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.

Fourth National Report on Human Exposure to Environmental Chemicals

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Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.5-Pentabromodiphenyl ether (BDE 99) 2. 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 (2.2'4.4-Tribromodiphenyl ether (BDE 17) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1. Table 1.1.4.1-Dichloroethene (Vinylidene chloride) cis-1.5'-Tetrachlorobiphenyl (PCB 49) 2.4.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2-Dichloroethane (Ethylene dichloride) 1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .3'.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4.6-Pentabromodiphenyl ether (BDE 100) 2.1.4'-Tetrabromodiphenyl ether (BDE 66) 2.2'. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.html.2.6'-Hexabromodiphenyl ether (BDE 154) 2.4'-Tetrabromodiphenyl ether (BDE 47) 2.2’.2'.4'-Tribromodiphenyl ether (BDE 28) 2.3.1.3.6'-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. Paradichlorobenzene) 1.4'-Pentabromodiphenyl ether (BDE 85) 2.4.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2'.2'.4'.6.4.4'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4.4.1-Trichloroethane (Methyl chloroform) 1.3-Tetramethylbutyl] phenol) Triclosan (2.5'-Tetrachlorobiphenyl (PCB 44) 2.4.1.4.5'.3.3-Dichlorobenzene (m-Dichlorobenzene) 1.5’.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2'.3’.5.What’s New in this Report What’s New in this Report In this Fourth Report.3.5'-Hexabromodiphenyl ether (BDE 153) 2.4’.cdc.4'.2'.6-Heptabromodiphenyl ether (BDE 183) 2.2-Dichloroethene trans-1.4.gov/exposurereport/chemical_selection.2'.2'. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4’.4.4-Dichlorobenzene (p-Dichlorobenzene.4'. The process for selection is described at http://www.5.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2-Dichloropropane 2.2'.4'.1-Dichloroethane 1.5.5.4.2'3.

g. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Data for other pesticides are included only for 1999-2000 and 2001-2002..1).. 2003-2004) have been re-computed by use of this improved procedure. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. and these data will be included in the next release of the Report. Explanations for each change are provided in Appendix B.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. Details of this procedure are provided in Appendix A. 2001-2002. urinary 2. five results that all have the value 90. the presence of an interference) that produced results of inadequate quality. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Only slight differences should be noted when one compares the recomputations to previous releases of the Report. Percentiles for all three NHANES survey periods (1999-2000.4-dichlorophenol and 2. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.5-dichlorophenol for the 1999-2002 survey periods.g.

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

gov/nchs/nhanes/ nhanes2003-2004/analytical_guidelines. Other racial/ethnic groups are sampled.S. the measurement of quality control samples in each analytical run to detect unacceptable performance in accuracy or precision. This design does not permit straightforward analysis of exposure levels by non-targeted strata such as locality. Results are reported here using standard units. The geometric mean is influenced less by high values than is the arithmetic mean.. Units: For chemicals measured in urine. Data were analyzed using the statistical software package Statistical Analysis System (SAS) (SAS Institute Inc. sample weights must be used to adjust for the unequal probability of selection into the survey. serum. or region. Laboratory measurements underwent extensive quality control and quality assurance review. 2001). inductively coupled plasma mass spectrometry. micrograms per liter). seasons of the year. Other racial/ethnic groups are included in estimates that are based on the entire population sample. This type of distribution is common in the measurement of environmental chemicals in blood or urine. Levels per gram of creatinine (i. and organochlorine pesticides. Age groups are as described for each chemical in each data table. 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.S. creatinine corrected) adjust for urine dilution.e. The Report presents descriptive statistics on the blood. including tolerance limits for operational parameters. or by use of particular products. For dioxins. 2002) and the statistical software package SUDAAN (SUDAAN Release 8.0. state. population. proximity to sources of exposure. Acrylamide and glycidamide adducts are expressed as the picomoles per gram of blood hemoglobin to which the adduct is bound. Serum levels reported per gram of total lipid reflect the amount of these compounds that are stored in body fat. gender. race/ethnicity is categorized based on the sample design as Mexican American. For these analyses. serum. For example. References for the analytical methods used to measure the different chemicals are provided in Appendix C.cdc. his or her urine output is likely higher and the urine more dilute than that of the other person. generally conforming to those most commonly used in biomonitoring measurements. Statistics include unadjusted geometric means and percentiles with confidence intervals. including the lipid in serum. and race/ethnicity as defined in NHANES. 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.htm. Data Analysis Because the NHANES is a complex. Units of measurement are important. Sample weights also are used to adjust for possible bias resulting from nonresponse and are post-stratified to U. and verification of traceable calibration materials. PCBs.Data Sources and Data Analysis metabolites in blood.. Table 2. stratified. probability-cluster design. Useful unit conversions are shown in Table 2. These compounds are lipophilic and concentrate in the body’s lipid stores. levels are presented two ways: per volume of urine and per gram of creatinine. and nonHispanic white. results are given for the total population as well as by age group. or urine levels for each environmental chemical. multistage. Guidelines for the analysis of NHANES data are provided by NCHS at http://www. SUDAAN uses sample weights and calculates variance estimates that account for the complex survey design. Census Bureau estimates of the U.g. 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. furans. In each table. and urine were based on isotope dilution mass spectrometry.. or graphite furnace atomic absorption spectrometry. serum levels are presented per gram of total lipid and per whole weight of serum. but the proportion of the total population represented by other racial/ethnic groups is not large enough to produce valid estimates. if one person has consumed more fluids than another person. Ninety-five percent confidence intervals around this Fourth National Report on Human Exposure to Environmental Chemicals 5 . 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. non-Hispanic black. Other mostly non-lipophilic chemicals measured in serum are expressed per liter of serum (e. Urinary levels are expressed both ways in the literature and used for different purposes. Gender is coded as male or female.

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

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

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

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

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

217 million pounds of acrylamide were produced commercially in the U. 2005). environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.2-59.9 (60. 2005).6-104) 82. 2004. pulp and paper production.7) 96.1-61.4-76.7) 75th 79.4) 100 (89. but can covalently bind to form adducts with proteins.1 (73. 2005). and cosmetics (NTP-CERHR.0-49.4 (51. Elimination occurs mainly in the urine as mercapturic acid conjugates.1) 55.8 (91.0 (53.1 (47.5 (74.5-80.4) 57.6 (56.0) 57.Acrylamide Acrylamide CAS No. gels.6) 73. widely distributed in tissues. population from the National Health and Nutrition Examination Survey.0 (69.1 (52. and from dermal contact with products that contain residual acrylamide. 2004).2 μg/kg/day (U. In humans. and binding agents.9 (54. EPA reference dose of 0.8 (57. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.4-60. 2005).6-65.4 (54. interval) 61.S. smoking. ocular and dermal irritation from direct contact with acrylamide containing materials. acrylamide has produced upper airway irritation following inhalation of high levels. 2005).4-83.6 (81. Animal studies indicate that acrylamide is well absorbed.8 (52. in permanent press fabrics.6-75.4 (59.6) 50.2-118) 98. and is either metabolized to the reactive epoxide.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 54.4-89.7 (65. are heated at temperatures used for frying and baking..9-105) 86. Natural substances in the food are converted to acrylamide.S.9) 75.2-93. EPA.5) 66.6-108) 61. Acrylamide is not thought to accumulate in the body at environmental doses.3-2. FAO/WHO.0) 85. 2006).1) 53.0-66. but are generally above the U. it was discovered that acrylamide is formed when starch-rich foods. 1990.9 (69.0-104) 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 61.5 (79. Polyacrylamides are useful water-compatible polymers used in water treatment. and an average daily intake is estimated as 0. glycidamide.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.S.2) 57.9) 58. or to glutathione conjugates (Calleman et al.7 (63.0 (57. in some sealing grouts. and in some cosmetics.2-91. acrylamide is synthesized and used in the production of polyacrylamide polymer.0 (67. In 1997. 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.9-52.1-57.3) 70.3 (53.5-85. 2005.2-70.6) 71.7-64. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.8-57. Survey Geometric mean (95% conf.1 (83. These estimated intakes are hundreds of times lower than occupational exposures.3) 86.6 (51. Recently.S.9-61.2-77.4-60. Estimated intakes in children are about twice that of adults (DiNovi and Howard.3-71.0-58. Fourth National Report on Human Exposure to Environmental Chemicals 11 .1) 46.2 (75.2) 57. see Data Analysis section) for Survey year 03-04 is 3. such as potatoes and some grains.0-108) 152 (139-175) 126 (111-142) 108 (86.4 (53.. soil conditioners.S.7) 58.6) 90.4) 57. Tareke et al.8-55. Since acrylamide has limited volatility and high water solubility. (NTP-CERHR.7-64. 2006.3) 63.2-67. and in the synthesis or compounding of dye materials.8 (81. FDA.7) 54. Commercially. People may be exposed to acrylamide from foods.2 (62. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.1 (88. 2002).7) 73. In the general population.7 (58. the main source of exposure is from the diet.4 (54. drinking water.1) 62.6-61.0.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.2 (58.9) 57. mineral processing. as an absorbent in disposable diapers. Fennell et al.3 (55. and well below doses known to cause nerve damage or carcinogenicity in animals.1-64.7-60. EPA.7 (55.5) 58.9) 63..6-66.1-64.1) 101 (95.5 (44.2-114) 163 (147-191) 96. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 1994).0 μg/kg for adults (FAO/ WHO.5 (52.

5) 75th 85. 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. 2005. 2005. U.int/ ipcs/food/jecfa/summaries/summary_report_64_final. 2006.7) 60.2) 87. 2005.8 (51.9-64. although different analytic methods can affect results. AHA levels have been shown to increase with dietary intake (Hagmar et al..4) 53. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).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. 2005) and sperm DNA adducts (Xie et al. 2008).9-138) 143 (130-159) 96. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 2005.3) 85. 2008). Puppel et al.1 (57. In addition.2-68..5 (42. fetal death..7) 90. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. respectively) are markers of integrated acrylamide exposure over the preceding few months.0 (80.who. 2004.. NTP-CERHR..5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. most non-smokers had levels less than about 100 pmol/gram hemoglobin.7) 61. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.5) 71.5 (83.epa.6 (90.5 (59.pdf.9-62. reproductive effects (reduced litter size.4-98.7 (87.3-78. 2005. dominant lethality).9) 65.9-77.. 2002.S..S. adrenal.0 (52. 2005). Vesper 2005) and smoking (Bergmark. 2003.1) 60.3) 59. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. 2005.1) 56.0) 94. Additional information is available from U.S.5-66.1 (66.9 (57.2) 65. Glycidamide has been shown to react with DNA (Doerge et al.2-90..4-65. After exposure ceases. Rice. see Data Analysis section) for Survey year 03-04 is 4. Klaunig et al.1 (70.6-64. 2005. thyroid. IARC classifies acrylamide as probably carcinogenic to humans..4 (61.0 (70. glycidamide (NTP-CERHR.2 (56.4 (81. altered gene expression in testicular tissues (Yang et al..8-61. Vesper et al. 2005) have been demonstrated in animals. 2005).5 (56..4 (51..9 (58. 12 Fourth National Report on Human Exposure to Environmental Chemicals .8 (44.7 (57. Axonal degeneration.1-62..8-48.9 (81.5) 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. uterine.9) 87. Maniere et al.3-101) 95. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.3) 59.4-59.. 2005).1) 62. Survey Geometric mean (95% conf. and neuronal DNA reactivity (Doerge et al. 2006) have been demonstrated after acrylamide dosing. EPA.2) 55. 2001).1-60. 2006). 2002. 2005.7-86. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. 2004).8) 60.2 (63.3) 59. EPA. Acrylamide is clastogenic and can produce dominant lethal mutations.9) 59.S.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. 2005. 2005).3 (56.1-70.8-49.6-62.7-62. Hagmar et al.4 (57. 2005.5) 87.1 (56. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. 1997. 2009).0.Acrylamide occupational exposures. presynaptic nerve terminal binding (LoPachin. U.1 (82. interval) 59.0 (75. 1997.4) 83. EPA at: http://www.2 (72. Schettgen et al.9-78.7 (84. 2005. probably through its epoxide metabolite.5-64.. scrotal. population from the National Health and Nutrition Examination Survey.0) 118 (103-126) 121 (112-134) 113 (94. Schettgen et al. Puppel et al...7) 74. male germinal cell injury. and other sites) (FAO/WHO.6-90.8) 45..7 (61. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.4) 46. and cancer (mammary.4-103) 79.4 (90.6 (66..0-93..9) 75.5-94.4 (56. 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.0-62.7-64. 2006).9-76. Mucci et al.1-56.5-92.2-91.

DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. da Costa GG. et al. Fennell TR. Wirfalt E. Doerge DR. Calleman CJ. gov/~dms/acrydata. Kamendulis LM. He F. Yang JS. Mutat Res 2005..56. 2004. Metabolism and hemoglobin adduct formation of acrylamide in humans. Andersen M. 1993. Rome. Scand J Work Environ Health 2001. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Zhang S. [Epub ahead of print] Dybing E. The Updated Exposure Assessment for Acrylamide.561:21-37.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Perez et al. Survey data on acrylamide in food: individual food products. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 054472. Chem Res Toxicol 1990. Fennell TR. Toxicol Sci 2005. smokers and nonsmokers. 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. 1999). Acrylamide intake through diet and human cancer risk. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. 64th Meeting: Summary and Conclusions (FAO/WHO). In another study. 2005. Maniere I. Available at URL: http://www. Snyder RW. Joint FAO/WHO Expert Committee on Food Additives. J Agric Food Chem 2008. Becher G. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. et al. DiNovi M and Howard D. LoPachin RM. et al. Granath F. 2001). Kautiainen A. Laurentie M.Acrylamide In occupational settings. February.pdf.126(2):361-371.html#u1004.43:365–410. Paulsen JE.27(4):219-226. Mechanisms of acrylamide induced rodent carcinogenesis. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Acrylamide neurotoxicity: neurological. Human exposure and internal dose assessments of acrylamide in food. Illinois. Duale N. McDaniel LP. Calleman CJ. Burgess J. Guffroy M. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. April 13-15. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose.gov/chemicals/ acrylamide/Acrylamide_Monograph.fda. 2004 Acrylamide in Food Workshop: Update Scientific Issues.85:447-459.Toxicol Appl Pharmacol 1994.niehs. et al. Beland FA. Mutat Res 2005.580(1-2):157-165. Axmon A. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Chem Res Toxicol 1997 Jan. Osterman-Golkar S. Available at URL: http://www. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al.. Bergmark E.561:49-62. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Wilson KM.. Godard T. 1994). 2006. et al. Churchwell MI. Paulsson B. Adv Exp Med Biol 2005. Farmer PB. Bergmark E.10(1):78-84.120(1):45-54. Costa LG. Food Chem. 2/3/09 Klaunig JE. Twaddle NC.cfsan. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 6013-6019. Hagmar et al. 2009 Jan 8. Food and Drug Administration (FDA). Nordander C. Toxicol Sci. 2/3/09 Perez HL.. 2/3/09 Hagmar L. Doerge DR. Chicago. References Bergmark E. 2001. Tian G. Rosen I. Bridson WE. Tornqvist M. Haugen M.3:406-412. Bergmark E. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.nih. Cheong HK. Bjellaas T. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. July. He F. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Summer SCJ.580(1-2):131-141. Available at URL: http://cerhr. Uncertainties. National Toxicology Program. Wu Y. CFSAN/Office of Plant and Dairy Foods. Magnusson AL. Malmberg B. 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. Bruze M.580(1-2):119-129. Tornqvist M. Toxicol 2005. Mucci LA. Adv Exp Med Biol 2005. Churchwell MI. Costa LG. 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. smoking habits and gender. Calleman CJ.. Aprea P. and Research Strategies. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Spicer R.who. NIH Publication No. Hagmar L. 8-17 February 2005. Alexander J. Toxicol Appl Pharmacol 1993. morphological and molecular endpoints in animal models.pdf. Italy. Mutat Res 2005.

Ingham L. Available at URL: http://www. Rydberg P. Available at URL: http://www. 1994. Mutat Res 2005 Feb 7. Drexler H. Rice JM. Toxicol Lett 2002.274(1):59-68. Tornqvist M. Washington (DC). Chemical Summary for Acrylamide. Schettgen T. Hallmans G.207(6):531-9. Eriksson S.163(2):101-8. Liu K. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Office of Pollution Prevention and Toxics. Slimani N. J Agric Food Chem 2002. Rossbach B.561:89-96. Puppel N. Broding HC. Meyers T. Drexler H.Acrylamide glycidamide by gas chromatography-mass spectrometry. Han DU.20(6):959-64. Int J Hyg Environ Health 2004. Licea-Perez H. revised 1/3/06. Hemoglobin adducts of ethylene oxide.txt.gov/iris/subst/0286. Anal Biochem 1999. Lee SH. 2/3/09. Vesper HW. Tareke E. et al.19(4):527-34. Karlsson P. Mutat Res 2005. Smith A. Toxicol Lett 2006. Schettgen T.S. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Ding X. Jin Y.580(1-2):3-20. Ospina M. Integrated Risk Information System (IRIS).50(17):4998-5006. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Angerer J. Gray JG. EPA).S. et al. 2/3/09 Vesper HW. Kutting B. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Toxicological effects of acrylamide on rat testicular gene expression profile. Drexler H. Sun H. Int J Hyg Environ Health 2003.S. Adv Exp Med Biol 2005. Environmental Protection Agency (U. Fu D. J Agric Food Chem 2008. Environmental Protection Agency (U. Meyers T. Benetou V. Yang HJ. Analysis of acrylamide. U. U. Marko D. propylene oxide. Angerer J. Tjaden Z. Schettgen T. Weiss T. Lee MH.htm. Vesper HW.134(1-3):65-70. Han CH.S.epa.gov/chemfact/s_acryla. Letzel S. Myers GL. Acrylamide. EPA). 14 Fourth National Report on Human Exposure to Environmental Chemicals . Reprod Toxicol 2005.206(1):9-14. Liu Y.epa. Ospina M. Choi JH. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Angerer J. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Agudo A. September. Chae C. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.56(15):6046-53.580(1-2):71-80. Rapid Commun Mass Spectrom 2006. Xie Q. The carcinogenicity of acrylamide. a carcinogen formed in heated foodstuffs. Tjønneland A. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Fueller F.

990) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.160 (.052 (<LOD-.047-.068) .65 (1. and various other disorders (U.060) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .060 (<LOD-.015 ng/mL.050-.120-.15 (2.21 (.220) .154-.187) .080) < LOD < LOD .080 (.47-3.99) 2.23 (.70) 2.68 (1.310) .44) 2.084) .920 (.360) .66-3.48-3.188) .19) 1.068) .30) 2. cardiovascular disease.160-.110 (.057-.370-.520 (.145) .690 (.02) 1. 2004).060-.S.34 (1.140-.148-.09-3.77 (1.960-1.216 (.39) 3.92 (1.17 (.180) .26-1.090-.131 (.104-.164 (.050 (<LOD-.126) .124 (.12 (2.44 (2.770) .Cotinine Cotinine CAS No.930 (.76 (1.130) .89) 1.32-2.060 (.062 (. Cigarettes contain about 1.42 (1.308 (.428-.190-.23 (1.175 (.150) .111-.180) .88 (.144 (.35 (2.050 (<LOD-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .088-..18-3.625) .066) .17 (1.770) .047-.040 (.190-.66 (1.540-.12 (1.075 (.30) 2.198) * .14) .350 (.21-1.260) 1.53-4.120 (.01) 3.120) .620-1. population from the National Health and Nutrition Examination Survey.63 (2. 1998).480-.710 (.142-.160 (.200) 1.840) 3.073) < LOD .5% nicotine by weight (Kozlowski et al. < LOD means less than the limit of detection.68) .087) < LOD < LOD .180) .059-. maternal exposure during pregnancy can result in lower birth weight.860 (.39 (1.312) .180) .120 (.153-.726) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.115-. emphysema.630 (.20 (.81-2.14) . ** In the 2001-2002 survey period.55 (1.09-3.43 (1.071 (.99) 2.060 (<LOD-.052 (<LOD-.220-.600-1.740-1.110 (.140 (.900-1.040-.110 (.620 (.09-2.670) .17) .080-.96-4.49) 1.93) .60-2.077) .050 (<LOD-.070 (<LOD-.75) 1.950-1.080-.510 (.50) 3.506 (.S.059-.058 (.30) * .197) .11) . 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.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 .120 (.77 (2.95) 1.820) .302) .030 (.54) 1.110-.120 (.230 (. DHHS. see Data Analysis section) for Survey years 99-00.12-4.310-1.050 (.320) .570-1.110-.190-.20) 1.38-2.070) .120-.997-3.180 (.066 (.22) 2.108) * .621-1.080-.14-1.030-. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.63-2. stroke.087-.061) < LOD .040-.05 ng/mL. 2004).83-2.180) .080-.540 (.33-2.140 (.450-.160 (.70-2.087 (.800 (.213) .990 (.00) .23 (2. ear problems. and 03-04 are 0.570 (.32) 1.50-4.110) .50 (1.05) 1.470-.580) .310) 90th 1.150) . 83% of measurements had an LOD of 0. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.050) .310-1.770-1.060-.053 (<LOD-.23-2.12) 1.94) 1.53 (1.430-1.350-.950 (.42-4.85 (1.040 (.02) 1.050-.193) .015.130 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.79) 3.201) .96 (1.62) 2.030-.089) Age group 3-11 years 99-00 01-02** 03-04 .660) .500 (.910-1.48-2.533-.050 (<LOD-.050) .260-1.20 (1.00) 1.28) .060 (.140-.28-1.580 (.040 (.19) .505 (.410) .160) .790) .086 (.054 (. respectively.01 (1.04 (1.030-.20) .080) < LOD .96) 2.139) * .220) .210 (.077) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.49) 1.32-2.S.110-. DHHS.163 (.05.060-.54 (1.50-1.730 (.630 (.180 (.45) 1. acute respiratory infections.100-.850 (.070-. Survey Geometric mean (95% conf.167 (.070) 75th .57) 2.110) . 2006). and exacerbated asthma (U.043-.110 (.071) .163) .070) .44) 2. Fourth National Report on Human Exposure to Environmental Chemicals 15 .20-2.137-.740-1.106-.020-.094) . 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.62 (2.076-.55-2.02 (.090-.44 (1.090-.160) .87-3.84-3.580-1.54 (1.68) 2.480-1.063) .110 (. which may vary for some chemicals by year and by individual sample.16) .230) . acute respiratory illness. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.234) .137 (.21-1.300) .400-.88 (1.77 (1.78) 2.630 (.66) 1.240 (.19-2.350-.15) 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. and 17% had an LOD of 0. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.164 (.080 (. and 0.280 (.066-.40) .120 (.

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

Tobacco Smoke and Involuntary Smoking.gov/ntp/roc/eleventh/profiles/ s176toba. available at URL: http://mtn. Tobacco Smoke. Pechacek TF. Brody DJ. 4/13/09 Centers for Disease Control and Prevention (CDC). Centers for Disease Control. Herrera B. Benowitz NL. and the United States.fr/ENG/Monographs/allmonos90. Ethnic differences in N-glucuronidation of nicotine and cotinine. Jacob P III. Exposure of the U. Pickett MA. Clin Pharmacol Ther 1994. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Strauss WJ.niehs. Centers for Disease Control and Prevention. Perez-Stable EJ. Am J Public Health 2004.280:135-140. Respiratory nicotine absorption in non-smoking females during passive smoking. Benowitz NL. Department of Heath and Human Services.280:152-156. Benowitz NL. Int Arch Occup Environ Health 1991.S. DHHS).niosh. Available at URL: http://monographs. Vogler GP. Giovino G. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.291(3):1196-1203. Pollack HA. Lewis PJ. Vol 83. Sweeney CT.php. Sosnoff CS. In Report on Carcinogens. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Tobacco related exposures. Caudill SP. Available at URL: http:// cancercontrol. Vol 38. Mehta NY. Kira S.iarc. References Armitage AK.S.S. Summary of Data Reported and Evaluation [online] 1986. 11th ed. Third National Report on Human Exposure to Environmental Chemicals. 4/13/09 Perez-Stable EJ. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Curtin LR.cancer. Department of Heath and Human Services.fr/ENG/Monographs/ allmonos90. George CF. Benowitz NL.56:483-493. JAMA 1998. Maurer KR. Nicotine metabolism and intake in black and white smokers. Available at URL: http://ntp. IARC Monogr Eval Carcinog Risks Hum.surgeongeneral.gov/tcrb/monographs/10/. National Center for Chronic Disease Prevention and Health Promotion.pdf. Bernert JT. Pharmacol Rev 2005. Absorption and metabolism of nicotine from cigarettes. Trends in the exposure of nonsmokers in the U. Pirkle JL.gov/eid/rmca/critdocs/ criteriadoc/33. 4/13/09 U. U. Jacob P.57(1):79115. Summary of Data Reported and Evaluation [online] 2004.php. 1988-1991. Richter PA. National Toxicology Program (NTP). iarc. Modin G. Tob Control 1998. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Caraballo R. Tob Control 2006. JAMA 1998.S. Pirkle JL. Dollery CT. et al. Fong I. Racial/ethnic differences in serum cotinine levels among adult U. 1999-2002. Coordinating Center for Health Promotion. Bernert JT. Aiba M. Jacob III P. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.4:313-316. Available at URL: http://www. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. DHHS).cdc. International Agency for Research on Cancer.S.15:302-307. population to secondhand smoke: 1988-2002. Coordinating Center for Health Promotion.114(6):853-858. Etzel RA. Available at URL: http://monographs. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. 4/13/09 International Agency for Research on Cancer. Soliman S. Epidemiol Rev 1996. National Institute for Occupational Safety and Hygiene (NIOSH).7:369-375. Giovino GA. Kozlowski LT.63:139-43. IARC Monogr Eval Carcinog Risks Hum. Flegal KM. U. et al.S. June. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. 1991. Warner K. the United Kingdom. Schwartz SS. cigarette smokers: the Third National Health and Nutrition Examination Survey. Centers for Disease Control and Prevention.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. JAMA 1996.S Department of Health and Human Services (U. 2004. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Hukkanen J. Jarvis MJ. Metabolism and disposition kinetics of nicotine. Schober SE. Jacob P III. U. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Atlanta (GA): 2005. Houseman TH. 1999. Mowery PD. 4/13/09 National Cancer Institute (NCI).pdf. Environ Health Perspect 2006.18:188-204. 4/13/09 Iwase A.gov/library/ secondhandsmoke/. Benowitz NL. Smoking and Tobacco Control Monograph 10 [online]. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. BMJ 1975. Pechacek TF. Herrera B. J Pharmacol Exp Ther 1999. 1988-1991.nih. Brody DJ.275:1233-1240.S. Turner DM. [online]. Office on Smoking and Health [online] 2006.94(2):314-320.S Department of Health and Human Services (U. Cotinine as a biomarker of environmental tobacco smoke exposure.

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

130 (. including seizures and encephalopathy. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. About 3-8% of dermally applied DEET is absorbed. DEET is also used in combination with dermal sun screens (U.110 (<LOD-. DEET is not genotoxic. There are over 225 insect repellents brands containing DEET.S. DEET is not a developmental or reproductive toxicant in animals (U.140-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. < LOD means less than the limit of detection.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 . People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.130-.100-..250) < LOD .100-. Additional information is available from U.S. 2003). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.560) < LOD .N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120-.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.110-.180 (.. and they range in concentration from 4% to 100%. 1995.449 and 0.EPA.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . (Kolpin et al.520) < LOD . EPA.180 (. Survey Geometric mean (95% conf. After absorption. Sudakin and Trevathan.150) < LOD . 134-62-3 General Information N.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 .S. 2003).190) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . 2002).EPA.epa. Neurological effects in humans.240) < LOD .180 (. which may vary for some chemicals by year and by individual sample.110 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.100-.N-Diethyl-meta-toluamide (DEET) CAS No.110 (. (U.110 (.1. Urinary N.130-. 1998).EPA at: http://www.100 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 19 .130-. 1998).110 (.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .S. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.110-. and it has not been rated by IARC or NTP with respect to human carcinogenicity.130) < LOD . 2002). DEET can be applied to clothing and the skin to repel biting insects. 2005).170 (.N-Diethyl-meta-toluamide (DEET) N.130 (.gov/pesticides/.100-.220 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.270) 688 678 518 700 598 956 Limit of detection (LOD.140) < LOD .120-.N.100-. DEET has low acute toxicity.180) < LOD .. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.160) < LOD .170 (.210 (. have been reported as result of self-poisoning by ingestion or excessive dermal application.S.140) < LOD . DEET is not registered for use on agricultural commodities.130 (. One survey detected DEET in 74% of sampled streams in the U.110 (<LOD-.130-.130) < LOD . population from the National Health and Nutrition Examination Survey. Its use is recommended for prevention of several vector-borne diseases.100-.140) < LOD .140 (.S.

150) < LOD . In this survey period.270 (<LOD-. 2007).N.170-.190 (. 2005).130 (<LOD-.250-.390-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.S.270) < LOD .350) < LOD .270-. population from the National Health and Nutrition Examination Survey.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 .230-. 20 Fourth National Report on Human Exposure to Environmental Chemicals .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.290-. 1992).500 (.270 (.410-.230) < LOD .320) < LOD .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 .370) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.350-.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 .250 (.640 (.140-.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.. 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. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.240-.320 (.480 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.280-1.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .630) < LOD .410 (.190 (.250) < LOD . Urinary DEET levels as high as 5.S.330 (.350) < LOD .190-.370-.150-. Urinary N. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .230-.330 (.200 (.190 (<LOD-.490) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.93) < LOD .240) < LOD ..440) < LOD . Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.300 (. Survey Geometric mean (95% conf. representative subsamples from NHANES 2001-2002.280 (.410 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

1993-1997.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. 1-118. Available at URL: http://www.S. Chen H. Lowry LK. Furlong ET. Chemical Summary.S. Toxicity and Exposure Assessment in Children’s Health. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. U. Third National Report on Human Exposure to Environmental Chemicals. pp. Quandt SA. Reregistration Eligibility Decision (RED): DEET. Absorption. Bell JW. Osimitz TG.gov/teach/chem_summ/ DEET_summary. Meyer MT.41(6):831-839.epa. Human exposures to N. EPA 738-R98-010. J Anal Toxicol 1992.N. Schoenig GP.S. Smallwood AW. 4/9/09 U.gov/oppsrrd1/REDs/0002red. Environ Sci Technol 2002. Fundam Appl Toxicol 1995.epa. Selim S.EPA.36(6):1202-1211. pdf. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . and other organic wastewater contaminants in U.S. Zaugg SD.115(8):1254-1260. DeBord KE. 2005 Kolpin DW. Centers for Disease Control and Prevention (CDC). N.S. and excretion of N. Hartnagel RE Jr. J Toxicol Clin Toxicol 2003.S. Available at URL: http://www. 2005.EPA). Environmental Protection Agency (U. Sudakin DL. hormones. Grzywacz JG. Diethyltoluamide (DEET). metabolism. Pharmaceuticals. Veltri JC.S. Tapia J. Int J Toxicol 2002. Environmental Protection Agency (U. Atlanta (GA).2:341352.16(1):10-13. Barr DB. DEET: a review and update of safety and risk in the general population. Trevathan WR.N-diethyl-mtoluamide following dermal application to human volunteers. et al.pdf.N-Diethyl-meta-toluamide (DEET) References Arcury TA. Gabriel KL. Environ Health Perspect 2007.EPA). September 1998. 1999-2000: a national reconnaissance. Thurman EM. EPA. Page BC.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Barber LB. streams. Washington (DC): U. U.25:95-100.

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

1999-2000: a national reconnaissance. Keimowitz AR.nih. Haighton LA. and Hardy MP. Endocrinology 2004. Hara K.Scientific Committee on Toxicity. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Needham LL. Environ Health Perspect 2005. 2/4/09 European Commission. Kim JC. Fujii S. J Am Dent Assoc 2006. Tsugane S.pdf.S. Kim CS. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Watanabe C. Timms BG. Zaugg SD. Han SY. Kawamura N. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite.nih. Brine DR. 2/4/09 Ouchi K.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Calafat AM. Cohen JT. Gender differences in the levels of bisphenol A metabolites in urine. Kolpin DW.J. 2007. Ye X. Leranth. Furukawa M. Chung MK. Cha SW. and other organic wastewater contaminants in U. Szigeti-Buck. Imai H. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. September. streams. 2008. et al.jrc. Barr JR. Barton L. Rat two-generation reproductive toxicity study of bisphenol A. National Toxicology Program.Environmental Phenols References Akingbemi BT. 4.pdf.europa. Research Triangle Park. Available at URL: http://cerhr.pdf .gov/chemicals/bisphenol/bisphenol. Kuklenyik Z. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Ecotoxicity and the Environment (CSTEE). Kroes R.59(4):403-408. N. bisphenol A glucuronide. Hanaoka T. Hum Ecol Risk Assess 2004. Serizawa S. Belgium. Available at URL: http://ec.780(2):365-370. Thomas BF. An evaluation of the possible carcinogenicity of bisphenol A to humans. Pyo MY. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. European Commission. Proc Natl Acad Sci USA 2005.69(22):2611-2625. et al.68(1):121-146. Marr MC. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Cunha G. Regul Toxicol Pharmacol 2002. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Rubin C. NC. Biochem Biophys Res Commun 2003. Life Sci 2001. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. 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. Available at URL: http://ecb. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Arakawa C. Department of Health and Human Services.59(9):625-628. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Klinefelter GR.312(2):441-448. Koulova AI. Ema M. and Hajszan. Brussels. May 22. Ikka T. 2/4/09 Fujimaki K. Reprod Toxicol 2001.149:988-994. Thurman EM. Koh WS. Yoshinaga J. Yang M. Bisphenol A. Bradley S. Environ Sci Technol 2002. Harazono A. Pharmaceuticals. Lynch BS.14(2):149-157. Howdeshell KL. Matthews JB. Kiguchi M. National Institute of Environmental Health Sciences. Zacharewski TR.35(2 Pt 1):238-254.10:875-921. Furlong ET.S.S. Ekong J. Kim YH. National Institutes of Health. niehs. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). McConnell EE. Needham LL. U. Human Health. Hughes C. Joskow R. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. In vitro and in vivo interactions of bisphenol A and its metabolite. Gray GM. Twomey K.pdf . 5: 505-523..gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Rhomberg et al. Italy.pdf. Nippon Eiseigaku Zasshi 2004.eu/ health/ph_risk/committees/sct/documents/out156_en. Sottas CM.. Exposure of the U. August 2001. Doull J. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Reidy JA. 2003.113(4):391-395. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). 2002.137(3):353-362.. Watanabe S. Ispra. DirectorateGeneral Health and Consumer Protection. Occup Environ Med 2002. Needham LL. with estrogen receptors alpha and beta. C. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Han SS. Barr DB. Meyer MT. niehs. Caudill SP. MacLusky.nih. Tyl RW.niehs.102(19):7014-7019. Munro IC. Endocrinology 2008. Reidy JA. Chem Res Toxicol 2001. Calafat AM. Park S. Joint Research Centre Institute of Health and Consumer Protection. et al.145:592-603. Richter CA. Hlywka JJ. Wong LY. November 26. vom Saal FS. Calafat AM. Barber LB.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Shin HC. Available at URL: http://ntp. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. T. Toxicol Sci 2002. hormones.116(1):39-44.36(6):1202-1211. Myers CB. K.gov/chemicals/bisphenol/BPAFinalEPVF112607. Available at URL: http://cerhr. Environ Health Perspect 2008.

Arch Environ Contam Toxicol 2003. Morgan MK. and nonylphenol at home and daycare. Biological monitoring of bisphenol a in a Korean population. Colnot T. Chuang JC. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Dekant W. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Food Chem Toxicol 2002. Environ Res 2007. Chem Res Toxicol 2002.Environmental Phenols Volkel W. vom Saal FS. Lordo RA. Endocrinology 2006. Yang M. Kawamoto T.113(8):926-33. Welshons WV. An observational study of the potential exposures of preschool children to pentachlorophenol.147(6 Suppl):S56-69. Large effects from small exposures. Wilson NK. Witorsch RJ. et al.15:12811287. Hughes C. Jang JY. III. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Csanady GA. Environ Health Perspect 2005. Lee SM. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.44(4):546-51. Sheldon LS. Chang SS. bisphenol-A.40(7):905-12. Vom Saal FS. Kim SY. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Filser JG. Nagel SC.103(1):9-20.

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 .Environmental Phenols 4-tert-Octylphenol CAS No...2..500 (. and through manufacturing waste streams (Warhurst.30 (1. population from the National Health and Nutrition Examination Survey. In 1999-2000. Indoor and to a lesser extent. During the 1980s and 1990s. and the polyethoxy chain may consist of up to 50 ethoxy units.50) 1.00 (1. In rats. and from contact with some personal care products and detergents. Laws et al. altered estrus cycles and reproductive outcomes.300 (<LOD-.400 (.40) 1. leading to inhalation as another potential exposure route (Rudel et al. 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) . Blake and Boockfor.300 (<LOD-.600-1.40) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.299-. 1996). 2000. 2006.40) 2.20-2.507) * < LOD .00 (.S.600-1.40 (1. which may vary for some chemicals by year and by individual sample.60-3.10 (. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. Survey Geometric mean (95% conf. 4-octylphenol monoethoxylate was detected in 43..600) 1. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.20-2.900 (..497) * . Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.80 (1.50-2. Katsuda et al.70 (1.30 (.60-3.10) 2.30) 2. orally administered 4-tert-octylphenol was well absorbed.268-. impaired steroidogenesis. Urinary 4-tert-Octylphenol (4-[1.60-3.800-1..900 (. over 500..500) 75th . Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.000 tons of alkylphenol ethoxylates were produced annually worldwide.300-.40) 2.10 (1. and some of their degradation products are toxic to aquatic life.600) .30 (1.20-2.60-3. is used to manufacture alkylphenol ethoxylates.70 (1.50) 1.400 (.600-1.200-.300-.900 (. to shorter chain alkylphenol ethoxylates.g.30) 1.600) . which are anionic surfactants used in detergents.369 (.500) . several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. Several alkylphenols.500-1. The alkylphenols can bioaccumulate in some fish. 1995. 2000. Disposition in humans has not been studied sufficiently.10-2. and some personal care products.900 (.20-2. Saito et al. Bian et al.60) . 2002).10 (.60) 1...600-1.20-2.10) 1.300 (<LOD-.477) .200-. Ying et al. have demonstrated estrogenic effects particularly when injected at high doses in animals.60-3.3.50) . see Data Analysis section) for Survey year 03-04 is 0. 1997.274-.500) . streams in 30 states (Kolpin et al.1.80 (1. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. textiles.30) 90th 1. did not bioaccumulate.400) 1.90) 2.70 (1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. and was quickly eliminated from the blood (Certa et al. and to alkylphenoxycarboxylates.00 (.20-2.20) 1. testicular atrophy.20) 2.g. the various alkylphenols have also been used as emulsifiers and modifiers in paints.389 (.5% of 139 U.50 (1.900 (.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. through sewage. industrial cleaners. fish) and drinking water.600-1.300 (<LOD-. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. and impaired spermatogenesis (e.50) 1.00) 1229 1288 03-04 03-04 03-04 * . 2002). Less frequently. an alkylphenol. The alkylphenol ethoxylates enter the environment through human use of products containing them.400 (.90) 2.30 (1.80) 2.. 140-66-9 General Information 4-tert-Octyphenol.20) 314 715 1488 03-04 03-04 * * . altered neonatal sexual development.30-2. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).357 (.60) 613 652 1092 Limit of detection (LOD.30 (1. pesticides.S.20 (1.700-1.80 (1. including 4-tert-octylphenol. 34 Fourth National Report on Human Exposure to Environmental Chemicals .500-1.60-3.600-1. 2004).50-3. 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.40) * 03-04 03-04 03-04 . and emulsifiers.500) . < LOD means less than the limit of detection.300 (<LOD-.70 (1. In the 1990s.50) .

910 (.S.00) 2. Urinary 4-tert-Octylphenol (4-[1.00 (. Nagao et al. In a small number of adult Japanese volunteers.08) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.730-1.25) 2. Kawaguchi et al.65-3. Fourth National Report on Human Exposure to Environmental Chemicals 35 .54) * 03-04 03-04 03-04 .24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. or their corresponding ethoxylates with respect to human carcinogenicity. Calafat et al.300 (<LOD-. population from the National Health and Nutrition Examination Survey.31 (1. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.31-2.00) 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 .620-1. 2000.96-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.199-.540-1. 2001. 2004.18-4.68-2.349) * < LOD . 2001).78) 1228 1286 03-04 03-04 03-04 * .380 (<LOD-.370 (<LOD-..3.29) 2.50 (2.68) 2.62 (1.22) .160-.410 (.03-6.43) 1.00) 2.11-2.640-1.S.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.81 (1. Sweeney et al.740 (.530) .00) 1..59 (1..41) .460 (. at lower or environmentally relevant doses (Blake et al. Tyl et al.14) 314 713 1487 03-04 03-04 * * .25-2.33) 3.337-.435 (. IARC and NTP have not rated octylphenol.64 (.420) . Yoshida et al.33 (2.Environmental Phenols Myllymaki et al.06 (2.620) .10-2.53-3.36-3. nonylphenol.270 (.384) * . 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.276 (.43) 1.40-4. 2005.17 (.570) .470) 75th .550-1. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.270-.207-.85 (1.1. representative subsample of NHANES 2003-2004.. 2003.02-4.610) .450) .05-2.630-1.280-.850 (. It is unclear if estrogenic or other effects occur in animals through oral dosing.11) 2.890-2. 4-tert-Octylphenol is not considered directly genotoxic.62) .03 (1.450) 1.60 (1.40 (1. 2004).260 (<LOD-.770 (.860 (.400) . Survey Geometric mean (95% conf.20 (1.170-.00 (.500-1.73) 2.470-1.62 (1.71) 2.740 (.15) 1.270 (.560) . the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.59) 1.320 (<LOD-. 1999).269 (.76 (2.25) 90th 1.78 (1.470-1.43-3.11) 1..67-2..78) 3.03 (1.

Available at URL: http:// www. Reprod Toxicol 2004. Boockfor FR.S. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Saito Y.15(6):683-692. Meyer MT. Izumi S.folliclestimulating hormone. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Sweeney T. Yoshida M. Taya K.141(7):2667-2673. Estrogenic activity of octylphenol. Toppari J. Taya K. Laws SC. Ferrell JM. et al. Makino T.207(1):59-68. streams. McCoy GL. Exposure of the U.Environmental Phenols References Bian Q. Anal Chim Acta 486:41-50. Kawaguchi M. and other organic wastewater contaminants in U. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Ye X. Two-generation reproduction study with para-tert-octylphenol in rats. Reidy JA. hormones.S. Environ Health Perspect 2008.37(20):4543-53. Marr MC. Maekawa A. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. and testosterone. alkylphenols. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Ono H. Watanabe G. Bolt HM. Takai N. Horie M. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Toxicol Appl Pharmacol 2005. Seto H. Seely JC. Wiegand HJ. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. bisphenol A and methoxychlor in rats. Pharmaceuticals. Ito R.799(1):119-125. Brine DR.18(1):43-51. Reprod Toxicol 2001. Onuki A. Indoor Air 2004. Fedtke N.121(1):21-33. Saito I. Myers CB. An environmental assessment of alkylphenol ethoxylates and alkylphenols.co. 2003. Xu L. Qian J. et al.30(2 Pt 1):81-95. Inoue K. et al. Karjalainen M. Maekawa A. Arch Toxicol 1996. Blake CA. 1995. Furlong ET. Haavisto TE. Brody JG. Cooper RL. Food Chem Toxicol 2006. Williams B. et al. Song L. Environ Sci Technol 2002. Yoshimura S.54(1):154-167.28(3):215-226. Korn LR. Phthalates. 2/4/09 Ying GG.pdf. Kawaguchi M.116(1):39-44.uk/resource/reports/ethoxylates_alkylphenols. Brooks AN. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Myllymaki SA. Katsuda S. polybrominated diphenyl ethers. Usumi K. Kolpin DW. Calafat AM. Warhurst AM. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. testis size. nonylphenol. Takenaka A.44(8):1355-1361. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats.165(3):217-226. Camann DE. Zaugg SD. Wang X. Toxicol Sci 2000. Blake CA. Tyl RW. Thurman EM. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Chen J. Needham LL. Kookana R. Environ Int 2002. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Paranko J. Environ Sci Technol 2003. Nicol L.foe. Watanabe G. Muller AM. Okada F. and sertoli cell number. Fail PA.71(1-2):112-122. Regul Toxicol Pharmacol 1999. and other endocrine-disrupting compounds in indoor air and dust. Katsuda S.57(2):255-266. Sakui N. Yoshimura Y. Nakagomi M. Yoshida M. Wong LY. Carey SA. Biol Reprod 1997. Toxicol Lett 2001. Spengler JD. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Endocrinology 2000. pesticides. Raychoudhury SS. Bodman GJ. Nair-Menon JU.14(5):325-332. Boockfor FR. Roche JF. 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. prolactin. Rudel RA. 1999-2000: a national reconnaissance. Barber LB. Certa H. Indoor air pollution by alkylphenols in Tokyo. Nagao T. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.36(6):1202-1211. Toxicol Appl Pharmacol 2000. Inoue K. Millette CF.

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

6) 31.6-37.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.4-19.2-58.48 (8.20-10.82 (8.8) 7.6-65.2 (13.7) 123 (36.9) 32.93 (7.3-15. Urinary Triclosan (2. interval) 12.7 (14.21 (6.48-10.0) 9.7) 292 (151-432) 132 (78.8) 9.1) 14.20-11.4) 73.72-13.Environmental Phenols Urinary Triclosan (2.40-11.86-12.3) 6.18 (5. see Data Analysis section) for Survey year 03-04 is 2.3 (8.S.20 (7.0-15. Survey Geometric mean (95% conf.1) 11.0 (34.8) 116 (39.9) 7.6-14.3 (11.5) 11.90-10.43-13.8-60.8-127) 37. interval) 13.94 (7.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2) 12.8-63.4) 51.8-112) 30.60 (8.40-17.30-14.4) 90th 249 (188-304) 03-04 03-04 03-04 8.10) 84.1-39.2 (10.9-236) 193 (90.5) 66.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.4 (12.0 (11.2-58.4) 7. population from the National Health and Nutrition Examination Survey.5 (11.4) 317 (231-433) 144 (96.45 (5.6) 90th 212 (172-241) 03-04 03-04 03-04 9.9 (33.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.2-14.6-20.11-11.8) 14.9 (50.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.29-12.5) 13.2 (25.1) 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 9.3-35.3-31.4 (11.92-12.1) 9.16 (6.32-14.6-111) 33.22-10.5-86.45-13.6 (30.0-213) 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 .9-61.50) 10.2 (37.38-18.5-14.7 (28.8 (21.0) 65.1) 9.2) 9.1) 9.3 (26.00 (4.0 (8.1 (8.0 (26.45-10.2-46.4.0) 49.6-14.9 (11.6) 39.0-15.4-18.2 (27.1) 9.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.6-15.10-9.4) 25.60 (6.1 (45.70-16.9 (8.9) 75th 47.7 (11.00-8.7 (9.3) 47.0-73.6 (9.3-67.7) 10.8-85.4) 75th 43.6) 10.4.6) 12.4 (38.80 (5.1) 7.0 (36. Survey Geometric mean (95% conf.0-19.7 (39.S.2 (11.6 (10. population from the National Health and Nutrition Examination Survey.50-10.54 (8.9) 8.74 (5.3 (9.4 (32.55 (4.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5) 20.1 (15.3) 10.1) 13.6 (12.3.20-13.1) 50.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.20 (7.2) 13.4) 357 (225-456) 203 (87.89-11.

J Toxicol Environ Health A 2006. Pharmaceuticals. Anal Chim Acta 1004.67(4):532-537. J Invest Dermatol 1976. Meyer MT. Fourth National Report on Human Exposure to Environmental Chemicals 39 . and phenols in girls. Katsura E. Toxicology of 2. Williams PE. Am J Infect Control 1996. Triclosan: applications and safety. Ebersole R. Watanabe N. Adolfsson-Erici M.28(9):1748-1751. Gunderson MP. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Mar Environ Res 2000. Moss T. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Readman JW. Clapson DJ. Leonard PA.115:116-121. Skirrow RC. Environ Sci Technol 2002. 4’-trichloro-2’-hydroxydiphenyl ether.38(4):361370. Howes D. 4.80(3):217-227. Ogawa H.24(3):209-218. Wolff MS. Pilot study of urinary biomarkers of phytoestrogens. Aguera A. Okui T. Kolpin DW.4’-trichloro-2’hydroxydiphenyl ether). Urinary concentrations of triclosan in the U. et al. Zaugg SD. Needham LL. Nagao Y.116(3):303-307. Pinney SM. Sandborgh-Englund G. Chelimo C. hormones. Teitelbaum SL. The oral retention and antiplaque efficacy of triclosan in human volunteers. Hernando MD. Ye X. Gilbert RJ. Bodey GP. Evidence of 2. Ishibashi H.45 Suppl 2:S137-S147. et al. Mezcua M. Barber LB. Kanetoshi A. Photolytic degradation of triclosan in freshwater and seawater. Chemosphere 2007. Thurman EM. Aranami K. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Bhargava HN. Furia T. Kaneshima H. streams. Biol Pharm Bull 2005. Ekstrand J. phthalates. Erratum in: Aquat Toxicol 2007. Environ Health Perspect 2008. et al.36(6):1202-1211. Gomez MJ. Shiratsuchi H. Benson WH. Wigmore H.7/2. Odham G.Environmental Phenols References Aiello AE. Furlong ET.S.23(5):579-583. Windham G. IMS Ind Med Surg 1969.66:1052-1056.17(5):637-644. population: 2003-2004. Calafat AM. Arch Environ Contam Toxicol 1988. Wong LY. and other organic wastewater contaminants in U.69(20):1861-1873. Lyman FL. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Matsumura N. Larson EL. Osachoff H. Hirano M. Fernandez-Alba AR. Veldhoen N. Percutaneous penetration and dermal metabolism of triclosan (2. 1999-2000: a national reconnaissance. Reidy JA. Williams FM. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Br J Clin Pharmacol 1987. Hong HC.83(1):84. Bennett ER. Foran CM. Pharmacokinetics of triclosan following oral ingestion in humans. Food Chem Toxicol 2000.50(1-5):153-156.38(2):64-71.4.S.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Aquat Toxicol 2006.. Britton JA. Environ Health Perspect 2007. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Levy SB.524:241-247. et al. Ferrer I.

70) 2.91 (1.67) 1..53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th . so it is relatively non-persistent.350) < LOD .500-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.94 (1.04) 1.350) < LOD .350-. population from the National Health and Nutrition Examination Survey. along with small amounts of tetrachlorohydroquinone and conjugates.350) < LOD .350 (.350-.62 (.990 (<LOD-2.30 (. other polychlorinated benzenes.90) 2.350) 90th .350) < LOD < LOD 75th .65 (.350 (.350) < LOD .18 (<LOD-1. 1997). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.S.960) 1.650) 1.10) 1.350) < LOD .. Acute.54-2.630 (.650 (. PCP is eliminated over a few days (Braun et al.350 (. utility poles and fence posts). 2002. algaecide and insecticide. with repeated or chronic exposure.73 (1.350-.350-. bactericide.90) 1.350-.350-2.350) .350 (.510-3. water and sediments because of the large amounts that were produced and used historically. PCP is absorbed rapidly and well by all exposure routes.30) 1. To-Figueras et al.94 (1.80) .350) < LOD .890-1.350) < LOD .350-.00) 1.350 (. The parent compound and conjugates.390 (.980 (.350 (. mollusicide.390 (. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.60) 1.350 (. air. Survey Geometric mean (95% conf.58-2.75) 2..350-2. 1979).33-2.350) < LOD .350-.30) 1.30 (1.30) .42) 696 680 521 696 603 951 Limit of detection (LOD.350-.350-1.65 (. the elimination half-life may be a week or more (Uhl et al..480-2.37) . and animals.530) 1. and it is used primarily as a preservative for wood to be used outdoors (e.350-. Since 1984.09) .350) < LOD .350) < LOD .47-3.350-.350-. which may vary for some chemicals by year and by individual sample.350-1.770 (.10 (<LOD-1. General population exposure to PCP may occur by inhalation of contaminated air. PCP is distributed to most tissues and is not extensively metabolized.860-2.25 and 0.350 (. After absorption.660 (.47-5. herbicide.350) < LOD .23 (.78) 1. PCP is degraded by sunlight and metabolized rapidly by microorganisms. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-. are eliminated in the urine. 1986).01 (<LOD-1.30 (.510-5.76) 1. hypertension.40 (.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-.350 (.350-.10) 1.00) 1. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.48-2.350 (. ingestion of contaminated food or water.64) 1. and possibly of lindane (IPCS.350-.50) 1. and dermal contact with PCP-treated products.45-2.350-2.32 (.350-2.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Kohli et al.350-2.350 (.990-2.350 (. Effects including hyperthermia.58-2.350-.350-1.350 (. PCP use in the U.70) .350 (.90 (1.350-.590-1.350-1. 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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Human exposure to PCP has become less common. has been restricted.350 (.350 (.48 (.850-2. In the environment. PCP has been detected in soils.83 (2.37 (.350) < LOD .33) .S.890 (.350-.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .5.00) 2. After a single dose.350-.350-.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350 (. 1976.08-3.51) 1.350 (.10 (1.350 (.350) < LOD .350) < LOD .76) .350-. < LOD means less than the limit of detection.60) 1.350) < LOD .00 (..350 (.350 (. and metabolic acidosis were observed in CAS No. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.g. plants.350-.350) < LOD .98 (1. PCP cannot be used on wood in residential or agricultural buildings.10 (.680-1. 40 Fourth National Report on Human Exposure to Environmental Chemicals .

75 (<LOD-2.82) 1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.94-3.730) < LOD . respectively) (Seifert et al. chronically administered high doses of PCP were hepatotoxic.270-.220-.650 (.420) < LOD .69 (1.11) 2.500-.270-.13 (. 2003).26 (1.360 (. children in the 1980’s.atsdr. OSHA has established an occupational standard.990 (..30) 1.30) 1.700-2. environmental levels) and health effects is available from the U.34 (.55) 1.79) 1.310-.36) .18) .S.. Survey Geometric mean (95% conf.240-.51) 1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.gov/ toxpro2.S.430) < LOD .21-2.00-1.94 (1.800-1.9 mg/L. 1989). The U.06-3.35-2.29-3. In a small sample of U. 2003). Fourth National Report on Human Exposure to Environmental Chemicals 41 . and the FDA has established a standard for bottled water.800) < LOD 1.900-1.500-1.40) 1. van Raaij et al.84) 1. inhalation.18 (1.290-.00) 1.92) 1. 1989).26 (1.35-2..19 (1.67-3.220-.40) 1. 2004.67 (1. In animals.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .290-. 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.Fungicides adults and children severely exposed to PCP through ingestion.250 (.84 (1.560-.6 and 14.830) < LOD . 1995).19) 2. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.300 (. 1991).57 (1.320 (.290) < LOD ..320) < LOD < LOD 75th ..950-1. 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.25-2.25-2..780) < LOD .360-.510-.19) 2.25 (1.30 (.35) 1.320) < LOD .340-.35) 1.430-.52 (1.57 (.0 mg/L.920 (.EPA.440 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67-3.82 (1.67-2.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .08 and 5.00-1.590) < LOD .90) 1.330-. Among adults in the NHANES 1999-2000 subsample.850 (.S.16 (.10 (1.52 (<LOD-1.73 (1. Death can result from seizures and cardiovascular collapse. Pentachlorophenol is not mutagenic or teratogenic.610 (. 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.950-1. More information about external exposure (i.56) 1.gov/ pesticides/ and from ATSDR at: http://www.910-1.67 (1.52 (<LOD-1.300 (.490) < LOD ..250 (.40) 1.06) 1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .78) 1.16-1.350) < LOD .370 (.30-2.950-1.400 (.48-2.630 (.94 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.09 (<LOD-2.780-1.710-1.560) < LOD .html.75) 1.25) 1. 2000).590-1.S.320) < LOD . the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.760 (.S.19) 2.40-2.510-.84-4.95) 3.epa. IARC has determined that pentachlorophenol is possibly carcinogenic to humans. or skin absorption.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . EPA has developed standards for PCP in drinking water and the environment.25-1.280) < LOD .570 (.cdc.52) 1. respectively) (Becker et al.09-1.25 (1.21 (. and adversely affected thyroid function (U.67 (1.08) 696 680 521 695 603 951 < 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.83 (1.40) 1.650 (.40) 1.310) < LOD .. carcinogenic. EPA at: http://www. In NHANES 2001-2002 subsamples.380-.260 (.300 (.580-.560) < LOD .67 (1.67 (1.06 (.10-2.78) 1.470 (.500 (.e.650) 90th 1.

Helm D. 4/21/09 Kohli J. Baker S. J Expo Anal Environ Epidemiol 2000. Seiwert M. 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. Cline RE. Barrot C. Sala M.4:289296. Pesticide residues in urine of adults living in the United States: reference range concentrations. Schulz C. Available at URL: h t t p : / / w w w.S. Can J Biochem 1976. Becker K. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Hill RH Jr. Bragt PC.18:475-481.71:99108. Engel R. Phillips DL. r e g u l a t i o n s . Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. available at URL: http://www. Jones D. PCP: Human Risk Characterization [online]. Notten WR. Pharmacokinetics of pentachlorophenol in man.105(1):78-83. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. U. Otero R. Schlatter C. Blau GE. hair.10:552-65. Dev Toxicol Environ Sci 1979.inchem. 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. Arch Environ Contam Toxicol 1989. htm.58:182-186. Needham LL. Lindane. et al.S. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. 206:15-24.org/documents/jmpr/jmpmono/2002pr08.54(3):203-208. Seifert B. Arch Toxicol 1986. Hill RH. Chenoweth MB. Gregg M. Uhl S. Hill RH Jr. To-Figueras J. References Becker K. Arch Environ Contam Toxicol 1989. Holler JS. van den Berg KJ. et al. Environmental Protection Agency (U.18(4):469-474. 11/30/2004. Environ Res 1995. The metabolism of higher chlorinated benzene isomers. Smith SJ.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. 4/21/09 van Raaij JA. Braun WH. Santiago-Silva M. Seiwert M. house dust. Shealy DB. Environ Health Perspect 1997. Schmid P. Int J Hyg Environ Health 2003. International Programme on Chemical Safety (IPCS). urine. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Schulz C. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Kaus S. To T. 2002. Seifert B. Fast DM. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Head SL. Needham LL. drinking water and indoor air. et al. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Safe A. Bailey SL. EPA). Krause C. Rodamilans M. Toxicology 1991: 67(1):107-16.

on ornamental plants and turfs. Survey Geometric mean (95% conf.570-2.20 (1. Cnubben et al. 2006). 1989).80) 1.34) 1. but OPP and SOPP are still used on pears and citrus (U.630) < LOD .390-.570-.60 (1.10) . In the past. 90-43-7 General Information Ortho-phenylphenol (OPP.560-8.10-1.28-3.80-3. 2002.970 (.800-3.30-7. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.00 (1.80 (2.490 (<LOD-.S. or apply these chemicals may be more highly exposed than the general population.30-2.27 (.50-2.22 (.509 (.S.Fungicides ortho-Phenylphenol CAS No.790) 2.490 (<LOD-.20 (.00-2.50 (1. however. fungicides.696) * .22) 2.30) < LOD 90th 1.466 (.50-4.386-.389-.10) 1.. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 .90) .600-1.23) 695 680 520 695 603 953 Limit of detection (LOD.30) < LOD 1. sodium ortho-phenylphenate (SOPP).770 (.580-1.20) 2.890 (.836) * .88) 1.S.890 (.40-5. < LOD means less than the limit of detection. Most agricultural food applications have been revoked.600) < LOD .90 (1.600) < LOD 75th .497 (.00 (1. Timchalk et al. leaving the chemical residue OPP. 2006).00) .770 (.570-1.567 (.364-.S.50 (1.20 (1.880-2.90) .493 (.20) < LOD 1.740 (.10) 1. interval) .30 (1.07 (.10-2.820 (.710-2.600-1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2. in paints.03) 1.80) 1.590-2. are antimicrobial agents used as bacteriostats.10) 2.02) 1.76) 1.370-. Available evidence suggests that OPP does not accumulate in the body.3.20) < LOD 2.520 (.10) .690) < LOD . OPP is considered to be moderately toxic after acute oral doses in animal studies.92 (.50) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600-1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.450 (<LOD-..33 (.638) * .370-. population from the National Health and Nutrition Examination Survey.600) < LOD 1.670) 2.540-2. Both chemicals degrade within hours to weeks in the environment (U. Estimated human intakes have been below recommended intake limits (U. and it has limited water solubility.14 (<LOD-3.450 (<LOD-.60-3. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.85) 2.470 (<LOD-.552 (.50) < LOD . such as fruits and vegetables.10 (1.860 (.3 and 0.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .40 (.780) < LOD .950) < LOD .496 (.636) * .20-2.50 (1. Chronic dosing in animals resulted in such systemic effects as weight loss and Urinary ortho-Phenylphenol Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60-2.610-1.890) 1.350-1. SOPP is applied topically to the crop and then rinsed off.640) < LOD .40-2.550-1.410-. it was used in home sanitizers for surfaces. and as a wood preservative.50-3. General population exposure can occur via dermal.624) * . OPP is still used as a disinfectant fungicide for industrial applications.10 (1.30) 1.17 (.00) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. formulate.490 (<LOD-.498 (. whereas SOPP is not volatile and is more water soluble. 1998).19 (. or 2-phenylphenol) and its water-soluble salt. 2006).420 (<LOD-.370-.389-.28 (.621) * .90) 1.570 (. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. Both have been used in agriculture to control fungal and bacterial growth on stored crops.760-2.402-.433-. which may vary for some chemicals by year and by individual sample.710) 3..490 (<LOD-. and sanitizers.40-5.60 (1.480-1. OPP is volatile.690-1.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .09) 2.EPA.60 (1.50) 1. Workers who manufacture.50) .90 (1.610 (. 1998.349-.570 (.500-2.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . inhalational. Fourth National Report on Human Exposure to Environmental Chemicals 43 .30) < LOD .508 (. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.50) < LOD .750-2.40-7.90) 2.00) < LOD .742) * .61) 2. EPA.10) .490 (<LOD-.830 (.EPA.645) * .00 (1.00 (1.930 (.450 (<LOD-.20-3.600) < LOD .850 (.840-1. 2006).

455-. less likely. Kwok et al.. 1999.61 (1. 1999.. 1984.96-4.33) ..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 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.81) 1. Ito et al. 2002.EPA at: http:// www.78 (2.311-.590) * .291-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. U.640-1.43) 3.21-2.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 . Volunteers exposed to 0.900-1.500) < LOD .750 (.301-.11 (. 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. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.17 (.343 (.epa..860 (.64 (2.43-2.940-2.96) 1. or developmental toxicity was observed (Bomhard et al.270-. Biomonitoring Information Urinary OPP levels reflect recent exposure.17 (.29) 1.24-2.75 (1.480-.385 (.09-6. 44 Fourth National Report on Human Exposure to Environmental Chemicals .32) 1.89 (1.18) 2.780-14..420 (<LOD-.410 (<LOD-.910 (<LOD-1.656) * .248-.08-2.840 (. Additional information is available from U. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.93) 1.. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.EPA 2006).550-.47) .670 (.27) < LOD .444 (.580) < LOD . OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.02 (.780 (.32) 3.382 (.93 (1.570) < LOD 1..S.46) < LOD 1.910-1.00 (1.453 (.S.38) 2. 1986).91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.514 (.40-13.86 (1.74 (1.900) < LOD .43 (1.33-2.08) 1..43-2. Zhao et al.61 (2.84 (1. or.600-1.93) .S. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.580-1.96 (1.361-.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.75 (1.59) 1.0) 1.950) < LOD .470 (<LOD-.650-1.31) < LOD .810-1.560-2.473) * . 1998. CDC.11-1.05-2.58) 2.12) < LOD 1.510-..06-5.496 (.Fungicides anemia.666) * .320 (<LOD-.410 (<LOD-.620-1.560) < LOD 75th . OPP was not found to be mutagenic.800-1.910 (.440 (. Murata et al.21) 1.08-1.04-4.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .38-3. and it has classified OPP as not classifiable with respect to human carcinogenicity.17) 2. Pathak and Roy.EPA 2006).610) < LOD 1.750-2.61 (.980 (.508) * .380 (.06 (1.96 (1. interval) . Smith et al.770-2.510 (<LOD-.97 (2.gov/pesticides/.329-.62) . 2000.460-.44 (1. 2002.07) 2.484) * .S.06-4. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. Bomhard et al. 2005).09 (1. population from the National Health and Nutrition Examination Survey.91 (1.403-.00 (.01) 1. 1992.52 (.990) < LOD .28 (<LOD-4.670 (.620-1. Survey Geometric mean (95% conf.38) 1.26) 1.53) 1.750 (.59) .550 (. Nakagawa et al.4) 3.970) 1.93) .550) < LOD . but no neurologic. Brusick.670) < LOD . by possible genotoxic mechanisms (Hagiwara et al.11) < LOD 90th 1.880-1. 1984. leading to production of two metabolites.360 (<LOD-.420 (<LOD-.470) < LOD . 2005. 2005). 1997.88-4.568) * .28 (2. Detectable levels were seen in over half the U.12-2.11) 4. In high dose animal studies.860 (. U.69 (1.11 (.980 (<LOD-1. 1993.791) * .24-2.20) < LOD 3.21 (.353-.13) 1.4 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.51-3.690 (.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . reproductive.25-6.29) 1. 2002). IARC has classified SOPP as a possible human carcinogen.810) < LOD ..09-3.

Buchholz BA. The carcinogenicity of the biocide ortho-phenylphenol. U. et al. Centers for Disease Control and Prevention (CDC). Glas K. Timchalk C. Crit Rev Toxicol 2002. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Toxicol Appl Pharmacol 1999. Roberts AL. Office of Toxic Substances. Bomhard EM. Smith RA. Fukushima S. U.50(11):3351-3358. Eadon G. van de Sandt JJ. Xenobiotica 1998. Vogel JS.pdf. Drugs. Arnold LL.159(1):18-24.S.17(8):411-417. Cnubben NH. St John MK.S.. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. rat and man. 4/9/09. 2006. Nakagawa Y. EPA 739 R-06004. Hum Exp Toxicol 1998.43(7):14311437. 1989. 4/13/09 Onstot JD. J Agric Food Chem 2006. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.(56):399-407. Elliott GR.gov/oppsrrd1/REDs/ phenylphenol_red. Available at URL: http://www. J Agric Food Chem 2002.S. Moriya K. Moldeus P. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Pathak DN.45(5):460-481. Mendrala AL. Mutat Res 1993. food additives and natural products as promoters in rat urinary bladder carcinogenesis. July 28.286(2):309-319. Brendler-Schwaab SY. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Bartels MJ. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Brusick D. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Turteltaub KW. Food Chem Toxicol 1984. Kawanishi S. Environmental Protection Agency (U.gov/ntp/htdocs/LT_ rpts/tr301.22(10):809-814. Imaida K. Hagiwara A. Richter M. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Coelhan M. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Roy D. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats.54(16):5731-5735. Bartels MJ. Selim S.28(6):579594. National Toxicology Program (NTP). Shirai T. J Chromatogr B Biomed Sci Appl 1997.74(2):61-71. Brzak KA. EPA-560/5-89-003. Bartels MJ. Fourth National Report on Human Exposure to Environmental Chemicals 45 .703(12):97-104. Hirose M. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Ito N.epa.pdf. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Inoue S. McNett DA. Fukushima S. Atlanta (GA). Narang A. Identification of SARA compounds in adipose tissue. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. et al. Sangha GK.20(5):851-857. Christenson WR. Bormett GA. Bromig KH. Hakkert BC. Environ Mol Mutagen 2005. Toxicol Appl Pharmacol 1998. Carcinogenesis 1999. Regul Toxicol Pharmacol 2002.niehs. Freyberger A. Third National Report on Human Exposure to Environmental Chemicals. Bartels MJ. Kwok ES. Timchalk C. 2005. Comparative metabolism of orthophenylphenol in mouse. Available at URL: http://ntp. Gierthy J.EPA). Leser KH. Environmental Protection Agency (U.nih.Fungicides References Appel KE. Biochem Pharmacol 1992. Ito N. Meuling WJ. Moore GA. Arch Toxicol 2000. IARC Sci Publ 1984. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No.S. Tayama S. Cano M. Christenson WR. Murata M.32(6):551-625. 90-43-7) in Swiss CD-1 mice (dermal studies). Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. EPA). Zhao S. Shibata M. Sangha G. Stanley JS. Herbold BA. March 1986. Eastmond DA.35(2 Pt 1):198-208. Hagiwara A.150(2):402-413.

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

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

population from the National Health and Nutrition Examination Survey. 48 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.S. < LOD means less than the limit of detection.1. 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.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2500 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 819 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1322 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 672 952 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf. 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. 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. population from the National Health and Nutrition Examination Survey.

Number 15.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Jefferies PR. Reynolds SJ. et al. U. Olsson AO.108(12):1151-1157. Hines CJ. et al. Ward EM. Coleman S. Comparative metabolism and elimination of acetanilide compounds by rat. Linhart SM.Herbicides References Ashby J. Barr DB.S. Lefevre PA. Tinwell H. J Agri Food Chem 1989. Bravo R. Hum Exp Toxicol 1996. Barr JR. and metolachlor herbicides in rats. 5/30/06. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Rose RL. Environ Sci Technol 2005. Centers for Disease Control and Prevention (CDC). imidazolinone. Kier L. Kinney PL. Burkhardt MR. Curwin BD. acetochlor. reservoirs and ground water in the Midwestern United States. Dialkylquinonimines validated as in vivo metabolites of alachlor. Andrews HF. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Xenobiotica 1994. Kolpin DW. Volume 65.S. Barr DB. Green T. Larsen GL. Occurrence of sulfonylurea. Sanderson WT. Quistad GB. Environ Health Perspect 2000. Peter CJ.S.39(17):6561-6574. Feil VJ.html. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. et al.37(4):10881093. sulfonamide. and other herbicides in rivers. Chem Res Toxicol 1998. Striley CA.S. Wilson AG.248(2-3):115-122.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Davison KL.EPA): http://pmep. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Acetochlor (Harness) Pesticide Petition Filing 1/00. Fourth National Report on Human Exposure to Environmental Chemicals 49 . EPA).111(5):749-756. Environ Health Perspect 2003. Hsiao JJ. Barr DB. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Available at URL: http://www. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. EPA). Third National Report on Human Exposure to Environmental Chemicals.15(6):500-508. Hodgson E.S. 1998. Deddens JA. 5/30/06 U.cce. EPA 738-R-00-009. Furlong ET. 2000. Roberts AL. J Expo Anal Environ Epidemiol 2005. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Sci Total Environ 2000.17(6):559-566. 2005. epa. Whyatt RM. Atlanta (GA). Available at URL(non U. Casida JE.24(10):1003-1012. Linderman R. Camann DE. Heederik D. Battaglin WA.11(4):353359.248(2-3):123-133. Thurman EM.cornell. Hein MJ. Alavanja MC. J Expo Sci Environ Epidemiol 2007. Environmental Protection Agency (U. pages 3682-3690. Feng PCC. Federal Register: January 24.15(9):702-735. Sci Total Environ 2000. Hladik ML. Wratten SJ.pdf. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Environmental Protection Agency (U. March 2006.

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

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

Hines CJ. Circular 1291. Hum Exp Toxicol. Environmental Protection Agency (U.usgs.S. Kinney PL. Henningsen G.int/water_sanitation_health/dwq/chemicals/en/alachlor. No. Whyatt RM. Tolos W. Brown KK. Tessier DM. Hull RD. Xenobiotica 1994. Heydens WF. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.gov/oppsrrd1/ REDs/0063. 86. et al. and other herbicides in rivers. EPA 738R-98-020. who. Hill RH Jr. Geological Survey (USGS). Available at URL: http://water. Lau H. Reregistration Eligibility Decision (RED) Alachlor. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .18(6):363-391. Deddens JA.Herbicides References Battaglin WA. Geneva. Environ Sci Technol 2005.39(17):6561-6574. Chem Res Toxicol 1998.pdf.24(10):1003-1012.111(5):749-756. Atlanta (GA).44(18):1325. 2005. Kimmel EC. Sacramento. Wilson AG. Casida JE. Erratum in: Life Sci 1989. World Health Organization (WHO). Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. J Agri Food Chem 1989. 2003. acetochlor. Casida JE. Dialkylquinonimines validated as in vivo metabolites of alachlor.248(2-3):115-122. Thake DC.11(4):353359.248(2-3):123-133. Casida JE. Available at URL: http:// www. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Kolpin DW. Feng PCC. Centers for Disease Control and Prevention (CDC). 1992-2001.org/documents/pds/pds/pest86_e. Camann DE. Wratten SJ. EPA). 4/2/09 U. Quistad GB. Third National Report on Human Exposure to Environmental Chemicals. Roberts AL.395(2-3):159-171. Occurrence of sulfonylurea. Geological Survey (USGS). sulfonamide. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Quistad GB. DNA adduct formation by alachlor metabolites. Am Ind Hyg Assoc J 1995. Environ Health Perspect 2003. U. 1997. Kier LD. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. revised February 15. 1999. et al. 2007. WHO/ FAO Data Sheets on Pesticides. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. California. Background document for development of WHO Guidelines for Drinking-water Quality.pdf. Shoemaker DA. Hladik ML. 1996.htm. Barr JR. Andrews HF. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. ALACHLOR.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Biagini RE.inchem. 98-4245 (by Barbash JE. Driskell WJ. Supplemental Technical Information (available on-line only). Linhart SM. Hsiao JJ. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Sci Total Environ 2000. Hines CJ. and metolachlor herbicides in rats. Thelin GP. Kolpin DW. Brown MA. Burkhardt MR.43(25):2087-94. Thurman EM. Bull Environ Contam Toxicol 1996. Feil VJ. Davison KL. reservoirs and ground water in the Midwestern United States. 2/27/09 Jefferies PR. Furlong ET.43(9):2504-2512.S. MacKenzie B. Ann Occup Hyg 2003. 1998.37(4):10881093. Peter CJ. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Sci Total Environ 2000. J Ag Food Chem 1995. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Life Sci 1988. Mutat Res.S. imidazolinone. Available at URL: http://www. International Programme on Chemical Safety (IPCS).S.56(9):883-889. Larsen GL. Striley CA. Alachlor in Drinking-water. December 1998.php. World Health Organization. Barr DB. Martens MA. Gilliom RJ). Hill AB. Biagini R. Sanderson WT. March 2006. Clark JM. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Comparative metabolism and elimination of acetanilide compounds by rat. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. 2/27/09 U. Jefferies PR.47(6):503-517. Shealy DB.56(6):853-859. 1999. Available at URL: http://www.epa.

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

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

The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function.html. et al. Collins A. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.atsdr. 2003. The geometric mean of urinary atrazine mercapturate was 1.. 2007).61(4):331-355. J Expo Anal Environ Epidemiol 2005. 2005). Striley CA. Third National Report on Human Exposure to Environmental Chemicals. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Biological monitoring of human exposure to atrazine. et al. Toxicol Lett 1993. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Vonk A. Blewett C. Gillis JH.76(1):190-200. 3/11/09 Arcury TA. Deddens JA. Centers for Disease Control and Prevention (CDC).30(2):244-247. Schmid J. Reynolds SJ. WHO/ FAO Data Sheets on Pesticides. Extrom PC. Ferrell JM.. Pest Manag Sci 2005. Sanderson WT. J Agric Food Chem 1982. et al. Shoemaker DA.15(6):500-508. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Toxicol Sci 2003.69(2):217-222. 2005. Lucas AD. Gammon DW. Goldman JM. Simpkins JW.gov/toxprofiles/tp153. Stoker TE. In the NHANES 2001-2002 subsample.cdc. Steroids 1999. Stevens JT. References Adgate JL. Goodrow MH. Lioy PJ. Bradway DE. Chen H. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Clayton CA. Wetzel LT. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. ATRAZINE. J Toxicol Environ Health 1994. 3/11/09 Laws SC. Grzywacz JG. Maroni M. Mendoza M. Proc Natl Acad Sci USA 2002. 2001 [online]. Toxicological profile for atrazine. International Programme on Chemical Safety (IPCS). In small studies of Maryland residents in 19951996 (MacIntosh et al. Hayes TB. J Toxicol Environ Health 1994. Brown KK. Stoker TE. Aldous CN.. 2000). Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Tyrey L.64(9):672-678. Perry et al.109(6):583-590. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.47(6):503-517. Quandt SA. 1993). Cooper RL. Ann Occup Hyg 2003. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Pfeifer KF. Sanborn JR.htm. Eberly LE. McElroy WK. World Health Organization.org/documents/pds/pds/pest82_e. A risk assessment of atrazine use in California: human health and ecological aspects. No.43(2):155-167.43(2):155-167. Barr DB. Agency for Toxic Substances and Disease Registry (ATSDR). Hines CJ. Tapia J. Hermaphroditic. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). levels of atrazine mercapturate were generally not detectable (CDC. atrazine was detected in only four children (Arcury et al. Carr WC Jr. Barr DB. Environ Health Perspect 2007. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Noriega N. Cottica D. Gillis JH. Available at URL: http:// www. Geneva. 2001). Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.inchem.. Ferioli A. Barbieri F. Environ Health Perspect 2001. Seiber JN. Toxicol Sci 2000. Lee M. Eldridge JC.58(2):366-376. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Catenacci G. Barr DB. Stuart AA. 82. et al. 2005). Freeman NC. Saiz SG. Available at URL: http://www. Breckenridge CB. Laws SC. Fleenor-Heyser DG.53(2):297-307.115(8):1254-1260. Heederik D. In a study of 60 farm worker children. diamino-S-chlorotriazine and hydroxyatrazine. Biomonitoring studies on levels of atrazine mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of atrazine than are found in the general population.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.. Biagini RE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Bersani M. Curwin BD. Eldridge JC. 1996. In a small number of field workers. Cooper RL. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Cooper RL. Stoker TE. Jones AD. Hein MJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.99(8):5476-5480.. Moseman RF. et al.. Atlanta (GA). Ferrell JM. Toxicol Sci 2000. Wetzel LT. et al. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.

1992-2001.27(6):599612. J Expo Anal Environ Epidemiol 1999. Environmental Fate and Effects Division.gov/oppsrrd1/REDs/ atrazine_ired.67(2):198-206. Toxicol Sci 2000. Hammerstrom KA. Available at URL: http://www. The Quality of Our Nation’s Waters.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Pesticides in the Nation’s Streams and Ground Water. Perry M. revised February 15. Ann Epidemiol 2000. Environmental Protection Agency (U. Available at URL: http://www. Urinary biomarkers of atrazine exposure among farm pesticide applicators.S. 2003b.php. A risk characterization for atrazine: oncogenicity profile. EPA). Cooper RL. Circular 1291. Toxicol Appl Pharmacol 2002. A review of epidemiologic studies of triazine herbicides and cancer.S. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .10(7):479.56(2):69-109. Available at URL: http://water. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.S. Timchalk C. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Needham LL. Stoker TE. Crit Rev Toxicol 1997. 6/1/09 U. 2007.S. Wood C. Lansbergen GW. Sathiakumar N. Case No. Dryzga MD. Supplemental Technical Information (available on-line only).195(1):23-34. van den Berg M. J Toxicol Environ Health A 1999.usgs. Cooper RL. Laws SC. Langvardt PW. Singzoni B. Chem Res Toxicol 1993. Toxicology 1990. Toxicol Sci 2002. Interim Reregistration Eligibility Decision For Atrazine.epa.S.61(1):27-40.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Ryan PB. Office of Prevention. Delzell E.182(1):44-54.9(5):494-501. Wetzel L. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.pdf. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. 0062. Dagenhart D. Osborne DW. Stevens JT. EPA).6(1):107-116. Environmental Protection Agency (U.58(1):50-59.epa. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Stoker TE. Tortorelli J. March 2006. Guidici DL. White paper on potential developmental effects of atrazine on amphibians. MacIntosh DL. Breckenridge CB. Sanderson JT.pdf. Boerma J. 3/11/09 U. Kastl PE. Guidici DL. Laws SC. EPA Office of Pesticide Programs. Geological Survey (USGS). Toxicol Appl Pharmacol 2004. Christiani D. Washington (DC).Herbicides development of a biomarker of exposure. Rayner JL. A longitudinal investigation of selected pesticide metabolites in urine. Fenton SE. Pesticides and Toxic Substances. May 2003a. U.

49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .4-D may occur during residential applications. 2004).48) < LOD 1. agricultural.Herbicides 2.07 (.740 (.952 and 0.2.910) 1. it acts as a plant growth hormone.550-1.910) < LOD .EPA in 1948. 2.EPA.560-. 2007). headache. in 2001 (U. myotonia. 2.10 (<LOD-1.490) < LOD < LOD < LOD . by direct contact with agricultural and residential areas after applications.21) 1.22) < LOD .250 (<LOD-.08) < LOD .4-Dichlorophenoxyacetic Acid CAS No.60) 1. Survey Geometric mean (95% conf. abdominal pain. Once absorbed.760 (.890) < LOD .890 (. and mecoprop).420) < LOD . MCPA. these herbicides can enhance plant growth.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.250 (<LOD-.4-D has low acute toxicity.S.210 (<LOD-. 94-75-7 General Information Widely used throughout the United States.660) 1. It is rarely detected in ground waters (USGS.80) 1.27-2.260 (<LOD-.4-D) controls broadleaf weeds in residential.S. and delayed Urinary 2.27 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. Human health effects from 2.4-dichlorophenoxyacetic acid (2. and aquatic environments. with a half-life of several days to several weeks.03) 695 659 520 668 589 892 Limit of detection (LOD.51 (1.EPA. It is not well absorbed through the skin. 1989.4-D or exposed for prolonged periods.370-.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. renal and hepatic injury. 2.20 (<LOD-1. 4-D. dizziness.930-1.00-2. It is poorly bound in soils.32 (1.10 (<LOD-1.4-D can be applied either as an aqueous salt or as oil-soluble esters. Similar to other chlorophenoxy herbicides.670-1.4-D is rapidly absorbed via oral and inhalation routes. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.690 (.730 (. which may vary for some chemicals by year and by individual sample. 1977). At low levels.16) < LOD .05-2. 2.S.540-.27 (1. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. hypotension.400) < LOD . nausea. General population exposure to 2.440-1..560-1.40) 1.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD .420-.10) < LOD 1..960-1. and by consuming food or drinking water contaminated with 2.490 (. Kohli et al.930 (.320) 90th .70) 1. It was first registered with U.S. but at higher levels they are herbicidal.S. Sauerhoff et al.810-1.680-1.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al..610 (.4-D were used in the U.55 (1. Recent estimates of chronic intakes of 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410) < LOD .4-D have been below recommended intake limits (U. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.690 (.310 (.43) 1.02-1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.24 (. the chlorophenoxy herbicide 2.690 (.13) < LOD .210-. 2005).350) < LOD < LOD < LOD .230 (<LOD-.610-.330 (.690-1. < LOD means less than the limit of detection. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.30 (<LOD-2.310) < LOD .66) < LOD 1. population from the National Health and Nutrition Examination Survey. As much as 62 million pounds of 2.230-.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1974.20 (. Fourth National Report on Human Exposure to Environmental Chemicals 57 .

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1..S.790) < LOD .. population (Hill et al.EPA. 2005).680) < LOD .610-.670 (.560-.570) < LOD .620-. Epidemiological studies have reported associations of several types of cancer..4-D production plant workers and a few forestry workers spraying 2.270-. liver. 2005. 1985.26) 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 .39) < LOD 1.EPA.440 (.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.550-.350 (<LOD-. population from the National Health and Nutrition Examination Survey.14 (. or to contaminants in the herbicide formulations (specifically 2.340-.930-1. Additional information is available from U. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. U.EPA.470) < LOD .520-. 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. Survey Geometric mean (95% conf. Hill et al.27-1.4-D reflect recent exposure. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. IPCS. Average post-application urinary levels of 2. thyroid.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .16) 1.gov/pesticides/.7. 2002. other exposures. 2005.4-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.Herbicides neuropathy (Bradberry et al.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.380) < LOD . Biomonitoring Information Urinary levels of 2. IOM.13 (.380-.270 (<LOD-.13 (.610-. U.05) .670 (. and of adults and children (Baker et al.17 (.S.790) 1.56) .4-D levels were detectable in less than a quarter of the individuals studied.990-1.4-D are eye irritants.980) < LOD 1.4-D does not have significant reproductive.560-.08 (. Post-application levels in farmers and home gardeners were dependent on Urinary 2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.epa.590 (<LOD-1.740 (. 2005.580-.410) 90th . 1995.32 (<LOD-2. IPCS.700 (. 2005). Frank et al.08 (. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660) < LOD .480 (.410 (<LOD-.890) < LOD 1. or teratogenic effects in chronic rodent studies (Charles et al. 2.S. 2005). 1995).640 (. Acute high doses administered to laboratory animals produced ataxia... 1996..660 (.490 (.780 (. 1989). U. 2.890-1. 1996.08 (.380 (<LOD-.S. 2005.S. 2. 2006.. eyes..410) < LOD 1. and evidence of histological injury to the kidneys. 2004). 2002. IPCS. CDC. 2000).850) < LOD .720 (.380 (<LOD-.810-1. myotonia.410) < LOD < LOD < LOD . 2003.820-1. 1992).920) < LOD 1.S. urinary 2.590 (<LOD-1.41 (1.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 1994). In previous samples of the U. It is unclear whether these associations are related to the chlorophenoxy herbicides. Knopp et al.EPA 2005).670 (<LOD-1. U. Pearce and McLean.3.780) .4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.780-1.19) .340 (.73) . developmental.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .EPA at: http://www.35) < LOD . Kolmodin-Hedman and Erne.24) 1. The acid and salt forms of 2. adrenals and gonads (NTP. in small samples of children (Hill et al.390) < LOD < LOD < LOD ..330-.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.810-1. 1996. Kutz et al.. 1980.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2001. 58 Fourth National Report on Human Exposure to Environmental Chemicals .

4-D than levels found in the general population.10(6 Pt 2):789-798. Occup Environ Med 1994.15(6):500-508.4-. Bailey SL.71(2):99-108. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Gregg M.4:427-435.5-T). 2006. Gupta BN.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. 3/17/09 Institute of Medicine (IOM). Arch Environ Contam Toxicol 1985.gov/index.4:97-100. 3/17/09 Knopp D. J Environ Sci Health B 1992. Tables. Baker BA. Baker S.18(4):469-474. Khanna RN.4-D were highest in the farmers who applied the 2. Shealy DB.4-D will result in an adverse health effect. 2005.org/documents/jmpr/jmpmono/v96pr04. Alexander BH. Holler JS. et al. Environ Res 1995. Centers for Disease Control and Prevention (CDC). Available at URL: http:// www.4-D): exposure and urinary excretion. To T. 2005). National Toxicology Program (NTP). cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4:318-321. Needham LL. In farm families. Toxicol Sci 2001. Harris et al. Scand J Work Environ Health 2005. Dichlorophenoxyacetic acid. Assessment of exposure to 2.4-D) epidemiology and toxicology. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Chapman P. Frank R. Selected pesticide residues and metabolites in urine from a survey of the U. Wilson RD. Hill RH Jr. Atlanta (GA). Absorption and excretion of 2. 2005 Charles JM. J Expo Anal Environ Epidemiol 2000.. Third National Report on Human Exposure to Environmental Chemicals. Kutz FW. et al. Veterans and Agent Orange: update 2002. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Biomonitoring of herbicides in Ontario farm applicators.32(4):233-257. Barr DB. Review of 2. the number of acres to which it was applied (Curwin et al.4-D in urine does not mean that the level of the 2.4-dichlorophenoxyacetic acid (2. Sanderson WT. Pesticides residues in food: 1996 evaluations Part II Toxicology.27(1):23-38.51(3):152-159.4-dichlorophenoxyacetic acid in man. Washington (DC): National Academies Press. Beeson MD.S. Arnold EK.Herbicides the time since application.37(2):277-291.4.. Philbert MA.31 Suppl 1:98-104. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Scand J Work Environ Health 2005. Survival and Growth Curves from NTP Toxicity Studies. Head SL.htm. 914. Carter-Pokras OD. Mandel JS. and the use of protective clothing or equipment (Arbuckle et al. TOX-63: TOXICITY REPORT CURVES. References Arbuckle TE. Developmental toxicity studies in rats and rabbits on 2. Beasley VR.php?record_id=10603. Sircar KP.nap. International Programme on Chemical Safety-INCHEM (IPCS). Barr DB. et al. Fast DM. van Ravenzwaay B..4-dichlorophenoxyacetic acid (2.niehs. Hill RH Jr. Erne K. Kohli JD. Biomonitoring studies of 2. Garabrant DH. Hein MJ.4-D). TOX-63 Peroxisone Project (2. Arch Toxicol Suppl 1980.. Updated March 7.edu/catalog. Harris SA. Brody D. 2003. Arch Environ Contam Toxicol 1989. Curwin BD. Acquavella JF. geometric mean urinary levels of 2. Stephenson GR. Hanley TR Jr. Cook BT. Available at URL: http:// www. Exposure of homeowners and bystanders to 2.4-D. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Biomonitoring for farm families in the farm family exposure study. Finding a measurable amount of 2.4-dichlorophenoxyacetic acid and its forms. Driskell WJ.nih. 1992). 2005). Sirons G J. Dhar MM. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Estimation of occupational exposure to phenoxy acids (2. Available at URL: http://ntp. Reynolds SJ.4-D and 2.4 dichlorophenoxyacetic acid (2. 2005. Murphy RS. Solomon KR. Heederik D.31 Suppl 1:90-97. Ritter L. Ripley BD. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. general population. Xenobiotica 1974. Vet Hum Toxicol 1989. Smith SJ.31(2):121-125. Crit Rev Toxicol 2002. Bus JS.60(1):121-131. Baker SE.4-D in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2. Honeycutt R. Kolmodin-Hedman B. Forestry workers involved in aerial application of 2. Cole DC. Needham LL. the amount of pesticide applied. J Expo Anal Environ Epidemiol 2005 Nov. Mandel et al. Board on Health Promotion and Disease Prevention. Pesticide residues in urine of adults living in the United States: reference range concentrations. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.inchem.4-Dichlorophenoxyacetic Acid). Campbell RA. J Toxicol Environ Health 1992. Tandon JS. 2.

Available at URL: http://www.EPA.S.2000 and 2001 market estimates. The Quality of Our Nation’s Waters. Available at URL: http://www.4-D RED Facts. Available at URL: http://water. May.EPA). Gehring PJ. Circular 1291. S. Supplemental Technical Information (available on-line only). 3/17/09. 2.pdf. 60 Fourth National Report on Human Exposure to Environmental Chemicals .S. Washington (DC): U. Environmental Protection Agency (U. Braun WH.EPA). March 2006. 2004. Pesticide industry sales and usage . Blau GE.S.4-dichlorophenoxyacetic acid (2.S. Office of Prevention Pesticides and Toxic Substances.Herbicides Sauerhoff MW. 1992-2001.8:3-1U. 2007.php. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Environmental Protection Agency (U. EPA 738 F-05-002.epa.htm. 4/2/09 U. Pesticides in the Nation’s Streams and Ground Water.gov/oppsrrd1/ REDs/factsheets/24d_fs. revised February 15.epa. Toxicology 1977. June 2005. Geological Survey (USGS).gov/nawqa/pnsp/pubs/ circ1291/supporting_info. 3/17/09 U. The fate of 2.usgs.S.4-D) following oral administration to man.

EPA. The geometric mean metolachlor mercapturate was 4. 2005. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. In animal studies. and on non-crop land for general weed control. sorghum and other crops.EPA. 2005). soybeans. 1995).S.. so applicators. U. metolachlor levels in water have exceeded lifetime human health advisory levels (U. USGS. 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. lacrimation. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish.S. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. 1995. and convulsions were observed at lethal doses in animal studies. It is absorbed by plants and inhibits plant protein synthesis. EPA at: http://www.S. WHO. WHO.EPA considers metolachlor to be a possible human carcinogen. 2000. 1995). Metolachlor did not show developmental or reproductive toxicity in chronic animal studies.200 μg/L (CDC. 2003). mercapturate conjugates were the predominant metabolites.. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. though the 95th percentile for males was 0. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. in both ground and surface waters (Battaglin et al. 1989. and field workers may have significant exposures via this route.EPA.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. Metolachlor has low potential for acute toxicity (U. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. including corn.S. Gilliom. and eliminated in urine and feces over two to three days (WHO. Metolachlor is well absorbed dermally. Occasionally in the past. Estimated human intakes have been below recommended limits (U.Herbicides Metolachlor available from U.. Jefferies et al.. and it was not mutagenic in mammalian cells (U. whereas 60% of applicators had detectable amounts. Davison et al.. Fourth National Report on Human Exposure to Environmental Chemicals 61 . 1995). 2000. 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. 2007.epa. EPA.S. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Feng and Wratten. Salivation. In animals. 2005). 2007. (2003) showed that 2. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect.. 2003).S. 1994. Hines et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998). General population exposure may occur through the consumption of contaminated food or drinking water. Kolpin et al. metolachlor was quickly absorbed after dermal or oral doses. 2003). Hladik et al.. 1999.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al.gov/pesticides/. Biomonitoring Information CAS No. Biomonitoring studies on levels of metolachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels metolachlor than are found in the general population. formulators. NTP and IARC do not have ratings regarding human carcinogenicity.

500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.670 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .2.200 (<LOD-.440 (<LOD-.240) 679 701 957 Limit of detection (LOD. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0.S.200 (<LOD-. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Survey Geometric mean (95% conf.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. 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 .740) 679 700 957 < 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. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.108(12):1151-1157. imidazolinone. Rose RL. Environ Sci Technol 2007.gov/oppsrrd1/ REDs/0001.248(2-3):115-122.11(4):353359.37(4):10881093.S. Roberts AL. 3/26/09 U. Coleman S.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Burkhardt MR. and metolachlor herbicides in rats. Barr DB. Biagini RE. Larsen GL. Feng PCC. Available at URL: http://water.gov/nawqa/ pnsp/pubs/wrir984245/text.php. Linderman R.usgs. Davison KL. sulfonamide. Hodgson E. World Health Organization (WHO). Available at URL: http://water. Supplemental Technical Information (available on-line only). U. 2005. Jefferies PR. 4/2/09 U. streams and groundwater.24(10):1003-1012. Pesticides in U. J Agri Food Chem 1989. Environ Health Perspect 2003. Sanderson WT. Thelin GP.pdf. Thurman EM. Peter CJ. Centers for Disease Control and Prevention (CDC). Reregistration Eligibility Decision (RED) Metolachlor.ESTfeature_gilliom.gov/nawqa/pnsp/pubs/files/051507. 1999. Casida JE.who. Brown KK.111(5):749-756. Chem Res Toxicol 1998.S. Occurrence of sulfonylurea.int/water_sanitation_health/dwq/chemicals/ metolachlor. Hsiao JJ. Sci Total Environ 2000. Sci Total Environ 2000. Kinney PL. Striley CA. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. usgs.S.Herbicides References Battaglin WA. 2003. 1992-2001. Metolachlor in Drinkingwater. Reynolds SJ. Kolpin DW. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Ann Occup Hyg 2003. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 6/1/09 Whyatt RM. Quistad GB. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.47(6):503-517. Environmental Protection Agency (U. revised February 15. Kolpin DW. EPA 738R-95-006. Geological Survey (USGS). Available at URL: http://water. Geological Survey (USGS). In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Xenobiotica 1994. Linhart SM. Wratten SJ. Andrews HF.41:3409-3414. Third National Report on Human Exposure to Environmental Chemicals. 98-4245 (by Barbash JE. Hein MJ. R.pdf 3/30/09 Hines CJ. 1998. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Ward EM. Camann DE. Gilliom RJ). April 1995. et al. Feil VJ. Gillion. Sacramento. Circular 1291.epa. Furlong ET. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Alavanja MC. Curwin BD. Hladik ML. reservoirs and ground water in the Midwestern United States. EPA). J Expo Anal Environ Epidemiol 2005.39(17):6561-6574.S.S. et al. Available at URL: http://www. March 2006. and other herbicides in rivers. Comparative metabolism and elimination of acetanilide compounds by rat. Available at URL: http://www. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Shoemaker DA. Atlanta (GA). Dialkylquinonimines validated as in vivo metabolites of alachlor.pdf.15(6):500-508. Environ Health Perspect 2000. Barr DB. 2007. Deddens JA.html. Background document for development of WHO Guidelines for Drinking-water Quality. California. Environ Sci Technol 2005. Barr JR.usgs.248(2-3):123-133. acetochlor. Heederik D. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.

At low levels. Kohli et al.4..4. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Although 2. population from the National Health and Nutrition Examination Survey.4.4.5-T is eliminated mostly unchanged in the urine. it is not well absorbed through the skin. Mohammad and St.7...4. hypotension. renal and hepatic injury. Agent Orange). 2. but higher levels are herbicidal.5-T use as a herbicide in 1985. Given the commercial unavailability of 2.4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2..4.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. these herbicides can enhance plant growth. which may vary for some chemicals by year and by individual sample. dizziness.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.5-T.5-Trichlorophenoxyacetic acid (2.1.5-T in soil varies with conditions. Epidemiological studies have reported associations of several types of cancer. Once absorbed into the body. nausea. myotonia.4. the general population is unlikely to be exposed to it. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. abdominal pain.4.5-T (Holson et al. with an elimination half-life of approximately 19 hours (Arnold et al. 2007). Nelson et al.5-trichlorophenol and other degradates.g. Human health effects from 2. < LOD means less than the limit of detection. 1992. and concern about contamination with 2. Chlorophenoxy herbicides act as plant growth hormones. ranging from several weeks to many months. Omer.4.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. 2004). with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 1974).5-T has been rarely detected in ground waters (USGS. 1989.4. 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-T was once applied as either an aqueous salt or as an oil-soluble ester.4. The half-life of 2.Herbicides 2.3.. 93-76-5 General Information 2..5-T and 2.4.4.5-T degrades to 2. headache.5T is rapidly absorbed via oral and inhalation routes. 2. 2. 1992). and delayed neuropathy (Bradberry et al. 64 Fourth National Report on Human Exposure to Environmental Chemicals . 1986. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.2 and 0. Survey Geometric mean (95% conf.5-Trichlorophenoxyacetic Acid CAS No.4-D were used as defoliants in the Vietnam War (e.S.4. Ester forms of 2.

3. Pearce and McLean.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. U.5-T itself is not mutagenic. 2005). 2002.4.4. Biomonitoring studies on 2. IPCS.EPA. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.5-T than levels found in the general population. or to contaminants in the herbicide formulations (specifically 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. urinary levels of 2.4.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 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. 2003.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.gov/pesticides/.5-T does not mean that the level will result in an adverse health effect. other exposures. Additional information is available from U.5-T were generally below the limit of detection.4. Mean urinary levels of 2. Survey Geometric mean (95% conf. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. Finding a measurable amount of 2.EPA at: http://www.epa.S.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 2.4. 2005. IOM.S.4.S. 1980).4.4. 2. Urinary 2. in which urinary levels of 2. similar to results of NHANES II (19761980)..5-T reflect recent exposure. Biomonitoring Information Urinary levels of 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.4.7.5-T also were below the limit of detection (Kutz et al. population from the National Health and Nutrition Examination Survey.Herbicides or contaminated herbicides. 2004). 1992). 1996.

org/documents/jmpr/jmpmono/v96pr04. Sircar KP.S. Fundam Appl Toxicol 1992. 3/17/09 Institute of Medicine (IOM). 914. Pesticide industry sales and usage . Pearce N. Dichlorophenoxyacetic acid. Scand J Work Environ Health 2005. Nelson CJ. Review of 2. Agricultural exposures and non-Hodgkin’s lymphoma. Office of Prevention Pesticides and Toxic Substances. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Kutz FW.4. Available at URL: http://www. Veterans and Agent Orange: update 2002. Multireplicated dose-response studies with technical and analytical grades of 2. Murphy RS. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. discussion 5-7. Sheehan DM. Third National Report on Human Exposure to Environmental Chemicals. 2005.4. Gupta BN. Bradberry SM.19(2):298-306. Washington (DC): National Academies Press.edu/catalog. Behavioral and developmental effects in rats following in utero exposure to 2. S. Dhar MM.EPA. Crit Rev Toxicol 2002. Developmental toxicity of 2.32(4):233-257. U. Wolff GL. International Programme on Chemical Safety-INCHEM (IPCS).php?record_id=10603.pdf. Tandon JS. II.4-D/2.Herbicides References Arnold EK. Beasley VR. Arch Toxicol Suppl 1980. Holson JF.5-T).2000 and 2001 market estimates. Pesticides residues in food: 1996 evaluations Part II Toxicology.S. et al. LaBorde JB. Philbert MA. McLean D. Poisoning due to chlorophenoxy herbicides.4.4:318-21. Carter-Pokras OD. et al. 3/17/09 Kohli JD.nap. Arch Int Pharmacodyn Ther 1974. St Omer VE. Available at URL: http:// www. 2004. J Toxicol Environ Health 1992.5-T in four-way outcross mice.5-trichlorophenoxyacetic acid (2.4-D) epidemiology and toxicology. Proudfoot AT. Atlanta (GA).4. Cook BT. Board on Health Promotion and Disease Prevention. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .htm. Washington (DC): U.5-T). I. Erne K. Mohammad FK. Toxicol Rev 2004.4-. 210:250-255.5-trichlorophenoxy acetic acid in man. Vale JA.4. Estimation of occupational exposure to phenoxy acids (2.inchem. Available at URL: http:// www.23(2):65-73.31(2):121-125. Kolmodin-Hedman B. 2.4-dichlorophenoxyacetic acid (2.31 Suppl 1:1825.4. Garabrant DH. McCallum WF.4-D and 2. Vet Hum Toxicol 1989. Nelson CJ. May. Selected pesticide residues and metabolites in urine from a survey of the U.5-t mixture. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Developmental toxicity of 2. 2003. Brody D.19(2):286-297. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Neurobehav Toxicol Teratol 1986. Khanna RN. Gaines TB. Absorption and excretion of 2.37(2):277-91. Holson JF.4.5-T). Gaines TB. Fundam Appl Toxicol 1992.4.EPA).epa.5-trichlorophenoxyacetic acid (2.S. LaBorde JB.8(5):551-60. Environmental Protection Agency (U. Gaylor DW. general population. Centers for Disease Control and Prevention (CDC).

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

Carbamate Insecticides

Carbofuran

CAS No. 1563-66-2 General Information Carbofuranphenol is a metabolite of four different carbamate insecticides: benfuracarb; carbofuran; carbosulfan; and furathiocarb. Only carbofuran is registered in the U.S. Carbofuran is a broad spectrum, restricted-use insecticide and nematicide applied to a variety of field, fruit, and vegetable crops for control of beetles, borers, nematodes, weevils, and similar pests. Recently, registered uses of carbofuran were cancelled except for the following: field corn; potatoes; pumpkins; sunflowers; pine seedlings; and spinach grown for seed (U.S.EPA, 2009). About 1 million pounds have been used annually (U.S.EPA, 2007). Carbofuran is not registered for use in residential settings or food-handling establishments. In soils of varying composition, carbofuran has a half-life ranging from one to three months. It can leach into ground waters, but it has been detected only infrequently in either surface or ground waters (Gilliom, 2007; USGS, 2007). Carbofuran

is very highly toxic to fish and aquatic invertebrates, and it is highly toxic to birds where granular applications are used, but such applications have been restricted since 1991 (U.S.EPA, 2007). General population exposure can occur through consumption of food contaminated with carbofuran. Because estimated acute intakes from some dietary components in young children may exceed recommended intake limits, the U.S.EPA is in the process of revoking current regulations that allow carbofuran residues in food (U.S.EPA, 2009). Pesticide handlers and applicators are at greater risk for exposure and a number of incidents of systemic poisoning have been reported. After absorption, carbofuran is metabolized to phenolic metabolites and 3-hydroxycarbofuran, which are quickly eliminated in the urine. Human health effects from carbofuran at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Carbofuran was very highly acutely toxic in animal studies, causing effects related

Urinary Carbofuranphenol
Metabolite of Benfuracarb, Carbofuran, Carbosulfan, and Furathiocarb

Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th .770 (<LOD-1.30) < LOD size 1994 2530

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.450 (<LOD-2.20) < LOD .570 (<LOD-1.20) < LOD .840 (<LOD-1.50) < LOD

482 578 681 827 831 1125

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

.740 (<LOD-1.50) < LOD .840 (<LOD-1.50) < LOD

973 1190 1021 1340

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.590 (<LOD-2.00) < LOD < LOD < LOD < LOD < LOD

1.90 (<LOD-5.10) < LOD .550 (<LOD-1.60) < LOD .740 (<LOD-1.50) < LOD

696 680 521 696 603 953

Limit of detection (LOD, see Data Analysis section) for Survey years 99-00 and 01-02 are 0.4 and 0.4. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

to acetylcholinesterase enzyme inhibition. In contrast, carbofuranphenol is not an inhibitor of acetylcholinesterase enzymes. Carbofuran was not teratogenic, but high chronic doses in animals produced nonspecific developmental effects, such as reduced weight gain and pup survival (WHO, 2004). Testicular toxicity at subacute doses was reported in adult rats, rat pups, and dogs (Pant et al., 1995, 1997; WHO, 2004). Carbofuran was found not to be mutagenic or carcinogenic in animals (U.S.EPA, 2007). It is not rated by IARC with regard to human carcinogenicity. Additional information is available from U.S.EPA at: http:// www.epa.gov/pesticides/. Biomonitoring Information Urinary carbofuranphenol levels reflect recent exposure. The level of this metabolite in urine may reflect exposure to carbofuran or to carbofuranphenol as a degradation product in the environment or food. In representative subsamples from NHANES 1999-2000 and 2001-2002, most urinary levels of carbofuranphenol were below the limit of detection (CDC, 2005). In a nonrandom subsample from NHANES III (1988-1994), the 99th percentile level of carbofuranphenol

was 2.1µg/L (Hill et al., 1995). In a previous study of U.S. farmers and their families, carbofuranphenol was detected in 6.7% of urine samples (Shealy et al., 1997); the 95th percentile value in that study was 0.73 µg/L. Urinary levels of carbofuranphenol in two applicators were three and sixfold higher than the detection limit for the NHANES 2003-2004 subsample (Petropoulou et al., 2006). Finding a measurable amount of carbofuranphenol in urine does not mean that the level of carbofuranphenol causes an adverse health effect. Biomonitoring studies on levels of carbofuranphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of carbofuran or related carbamates than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Urinary Carbofuranphenol (creatinine corrected)
Metabolite of Benfuracarb, Carbofuran, Carbosulfan, and Furathiocarb

Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th .780 (<LOD-1.00) < LOD size 1994 2529

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.990 (<LOD-2.80) < LOD .480 (<LOD-.850) < LOD .880 (<LOD-1.06) < LOD

482 578 681 826 831 1125

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

.670 (<LOD-1.08) < LOD .880 (<LOD-1.13) < LOD

973 1190 1021 1339

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.780 (<LOD-1.94) < LOD < LOD < LOD < LOD < LOD

1.83 (<LOD-4.16) < LOD .700 (<LOD-1.08) < LOD .740 (<LOD-.930) < LOD

696 680 521 695 603 953

< LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

References Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). 2005. Gillion, R. Pesticides in U.S. streams and groundwater. Environ Sci Technol 2007;41:3409-3414. Available at URL: http://water. usgs.gov/nawqa/pnsp/pubs/files/051507.ESTfeature_gilliom. pdf. 4/9/09 Hill RH Jr, Head SL, Baker S, Gregg M, Shealy DB, Bailey SL, et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995;71(2):99-108. Pant N, Prasad AK, Srivastava SC, Shankar R, Srivastava SP. Effect of oral administration of carbofuran on male reproductive system of rat. Hum Exp Toxicol 1995;14(11):889-894. Pant N, Shankar R, Srivastava SP. In utero and lactational exposure of carbofuran to rats: effect on testes and sperm. Hum Exp Toxicol 1997;16(5):267-272. Petropoulou SS, Gikas E, Tsarbopoulos A, Siskos PA. Gas chromatographic-tandem mass spectrometric method for the quantitation of carbofuran, carbaryl and their main metabolites in applicators’ urine. J Chromatogr A 2006;1108(1):99-110. Shealy DB, Barr JR., Ashley DL, Patterson DG Jr, Camann DE, Bond AE. Correlation of environmental carbaryl measurements with serum and urinary 1-naphthol measurements in a farmer applicator and his family. Environ Health Perspect 1997;105:510513. U.S. Environmental Protection Agency (U.S.EPA) Carbofuran cancellation process. March 28, 2009. Available at URL: http:// www.epa.gov/pesticides/reregistration/carbofuran/carbofuran_ noic.htm. 4/10/09 U.S. Environmental Protection Agency (U.S.EPA). Reregistration Eligibility Decision for Carbofuran. September 2007. Available at URL: http://www.epa.gov/pesticides/reregistration/REDs/ carbofuran_red.pdf. 4/10/09 U.S. Geological Survey (USGS).The Quality of Our Nation’sWaters: Pesticides in the Nation’s Streams and Ground Water, 1992-2001. Circular 1291. Supplemental Technical Information (available on-line only). March 2006, revised February 15, 2007. Available at URL: http://water.usgs.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.php. 4/2/09 World Health Organization (WHO). Carbofuran in DrinkingWater. Background document for development of WHO Guidelines for Drinking-water Quality. 2004. Available at URL: http://www.who.int/water_sanitation_health/dwq/chemicals/ carbofuran.pdf. 4/9/09

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Carbamate Insecticides

Propoxur

CAS No. 114-26-1 General Information 2-Isopropoxyphenol is a metabolite of propoxur, a carbamate used to control ants, roaches, hornets, and similar pests in residential areas and around commercial food-handling establishments. Propoxur has also been used in pest strips and pet flea collars. Like several other pesticides, propoxur has been used outside the U.S. as a replacement for DDT in malaria vector control. Propoxur may remain in the environment for weeks to several months, longer than most carbamates (U.S.EPA, 1997b). Despite its mobility in soil and its potential for leaching into groundwater, propoxur has been rarely detected in U.S. surface or ground waters (Gilliom, 2007; USGS, 2007). Although propoxur is toxic to birds and aquatic life, ecologic exposures are unlikely due to current outdoor use restrictions. General population exposure to propoxur through the diet is likely to be limited because of usage restrictions (U.S. EPA, 1997a). Estimated human intakes have been below recommended intake limits (U.S.EPA, 1997b). Pesticide applicators are likely to have the highest exposures. Propoxur can be absorbed through the skin, lungs, and gastrointestinal tract. Propoxur does not accumulate in blood or tissues and is eliminated rapidly from the body (Leenheers et al., 1992; WHO, 2003). In animal and human studies, 2-isopropoxyphenol was one of several urine metabolites (U.S.EPA, 1997b). Human health effects from propoxur at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In animal studies, propoxur has moderate acute toxicity consisting of anticholinesterase effects (U.S.EPA, 1997b). 2-Isopropoxyphenol does not inhibit acetylcholinesterase enzymes. Propoxur is not considered mutagenic, embryotoxic, or teratogenic (WHO, 2003). U.S. EPA considers propoxur to be a probable human carcinogen, based on bladder tumors in male rats (U.S. EPA, 1997b). The human carcinogenic potential of propoxur has not been evaluated by IARC or NTP. Additional information is available from U.S.EPA at: http:// www.epa.gov/pesticides/. Biomonitoring Information Urinary 2-isopropoxyphenol levels reflect recent exposure. The level of this metabolite in urine may reflect exposure to propoxur or to 2-isopropoxyphenol as a degradation product in the environment or food (U.S.EPA, 1997b). In the U.S.

representative subsamples from NHANES 1999-2000 and 2001-2002, most 2-isopropoxyphenol levels in urine were below the limit of detection (CDC, 2005). In a nonrandom subsample from NHANES III (1988-1994), the 95th percentile level of 2-isopropoxyphenol was 1.7 µg/L (Hill et al., 1995). Higher urinary levels of 2-isopropoxyphenol have been measured in a few pesticide applicators, with a range of 45-306 µg/g creatinine (Hardt and Angerer, 1999). Finding a measurable amount of 2-isopropoxyphenol in urine does not mean that the level of 2-isopropoxyphenol causes an adverse health effect. Biomonitoring studies on levels of 2-isopropoxyphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of propoxur than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

456 574 655 820 806 1109

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

664 677 500 696 585 931

Limit of detection (LOD, see Data Analysis section) for Survey years 99-00 and 01-02 are 1.1 and 0.4. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

456 574 655 819 806 1109

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

664 677 500 695 585 931

< LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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Carbamate Insecticides

References Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). 2005. Gillion, R. Pesticides in U.S. streams and groundwater. Environ Sci Technol 2007;41:3409-3414. Available at URL: http://water. usgs.gov/nawqa/pnsp/pubs/files/051507.ESTfeature_gilliom. pdf. 4/9/09 Hardt J, Angerer J. Gas chromatographic method with massselective detection for the determination of 2-isopropoxyphenol in human urine. J Chromatogr B Biomed Sci Appl 1999;723(12):139-145. Hill RH Jr, Head SL, Baker S, Gregg M, Shealy DB, Bailey SL, et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995;71(2):99-108. Leenheers LH, van Breugel DC, Ravensberg JC, Meuling WJ, Jongen MJ. Determination of 2-isopropoxyphenol in urine by capillary gas chromatography and mass-selective detection. J Chromatogr 1992;578(2):189-194. U.S. Environmental Protection Agency (U.S.EPA). RED Facts. Propoxur. August 1997a. EPA 738 F-97-009. Available at URL: http://www.epa.gov/oppsrrd1/REDs/factsheets/2555fact.pdf. 4/9/09 U.S. Environmental Protection Agency (U.S.EPA). Reregistration Eligibility Decision (RED) Propoxur. August 1997b. EPA 738R-97-009. Available at URL: http://www.epa.gov/pesticides/ reregistration/REDs/2555red.pdf. 4/9/09 U.S. Geological Survey (USGS). The Quality of Our Nation’s Waters. Pesticides in the Nation’s Streams and Ground Water, 1992-2001. Circular 1291. Supplemental Technical Information (available on-line only). March 2006, revised February 15, 2007. Available at URL: http://water.usgs.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.php. 4/2/09 World Health Organization (WHO). WHO Specifications and Evaluations for Public Health Pesticides. Propoxur. FAO/WHO Evaluation Report 80/2003. 2003. Available at URL: http:// www.who.int/whopes/quality/en/propoxur_eval_spec_WHO_ October_2005.pdf. 4/9/09

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Organochlorine Pesticides
General Information Organochlorine pesticides, an older class of pesticides, are effective against a variety of insects. These chemicals were introduced in the 1940s, and many of their uses have been cancelled or restricted by the U.S. EPA because of their environmental persistence and potential adverse effects on wildlife and human health. Many organochlorines are no longer used widely in the U.S., but other countries continue to use them. Hexachlorobenzene has been used primarily as a fungicide or biocide. Organochlorine pesticides can enter the environment after pesticide applications, disposal of contaminated wastes into landfills, and releases from manufacturing plants that produce these chemicals. Some organochlorines are volatile, and some can adhere to soil or particles in the air. In aquatic systems, sediments adsorb organochlorines, which can then bioaccumulate in fish and other aquatic mammals. These chemicals are fat soluble, so they are found at higher concentrations in fatty foods. In the general population, diet is the main source of exposure, primarily through the ingestion of fatty foods such as dairy products and fish. Usage restrictions have been associated with a general decrease in serum organochlorine levels in the

U.S. population and other developed countries (Hagmar et al., 2006; Kutz et al., 1991). Contaminated drinking water and air are usually minor exposure sources. Infants can be exposed through breast milk, and the fetus can be exposed in utero via the placenta. Workers can be exposed to organochlorines in the manufacture, formulation, or application of these chemicals. The FDA, U.S. EPA, and OSHA have developed standards for allowable levels of certain organochlorines in foods, the environment, and the workplace, respectively. Attributing human health effects to specific organochlorine chemicals is difficult because exposure to multiple organochlorine chemicals occurs often and these chemicals may have similar actions. The table shows selected parent organochlorines and their metabolites that can be measured in serum or urine. Measurements of these chemicals can reflect either recent or cumulative exposures, or both. Some of the metabolites can be produced from more than one pesticide. The level of a metabolite in a person’s blood or urine may indicate exposure to the parent pesticide as well as to the metabolite itself.

Organochlorine Pesticides and Metabolites in this Report
Organochlorine Pesticide (CAS number) Serum pesticide or metabolite(s) (CAS number) Urinary pesticide or metabolite(s) (CAS number)

Aldrin (309-00-02) Chlordane (12789-03-6)

Aldrin (309-00-02) Dieldrin (60-57-1) Oxychlordane (27304-13-8) trans-Nonachlor (3734-49-4) p,p’-DDT (50-29-3) p,p’-DDE (72-55-9) o,p’-DDT (789-02-6) Dieldrin (60-57-1) Endrin (72-20-8) Heptachlor epoxide (1024-57-3) Hexachlorobenzene (118-74-1) Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4) Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4)

Dichlorodiphenyltrichloroethanes Dieldrin (60-57-1) Endrin (72-20-8) Heptachlor (76-44-8) Hexachlorobenzene (118-74-1)

Hexachlorocyclohexanes Mirex (2385-85-5) 2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)

beta-Hexachlorocyclohexane (319-85-7) gamma-Hexachlorocyclohexane (58-89-9) Mirex (2385-85-5)

2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)

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Organochlorine Pesticides

References Hagmar L, Wallin E, Vessby B, Jonsson BA, Bergman A, Rylander L. Intra-individual variations and time trends 1991-2001 in human serum levels of PCB, DDE and hexachlorobenzene. Chemosphere 2006;64(9):507-513. Kutz FW, Wood PH, Bottimore DP. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rev Environ Contam Toxicol 1991;120:1-82.

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

but dieldrin has been detected in meats, dairy products, and in crops grown in soils that have been contaminated, usually by application, manufacturing, or disposal. General population exposure to these chemicals occurs through the diet, and detection of dieldrin residue in foods has decreased over time (FDA, 2008). Inhalation exposure may occur among people living in residences where aldrin was applied historically as a pesticide. Aldrin and dieldrin are absorbed following ingestion, inhalation, and dermal application. After absorption, aldrin is metabolized to dieldrin so rapidly that aldrin is rarely detected. Dieldrin accumulates in fatty tissues, and its metabolites are excreted in bile and feces (ATSDR, 2002). It is also excreted in breast milk and can cross the placenta. The elimination half-life of dieldrin is approximately 1 year (IPCS, 1989; Jorgenson 2001). Human health effects from aldrin and dieldrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses, aldrin and dieldrin block inhibitory neurotransmitters in the central nervous system (Narahashi et al., 1992). This blocking action can cause abnormal excitation of the brain, leading to symptoms such as headache, confusion, muscle

Dieldrin

CAS No. 60-57-1 Also a Metabolite of Aldrin General Information Aldrin and dieldrin are no longer produced or used in the U.S. From the 1950s to 1970, both chemicals were applied mainly as a soil insecticide or seed dressing for food and commodity crops. Dieldrin was also used for mothproofing clothes and carpets. In tropical countries, dieldrin was used as a residual spray in residential dwellings to control vectorborne diseases such as malaria. The U.S. EPA cancelled agricultural uses of both pesticides in 1970; termiticide uses were cancelled in 1987. Aldrin is readily converted to dieldrin in the environment and in plants that take up the chemical. Aldrin volatilizes after agricultural soil applications or is converted to dieldrin, which volatilizes more slowly. These chemicals persist in the environment and bioaccumulate in foods (Jorgenson 2001; USGS, 2007). Aldrin is rarely detected in plants or animal tissues,

Serum Aldrin (lipid adjusted)
Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

559 456 512 485 1045 881

Limit of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 5.94 and 7.8. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

77

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

1-24.6) 19.110) .7-22.242) . 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.2) 15.8 (18.147) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .8) 14.130) .138) .062 (.7-19.077 (.110) .100 (.117) < LOD . < LOD means less than the limit of detection.100) .058) < LOD .130) .4) 95th 20.8-24.160 (.4 (12.9-23.4-17.112-. which may vary for some chemicals by year and by individual sample.170) .112) 95th .130 (.120-. 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 9.062-.1) 20.077-.1-19.048 (<LOD-.108-.6 (15.054-.090-. Survey years 01-02 03-04 Geometric mean (95% conf.090-. Fourth National Report on Human Exposure to Environmental Chemicals 79 .059 (.50 (8.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .5) 19. see Data Analysis section) for survey years 01-02 and 03-04 are 10.064 (.0 (10.130) .3 (19.054-.40-10.064) 90th .096-.110-.084-.S.124) .0-25.8 (9.149) .054-.9-22.8 (11.138 (.180) .2) 12.160 (.6-24.088-.160) .6-24.8) 15.8-17.120) . population from the National Health and Nutrition Examination Survey.9 (13.056-. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1-18.103 (.090 (<LOD-.075) < LOD .1 (18.5-15.053 (<LOD-.0-21.4) 20.1) 13.0 (15.80-10.5) 15.80 (<LOD-10.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 (15.110 (.3 (18.60-10. which may vary for some chemicals by year and by individual sample.6-33. Survey years 01-02 03-04 Geometric mean (95% conf.4) 14.120 (.5) 21.0 (11.8-25.8-19.9 (12.090 (.130-.8.1-16.110 (.4) 21.40-9.060) .9 (14.1) 14.103 (.6 (14.3 (18.120 (.101) .S.1) 15.2-15.0 (10.098 (.0) < LOD 9.089 (.139 (.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .3 (13.4) 539 456 484 487 980 885 Limits of detection (LOD.190) .2) 11.100-.150 (.070-.150 (.80-9.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.140 (.7 (<LOD-15.1) 10.080) .147 (.0) 21.080-.1) 15.4-18.5-17.102 (.069) < LOD < LOD .055 (.5 (16.113 (.139 (.50) 15.080 (.109-.6) 16.4) 19.0) 19.9 (13.00-14.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.5 and 7.10 (<LOD-16.1 (13.9 (12.1) < LOD 9.4) < LOD < LOD 16.070) .7 (14.00 (8.120 (.093) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190) .049-.70 (7.3 (14.109 (.086-.100) .090-. 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 .3-21.5-17.130-.109-.8) < LOD 8.6 (15.6) 9.4 (12.073-.2) 14.30 (8.4) 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 8.8-17.116) .5 (<LOD-11.062 (.7) 15.140) .180) .90) 90th 15.063-.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.30 (8.083-.100-.140-.100-.070 (<LOD-.110 (.9-38.130-.158) .

4/21/09 Bates MN. 4/21/09 Hoyer AP. Demographic and seasonal influences on human serum pesticide residue levels. 4/21/09 Jorgenson JL.gov/toxprofiles/ tp1. Aldrin and Dieldrin [online].103(Suppl 7):113-122. Available at URL: http://www.inchem. Tully DB. PA. Corrigan FM. Environ Health Perspect 2001. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. 2007 [online]. 1991. Serrano FO.gov/ circ/2005/1291/. Jorgensen T. Exp Neurol 1998. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Carlson JN. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. United States Geological Survey (USGS). Grandjean P. Kanthasamy AG.cfsan. References Agency for Toxic Substances and Disease Registry (ATSDR). Anantharam V. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.14:95-102. David VL. 1989. Shore RF. McIntosh LJ. Jr and Laws ER. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Cox. Organochlorine exposure and risk of breast cancer. 731-915. Sanchez-Ramos J.66(4):229-234. Garrett N. pp. Jr. August 2008. Patterson DG Jr. Chemosphere 2004. Environ Health Perspect 1995.gov/~dms/ pesrpts.atsdr. Priestly BG. Facca A. Kanthasamy A.usgs.9:1357-1367.109(Supp1):113-139. Lancet 1998. Available at URL: http://www. Six high-priority organochlorine pesticides.fda. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Narahashi T. Pesticides in the Nation’s Stream and Ground Water. September 2002. Inc. Stehr-Green. Neurotoxicol 2005. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Mann D. Part A 2000. plasma dieldrin. Grajewski B. Andersen A.64-65 Spec. Schulte P. Ginsburg KS. 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. VT. Effect of occupational exposure to aldrin on urinary D-glucaric acid. and epidemiology in the United States. New York. Finley B. Rosellini RA. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. et al. Soto AM. Hartvig HB. Reprod Toxicol 2000. Song S. are nonestrogenic in transfected HeLa cells. International Programme on Chemical Safety (IPCS). Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Wienburg CL. Olea N.150:263-271. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. 2 Classes of Pesticides. Needham LL. No:429-436. Eds. Environmental Health Criteria 91. Li AA. 1992-2001. Brock JW. 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. 15.26:701-719. Psychopharmacology (Berl) 1987.54:1431-1443. Toxicol Lett 1992. Chung KL. bioaccumulation. Buckland SJ. J Toxicol Environ Health 1989. Toxicological profile for aldrin/dieldrin [online]. Daniel SE. Int Arch Occup Environ Health 1994.org/documents/ehc/ ehc/ehc91.html. 6/1/09 Ward EM. Handbook of Pesticide Toxicology. Teta MJ.cdc. Basit A. toxicology. et al. Vol. Kitzazwa M. J Toxicol Environ Health.html. Smith AG. Available at URL: http://www. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Roy ML. Patterson DG Jr. Sonnenschein C. Academic Press. and lymphocyte sister chromatid exchange. Food and Drug Administration (FDA). Fernandez MG. Revised Feb. Ellis H. Available at URL: http://pubs. Edwards JW. J Occup Environ Med 2005. Turner W.27:405-421. Cancer Epidemiol Biomarkers Prev 2000.htm. In Hayes WJ. Chlorinated Hydrocarbon Insecticides. Chapin RE.59:229-234.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Organochlorine insecticides in substantia nigra in Parkinson’s disease. Mumtaz MM. Frey JM. Mink PJ.47:1059-1087.352:1816-1820. either singly or in combination.91(1):122-126.

interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.7) 19.5 (31.3-45. see Data Analysis section) for Survey years 99-00.2) 33.9) 13.9) 37.8) 18.5-13.4-21.4 (30.1) 16.4) 37.5-47.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.5-32.9 (11.0-61.4) 22.7 (34.6 (9.8) 52.7) 35.3-24.4-40.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.7 (43.3 (27.2-49.8-43.2) 34.0) 27. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8. Since 1992.8-61.5) 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. 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.0-33.4 (35.0-13.8) 53.8-33.8-73.9 (31.8 (17.2 (9.7) 42.5.8-32.9-40.0-12.3) 18.30-11.9 (26.37 (8.74 (<LOD-10. Fourth National Report on Human Exposure to Environmental Chemicals 81 .6) 39.7-14.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11. 01-02.3) 18. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.8 (17.7 (42.5-43.4) < LOD 11.7-56.70 (<LOD-10.7 (32. which may vary for some chemicals by year and by individual sample.8 (40.5) 9. Chlordane is not currently produced or used in the U.4 (10.8 (10.9) 23. chlordane was used to kill termites and other insects on agricultural crops.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (33.10 (8.5 (34.1-65.1-50. Consequently. population from the National Health and Nutrition Examination Survey.7 (<LOD-32.9) 39.1 (25.9) 36.7 (19.5-65.7) 31. and in soil.1 (40.5) < LOD < LOD < LOD < LOD 13.1-25. buildings.5) 10.0-18.0 (32. and 03-04 are 14.7) 28.4) 39. from the early 1950’s until the mid-1980’s.5-38.36-11.3) 10.5 (41. Technical grade chlordane had contained 7% trans-nonachlor.6-45.8 (42.7-12.3-43.2-28.1-19.6) < LOD 11.9-42.9-21.20-10. heptachlor use has been limited to treatment of fire ants near power transformers.6-12.0 (20.4) < LOD < LOD < LOD 23. < LOD means less than the limit of detection. and 7.7 (17.3 (28. fish.4 (22.2 (36.6-24.Organochlorine Pesticides Chlordane CAS No.1 (15.2) 46.7-39.8) 52.9) 47.4 (<LOD-12.69-10.3-45.1-25.3) 37.5) 37.10-18.1) 22.2 (10. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.2 (37.0 (37.1) * 11.3-49.6) 36. the technical grade product of each chemical contains 10%-20% of the other chemical. As a result of the manufacturing process.6) 11.1 (<LOD-12.8-23.1-51.1 (44.1 (20.89-10.4) 12.1 (<LOD-12. 2007).2-49.7 (10.1 (16.5-41.6) 49.6) 20. lawns.7 (34.3) 41.2) 36.4) 29.6) 9.7) 19.2) < LOD 11.0 (16.9 (11.8-31.2-21. 2007).9 (15.4 (30.1) * 11.8 (18.5) 38.3 (20.6 (16.0 (26. foods high in fat such as meat.2) 37.7-25. 1994).5-42.9) 23.5) 56. Survey Geometric mean (95% conf.3 (25.9 (15. 1994.3 (9.90 (8.9-21. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.5-40.2-56.9 (21.9-38.6) 48.S.2 (41.S.5) 44.0 (<LOD-12.6 (25.0-67.8-20.5) 21.9 (17.5 (8.8) 27.1) 30.4-45. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.4) 18.9) 10. 57-74-9 Heptachlor CAS No.7 (<LOD-13.1) < LOD < LOD < LOD < LOD < LOD 8. 10.3 (<LOD-19.63 (8.6) 9.5-44.3 (11.2) < LOD 11.9) 11.8) 44.S.0-25.5) < LOD < LOD 9.6-18.6-24.20-11.3) 10.0) 31.6-53.9 (26.9 (18.5 (<LOD-12.2-26.1 (<LOD-12.9 (36.7-70.0) 20..2 (21.5.1 (11.4-51.9) 17. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.6 (43.2 (39.9) 31.2) 22. Until 1988.0) 41. in addition to trace amounts of numerous other related compounds (ATSDR.7) 9.6) 8.2 (28.1) 90th 34.8-33.3-32.9) 11.8 (10.4 (31.20 (<LOD-11.1 (27.2) * 12.9 (29.6 (9.1) 30.6) 23.6) 48. and dairy products are the usual sources of exposure to these chemicals in the general population.0) 21.1-15.3 (26.1 (17. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.0) 75th 20.4-14.8-42.10-11. respectively.0) 37.3 (21.82-11.

320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .130 (.080) .090-.048-.100 (<LOD-.280-.100-.056 (.430) . 1986). heptachlor.380) .200-.430) .060 (<LOD-.240-.203-.227) < LOD .250 (.310) .310 (.373) .150 (.047 (<LOD-.130-.170) .130-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .100 (.073) < LOD < LOD < LOD < LOD .180) .077) . Acute.290-.440) .066-.560) .240-.400) .082 (.057-. and the U.133) 90th . to heptachlor. In laboratory animal studies.331) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .189-.320 (.340) .070 (.199-. which is also persistent in the body (ATSDR.090) .068-.120-.230-.140 (. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility. interval) Selected percentiles ( 95% confidence interval) Sample 95th . The U. and heptachlor epoxide in foods and bottled water.070) .062) < LOD .150 (.450) .170) .190-.073 (. Shindell and Ulrich.207 (.225 (.068) .245-.280-.230 (.069 (<LOD-.083 (.320) .100-...330 (.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.104-.350) .270 (.083) .410) .270 (.200 (.130-.063) .119 (.290-.300) . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.170) .140 (. Chlordane and heptachlor are absorbed after oral.189 (.170-.280 (.067 (. FDA established allowable residues of chlordane.149 (.130) .076) < LOD .190-.260 (.140) .148) .370 (.115 (.370 (.180) . and inhalation exposure.207) .300) .220-.074-.246-.310) . population from the National Health and Nutrition Examination Survey.300-.230-.063 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.260-.210 (. and alterations in immune function of offspring.079) .200-.180-. and breast milk is a major excretion route in lactating women.070 (<LOD-. 2006).210-. 1981).104) .160) .077) .110 (<LOD-.063 (.223) . EPA has established environmental criteria for chlordane and heptachlor.050-.290-.140-.087-.280 (. which may vary for some chemicals by year and by individual sample.230-.049 (<LOD-.242-.066 (<LOD-.126 (.208 (.053-.130 (.066-.S.050 (<LOD-.240 (.370 (. Le Marchand et al.S. 2007).280) .063 (.510) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.240) .070) < LOD < LOD < LOD < LOD < LOD .080 (.168-.150) .Organochlorine Pesticides (Dallaire et al.320 (.253-.286 (.140 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.058-.340) .063) * .077) .300) .213) * .310) .120 (. chronic doses of heptachlor have produced liver enlargement and injury.271 (.068) 75th .. dermal. neonatal mortality.190-.070-.091) .130) . Elimination of all these chemicals from the body occurs over months to years.290) . OSHA has established occupational exposure criteria.250-.115-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.148-.120-. 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.165-.231) .130 (.400) .150-.136) .230 (.160 (.S.130-.070-.315 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. IARC. Takahashi et al.320) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.106-.128 (. 1991.058-.. Rogan. 1986).160) . 1977b.170) .286 (.220-.071 (.300) .160) .090) .290 (.170) .280-.066 (.350 (.070 (<LOD-.287) .250 (.110-. 1996.269 (.064) < LOD .070 (<LOD-.108-.310-.112 (.057 (. 2001.180-.140 (.063-.065-.126) . characterized by seizures and paralysis.260 (.230) .120-.140-.220 (.258-.348) .077) .320 (.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. Smith.055-.079) < LOD < LOD < LOD .270 (.146) .300 (.092) .150 (.350 (.080 (. 2007. 1977a.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * . 82 Fourth National Report on Human Exposure to Environmental Chemicals .210 (.146) < LOD < LOD .057) * . Chlordane is metabolized primarily to oxychlordane and to a lesser extent. The major metabolite of heptachlor is heptachlor epoxide.080) .320 (. 2002.063 (.053-.130-.260 (. Survey Geometric mean (95% conf.216-.075 (.070 (<LOD-.204 (.290) .061-.360) .258 (.058 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.302) .080) .070-. 1991).450) .

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

6-21.2-17.9-29.9) * * * 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. see Data Analysis section) for Survey years 99-00. and 7.9) 15.20 (<LOD-9.3 (<LOD-25.8) 13.6 (16. < LOD means less than the limit of detection.4) 21.5 (11.8 (13.3) 18.S. and 03-04 are 14.4 (15.4 (<LOD-19.8 (15.8) 15. 01-02.8-46.1 (19. which may vary for some chemicals by year and by individual sample.2) 15.8-24.8-24.6 (<LOD-27.7-18.2-16.0-16.1) 20.2 (<LOD-25.8) 16.9 (12.6) 13.5 (11. Survey Geometric mean (95% conf.1-15.6) 14. 10.1-16.8) 13.3) 23.9 (15.6 (11.3-18.3) 18.6 (12.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.1-38.5 (18.2 (<LOD-16.8 (<LOD-23.8) 20.2) 20.7-19.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.7 (16.4 (11.1-29.3 (13.0-19.1) 13.8) 21.5) < LOD 14.8) 14.9-25.4) 18.9-16.2-27.8) 19.0 (11.6 (13.4 (11.4 (<LOD-54.6) < LOD < LOD < LOD 27.0) 13.0-17.8.6 (8.10-13.6 (14.2-27.90 (<LOD-9.40) 15.50) < LOD < LOD < LOD 17. 84 Fourth National Report on Human Exposure to Environmental Chemicals .1 (16.3) 18.6) 22.5) 19. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.5 (<LOD-21.0) 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 13.3) 10.6-17.8-23.0 (15.9-23.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) 19.5. population from the National Health and Nutrition Examination Survey.3) 27.6 (16.5 (<LOD-32.3) 16.8) 14.9-29.1) 23.8 (18.7 (10.0-54.2) 26.2 (18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 (<LOD-62.0-17.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7-25.6.5 (10.3) 22.8 (13. respectively.7 (13.8-24.2) 13.8 (18.

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

9 (47.6 (56.9) < LOD < LOD < LOD 20. and 7.4 (30. 10.0-24.1) 32.3-50.6-20.9 (<LOD-14.5-69.6) 56.2) < LOD 10.9-65.3 (14.2) 59. and 03-04 are 14.4 (11.9 (51.5) 19.4-67.6) 60.2-88.8 (45.7) 17.2-18.10 (<LOD-11.5-17.4 (67.1-51.8 (11.0 (16.8 (16.9 (15.5-20.7 (16.5-95.1-34.4 (16.0-93.0-20.1 (48.1) 17.5) 14.3) 32.7-17.9-64.8 (42.7-18.3-86.5 (13.5-111) 68.4) 48.7) 78.4-23.5) 36.8-129) 74.8-41.5) 30.9-40.7-29.4 (28.7-35.2) 20.2 (25.8-21.7 (11.7-113) 68.8 (71.8) 80.5 (15.3 (49.0) 33.7) 52.6 (32.0 (19.7 (74.8 (49.7-23. population from the National Health and Nutrition Examination Survey.3-39.8-67.7 (28.8 (17.7 (59.7 (59.9) 51.6) 56.4) 16.4 (12.3) 36.5) 90th 55.9-22.2 (19.2-21.0-22.0-113) 68.2 (59.6 (56.9-69.3) 32.7) 56.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.2 (60. 86 Fourth National Report on Human Exposure to Environmental Chemicals .4) 19.0 (14.1) 14.7-34.9) 14.5) 48.1 (65.7-22.3-30.3 (56.9-35.3 (17.8-90.1-20.1) 78.0 (60.7-32.1 (22.8 (30.9-45. 01-02.2 (27.0 (13.4) 55.9-36.8 (28.0-143) 112 (68.8 (15.6 (<LOD-14.3) 16.1-55.5-36.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.5 (44.2 (14.1) 31.6 (15.1-18.5 (25.70 (<LOD-12.0) 13.5) 26.6) 25.7) 73.6) 10.2 (7.5) 14.2) 39.5) 78.8 (<LOD-20.8 (26.6 (12.6 (50.6) 34.8 (13.0 (29.7) 59.3 (58.3) 15.6-66.0-123) 74.1) 17.7-21.4) 107 (84.1) 16.0) 40.0 (62.8 (13.7) 78.0-38.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.0) 18.5) 77.5.9-65.9 (19.1-22.4-52.1-16.7-160) 86.7-20.0 (42.8-77.0-23.9-20.3 (16.2 (36.2-37.5) 35.4) 59.3) 18.9-58.8 (28.6-88.9 (15.1) 62.6-54.8 (28.8) 51.2) 19.0-93.1-34.7) 28.1) 18.9 (16.9) 14.9 (36.7 (30.8-19.0 (42.1) 17.9) 51.8 (19.2 (14. < LOD means less than the limit of detection.1 (41.3-57.3-32.1 (17.0) 49.3-74.8-90.0 (15.7 (35.1) 17.0) 19.7) 15.6) 84.0 (13.5 (15.9-89.1) 17.4) 20.1-16.3) 18.6 (52. respectively.2-23.3) 25.3) 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. interval) 18.8-16.2 (26.1) 17.6-19.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. Survey Geometric mean (95% conf.9 (66.8.0) 75th 31.8 (26.5-87.6 (16.5-19. which may vary for some chemicals by year and by individual sample.0 (16.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.5) 22.1) 78.3 (14.3) 19.1) 18.2 (15.7 (13.4-22.7) 14.8 (26.4-62.7-38.3) 30.3-21.6) 82.0-68.3) 30.0-37.0-23.7-77.7) 35.5) 9.1-126) 67.9 (51.3 (45. see Data Analysis section) for Survey years 99-00.8-110) 59.8) 47.1 (10.6 (57.6-22.2 (64.9 (28.0-59.5.2-16.8-79.1) 30.0 (48.4 (45.5) 20.1) 17.0) < LOD < LOD 8.6) 13.S.2-18.8) 19.7 (18.6-82.9 (29.3-58.6) 54.1-28.1 (47.2-17.5 (45.8-19.2) 34.2) 30.4-35.86-13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (12.4-36.0 (15.2) 17.8-16.4-18.

510 (.270-.210) .280) .110 (.210-.580 (.090-.130 (.084-.630) .580 (.060 (<LOD-.061-.120 (.113) < LOD .240 (.150) .680 (.684) .330 (.288-.590) .360-.390 (.288 (.260) .565) .630) .128 (.630) .330-.190-.430-.069-.116-.310-.390 (.210 (.093-.090 (<LOD-.116) .100-.106 (.690) .690) .520) .830) .367) .240) .460-.041 (<LOD-.177-.340-.120-.285-.343 (.390) .091) . population from the National Health and Nutrition Examination Survey.559) .110 (.324 (.237) .320-.220 (.124) .279-.129) .490 (.191 (.170 (.062 (.092 (.380 (.600 (. which may vary for some chemicals by year and by individual sample.327 (.410-.580 (.054-.190-.210) .458 (.150) .098-.300) .060) .260) .090-.210 (.085-.130) .340) .301-.090-.220 (.470-.460) .090 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .140) .370 (.130) .092 (.120-.590 (.100-.110 (.320-.350-.093) .310-.125 (.100 (.397-.240) .116 (.232) .220) .20) .520 (.490) .310) .094 (.450) .103 (.190-.110 (.100 (.108 (.409-.130) .158-.590 (.640 (.400 (.096) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190-.090-.120) . interval) .068-.119) < LOD < LOD < LOD .186-.600) .350 (.417 (.500) .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.160 (.055 (<LOD-.080-.141) .112 (.510-.141) .122) .087 (.520 (.108) .405) .100-.106 (.237) .210) .390 (.330-.126) .317 (.461 (.S.078 (.651) .080) .098 (.081-.220 (.410-1.114) .286-.310-.060-.497-.090) .096-.161) .130) .202 (.171-.180-.440) .300-.290-.091-.400-.594) . Survey Geometric mean (95% conf.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .180-.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. Fourth National Report on Human Exposure to Environmental Chemicals 87 .120) .080 (.250) .220 (.173-.081 (.800) .180-.119) Selected percentiles ( 95% confidence interval) Sample 95th .109 (.130) .220 (.071 (<LOD-.069) .470 (.470 (.098) .134) .183 (.395) .111 (.205 (.120) .080-.220 (.109 (.122) .106 (.440-.070 (.105 (.120 (.047-.145-.430-.104-.125) .104 (.490-.110) .340-.240) .390) .100-.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 .234) .760 (.079-.390-.395-.830) .095-.960) .370 (.310-.120-.130 (.210-.082) .550 (.240-.460) .250) .127) < LOD < LOD .490 (.400) .085-.220 (.840) .135 (.355 (.470 (.250) .400-.131) .130) .470-.390 (.161-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .130) .099-.117) .120 (.371) .090-.420) .480) .093-.103 (.242) .680) .160-.099-.111-.190-.360-.080-.110-.930) .120) .210 (.540) .400 (.096-.186 (.098 (.085-.430-.420 (.112 (.108) 75th .078-.080-.272-.089 (.220 (.110 (.230 (.113) .090-.110 (.093-.211) 90th .190-.414 (.079-.310 (.097) .573 (.

Royce W. 4/21/09 James RA.9:1-109. Covaci A. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.150:981-990. Poland.gov/toxprofiles/tp31.atsdr. Available at URL: http://www.372:20-31. Willman E. Arch Environ Health.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Available at URL: http://www. Dendle WH. Available at URL: http://www. Jaraczewska K. 1994-1997 organochlorine compounds. Bleiweiss IJ. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Brower S. Dewailly E. Available at URL: http://www. et al. Smith AG. Wohlleb JC. Academic Press. Voorspoels S. A Report to the Hawaii Heptachlor Research and Education Foundation.110:617-624. Baker DB. Available at URL: http://ntp. et al.htm. gov/toxprofiles/tp12. Takahashi W.110(8):835-838. Saidein D. Chlorinated Hydrocarbon Insecticides. Keller JA. Vol. 6/1/09 Rogan WJ. Odland JO. Canada). Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Ayotte P. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). JAMA 1988. Environ Health Perspect 2003. 1993. Barker J. Available at URL: http://www. Vol. Muckle G. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. 79. 1991 pp. 9/25/07 International Programme in Chemical Safety (IPCS).50(3):108-118. Lawrence River (Quebec.htm. 1963-1967.inchem. Arch Pediatr Adolesc Med 1996. maternal serum and milk from Wielkopolska region. Available at URL: http://ntp. Jr. Bjerselius R.8:1-123. Laliberte C. Bull Environ Contam Toxicol 1981:27:506-511.259(3):374-377. Handbook of Pesticide Toxicology. Darnerud PO. Mortality of workers employed in the manufacture of chlordane: an update. et al. Dewailly E. Concise International Chemical Assessment Document 70 Heptachlor [online].niehs.atsdr. Environ Res 2000.org/documents/iarc/ vol79/79-12.pdf. May 1994. Takei G. 4/21/09 Dallaire F.inchem. 2001. J Occup Med 1986. Shindell S and Ulrich S. Hawaii Med J 1991. International Agency for Research on Cancer (IARC). Granath F. In Hayes WJ. Eds. Organochlorines in Swedish women: determinants of serum concentrations. KalubaSkotarczak A.84:151-161. Organochlorine exposures and breast cancer risk in New York City women. Hansen JC. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. 1979-1980. Van Oostdam JC. 2006. Circumpolar maternal blood contaminant survey.gov/ntp/ htdocs/LT_rpts/tr009. Senie R. Head SL. Glynn AW. Inc. Toxicological profile for heptachlor and heptachlor epoxide [online]. 1986.111:349355. Organochloride pesticide residues in human milk in Hawaii. Kolonel LN. International Agency for Research on Cancer (IARC) . Gilman A.41:145–148. Tartter P. 4/21/09 Baker DB. Bioassay of heptachlor for possible carcinogenicity. 731-915. August 2007.heptachlor. Bioassay of chlordane for possible carcinogenicity.nih.Summaries & Evaluations. Wolff MS. Chlordane and heptachlor [online]. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. LeMarchand L. Environ Health Perspect 2002.org/site/foundation/ research/projects2. Loo S. New York. Charles MJ. Siegel BZ.cdc. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Aune M. National Toxicology Program (NTP). Berkowitz GS. et al.28:497501.org/ documents/cicads/cicads/cicad70.html. Lulek J. Jr and Laws ER. Natl Cancer Inst Carcinog Tech Rep Ser 1977b.cdc. Hertz-Picciotto I. Chashchin V.html.pdf.html.niehs. Environ Health Perspect 2002. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Atuma S. Distribution of polychlorinated biphenyls.nih. Sci Total Environ 2004. 6/1/09 National Toxicology Program (NTP). Drews K. 2 Classes of Pesticides. Wong L. Toxicological profile for chlordane [online].gov/ntp/ htdocs/LT_rpts/tr008. Sci Tot Environ 2006.330:55-70. Stehr-Green P. Pollutants in breast milk.

1991).0-155) 83.7 (15. Food imported from countries that still use DDT may contain the chemical or its residues.8.6 (22. These chemicals are highly persistent in soil. and 03-04 are 20.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. In the general U. Smith.90 (<LOD-12.0) 40.7.9 (21.9 (<LOD-20.1’-(2.0 (21.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.0-35. food. or dermal exposure.8) 36.5 (14.5) 23.p’-DDT (15%-21%).1-71. Only a small proportion of DDT is metabolized and excreted (Smith.0-53.8-26. It was produced and used in the U.S. inhalation.3 (<LOD-21.2) 155 (59.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.5) < LOD < LOD 9.9) 17. air. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. Fourth National Report on Human Exposure to Environmental Chemicals 89 .7) < LOD 18.2 (<LOD-40.8) 15. p.1 (23. which may vary for some chemicals by year and by individual sample.9-28.1) 31.2) 30. In the body.00 (<LOD-10.3 (<LOD-31. see Data Analysis section) for Survey years 99-00.2) < LOD < LOD 9.S. particularly for endemic vector and malaria control. fish.7-16. sediments.5 (23. and dairy products.5-36.4) < LOD 17.0 (18. 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.3-236) 24.0-27.0-15.8) 30.0 (10.2-bis(p-chlorophenyl) ethane (DDD).6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 7.10-13.3) 28. depending on conditions.9 (10.1-27.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.1 (<LOD-39. population.6 (9.4.6 (25.7) 12.3) 22. particularly meat.0-37.50-11. o.4) < LOD < LOD < LOD 61.0) 26. and water.9 (10.S.0) 19. DDT and DDE can cross the placenta. 1988). resulting in fetal exposure. 2002.9-34.5-54.1 (33.3 (27. as well as in plant and animal tissues. DDT can be absorbed after ingestion. although DDT and DDE intakes have decreased over time (FDA. DDT is converted to DDE and several other metabolites.1’-dichloro-(2.3) 21. after World War II until 1972.9 (10.7) 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) 25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (<LOD-12. DDT usually refers to the technical product.6-33. continues to be the primary source of DDT exposure. respectively. when virtually all use of it was banned. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.9) 14.6 (<LOD-25. The biodegradation half-life of DDT in soil varies from 2 to 15 years.9) 29. 2008.8) 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 8.3) 21. including 1. It is still used in some countries. 01-02.3-590) 293 (104-541) 48. 17. population from the National Health and Nutrition Examination Survey.8-17. which is a mixture containing p. Gunderson.8-23. DDT is converted in the environment to other more stable chemical forms.2-65. Both Serum p.p’-DDD (4% or less).0) 20.9) < LOD < LOD 9.7 (19. DDT was used at one time as a treatment for head and body lice. 1991).3-16.p’-DDT (65%-80%).2 (11.1) 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 12.6 (31.2-95.4 (23.5 (15. and trace amounts of several related compounds.5 (23.0 (18.70 (8. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.8-39.

2004. and altered behavior after neonatal exposure (Eriksson and Talts.180) .627) . and duration of lactation.400 (.051 (<LOD-. 2006.079) < LOD < LOD .097) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00) .071 (.260) .190 (. Beard.Organochlorine Pesticides chemicals are excreted in breast milk. 2000. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.240 (.250 (.106) < LOD < LOD . Calle et al. premature delivery.170) .087 (.420) . 2002.150-.230) .143) < LOD < LOD . 2001). resulting in exposure to nursing infants (Rogan. population from the National Health and Nutrition Examination Survey.. 2006).074-.170 (.061) < LOD < LOD < LOD .p’-DDE can produce anti-androgenic effects (Gray et al.220) . 1997). 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.065-.. Gladen and Rogan. reproductive organ abnormalities... A workplace standard for DDT has been established by Serum p.114-.530) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .290) .400) . lung cancer.069) . It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 1998). 2001).130-. Studies of DDT exposure and pancreatic cancer.063 (<LOD-.190 (.. 1995.059-.201 (.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.62 (.p’-DDD and p.075) 1.570-4.220) . 2006.343) < LOD . Gray et al.240) .054-..190-1. 2006.189-.00 (. Longnecker et al..530 (.200 (.150) . Mariussen and Fonnum. dioxins and furans).140) . tremor.120-. and o. Snedeker. Jusko et al.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 .160-.146 (. 1956).180) . have not been consistently demonstrated (Beard. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. accidental exposures.142 (.230) . Reproductive effects in humans affecting birth weight. Jusko et al.34) .. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.26) 1.108 (...180 (. 2002. overt signs of acute human toxicity include vomiting.106) .130 (<LOD-. 2002.150 (<LOD-.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 . and seizures.330-4. 2001). Animal studies reported reduced fertility.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .g.095) < LOD .098-.128 (. 90 Fourth National Report on Human Exposure to Environmental Chemicals ..080-.250-1.170-.078 (.120 (<LOD-.150 (<LOD-.112 (.105-.150-.132-. DDT may bind to estrogen receptors (Chen et al.180 (. 2006).084 (.064 (. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S.130 (<LOD-. fertility. In laboratory animals. In high dose. polychlorinated biphenyls. and leukemia have also been inconclusive (ADSDR.203) . although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.140-. 2002.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.01) .048 (<LOD-. other organochlorines. 2006). Survey Geometric mean (95% conf.078-.180-. 1996). which may vary for some chemicals by year and by individual sample.130 (<LOD-.146 (.313 (.086 (.071-.106-. Hayes et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..068-. 2001).

6. NTP considers DDT as being reasonably anticipated to be a human carcinogen. In a population-based sample of men and women from eastern Slovakia. Fourth National Report on Human Exposure to Environmental Chemicals 91 . 1989). Compared to females in the NHANES 1999-2000 subsample..cdc.. see Data Analysis section) for Survey years 99-00..7-119) 113 (100-140) 93.atsdr. mean serum levels of DDT and DDE in the U. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR..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. 1998.html. environmental levels) and health effects is available from the U.epa. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 2004).. 2002.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. Since the 1970’s. population from the National Health and Nutrition Examination Survey. 2003. 8. and 7. 1991). and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. More information about external exposure (i.6 (81. Biomonitoring Information DDE persists in the body longer than DDT. 2002..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. Smith.e.. Heudorf et al. 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. 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.gov/ pestcides/ and from ATSDR at: http://www. compared to levels observed in this Report (Anderson et al.S. In general. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. 2003). respectively. Survey Geometric mean (95% conf.S.8. 2004). population declined by about fivefold to tenfold. EPA at: http://www.S. 2005). 01-02. 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.3. respectively. and 03-04 are 18. Stehr-Green. Link et al. IARC classifies DDT (p. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.Organochlorine Pesticides OSHA and a guidance established by ACGIH..p’-DDT) as a possible human carcinogen. Declining DDE levels over time have also been observed in the German population.gov/ toxpro2. for males and females in the NHANES 19992000 subsample (Pavuk et al.

34-11.11 (2.56) 2.18-1.78 (4.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.92) 1.32) 1.10) .01) 1.3 (8.32-1.91-2.8 (13.39-2.635) 1.02 (2.4 (12.40-4.66) 4.1) 7.16-1.3-43.82) 1.37 (1.58) 75th 3.25-14.2 (9.9 (26.21) 90th 7.05) 1.91-3.46-2. interval) 1.29 (1.64) 3.84-3.2-32. or p.3) 16.611-1.19) 4.51 (1.36-1.516 (.01-15.22-1.15-4.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.820-1.6 (17.31-2.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.6 (8.57-13.25) 1.24-17.52 (3.91) 3. 1971).57 (1.07) 1.9) 7.Organochlorine Pesticides nearby agriculture (Botella et al.41-12.60-13.96) .66-4.870 (.77 (1.54 (1.32 (1.00-1.75) 1.500-.S.69 (1.58) 1.520 (.488-.97-4.p’-DDT.17-3.01-1. considerably higher than levels in this Report (Smith.01) 1.385-.28) 1.57-3.64-2. serum levels of o.13-2.14-1.26) 3.66) 1.4) 9.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .14) 2.646) .34) 6.52-6.48 (6.33-1.6) 9.44) 1.14 (1.81-5.03-4.6 (9.534-.51) 1. Finding a measurable amount of p.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.65 (1.82 (1.3) 13.38 (1.18) 1.48-4. High mean levels of whole blood DDT (about 3.57 (3.93 (7.39) 1.8 (14.419-.51-49. 2004).26-10.3) 10.53-15.34-3.97 (3.04 (6.54) 8.796 (.53) 7.43-8.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.49 (1.6) 13.06) 3.5) 22. 2005).34) 2.27) 3.56-3.6) 9. Survey Geometric mean (95% conf.3 (9.56-6.6 (7.59 (1.01-5.20 (. 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. population from the National Health and Nutrition Examination Survey.83 (1.96) 1.26 (1.07) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6) 9.p’-DDT.51-8..59 (4.80) 1.45 (1.623 (.81) 11.88-35.4 (8.02) 1.36-2.43-4.07 (5.0) 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 .2 (19.37-10.05 (3.18 (6.13 (1.32-9.59) 3.85-10.01-1. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.5) 10.7) 13.39-1.9-38.40-4.69 (2.860 ng/L) and DDE (about 14.17 (3.2) 19. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.10) 2.49) 8.81 (1.2 (6.76) 1.68-4.72) 1.9-17.7) 9.92 (3.03-1. 1991).27-1.0 (9.24 (1. o.p’-DDT (Stehr-Green.52 (1.80) 1.79) 4.726) .18-3.71 (5.13) 4.8 (9.80 (2.37-1.55-9.50 (2.76 (2.1) 40.63-15.00 (.99) 1.30-1.57) 2.75 (4.430-.9 (15.10-5.41 (1.55 (2.88 (2.9) 5.06) 1.84 (3.35) 1.66) 1. less than one percent had detectable serum levels of o.00) 7.01-11..890-1.25 (1.50-17.36 (3.12 (6.36) 3.4) 13.2) 26.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.6) 8.57 (1.456 (.26-2.8 (13.561 (.6) 9.30-1.680-1.45 (1.p’-DDT were below the limits of detection.58) 1. 1989).34 (7.61 (1.76-3.43 (5.18-4.5) 16.0 (12.18-1.46 (1.22 (7.71 (6.7-20.09-1.68) 2.0) 2. 2001-2002 and 2003-2004 subsamples.91 (6.6) 11.70) 1.63 (1. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.02-8.8-90.8) 15.22) .10-1.557) 1.4) 14.31 (1.56-2.963-1. In the NHANES 1999-2000.5) 5.75) 2.85 (1.7 (8.600) .53) 1.59 (1.37-16.12-1.4-19.730) .12 (.81 (7.72) 1.61-2.00 (6.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.51) 3. Serum p.47 (1.37-4.23 (7.6) 12.32-1..76) 1.1 (9.90-8.25 (.39 (3.68 (2.1) 12.21) 3.75 (8.965-1.71) 12.5) 7.66) 3.65) 1.54-7. 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.43-4. 2004).81-18.47) 3.85-4.25-16.75) 6.59) 6.30 (1.04-1.87-16.66-2.16 (2.36-11.994-2. 309 versus 268 ng/g lipid.69 (.31-12.49 (1.7-48.87 (5.01-11.69) 4.80) 3.77 (1.51-15.92 (3.70-3.25) 8.57-2.38 (1.63 (6.14) 2.1 (8.2 (9.7) 16.62-6.49 (6.24) 1.90) 22.63 (1.19-14.71) 32.46 (1.590 (.53 (2.66-17..30 (1.40 (3.32 (1.40-8.69) 8.11-1.14-9. In a subsample of NHANES II (19761980) participants.7-19.

< LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 93 . respectively. 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. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.Organochlorine Pesticides Serum o. and 7.8. and 03-04 are 20.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. 17. 01-02.7. see Data Analysis section) for Survey years 99-00.S. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.

94 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.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.Organochlorine Pesticides Serum o.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.

Int J Hyg Environ Health 2003. Ellis H. Hediger ML. and DDD [online]. Epidemiology 2006. Needham LL.97(2):178192. Lancet 2001. Klebanoff MA.112(17):1761-1767. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Angerer J. Maternal serum level of 1. 4/21/09 Gladen BC. Fourth National Report on Human Exposure to Environmental Chemicals 95 . selected elements.html. Organochlorines in Swedish women: determinants of serum concentrations.72:261265. Botella B. Granath F. et al. Kulkarni PK. Vena JE. Environ Health Perspect 1998. 4/21/09 Anderson HA. hexachlorobenzene. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.206:485-491. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.gov/~dms/ pesrpts. Becker K.1-dichloro2. Falk C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. et al.355:7889. Durham WF. Baker RJ. Gunderson EL. Effects of environmental antiandrogens on reproductive development in experimental animals. Frumkin H. et al. dietary intakes of pesticides. DDT and human health. Chen CW. et al. Rogan WJ. Food and Drug Administration (FDA). Eriksson P. Profiles of ortho-polychlorinated biphenyl congeners. Thun MJ. Henley SJ. Olson J. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Cerrillo I.cfsan. Garrett N. Hayes WJ. Buckland SJ. Patterson DG Jr. Biomonitoring of persistent organochlorine pesticides. Chemosphere 2004. Katz SH. Beard J. Heudorf U. Aune M. and polythelia among male offspring. Savitz DA. CA Cancer J Clin 2002. The Great Lakes Consortium. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Arnold SF. Int J Hyg Environ Health 2002. Jr. Darnerud PO. September 2002. Vorojeikina DP.162:890-897.html. Lambright C. hypospadias. Olson JR. Ostby J. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Environ Health Perspect 2003. dichlorodiphenyldichloroethylene. Bjerselius R. Longnecker MP. and dichloro(diphenyl)ethylene (DDE). Herrman T. lindane (g-HCH).85:504508. Barr DB. Schulz C. Jr. DDE and shortened duration of lactation in a northern Mexican town. Moysich KB. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Davis MD. Koepsell TD.106(5):279-289. Kaus S.58:1185-1201. Klebanoff MA. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Bloom MS. Drexler H. Hanrahan L. Hurd C. August 2008. and HCB residues in human blood in Ahmedabad. Environ Health Perspect 2004. Available at URL: http://www. Am J Epidemiol 2002. Toxicological profile for DDT. Zhou H. Jusko TA.96:34-40.358:110-114. Needham LL. Olea N. et al. Organochlorines and breast cancer risk. et al. Charles MJ. Klebanoff MA. Exposure of women to organochlorine pesticides in Southern Spain.155(4):313-322. Zaidi SS.7(3):248-264.cdc. India. Am J Public Health 1995.fda. J Assoc Off Anal Chem 1988. Brock JW. et al. Furr J.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Paepke O. Talts U. Gray KA. Olea-Serrano MF.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Parks L. Zhou H. April 1982 to 1984. Greenfield TA. Hum Reprod Updat 2001. Biochem Pharmacol 1997.21(1-2)37-48. Sci Tot Environ 2006. Bates MN. Rivas A. Environ Res 2005. Kashyap R.205:297-308.. DDE. HCH. Wolf CJ. Link B. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. et al. Willman EJ. Longnecker MP. Notides AC. Glynn AW. Cueto C. JAMA 1956. Zoellner I. Gabrio T. Chemosphere 2005. Gladen BC. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. FDA total diet study.gov/ toxprofiles/tp35. Seiwert M. Maternal DDT exposures in relation to fetal and 5-year growth. Swanson MK. Environ Res 2004. Neurotoxicol 2000.17(6):692-700. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Krause C.71(6):1200-1209.atsdr. Saiyed HN.54:1431-1443. Crespo J.111:349355. Bhatnagar VK. Calle EE. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Piechotowski I. et al. Bull Environ Contam Toxicol 2004.52:301-309.53(8):1161-1172. Gray LE Jr. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Lepom P. Brock JW. Levels of DDT. Atuma S. Needham LL. and other chemicals. Available at URL: http://www. Burse VW.

731-915. DDE. Snedeker SM. Neurochemical targets and behavioral effects of organohalogen compounds: an update.20(2):186-193.27:405-421. Fox S. Rey AA. New York. Vol. Chemosphere 2004. Chlorinated Hydrocarbon Insecticides. In Hayes WJ. Stehr-Green. Lynch CF. Toxicol Appl Pharmacol 1971. Schecter A. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Rogan WJ. PA. Lubet R. Environ Health Perspect 2001. Academic Press. Handbook of Pesticide Toxicology. Fonnum F. Chovancova J. et al. Pesticides and breast cancer risk: a review of DDT. Pavuk M. Astolfi E. Eds. Petrik J. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Jr. et al. Smith AG. children and newborn infants. J Toxicol Environ Health Part A 1998. DDE. 2 Classes of Pesticides. J Toxicol Environ Health 1989.Organochlorine Pesticides Mariussen E. Nims R.54:1509-520. Arch Pediatr Adolesc Med 1996. Jones CR. 1991 pp.53:455-477.109:35-47. Crit Rev Toxicol 2006. Cerhan JR. Reddy AB. Comparative pharmacodynamics of CYP2B induction by DDT. Inc. Deichmann WB.36:253-589. and DDD in male rat liver and cultured rat hepatocytes. Pollutants in breast milk.150:981-990. and dieldrin. Radomski JL. Thomas PE. Jr and Laws ER. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Demographic and seasonal influences on human serum pesticide residue levels.

Ketoendrin is a major photodegradation product (IPCS. have been cancelled by the U. Because it is metabolized so rapidly. 1981). Smith. 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. a stereoisomer of dieldrin. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. or from contact with contaminated soils and sediments in areas where endrin was applied.30 (<LOD-6. unless the dose is high and the exposure is very recent. endrin can persist for years. Endrin does not accumulate in body tissues (IPCS.09 and 7. total diet surveys (FDA.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. Kavlock et al. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. All uses of the pesticide in the U. Survey Geometric mean (95% conf. or discarded. Depending on soil conditions.40 (<LOD-6.S. In the body.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. 1996. Endrin has been detected in soils. manufactured. inhalation or dermal exposure routes. fatty infiltration.50) < LOD < LOD < LOD 5. 1992. Hepatic effects of endrin exposure have included necrosis. EPA. 1991). endrin has been detected with declining frequency in U. is no longer manufactured in the U.S.Organochlorine Pesticides Endrin CAS No.60 (5. population from the National Health and Nutrition Examination Survey. Endrin was used as an insecticide. Over time.S. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. < LOD means less than the limit of detection.S. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. unlike aldrin and dieldrin.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.50) < LOD 5. which may vary for some chemicals by year and by individual sample. 1992). characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.. 1987).. and occasionally at low levels in sediment and surface waters. An epidemic of acute endrin poisoning. 1992). Endrin is absorbed rapidly after ingestion.10 (<LOD-5. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.10 (<LOD-5.8.. 72-20-8 General Information Endrin. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. and inflammation (Smith. IPCS. endrin is converted rapidly to its major metabolite. rodenticide and avicide.40-5.S. anti-12hydroxyendrin. 1979. endrin usually is not detected in serum of exposed individuals.20 (<LOD-5. 1991)..30) < LOD 5. Endrin was not widely used as a termiticide.20 (<LOD-5. 1992).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. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 2008). At high doses. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.

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

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

particularly by consuming fish.6 (21.7) < LOD < LOD 24.4) < LOD < LOD 33.9-15.S.6 (24. 100 Fourth National Report on Human Exposure to Environmental Chemicals .0) * * 15.8-15.1 (13.7) * * 14. and has been detected in soil.6-trichlorophenol (2. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. 31.5-18.4. Survey Geometric mean (95% conf.1-16.0-28. 1988). distributes widely throughout the body.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.6) < LOD < LOD 26.4) < LOD < LOD 18.0-25.5 (13.9-30. Although it is not manufactured as an end-product in the U. and sediment (Barber et al.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and foods with a high fat content.7-30.0) < LOD < LOD 15.9) < LOD < LOD 20. air.3 (22.6) < LOD < LOD 24.2-15.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.0 (25.3-22.1 (17.9 (25. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. Urinary metabolites include pentachlorophenol (PCP).7 (27.4 (18..7 (15.7-16.S.4 (22.7-22.3) 24.5) < LOD < LOD 18.3-20.5-trichlorophenol (2..4) < LOD < LOD 14.8) < LOD < LOD 27. The FDA dietary surveys have shown that over time.5-14. 1997). Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.9) < LOD < LOD 15.5-15. or game taken from areas with HCB contamination. < LOD means less than the limit of detection.0) < LOD < LOD 24.2-31.9 (23.4) < LOD < LOD 23. primarily as a fungicide and seed treatment until the U.4.9 (25.7-15. The general population may be exposed to HCB through diet. 2.3 (16.3 (12. 2005).6-19. 2002).8 (15.2) < LOD < LOD 13.S. Gunderson. respectively. water.1 (14.3) < LOD < LOD 20. HCB has been detected in fewer foods since the 1980s (FDA.0 (14.9) < LOD < LOD 16.4.4 (11. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. which may vary for some chemicals by year and by individual sample.8. 1976).6-33.4) < LOD < LOD 22. 01-02.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.2) < LOD < LOD 29.4 (18.5-TCP) and 2. Therefore. wildfowl.1-20.2 (14.6) < LOD < LOD 25.5-15.1 (14.6-44.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.9-17.9) < LOD < LOD 28.1) * * 15.5 (13.4. EPA cancelled its use in 1984. and elimination occurs by renal and fecal routes.6-26.6) < LOD < LOD 26.8 (26.2 (17.0-16.3 (22.3-26.5-33.Organochlorine Pesticides Hexachlorobenzene CAS No. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.3 (20.6-32.9 (14. and 7..7 (19.9) < LOD < LOD 19.6 (23..3) < LOD < LOD 29.0) < LOD < LOD 15. and accumulates in fatty tissues where it persists for years.0 (18.3) * * 15.7 (15.6-TCP) (To-Figueras et al. 2008.4.0-19.6) < LOD < LOD 14.2-15.0 (18. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.8 (22.4-16. breast milk is an additional route of elimination in nursing women.2 (24.2 (14.0.9) < LOD < LOD 20.5-14.4) < LOD < LOD 19.9-32.7-21.7-16.7-29.7-26.1) < LOD < LOD 15.4-15. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.5 (14. and 03-04 are 118. HCB is slowly metabolized. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-20.S.9) 19.9-24. population from the National Health and Nutrition Examination Survey. HCB is well absorbed after oral administration.3 (14. see Data Analysis section) for Survey years 99-00.2 (13. 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.

190 (.175) < LOD < LOD .163) < LOD < LOD .160 (. very high.086-.090 (.S. More information about external exposure (i.090 (.163 (.092-.152) < LOD < LOD .125 (.073-.182 (.088-.078 (. acute doses produce central nervous system depression and seizures.225 (.145-.089-.173) < LOD < LOD .091-.258) < LOD < LOD .176) < LOD < LOD .092 (. population from the National Health and Nutrition Examination Survey. and liver and thyroid cancers (ATSDR. immunologic abnormalities.145-.123 (. In humans.140 (.102 (.111) < LOD < LOD .109) * * . IARC classifies hexachlorobenzene as possibly carcinogenic to humans.114-.157-.072-.095 (. environmental levels) and health effects is available from the U.html.085) * * .099) < LOD < LOD .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 * * .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * . HCB interferes with normal heme synthesis.097) < LOD < LOD . and the FDA has established a bottled water standard for HCB.147 (. Biomonitoring Information Serum concentrations reflect the body burden of HCB. Infants were exposed transplacentally and through breast milk.113-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.130) < LOD < LOD .203) < LOD < LOD .203) < LOD < LOD .132) < LOD < LOD .155) < LOD < LOD ..186 (.127-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda. which may vary for some chemicals by year and by individual sample.079 (.081-.epa.094) < LOD < LOD . and many died before 2 years of age (Peters et al.090 (.100) < LOD < LOD .064 (.088-.179 (.Organochlorine Pesticides chemical.157 (.095 (.083) < LOD < LOD .118-.171 (.169-.167 (.089-. Schmid.092 (.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .159-. Chronic feeding studies in animals have demonstrated kidney injury.gov/pesticides/ and from ATSDR at: http://www.122) < LOD < LOD .126) .099) < LOD < LOD .069) * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .094 (.090-.086-. and weakness.120 (.082-.099) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.088-.cdc.107-. as well as hypertrichosis. This condition.069) < LOD < LOD .163-.121 (. arthritis.107) < LOD < LOD .141) < LOD < LOD . reproductive and developmental toxicities.095-.102) < LOD < LOD . anorexia. With chronic exposure.086) < LOD < LOD . HCB levels were generally below the limits of detection Serum Hexachlorobenzene (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.115 (.081 (.095) * * .111-. EPA at: http://www.092 (. thyromegaly.085-.077-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.148-.118-..191 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 . 1982.218) 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 (.147-.118) < LOD < LOD .196) < LOD < LOD .135-.097) .174-.098 (. ACGIH has developed workplace exposure limits for HCB.095) < LOD < LOD 75th < LOD < LOD 90th * * .156 (. 1960).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 * * .104 (.e.129) < LOD < LOD .S.178-.143-. The U. 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. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.060-.114-. 2002).062-.087 (.123 (.atsdr.065 (. EPA has established a drinking water standard.S.gov/toxpro2. Survey Geometric mean (95% conf.176-.123 (.

FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 2006). Safe A. Bryan GT. Atuma S. Herrman T. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. J Exp Sci Environ Epidemiol 2007. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.81(2):82-85. Piechotowski I. Lackmann. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. et al. Kohli J..39(12):744-749.110(8):835-838. Cripps DJ. 2005).. selected elements. Dogramaci I. Gunderson EL. trends and processes. Gocmen A. but overall. Biol Neonate 2002. Muckle G. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Laliberte C. HCB levels were directly related to age.gov/~dms/ pesrpts.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. 4/21/09 Glynn AW. Ayotte P. 2005. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. IARC Sci Publ 1986. August 2008. Krause C. Gabrio T. September 2002. 1989). and the geometric mean concentration of HCB in whole blood was 0.44 mg/L. respectively.. In the 1976-1980 NHANES subsample. Arch Neurol 1982. and other chemicals. 2002). FDA total diet study. 1999). Fenster L. In a representative sample of the 1998 German adult population. Seiwert M. Biomonitoring of persistent organochlorine pesticides. Dewailly E. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.58:1185-1201. Granath F. Barr DB. Available at URL: http://www. Bradman et al.cfsan. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Bertram et al.17:388–399.9% of participants had quantifiable levels (Stehr-Green. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Kaus S. Arch Dermatol 1999. In Spain. Can J Biochem 1976. Sweetman AJ. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. J Assoc Off Anal Chem 1988.. et al. van Wijk D. Lackmann GM. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. References Agency for Toxic Substances and Disease Registry (ATSDR). Food and Drug Administration (FDA). Peters HA. Hexachlorobenzene in the global environment: emissions. Schwartz JM. The metabolism of higher chlorinated benzene isomers. 2002. Sci Tot Environ 2005.atsdr. only 4. Int J Hyg Environ Health 2002. Holland NT..349:144. Lawrence River (Quebec. Muller C. Kemper FH. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene.cdc.. 2002) and among children (Link et al. As a result of the lower limit of detection in NHANES 2003-2004. Glynn et al.54(3):203-208.gov/ toxprofiles/tp90. 102 Fourth National Report on Human Exposure to Environmental Chemicals . 2003). distribution. 2002.fda. Reference values updated. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Jones D. Available at URL: http://www. Zoellner I. Dallaire F. Lackman. Jones KC. Darnerud PO. April 1982 to 1984. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Biomonitoring studies on levels of HCB provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of hexachlorobenzene than are found in the general population. Chemosphere 2005. Environ Health Perspect 2002.html. Link B. Paepke O. Eskenazi B. 1986. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Otero R.. Over the past two decades. Bjerselius R. Canada). Link et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 4/21/09 Barber JL. levels. 2002. more HCB levels were quantified. Organochlorines in Swedish women: determinants of serum concentrations. Lepom P. Ozalla D. Santiago-Silva M. Becker K.. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. dietary intakes of pesticides. Toxicological profile for hexachlorobenzene update [online].. 2002. Environ Health Perspect 2003. Aune M..html.111:349355. Herrero C.135(4):400404.71(6):1200-1209. however. et al.77:173182. Schulz C. Bertram HP.205:297-308. Sala M. 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. HCB detection in serum also was proportional to age. Lecha M. 2005).. Bradman A.

105(1):78-83.263:397-398. Barrot C. Environ Health Perspect 1997. J Toxicol Environ Health 1989.27:405-421. Cutaneous porphyria in Turkey. Rodamilans M. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Stehr-Green. Otero R. N Engl J Med 1960. Demographic and seasonal influences on human serum pesticide residue levels. Sala M. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Santiago-Silva M.Organochlorine Pesticides Schmid R. PA. To-Figueras J. et al.

respectively.4 (16.4-111) 84.5-29.0 (14.2) 13.87 (9.8 (33.0) 41.4 (50.9 (40.5) 40.6) 653 758 589 1240 1533 1370 20 years and older 10.0 (33.3-38.70-19.0-21.5 (43. gamma.4) 51.7-26.4) 44.1) 12.6) 35.2 (48. population from the National Health and Nutrition Examination Survey.4) 27. 58-89-9 General Information Hexachlorocyclohexane (HCH).Organochlorine Pesticides Hexachlorocyclohexane CAS No.0-20. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.2) 36. particularly alpha and gamma have been detected widely in air.1 (21. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. Technical grade HCH is a mixture of all four isomers.8) 12.4-50.S.8 (32.8) * * * * * * 15.2) 142 (99.7 (29.2) 62.4) < LOD 9.1-37.5) 90th 42.8 (10. and 7.7 (25.2-22.7) 27. beta.80 (6.7-166) 70.0-70.4) 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 21.43 (<LOD-9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 6.46-11.8) 7.6-62. 608-73-1 beta-Hexachlorocyclohexane CAS No.4) 21.2) 9.4) 11.1) 12.0-70.50) 8.3) 37.8 (17. 2005). which may vary for some chemicals by year and by individual sample.9-56. including alpha.7 (13.5) 29.8 (21.9 (50.1-49.7) 97.4) 901 1067 952 992 1224 1007 Females 11.9 (9.4-73.1) 13.3) 34.1 (27.04-10. HCH isomers.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.2-52.2-42.9) 17.6 (16.9) 45.8-19.7-96.6) 16.3) 51.4 (11. and 03-04 are 9. formerly referred to as benzene hexachloride.8) 39.0) 35.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.6 (10.6-89. < LOD means less than the limit of detection.6 (17. See the section “What’s New” at the beginning of this Report for details.6) 50.2-17.1) 71.1 (18.7) 10.8-199) 134 (85.8-16. and sediment as a result of historic production and use. EPA cancelled agricultural uses of lindane (ATSDR.5528.0 (19.80 (<LOD-14.4 (12.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.2 (31.7) 10.1-36.4) 10. exists in several isomeric forms.9) 81. 01-02.2-98.5 (16.7 (35.1 (9.3 (62.9) 15.76.7) 23. environmental levels declined.9-24.70-12. 319-85-7 gamma-Hexachlorocyclohexane CAS No.6-37.5 (11.5) 11.0-111) 70.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.4) < LOD < LOD < LOD 46.8) 27.4-45.7) 18.3 (42. The other isomers can be formed during the synthesis of lindane.0-34.1 (12.6-18.5-123) 49.1 (16.2 (9.7-20.36.90-8.89 (<LOD-9.6-135) 69.68 (<LOD-10. and have been used either as fungicides or to synthesize other chemicals.5 (37.0 (35.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. each result has been multiplied by 1.9-81.61-12. However.66-12.5) 67.1 (30.8) 95th 68.9 (30.1 (9.1-15.6 (22.6-20.7 (62.1-32. As pesticide applications of HCH were increasingly restricted or eliminated.0 (8.5 (14.6) 18.2-55.0) 17.S.8-87.5) 14.8) 52. Lindane has a half-life of about two weeks in soils and water.60-13. **In survey period 2001-2002.7-96.6) 36.1-32.7-69.1) 31. soil.5 (24.3-85. the U.2-20.4 (8.0) 7. In 2006.9 (62.S.6) 47. 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.70 (8.6-42.0) 71.6 (33.6 (40.9-21.8 (23.9-14.9-178) 48.70 (6. see Data Analysis section) for survey years 99-00.5) 16.2 (18.2-46.90-8. The gamma isomer.9 (11.8) < LOD 10. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.2-87.0 (<LOD-12.2 (34.7-69.3 (13. commonly known as lindane.2-67. It is no longer produced or sold in the U.8 (9.8-68.7 (<LOD-16.2 (50.2 (29.7) 73.3) 25.7 (53.6-14.1 (11.7) 56. HCH isomers are lipophilic. containing about 64% alpha and 10%-15% gamma isomers.0) 8. interval) 9.56-12.8-54.7 (30.0-23.3 (42.0 (37. so they can accumulate in fatty tissues of animals.5) 22.8. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. water.3-56.1-16.30-11.9 (32.6-47.3 (26. and delta.7) 32. 2005).20-16.3) 14.1-27.9-51.4 (52.9 (26.90) 7.5 (8. 104 Fourth National Report on Human Exposure to Environmental Chemicals .8 (64.

280-.175 (.070-.056-.37) 1.300-. Workers who directly handled HCH have complained of headache.230-.410) .260) . ataxia.100) .119) .191-.680) .910 (.222 (.01 (. and memory loss (Nigam et al.310) .350 (.103 (.103-.410-.081-.410) .150-. HCH crosses the placenta and is also excreted in breast milk (Radomski et al. from 6% of samples in 1982-1984 to 2% in 1994 (FDA. 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. probably by blocking inhibitory neurotransmitters in the central nervous system.050-.057 (<LOD-. Saxena et al.092 (.200-.080) * * * * * * .710) .216 (.098 (.110) .600) .308-.100-.400) .250-.120-.260) .661) 901 1067 952 992 1224 1007 Females .700) .050 (<LOD-.170-.070-.100-.160) . each result has been multiplied by 1.065 (. Gunderson 1988). Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.32) .170-.521 (.080 (.370-.070) . HCH isomers are absorbed after inhalation.180-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .072 (.340) .814) .320 (.410 (.062 (.089) . 1983).220 (.442 (.191-.331 (.051-.360 (.214) .140) .470 (.450 (..125) < LOD < LOD < LOD . 1971.450) .174) .120 (.100 (.400) .083 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .560 (.065 (. and nephropathy developed (IPCS.210-.310) .050 (.250-.110-. enlarged livers.130) .048 (<LOD-.. After dermal application of lindane 1% lotion. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.073-.100 (. resulting in a half-life of about seven years. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.250 (.297-.281 (.089-.360) .380 (.080-.167 (.120-.210 (.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 .620-1.360-.067 (.077) < LOD .5528.350) .220-.254) 95th .330 (.040-.Organochlorine Pesticides exposure to HCH is through the diet.270 (.240 (.050 (<LOD-.090 (..091) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .382-.160-.190) . or dermal exposure. The U.096) .150 (.120-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.190) . When animals were chronically fed lindane at high doses.200 (.319) .234 (.294-.090-.064 (.120) .305) .064) .460 (. 1981)..250 (. respectively.062 (.110) .210 (.068-.100) . Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.110) .150) .120 (.460) .050) .050 (.05) .057-.480 (. U.160 (. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.130-.340-.250 (.450-. 1977).480) ..173-.139 (.120) .220) .080-.501) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.050-. population from the National Health and Nutrition Examination Survey.190-1. 1986).250) .047-.287 (.570 (.070 (.144 (.620) .372 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .078 (.S.240-. EPA has established a drinking water standard.S.470) .290 (.059-.130 (.560) .S.310 (.050-.070 (.390-.060) .390 (.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.077) < LOD . Distribution is mainly to fatty tissues.146-. ingestion.150) .080 (.290) .210) .090 (.140 (.690) .080) .140) .070-.100-. tremors.200-.118-. and FDA has established a bottled water standard and food residue tolerances for lindane.290 (.290 (. the serum half-life was about 20 hours among children (Ginsburg et al.840) .069) . **In survey period 2001-2002.080-.058 (<LOD-.051 (<LOD-.124-.090 (.587) 653 758 589 1240 1533 1370 20 years and older . 1996.057-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.412 (. and seizures.330-. interval) .083) .260-.120 (.131-. for lindane.580 (.220-. OSHA and ACGIH have established workplace standards and guidelines.103) 90th .086) < LOD < LOD < LOD < LOD < LOD < LOD . See the section “What’s New” at the beginning of this Report for details.118 (.221-.244-. which may vary for some chemicals by year and by individual sample. paresthesias.290) .140) .510) .050-.190-. hepatic enzyme induction. 2002). Rogan. 2008.056-.580-1.067) .420-.404) .280-. The beta isomer accumulates in fatty tissues and is metabolized more slowly.480 (.

More information about external exposure (i. Link et al.epa. Biomonitoring Information Because of its longer half-life.e.. 1989.. 2005. 1991. 2004). older age. and 2003-2004.gov/toxpro2. Kutz et al. male sex. Sturgeon et al. Radomski et al. were similar to the 95th percentiles in this Report. 2004.. Bates et al. 2002).S. In recent years. 10. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al.. which may vary for some chemicals by year and by individual sample..8. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al.. 2002. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR..atsdr. 1989). beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers.. environmental levels) and health effects is available from the U. population from the National Health and Nutrition Examination Survey.. 1998. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/pesticides/ and from ATSDR at: http:// www. aged 9-11 years. and 7. and a diet that includes meat (Becker et al. 2004) and India (Bhatnagar et al.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. Becker et al. 2005.html. In populationbased studies of New Zealand adults and German adults and children. respectively. the maximum and 95th percentile beta-HCH values. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. < LOD means less than the limit of detection. 1971. In NHANES 1999-2000. the 95th percentile of betaHCH levels was twofold to threefold higher than the 95th percentile of 12-19 year olds in the comparable NHANES Serum gamma-Hexachlorocyclohexane (Lindane) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. respectively.5. Additional factors associated with higher beta-HCH levels include rural residence. 1991. 1998). EPA at: http://www. and 03-04 are 14. serum levels of lindane were generally below the limits of detection. 2001-2002.. see Data Analysis section) for Survey years 99-00.. Stehr-Green.. Kutz et al. 01-02. Survey Geometric mean (95% conf. In an earlier (1996-1997) sample of German children. 106 Fourth National Report on Human Exposure to Environmental Chemicals .cdc.S. Stehr-Green.5.

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. population from the National Health and Nutrition Examination Survey. respectively. which may vary for some chemicals by year and by individual sample. in this Report (Nigam et al... * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1971). 2005)... 1998). Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. Beta-HCH and lindane levels in workers involved in HCH production have been more than 1000-fold higher than the 95th percentile and limit of detection (lipid adjusted). 2003). the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al. Radomski et al.Organochlorine Pesticides 2001-2002 survey period (Link et al. 1986.. In a small study of adults who consumed sport fish from the Great Lakes.S. 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. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 107 . Serum gamma-Hexachlorocyclohexane (Lindane) (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Demographic and seasonal influences on human serum pesticide residue levels. Lindane. Krishna Murti CR. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Olson J.111:349355.fda. Occupational exposure to hexachlorocyclohexane. Rev Environ Contam Toxicol 1991. Brock JW. Brinton LA. FDA total diet study.58:1185-1201. August 2008. Aune M. Chemosphere 2004. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Atuma S. April 1982 to 1984. Levels of DDT. VI.91:998-1000. J Pediatr 1977. J Toxicol Environ Health 1989. Zoellner I. Becker K.27:405-421. Bottimore DP.54:1431-1443.html. The Great Lakes Consortium.71(6):1200-1209. Arch Pediatr Adolesc Med 1996. International Programme on Chemical Safety (IPCS). Rothman N. 2002.106(5):279-289.52(1):59-67. Exposure of women to organochlorine pesticides in Southern Spain. Environ Health Perspect 1998. Angerer J. Krause C. Darnerud PO.72:261265. Bull Environ Contam Toxicol 2004. Bhatnagar VK. Placental transfer of pesticides in humans.inchem. et al. Kaus S. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Maass R. Toxicological profile for hexachlorocyclohexanes update [online]. Stehr-Green. Reisch JS.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).9(4):417-424. Link B. Falk C. Garrett N. Patterson DG Jr. Herrman T. Botella B. Lowry W. Available at URL: http://www. Environ Health Perspect 2003. et al. Needham LL. India. Gabrio T. Saxena MC. Pollutants in breast milk. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Olea-Serrano MF. et al. Cerrillo I. Olea N. Sturgeon SR. Rivas A. Seiwert M. available at URL: http://www.120:1-82. Buckland SJ. Radomski JL. Schulz C. Heinrich R.150:981-990.cdc. Toxicol Appl Pharmacol 1971. Bjerselius R. Bai KM. Zaidi SS. children and newborn infants. Raju GS. Environ Res 2004. Int Arch Occup Environ Health 1983. Bhargava AK. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www. Needham LL. Visweswariah K. dietary intakes of pesticides. 4/21/09 Anderson HA. Cancer Causes and Control 1998. Majumder SK. Karnik AB. et al. Saiyed HN. Wood PH.205:297-308. Siddiqui MKJ. et al. 4/21/09 Kutz FW. selected elements. 4/21/09 Ginsburg CM. Deichmann WB. org/documents/jmpr/jmpmono/2002pr08. Bates MN. Int Arch Occup Environ Health 1986. gov/toxprofiles/tp43. Gunderson EL. Astolfi E. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant.cfsan. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Hanrahan L. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Chemosphere 2005.atsdr. et al. Glynn AW. Rey AA.48:127-134. and HCB residues in human blood in Ahmedabad. Crespo J. Potischman N. Arch Toxicol 1981. Int J Hyg Environ Health 2002. Burse VW. and other chemicals. Kutty D. August 2005. Piechotowski I.57(4):315-320. Granath F.html. PA. Biomonitoring of persistent organochlorine pesticides. Ellis H.20(2):186-193. J Assoc Off Anal Chem 1988. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Absorption of lindane (g benzene hexachloride) in infants and children. Needham LL.gov/~dms/pesrpts. Nigam SK. Organochlorines in Swedish women: determinants of serum concentrations. Kashyap R. Rogan WJ. HCH. Kulkarni PK.96:34-4Food and Drug Administration (FDA). Lepom P. Paepke O. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.htm. Metabolism of gammahexachlorocyclohexane in man.

Formerly.6) < LOD < LOD < LOD < LOD 71. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.7) < LOD 66. aquatic organisms.10 (<LOD-15.40 (<LOD-13.1 (8. and 03-04 are 14. (Kutz et al.7 (<LOD-47.0) * * * 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 19.2) 51.1 (13..10-37.5-291) 11.70 (<LOD-15.5 (<LOD-42. since 1977.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. 1995).3 (15. soil. animals. respectively. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. which may vary for some chemicals by year and by individual sample.0 (14. Mirex is absorbed through the skin and from the gastrointestinal tract.3-225) 15.5 (<LOD-115) 153 (30.4) < LOD 63. sediments.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. where it was applied directly to soil and by aerial spraying.6 (<LOD-23. Mirex has been detected in air.0-374) 11. resulting in exposure to newborns and nursing infants. after which it is widely distributed in the body and stored in fat.6.8 (<LOD-73.5.5-82. and foods.3 (15. Mirex can cross the placenta and be excreted in breast milk.70-24.90-29. it is a highly persistent chemical in the environment. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. 1991).8 (12.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.6-305) 15. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4-230) 18.S. mirex was detected in human adipose samples. In studies conducted in the 1970’s and 1980’s.8. 10.7 (12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..Organochlorine Pesticides Mirex CAS No.70-40. Occupational exposure is limited to workers at sites where mirex contamination is present.S. Some states and the U. 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.6 (<LOD-31.6 (<LOD-108) 9. especially those from persons living in the southeastern U.5-425) 40. population from the National Health and Nutrition Examination Survey. water. where it has a half-life of 12 years.0 (<LOD-108) < LOD < LOD 50.S.6) 9.3) 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. 2385-85-5 General Information Mirex has not been produced or used in the U.1 (<LOD-65.5 (9. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. 1985. Survey Geometric mean (95% conf.S.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.2-230) 13. and 7. Fourth National Report on Human Exposure to Environmental Chemicals 109 .2 (7. 01-02.4 (8.0 (12.8) < LOD 15. or pesticide application. see Data Analysis section) for Survey years 99-00. disposal.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Mirex binds strongly to soil.4) < LOD 15. < LOD means less than the limit of detection.S.7) 8. Mirex is not metabolized in the body. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.

450) 1.256 (.090 (<LOD-.079 (<LOD-.064 (<LOD-. 7. 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. Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions.430 (.077 (<LOD-.110 (<LOD-. 2004).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 .e. EPA has established environmental standards for mirex.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 .240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 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.610) < LOD < LOD < LOD < LOD .102) < LOD < LOD < LOD < LOD .090 (<LOD-. 2005). In samples obtained between 1994 and 1997. reproductive toxicity included decreased fertility and testicular damage.090-1. 1989).100 (<LOD-.470 (.690) .atsdr.090-1.052-.268) < LOD .7 ng/g of lipid.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .450 (. 1991).093 (.059 (<LOD-.41) .S. serum mirex levels were generally below the limits of detection (Stehr-Green.73) .220) .053-. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. as well as in a subsample of NHANES II (1976-1980) participants.220 (<LOD-.112 (.Organochlorine Pesticides exposures are unknown.080-1.92) . Smith. 1995.8.106) < LOD . Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .106 (..gov/toxpro2.090-1. More information about external exposure (i.79) .635) < LOD .108 (.S. and 2003-2004 subsamples. which may vary for some chemicals by year and by individual sample.08 (.062-.170) < LOD . 110 Fourth National Report on Human Exposure to Environmental Chemicals .090 (<LOD-. The U.02) .410 (.cdc.054 (<LOD-. Laboratory animals fed high doses developed liver enlargement and liver tumors.100 (<LOD-. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.080-1. The geometric mean mirex levels of the Inuit mothers were 8.070-1.470) .089-.html.310 (.510) < LOD < LOD . Biomonitoring Information In the NHANES 1999-2000.170-3. IARC classifies mirex as possibly carcinogenic to humans.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 .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. 2001-2002. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140 (<LOD-..470) .37) . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.055-.79) .370 (. environmental levels) and health effects is available from the ATSDR at: http://www.. In addition. and 4.

Moysich KB. Swanson MK.cdc. Toxicological profile for mirex and chlordecone [online]. 1994-1997 organochlorine compounds. Van Oostdam JC. Strassman SC. J Toxicol Environ Health 1989. August 1995. Eds.330:55-70.27:405-421. Stehr-Green. Available at URL: http://www. Dewailly E. Profiles of ortho-polychlorinated biphenyl congeners. Watts DL. Smith AG. Inc. Wood PH. Stroup CR.html. hexachlorobenzene. References Agency for Toxic Substances and Disease Registry (ATSDR). Olson JR.Organochlorine Pesticides effect. 2 Classes of Pesticides. Chashchin V. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Academic Press. Handbook of Pesticide Toxicology.97(2):178192.gov/toxprofiles/ tp66. The human body burden of mirex in the southeastern United States. Leininger CC.120:1-82. J Toxicol Environ Health 1985. et al. New York. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Fourth National Report on Human Exposure to Environmental Chemicals 111 . 731-915. 1991 pp. Environ Res 2005. Sci Total Environ 2004. Circumpolar maternal blood contaminant survey. Demographic and seasonal influences on human serum pesticide residue levels. et al. dichlorodiphenyldichloroethylene.15:385-394. Kutz FW. Hansen JC. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Vena JE. Chlorinated Hydrocarbon Insecticides. PA. Rev Environ Contam Toxicol 1991. Odland JO. In Hayes WJ. 4/21/09 Bloom MS. Jr and Laws ER. Bottimore DP. Vol. Kutz FW. Gilman A. 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.atsdr. Jr. Carra JS.

Trichlorophenols are no longer manufactured commercially.900-2.Organochlorine Pesticides 2. and sediments.80 (2.60 (2. Such workers would probably Urinary 2.4.40 (1.3.30-27.71 (<LOD-8.30) < LOD < LOD < LOD < LOD < LOD 1.20 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) < LOD 1.5-TCP) and 2.9.980-3.4.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.0) 2.8) 21.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.6-TCP).5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (3. other organochlorines.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.6-TCP were used as intermediates in the production of certain pesticides.4.71 (<LOD-8. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.0) 14.50-63.0 (3.60 (4.50-25. Formation of 2.0) < LOD 11.30 (. Exposure to trichlorophenols also may result from metabolism of lindane.40 (1.0) < LOD 21.00 (3.50) < LOD 1.0) < LOD 5.0) 2.60) < LOD 8.80 (1. 1976). may occur by inhalation or dermal routes.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.50-16.20-71.4. are metabolites of several organochlorine chemicals.9 and 0.27) 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 1.03) 9.40 (2.5-trichlorophenol.5-Trichlorophenol CAS No.00 (2. public drinking water systems did not detect 2.50 (.30-40.4.20) < LOD 90th 5. which may vary for some chemicals by year and by individual sample.S.00-3. usually at herbicide production or waste incineration facilities. 95-95-4 2. EPA.40-18.40) < LOD 6.72) < LOD 1. 1999).00-8.0 (4.40 (. Occupational exposures.0) 5.60 (.7) 24.4.7.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .80) < LOD 1. including hexachlorobenzene and hexachlorocyclohexanes.940-3.30) < LOD 4.9 (<LOD-121) 9.50 (2.0) < LOD 5. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.10-3. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.0) < LOD 5.40 (2.30-11.30-27.6-Trichlorophenol CAS No.80-41. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.40 (2.0) 2.0) 2.30-44.42 (<LOD-8.30-3. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.0 (8.4.00-3.0) 2.4.4. 2.20) < LOD 1.60-18. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.27) 696 661 521 696 603 939 Limit of detection (LOD.980-3.40 (.57 (<LOD-15.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.50 (1.40-11.0) < LOD 11. Historically. hexachlorobenzene. Both chemicals have been detected in air.63) 18. Survey Geometric mean (95% conf.920-3.20-36. 2. population from the National Health and Nutrition Examination Survey.0 (4.40 (2.42 (<LOD-12. recent sampling of U.S.4.S.19 (<LOD-6. surface water.5TCP and 2.90-33. 1999).40) < LOD 4. 2.0 (4. 2006).950 (<LOD-1.5-trichlorophenol (2.31 (<LOD-9.60-8..20) < LOD 5.6-TCP in any of the samples (U. however. soils.0) 2. 112 Fourth National Report on Human Exposure to Environmental Chemicals .30-27.6-trichlorophenol (2.4. < LOD means less than the limit of detection.0 (5. and polychlorinated benzenes (Kohil et al.

Laboratory animals chronically fed high doses of 2.78-19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-TCP as reasonably anticipated to be a human carcinogen.S. leukemias.820-2.57 (<LOD-7. 2003).29 (1.2 (2. Survey Geometric mean (95% conf.43 (2. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.95 (3.6-TCP levels at the 95th percentile were up to eight times higher than 3. population from the National Health and Nutrition Examination Survey.37) 16.4) 5.6-TCP had increased rates of hepatic tumors.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. IARC classifies combined exposures to polychlorophenols..90 (4.4 (6. 1995) and up to 19 times higher than the 95th percentile value of 1.4.53-3.37-11.16) < LOD 90th 5. environmental levels) and health effects is available from ATSDR at: http://www.5-TCP or 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.4.75 (<LOD-6.4.24-11. Among 6-11 year old children in NHANES 1999-2000.64 (4.17) 9.68-4.46 (1. At lower doses.7 (4. Fourth National Report on Human Exposure to Environmental Chemicals 113 .1 (<LOD-58.69-18..0 mg/L.78 (3. the 95th percentile urinary 2. 7.67 (1.43) < LOD 12.8 (5.53-3.4. furans.81 (<LOD-9.68 (<LOD-8.00) < LOD 4.5-TCP and limited for 2. urinary 2. Neither 2.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). as being possibly carcinogenic to humans.1) 2.24) < LOD 5.31) < LOD 2.49 (1.05-8.4) < LOD 3. and other chlorinated compounds.atsdr.28-25. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.82 (<LOD-32.8) < LOD 9.02) < LOD 7. The 95th percentiles for 2.60-3.e.69 (2. However. 2003.0) 7.4.15) < LOD 2. In the same 2-6 year old children.19-12.Organochlorine Pesticides be exposed to mixtures of chlorophenols.74) 11.78) < LOD 1.. More information about external exposure (i.00-29. and lymphomas.44 (1.33) < LOD < LOD < LOD < LOD < LOD 2.6) 4.5) < LOD 12.02-3.57 (3.4.05-17. the 95th percentile urinary 2. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.9 (5.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.2) < LOD 5.19-4.00-19.55 (4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11..5) 11.6-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.47-8. NTP classifies 2.. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.4.57 (<LOD-7.88-16. Human health effects from 2.20-6.4.gov/toxpro2. 1989)..27-17.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .36 (1.24) < LOD 1.16 (.2) 2. Radon et al.6) 4.73 (<LOD-8..4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.80 (1.980 (<LOD-1. Urinary 2.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1989).44 (.920-2.4. which includes trichlorophenols.6-TCP.83-12.4.50) < LOD 2.67 (1..37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 1995) were similar.32) < LOD 4.4) < LOD 3.8) 4. in addition to dioxins.79-4. animals showed hepatocellular abnormalities.93-11.5-TCP.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 2.4.86 (3.13-13.24 (3. 2003).62-20.4.3 (5.cdc.5-TCP nor 2.6) 4.75 (3. 2004).html.9) 12.3 mg/L reported in German adults aged 18-69 years (Becker et al.24) < LOD 6..

4.0) 15.36 (1.70) 1.5-TCP (0.0) 9.70-6. Biomonitoring data will also help scientists plan and conduct research about 2.70-6. similar to the limit of detection for this Report (Anderson et al.73-9.80) 1. < LOD means less than the limit of detection.60) 6.6 (11.98-7. Biomonitoring studies on levels of 2.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.40) 2.09-7.80 (2.0) 11.85 (2.63) 90th 15.76) 3.23) 3.20 (3.20-23.9 (11.9) 694 677 519 696 602 931 Limit of detection (LOD.1 (10.6-TCP (0.4 (17.0) 10.7 mg/L.4. was about six times lower than the median urinary levels for males in this Report (Radon et al.36-5.0) 19.47 (3.0) 13.0) 12.3) 23.90 (3.5-TCP or 2.95 (4.7) 33.4.18-3.14 (2.0) 13.4.28) * 2.60 (2.9 (13.08 (2.67-12.23) 2.49 (6.70) 5.32) 3.40) 3.40) 4.0 (11.04) 2.40-14.80-25.8 (9.4.80-20.60-21. Survey Geometric mean (95% conf..98-11.0 (6.10) 2.0-68.40 (2.0) 14.20 (3.78 (2.45 (2.6TCP values.6TCP causes an adverse health effect.40) 2.9) 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 2.48-26.40-32..32) * 3.55-3.06) * 2.10) 6.90 (4. for males in NHANES 19992002 (Agramunt et al.24 (2.2 (14. Urinary 2.70) 5.45) < LOD 11.4-17.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.0) 10.0 (12.6-22.60-3.75 (8.3-26.4.45 (5.58 (1.2) 25.6-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.4.40-2.0 (16.10-3.5-TCP and 2.6-TCP exposure and health effects.65 (5.6 mg/g creatinine) and 2.0-50.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.36 mg/g creatinine.00-4.0-41.80-6.1-25.0 (8.5-TCP or 2.40-2.6-17.4 (8.26 (2.3) 20. interval) 2.60 (3.4.99) 6.7) 21.4.07 (<LOD-3.0 and 1.53) 2.0 (14.69 (3.0) 13. 114 Fourth National Report on Human Exposure to Environmental Chemicals .2) 12.5-TCP and 2.79 (5. the median urinary 2.6-TCP than are found in the general population.3) 37.35-3.6-TCP in urine does not mean that the level of 2.30-2.0) 7.78 (2.6-TCP level.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.59-6.7 (13.23-2.0) 13. In harbor workers exposed to chlorophenol-contaminated river silt.5-TCP or 2.4 (9.12) 2.5-TCP or 2.5-TCP and to the median 2.3-17.40 (2.0-54.0 (9.4.0 (6.33-4.4.4. 0.65) 15.3 (11.3.0 (14.0-37.51-12.90) 2.2-0.40-4.95) 3.70 (2.8-13.80 (2.85) * 3.0) 9.0-44.80-7.53) 4.0 (15. 2003).20) 4.52 (2. which may vary for some chemicals by year and by individual sample.91-4.0) 6.4.74-3.10-2.00 (2.0 (20.09) 15. 2004).3 (11.30-2.70) 3.0-18.0) 19.25-11.30-33..80 (3.5-TCP level of 0.7-16.10-3.90-8.7 (9.60) < LOD 5.7-3.68 (<LOD-2.40-7.20-6.60 (3.00 (1.50 (2.8) 32.72-10.4 (10.4.0-38.58-3.6) 21. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.30) 4.0-38.89-6.8) 18.95-6.28) 24.0 (20.32-4.1 (8.4.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.84) 2.70-3.0) 14.0 (14.57 (<LOD-2.4. 1991). population from the National Health and Nutrition Examination Survey.56 (3.30-11.00 (4.6) 26.9) 13.0 (6.8-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-21.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.4.. respectively. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.31 (3. Finding a measurable amount of 2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.0) 17.8-15.4.02) 2.0) 17.0) 11.0 (15.5 mg/g creatinine) were similar to the limit of detection for 2.0 (4.60-37.74 (2.46-3. Mean values of 2.50-5.92 (2. Urinary 2.66 (8.4.59) 4.6-19.5-46.52-3. 1998).0) 7.1) 16.67) 4.31) * 2.20-3.4.0 (8.6 (12.0 (7.89 (3.70 (2.10 (5.S.01-6.54) 6.0 (13.0-43.45-9.44) 75th 4.87-14.

25-2.2) 19.1 (8.10 (6.0 (11.11) 10. population from the National Health and Nutrition Examination Survey.1) 14.63 (<LOD-2.0) 8.4) 8.6) 8.98 (1.91 (3.63-13.8 (8.44 (3.6 (22.83-6.79-17.22 (3.35 (3.88 (2.25-15.4 (11.32 (2.91-2.17) 13.2 (12.40 (2.52) 2.63-15.83-6.38 (4.87 (3.87) 2.3 (9.55-2.42 (2.38-5.76) 4.24 (1.46-14.22-2.51) 18.65-21.56-5.13 (1.94-13.3-23.8) 12.77) 2.9 (9.5 (8.20-2.82 (8.2 (7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88-7.49) 4.14-13.15 (1.52 (5.1-21.5) 12.95-2.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.10-9.3) 8.04-2.16-10.06-2.65-2.9-29.02) 3.1) 11.52 (3.88) 5.60 (4.87-6.62-15.78) 90th 12.50-8.8 (7.02 (1.38) 22.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.25-17.63) * 4.8) 19.17) 2.73) 5.29 (6.6 (12.18-4.13-6.78) 2.9) 7.33-2.43-7.04-16.76) 1.00 (2.5 (7.98) 10.51-21.7) 25.82) 2.87) * 2.89) 10.18-2.5) 11.76-8.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.9-64.92) 4.82 (3.6 (9.63) 4.05 (6.88) * 2.76) 2.4) 4.S.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.38 (2.42) 2.6-31.56 (7.7-36.3-37.17-4.83 (3.88) 1.6 (6.6 (5.96) < LOD 4.53) * 2.40 (7.6) 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 2.43 (2.9-34.70-9.41 (3.06) 11. Survey Geometric mean (95% conf.87-7.10) 4.27-9.5 (10.00) 4.43 (<LOD-2.1-32.66-4.71 (3.19-5.32-19.26-13.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.63 (2.58 (4.25 (3.2 (8.Organochlorine Pesticides Urinary 2.33 (7.8) 11.67-17.6) 13.53 (3.28-4.00 (3.5-28.89-2.33 (1.49-3.90 (1.78 (2.54 (2.75) 75th 4.41-6.91 (7.5) 11.59 (2.09-3. interval) 2.51 (2.08-2.9 (9.99-2.01 (3.68) 2.7 (14.0 (9.29-4.53) 4.0) 10.56) < LOD 11.47-5.2 (13.25 (3.06) 4.60-2.65) 2.72) 32.5) 8. Fourth National Report on Human Exposure to Environmental Chemicals 115 .50 (2.22 (1.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.83-5.21-11.88) 4.90) 2.26 (6.00) 4.9) 8.6) 12.82-2.77-4.9) 8.68) 2.52) 2.73-22.9) 19.22 (<LOD-2.65) 18.15 (6.0 (6.88) 4.9-32.29-4.8) 21.1 (13.53-11.14-2.81-9.48-2.23) 4.22-9.33) * 2.72-16.6 (9.4) 9.7) 6.4.81) 2.30-2.4 (12.5) 9.6 (10.23 (1.05 (3.

Radon K.EPA). The metabolism of higher chlorinated benzene isomers. Hill RH Jr. html. Schulz C.epa.54(3):203-208. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Can J Biochem 1976.cdc. Shealy DB. Holler JS. Kohli J. Wegner R. Poschadel B. Falk C. Available at URL: http://www. S. December 2006 Draft. Urinary excretion of chlorinated phenols in saw-mill workers.S. Pekari K. Baur X. Olson J. Domingo JL. et al. Seifert B. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Szadkowski D.45:440-445.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Toxicol Lett 2003. U. Environmental Protection Agency (U. Safe A. 206:15-24. Int Arch Occup Environ Health 1991. Chlorophenol exposure in harbor workers exposed to river silt aerosols. To T. Heinrich-Ramm R. Needham LL. Anderson HA. Jarvisalo J. Jones D. Arch Environ Contam Toxicol 1989.gov/toxprofiles/tp107. Smith SJ. Environ Res 1995. Lindroos L. Hanrahan L. Am J Ind Med 2004. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Fast DM. Hill RH Jr. Bailey SL. July 1999. Toxicological profile for chlorophenols [online]. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Burse VW.71:99108. Corbella J. Environ Health Perspect 1998. Aitio A. Domingo A. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. et al. Needham LL. 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]. Seiwert M.18(4):469-474. Kaus S.63:57-62. 4/21/09 Agramunt MC. Available at URL: http://www. et al. Gregg M. Head SL. Luotamo M. Int J Hyg Environ Health 2003.106(5):279-289.146:83-91. Baker S.atsdr. The Great Lakes Consortium.pdf. Becker K. Pesticide residues in urine of adults living in the United States: reference range concentrations.

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

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

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

40-16.86 (1.56-13.10-7.52) 6.4 (7.15) 14.599-1.0 (7.0) 9.10 (2.48-7.0-28.6) 18.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.27-15.21 (.290 (<LOD-.68-7.490-2.56 (4.8-32.20 (2.1-23.07-10.34-7.26-6.0 (8.717-1.30 (2.42) .1 (9.66) * * 1.9) 8.82-12.13 (2.70 (2.19) 9.757-2.80-22.00-12.47) * * 1.0) 6.28) 1.53) 4.54 (3.954 (.50 (2.9) 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 1.71 (2.45 (2.9-18.70) .83 (5.10 (.0 (9.04) < LOD 1.86-15. and 0.5) 15.47) 5.700-1.72) 5.08-15.0 (12.60 (5.90-4.60 (1.2.9) 14.61) 4.71-9.80) .4 (9.740-2.80) 2.36-4.96-3.39 (8.79-7.70-11.79 (5.0 (7. which may vary for some chemicals by year and by individual sample.890 (<LOD-2.40-5.00-19.20-30.12) 4.1) 95th 13.58 (3.0 (7.00) 3.80) 2.20-4.2 (14.70) < LOD < LOD 75th 3.0) 11.0) 7.0) 11. 01-02.90 (1.20 (.40-11.7) 11.2) 14.97) 8.80) .4 (9.0) 11.530 (<LOD-2.2 (9.10 (2.0) 6.89) 9.00-12.1.80-4.00 (5.2) 16.50) 2.9 (8.0 (5.8) 7.63) 1.46) 10.56 (1.90) 2.44-38.0-27.830 (<LOD-3.860-2.0 (6.981 (.98-12.80-24.2) 16.40-1.60-11.32) 1. interval) 1.17-3.90-5.0 (7.22 (.90) 3.50-5.13-2.00-27.30-6.60) < LOD < LOD 4.8 (14.98-5.0) 10.97) 90th 7.99 (5.8 (9.4 (7.00-7.20 (.91) 4.623-1.08-2.2 (7.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.85 (3.56 (6.750-1.00 (1.620-1. population from the National Health and Nutrition Examination Survey.70 (4.5-17.13 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (4.2) 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 1.58 (5.0) 10.81) 1.32 (.61 (3. 0.80 (4.5 (11.2) 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 1.00-27.3) 17.80) 3.02) 4.29) * * 1.2 (9.4) 17.1) 10.67) 3.80) 11.8) 11.1) 13.0) 20.0 (6.33 (5.70-23.0) 10.02-5.26-8.290 (<LOD-1.26 (5.3) 14.6) 7.5-16.0 (8. respectively.7 (14.5) 20.82) 10. see Data Analysis section) for Survey years 99-00.94) 3.27-3.2 (7.1-17.70) < LOD < LOD 1.40-19.0) 5.35-11.40-14.01) * * 1.80) 4.52) * * 1.8) 7.20-7.05-7.93-24.93 (4.0 (9. < LOD means less than the limit of detection.40 (.76 (2.60-25.2 (7.37 (3.74 (8.0) 10.8 (12.23-5.20 (.70-19.8) 19.11 (.8 (8.2 (11.16) 4.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (.50-36.80 (2.840-1.81) 11.50 (.0) 5.0) 5.0) 11.74 (8.810-1.00) 3.30 (2.3) 16.70-14.0) 10.4) 18.55-6.758-1.14) * * .10 (.0) 12.55-8.57-7.10) < LOD .12-19.970-2.33-18.43-12.7 (12.08 (<LOD-2.3-15.2-20.2 (14.0) 15.0 (8.1 (10.780) < LOD 3.44-3.44 (2.5 (8.60) .35-16.94) * * .00 (4.2.0) 6.30 (4. 120 Fourth National Report on Human Exposure to Environmental Chemicals .955 (.80) 2.73) * * .35-12.670-1.51) 2.58 (2.600 (<LOD-1.95) 5.39 (3.30-4.579-1.34-3. and 03-04 are 0.15-12.S.60-18.10) < LOD < LOD 4.03 (.42-3.0 (4.81) 11.38-5.52-11.16 (2.21) 9.4) 20.

960 (<LOD-2.28 (5.00-19. population from the National Health and Nutrition Examination Survey.56) .46) 2.8) 7.37 (5.710 (<LOD-1.34) < LOD < LOD .5 (4.2 (10.69 (4.28-9.66 (5.36) * * 1.01-2.54-2.9-28.66-15.35) < LOD < LOD 3.00-13. interval) .93-9.5) 11.40-14.57) 4.89-3.45-11.40-28.95 (3.81 (1.90-8.46-5.85) 2.41) Selected percentiles ( 95% confidence interval) Total * * 50th .53) 9.56-13.1 (8.0) 6.2) 7.47) * * .75) 14.09 (.6) 8.57-10.37-3.7 (10.890 (<LOD-1.71-2.79-9.80) 9.75 (3.5-32.780 (<LOD-1.43 (.37 (4.62-5.74) 4.82-14.9 (9.6 (9.41) .76-4.24-3.88) 2.870-2.05 (.87 (1.6) 11.440 (<LOD-2.52) 4.41-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.42) 12.84 (5.7 (9.650-1.4 (9.9) 16.06-2.03-6.2) 95th 12.83) 8. Fourth National Report on Human Exposure to Environmental Chemicals 121 .69-10.98) .04 (1.75-7.00 (4.80 (2.9 (5.830-1.S.30) 2.67) 1.540-1.1-15.03 (7.03 (2.37) 9.574-1.42 (3.53-11.5) 7.820 (.58) * * 1.79-3.67-19.1 (11.93-5.28 (4.43) 2.68-4.98) .40-5.4) 4.47 (1.2 (8.533-1.996 (.633-1.81-5.60-9.3) 5.66-34.21-23.54) .00-17.0) 7.18 (.3) 15.61-29.69) 4.02 (7.94 (4.09-11.87 (3.51-5.82-6.69) 2.11-6.7) 18.19 (4.80 (7.78 (2.40-3.773-1.57 (4.14 (3.02-14.66 (2.27) < LOD 2.860 (.818 (.23) 4.02-2.2) 8.98) 9.82-26.88-15.60) * * .77 (6.9 (9.430-1.2 (6.4) 13.15-10.02 (2.510-1.34 (6.790 (.45-5.43 (3.61-13.7) 5.920 (.5) 8.8) 12.10-13.2) 9.55-20.72) 11.34) * * .10 (3.40 (3.3) 16.64-5.31-14.2) 13.54-15.40) 4.68) < LOD < LOD 3.32-12.9) 11.44 (2.13) 4.620-1.560-1.28) 10.09) 2.1) 4.1) 4.1 (9.83 (7.82-14.5) 7.1 (10.40-12.4) 4.7) 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 .94 (2.94-22.05 (1.73 (1.89) * * 1.28 (2.98-22.750 (<LOD-1.3) 12.88 (5.47 (3.2) 5.1 (6.56) 7.47 (3.94-23.5) 12.45-5.47) 2.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.883 (.608-1.71) 10.92-2.549-1.67) 4.39 (2.0 (8.8) 6.8) 16.25) 6.61 (1.74) 90th 7.54-4.98-5.53 (6.88-10.60) 2.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.37-5.80 (6.92-5.38 (1.61 (1.66 (1.924 (.54-11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.26) * * .98 (3.03) 2.57 (6.87-5.76) < LOD .6) 9.31 (3.1 (7.932 (.9) 12.75) 2.5-20.2) 5.7) 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.8) 8.6 (10.500-1.35 (1.4 (4.94-10.25) < LOD .29 (2.855 (.75 (7.07 (.85 (6.40) < LOD < LOD 75th 2.00) 8.3) 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 1.8 (10.20-8.90-5.30 (1.7) 12.04-6.94-9.95) 2.62) .29) * * .93) 9.50) 7.7 (8.5-13.05) .6) 13.960 (.570-1.38) .5-16.00 (4.900 (.566-1.84) 7.23 (4.34 (6.890 (<LOD-1.56) 4.03) 2.

9-15.35-3.7 (11.95 (2.6) 14.00) 7.80-12.670 (<LOD-1. see Data Analysis section) for Survey years 99-00.00 (.11-6.30) 8.89 (2.10 (.30) < LOD < LOD 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 11.45 (3.30) < LOD < LOD . which may vary for some chemicals by year and by individual sample.24-5.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.22 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.82) 8.86-10.0 (5.3 (9.20) 3.00-4.0-29.00-16.580-2.0 (10.34-10.01 (2.90) 4.24 (2.90 (5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9-17.34-5.00-18.5.75 (2.7 (10. 0.90 (6.39-13.88) 10.5 (8.98-9.29) < LOD < LOD < LOD < LOD 3.650-1.0) 6.0) 11.92-17.27) .9 (12.0-24.3 (12.00-9.9 (7. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .50-5.66) 4.80-3.28 (7.3) 14.50-4.7) 10.680 (<LOD-1.30) 3.40 (2.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (13.0) 14.8 (12.88) 3.95-9.8-21.25 (2.60 (6.90-31.30) 3.40 (2.0 (15.5 (9. 01-02.46-4.72) 2.90 (2.6) 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 * * * 1.52 (6.90) 8.95 (5.20 (<LOD-2. < LOD means less than the limit of detection.2) 14.5-26.90 (6.3 (7.61-32.37) 2.89) 2.90 (2.74) * * * * * 1.20-8.7-21.1 (10.35) 4.1-23.20) .90 (1.20-4.18) * * * * * * * * 1.0) 13.9) 10.90-15.5) 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 * * * * * * .8 (12. and 03-04 are 0.0) 18.51) < LOD 1.7) 14.81-6.0-33.2 (9.77-3.2 (7.96) 90th 7.3) 20.3) 22.97-4.1) 11.90-9.0 (9.15-6.60 (2. respectively.80 (5.6) 14.6 (10.9) 16.9) 95th 14.4 (10.10-10.0 (10.10-4.80-21.53 (3.62-17.80 (2.60 (5.4-17.740 (<LOD-1.6) 11.27 (7.27) 9.20) 3.970 (<LOD-2.670 (<LOD-1.6-41.6) 18.31-12.35 (6. and 0.14 (6.7) 16.7) 15.70-8.3 (11.42 (1.10-15.47-6.61 (3.4) 7.6 (10.41) 3.58 (1.90-15.00) 3.670 (<LOD-1.00-18.80-14.3 (9.00) < LOD .22-12.5) 21.04 (3.31) 1.0) 23.41-5.63-14.0) 9.0-19.27) 4.33-11.5 (8.0 (9.80) .92) 9. population from the National Health and Nutrition Examination Survey.80-6.96) 3.59-3.4 (10.0) 9.0) 12.9) 9.16-1.70-9.34 (6.39 (5.790 (<LOD-1.90 (6.90 (2.9-14.12 (4.67) 3.80) .66-13.0) 13.0) 7. 122 Fourth National Report on Human Exposure to Environmental Chemicals .00-4.22) 8.3) 8.50) 5.7-19.22 (6.67-10.70-5.8-20.6-19.29-4.37 (3.70-9.73) 7.10) 6.3) 10.1 (10.80) 5.0) 19.50) .0 (14.75 (3.84-4.70) 2.7) 22.20-18.46-28.0) 14.18 (3.670 (<LOD-1.0 (8.40) < LOD < LOD 75th 2.S.67) 4.80-8.0) 12.58.77-14.06 (2.4 (14.00) 3.34-3.64) 10.17 (7.27 (3.99 (3.80-4.50) 3.60) < LOD < LOD 2.31-7.0) 11.15-2.10 (<LOD-1.8) 9.70 (8.49-4.910 (<LOD-2.8) 8.8-20.0-24.90 (6.3 (6.5.0) 12.70 (1.8-17.00) 8.78) 5.80 (2.0 (7.

54) 9.21) * * * * * 1.33-10.07) 2.2) 12.89 (2.44-6.8) 11.54 (7.71 (1.86 (3.8 (8.03) 3.6) 7.7-23.88-7.2) 12.7 (10.91-9.4) 9.7 (8.93 (6.01-5.89-3.3-34.4-18.7 (11.78-10.97-4.92 (5.2-15.0) 14.51-7.34) < LOD < LOD < LOD < LOD 3.9-25.30-5.04) 9.45) 6.5) 10.85-17.00 (7.5-17.3) 12.27) * * * * * * * * 1.1) 20.50-17.80) 3.54-5.82-11.3-21.2 (9.67 (7.7) 9.530-1.5 (8.1) 13.05-3.93 (2.25 (4.2 (9.50 (6.42) 8.38 (2.5 (11.09-11.6) 14.9-17.72-4.7) 12.25-9.55) .29) 3.00 (5.99) 2.06) .00) 8.07) 2.03 (2.810 (<LOD-1.64-11.68-10. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .37) 3.09-11.86-3.41 (7.47-9.5) 22.06 (<LOD-1.96-10.29 (5.38-13.55) 16.00) 2.37-5.6) 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 * * * .81 (7.36 (2.89-10.940) < LOD < LOD 1.91) 3.38 (1.5) 8.78 (6.9 (9.2) 16.83 (7.760 (<LOD-1.2) 10.86) 9.620 (<LOD-.6 (11.34-18.23-3.30) 2.30) 7.4-16.77 (2.75-3.61 (2.4) 16.74-4.39-17.910 (<LOD-1.11 (5.0-19.29 (2.6 (10.95) 90th 8.00 (<LOD-1.920 (<LOD-1.69-11.94-14.3-17.95) 3.6 (13.77) 3.77 (2.52-3.0 (11.27) 1.890-2.79-6.780-1.18) 2.7) 15.11-3.63 (6.4) 6.53-8.89 (3.99 (4.7) 14.2-30.4) 7.59-3.16 (3.2) 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.67 (1.72) 4.950) .78) 4.78 (4.590 (<LOD-.68-19.51-10. Fourth National Report on Human Exposure to Environmental Chemicals 123 .6) 12.82-8.6) 95th 16.6 (11.S.16-14.07-3.68) .3) 6.9 (9.6-19.1) 10.88 (1.5 (10.2) 12.43 (2.92) 3.00 (<LOD-1.6) 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 * * * * * * .30) 8.85-8.5 (9.19) 3.96-11.2) 15.2) 19.4) 7.07 (5.97) < LOD .3-17.89) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48 (2.32-8.14 (2.9) 16.71) < LOD < LOD 2.70-35.6 (13.7) 14.15) < LOD < LOD 75th 2.6) 6.4-15.42-19.8 (10.1 (13.21-21. population from the National Health and Nutrition Examination Survey.2) 8.7-19.6) 13.02-4.20-3.00 (2.87 (3.3 (7.9) 19.63 (2.89-13.03 (6.27) < LOD .83 (6.45) 3.850 (<LOD-1.5) 13.38 (.95 (2.27) 5.15 (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.690 (.28 (1.6) 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 1.8) 16.55 (2.9 (9.1 (8.33) 3.28) 6.0 (8.4) 15.4 (11.58 (4.3-15.70-2.73 (5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (15.94 (5.00 (3.93 (<LOD-2.38) 1.4-16.0 (13.12 (7.89-3.7 (10.74-19.3) 9.29-2.27-13.28-12.12) < LOD < LOD 4.68-4.0-21.3) 8.4) 7.973 (.8) 14.32) 2.75-3.79-9.6 (12.93-10.1 (19.42) 7.0 (10.

19-1.54-2. 0.31-3.95-5.59-2.440-.940) < LOD .592) * 50th .15) 2.26) .17) 1.800 (.70 (1.26 (2.70-7.30 (.730) .20 (1.50 (1.618) * .820 (.20-2.32-1.280-.740-.50 (1.91) 2.860) < LOD < LOD .20-3.20 (2.587) * * .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 * .73-5.1.780 (.580-1.94 (3.450 (<LOD-.398-.32) 3.710 (.30) 1.600-1.201-.592) * .720 (.750) 1.350-.90 (1.490 (<LOD-.03) 1.960) .41 (2.54 (2.01-3.60 (2.83) .600 (<LOD-.570-1.05-2.90) 3.97 (2.09 (.80) 2.880 (. 124 Fourth National Report on Human Exposure to Environmental Chemicals .400) .10-1.83) 1.690) .650-.540 (.580-.45 (1.60-4.990-1.49) .18 (1.30 (.20) 3.780) . which may vary for some chemicals by year and by individual sample.380-.77 (1.89) 1.80 (1.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .690-.88) 1. interval) Selected percentiles ( 95% confidence interval) Total * .46-3.759) * .425 (.460-.20 (1.910-1.98 (2.76 (1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.94 (2.16-3.710 (.390-.00) 1.74) 3.45 (1.960-1.30) 4.31) 95th 2.22-3.720-1.29-2.45 (2.880) < LOD 75th .930) 1.50-2.61 (1.20) 2.55 (3.30 (.380) .10) 3.850) < LOD .37-2.820 (.457 (.22-8.95 (2.46 (2.970) 1.50 (1.60) 3.790 (.740-1.46) 1.560-.160 (<LOD-.89-6.20) 2.00) 2.459 (.21) 3.32 (1.96-5.33-2.80) 3.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.49) 2.353-.34) 2.80) 5.31) 2.810) .700) .260 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.680-1.31-3.50-2. respectively.30) 2.58 (1.657) * * .720-1.50) 1.35) 1.38) 1.16) 2.47) 2.34) 2.680-1.47 (1.90) 2.340-.74-5.48 (1.960 (.01-1.30-3.20) 1.13) .388-.17) 1.27 (2.690-1.740 (.14-1.13) 2.23-3.83) 2.240 (<LOD-.930) < LOD .20) 3.590-.10) 1.749 (.30) 4.16) 1.95) 2.73 (1.80) 3.11-3.390-.597) * .980) 1.87-3.910) 1.40 (1.336-.14 (1.600-.50 (1.64 (1.510 (.840 (.592-.40 (1.18 (.73 (2.30-1.570 (.343 (.98) .60) 2.80 (2.910 (.11-3.930-1.41-5.57 (2.960) .22-2.77-2.20) 1.96-3.50 (1.80) 2.455 (.89) .69-4.549 (.75 (2.15) 2.63 (1.86 (1.70 (1.780 (.01) .27 (3.68-5.584) .S.09.10) 1.08 (2.960) 1. population from the National Health and Nutrition Examination Survey.75-2.880) < LOD . and 0.05-3.500 (<LOD-.760 (.00 (1.22-3.670) .380-.585) * * .570 (<LOD-.25-1.620-1.700) .80) 3.29) 1.48 (2.10) 1.42-2.949) .20 (1.00-2.04) 1.39) 2.76-6.690 (.830 (.570 (<LOD-.00-4.04) .94) .467 (.22 (1.57 (1.08 (2.98-3.449 (.550 (. see Data Analysis section) for Survey years 99-00.70 (1.570) * .382-.78) .2.83 (2.17-4.30-3.510 (<LOD-.210 (<LOD-.70-2.59-6.90-4.303-.970) . < LOD means less than the limit of detection.54) .20-2.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .79) .46 (1.90) 2.359-.750-1.930 (.10-1. and 03-04 are 0.30 (1.36-4.740 (.45-4.570 (.65 (2.86) 3.83 (2.20-1.710) .453 (.350-.79) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.950) 90th 1.505 (.550 (. 01-02.

39 (1.20) 1.14 (2.61 (3.43) 1. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 125 .07) 1.830) 90th 1.S.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 * .23) 2.460 (.11) 1.08 (.870) .02-3.77 (3.42-8.79 (1.471-.470 (<LOD-.07) 1.07-2.830 (.550-1.47 (1.50) 1.05 (1.30) 3.515) * * .60 (2.310-.55-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60 (1.92 (1.18-2.97) 2.43) 2.740) .49 (1.30-2.590-1.75) 6.16-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75 (2.700 (.900) 1.02-6.71) 2.77-4.42 (.61-3.320-.63 (1.800-1.61) 2.280 (<LOD-.38-3.97) 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.60) 1.32 (.710 (.08-2.00-3.08 (2.98) 1.00 (3.640 (.440-1.04-5.38 (1.742) * * .580) .29-4.25-3.710 (.597) * .11 (.700 (.71) .760) .535 (.350) .57-4.370-.500-.320-.07) 1.490 (.08-3.77-3.82 (2.99) 2.720-1.08-3.47 (1.680 (.44-2.700 (.55 (1.07) 5.44) 2.23) 1.520 (.57 (1.42-6.97 (1.75 (1.04-1.05) < LOD .510 (.97 (1.520-.348-.24) 4.60) .870 (.00-1.590 (.49-4.61-3.645) . interval) Selected percentiles ( 95% confidence interval) Total * .20-7.66) .10) 2.64 (2.67) 1.910) < LOD .33) .17) 2.38 (2.69 (1.880) 1.840) .39) 2.73-3.580-.07-3.591 (.453 (.16-2.234 (.318-.412-.485) * * .390-1.305 (.16) 1.05-2.940-1.04) 95th 2.372 (.460) .45 (2.950-2.91 (1.330-.05) 1.380-1.73 (2.920) .590) * 50th .72) 1.460-1.03-2.99) 1.90) 2.70 (2.67-3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.310 (<LOD-.540-.28 (1.78) 3.97) 1.08) 1.43) 2.62 (2.510-.377-.87 (2.32) 2.50 (1.980-1.32-1.89 (1.300-.66 (2.32) 1.180 (<LOD-.08) 2.560-.88 (1.400-1.52 (1.310 (<LOD-.285-.640 (.253-.447 (.480-1.41 (.739) * .250 (<LOD-.630) * .393 (.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 * .71 (1.23) 2.740) < LOD 1.390) .69 (3.580 (.17) 2.88) .850) 1.330 (<LOD-.08-2.62 (1.270-.94) .448 (.58) 3.43 (1.07 (.06) 4.70 (3.690) < LOD < LOD .06-2.80) 2.380) .33 (1.23) 3.58 (1.02-3.57-2.64 (2.688) * .400) .22) .81) 2.52) 3.20-2.550-.67 (1.05-4.22-2.760) < LOD 75th .560 (.790) .840) 1.550-.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 * .23 (.730) .444-.22-3.335-.75-3.820) 1.32) 5.560-.84 (2.72-4.31-1.89-3.22-3.136-.368) * .403) .03-1.53) .09) .640 (.552 (.270 (<LOD-.92) 3.57 (3.72 (2.47-4.67) .76) 1.08-2.13 (1.750 (.930-1.22) 1.660-.300 (<LOD-.800) < LOD .22) 4.480) .530 (.990-1.790 (.79) 1.34 (1.36) 3.17-2.82) 2.67 (1.22 (2.230 (<LOD-.270-.19 (1.58-6.550) .840) 1.95) 1.380-.820) .720 (.08-3.42) .509 (.470) .670 (.750 (.250 (<LOD-.08-3.65) 2.72 (1.45 (1.84-6.510 (.11-2.710 (.92-8.

54 (1.7 (12.00 (.58) 16.5) 30.4) 38.9) 17.45) 2.70 (1.2-27.05-3.70 (.46-2.1 (22.1) 18.1-19.8 (12.0) 19.44-7.00 (.0 (11.830-3.9 (10.4) 19.18) 20.70 (7.600-2.0 (24.85 (1.80) 90th 38.18) 6.0-110) 42.40) 50th 2.60 (2.65 (4. 0.3) 31.41 (1.50-17.0-41. 126 Fourth National Report on Human Exposure to Environmental Chemicals .77 (1.90-8.79-2.42) 1.5-45.0 (26.70-6.0) 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 2.0) 6.53 (1.46 (.5-20.90) 11.660-2.690-3.21 (4. respectively.1 (25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 140 (46.12) 1.9) 48.0) 15.6 (11.27-6.21 (1.5) 69.13 (1.0 (19.30-14.0) 4.0-52.8-21.44) 3.0) 3.83 (3.4.07-5.9 (27.44) 2. < LOD means less than the limit of detection.46-6.26) 75th 11.0) 45.0) 32.16) * 1.20-4.32 (2.2) 16.40-4.1 (26.26 (.79 (1.0) 5.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.29) 2.0) 3.0) 31.0-58.88) 1.87-7.0 (6.50 (2.0-69.3 (12.0) 15.2-27.05) 1.41-4.0-62.81-3.13) 12.0-49.530-4.470 (<LOD-1.4 (15.92-5.52 (4.4 (19.3 (10.78 (1. population from the National Health and Nutrition Examination Survey.35-6.85) * 2.S.90 (1.2-33.66-5.02 (2.9) 38.72 (1.0) 16.63-6.6 (26.10 (1.36-2.04) 3.5-74. see Data Analysis section) for Survey years 99-00.3 (23.0-43.7-22.64-3.61 (1.0-53.99 (2.23-2.0 (38.7 (28.0) 42.33 (5.4-76.0-31.70) 1.0) 16.1 (11.1 (25.69) 2.58-2.30) 4.80-18.40) < LOD 2.0 (33.1-46.8) 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 1.53) 1.11) 2.0 (25.5.3) 33.0-39.10 (7.9 (19.53) 40.31-6.70 (1. interval) 1.30 (.0) 3.97) 6.29-4.3) 26.98 (1.0-53.10 (1.59 (1.8 (12.0 (21.3 (24.0) 18.53) * 2.17-2.0 (13.0 (8.0-41.50-20.8-24.1 (10.21 (3.7 (12.81-2.50-7.71-2.64-8.41) 1.6 (15.70-17.0 (38.41) 5.0 (38.0) 28.610 (<LOD-1.18) 14.0) 20.6-45.70) 5.5 (24.91 (4.0-260) 34. which may vary for some chemicals by year and by individual sample.9) 18.48-2.48) 5.29-9.0 (38.0) 8.80) < LOD 1.0 (38.0) 30.1-40.50-2.90 (1.0-50.0) 28.71 (4.0) 3.10-4.0-58.13 (1.06 (1.09 (4.0 (20.80-2.12 (3.2 (12.59 (1.3) 38.40) < LOD 1.77) 38.76 (2.95 (5.94 (1.0 (40.0) 4.86-3.7-41.4 (10.0 (37.00-24.49-2.79 (2.0 (20.2-47.41) 1.48-2.83 (1.83-2.6-54.9 (23.11 (4.60) < LOD 1.8) 32.3 (14.0-92. 01-02.57-2.61-2.1) 95th 48.0 (38.10) 39.06) * 2.16) 2.80) 1.19-2.30) 11.98) * 2.1) 38.19) 2.04-8.23) 9. and 03-04 are 0.25-3. and 0.1-20.82 (1.93-3.45) 2.3 (12.0 (8.86 (1.8 (26.2) 31.6-22.10 (1.0-110) 34.9 (19.10 (1.0-47.74-2.05) * 2.830-4.3) 28.50-5.7) 20.6-27.5-27.2-26.0) 17.40-16.1-47.0-39.5-40.0) 17.9-21.0-62.0 (32.0-41.6) 52.76 (2.0 (17.0) 33.10) .0) 13.75-14.9-51.0) 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 2.92) * 2.2-80.44) Selected percentiles ( 95% confidence interval) Total * 2.4-22.8) 39.0) 20.71) 5.0-230) 35.80) .14) 5.20) 1.2 (19.1-25.70) 1.78) 9.23-2.43-7.0 (8.83-2.20 (2.0 (38.7) 47.88) 3.04 (<LOD-2.0-29.8) 62.18.67 (1.8) 41.2-39.57-2.1) 38.8 (22.10-13.0) 4.2-62.54 (3.96) 5.0 (7.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6 (9.

5 (8.50 (2.61-2.1-22.6-51.61 (1.9) 3.4 (9.4-39.47 (3.2) 36.37 (1.0 (17.860 (<LOD-1.0 (23.97 (1.3) 28.79 (2.7-37. population from the National Health and Nutrition Examination Survey.5) 70.33) 2.2 (9.7 (11.32-3.60 (.40-7.46-22.62 (2.4 (25.35 (2.95-16.19) 5.2) 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 2.6 (7.7-20.48 (4.0 (19.57) 4.6) 23.38-5.6) 7.16 (1.67-16.0-118) 29.27) 50th 2.8) 32.2) 4.27 (6.83) .2) 13.71-2.68) 47.7) 34.51) .4) 12.08) 1.4 (11.15 (.28) 1.46) 1.2-34.7) 95th 51.61-22.7) 61.5-36.0) 13.88 (4.0) 48.4 (21.07-2.95-16.36) 10.00) 1.8) 11.2) 13.71 (1.0 (25.54-2.30) 28.1) 52.1) 17.48) 1.66 (1.25-3.1) 25.9-37.67-3.5-97.29-5.9 (39.41 (2.7 (18.67 (1.28 (1.86) * 2.16 (1.46-6.11-2.4 (12.37-2.4 (5.4-34.72) 2.59-15.56) 1.33) 1.20) Selected percentiles ( 95% confidence interval) Total * 1.8) 3.14 (.02) * 1.9-52.8-26.9 (26.44) 9.60) 4.2 (21.50-5.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.3-19.91 (6.2-70.53) 1.45-1.52 (1.84-13.99-4.20-5.06) 1.7-43.0) 25.6 (27.70-4.8-37.00) 6.899-2.16-2.5-43.43) * 2.02 (.95) 90th 32.14-8.5 (13.16 (1.06) 1.69-18.2 (8.4-71.7-47.62) 4.2 (15.0-71.6) 19.3 (8.7) 23.35) 1.1) 15.2-28.1 (34.9) 54.88 (1.58-2.7-38.6) 3.3-27.93) 5.56 (2.3 (20.890-4.6 (24.94-20.19-14.3 (10.23-1.63-5.670-1.8) 15.94) 1.0) 3.67 (1.8 (7.3 (9.870-3.5) 27.75 (1.33-5.51) < LOD 1.1) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (1.9 (7.07) 9.2) 33.2-38.82 (2.7) 15.9 (10. interval) 1.7-19.17-3.1-63.2-47.5 (34.54-15.0 (14.08 (1.03) 1.9-36.2) 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 1.90 (.06-1.47 (1.888-1.01 (.66 (1.86) * 3.57 (6.26-2.38 (3.6) 112 (40.5-190) 30.70 (1.27-3.40 (5.43-12.88 (4. Fourth National Report on Human Exposure to Environmental Chemicals 127 .03-2.9) 24.8-43.69-5.33) < LOD 1.0) 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 1.95 (2.5 (15.12 (1.1) 27.7 (10.40-4.1 (12.19) 5.22-2.8-45.6-38.9-18.0 (6.7 (24.22-3.2) 41. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9) 24.4 (25.58-17.5 (41.1 (25.18) 3.23) 37.5 (15.7) 30.47-17.09 (5.00 (4.4) 3.18-1.8) 31.0) 47.26-4.9 (13.75) * 1.7-109) 22.1) 13.3-22.870-3.680-4.02) 1.9-41.27) 10.18) * 2.8-34.930 (<LOD-1.6 (11.91-2.3-42.2) 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.1) 27.0-40.19 (1.34) * 1.39 (1.1 (50.7) 66.5 (6.22 (2.21 (4.83 (.55 (2.9) 12.4-67.31) 2.1-60.40 (2.0 (23.68 (1.46-5.06) 75th 9.64 (1.4) 12.22 (.00-16.0 (32.9) 3.36-13.7) 26.32 (3.6) 3.4 (19.75 (1.750 (<LOD-1.79-17.1 (39.43-2.71) 8.3) 13.96-16.80-8.23) < LOD 2.0) 10.4) 14.9 (19.35) .94) 19.82) 1.75-6.45 (1.38-1.S.6-49.0) 30.07-2.7 (18.36 (4.38) 5.66) 8.19-6.59-2.1) 36.4-21.1 (33.76-2.2 (16.9-95.0 (39.8) 23.2 (22.5 (17.88 (1.59-2.0-70.24 (1.11) < LOD 1.3 (10.52-4.17) 2.6-32.1) 25.870-3.12) 3.96) 2.6) 11.

360-.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 * * * * * * * * * .510-1.660 (.300-.730) .450 (.820 (.310 (.870 (.640) .130 (.140) .450 (.120-.830 (.230) .162) * * * * * .320 (.350) .210 (.320-.680-1.580) 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 * * * * * * .870 (.080 (<LOD-.270 (.780) < LOD 1. population from the National Health and Nutrition Examination Survey.190 (.840) .680) .1.350) < LOD < LOD < LOD < LOD .700-1.860-1.310) < LOD < LOD < LOD < LOD .130-.090 (<LOD-.32) .540) .090 (<LOD-.380-.830 (.60) 1.130-.540) .610 (. 01-02.720) .820 (.650) .680-1.200) < LOD < LOD .630 (.30) .870 (.630 (.05.900 (.830) .170-.390 (.700-1.990) .840) .10) .099-.870) < LOD .13) .680 (.550) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.130) .650 (.300-1.084-.40) .490 (.470-1. and 0.190 (.42) .410-.410-.610-.740) < LOD . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.190 (.990 (.650-1.640 (.050-.240 (<LOD-.12 (.330-.430-.470 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.42) .210 (.720-1.160-.220 (.160) .770 (.720 (.280) < LOD < LOD < LOD < LOD .530-.930 (.690-1.640-1.370-.450 (.090 (<LOD-.110-.10 (.560 (.150 (<LOD-.290 (<LOD-.090 (<LOD-.730-.990) .560 (.460 (.570) .390) < LOD < LOD .380-.58) .130-.400-.260 (.20) .700-1.290) < LOD < LOD < LOD < LOD 90th .230-.410-1.620 (. respectively.700-1.10) .120 (<LOD-.140-. and 03-04 are 0.00) .770) < LOD 95th .310) < LOD < LOD < LOD < LOD .380-.130) .830) < LOD .850) < LOD . 128 Fourth National Report on Human Exposure to Environmental Chemicals .640) .15) .460-. see Data Analysis section) for Survey years 99-00.860) .440-1.760) < LOD .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .370-.080 (<LOD-.160) .10) .090 (<LOD-.117 (.290) < LOD < LOD < LOD < LOD .360-.940 (.36) .100 (.850 (.600 (.610-1. which may vary for some chemicals by year and by individual sample.150) .220 (<LOD-. < LOD means less than the limit of detection.310-.1.S.540 (<LOD-.420-. 0.30) .850 (.410) < LOD < LOD < LOD < LOD .310 (.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 .171) * * .140-.430 (.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.090 (<LOD-.650) .30) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .610 (.650-1.870 (.870 (.120-.140-.180) .03) .

780) < LOD 1.380-.580) .110-.290) < LOD < LOD < LOD < LOD 90th .400 (<LOD-.110) .03 (.510-.140) .36 (1.760) .78) .960) .210 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.450) .111) * * * * * .500 (<LOD-.080) .440 (.20) 1.740) < LOD 1.190 (.67) .500) .850 (.084-.58) 1.700 (.170 (.580 (.660-1.380-.260) .140-.570-.410 (.330 (.560 (.S.580 (.600) .100 (<LOD-.540) .460 (.02-1.540 (.057-.890 (.09) .410-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .270) < LOD < LOD < LOD < LOD .43) .450 (.12) < LOD .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.220 (.720 (.070 (<LOD-.410) < LOD < LOD .970) .390-.170 (.070 (<LOD-.070 (<LOD-.02) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (.170) < LOD < LOD .01 (.540 (.360) < LOD < LOD < LOD < LOD .19 (.116 (.990) .860-2.370 (<LOD-.640) 952 1187 945 997 1328 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .140-.070 (<LOD-.60) .300 (.670-1.720 (.670 (.500-1.880-1.410) .550 (.550 (.360-.880 (.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 * * * * * * .610-1.440-1.410-.600-1.410 (.38) 1.060-.570 (.520-.780 (.380-.870) . population from the National Health and Nutrition Examination Survey.400) .180-.280) < LOD < LOD < LOD < LOD .940) .750) < LOD 95th .990) .250-.090 (<LOD-.66) 1.86) .730) .700-1.700 (.860 (.100-.230) < LOD < LOD < LOD < LOD .650-1.940) .140-.330-.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 * * * * * * * * * .710-1.260-.390-.110) .120) .570-1.03 (.310) < LOD < LOD < LOD < LOD .730 (.740 (.330-.080 (.230-.340-.380-1.330 (.110) .86) .220) < LOD < LOD < LOD < LOD .00) < LOD .24 (.800-1.360 (.650) < LOD .300-.140-.080 (<LOD-.860 (.150-.380 (.29 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.730) .810 (.700) .161) * * .050 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .62) 1.240-. Fourth National Report on Human Exposure to Environmental Chemicals 129 .300-.200 (.640-1.140-.14) 1.03 (.110) .670 (.230 (<LOD-.330-.580) < LOD .03) .120) .190-.24) .090 (.270 (.490-1.360-.190 (.580-1.320 (<LOD-.470 (<LOD-.730) .

05 (2.20 (1.29-10.38-3.0) 4.05-3.07 (1.46 (1.68) 2.00) 1.51-8.40) 1.99 (1.10 (3.97) 20.0 (13.1.30 (1.0-44.99) 19.60) .53) 20.40-7.63) 32. respectively.80 (4.14) 2.52 (1.610 (.0 (7.840 (<LOD-1.10 (.260-.83-3.600 (.87) 5.0 (16.30-6.74 (3.730 (.0-38.12-1.750-2. which may vary for some chemicals by year and by individual sample.110 (<LOD-.90-9.49 (1.35) 11.770) 2.76 (1.400-1.52) 5.01) 5.94-8.800) 90th 13.45 (2.07 (3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350-.690 (.0-40.53 (2.12) * * * * * * * * .07 (3.20) < LOD < LOD < LOD < LOD < LOD 1.0) 4.0) 4.6) 5.1.0 (4.67 (2.0) 4.840 (.640 (.70-50.840-3.0 (17.0 (4.800) 17.10-3.0) 2.55-4.24-7. 01-02.0 (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 * * * * * * * * * .620-1.960 (.60) 1.90) .47 (3.10-9.880) 5.10-3.800-4.28) .0) 2.28-9.0 (5.49) 17. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2. and 0.05 (3.85-3.0 (17.26 (2.03 (.96 (1. 130 Fourth National Report on Human Exposure to Environmental Chemicals .90) .30) 95th 19.590 (.83-3.750-1.40-8.360-1.08.14) .870) < LOD < LOD .0 (5.0-38.39 (2.42) .890 (.380-.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 .30 (2.10 (3.40-20.43-4. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.0-40.90-37.0) 2.691 (.90-28.94 (1.70-17.52 (1.63 (3. 0.74) 5.00 (1.11 (1.70-30.70) 2.55-8.31-10.82-4.48) 13.36-3.350-.94-3.0) 7.20 (1.30 (.49 (1.20-4.32-9.0) 5.53-7.33 (4.11) .480-.30-3.190-1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (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 * * * * * * .0 (17.00 (.850) 16.11) 13.90 (2.00) .35-10.30 (1.18) 1.70-7.40 (1.900 (.20-17. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 2.640 (.07-3.40 (1.510-.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.425-1.20-4.0 (6.21) 3.00-17.30 (1.210-1.0-39.910) 2.0) 3.83) 2.50) 2. and 03-04 are 0.50) .370-.0 (5.S.23-6.610) < LOD < LOD < LOD < LOD < LOD 2.07-3.0 (5.70-3.65) 1.830 (.67 (1. population from the National Health and Nutrition Examination Survey.0-38.88-3.90-20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170-1.30) .0 (17.40-4.32 (1.0) 2.99) 11.00-17.90) .960 (<LOD-1.42) 2.07) 1.30-7.080-1.720) 2.61 (1.35) 5.580 (.31) .0 (3.00) .770 (<LOD-1.62-8.250 (<LOD-.97) 20.0) 5.14-5.37) .15) 14.36-3.40) 2.59-5.90 (1.0) 2.0) 5.13 (3.51 (2.0) 2.740 (.28) 1.15) 19.0) 5.21-3.48 (2.0 (17.67) .87) 12.39) .86) 4.66) 4.330 (<LOD-1.

25-9.740-1.474-1.7 (12.390-.9) 5.96) 2.47) 5.86) .31-7.620-3.57-40.91-4.02) .770) .47) .80) 3.66-47.580) 1.07-21.5 (9.730-3.85 (1.260-.50) 11.64-4.430 (<LOD-.9 (11.6) 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 * * * * * * * * * .17 (1.930) .00-19.940-4.57) 1.3) 3.8-33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.59 (1.340-.10 (2.1) 2.14-6.580 (.650 (.7 (6.53) 27.40) 1.83 (4.89 (2.44) .35 (.31) .71 (.03) 2.18) 95th 21.450 (.7) 4.260-. Fourth National Report on Human Exposure to Environmental Chemicals 131 .4-34.1 (7.97) .0) 4.2 (8.10) 2.79 (.630-1.85-3.38 (2.190-1.80 (.28-6.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.88 (2.270-.51-4.33 (1.25-38.5-40.64) 30.47-10.69-7.67) 1.15) 9.56) 2.150 (<LOD-.39) 20.48-7.5) 7.340-.01 (1.92 (2.430) 1.780-4.840-3.88 (.67-6.790) 11.62-17.790 (.580) 16.06 (.51-44.7) 6.40 (.53) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.55) 21.55) 21.580-1.47-10. population from the National Health and Nutrition Examination Survey.7) 5.82-11.470 (.30 (4.11-5.650) 90th 10.90-6.670 (.310-.31-18.8 (20.0 (9.74 (2.55 (3.86 (3.8) 1.88) 17.3) 2.33-3.96-25.1) 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.98 (4.860-2.12-4.77 (.560 (.13 (2.50 (4.12 (4.4 (4.800-2.270 (<LOD-.370-1.02 (1.11) .48-42.1 (5.50) .500 (.40-2.22) 2.02 (.890 (.700) 6.04 (1.88-3.700) < LOD < LOD < LOD < LOD < LOD 1.820 (.29 (4.21-3.57 (.32) 9.17) 5.820) .27 (2.25 (1.49-2.370) < LOD < LOD < LOD < LOD < LOD 1.50 (2.7) 3.33 (3.05) .5 (11.84) 9.10-3.69) 2.18) 1.S.850-3.75) 5.37) 4.91) 2.960 (.370 (.8) 7.81-17. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.24) 3.8) 4.02-4.340 (.600 (<LOD-1.340-.14 (1.56) .40-12.67) 2.73 (4.240-.22-27.61) 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 .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 * * * * * * .690-5.56 (1.57) 8.5) 2.52 (.4) 2.830 (.970-3.320-1.33-4.62 (1.71 (2.590) 2.660) < LOD < LOD .31) .540 (.48 (4.36 (.5) 2.03) 16.45 (1.07 (2.18) * * * * * * * * .41) 18.67 (2.23-7.43) .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.2-38.710 (<LOD-1.8) 2.32-6.830-3.8) 2.0 (4.00) .250 (<LOD-.330-1.5 (8.360 (.60 (1.33-5.29-4.9) 6.65 (2.41 (4.09-3.44-11.96-8.540-1.08) .748 (.04-16.83-11.8) 7.

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Calvert IA. Stephens R.338(8761):223-227. Beach J. Lasarev M. O’Malley M. Frasca G. Scherer J.52(10):648-653.S. Am J Public Health 1994.52(2):190-195. Phillips J. Masala G. Salvini S. et al. Arch Environ Health 1975. Muniz J.edu/ openbook. Narang A. Kidd M. Russo J. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Available at URL: http://books. Robson MG. Bradman A.332(1-3):71-80. EPA). Pesticides in the Diets of Infants and Children. London L.43(1):38-45. Pedersen L. Santana J. Bravo R. Weisskopf C. Occup Environ Med 1995. Rothlein J. Chronic neurological sequelae to organophosphate pesticide poisoning. Myers JE. Wickremasinghe AR. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Daniell WE.2000 and 2001 market estimates. The Pesticide Health Effects Study Group. Stokes L. discrimination. Smit LA. Thompson ML. Scand J Work Environ Health 1998. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Int J Occup Environ Health 2006.12(2):153-172.nap.38(4):546-563. Lancet 1995.114(5):691-696. Environ Health Perspect 2005.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Samuels S. and spatial learning in monkeys and rats. Terry AV Jr. Schenker M. Neurotoxicology 2005. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Lambert WE. Dinoff TM. Arch Environ Contam Toxicol 2000. Am J Ind Med 1987. Berry H. Environ Health Perspect 2006. gov/oppbead1/pestsales/01pestsales/market_estimates2001. McCauley L. Available at URL: http://www. Nell V. Jenkins B. Savage EP. Burcar PJ. vibration sense and tremor among South African farm workers. Buccafusco JJ. J Toxicol Environ Health A 2005. U. et al. Hansen S. 1993 [online]. Keefe TJ. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments.20(2):115-22. Rosenstock L. J Occup Environ Med 2002. Aprea C. Lewis JA. Rothlein J.S. Saieva C. A behavioral evaluation of pest control workers with short-term. Visuthismajarn P.68(3):209-227 Maizlish N. Petchuay C. Eskenazi B. Neurotoxicity among pesticide applicators exposed to organophosphates. Washington (DC): U. Stark A. Lasarev M. Rodnitzky RL. metabolite clearance. Occup Environ Med 2001. S. Barr DB. Chrislip D.pdf. Neurotoxicol Teratol 1998. 1991. McConnell R. Bull Environ Contam Toxicol 1994. Keifer M. Vitayavirasak B. et al. Caltabiano LM. 1/12/09 Peiris-John RJ.php?record_id=2126&page=1. Irish RM. Spurgeon A. Jamal GA. Gladstone EA. Ruberu DK. Buchanan D.345(8958):11351139.84(5):731-736. Mounce LM.26(2):199-209. Steenland K. Johnson C. 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. Takamiya K. Chronic neurological sequelae of acute organophosphate pesticide poisoning. et al. Weerasekera G. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Ames RG. Pesticide industry sales and usage . National Research Council (NRC).44(4):352-357. Lu C. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Heaton RK. Pilkington A. Marshall E. Hore P. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). 4/7/09 Young JG. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Tumino R. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Effects of long-term organophosphate exposures on neurological symptoms. Gillham R. Seiber J. Arch Environ Health 1988. Effects of chronic. Muniz J.58(11):702710. Rohlman D. and cholinesterase status of date dusters and harvesters in California. Malathion deposition. May. 2004. low-level exposure to the organophosphate diazinon. EPA.epa. et al. Levy LS. Claypoole K. Lancet.24(1):18-29. Prendergast MA. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.12(2):134-141. Office of Prevention Pesticides and Toxic Substances. Sci Total Environ 2004. low-level organophosphate exposure on delayed recall. Washington (DC). Environmental Protection Agency (U. National Academy of Sciences.30(2):98-103.113(4):504-508. van der Hoek W.

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

20-16.95) 7.5 (8.9 (9.04-10. and on plants for days to several weeks. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50 (1.50-4.0 (7. USGS.44-5.47-13.37) 5.8) 9. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.72-4.7) 13.0) 12.70 (1.99-4.97) 4.87-6.63 (1.00) 2.70-17.05-5.30) 4.4 and 0.3) 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. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.70-11.80-10.5-24. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn. 2005).47-9.71 (1.00) 3.29) 90th 7.00-8.16) 2.9-18.9 (7.30-5.60-3.20-14.0) 8.0) 12.30-9.0) 10. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low. 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. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.53 (1.0) 6.40 (5.44 (3.26) 7.47) 1.10 (5.78 (7.25) 1.67 (1.50 (2.0) 12.45 (1.50 (2.51) 1.57 (2.92 (1.20) 10.94 (4. air.52-2.97-7.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.4 (9.20 (4. Estimated intakes from diet and water have not exceeded recommended intake limits.37 (1.60-4. The general population may be exposed to chlorpyrifos via oral.67 (2.50 (1.35) 1.61 (1.68-2.17 (1.90 (1.0 (7. but can be detected in streams receiving runoff from application sites.80) 1.0) 12.30) 5.44-2.01) 1.77-15.66-15.95 (4.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.4-15.5.40) 2.09 (3.S.97) 2.4 (10.96) 3.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (13.86) 4.90 (6. It also has been applied directly on animals to kill mites.70 (1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.61-7.60 (2.76 (1. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.39-2.27 (7.09 (2. pre.81-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.30) 4.32) 2.59) 2. and inhalation routes.05) 1.88 (1. 2921-88-2 Chlorpyrifos-methyl CAS No.70-16.60-3.7) 8.0 (7.46-2.50-2. For instance.38 (3.02) 1.90-8.10) 2.7-23.50-5. Survey Geometric mean (95% conf. and is infrequently detected in ground water (IPCS.03) 1.30 (2.63 (2. Approximately 80.30-12.3) 8.34) 1.51 (1.50-14.63 (8.19-3.0) 10.13-3.0) 14.25) 3. Fourth National Report on Human Exposure to Environmental Chemicals 135 .S.0) 18.20 (2. Exposure can also result from contact with contaminated surfaces.04-10.30-11.60 (5.22 (1.2 (10. 2002).4. population from the National Health and Nutrition Examination Survey.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.28-3.79-2.40) 9.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.1) 5. dermal.50-8.5) 7.0 (9.40 (6.43-2.90-4.70) 1.15 (1. interval) 1.51-2.80 (7.8-15. and dust.62-2.52-12.43-2.19 (1.90) 7.10 (4.77) 1.29-1.60 (4. applied to structures to kill termites.83) 1.20) 2.0 (7.55-5.80) 2.47-11.0) 12.0) 9.0) 10.30 (2.47 (4.S.90 (2.39) 4.000 pounds are used per year.70-15.30-2.02 (1.0 (10.66-4.7) 9.80 (1.40-2.64) 3.3 (10.90) 3.0 (7.40 (5.35) 2.74-9.91 (1.1-16.90 (1.20) 2.60-2.84) 1.24-1.70-5.97) 7. It has low leachability.02 (7.0) 15. chlorpyrifos was no longer registered for indoor residential uses in the United States.3 (11.28) 2. 1999.37 (4.50-2.80) 4.89-2.31-2..22) 2.50-4.67 (2.6) 7.20) 4. and sprayed to kill mosquitoes.10 (1.98-15.90 (3.0) 7.71 (2.00) 1.21) 3.74 (1.40-26.36 (4.32-1.0) 11.9) 11.0) 8.76 (1.91) 16.31-2.40-13.9) 697 660 521 701 602 947 Limit of detection (LOD.97) 2.30-1.40-10.20-11.8) 10. in 142 urban homes and preschools in North Carolina.30 (4.13 (1.80-8.80) 12. staying bound to soil particles.EPA.71 (6.10-17.20-2.EPA.24-3.68 (7.10 (3.and post-construction structural applications for termite control were to be phased out by 2005 (U.50 (2.77 (1.20-3.89 (2. Chlorpyrifos is Urinary 3.59-2.10) 6. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators. After 2001.5. 2002).90-2.60) 5.3 (8.77-6. 2007).4 (8.9 (10.61) 75th 3.90-7. 5598-13-0 General Information The chemical 3. Approximately 21-24 million pounds per year were used domestically from 1987-1998.20-4.0-28.00-24.72) 2.

53-5.92 (1.00 (7.72-2.91) 10. Once absorbed.88-10.20 (2.2) 6.12-3.09-1.3) 8.01) 3.3) 8.91) 1.19-2. Urinary 3.87-3. 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.35) 2.3) 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 1.1 (7.56) 2. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.19-1..80-6.29 (3.37 (1. interval) 1. 2006.25-1.00-8.89) 4.79-13..95 (3.85) 4.63 (4. and other metabolites.58-5. vomiting. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.82) 8. resulting in excess acetylcholine at nerve terminals.81 (3.11-9. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.24) 5.46 (1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.6) 10.06 (1.98 (6.940-1.59) 3.60-3.33 (.24-1.64 (1.47 (1.00) 1.30-4. Roy et al.88-9.57) 2. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.94-12. neurotransmission.33 (1.56 (1.55) 1.60 (1.85 (2.30-1.11 (2.44 (6.72) 1..7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .96) 3. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.6) 9.17-4.22-6.93 (4.92-2.01) 1.22 (6.88 (1. 1984).09 (1.12) 1.91-13.58) 5.20-1.43 (4.46 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).97 (2.05-4. Based on animal data and human cholinesterase monitoring during occupational exposure. TCPy can also occur in the environment from the breakdown of the parent compounds.23-1.99-8.82 (2.0) 6.77) 1.57-2.11) 7.47-2.59-2. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. Slotkin et al.91-4.07) 1.93 (2.36) 1.28) 2.49-2.58) 1.47 (1.57-2.5 (6. and producing acute symptoms such as nausea.91 (4.06-4. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.78 (1.25-12.24) 75th 2. Thus..33) 2.8) 9. 2002).21-1.62) 90th 5.54 (2. 2000).9 (12.09-3.5) 5.49-2.3 (7.68) 1.75 (1.66) 1.33-7.28) 2.0) 10.2 (7.44 (1.97 (3.14) 1.66-11.52 (5.42-2.80-4.15 (4. paralysis.S.. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.17-4.03) 1.07) 5. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1..76 (2. 2005.88 (1.95 (1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.02) 7.74) 1.24-24.35) 1. population from the National Health and Nutrition Examination Survey.44 (1.93) 2.83-2.88-8.55 (1.43-10.08) 6.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.24-5.82-4.71) 3. cholinergic effects.80) 3.90-9.31-4.39) 6.64-7.88) 6.75) 6.88-8. and seizures.58 (4.56 (4.91) 1.45 (1.S.66 (1.86 (1.51 (1.65-15. Metabolic hydrolysis leads to the formation of TCPy.55 (4.91 (3.49-2.69 (1.01) 3.65-11.22 (4.56) 5.62) 1.31-1.0) 16.94-14.19) 6.27-1. Survey Geometric mean (95% conf.83) 1.73 (1. Howard et al.25-11.14-8.57) 9.35-1.0) 12.12-1.56-2.86 (1.83-11.93 (1.62-7.23) 14.85) 1.85 (3.93) 5. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.32) 1.16 (4.6-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.85-4.42 (5.40) 1.99) 1.05) 3.50 (4... 2006b).84-6.44-6.82 (3.44 (5.97) 3. TCPy is more persistent in the environment than chlorpyrifos itself (U.86 (3.02 (5.64-2..49 (1.33 (5.72) 2.41 (1.81) 2.68) 6.80-11.54) 5.58 (1. 2006.22) 1.48 (2.05-1.00-13.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.26-14.4) 4.39-1.1-21.48 (1.06 (5.34-1. Ricceri et al. weakness.63 (5.EPA.24 (1. In pesticide applicators.24-4.71 (1.05-3.1-38.47 (5.27-7.98 (7.1 (10.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.39 (2.63-2. 2005.7) 7.21-6. Betancourt et al.92) 3.97) 3.39 (4.44 (5.76 (3.09-2.31) 1.53 (2.97-3. 2005.58 (1.45-1.19) 3.42 (6. 2006a.70-4.05-8.16) 6.91) 2.38) 3.5.3) 9.11 (2.

63(3):218220. Lotti A. Biomonitoring Information Urinary TCPy levels reflect recent exposure. 2006). Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Levels of TCPy in the U. Of 482 pregnant women living in an agricultural community.S. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. In Minnesota and South Carolina farmers who used chlorpyrifos. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure.. Aldridge JE.S. 2004). In Iowa farm families using several different pesticides. 2005). 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. Chlorpyrifos exposure and biological monitoring among manufacturing workers. Barisano A. Haidar S. 1992. Additional information about external exposure (i. 2001).Organophosphorus Insecticides: Specific Metabolites 2004. Giordani B. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections.109(6):583-590. urinary TCPy levels in children were reported not to have increased (Hore et al. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. 2005). but levels were roughly four to six times higher than the geometric means in the U. 2005. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U.92(2):500-506.epa. 2000). 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Perera et al... population (CDC. the geometric mean urinary TCPy levels were similar in parents and children.html and from U. Betta A.e. Aprea C.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study).. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Koch et al..gov/toxpro2. 2002). Eberly LE. Toxicol Sci 2006.. J AOAC Int 1999. 1999). Barr DB.Reference values of urinary 3. 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.. Clayton CA. In a probability-based sample of 102 Minnesota children aged 3-13 years. Carr RL. Seidler FJ. Burgess SC. et al. References Adgate JL.cdc. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Garabrant D. Betancourt AM. representative subsample of NHANES 19992000 (CDC. Meyer A. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Environ Health Perspect 2001. Freeman NC. et al.. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. 2003. 2001) and Italy (Aprea et al.gov/pesticides/. Burns CJ.82(2):305-312. Magnaghi S. Environ Health Perspect 2005.5. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Occup Environ Med 2006. Slotkin TA. Berent S.. 2005). 2005). Albers JW. 2005). et al. CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..113(8):1027-1031. Fourth National Report on Human Exposure to Environmental Chemicals 137 . MacIntosh et al. environmental levels) and health effects is available from ATSDR at: http://www. Following crack-and-crevice application of chlorpyrifos in their homes.EPA.S. Lioy PJ. 2005). 2004). median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al.. Curwin et al. Whyatt et al. 2005. 2007).. Catenacci G. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. 2005. EPA at: http://www. subsamples of NHANES 1999-2000 and 2001-2002 (CDC.. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al..S.S..atsdr.

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Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Jones PA. Howard AS. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Chlorpyrifos: pharmacokinetics in human volunteers. Executive summary of safety and toxicity information. Zhang J. Available at URL: http://ntp. et al.5. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Hore P. et al. Scand J Work Environ Health 2005. Capone F. Urinary pesticide concentrations among children. J Expo Anal Environ Epidemiol 2000. Tsai WY.204(2-3):175-180. Shealy DB. Gregg M. Fortuna S. Robson M. Chrislip DW. Adgate JL.inchem. Environ Res 1995. Ryan PB. Howell RJ. 2921-882. Toxicol Appl Pharmacol 2005.niehs. Mandel JS. Hill RH Jr. Angerer J. et al. et al. Dick RB.6-trichloro 2-pyridinol in their everyday environments. Steenland K. Exposures of preschool children to chlorpyrifos and its degradation product 3.15(4):297-309. MacIntosh DL.93(1):105-113. Edwards RD. Yang D. Seidler FJ. Chapman P. Freeman N. Neurologic function among termiticide applicators exposed to chlorpyrifos.

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

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

560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .270) < LOD 659 701 920 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.200 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 141 .S. * 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.670 (<LOD-1. 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 .2. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. 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.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 .200 (<LOD-.380 (<LOD-.S.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.

September 2000. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Centers for Disease Control and Prevention (CDC). Sadowski MA. Barr DB. Reprod Toxicol 1998. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www.gov/oppsrrd1/ REDs/0018tred.epa. Third National Report on Human Exposure to Environmental Chemicals. Nguyen JV. Olsson AO.Organophosphorus Insecticides: Specific Metabolites References Astroff AB.12(6):619-645. Eigenberg DA. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Anal Bioanal Chem 2003.376(6):808-815. Atlanta (GA). 2005.S. U. EPA).S. Environmental Protection Agency (U. Freshwater KJ. EPA 738-R-00-010.pdf. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.

an organophosphorus insecticide that is used to control insects on nuts. Most granular formulations. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.EPA. It is toxic to birds. 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. and other metabolites. 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. in some pest strips. 2004). fruits. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Prior to 2000. aerial. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. but is rapidly absorbed orally (IPCS.EPA. 1998.S.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.11) < 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. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. since 2004.2 and 0. Inhalational and dermal routes of exposure can be significant for pesticide applicators. * 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. seed and foliar applications are planned to be phased out (U. Survey Geometric mean (95% conf. Diazinon is not well-absorbed through the skin. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. USGS. 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. vegetable. diazinon cannot be sold for residential use.45 (<LOD-3. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. diazinon was widely used in residential and garden application. Once absorbed. and forage crops. and particularly when it was ingested in granular form. < LOD means less than the limit of detection. in the past. 2004). dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). but these uses have been phased out. Before these restrictions. 2007). It is also used for cattle ear tag applications to control flies and ticks and.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD.49 (<LOD-2. 1998). diazinon produced wild bird kills before use restrictions were in place.S. Estimated intakes from diet and water do not exceed recommended intake limits (U. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 143 .Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.7.

Survey Geometric mean (95% conf. EPA at: http://www. 2002). diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.76 (<LOD-3.45) < 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..html and from U. In two nonrandom samples of United States adults and children. 1998). respectively..S. paralysis. Olsson et al. population from the National Health and Nutrition Examination Survey. Seifert and Pewnim. 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. Additional information about external exposure (i.S. environmental levels) and health effects is available from ATSDR at: http://www. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. vomiting. 144 Fourth National Report on Human Exposure to Environmental Chemicals . There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. agricultural.72 (<LOD-4. resulting in excess acetylcholine at nerve terminals. weakness. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. respectively (Baker et al. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. 2000.gov/pesticides/. Thus. In the U. 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.. 1992). Intoxications in humans from intentional overdose. Diazinon is not considered to be a mutagen. in the 2001-2002 subsample (CDC.epa. diazinon does not accumulate in tissues (IPCS. In animals. In addition to being a human metabolite of diazinon.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.atsdr. cholinergic effects.45 and 1. 2003). Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown.cdc.S. animal carcinogen. 1986 Rajendra et al.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al..49 μg/L. or reproductive toxicant (IPCS.e. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.EPA considers diazinon unlikely to be carcinogenic in humans.S.gov/toxpro2.. and seizures.. and indoor applications have been documented. and producing acute symptoms such as nausea. The U. Diazinon has moderate acute toxicity in animal studies. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. 1998). Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. At high doses. teratogen. 1986. subsamples of NHANES 1999-2000 and 20012002.

Cocker J. Environ Health Perspect 2003. Bravo R. Toepel K. Interim reregistration eligibility decision (IRED. EPA). May 2004. Pesticides in the Nation’s Streams and Ground Water. Noisel N. Barr DB. The Quality of Our Nation’s Waters. Geological Survey (USGS). Mason HJ. Available at URL: http://www. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 2006). 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Rajendra W. J Expo Anal Environ Epidemiol 2000.376(6):808-815. Drobnis EZ. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Seifert J.. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon.134(1-3):105-113.44(11):2243-2250. Oloffs PC.114(2):260-263. Barr DB. Carrier G. Sadowski MA. Oloffs PC. In 54 Canadian greenhouse workers. Study for Future Families Research Group. Diazinon.usgs. Bouchard M. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Third National Report on Human Exposure to Environmental Chemicals.S. Atlanta (GA). 2007 [online]. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Bull Environ Contam Toxicol 1986.9(2):117-131. 1992-2001. U. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.111(12):1478-1484. Environmental Protection Agency (U. References Anthony J. Brunet RC. Needham LL.37(4):501-507. Garfitt SJ. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Kruse RL. International Programme on Chemical Safety-INCHEM (IPCS). 1/14/09 U. Barr DB. Swan SH.50(5):505-515. Banister EW. Diazinon. Biochem Pharmacol 1992. Finding a measurable amount of 2-isopropyl-4-methyl-6hydroxypyrimidine in urine does not mean that the level will result in an adverse health effect. Liu F. Redmon JB.pdf.S. Available at URL: http://www. Olsson AO.epa. 2006). Available at URL: http://pubs. 1998. 2005. Barr DB.10(6 Pt 2):789-798. Semen quality in relation to biomarkers of pesticide exposure. Jones K.inchem. Banister E. Effect of sublethal levels of diazinon: histopathology of liver. Dumas P. Swan et al.htm. Biomonitoring studies of 2-isopropyl-4-methyl-6-hydroxypyrimidine provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of diazinon than are found in the general population. et al.org/documents/ehc/ehc/ehc198. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. 4/7/09 Lu C. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. In 23 children.S.gov/circ/2005/1291/. In a small number of men visiting fertility clinics in Missouri and Minnesota. Drug Chem Toxicol 1986. Driskell WJ. Anal Bioanal Chem 2003. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. revised February 15. Irish R. Beeson MD. March 2006. Pewnim T.Organophosphorus Insecticides: Specific Metabolites 2005). Environ Health Perspect 2006. Nguyen JV.. Fenske RA. Toxicol Lett 2002. Environmental Health Criteria 198. Baker SE. EPA 738-R-04-006. Ann Occup Hyg 2006. Centers for Disease Control and Prevention (CDC).gov/ oppsrrd1/REDs/diazinon_ired.

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

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

Lu C. et al. Flessel P.445(2):275-283. Lioy PJ. Sharma GD. Goldhaber M. Grether JK. The Quality of Our Nation’s Waters. Neutra R.inchem. Atlanta (GA).pdf. Hooper K. Bradman A.38(4):546-553. U. Barr DB. Bravo R. Thomas D.112(10):1116-1124. revised February 15.56(10):2393-2399. Jaloszynski P. Barr DB.514(1-2):223231.9(5):494-501. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.132(4):794-795. Petitti D. Needham LL.S. Toepel K. Eskenazi B. Genetic toxicity of malathion: a review. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Barr DB. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Ryan PB. Mutat Res 2002. Barr DB. EPA 738-R06-030. Environ Health Perspect 2004. Brunet RC. Nicklas JA. Reproductive outcome in women exposed to malathion. Weltzien E.epa. Environmental Protection Agency (U. Gosselin NH.usgs. O’Neill JP. Malathion deposition. Swan SH. EPA). Dinoff TM. Irish R. Reregistration eligibility decision (RED) Malathion. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . 2007 [online].114(2):260-263. Third National Report on Human Exposure to Environmental Chemicals. Cancer Res 1996. March 2006. MacIntosh DL. Krieger RI. J Expo Anal Environ Epidemiol 1999. Kedan G. Freeman NC. Quintana PJ. Erratum in: Toxicol Sci 2003 Aug.org/documents/jmpr/jmpmono/v2003pr06. Environ Health Perspect 2001. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. et al. 1992-2001.S. Jewell NP. Giri A. Eberly LE. Griffith W. Szyfter K. Pluth JM.15(2):164-171. Am J Public Health 1987. Pesticides in the Nation’s Streams and Ground Water. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. July 2006.gov/oppsrrd1/REDs/ malathion_red. Malathion (addendum). et al. htm. Albertini RJ. Giri S. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Rappaport E. 4/7/09 Kissel JC. Lu C.74(2):following table of contents. Hertz-Picciotto I. Environ Health Perspect 2006. Clayton CA. Samuel O. Bouchard M. Dumoulin MJ. Available at URL: http://www. Prasad SB. Am J Epidemiol 1990.gov/circ/2005/1291/. A longitudinal investigation of selected pesticide metabolites in urine. Centers for Disease Control and Prevention (CDC). Environ Mol Mutagen 1993. Blasiak J. Available at URL: http://pubs. Mutat Res 1999. Arch Environ Contam Toxicol 2000.22(1):7-17. Available at URL: http://www. J Expo Anal Environ Epidemiol 2005.77:1009-1010. 2005. Fenske RA. Carrier G.109(6):583-590. Curl CL.S. and cholinesterase status of date dusters and harvesters in California. Hammerstrom KA. International Programme on Chemical Safety-INCHEM (IPCS). 6/1/09 U. metabolite clearance. Trzeciak A. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Geological Survey (USGS).Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Harris JA. Toxicol Sci 2003 May. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.73(1):182-94. Harley K.

. more slowly absorbed through the skin.32 (1.48) 90th 2.79) 4.50-9.70-3.02-6.50 (2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70) 2.40-4. and oral routes can occur in pesticide and agricultural workers (Muttray et al.90 (1.10-1.0) 4.40) 4.0) 2.67 (1. Once absorbed.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . 1977).50) 1.10 (3.46 (3.70 (3.33 (1. Increased risk of exposure via dermal. pulmonary.32-1.1. Estimated intakes from diet and drinking water have been below recommended limits.58) 3.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .66 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.850) < LOD . Both are toxic to birds.30-3. methyl parathion was rapidly absorbed after ingestion.33) 2.90-9.69 (2.71 (3. Many previous registered agricultural uses of methyl parathion have been cancelled (U.10 (3.50 (1.69) 4.45) 5. 2002.19 (.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. with limited applications in agriculture.70 (2.40 (1.90-11.34 (3.50 (1.16) < LOD 1.40) 2. < LOD means less than the limit of detection.60-24. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.37-4.0) 3.15-3. Methyl parathion is not registered for residential use in the United States.37) 2.910) < LOD < LOD < LOD 1.22-3.60) 1.70-6.18-3. population from the National Health and Nutrition Examination Survey.20-5. Fourth National Report on Human Exposure to Environmental Chemicals 149 .37-4.770 (.EPA.01-4.298-00-0 Ethyl Parathion CAS No.50) 3.61) < LOD 1. 2006).02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .0) 3.50 (1.67) < LOD 1.10-11.EPA. binds tightly to soils resulting in low leachability.40-4.20) 5.30 (2. fish.21 (2.41-4.910) < LOD < LOD .28-4. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.70 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50-14. and of the chemical nitrobenzene.60-19.80) 2.0) 3.40-3.20 (2.10) 4. In animal studies.50) 2. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.70-6. on cereal grains.70 (<LOD-3.0) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.47) 2.8 and 0.05) 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. ethyl parathion.50) 3.11-4.910) < LOD .37-2. Methyl parathion use is highly restricted.0) 3.26 (1. and has a short half-life in soils and on plants.57) 1.62 (1.61) < LOD 1. Morgan et al.12) < LOD < LOD 1.50 (1. 2003). Ethyl parathion. but by 2003.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.700 (<LOD-.00) 3.09-1.74) 5.13-1. 2007).27) 2. peak domestic use was as high as 5-6 million pounds per year.10 (<LOD-6.940 (<LOD-2.70-3.40) 1.70 (2.60-36.790 (<LOD-. 2000).45 (1.60-5. Given its limited use. and aquatic invertebrates.70-6.91-3.36-1.00 (2. In the 1990s.72 (3.80 (2.70) 2.30-5.80 (1.860 (<LOD-1. and eliminated rapidly from the body after absorption (Kramer et al.60 (4. was once a restricted-use insecticide with limited applications on certain agricultural crops.49 (1.S.0 (3.50 (2.21-1.44) 2.S.28 (1.80 (2.32-3.89 (2. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. Survey Geometric mean (95% conf.S.92-2.28 (1.01) 4.10) 22.92) 5.11) 2.01) 695 660 518 679 603 941 Limit of detection (LOD.730 (<LOD-.85 (2...71 (2. It had been applied to cotton.300-.00 (2. first registered in 1948.70) 2. Methyl parathion has low water solubility.30-16.20 (<LOD-2. and to a lesser extent.57-4. all registered uses were voluntarily cancelled (U.990-1.30 (1.32-1. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. which may vary for some chemicals by year and by individual sample. Methyl Parathion.

930 (.57-2.82 (2.96 (1..48-4.13-12.26) 17.97 (2.05) 4.71) 1. Thus.89 (2. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.77-7.61) 4.. paralysis.79) 1.84) 3.e.720 (<LOD-.atsdr.13) 4. 2006. Additional information about external exposure (i.4 (3.21) 1.78-2. vomiting.44-3. Orsorio et al.76-14.60) 2.95) 1.940 (<LOD-1. and seizures.93 (2. gov/pesticides/.09) 2.80 (1.78 (2.3) 2.840 (.640) < LOD < LOD 1. 1990.35-3.20 (3.44-3. 150 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf.83 (1.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. weakness. and producing acute symptoms such as nausea.57) 6.56-2.96 (1. In addition to being a metabolite of methyl and ethyl parathion. accidental exposure.67 (3.67-2. teratogenic. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.01 (2. U.530) < LOD < LOD < LOD . Methyl Parathion.20) 3.97 (<LOD-4.72-2.39) 1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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. population from the National Health and Nutrition Examination Survey.10) 90th 2. Slotkin et al. and unintentional acute or chronic high-level occupational exposure (Hill et al.20) .31-3.97-10.88 (1. In large doses.79 (1.35-3.91 (1.94-4.. but lists ethyl parathion as a possible human carcinogen.370 (<LOD-.790-. cholinergic effects.29 (2.31) < LOD . the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. WHO.1) 2.87 (1.89 (2. Lores et al.14-3.33-3.73 (1..29) 2..930 (..00 (1.970 (.500) < LOD < LOD . ethyl parathion.17) .21-21.92 (2.S.98-7. The metabolite.15-10. EPA at: http://www.00 (1.71 (1.11) 1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.41-2..730-1.25) 1.88) 1.15) 3.S.800-1.790-1.57-7. Zurich et al. 1995. 1995).39 (1.880 (.690-1.430 (. 1991).37-1. 2005.86 (2.78) 2.310-.680 (<LOD-1. resulting in excess acetylcholine at nerve terminals.04) 1.720-1.55) 2. 2004). and other metabolites.43) 4. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.epa. 2003.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .950) < LOD .94-47. 2006.29) 1.07) 2. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.970 (.9) 1.30) 3.540) < LOD . Methyl parathion is not considered genotoxic.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 .10 (1.S.980 (.7) 3. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2004).60 (1.55 (<LOD-3.26 (1.08) < LOD .33-3.16-4.08-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.01 (. does not inhibit acetylcholinesterase enzymes.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .html and from U.830-1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.01-3.30-1.11-4.870) < LOD .850-1.60-2. Parathion and methyl parathion have high acute toxicity in animal testing.33-6. At high animal doses of methyl parathion.70) 3.17-4.00) 2.07 (1. methyl parathion.2) 2.23) 1.78-2.90 (1.38-3.82) < LOD .91) 1.400 (<LOD-.EPA considers methyl parathion unlikely to be carcinogenic to humans.2) 2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.59 (1.80 (1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .04 (2. Jaga and Dharmani.440 (<LOD-.cdc.Organophosphorus Insecticides: Specific Metabolites Metabolites”).25 (2. paranitrophenol. environmental levels) and health effects is available from ATSDR at: http://www. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. 1978. gov/toxpro2. Karanth and Pope et al.08 (1.

14(4):213-216.. 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. population (Olsson et al. 2005). Cline RE. a range of values several hundred times higher than levels found in the U. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. et al. Alley CC. general population (CDC. Hetzler HL. Morgan DP. Weltzien E.71:99108.S. Giordano G. Rev Environ Health 2006. Hill et al. Turner WE. Available at URL: http:// www. Pesticide workers may have much higher levels following pesticide applications. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Parathion-Methyl (addendum). Toxicology 2005. Baker RC. Rockhold RW. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. oral or dermal administration.5 mg (500 µg)/g creatinine for workers at the end of shift. Griffith W. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Curl CL. et al. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. 1995. Runkle KD. CDC. Third National Report on Human Exposure to Environmental Chemicals. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Environ Health Perspect 2002. McCann et al. International Programme on Chemical Safety-INCHEM (IPCS). Lewalter J. Arch Environ Contam Toxicol 1977.. Neurotoxicol Teratol 2003. Lores EM. Atlanta (GA). Role of individual susceptibility in risk assessment of pesticides. McClure PC. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion.215(3):182-190. Head SL. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. 1995).. Fourth National Report on Human Exposure to Environmental Chemicals 151 . References Barr DB. 2005).6(2-3):159-173. McCann KG. Costa LG. 2002. DiPietro E. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.15(2):164-171. 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. Jewell NP. Pathak S. J Biomed Sci 2002. et al. Environ Res 1995. Wellman SE. Hryhorczuk DO.. Environ Health Perspect 2004. Barr DB. 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. Leng G. Kissel JC. Occup Environ Med 1999.S. Environ Health Perspect 2002. Moomey CM.112(10):1116-1124.25(5):599-606. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Methyl parathion: an organophosphate insecticide not quite forgotten.110 Suppl 6:1075-1078. Baker SE. Laboratory investigation of a poisoning epidemic in Sierra Leone. Arch Environ Health 1978.. Rubin et al.. Centers for Disease Control and Prevention (CDC). ACGIH recommends a BEI of 0. 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. Gregg M. Hill RH Jr. et al. Slach EF. Ashley DL. Barr JR.33(5):270-276. Shealy DB. 2005. Karanth S. Barr DB. Chicago area methyl parathion response. Kedan G. Hill RH Jr. In a study of workers who handle parathion. Pesticide residues in urine of adults living in the United States: reference range concentrations. Clark JM.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. 2004). J Anal Toxicol 1990.9:311-320. Kramer RE. 2005. Bradway DE.110 Suppl 6:1085-1091. 1999).56(7):449553. Lin LI. Baker S. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Eskenazi B. Bradman A. and many residents were symptomatic (Barr et al. Barr DB.inchem. Needham LL. 2005. 2002. Guizzetti M. and levels were similar or slightly lower that those in a small convenience sample of the U. Lu C.21(1):5767. 2002). 4/7/09 Jaga K.org/documents/jmpr/jmpmono/v95pr14. Dharmani C. Moseman RF. J Expo Anal Environ Epidemiol 2005.. Harley K. Pope C. et al.htm. Head SL. Bailey SL.

U. Osorio AM.D. Methyl parathion in drinking water.S. Jung D. Schilter B.S. Available at URL: http://www.usgs.int/water_sanitation_health/dwq/chemicals/ methylparathion.pdf.20(4):533-546. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Investigation of a fatality among parathion applicators in California. March 2006. Environmental Protection Agency (U. Toxicol Lett 2006. et al.04/106. Esteban E. Pesticides in the Nation’s Streams and Ground Water. Nguyen JV. Ryde IT. Yacovac R. Available at URL: http://www. 1995-1996. Toxicol Appl Pharmacol 2004. Am J Ind Med 1991.S. gov/oppsrrd1/REDs/methylparathion_ired. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.114(10):1542-1546. Ohio. Levin ED.110 Suppl 6:1047-1051.gov/circ/2005/1291/.201(2):97-104.pdf. 2004. Seidler FJ. 6/1/09 World Health Organization (WHO). Interim reregistration eligibility decision (IRED) for Methyl Parathion. Case No. 152 Fourth National Report on Human Exposure to Environmental Chemicals . revised February 15. Environmental Protection Agency (U. Mengle DC. EPA-738-FOO-009.who.epa. Kieszak S. 1/12/07 U. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Honegger P. Rosenberg J. Rubin C. 1992-2001. EPA). The Quality of Our Nation’s Waters. External and internal exposure of wine growers spraying methyl parathion. Barr DB. Environ Health Perspect 2006. Dunlop B. pdf. WHO/SDE/WSH/03. Facts. Ethyl parathion. R.162(2-3):219-224. Available at URL: http://www.gov/oppsrrd1/REDs/factsheets/0155fct. Available at URL: http://pubs. Hill RH Jr. Costa LG. Hill G. Backer G. Ames RG. Tate CA.E. Slotkin TA.S.epa. Letzel S. Geological Survey (USGS). Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition.S.Organophosphorus Insecticides: Specific Metabolites Muttray A. Olsson AO. Monnet-Tschudi F. 2007 [online]. 0153. May 2003. Sadowski MA. Anal Bioanal Chem 2003.376(6):808-815. Environ Health Perspect 2002. 5/19/09 Zurich MG. September 2000. EPA). 1/14/09 U.

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

840 (.500 (. population from the National Health and Nutrition Examination Survey.300-1.770) 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 . < LOD means less than the limit of detection.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.17 (.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.780 (.760 (<LOD-.470 (.820) < LOD < LOD .700-1.780 (.64) .430 (<LOD-. 154 Fourth National Report on Human Exposure to Environmental Chemicals .780 (<LOD-1. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.21) < LOD .210 (<LOD-.850 (.31) .200-.700-.840) 669 687 929 Limit of detection (LOD.S.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.210-1.250 (<LOD-.27) .740 (. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .740-1.580-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Survey Geometric mean (95% conf.610 (<LOD-1. 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.950) < LOD < LOD 1.94) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07) .780 (<LOD-1.410 (<LOD-1.670 (<LOD-1.55) .930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .210-.15) < LOD .680 (<LOD-.

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

Soderlund et al. and sumithrin) are also registered for use in mosquito-control programs in the United States. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. 2002).2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. 2005. solvent oils. 2003.. WHO. and synergists. 2003. followed by conjugation. 2006b). 2002. Leng et al. Generally..2-Dichlorovinyl)-2. or carbamate pesticides. Unmetabolized pyrethroids have been measured in breast milk. Certain pyrethroid insecticides (such as permethrin. which are natural chemicals found in chrysanthemum flowers. such as piperonyl butoxide... Woollen et al. and are rarely detected in ground waters (USGS.2-Dichlorovinyl)-2. and then eliminated over several days in urine and bile (Kuhn et al. cypermethrin. Soderlund et al. 1992).2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. 2002). in some situations replacing the use of DDT. but pyrethroids are highly toxic to fish and some aquatic invertebrates. deltamethrin has been used for indoor protection against mosquitoes that carry malaria.. 2006a.. 1992). so usage is restricted near water (U. by either ester hydrolysis or hydroxylation. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. organophosphorus. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations..S. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides.2-Dibromovinyl)-2. Woollen et al. and deltamethrin have been used frequently on cotton. warehouses. 1999. they are not persistent in the environment due to their rapid degradation within days to several months. They are also applied on livestock to control insects. pyrethroids are rapidly metabolized. Pyrethroids are not well absorbed through the skin (ATSDR. They are ranked as having moderate acute oral toxicity. but may be poorly transferred across the placenta (ATSDR. and greenhouses. cyfluthrin. Compared with other classes of insecticides such as organochlorines. Estimated intakes from diet and drinking water are below recommended limits. 1997.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. resmethrin. EPA.S. 2007). animal facilities.. There are about 30 different pyrethroid pesticides in use. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. 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. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. 2005).S. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. Pyrethroid pesticides have low volatility. Outside the U. This class of pesticides has low toxicity in birds and mammals. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. pyrethroid pesticides have less acute toxicity in animals and people. agricultural fields. bind to soils.EPA. After absorption from inhalation or ingestion. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. In agriculture. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. The table shows the urinary pyrethroid metabolites measured in this Report.

2005). Spinosa HS. Eriksson and Fredriksson. 2005).8(1):18-21.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Shafer. Int J Hyg Environ Health 2002.23(6):665-673. 2002). 2006. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Available from URL: http://www.S. McCarthy et al. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Toxicological profile for pyrethrins and pyrethroids.html. Kamita Y.. Kang IH. Sugiri D. Kuhn K. Seth PK. 1999.62:101-108. Thomson BM.. J Environ Monit 2006. Bull Environ Contam Toxicol 1999. Leng G.27(12):1273-1283. Garey and Wolff. Soderlund et al. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.atsdr. Kunimatsu et al. 2006.. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Caudle WM.50(2):245-255. 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. fenvalerate.. tremor. Neurotoxicol Teratol 2001.108(1):78-85. In developing rodents. Levsen K. 2002).gov/pesticides/ and from ATSDR at: http://www. Wolff MS. Bernardi MM. cdc. Okuno Y. Lazarini et al. Garey J. Shin JH.. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. 2001.107(3):173-177. 2005). on immature and adult mice: changes in behavioral and muscarinic receptor variables. Miller GW.cdc. Yamada T.. Kim TS.35(2 Pt 1):227-237. Florio JC.27(4):609-614.gov/toxprofiles/ tp155. Eriksson P. References Agency for Toxic Substances and Disease Registry (ATSDR). 2003. Sunami O. dopaminergic. Leng G. 1991. Generally.. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. September 2003. epa. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Shukla Y. Ose K. Idel H. choreoathetosis. Pyrethroid pesticide-induced alterations in dopamine transporter function. Toxicol Appl Pharmacol 1991.251(3):855-859. Toxicol Appl Pharmacol 2006. Additional information about pesticides is available from U.205(6):459-472. Song L. Hu et al. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. et al. Lemonica IP. WHO. Ranft U. Regul Toxicol Pharmacol 2002. Fredriksson A. Kim et al. 2003. Pogo BG. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley.. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. EPA at: http://www. Varoli FM. Kim HS. Yang J. Elwan et al. 2001. Bernardi MM. Chen JH. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. et al. 2005). neurochemical changes in cholinergic. 2003. Lee SJ. Biochem Biophys Res Commun 1998..gov/toxpro2.1/15/09 Aziz MH.. salivation. Idel H. Shaw IC.atsdr. Abell AD... 1998.300(3):161-165. motor activity. and permethrin) in the Hershberger and uterotrophic assays. Moniz et al. McCarthy AR. Wolff MS. 2004. 2002. and striatal dopamine levels in male and female rats. Lazarini CA. Hu JY. and seizures (ATSDR. Leng G. Garey J. 2006). Moniz AC.html. Pauluhn J. J Reprod Dev 2004. Environ Health Perspect 1999. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Go et al. Cruz-Casallas PE. Wieseler B. bioallethrin and deltamethrin. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. et al. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Guillot TS. In California. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Berger-Preiss E. 2000. hypersensitivity. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Neurosci Lett 2001. Elwan MA.. Go V. Ray et al. 2003. Agrawal AK. Estrogenicity of pyrethroid insecticide metabolites. Salzgeber SA. et al.8(1):197-202. Wang SL. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Neurotoxic effects of two different pyrethroids. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Kim IY. Zhao RC. Leng A. Lewalter J. Kunimatsu T.211(3):188-197. Neurotoxicol Teratol 2005. Kuhn KH. Richardson JR. Xenobiotica 1997. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Adhami VM.

Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .10. Available at URL: http://pubs. 1992–2001. 19962002. EPA). World Health Organization (WHO).epa.S. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. U. Mullin LS. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). pdf. 5/26/09 U. 2005. Toxicology 2002.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. EPA). Forshaw PJ. March 2006. Piccirillo VJ. April 2002.Pyrethroid Pesticides Ray DE. June 2006b. Meyer DA. 5/26/09 U. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. and therapy.gov/ circ/2005/1291/. Permethrin.epa.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Sargent D. sumithrin synthetic pyrethroids for mosquito control. Geological Survey (USGS).S. synergies. Rev Environ Contam Toxicol 2006.htm. June 2006a.S. Spencer J. Marsh JR. Available at URL: http://www. Available at URL: http://www. Sheets LP. Reregistration Eligibility Decision for Cypermethrin. resmethrin.38:95-101. Pyrethroid insecticides: poisoning syndromes.who.S. Shafer TJ. Pesticide and Evaluation Scheme.pdf. Environmental Protection Agency (U. Lesser JE.S.S. J Toxicol Clin Toxicol 2000.htm. Clark JM. 2007.186:57-72.171:3-59. Xenobiotica 1992. Environmental Protection Agency (U.113(2):123-136. Pyrethroid illnesses in California. 5/26/09 U. Available at URL: http://www. 5/26/09 Woollen BH. O’Malley M. Soderlund DM. Revised February 25. Laird WJ. EPA). Environ Health Perspect 2005. Safety of pyrethroids for public health use. Available at URL: http://whqlibdoc.gov/oppsrrd1/REDs/cypermethrin_red. Crofton KM. Environmental Protection Agency (U.22(8):983-991.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.usgs.S.epa. et al. Pesticides in the Nation’s Streams and Ground Water.

Following an indoor application exposure. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. 2003). Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al.S... representative 2001-2002 NHANES subsample (CDC. 2006) and 1177 urban adults and children (Heudorf et al. Finding a measurable amount of 4-fluoro-3-phenoxybenzoic acid in urine does not mean that the level will result in an adverse health effect. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin.. 2005). 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. representative subsample in NHANES 2001-2002 (CDC. Studies in Germany of 396 children and adolescents (Becker et al..2 μg/L) in the U. 2004). (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. 2003). 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. Baker et al.Pyrethroid Pesticides Cyfluthrin CAS No. Cyfluthrin is rapidly metabolized and eliminated from the body. Fourth National Report on Human Exposure to Environmental Chemicals 159 . 2005). Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population. most of which were dermal and respiratory irritations (Spencer and O’Malley. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.. 2006). 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. 2001. Urinary levels for adults and children in these studies were similar (Heudorf et al.. 2003). Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002.95 µg/L. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment.. 2005.S. Thus. Leng et al.

< LOD means less than the limit of detection. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 and 0. population from the National Health and Nutrition Examination Survey.S. 160 Fourth National Report on Human Exposure to Environmental Chemicals .2. which may vary for some chemicals by year and by individual sample.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 161 .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Idel H. Centers for Disease Control and Prevention (CDC). Leng G. Ranft U. Krieger RI. et al. Hadnagy W. Int J Hyg Environ Health 2003. Williams RL.Pyrethroid Pesticides References Baker SE. Bernard CE. Pyrethroid illnesses in California. Olsson AO. J Expo Anal Environ Epidemiol 2003. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Sugiri D. Heudorf U. Heudorf U. Spencer J. Int J Hyg Environ Health 2006. Barr DB. Schulz C. Angerer J. Becker K. Heudorf U. 19962002.77(1):67-72. Int Arch Occup Environ Health 2004.13(2):112-119. 162 Fourth National Report on Human Exposure to Environmental Chemicals . GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.206(2):85-92.186:57-72. Seiwert M. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Arch Environ Contam Toxicol 2004. Drexler H. 2005.209(3):221-233.109(3):213-217. Atlanta (GA). Ball M. Rev Environ Contam Toxicol 2006. Environ Health Perspect 2001. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Int J Hyg Environ Health 2006.46(3):281-288. Kolossa-Gehring M. Human exposure to indoor residential cyfluthrin residues during a structured activity program.209(3):293-299. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Hoppe HW. Angerer J. Berger-Preiss E. Third National Report on Human Exposure to Environmental Chemicals. Butte W. Angerer J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. O’Malley M.

2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.68 (.200-.670-2.460-1.13 (. 1985. which may vary for some chemicals by year and by individual sample.380 (.610) .330 (.950-2.270-.690) .340) .630) .250 (.300 (.410) .12 (.10) size 1951 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .44 (. transcypermethrin and trans-cyfluthrin.24) 1.160 (.11) .250-.490-1.730 (.200) < LOD < LOD < LOD .510 (.47 (.900 (.740) 1.280 (.470-1.1 and 0. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.580) 1.530 (.890 (.2-dichlorovinyl)-2.380-.340) .1. the presence of trans-3-(2. cis-3-(2. Kuhn et al.120-.210) 90th .340-.300-.740-2.300-.380) .410) . but it can also reflect exposure to cis-3-(2. population from the National Health and Nutrition Examination Survey.650-1.80) .2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.43) .500 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.08) .600 (.120-.730 (.420-.630 (.920) 1.S.07 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.380-. Generally.790 (.700) .68) .110-.400-. Similarly.240) .160 (.200) .850 (.630) . Fourth National Report on Human Exposure to Environmental Chemicals 163 . ciscypermethrin and cis-cyfluthrin.53) .680-3.430-. Survey Geometric mean (95% conf.380-.240) .490-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220-.140 (.210) .470 (.35) .350) .77 (.2-dichlorovinyl)-2.790) .310) .150 (. cis-cypermethrin.890 (.270 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-dichlorovinyl)-2.910-5.262) * * * < LOD < LOD .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.740 (.220-.630-.550) .270 (.280-.370 (.120-.28) 671 680 518 701 591 957 Limit of detection (LOD.32) . and trans-cyfluthrin. more of the trans-metabolite than Urinary cis-3-(2.270 (.640 (.670-1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.460 (.210-.202 (.180) .2-dichlorovinyl)2. 1999).28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .520) . Cyfluthrin.300 (.330) .580-1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin. 52315-07-8 CAS No.170 (.155-.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .740-1.790-1.230) .2dichlorovinyl)-2.2-Dichlorovinyl)-2. < LOD means less than the limit of detection.110-.370-.and trans-isomers.610) .2-dichlorovinyl)- CAS No.780) .220-.670-1. The chemical trans-3(2.710-1.200-.68) . trans-permethrin.820 (.220-.200 (.50) .2dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.110 (<LOD-. The presence of cis-3-(2.200) .54) .200-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. 1985.460-.160 (<LOD-.21) .260 (.440 (. and ciscyfluthrin. In the body.600-1.490-1.or trans-3-(2.110-.770) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. trans-cypermethrin.510 (.570 (.510 (.710) .870) 1.600) .680 (..68359-37-5 Cypermethrin Permethrin CAS No.15) .35) 1. but can also reflect exposure to trans-3(2.140 (<LOD-.730 (. Biomonitoring Information Urinary levels of cis.670 (.960 (.490-.790-1. cis-permethrin.880 (. 1999). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1..220) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. Kuhn et al.770-1.570-.180 (.120-.500 (.

2-dichlorovinyl)-2.360-1.250-.380 (.270 (.580) ...840 (.450-.300) .260 (.540 (.400 (.170) < LOD < LOD < LOD .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U. the median and 95th percentile of urinary levels of cis-3-(2.230 (. Lu et al.182) * * * < LOD < LOD .580-1.190 (.450-1.220 (.890) . 2004).290) .430-1. In a study of urban residents in Germany (Berger-Preiss et al.550-1.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .550 (.780 (.530 (.260 (. Other studies have provided evidence that urinary levels of cis.250 (<LOD-.800 (.340) .290 (.380) .Pyrethroid Pesticides 2.540) .700) .S. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.340-.710 (.260 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates..640-1. 2005).2-dichlorovinyl)-2.2-dichlorovinyl)-2.160 (<LOD-. In the same residents.300) .420 (.230-.24) . 2003).. post- Urinary cis-3-(2.11) . 2005). Studies in Germany of 396 children and adolescents (Becker et al.2-dichlorovinyl)-2.220) .104-.690-1. median urinary levels of trans-3-(2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.. Cyfluthrin..230-.890 (.290-.410) .450 (.250-.180-. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.150-.and trans-3(2.300 (. In these volunteers.29 (. population from the National Health and Nutrition Examination Survey.920 (. 2006) and 1177 urban adults and children (Heudorf et al.11 (.11) 1. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.710-3.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.49) .530 (.570) . 2003).12 (.370-.280-.200-.750-1..2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.2-Dichlorovinyl)-2.190) .300-.180 (.250) 90th .700-2. representative NHANES 2001-2002 subsample (CDC. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. 2006).270) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (.340) .138 (.260-.300 (.080-.380-.220 (.640) 1. 2002).840 (. 2005).and trans-3-(2.21) .600 (.700) .320) .12-2.440 (.210-.500 (.2dichlorovinyl)-2.550) .560) 1.80) ..2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al..830) .440-.540 (.390 (. 2006.250-.150-.250) . 2001.550-1.130-.430 (.680-1.190) .59) . 2001) showed urinary levels of cis.390-.120 (.900 (.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.2dichlorovinyl)-2.31) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.S.59 (1.550) .200-.640 (.510-1. Survey Geometric mean (95% conf. 164 Fourth National Report on Human Exposure to Environmental Chemicals .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC. urinary levels of cis-3-(2.03) 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 .37) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2002).350) . Schettgen et al.2-dimethylcyclopropane carboxylic acid did not increase.780) 1.170 (. urinary trans-3-(2.290) .370-. In a study of volunteers.430-.11) .140-.590 (.370-.750 (..590) .390-. 2004.59) .200) .440 (.270) .03) 1.440-. 2005).270-.320-. 2006).67 (.150-.33) .880) .640-1.560) .170 (.640-.280 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.250) .350 (.260) . 2005) In a small group of indoor pest-control operators.680 (.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .680-1.240 (<LOD-.33 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .67) . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. 2006.470-1.810 (.400-1.230-..

56 (1.19 (2.800-1.910-1.780 (.19 (3.S.28 (1.Pyrethroid Pesticides application median urinary levels of summed cis.920-1.62 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60) .570) 90th 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.76-3.70) 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 .58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-Dichlorovinyl)-2. Survey Geometric mean (95% conf.01 (1.90) 1.5) 2.63) 1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.20 (.710 (.10) 2.49-3.42) 1.830-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.48) 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.40 (1. Urinary trans-3-(2.400 (<LOD-. however.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.94 (1.22 (1.14-6.7) 2.850-1. 2005).91 (1.840-1.520-.55-4.17 (.59 (1.460-. < LOD means less than the limit of detection.89 (2.23) 2.440 (<LOD-.95) 2.77) 2.470 (.410-.69 (1.23 (.760) .60) 1.39 (1.69) 1.56 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .17-1.26 (.81) 2.66) .41 (1.14-2.11-1.85) 4.490 (<LOD-.56) 2.19) 1.400-.42 (2.43) 2.460-. Fourth National Report on Human Exposure to Environmental Chemicals 165 .700) .27 (1.500) .76-4.490-1.500-.56) 2.87 (1. population from the National Health and Nutrition Examination Survey.or trans-3-(2.20 (.09 (.410 (<LOD-.550 (.and trans-3-(2.68) 1.660) 1.97-11. The maximum post-application urinary levels.620) < LOD 2.49-3.530) .750) .16) 1.11-2.730) . 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.560 (.420 (<LOD-.07 (1.95) 3.2dichlorovinyl)-2.01) 4.28 (2.08) 1.520) .54 (1.25-3.07-3.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.68) 1.25 (1. 2005).54) 4.77 (1.410 (<LOD-.480-.35) 1.970 (.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.03-1.37 (1.08-6.55-3.66) 691 680 518 690 595 954 Limit of detection (LOD. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.68-3.77) 1.68-2.810-1.12-6.560 (.03-1.4.860) .2-dichlorovinyl)-2.4 and 0.560 (.610) 1. Finding a measurable amount of cis.500 (.410-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.700-1.64-4.20 (.14) 1.820) .13) . which may vary for some chemicals by year and by individual sample.41-14.670) .940 (.2-dichlorovinyl)-2.470 (<LOD-. Biomonitoring studies on urinary levels of cisor trans-3-(2. trans-Cypermethrin.84 (1.49-5.17 (.55-5.680-1.39-5.63) 1.580 (.68) 2.910-1.670) .50 (1.60-4.08-4.

930-1.560 (.74) 2.07) 2.55 (2.22) 1.65) 1.26 (1.75 (1.87-8.20 (1.970 (.56-2.30-6. trans-Cypermethrin.720 (<LOD-.31 (2.86 (2.15 (1.27-2.15-3.74) .29) 1.39) 1.31 (.87) 1.410-.880 (.470 (.48-2.15) 3.480-.440-.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.89) 2.Pyrethroid Pesticides Urinary trans-3-(2.700 (.15) 2.750) .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.40-2.57 (1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .47 (1.880-1.65 (2.530 (<LOD-.15-3.S.22-1.880 (<LOD-1.47-2.60 (1.13) .64 (1.19 (1.31) 1.780 (<LOD-.37 (1.670) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.570-.68) 3.800-1.28) 2.87) 1.470-.580) . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.91) 1.12 (.850) 1.11) .34-4.02-1.56-5.45-2.87-3.33 (1.41) 1.13) 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 .12-1.35 (1.55 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1.87 (1.91 (1.580 (.570 (.770) < LOD 2.20-2.00) 5.98 (1.00-5.42) 1.08 (.27-2.48 (1.740) .640) .22-2.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .07-2.900 (<LOD-1.00) 1.720-1.08 (.850) .520 (<LOD-.61) 1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.610-.42 (.67 (2.33-2.760 (. 166 Fourth National Report on Human Exposure to Environmental Chemicals .500-.07-1. Survey Geometric mean (95% conf.850-3.07-3.780) .3) 2.80) 1.2-Dichlorovinyl)-2.800-1.39 (1.540) .55 (2.780) 90th 1.91-11.56 (1.81 (2.60) 2.700 (.33-1.16 (1.45 (1.19) .36 (1.570 (<LOD-.44) 2.700-.57) 3.730) .30-3.660) .47-2.34-3.60) 2.35) 1.36) 2.15-3.70 (.530 (.720-1. population from the National Health and Nutrition Examination Survey.00 (1.07) 2.820-2.

Angerer J. Sugiri D. Fourth National Report on Human Exposure to Environmental Chemicals 167 . 2005. Drexler H.109(3):213-217.206(2):85-92. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Schulz C. Environ Health Perspect 2006. Sugiri D. Idel H. Hoppe HW. J AOAC 1985. Leng G. Int Arch Occup Environ Health 2003. Heudorf U. Permethrin and its two metabolite residues in seven agricultural crops. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Schettgen T. Environ Health Perspect 2001. Lu C.77(1):67-72. Kolossa-Gehring M. Seiwert M. Centers for Disease Control and Prevention (CDC). Ranft U. Idel H. Berger-Preiss E. Barr DB. Int J Hyg Environ Health 2006. Levsen K. Ball M.209(3):221-233. Int J Hyg Environ Health 2003. George DA. Leng G. Atlanta (GA).62:101-108. Angerer J. Leng G. Bartell S. Third National Report on Human Exposure to Environmental Chemicals. Idel H. Hadnagy W. Bull Environ Contam Toxicol 1999. Bravo R. Int J Hyg Environ Health 2002.205(6):459-472. Biological monitoring of workers after the application of insecticidal pyrethroids.76(7):492-498. et al. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Int J Hyg Environ Health 2006. Butte W. Drexler H. Wieseler B. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Pearson M. Heudorf U. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Hardt J. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Heudorf U.209(3):293-299. Angerer J. Int Arch Occup Environ Health 2004.114(9):14191423.Pyrethroid Pesticides References Becker K. Ranft U. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Berger-Preiss E. Kuhn K. Heudorf U.134(1-3):141-145. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.68(6):1160-1163.

2-dimethylcyclopropane carboxylic acid of 0. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2dimethylcyclopropane carboxylic acid formed in the environment.1 μg/L) for the NHANES 2001-2002 subsample (CDC. Baker et al..2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.S. 1990). 2001. 2006) and 1177 urban adults and children (Heudorf et al.2-dibromovinyl)-2.2-dibromovinyl)-2.2-dibromovinyl)-2.3-0. Studies in Germany of 396 children and adolescents (Becker et al.2-dibromovinyl)-2.. Thus. Outside the U. 2004). in some situations replacing the use of DDT.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al. Deltamethrin can degrade to cis-3(2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. In the NHANES 2001-2002 subsample. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Biomonitoring Information Urinary levels of cis-3-(2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population. 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. Urinary levels for adults and children in these studies were similar (Heudorf et al.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. 2005). Finding a measurable amount of cis-3-(2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.. 2005).5 μg/L) than the detection limit (0.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2. 2005). mean peak urinary levels of cis-3-(2.Pyrethroid Pesticides Deltamethrin CAS No... in detection of cis-3-(2..2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dibromovinyl)-2.2-dibromovinyl)-2. urinary levels of cis-3-(2. 52918-63-5 General Information Cis-3-(2.2-dibromovinyl)2. Following residential spraying with deltamethrin for malaria protection in Mexico. (2004) reported a geometric mean concentration of cis-3(2. deltamethrin has been used against mosquitoes that carry malaria.

Pyrethroid Pesticides Urinary cis-3-(2. which may vary for some chemicals by year and by individual sample.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < 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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S.2-Dibromovinyl)-2. population from the National Health and Nutrition Examination Survey.1 and 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

2-Dibromovinyl)-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. 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.Pyrethroid Pesticides Urinary cis-3-(2. Survey Geometric mean (95% conf.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. 170 Fourth National Report on Human Exposure to Environmental Chemicals .

Deltamethrin. Environ Health Perspect 2005. 2005. Centers for Disease Control and Prevention (CDC).inchem. Angerer J. Atlanta (GA). Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Grimaldo M. Seiwert M. Carranza C. Environmental Health Criteria 97. Int J Hyg Environ Health 2006. [online] 1990. Angerer J. Schulz C. Lopez-Guzman OD. Third National Report on Human Exposure to Environmental Chemicals. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Fourth National Report on Human Exposure to Environmental Chemicals 171 . et al. toxicokinetics. Angerer J. Environ Health Perspect 2001.209(3):293-299. Kolossa-Gehring M. et al.Pyrethroid Pesticides References Becker K.77(1):67-72. International Programme On Chemical Safety (IPCS). Ball M. Available at URL: http://www. Angerer J. Batres LE.org/documents/ehc/ehc/ ehc97. 5/26/09 Ortiz-Perez MD.209(3):221-233. Hoppe HW. Heudorf U. Int J Hyg Environ Health 2006. Butte W. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Drexler H.113(6):782-786. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.htm. Torres-Dosal A. Int Arch Occup Environ Health 2004. Heudorf U.109(3):213-217. and genotoxicity in exposed children.

68359-37-5 Cypermethrin Deltamethrin CAS No. In the New York City study. Hardt and Angerer. Fenpropathrin Permethrin CAS No. 39515-41-8 CAS No. 2005).. representative NHANES 2001-2002 subsample (CDC.. 2003. A study of 396 German children (Becker et al. 2006) showed that urinary levels of 3-phenoxybenzoic acid at the 95th percentile were similar to levels at the 95th percentile for children in the U. In one study of 145 urban residents in 80 private homes in Germany.. A small sample of occupationally unexposed Italian residents had median levels of urinary 3-phenoxybenzoic acid that were about fourfold higher than for adults in the NHANES 2001-2002 subsample (CDC. In a small group of indoor pest-control operators. 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).. 2004). 52645-53-1 Tralomethrin CAS No. 2005). 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. CDC. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect.. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid 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 .S. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 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. 2002.52315-07-8 CAS No. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. 2005. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. Baker et al. 2005). 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. Following residential spraying with deltamethrin for malaria protection in Mexico. 2003). but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 52918-63-5 use and house dust levels (Lu et al. Saieva et al. 2005). Thus. 2006. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Becker et al.. 2005). CDC.Pyrethroid Pesticides Cyhalothrin CAS No. 2005. 2003.. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2005). CDC. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. 2005)..

42-2.27-2.32 (1.250-.49-2.18 (1.292 (.330) .600 (.60) .295) .35) 2.288 (.373) .490) .16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .260 (.13 (.41) 3.740 (.230-.30 (1.700-1.233-.530-.35 (2.800) 1.340) 75th .35) 2.63 (3.590 (.362) .280 (.72 (1.350-.870 (.8) 3.44) 5.05) .780) 4.247-.417 (.601) .440) .850) .230 (.454 (.253-.320) .34 (2.18 (2.800 (.226-. interval) .550-.265-.25-1.1) 3.510-.62) 5.510-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .1) 3.53) 1.30) 3.30 (.48-2.65 (1.288-.430-.79) 3.520 (.02-6.1) 3.750) .16-1.740 (.190-.49 (1.04-5.590-.46) 2.05) 1.830-2.54) 1.03 (3.230-.39) 2.52-4.352-.355) .32-21.190-.320) .210-. population from the National Health and Nutrition Examination Survey.320) .586) .46) .55 (1.610) .300) .330) .29-1.320 (.630) .48-2.25-7.33 (2.820) .260 (.25 (2.370) .26) 2.45-5.710 (.298 (.340) 1.S.78) 1. Survey Geometric mean (95% conf.266-.650 (.71 (1.336 (.64) 697 680 524 701 603 957 Limit of detection (LOD.27-2.810) 1.83-11. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.700 (.26-2.36) 1.328 (.760 (.81 (1.26) 2.267 (.297 (.35) 1.41-2.710 (.56-5.250 (.200-.420) .250 (.369) .428-.63-3.43) 3.240 (.340) .570-1.434) .364) .90) 1.730 (.321 (.38 (2.92-3.65-2.14-6.290 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .470-.960 (.73) 1. Deltamethrin.200-.190-.200-.190-.52-5.49-2. Fourth National Report on Human Exposure to Environmental Chemicals 173 .530-.560-1.01 (1.300 (.260-.750) .940) 1.38 (2.240 (.427) .750-1.78 (1.25-4.570-.406) .78) 1.34) 8.210-.507 (.276-.273 (.23 (2.04) .620-1.62-8.32 (2.680 (.670 (.314) .1 and 0.50 (2.227-.35 (1.271-.12) 4.51-3.387) .41-3.89-71.390) .246-.49 (1.62-6.53-3.75 (1.28) 1.41 (1.27-11.325 (.13) .69) 3.230-.45 (2.840-1.21 (2.25) 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 .33 (1.300 (.595) .490-.830) 90th 1.311 (.33) .250 (.12 (.990) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.238-.69 (1.160-.850) .51-6.292-.86 (1.230 (.160-.277-.450 (.640 (.1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.16) 1.430-.320) .560-.180-.76 (1.820) .560-.270 (.360) .300 (.78) 6.93 (1.220-.34-6.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.315 (.25 (2.270) .12) .384) .260 (.353 (.314 (.

440-.36-6.04 (.41-4.05-3.437) .240 (.190 (.13 (.200-.06-3.309) .178-.321-.22 (1.440-.860-1.240-.490 (.330) .380 (.490-.250 (.19 (2.264 (.49-2.173-.450 (.49) 1.490 (.230-.362 (.370-.19-6.32 (2.60) 1.730-1.200-.534) .75-8.280) .320) .760) .21-4.590-1.590) .300-.261 (.83 (1.372) .328) .274 (.480-.329) .53 (1.246 (.390-.11 (.510 (.300-.216-. Deltamethrin.43 (2.190-.35) .720 (.67 (1.530-.400-.357) .272 (.590) .278) .09-2.41) 1.550 (.810) 1.272) .25) 2.670) 3.37 (1.74) 3.310) .73-4.73) 1.677) .17 (.230-.83) 1.190-.280-.530-.350) .92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .560 (.329) .423 (.410) .S.378 (.35 (1.40 (1.03-1.62) 1.03 (. Survey Geometric mean (95% conf.11 (.670) .61-2.25-2.570) .44) 2.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.400) .35-3.88) 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 . interval) .240 (.15-2.17-1.640 (.323 (.00) 1.84 (1.270) .35) 1.271-.720) 90th 1.480 (.19) 2.94 (1.387) .280 (.240-.91-4.210 (.39) 1.270-.21 (1.225-.700-1.49 (1.210 (.960-1.580 (.200-.240 (.37) 1.0) 3.00) 5.62) .930) .270 (.55) 3.80) 4.460-.250 (.234 (.200-.730) .240-.730) .19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .280) .229-.350 (.55 (1.91) .91) 9.04 (3.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.640 (.13-1.370 (.230) .410-.07) 2.81 (1.311 (.210-.02 (2.43 (1. population from the National Health and Nutrition Examination Survey.67 (1.420-.440-.88-5.202-.52 (1.13-1.580) .400-.49) 3.401) .48 (1.250) .224-.275 (.261-.750-1.309 (.10 (2.550 (.270) .02-1.54 (1.510 (.60-4.930) 1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .238-.27) 1.220 (.590) .240-.650) .330) 1.253) .16-4.860 (.365) 99-00 01-02 99-00 01-02 99-00 01-02 .840-1.330) 75th .540 (.63-3.299-.86 (1.90) 3.280 (.335-.740) .160-.07-5.240 (.95) 1.91 (2.330 (.226-.09) 3.290-.150-.09 (.280 (.610 (.64-5. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.44 (1.550 (.274-.63) 1.290) .52) 2.96 (1.72 (1.67) 1.51-7.25-5.630) .270 (.40) 2.380-.220-.460-.860-1.290) .330) .316 (.500) .510 (.446) .312 (.09-2.227 (.36 (1.43) 1.43-64.00) 1.

Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Third National Report on Human Exposure to Environmental Chemicals. Berger-Preiss E.113(6):782-786. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Arch Environ Contam Toxicol 2004. Hoppe HW. Angerer J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Hardt J. Bartell S.209(3):221-233. Idel H. Lu C. 2005. Int J Hyg Environ Health 2002. Leng G. Pearson M.111(1):79-84. Grimaldo M.76(7):492-498. toxicokinetics.Pyrethroid Pesticides References Baker SE. Environ Health Perspect 2005. Sugiri D. Deych E. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Leng G.46(3):281-288. Ranft U. Exposure to indoor pesticides during pregnancy in a multiethnic. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Atlanta (GA). Torres-Dosal A. et al. Ortiz-Perez MD. et al. Int J Hyg Environ Health 2003. Becker K. Berkowitz GS. Obel J. Idel H. Ball M. Barr DB. Environ Health Perspect 2003. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. urban cohort. Seiwert M. Lopez-Guzman OD. Environ Health Perspect 2006. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Kolossa-Gehring M. Biological monitoring of workers after the application of insecticidal pyrethroids. Levsen K. Berger-Preiss E.205(6):459-472. and genotoxicity in exposed children. Centers for Disease Control and Prevention (CDC).114(9):14191423. Bravo R. Int J Hyg Environ Health 2006. et al. Liu Z. Int Arch Occup Environ Health 2003. Carranza C. Olsson AO. Godbold J. Lapinski R. Hadnagy W. Sugiri D.206(2):85-92. Barr DB. Ranft U. Batres LE.

270 (.178) .170) .170-.470) .120-.137) . water.210 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.220) .300 (.280 (. sheet and pipe metal.230-.310 (.154-.290 (.156-.280 (.430 (.190 (.270 (.210 (.180) .270) .200-.300) .190) .145) Selected percentiles ( 95% confidence interval) 50th .095 (.350-.230 (.320-.440 (.350-.120-.150) .160 (.120-.400-.140-. Urinary excretion appears to be greater for pentavalent antimony Urinary Antimony Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.130-.290-.230-.310) .220-.390) .180 (.108-.150) 90th .330 (.150 (.370-.098-.141-.400 (.350) .390-.210) . population from the National Health and Nutrition Examination Survey.090) 75th .130) .350 (.080) .130-.150-.120-.390 (.120 (.250 (.180 (.130-.220-. distribution.180 (.350) .130) .130 (.Metals Antimony CAS No.220 (.530) .320-.150) .120-.320) .130-.230 (.180 (.160-.105 (.07. People are exposed to antimony primarily through food and.160) .250-.080 (<LOD-.350 (.240-.087-.200-. and as a fire-retardant in textiles and plastics.330-.100-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.128 (.360 (. and refuse incinerators that process or release antimony.200 (. metal bearings.140) .160-.120-.190-.350-.330-.090 (.240 (.340) .210) .150) .510) .190 (.400) .130 (.122 (.180 (.095-.169 (. +3.200 (.080-.220-.154) .126 (.180-.161) .134-.148-. which may vary for some chemicals by year and by individual sample.400 (.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 .160 (.360) .200-.270 (.310-.250-.120 (.260 (.400) . storage batteries.123 (.190-.132 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals . from air and drinking water.260-.120-.570) .210) .131-.136) * .200) .120) .310 (.128 (.04.170-.160 (.150-.360 (. see Data Analysis section) for Survey years 99-00.140) .220) . 0.410) .410) .390-. or other substances containing antimony is another means of exposure.160) .250 (.220) .200 (.330) .560) .190 (.120 (.240 (.04.112-.310 (.200 (.130 (.180-.260) .200) .350) . < LOD means less than the limit of detection.230) .260 (.340 (.142 (.190) .210-.130 (.280-.250 (.117-.280) .250-.119-.320 (.160) .207) .350 (.490) .114) .440) .430 (.360) .176 (.400) .140) .390-.310) .120 (.130-.090-.190) .132 (.370) .090-.300 (. Antimony enters the environment from natural sources and from its use in industry.160-.280-. The absorption.130 (.260 (.130 (.130 (. It is also used in paints.180-.270-.130-.103) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.099 (. and excretion of antimony vary depending on its oxidation state.410-.170-.093 (.270) .140 (.180 (.320 (.230) .110-.070 (<LOD-.180-.137) .110-.500) .140) .280-.240 (.120-.120) .280-.190) .117-.110 (.300-.330) .220-.130 (.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 .240 (.190 (.150-.210-.160) .470 (.220 (.S.220-.220) 95th .184) .145 (.150 (.110) .230 (.115) .109-.170-.230-. 01-02.390) .160-.164-.420) .460 (. ammunition.190-.280) .133) * .140 (.070 (<LOD-.180) .120 (.200) .120) .400 (.460 (.170 (.200 (. enamels. and +5.350 (.460 (. ceramics. interval) . Dermal contact with soil.330) .220-.250) .260) .119) .230) .350) .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 .240 (.300) .115-. and 03-04 are 0. 0. and pewter.160) .280-.310 (.150-.320) Total .320-.190-.330 (.143 (.390) . It is used in metal alloys.140 (.170-.290-.150 (.120-. 7440-36-0 General Information Antimony is found in ores or other minerals.175 (.180-.300-.126-.130-.210) .079-.200-.460) .230-.300-.100-.120) .157) .600) .320-. respectively.158 (.144) .197) .070-.190 (. Workplace exposures can occur at smelters.088-.470) .430 (.136-.190-.150-.140 (.240-.280) .270 (.260) .125 (. castings.200 (.390) . and glass. coal-fired plants.280) .710) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240) .100 (.210) . fireworks. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.350 (.140) .135) * .110-.146 (.310-.500) .100 (.170 (.230-.360-.260-.200) .154) . solder.330) .340 (.330 (.190) . Stibine is a metal hydride form of antimony used in the semiconductor industry.108 (.160) .250-.080) .100) .300) . and 0. to a lesser extent.440) .490 (.130) < LOD .090 (<LOD-.130) .134 (.110-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.140) .

228 (. skin.471) .173) .143) Selected percentiles ( 95% confidence interval) 50th .135) .310) .175 (.164) .391) .276 (.230-.261) .114 (.429) .092-.140) < LOD .124-...500) .310 (.159-.268) .104-.151) .167 (.182 (.194-.214) .248-.247) .143) .244-.076-.239-.140) .228-.107-.152) .126-.117-.277 (.143) 90th .176 (.061-.256 (.143) .225) .228 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.317) .430) .113) .S. myocardium.286 (.115-.191 (.255) .138 (.417) .233-.098) .069-.131) .130) .113-.250 (.421) .115 (.120 (.267 (.253 (.200) .100 (.120 (.224 (.106-.Metals than for trivalent compounds (Elinder and Friberg. interval) .127 (.317) .121) . 1944).109 (.233) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.265 (.146-..227-.161) .222 (.207) .248) .226 (.266 (.149) .139 (.295 (.099-. 1953).320 (.318-.127) .069-.130 (.133) .333-. abdominal pain.146) ..172-.178 (.143 (.145) .357) .209) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.127) . 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.159-.132 (. 1973).176 (.121 (.108-.135 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.211) .124) . resulting in hemolysis with abdominal and back pain (Dernehl et al.082 (<LOD-.480) .131-.238) .308) .077) .320-.080 (.085) .380 (.300 (.095-.150-.188-.199-.352 (.105-.167 (.147-.333 (.233 (.192-.160 (.120 (.318-.176-.127) .150-.280-.333 (. and ulcers (Werrin. diarrhea.111 (.281-.198) .108 (.741) .170 (.250-.257) .098-.385 (.146-.185 (.405) . and kidney have been demonstrated in high dose animal studies depending on the dose.103-.108-.167-.181) .163 (.112 (.438) .148) * .230) 95th .119-.122 (.089) .30) .333-.082) .255-.102-.333) . and gastrointestinal symptoms such as vomiting.116 (.217 (.447 (.068-.444) .130) .320 (.294) Total .112-.119 (.121 (.300) .161) .250-.188) .126) .187) .185-.118 (.074 (.136) .153 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.109-.106-.086 (.313-.084) .259 (.111-.134) .741 (.125-.242-.178-.156-.149-. 1954).263 (.138-.125 (.137 (.183) .200-.280 (.189 (. Inorganic antimony salts irritate the mucous membranes.485) .079 (<LOD-.193) .144-.129) .135) .195-..263-.206-.371 (.179-.131 (.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 .104-.308-.128-.099-.095-. and route of exposure (Elinder and Friberg.471 (.203) .087) .098-.272) .269 (.173 (.236 (.338) . Ming-Hsin et al.417) .727) .185 (.267-.117-.338 (.253-. species.114 (. 1995). Acute antimony poisoning may cause a metallic taste.135) .156 (.338 (.113-.400 (.294) 316 368 290 663 762 725 1297 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .373) .271-.119-.068 (.092) .116-.250 (.315) .317) .148-.288 (.129 (.115) .333-.148-.123) .298 (.081) .321) .107-.429 (.203) .320-.186) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120 (.129 (.220) .102-.209 (.076-.124 (.265-. Histopathologic inflammatory and degenerative changes in the lung.112 (.152) .159-.364 (.127) .333) 1132 1334 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .444) .138-.130) .132) .181) .213 (.107-.391) .352) .192 (.163 (.147) .195 (.250-.081 (<LOD-.225 (.115 (.300) .115-.164-.164 (.204-. 1986). Fourth National Report on Human Exposure to Environmental Chemicals 177 .181) .205-.192) .320) .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.200-. liver.238) . 1962).146-.118 (. 1988.414) .071-.196 (.241-.096-.173 (.167 (.115 (.153-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes. population from the National Health and Nutrition Examination Survey.267) .208 (. 1958) and occupational exposures (Briegner et al.126 (.109 (.123 (.138) * .229-.209-.245) .250) .209) .122 (.114 (.082) .162-.171) .208-.238 (.193 (.195-.075 (.333-1.357-.117-.097-.173-.124-.235-.078 (.080 (<LOD-.241-.250-.135 (.154-.075 (.364 (.343 (.333 (.086) 75th .310) .103-.108-.278 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.129) * . 1986).425) .278) . and eyes.139 (.200-.

Pilgrim L. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Iavicoli I..67:119-123. gallium. Yu H-S. Van der Venne MT. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. J Trace Elem Med Biol 2002. Stead FM. Information about external exposure (i.)1954. et al. stibine. Chest 1973. Ju-Sun P. Chemotherapy for leishmaniasis: Biochemical mechanisms. and 2003-2004. even when exposure levels were below workplace air standards (Bailly et al. Nordberg GF. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.cdc. Petrucci F. Chin Med J 1958. Carelli G. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. 1998). Pozzoli L.. Liao Y-H. Dunkelberg. Br J Ind Med 1991.10(3):560-586. or exposure differences. Dernehl CU.. Cordasco EM. Kuo-Juie Y. environmental levels) and health effects is available from ATSDR at: http://www. Yang C-Y. Dezateux et al. Friberg L. which may be due to methodologic. Semisch CW. 1998.. Int Arch Occup Environ Health 1995. and future strategies. Wade A. Sabbioni E.48:93-97. Vouk VB. Arsine. Dezateux C. VI. Stone FD.158:165-190.64(2):182-185.. and antimony in optoelectronic industry workers. 20012002. Luedersdorf R. Paschal et al. O’Regan M. Antimony trioxide is rated by IARC as a possible human carcinogen. Bolten C. Biomonitoring of a worker population exposed to low antimony trioxide levels. Alimonti A. Nau CA. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Gebel TW. Leinemann M. 2005.51:238-240. Industrial Medicine 1944. Minoia C. Biological monitoring of exposures to aluminum. Ming-Hsin H. Sabbioni E. Fuchs A. Costeloe K..13:361-362..59:469-474. Centers for Disease Control and Prevention (CDC). et al. Kentner M. Review of elements in blood. Industrial Medicine and Surgery (Dec. Bailly R.76:432436. Konings J. Industrial antimony poisoning. Delves HT. Apostoli P. Mahieu P. Int Arch Occup Environ Health 1987. Delves HT.. Shao-Chi C. Roland H. plasma and urine and a critical evaluation of reference values for the United Kingdom population. 1987). Mayer P. pp. Skulsukai G. Environ Health Perspect 1998. Rev Infect Dis 1988.Metals to antimony have been established by OSHA and ACGIH.. Wu M-T. Pulmonary edema of environmental origin. Liao Y-H et al. Cheng-Wei L.e. Ludersdorf et al. J Clin Pathol 1998. Buchet JP. 1994) have reported values slightly higher than those in this Report. EPA. Urinary antimony in infancy. Schaller KH. Chen J-R. indium. 1995. 2004. External and internal antimony exposure in starter battery production. Biomonitoring Information Levels of urinary antimony reflect recent exposure. population. Schacke G. Cullen A. 1991. Iavicoli et al.. New York: Elsevier. Third National Report on Human Exposure to Environmental Chemicals. gov/toxpro2. 1997). Kentner et al. 1990. 1986. References Berman JD. Hamilton EI. 2002.html.S. Element reference values in tissues from inhabitants of the European community. Handbook on the toxicology of metals. respectively.16: 33-39. Elinder CG. arsenic. Arch Dis Child 1997. 26-42. In: Friberg L. Biological assessment of exposure to antimony and lead in the glass-producing industry. Antimony. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2nd ed. Chia-Yu H. Trace element reference values in tissues from inhabitants of the European community I. J Occup Environ Med 2004. Antimony in blood and urine of infants. Lauwerys R. HH. Matthews T. Stocks J. Kiberd B. Stasney J. 1998) or compiled reference ranges (Hamilton et al. et al. Suchenwirth R. and a drinking water standard has been established by the U. Ho C-K.. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Caroli S.46:931-936. Pietra R. Earlier measurements in general populations (Minoia et al. Briegner H.76(2):103-115.. eds. Sci Total Environ 1994. Gallorini M. clinical efficacy. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Piatnek DA.106:33-39. Mayne P.atsdr. 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.521-523. Lenert G. and hydrogen sulfide. Atlanta (GA). Weltle D.

Pirkle JL. Paschal DC. blood. Chemical food poisoning. Sampson EJ. Renes LE. Trace metals in urine of United States residents: reference range concentrations. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Industrial Hygiene and Occupational Medicine 1953. 27:38-45. Werrin M.95:89-105. Jackson RJ.Metals in urine. Environ Res 1998. Ting BG. et al. Morrow JC. Antimony poisoning in industry.76(1):53-59. Quarterly Bulletin of the Association of Food and Drug Officials 1962. and serum of Italian subjects.99-108. Sci Total Environ 1990.

70) 8.8) 7. meats.6) 618 722 1074 Limit of detection (LOD. Arsenic is measurable in most soils. lead.12-10.3) 10.4 (31. such as arsenopyrite (FeAsS) and realgar (As4S4).2 (41.8 (48.00 (6. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.Metals Arsenic CAS No.6 (32.50-14.10-10.4 (7.50 (8.10-7. General population exposure to inorganic arsenic can occur through consumption of drinking water and.5-41.7-95.1-40. mental disorders.5 (14.6 (9.34-10.5 (36. mostly for use in wood preservation (ATSDR.4-65.8-61. see Data Analysis section) for Survey year 03-04 is 0.5) 43.90-8. cancers. and indium arsenides are used in the semiconductor industry.8) 29.25-9.9-62. 2001). and as homicidal poisons. +3 and +5). or rarely as elemental metalloids (yellow. particularly arsenic trioxide. arsenites. arsenic as elemental metalloids may be used in some ammunition. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5-178) 46. semiconductors.80 (5. Since the 1940s. though in some locations arsenite may be prevalent (WHO.5) 41.20 (8. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. In the last century. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.5) 95th 65.8-77.2 (13. aluminum.29 (8. were used as treatments for syphilis. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.0 (22. In nature. to a lesser extent.5) 66.10) 10.6 (15. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.7) 24.1) 1281 1276 03-04 03-04 03-04 9.2 (12.3-19. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.2) 46.90) 75th 16. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. The United States no longer produces arsenic from mining but imports about 22.9-46.41 (7.2-93. interval) 8. arsenic compounds.4 (26.90-8. the smelting of copper. 2005).4) 13.6-141) 53.8) 30.80-9. from coal burning.2 (51. and gray forms).8) 17.2-61. arsenocholine.000 metric tons annually. ocean and fresh waters. Also.6-35. and other metals. sodium arsenite.90 (7. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. Before the 20th century. population from the National Health and Nutrition Examination Survey.66-8.6) 11.0 (14.1) 7.7-83.1) 290 725 1542 03-04 03-04 9. and arsenates (oxidation states of -3. Arsenic and its compounds have had many uses in the past and present as medicines.90) 16.84) 8.08 (5. Arsenic trioxide is approved to treat acute promyelocytic leukemia.9) 68. 180 Fourth National Report on Human Exposure to Environmental Chemicals .7) 65.84) 8. black.4 (24.90-7. Survey years 03-04 Geometric mean (95% conf.12 (6. trimethylarsine oxide.4) 60.4 (48. and play sets.0 (11.90 (7.90-11.5 (40.40) 7. psoriasis.1) 15.9-34.80) 6.57) Selected percentiles ( 95% confidence interval) 50th 7. and in lead-acid storage battery grids.S.77) 6.10 (6.13-8. copper arsenates. Arsenic trioxide (As2O3. gaseous hydride manufactured in small quantities for use in the semiconductor industry. cacodylic acid. and produce. pesticides.0 (43.6 (13.02-8. it is found in over 200 crystalline or mineral forms. and foods. Arsine (AsH3) is a reactive.9 (8.2-17.3-111) 78.90 (5.9 (17.3) 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 7.5-52.0-19.27) 9.2-20.8) 7.34-9.5-19.8) 34.97) 8. and. retaining walls. Although it is still widely used in the United States. referred to as inorganic arsenic compounds.1 (38. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. as alloy in metal bearings.7 (11.00-9.1 (32.74. alloys. lead hydrogen arsenate.6-43. and as a cosmetic to lighten complexion.30) 17.30 (6. Water sources contain mostly inorganic arsenate.19-9. Various arsenic compounds were used in paint pigments and for tanning animal hides.5 (34.55 (7.1-18.8) 33.70-9.70 (6.4) 40.9) 21.2) 15.5 (23.0 (15. grain. solders.3-15.90-14.30 (7. and arsenosugars. to a lesser extent.0-60.7) 90th 37. Gallium.

28-7.7) 95th 50.g.. and arsenosugars. interval) 8. and some other seafood can contain organic forms of arsenic including arsenobetaine.9-56.0-26.5) 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 8.61 (7.2-15. U.7-17.66-8.04 (5.32 (5.7-188) 27.8 (12. 2001).1) 6. 2001). Some studies suggest that variation in the degree of methylation among persons is related to the susceptibility of arsenicinduced disease and may involve consideration of genetic polymorphisms.4 (11.4 (42.9) 13.5-120) 40.6 (17. Fish. Tseng. After absorption. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.7-34.30-9. are used in enclosed ultraclean operations within the semiconductor industry.47 (7.66 (7.44) 6.50 (6.1) 8. 2001)..93-8. and contact with CCA-preserved wood structures.4 (24.99-9.47-6.18 (5.6) 45.9) 53.7 (25.59) Selected percentiles ( 95% confidence interval) 50th 7.4-64.0) 14. Inorganic forms of arsenic demonstrate high acute toxicity. kelp.01) 11.47 (6. WHO.1-36.8-75.6-17.9 (45. inorganic arsenic is widely distributed within the body. NRC. so exposure to the general population is extremely limited. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.45) 5.2) 40.0) 1281 1276 03-04 03-04 03-04 8.7 (9. shellfish.1) 58.7 (11.7-18. organic arsenic can be converted back to methylated and inorganic arsenic. dose level. Arsenate is reduced in the body to arsenite (oxidation state +3).38-10.0) 26.06 (4. Children may have additional exposures from ingestion of contaminated soils (e.58-10.7) 28.3 (27. 2001. EPA.8 (21.2-46. arsenocholine. In aquatic organisms.0 (17. Though modest bioconcentration occurs in some aquatic life.51) 75th 14.33-10. trimethylarsine oxide (TMAO).3) 9.64 (7.0) 33.76 (6. Direct exposure to DMA and MMA may result from use of the two pesticides.5 (9.88 (5.81-9.75) 13.44-11. 2006.0-69.2) 15.1) 24.35) 7.3-41.8-32.4 (12. population from the National Health and Nutrition Examination Survey.2) 90th 30..0-18.10-16. 2001).0) 42.4 (40. WHO.86-17. selenium.1 (11.3-62. 2001).3) 6. 2006.75 (5. Extremely high groundwater arsenic levels. arsenic does not show biomagnification in the food chain (WHO.12-10.13) 8.41) 6. Steinmaus et al.1) 7.8-62.66-8.10-8.24 (7..40) 8.07-9. 2001). 1988).33 (6. 2007. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA..31 (6.25-9.25 (6. age. Survey years 03-04 Geometric mean (95% conf.8) 27.8) 22.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. have caused clinical arsenic poisoning.3-64.5-17.5) 290 725 1542 03-04 03-04 8.5) 17. and folate status (Chen et al.23-7.S.8 (11.4 (26. In aquatic sediments. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. cacodylic acid and monosodium methyl arsenate. Gamble et al.04) 7. gallium arsenide and indium arsenide.93-9. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. 2001.S. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. 2007.4) 54.8 (27.0) 12.96) 12. Smoking tobacco is also a source of inorganic arsenic.8 (20.0 (31.4) 32. as observed in Bangladesh where millions of people have been exposed.S. dust.88) 7.20-9.01) 7. EPA’s maximum contaminant level (Hughes. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.0-38.3 (24.3-53.11 (5.1 (14.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . 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. 2003. but is poorly absorbed dermally (WHO. 2001).7-35.6 (10.00 (6. though some reduction may occur in the gut prior to absorption. 2007. The semiconductor dopants. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.6 (35.2 (12. 2001). Chowdhury et al.. mine tailings).

and altered gene expression. 2001).20 (<LOD-1. leading to a decrease in adenosine triphosphate energy production. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.. 2001). 2007.10 (<LOD-1. interference in signal transduction pathways. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.20 (<LOD-1. peripheral vascular disease. and diarrhea. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. drinking water have not been associated with increased cancer rates (Schoen et al.20 (<LOD-1. 2001. Chronic arsenic exposure in humans is considered to be a cause of skin.50) 621 725 1078 Limit of detection (LOD. fatty acid oxidation. hepatotoxicity. NRC. substitution in phosphate metabolism.S. including inhibition of numerous enzymes. Bredfeldt et al. WHO. 2007). Although arsenate is reduced in the body to arsenite. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.20 (<LOD-1.. which can lead to dehydration and shock.S.g. Taiwan. hypertension. hyperkeratosis.. 2006. 2001). 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. The U.60) 1. 1998.EPA. some of these effects may take years to develop. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2006. food residue. but additional or confirmatory research is needed (Kapaj et al. WHO.10 (<LOD-1. lung.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. 2000. and production of glutathione may be affected as well. Bangladesh. Cohen et al. WHO. Cardiac arrhythmias. hematocytopenias. gluconeogenesis. and by uncoupling oxidative phosphorylation (NRC. WHO. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. and it also will inhibit succinate dehydrogenase. noncirrhotic portal hypertension..30) 1.10 (<LOD-1.. Arsenic has many actions demonstrated in cellular studies.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. see Data Analysis section) for Survey year 03-04 is 1. including drinking water sources with elevated arsenic levels (e.g. arsenic trioxide) includes hemorrhagic gastritis with nausea. NRC. Chile).S.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. can cause peripheral sensorimotor neuropathies. vomiting. < LOD means less than the limit of detection. Cellular glucose uptake. and endothelial injury (Kumagai and Sumi..60) 1.. apoptosis.10 (<LOD-1.. 2001). increased oxidative stress.. 2001. and bladder cancer (IARC. With chronic exposure.80) 1. 2001). renal failure. 2006) or when exposure occurs in smokers (Chen et al. 2004).0. 2004. 2001). The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. cell transformations.S. U. Raml et al. 182 Fourth National Report on Human Exposure to Environmental Chemicals . and childhood neurodevelopmental effects in observational human studies. respectively. Such actions may lead to decreased energy production.10 (<LOD-1.EPA has established drinking water. The organic forms of arsenic occurring in seafood have little known toxicity. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 2006. cytotoxicity. and hyperpigmentation of the skin (NRC. 2004).50) 1... Chronic elevated arsenic intakes have been associated with diabetes. Acutely. Studies of arsenic at levels typical of U. which may vary for some chemicals by year and by individual sample. 2007. Survey years 03-04 Geometric mean (95% conf. and DNA repair inhibition (Cohen 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 1. population from the National Health and Nutrition Examination Survey. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 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.

Pellizzari and Clayton. 2006.. 2001).. 1999. 1998.S. 2000)...html. but generally only at maternally toxic doses (WHO. population (Rubin et al. 2006. 2004. 2001).89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population in NHANES 2003–2004 (Schulz et al.. Offergelt et al.S. 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. 2008. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2007. Vahter et al. 2007...33 (<LOD-3.Metals compounds. environmental levels) and health effects is available from ATSDR at: http://www. 1992.. In animal studies. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Additional information about external exposure (i.e..S.. Caldwell et al.00) 1.33 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 1999..50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 1999). Valenzuela et al. Shalat et al. had decreased since the prior 1990– 1992 survey.18) 3. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. In the German Environmental Survey III of 1998. and the FDA has established a bottled drinking water standard.S.75 (<LOD-2. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.50) 1. 2004. Caldwell et al. 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. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Shalat et al.atsdr. 2006).75 (<LOD-2.04 (<LOD-3..18 (<LOD-3. WHO.80 (<LOD-4. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.61 (<LOD-3.cdc. DMA produced bladder cancer in some chronic rat studies (Cohen et al. Survey years 03-04 Geometric mean (95% conf. 2008). 1986). 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. Pellizzari and Clayton 2006). 2006).41) 3. In a Nevada town where groundwater levels were naturally elevated. 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. 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.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2008). median urinary total arsenic levels in 4052 adults varied with seafood intake.. 2006). 2006). 2001)...19) 3.. Compared with this Report. 2003.69 (<LOD-3. arsenic has been fetotoxic and teratogenic. Josyula et al. Pellizzari and Clayton. Consequently. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. although urinary arsenic levels were not associated with CCA contact (Shalat et al. population from the National Health and Nutrition Examination Survey.. Meza et al. 2006. Levels of total urinary arsenic in the U.. 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. 2000.. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.. and were about two-fold lower than those for the U. gov/toxpro2. Fourth National Report on Human Exposure to Environmental Chemicals 183 . Calderon et al..

19 (.g.5 (26.10 (4.9) 13. 2006).1-25. geometric mean levels were about 70-fold higher than for the U.800 (.900-1.400-. population (Sun et al.48-2.. 2008). 2007).70 (3. when seafood organic arsenic is subtracted). Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.4.10) 8. 2000.871-1. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Sun et al.90-29.7-22. arsenobetaine.S.0 (27. In the late 1980s. 2005..40-6.50) . and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.30) 10.28) 1. methylation capacity. respectively.90-7.e. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.93) 1.70-21. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.4) 23.0) 4. and TMAO were detected in only 7..3 (9.5) 292 728 1548 03-04 03-04 1.600 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals other areas of the world (Ahsan et al.. interval) 1.62) 2. arsenite. in NHEXAS 1995–1996.500-1. In the residents of a Chilean town who consumed water with high levels of arsenic.68) . DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. arsenocholine.800-4.6.0) 29.2 (6.8-50.. and other factors such as nutrition.20) 18. vasospasm. Valenzuela et al. 2005. which may vary for some chemicals by year and by individual sample. 184 Fourth National Report on Human Exposure to Environmental Chemicals .40) 75th 5.8-40.8. 2008). arsenocholine.S. Survey years 03-04 Geometric mean (95% conf. and duration of exposure are also considered important.70-21.6 (13.7) 13. Caceres et al.1-94.. Individually measurable species resulting from inorganic arsenic exposure are arsenate.66 (1..20) 7.S.6 (11.800 (. For residents of Inner Mongolia.4-35. see Data Analysis section) for Survey year 03-04 is 0.6-44.45 (1.20 (.9-23.3) 1284 1284 03-04 03-04 03-04 1.S. population showed a higher contribution of arsenobetaine (Caldwell et al.. 2005.80 (.37 (1.9 (7. The higher percentiles of total urinary arsenic levels in the U.5 (14.8 (12.00-12.60) 1. dermal keratosis. In most human studies. Blom et al. and 0.00-4.00-1. Caldwell et al.800-1.20) 3.05) < LOD . and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.20-25.3-39. DMA and MMA. 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.3% of a representative sample of the U.9 (6.00) 3.29 (1.30) 2.3) 95th 35.50-6.. China.20 (1.. Some noncancer effects of arsenic (e..55 (1.0 (26.4) 31.2-38. These associations are stronger at higher urinary levels.5) 621 725 1078 Limit of detection (LOD. 1985. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. 1996. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. Aposhian et al.7) 15.20 (2. 1990.50) .1-51.80 (3. Tseng et al.74 (1.7 (13.30 (2.1) 18. 2008...40) 5. MMA. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.00-6.50) 90th 16...17-1. 2001).1) 45.30 (1.3) 35..31-1.83) Selected percentiles ( 95% confidence interval) 50th 1.7 (21. After recent seafood ingestion.6. 2000. Arsenate.00 (1. 2000. and two methylated metabolic products. 2008). a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. population in the NHANES 2003–2004 subsample. Caldwell et al.70) 6.700-1. 2007) with higher levels of arsenic in the drinking water.40-7.700-1. 2001.70 (5.20 (4. 1.3 (21.80-5. < LOD means less than the limit of detection.80 (4.4 (16.5) 29. 4. 2008). When seafood intake is avoided.00 (. population (Ahsan et al. 2003).20-3.11-1.8 (17. WHO.900 (. arsenite.8) 35. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. 2008. Pellizzari and Clayton.20-190) 31. population from the National Health and Nutrition Examination Survey.43-1. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.80) 1.6 (25. with DMA. Chowdhury et al. and TMAO..S.2-35. Caldwell et al. Also...5) 32.800) 1.6) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1.60-3.0-23. Measurable organic arsenic species in this Report are three biologically generated environmental forms..10) 4.

Sun et al.47 (2.25-7.531 (. 2008).18-1.6-29.82) Selected percentiles ( 95% confidence interval) 50th 1.0-36.51-2.81 (4.786-1..93 (1..54 (1.638) 1. Offergelt et al.9) 14.15-4.80-153) 17.44 (1. which is below the ACGIH BEI (Caldwell et al.1) 26.53 (.4-82. Survey years 03-04 Geometric mean (95% conf. 1998.6 (9.13-39.43) 75th 5.1-36.400-.0 (9.83) 2. 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. The 95th percentile of the U.2 (13. 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.36) 2.30) 1.00 (3.21) 5.55) 1.68 (1.4) 32.78-5.88) 2.6-46.4-21.40 (1.43) 14..65 (1..82) 4. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.612-1. 2001).32-7.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2 (4. WHO. Caldwell et al...58 (3.5) 17. 2003. 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.67) 4.64-29. Fourth National Report on Human Exposure to Environmental Chemicals 185 .73-6.4) 292 728 1548 03-04 03-04 1.877 (. 2008).10 (. population for the sum of inorganic related species was 18.2 (12.39-3.50-15.30-1.7) 30.91 (4.15-1.28) 1.938-1.4-28.45) 1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.16 (.959-1.15-1.3) 1284 1284 03-04 03-04 03-04 1.37-2.7) 9.8) 29.3 (10. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In recent years.51) 5. 2007).4 (24.6-32.88 (5.1-18.S. Vahter et al.4 (11.91) 90th 16.Metals as with DMA. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. interval) 1.833-1.05) 1. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.1 (26.80) .12) < LOD . 2006. not to imply a safety level for general population exposure. 1986.29-14.5 (18.5 (18. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. 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.3-24.901-2.72) 12.67) 1.40) 1...76-27.5-20.9 μg/L.6) 19.4) 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 * * 1.05 (. Information about the biological exposure indices is provided here for comparison.14 (1.3) 95th 29. 2001).9-18.19-2.5) 26.70) 5.29 (4.6 (6.9 (13.61-6.9) 32.25 (.83) 8.11 (. 1992.7) 17.2 (12.79 (1.50-7.4) 13.47 (1.62-6.78 (3.3 (10.9 (25.909-1.00 (1. population from the National Health and Nutrition Examination Survey.

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

S.44) 2.S.20 (<LOD-1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. which may vary for some chemicals by year and by individual sample.08 (<LOD-4. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.80) < LOD 621 725 1078 Limit of detection (LOD.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2.00 (<LOD-2. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.95 (<LOD-2. Fourth National Report on Human Exposure to Environmental Chemicals 187 .76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.70) < 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. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1.40 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.00 (<LOD-3. Survey years 03-04 Geometric mean (95% conf.

29-4.20-12.00-7.72 (4.60-3.57-5.60-6.0 (13.8) 7.74) 90th 9.14) 3.10) 6.34 (3.89 (3.84-18.0) 13.3 (7.00) 6.00-5.05) 10.45) 8.77 (3.59 (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 Sample size 2568 03-04 03-04 03-04 4.88 (4.0 (10.00) 7.00-4.0) 292 728 1548 03-04 03-04 4. see Data Analysis section) for Survey year 03-04 is 1.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .0) 9.52) 3.30) 3.5) 95th 13.80) 2.00-3.00 (5.06) 5.0 (9.81 (5.67) 9.0 (10.0-19.17-6.6) 1284 1284 03-04 03-04 03-04 4.0) 621 725 1078 Limit of detection (LOD.71 (3.00-11.5) 12.0-12.15) 4.61-16.00-11.0 (10.86-21.70-3.00 (3.45 (8.97-3.0 (8.86 (2.9) 5.00 (3.32 (8.00-4.94-3.0) 13.00-13.00 (7.03 (3.0-25.0) 9.16-11.00) 90th 11.0) 10.0-16.69 (3.80-3. interval) 3.70-4.S.00 (3.78 (4.00 (6.70) 5.0-18.1-22.34-4.37 (2.0 (12.00) 6.2) 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 3.90) 5.0) 17.33) 3.3 (8.71-4.55 (2.61-11.0) 16.92-12.0) 14.1 (8.48 (3.19) Selected percentiles ( 95% confidence interval) 50th 3.05) 3.16 (2.0 (9.9) 11.00) 75th 6.27 (3.0 (14.69 (3.28) 2.00) 5.22) 4.50 (4.34 (3.78) 4.16 (4.14) Selected percentiles ( 95% confidence interval) 50th 3.00-15.95-3.7) 13.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 11.1-15.79 (3.00 (6.0 (9.27-5.85 (3. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (5. population from the National Health and Nutrition Examination Survey.00 (3.00-3.49) 10.00-4.00) 3.0-16.0) 95th 16.31-4.80-5.49-4.7) 1284 1284 03-04 03-04 03-04 4.00) 3. Survey years 03-04 Geometric mean (95% conf.09 (7.00-15.80 (4.69-3.00 (5.91) 75th 5. Survey years 03-04 Geometric mean (95% conf.11 (3.71) 3.50-15.37 (3.38 (3.65-6.9 (11.9) 12.34-4.46 (4.90 (3.12 (3.95-4.82-9.94) 3.00-22.62) 4.0) 11.92) 3.90) 2.00 (6.25 (4.6-18.0) 16.27 (2.82-5.0 (8.9 (7.70 (3.00-12.44 (2.74 (2.0) 17.S.73 (3.60-4.00-8.00-7.17-4.95 (4.71 (4.00) 6.0-17.98) 4.82) 3.00-4.95-6.67) 8.20) 11.00-4.00) 9.11) 4.12-4.6 (9.0 (10.00-9.7 (10.0 (11.03-6.0 (12.18 (6.7) 12.73) 6.86-7.00-7.57 (3.0 (13.00-4.00) 6.00) 4.65-8.00-12.6) 292 728 1548 03-04 03-04 3.39-3.70-12.00-10.00 (4. interval) 3.33-4.27-2. population from the National Health and Nutrition Examination Survey.69-6.1-18.0-17.00 (7.44) 5.0) 12.00 (5.5 (11.7.9) 13.84-8.00 (5.32 (4.10) 3.3 (8.0) 9.34) 3.24-4.50-5.60-7.00-11.08 (2.31) 4.7-16.00-7.00) 4.42) 3.30 (7.8) 7.45) 3.00 (3.20-4.24) 3.4 (7.80-6.48 (2.00) 12.32-10.80) 7.00-15.00 (3.13-4.17 (2.05) 5.

30) 2.50 (1.00) 1.00-1.20 (1.20 (1.00) 2.34) 2.10 (.28 (1.50) 1.00 (<LOD-1.50 (1.90) 1.40-2.00 (<LOD-1.00-2.20-3.15-1.60) 2.40 (1.20) 2. * 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.10-1.985) 1.61) 2.20 (1.00 (2. < LOD means less than the limit of detection.50 (<LOD-1.86) 2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.85) 1.50-2.90) 2.40 (2.853-1.20-1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.81) 1.86 (2.53-2. which may vary for some chemicals by year and by individual sample.11-1.79) 2.20 (1.00) 2.S.900-1.54) 90th 2.40) 1.05-1.60 (2.52 (2.73-2.23) 1.71-2.10 (.77) 1.10-1.07) 2.35-3.22) 3. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.36) 1.30 (1.30 (2.80) 1.33 (1.30-1.17) 2.60-2.30 (1.60) 1.36 (1.18-1.10-3.84-3.30) 1.82-2.70-2.90) 2.46-2.33 (1.88-2.00-4.88 (1.70) 2.20 (1.31 (1.90 (1.80 (1.18-1.10) 2.07 (1.50) 621 725 1077 Limit of detection (LOD.82-2.85) 2.80-2.86 (2.80 (2.16 (2. population from the National Health and Nutrition Examination Survey.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00) 1.30 (1.816 (<LOD-.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.53 (1.30-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88 (1.70-3.10) 95th 2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.58) 2.37 (1.80) 1.93) .00 (2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.62) 2.57) 95th 2. population from the National Health and Nutrition Examination Survey.10 (<LOD-1.40) 1.80-2.43-3.30-1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.20 (1.40-3.30) 90th 1.70-2.70-2.80 (1.40) 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. 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 1.60 (1.86) 3.14-1.07-3.80 (1. Survey years 03-04 Geometric mean (95% conf.40-3.80 (1.60) 2.96-2.40-2.9.00-1.00) 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.00 (1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .50 (2.45) 3.90 (2.S.46 (1.61-3.10 (1.30) 1.63 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 0.28 (1.70-2.00-2.10 (1.31-3.22 (1.

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

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30-1.98) 1.19-1.60-2.71 (2.26-7.75) 2.70-8.20-1.70 (5.71) 1.51 (1.65-8.81-2.49) 8. are high in barium (Genter.37-1. Barium salts have also been available as rodenticides.65-1.56) 1.48) 1.36 (1.09 (1.73) 1.30) 8.68 (1.96-2.22) 6.32) 8.88 (5. respectively.86 (4. 01-02.76-7.87 (6.51) 1. such as brazil nuts.25 (1.90) 2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.65-5.70) 3.78) 1.8 (6.30) 4.40 (1.36-1.50 (3.30) 5.60) 1.18 (6.54) 1.31 (2.86 (4.19) 2.29) 5.40 (5.47-1.63 (2.73 (6.61 (2.g.87-14.66) Selected percentiles ( 95% confidence interval) 50th 1.12) 6.78) 1.91) 6.87 (5.91 (2.39) 1.70) 5.8) 9.20-5.15-11.61 (1.11-1.15-1.20-8.35-1.10-4.4) 9.12-1.00 (2.20-1.20-1.40) 3.25-1.80-2.50 (5.21-2.70-6.48-4.35 (2.56 (1.50-6.90 (6.87-9. such as barium chloride.94-6.67) 6.50 (1..35 (1.25-11.77) 1.00-3.15-1.93 (4. and 03-04 are 0.35 (3.20) 2.57-7.29-5.39 (1.91) 2.08 (6.55-3.50) 4.06-1.00) 4.01 (4.95 (4.49-1.35-4. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).4) 6.60) 1.43 (1.22-1.30-5.50) 1. and ceramics.93-2. tiles.17-1.26) 5. Some barium salts are freely soluble in water. 7440-39-3 Medically.30-1.50 (4.20-8.72) 75th 3.06-2.40 (1.50) 2.60 (2.80 (5.80-3.37) 1.90) 1.85 (2.80) 7.70-2.30-2. population from the National Health and Nutrition Examination Survey.63) 1.29-1.43 (1.26-1.51) 2.46) 1.70 (1.56 (1.99-5.82) 1.11 (3.37-8.02 (7.56 (2.10 (4.63) Total 1.28-1.59-11. depilatories.54-1.00) 1.53-5.37) 5.31. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.49) 4.62 (1.82) 2.24-1.00) 1.72) 1.72) 4.34 (2.18) 3.65 (5.4) 7. Barium compounds are also used commercially in paint.30 (5.8) 5.21 (1.50-1.20-6.41-1.43) 2.90-9.62) 1.86-4. glass.52 (4.43 (5.45) 7.63) 1.82-6.99 (4.76) 1.87) 7.21-8.16 (1.59) 3. whereas others are practically insoluble (e.41-3.60-6.50 (2. rubber.54-1.66 (4.71-9.53) 1.54 (2.20-1.28) 90th 5.30-2.50 (4.40 (4.10-5.30 (5.80 (1.70-5.62 (1.40 (5.10) 3.50 (1. see Data Analysis section) for Survey years 99-00.10) 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 1.90 (4.44 (1.12 (2.65) 1. Small amounts of barium can be released into the air during mining and other industrial processes. The general population can be exposed to low amounts of barium in air. and 0.65) 3.57) 3.49) 2.42 (1.00-76.61 (3.54-8.70-2.74) 3.80 (1.34 (1.22-1.88) 1.56) 4.30 (1.77 (3.21 (1.70) 7.50-1. barium sulfate and barium carbonate).88) 7. In single dose animal studies.57 (5.38 (1.14 (6.44-2. Workers employed by industries that make or use barium compounds can be exposed to barium dust.75-3.07 (2.90-13. interval) 1.39) 4.30) 2.74-3.46-1.70) 4.69 (1.86) 6.85) 1.15) 5.50 (4.15 (6.93-8.S.30) 5.00) 6.37 (4.55-7. 2001).12 (2.16) 5.11 (2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90) 4.44-5.35-1.51) 7.31-2.64-3.52 (1.90) 2.81-3.92) 2. Certain foods.20 (3.04-2.97 (1.15 (2.90-2.74-2.62) 1.10) 5. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.50 (1.50 (1.63 (1.73 (5.60-10.87-7.78-3. water.81-2.00-8.35) 5.48-4.40-13.10 (3.80 (2.88) 4.30) 3.70) 1.30) 5.61-8.80-7.20 (1.09 (2.80) 1.78-2.77-3.14-6.40) 7.43) 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 1.20 (4.70) 1.60 (1.95-6.47-1.50 (1.80 (2.50) 2.53) 2.27) 2. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.60-6.27 (1. fireworks.08-8.64) 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 2.20-8.50-6.65) 1.9) 5.40 (1.76-2.90 (1.33 (1.34 (1.76-3.71) 2.54 (6.47) 4.24 (4.70-3.30 (3.38 (1.Metals Barium CAS No.04-6.60-3.32-7.49) 11.71) 95th 6. In nature. Fourth National Report on Human Exposure to Environmental Chemicals 193 .43) 6.56 (6.12.27 (1.61 (5.63 (5.41) 1. bricks. Barium compounds are used by the oil and gas industries to make drilling muds.30-3.03 (1.12.2) 6.40) 7.15 (1.40 (5.48 (6. soluble forms of barium.32-1.73-5.00 (1.26) 2.80 (1.49 (1.18-1.49-9.54) 1.12) 7.84) 5.11 (3.38) 2.45 (1.05-2.10 (2.39-1.63 (8. 0.38) 8.80-5.54) 2.05% of the earth’s crust.39 (1.60) 3.36-1.36 (4. it combines with other chemicals such as sulfur or carbon and oxygen.73) 3.87-3.01-7.64 (1.30 (2.50 (6.61 (1.34) 2.85) 1.76 (3. and food.80) 6.86-5.48) 1.60) 4.24-1.36) 5.14-1.46) 1.1) 9.

19-2.42) 1.58) 75th 2.2) 6.45-1.72) 4.92) 2.72 (2.47) 4.09) 6.39-5.84) 2.36 (5.55 (1.48-5.39-1.23-1.24-3.36-1. water solubility.58 (2.62) 2.71 (5.66 (1.22-1.31) 5.64 (1.68-3.65 (5.72) 6.35-1.52) 2.16 (1.00) 6.51) 6.56 (1.00 (2.96 (4.03) 2.28-1.31-1.03-1.20 (1.75-3.19-1.10 (6.54 (1.28) 5.24-6.39) 4.41) 5.06) .90-2.32 (2.64 (1.53-21.11) .52) 1.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .01) 1.62 (1.97 (4.23-2.38) 4.63) 1.28 (1.55 (1.37-2. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.80-6.60 (2.29-4.99 (2.16) 11.45-1.10-1. 1994.97) 1.00 (3.68 (2.08-2.22-4.0) 7.78 (2.62 (2.33 (1.3 (6.97-4.703-1.41 (1.77) Total 1.68-3.34) 1.710-1.68) 3. NTP.84-5.55-6.82) 1.26-1..60 (2.55 (4.58-6.05-1.11) .69-9.51-3.32) 2.99 (4.921 (.96) 4.03-1.38-7.38-1.47-8.24 (3.42) 1.86 (2.45-8.39-1. and route of exposure.51) 4.24-11.13-2.38-5.33-4.55-5.28-6.02) 4.91-2.19-1.20-2.20-8.5) 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. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.68 (3.46) 2.00) 1.54 (2.50) 2.27-3.33-1.57) 2.22-2.880-1.42 (4.754-1.39 (3. population from the National Health and Nutrition Examination Survey. are not absorbed when administered.76 (3.37) 2.891 (.97 (5.59 (1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter. such as those used in medical radiographic procedures.76 (4.43-6.80) 4. Wones et al.47 (5.91 (3. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.79-5.96) 7.29 (1.50) 1.48 (1.91 (3.19-1.45 (3. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.58) 1.60 (1.31 (4.2) 5.15-4. Following intravenous injection in animals.31-1.04) 5.00) 4.48-3.29-3.34-1.73-2. Chronic high doses in animals resulted in kidney damage (McCauley et al.33 (5.47) 1.06) 2.14-2. Barium is not rated for human carcinogenicity.4) 5. 1990).26-4.55 (5.70) 10.02-5.23-5.85-5.34-3.75-22.75) 2.28-7. hypertension.13-3.34 (1.51 (3.0) 5.68 (3.44 (1.29 (3.49-1.74) 1.25-11.S.75) 1.91) 2.28-11.29-7.30 (1.37 (1.905 (.76 (2.8) 4.45) 95th 6.87) 1.29-4.46-22.88 (2.77) 1.52-10.80) 3.58) 4.83) 2.00-7.40-1.49 (1.30 (1.89) 90th 4.08-1.52-4.81-6. weakness.74 (5.69 (5.63-4.76-3.48-1.48 (1.49 (1. interval) 1. The health effects of exposure to barium compounds depend on the dose.777-1.33) 6.59) 1.35-1.51 (1.97-3.61 (4. in urine.55) .64 (1.22-1.98 (2.02) .36 (1.50) 1.53 (2.0) 6.73-4.39-10.. Toxicity from soluble barium salts is rare.51) 4.39 (2.83) 3.99) 1.03) 3. 1984.39 (2.31-1.04 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.03) 1.24) 3.36 (3.01 (5.84-2.86) 5.96-6.58 (4.96) 4.18 (1.21 (1.25) 4.47 (2.88 (6.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.26-1.33) 1.41 (2.56) Selected percentiles ( 95% confidence interval) 50th 1.29-1.4 (5.76) 2. a benign condition that may occur among barite ore miners. Symptoms following acute high dose include perioral paresthesias.33 (1.84 (3. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.56) 4.62 (4.38 (4.48) 2.45-6.24-1.79) 1.52) 7.10) 6.40 (1.27-1.56 (1.47) 10.00 (5.34-5.53) .65 (2.54) 2.38) 1.77) 5.70) 1.36 (3.43) 1.32 (1.45) 1.76) 1.18 (1.44-2.963 (. 2001).76) 2.70) 4.915 (.57-7.59-7.49-1.64) 7.64) 7.89 (2.35-3.38) 1.77) 1.68) 1.81-6.04) 1.00 (3. chemical form. 1985.31 (1.51 (1.26) 4. Insoluble barium salts.26-1.36-1.37 (1.44-2.39 (2.54) 1.57 (6. vomiting.832-1.52 (3.30) 2.32) 2.57-10.59 (1.46) 3.96) 4.36 (1.47) 1.32 (1.41 (1.20) 4. 1989).27 (2.25 (1.61) 2.00-1.00) 4.20-1.3) 6. paralysis.2 (3.81-7.75) 1.10) 3.59) 2.02 (3.38 (1.60 (1.16-1.881 (.49-1.86-7. and cardiac dysrhythmias.Metals was eliminated primarily in feces and to a lesser extent.57-5..11-2. diarrhea. Perry et al.40 (1.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.37-1. 1986).36-2.92 (4.38 (1.82) 1.96 (4.77) 1.27) 7.26-1.24-6.67-6.75) 2.77-5.64 (1.60 (5.01 (4.48 (1.73) 2.12) 2.56-3.41) 4.45 (1.50 (4.24 (5.59) 1.29) 1.40 (1.10-2.38 (4.24-1.74) 1.46) 1.46 (2.

p. Jr. Perry HM. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Int Arch Occup Environ Health 1992. National Toxicology Program (NTP). Inc.. J Toxicol Environ Health. Laurie RD. Exposure to soluble barium compounds: an interventional study in arc welders.296(1-2):71-90. 84-94. ed. NTP. Frohman. eds. In: Calabrese EJ.e. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Costa R. and a drinking water standard has been established by U. References Brenniman GR. 231-249.. et al. Pirkle JL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.197210. Barium. EPA. blood.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Trace element reference values in tissues from inhabitants of the European community I. Princeton NJ: Princeton Scientific Publications. the welders had no obvious adverse clinical effects (Zschiesche et al. calcium. 4/8/09 Paschal DC. Comparison of representative ranges based on U. New York: Elsevier. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Wones RG. Vouk VB. Jackson RJ. Douglas BH. pp. Advances in modern toxicology. et al. 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.. and radium In: Bingham A. Minoia C. eds. Nordberg GF. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. and 2003-2004 (CDC. Centers for Disease Control and Prevention (CDC). Morrow JC. PS. 2005.95:89-105.. 1985.85:355-359. Minoia et al. Sci Total Environ 1990. Howerton K. 221-252 Komaromy-Hiller G. Epidemiological study of barium in Illinois drinking water supplies.niehs. A study of 46 elements in urine. Patty’s toxicology. Investigations into the effect of drinking water barium on rats.. 2001-2002. Ting BG.. Perry EF. Cohressen B. Weltle D. Paschal et al.S.nih..28(3):373-388. p.. 2000) to levels in NHANES 1999-2000 and 2001-2002. [online]. 2nd Ed. New York: John Wiley & Sons.64(1):13-23. strontium. p.html. Pozzoli L. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. ed. Environ Res 1998. Genter MB.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA.atsdr. Atlanta (GA). Pietra R.gov:8080/cs. Reeves AL. Powell C. Fourth National Report on Human Exposure to Environmental Chemicals 195 . 1994. Schaller KH.html?charset=iso-88591&url=http%3A//ntp.cdc. patient population and literature reference intervals for urinary trace elements.niehs. barium. In Friberg L.S. Biomonitoring Information Levels of urinary barium reflect recent exposure. Sabbioni E. Ash KO. 2001. environmental levels) and health effects is available from ATSDR at: http://www. 1990. Available at URL: http://ntp. Vol 2: Specific Metals.gov/toxpro2. et al. 1998). 5th ed. Kopp SJ. Trace metals in urine of United States residents: reference range concentrations. et al. Information about external exposure (i. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.. Calabrese EJ. 1989. Magnesium. Stadler BL. Gallorini M. Clin Chim Acta 2000. 1984. LA. 2005. In: Inorganics in drinking water and cardiovascular disease.nih. McCauley PT. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding.76(1):53-59. Levy.gov/ntp/htdocs/LT_rpts/tr432. Apostoli P. and serum of Italian subjects. 1986. Environ Health Perspect 1990. Lack of effect of drinking water barium on cardiovascular risk factor. Handbook on the Toxicology of Metals. Third National Report on Human Exposure to Environmental Chemicals. 1992). Princeton (NJ): Princeton Scientific Publications. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Zschiesche W. Sampson EJ.

S. electrical. and machine-parts industries. nuclear. coal. Beryllium compounds are commercially mined.13. 0. Low-level beryllium exposure in the general population can occur through breathing air.13. In studies of laboratory animals.Metals Beryllium CAS No.150) < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .13.130 (<LOD-. In medicine. bertrandite and beryl. and volcanic dust. Two types of minerals. beryllium is used in instruments. soil.140 (<LOD-. and can be found in mineral rocks. near some hazardous waste sites. see Data Analysis section) for Survey years 99-00. which may vary for some chemicals by year and by individual sample. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. 196 Fourth National Report on Human Exposure to Environmental Chemicals . less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. 01-02. respectively. population from the National Health and Nutrition Examination Survey. Exposure to beryllium occurs mostly in the workplace. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. are mined for commercial recovery of beryllium.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. the lightest of all metals. and refined beryllium is used in mirrors and special metal alloys for the automobile. and 03-04 are 0. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. and 0. < LOD means less than the limit of detection. computer. and from breathing tobacco smoke. eating food. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 . and dental bridges. 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 . aircraft. x-ray machines. 7440-41-7 General Information Pure beryllium is a hard gray metal.130 (<LOD-. or drinking water containing the metal.

273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1990). 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.231 (<LOD-. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. 2002). * 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 197 . including contact dermatitis and subcutaneous nodules. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.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 .S. Chronic beryllium disease. respectively. S. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. and drinking water and environmental standards have been established by U. IARC has classified beryllium as a human carcinogen. Maier. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. 2003. which produces pneumonitis. Skin exposure can result in delayed hypersensitivity reactions.346 (<LOD-.391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. based upon excess lung and central nervous system cancers in studies of workers. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. population from the National Health and Nutrition Examination Survey. or berylliosis.281 (<LOD-. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. NTP considers beryllium to be a known human carcinogen. EPA.

Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. and serum of Italian subjects. Sci Total Environ 1990.cdc. International Programme on Chemical Safety (IPCS). Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. environmental levels) and health effects is available from ATSDR at: http://www. Centers for Disease Control and Prevention (CDC). Am J Epidemiol 2003. Hamilton EI. and 2003-2004. Paschal et al. In other studies. Pietra R.12 to 0. Jackson RJ. 2001). Atlanta (GA) 2005. Sci Total Environ 1994. Given these results.htm. 106. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Beryllium [online].gov/toxpro2. Trace element reference values in tissues from inhabitants of the European community I.1 μg/L). Minoia C. Genetic and exposure risks for chronic beryllium disease.org/documents/ehc/ehc/ ehc106. 20012002. Andrew M. plasma and urine and a critical evaluation of reference values for the United Kingdom population. et al. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Biomonitoring studies on levels of beryllium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of beryllium than are found in the general population.e. HLA-DPB1 and chronic beryllium disease: a HuGE review. 1990. Gallorini M.e.74:162-166. Comparison of representative ranges based on U. Van der Venne MT. Clin Chest Med 2002. Sabbioni E. 1990. it is likely that urinary beryllium levels in the U. They reported urinary beryllium levels ranging from 0. 2000. and the 95th percentile for males in NHANES 2001-2002. Kriess K.. Minoia et al.Metals (i.13 μg/L. McCanlies EC. Review of elements in blood. Element reference values in tissues from inhabitants of the European community.. Schaller KH.76(1):53-59.23:827-839. 3/27/08 Komaromy-Hiller G. Morrow JC. Paschal DC. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Trace metals in urine of United States residents: reference range concentrations. Sabbioni E.S. Ting BG.296(1-2):71-90. 1998). Levels of beryllium in urine for the U. blood. and the fact that most NHANES participant levels were undetectable. 0.atsdr.158:165-190.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Hamilton et al. Pozzoli L. References Apostoli P. VI. A study of 46 elements in urine. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Howerton K..S. patient population and literature reference intervals for urinary trace elements.. Environ Res 1998. Costa R. population are lower than levels in workers..157:388-398. Environmental Health Criteria. Sampson EJ. Apostoli P. population were generally undetectable in NHANES 1999-2000. Int Arch Occup Environ Health 2001. Clin Chim Acta 2000.inchem. Weston A. Available at URL: http://www. less than 0. Pirkle JL. which approximate this Report’s limit of detection. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. et al. Maier L.S.95:89-105. Third National Report on Human Exposure to Environmental Chemicals.html. Ash KO.

30-1. respectively.10 (1. malleable.500 (.368-.900-1.513) .900-1.60 (1.400 (.70) 1.344) .400) .20-1.300 (.400) .300-.600 (.333 (.296-. Since 2001.600-1.427) * .600 (.382 (.400 (.235 (.00 (.300-.300-. during refining of lead and copper from sulfide ore.300 (.300-.398) < LOD < LOD < LOD < LOD < LOD < LOD .200-.40) 1.386-.300 (.10) 1.60) 1.500-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (.300-.400-.40 (1. < LOD means less than the limit of detection.500-.00 (1.200) . interval) .400-.40 (1.400-. and incineration of municipal waste materials.500 (.20) 1.00) .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 * * * * * * .500) .400-.600) .300 (.80 (1.300 (.600) .500 (.30) 1.460) .600 (.20) 1.600) .10) 1.Metals Cadmium CAS No. and 03-04 are 0.600 (.30-1.500-.400-.313 (.300-.50 (1.400 (.10) 1.500-.800) .216-.400) .14.50-1.00-1.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .700) 1.S.400 (.500-.900-1.400) .00 (.200 (<LOD-.600) 1. Fourth National Report on Human Exposure to Environmental Chemicals 199 .50-1.800-1.200 (.90) 1.30-1. see Data Analysis section) for Survey years 99-00.300 (.60 (1.300-.00-1.300-.500-.393 (.900-1.449) Selected percentiles ( 95% confidence interval) 50th .20-1.362-.300) .400) .412 (.20) .200-.300-.400 (.403 (.600 (.00-1.289-.378-.10) 1.400 (.10 (1. and 0.400) .600-.300-.40-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) 1.10 (1.424) * .20) .300) .403) .20-1.50 (1.300) .378 (.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 01-02.700) . Cadmium also may be emitted into the air from zinc.304 (.30) 1.20) 1.800 (.600) .400) .10 (1.300-.300) .500) .400) .3.400) .400) < LOD .300 (<LOD-.700) .400 (.400 (.283 (.500-.420 (.500-. U.50 (1.395 (.00-1.600) .400) .10) 1.500-.20-1.600) .400 (.500 (.361-.400-.500 (.400) .500-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.266-.400 (.304 (.300-.900 (.50-1.70) 1.900 (.700) .00 (.300-.900-1.400-.30-1.20-1.300 (.00 (1.600) 90th 1.400 (.60) Total * .00-1.326 (. The predominant commercial use of cadmium is in battery manufacturing.10) 1.20) 1.50) 1.200 (.300-.700) .400) .60) 1.500-.500-.20) 95th 1.00 (.200-.500 (.900-1.900-1.400) < LOD < LOD < LOD .300) .500-.800) .60 (1.400 (.304-. Other uses include pigment production.700-1.70) 1.20) 1.200 (<LOD-.S.10 (.300 (. as zinc sulfide) and to a lesser extent.500-.300) 1.200) .00 (.600-.00 (.300 (.80) 1.300) .500 (.500) .337) .300 (<LOD-.426-.40 (1.50 (1.40 (1.20 (.00-1.359-.400 (.452) .425 (.800 (.500-.300) .50) 1.300-. EPA.700-1.367-.300 (.441) * .500-.309-.S.400-.331) .40 (1.60 (1.50-1.3.500-.500) .400) . cadmium use has declined in response to environmental concerns (http:// minerals.00 (.600 (.60 (1.400) < LOD .255) .00 (.800) 1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.400 (.900-1.500 (.468 (.20) 1.60) 1.10 (1.90) 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 .30-1.400 (.300-. coatings and plating. 0.usgs.00-1.700) .60-1. lead.400 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300) .700 (.30 (1.300 (.700) .20-1.gov/minerals/pubs/commodity/cadmium).421 (.10) 1.20 (1.900-1.70) 1.300 (<LOD-.700) . population from the National Health and Nutrition Examination Survey.366) * * .00) .500) . which may vary for some chemicals by year and by individual sample.500) .600-.600 (.300 (.300) .600 (.500-.00-1.300 (.10 (1.600 (.300-.275-.40 (1.300) .00-1.300 (.30) .400) .30) 1.400) < LOD .200-. and nonferrous alloys.40) 1.700-1.20) 1.600 (.376-.50) 1.40 (1.500 (.300) .600) .400-.900-1. 7440-43-9 General Information Cadmium is a soft.300) .400-.20-1.500) .600) .470) * .600 (.300-.300-.300-.20) 1.300-.400 (. plastic stabilizers.300-.00 (.300) .40-1.600) .300 (<LOD-.600 (.800-1.600 (.10 (1.600 (.200-.700) .400-.80) 1.300) 75th .200 (. or copper smelters (U.

092 (. Horiguchi et al.190-.22 (1.390-.170-.366-.282 (.366) .360) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.230 (.680 (.316 (.10 (1.279 (.753-.481) .135-. Cadmium absorption may be increased with iron deficiency (Berglund et al.141 (.322 (.479) .329 (.390 (.204 (.187 (.539) .061-.28) 1.280 (.295) . and 0. 2003).610) .843-1.255) .249) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.790 (.559 (.261-.219 (.06) .74) 1. The kidney is a critical target and shows the earliest sign of cadmium toxicity.270 (.200-..065-.090) .855-1.233) .090) .200 (.112-.17) .20 (1.107-.257) .243-.283 (.289-.24) 1. and various seeds.13 (.214-.748-1.199 (.179-.41 (.136) .04 (.390-.450 (. With chronic exposure.220) Selected percentiles ( 95% confidence interval) Sample 95th 1. respectively.061 (<LOD-.265) .07-1.175 (.492 (.06-1. copper) and protein.713) .220 (.633 (.233) .200 (.210 (. zinc.211-.43) 1.157) .426 (.. 2003.714-1.810-1.540) .171-.445 (.25 (1.498-.400-.160 (. calcium. For nonsmokers who are not exposed to cadmium in the workplace.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 .170-.918-1.507) .191-.01) .700-.257-.230) .972 (.381-.36) 1.480) .38) .32 (1.790 (.623) .388-. Diamond et al.339) .817 (.190-.06.490) 1.766 (.48 (1.239 (. To a lesser extent.519) . an inducible metal binding protein.078 (.17 (.192-.763-.265 (.13) .820 (. drinking water is a source for cadmium intake.178-.733) .800 (.700-.980) .135 (.336) .890 (.170 (.870) .151-.817 (.183-.207-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.206) .82) 1.235) .860) 1.633-1.238) .219 (.963-1.836-1. including many food crops such as cereal grains.100-.210) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.210 (.081) .189-.858 (.220-.470-..240) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.201 (.247) .38) 1.15 (.140 (.03) . whose body burdens of cadmium can be approximately twice that of nonsmokers.28-1.580) .216 (.240-.196-.519) .277 (.210 (.109-.813 (.165-.462 (.447 (. 1994). 0.20 (1.192-. however.221 (.733-.157-.354) .30-1.551 (.01 (.313) .892 (.189) .203) .980) .450 (.221) .302 (.730-.06-1.350 (.270 (.167-.820-1.455 (.** Survey Geometric mean (95% conf.198) . 01-02.551) .246) .060-.191-.261-.886) .510) ..284) .13-1.20) 1.260-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .153-.222) .203 (.S.466 (.128 (.607) .17 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.57) 1.229) .530 (.28 (1.249-.210 (.440 (.530) .890-1.160-. potatoes. interval) .191 (.173) .892-1.110-.34) 1.686-.195-.596) .184-.148-.940-1.194-.452 (.330-.262) .445 (.251) .211 (.15) . 2004a.077 (.820) 1.980-1.160) .177-.169-.320) .220-.09-1.387) . see Data Analysis section) for Survey years 99-00.260 (.456-.281 (.12 (.800-. 1999.741-1.717-.589 (.077 (.219 (.210 (.209 (.919) .52 (1. and 03-04 are 0.493-.17 (.38) 1.38) .47) 1.327 (.430-.134) . Renal tubular and glomerular damage.545 (.520-. rice.393-.310 (.180 (. Kikuchi et al.150) .412) .02-1.989-1.208-.223 (.01-1.433-.440-.181 (.700-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .126) .092) .Metals 2000). Cadmium in soil is absorbed by plants.640) .19) 1.202-.226) .326) .550 (.273 (.227 (.300) . 2001).25) 1.22 (.300 (.229-.394-.400-.130 (.220) . population from the National Health and Nutrition Examination Survey.272-.255) .490) . 2003).299) .12-1.990) .067-.232 (.72) 1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.160) .114-.080 (.372) .848 (.210) .482) .977) .237-.806) .306 (.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-.232) .839 (.510-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.109 (. Cadmium is absorbed via inhalation and ingestion.475 (.875 (.15) 1.238-.202 (.20-1.308) .705-.886-1.20 (1.818 (. ingestion through food is the largest source of exposure.230) 75th .263) .241) .500) 90th .83) 1.253-.875) .148) ..458 (.150-.06.04 (.436-.880) .087-.193 (.120 (.255) .121 (.960 (.06.362) .101) .200-.351-.206 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th . Inhalation of cigarette smoke is a predominant source of exposure in smokers.423-.175 (.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 .440 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.229) .476-.285-.310) .980 (.960) 1. wheat.193-.51 (1.115-.260-.290-.190-.231) .234 (.980-1.500) .366-.430) ..067-. 2003).

222-.631) .185 (.266-.387-.607) .364) .173 (.754) .300-..909-1.650-.470) .168-.444-.481 (.208-.316 (.077-.156 (.191-.795) 1.382) .159 (.491-.227-.10) 1.182) .678 (.560-.653) .228-.329 (.998) .175 (.767) .06 (.078 (.446) .263 (.232) .686 (.232) .09 (.106) .091 (.156) .112) .225) .187-.536 (.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 .091) .196 (.507-.162 (.111-.181 (.261 (. 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..941 (.476) .962) .350) .144-. 2004b).449) .00 (.143-.084 (.226) 75th .830) .143-.242) .085 (..096) .338 (.236-.438-. 1999). Noonan et al.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .278) .630-.094) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.884) .063-.224 (.537-.917) .225) . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.07 (.178-.212 (.415) .418-.716-.083-.266) .181) .757) .906) ..304-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.098) .292) .719 (. 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.130-.818) .051-..783 (.591 (.00 (. 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.218) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .431) .712 (.205 (.090 (.927-1.159 (.192) .201-.727-.931 (.268 (.147-.229) .17) .161-.219 (.303) .171-.336-.221 (.288-.622 (.154-.067-. However.352) .414 (.245 (.148 (.839) .516-.091 (.283 (.234 (.940 (.190 (. Jarup et al.281) .136-.784) .678-..210 (..150-.176 (.421 (.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 .441-.434 (.690-.170-.182) . 1996.104) .200 (.101) ..126 (.184) .289) .418) .470) .404 (.381-.789 (.140-. can result from high dose chronic exposure. **All results are corrected for molybdenum oxide interference in the ICP-MS method.708-1.221-.700 (. 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.267 (.779 (.** Survey Geometric mean (95% conf.247-.500-.691-.204-.38) .645-.873 (.253 (.806-1.850) .250) .490 (.722-.168-.154 (.979 (.198) . Olsson et al.423 (.156-.874-1.220 (.208 (.207-.865 (.856) .207) .216-.05) 1.104) .690-.123-.438) 90th .181 (.182) .541) .085-.792 (.929) . During the 1950’s and 1960’s.687 (.140-.247-.194-.826-1.614) .950) .559-.100 (.241) .273 (.690 (.562-.02 (.767 (.174-.191) .187) .074-.687-.693 (.426-.479 (.501 (.940-1.412 (.783) .122 (.533) .325 (.827) .084-.331 (. population from the National Health and Nutrition Examination Survey.382-.538) .086 (.398-.135) .202 (.157-. 2002.297) .769 (.667) .239-.316) .16) 1.183 (. 2004).281) . most often a result of occupational exposure (Roels et al.432 (.210 (.296 (.484 (. 2000.304) .191 (.308 (.802 (.282 (.340) .270 (.293-.256-.813-.318 (.740 (.818) .113-.183) .166 (.16) .288) .211 (.184-.473 (..666-.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.387 (.12) 1.178) .343-.377-.518) .177) .274) 1.173-.157-.335 (..263-.267 (.531 (.985 (.215 (.404) .199-.163) .147-.078-.199 (.663 (.850) . 2002.440) .185) . 2002.093 (.238-.181-. 2003.206-. interval) .247-.729 (.617 (.388-.289) .414-.209) .545) .688-.826-1.813-1. 1999).163 (. Horiguchi et al.071 (.07) .S.137 (.674-1.219 (.123-.240) .107) .433-.136-.261-.311) .175-.210) .08) . At lower environmental exposures.919 (. Staessen et al.830-1.234) . 1999).280 (.917 (.147 (.189-.551) .176 (.097) .143) .696-.757 (.238) .668-.235) .647-.190 (.252 (. 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.184-.223) .146-.234-.716) .209) Selected percentiles ( 95% confidence interval) Sample 95th .828) .261) .391-.487 (.240) .075-.472) .233 (.833-1.288 (.255-.321) .170 (.197-.253) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .423-.13) .440) .876-1.725-1.308) .856 (.168 (.700) .175 (.158-.075 (<LOD-.137-.131-.718 (.

Friedman et al. In postmenopausal women.. Animal studies have demonstrated reproductive and teratogenic effects. 2004b).26 and 3. 2002). potentially fatal pneumonitis (Fernandez et al. Becker et al. environmental levels) and health effects is available from ATSDR at: http://www... as may occur from welding cadmium-alloyed metals. 2003.. Occupational standards are provided here for comparison only.. 2005). 2006. Further research is needed to address the public health consequences of such exposure in the United States.. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. Wilhelm et al. Wennberg et al. 2002.. 2004. 2004.. Olsson et al. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. 2006).S. 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). Acute and heavy exposure to airborne dusts and fumes. Information about external exposure (i. 1996.gov/ toxpro2. 2002). 1996). Jin et al. 2006). 2000. For NHANES 19992000. 2005. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. 2000. data (CDC.. Becker et al. with peak values observed in the fifth to sixth decades (CDC... 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.. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. Cadmium can produce lung. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. approached these values associated with subclinical changes in renal function and bone mineral density. Moriguchi et al. 2003. 2004). decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al... Horiguchi et al. 2002.atsdr. 2000. 2002. Ezaki et al. 1999)..1 mg/L (Alfven et al. 2005. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al.. 2005.. 1988).. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.. intermediate in former smokers and lower in never-smokers (Becker et al. 2004. 2002) and length at birth (Nishijo et al. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U. Wennberg et al.S.. Becker et al. and drinking water and environmental standards have been established by U.. Noonan 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.. 2003. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.. 1999. 2003.. 2000). Mannino et al.. Staessen et al... respectively.html. Women had higher blood and urine cadmium levels compared to men of similar ages. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al... 1999). 2005.. Salpietro et al. Staessen et al. 2004.. EPA. Horiguchi et al.. 2002).cdc. 2004b. 2003). Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 2006.e. Jarup et al.. 2002). 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.. maternal blood or maternal urine and birth weight (Nishijo et al. Ezaki et al. 2002. 2002. Komaromy-Hiller et al. However. 2003.. CDC. 2002). respectively. Creatinine-corrected urine cadmium values in U. Olsson et al.. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies.S. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood.46 mg/gram of creatinine) (Ezaki et al.. Staessen et al. 2003. Suwazono et al. not to imply a safety level for general population exposure. In the typical environmental exposure. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. Jarup et al. 2002. Zhang et al. has resulted in severe. In adults aged 60 years and older.. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population.. Olsson et al. Both IARC and NTP consider cadmium a human carcinogen.

Comprehensive study of the effects of age.110:699-702. Serra J. Alfven T. Environ Health Perspect 2002. Mascagni P. 196:114-123.1(8587):663-667. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. et al. Seiwert M. et al. Lepom P. Howerton K. 2005. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002.000 women in the Japanese general population: a nationwide large-scale survey. Machida M. Chislovska NV. Int Arch Occup Environ Health 2003. Grubb A. Kikuchi Y. Schulz C. Olfactory function in workers exposed to moderate airborne cadmium levels. Fatal chemical pneumonitis due to cadmium fumes. environmental. References Akesson A. Savage-Brown A. Friedman LS. Krause C. Lundh T. 4/8/09 Alfven T. J Occup Health 2003.S. 102:10581066. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Atlanta (GA).24:717-724. Akesson A. Mannino DM. Consonni D. Available at URL: http://www. Costa R. Kumagai N. Komaromy-Hiller G. Lancet 1988. Vahter M. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers.102:83-89. Jones RL. Bregante G. Fourth National Report on Human Exposure to Environmental Chemicals 203 .13(11):1627-1631. Nomiyama T. Nerbrand C.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. Becker K. Comparison of representative ranges based on U. Becker K. Environ Health Perspect 1994.S.cdc. et al. et al. et al. Third National Report on Human Exposure to Environmental Chemicals. J Toxicol Environ Health 2003. Nermell B. Lidfeldt J. Uemura T. Kundiev YT. Mucha A.45:43-52. Tsukahara T. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers.148(1-2):11-20. Fukui Y. Bernard A. Int J Hyg Environ Health 2002. Environ Res 2004b. Diamond GL. Venables KM. Neurotoxicology 2003. Stock AL. diabetes mellitus.html. Clin Chim Acta 2000. Oguma E. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Ezaki T. Chiappino G. Nordberg G. Lukyanova EM. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Ezaki T.46:372-374. Oguma E. Jarup L. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Ye T. Darbyshire J. Berglund M.59:194-8.atsdr. Hotz P. Moriguchi J. Anthropometric. Sanz P. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.95:20–31. ShkiryakNizhnyk AZ. Ikeda Y. iron deficiency.57:668-672. et al. et al. Horiguchi H. et al. Environ Res 2006. Environ Health Perspect 2005. Lison D. Bellerup P. Centers for Disease Control and Prevention (CDC). Toxicological profile for cadmium update. Seiwert M. Takebayashi T.296(1-2):71-90. Jarup L. Ikeda Y. Thorax 2004. Occup Med 1996. Lancet 1999. Kaus S. Schulz C.76:186-196. Horiguchi H. Occup Environ Med 2000. Moriguchi J. Choudhury H. Davison AG. Carlsson MD. Machida M. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Gadea E. Toxicol Lett 2004.205:297-308. Agency for Toxic Substances and Disease Registry (ATSDR). German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.66(Pt A):2141-2164. Furuki K. Ukai H. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Persson B. Sasaki S. Hellstrom L. Toffoletto F. Wang H. Miyamoto K. Buchet JP. Pickering CA. et al.354:1508– 1513. Ash KO. possibly better than b2microglobulin. Kaus S. Okamoto S. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Taylor AJ. Lauwerys R. Elinder CG. Zhu G. 1999 [online]. Holguin F.59:497]. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria.gov/toxprofiles/tp5. 206:15-24. Int J Hyg Environ Health 2003. patient population and literature reference intervals for urinary trace elements. Jin T. Bo M. Palomar M. Vahter M. Sasaki S. Greves HM. population. Dekio F. Environ Res 2004. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Fernandez MA.96:353-359. Tsukahara T. Fayers PM. Furuki K. Toxicol Appl Pharmacol 2004a. et al. Thayer WC. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Seifert B. Fukui Y. Miyamoto K. et al. Cadmium fume inhalation and emphysema.

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57-5.9) 8.7 (11.38) 5.09-5.1-12.36 (3.79 (4.23-4.3) 9.71-5.53-11.84) 8.01-8.64-5.00) 4.1 (10.0) 12.81 (4.80 (4.20) 7.59 (5.3) 10.90-10.1 (9.80 (8.74-5.90) 7. population from the National Health and Nutrition Examination Survey.3) 10.64) 5.20 (4.87 (4.8) 9.Metals Cesium CAS No.05) 5.81-14.32 (3.61-6.50 (7.07-11.5) 10.9) 11.90 (6. 01-02.5-13.68 (7.40-5.00-10.55 (7.97) 4.25 (3.6) 10.91-8.40-7. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04 (4.40 (4.5-14.12-5.70-8.56 (4.9 (11.50 (6.83) 6.66 (7.40) 7.03 (4.60-5.50) 9.01-6.70-5.0 (10.6 (9. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.80 (8.4) 10.13 (5.92-13.81) 4.4) 10.0) 10.1) 11.71 (8.40-5.1) 10.7 (8. For absorbed cesium salts.59-5.7 (9.2.59-5.2 (9.3) 10.00) 6.60-6.60) 7.4) 12.95) 5.33 (6.63-4.10-9.1-12.09) 5. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.50-7.80-6.14.30) 5.8-13.80) 7.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.39-4.16-6.77 (9.8 (10.2-13. although cesium was generally of low toxicity when given to animals.49 (5.00 (7.08 (6.94) 4.5 (8.82-4. and high-power gas-ion devices.20) 5.34 (4.13-8.20-7.64 (4.0 (9.5) 12.90-10.55 (4.30 (6. see Data Analysis section) for Survey years 99-00.4) 11.23) 9.08-5.95 (3. the body half-life is estimated to be 70-109 days based on 137Cs exposures.3) 10.56) 5.84) 5.80 (4.4-13.4 (9.1) 11. and as polymerization catalysts.9 (10.82) 5.17-6.10-7.30-5.47-8.50 (4.52) 7.80 (4.70 (6.40-11.70 (6.04) 7.16-6.0-13.95-4.4) 9. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.71) 4.77-8.86-12.54) 4.4) 12.88 (8.05-5.35-5.40-5.3-13.20-5.43-8.10-5.7 (10. scintillation counters.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. and 03-04 are 0.3) 12.00-4.45-8.60-7.32-5.0) 9.70 (5.56 (4.22 (4.60) 7.90) 5.30 (6.90) 4.3-13.39) 7.70) 5.20) 8.35 (4.12-11.94 (4.52-9.17 (6.14 (4.00) 7.47-4.12) 5.9) 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 4.71-9.2-13.37) 5.8) 11.S.25) 4.21) 90th 9.6 (11.64-10.10 (6.03-4.54-11.8 (11.60) 5.6) 11.26) 4.9 (11. nausea.7) 10.61) 7.02 (4.00-8.44 (8.9 (10.90-8.8) 9.93 (4.17) 4.96 (6.7 (9.01) 7.26-11.89-5.9 (11.84-5.8 (10.42-7.70 (4.60-12. and cardiac arrhythmia (ATSDR.8) 12.8) 11.2-12.43 (5.72) 4.6 (11. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.70 (8.5 (10.30-10.89) 5.5) 9.24) 4.3 (8.0-15.60 (7.59) 7.49 (4.13 (8.72-7.1) 9.05) 5.2 (9.59-5.77 (4. infrared lamps.42) 6.69-6. Fourth National Report on Human Exposure to Environmental Chemicals 205 .7) 11.46) 7. soil. semiconductors.50 (4.07) 4.56-11.13 (7.7 (10.50) 5.73-5.34) 9.70 (9.2) 12. cesium hydroxide is corrosive and irritating at high concentrations.27 (7.98 (7.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. photographic emulsions.70 (8.90) 5.20-4.10 (6.26) 7. diarrhea.10 (8.36) 3.6 (9.21 (4.83-4.0) 12.6 (9.62 (5.99) 9.7 (10.71-8.27) 4. Whether cesium compounds are carcinogenic is unknown.2-13.74) Selected percentiles ( 95% confidence interval) 50th 4.97 (7.99-11.97-7.03 (4.8) 12. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.87) 5.33-5.0) 12.35 (4.1-13.33 (5.90-12.15-8.20-8.40-5.49) 4.87 (4.87 (4.7-14.94 (4.10-8.32) 4.08 (7.08) 7.12 (4. Little is known about the health effects of this metal.37) 7.9) 12.08-5.84 (4.7) 11.40) 5.29) 4.49) 75th 7. However.81) 4.42) 7. 0.20 (6. Most human exposure to cesium occurs through the diet. respectively.74 (4. interval) 4.30) 7.4 (10.63 (4.8) 12.4) 95th 11.90) 9.45-5. 2004).60-6.71 (4.31-8.50 (4.68) 9.1 (11.20) 4.53 (6.26 (3.0) 11.00-8.80 (8.99-11.94-4.91 (7.7) 10.29 (4.89) 4.0) 11.2) 11.80-10.63) 6.90 (4.80-13. and 0. Radioactive 137Cs has been used medically to treat cancer.80-11.70) 7.55-11.36 (6.1) 9.98 (7.05-5.64) 5.62 (5.86-11.4 (9.86 (7.60-7.76-6.67 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.99) 7.9) Total 4.00-9.87-7.80-10.80-10.90-12.81) 9.9 (11.2-14.10 (8. and clay.5-14.27-5.14.64) 4.7 (9.99-6.60 (8.3 (8.5-16.84-9.73-11.70) 5.77 (9.25-5.62) 4.3-15.90-10.40) 5.6 (9.40-11.22-4.

46-8.46-4.85) 5.87 (5.48-6.41) 9.45-6.05-4.17 (6.68) 6.7) 10.28 (5. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.37-3.38-12.00-8.60 (5.7-12.35 (4.50 (6.40-5.46 (8.44) 3.30 (3.25) Selected percentiles ( 95% confidence interval) 50th 4.17) 9.54 (3.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.95) 4.91-6.73 (3.98 (6.31-4.09) 4.78 (3.83-7.41 (8.42-4.29) 4.11 (5.60-20.75-11.72-5.05) 6.96 (4.44-5.77 (4.00-5.15 (7.0) Total 4.64) 5.3) 9.6 (9.19-3.43 (4.47) 7.20-4.36-6.88-4.84-9.35-7.20-4.3 (8.65-3.64) 9.27 (8.65 (6.99-9.50) 4.74-11.39 (5.76-6.84-7.38 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.77 (7. Komaromy-Hiller et al.19-6.55-5.91) 5. interval) 4.51 (3.60 (3.3-15.92) 3.94) 7.90-8.95) 10.20-4.43 (3. population from the National Health and Nutrition Examination Survey. Two small studies of European populations reported urinary cesium levels similar to U.2 (8.1) 11.S.07 (5.10 (5.00-10.27-4.42-4.17-4.16-5. population results shown in this Report (Alimonti et al.95-12.03-6.00 (8.70 (7.26-6.3) 11.13-9.14 (6.66 (5.14-7.05-3.03) 6.50) 8..06) 4.31 (4.27 (6.9 (10.86 (4.38 (3.12-6.50 (7. 2005.47) 6.10-4.03) 5.87) 5.14) 4.63) 6. 1990).41) 4.50-5.50 (5.56-10. population.54 (4. 2004).95-6.51 (7.49) 3.54 (5.6) 6. Minoia et al.0) 7.74 (4.21-4.41-4.8) 5.64-6.16) 5.53 (4.14-4.15-11.47 (7.24-10.8 (9.2) 11.96) 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 3.08) 4.58-5.16-8.40) 6.97-5.72) 4.64 (4.8) 10.5 (9.91 (5.59) 4.27) 4.80) 6.35-11.40) 7.96) 4.20-8.9 (9.29) 4.30 (7.67 (5.31-6.56 (4.8) 6.84-7.77 (6.42-6.22 (3.09 (4.5) 9.46) 6.91-9.66-6.51) 4.68 (4.06 (5.41-7.21-3.S.63 (7.45 (4.64) 4.74 (5..11 (5.93-7.13 (3.99-9.41 (4.10) 7.92 (5.91) 5. (2000) found urinary cesium levels that were slightly lower than those reported for the U..06 (3.21 (2.74) 3.67) 5.06) 5.13) 7.58 (6.01-8.53 (6.28) 7.15-4.07) 8.43-11.63 (6.34 (5.44 (4.78) 4.68) 3.98) 5.08 (6.46 (7.05 (4.20) 5.31 (4.51 (4.87-4.95 (3.84-11.26 (3.38) 10.09) 8.30-4.7) 10.42 (4.05) 3.56) 3.29-3.47) 4.82) 7.57) 3.71) 6.18) 8.91-7.02 (5.76-9.95 (5.44 (8.07-4.24 (3.22-11. Using clinically submitted specimens.79 (5.60-10.98 (7.33 (5.30) 10.14-6.08 (3.04) 5.02-4.28 (4.52-5.70) 7.21-5.5) 9.27-6.63-6.68-11.53) 3.79) 9.94 (5.55) 4.43 (8.33 (5.61 (7.48) 7.33-8.36-3.51 (4.47) 6.58) 8.00-5.23 (7.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.05-3.81 (4.63-6.98) 5.08-7.56) 4.00-4.50) 4.2 (8.78 (3.96-4.73-4.53) 6.S.81 (4. and were also roughly similar to those in this Report. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.29) 5.04-11.79) 6.03-5.67 (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 .90 (7.66 (5.04) 6.91) 4.42 (5.97) 8.85-4.83-6.44-9.62) 5.39) 5.08-3.14) 4.26 (4.85) 4.95) 8.97-4.78) 4.35) 3.6 (9.56) 4.75 (7.9) 10.15) 95th 8.25) 4.43 (4.3) 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 3.12) 3.37) 4.30) 10.62-8.71 (7.5) 7.77) 4.74) 75th 5. 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.70) 6.27 (6.93-9.58 (4.63 (4.90-3.04-5.91 (5.83) 8.60) 3.43) 8.30 (4.00-9. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.59-8.08) 4.75 (6.35 (3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.08) 3.3 (9.22) 6.99-4.3 (10.36-10.10 (3.07) 8.89-4.99 (3.38-7.43-6.65-4.39) 8.18-6.08 (5.13-9.72 (4.88-10.00) 6.10 (3.84-9.18 (7.55 (3.54 (4.79) 4.17) 4.58) 3.47 (4.51 (3.28) 8.16-8.96-4.99) 4.24-4.41 (5.48) 90th 7.18-7.61-3.68) 4.0 (7.64 (8.4) 10.79-5.12 (3.50) 4.30-4.82-4.66 (6.29-3.90-8.33-3.77-5.

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

12) 1.369 (.46 (1.490-.427-.470) .32) 1.340-.15 (1.980-1.680 (.92) 1.394) .08-1.19) . and kitchenware.371 (.730) 1.280-.900) . Cobalt is used as a drying agent in paints.13) 1.47 (1.487) .670 (.660-.850-1.331-.860 (.320 (.379 (.316-.06 (.540-. seawater.330) .515 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.333-.900-1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.352 (.543) .410 (.950 (.410 (.470 (.450) .01 (.04-1.920-1.05 (.820 (. Cobalt compounds are used as catalysts in producing oil and gas.17-1. and fertilizers.520 (.380 (.47 (1.460 (.02-1.16) 1.800-.300-.355-.417) .850-1.430-.50) 1.630 (.390 (.430 (.23-2.340) .339 (.950-1.424) .350-.48) 1.340-.399) .419) Selected percentiles ( 95% confidence interval) 50th .379 (.16 (1.740 (.25-1.790) .431) .285 (. hard metal or in combination with other elements.360-.380-.410-.900-1.550 (.580 (.53) 1.410 (.390-.430 (.880-1.17 (1.06 (.670-.26) 1.22-1.16-1.950 (.300 (.930 (.03-1.360-.05 (.24 (.890) .410 (. large appliances.590-.700) . blue-colored pigments.374 (.350-. varnishes.52 (1.09 (.308-.420) .430 (.581) .330-.630-.12) 1. diamond-polishing wheels.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 .900) .450-.17 (1.340) .583) .760 (.29 (1.42) 1.410) . and magnetic recording media.496) . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.520 (.01-1.26-1.364-.316 (.460) .414) .375 (.291-.32) 1.45 (1.405-.410 (.900) .03) 1.56) 1.16 (.550) 90th .710 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.372) .660) .36) 1.380-. and inks.670 (.450) .750-.560 (. Cobalt occurs naturally in airborne dust.590-.S.14) .520-.17 (.32-2.570 (.460-.570) .520-.410-.570-.20 (1.294 (.890-1.890) 95th 1.68 (1.33 (1.460) .630 (.398) . shiny. Cobalt compounds are also used in manufacturing battery electrodes.28 (1.710) . interval) . industry is imported or obtained by recycling scrap metal that contains cobalt.48) 1.400-.570-.367 (.420 (.39) 1.07 (.440-. It is emitted into the environment from burning coal and oil and car and truck exhaust.431) .05) 1.14-1.388-.26-2.870 (. The cobalt used in U.810) .940-1.47) 1.410-.377-.435 (.430) .23) .09) .650 (.960-1.16) 1.600-.461 (.520 (.434 (.690 (.680) .07.950) .360-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.15-1.33-1.580 (.22) 1.460) .24 (1.600 (.810-.370) .370 (.680) .404) .386) .670-.373) .08) .520) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.800) .740-.770) .67) 1.520-.454 (.760) . population from the National Health and Nutrition Examination Survey.540-.480-.03 (.740-.500) .290-.348-.75 (1.523) .610) .750 (.01-2.370-.700) .03) 1.640) .370-.04-1.520 (.940 (.S.09 (.21) 1.465) .600) .416) .530 (.820 (.550-.334) .590) .710) 1.44) 1.319) .540) 1. Usual human exposure is from food sources.610 (.570) .393-.390) .870-1.660) .350 (.390 (.03) .50 (1.750 (.450) .620) .259-.73) 1.64) 1.580 (.313) .65) 1.530) . steel-belted radial tires. 0.480 (.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 .22 (1.930) .540-.305-.620-.670 (. and soil.680 (.790 (.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 .450-.510) 1.338-.810) .840) .37-1.620-.16 (1.610) .520-.28-2.620-.450) .370-.420) .920) 1.800-.04) 1.610-.690-. automobile airbags.830-1. 01-02.410) .270-.950-1.380 (.28 (1.359 (.890-1.640) .81) 1.930-1.650-.330 (.502) .398 (.590 (.04 (.650 (.01 (.60 (1.270-.32 (1.499 (.310-.16-1.336-.301 (.81) 1. hard metal (alloys of cobalt and tungsten carbide).540-.490-.790-.47) 1.07-1.890-1.327-.500 (.820 (.350-.519 (.343 (.Metals Cobalt CAS No. see Data Analysis section) for Survey years 99-00. respectively. 208 Fourth National Report on Human Exposure to Environmental Chemicals .750 (.460 (.348-.380 (.06-1.880 (.530-.26) Total .99) 1.333-.07.07-1.373-.430) .520) .940-1.04-1.350) 75th .850) 1.270-.640) .418 (.59 (1.850) .428-.870 (.390 (.310 (.03 (.480 (.690-. and 03-04 are 0.910-1.08.340 (.980) .469-.564) .32 (1.463-.28 (1. and in synthesizing polyester and other materials.00) . 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. and 0.452 (.

50) 1.215-.259-.02 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.333-.378-.368) .272-.S.17) .785) .275-.239-.434-.291 (.960 (.550-.900-1.595) .333-.449-.417) .990) .975 (.35) .257-.723 (.487-.12 (. 1994. 1979).24) .707) .513-.29) 1.353 (.804) 1.838 (.352) . an essential human nutrient..727 (.44 (.786-. refining or processing alloys.481) 90th .929) .16 (.905) .237-.562) .821-3.955) .444 (.06 (.554 (.635 (.634-.316 (.581) .29 (1.10) .488) .429) 1.372) .647) . Cobalt is absorbed by oral and pulmonary routes.35) 1.495 (.289) .848 (.872 (.302-.452-.362-.393 (.256-.593) .703-.479-.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 .983-1.792 (.461) .327 (.753-.296) .33) 1.268 (.11-1. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.324-.396) .313-.337 (.615) .669) .346 (.326-.438) . Once absorbed and distributed in the body.376 (.462) .792-1.03-1.381) .700 (.259 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.271 (.542 (.382-.829-1.543) .738 (.582-.547 (.574-.821 (.323) .737 (.303-.365) .54) 1.327-.467-.27) 1.313-.393-.404-. using hard metal cutting tools.360) .523 (.469-.339-.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 .297) .857-1.363) .402 (.850 (.328) ..384) .333-.683-.435-.983) .753) 1.25 (.296-.333 (.329 (.963-1.310) .640) .361-.279 (.552 (.500 (.04 (.11-1.348) .850-1.407 (.740-1.500-.251-.304-.457 (.457) .298 (.400 (.248-.392 (.306) 75th .638-1.15 (.04-1.760-1.306 (.274-.09) 1.750) ..861-1.10) 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 .591 (.257 (.328 (. 1972). or using diamond-polishing wheels that contain cobalt metal.533 (.29 (1.337) .281) .14 (.290 (.369 (.833-1.55) .280-.694) .60) 1.895-1.963) . with pulmonary clearance half-lives of from one to two years (Hedge et al.630-..83) 1.300) .343 (.425-.365-.879-1.990-1.294-.301) .937 (.278 (.468) .36) 1.898 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.662) .955) .362 (.756 (.522) .313 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).368) .247 (.455 (.29) .630-. cobalt is excreted predominantly in the urine.439) .917) .563-.632-.358 (.513) ..408 (.449) .342-.585) .964 (.16 (1.10 (.50) 1.60) 1.513 (.830 (.952 (.334) .33) .515 (. Smith et al.844 (.963) .594) .313-.391) Selected percentiles ( 95% confidence interval) 50th .861 (.234 (.386 (.00 (.391 (.599) .25 (.290 (.23 (1.736-.503-.826-1.609) .700 (.309) .608 (.471 (.824 (.419) .471-.781) 95th 1.744) 1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.301-.842) .548 (.49) 1.508-.689 (. 1972).911-1.728) .344-.16) . Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.500-.362) .421) .394) .314 (.50 (1.757-1.282 (.73) 1.829) .471-.598 (.12-1.03 (.378-.27) 1.28) 1.963-1.278-. in the feces.282-.523 (. A portion of cobalt retained for long periods is concentrated in the liver.606 (.250) .388 (.293 (.361 (.949) .616-.644 (. 2003).317 (.328 (.777-.534 (.463-.331-. population from the National Health and Nutrition Examination Survey.361 (.479) .895-1.476-.00 (.667-1.352 (.319-.851 (.304) .691 (.248-.00) .324) .343-. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.774 (.277-.425) .407) .00-1.313-.00) .505) .673-.15) 1.426 (.349) .667-1.378 (.335 (.537 (.475 (.313-.10-1.275-.409) .368 (.600-.16 (.487-.733-1.417 (.560-.611) .435 (.976 (.355) .781-1.750-.611) . 1994).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 .329-.728 (.679-.00 (. and to a lesser extent. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.847) .378-.00 (.660-.457-.352 (.279) .529 (.626-. respectively.938-1.29 (1.10) Total ..361-.243-.534-.297-.442-.428-.353-.708) .938) .738 (.19) .57) 1.Metals fabricated from cobalt alloys (Lhotka et al.433) .396) .36) 1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.554 (.290 (.562) .561) .30 (1.259) .286) .932-1. Exposure in the workplace may come from electroplating.380-.273 (.704-.387) .388 (. interval) .

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

Thakker DM. Sci Total Environ 1997. J Rheumatol 2001. Hedge AG. Outcome of occupational asthma due to cobalt hypersensitivity. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Sci Total Environ 1998. Int Arch Occup Environ Health.148:241-248. Lauwerys R. Palmroos P. Science 1988. Weber A. 3rd ed. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust.242:1412-1415. J Bone Joint Surg Br 2005. Moulin JJ. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Kusaka Y. Clin Orthop Relat Res 2003. Unwin P.58(10):631-634. Bunn HF. et al. Zhuber K. Kirsch-Volders M.150:177-183. Robinson C. Sci Total Environ 1994. Mosconi G. Dickel H. Weyher I. Jarvis JQ. Sabbioni E. et al. X. Lison D. Barnaby CF. Diepgen TL. Health Phys 1979.(1-3):133-139. Thomassen H. Kriss JP. De Boeck M. McMinn DJ. Kato M. Lasfargues G. Thabe H. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Linna A. Sabbioni E.150.28(5):1121-1128. Rorabeck CH. Lauwerys R. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Gross RT.157:117121. Kraus T. Co-sensitivity between cobalt and other transition metals. Cobalt and antimony: genotoxicity and carcinogenicity. Absorption and retention of cobalt in man by whole-body counting. White MA. J Orthop Res 2003. Sci Total Environ 1994. et al. 2001. Stanescu D. Peltier A. Lisi P.48:172-173. Shirakawa T. Dunning SP.50(9):835-842. Fujimura N. Szekeres T. Pisati G.44:124-132. salt.87(5):628-631. et al.69(3):193-200. Vitali MT. Leghissa P. Kuska Y. Angerer J. A report of two cases from mineral assay laboratories and a review of the literature. Carnes WH. and cobalt metals.21(2):189-195.Metals effects of cobalt. Wild P. Dunstan E. Roto P. Iversen BS. Falcone G. Buchet JP. Swennen B. Ziaee H. Christensen JM. Blunn G.533:135-152. Goldberg MA. Alessandrelli M. Hoher T. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Tilley S. Zweymuller K. Sabbioni E. Cannon SR. Molders J. Edmonds CJ. Int Arch Occup Environ Health 1997. Cleland D. Uitti J. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Lung cancer risk in hard-metal workers. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Bourne RB. et al. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Daniel J. Health Phys 1972. Steffan I. Lauwerys RB. 1985. Contact Dermatitis 2003. Schramel P. Lison D. Hoet P. Smith T. The release of metals from metal-onmetal surface arthroplasty of the hip.22:359367.204:147-160. Epidemiological survey of workers exposed to cobalt oxides. Arch Intern Med 1990.34:620-626. and hard metal dust. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Hammon E.” Contact Dermatitis 2001.216:253-270. Occup Environ Med 1994. Cresti R. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Lhotka C. Cobalt cardiomyopathy. Am J Ind Med 2003. Schank M. et al. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Meyer zum Buschenfelde K-H.51(7):447450. Am J Epidemiol 1998. Chest 1989. J Trace Elem Med Biol 2006. Goto S. Goto S. cobalt salts. Buchet JP. Iavicoli I. Swennen B.36:732-734.55(4):269-276. Boca Raton (FL): Lewis Publishers. Heki S. Oksa P.150(1-3):167-171.20(1):25-31. Pradhan C. Lison D. Ichikawa Y. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Long-term clearance of inhaled 60Co. Bozec C. Biological monitoring of workers exposed to cobalt metal. Br J Ind Med 1993. a study of 13 elements in blood and urine of a United Kingdom population. Zobelein P. Bacis M. Schaller KH. Mutat Res 2003. Salvatori S.95:29-37. oxides. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Ghat IS. Respiratory health of cobalt production workers. Zedda S. DeSantis V. Trace element reference values in tissues from inhabitants of the European Union. Sanghrajka AP. J Occup Med 1992. Radulescu M. Occupationallyinduced “isolated cobalt sensitization. Linnainmaa M. Laippala P. McCalden RW. Occup Environ Med 2001. MacDonald SJ. J Bone Joint Surg Br 2006.88(4):443448. Meier R. Kristiansen J. Chess DG.45:246-247.406:282-296. Kiilunen M. Romazini S. HoffmannB. Salama A.

30-2.52 (1.30-1.70-3.30 (4.10) 3.50-2.43-1.50-1.00 (3.900 (. Lead is most often mined from ores or recycled from scrap metal or batteries.70-2.37-1.34-1.90-2. solders.10-3.60) 3.40) Total 1.10 (1.90-4.80) 1.80 (4.S.70 (1.30 (2.70 (3. and 03-04 are 0.50-1.80-4.00) 3.52-1.62) 1.39) 1.10) 3.942 (.90) 3.60-6.83 (1.30) 2.14-1.65 (1.80) 1.80) 1.10 (2.70-1.20 (3.20 (3.30-1.60) 3.50-5.40) 2.80 (1.80 (1.50) 7.60 (1.20 (1.70 (2.60 (1.87 (1.60) 1.95) 1.43 (1.40-2.50 (1.70) 1.66) 1.70 (1.62 (1.90) 5.40-1.23 (1.70-5.80 (1. 01-02.70 (1.800-1.50-1.50-5.51) 1.50) 75th 2.40) 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 1.70) 3.93-2.32-1.80) 2.00-2.20) 1.60-3.62-1.90 (3.40-1.80-3.90) 2.60) 2.30 (4.900 (.00) 2.10-4.60 (3.20) 90th 3.80 (3.30 (2.S.10) 4.81) 1.20 (1.00-4.10-8.878-1.90 (3.40 (1.96-2.00 (2.55-1.g.00) 1.40 (1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Before the 1980’s. 0.68-1.80 (4.10) 2.10-2.50-1.60-2.00) 1.90 (3.22 (1.60 (4.80 (5. Lead was used in plumbing for centuries and may still be present.40) 4.75 (1.70) 3.40) 3.10) 5. interval) 1.10-3.69) 1.70-4.20 (3.75-2.90-4.60-4. antique-molded or cast ornaments.39-1.50 (2.50 (4. and for radiation shielding.30) 1.02) 1. malleable.32-1.00-5.40 (1.30 (2.89) 1. bronze).90) 3.40-6.20 (3.40) 2.50) 3.20-6.50) 2.80-5.20-3.50 (1.45 (1.90 (3.70) 4.87) 1.50-2.60 (1. see Data Analysis section) for Survey years 99-00.10-1. blue-gray metal that occurs naturally in soils and rocks.31) 1.60) 1.30) 5.00 (1. Lead has a variety of uses in manufacturing: storage batteries.900-1.90) 2.30-1.60) 2.60 (2.60) 4.55 (1.10 (4.00 (4.10 (2. metal alloys (e.30) 95th 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 2.36-1.50) 2.10-6. and 0.40-4.40-1.90-2.30-6.20) 3.40-3.20-2.20) 4.50 (1.60 (2.60 (2.17) .71-1.10-4.50) 5.3.10-3.48) 1.60) 4.90) 1.00) 2.30 (1.70-2.20-1.00 (5.40 (2.70-1.09) 1.12-1.20 (3.70) 1. brass.25 (1.20-2.80-4.20-3.10-2.30 (1.69 (1.10) 1.60) 2.50-6.50 (4.40 (4.50 (2.60 (3.20) 5.77 (1.60 (3.20-3.14-1.80) 2.50-4.25) 1.40) 1.60 (2.40-3.30) 2.50) 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 (1.30 (1.20) 3.60) 1. the main source of lead exposure for the general U. lead was added to gasoline and residential paints and used in soldering the seams of food cans.60 (1.00 (4.00) 6.30-2.00-1.51 (1.Metals Lead CAS No.50) 1.40) 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.49-1.60-1.70) 4.10-2. ceramic glazes. Elemental lead can be combined with other elements to form inorganic and organic compounds. leaded glass.40 (5.80) 2.60) 1.90 (3.90) 2.60) 2.30-1.20) 4.20) 3.10-1.70 (2.50 (1.60 (1.40-1.01 (1.50-2.70 (3.50) 5.40-1.50-2.70 (1.20 (1.80) 1.30-4.40-2.00) 1.90) 2.30 (2.30-5.10) 3.50-4.70) 4.00) 2.70) 1.69) 1.10) 2.37 (1.30 (3.20-4.80-3.60-1.90-6.91) 1.30 (2.30-2.70) 1.80 (2.45-1.10-2. Since lead has been eliminated from gasoline.20) .60) 4.00) 5.75-1.50 (2.50-3.90-3.90 (1. 7439-92-1 General Information Elemental lead is a soft.19 (1.20-3.56 (1.70 (5.60-1.20 (2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .53) 1.10-2.60-1.30-2.70) 2.52-1.80-3.80-4.10 (3.00-4.80 (5.50) 1.90) 1.40-6.90-2.00) 2.00-1.30) 2.80 (1.60) 2.40) 5.60) 5.90) 2.40-5.3.25 (1.60) 1.80-3.986) .50) 4.60-4.80-2.40 (1.20 (4.66 (1.60) 3. dense.20 (3.10 (2.60 (1.20) 2.43 (1.50 (3.40-2.00) .70-1.78 (1.70-6.60) 3.899-.50) 4.36) 1.00) 1. respectively.50) 1. In the past.20 (2.20-1.10-2.00) 3.60) 5.90 (2.36-1.50) 1.50-3.40) 2.10-1.90-4.04-1.60-2.20 (1.10) 1.00-6.40-3.00) 1.10) 1.72) Selected percentiles ( 95% confidence interval) 50th 1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.00) 4.40-1.60 (2.40) 1.60 (3.90-2.00 (6.80 (1.10 (1.90 (1.90-4.20 (3.80) 1.75) 1.40 (2. ammunition.10-6.20) 3.30 (4.20 (1.90 (2.50-1.60) 4.50 (3.70) 1.00 (1. such as lead phosphate and tetraethyl lead.10 (1.60 (2.80 (2.37 (1.70) 4.30-1.80) 2.43) 1.86) 1.30-1.60 (1.946 (.70) 3.90 (4.30 (1.30 (2.10-3.80) 3.70-2.30 (2.50 (2.46 (1.80 (2.80 (1.43) 1.28. plastics.55-1.90) 1.50 (2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.00) 4.70 (2.40 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00-4. population from the National Health and Nutrition Examination Survey.14-1.

600-.20) 1.12) 90th 2. older plumbing systems with leaded pipes or lead soldered connections.33.749) .661-.80) 1.86) 95th 2.00) .680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.80) 2.19 (1.30) .50 (2.690) 75th 1.21 (2.50-3.40) 1.33-2.931) . 01-02.710-1.66 (2.44-2.40 (1.800-.90) 2.40-1.40 (1.553-.20-1.30) 2.80) 2.17 (1.660) .10) .50-1.1.700 (.30) 1.04 (.07-1.20) .00-1.60 (2.00-1.640-.540-. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.89) 2.40) 1.29) 2.23) .526-.589-. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.90 (1.60 (1.60-1.680-.556-.40 (1.64) 2.23-4.29 (2.78-2.700-1. see Data Analysis section) for Survey years 99-00.900 (.90-2.50) 1.70) 3.640 (. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.840 (.815 (.13-3.636 (.790 (.90 (2.625-.20 (1. or water contaminated by mining or smelting operations.20) .90) 2.22) 1.745-.910-.30-3.30) 2.90-2.572-.80-2.900) .850 (.62) Total .00) .10-1.70) 1.625 (. pewter utensils and drinking vessels.20-1.80) 1. 1991).828) Selected percentiles ( 95% confidence interval) 50th .10-1.900) .75) 3.766 (.09) 1.04) 2.1.31 (1.14 (1.20) .50) 2.680-. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.20 (1.785) .941) .700-.00-2.822-1.10-3.60 (1.940 (.50 (1.30) 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 1.800-1.18-1.20 (1.40 (2.g.610 (.10-3.30 (1.00 (.960-1.82 (1.32 (1.00-2.40) 2.80 (2.80) 3.11) 2.03-2.10-5.986) .80) 2.820-1. CDC.650) 1.620) 1.600 (.857) .651) .573 (.40) 2.642 (.848 (.50 (2.80) 2.960-1.04) .30) 2.570-.800) .970-1.70) 2.30) 1.02) 1.862) .90 (1.40-3.900-1.691-.600-.00 (2.630 (.800) . In the blood.72) 1.52-1.752 (.710-.20 (2.40 (2.Metals occupational (e.753 (.900) .605) .00) 1.90-4.91) 2.800 (. lead-containing folk remedies and cosmetics.70) 1.800 (. and 0.729-.10) 2.990) 1.70-3.50-2.637-.10) 2.49) 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 .579-.818) .10-3. 0.558 (.70 (2.40 (1.40) 2. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.20-1. imported children’s trinkets and toys. and 03-04 are 0.935) 1.730 (..900 (.90-3.60 (1. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR. lead-based painted surfaces undergoing renovation or demolition.86-2.40-1.900-1.700-.80 (1.920 (.40) 1.604 (.700) .30-1.659 (.80) 2.30) 1.671-.31-3.10) . bullet fragments retained in human tissue. lead-contaminated dust in indoor firing ranges.90-3.20) 1.480-.600 (.695 (.06) .579-. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.580-.30 (2.641-.00 (1. 2007.60-3.00-1.718) .674) 1.24-1.10 (1.90) 2.680) .S. battery and radiator manufacturing) and recreational sources.27 (1.923 (.620 (.20 (3.41) 2.30) 1. However.900-1.688 (.20 (1.30-1.00) 2.30 (3.04-2.80-3.33 (2.50 (1.00 (1.616) .10 (1.50) 2.900-1.20 (2.14-1.595-.900) .90-2. 2000).60-2.590 (.700 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90 (1. interval) .90 (2.90) 1.506-.60) 2. Approximately half of the absorbed lead may be incorporated into bone. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.80) 3.795 (.800) .700 (.700-.20-2.955-1.30) 1.800-.700 (.52 (1.13) . respectively.535-.60 (1.701) .03 (1.66 (2.70 (1.757-.30-1.800-1.14 (1. population from the National Health and Nutrition Examination Survey.80 (1.27) 1.00-2.70) 3.90 (2.810-1.97) 4.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10-1.800) .70 (2.90-2.10-1.60-3.70 (2.04 (.00) 2.10 (.20) 1.50) 1.700 (.920 (.40 (2.86 (1. or after soluble lead compounds are ingested.700) 1.10 (.40) 3.960 (.40-5.800 (.731 (.500-.82 (2.677 (.49 (1.40-2.600) .52-1.78-2.700 (.59-2.50-2.00 (1.10) 1.628) 1.70-2. and contact with soil.50) 3.700-.900 (.00) .40 (1.80-2.02 (.00) .990) 2.591 (.808 (.30-5.540 (.10-1.50) 1.40) 1.10 (.50 (2.07 (.564 (.600-.40 (2.700-.10 (1.560-.613) .59) 1.833 (.20 (1.40-1.30-1.00 (1.86) 1.62-4.708-. dust.773) .70 (2.40-1.80) 1.30-2.50-2.60-2.600) .800 (.73 (1.75) 4.20 (1.20) .900) .40) 2.70) 1.20 (2.900) .600-..915-1.11 (1.40) 1.833-1.20-2.800) . Fourth National Report on Human Exposure to Environmental Chemicals 213 .78-2.600-.35 (.10 (1. stained glass framing.738) .

638 (. with a half-life of years to decades.50 (1.98 (1.97) 1. In 1991.88) 1..887 (.608-.10 (.615 (. 1993). Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.18) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.43-1.17-1.734) .08) . 1991.593 (.617-.03) 90th 1.33 (1.841-1.605-.74 (1.05-1.635 (.03) 1.698) .06 (.69 (1.559-.03) . and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.492-.07-1.89-5.870 (.63) 4.742) .66) 2.731-.71-2.87) 1.72) .25-1.00 (. population from the National Health and Nutrition Examination Survey.682) .64) 2.709 (.31 (1.720 (.703) .37-1.707 (.655-.828-1.18) 2.23 (1.40-1.702) .88) 2. zinc.644 (.35) 2.625 (.38 (2..89-2. and iron.00 (1. For instance.975-1.657) 1. interval) .739) .988-1.918-1.15-2.992-1.79) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.43 (2.04) 2.15) 1.623 (.04-3.763) .19) 1.26) Total .41) .679) 1.03) 2.31 (1.25-1.774 (. encephalopathy.971 (.72-2.55 (1.583-.51 (1.06) .838) .22) 1.579-.19-5. CDC. through the inhibition of certain enzymes.47 (1.10 (1.62-1.742) Selected percentiles ( 95% confidence interval) 50th .696 (.15-3.88) 2.708 (.22-2.671 (.51) 1.85 (1.38 (2.693 (.68 (1.380-.50-2. scant amounts are lost through sweat.461) . The toxic effects of lead result from its interference with the physiologic actions of calcium.652 (.700-.49 (1.31) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.645-.755 (. and through binding to ion channels and regulatory proteins.48 (1.594-.793-1.92) 2.633 (.03) 2.03 (.997-1.571-.03) 1.20) .77) 2.S.933-1. O’Flaherty.11 (1.639) .588-.11) 1.12-1.38 (2.383-.677-.37-1.683-. 2007).94 (1.27 (1.644) .790) .561-.08) .698) .67-4.677 (.09) 1.0) 3.460-.603-.681-.41-1.979 (.50-2.24 (1.673) .604-.722 (.62) 2.667-.73-2.61) 1.428) .09-1. and nails (Leggett.914-1.53) 1.702) .658 (.64-2.432 (.623 (.990 (.603 (.17 (.07) .612-. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.722 (.65 (1.41 (1.938 (.667) . Large amounts of lead in the body can cause anemia.88 (1.601-.676) .18) 1.39-1.404 (.66 (1.50) 1.654) .53-1.20) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .753) .03 (.22) .78-4.618 (.56 (1.721 (.920-1.810 (.541-.61) 1.408-.22) 1.14 (1.796-1.862-.61) 3.800-.893) .15-2. kidney injury.78 (2.47) 1. Schwartz.01) .18 (1. Approximately 70% of lead excretion occurs via the urine.83) 1.03-2.79) 2.50-1.622 (.61) 1.08-2.75-2.603-.47 (2.677) .436) .606-.05 (1.44) 1.914 (.00 (1.746) .655) 75th 1.876-1.10) 1.55 (1. BLLs and associated toxic effects differ in children and adults.Metals 90% of the body lead burden in most adults.569 (.639 (.587-.15) 1.64) 95th 2.03) .88-2.11-1.97 (1.63) 1.82) 1.43) 2.720 (.725) .05-1.609 (.342-.701) .649 (.94-2.18) 1.933) .46 (1.701 (.508) .33-1.718) .681-.940 (.97) 1.06) 1.496 (.963-1.56-3.07 (.44 (1.679-.588-.725) .11) . 2004. Nash et al.31 (2.641 (. The skeleton acts as a storage depot.655) .853-1.44 (1.851) . seizures. 1993.639 (. Staessen et al.710) .85-2.510-.946-1.50-2.05 (.52 (1.586-.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 1.828) .86 (1.45 (1.648 (.36-2.73) 2.375 (.06 (1.900 (.31) 1.668-.28) .46 (2.66 (1. 1995).33) 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.981-1.917-1.28-1.61) 1.00 (1.404-.988 (.571-.43 (1. 1996).469 (.65-2.765) .34-1.686) .670) 1.20) .592-.712 (.977) 1.70 (1.58) 1.962 (.33) 2.01 (.56-2.11 (.62-3.28) 2.551-.64 (1.97-18.11 (.639 (.918 (. and paralysis.11 (1.615 (.529-.29 (1.14) 1.09-1. 1995.898) .56) 3.730) 1.608 (.20-3.83 (2.621 (.926 (. hair.812-1.79 (1.03 (1.85-2.22-1.882-1.607-.659-.914 (. abdominal pain.938-1.404 (. based on prospective population studies.632 (.00) .781-1.72-2.62-2. Lead can cross the placenta and enter the developing fetal brain.645-. 2003.702-.26) 2.992-1.85) 1.12) 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .688) .59-3.71 (1.02-1.52) 1..535) .98) 2.43) 1.96 (1.98-2.957-1.09-1.02) 1. with lesser amounts eliminated via the feces.718) 1.758) .667-.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 .594-.75 (2.03 (.400) .

CDC. Muntner et al. and peripheral neuropathy generally occurring at much higher levels (e. approximately 11. particularly in the skeleton.cdc. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. reduce sperm count. 1998). 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. may alter sperm morphology. the geometric mean BLL was 3. environmental levels) and health effects is available from ATSDR at: http://www. 1995.3 million children tested had BLLs of 10 mg/dL or higher (http://www. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. More recently.. 1999). when the geometric mean BLL was 2. In occupationally exposed adults. 2007). High dose occupational lead exposure. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample. 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. In NHANES 1999-2002 in children 1-5 years old. EPA. Schwartz et al. Both drinking water and ambient air standards for lead have been established by the U.S. 2001). 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.. premature delivery. 2005b. 1994). 2002). At low environmental exposures. Jones et al. Payton et al.S. the prevalence rate has declined annually since 1994 (CDC. 1987. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. However. with overt encephalopathy. Staessen et al. 1996. Data submitted through state public health programs from 2006 showed that 1.g. 2009).. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al..21% of approximately 3. 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. respectively. though there is greater individual variation in urine lead than in blood and greater potential for contamination. and spontaneous abortion (Baghurst et al. including minority race or ethnicity. usually with BLLs greater than 40 mg/dL. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. both the geometric mean (1. 1996. 2005b). Surveillance data reported by U.7 µg/dL and 4. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.07 µg/dL (Becker et al... which is an 84% decline. residing in housing built before the 1950’s. adults in the 1999-2000 NHANES sample. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.4% of children had BLLs of 10µg/dL or higher (CDC.S. Borja-Aburto et al.4% in NHANES 1999-2004. Bellinger 2005. and low family income (CDC.. IARC considers inorganic lead compounds probable human carcinogens. seizures.gov/toxpro2. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.. 2003). 2006). the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.S. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. almost double the geometric mean of 1..html. 2003. adults in the 19992000 NHANES sample (Apostoli et al. Korrick et al. 1996.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. Fourth National Report on Human Exposure to Environmental Chemicals 215 . BLLs reflect both recent intake and equilibration with stored lead in other tissues. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects...gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. urban residence.. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.Metals µg/dL or higher as the level of concern in children.S. lead in women may be associated with hypertension during pregnancy.6%) were lower than those from NHANES 1991-1994.. Urine levels may reflect recently absorbed lead. Telisman et al.atsdr. 2003..0 µg/dL in females (Soldin et al. 2002. Information about external exposure (i.75 µg/dL in U..2 µg/dL in males and 3.. The U. 2006). 2000)... Overall. For example.5 per 100.e.xls). higher than 100-200 µg/dL). and organic lead compounds not classifiable with respect to human carcinogenicity. adult residents. Pirkle et al.cdc. 1999). and decrease fertility (Alexander et al.6% in NHANES 1988-1991 to 1. Lanphear et al.. 1991.. 2000).S. 2003.. 2002a). 2005a).. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.. 1984. Schwartz.000 adults.

Cory-Slechta DA. Atlanta. JAMA 1996. Payton M. Lepom P. Atlanta (GA). Blood lead levels—United States. Rotnitzky A.htm. Roberts RR. Lead and hypertension in a sample of middle-aged women. Hu H. Becker K. Lead.275(15):1171-1176. Teratogen update: lead and pregnancy. Cox C. MMWR Morb Mortal Wkly Rep 2006. Angle CR. Am J Epidemiol 1999. Robertson EF. Occup Environ Med 1996. Brody DJ.287:1-11. Canfield RL. Hertz-Picciotto I. Available at URL: http://www. Vupputyuri S. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas.gov/mmwr/preview/mmwrhtml/ mm5532a2. Age-specific kinetic model of lead metal in humans.115:521-529.53:411-416. 1991 [online]. Hu H. Apostoli P. Hernberg S. Seiwert M. Acquisition and retention of lead by young children. Centers for Disease Control and Prevention (CDC).htm. gov/mmwr/preview/mmwrhtml/mm5420a5. Toxicological profile for lead. Jones RL. The relationship of bone and blood lead to hypertension. Scand J Work Environ Health 1984. Adult blood lead epidemiology and surveillance—United States. 4/14/09 Centers for Disease Control and Prevention (CDC). 1999-2002. et al.275:1177-1181. 4/14/09 Centers for Disease Control and Prevention (CDC). Pediatrics 2009. Sparrow D. Ewers TG. Environ Health Perspect 1993. et al. McMichael AJ. Neri A. van Netten C. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Wigg NR. Blood lead levels measured prospectively and risk of spontaneous abortion. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention.113(4):1016-1022. Chiodo LM. Coresh J. Korrick S. Cox C. Henderson CR. Available at URL: http://www. Kuehnemann TJ. Farias P. Neurotoxicol Teratol 2004. Birth Defects Research (Part A).cdc. Batuman V. Korrick SA. Bellinger D. Leggett RW. Available from URL: http://www. Baj A.82:60-80. Borja-Aburto VH. 2005b. Blood lead reference values: the results of an Italian polycentric study. References Agency for Toxic Substances and Disease Registry (ATSDR).123:e376-e385. Ga. Hänninen H.8(3):395-401. et al. Wager C.atsdr. Preventing Lead Poisoning in Young Children.1542/peds:2007-3608.cdc. Aug 2007 [online]. Kaufman JD. Weiss ST. IARC Monogr Eval Carcinog Risks Hum 2006.cdc. 1988-2004. Managing Elevated Blood Lead Levels Among Young Children.205:297-308. Int J Hyg Environ Health 2002.10:43-50.89:330-335. Jusko TA. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Bavazzano P. Muntner P. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Jacobson SW. doi:10.gov/nceh/lead/ CaseManagement/caseManage_main.55(32):876-879. Mantere P. JAMA 1996. Bellinger D. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Aro A.gov/nceh/lead/publications/ books/plpyc/contents. Kaus S. Stanek KL. Kim R. Available at URL: http://www. Available at URL: http://www. Hu H. Checkoway H. Manton WI. Jacobson JL. Sparrow D. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Rojas LM. et al. Hunter DJ. Schulz C. MMWR Morb Mortal Wkly Rep 2005a. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Neurodevelopmental effects of postnatal lead exposure at very low levels. 2002 [online]. Auinger P. Atlanta (GA). Ronchi L. et al. Dietrich K.cdc. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Ganzi A.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.htm. Luukkonen R. Am J Public Health 1999. Third National Report on Human Exposure to Environmental Chemicals. Semen quality of men employed at a lead smelter. Caldwell KL.htm. Reese YR. Environ Res 2000.101(7):598-616. 2003-2004. Krause C. Lanphear BP.gov/toxprofiles/tp13. Pediatrics 2004. Inorganic and Organic Lead Compounds. Sci Total Environ 2002. 2005.cdc. Weiss ST. 4/14/09 Alexander BH. Vimpani FB. 4/14/09 Centers for Disease Control and Prevention (CDC). Lanphear BP. Baghurst PA. Muller CH.348:15171526. Homa DM. N Engl J Med 2003.150(6):590-597.87:1-471. Meyer PA. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Blanco J.54(20):513-516.html. CDC. Rios C. Rotnitzky A. Public Health Rep 2000. Speizer FE.26:359-371. Pirkle JL. 4/14/09 Centers for Disease Control and Prevention (CDC).73:409-420. Neurotoxicol 1987.

9:303-327. blood pressure. Osterloh JD. Pirkle JL. cadmium.108(1):45-53.118:16-29. Roels H. Rocic B. Am J Epidemiol 1994. dimercaptosuccinic acidchelatable lead. Brody DJ. Kinetics of lead disposition in humans. Schwartz J. Lead. Jurasovic J. Schwartz BS.140:821-829. Environ Health Perspect 2000. Gunter EW. Exposure of the U. Smith DR. Soldin SJ. and copper in men.289(12):1523-1531. Pizent A. Low-level lead exposure and blood pressure. Environ Health Perspect 1998. Hanak B. Amery A.Metals results from NHANES III. lead. Lee BK. Lauwerys RR. Wilhelm M.S.106:745-750. Revised and new reference values for arsenic. Hickman T. Soldin OP. Hwang KY. Weiss ST. and tibia lead with neurobehavioral test scores in South Korean lead workers. Lee GS. Schwenk M.153(5):453464. Sherwin R. Flegal AR. Staessen JA. Telisman S. cadmium. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Hu H. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Gavella M. Paschal DC. Use of endogenous. stable lead isotopes to determine release of lead from the skeleton. Arch Environ Health 1995. et al. Sparrow D. Low-level lead exposure and renal function in the Normative Aging Study. Kidney Int 2003. Blood lead. J Hum Hypertens 1995. Toxicol Appl Pharmacol 1993. population to lead: 1991-1994. zinc. JAMA 2003. blood pressure and cardiovascular disease in men. 50:31-37.104(1):60-66. Kaufmann RB. and hypertension in perimenopausal and postmenopausal women. Blood lead concentrations in children: new ranges. Nash D. Lee SS. Am J Epidemiol 2001. Clin Chim Acta 2003.209:301305.63:1044-1050. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Schulz D. Kaufmann R. Environ Health Perspect 1996. IV. Int J Hyg Environ Health 2006.327:109-113. Rubin R. Association of blood lead. et al. O’Flaherty EJ. Magder L. Cvitkovic P. Stewar WF. Lustberg M. Payton M. Physiologically based models for bone-seeking elements.

60 (1. thermostats and switches).60) 2085 2293 3478 Limit of detection (LOD..80) 4.781 (.700-.00 (2.776 (. 1994.700-.50) 4.00 (. Also. and mercury compounds are still used as preservatives (e. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.60-5.00-5.90) 90th 3. with the highest concentrations occurring in the kidneys (Barregard et al. or oxygen.00 (.800 (.2.10) . electrical lamps.689-.00 (1.00) 3. The kinetics of the different forms of mercury vary considerably.900 (.30-6. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).655-.50) 2.60 (2. Hursh et al.00) .30) 1..Metals Mercury CAS No.300) .800 (.S.372) .50) 5.326 (. Poorly absorbed from the gastrointestinal tract.900) . Accidental spills of elemental mercury.20 (2.600) 1. Woods et al. thermometers.80 (1.20-3.g.400-.797 (. interval) .500-.703-. Other major uses include electrical equipment (e.00 (2.80) 3.877 (.20) 2. Kingman et al.80 (1.00 (.672) .30-2.30-5.860-1.400-.10-3.70) 911 856 2081 4525 03-04 03-04 .800-1.800-1. 2007).60-6.800 (.40-3.40-1. The ingestion of methyl mercury.30) 5.90 (4.50) 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 . and is distributed to most tissues.60) 1. which can bioaccumulate in aquatic and terrestrial food chains.12) . to form inorganic mercury compounds or salts.60-3.700-.90 (1.484) .700) .574) .40 (4. inorganic.900) 1. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. 2002).60-6.563 (.50-1.. Survey years 03-04 Geometric mean (95% conf. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.927) .900) 75th 1.S.90) 95th 4.40 (4. Apart from methyl mercury.60 (1. mercuric chloride). 1999 .814 (. and dental amalgam. 1980. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).900) 1.753-1.30) 4132 4241 03-04 03-04 03-04 . solid-waste incineration. In addition.40) 1.500 (.979 (.600 (.30) 3.472-.00 (2.900) 1.700) . such as chlorine (e. and mining and smelting.70 (1.70 (4. elemental mercury is absorbed mainly by inhaling volatilized vapor. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.363-.800 (.800-1.30 (2.418-. thimerosal.50-3..00-1.60-2.00 (.. and organic forms.60) 1.419 (. may contain inorganic mercury. 218 Fourth National Report on Human Exposure to Environmental Chemicals .919) .20-4. predominantly from fish and other seafood.30) 1. which create an episodic potential for volatization and inhalation of mercury vapor. Atmospheric elemental mercury can be deposited on land and water. IARC.700-.90 (1.40-2. constitutes the main source of dietary mercury exposure in the general population.903) Selected percentiles ( 95% confidence interval) 50th . elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. sphygmomanometers and barometers. have often required public health intervention (Zeitz et al. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.700-.714-.00) 1.70 (3.00) 4.490 (.50-2.02) . synthetic organomercury compounds were once used in pharmaceutical applications. Elemental mercury is a shiny. see Data Analysis section) for Survey year 03-04 is 0. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.70 (1. After elemental mercury is absorbed.. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. Some cosmetic skin creams from countries other than the U.285-.886) . Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.80 (3.90-3.400 (.20-4.40-1.40-2.g.40) 3. phenylmercuric acetate) or topical antiseptics (e.80 (1.90) 3. population from the National Health and Nutrition Examination Survey.g.300 (.500 (.50) 1.g..700 (. sulfur.800-1.800-1. merbromin).40 (3.40 (3.30-4. 1998. an organic form of mercury.00) 1..300-.30) 3.70-2. 1993).30 (1.80) 1..500) .500-.

Metals the tissues to mercurous and mercuric inorganic forms. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.500-..70 (1.395) .00 (2.30-11.10-3..50-3. 1971). Miettinen et al.70-6.317 (. After exposure to elemental mercury.40) 2.60) 1.10 (1.10) 1.06-1. National Health and Nutrition Examination Survey.20) .700-.299-. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. Jonsson et al.00) 7.269-.. Fourth National Report on Human Exposure to Environmental Chemicals 219 ..256-.726-1.00) 1.20) .60 (1.268-.871-1.35 (1.30-5.800-1.10 (5.90 (3.80-3..20-3. 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. 1975.944 (.00-6.30-2. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. 1973).70 (1. 1996.7) 4.30 (1.667 (.700 (.300) .700) 2.90) 2.30 (.10 (1. for both acute and chronic exposures.940) Race/ethnicity (females.90) 3.30) 3.200-.900-1. Smith et al. a measure of accumulated dose (Cernichiari et al.374) .50 (1.50-12. 1999).30) 1.700-1.20-2.600 (.265-.800-1.00 (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 .40) 1.00) 6.60) 1.00-2.300) .50) 1..3) 4.700 (. 2005).300 (. 1984. 2003).600) .. 1999-2002. McDowell et al.29) . Sandborgh-Englund et al. 1991.300) .20 (2.60 (3. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.300 (.02 (.00 (2. 1994.200 (. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.700-.00) 1.30-6. 1995.600) . Myers et al.541-..00-1.00 (2.70-3.50-2. 1990).40) 5.14 and 0.10) . 1998).700 (. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.S.10 (.800) 1.30 (1.900-1. 1996).0) 4.70-5.300) .500-..27) .00) .300) .60) 3.00-3.500-1.900 (.30-6.200-.500-.40-2.23) .70-3.70) 4. thereafter. 1993).40 (1.500-.. Geometric mean Survey years (95% conf.800 (.200-. 1993).70-5.90 (4. 1992.73) 1.475) .700 (.343 (.664-1.30-4.50 (2.300 (.60 (1.70) 1.825-1.800) .200-.50) 3. with most elimination occurring through in the feces (Sherlock et al.10 (1. Vahter et al.20 (. 1994) and then undergoes slow dealkylation to inorganic mercury.200-.820 (. 1994).40 (1.50) 2.80 (3.10 (3.06 (. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.90) 5.30 (1.60 (3..300 (.800 (.60 (1.377 (.20-3. population.20) 1.30-3.200-.824) 1.30-6. 1969. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al... 1998).377) .800) .00) 2..20-3. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.900 (.500-.00) 4.738-.200 (.30-4.329 (.300) . 2003). Smith and Farris.800 (. and a useful marker of exposure in epidemiologic studies (Grandjean et al. Suzuki et al.20-11.90) 2.. interval) Selected percentiles (95% confidence interval) 50th .900 (.90 (1.00-2.60) 2.10) . 2004. Methyl mercury is incorporated into growing hair.297-.800) 1.80) 579 527 370 436 588 806 Limit of detection (LOD.40-2.90 (1.70 (1.318 (.80 (1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.500 (.919) .90 (4.10 (. Methyl mercury enters the brain and other tissues (Vahter et al.90) 90th 1. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . Vimy et al.50) 95th 2.50) 1.400-.30) 1.70) 4.800-1.500 (..60 (2..10-1.80) 1..369) 1.800) 75th . 1992 and 1999. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40-1.407) .700-1. Excretion occurs by renal and fecal routes.01) .. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.697-.00 (3. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.00-2..14. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.307 (.. 1992).833 (..

. and sleep disturbance (Bidstrup et al. lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC.500-.500-. population from the National Health and Nutrition Examination Survey.500 (.700 (.700 (. Inorganic mercury exposure usually occurs by ingestion.700 (. 1995.. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600) .. 2005). depression.500 (<LOD-. Smith et al. short-term memory loss. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.500 (<LOD-.. pain in the extremities. 220 Fourth National Report on Human Exposure to Environmental Chemicals . 1951. Rissanen et al.600 (.600 (. typically after a latent period of weeks to months.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Drexler and Schaller. 2000.600 (. Smith et al. In recent epidemiologic studies. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.. 1987)..600) . Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 2004). and cerebral palsy (NRC. maculopapular rash.700 (. cerebellar ataxia. Survey Geometric mean (95% conf.500-.800) . 2006. gingivitis. < LOD means less than the limit of detection. Sakamoto et al... dysarthria.. sensory impairments. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. 2006. 2004.600 (.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .600 (.700) 2007 2240 3406 Limit of detection (LOD.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 . 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. Vupputuri et al. causing parasthesias.700-. Once absorbed.600-. 2004.600) .42.600-. particularly irritability. anorexia.600) .500) .500-.500 (. insomnia. fatigue. 1996). altered physical growth.S..600-. 1998. irritability.500-. 2005. 2000). 1995.600 (. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.600) . overt signs and symptoms of chronic inhalation may include tremor. hypertension. At levels below those that cause acute lung injury. ataxia. and progressive constriction of the visual fields.500-. Rice.600-. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al... High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. 1983).800) .700-. Salonen et al. The constellation of findings may include anorexia. limb deformities. * 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 0.500-.700 (. Factor-Litvak et al.600) . 2002.500-. 2003). interval) Selected percentiles ( 95% confidence interval) Sample 95th .. the existence of a causal relation is unresolved (Chan and Egeland.700 (. Oskarsson et al. and pinkish discoloration of the hands and feet (Tunnessen et al.. DeRouen et al. Stern 2005. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.700-. 1970. 1963). Overt poisoning from methyl mercury primarily affects the central nervous system..700) . Bellinger et al. 1993).600) .600 (. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. 2000..600) .600) . Sakamoto et al. and neurocognitive and behavioral disturbances.500-. Acute. which may vary for some chemicals by year and by individual sample..600 (. hearing impairment.Metals may be more efficient for inorganic mercury (Grandjean et al.. 2004). dysarthria.

85-2..330-.24 (2. Survey years 03-04 Geometric mean (95% conf.840-1.530-.31) 1266 1272 03-04 03-04 03-04 .S. the total blood mercury concentration is due mostly to the dietary intake of organic forms.433 (.61) 1.430 (.78-2.476 (.07 (.410-.. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.epa.358 (.382-. 1997...463) .360-.770-1.430) .76-4. 1998).. who participated in a 1998 representative population survey (Becker et al.870-1.304) .Metals standard for inorganic mercury has been established by U.330-.00 (. From 1996 through 1998.442-.534) .14-2..200 (.99-6.405-.313-.530) .89) 3.520) .330-. 758 children.580) .24) 1.890 (. total blood mercury geometric mean levels in females aged 16-49 years did not change.360 (.60 (1.340-.29) 1.34-3.S.33 (2. Mahaffey et al. Among the three racial/ethnic groups. 2001..254 (.. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.42) 95th 3. population from the National Health and Nutrition Examination Survey.18) 2.52) 2.. In NHANES 19992002.63-2. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.88) 287 722 1529 03-04 03-04 .416 (.46 µg/L for children.330 (. EPA at: http://www.S.13-2. However.840) 1.492) Selected percentiles ( 95% confidence interval) 50th .460) .96 (1.530) .54 (2.atsdr. 2006).480 (.20 (1.19 (2. 2001.460 (. 2009). Biomonitoring Information In the general population.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 . 1998).58 µg/L for 4645 adults.413-. 1995.16 (1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.440 (. Information about external exposure (i. Sanzo et al.30) 3. Schober et al.960 (.509) .16 (.408) .gov/mercury and from ATSDR at: http:// www.97) 2. Total blood mercury levels increase with greater fish consumption (Dewailly et al. military veterans (mean age 52.26 (1.930-1.55 µg/L.940 (. EPA.08 (1.213-.66) 3.406-.420 (.14. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.23) .441 (. Kingman et al. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.19 (1. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. interval) .68 (2. et al.610-1.46) 3. Fourth National Report on Human Exposure to Environmental Chemicals 221 .e. In Germany the geometric mean for blood mercury was 0.65) 1.90) 2.09 (2.250) .9 years). Benes et al.549) .700 (.S.88-3.14) 90th 2.360-.76-3.12 (. total blood mercury increased with age.495 (. environmental levels) and health effects is available from the U.08 (1.870-1.96 (1.93 (1. average age 33 years..01 (. average age 9. 2003). During the same survey periods. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U..31) 2.77-2. 2004.509) .67-2. A cohort of 1127 U.8 years.00) 1. 2009). These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. 2000). 2002). 2003). particularly methyl mercury. Over the NHANES 1999-2006 survey periods.28) 1.S. and the age-related changes differed across the groups (Caldwell et al.350-..67-3..555) .23) 2.39-3.700-1.160-.03-4.76-3.280-. the median concentration of blood mercury was 0. see Data Analysis section) for Survey year 03-04 is 0.290-.cdc. slightly higher total blood mercury levels were found in U.840-1. range 40 years to 78 years) had an average total blood mercury concentration of 2.420 (. 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.88 (1.78 µg/L for adults and 0. adult women in several ethnic subgroups (Hightower et al.05) 3..400 (.05) 1.370) .396-. Grandjean et al.480) 75th 1. These distinctions can help interpret mercury blood levels in people.447 (.60-2. aged 18 to 69 years.60) 619 713 1066 Limit of detection (LOD.570) .gov/toxprofiles. and increased slightly in non-Hispanic white children (Caldwell.430 (.

2009).385-.391) . Information about the biological exposure indices is provided here for comparison.463 (.39) 1.970 (.01) 2.28 (. not to imply a safety level for general population exposure.417) .480) . et al.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 .784) 1.476 (.35 (1.41-2.40 (1.532 (.79) 1.800-1.652) . reversible increase in urinary N-acetyl-glucosaminidase.365 (.S.307-.525 (.S.30) 1.65 (1.535) 1. Department of Health and Human Services noted that several studies have observed a modest.23-2.00) 90th 1.S.376-. Levels in U.246-.472-. 2003).1 µg/L for each surface with a dental amalgam (Kingman et al. women of childbearing age have generally been much lower than these levels (CDC..225-. 1992).56) 1266 1271 03-04 03-04 03-04 .486) Selected percentiles ( 95% confidence interval) 50th .44) 1.78-4.276 (..455) . Urine mercury and the number of dental amalgams were correlated..16) 1..404-. 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..87) 2.25 (.07) 1.455-.990) . population from the National Health and Nutrition Examination Survey. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. and on average.400-.. Urinary mercury levels in recent German (Becker et al.447-.00 (.32 (1.333-.275) .768 (.714-1.255 (. An expert-panel report recently prepared for the U.301-. and Italian (Apostoli et al. interval) .13 (1.964-1.03) 2.63) 1.280-.566) .522-.391-. 2006).88 (1.64-2.362 (. 2006.62 (1.217 (.32-2. Langworth et al.46-2.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .289) . mean urinary mercury was 3.86) 95th 2.87 (1.785-1.11) 2..392-..79 (1.464 (. 2005). 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.545 (.30) 2.208-.616) .51-2.00) 286 722 1529 03-04 03-04 .76 (1.06 (.485 (.S.588) . Czech (Benes et al.343 (.18-1. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.687) .358) .447 (.. In the study of U.1 µg/L. 1998).667-1. Survey years 03-04 Geometric mean (95% conf.599) .88-2.13-2.11-2.443 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.620-.365 (.696 (.196-. 2002) adult population surveys were similar to those in a U. et al.455-.400) . 2002).77 (2.969-1. military veterans with dental amalgams. a biomarker of perturbation in renal tubular function.508 (. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.619-. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. the urine mercury increased by approximately 0.67 (1.S.630) .88-2.54 (2.61) 1..31 (1.587 (.306 (.875-1.537) . 1988.04-3.498) 75th . 2009). representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.06 (.368) .11) 1.309-.265-.909 (.21) 1.Metals 2000).12-3.297 (.40-1.09) 1. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.384 (.67 (1. DeRouen et al. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.347) .

06 (.46 (1.516 (. 1999-2002.56) 3.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .592 (.03) 1.721 (.632 (.25) 2.850-1.387-.24) 6.07-5.31-1.91-7.892) .10-4.87-4.65) 1.557-.582-.84 (2. 16-49 years) 99-00 01-02 .69-3.870) .831) .37 (1.14-2.70 (2.809) . National Health and Nutrition Examination Survey.790) .69 (1.03 (.62 (1.580 (.615 (.68 (3.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .35 (1.00 (2.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.540-. Geometric mean (95% conf.41-6.706 (.55-3.45-2.59-5.27-1.61) 1.501-.685 (.23-1.14.560-.56 (1.62 (4.686) .624-.07) 1.46-4.420-.508-.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.553-.54) 595 531 381 442 594 826 Limit of detection (LOD.45-3.21 (1.42) 90th 2.61-6.13 (2.520-.37) 1. population.45) 2.744) 1.622-.16) 5.719 (. National Health and Nutrition Examination Survey.09-1.85) 4.620 (.578-.45 (1.47) 1. 1999-2002.S.51 (3.04-1.655 (.18 (3.709) .606 (.00) 2.99 (2.98 (5.670) 75th 1.92) 3.426-.14 and 0.94) 1.04-10.526-. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.39-3.610-.97) 2.81-6.42) 2.97) 2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .810) .84 (2.27 (2.650) 1.27 (1.23-1.79) 1.13-4.410-.47) 1.32-3.95 (2.41 (2.41 (1.46) 3.28 (1.89 (2.824) . interval) Selected percentiles (95% confidence interval) Survey years 50th .657 (.07-2.774) .502-.665) .658 (.57-4.68) 3.51) .596 (.83-3.38) 4.650 (.50 (2.32) 2.579-.799) .909-1.691) .520-.03-2.Metals Urinary Mercury−Females Aged 16-49 Years Old.30 (2. interval) Selected percentiles (95% confidence interval) 50th .76) 2.560 (.831) .97 (1.15 (2.09-1.636-.99 (3.475-.30 (2.22 (.00 (3.65-4.540 (.05 (2.24-1.846) .42-3.600 (.631-.605-.21 (2.43-1.50-4.14) 3.16-5.966) .569-.656-.85-3.580-.14-1.930) .637) .910) .30-2.832-1.31 (1.68-3.650 (.699) 1.99-2.664) .53-3.55) 90th 3.56) 4.79) 3. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.772 (. population.15-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 16-49 years) 99-00 01-02 .17) 95th 5.450-.35) .81 (3.50 (1.76-5.41 (1.30 (1.77) 2.45) 2.45) 95th 3.710 (.92) 4.500-.18) 3.S.639 (.05 (3.77) 1.3) 5.565 (.21-3.742-1.709) 75th 1.72) 1.740 (.52) 3.91 (2.724 (.833) .22-3.522 (.62 (3.03 (. Geometric mean Survey years (95% conf.76 (1.760 (.10-2. 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.92) 2.710) 1.97) 2.806) .48 (2.616-.710 (.723 (.32 (1.99) 1.44) 3.

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Toxicol Appl Pharmacol 1994. Most B. Baser M. et al. Nakazawa M. Methyl mercury pharmacokinetics in man: a reevaluation. Hall LL. Smith JC. Sherlock J. Mooney TF.128(2):25125-25126.115(10):1527-1531. DeRouen TA. et al.48(4):221229.97(2):195-200. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Azpiri MA. Effects of occupational exposure to elemental mercury on short term memory. Smith PJ. Whittle K. Kaye WE. Environ Res 2005. Stern AH. Zeitz P. Lorscheider FL. McDowell M. Effects of exposure to mercury in the manufacture of chlorine. Woods JS. Vupputuri S. 1999-2000. Bolger PM. Sinks TH. Smith JC. Martin MD. Pediatrics 1987. Mottet NK. Acrodynia: exposure to mercury from fluorescent light bulbs. Patil LS.2:117-131. Newton G. Toxicol Appl Pharmacol 1994. Fisher HL.258(4 Pt 2):R939-945.289(13):1667-1674.31:687-700. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Toxicol Appl Pharmacol 1996. Osterloh J. Public Health Nutr 2001. Dorronsoro M. Orr MF. The contribution of dental amalgam to urinary mercury excretion in children. Schober SE. Smith RG. Environ Res 2005. Allen PV. Goldberg J. Guo S.111(12):1465-1470. JAMA 2003. Aguinagalde FX. Am J Physiol 1990. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Am Ind Hyg Assoc J 1970.98(1):133-142. Takahashi Y. Amiano P. Vimy MJ. Environ Health Perspect 2003. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.124:221-229. The hair-organ relationship in mercury concentration in contemporary Japanese. Leroux BG. Vorwald AJ. Smith AE. Jones RL. et al. Br J Ind Med 1983. Farris FF. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Topping G. Bernardo MF. Arch Environ Health 1993.40:413-419. Tunnessen WW. Sandler DP. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Hislop D. Matsuo N. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Friberg L. Lind B. Langolf GD. Suzuki T. Blood mercury levels in US children and women of childbearing age.Metals Sanzo JM.4(5):981-988. Longnecker MP. Amurrio A. Turner MD. Environ Health Perspect 2007. McMahon KJ. Environ Health Perspect 2002. Shen DD. Imai H. Hum Toxicol 1984. Stern AH. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment.37:245-252.110:129-132. Vahter M. 1993-1998. Hongo T. Leitao JG. Yoshinaga J. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. The kinetics of intravenously administered methyl mercury in man.79:786789. Burbacher T. Daniels JL.

3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.2-53.6) 53. hydrogenation catalysts.6 (52.7-92.9 (37.7 (45. inks.2) 37.1 (71.1-88.2-59.7) 45.7-68.9) 34.0 (76.3) 54.0) 39.3) 37.7-84.1) 59.9 (33.7-105) 69.0 (48. and 03-04 are 0.9 (40.0-71.0-85.0-62.4) 52.7-60.5-65.2-42. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.8 (85.7-51.5) 80.4-75.6) 51.7-91.6) 93.3 (55.8 (42.0-56.5-91.0-77.6) 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 (99.5-68.5 (37.3-47.5) 80..3) 65.8) 44. lubricants.0-100) 63.0) 97.5 (49.3 (79.4-82.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.8 (67.2 (61.1) 35.0 (43. see Data Analysis section) for survey years 99-00. respectively. and xanthine oxidase (Kisker et al. 7439-98-7 General Information Elemental molybdenum is a silver-white.9-55.4) 76.1-48.0) 62.5-46.4 (80.3 (47.1) 82.3) 41.7 (44.3 (37.0-65.3) 85. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2) 79.1-55.3 (55.6-111) 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 52.6 (55.7 (73.1) 57.7) 78. More recently.3 (53.3 (46.2) 40.3 (71.2 (63.8-106) 88.0-110) 90.9 (34.5-41. which exert homeostatic regulation over molybdenum balance.8) 46.7 (51. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.4) 56.5 (41.7) 77.6-82.3-108) 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 47.3 (64.3) 83. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.7-122) 93.6-72.4-61.7-39.4) 42.2) 48.6-62. semiconductor and battery industries have begun to use molybdenum.9) 62.7-73.2 (55.5 (48.1-51.8-90.8-108) 87.6-46.6-96.9-56.1) 126 (106-147) 109 (94.5 (43.3 (84. At a daily oral molybdenum dose of 24 µg.5 (67.0) 45.8) 40. and paints.1-44.0-53.3 (38.5) 47.2) 52.8-46.7 (50.9 (78.8-94. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM. and in pigments for ceramics.9-82.1 (38.5) 60.0) 54.2 (49.2) 41.4 (72.8) 75.0 (42.2) 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 (98.9-55.6) Selected percentiles ( 95% confidence interval) 50th 50.5 (81.1-59.6 (73.1-52.7) 75th 84.5.5-124) 108 (92.9-83.S. and 1.7) 78.2-91. 2001).1) 60.5-52.6) 71. interval) 45.3 (73.2 (49.7) 86.3-91.6) 71.8. In humans.0 (46.1 (91.6-55.0 (41. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.6 (55.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.3-75. urinary excretion over six days CAS No.2 (83.7-47. population from the National Health and Nutrition Examination survey.3) 47.7 (71.9 (32.8 (82.2 (56.0) 84.8. 0.7) 46.0-38.4) 45.0 (42.0 (81.4-52.4 (48.Metals Molybdenum or ore deposits.1-52.8) 39.9 (52.7 (36.4 (48.4) 49.6 (40.2-79.9 (73.2-37.7 (58.3-115) 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.1 (34.4) 41.0-101) 82.4 (79.9) 67. aldehyde dehydrogenase.6-42.2-70.9-85.8-49. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (41.2 (69.2) 53.6 (40. chemical reagents in hospital laboratories.0) 55.5-52.7-96.5) 85.1) 46.9 (44. Fourth National Report on Human Exposure to Environmental Chemicals 227 .2 (38. WHO.5-66.9-109) 97.7) 57.7) 51. 01-02.0) 60. 1996). 2001. Compounds of molybdenum are also used as corrosion inhibitors.4 (34.8) 48.1-63.6-58.2 (40. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5 (74.2-59.7 (37.6 (43. Excretion occurs predominantly via the kidneys.7-50.7-41.3-44. 1997).5) 44.

8) 38.8-47.1) 37.1-43.1 (33.1-67.2) 42.5 (40.0) 39.1-100) 86.2 (57.5) 63. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0. Biomonitoring Information Molybdenum is an essential element for health.4) 89.0) 44.3 (55.7 (77. and clinical or epidemiologic evidence of adverse effects is limited.6 (36.9-68.2 (37..5-62.8) 37.5-44.6) Selected percentiles ( 95% confidence interval) 50th 41.8 (37.3) 43.9-41. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.3) 40.9-61.4-66.3 (51.6 (38.Metals was 18% of the ingested dose.1-39.9 mg/kg/day and established a tolerable upper intake level of 0.2 (52.9-117) 57.6) 48. respectively. at daily oral doses of 95 µg and 428 µg.0-46.2-96.9) 40.3 (37.4-41.3 (71.4) 58.7) 112 (95.8) 45.8-42.7) 53.3 (71.3 (83.2 (36. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 75th 63.9) 79.4 (53.9-118) 91.6-45.1-81. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.9 (36.3 (36.6-63.1-41.4 (56.1 (49. population from the National Health and Nutrition Examination survey.1 (42.8-52.1-109) 89.1) 101 (83.6-61.1-40.4-185) 106 (94.7-62.8) 39. EPA.9 (79.8 (90.0 (58.1 (40.9) 92.8-65.4 (44.0) 38.4 (40.3) 44.1 (38.03 mg/kg/day in humans (IOM.9-96.4) 47.5 (40. urinary excretion over six days rose to 50% and 67%.1-45.2-49.5 (80.2 (40.2 (50.9 (64.1 (39.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.1) 37.3-44.2) 58.0 (35.0-41.7-43.7-52.4 (78.8) 62.4 (55.4-118) 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 .2-47.4 (67.1-39.4) 122 (107-133) 109 (99.8-67. Molybdenum is generally considered to be of low human toxicity.4-76.6 (57.9 (73.5) 71.2-41.5-99.5 (38.5) 90th 108 (97.1-43.1) 65.0) 62.0-120) 85.9) 31.0) 33.8-47.9-71.7) 41.0) 39.4 (59.2 (33.5) 73.8-46.0-103) 103 (90.3) 57.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.8) 79.3 (53.9 (64.3-46.9-42.1-79.1) 56.5 (37.5 (65..4-42.3-56.5 (54.S.2-65.4-120) 101 (84.7-38.0-46.5) 72.6) 39.5-35.7) 62.2) 37.5 (36.3 (37.2-96.7) 115 (93.9-45.3 (36. 2001).0 (74.6-41. Based on studies finding adverse reproductive effects in rats and mice.2) 37.7 (30. interval) 43.5 (41.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.3) 37.6) 43.6) 36.9) 44.4) 44.1-127) 90.5 (65.0) 53.8-84.4) 48.1-38..8 (36.1 (82.4-39.5 (37.3-102) 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 40.0 (80.8 (75.3-45.2) 55. 1993). dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.5 (39.6 (36.3-115) 98.5 (50.2 (73.2 (43.2) 43.4) 77.1 (44.3-43.3-68.1) 40.9-40.6-78.1 (54.9 (39.0-38. but available epidemiologic data are scant.1-34.5 (59.5 (39.6 (42.5 (78.9 (39.7-44.9 (49.5-45. 1999).3-59.5-92.2-40.7 (66. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.1) 43.8 (56.9 (35.6-76.8-66.2) 39.7) 45.6) 39.1 (38.0) 36.1-112) 78.6-61.2) 38.5-50.2) 42.3) 61.7-93.4) 60.9-45.3) 41.8 (57.3) 64.5 (35.5 (35.5-97.7 (75.7-137) 129 (109-155) 112 (97.4-106) 85. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (37.5-119) 90.5 (79.4 (37.4-107) 85.2-46.8) 38.6-63.3-52.2-80.5 (83.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.5) 60.7-120) 87.9 (40.6-88.1 (30.2) 39.3 (58. In industry.9) 41.7) 57.3-141) 109 (81.2-121) 107 (92.0) 88.2 (69.5 (41.4) 116 (101-126) 104 (88.8) 71. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.6 (71.8) 61. 1995).2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.5-46.3) 56.9-87.7-40.S. 1961.5-70. U.5-69. 1997).5-60. of the ingested dose (Turnlund et al.4) 40.8-118) 81.2 (40.6 (59. and urinary levels reflect intake from all sources.7-100) 77.5 (34.0) 72.2 (40.7) 42.5-48.0-56.0-133) 119 (88.4) 61.

boron. Sci Total Environ 1998. World Health Organization (WHO). X. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Molybdenum 1993 [online]. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. vitamin K. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Yarovaya GA. 4/14/09 Iversen BS. Rapid Comm Mass Spectrom 2002.62(4):790-796.Metals in urine for the U. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC.nap. Schindelin H. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. 56:322-327. Schaub J. 1996. Ronchi A. U. 1998. Occupational risk factors of lung cancer: a hospital based case-control study. Koval’skiy GA. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Available at URL: http://www. EPA). 2001). Inductively coupled plasma mass spectrometric determination of molybdenum in urine.S. J Trace Elem Med Biol 2001.216:253-270.niehs. Menne C.. White and Sabbioni. Schleyerbach U. iodine. Occup Environ Med 1999. References Centers for Disease Control and Prevention (CDC). Minoia et al.htm. Available at URL: http://ntp. Sabbioni E. 1998). Third National Report on Human Exposure to Environmental Chemicals. Analyst 1998. Van Meerbeeck JP. Turnlund JR. Atlanta (GA). Kristiansen J. molybdenum. Sabbioni E. Available at URL: http://books. 2001. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Trace element reference values in tissues from inhabitants of the European Union. Droste JHJ.123(1):81-85.22(3):179-191. and zinc: a report of the Panel on Micronutrients. Rees DC. 2005). Ann Rev Biochem 1997. 420-441. excretion.gov/index. Molybdenum absorption. 2005. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Institute of Medicine (IOM). et al. Weyler JJ. 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. In: Trace elements in human nutrition and health. Turci R.S. iron. edu/openbook. Zhurnal Obshchey Biologii 1961. pp. Peiffer GL. arsenic. manganese. Aprea C. (DC): National Academy Press. Gatti A. copper. Christensen JM..php?record_id=10026&page=420. Molybdenum-cofactorcontaining enzymes: structure and mechanism.66:233-267. 144-154.15(2-3):149-154. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. White MA. Molybdenum in infancy: methodical investigation of urinary excretion. National Toxicology Program (NTP).nih. Molybdenum. vanadium.gov/iris/ subst/0425. Am J Clin Nutr 1995. Kisker C.. Vermeire PA. TR-462.epa. van Sprundel MP. Geneva: WHO. Keyes WR. Washington. 16:1313-1319. Environmental Protection Agency (U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Dietary reference intakes for vitamin A. pp. 4/14/09 White MA. A study of 13 elements in blood and urine of a United Kingdom population. nickel. Shmavonyan DM. Minoia C. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. silicon. 4/14/09 Sievers E.S. Sciarra G. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. chromium. 2002. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Food and Nutrition Board.

population from the National Health and Nutrition Examination Survey. the ambient air concentrations of platinum associated with its use in automotive engine catalytic converters are estimated to be thousands of times lower than occupational exposure limits. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. 01-02. strength at high temperatures. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and high catalytic activity..04. Important properties of platinum are resistance to corrosion.Metals Platinum CAS No. < LOD means less than the limit of detection.04. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.07.g. see Data Analysis section) for Survey years 99-00. 0. copper.S. and iron. 7440-06-4 General Information Platinum is a silver-gray. as oxidation catalysts in chemical manufacturing. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. and 0. Human health effects from platinum at low environmental Urinary Platinum 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. and 03-04 are 0. thick-film circuits printed on ceramic substrates. jewelry. however. Platinum compounds are used in electrodes. and as drugs (e. carboplatin) in the treatment of cancer. respectively. dental alloys. cisplatin.. 230 Fourth National Report on Human Exposure to Environmental Chemicals . 1998). lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

Hebert R. International Journal of Hygiene and Environmental Health 2003. Schulz C. eds. Levels of platinum in urine for the U. Senofonte O. Thornton I. Ruff F: Platinum and platinosis. Arch Environ Health:1969. 232 Fourth National Report on Human Exposure to Environmental Chemicals . 206:15-24.13(1):24-30. Environmental Health Criteria 125. Herr et al. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.htm. et al.inchem. Ensslin AS. Duneman L:Long-term urinary platinum. Neuendorf J. References Becker K. which elevate urinary platinum by five to twelve-fold (Begerow et al. Uptake of antineoplastic agents in pharmacy and hospital personnel. Analyst 1998.. Kelly J. Environ Health Perspect 1975b.9:152-158. Platinum. palladium. 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. New York: John Wiley & Sons.61(7):636-9.S. Available at URL: http://www. Ruff F: Histamine release by sodium cholorplatinate. Parrot JL.. Schierl. Herr et al. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. J Expo Anal Environ Epidemiol 2003. Boos KS.org/documents/ehc/ehc/ ehc125. Czerczak S. 1999. palladium.. Environ Res 1975a. In: Bingham E.. 1991 [online]. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Occup Environ Med 1998.35:313-321. Schierl R. Kaus S. Seiwert M. Biomarkers 1999. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Angerer J. Seifert B.. Raab W. Wilhelm et al. and platinum.. Saindelle A. Saindelle A. 3/31/08 Moore W Jr. Schierl R... Hauff K. Pethran A. Begerow J.inchem. ruthenium. Turfeld M.04 µg/L) in this Report.. 2001). Urinary platinum levels associated with dental gold alloys. 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. Biomonitoring Information Urinary platinum levels reflect recent exposure. et al. Stilianakis NI. Several studies have shown that background concentrations in general populations were usually less than 0. Nickel. Moore W Jr. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. 1997. Cohrssen B.19:685-691. Schierl R. Gromiec JP. Crocker W. Occup Environ Med 2004. Br J Pharmacol 1969. Schierl R. 2003. Fries HG. Kuster W. Kulka U. Hysell D. Part 1: monitoring of urinary concentrations. Urinary excretion of platinum from platinum-industry workers. Herr CE. 2004) or less than 0. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. population were below the limit of detection (0. 1998).70(3):205-208. 2003. Schierl et al.123(3):451-454. Ewers U. Pethran A. 2003. osmium. et al.55(2):138-140. Blanks R. 1998).005 µg/L (Iavicoli et al. 2000. Pethran et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Iavicoli I. Patty’s Toxicology. Arch Environ Health 2001. 2003). and in blood and urine in the United Kingdom. rhodium. Schulz C. Platinum concentrations in urban road dust and soil. Gieler U. Fruhmann G. Hall L. 2004. Jankofsky M. Petrucci F. pp.207(1):69-73. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.56(3):283-286.76(1):5-10. Nowak D. Rommelt H. Allergy and histamine release due to some platinum salts. Alimonti A.org/documents/ehc/ehc/ehc125. 2004). Huber R. Hysell D. Powell CH. Bocca B. Biomonitoring of traffic police officers exposed to airborne platinum. 5th ed.. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al..10:63-71. Int Arch Occup Environ Health 1997.01 µg/L (Becker et al. Influences on human internal exposure to environmental platinum. International Programme on Chemical Safety (IPCS). Grimm CH. Farago ME.htm. Kazantzis G. Wilhelm M.Metals the International Programme on Chemical Safety at http:// www. van de Weyer C. Campbell K.4(1):27-36. Int J Hyg Environ Health 2004. and gold excretion of patients after insertion of noble-metal dental alloys. 289-380. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Kavanagh P. Int Arch Occup Environ Health 2003. Carelli G.

400 (. the latter being the current major industrial consumer of thallium in this country.170) .420-.200-.160-.350-.225) .450) .470) .440) .170 (.145-.500) .380 (.260 (.320) .182-.360-.370 (.360 (.183) .184 (.240) .410-.170-.480) .240-.440-.350-.210-. 01-02.188) .160-.260-.490) .210 (.280) .360 (.270 (.137-.160-.500) .180 (.197-.420) .480) .410-.230 (.310 (.450 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.320 (.450 (.144 (.420) .400-.167 (.160 (.400 (. 0.400 (.390) .380 (.420 (.410 (.220) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .243) .200-.220) .290) .220) .250-.180-. In addition.430-.330-.250-.S.200 (.390 (.590) .390 (.440 (.178) .250-.140-.280 (.460-.420-.159 (.160 (.520) .380-. representing distribution into other tissues.370-.290) .145-.150-.260-.180) .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 .200 (.310 (.134-.150-.400) .167-.147-.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 .154-.260-.260 (.490) .153-.370) .177) .196) .300) .170-.520 (.450 (.170 (.500 (.330-.410) .160 (.520) .220 (.410-.156-.250-.201 (.370 (.370 (.470) .157-.217 (.180 (.159 (.340-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.280) .430 (. 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.220 (.180 (.170 (.330) .410 (.420) .290 (.300-.192) Selected percentiles ( 95% confidence interval) 50th .400-.218) .290-.290 (.340) .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 . thallium was obtained as a by-product of smelting other metals.156) .173-. however.170) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.300) .310-.550 (.410 (.240) .200) .350-.230) .410 (.410-.210 (.510 (.220) .149 (.215) .330) .390-. population from the National Health and Nutrition Examination Survey.690) .480) .260-.280-. respectively.430 (.430-.360-.370 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.490) . interval) .240) .290 (.171 (.196) . it has not been specifically mined or refined in the United States since 1984.330-.210) .290) .240-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.180-.230) .200 (.250) .230-.470 (.410-.180-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al. see Data Analysis section) for Survey years 99-00.173) .350 (.170) .370-.330) .300 (.172) .217) . and 0.239) .02.158) .250-.02.160-.330-.330-..150-.360-.270) .156) .270 (.640) .270 (. In the past. 2005).230-.220 (. and 03-04 are 0.163) .400) 95th .170-.250-.390-.340-.440) .162-.270-.270) .460) .167-.350) .480) . Thallium disappears from the blood with a half-life of several days.190 (.202 (. Human health effects from thallium at low environmental CAS No.590) .230) .220) .420-.183) .175) .490) Total .200) .240-.370-.180-.330-.310 (.146 (.148-.400 (.450 (.420) .390) .Metals Thallium depilatory cosmetics.500) .390) .190 (.133-.150-.190 (.400) .170-.147-.280-.290) 90th .400-.430 (. In the United States.280) .450 (.202 (.191 (.280 (.310) .300) .460 (.159 (.350 (.250 (.320) .320) .420) .400-.230) .300) .370 (.350-.170-.420-.145 (.360 (.400 (.370 (.410 (.300 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.330-.220-.218) .400) .370-.290-.360) .390) .340-.270-.170-.390-.206) .390-.380-.200 (.181-.560) .155 (.160-.185 (.147-.170-.270-.450 (.350) .450 (.340 (.360-.200-.270 (. thallium readily crosses the placenta and also distributes into breast milk.440 (.250 (.430) .290 (.220) .190 (.430) .470 (.260-.220 (.190 (.370) .200) .220 (.290) .430-.190 (.150-. From these and other sources.260) .520) .201 (.185-.200 (.02.410 (.200-.440 (.135-.280 (.190-.450 (.420) .173) .172 (.340) .430 (.290 (.179-.200) .187-.200) .200 (.360-.360 (.260 (.230-.440) .172 (.165 (.300 (.380) .250-.270 (.250-.410-.290 (.200) .510) .197 (.420) .202) .150-.176 (.400-.490 (.480) .350-.440 (.330) .450 (.370 (.630) .180) 75th .340-.470) .320-.160 (.400) .160 (.350-.

environmental levels) and health effects is available from ATSDR at: http://www.140-.146) .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 .156 (.260-.297 (.278) .171) .149-.333-.236) .278) .214 (.161 (.122-.162) .282 (.254 (.278 (.348-.291-.402) .286 (.133-.469) .146-.258-.365) .161) .333) .162) .179-.135-.153) .197-.151) .204 (. Chronic high-level exposures have been associated with weight loss.173) Selected percentiles ( 95% confidence interval) 50th .356-.286 (.153-.143-.369) Total .389) .166 (.458) .184-.282-.338 (.146) .208) .214) .333) .250-.atsdr.184-.333-.318-.162) .231-.600) . Severe accidental thallium poisonings from ingesting of rat poisons that contained water-soluble thallium salt have occurred.223 (.137-.387) .125-.210 (.307) .304) .135-.144-.271-. Peripheral neuropathy and alopecia are well-documented effects of acute and chronic exposures.154 (.307 (.207 (.196 (.330-.131-.150) .180) .273-.156 (.456) .312 (.151-.176) .269) .366 (.221 (.197) .532) .292 (.214) .160-.200 (.192-.238) .189) .286 (.377) .129-.370 (.264 (.255 (.278-.412 (.349 (.299-.168 (.424 (.297) .179) .143 (.363) 861 674 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites 234 Fourth National Report on Human Exposure to Environmental Chemicals .283 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.361 (.145) .167-.289) .218 (.204) .234-.160) .265-.329) .271-.273-.152) . Biomonitoring Information Urinary thallium levels reflect recent exposure.300-.169) .217-.221) .343 (.164) .152) .198-.169 (.402) .304) . population from the National Health and Nutrition Examination Survey. and polyneuropathy.169-.191-.462) .153 (.207) .229) .254-.306-.233 (.145 (.173 (.184-.356) .326-.278) .138 (.348) .133 (.238-.143) .153 (.462) . interval) .196-.266-.206 (.244 (.157 (.217-.gov/toxpro2.147-.155-.280) . although additional mechanisms of action are possible.222 (.458 (.297 (.301-. (ATSDR.S.383 (.222-.313 (.148 (.149-.143 (.286-.178 (.156) .369 (.286) .304) 95th .340-. 1992) Workplace air standards and guidelines for external exposure are established by OSHA and ACGIH.167 (.153-.227 (.321) .230) .167) .146-.217) .387) .306-.119-.144-.222 (.148-.362) .149 (.154 (.145-.170) . Levels of thallium in urine for the U.185 (.176) .317 (.141-.378 (.191-.167 (.145-.287-.213 (.222) 90th .147-.321 (.224 (.167) .216 (.208-.375 (.171) .202 (.182 (.389) .128 (.S.289) .214-.146 (.246-. EPA.350 (. IARC and NTP consider the evidence for the carcinogenicity of thallium as inadequate or unclassifiable.256 (.383) .158-.194 (.364 (.167 (.287 (.153 (.293 (.160) 75th .153 (.304) .162-.162-.167 (.200-.259) .300 (.323 (.272-.350) .286-.278-.134-. Information about external exposure (i.229-.136 (.207-.424) .263-.364) .181) .160) .135-.258 (.269 (.243) .173) .157) .214 (..215-.149) .223) .156 (.e.180-.278 (.155) .346-.148-.300) .342) .171-.155-. 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.142-.286 (.271-. neurologic injury.248) .237) .313-.198) .343 (.328 (.328-.150) .142 (.274-.389-.147-.170) .154 (.200) .212) .148-.176) .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 .364 (.146 (.146-.231) .273 (.194 (.148 (.327) .192 (.313-.333 (.187-.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 .177) .192-.176) . respectively.333-.172) .272 (.281-.221) .260 (.226) .368 (.170-.148-.240) .153 (.250) . and a drinking water standard has been established by U.250-.338-.128-.319) . arthralgias.304 (.164) .211 (.412 (.280-.346) .364) .153) .198-.271-.Metals doses or at biomonitored levels from low environmental exposures are unknown.143-.html.422) .380 (.235-.325-.140 (.293) . Thallium produces toxicity by replacing intracellular potassium in the body.159 (.142 (.241) .313 (. Relatively high-dose intentional or accidental ingestion can result in gastrointestinal symptoms followed by multiorgan failure.140 (.324) .161) .244-.237-.200-.219) .226-.233) .348 (.235 (.161 (.211 (.156 (.200-.267-.153-.159-.158 (.159) .300) .166 (.377) .317 (.215) .cdc.160 (.157-.155 (.306 (.S.203-.366) .152) .317) .400-.154 (.188 (.215 (.198-. and death.167-.162 (.222) .208-.205 (.333 (.337-.

76(1):53-59. Ewers U. Radiat Prot Dosim.gov/toxprofiles/tp54. Celier D. et al.47(3):223-231. Martin J-C. 7/15/09 Blanchardon E.1 mg/m3 (Marcus. population) are thought to correspond to workplace exposures at the threshold limit value of 0. 2005. 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. Toxicological profile for thallium. White and Sabbioni. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Minoia C. A study of 46 elements in urine. 1992 [online]. Schaller et al.95:89-105. 1998). 1998. Cassot G. X. Ting BG.5 μg/L. Apostoli P. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Kramer U. with concentrations ranging up to 76. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Morrow JC. Soddemann H.. Investigations of thallium-exposed workers in cement factories. Paschal et al. Trace metals in urine of United States residents: reference range concentrations. blood. Boisson P. White MA. References Agency for Toxic Substances and Disease Registry (ATSDR). These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al.. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Schmidt M. Raithel HJ. 1990. Minoia et al. 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. Marcus RL.48(4):375-389.atsdr. Sci Total Environ 1998. Investigation of a working population exposed to thallium.113(1):47-53.S. J Soc Occup Med 1985. Valentin H. 1981. Paschal DC. Buhlmeyer G. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. 2005.cdc. (1981) studied 1.216:253-270. Sabbioni E. Trace element reference values in tissues from inhabitants of the European Union. et al. Centers for Disease Control and Prevention. A study of 13 elements in blood and urine of a United Kingdom population. Jackson RJ. Manke G. 2005) and are shown with results from NHANES 2003-2004 in this Report. 1980. Sampson EJ. Sci Total Environ 1990. Pietra R. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Trace element reference values in tissues from inhabitants of the European community I. et al.. Sabbioni E. 1985). and serum of Italian subjects. Brockhaus A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Metals (CDC. Available at URL: http://www. Int Arch Occup Environ Health 1980. Atlanta (GA). Int Arch Occup Environ Health 1981. Schaller KH.35(1):4-9. Brockhaus et al. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Pirkle JL. Challeton-de Vathaire C.. Environ Res 1998. Gallorini M. Third National Report on Human Exposure to Environmental Chemicals. Dolger R.html. Pozzoli L.265 people living near a thallium-emitting cement plant in Germany. Wiegand H.

350) .064-.310-.460) .250) . see Data Analysis section) for Survey years 99-00. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.160 (.500 (.070) .310-.116) .060-.160 (.470-.082 (.090) .160) .260 (. Tungsten compounds are used as lubricating agents.470 (.550 (.158 (.Metals Tungsten CAS No.062 (.120) .180) .080-.400 (.460 (.380-.090-.120-.340-.200) .080 (.078-.570 (.350 (.130 (.240-.310 (.130) .160-.109) .110) .800) .110 (.470) .460 (.058-.270 (.260 (.126) .470) .620) .330) .330) .380-.050-.100 (. population from the National Health and Nutrition Examination Survey.090) .430-.190-.530 (.350) .620) .510-1.180) .300 (.410 (.087) .270-.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.220) .320-.490 (.310-.180) .480) Total .080) .062 (.560 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.280 (.190 (.120) .069) .260-.060 (.066-.150) .300) 95th .105 (.230) .300-.290 (.300 (.190-.110-.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 .380-.180-.130) .087-.130 (.230-.170 (.070 (.060 (.140 (.080 (.360-.060-. and for producing ferrotungsten.160 (.630) .310-.430-.130) .220) .370-.100) .230) .101-.097-.060-. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.270 (.091) .260-.360 (.120) .210 (.190-.350) .080 (.320-.570 (.560) .137 (.084-.069-.113 (.110 (.110 (.093-.056-. Occupational exposure is from dusts released during grinding or drilling of hard metals.068) .340) .090-.081 (.150 (.122) .420-.084) .074-.101 (.105) .073 (.450-.140 (.180) .560) .310) . Tungsten is used mainly for producing hard metals.430 (.290-.380) .093 (.080 (.250) . and 03-04 are 0.090 (.113 (.100-.430 (.100) Selected percentiles ( 95% confidence interval) 50th .260) .440) .080) 75th .170) .073) .410-.310-.113 (.132) .080-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.133) .151) .230-.090 (.290) .071 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .160) .120) .120-.360-.160 (.550) .460) .790) .090-.510-. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.250) .180 (.110-.090-.100) .092) .070 (.460 (.100 (.210 (.090-.380 (.150 (. mainly as scheelite (CaWO4).230-.530 (.330-.250-.280 (.204) .080 (.060 (.220-. 01-02.090 (.230 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).520) .S.360) .230-.520) .095-.360 (.200 (.076 (.400 (.270-.170-.160-.670) .770 (.400-.140) 90th .370 (.113 (.065 (.104) .060-.400) .520) .082) .060-.070-.050-.086 (.950) .290) .04.800) .071-.107 (.120) .090-.070-. which are used in rock drills and metal-cutting tools.100) .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 . Little information is available on the toxicity of tungsten.470 (.050-.080) .096 (.100 (.830) .130) .500) .400 (.180-.135) .330-.210 (.370-.130-.390) .510 (.250-.082 (.430) .53) .060 (.100) .120-.490) .370 (.096-.04.250) .084 (.190-.590) .270-.100) .110) .380-. filaments for incandescent lamps.180 (.250) .200-.150 (.550) .320 (.130) .060 (.650) .270 (. and as catalysts in the petroleum industry. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120-.065-.320) .810) .070 (.140 (.050-.210) .370 (.530 (. and 0. interval) .450 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.180-.620 (.120-.560) .170) .290-.240 (.070-.420-.090-.095-.210 (.350-1.120 (.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 .550) .00) .170 (.090) .070) .077-.340-.130-.390 (.580) .150-.170) .500 (.092 (.370) .430 (.560) .110 (.320 (.160 (. Evidence is lacking for the carcinogenicity of tungsten.280-.073-.04.690) .110 (.082-.180-.110-.076 (.070) .340-.080-.100 (.070) .380 (.111-.088) .070-.220 (.300 (.360 (.120-.300) . 0.190 (. respectively.290-.123-.210-.330 (.270-.070-.093) .140-.640 (.190) .130-.160-.100-.210 (.160-.170) .092 (.250) .130-. which is used in the steel industry.140-.088 (.140 (.060-.080) .060 (.090) .100-.260-. bronzes in pigments.400 (.220) .090-.056-.073-.120) .

218 (.056-.S.081 (.285) .091 (.079 (.308) .121 (.078 (.354-.431) .064-.109 (.216 (.098 (.278-..059-.120) .122-.301) .099-.392) .080-.088) . 2001-2002.073 (.153-.065 (.109-.199 (.061-.359 (.208-.333-.103-.214-.206-.255 (.091) .237) .146) .098) ..179-.386) .063-.117 (.122 (.270 (.181 (.116 (.148) .081-.093) .086) .091) .060-.148 (.100) .364 (.287) .167) .138) .074-.075) . population from the National Health and Nutrition Examination Survey. 1998).066 (.084) .049-.071) .133) .279 (.431) .093-.329-.108) . population.061-.258-.086-.131-.302-.100 (.217-.179-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.188-.087) .174 (.154) .465) .105 (.200-.157) .293 (.216-.063-.300 (.065) .071 (.138 (.216-.074 (.426) .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 .354) .359 (.317-.582) .214) .094) .414) .344-.308) .300) . 2003.231 (.267) .431) .122-.082) .353 (.136-.301) .057-. 2005).133) 90th .059 (. or exposure that a control group of non-metal workers had mean levels differences.150-.201 (.106 (.255-.200-.088) .091) .165) .237) .061-.104-.081 (.379 (.329 (.057-.333-.085 (.176-.084 (.084 (.497 (.067 (.108-.065-.111 (.075) .436) .073 (.253-.439 (.086) .075 (.138 (.231-. Nicolaou et al.136-.074) .087 (.071-.184 (.083-.250-.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 .094-.119 (.133) .465) .063 (.063-.075 (.253) 95th .353 (.164 (.078) . 1997).077) .279 (.667) .439) Total .070 (.170-. 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.261-.250 (.082 (.083 (.116-.058-. measure urinary tungsten. Using neutron activation analysis to 2000.072-. Patients with medically-inserted tungsten found at increased levels in drinking water.065-.072-.727) .294 (.199 (. 2001)..667 (.063-. similar to those in this Report (Schramel et al.054-.197-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.158) .078 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.381) .091) .224) .053-.169 (.063 (.S. population (CDC.059-.283) .S.315-.253 (.201) .300-.358) .153) .062 (.341 (.331-.306) .190) .300-.169) .605) .255 (.168 (.121-.554) .079) .120) .060-.068 (.086) .216 (.299 (.079 (.107-.197) .089 (.174) .139) .158) .383 (.085-.797) .136-.459) .(Kraus et al.090-.258 (.333 (.146 (.094) .187) .333) .077) .060 (.096) .084) .065 (.452-.267-.056-.090-.130 (.426) .074-.215) .217-.347 (.317) .144-.143 (.136-.071 (.080 (.069 (.155-.484) .124 (.410-.071) .139-.091 (.054-.198-.074) 75th .146 (.098-.080 (.073 (.739) .197 (.151 (.067 (.205-.085) .083 (.245-.073 (.333) .439 (.079) .634 (.284) .275 (.150-.302-.078-.333 (.158) .28) .340 (.068-. (1987) found possibly due to methodologic. interval) .222-.317 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.197) .092) .265 (.161) .462) .130-.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 .079) .333 (.215 (.375) .098-.240-.095) Selected percentiles ( 95% confidence interval) 50th .071) .079) .072 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.500) .823) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.186 (.216-.152-.333 (.080-.098-.125) .069 (.075-.154) .078) .180-.538) . and 2003-2004 (Paschal et al.453) .301) .272-.145 (.167) .203-.412 (.105 (.326) .209-.083) .158 (.360 (.059-.077-.083) .198) .150 (.077-.555 (.222) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.143-.100) .237-.089) .279 (.286-.176-.116) .070 (.125 (.119-.250 (.233-.126-.139 (.082) .436-1.065-.385 (.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 .339 (.055-.124-.167-.136 (.095-.117) .069-.064-.067-.066 (.880) .081) .484 (.075-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.482 (.211 (.144 (.339 (.167-.071 (.

tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Int Arch Occup Environ Health 1997. Churchill County (Fallon). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Weber A. platinum. Paetzel C. Sampson EJ. [online] 2003. 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.cdc.(2):73-77. Schramel P. Manke C.gov/nceh/clusters/Fallon/study. Schaller KH. Jackson RJ. Nevada Exposure Asssessment. Wendler I. Paschal DC.. Trace metals in urine of United States residents: reference range concentrations. 2004). Centers for Disease Control and Prevention. palladium. Available at URL: http://www. mercury. J Trace Elem Electrolytes Health Dis 1987. Lenhart M.76(1):53-59. Third National Report on Human Exposure to Environmental Chemicals. Occup Environ Med 2001.62:380-384. and hair (Bachthaler et al. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Catheter Cardiovasc Interv 2004. Morrow JC. Kraus T. Angerer J. Angerer J.58(10):631-634. Cancer Clusters. thallium. Ting BG. Environ Res 1998.Metals blood. Nicolaou G. Pirkle JL. Cassina G. Atlanta (GA). Feuerbach S. tellurium. 2005. Link J. lead. The determination of metals (antimony. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. National Center for Environmental Health. Sabioni E. Pietra R. bismuth. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Zobelein P. 238 Fourth National Report on Human Exposure to Environmental Chemicals .htm. Schramel P. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. References Bachthaler M. et al. urine. cadmium. Mosconi G. Seghizzi P. 4/15/09 Centers for Disease Control and Prevention.69(3):219-223. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis.

010) * .014 (.031 (.012 (.013-.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 .010) .008) .009-.045) .030 (.005-.016-.009) .015 (.013 (.018) .007-.026-.008 (.007-.036-.017-. and 234U.013-.008 (.007 (.009) .021-.007 (.004.027-.017 (. In workplaces that involve uranium mining.040-.026 (.056) .72%).008 (.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 .008 (.031-.021-.020-.004.022-.028-.049) .007-.009) .046) .007 (. population from the National Health and Nutrition Examination Survey.019-.037-.009) .005.006 (.014 (.158) .006-.020-.031 (.053 (.048 (.022 (.127) .012 (.020-.012 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.007 (.033 (.017-.012) .009-. and 0.027 (.007-.008-.010-.017) .016) .013 (.027 (.040) .027 (.011) .050) .010-.007-.015) .013 (.039) .006-.010 (.036) .024 (.026-.008) .008 (.066) .041 (.062) .042 (.006-.017) .037) Total .036) . 235U (about 0.011) .009) .008 (. and 03-04 are 0.010) .012 (.008 (.007-.006-.S.006 (.008 (.009) .011-.007-.036 (.007-.006-.009) .007-.009-.028 (.009-.037 (.009-.046 (.020-.054-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.026) 95th .012-.008 (.006-.011-.013 (.028 (.017) .020 (.030) .049) .046 (.069) .063) .023) .008 (.006-. see Data Analysis section) for Survey years 99-00.031 (.012-.010 (.010) .054) .007) .009 (.011-.011) .005-.040-.013-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.023 (.031 (.039-.027) .021 (.036 (.030 (.016) .051) .009-.009 (.020) .009 (.023) .009) Selected percentiles ( 95% confidence interval) 50th .055 (. 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.027 (.008 (.010) . Since the 1990’s.011-.008-.010) .018) .030 (. 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.034-.010-.027) .065) .009) .009-.007 (.007-.017) .011) .029-.011 (.009-.013 (.011-.008-.010-.019 (.028 (.008 (.012-.007-. 01-02.028-.046 (.016) .008 (.015) .009) .027) .007 (.006-.037) . milling.022-.007) .007-.012) .006-. Variable concentrations of uranium occur naturally in drinking water sources.024-.010-.018 (.020-.012-.016) .007-.008) .029 (.018-.009 (.032 (.007-.065) .021) .013) .026 (.011) .007-.007-.010 (.035) . 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.009-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.015 (.036-.007) 75th .022-.045) .039) .008-. interval) .008) .009 (.048) .023 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).011 (.009 (.017-.031 (.015 (.023-. or processing. Fourth National Report on Human Exposure to Environmental Chemicals 239 . nuclear fuel.022) .053) .054) .008-.006-.009) .019-.027-.064 (.023-.008 (.021 (.008) .008 (.033-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.009 (.067) .056) .033 (.088) .018) .016-.037) .009) * .038) .007-.024-.011-.026 (.067) .042) .016) .012 (.011-. in some ceramics.016-.015-.013 (.019-.007-.012-.017-.023-.021 (.017-. 0.009) .046 (.018 (.007 (. respectively.007 (.037) .021) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.015 (.007 (.029-.007 (.009 (.279) .023-.014 (.040 (.033) .014 (.060 (.035) .006-.026) .Metals Uranium CAS No.043 (.038 (.010-.012) .016 (.018) .008-.017) .014 (.041 (.010 (.006-.007) .034-.047 (. human exposure occurs primarily by inhaling dust and other small particles.012) .023) .009 (.019-.016) .005-.027-. including nuclear weapons.009 (. Uranium has many commercial uses.008 (. and as an aid in electron microscopy and photography. Thus.040 (.010) .006 (.007 (.043) .014 (.009-.034) .008-.005-.017 (.007) .030-.008 (.027) .046-.007) .010) * .073) .017-.006-.012-.023 (.025-.050) .013) 90th .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 .024-.010) .011) .006 (.008-.010 (.021) .009) .040) .072) .009) .026) .020) .013 (.010) .005-.012 (.011) .114 (.035-.044 (.052 (.

080) .020-.007 (.013 (.007-.010) .008-.006-.Metals impact.024) .011) .006-. In cases of retained DU shrapnel.012 (.008 (.022 (.007 (.012 (.016) .032) .012 (.007 (.006-.050 (.021-.015 (.053) .011-.009) .009) .007 (.016) .019-.015) .009 (.030) .006) .008-.. 240 Fourth National Report on Human Exposure to Environmental Chemicals .024 (.007 (.050) .010 (.025-.020 (.025) 95th .006 (. After exposure to soluble uranium salts.019-.008 (.019 (.017) .011-.013) .008-.012 (.025 (.021 (. interval) .031-.025-.016) .011-.018-.007 (.007 (.007-.007-.014) .011) * . which represents distribution and excretion.009) .020) .012 (.016 (.042) .027 (.033 (.011-.045 (.013 (.005-.012 (.028) .007 (.023-.016-. low level exposure.026 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.007 (.030 (.009) * .051) .029 (.006-.007 (. After inhalation.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 .013-.018-.014 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.050) .008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .007) .010 (.010) .015) .010-.044) .022 (. 1992).027-.028-.013 (.034 (.011-.006) .008) .005-.034-.025-.019) .026 (.028) .059 (.006) .008) .034 (.008-.027 (. After long term or repeated exposure.008) .015-.004-.017 (.029 (.039) .009 (.010) .009) .025-.015 (.006-.024) .026-.053) .006 (.043 (.006-.008) .019) .067) .006 (.029) .007 (.006-.019 (.009 (.022-.008 (.012 (.024) .005 (.030 (.016) .008 (.028) .014) .029) .039) Total .010-.006-.014-.054) . 2003).011-.007 (.006 (.270) .010-.009 (.018 (.074) .024) .016-.007-.035 (.010-.027-.013 (.028) .009) .019-.013) .018) .S.017 (.007 (.019 (. 2005).020-.007 (.007 (. Radiation risks from exposure to natural uranium are very low.024-.009-.013) .027 (.006-.008) .008) .013 (.013 (.005-.008) 75th .019-.008) .033 (.027) .007 (.033) .011) .009-.051) .032) .017-.034 (.021 (.008 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.048) .005 (.026 (.011) .1%-6% of an ingested dose may be absorbed.029) . the shrapnel acts as a source of chronic.009) .014 (.033 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours. population from the National Health and Nutrition Examination Survey.005 (.029) .017-.030 (.014) .006-.011 (.024-.005 (.058) .008 (.077) .013 (.014-.016-.017) .040 (.009) .013 (.040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result.007 (.015 (. liver.012-. with much slower elimination from bone.015) .020-.047) .009) Selected percentiles ( 95% confidence interval) 50th .006-.020 (.012) .006-.018-.006-.017-.011-.018-.033 (.009) .007 (.020 (.018-.007-.010) * .009 (..015-.005-. where limited absorption occurs (less than 5%).007-.051 (.009) .007-.010 (.009) .031 (.006-.041) .030) .010) .007 (.037 (. 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.008 (.039) .021 (.011-.010-.010-.027-. Inhaled uranium-containing particles are retained in the lungs.006-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.012) .027) .016) .146) .008) .015) .042-.019-.014-..021 (.008 (.015-.005-.007 (.016) .025 (.029 (. kidneys.009-.006 (.063) .007 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.100 (.005-.034 (.028 (.008-. Uranium is eliminated in feces and urine.016-.024) .005-.058) .006-.006) .013 (.010-.009-.056) .011 (.015-.008) .006 (.021) .011-.024 (.030-.024 (.006-.024-.009-.051) .008 (.007-.034) .041) 1227 1334 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .010-.010-.008) .007) .006-.007-. 0.030-.013 (.022-.006-.015 (.034 (.017) .006-.006-.015-.008) .010) .034-.006-.016) .016) .017-.061) .014) 90th .008 (.027-.039) .006-.012) .010-.026) . which can occur occasionally from high occupational exposure.010-.035 (.010) . Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.012-.004-.007-.048) .009) .028 (.006) . Depending upon the specific compound and solubility.010 (.022-.042) .022) .022 (.010 (.008-. Health effects from uranium exposure result from chemical toxicity to the kidney.009-.006-.007) .020-.

2001-2002. Zimmerman I.. NRC. 1991.168(8):600-605. In 17 U.. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. but in whom no shrapnel was embedded. 2003. Thomas RG..e.. 2006). 2005. Six workers in a depleted uranium program showed concentrations of 0. 2004).. Volf V. Breitenstein BD. In: Gerber GB.110 to 45 μg/L (Ejnik et al.S.078 μg/L (ranging up to 5. (Kurttio et al. eds.. Carmichael AJ. IARC and NTP have no ratings for uranium human carcinogenicity. 1992. Health Phys 2000.S. McDiarmid et al. McDiarmid M. 2006).. Kent (England): Nuclear Technology Publishing. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Dietz LA. Ejnik JW. Metivier H.066 μg/g creatinine (Gwiazda et al.. urinary levels of uranium were as high as 9.. had a mean urinary uranium concentration of 0. Uranium content of blood.61 μg/g creatinine.gov/ toxpro2. 2004). Stradling GN. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Boyd P. Hamilton MM. 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. 2000). Drinking water and other environmental standards have been established by U. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.107:143-157. Pillai KC. ingestion. although slightly increased during and after deployment. in that the levels were below their respective detection limits (Byrne et al. and after deployment had geometric mean urinary uranium concentrations that were less than the NHANES 1999-2000 and 2001-2002 geometric means at all three time periods.62:562-566. 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. soldiers evaluated before. respectively.. 41 (1). 2004)..162 μg/L) (Orloff et al. Fourth National Report on Human Exposure to Environmental Chemicals 241 . the median urinary uranium concentration was 2. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 2000).. Hamilton et al. 1994.011 μg/L (McDiarmid et al. the median urinary concentration was 0. Squibb K. Atlanta (GA).. 1-49. 1978). 2004). Durakovic A. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.55 μg/L (median 0. during.Metals injury associated with elevated urinary uranium levels (Kurttio et al. 2006). 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.S.65 μg/L). soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Health Phys 1992.. Muggenburg BA. Radiation protection dosimetry.78:143-146. the geometric mean urinary uranium concentration was 0. In a study of 105 persons exposed to natural uranium in well water. Horan P.atsdr. Komaromy-Hiller et al.. Information about external exposure (i. A cohort of 46 U.1996. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. and no consistent effects on multiple endpoints of kidney function were found. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. and 2003-2004 (Dang et al. Karpas et al. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Tolmachev et al. et al. Galletti. pp. with emphasis on quality control. The U. 2006). References Bhattacharyya MH.. Vol. (May et al. EPA. environmental levels) and health effects is available from ATSDR at: http://www. Third National Report on Human Exposure to Environmental Chemicals. Benedik L. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.S.S. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.. 2002). Mil Med 2003. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In the same study. 2006. 28 soldiers who may have been exposed to DU by inhalation. Sci Total Environ 1991. Centers for Disease Control and Prevention (CDC).cdc. 2002.html.. Byrne AR. Pullat VR.1992. 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. Dang HS. population. or wound contamination.S. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.

et al. Katorza E. Andrews WS. Metcalf S. Ting BG.82(4): 527-532. Sampson EJ. Komulainen H. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Paretzke HG. Shelly T. et al. Saha H. Comparison of representative ranges based on U. Washington (DC): NRC. Health Phys 2004. Cordero S. Salonen L. Human exposure to uranium in groundwater. Health Phys 2002. Karpas Z. Noguchi H. Kalinsky V. Inductively coupled plasma mass spectrometry as a simple. Kane R. Biologic monitoring for urinary uranium in Gulf War I veterans. Health Phys 2003. Pinto V. Radiat Environ Biophys 2005. Sci Total Environ 1994. Lorber A. Mistry K. Lewis BM. et al. U. et al. May LM. Van der Venne MT. Roiz J.296(1-2):71-90. Auvinen A. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Kurttio P. Marko R. Biokinetic modeling of uranium in man after injection and ingestion. U.S. Marino R.87:51-56. Gwiazda RH. Pirkle JL. Wahl W. Karpas Z. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Renal effects of uranium in drinking water. Paschal DC. Pekkanen J.94:319-326. Harmionen A. Ejnik J. Jackson RJ. Charp P.86:12-18. McDiarmid MA. VI. Kuwabara J. Makelainen I.71(6):879-85.91(2):144-153. D’Annibale L. Health Phys 2004. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Saha H. Element reference values in tissues from inhabitants of the European community. Englehardt SA. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Squibb K. Halicz L. J Toxicol Environ Health A 2004. Orloff KG. Clin Chim Acta 2000. Hollriegl V. et al. Health Phys 2006. Environ Res 2004. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Scott K. Hamilton EI. Costa R. Health Phys 1996. Nuclear Regulatory Commission (NRC) Guide 8. patient population and literature reference intervals for urinary trace elements. Auvinen A. Ash KO. Li WB. Oberbroekling KJ.S.47(6):972-982. Cremisini C. Oeh U. Smith D. Squibb K. July 1978. Am J Kidney Dis 2006. Kurttio P. Roth P. Environ Res 1999. Hancock RG.85:228-235. Int Arch Occup Environ Health 2006. Kidney toxicity of ingested uranium from drinking water. Komaromy-Hiller G. Review of elements in blood. Bennett LG. Sabbioni E.44:29-40. Howerton K.Metals Galletti M.S.81:45-51. Wilson PD. Uranium daily intake and urinary excretion: a preliminary study in Italy. McDiarmid MA. Ough EA. Environ Health Perspect 2002.22–Bioassay at uranium mills.S.67(8-10):697-714. Salonen L. McDiarmid M. Heller J. Jarrett JM. Engelhardt SM. Oliver M. Gucer P.110(4):337-342. Uranium and thorium in urine of United States residents: reference range concentrations. et al.158:165-190. Nuclear Regulatory Commission (U.79(1):11-21. rapid. concentration and daily excretion of uranium in urine of Japanese. NRC). Tolmachev S.

10-11.39-4.0) 19.74-3.51 (3.80-4.20 (7.40) 3.30-6.45-4.90-9.87-3.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.10-12.00) 5.0) 11.30) 6.50-7.0 (8.90 (5.40) 6.20 (6.90-3.0-15. Other manufactured uses include fireworks.0 (9.S.19 (3. leather tanning.30 (2.0-18.40) 4.0-17.11) 3.0-17.80-15.0) 10.00) 3.20) 3.0 (9.02 (3.0 (8.0) 15.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.93-3.0-17.22-5.0 (12. 2005).40) 3.05 (2.40-13.30 (5.0) 8..50-11.20 (4.07-4.08-3. Survey years 01-02 03-04 Geometric mean (95% conf.40) 3.0-29.26 (2.60) 8.90-3.0) 13.70-5.40 (4.20 (2.10) 5.90 (2.90 (5.22 (2.10) 5.50) 11. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.66) 3.70 (3.0) 13.35 (3.76 (3.40-11.60-7.56) 3. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.70-6.0) 11. laboratory analysis.93 (4.10-11.68) 4. 2002). and electroplating.0) 14.0 (9.00) 3.0 (9.80-6.10 (7.40-7.30 (2.46) 3.g.51 (3. population from the National Health and Nutrition Examination Survey.75 (3. It is normally found and produced as the anion of a sodium.96 (3.0 (8.0 (11.40 (3.84) 14.60) 5.40 (5. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.40-5. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.76) 4.60-6.0) 8.80) 75th 6.30-19..70 (3.40 (3. 2007).0) 15.20 (4.10 (5.49-3.00) 7. fabric dyeing.90) 6.0-20.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0) 14.21 (2.00-5.0) 9.12) 3.S.90-11.47-4.00-6.0 (9.10 (2.31) 2.0-19. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 11.30-17.90) 5. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0-17.60 (4.44-4.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.30-7.50) 6.60 (7.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.Perchlorate Perchlorate (Urbansky.0-17.05.0) 9.0) 13. 1998). In addition.80 (7.75-3.70-3.0) 10.0) 9.70-9.90-6.40 (4.50-4.70-7.60) 3.50) 5.90 (3.50) 5.0 (11.00) 4.0 (10.50 (8.80 (3. or ammonium salt. certain catalytic metals. 2005).0) 9.80 (6.0 (11.0 (8.65) 3.11) 4.10) 3.19-4.00-6.90 (5.0 (11. but has strong oxidant properties in the presence of concentrated acids.0 (11.20-11. and limited applications in pharmaceutics.30) 6.70 (3.20-4. lettuce) can be the main sources of intake for humans (FDA.70-11.20-3.10) 3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0) 13.0) 13.40-4.03) 3.0-17.0 (9.0) 95th 14. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.50 (3.70-3.10-4.0) 13.70) 3.0 (13. Drinking water.62 (3.81-16. interval) 3. and reducing agents.0 (12.S.67-5.40) 2.80) 3.90-9. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.90-11.90 (4.89-3.40 (5.29-3.10) 12.5 hours and has a small estimated volume of distribution (Crump and Gibbs.80-4.0 (11. potassium.20 (5.79 (2.80) 7.40 (8.0 (8.80 (3. Perchlorate is stable under most environmental and physiological conditions.10 (6.54 (3. 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.40-6.0-15.0 (12.40 (5. 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.30-7.0-18.0 (11.38) 5.0) 10.90-12.20) 7. milk.0-14.EPA.0) 12. matches.10-7.0 (9.10 (6.80) 12.0 (11.70-12.0) 16.80-12.0 (12.09) 3.30 (5.0) 9.0 (11.80-8.88) 3.20-12.0) 14. Perchlorate was added to the U.40) 90th 10.20 (8.20 (2.0) 13.50-4.40-4.60 (4.50-3.16) 3. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (5.90-10.0) 13.93-4.0-18.20) 4.01 (2.50) 3.05 and 0.18-3.32 (3.0-23.0 (11. and certain plants with high water content (e.0) 9.20-4.81) Selected percentiles ( 95% confidence interval) 50th 3.

90-20.90-2.09 (7.64) 5.20-4.80-3.76 (3.3-14.45) 3..40) 17.1-14.30) 5.4-16.0 (8.50) 6.74) 7.25) 5.91) 4. levels.22-4. During gestation and infancy.50) 2.30) 75th 5.4) 13.10 (4.60) 10.87 (7.99-3.90-11..99 (5.1-13.0) 10. interval) 3.76-3.95 (2.90 (7.37 (4.90) 5. However.60-8.52 (8.89-3.43) 6. up to 68% RUI has been demonstrated.14 (2.1-16.56 (3.10) 4.82 (5.26) 4.39-4.80) Selected percentiles ( 95% confidence interval) 50th 3.51-4.26 (3.72 (3. NAS.0 (11.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 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.6-17.19-6.0-44. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.35 (4.93-8.60-11.25) 5.90-3. U.24 (4.6) 20.S.3) 11.54 (3.60-8.02-4.. Li et al. In the U..0) 9.70 (2. 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.20 (2.67) 5. Steinmaus et al. perchlorate is negative in most genotoxic assays (U. and the presence of other substances known to affect thyroid function (e. 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.1) 8.30-5.0 (9.51 (3.S.93) 3. gender.60 (3. Survey years 01-02 03-04 Geometric mean (95% conf. thiocyanate. 2005.S.12 (6.3 (10.53 (2.0) 7.71 (5. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.70-4.35) 3.33 (7.00-3.54 (2.50) 95th 12.80 (4.Perchlorate inhibition (RUI).52-9. in a representative sample of U.41-9.90 (4.60-5.00 (4.2) 8.00-11.56-3.10 (6. Lawrence et al.40 (7.45-2. women with urinary levels of iodine less than 100 micrograms per day.50-9.0-14.20-3.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.0 (11.60) 3.S.19-10.20) 3. 1999.75) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.87 (5.61 (5.20-3. 2005).02) 3.32) 5.20-10.25 (3.40-10.70-15.0 (9. 2003.2) 8.4 (10.42 (3.20 (3.30-10.10 (4.80-3.00) 4.36 (8.00) 9.20) 8.18-3.50 (3.50) 5.8 (11.60-5.0-19.70-3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.S.40 (3.S. 2000).89 (2.30-5. population from the National Health and Nutrition Examination Survey. menopausal status.1-22.58) 2.86) 4.44) 3.70) 10. 2002). Greer et al.20 (7.81-3.35 (2.60-15. levels and sufficient in most participants (Tellez et al.50-3.10 (1.93-5.80 (7.50 (6.87) 2.20-9.16-3.0) 13.0) 12.50-5.40) 5.3) 8.0) 14.0-17.EPA.73) 3. 2005).46 (3. nitrate.5 (13. 2002. 2007).77 (3.7 (11.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .10) 3.39 (3. 2002.60-11.40) 3.22-4.0 (10.00 (6. Also.61-10.0) 12.10-7. chronicity of exposure.07 (2.70 (4.90 (2..0) 12.21 (2. 2005).0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.0) 9. although iodine intake was higher than U.66) 3.09) 3. dietary iodine intake.1 (8.10) 6.0 (8.15-12.50) 2.30) 90th 9.98) 3.0) 11.30 (5.4 (8.20 (6.00-2.05 (4.30 (6.22 (2.60) 8.90-15.93-7.5) 8.10-3.S. 2001.84) 2.03 (2..04-3.4) 8.g.3) 12.6) 12.70) 2.12-2.39) 2.10 (2.70-5. Many factors may be important in consideration of perchlorate action on the thyroid: dose.04-3.33-6.00 (2..90-9.29) 2.. Lamm and Doemland. 2006.47) 2.96) 2. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.87) 7.40 (3.93-5.4 (11.08 (3. age. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.29-6. 2005.0) 6.24-2.97-5.0) 4.80 (7.0 (11. medications).46-13.64-3..20 (4.90 (2..1 (11.22-6.0 (9.61-5.30) 3.33-12.87-3.50) 9.0) 12.70 (2.25) 5.30 (3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.60-6.59) 3.0-14.46-4.34-3.60-3.0) 13.EPA. 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.4 (11.37-13.83 (5.40 (4.44-6.00) 3.10) 13.08) 3.

Landingham CB.S. Blount et al. Erratum in: J Occup Environ Med 2004. 2007). Braverman LE. Pino S. Steinmaus C.40(21):6608-6614. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Blount BC. Kelsh MA. Goodman G.atsdr. 2005). Caldwell KL. Lamm SH.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis.. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Analysis of relative source contributions to the food chain. Sesser DE. Perchlorate in the United States. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Jackson WA. Valentin-Blasini L. Lamm SH. Additional information about exposure and health effects is available from the U. Tellez RT.113(8):10011008. Barnard JC. Crump KS.gov/toxpro2. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.110(9):927-937. Lau EC. and nitrate on thyroid function in workers exposed to perchlorate long-term. et al. Biomonitoring studies of urinary perchlorate provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of perchlorate than levels found in the general population. Primary congenital hypothyroidism. epa.. J Occup Environ Med 2003.17(4):400-407. Braverman LE. 2001-2002.10(8):659-663.. 2005). Food and Drug Administration (FDA). Braverman LE. The effect of perchlorate. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.cdc. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Environ Sci Technol 2006. Deyhle GM. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. 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.html and from ATSDR at: http://www. Cross M.S. Environ Health Perspect 2002. Mauldin JP. et al. most of the population is considered to be below the U. Erratum in: Environ Health Perspect 2005. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. National Research Council of the National Academies. Pirkle JL. National Academy of Sciences (NAS).S. Abarca CR. 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. Osterloh JD.46(5):509. Buffler PA. Kirk AB. Environ Health Perspect 2006. Environ Health Perspect 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Health Perspect 2007. Low dose perchlorate (3 mg daily) and thyroid function.html. newborn thyroid function. population. Lawrence J. Daaboul JJ.gov/safewater/ccl/perchlorate/perchlorate. et al. Dasgupta PK. CFSAN/Office of Plant & Dairy Foods. Benchmark calculations for perchlorate from three human cohorts. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. et al. Lamm SH. He X. (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.114(12):1865-1871. 6/2/09 Greer MA. Richman K. Rutherford GW. Health Implications of Perchlorate Ingestion. Blount BC.11(3):295. Pleus RC.EPA at: http://www.45(10):1116-1127. J Expo Sci Environ Epidemiol 2007. Li FX. Gibbs JP.90(2):700-706.115(9):1333-1338. Greer SE. Li Z. Washington (DC): National Academy Press. J Occup Environ Med 2000.41(5):409-411. Pirkle JL.htm. Byrd D. Miller MD. Dyke JV. May 2007. Page Last Updated: 05/28/2009. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Lawrence JE. EPA reference dose (Blount et al. Crump KS. Osterloh JD. Available at URL: http://www. J Clin Endocrinol Metab 2005. References Blount BC. thiocyanate. Neonatal thyroxine level and perchlorate in drinking water. Magnani B. Doemland M. and environmental perchlorate exposure among residents of a Southern California community. 2005. Chacon PM. Also. Howd R.113(11):A732. Valentin-Blasini L.fda. Skeels MR. Lamm S. Perchlorate Exposure of the US Population. Pino S. Thyroid 2001. Thyroid 2000. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.42(2):200-205.

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

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

2004.4.. < LOD means less than the limit of detection... may metabolize or degrade to PFOA (Dinglasan et al. 2005). 2006. heptadecafluoro-1-decanol. 2005. the 8-2 telomer. environmental fate... All sources of human exposure are uncertain. C6. Taniyasu et al.. kidney. there is limited information on the sources. U.. C5. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i.. Guruge et al. PFOA is mostly excreted in the urine in animal studies. 2007).S. 2002.. pancreas.. human toxicokinetics.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004. in a wide variety of marine and land animals (Kannan et al. Survey Geometric mean (95% conf.e. which may vary for some chemicals by year and by individual sample. 2000. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. Prevedouros et al. The PFCs often measured in human serum are listed in the table. 2004.. EPA. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. Lau et al. 2004).. but probably include dietary sources (Kannan et al. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. 2005).. Olsen et al. endocrine and immune effects. Lau et al. It is unclear if environmentally degraded telomer products are a major source of other PFCs. peroxisomal proliferation.. thymus and spleen. see Data Analysis section) for Survey year 03-04 is 0.S. Bookstaff et al. Tittlemier et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. Unlike many organohalogen contaminant chemicals. 2003. 2006a.. 2004.. 1995. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al... 2003a and 2004a).5 years and for PFOS. 2007a). Some of the effects in animals may be mediated through peroxisomal proliferation. but still can have long residence times in the body.8 years (Olsen et al. For instance. including immunologic effects and tumor induction. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. Vanden Heuvel et al. Excepting PFOS and PFOA.. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. in part. by high protein binding in plasma and other proteins. 2005. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. population from the National Health and Nutrition Examination Survey.. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. 1993). approximately 4.. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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. The elimination half-life of PFOA in humans is roughly estimated to be 3. and in offspring. or effects of other PFCs. Kannan et al. In some cases. Keller et al. hepatotoxicity. 2005). 2003).Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). 1990). and in human blood and semen (Calafat et al. C7). 2005. 2004).... and β-oxidation of lipids (Kudo et al. growth retardation and delayed sexual maturation (Kennedy et al. PFOA has been reported to cause liver. 2003). 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. 248 Fourth National Report on Human Exposure to Environmental Chemicals .

2003.00 (.. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.400-1.400-1. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear....900 (.900 (.500-3.400 (<LOD-. 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. 2001. PFOS. which may vary for some chemicals by year and by individual sample.400 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Survey Geometric mean (95% conf. monkeys..400-.600-2. reproductive. At doses causing maternal toxicity. possibly related to lung immaturity (Lau et al.400-1. elderly and children.500-1. 2003a).700 (.700) . 2003a).S. Animal studies of PFOS have demonstrated weight loss. 2004. perfluorohexanesulfonate (PFHxS). Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.800 (..3. 2004).600 (.800) 1.500-1. 2003). PFOS...S.80) 485 538 962 Limit of detection (LOD.600 (. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. EPA. 2007b). thyroidal).. Olsen et al. 2003. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 2004a. Olsen et al. Olsen et al. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . Cook et al. Harada et al. 2007. In such studies.300 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2007).20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .20) . 1999.10 (..108 times higher than background serum levels in humans (Butenoff et al. However. 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. U..S.400-1.500) . and humans. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2005).500-. 2003). 2007b. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 2003a. 2004. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 1992. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. 2007a..00) .600 (. 2003a.500 (. 2004b).80) 640 1454 03-04 03-04 * * < LOD < LOD . PFOA. Fei et al.500) . At high but non-toxic maternal doses of PFOS.00) .10) .00) .300-1.500-1.40) . or increased cancer rates (Alexander et al. population from the National Health and Nutrition Examination Survey. 2007a. Thibodeaux et al. development in offspring was stunted and hypothyroxinemia was observed.. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.. hepatotoxicity. EPA.. 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. < LOD means less than the limit of detection.300 (<LOD-.800 (.500) . developmental and teratogenic effects were demonstrated in offspring.400-.500 (<LOD-1.800 (.500) 90th ..10) * 03-04 03-04 * * < LOD < LOD < LOD . 2003a. Lau et al.800) 1. see Data Analysis section) for Survey year 03-04 is 0. the potential to estimate risks to humans from animal doses is uncertain. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 2004).400 (<LOD-. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. 2005). Kennedy et al. U. 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.800 (.500-1. population.50) .300 (<LOD-..400-1.900 (.400) .10) .500) . In comparing three separate reports on adults..500 (...S. PFOA. 2003. and changes in thyroid hormone concentrations (Grasty et al. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 2003)..

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

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 . Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.300-.400 (.S.500) 485 538 962 Limit of detection (LOD.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.3. population from the National Health and Nutrition Examination Survey.600 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400) .900) < LOD .400 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 251 .600) < LOD .600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (<LOD-.S.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .300 (<LOD-. which may vary for some chemicals by year and by individual sample.500 (<LOD-.500-. see Data Analysis section) for Survey year 03-04 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th .

00-7.67-2.20 (6.20 (1.900 (.80 (1.80-8.20 (1.70) 2.00 (.10 (.6) 7.600-.00) 3.40-3.90) 1.90) 3.900-1.00) 1.00 (1.984 (.30 (2.92 (1.50 (1.12) .90-10.50 (6.30-12.900-1.20) .0) 8.S.10) 6.00-1.3 (9.80) 4.10 (.800 (.90 (2.91) 2.80-3. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50-6.90 (1.30 (1.10-9.30) 3.70) 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 1.70 (2.80-4.16) .700 (.00-6.44 (2.90 (4.93 (1.42 (1.17 (1.20-3.3.20-1.20-1.80-4.00) 2.900) 1.700-1.60-2.20) 1.00 (1.62-2.852 (.30-9.586-.20) 03-04 03-04 2. interval) 1.721-1.80) 1.30 (1.26) 2.04) .86 (1.30) 3.60-3.90) 1.80-2.70-10.90 (1.50 (1.10) 6.30-6.00 (1.60 (6.10) 8.10) 75th 3.73-2.90) 8.60-8.40 (1.80-7. interval) .72) 1.54) .60) 3.50 (1.30) 03-04 03-04 .60-4.912-1.72 (1.30-2.50-10.80-8.697-1.50 (4.10-5.816-1.963 (.70) 1.80 (4.800-1.20) 2.70) 1.60 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.01 (1.900-1.10) 4.00) 1.40) .20-1. see Data Analysis section) for Survey year 03-04 is 0.90-2.51) 1.70) 2.70 (1.00-1. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.40) 1.00 (2.90 (1.10) 1.10 (4.77-2.70-5.50) 6.5) 8.10 (.70-2.30 (3.40-1.90) 90th 5.00-8.70-7.809) 1.689 (. see Data Analysis section) for Survey year 03-04 is 0.50) 2.80) 3.87-2.10) 75th 1.70) 3.90) 1.50 (1.80-6.20 (1.40 (2.14 (.10) 4.40-1.80-4.50) 2.80 (1.40) 2.60 (1.70-6.826-1.50 (4.10 (4.20-2.40 (1.10) 1.40) 640 1454 03-04 03-04 2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.10 (1.05-2.60-3.08) 2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.40) 4.60-7.834-1.20 (6.1) 485 538 962 Limit of detection (LOD.900 (.40 (1.5) 5.56-1.861 (.90-19.40) 1.30 (7. 252 Fourth National Report on Human Exposure to Environmental Chemicals .1.900-1.03) 1.30) .90 (4.30 (1.09 (.60-4.20 (1. population from the National Health and Nutrition Examination Survey.20) 1.70) 13.30 (2.00 (1.00 (.60-2.50 (2.17-1.60-2.60) 9.20-1.30) 3. Survey Geometric mean (95% conf.10) 5.80-7.50 (6.10-9.50-6.60) 1.10) 1053 1041 03-04 03-04 03-04 .900-1.0) 1053 1041 03-04 03-04 03-04 1.60) 2.50-3.30 (1.40 (1.70-2.80) 90th 2.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900-1.966 (.00 (5.90 (1.40) 640 1454 03-04 03-04 1.30 (6.835-1.80-3.27) 1.S.60 (1.80) 5.20) 485 538 962 Limit of detection (LOD.80-12.

Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) 10.80 (6.60-14.8-22.7-69.8-81.5) 18.3-61.1-24. population from the National Health and Nutrition Examination Survey.1) 57.4) 21.20) 5.6) 9.1-33.90) 6.80-9.5-33.2 (16.30-6.5) 57.9-23.4 (28.8) 27.3 (17.6 (19.6) 42.70 (5.40) 5.2 (21.0) 485 538 962 Limit of detection (LOD.70-5. Fourth National Report on Human Exposure to Environmental Chemicals 253 .0) 36.3-22.50-13.7-49.2-22.50 (4.2 (18.40 (6.40-14.4-17.7 (43.80) 8.50-4.0) 03-04 03-04 19.7-30.2-57.1-25.8) 46.70-10.89 (3.10) 5.00 (3.50-6.5-21.4 (17.85-4. see Data Analysis section) for Survey year 03-04 is 0.84-3.10 (3.1 (23.9) 27.2 (27.20-4.6) 7.40) 75th 5.70) 4.10-3.8-30.3 (35.4-25.8-78.60 (5.1 (19.00 (5.35) 3.0 (27.67-4.30-8.2) 30.70) 6.4 (19.07-4.0) 43.3 (28.65-4.2) 30.96 (3.7 (13.7) 39.3 (44.50) 7.30-3.80-4.30-5.95 (3.70 (3.8-22.80 (7. Survey Geometric mean (95% conf.82) 4.1 (24.60-13.20-5.90 (7.60) 8.20) 4.1-35.4 (23.8 (37.6) 35.20-9.10 (6.80 (5.S.6 (44. Survey Geometric mean (95% conf.9) 22.4) 75th 30.5-62.9 (19.18 (3.9 (13.0) 21.20) 5.27) 4.3) 485 538 962 Limit of detection (LOD.30 (3.50 (3.1.70) 3.5 (28.20 (4.7 (35.1-52.6 (42.99-3.5) 19.5 (28.40) 90th 7.6) 62.2 (19.40-10.4 (19.6 (35.9 (17.6) 1053 1041 03-04 03-04 03-04 3.5) 1053 1041 03-04 03-04 03-04 14.7 (7.27) Selected percentiles ( 95% confidence interval) Sample 95th 9. interval) 20.20 (4.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.30 (5.90 (7.50) 4.30) 7.0) 23.8 (45.5) 7.6-45.1-36.91) 3.5) 32.90-12.3 (35.2 (28.70 (5.60 (4.7-23.60 (6.4.4) 20.40-6.53) 3.40 (4.9) 9.79) 4.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.47-4.5) 9.90 (5.6-50.8) 32.3) 42.9-19.7 (19.9-38.40-17.6-24.9) 22.10 (3.60 (3.21-3.20) 7.70-7.8-22.80 (6.20) 7.30) 6.11 (2.5-23.4-42.5) 8.9 (22.2) 45.60 (7.90-4.7 (35.47 (4.30-11.6) 18.1) 15.00 (5.4) 56.4) 640 1454 03-04 03-04 23.2) 640 1454 03-04 03-04 4.6) 21.0-66.3) 41.60 (6.00) 3.60-6.0) 21.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.0-16.60) 03-04 03-04 3.37 (2.90 (7.40) 3.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-12.7-53. interval) 3.0 (20.60-9.7-33.40-6.70-7.S.30 (3.7 (43.90-4.0) 90th 41.0-70.3) 28.8-35.0-20.70-9. see Data Analysis section) for Survey year 03-04 is 0.8 (34. population from the National Health and Nutrition Examination Survey.

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

10-1.600 (<LOD-1.90) .700) 90th 1.40) 1. < LOD means less than the limit of detection.700) .700 (<LOD-.700 (<LOD-.10) 1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .900-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .10-1.10 (1.600) .3. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40) < LOD < LOD .600 (<LOD-1.900-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) * 03-04 03-04 * * < LOD < LOD .50 (1.00 (.400 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.700 (<LOD-2.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00-1.30 (1. population from the National Health and Nutrition Examination Survey.20) 1.700) 1. population from the National Health and Nutrition Examination Survey.900) .800) .6.60) 640 1454 03-04 03-04 * * < LOD < LOD .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. which may vary for some chemicals by year and by individual sample.500 (<LOD-.800 (<LOD-.60) 485 538 962 Limit of detection (LOD.20 (1.10-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.900-1.900-1. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th .10-1. which may vary for some chemicals by year and by individual sample.00 (.900) 485 538 962 Limit of detection (LOD.00) < LOD .900-1.80) 1.800) .30) .10 (.400 (<LOD-1.600 (<LOD-.900-1.300 (<LOD-.70) 1.30) 1.30) 1.30 (1.900 (<LOD-1.900) 1.300 (<LOD-1.00 (.10 (.10) .00 (.700 (<LOD-.20-1.10) .10) 1.700 (<LOD-.700) 1.700 (<LOD-.900 (.300-2. < LOD means less than the limit of detection.50 (1.700 (<LOD-.S.S.600 (<LOD-1. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 0.900-1.10 (.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 .

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Kannan K. Church TR. Thibodeaux JR. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. J Occup Environ Med 1999. Olsen GW. Biol Pharm Bull 2003. Kawashima Y. Church TR. Butenhoff JL. Rogers JM. Lau C. Environ Health Perspect. Richards JH. (Erratum in: Toxicol Sci 2004. Hansen KJ. perfluorooctanoate andother fluorochemicals in human blood. Huang HY. Helzlsouer KJ. Seacat AM. Olsen GW. 2003.1177(2):183-190.40(1):32-44. Toxicol Sci 2003.gov/opptintr/pfoa/pfoara. Grey BE.41(9):799-806. Mandel JH. Peterson RE. Environ Sci Technol 2003. Stanton ME. fate and transport of perfluorocarboxylates. Toxicol Sci 2002. Mar Pollut Bull 2005. Horii Y. Mair DC. 2007a. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Gamo T. Environ Health Perspect 2005. Chemosphere 2007b.198(2):231-241. Froehlich JW. Kannan K. Historical comparison of perfluorooctanesulfonate. Church TR. Cousins IT. Prevedouros K. Buck RC.Perfluorochemicals Kudo N. Hansen KJ. Environmental Protection Agency (U. Miller JP. Burris JM. birds. Seacat AM. Olsen GW. A global survey of perfluorinated acids in oceans. Hansen KJ. Lau C. Ehresman DJ. Chemosphere 2004a. Toxicol Sci 2003. and humans from Japan.S. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. fast foods. Lundberg JK. J Ag Food Chem 2007. Reagen WK. and perfluorooctanoate in retired fluorochemical production workers.2(1):53-76. fish.51(8-12):658-668. et al. Burris JM. Cao XL et al. Environ Health Perspect 2003a.perfluorohexanesulfonate. Nesbit DJ. van Belle G.55:3203-3210. Butenhoff JL. Butenhoff JL. Taniyasu S. Sterchele PF. Ellefson ME. Sources.26(1):47-51. et al. I: maternal and prenatal evaluations. et al.45(3):260-270.S. Ehresman DJ.54(11):1599-1611. Fourth National Report on Human Exposure to Environmental Chemicals 257 .68(1):249-264. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Burlew MM. Burris JM. Olsen GW. II: postnatal evaluation. Butenhoff JL. Thomford PJ. Burris JM. Hansen KJ. U. Available from URL: http://www. Olsen GW. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations.) Tittlemier SA. Washington. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Olsen GW. Coordinate induction of acyl-CoA binding protein. 2003a. Moisey J.68:105–111. (Erratum in: Environ Health Perspect. htm. Taniyasu S. Hanson RG. Environ Sci Technol 2006.74(2):382-392. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Case MT. Rogers JM. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.111(16):1900) Olsen GW. Mandel JH. Petrick G. Thibodeaux JR. J Children’s Health 2004b. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Butenhoff JL. Bronson R. Larson EB. and food items prepared in their packaging.111(16):1892-1901. Burris JM. et al. Biochim Biophys Acta 1993. The developmental toxicity of perfluoroalkyl acids and their derivatives. Seymour C. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Mandel JH. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Rogers JM.74(2):369-381. Zobel LR. EPA)..82(1):359. Grey BE. Pepper K. Hanari N. et al. Butenhoff JL. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. J Occup Environ Med 2003b.113(5):539-545. Korzeniowski SH. Olsen GW. Yamashita N.37(12):2634-2639. et al. Mandel JH. 1/15/06 Vanden Heuvel JP. Barbee BD. Hansen KJ.epa. Horii Y. Half-life of serum elimination of perfluoroo ctanesulfonate. Lundberg JK. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Hanson RG. fish. Yamashita N.115(9):1298-1305. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Olsen GW. Toxicol Appl Pharmacol 2004.

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

Also. Environ Health Perspect 1982.. However.. variation also occurs in the same person during repetitive monitoring (Fromme et al. Silva MJ. The Handbook of Environmental Chemistry.atsdr.nih. 227-262. 2001. and race/ethnicity (Silva et al. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. efficiency of intestinal absorption. These differences may contribute to species-specific differences in toxicity (ATSDR. and extent of metabolite conjugation to glucuronide (Albro et al. atsdr. Available at URL: http://www.niehs. Matthews HB. Toxicological profile for di-n-butyl phthalate update [online].atsdr. 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. Kessler et al. Slakman AR. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.. 2005. Environ Health Perspect 1997. pp.. The monoester metabolites are thought to mediate toxic effects for some of the phthalates.. J Chromatogr B 2004. 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. Drug Metab Rev 1989.805:49-56.e. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.cdc. 2006). Mackay D. Hauser et al. 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. Massey RC.gov/ toxprofiles/tp9. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . van der Broek PH. Hoppin et al. Pharmacokinetics. gender. 2003. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. 2007. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. but there are known species-related differences in the hydrolysis of diester phthalates.. 2004..gov/ reports/index. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. and Sertoli cell abnormalities in the male animals and. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 105:734-742. interactions with macromolecules and species differences in metabolism of DEHP. Dirven HA. 2000b. Assessment of critical exposure pathways. testicular atrophy. 2004). phthalates have been shown to induce peroxisomal proliferation in rodents. Silvapathasundaram S. 2004. Herbert AR. Springall C.. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. 2001. References Agency for Toxic Substances and Disease Registry (ATSDR). Clark K.gov/toxprofiles/ tp135.html). 2001). Calafat AM. which may be a pathway to the development of liver toxicity and cancers in these animals. 2004. Population estimates of concentrations of specific phthalate metabolites may differ by age.gov/toxpro2. Lovekamp-Swan and Davis. reducing estrogen production. 2005). 2006). Schroeder JL.cdc.html.. Part Q: Phthalate Esters. Metabolism of di(2-ethylhexyl) phthalate.html. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 2002. 1982). Hauser et al. Connor C. 1985. Information about external exposure (i.cdc.. 2003. Evaluation of a recombinant yeast cell estrogen screening assay. Rhodes et al.45:19-25.3.html. 2002).. Scotter MJ. Jongeneelen FJ. In animals.. Peck and Albro. Springer. Castle L. Available at URL: http://www.18(12):10681074.. Coldham NG..New York.. Jordan S.Phthalates and metabolites have been tested. 2002). Needham LL. phthalates produced anti-androgenic effects by reducing testosterone production and. Dave M. 2007). A biomarker approach to measuring human dietary exposure to certain phthalate diesters. at very high levels. McKee et al. McDonnell DP. Albro PW and Lavenhar SR. NTP-CERHR. 1982. 1986). High doses of di2-ethylhexyl phthalate (DEHP). 2000c. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). 4/20/09 Albro PW. Vol. In Staples CA (ed). 2004.21:13-34.. Anderson WA. Sauer MJ. dibutyl phthalate (DBP). Food Addit Contam 2001. Corbett JT. 2000a. ovarian abnormalities in the female animals (Jarfelt et al. Cousins IT. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. at higher doses.

Environ Health Perspect 2003. Akesson B. Environ Health Perspect 1997.nih.111(2):139-145. Leffers H.195:142-153. Reynolds T. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.niehs.nih. 6/2/09 Okubo T. Int J Hyg Environ Health 2007. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Reprod Toxicol 2004.niehs. Anal Bioanal Chem 2005. Brock JW. Skakkebaek NE. Hauser R. Bolte G.382:10841092. Yokoyama Y.18(1):122. 2000a [online].112(17):1734-1740. Environ Health Perspect 2004. Jobling S. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Butala JH.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. 6/2/09 NTP-CERHR. Stringer WT.210:21-33. Ladefoged O. Zhang S. et al.niehs. Toxicol Appl Pharmacol 2004. Mortensen GK. David RM. 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Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Hanaoka T. Int Arch Occup Environ Health 1993. Determination of phthalate monoesters in human milk. Biol Pharm Bull 2003. Nielsen J. Main KM. Numtip W. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Boehmer S. Pan G. Environ Health Perspect 2002. Duty S. Hauser R.16(4):487-493.25(2):293-302. Environ Health Perspect 1995. Hartle RW. Davis BJ.Phthalates in human urine samples.gov/chemicals/dehp/dehp-eval. Environ Health Perspect 1998. Reprod Toxicol 2005. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. 2000b [online]. Scand J Work Environ Health 1985.html. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Chen Z. Gans G. Suzuki T. Balasubramanian AV. Tsukino H. 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4 (10. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.4) 108 (96.3-82.6-92.6) 13.4) 80.0 (34.5) 82.6) 63.5) 15.3) 13.1) 76.6 (12.1-120) 52.5-41.8) 28.0-85.5-25.7-170) 169 (134-198) 152 (99.2-19.8-41.2 (43.9-27.3-18.8-16.4-16.2-17.5) 16.4) 14.4) 75th 35.3 (54.9) 49.8 (14.9) 15.3-125) Total 15.3 (44.3-74.0 (11.2-116) 122 (102-143) 101 (84.2 (11.6 (13.1 (10.3-130) 122 (88.2-183) 101 (78.4-127) 80.7-58.8-76.3 (12. Food crops take up BzBP.6-92.8) 33.0) 70.9) 11.0 (43.6-72.6 (41.7) 40.0-106) 58.4 (63.1) 67.8 (50.0) 20.7-172) 103 (74.8 (12.4) 33.2) 33.2-39.6-17.1) 12.9 (21. 2004.4-25.0 (15.1-116) 122 (93.S.2-155) 91.3-161) 99.9 (39.0) 23.7-16.1 (14.6 (66. and 03-04 are 0.0) 34.1 (13. car care products. interval) 15.2) 15.1-15.2 (25.0 (23.8-35.1-90.9-49.0 (26. High dose BzBP and its monoester metabolites.6-38.5-18.2-38.6) 13.3 (22.4) 12.7-13.8-14. 2000).1) 13.6-79.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.8 (71.7-16.4 (53.3-91.4-92.0 (20.9-190) 86.1.9 (22.2-16.4) 35.8-64.4 (13.5-14. IARC considers BzBP not classifiable with respect to human carcinogenicity.6) 35.1 (55.4 (10.5 (66.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.3-43.9) 18.9 (11.4) 98.6-43.8) 14.6-39.3 (30.1-38. vinyl tile.5) 55.1) 68.4) 65.5-94.9-62.4-62.1 (32.8-17.6-150) 94.3) 37.2) 14..1 (13.5-62.8 (30.9 (16. 262 Fourth National Report on Human Exposure to Environmental Chemicals . 2000).0 (30.4 (32.6) 95th 103 (94. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (27.8-16.8-14.3) 13.5 (13.9 (12.6-132) 103 (84.2 (14.7) 38.2 (19.5) 27.6-29.0-55.5) 23.7-35.3 (13.2-31.7 (51.5 (27.8-72.9-47.6) 67.S.8) 24.5-145) 138 (106-241) 143 (127-179) 120 (99.9-14.5-84.8 (53.3.4) 71.3-18.3-75.5-97.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 69.4-24. particularly male animals (McKee et al.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 13.8 (71. 0. population from the National Health and Nutrition Examination Survey.6) 37.1-39.9 (12.8 (80.6) 24.7-119) 99.4) 35.2) 14.7 (13.8 (10.4) 81.2-33.9-87.8-98.9 (13.4 (32.3 (12. some personal care products.2) 13.1) 31.5 (26.9) 14.7 (53.8 (21.0) 90th 67.3-34.5 (76.9-16.0) 33.5-33.5) 65.2) 22. and to a lesser extent.6) 15.1-16.4) 38.6) 16.4 (48.6 (13.3) 94.8-17. 01-02.0 (12. NTPCERHR. respectively.2-16.3) 63. because it is not bound to products in which it is incorporated.0 (33. BzBP can be released into the environment during its production and.9 (70.0) 24.2-115) 113 (91.8. it can be released into the ambient air during use or disposal of the products.6 (13.3-88.9) 13.8-121) 79.3 (12.2) 17.0 (14.6) 25.7-15.6) 29.6) 14.2 (10.1-214) 166 (116-191) 145 (110-213) 88.1 (14.9-30. and 2003-2004 were generally similar those reported in U. 2001-2002.3) 15.2 (47.2) 32.7 (80.8) 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 16.5-35.6) 50.2) 78.9) 43.6 (13.5 (47.5) 30.9) 14.7 (70.0) 32.4 (31.8 (38.9 (28.8-133) 89.2) 12. and diet is the major source for general population exposure.5-36. see Data Analysis section) for Survey years 99-00.7 (15.7-16. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1-18.1-43.4 (68. and 0.7-17.1) 14.6 (32.0-26.5-40.3 (29. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.8-18.1 (58. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.1-61.9) 12..7 (82.4 (29.2-20.8) 63.6-116) 122 (102-142) 101 (85.7 (12.7-25.3-21.0 (15.0 (30.6 (53.1-35.3 (29.2 (19.0 (55.0) 16.8 (86.1-16.1) 29.5 (57.6) 14.4 (53. sealants.5) 15.7) 23.6-18.1 (19.7 (11.3) 54. can produce developmental and reproductive toxicity in rodents.5-36.4) 49. including MBzP.5 (55.1) 32.2) 66.0-130) 101 (86.7-82. residents (Blount et al.6) 35.4-15.3 (33.3) 23.3-12.1 (20.5 (67.4 (59.6 (21.1-15.1) Selected percentiles ( 95% confidence interval) 50th 17.5 (61.7-14.4 (27.8-48.4) 129 (98.9-28.3-27.8 (28.8-13.Phthalates Benzylbutyl Phthalate CAS No.4) 51.2-40.

7-12.4) 60.9) 52.1 (13.9-16.8 (11.9-104) 62. Weuve et al. 2003).7-69.6-81.9-83.0) 12.4-99.5) 17.5 (9.2) 32.4-116) 73.3-64.0 (10.7-20.8 (57.6 (22.4-79.8-27.1 (41..2) 11.4) 15.5 (10.3 (35.5) 23.7 (12.2-78.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .1) 12.9) 24.7-61. In NHANES 1999-2000.6-99.3) 37.7) 25.4 (11.9) 100 (80.7-31.. A small study of African-American women in Washington.5) 41.9 (39.2 (27.5) 20.4-15.4) 21.9) Total 14.9 (10.0 (33.8-13.1) 24.7-397) 70.95-14.7) 11.8-173) 195 (121-305) 229 (99. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6 (11.3) 13.8) 68.9 (55.3-11..6) 12.4) 14.5 (56.3) 13.8) 26.8) 108 (75.5) 10.7-14.6-12.1 (15.1-35.6) 30.4-42.4) 13. in young Swedish men (Jonsson et al.8) 16..8-16.6 (36.2) 15.5-58.6) 58.0-90.6) 73.7) 19. 2004).0-26.6) 53.5) 16.7 (54.1 (53.4 (10.2-15.0 (49.3-38.1-79.7 (11.4 (13.9-14.8-14.1 (46.5-16.8-64.5-58.0 (12.4-18. and females compared to males (Silva et al. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al. in men attending a Boston infertility clinic (Duty et al. 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.3) 36.8-15.3 (23.2) 12.1) 80. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7-20.0-15.6) 25.5-26.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.4-142) 134 (116-176) 136 (85.0 (11.8-14.4 (34.0) 24.9 (22.3 (60.9 (51.7-14.1 (43.2) 11.9 (12.3) 21.1 (21.3 (38.6-40.6 (30.4) 104 (89.8) 15.5-76.5-38.4 (21.6 (11.1 (34. and in a small sample of German residents (Koch et al.2 (41.8-34.8-15.7) 46. 2005).1) 39..9) 11.5-61.1 (18.8) 56.4) 90th 50.8) 13.2-26.0 (41.6 (24.4 (46.2-13.7 (38.8) 24.3) 14.5 (12.7 (18.9-69.8) 71.2-12.8) 33.1-125) 86.9 (54.0 (12.4 (25.4 (74.6 (14.2-15.69-11.3) 18.6-20.1 (21.8 (10.0) 60.1) 27.9 (24.9 (10.0) Selected percentiles ( 95% confidence interval) 50th 13. 2006).8) 33.4-60.8 (12.6 (30.2 (69.9) 64.0) 49.3) 14.3) 73.7 (11.6 (51.6) 13.4-17.0 (13.1-27.3 (24.8) 34.2) 11.3) 29.3-34.9) 12.3) 16.8-13.1 (21.3) 67.7-19.4) 17.9-28.6-26.8 (69. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.1) 35.7-19.1 (25.0-53.1 (19.9 (24.9-23.9 (15..1 (13.4-27.6-15.1-12.8 (30.4) 50.5-31.9 (12.5-213) 49.7-15.8 (64.Phthalates York City (Adibi et al. 2004.1-58.0 (67.3) 13.9) 11.8-48.8-69.7-90.7 (13.9-40.1 (21.1-120) 77. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.8 (50.4) 12.4 (33.4-14.6-116) 74.2-51.3 (39.0-109) 65.0) 11.9 (15.9-13.9 (43..3 (12.1) 24.8-85.6 (19.6 (15.2-13.5 (35.7 (23.5 (42.8) 46.6-13.6 (11.2-57.1-12.5) 78.8-39.2-49.8-60.0 (41.8) 11.6 (34.5 (49.7 (21..3-16.0-27.8-42.6) 75th 25.9-13. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.5 (10.6-47.3) 89.2-21.0) 24.4 (60.7 (55.7 (59.1-29.7-123) 77.4-93.4) 51.8-80.7-15.3) 55. 2007). population from the National Health and Nutrition Examination Survey. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al. Hoppin et al.4 (26.1 (9.4) 25.5 (48.7 (19.6) 12.7 (13.1) 142 (99. 2002).9-115) 57. 2005.5 (11.8) 80.3 (15.4 (11.3) 12.8) 53.0) 15.0 (38.5) 95th 77.7 (14.9) 42.1) 23.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.8 (46.0) 13.S.4 (11.8 (13. 2003).5-23. Hauser et al.6 (57.5-29.7) 56.5) 13.0 (62.6-86.9 (29.6) 38.4) 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. 2007).5) 46.4 (63.1 (11.4) 28.7-56.1) 17.8) 53. 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. 2002.9 (9.0-48.1 (14.4-102) 70.2 (56.5) 14.9) 12.5-79.5-26.2) 67.9) 12.7) 38. interval) 14.73-12.4-90..1-14.7-29.3) 90.2-17.3-73.4) 44.8-13.4-23.3 (13.4 (12.5-99.8) 54.1 (23. In an annual sample of German university students.4-14.5-57..2 (40.5-13.0-51.4) 13.4 (69.7 (11. adolescents compared with adults.9-62.8 (49.2) 26.4-19.5-42.2-117) 95.

Weuve J. Hu H. et al.niehs. Blount BC.16(4):487-493. Wiesmuller GA. Duty S. Sanchez GN. Silva MJ. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Levels of seven urinary phthalate metabolites in a human reference population.S. Silva MJ.210(3-4):319-333.nih. Prenatal exposures to phthalates among women in New York City and Krakow. Jonsson BAG. Brock JW. Caudill SP. Jedrychowski W. NTP-CERHR. Helm D. et al. Gans G. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Atlanta (GA). Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Green RA.25(2):293-302.Phthalates References Adibi JJ. Hum Reprod 2007. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.22(3):688-695. Angerer J. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.112(3):331-338. Drexler H. Environ Health Perspect 2002. et al. Jacek R.18(1):122. Environ Health Perspect 2006. Rossbach B. Environ Res 2003. Available at URL: http://cerhr. Needham LL. Barr DB. 2000 [online].111(14):1719-1722.108(10):979-982. Davis BJ. Richthoff J. Calafat AM. Environ Health Perspect 2004. Camann DE. Butala JH. Reproducibility of urinary phthalate metabolites in first morning urine samples. McKee RH. Int J Hyg Environ Health 2007. Hodge CC. 2005. Hilborn ED.110(5):515-518. Singh NP. Brock JW. Barr D.114(9):1424-1431. Giwercman A. Eckard R. 112(5):A270]. Third National Report on Human Exposure to Environmental Chemicals. Dobler L. Hagmar L. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Rylander L. et al. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Centers for Disease Control and Prevention (CDC). Hoppin JA. Malek NA. Ryan L. Schettler T. Perera FP. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Koch HM. Needham LL. Research Triangle Park (NC). Caudill SP. Poland. Epidemiol 2005. et al. et al. Sampson EJ. Silva MJ. Phthalate monoesters levels in the urine of young children. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Duty SM.html. Baird DD.93:177-185. J Androl 2004. David RM. et al. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.68:309-314. 4/20/09 Silva MJ. Wittassek M. Calafat AM. Hauser R. Caudill SP. Ryan L. Reidy JA. Pirkle JL. Bull Environ Contam Toxicol 2002. Urinary levels of seven phthalate metabolites in the U. Koch HM. Chen Z. Reprod Toxicol 2004. Environ Health Perspect 2003. Environ Health Perspect 2000. Silva MJ. Meeker JD. Brock JW.

6 (14.63) 3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.6) 26.10 (3.2-22.S.46 (2.55 (3.3-20.40-3.30-13...1 (13. Survey Geometric mean (95% conf.20 (7. Fourth National Report on Human Exposure to Environmental Chemicals 265 . Koch et al.40-12.80 (3.7) 18. DBP can produce reproductive toxicity in male rodents (McKee et al. Hauser et al.6 (9.40-4.3-18.60 (5.6) 17.11-3. 2000).6 (29.3) 33.10) 2. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.40 (2.80 (5.3-43.40 (3.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.0-38.2-14. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.84) 4.00) 10.97-7.20-9.5-29.00-11. and in a small sample of Japanese adults (Itoh et al.20-6.10 (4.26 (2.72-3.56-4.70-4.60-6.00) 6.7 (17.00) 4.30-2.55) 2.6 (13.49-2.7 (18.50) 2. Studies of children found age-related differences in urine MBP levels.7-20.81 (3. they have been referred to as monobutyl phthalate (MBP). 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.22) 3.90 (6. When total DBP metabolites have been measured.00-6.10-9.90) 12.71 (2.40-17.56 (3.2) 5.0-18.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.5 (10.5) 22.73 (2. 2007).5-16. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine. mostly as MnBP (Anderson et al.2 (11. in a small sample of pregnant women in New York City (Adibi et al. 2004.2-33.70-4.22 (3.3-30.4-12.8) 677 652 703 699 1216 1088 Limit of detection (LOD.30-6. and insecticides.19-3.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.90-4..30) 10.9) 10.0 (13.6 (10.97) 4. about 65% to 80% of a dose is eliminated in urine within 24 hours..1-17.3 (18.5) 14.85-6.50-10.44-2.3 (11.90-4.8 (9.80 (5.46 (3.20-12.50-2.1-20.10 (4.6) 10.3 (16.5) 18.7) 14.10) 8.6) 12. 2000.20-2.0) 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 2.7) 7.5) 19. 2004.3-24.4 (20.2 (12. 2003).40 (6.70-8.6) 16.40-3.80 (2.56) 3.3 (13.3) 3.5) 25.6) 16.00) 4.4) 12.66) 2. in men attending a Boston infertility clinic (Duty et al.6 (14.5) 12.6) 17..48 (2.30-3.1) 16.91) 4. residents (Blount et al. 2005.70) 5. 2005).8) 21.3-19.10) 11.1-12. 2003).3) 18. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.90-7.02) 4.4) 22.67 (5.00-6. population from the National Health and Nutrition Examination Survey.4) 5. In addition.9 (16.50 (6.40-4.90 (3.40-5.80 (2. 2005).50) 18.7-18.90 (4.0 (19.9) 15.3 (13. 84-74-2 Di-isobutyl Phthalate CAS No.00 (7.0 and 0.30-11. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC. Following oral administration of DBP to humans.. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.5 (20.7-31.8) 40.50) 5.37) 6.4 (14.30 (1. CDC.7 (7.20-12.7 (9.17 (2.82-3. and also in some printing inks. 2001).2 (8.30) 2.96) 3.7 (16.5) 23.80-5.9-23.46-5.60 (2.00-9.1 (8.6-18.3-48.10-9.73-5.6 (13.9-14.30) 5.68 (2. NTP-CERHR.80) 75th 5.30-6. 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. OSHA has established a workplace air standard for external exposure to DBP.50 (3.6-34.0 (11.30 (3.0) 24.60 (4.10) 9.3.00) 7.30) 10.7) 15.5 (17.0-25.0) 20.60 (8.9 (16. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.90-2.4-27.50-6.28-5.80-5.10) 3.24-8.7) 4.5-24.60) 3.56 (5.07 (3.50) 8.0 (13.20) 4. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.6-20.7-31.46) 2.3 (16.5-16.10-2.20 (6.20 (3.7 (17.00 (5.5) 18.30-7. pharmaceutical coatings.40) 5.5 (27.0) 12.20) 7.50) 90th 12.Phthalates Di-n-butyl Phthalate CAS No.6 (10.50-4.00-4.59) 3.17) 4..40 (7.1) 22.40 (2.0-14.0) 13..70 (2.30) 6.3 (19.43) 6.S. 2005).97) 2.6-26.33 (2.6-14.50) 7..0) 9.30 (4.70 (5.70) 3.1-25. interval) 2. Biomonitoring Information Median concentrations reported in the NHANES 19992000.90 (4.5 (11. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.40-9. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.6 (11.1) 25.

79 (4.20-2.3) 13.1-24.33 (3.53-4.84 (8.17-12.30) 2.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.5 (11. ranging from more than one-tenth the NHANES median (Itoh et al..7) 11.5) 13.1 (11.80) 7.1-15.7 (11.76-3.68) 3.97-2.32 (3.2 (11. to about two to fourfold higher (Fromme et al.89) 6.38 (6.76 (3.6-19.76-15.76-3. Between 1998 and 2003.02-10.31) 2.54) 2.6 (8.83 (2.56-15.89 (3.21 (5.1) 15.41 (2.09-2.0 (8. 2007).57-4.55-6.11 (5.S. samples from German university students had consistently higher median urine levels of MnBP and MiBP. 2005).92 (7. than adults in NHANES subsamples during the same time period.4-16..18-4.5) 15.08-2.69) 4.9 (11. interval) 2.24) 3.0 (12.75 (6.22 (2.72) 5.33) 3.43) 3.6) 11.64-7.3) 16.33-9. while MnBP declined (Wittassek et al.0) 15.9-16.69) 6.6 (9.81 (6.51) 2.93-6.56) 5.20-3.35) 3.00-3.10-5.58-3.80-3.86) 6.18) 4.94 (5.9 (9.05) 2.98 (2.04) 7.62 (6.85 (2.64-7.99) 7.84 (4.29-8. 2004).2-13.28 (4.6 (10.20-4. 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.7 (9.95-3.36-7.88 (2.8) 10.8-13.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .2) 9. 2005).78) 9.and gender.1) 7.4) 7..65 (4.6 (8.80 (3.68 (2.52-20.20 (2..36-2.0-18.91-6.54 (2.54 (4.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.11-2.51) 5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In an analysis of NHANES 1999-2000.2-15.0 (10.8 (8.6 (12.8-18.3) 28.39-3.8 (10.62-12.26 (2.46-11.86-4.46 (2. Over this time.7) 19.5-19.95) 10.81) 9.73 (5.31) 2.9 (15.26-2. Survey Geometric mean (95% conf.4 (12.18 (1.34 (3.18-10.18 (4. 2002.2) 24.. the students’ median values for MiBP levels remained relatively unchanged.9-40.25) 5.52-3.0) 11.17 (2.03 (5.0) 3.28-13.1) 10.6 (15.00 (3.07-5.21) 10.8-36.2) 8.1-12.04-5. up to four and 13 fold.4) 15.45) 3.31 (7.52) 3. Biomonitoring studies on levels of MnBP and MiBP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of dibutyl phthalates than are found in the general population.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.44 (3.66) 10.65-4.66 (8.04) 3.53-3.7-28.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.19 (2.67-5.0) 7.00-7.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.47 (3.32) 7.72-7.8 (9.64-10.68) 5.42) 2. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.07 (2.8-18.59 (4.20 (7.46) 3.37) 3.01-2.7 (21.03-7.02 (7.38-10.95) 2.6) 13.53-5.1 (10. 2004).7 (13.51) 15. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.81 (3.66) 4.74-3.81) 4.20 (2.1) 13.32 (7.75 (4. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.1) 4.18) 3.6) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.47-12.56) 2.47-5.58-4.30 (6.57 (3.27-12.1-25.69-7.56-4.96 (3.65-11.29-3.74 (4.1) 11.61-3.82) 4.94-12.94) 6.78) 8.43) 3.9) 12.39) 5.17) 90th 8.13-6.3 (13.00-3. population from the National Health and Nutrition Examination Survey.79-8. Weuve et al..14 (4.79-6. 2007).89-5. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..08) 75th 4.78-8.69 (2.2 (10.43) 3.3 (17.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.66) 2. 2006).57 (3.33 (2.99-4.15) 3.7) 10. respectively.82 (4.4) 23.31 (2.9-26.7) 3.3) 13.15-4.5 (9.13 (2. An analysis of NHANES 2001-2002 showed similar age.3) 18.52 (2.6-19.11) 5.03-11.

2 (18.2-56.7) 52.0) 120 (98.2 (21.0 (78.1) 36.6-29.0-21.S.2) 68.6-113) 108 (90.0-58.3) 24. referred to as monobutyl phthalate (MBP).3) 26.1 (36.3 (51.5-53.8-22.3 (37.9-53.1 (62.6-48.2-49.5-47.8) 23.7 (70.6-69.5 (59.5 (28.2 (74. 01-02. 1.1) 47.5 (59.0 (31.0 (23.0-24.5) 17.7 (51.0-19.5-121) 106 (94.1-20.8-25.0 (15.5) 37.6) 35.4-42.6-37.4) 20.3) 40.9) 18.9-101) 77.6-143) 127 (99.3-40.7-106) 69.5-60.9-92.4-159) 107 (84.2 (78.7 (28.6 (55.6-40.7-26.7 (43.5) 24.2) 32.5) 85.6 (44.5) 36.9-114) 116 (97.0 (25.7) 92.2 (20.7) 42.9-22.0 (30.2 (58.5) 47.1) 23.3-96.7-34.5) 95.9 (17.8-119) 90.6-33.6) 38.9) 75.3 (30.5) 31.0-32.5) 34.0 (72.1-29.4 (72.9) 36.1) 30.1 (16.7-53.1 (41.8-29.5 (74.9 (79.5-47.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.1-22.0-24.7 (64.7-91.1 (26.4) 52.4 (38.6 (65.9) 26.0 (18.1 (58.7 (18.2-32.8 (57.2-114) 73.7-34.0-19.6 (19.7 (16.2) 90th 98.6 (48.5-117) 95.3 (30.4) 22.0-26.7-20.9) 29.6-44.2) 20.2-63.0) 27.4 (25.2 (79.6) 20.5-44.6 (22.3-145) 85.4 (84.6) 71.5) 78. *In the 1999-2000 survey period.7 (38.7-42.6-49.2-159) 92.1.3 (17.0) 20.2 (25.6 (32.9 (17.1) 20.7-24.0) 38.4-26.8) 58. respectively.4 (35.8-132) 95.5 (30.2-87.4-25.9) 71.8) 19.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.6-31.2 (21.2-93.3-85.5-43.6) 46.6 (61.9-33.2 (75.2-23.3-67.3) 18. population from the National Health and Nutrition Examination Survey.8) 43. interval) 24.1 (19.1) 19.1) 17.3) 19.9-22.8) 48.7-121) 97.5) 20.0) 30.5) 21.6) 21.4 (21.1 (51.1-51.7-111) 64.3 (42.0) 84.7 (18.4-44.6 (26.0 (36.6) 80.4-31.6) 17.6-20.2-22.1) 23.8) 75th 51. and 0.1-92.2) 26.2) 42.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.4-18.3 (23.3-136) 137 (107-162) 119 (90.0) 21.7) 124 (98.3-21.9 (20.9) 46. and 03-04 are 0.4) 59.1-75.6 (16.9 (79.1 (19. Fourth National Report on Human Exposure to Environmental Chemicals 267 .2 (19.7-116) 95.1 (17.4 (35.4-60.7 (33.6-24.1 (34.4) 64.4-20.6-36.9-28.1) 23.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.1) 31.5) 65.4.5 (29.3-79.3) 21.0) 117 (104-131) 112 (84.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94. Survey Geometric mean (95% conf.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.5) 26.8) 62.8-42.7 (22.2-24.4 (35.2 (59.3-24.0 (17.5-27.8-123) 101 (90.3-76.0 (20.3 (60. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1-24.8 (19.5-42.7-117) 118 (108-143) 93.1-82.3 (23.5) 19.4 (19.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.6 (90.7) 74.3 (36.3) 23.1) 25.1 (21.3-60.2-33.7) 28.3 (56.1 (54.2 (17.0 (45.0) 31.7-127) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 22.4 (71.9-87.7-42.9-42.2-21.1 (31.1) 46.1-80.7-92.0-51.1 (19.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.6) 39.1 (28.6-29.4 (23.7 (19.1 (18.0-73.3) 36. see Data Analysis section) for survey years 99-00.2) 62.9.4 (36.2) 38.1-27.9) 21.4 (35.5) 36.9-79.1 (19.5) 40.7 (24.

3) 59.4 (68.0 (61.4 (31.4-65.8) 20.4 (19.9) 91.3-40.3 (76.2) 16.3-78.3-32.4-164) 96.3) 17.7 (43.5-16.1) 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 17.5 (15.5) 17.8) 28.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 (27.9) 39.2-27.6) 65.0) 53.4-47.6) 39.2-73.4-135) 71.7 (60.6 (17.8-23.3 (48.6 (74.3-39.3 (46.8-32.8) 63.4-72.7) 42.4) 21.9-38.6-42.8) 20.6 (72.0) 19.3 (17.3-49.6-92.7 (60.4 (31.4-76.3-20.1-83.3-23.4) 19.6 (19.8 (17.9) 62.7-51.6 (27.3-106) 74.9-100) 86.6) 37.0) 28.4 (18.1 (21.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.2) 59.6 (57.1) 20.6-32.3-38.6-22.9 (56.0 (20.4 (37.7-19.8) 17.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.9-49.3 (24.3 (28.9-36.3) 20.2-22.0) 59.0 (26.9 (58.9-26.3-21.6) 14.0) 108 (71.9-105) 85.0 (69.2-16.1) 61.0) 70.1 (46.5-15.6-44.3 (55.9 (39.7 (12.9-84.2-28.4 (16.9) 24.5-41.6-26.0 (15.8) 35.1) 22.3-21.8-43.3-26.5) 84.8) 75th 38.6-74.6 (41.7) 19.0-17.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.9) 52.8 (13.2 (16.3 (42.3) 19.9-14.1 (29.3-71.5-18.2-179) 84.7 (57.2 (19.3 (16.8 (33.0) 29.4) 53.2 (35.S.2) 31.4 (33.1-23.7 (19.5-142) 89.8) 30.0 (71.4-24.8-235) 137 (108-198) 88.7-78.7-21.4) 15.6-23.2) 21.6) 38.3) 67.8 (65.9 (37.3 (17.6) 34.0) 26.0 (52.7 (20.3) 33.4) 16.5) 90th 68.9-56.6) 31.1) 42.0-90.5-22.6) 25.9-68.8) 23.2) 74.2-86.6-23.9 (30.5 (30.3) 33.8-24.9) 28.6-53.3 (71.3) 52.4 (17.5) 39.6 (25.3) 21.7) 20.0) 75.1) 21.3) 35.6) 83.8) 13.0) 55.2-106) 64.6) 24.9 (16.1 (56.1-32.6-24.6-50.8) 22.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9 (21.1) 50.7-28.7 (81.7-37.8 (25.3 (69.2-22.6-155) 91.2 (83.6-16.9-68.9 (20.5 (18.6) 23.3 (17.4 (23.0-41.6 (29.2) 65.0 (16.6) 18.6-128) 96.1) 37.6-24.0) 94.0-19.3) 19.7-23.3 (52.6 (25.1-21.1 (61.3-18.3 (19.3 (52.7-20.1 (32.5-23.7-42.2 (38.8 (18.6 (61.9) 30.1 (15.5) 60.3 (60.4-131) 81.9) 19.6-28.8) 34.9) 20.0-75.2 (19. population from the National Health and Nutrition Examination Survey.6) 24.6) 64.5-30.1-99.0-113) 104 (83.9 (30.7 (54.2-18.8 (18.7) 36.4 (45.8 (22.7-80.5 (81.5 (18.7-19.0) 25.0 (19. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0 (18.3-81.5-64.1) 35.3) 18.8) 19.0-60.8) 17.6-119) 63.0-38.3 (21.4 (50.1-62.9) 14.9 (64.2-61.9 (35.4 (50.5-76.2-48.3-17. interval) 22.2) 159 (102-263) 147 (93.5) 21.0 (34.7 (14.4 (13.6 (31.6-44.8) 17.0-47.4) 51.0 (50.0 (18.0 (27.5-70.8 (16.9) 49.4 (16.8 (50.2-85.7-39.9 (35.5) 134 (93.4 (56.4-61.5 (64.5-21.8 (18.1-128) 97.9 (30.4) 15.4-103) 117 (83.0 (43.7 (73.5-142) 81.4 (53.1) 17.5) 91.4-34.4 (31.2-21.1-18.0) 81.7 (28.4 (47.0) 41.6-43.7-26.5-37.8) 40.0-92. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1) 44.9 (19.5) 82.8) 34.1 (34.1) 53.9 (73.4 (20.7 (16.2-108) 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.6-19.0 (70.9-70.5 (14.6-27. Survey Geometric mean (95% conf.8-24.4) 62.0) 35.4) 20.1-99.2-22.4 (17.9-34.

Gans G. Jonsson BAG. Drexler H. Brock JW. Atlanta (GA).18(1):122.22(3):688-695. Environ Health Perspect 2004. et al. Boehmer S. Massey RC. Bull Environ Contam Toxicol 2002. Chen Z. et al.111(14):1719-1722. Fourth National Report on Human Exposure to Environmental Chemicals 269 .93:177-185. Reprod Toxicol 2004. Jedrychowski W. Helm D. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Silva MJ. et al. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Silva MJ.16(4):487-493. Hum Reprod 2007. Calafat AM. Caudill SP. 4/20/09 Silva MJ. Hodge CC. et al. Caudill SP. Urinary levels of seven phthalate metabolites in the U. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Hagmar L. Int J Hyg Environ Health 2005. Castle L. Levels of seven urinary phthalate metabolites in a human reference population. Malek NA. Sampson EJ. Koch HM. Hu H. Prenatal exposures to phthalates among women in New York City and Krakow.210:21-33. Angerer J. Duty SM. Rossbach B. Poland. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Silva MJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Ryan L. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Perera FP. et al. Dobler L.108(10)979-982. 112(5):A270]. Giwercman A. Singh NP. et al. Phthalate monoesters levels in the urine of young children. Drexler H. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. NTP-CERHR.25(2):293-302. Available at URL: http://cerhr. 2005.208:237-245. Barr DB. Needham LL. Eckard R. Scotter MJ. Needham LL. Anderson WA. Centers for Disease Control and Prevention (CDC). Pirkle JL. Brock JW.210(3-4):319-33. Reidy JA. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Itoh H. Research Triangle Park (NC). Rylander L. Springall C. Meeker JD. Environ Res 2003.gov/chemicals/ phthalates/dbp/dbp-eval.nih.html. Calafat AM. Masunaga S. Koch HM. Silva MJ.112(3):331-338. Third National Report on Human Exposure to Environmental Chemicals. Fromme H.niehs. Caudill SP. J Androl 2004. Hilborn ED.114(9):1424-1431. Environ Health Perspect 2006.18(12):10681074. Camann DE. Wittassek M. Hauser R.S. Blount BC. et al. Food Addit Contam 2001. 2000 [online]. Barr D. Environ Health Perspect 2000. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Bolte G. Int J Hyg Environ Health 2007. Schettler T. Sanchez GN. Koch HM. David RM. Wiesmuller GA. Green RA. Environ Health Perspect 2003. et al. Weuve J. Richthoff J. Epidemiol 2005.68:309-314. Jacek R. Angerer J.Phthalates References Adibi JJ. Butala JH. Ryan L. Int J Hyg Environ Health 2007. Urinary phthalate metabolites and biomarkers of reproductive function in young men. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. McKee RH. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Duty S. Yoshida K.

20) .400 (.300 (.10 (<LOD-2.400) 1.400-.200-.600) .3.200 (<LOD-.500 (.500) 1.500 (.500) < LOD 1.300-. 01-02.500 (. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.400-.600 (. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.400 (.300-.700) .500) .300-.300 (.400-.400 (<LOD-.600) < LOD .500 (.400 (.500 (. resins.400-. and 03-04 are 0.300 (. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.00 (<LOD-1. see Data Analysis section) for Survey years 99-00.400) 1.300-.500) 1.300-. 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.50) .200-.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively.500) .70) .500 (.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 .300 (.S.10) .400 (.00) .300) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.00 (<LOD-1.10 (<LOD-1.500-.400-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300) < LOD .300-.700) .300 (.500) < LOD < LOD .200-.500) 1.400) < LOD < LOD . Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.00-3.400 (.400) < LOD 1.600) .9. < LOD means less than the limit of detection.600) . which may vary for some chemicals by year and by individual sample.300 (.Phthalates Dicyclohexyl Phthalate CAS No. only levels at or above the 90th percentile could be characterized.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 1.400 (.00-2.500 (. and polymers.2.500) .300-.00 (<LOD-1.10 (.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70) . including nitrocellulose.400 (<LOD-.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.500) < LOD < LOD .400-.400-.400 (<LOD-. polyvinyl acetate.700) .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-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.900-1.200-.500 (.400 (. In this Report.80) .400 (<LOD-.600) .90) .300 (<LOD-.70 (1.500) .70 (1. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.200-.600) .300 (.300-.500 (.10 (<LOD-1. 270 Fourth National Report on Human Exposure to Environmental Chemicals . and 0.200-.300-. and polyvinyl chloride.

18) .54 (<LOD-2.690-1.630 (<LOD-. Survey Geometric mean (95% conf.06) .910 (.800-1.S.740) .43 (1.910 (.770-1.630 (<LOD-.530-.470) 3.420-.370 (<LOD-.270) < LOD .22 (<LOD-1.34) .490) .44) .480 (.510 (.530 (.330 (.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 (.400-.910 (.940 (.410 (.380-.400-.250 (.770 (.610 (.16 (<LOD-3.590 (.53) .16) .310-.590 (<LOD-.36-1.660) .470 (.910 (.770) < LOD 2.240-.500-.510-.390 (.950 (.11) .14 (<LOD-3.350-.660) < LOD < LOD .450 (. population from the National Health and Nutrition Examination Survey.260-.880 (.00 (<LOD-3.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .770-1.67 (1.05) .500) 3.690) < LOD < LOD .82) .06) .560) 1.690 (.620) < LOD .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.220 (<LOD-.690) < LOD 2.740) < LOD < 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 .54-6.530) 1.670-1.530-1.82 (1.12-1.330 (.360-.710) .830) 1.170-.420-.74) .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.10) .380 (.290-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33 (<LOD-3.420-.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 1.17) .53) .450 (.310) < LOD .33) .00) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. Fourth National Report on Human Exposure to Environmental Chemicals 271 .770-1.670 (<LOD-.790-1.54) .

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. 01-02. shampoos. 2002).3 (74. 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. population from the National Health and Nutrition Examination Survey.7) 71.4 (62.9. 0. and also in men attending a Boston infertility clinic (Hauser et al. deodorants. particularly those containing fragrances. 2001-2002. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. and 03-04 are 1. colognes. and hand lotions.4. 2003) and African-American women in Washington. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. 272 Fourth National Report on Human Exposure to Environmental Chemicals . 2007). DC (Hoppin et al.. 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.S.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.Phthalates Diethyl Phthalate CAS No.2..9-92.1 (71.7 (70.3 (82.1-93. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. Products that may contain DEP include perfumes. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. 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. and 0. respectively. Biomonitoring Information MEP levels in the NHANES 1999-2000.2-102) 95.9 (61. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-111) 85. see Data Analysis section) for Survey years 99-00. soaps. In contrast.5) 81.

7-110) 81. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.S. Median MEP levels found in a small sample of German residents (Koch et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Other population estimates also differed by sex and race ethnicity (Silva et al.9 (82.Phthalates 2002 (Brock et al.5-114) 101 (87. In an analysis of NHANES 1999-2000.3-105) 87. 2004).. 2005). 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. 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.. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..6 (65.9-110) 96.0-156) 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 . 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.6 (77. This age-related trend is opposite the direction seen for other phthalates. 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.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.5-113) 122 (93.2 (66. 2003) were slightly lower than levels found in NHANES 2001-2002. 2002). 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. Analysis of NHANES 2001-2002 showed similar findings.0 (66.

Malek NA. Singh NP. Centers for Disease Control and Prevention (CDC). Brock JW. Needham LL.22(3):688-695. Rossbach B. 112(5):A270]. Brock JW. Environ Health Perspect 2004. Perera FP.110(5):515-518. Phthalate monoesters levels in the urine of young children. Meeker JD. Third National Report on Human Exposure to Environmental Chemicals. Hoppin JA. Poland. Davis BJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Jacek R. Jedrychowski W.S. Bull Environ Contam Toxicol 2002. Reproducibility of urinary phthalate metabolites in first morning urine samples. Prenatal exposures to phthalates among women in New York City and Krakow.111(14):1719-1722. Barr D. Hum Reprod 2007. Hodge CC. Environ Health Perspect 2002. Hilborn ED. 2005. Camann DE. et al. Baird DD. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Hauser R. et al. Caudill SP. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.68:309-314.93:177-185. Ryan L. Silva MJ. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Caudill SP. Urinary levels of seven phthalate metabolites in the U. Drexler H.112(3):331-338. Koch HM. Silva MJ. Environ Res 2003. Atlanta (GA). Silva MJ. Barr DB.Phthalates References Adibi JJ. Reidy JA. et al. Duty S. Environ Health Perspect 2003. Angerer J.

4 (13.70-3.6 (20.0 (21.3) 28.6 (16.5-27.9) 5.51) 4.31 (3.14 (1.3-57.56 (2.1 (8.90-11.8) 15.5) 37.00-5.10) 4. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics. Following ingestion.40-8.4 (16.6 (11.4-40.7) 18.9-48.23 (2.60) 7.35) 4.62) 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 5.12 (4. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9-26.9 (17.23) 3.S.0-18.70 (1.24-4.60) 4.70 (2.5-28.40) 4.42-5.50-5.4-20.8 (19. 1989.70 (5.60-7.10 (4.5 (24.60) 8.90-8.80 (2. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.9) 13.5) 19.7) 37.5 (18.90) 4.54) 4. 1982.30-11.27) 2.1 (10.4) 6.4) 22.25-3.21 (2. After parenteral administration.00-4.30 (4.4) 23.50-8.10 (2. and in humans.80-27. Peck and Albro.50-20.50-14.5 (25.00) 5.82) 3.9) 15.31-4.50 (7. as glucuronide conjugates (Albro et al. packaging film.9 (7.Phthalates Di-2-ethylhexyl Phthalate CAS No.20 (3.5-41.00) 19. which is used for many consumer products.10-11.10 (3.50-2.6 (9.41) 3.00) 11.90) 4.86) 2.46) 3.4) 20.7-58.70) 16.90-5.1) 29.67-4.50-3.7 (17.6) 15.69) Selected percentiles ( 95% confidence interval) 50th 3.40-1.5 (12.2-17.20 (1.30 (3.5) 32.10) 3.5) 40.9 (29.1-29.20 (3.3 (15.50 (3.10 (3.16 (2.10 (6.9 (17.0 (13. and 0.2 (7.10) 3.92-5.9-57.00) 9.0-84.7) 19.1 (8.42) 3.2 (11.57-7.4-53.4) 7.80 (8.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7 (14.5-28.40-9.0) 31.0 (9.1 (11.5 (18.40 (2.0 (19.70-2.96-5.90-4.27 (3.41 (3.0) 23.80-4.5 (12.40 (6.50) 4.9-55.50 (3.3-49.4-20.5) 23.30) 2.00 (2.40) 75th 7.5) 43.0 (14.84 (2.2) 23. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.40) 11.70-2.70-6.10-5.80 (8.90 (4.6) 14.30 (6.37-4.93) 6.30 (7.7) 6.4) 15.9 (29.10-2.90) 1.3-26.0) 35.30-8.19-3.2-28.34 (2.6 (12.35 (1.84-4.50 (8.6 (10.6 (41. see Data Analysis section) for Survey years 99-00.80-5.6) 14.10) 3.9-29.70 (7.96) 4.9.70) 7.98) 2.7) 8.4-42.00 (5.85 (3.10 (4.10) 2.70 (3.90) 4.50) 9.00 (7.00-3.2) 4.70-8.85) 4.30-6.0 (17.5 (11.10-3.60) 4.75-4.2 (29.0.5 (20.40-8.60) 10.3 (24.80-9.5-40.15 (1.86) 2.32 (3.70-5.50 (7.90 (3.3 (19.1982).1-17.8-50. Albro and Lavenhar.4) 33.03-2.92) 4.9-49.8 (19.40 (4. mainly polyvinyl chloride.70-4.3-64.0-19.0-29.5 (31..2-35.6-23.50-5.60) 3.10-11.5-17.6-25.0) 23.91-3.00-3.9) 18.2. ATSDR.1) 19.00) 2.40) 1.21 (2.1) 22.1-27.90-3.00 (4.80) 9.49 (3.90) 3. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (M