Adibi JJ. Brock JW. Third National Report on Human Exposure to Environmental Chemicals. Hilborn ED. Bull Environ Contam Toxicol 2002. Research Triangle Park (NC). Rossbach B. Hoppin JA. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Duty S. Wiesmuller GA. J Androl 2004. Silva MJ. Meeker JD. 4/20/09 Silva MJ. et al. Davis BJ.110(5):515-518. Eckard R.108(10):979-982. Silva MJ. Reproducibility of urinary phthalate metabolites in first morning urine samples. et al. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.nih. Koch HM. Caudill SP.18(1):122. Angerer J.210(3-4):319-333. Environ Health Perspect 2003. Green RA. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Singh NP. Environ Health Perspect 2000. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Giwercman A. Available at URL: http://cerhr. Schettler T.22(3):688-695. Baird DD. et al. Wittassek M. Gans G. Helm D. Rylander L. Epidemiol 2005. Silva MJ.114(9):1424-1431. Urinary levels of seven phthalate metabolites in the U. Reidy JA. NTP-CERHR.68:309-314. Blount BC. Phthalate monoesters levels in the urine of young children. Hu H. Environ Health Perspect 2002. Perera FP. Levels of seven urinary phthalate metabolites in a human reference population. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Int J Hyg Environ Health 2007. Ryan L.111(14):1719-1722. David RM. Environ Health Perspect 2004. et al. Hodge CC. Sampson EJ. et al. Hagmar L. McKee RH. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Prenatal exposures to phthalates among women in New York City and Krakow. Weuve J. Caudill SP. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2006. Koch HM. Drexler H. Butala JH. Calafat AM. Richthoff J. Pirkle JL.html.25(2):293-302. Atlanta (GA).S. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Needham LL.

2004.81 (3.30-11.97) 4..40) 5.30 (4.0 (13.S.7) 4.5) 18.00 (7.3 (16. Biomonitoring Information Median concentrations reported in the NHANES 19992000.20-12.6 (11..7) 18.3 (11.00 (5.50) 90th 12.40-3.70) 3.50) 8.60) 3.0-25.63) 3.10-9. OSHA has established a workplace air standard for external exposure to DBP.72-3.97-7.20 (6. In addition.91) 4.0 (19. 2000.3 (16.5 (27.40-4.80 (5. 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..1-25.30-3.50) 5.60 (2.3-18.8) 677 652 703 699 1216 1088 Limit of detection (LOD.7 (16.4) 22.6 (13.7 (7.4-27. 2007).85-6.30 (3.2 (11.55) 2. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.0) 13.10 (4.1-12.20) 4.0) 12.20-2.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.6) 10. pharmaceutical coatings. Studies of children found age-related differences in urine MBP levels.96) 3.48 (2.70-4.5) 22.17 (2. residents (Blount et al.80 (3.6) 16.30-6.40-9. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates..6) 26.59) 3.9 (16.6) 12.0-14.6-34.7 (18.40 (7.43) 6.37) 6.4) 12.00-9.30-7.80 (2.90 (4. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.7-18.3 (13.40-3.40-4.7-31.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.24-8.5) 14.5) 18.4 (14.22) 3.40-12.0-38. Fourth National Report on Human Exposure to Environmental Chemicals 265 .6-20.5-16.90-4.6 (14..5-24.80 (2.10 (4. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.10-9.49-2.20 (3.02) 4.7 (9.50-2.30-6.19-3.7 (17.6) 17. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.50) 7.0 (11.20) 7.70-4.17) 4.5-16.50-6.80-5.5 (17.6 (10.5) 19.7-31.00-6.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.3-43.82-3.60 (4.90 (3.56 (5.46 (2.84) 4. they have been referred to as monobutyl phthalate (MBP).1 (13.28-5. Hauser et al.5) 23.3-30.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.3) 33.10) 3.1 (8.3 (19.. 2005).0 (13.33 (2.40 (3.6) 17.40 (6.3 (13.3-48.1) 25.50 (6.10) 9. Survey Geometric mean (95% conf.90) 12. 2005).6 (29.68 (2.5 (20.00-6.3-24.9 (16. Koch et al.9-23.80 (5.30) 6.80-5.22 (3. in men attending a Boston infertility clinic (Duty et al. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.7) 7.2-22. 2004. 84-74-2 Di-isobutyl Phthalate CAS No.00-4.Phthalates Di-n-butyl Phthalate CAS No.5 (11.50) 18.4-12.10 (3. 2003).11-3.30) 10.00) 10.30) 10.5) 25.90-4.40-17.8) 40.5 (10.56 (3.6-18.00) 4.1-20. Following oral administration of DBP to humans.7 (17.1-17.6-26.60 (8.60 (5.6-14.46) 2. NTP-CERHR..3.20-12.2-14.2) 5. and in a small sample of Japanese adults (Itoh et al.30) 5.46-5. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.10-2.2 (8.00) 4.2-33.0) 24. 2005.5) 12.40-5.90 (6. and also in some printing inks.07 (3.71 (2.5-29.S.70 (2. interval) 2.10) 11..00-11.6 (10.50 (3.44-2.50-4. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.8) 21.3-19.4) 5.50) 2.30-13. 2001). in a small sample of pregnant women in New York City (Adibi et al. 2000). see Data Analysis section) for Survey years 01-02 and 03-04 are 1.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.67 (5.0-18.10) 2.90-2.2 (12.7) 14.6 (9. When total DBP metabolites have been measured.3) 18.73-5.9-14. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al. DBP can produce reproductive toxicity in male rodents (McKee et al.40 (2.9) 15.6 (13.46 (3.40 (2.3-20.66) 2.60-6.70) 5. population from the National Health and Nutrition Examination Survey.55 (3.70 (5.73 (2.7) 15.0 and 0.30-2.6) 16.26 (2.30 (1.3) 3.8 (9.80) 75th 5. CDC.20 (7.1) 16. about 65% to 80% of a dose is eliminated in urine within 24 hours.7-20.00) 6.9) 10.97) 2.90 (4.70-8.56-4.20-6.30) 2. mostly as MnBP (Anderson et al.4 (20.20-9.10) 8. 2003).56) 3.3 (18.1) 22.90-7.6 (14. 2005).50-10.00) 7.0) 9. and insecticides.0) 20.

17 (2.3 (13.1) 4.8 (8..37) 3.45) 3.20-4.76-3.92 (7.39) 5.33 (2.00-3.S.46) 3.83 (2.55-6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3) 13.10-5.7) 10.72) 5.91-6.6-19.9-16.43) 3.20-2.8-18.1-12.7) 11.89) 6.32) 7.43) 3.07 (2.88 (2.05) 2.51) 2.1-24.20 (2.07-5. In an analysis of NHANES 1999-2000.78) 9.28 (4.15-4.26 (2.81 (3.26-2..18 (1.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.89-5. 2002.62 (6.68 (2.24) 3.31 (2.99-4.1) 11. 2006).4) 7.20 (7.58-4.95) 2.03-7.15) 3.57-4.86) 6.52 (2.5-19.20-3.08) 75th 4.3) 18.21 (5.6-19.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .30) 2.31) 2.64-7.84 (8.22 (2.74 (4.68) 3.00-3.94) 6.2) 9..34 (3. respectively.64-10.46 (2.69 (2.47-5.18-4.94 (5.0 (12. while MnBP declined (Wittassek et al.19 (2.5) 13.44 (3.04) 7.51) 5.4) 23. 2005).3) 28.54 (2.21) 10.8) 10.11-2.68) 5.93-6. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.0) 3.1) 10.0) 11. 2004). 2007). Between 1998 and 2003.6) 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 2.65-4.52) 3.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.01-2.7 (13.97-2.33-9.5 (11.79-8.76-15.65 (4.03 (5.58-3. 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.31) 2.56) 2.7) 3.8-18.56-4.4) 15. 2004).76 (3.6 (10.3) 16.5 (9.30 (6.11) 5.6 (12.02-10.82) 4.0) 15.67-5.75 (6. Weuve et al. 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.42) 2.32 (3.81) 9.0 (10.and gender.29-8.84 (4.52-20.59 (4.09-2.17) 90th 8.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.57 (3..6) 13.53-5. population from the National Health and Nutrition Examination Survey.66) 10.5) 15.47 (3.04-5.32 (7.80-3.27-12.75 (4. ranging from more than one-tenth the NHANES median (Itoh et al.1) 15. 2005).62-12.39-3. interval) 2.2) 24.95-3.08-2.38-10.2 (11.14 (4..43) 3.20 (2.18-10.18) 3.79-6.41 (2.28-13.81 (6.64-7.9 (9.80 (3.85 (2.78-8.3 (17.80) 7.54 (4.6 (8.1 (10.61-3. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.18) 4.1) 7.2 (10.46-11.54) 2.38 (6.7 (21.4 (12. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.36-2.82 (4.98 (2.4-16.56-15.95) 10.8 (10.0-18.66) 2.1) 13.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC. 2007).47-12.69-7.18 (4.6) 11.76-3.94-12.13-6.13 (2.66) 4.7) 19.8-36.11 (5.1 (11.9 (15. than adults in NHANES subsamples during the same time period.36-7.9-26.9-40.7 (11.8 (9. to about two to fourfold higher (Fromme et al.2-13.89 (3.51) 15.0 (8.81) 4.35) 3.69) 4.96 (3..33) 3.52-3.03-11.86-4.1-15.25) 5.04) 3.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.7-28.3) 13.00-7.57 (3. Over this time.2) 8.69) 6.0) 7.56) 5.7 (9.53-3.79 (4.65-11. samples from German university students had consistently higher median urine levels of MnBP and MiBP.33 (3.6 (8. 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.02 (7. Survey Geometric mean (95% conf.17-12.6 (15.53-4. up to four and 13 fold.78) 8.29-3.66 (8.1-25.9 (11.6 (9.. An analysis of NHANES 2001-2002 showed similar age.8-13.99) 7. the students’ median values for MiBP levels remained relatively unchanged.2-15.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.74-3.00 (3.73 (5.31 (7.72-7.9) 12.

2 (21.6) 39.6 (19.5) 37.5) 34.1 (18.0-32.3 (37.0 (23.6-31.6) 80.7-92.6-37.2-33. *In the 1999-2000 survey period.4 (21.7) 52.3 (56.2 (79.1 (34.5) 17.7-111) 64.4-26.3-85.9 (17.3) 36.7-127) 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 22.2-87.3) 23.6-44.9) 75.1-51.0 (18.1 (51.8) 48.2 (58.6-69.3) 19.0 (78.6-143) 127 (99.7-53.6 (32.7) 92.5-44.5 (28.9-79.3-145) 85.1 (19.1) 31.0) 31.4 (36. Survey Geometric mean (95% conf.8) 19.6-29.2-21.6-24.7-34.3-40.7-91.2) 90th 98.9 (79. population from the National Health and Nutrition Examination Survey.4-20.1-27.7-34.3-67.9) 26.6-49.7-106) 69.3 (30.9) 29.5 (59.1 (17.5) 26.3) 24.0 (15.2-159) 92.0) 20.8) 43.4 (35.0-21.6 (48.2) 26.9-22.7-26.0) 120 (98.1-22.3) 26.2-56.7 (51.7 (64.2 (59.9 (17.2 (74.5) 78.3-96. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.5-47.1 (31.2-114) 73.0-24.1) 17.6) 35.5) 36.7-20.9-22.4) 20.5) 20.3 (30.1) 46.3) 21.8-25.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1) 19.1) 25.9-87.6 (90.4-25.0) 84.9-92.7) 74.9-114) 116 (97.6) 71.8) 62. respectively.2-24.8) 75th 51.4 (35.S.8) 58.2-93.2 (25.2 (19.0-19.0-58.9.0) 21.1) 23.7-42.1-82.2 (20.7-124) 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.7 (43.0) 30.0 (17.8 (57.1 (36.1) 23.4 (72.2) 38.4) 22.4 (19.7-24.0 (45.8) 23.7-121) 97.8 (19.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2-23.7 (18.1-80.2-32.5-121) 106 (94.9) 18.4.8-119) 90.9-33.5) 21.6 (44.4-44.9-28.5) 65.7 (28.2) 68.1 (41.5) 31.7) 42.7 (33.4 (23.5) 47.9 (79.2) 62.7-42. referred to as monobutyl phthalate (MBP).3 (60.0) 27.0-73.6-20.6 (16.1-75.2) 32.5-27.3) 18.4-42.6-33.5) 36.5-53.4 (35.5-60.1 (19.1 (62.5-117) 95.6-36.9-53.8-132) 95. Fourth National Report on Human Exposure to Environmental Chemicals 267 .6-113) 108 (90.1-29.3 (51.4-159) 107 (84.2 (21. and 0.6 (22.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95. interval) 24.0) 38.0 (72.1 (26.4 (38.1 (21.3 (42.5 (74.9) 46. 1.0-51.1 (19.9-101) 77.3 (23.5 (30.3 (23.2) 42.5) 40.5 (29.6) 17.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.4-31.6) 46.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.7-116) 95.0 (30.3-76.8-111) 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 23.8-22.6 (26.6) 20.4-60.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.5-43.9 (20.4) 52.9-42.2 (17.0-26.7 (70.6 (55.0 (20.1) 23.5 (59.7 (38.9) 71.1.2-49.2 (18.9) 36.1) 47.5) 95.2-63.0-24.1) 36.5) 24.3-24.4 (35.7 (16.1 (58.2-22.5) 19.8-42.3 (17.4-18.1) 30.0 (31.8-29.8-123) 101 (90.6-48.6 (65.2 (75.3-21.7 (22.7-117) 118 (108-143) 93.1 (19.4) 59.7 (18.1 (54.6 (61.3-60.1-92.1) 20.7 (19.3-79.0 (36.0) 117 (104-131) 112 (84.7) 124 (98.4 (25.3) 40. and 03-04 are 0.7) 28.2 (78.3-136) 137 (107-162) 119 (90.9) 21.6-29.3 (36.5-47.1 (28. see Data Analysis section) for survey years 99-00.1 (16. 01-02.0 (25.6-40.0-19.1-20.5-42.5) 85.2) 20.4 (71.6) 38.6) 21.1-24.4) 64.7 (24.4 (84.

9) 19.4 (16.9 (35.9 (19.1 (46.6-32.6) 34.0-113) 104 (83.9) 91.2) 21.3-21.3 (76.6) 64.6-44.9 (35.8 (17.2 (19.3) 67.9 (39.4 (17.8 (65.5) 60.2-86.0) 94.9-84.3-20.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.8-43.4 (50. interval) 22.0-60.3 (69.7 (81.2 (35.4 (33.3) 21.7-51.7 (54.3 (55.5) 90th 68.5-18.5 (18.9 (30.5 (15.3-38.6-24.4-34.7-28.3 (52.1-62.4 (17.3) 20.0 (15.0 (18.7 (27.7 (28.3) 19.8-24.0) 59.2-61.2-22.5 (30.9) 14.9 (73.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9) 62.5-30.6) 18.4) 62.0 (50.2) 16.6 (17.7 (73.0) 28.3 (17.4) 21.6-50. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.7-19.4-47.5 (14.9) 39.6 (19.4-103) 117 (83.7-80.3 (17.9) 52.3-26.4 (19.4) 20.9 (16.7 (57.7 (19.0) 25.2) 59.8) 20.3-23.3) 33.6) 65.5-64.5-142) 81.0) 19.4 (68.4) 19.4 (50.7 (20.8) 35.5-142) 89. population from the National Health and Nutrition Examination Survey.9) 49.1 (34.8) 40.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.9-26.2) 65.1) 53.0 (26.1 (21.5) 91.S.6-27.9 (37.7-26.0) 35.1-21.0) 29.7 (43.7-19.8 (33.0-90.3 (42.0 (61.2-106) 64.3) 35.4 (23.6) 24.0) 70.4-24.4-164) 96.6-43.9-100) 86.3 (71.3 (60.1) 17.4 (31.6 (57.0-17.9 (21.6 (27.9) 30.1-99.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.0 (27.9-105) 85.6 (74.8) 13.3 (28.0) 55.3-18.6-16.3-40.2-48.5-70.0 (34.8 (18.2-18.3 (17.6-53.6-44.9 (20.3) 33.6) 39.4 (20.3 (16.0) 53.6-74.4 (18.6-19.1-32.1 (56.9-36.3-21.4 (31.8) 63.6 (29.0) 108 (71.7 (60.5-22.6-26.8 (50.3 (21.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7) 19.8) 34.0 (43.8 (16. 268 Fourth National Report on Human Exposure to Environmental Chemicals .8-32.8-23.8) 19.1) 37.5 (18.6 (25.5 (64.4) 53.7 (60.2-16.9-70.0-41.3 (46.8) 17.2 (38.1 (32.1-99.8) 28.9) 24.1) 42.0) 41.6-28.6-22.7 (12.8-235) 137 (108-198) 88.6 (61.3) 52.2-21.3 (19.8 (18.2-179) 84.3) 17.4 (31.6 (41.0-47.4 (45.9-34.9) 28.4-135) 71.7-42.4-72.7-23.7-21.9-56. Survey Geometric mean (95% conf.1) 20.6 (72.7-20.3-114) 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 17.2 (16.3-39.6-155) 91.6) 37.4-61.3) 18.8 (25.2-73.5) 21.1-23.1) 61.6) 24.4) 15.3-71.5) 82.5-37.5-21.9-14.6) 31.1) 21.0) 26.1 (29.2-85.2-22.1-128) 97.4 (37.2) 159 (102-263) 147 (93.4 (16.7) 20.0 (71.0-38.4 (13.1) 50.8) 23.2-27.4 (53.4 (47.5-16.4) 15.6-128) 96.3) 59.6-24.2-22.6) 14.6 (31.7-39.1) 22.8 (22.6 (25.3 (48.6-42.5-41.3-81.3-106) 74.4-65.7) 42.0-75.0 (69.1 (15.9) 20.2 (19.6) 23.9-68.2 (83.7 (14.4-131) 81.8-24.0) 75.0 (18.0 (52.9-49.6-119) 63.5 (81.8) 30.9 (30.3-78.8 (13.7) 36.5) 39.5-15.7-37.0 (19.2-28.6-92.8) 34.8) 17.3-49.5) 134 (93.8 (18.9-68.3) 19.9-38.1-83.7 (16.1-18.0 (70.2) 31.8) 75th 38.1) 44.5-76.3-32.0-92.6-23.6) 83.6) 38.9 (64.7-78.6-23.8) 20.0 (20.3 (52.9 (56.6) 25.1 (61.4) 51.0-19.3 (24.9 (58.1) 20.1) 35.5) 84.2) 74.5-23.8) 17.0) 81.8) 22.4-76.2-108) 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.0 (16.4) 16.5) 17.3-17.4 (56.9 (30.

J Androl 2004. Needham LL. et al. Blount BC. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Springall C. Jacek R. Schettler T. Massey RC. Itoh H. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Phthalate monoesters levels in the urine of young children. Weuve J.210(3-4):319-33. Perera FP. Singh NP. Hodge CC. NTP-CERHR. Calafat AM.html. Atlanta (GA). 2005. Camann DE. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Duty SM. Malek NA. Chen Z. Calafat AM. 2000 [online]. Hu H. Masunaga S. David RM. Drexler H. Sampson EJ. Jonsson BAG. Brock JW. Fourth National Report on Human Exposure to Environmental Chemicals 269 .210:21-33. 112(5):A270]. Butala JH. Koch HM. Anderson WA. Yoshida K. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.gov/chemicals/ phthalates/dbp/dbp-eval. Environ Health Perspect 2004.22(3):688-695. Sanchez GN. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Environ Res 2003. Epidemiol 2005. Dobler L.208:237-245. Brock JW. Centers for Disease Control and Prevention (CDC).Phthalates References Adibi JJ. Angerer J.68:309-314. Silva MJ. et al. Barr D. Koch HM. Barr DB.niehs. Reidy JA. et al. et al.18(1):122. Environ Health Perspect 2003. Int J Hyg Environ Health 2005. Needham LL.112(3):331-338. Rylander L. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Rossbach B. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Environ Health Perspect 2000. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Fromme H. Pirkle JL. Green RA. 4/20/09 Silva MJ. Caudill SP. Hum Reprod 2007. Jedrychowski W. Eckard R. Silva MJ.108(10)979-982. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Food Addit Contam 2001.18(12):10681074. Giwercman A. Int J Hyg Environ Health 2007. Hilborn ED. Reprod Toxicol 2004. et al. Richthoff J. Silva MJ. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Scotter MJ.111(14):1719-1722. Levels of seven urinary phthalate metabolites in a human reference population. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Drexler H. Ryan L.16(4):487-493. Koch HM. Caudill SP. et al. Caudill SP.93:177-185.25(2):293-302. Third National Report on Human Exposure to Environmental Chemicals. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Meeker JD. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Urinary levels of seven phthalate metabolites in the U. Boehmer S. Silva MJ. Poland.114(9):1424-1431.S. Helm D.nih. et al. Available at URL: http://cerhr. Environ Health Perspect 2006. Int J Hyg Environ Health 2007. et al. Duty S. Ryan L. Wittassek M. Bolte G. Hauser R. Hagmar L. Research Triangle Park (NC). Wiesmuller GA. Gans G. Castle L. Prenatal exposures to phthalates among women in New York City and Krakow. Angerer J. Bull Environ Contam Toxicol 2002. McKee RH.

400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .600) . population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00.400-.10 (<LOD-1.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300-.400 (<LOD-.400 (.600) . Survey Geometric mean (95% conf. and 0.500) .300 (.200-.70 (1. In this Report.600) .300-.400) < LOD 1. and polyvinyl chloride. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.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 1.600) < LOD .400 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.10) .500) 1.00) .500) < LOD 1. respectively. only levels at or above the 90th percentile could be characterized.500 (. 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.200-.400 (.400 (<LOD-.300 (.10 (<LOD-2.500 (.500 (.70) .50) .700) .300-.300 (<LOD-.300 (.500) .300 (.00-2. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400-.700) .500) 1. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. and 03-04 are 0.300-.2. 0.200-. polyvinyl acetate.500) < LOD < LOD .400) 1.400) < LOD < LOD .300-.500 (.00-3.300-.70) .300-.300-.400-. < LOD means less than the limit of detection.900-1.400 (<LOD-.700) . and polymers.300-. resins.300) < LOD .300-.500) 1.400-.200-.10 (.10 (<LOD-1.500) < LOD < LOD .400-. including nitrocellulose.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400 (<LOD-.300 (.400) 1. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.3.Phthalates Dicyclohexyl Phthalate CAS No.500) .500 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.400-.300) < LOD .500) .00 (<LOD-1.500 (.00 (<LOD-1.S.600 (.20) .400 (. 270 Fourth National Report on Human Exposure to Environmental Chemicals . 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.50) . 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.300 (.600) .400-.300 (.9.500-.400 (.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600) . 01-02.400 (.90) .500 (.200-.500 (.500 (.00 (<LOD-1. which may vary for some chemicals by year and by individual sample.200 (<LOD-.400 (.80) .70 (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.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.490) .670-1.740) < LOD < LOD .16) .11) .770-1.380 (.690) < LOD < LOD .530) 1.350-.950 (.54-6.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .380-.690-1.790-1.630 (<LOD-.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 .67 (1.910 (.06) .82 (1.530-.510-. Survey Geometric mean (95% conf.940 (.14 (<LOD-3.12-1.420-.770-1.240-.690 (.450 (.620) < LOD .00) .170-.34) .690) < LOD 2.420-.18) .800-1.10) .510 (.43 (1.250 (.660) < LOD < LOD .53) .710) .740) .330 (.590 (<LOD-.670 (<LOD-.630 (<LOD-.53) .44) .500) 3.74) .33) .770) < LOD 2.330 (.880 (.400-.54 (<LOD-2.910 (.82) .06) .S. population from the National Health and Nutrition Examination Survey.22 (<LOD-1.410 (.54) .910 (.360-.470 (.260-.590 (.16 (<LOD-3.310-.36-1.310) < LOD .830) 1.530) 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.660) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.500-.560) 1.610 (.480 (.450 (.420-. Fourth National Report on Human Exposure to Environmental Chemicals 271 .770 (.370 (<LOD-.770-1.910 (.390 (.400-.220 (<LOD-.17) .270) < LOD .33 (<LOD-3.590) 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 .500 (.290-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.530-1.00 (<LOD-3.530 (.470) 3.05) .

. Biomonitoring Information MEP levels in the NHANES 1999-2000. deodorants. and 03-04 are 1.2. DC (Hoppin et al. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.3 (74.3-103) 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. and 0.Phthalates Diethyl Phthalate CAS No. and also in men attending a Boston infertility clinic (Hauser et al.3 (82. and hand lotions. 01-02.4 (62.2-102) 95. 2002).8-111) 85. 2003) and African-American women in Washington.4.9 (61.S.9. and 2003-2004 subsamples were similar to median or geometric mean levels in small samples of pregnant women in New York City (Adibi et al. colognes.1-93.7) 71.9-92. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. soaps.7 (70. respectively. 0. 2001-2002.3-110) 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. 2007).. In contrast. 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. see Data Analysis section) for Survey years 99-00. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. particularly those containing fragrances. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (71. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.5) 81. population from the National Health and Nutrition Examination Survey. 272 Fourth National Report on Human Exposure to Environmental Chemicals . shampoos. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.

6 (65.0 (66.7-110) 81.3-105) 87.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9-110) 96. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. This age-related trend is opposite the direction seen for other phthalates. Analysis of NHANES 2001-2002 showed similar findings.S. Median MEP levels found in a small sample of German residents (Koch et al.9 (82. 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. Other population estimates also differed by sex and race ethnicity (Silva et al. 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. 2005). Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups. 2003) were slightly lower than levels found in NHANES 2001-2002.5-114) 101 (87. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-113) 122 (93. 2002). In an analysis of NHANES 1999-2000.2 (66. population from the National Health and Nutrition Examination Survey. 2004).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 .Phthalates 2002 (Brock et al.6 (77...

Hilborn ED. et al. Reidy JA. Jacek R. Duty S. Silva MJ. Silva MJ. Perera FP. Brock JW. Angerer J. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Caudill SP. et al. Silva MJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Malek NA.93:177-185. Singh NP. Jedrychowski W. Centers for Disease Control and Prevention (CDC). Hum Reprod 2007. Baird DD. Caudill SP. Barr DB.112(3):331-338. 112(5):A270]. Environ Health Perspect 2002. Meeker JD. Hoppin JA. Brock JW. Camann DE.110(5):515-518. Barr D.Phthalates References Adibi JJ. Prenatal exposures to phthalates among women in New York City and Krakow. Hodge CC. Ryan L. Reproducibility of urinary phthalate metabolites in first morning urine samples. 274 Fourth National Report on Human Exposure to Environmental Chemicals .68:309-314. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Needham LL. Phthalate monoesters levels in the urine of young children. Environ Res 2003.111(14):1719-1722. Third National Report on Human Exposure to Environmental Chemicals. Davis BJ. Bull Environ Contam Toxicol 2002. 2005. et al. Atlanta (GA). Hauser R. Drexler H. Rossbach B. Environ Health Perspect 2003. Koch HM.S. Urinary levels of seven phthalate metabolites in the U. Poland.22(3):688-695. Environ Health Perspect 2004.

6 (20.5) 23. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.37-4.1-48.1) 29.40 (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 5.00) 2.2 (29.30 (3.42-5.1) 25.60) 4.9 (7.80) 6.9 (29.00) 1.0 (9.10 (3.21 (2.0) 23.7-32.7 (14.2 (11.5-17.9-28.69) Selected percentiles ( 95% confidence interval) 50th 3.80 (1.80 (4. 1982.9) 15.80-4.10-5.90) 3.10-3.44) 4.9 (26.6) 14.30) 2.00-4.60) 10.50-14.70-5.50) 4.3) 28.34 (2.80-5.50-11.5-27.40 (2.2.23 (3.5) 21.4) 5.7) 19.87-2.90-8. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).9 (29.80 (8. mainly polyvinyl chloride.40) 4.27 (3.1982).5) 37.80-9.67-4.80-8.89-3. population from the National Health and Nutrition Examination Survey.00-3.6 (11.90-4.70) 7.9-57.03-2.10-3.90 (3.2) 4.90) 4.7) 35.4-42. Concentrations in plastic materials may reach 40% by weight.8) 15.57 (3.16 (2.3 (11.0 (14.7) 22.1) 22.56 (2.07-4.0-18.0 (19.00 (7.10) 3.4) 33.60) 3.79) 2.46) 3.6 (9.68 (3.90-5. 1. respectively.2-17.00) 2.40-9.10) 3.10 (4.5) 43. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.16-3.40-9.30-11.63-4.7 (17.9-55.40-8.70-5.8-36.10 (6.2 (31.35) 4.70 (1.40-8.84) 3.80-3.5 (11.92-2.6) 95th 23.70-4.9) 5.7) 6.3-57.7) 8.7) 18.1-17.10) 2.1-27.84-4.25-3.90) 7.40) 2.6) 15.40 (4.S.40-11.50 (3.23) 3.82) 3.5-36. and 03-04 are 1.00 (4.0) 39.30 (4. DEHP has been removed from or replaced in most toys and food packaging in the United States.6) 14.00-3.70 (3.3 (19.9 (15.2) 6.70 (2.24-4.70 (8.00 (2.1-29.4-20.94-3.00) 11.3 (10.90) 1.5 (24.84 (2.7-18.26-2.50-2.70 (1.90-3.50-8.49 (3.50-5.50 (7.50 (2.80 (8.4-40.50-6. Peck and Albro. Albro and Lavenhar.6 (16.10-2.4-27.8-50.0.5-28.60) 4.41) 3.51) 4.9-26.0 (13.5 (25.2 (7.60 (6.80-27. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.90 (1.20 (1.6-28.70-6.0-29.10) 3.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80 (2.50-3.00-5.50-16.5 (12.4-53.6 (12.30 (6.54) 4.8) 17. toys.92-2.70-8.50-3.9-49.9-19.8 (19.40) 11.10-11.93) 6.50 (7.70 (3. Following ingestion.3-25.50 (8.00) 1.0-18.80-4.50-5.4) 23.0 (18.8-47.70 (5.3 (24.90) 4.9) 13.10-5.5) 32.40-12.40 (4.31 (3.57-7.85) 4.20 (3.50 (3.21 (2.40) 8.60) 7.00) 3.10 (3.40-1.5 (18.2) 42.4) 15.6 (10.7) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.2) 23.0) 31. interval) 3.1 (8.20 (4.27) 2.0 (17.41 (3.3-26.60 (5. packaging film.5 (31.9-2