2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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4'-Pentabromodiphenyl ether (BDE 85) 2.cdc.2'.2'.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .5'-Hexabromodiphenyl ether (BDE 153) 2.1.2-Dichloroethane (Ethylene dichloride) 1.1.3’.3.4'.4-Tribromodiphenyl ether (BDE 17) 2.1-Trichloroethane (Methyl chloroform) 1.4.4.3.4.2'.4’.4. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2-Dichlorobenzene (o-Dichlorobenzene) 1.2’.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2'.2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4.3.5-Pentabromodiphenyl ether (BDE 99) 2.5.3.2'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4'-Tribromodiphenyl ether (BDE 28) 2.5.2'.2-Dichloropropane 2.5.4'.4-Dichlorobenzene (p-Dichlorobenzene.4'. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4'.3-Tetramethylbutyl] phenol) Triclosan (2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4.4.2-Dichloroethene trans-1.What’s New in this Report What’s New in this Report In this Fourth Report.html.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.5.5'-Tetrachlorobiphenyl (PCB 44) 2.4.1.1. The process for selection is described at http://www.5'-Tetrachlorobiphenyl (PCB 49) 2.2'.2'4.6-Pentabromodiphenyl ether (BDE 100) 2. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.3-Dichlorobenzene (m-Dichlorobenzene) 1.4. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.4. Table 1.4’.5'.6'-Hexabromodiphenyl ether (BDE 154) 2.2'.5’.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4. Paradichlorobenzene) 1.2'3.1-Dichloroethane 1.4'-Tetrabromodiphenyl ether (BDE 66) 2.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.6-Heptabromodiphenyl ether (BDE 183) 2.4'.2'.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 2.1-Dichloroethene (Vinylidene chloride) cis-1.4'-Tetrabromodiphenyl ether (BDE 47) 2.6.3'.gov/exposurereport/chemical_selection.

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

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

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

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

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

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

Geological Survey (USGS) • (http://www/usgs. Where can I find more information? For more information about environmental chemicals. and public government documents. Signature Publications. This organization notes that these values are for workers and that it is not appropriate to apply them to the general population.cdc.asp) U. 2007.gov/niosh/database.html) o Registry of Toxic Effects of Chemical Substances (RTECS) (http://www.gov/nchs/nhanes. and pathways of human exposure.cdc.S. sources. the U.S. 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. the information was compiled from many publicly available sources. Links to nonfederal organizations are provided solely as a service to our readers. including documents from national and international agencies and organizations. and comparative blood or urine levels from other studies.gov) • National Center for Toxicological Research (http://www. not to imply that the BEI is a safety level for general population exposure.gov/nctr) U.gov/opptsmnt/index.S.gov) 9 Fourth National Report on Human Exposure to Environmental Chemicals . or concordance among multiple scientific papers and sources. generally recognized guidelines for blood or urine levels are presented in the text.S.S.fda.gov/niosh/rtecs) Agency for Toxic Substances and Disease Registry (ATSDR) • Toxicological Profiles and ToxFAQs (http://www. refer to the list of web links below and the references given in the text. CDC is not responsible for the content of an individual organization’s Web pages found at these links. Advances in analytical methods allow us to measure increasingly lower levels of environmental chemicals in people.gov/substances/index.S. U.htm) • National Institute for Occupational Safety and Health (NIOSH) o Databases and Information Resources (http://www.gov/toxpro2. consensus agreement among experts. and the agencies of the World Health Organization.atsdr.cdc.gov/nchs) o National Health and Nutrition Examination Survey (NHANES) (http://www. Cincinnati (OH). Separate studies of varying exposure levels and health effects associated with these levels are required to determine whether blood. and Toxic Substances (OPPTS) (http://www. Governmental Sources Centers for Disease Control and Prevention (CDC) Resources: • National Center for Health Statistics (NCHS) (http://www. Some guidelines are from federal agencies. such guidelines are not available. 2007). serum.epa. One exception is the American Conference of Governmental Industrial Hygienists (ACGIH). Generally.cfsan.gov/iris) • Office of Prevention. nor do they create guidelines. disposition within the body.cdc. These links do not constitute an endorsement of these organizations or their programs by CDC or the federal government.fda. Examples of common institutional sources of information include the Agency for Toxic Substances and Disease Registry.cdc. population to environmental chemicals. and urine levels result in disease or adverse effects. Pesticides. The data and information in the Fourth Report do not establish health effects.epa.Chemical and Toxicological Information Chemical and Toxicological Information The Fourth Report presents biomonitoring data on the exposure of the U. If available. American Conference of Government Industrial Hygienists (ACGIH). a private organization that publishes biological exposure indices (BEIs) that “generally indicate a concentration below which nearly all workers may be repeatedly exposed without adverse health effects” (ACGIH. and it is not intended as a comprehensive review of each chemical.atsdr. For most chemicals in this Report. Environmental Protection Agency (EPA) • Integrated Risk-Information System (IRIS) (http://www. Statements are based on common general information. BEIs can be the blood or urine levels of a chemical that correspond to air-exposure limits for workers set by ACGIH. peer-reviewed scientific papers obtained from electronic searches. The information in the text is provided as an overview. effects in animals or humans. The Fourth Report provides descriptive information about each chemical or chemical group including uses. 2007 TLVs and BEIs. Food and Drug Administration (FDA) • Center for Food Safety and Applied Nutrition (http://www. Information about the BEI level is provided here for comparison.html) • Toxic Substances Portal (http://www. Environmental Protection Agency.cdc.htm) U.

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

2-77.6) 73.4 (51.7) 96.6) 90. Commercially.6) 50.6-65. EPA reference dose of 0. FAO/WHO.8-55.7) 75th 79.6-104) 82. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. Since acrylamide has limited volatility and high water solubility.3 (53. Fennell et al.4-60. Fourth National Report on Human Exposure to Environmental Chemicals 11 .2-59.0 (53.8 (57.2) 57. acrylamide is synthesized and used in the production of polyacrylamide polymer. EPA.7-60. People may be exposed to acrylamide from foods. pulp and paper production. mineral processing.7 (55.2-118) 98.2-93.5 (79.2-114) 163 (147-191) 96. interval) 61. 2002).9) 58. 2005).4-76.0 μg/kg for adults (FAO/ WHO.0. in some sealing grouts. widely distributed in tissues.1-64. it was discovered that acrylamide is formed when starch-rich foods.1 (52.3 (55.0-66. are heated at temperatures used for frying and baking. In the general population. gels.6 (81. Survey Geometric mean (95% conf.9-105) 86. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. in permanent press fabrics. acrylamide has produced upper airway irritation following inhalation of high levels. as an absorbent in disposable diapers.3) 70.0 (69.7) 73.2-67. Natural substances in the food are converted to acrylamide. and binding agents.9 (54.4 (53.2-91.1) 46.6-66.3-2.8 (52. 2004. Polyacrylamides are useful water-compatible polymers used in water treatment. 2006.6-75. and from dermal contact with products that contain residual acrylamide.1-57.4-83.1 (83.5 (74. Tareke et al.1 (47.1 (73.1-61.3-71. Recently. Estimated intakes in children are about twice that of adults (DiNovi and Howard.5 (44. These estimated intakes are hundreds of times lower than occupational exposures.1) 55.S.0-49.1) 53.. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.4-89. 1994). 2005). In humans. or to glutathione conjugates (Calleman et al.7 (58. EPA.0 (57.8-57.8 (91. soil conditioners.7) 54. Animal studies indicate that acrylamide is well absorbed.9 (60. 2005.4) 57.0) 57.0 (67.3) 63. but can covalently bind to form adducts with proteins.5-80.1 (88.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. (NTP-CERHR.9) 63. FDA.9-52. and an average daily intake is estimated as 0.4 (54.5) 66. and well below doses known to cause nerve damage or carcinogenicity in animals.4) 100 (89. Acrylamide is not thought to accumulate in the body at environmental doses. such as potatoes and some grains.2-70.5 (52.4) 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. see Data Analysis section) for Survey year 03-04 is 3. and is either metabolized to the reactive epoxide. and in some cosmetics.7 (65.S.6 (56.5) 58. smoking. 1990.1) 101 (95.4) 57.4 (54.S.7-64.6) 71.9-61.7 (63.0-108) 152 (139-175) 126 (111-142) 108 (86.6-61. 2004). drinking water. 217 million pounds of acrylamide were produced commercially in the U.6-108) 61.8 (81..S.2 (58. and in the synthesis or compounding of dye materials. In 1997.9) 75.4-60.. 2005).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. population from the National Health and Nutrition Examination Survey. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. 2005). Elimination occurs mainly in the urine as mercapturic acid conjugates.9) 57.4 (59.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.2 μg/kg/day (U.7) 58. 2006).5-85.2) 57.2 (75. and cosmetics (NTP-CERHR.3) 86.0) 85.1-64. 2005).Acrylamide Acrylamide CAS No.1) 62.6 (51. ocular and dermal irritation from direct contact with acrylamide containing materials.S. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. but are generally above the U.2 (62.7-64.9 (69.0-58. the main source of exposure is from the diet. 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. glycidamide.

2005.3-78.1 (70.3) 59. 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.5) 75th 85... Axonal degeneration. presynaptic nerve terminal binding (LoPachin. 2005. 2006). gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. U.5-64.7) 61.3-101) 95.4 (57. 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.0-93.4 (90. Puppel et al..9-62.9-64. 2005) and sperm DNA adducts (Xie et al.S. Survey Geometric mean (95% conf. 1997. U. 2005.epa. 2005.0 (70.9 (58.2 (72. altered gene expression in testicular tissues (Yang et al.5) 87..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 59.7 (84. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.4 (81.0. probably through its epoxide metabolite.6 (66.0 (80.4 (51. 2006.9 (57. Acrylamide is clastogenic and can produce dominant lethal mutations. 2006). 2005. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). AHA levels have been shown to increase with dietary intake (Hagmar et al.9) 75.0 (52.0) 118 (103-126) 121 (112-134) 113 (94.S.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.1-70..who. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.7 (87.9-78.9) 59.5 (59.9-138) 143 (130-159) 96..4-98.0) 94.. Klaunig et al.7) 74. 2005..5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. and other sites) (FAO/WHO.0-62.4 (61. most non-smokers had levels less than about 100 pmol/gram hemoglobin. fetal death.2-68.8 (44.. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.. 2005) have been demonstrated in animals. male germinal cell injury. Vesper et al.9) 87.7 (61.. Schettgen et al. NTP-CERHR. IARC classifies acrylamide as probably carcinogenic to humans.3) 59. 2005. EPA at: http://www. uterine..9-76. After exposure ceases. EPA..7-62. dominant lethality).3 (56. 2001)..0 (75.8-61. 2005. 2005). 2005). Maniere et al.2-90. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2002.5 (56.6-62.S.2 (63. 2004.1 (56. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.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. 2002.. Puppel et al.2) 65.4) 46. Glycidamide has been shown to react with DNA (Doerge et al. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.6 (90. In addition. reproductive effects (reduced litter size. scrotal.8 (51.2-91.8) 60.4-103) 79.8-48.2 (56.1 (66.. Rice. 2003.. Vesper 2005) and smoking (Bergmark.8-49. 2009). 2006) have been demonstrated after acrylamide dosing. and cancer (mammary.9 (81.1) 62. thyroid.int/ ipcs/food/jecfa/summaries/summary_report_64_final.5 (42. interval) 59. see Data Analysis section) for Survey year 03-04 is 4. Schettgen et al.1) 56.4) 83. Mucci et al.3) 85.9-77.4-65. EPA. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.5-66.4) 53. 2008).7) 90..pdf.1-56.5-92.3) 59.S.5 (83.4-59.7 (57. Hagmar et al. and neuronal DNA reactivity (Doerge et al. 1997.6-64. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. glycidamide (NTP-CERHR.1) 60. respectively) are markers of integrated acrylamide exposure over the preceding few months.7-64.9) 65.2) 55. 2005).7) 60. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.. population from the National Health and Nutrition Examination Survey. 2004). 2005. 2008). 2005.. adrenal.2) 87. 2005).5-94.1-60. Additional information is available from U.4 (56.8) 45. 2005.5) 71.1 (82.7-86.6-90.Acrylamide occupational exposures.1-62. although different analytic methods can affect results.1 (57.

Mutat Res 2005.10(1):78-84. 1993. Acrylamide intake through diet and human cancer risk.fda. Bergmark E. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Tian G. Hagmar et al. Food Chem. Wilson KM. Perez et al. Cheong HK. Godard T. Toxicol Sci. Metabolism and hemoglobin adduct formation of acrylamide in humans. Adv Exp Med Biol 2005. Available at URL: http://www. Chem Res Toxicol 1997 Jan. Food and Drug Administration (FDA). 6013-6019.56. 1999). Acrylamide neurotoxicity: neurological. Granath F. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide.cfsan. 2001. et al.niehs. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. 2004. 2/3/09 Klaunig JE. Toxicol 2005. Costa LG. et al. July. Chem Res Toxicol 1990. Becher G.580(1-2):119-129. Mucci LA.85:447-459. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Alexander J. 8-17 February 2005. Yang JS.43:365–410. April 13-15. Churchwell MI. Laurentie M. et al. 2006.. The Updated Exposure Assessment for Acrylamide. Summer SCJ. 054472. Tornqvist M. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Burgess J. February. da Costa GG. Magnusson AL. Tornqvist M. Paulsson B. Toxicol Sci 2005. He F.. 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.27(4):219-226. Kautiainen A. smoking habits and gender.Toxicol Appl Pharmacol 1994. Nordander C. Survey data on acrylamide in food: individual food products. Scand J Work Environ Health 2001. Fennell TR. NIH Publication No. Axmon A. Available at URL: http://cerhr. Duale N. Kamendulis LM. 2009 Jan 8.. J Agric Food Chem 2008. DiNovi M and Howard D.3:406-412. CFSAN/Office of Plant and Dairy Foods. 1994). Chicago. et al. Costa LG. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Bridson WE. Bruze M. 2005. morphological and molecular endpoints in animal models. Italy. Calleman CJ. Andersen M.html#u1004. Zhang S. and Research Strategies.. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al.126(2):361-371.gov/chemicals/ acrylamide/Acrylamide_Monograph. Hagmar L. Spicer R.Acrylamide In occupational settings. Twaddle NC. gov/~dms/acrydata. 2004 Acrylamide in Food Workshop: Update Scientific Issues. 2/3/09 Perez HL. In another study. Human exposure and internal dose assessments of acrylamide in food. National Toxicology Program.pdf. 2/3/09 Hagmar L. Mutat Res 2005. Toxicol Appl Pharmacol 1993. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Calleman CJ. Calleman CJ. He F. Rome. Bjellaas T. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Doerge DR. Maniere I. Farmer PB. [Epub ahead of print] Dybing E. Mutat Res 2005. Aprea P. 64th Meeting: Summary and Conclusions (FAO/WHO). Illinois. AHA levels correlated with a neurologic symptom index and specific physiologic measures in an occupational setting and correlated better with clinical signs and symptoms than urinary excretion of the mercapturic acid metabolite (Calleman et al. Beland FA. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Osterman-Golkar S. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Bergmark E.580(1-2):131-141. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. 2001). Adv Exp Med Biol 2005. 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. Malmberg B.nih. Doerge DR. LoPachin RM. Rosen I. et al. Haugen M.pdf. McDaniel LP. Bergmark E. Churchwell MI..561:49-62. Wu Y. Wirfalt E.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Uncertainties.who. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Fennell TR.580(1-2):157-165. Paulsen JE. Available at URL: http://www. Snyder RW. Joint FAO/WHO Expert Committee on Food Additives. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. References Bergmark E. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Mechanisms of acrylamide induced rodent carcinogenesis. smokers and nonsmokers.120(1):45-54.561:21-37. Guffroy M.

Anal Biochem 1999.epa. Choi JH. Ingham L. 2/3/09 Vesper HW. Eriksson S. Rydberg P. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Tjaden Z. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Ospina M. Meyers T. Toxicol Lett 2006. EPA).50(17):4998-5006. Gray JG. Tjønneland A. Drexler H. Sun H. 1994. et al.580(1-2):71-80.gov/iris/subst/0286. Washington (DC). Schettgen T. Tornqvist M. Vesper HW.S.S.txt.207(6):531-9. Toxicological effects of acrylamide on rat testicular gene expression profile.S.19(4):527-34. Office of Pollution Prevention and Toxics.Acrylamide glycidamide by gas chromatography-mass spectrometry.56(15):6046-53. Vesper HW. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Toxicol Lett 2002. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Tareke E.S. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Ospina M.htm. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Schettgen T.epa. Ding X.580(1-2):3-20. Meyers T. Broding HC. Letzel S. Rossbach B. EPA). Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Hallmans G. Mutat Res 2005 Feb 7. Rice JM.274(1):59-68. Kutting B. Liu K. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. 2/3/09. Drexler H. Jin Y. Int J Hyg Environ Health 2003. Slimani N. Acrylamide. Integrated Risk Information System (IRIS). Liu Y. Han DU. Available at URL: http://www. Adv Exp Med Biol 2005. Drexler H. Hemoglobin adducts of ethylene oxide. Schettgen T. Han CH.gov/chemfact/s_acryla.163(2):101-8. Chemical Summary for Acrylamide. Mutat Res 2005. Puppel N. Lee SH. Agudo A. U. Fu D. Angerer J. September. J Agric Food Chem 2002. Weiss T. Analysis of acrylamide.561:89-96. Smith A. Angerer J.206(1):9-14. Chae C. propylene oxide.134(1-3):65-70. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Fueller F. Environmental Protection Agency (U. Lee MH. U. Benetou V. Environmental Protection Agency (U. Int J Hyg Environ Health 2004. a carcinogen formed in heated foodstuffs. Angerer J. Rapid Commun Mass Spectrom 2006. et al. Marko D. Karlsson P. Licea-Perez H. The carcinogenicity of acrylamide. Reprod Toxicol 2005. Myers GL. Available at URL: http://www. revised 1/3/06. J Agric Food Chem 2008. Yang HJ. Xie Q.20(6):959-64.

cardiovascular disease.145) .63 (2.57) 2.14-1. population from the National Health and Nutrition Examination Survey.21-1.015.080) < LOD .190-.140-.066 (.188) .49) 1.17) .93) .09-3.43 (1.040 (.630 (.240 (.430-1. see Data Analysis section) for Survey years 99-00.040 (.130 (.230) .110) .580) .110 (.090-.110 (.740-1.38-2.05 ng/mL.32-2.030-.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 . 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.48-2.090-.077) .180) .505 (.621-1. Survey Geometric mean (95% conf.050 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 15 .080) < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.080-.690 (.49) 1.30) 2.S.533-.060 (<LOD-.990) .23 (2.20 (.997-3.66 (1.44) 2.840) 3.50 (1. 2006).79) 3.142-.19-2.060-. and 0.071 (.058 (.20-2.770) .480-1.086 (.770) . 83% of measurements had an LOD of 0.054 (.350-.050 (.260-1.059-.230 (.54) 1.660) .44 (2.23-2.77 (2.580 (.059-.052 (<LOD-.120 (.040 (.12) 1.60-2.060 (.68 (1.12-4. emphysema.02 (.167 (.220) .26-1.62) 2. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.163) .44) 2.110-.04 (1.124 (.00) .213) .09-2.108) * .308 (.21-1.99) 2.088-.21 (.32-2.81-2.216 (.080 (.110 (.115-.63-2.620 (.96-4.068) .950-1.11) . which may vary for some chemicals by year and by individual sample.260) 1.080 (.180 (.670) .070) 75th . stroke.050-.160 (.990 (.094) .S.040-.047-.20 (1.139) * .120 (.060-.220) .080-.137 (.062 (.625) .160 (. 2004).160-.68) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .96) 2.073) < LOD .66) 1.860 (.02) 1.28-1.148-.01 (1.14) .630 (.110-.193) .23 (. and 03-04 are 0.110 (.15) 2.33-2.428-.370-.28) .063) .060 (.19) 1.220-.35 (2.180) .164 (. < LOD means less than the limit of detection.084) .45) 1.950 (.087) < LOD < LOD .14) .060) .040-.150) .19) .070 (<LOD-.144 (.850 (.410) .089) Age group 3-11 years 99-00 01-02** 03-04 .02) 1.49) 2241 1878 1707 1333 1602 1704 1950 2847 2500 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02** 03-04 Limit of detection (LOD.110 (.160 (.920 (.190-.710 (.120) .180) .050 (<LOD-.164 (.030-.99) 2.54 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50-1.057-.020-.160) .480-.S.15 (2. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. Cigarettes contain about 1.470-.066) .080-. DHHS.061) < LOD .302) .140 (.068) .180) .12 (1.050 (<LOD-.130) .88 (.770-1.78) 2.066-.18-3.92 (1.42-4.89) 1.120 (.40) .39) 3.34 (1. ear problems.600-1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.310) .090-.163 (.310-1.20) .54 (1.01) 3.030 (.910-1.726) .131 (.87-3.030-.96 (1.76 (1. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.05. ** In the 2001-2002 survey period.32) 1.120-.39 (1.310-1.140-.960-1.360) .506 (.050 (<LOD-.070-.540 (.310) 90th 1.00) 1.44 (1.570-1.320) . Children exposed to ETS are at increased risk for sudden infant death syndrome. 1998).190-.730 (.75) 1.400-.820) .052 (<LOD-. 2004).110-.12 (2.540-.137-.106-.175 (.09-3.Cotinine Cotinine CAS No.790) .187) .126) .50-4. respectively. DHHS.47-3.210 (.198) * . maternal exposure during pregnancy can result in lower birth weight.510 (.050) .140 (.076-.88 (1.77 (1..05) 1.154-.84-3.62 (2.350-.180 (.120 (.153-.060-.570 (.16) .900-1.55 (1. and 17% had an LOD of 0.450-.94) 1.087 (.53-4.68) 2. and exacerbated asthma (U.201) .015 ng/mL.30) * .312) .42 (1.800 (.075 (.95) 1.65 (1.111-. acute respiratory infections.104-.180) . and various other disorders (U.100-.077) .070) .050) .050-.350 (.70-2.080-.53 (1.197) .30) 2.200) 1.280 (.234) .17 (1.071) .740-1.300) .22) 2.85 (1.070) .500 (.83-2.520 (.66-3.060 (<LOD-.150) .55-2.50) 3.5% nicotine by weight (Kozlowski et al.630 (.620-1.48-3.160) .70) 2.087-.120 (.930 (.580-1.110) .17 (.20) 1. acute respiratory illness.043-.047-.053 (<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 * .23 (1.120-.77 (1.

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

Summary of Data Reported and Evaluation [online] 2004. U. the United Kingdom. 11th ed. Vol 38.280:152-156. BMJ 1975.56:483-493. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Centers for Disease Control and Prevention. Giovino GA. 4/13/09 International Agency for Research on Cancer.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population.cdc. Pirkle JL. U. Available at URL: http://www. JAMA 1998.18:188-204. DHHS). Trends in the exposure of nonsmokers in the U. Department of Heath and Human Services. Mowery PD. Tobacco Smoke. 1988-1991. National Institute for Occupational Safety and Hygiene (NIOSH). Vol 83.niosh. Available at URL: http://monographs. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Mehta NY.gov/eid/rmca/critdocs/ criteriadoc/33. Sweeney CT.S Department of Health and Human Services (U. Warner K. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Racial/ethnic differences in serum cotinine levels among adult U. Etzel RA. Jacob P III. Department of Heath and Human Services. Metabolism of nicotine to cotinine studied by a dual stable isotope method.gov/tcrb/monographs/10/. Brody DJ.fr/ENG/Monographs/ allmonos90. Cotinine as a biomarker of environmental tobacco smoke exposure.gov/ntp/roc/eleventh/profiles/ s176toba. Ethnic differences in N-glucuronidation of nicotine and cotinine.nih. Jarvis MJ. Sosnoff CS. Herrera B. Modin G. Bernert JT. Strauss WJ. Soliman S. Lewis PJ. Fong I. Pirkle JL.php. International Agency for Research on Cancer. Bernert JT.fr/ENG/Monographs/allmonos90.275:1233-1240. June. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.S Department of Health and Human Services (U. In Report on Carcinogens. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Hukkanen J. Tobacco Smoke and Involuntary Smoking. et al. 1999-2002. Am J Public Health 2004. Dollery CT.7:369-375. 4/13/09 Centers for Disease Control and Prevention (CDC).php.280:135-140. 2004. National Center for Chronic Disease Prevention and Health Promotion. Absorption and metabolism of nicotine from cigarettes. Atlanta (GA): 2005.57(1):79115. Caudill SP. Pickett MA.pdf.S. Summary of Data Reported and Evaluation [online] 1986. Pechacek TF. Perez-Stable EJ. Office on Smoking and Health [online] 2006. Respiratory nicotine absorption in non-smoking females during passive smoking. Caraballo R. References Armitage AK. Benowitz NL.S. Flegal KM.S. Coordinating Center for Health Promotion. JAMA 1998.cancer. Kira S.S. Centers for Disease Control and Prevention. Schober SE. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Coordinating Center for Health Promotion. Jacob III P. Benowitz NL. [online]. JAMA 1996. Pollack HA. cigarette smokers: the Third National Health and Nutrition Examination Survey. population to secondhand smoke: 1988-2002. Jacob P III. Jacob P.S. Metabolism and disposition kinetics of nicotine. Tobacco related exposures. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Aiba M. Available at URL: http:// cancercontrol. Herrera B.291(3):1196-1203. Epidemiol Rev 1996. George CF. Turner DM. 4/13/09 Iwase A. Houseman TH. Richter PA. Nicotine metabolism and intake in black and white smokers. Benowitz NL. Available at URL: http://ntp.niehs. Available at URL: http://monographs. Exposure of the U. Vogler GP. Giovino G. Int Arch Occup Environ Health 1991.S. Schwartz SS. Maurer KR.94(2):314-320. IARC Monogr Eval Carcinog Risks Hum. available at URL: http://mtn. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. IARC Monogr Eval Carcinog Risks Hum.gov/library/ secondhandsmoke/. 1988-1991.surgeongeneral. Tob Control 1998. Benowitz NL. Kozlowski LT. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.63:139-43. Benowitz NL.15:302-307. U. Curtin LR. DHHS). National Toxicology Program (NTP). Environ Health Perspect 2006.iarc. 4/13/09 U. 1991.114(6):853-858. Brody DJ. Pharmacol Rev 2005. 4/13/09 National Cancer Institute (NCI).pdf. 4/13/09 Perez-Stable EJ. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. and the United States.S. Smoking and Tobacco Control Monograph 10 [online]. et al.4:313-316. iarc. Pechacek TF. J Pharmacol Exp Ther 1999. 1999. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Tob Control 2006. Clin Pharmacol Ther 1994.

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

170 (.100-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. DEET is not genotoxic. There are over 225 insect repellents brands containing DEET.250) < LOD . population from the National Health and Nutrition Examination Survey. 2002).560) < LOD .120-. 1998). EPA.100-.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 .130 (. (Kolpin et al. About 3-8% of dermally applied DEET is absorbed.130-. and they range in concentration from 4% to 100%. Neurological effects in humans.130-.EPA at: http://www. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140) < LOD .130 (.140-.N-Diethyl-meta-toluamide (DEET) N..N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 19 . 2003).130) < LOD .S.190) < LOD . including seizures and encephalopathy.100-.110 (<LOD-.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .110 (.180 (.110-.110 (. DEET is also used in combination with dermal sun screens (U.110 (.EPA. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .EPA. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.N-Diethyl-meta-toluamide (DEET) CAS No.. Additional information is available from U. Urinary N. < LOD means less than the limit of detection. DEET can be applied to clothing and the skin to repel biting insects.180 (.220 (. 2003). DEET has low acute toxicity.180 (.100-. (U.520) < LOD . 2002). 1995.S. Sudakin and Trevathan.210 (.449 and 0.130) < LOD . Survey Geometric mean (95% conf.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .epa.130-. 2005).130-. DEET is not a developmental or reproductive toxicant in animals (U.140) < LOD .N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.S. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.S. Its use is recommended for prevention of several vector-borne diseases.170 (.130 (.140 (. and it has not been rated by IARC or NTP with respect to human carcinogenicity. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.100-.110 (<LOD-.120-. DEET is not registered for use on agricultural commodities.100-.150) < LOD .110-.180) < LOD . Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.N. After absorption.140) < LOD .110 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. 1998).S. have been reported as result of self-poisoning by ingestion or excessive dermal application.S.160) < LOD . but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.240) < LOD . 134-62-3 General Information N. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .100 (<LOD-..1.270) 688 678 518 700 598 956 Limit of detection (LOD. One survey detected DEET in 74% of sampled streams in the U.gov/pesticides/.

N.270 (.200 (.230-.130 (<LOD-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .320) < LOD .350-.190 (<LOD-.250) < LOD .410 (.300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .330 (.390-. 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.140-.300 (.280 (. 1992). In this survey period.280-1. Survey Geometric mean (95% conf.500 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Urinary N.270) < LOD .350) < LOD .150) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.480 (.240-.190 (.630) < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.270-.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.370) < LOD .150-. 2005). the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.. 20 Fourth National Report on Human Exposure to Environmental Chemicals .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 .250 (.330 (. Urinary DEET levels as high as 5. representative subsamples from NHANES 2001-2002.240) < LOD . population from the National Health and Nutrition Examination Survey.250-.93) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .290-.170-.230-.410 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.410-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.190 (.S.270 (<LOD-.440) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2007).230) < LOD .350) < LOD . Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.S.640 (.370-.490) < LOD .190-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..320 (.

Thurman EM. metabolism. Zaugg SD.S. pp.41(6):831-839. 2005.16(1):10-13. Furlong ET. et al. Atlanta (GA). 1993-1997.epa.EPA).N.S. U. Diethyltoluamide (DEET). Toxicity and Exposure Assessment in Children’s Health. pdf. Environmental Protection Agency (U.S. Meyer MT. Absorption. streams. Barber LB.pdf. 4/9/09 U. and excretion of N. Chemical Summary.115(8):1254-1260. Third National Report on Human Exposure to Environmental Chemicals. Lowry LK. Environmental Protection Agency (U. Sudakin DL.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography.EPA. Washington (DC): U. Human exposures to N. Schoenig GP. September 1998.25:95-100. Chen H. Osimitz TG. Available at URL: http://www.N-Diethyl-meta-toluamide (DEET) References Arcury TA.36(6):1202-1211. and other organic wastewater contaminants in U.gov/oppsrrd1/REDs/0002red.gov/teach/chem_summ/ DEET_summary. DEET: a review and update of safety and risk in the general population. EPA. Trevathan WR.S. Veltri JC.S. EPA 738-R98-010. 1-118. Centers for Disease Control and Prevention (CDC). DeBord KE. Hartnagel RE Jr. Int J Toxicol 2002. Pharmaceuticals. J Toxicol Clin Toxicol 2003. hormones. U. Reregistration Eligibility Decision (RED): DEET. Environ Sci Technol 2002.EPA).2:341352. Fundam Appl Toxicol 1995. Environ Health Perspect 2007. Quandt SA. Selim S. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Smallwood AW.S. Gabriel KL. 1999-2000: a national reconnaissance.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.N-diethyl-mtoluamide following dermal application to human volunteers. N. Available at URL: http://www. Barr DB. J Anal Toxicol 1992. Page BC. Grzywacz JG.epa.S. 2005 Kolpin DW. Bell JW. Tapia J.

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

K. T.nih. Furukawa M. streams. NC. U.14(2):149-157. Brine DR. Kawamura N. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. 2003. Hum Ecol Risk Assess 2004.pdf. 2/4/09 European Commission.eu/ health/ph_risk/committees/sct/documents/out156_en. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Joskow R. National Institutes of Health. and Hajszan. vom Saal FS. Available at URL: http://ecb. Biochem Biophys Res Commun 2003. Ema M.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. et al. 1999-2000: a national reconnaissance.europa.137(3):353-362. Brussels. Available at URL: http://ntp. Proc Natl Acad Sci USA 2005.102(19):7014-7019.145:592-603. Serizawa S. Caudill SP. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Pharmaceuticals. N. Ekong J.nih. Howdeshell KL. Richter CA. Twomey K. Kim CS. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Han SS. Research Triangle Park. Imai H.35(2 Pt 1):238-254. Calafat AM. In vitro and in vivo interactions of bisphenol A and its metabolite. Ecotoxicity and the Environment (CSTEE).gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. DirectorateGeneral Health and Consumer Protection. et al. August 2001. Rat two-generation reproductive toxicity study of bisphenol A. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Toxicol Sci 2002. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). McConnell EE. September. Gray GM. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.J.10:875-921. Hlywka JJ. Klinefelter GR. National Toxicology Program. Ye X. Doull J.. Marr MC. niehs. 5: 505-523. hormones. Yang M.116(1):39-44. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Available at URL: http://cerhr. Sottas CM. Shin HC. Ikka T. Ispra. Harazono A. Life Sci 2001.68(1):121-146.pdf. Cohen JT. Leranth. Park S. May 22. Endocrinology 2004. National Institute of Environmental Health Sciences.niehs. Zaugg SD. MacLusky. Environ Sci Technol 2002.59(4):403-408. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection..36(6):1202-1211. Regul Toxicol Pharmacol 2002.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. An evaluation of the possible carcinogenicity of bisphenol A to humans. 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.113(4):391-395. Watanabe S.S. Available at URL: http://cerhr. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Chem Res Toxicol 2001. 2002. Szigeti-Buck. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Lynch BS.69(22):2611-2625. Hughes C. Arakawa C.jrc. C. Department of Health and Human Services. Furlong ET.S. Calafat AM.gov/chemicals/bisphenol/BPAFinalEPVF112607. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).nih. 2008. Needham LL. Thurman EM. Wong LY.S. Hara K. Needham LL. Pyo MY. Barton L. Han SY. Matthews JB. Belgium. Environ Health Perspect 2005. Haighton LA. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A.Scientific Committee on Toxicity. and other organic wastewater contaminants in U. Calafat AM.pdf . Nippon Eiseigaku Zasshi 2004. Yoshinaga J. Fujii S. Barber LB.gov/chemicals/bisphenol/bisphenol. Kuklenyik Z. Cunha G. 4.. Reidy JA. European Commission. Kroes R. 2/4/09 Fujimaki K. Cha SW. Munro IC.59(9):625-628. 2/4/09 Ouchi K. Reprod Toxicol 2001. Barr DB. Environ Health Perspect 2008. 2007. Needham LL. Keimowitz AR. Watanabe C. and Hardy MP. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite.pdf. Human Health.780(2):365-370. Tsugane S. Kiguchi M. niehs. Gender differences in the levels of bisphenol A metabolites in urine. Hanaoka T. Bradley S. Kim YH. Barr JR. Exposure of the U. Timms BG. Tyl RW. Myers CB. Italy. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Joint Research Centre Institute of Health and Consumer Protection. J Am Dent Assoc 2006. November 26. Bisphenol A.pdf . Kim JC. Koulova AI. Rubin C. Kolpin DW. Occup Environ Med 2002. Meyer MT.149:988-994. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Koh WS. Reidy JA. bisphenol A glucuronide. Rhomberg et al. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Chung MK.312(2):441-448. Zacharewski TR. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.Environmental Phenols References Akingbemi BT. Endocrinology 2008. et al. Thomas BF. Available at URL: http://ec. with estrogen receptors alpha and beta.

Environmental Phenols Volkel W. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. vom Saal FS. Sheldon LS. Witorsch RJ. Kim SY. et al. III. Kawamoto T. Endocrinology 2006.40(7):905-12. Nagel SC. Welshons WV.15:12811287. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration.103(1):9-20. Morgan MK. Large effects from small exposures. Environ Health Perspect 2005. Hughes C. An observational study of the potential exposures of preschool children to pentachlorophenol. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Chem Res Toxicol 2002.113(8):926-33. Chang SS.44(4):546-51. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Jang JY. Arch Environ Contam Toxicol 2003. Csanady GA. Chuang JC. Wilson NK. Environ Res 2007. Lordo RA. Food Chem Toxicol 2002. Yang M. Dekant W.147(6 Suppl):S56-69. bisphenol-A. Lee SM. Filser JG. and nonylphenol at home and daycare. Vom Saal FS. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Biological monitoring of bisphenol a in a Korean population. Colnot T.

30 (1.g.40) * 03-04 03-04 03-04 . outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.20) 314 715 1488 03-04 03-04 * * .800-1. impaired steroidogenesis. 2006.20-2.00 (. 34 Fourth National Report on Human Exposure to Environmental Chemicals .50-2.200-. In the 1990s.60-3. In rats.300 (<LOD-.10-2.60) 613 652 1092 Limit of detection (LOD. Saito et al.20) 2. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).1. 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) 2. 140-66-9 General Information 4-tert-Octyphenol.50) 1.400 (.50 (1. Blake and Boockfor.00 (.000 tons of alkylphenol ethoxylates were produced annually worldwide.900 (.900 (. 1995..60-3.60-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2..600) 1. 2002).20-2.300 (<LOD-. 2002).70 (1. industrial cleaners.80) 2.20-2.60) 1. altered estrus cycles and reproductive outcomes.500 (. through sewage.357 (. did not bioaccumulate. which are anionic surfactants used in detergents. altered neonatal sexual development..900 (.500) ..600-1. The alkylphenol ethoxylates enter the environment through human use of products containing them.60) .400 (. Katsuda et al.70 (1.00 (1.g.10) 2. population from the National Health and Nutrition Examination Survey. the various alkylphenols have also been used as emulsifiers and modifiers in paints.20-2.60-3.30-2.40 (1.497) * .500) .90) 2.300 (<LOD-. 1996).3.30 (1. 2004).600-1.500) 75th . Ying et al. an alkylphenol.900 (.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Less frequently. The alkylphenols can bioaccumulate in some fish.299-. and was quickly eliminated from the blood (Certa et al.600) .600) . see Data Analysis section) for Survey year 03-04 is 0.300 (<LOD-. 4-octylphenol monoethoxylate was detected in 43.10 (. and some of their degradation products are toxic to aquatic life.10 (1.600) .500-1..20) 1.50) 1. and the polyethoxy chain may consist of up to 50 ethoxy units. Bian et al.30 (1. have demonstrated estrogenic effects particularly when injected at high doses in animals. Urinary 4-tert-Octylphenol (4-[1.300 (<LOD-. over 500. which may vary for some chemicals by year and by individual sample. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. Survey Geometric mean (95% conf. is used to manufacture alkylphenol ethoxylates.30) 90th 1.80 (1.500) .70 (1.. pesticides..10) 1.50) 1.80 (1.S.60-3.600-1..50) .300-. and to alkylphenoxycarboxylates.90) 2.10 (. Laws et al. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. to shorter chain alkylphenol ethoxylates...600-1.500-1.20-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. streams in 30 states (Kolpin et al.477) .30 (.2.507) * < LOD .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 . and some personal care products. leading to inhalation as another potential exposure route (Rudel et al.600-1. and emulsifiers.40) 1.369 (. and from contact with some personal care products and detergents. Several alkylphenols. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.30) 1.400) 1.30) 2. including 4-tert-octylphenol.70 (1.40) 2. textiles.60-3. < LOD means less than the limit of detection. During the 1980s and 1990s.50) . 2000.40) 1. testicular atrophy. and impaired spermatogenesis (e. and through manufacturing waste streams (Warhurst.80 (1.274-. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.268-.300-. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.20-2.900 (.600-1.S.700-1. 2003. orally administered 4-tert-octylphenol was well absorbed.50-3.200-.30 (1.389 (. In 1999-2000. Indoor and to a lesser extent. 1997.20 (1.00) 1229 1288 03-04 03-04 03-04 * . fish) and drinking water.5% of 139 U. Disposition in humans has not been studied sufficiently.400 (.Environmental Phenols 4-tert-Octylphenol CAS No. 2000.

00) 2. 2003. at lower or environmentally relevant doses (Blake et al.08) 1.71) 2. Kawaguchi et al.620-1. 1999). Yoshida et al.S.25-2.270 (.740 (.470-1.300 (<LOD-.S.31 (1.3.850 (. Sweeney et al.68) 2.370 (<LOD-.500-1.22) . IARC and NTP have not rated octylphenol.06 (2.96-4.170-.40 (1.269 (. 2005.270 (.770 (.64 (.43-3.29) 2.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.03-6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.270-.33 (2.18-4. 4-tert-Octylphenol is not considered directly genotoxic.11-2.78 (1. or their corresponding ethoxylates with respect to human carcinogenicity.640-1.435 (.610) .62 (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.550-1. 2001.730-1.420) .1.530) .76 (2. 2004.36-3.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40-4.470-1.260 (<LOD-.62) .349) * < LOD . 2004).. Survey Geometric mean (95% conf.78) 3.67-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.630-1.Environmental Phenols Myllymaki et al.00 (.68-2.20 (1. In a small number of adult Japanese volunteers.59 (1.450) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.54) * 03-04 03-04 03-04 ..560) .160-.410 (.00 (.540-1.03 (1.570) .65-3.03 (1.53-3.910 (.85 (1. It is unclear if estrogenic or other effects occur in animals through oral dosing. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.11) 1.60 (1.25) 2. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.33) 3. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.78) 1228 1286 03-04 03-04 03-04 * . Tyl et al..31-2.25) 90th 1.14) 314 713 1487 03-04 03-04 * * .17 (.81 (1.10-2..43) 1. nonylphenol.73) 2. Nagao et al.384) * .276 (. Fourth National Report on Human Exposure to Environmental Chemicals 35 .02-4.400) ..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 .320 (<LOD-.380 (<LOD-.62 (1.05-2. Calafat et al. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.740 (.470) 75th .460 (.50 (2.860 (.41) .337-.207-. 2001).00) 2.11) 2. 2000. Urinary 4-tert-Octylphenol (4-[1.199-.43) 1. population from the National Health and Nutrition Examination Survey.59) 1.00) 1. representative subsample of NHANES 2003-2004..280-.620) .15) 1.450) 1.890-2.

141(7):2667-2673.121(1):21-33. Onuki A. Indoor air pollution by alkylphenols in Tokyo. Qian J. hormones. Yoshimura Y. Zaugg SD. Arch Toxicol 1996. Camann DE. Katsuda S. Spengler JD. Toxicol Appl Pharmacol 2005. Blake CA. Blake CA. Yoshida M.S. Inoue K. Horie M. Kawaguchi M. and sertoli cell number. Food Chem Toxicol 2006. Fail PA. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Biol Reprod 1997. polybrominated diphenyl ethers. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Carey SA. Brody JG. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. and other endocrine-disrupting compounds in indoor air and dust. Estrogenic activity of octylphenol. Bolt HM. Brine DR. Ito R. Environ Health Perspect 2008. 2003. Laws SC. Phthalates. Reprod Toxicol 2001. Two-generation reproduction study with para-tert-octylphenol in rats. et al. McCoy GL. Yoshimura S. alkylphenols. Watanabe G.30(2 Pt 1):81-95. An environmental assessment of alkylphenol ethoxylates and alkylphenols.37(20):4543-53. Raychoudhury SS. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Reidy JA. Muller AM. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Song L. Inoue K. Maekawa A. Saito Y. Williams B. Wang X. Seto H.S.14(5):325-332. Izumi S. Makino T. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Thurman EM. Bodman GJ. Millette CF.207(1):59-68. Kolpin DW.15(6):683-692. Maekawa A. and testosterone. Katsuda S. Reprod Toxicol 2004. Roche JF. Paranko J. 1995. Endocrinology 2000. Toxicokinetics of p-tert-octylphenol in male Wistar rats.799(1):119-125. nonylphenol. Warhurst AM. Rudel RA. Kawaguchi M. and other organic wastewater contaminants in U. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Sweeney T. Calafat AM.pdf. Haavisto TE. Furlong ET. Indoor Air 2004.44(8):1355-1361. Takai N. Toxicol Appl Pharmacol 2000. Takenaka A. streams. Boockfor FR. 2/4/09 Ying GG. testis size.Environmental Phenols References Bian Q. Stir bar sorptive extraction and thermal desorption-gas chromatography-mass spectrometry for the measurement of 4-nonylphenol and 4-tert-octylphenol in human biological samples. et al. Saito I. Ferrell JM. Myers CB. Anal Chim Acta 486:41-50. et al. Korn LR. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Regul Toxicol Pharmacol 1999. Exposure of the U. Sakui N. 1999-2000: a national reconnaissance. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Toppari J. Xu L.36(6):1202-1211. Fedtke N. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Ono H. Karjalainen M. Pharmaceuticals.28(3):215-226. Wong LY.57(2):255-266. Usumi K. Environ Int 2002. Cooper RL. Brooks AN. Taya K. Myllymaki SA. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.co. Nair-Menon JU. Available at URL: http:// www. Meyer MT.71(1-2):112-122. Nicol L. Tyl RW.116(1):39-44. Taya K.foe. Toxicol Sci 2000. Barber LB. Okada F. pesticides. prolactin.uk/resource/reports/ethoxylates_alkylphenols. Needham LL. et al.165(3):217-226. Certa H.folliclestimulating hormone. Seely JC.54(1):154-167. Environ Sci Technol 2002. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. bisphenol A and methoxychlor in rats. Boockfor FR. Toxicol Lett 2001. Nakagomi M. Yoshida M. Environ Sci Technol 2003. Watanabe G. Marr MC. Wiegand HJ. Ye X. Chen J.18(1):43-51. Nagao T. Kookana R.

In the body it is conjugated to glucuronides and sulfates (Bodey et al.S.S. mouthwashes. 1969). Calafat et al. In 1999-2000. the median urinary triclosan level of 7. Triclosan formulations may rarely cause skin irritation. 1976. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect.. Some reports show endocrine effects are observed in amphibians and fish (Foran et al.. Biomonitoring Information Urinary triclosan levels reflect recent exposure. It acts by inhibiting bacterial fatty acid synthesis.. 2005. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2007. 1988.. 2000). 2006). 1987). Triclosan has a low bioaccumulation potential in fish. General population exposure results from dermal and oral use of products containing triclosan. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. 2007).2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. Calafat et al.. Veldhoen et al. representative subsample of NHANES 2003-2004.. 2000.8-dichlorodibenzo-p-dioxin (Aranami et al. In a U. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. toothpastes. In a study of 90 U. IARC and NTP do not have ratings with respect to human carcinogenicity. toys. young girls. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. Lyman and Furia. and wound disinfection solutions. Triclosan is not considered teratogenic at maternally toxic doses. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. Triclosan enters the aquatic environment mainly through residential wastewaters. 2008 has shown higher levels during the third decade of life and among people with the highest household income.Environmental Phenols Triclosan CAS No. (Sandborgh-Englund et al.. 2007. triclosan was found in 57. a process that can result in the formation of small amounts of 2..S.. but not by race/ethnicity and sex.. Triclosan can be absorbed across skin into the blood stream. it has low acute toxicity. Matsumura et al. Mezcua et al. and medical devices. 2004). 2002). 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. streams sampled in 30 states (Kolpin et al. Fourth National Report on Human Exposure to Environmental Chemicals 37 .. acne medications. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2008). 1996. 2007). In animal and human studies.2 µg/L was comparable to the median level (8. In animal studies. Moss et al.... and has also been impregnated into some kitchen utensils. Triclosan has been added to soaps. deodorants.6% of 139 U. It can be photochemically and biologically degraded.. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al.

8-63.45-10.86-12.7 (28.2-46.1 (8.60 (8.3-31.4.1) 9.6) 39.4) 51.50) 10.8-127) 37.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9) 32.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8) 14.3 (8.6-14.94 (7.20-10.3 (11.1) 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 (9.6 (12.1) 14.8) 116 (39.38-18.9 (50.6 (10.3) 6.3) 47.2 (27.45 (5.50-10.1 (45.90-10.2) 9.8 (21.2 (37.1) 9.2 (11.5) 13.0 (11. Survey Geometric mean (95% conf.0-19.6) 90th 212 (172-241) 03-04 03-04 03-04 9.4) 357 (225-456) 203 (87.9) 75th 47.6-37.0 (36.6-20.8-60.1) 9.8) 9.4-19.0 (8.30-14.11-11.4) 90th 249 (188-304) 03-04 03-04 03-04 8.3-15.00-8.20 (7.4) 75th 43.18 (5.9 (11.4-18.3-67.1) 7.6) 31.7) 292 (151-432) 132 (78.1-39.2-58. population from the National Health and Nutrition Examination Survey.1) 50.5-86.93 (7.6-65.72-13.8-112) 30.4) 25.54 (8.82 (8. interval) 12.9 (8.3) 10.0-15.4 (11.5) 20.Environmental Phenols Urinary Triclosan (2.2 (10.9-236) 193 (90.48-10.40-17.40-11.7 (39.5 (11.6 (9.1) 11. see Data Analysis section) for Survey year 03-04 is 2.20-11.16 (6.4 (12.5) 11.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13. Survey Geometric mean (95% conf.4 (38.5) 66.20-13.3.4.89-11.1) 13.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14. population from the National Health and Nutrition Examination Survey.3 (26.0 (26.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.8) 7.2-14.4 (32.7) 123 (36.4) 73.3-35.45-13.20 (7.6-111) 33.7 (9.S.00 (4.5-14.9 (33. interval) 13.0) 65.43-13.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.55 (4.6-15.8-85.7 (14.70-16.0) 9. Urinary Triclosan (2.0-15.0-213) 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 .32-14.9-61.92-12.6) 10.0-73.6) 12.2) 13.60 (6.2-58.7 (11.6-14.4) 7.9) 7.0) 49.1 (15.48 (8.10) 84.74 (5.0 (34.S.2) 12.9) 8.1) 9.21 (6.4) 317 (231-433) 144 (96.2 (13.7) 10.6 (30.2 (25.6) 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 9.29-12.80 (5.22-10.10-9.

Ferrer I. Moss T. Environ Health Perspect 2008. Aquat Toxicol 2006. Hernando MD. Ye X.116(3):303-307. Erratum in: Aquat Toxicol 2007. Bennett ER. Mar Environ Res 2000. Larson EL. Skirrow RC. Adolfsson-Erici M. The oral retention and antiplaque efficacy of triclosan in human volunteers. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Chemosphere 2007. Wolff MS. Aranami K. 1999-2000: a national reconnaissance. Pharmacokinetics of triclosan following oral ingestion in humans.38(4):361370. Matsumura N. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Leonard PA. Kaneshima H. J Invest Dermatol 1976. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. and other organic wastewater contaminants in U.69(20):1861-1873. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Triclosan: applications and safety. Needham LL. et al. Biol Pharm Bull 2005. Arch Environ Contam Toxicol 1988. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Gilbert RJ.23(5):579-583.38(2):64-71. Hong HC. et al. Barber LB. Shiratsuchi H. Am J Infect Control 1996. Foran CM. Nagao Y. Meyer MT.7/2. Katsura E. Gomez MJ.4’-trichloro-2’hydroxydiphenyl ether). Anal Chim Acta 1004.83(1):84. Bodey GP. Williams FM. J Toxicol Environ Health A 2006. population: 2003-2004. Readman JW. phthalates. Furia T. et al.115:116-121. Kanetoshi A.24(3):209-218.17(5):637-644. Britton JA. Lyman FL. Calafat AM. Aguera A. Urinary concentrations of triclosan in the U. Developmental evaluation of a potential non-steroidal estrogen: triclosan.36(6):1202-1211. Photolytic degradation of triclosan in freshwater and seawater. streams. Sandborgh-Englund G. Thurman EM. Food Chem Toxicol 2000. Windham G. Zaugg SD. Bhargava HN. Percutaneous penetration and dermal metabolism of triclosan (2. Wong LY. et al. Howes D.S. Pinney SM. Williams PE. and phenols in girls. Teitelbaum SL. Pharmaceuticals.80(3):217-227. Okui T.4. Gunderson MP. hormones. Toxicology of 2.28(9):1748-1751. Osachoff H. Environ Health Perspect 2007. Kolpin DW. IMS Ind Med Surg 1969. 4’-trichloro-2’-hydroxydiphenyl ether. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Ishibashi H. Furlong ET.Environmental Phenols References Aiello AE. Mezcua M.67(4):532-537.50(1-5):153-156. Environ Sci Technol 2002. Ekstrand J.S. 4. Veldhoen N. Ogawa H.66:1052-1056.524:241-247. Ebersole R. Pilot study of urinary biomarkers of phytoestrogens. Chelimo C. Odham G. Reidy JA.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Fernandez-Alba AR.. Clapson DJ.45 Suppl 2:S137-S147. Benson WH. Evidence of 2. Hirano M. Levy SB. Wigmore H. Watanabe N. Br J Clin Pharmacol 1987.

g.58-2.350 (. After a single dose. population from the National Health and Nutrition Examination Survey.67) 1.91 (1.54-2..350 (.37) .53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350-.37 (.960) 1.01 (<LOD-1.680-1.53) 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 .500-2. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.33) . After absorption.350 (.350-.32 (.350) < LOD .78) 1. utility poles and fence posts).50) 1.350-.75) 2.350) 90th .350-1.850-2. are eliminated in the urine. other polychlorinated benzenes. herbicide.64) 1...76) 1. bactericide.350 (.980 (. hypertension.90 (1.350 (.33-2.510-5.S.350-2.10) 1.08-3.770 (.350 (.10 (. PCP is distributed to most tissues and is not extensively metabolized. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350) < LOD . and dermal contact with PCP-treated products.350 (. and possibly of lindane (IPCS. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350) < LOD .51) 1.10 (1.350-1.58-2. Since 1984.62 (.30 (1.590-1.94 (1. In the environment.390 (.76) .90) 2. Kohli et al.350-.09) .530) 1.350-. water and sediments because of the large amounts that were produced and used historically.42) 696 680 521 696 603 951 Limit of detection (LOD. so it is relatively non-persistent.350) < LOD . Effects including hyperthermia. ingestion of contaminated food or water. The parent compound and conjugates.350) < LOD < LOD 75th .350-.350 (.04) 1. and metabolic acidosis were observed in CAS No.350) < LOD .00) 2.23 (.350) < LOD .350 (.350) .S.350) < LOD .45-2.65 (.. which may vary for some chemicals by year and by individual sample.70) 2.70) .350-. 2002.350-. air.47-5. algaecide and insecticide.350-. Human exposure to PCP has become less common. and it is used primarily as a preservative for wood to be used outdoors (e.630 (.350 (.18 (<LOD-1. and animals. Acute.990 (<LOD-2.350) < LOD .350-2.40 (. General population exposure to PCP may occur by inhalation of contaminated air..350 (.30) 1.350-. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. PCP is eliminated over a few days (Braun et al.48-2.390 (.10 (<LOD-1. along with small amounts of tetrachlorohydroquinone and conjugates.350-2.660 (.350-.350-1.30 (. 1986).00) 1.30) . 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.650) 1.350-.60) 1.60) 1.350-.30) 1.350) < LOD .76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) < LOD .00) 1.5.350-. mollusicide. 1979). with repeated or chronic exposure.350 (.47-3.350 (.98 (1.350) < LOD .350) < LOD .350-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350-.990-2. plants.350-.48 (. PCP is absorbed rapidly and well by all exposure routes.350) < LOD . 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350 (.30 (.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-. PCP has been detected in soils. PCP use in the U.350-.890-1.350 (.510-3. PCP is degraded by sunlight and metabolized rapidly by microorganisms.350 (. has been restricted.350 (.350 (.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350 (. < LOD means less than the limit of detection. the elimination half-life may be a week or more (Uhl et al.350-. 1976.90) 1.94 (1.350) < LOD . To-Figueras et al.480-2.650 (.890 (. PCP cannot be used on wood in residential or agricultural buildings.350) < LOD . 1997).80) .25 and 0.350-2.350 (.00 (.350) < LOD .350-2.350-.83 (2.350-1.73 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.860-2.350-.65 (.10) 1.350 (.

atsdr.650 (.52 (<LOD-1..94 (1.300 (.510-. In animals. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.320) < LOD ..19) 2.06-3.570 (.30) 1..900-1.67-2. Pentachlorophenol is not mutagenic or teratogenic. 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.25-2.560) < LOD .800) < LOD 1.40-2.S. 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. 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.290-.84 (1.25 (1.990 (.55) 1.500-.52) 1.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25-1.240-.69 (1.21-2. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. or skin absorption.gov/ pesticides/ and from ATSDR at: http://www.310) < LOD .92) 1.35) 1.440 (.920 (.67 (1.html.67 (1.78) 1.30-2.760 (.18) . 1991).250 (.e.79) 1.830) < LOD .67 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.580-.10-2.6 and 14. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.290) < LOD . Death can result from seizures and cardiovascular collapse.26 (1. and the FDA has established a standard for bottled water.52 (<LOD-1. respectively) (Seifert et al.16 (. environmental levels) and health effects is available from the U.40) 1.300 (. 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 (4.380-. population from the National Health and Nutrition Examination Survey.82 (1.35-2.340-.S. Survey Geometric mean (95% conf.75 (<LOD-2.780-1. 1989).590) < LOD . respectively) (Becker et al. 1989).48-2.360 (.360-. EPA has developed standards for PCP in drinking water and the environment.330-.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.350) < LOD . More information about external exposure (i.400 (.40) 1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .630 (.67 (1.S.850 (.310-.94-3.21 (.57 (1.260 (. 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.220-.780) < LOD . chronically administered high doses of PCP were hepatotoxic.950-1.08 and 5.75) 1.19) 2..cdc.67-3.610 (..430-.270-.29-3.10 (1. The U.73 (1. children in the 1980’s.0 mg/L.950-1. 2004.910-1. EPA at: http://www.590-1.Fungicides adults and children severely exposed to PCP through ingestion.730) < LOD .82) 1.EPA.00) 1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .25 (1.40) 1.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .epa.09 (<LOD-2. In NHANES 2001-2002 subsamples.700-2.78) 1..500-1. OSHA has established an occupational standard..420) < LOD .35) 1.34 (.06 (.25) 1.560) < LOD . In a small sample of U.320) < LOD < LOD 75th . van Raaij et al.95) 3. 2003).67-3. and adversely affected thyroid function (U.18 (1.84-4.56) 1.35-2.00-1.40) 1.500 (. Among adults in the NHANES 1999-2000 subsample.30 (.19) 2.30) 1.S.280) < LOD .220-.06) 1.430) < LOD .19 (1.25-2.51) 1.83 (1.09-1.270-.00-1.950-1.11) 2. 1995).13 (.710-1. carcinogenic.490) < LOD . 2003).52 (1.650 (.57 (. 2000).510-.90) 1.67 (1.26 (1.650) 90th 1.S.36) .370 (.84) 1.94 (1.320 (.560-.250 (.470 (.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .290-.gov/ toxpro2. inhalation.9 mg/L.40) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .16-1.320) < LOD .800-1..

International Programme on Chemical Safety (IPCS). Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. EPA). Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects.S.inchem. Fast DM. Arch Environ Contam Toxicol 1989. Baker S. Helm D. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Environ Health Perspect 1997. U. To-Figueras J. Schulz C. Bragt PC. drinking water and indoor air. Phillips DL. Kaus S. Otero R. Hill RH. References Becker K. Uhl S. Arch Environ Contam Toxicol 1989.org/documents/jmpr/jmpmono/2002pr08. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Environ Res 1995.58:182-186. Can J Biochem 1976.71:99108. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Shealy DB. Jones D. To T. et al. Cline RE. J Expo Anal Environ Epidemiol 2000. Lindane. urine. The metabolism of higher chlorinated benzene isomers. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402. Dev Toxicol Environ Sci 1979. van den Berg KJ. Environmental Protection Agency (U. Gregg M. Head SL. available at URL: http://www. htm. Santiago-Silva M. Pharmacokinetics of pentachlorophenol in man.18(4):469-474. Schmid P. Int J Hyg Environ Health 2003. Pesticide residues in urine of adults living in the United States: reference range concentrations. 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. Safe A. Needham LL. hair. Seiwert M. Braun WH. et al. Available at URL: h t t p : / / w w w. Schulz C. 206:15-24. Needham LL. 4/21/09 van Raaij JA. Engel R. PCP: Human Risk Characterization [online]. Notten WR. Seifert B. Toxicology 1991: 67(1):107-16. Chenoweth MB.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. house dust. Seiwert M.10:552-65.105(1):78-83. r e g u l a t i o n s .4:289296. 2002. Seifert B. Arch Toxicol 1986.S.54(3):203-208. Rodamilans M. Krause C. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Barrot C. Hill RH Jr. Hill RH Jr. 11/30/2004. Bailey SL. et al. Holler JS. Sala M. Smith SJ. Becker K. Blau GE. Schlatter C. 4/21/09 Kohli J. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.18:475-481. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood.

466 (.10-2.40-7.552 (. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.760-2.389-.23) 695 680 520 695 603 953 Limit of detection (LOD.493 (.364-.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .624) * .490 (<LOD-.S.496 (.500-2. Available evidence suggests that OPP does not accumulate in the body. Estimated human intakes have been below recommended intake limits (U.28-3.EPA.470 (<LOD-.22) 2.S.497 (. General population exposure can occur via dermal.610 (.560-8. however.890 (.76) 1.520 (.570-1. on ornamental plants and turfs. and sanitizers.50) < LOD .40-5. Most agricultural food applications have been revoked.740 (.850 (.60-3.490 (<LOD-.970 (.836) * .621) * . < LOD means less than the limit of detection.420 (<LOD-. sodium ortho-phenylphenate (SOPP).40-5.820 (.20) < LOD 2. are antimicrobial agents used as bacteriostats.80-3.85) 2.490 (<LOD-. Survey Geometric mean (95% conf.22 (.20-3.20) < LOD 1.17 (.88) 1.00-2. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.830 (.350-1..20-2.50-3.750-2.20) 2.860 (.34) 1. Both chemicals degrade within hours to weeks in the environment (U.780) < LOD .490 (<LOD-.890) 1.880-2.840-1. Timchalk et al.30) < LOD 90th 1.90 (1.19 (.S. 2006).10) .90) 1. or apply these chemicals may be more highly exposed than the general population.92 (.90 (1. In the past.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 . interval) .770 (. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.600-1.50) < LOD . or 2-phenylphenol) and its water-soluble salt. it was used in home sanitizers for surfaces. inhalational.498 (.370-.490 (<LOD-.40-2.30) < LOD 1.480-1.800-3.742) * .630) < LOD .590-2. Cnubben et al. formulate. OPP is still used as a disinfectant fungicide for industrial applications..690-1. OPP is volatile. such as fruits and vegetables.10 (1.90) . 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.00) .600) < LOD .790) 2.580-1. in paints.10-1. whereas SOPP is not volatile and is more water soluble.450 (<LOD-.370-.10) .508 (.890 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.550-1.710) 3.386-.20 (.33 (. Fourth National Report on Human Exposure to Environmental Chemicals 43 .03) 1.60-2. Both have been used in agriculture to control fungal and bacterial growth on stored crops.30-7.00 (1.570 (.90) 2. 1998.509 (.10) 2.20 (1.690) < LOD .433-.600) < LOD .00 (1. EPA. 1989).00 (1. but OPP and SOPP are still used on pears and citrus (U.00 (1.00) .50 (1.27 (. 2006). SOPP is applied topically to the crop and then rinsed off.696) * . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.61) 2. leaving the chemical residue OPP.950) < LOD .14 (<LOD-3.50 (1.85) 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) 1.640) < LOD . 90-43-7 General Information Ortho-phenylphenol (OPP.50) .570 (. Workers who manufacture.930 (.80 (2.370-.450 (<LOD-.80) 1.20 (1.349-.3 and 0.60 (1.390-. 2002.570-.30-2. population from the National Health and Nutrition Examination Survey.770 (.540-2.600) < LOD 75th . 2006).10 (1.00) < LOD .10) . OPP is considered to be moderately toxic after acute oral doses in animal studies.389-. and as a wood preservative.EPA.600) < LOD 1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.670) 2.600-1.30) < LOD .860) * 99-00 01-02 99-00 01-02 99-00 01-02 . which may vary for some chemicals by year and by individual sample.50 (1.50) 1.50-4.610-1.02) 1.710-2.10) 1.28 (..3.636) * .570-2. fungicides.638) * .50-2.09) 2.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.90) .40 (.30 (1.80) 1.Fungicides ortho-Phenylphenol CAS No.567 (.60 (1. 1998).60 (1.50) < LOD . and it has limited water solubility.645) * .410-.600-1. 2006).30) 1.S.07 (.450 (<LOD-.402-.

59) 1.24-2.380 (.89 (1.38) 2.550) < LOD .558) Selected percentiles ( 95% confidence interval) Sample 95th 2. Kwok et al.320 (<LOD-.11-1..21) 1. 1984. In high dose animal studies.05-2.EPA 2006)..666) * .900-1..06-5.40-13.514 (.S.96 (1.570) < LOD 1. 2002.epa.484) * .480-.610) < LOD 1. Additional information is available from U.900) < LOD .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 .880-1. CDC. U.403-.97 (2.670) < LOD . Biomonitoring Information Urinary OPP levels reflect recent exposure.0) 1.810-1..670 (.910 (. Brusick.750 (.440 (. Survey Geometric mean (95% conf. 44 Fourth National Report on Human Exposure to Environmental Chemicals .780-14.860 (.420 (<LOD-.S.09-6.360 (<LOD-.590) * .21-2.. OPP was not found to be mutagenic.29) 1.500) < LOD .Fungicides anemia.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2005). ortho-phenylhydroquinone and ortho-phenylbenzoquinone.910-1.17 (.329-.568) * .800-1. Ito et al.33-2.11 (. 2005).13) 1.11 (.53) 1. 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. Smith et al.980 (<LOD-1.52 (.28 (<LOD-4.06-4.4 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.01) 1.353-.24-2.470) < LOD .17) 2. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.00 (.58) 2.43-2..28 (2. 1986).291-.410 (<LOD-.4) 3.00 (1.46) < LOD 1.26) 1.940-2.810) < LOD .25-6.510-.78 (2.33) .770-2.. 2000.09-3.32) 1.690 (.343 (.32) 3.640-1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .382 (. leading to production of two metabolites.270-. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.61 (2. Zhao et al.59) . Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.620-1.47) .410 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.04-4. 2002).550-. reproductive.09 (1.91 (1.910 (<LOD-1. population from the National Health and Nutrition Examination Survey..93) 1.361-.650-1. 1998.38) 1. 1997.96) 1. Detectable levels were seen in over half the U. U. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.08) 1.580-1.75 (1.550 (.17 (.750-2.840 (.453 (.07) 2.38-3..455-.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .580) < LOD .75 (1.460-. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1984.31) < LOD .980 (.61 (.510 (<LOD-.950) < LOD . Volunteers exposed to 0.93) . 1999.248-.444 (.06 (1.51-3. and it has classified OPP as not classifiable with respect to human carcinogenicity.656) * .970) 1.11) < LOD 90th 1. 2005.EPA at: http:// www.780 (.EPA 2006).29) 1.496 (.64 (2. 1993. or developmental toxicity was observed (Bomhard et al.96 (1.S.301-.43 (1.791) * . 1992.44 (1.74 (1.81) 1.311-.43) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.69 (1.473) * .02 (.93 (1. 2002. 1999.750 (. but no neurologic.20) < LOD 3.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . interval) .93) . by possible genotoxic mechanisms (Hagiwara et al.11) 4. IARC has classified SOPP as a possible human carcinogen.385 (. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.12) < LOD 1.. Pathak and Roy.27) < LOD .12-2.990) < LOD .21 (.61 (1.508) * .62) .470 (<LOD-. less likely.S.420 (<LOD-.08-2.670 (.84 (1.18) 2. Nakagawa et al.96-4.620-1. Bomhard et al.860 (.560-2.600-1.S. Murata et al.88-4.43-2.560) < LOD 75th .86 (1.gov/pesticides/. or.08-1.

Meuling WJ. Arch Toxicol 2000. IARC Sci Publ 1984. Kwok ES.35(2 Pt 1):198-208. Christenson WR.pdf.50(11):3351-3358. Zhao S. Mutat Res 1993. Nakagawa Y. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Cano M. J Agric Food Chem 2002.epa. Bormett GA. Imaida K.32(6):551-625. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Arnold LL. 4/13/09 Onstot JD. EPA). EPA-560/5-89-003. Christenson WR. 2006. Environ Mol Mutagen 2005. St John MK. Stanley JS. Hirose M. Centers for Disease Control and Prevention (CDC). Bartels MJ. Available at URL: http://ntp. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. et al. Glas K.703(12):97-104. Tayama S. Identification of SARA compounds in adipose tissue. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Mendrala AL.159(1):18-24. Drugs. Carcinogenesis 1999. Comparative metabolism of orthophenylphenol in mouse. 4/9/09. Pathak DN. U. rat and man. Ito N. J Agric Food Chem 2006. Bartels MJ. Narang A. Shirai T. Food Chem Toxicol 1984. 90-43-7) in Swiss CD-1 mice (dermal studies). Brzak KA. Richter M. Bartels MJ. Moldeus P.gov/oppsrrd1/REDs/ phenylphenol_red. Inoue S. Smith RA.22(10):809-814.gov/ntp/htdocs/LT_ rpts/tr301.. 2005. J Chromatogr B Biomed Sci Appl 1997.54(16):5731-5735. Sangha G. EPA 739 R-06004. July 28. Environmental Protection Agency (U.286(2):309-319. Kawanishi S. Selim S. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol.EPA). Leser KH. Roy D. Coelhan M. Eastmond DA. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Toxicol Appl Pharmacol 1999. Bromig KH.45(5):460-481.pdf. Hagiwara A. Xenobiotica 1998. Hakkert BC. Environmental Protection Agency (U. McNett DA. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. et al. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP).74(2):61-71.150(2):402-413. Brusick D.20(5):851-857. Fukushima S. Moore GA. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Cnubben NH. Moriya K.S. 1989. Elliott GR. Timchalk C.Fungicides References Appel KE. Bomhard EM. Sangha GK. Regul Toxicol Pharmacol 2002. Hagiwara A.(56):399-407. Timchalk C. Roberts AL. Vogel JS. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Atlanta (GA). Biochem Pharmacol 1992. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Brendler-Schwaab SY. Available at URL: http://www.17(8):411-417. Murata M. Freyberger A. van de Sandt JJ. Eadon G.S. Toxicol Appl Pharmacol 1998. U.28(6):579594. National Toxicology Program (NTP).nih. Crit Rev Toxicol 2002. Turteltaub KW. food additives and natural products as promoters in rat urinary bladder carcinogenesis. March 1986.niehs. Office of Toxic Substances. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Shibata M. Gierthy J. Herbold BA. Fukushima S. Ito N.S. Third National Report on Human Exposure to Environmental Chemicals. The carcinogenicity of the biocide ortho-phenylphenol. Bartels MJ.43(7):14311437.S. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Hum Exp Toxicol 1998. Buchholz BA.

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

this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. 2000.. Acetochlor is moderately toxic to fish and honey bees. However. 2007).EPA. 2006). Jefferies et al. but other pathways occur. including one that produces 2-methyl-6ethylaniline and its reactive metabolite. 2000. and hydroxymethyl ethyl aniline (U.S. Additional information about external exposure (i. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.gov/ pesticides/. It is absorbed by plants and inhibits plant protein synthesis. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.epa. 2006). Biomonitoring studies on levels of acetochlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acetochlor than are found in the general population. 1998). however. but it has produced testicular atrophy. Acetochlor is microbiologically degraded..Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure.S.EPA. Fourth National Report on Human Exposure to Environmental Chemicals 47 . Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. animals have demonstrated tumors of the lung. General population exposure to acetochlor may occur through diet or drinking water... 1996). U. a major pathway for acetochlor metabolism involves mercapturate conjugation. NTP and IARC do not have ratings regarding human carcinogenicity. the latter which may account for some observed effects (Coleman et al.EPA considers acetochlor likely to be carcinogenic in humans.. 1994.EPA 2000.S. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. 2000). 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. and thyroid (U. People exposed to acetochlor will excrete acetochlor mercapturate in their urine. and has been detected in watersheds of agricultural lands (Battaglin et al. Estimated human intakes of acetochlor have been below recommended limits (U..EPA. Acetochlor has low acute toxicity.S. remains in soils for up to 3 months.e. which are often more prevalent in the environment. Feng and Wratten.. 2005). 2005. 2005). 2006). Hladik et al. 1989. Kolpin et al.S. in some species and at doses above maximum tolerated doses. nasal epithelia. and it is unlikely to be genotoxic at relevant doses (Ashby et al. renal injury. In animals.S. 2000. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. 2006). Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. environmental levels) is available from U. mainly corn. Urinary acetochlor mercapturate levels of 0.. and neurologic movement abnormalities (U. Acetochlor is not mutagenic.0 μg/L (Curwin et al. CAS No. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. EPA at: http://www.. Davison et al.. 2-hydroxyethyl-6-methylaniline.

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

Hines CJ. Alavanja MC. Lefevre PA. Larsen GL. pages 3682-3690.248(2-3):115-122.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. et al. J Agri Food Chem 1989. Striley CA. Linderman R. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Feng PCC. imidazolinone. 5/30/06 U. Hladik ML. Heederik D. Sci Total Environ 2000. Tinwell H. Hein MJ. Kolpin DW.24(10):1003-1012. Wilson AG. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Peter CJ. Barr DB. Coleman S. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. sulfonamide.15(6):500-508.cornell.cce. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. J Expo Anal Environ Epidemiol 2005. 1998. Green T. U.11(4):353359.pdf. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Rose RL. Wratten SJ.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Kier L. Reynolds SJ. Olsson AO. Occurrence of sulfonylurea. Available at URL: http://www. Hsiao JJ. 2005. Environ Health Perspect 2000. Environ Sci Technol 2005.15(9):702-735. Quistad GB. Dialkylquinonimines validated as in vivo metabolites of alachlor. Sanderson WT. 5/30/06. Hum Exp Toxicol 1996. Curwin BD.17(6):559-566. Barr JR. Whyatt RM. 2000. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Jefferies PR. EPA). Volume 65. Deddens JA. Bravo R. Barr DB. Federal Register: January 24. and metolachlor herbicides in rats. Andrews HF. March 2006. Ward EM.html.Herbicides References Ashby J. Number 15.248(2-3):123-133.37(4):10881093. Burkhardt MR. Barr DB. Feil VJ.S. Linhart SM. Atlanta (GA).39(17):6561-6574.S.S. Comparative metabolism and elimination of acetanilide compounds by rat. et al. Hodgson E. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Xenobiotica 1994. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. EPA). EPA 738-R-00-009. Kinney PL. et al. Environmental Protection Agency (U. reservoirs and ground water in the Midwestern United States. Thurman EM. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention (CDC). Casida JE.108(12):1151-1157. Sci Total Environ 2000.S. Chem Res Toxicol 1998. and other herbicides in rivers. Environmental Protection Agency (U.111(5):749-756. Camann DE. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Available at URL(non U. acetochlor. Battaglin WA. Furlong ET. J Expo Sci Environ Epidemiol 2007.S. Davison KL. Environ Health Perspect 2003. Acetochlor (Harness) Pesticide Petition Filing 1/00. epa. Roberts AL.EPA): http://pmep.

1998. In a study of applicators and workers exposed to alachlor. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. 2005. 2005). 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.EPA. Because it can be absorbed through skin. mercapturate conjugates were predominant metabolites. 2003).EPA.1 to 1. Alachlor has low potential for acute toxicity. Kolpin et al. stomach. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. 1988.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. U. alachlor has demonstrated hepatotoxicity. including corn. Since the late 1980s alachlor use has been declining. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. 1998). as measured through conversion to deethylamine. and uveal degeneration. 1998). alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. and on non-crop land for general weed control. Jefferies et al.. U. In 1993-1995. 2000. Hladik et al. In animal studies. WHO. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. but shows little bioaccumulation.. 2003). 2003). Additional information about is available from U. about 20-25% of the U. WHO. Alachlor itself is not considered mutagenic.. hemosiderosis. Hill et al. corn cropland was treated with alachlor. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. EPA at: http://www.S.1 mg/L at various collection times (Sanderson et al. and field workers. but another metabolic pathway can produce 2.EPA considers alachlor to be a probable human carcinogen at high doses. 2000. 1999 and 2007. Tessier and Clark.EPA. mean values of urinary concentrations of alachlor metabolites. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. 1996. 1998).. U. 1997. soybeans. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. 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.6-diethylaniline and its reactive metabolite.. In animals.S. the latter may account for some observed effects (Davison et al.epa. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment.S. It is absorbed by plants and inhibits plant protein synthesis. peanuts and other crops. 1989. NTP and IARC do not have ratings regarding human carcinogenicity. 1996).S.. 1995). whereas 60% of applicators had detectable amounts.S.S.. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. 1998. In chronic animal testing. but not likely at low doses. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. 1998. Estimated human intakes have been below recommended limits (U.S. the dermal exposure route is potentially significant for applicators.. WHO. 2003). People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al.gov/pesticides/. Hines et al. IPCS. U.EPA. but has not shown developmental or reproductive toxicity in mammalian systems (U. 1999. 1995. 1994. ranged from 0. Alachlor has a soil half-life of a few weeks. WHO..EPA. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. (2003) showed that 2. formulators.. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. Feng and Wratten. 50 Fourth National Report on Human Exposure to Environmental Chemicals . 1996. USGS.Herbicides Alachlor CAS No.

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

EPA). J Agri Food Chem 1989. Environmental Protection Agency (U. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .int/water_sanitation_health/dwq/chemicals/en/alachlor. Jefferies PR.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Gilliom RJ).395(2-3):159-171. who. 1997.usgs. 2/27/09 Jefferies PR. An evaluation of the carcinogenic potential of the herbicide alachlor to man. 2/27/09 U. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Hladik ML.24(10):1003-1012. 4/2/09 U. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Hines CJ. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Furlong ET. Henningsen G. Available at URL: http://water. Environ Health Perspect 2003.18(6):363-391. 1999. December 1998. Casida JE. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Erratum in: Life Sci 1989. Alachlor in Drinking-water.S. Quistad GB. J Ag Food Chem 1995. 1992-2001. Tolos W. 1996. Sanderson WT. DNA adduct formation by alachlor metabolites. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Camann DE. Geological Survey (USGS). Striley CA. Wilson AG. Andrews HF. Feng PCC. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Circular 1291. World Health Organization (WHO). Kimmel EC. Biagini R. Casida JE. Kinney PL. Atlanta (GA). Geological Survey (USGS).37(4):10881093. Am Ind Hyg Assoc J 1995. U. Barr DB. 1998. Available at URL: http://www. 1999. 2005.epa. International Programme on Chemical Safety (IPCS).11(4):353359. Larsen GL. Kier LD.39(17):6561-6574. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Hill RH Jr. sulfonamide. Brown MA. Environ Sci Technol 2005. EPA 738R-98-020. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. imidazolinone. Roberts AL. Reregistration Eligibility Decision (RED) Alachlor. and metolachlor herbicides in rats. World Health Organization. Bull Environ Contam Toxicol 1996.pdf. Sci Total Environ 2000. Wratten SJ. Mutat Res.111(5):749-756. WHO/ FAO Data Sheets on Pesticides. Lau H. Sacramento. Casida JE.gov/oppsrrd1/ REDs/0063. Supplemental Technical Information (available on-line only). Peter CJ. Heydens WF. 86. Burkhardt MR.org/documents/pds/pds/pest86_e.php. Hines CJ.248(2-3):123-133. Driskell WJ. Centers for Disease Control and Prevention (CDC). Biagini RE.S.47(6):503-517. Thelin GP. Shealy DB. Background document for development of WHO Guidelines for Drinking-water Quality.43(9):2504-2512. Sci Total Environ 2000. Available at URL: http://www.pdf. Occurrence of sulfonylurea. Deddens JA. Hum Exp Toxicol. Life Sci 1988. Third National Report on Human Exposure to Environmental Chemicals. Kolpin DW. 2007.S. March 2006. revised February 15.Herbicides References Battaglin WA.43(25):2087-94. Davison KL. Hsiao JJ. Martens MA. Geneva. Available at URL: http:// www. et al. MacKenzie B. No. California. Clark JM.S. Dialkylquinonimines validated as in vivo metabolites of alachlor. Hill AB. Tessier DM.htm. and other herbicides in rivers. Whyatt RM. Thake DC. Kolpin DW. Feil VJ. Hull RD.44(18):1325. Ann Occup Hyg 2003.56(6):853-859. Comparative metabolism and elimination of acetanilide compounds by rat. Barr JR. reservoirs and ground water in the Midwestern United States. ALACHLOR. acetochlor. et al. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Brown KK. Linhart SM.inchem. 98-4245 (by Barbash JE. Chem Res Toxicol 1998. Shoemaker DA. Thurman EM. 2003. Xenobiotica 1994.56(9):883-889.248(2-3):115-122. Quistad GB.

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

and reduced levels of luteinizing hormone. 54 Fourth National Report on Human Exposure to Environmental Chemicals . In addition to being human metabolites of atrazine. increased pituitary weight. 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. Rayner et al. the dealkylated atrazine metabolites and hydroxyatrazine can occur in the environment from the breakdown of the parent chemical. 2003. Gammon et al. EPA at: http://www. Survey Geometric mean (95% conf. Sanderson et al. and cyanazine. 2000. Sathiakumar and Delzell. 2002. IARC considers atrazine not classifiable with respect to human carcinogenicity.epa. 2005). 2003). and U. impaired fertility. 2005.S.EPA considers atrazine unlikely to be a human carcinogen.gov/pesticides/ and from ATSDR at: http://www..gov/toxpro2.S. including simazine.. Dealkylated metabolites from atrazine can also result from metabolism of other chlorotriazine pesticides. population from the National Health and Nutrition Examination Survey. Atrazine is not considered genotoxic. propazine. Thus.. 1997). Chronic high dose toxicity observed in animals includes decreased body weight.atsdr. 2000 and 2003. Stevens et al. Laws et al.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 808 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1314 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 683 550 918 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.. altered estrus cycles. 2004.EPA. Human health effects of atrazine at environmental doses or at biomonitored levels from environmental exposure are unknown. liver toxicity. Atrazine and the dealkylated chlorinated metabolites did not have estrogen receptor activity. Estimated human exposures are thousands of times lower than doses that caused effects in animals (Gammon et al. detection of these dealkylated metabolites in a person’s urine may also reflect exposure to these degradates in the environment. atrazine is rated as having low acute toxicity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Some human ecologic and epidemiologic studies of reproductive and cancer outcomes have shown either positive or no associations. Additional information is available from U.. may mediate some effects of atrazine (Laws et al. 2005. but the effects are difficult to attribute due to lack of exposure markers or due to mixed chemical or pesticide exposures (ATSDR.. 2003b). In mammalian studies. prolactin...html.S. 1994. Stoker et al. developmental ossification defects.. delayed onset of puberty. 2000 and 2002.S. and testosterone (Gillis et al.cdc.. 1994 and 1999. Urinary Atrazine mercapturate (creatinine corrected) Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. Atrazine product formulations can be mild skin sensitizers and irritants. myocardial muscle degeneration.Herbicides particularly diaminochloroatrazine (the main dealkylated product). U. Eldridge et al. 1999). Gammon et al.

Moseman RF. Biagini RE. J Agric Food Chem 1982. Maroni M. Bersani M.inchem. Vonk A. In a study of 60 farm worker children. Gillis JH. Environ Health Perspect 2007.htm. Toxicological profile for atrazine. et al. Cooper RL. 2007). Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. ATRAZINE. 2000). Stoker TE. 1993). Hayes TB. Atlanta (GA). atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Stuart AA. Heederik D.53(2):297-307. Gillis JH. atrazine was detected in only four children (Arcury et al. Proc Natl Acad Sci USA 2002. Goldman JM. No. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). 2001 [online]. J Expo Anal Environ Epidemiol 2005. Shoemaker DA. Curwin BD.org/documents/pds/pds/pest82_e. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Goodrow MH. Wetzel LT. Freeman NC. Laws SC. 2005. Available at URL: http://www. Reynolds SJ. 3/11/09 Laws SC. Barbieri F. Ann Occup Hyg 2003.47(6):503-517. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. et al. References Adgate JL. Environ Health Perspect 2001. J Toxicol Environ Health 1994. Tyrey L. 82. Stevens JT. Sanderson WT. Agency for Toxic Substances and Disease Registry (ATSDR).15(6):500-508. Grzywacz JG.43(2):155-167. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.gov/toxprofiles/tp153.109(6):583-590. Barr DB. The geometric mean of urinary atrazine mercapturate was 1. Hines CJ. Eberly LE.58(2):366-376. Deddens JA. et al. Quandt SA. Sanborn JR. Lioy PJ. et al. Toxicol Sci 2000. Third National Report on Human Exposure to Environmental Chemicals.html. Barr DB.. Blewett C. Centers for Disease Control and Prevention (CDC). Available at URL: http:// www.99(8):5476-5480. In small studies of Maryland residents in 19951996 (MacIntosh et al. et al. McElroy WK. 1996.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. In the NHANES 2001-2002 subsample. Clayton CA.cdc. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Pfeifer KF. Ferrell JM. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. International Programme on Chemical Safety (IPCS). Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Simpkins JW. diamino-S-chlorotriazine and hydroxyatrazine. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Tapia J. Toxicol Sci 2000. Perry et al. Hein MJ. Geneva. et al.. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Noriega N. Extrom PC. Collins A. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. 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. A risk assessment of atrazine use in California: human health and ecological aspects. 2003. Cottica D. Mendoza M.. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Lucas AD. Brown KK. Wetzel LT. urinary concentrations ranged from 5-1756 μg/L (Lucas et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicol Sci 2003. J Toxicol Environ Health 1994.30(2):244-247. Ferioli A.61(4):331-355. Eldridge JC.atsdr. Eldridge JC. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Aldous CN. Breckenridge CB. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Hermaphroditic. In a small number of field workers.69(2):217-222.. Striley CA. Jones AD. Ferrell JM. Cooper RL. Cooper RL. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Bradway DE. levels of atrazine mercapturate were generally not detectable (CDC. 2005). Biological monitoring of human exposure to atrazine.64(9):672-678. World Health Organization. 3/11/09 Arcury TA. Toxicol Lett 1993. Gammon DW. Stoker TE.. Seiber JN. Saiz SG. Lee M. Steroids 1999.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Chen H. Catenacci G. Schmid J. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function.76(1):190-200. WHO/ FAO Data Sheets on Pesticides. 2005). Fleenor-Heyser DG. Pest Manag Sci 2005. Barr DB.115(8):1254-1260. 2001). Carr WC Jr..43(2):155-167. Stoker TE. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.

White paper on potential developmental effects of atrazine on amphibians.usgs. Delzell E. Perry M. March 2006. Toxicology 1990.Herbicides development of a biomarker of exposure. Timchalk C.182(1):44-54. Boerma J. 2007. Dryzga MD. 3/11/09 U. Available at URL: http://www. Sathiakumar N. 6/1/09 U. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Tortorelli J. EPA). Supplemental Technical Information (available on-line only). Toxicol Sci 2002. Sanderson JT. Langvardt PW.27(6):599612.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Circular 1291. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Pesticides and Toxic Substances.pdf. Laws SC. Environmental Fate and Effects Division. Rayner JL.195(1):23-34.10(7):479.S. 0062. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Ryan PB. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Geological Survey (USGS). van den Berg M.gov/oppsrrd1/REDs/ atrazine_ired.6(1):107-116.61(1):27-40.S. May 2003a. Christiani D.pdf. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www. Toxicol Sci 2000. J Toxicol Environ Health A 1999. revised February 15. U.S. Wetzel L.S. EPA Office of Pesticide Programs.56(2):69-109. Needham LL. Laws SC. MacIntosh DL. A risk characterization for atrazine: oncogenicity profile. Guidici DL. 1992-2001. Dagenhart D.php.epa. Case No.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.S. Chem Res Toxicol 1993. Cooper RL. The Quality of Our Nation’s Waters. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Stoker TE. Environmental Protection Agency (U. 2003b.9(5):494-501. Guidici DL. Cooper RL. Lansbergen GW. Singzoni B. Environmental Protection Agency (U. Fenton SE. Washington (DC).67(2):198-206. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Wood C.epa. J Expo Anal Environ Epidemiol 1999. A review of epidemiologic studies of triazine herbicides and cancer. Osborne DW. Crit Rev Toxicol 1997. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.58(1):50-59. Toxicol Appl Pharmacol 2004. Hammerstrom KA. Ann Epidemiol 2000. Stoker TE. Interim Reregistration Eligibility Decision For Atrazine. Office of Prevention. Available at URL: http://water. A longitudinal investigation of selected pesticide metabolites in urine. Breckenridge CB. Toxicol Appl Pharmacol 2002. Kastl PE. EPA). Stevens JT.

740 (.S.4-Dichlorophenoxyacetic Acid CAS No.210-.20 (.30 (<LOD-2.610 (.43) 1.952 and 0.27 (1.960-1. General population exposure to 2.4-dichlorophenoxyacetic acid (2.48) < LOD 1.EPA. Sauerhoff et al.66) < LOD 1. 2.690 (.EPA in 1948..51 (1.810-1. 1974. Kohli et al.560-. Once absorbed.490 (.40) 1. by direct contact with agricultural and residential areas after applications. 1989.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.4-D is rapidly absorbed via oral and inhalation routes. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.760 (.420) < LOD . and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.560-1.02-1.S. 2.07 (. Fourth National Report on Human Exposure to Environmental Chemicals 57 .540-.4-D have been below recommended intake limits (U. MCPA.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.230-. the chlorophenoxy herbicide 2.70) 1.690 (.21) 1.S.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 . It was first registered with U.680-1.32 (1.690-1. it acts as a plant growth hormone. population from the National Health and Nutrition Examination Survey. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms. abdominal pain. 94-75-7 General Information Widely used throughout the United States.10) < LOD 1.440-1.00-2. 2004).4-D has low acute toxicity.S.4-D) controls broadleaf weeds in residential.20 (<LOD-1.660) 1.27 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.490) < LOD < LOD < LOD ..310) < LOD . and aquatic environments. which may vary for some chemicals by year and by individual sample. At low levels.16) < LOD .690 (. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.890) < LOD .370-.250 (<LOD-. but at higher levels they are herbicidal. and by consuming food or drinking water contaminated with 2. myotonia.420-.03) 695 659 520 668 589 892 Limit of detection (LOD.4-D may occur during residential applications. dizziness.890 (. Similar to other chlorophenoxy herbicides. 2.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-D or exposed for prolonged periods. 2007). It is poorly bound in soils. headache. It is not well absorbed through the skin.08) < LOD .930 (. Survey Geometric mean (95% conf. hypotension.400) < LOD .05-2. 2005).22) < LOD . < LOD means less than the limit of detection. and delayed Urinary 2. 4-D. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. agricultural.80) 1.10 (<LOD-1.Herbicides 2.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.4-D were used in the U.EPA.610-.670-1.350) < LOD < LOD < LOD . 1977).230 (<LOD-.24 (.330 (.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .730 (.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. with a half-life of several days to several weeks.60) 1. and mecoprop).250 (<LOD-.4-D can be applied either as an aqueous salt or as oil-soluble esters.27-2. renal and hepatic injury. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.910) 1. Human health effects from 2. these herbicides can enhance plant growth..210 (<LOD-.S.13) < LOD .910) < LOD . in 2001 (U.260 (<LOD-. 2. It is rarely detected in ground waters (USGS.550-1.410) < LOD . Recent estimates of chronic intakes of 2.930-1.310 (. As much as 62 million pounds of 2.320) 90th .55 (1.10 (<LOD-1. nausea.

13 (. 2001.610-.08 (.620-.27-1.590 (<LOD-1.S. liver.810-1. developmental. myotonia.380-. 2002.670 (<LOD-1.780 (. 1994).410 (<LOD-.560-. thyroid. other exposures.08 (. population (Hill et al.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 .480 (. Average post-application urinary levels of 2.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.700 (.S.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . and of adults and children (Baker et al.610-.570) < LOD . 2002. Survey Geometric mean (95% conf.73) . and evidence of histological injury to the kidneys.820-1. IPCS. 1989).470) < LOD . IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4-D are eye irritants. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.32 (<LOD-2.890-1.41 (1. Epidemiological studies have reported associations of several types of cancer.550-. 1995. IPCS..640 (. 1995).810-1. urinary 2.890) < LOD 1.720 (. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.13 (.270 (<LOD-. 2000).850) < LOD ..680) < LOD . It is unclear whether these associations are related to the chlorophenoxy herbicides.24) 1.35) < LOD . Additional information is available from U.670 (.S.4-D reflect recent exposure.350 (<LOD-.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. Kolmodin-Hedman and Erne.S. 2005). 2.380 (<LOD-.410) 90th . U. 2005. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.S.S. U. Hill et al.790) 1.340-. or to contaminants in the herbicide formulations (specifically 2. 2. 1996.980) < LOD 1. 1996. adrenals and gonads (NTP.590 (<LOD-1. IPCS.. 2005).930-1.410) < LOD < LOD < LOD .4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 2003.330-. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.7..410) < LOD 1.3. IOM.EPA.56) .08 (.4-D does not have significant reproductive.4-D levels were detectable in less than a quarter of the individuals studied.740 (.660) < LOD . Post-application levels in farmers and home gardeners were dependent on Urinary 2.340 (. CDC.380) < LOD .S.790) < LOD .. 2004). Acute high doses administered to laboratory animals produced ataxia.EPA...16) 1.14 (.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 1996. Frank et al. 2.920) < LOD 1.660 (. 58 Fourth National Report on Human Exposure to Environmental Chemicals . 2005..EPA at: http://www. Pearce and McLean. 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.Herbicides neuropathy (Bradberry et al.390) < LOD < LOD < LOD .490 (..EPA 2005).990-1. The acid and salt forms of 2. or teratogenic effects in chronic rodent studies (Charles et al. eyes.EPA. Knopp et al.780-1.05) . 1985. U.440 (.270-.780) . 2006.520-. Kutz et al. 2005. in small samples of children (Hill et al.17 (.epa. 2005).40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Biomonitoring Information Urinary levels of 2. 2005. 2005).380 (<LOD-.39) < LOD 1.580-. 1980. population from the National Health and Nutrition Examination Survey.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-D production plant workers and a few forestry workers spraying 2. In previous samples of the U. 1992).670 (. U.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .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.19) .gov/pesticides/..560-.

Driskell WJ. Developmental toxicity studies in rats and rabbits on 2. In farm families. Alexander BH. Gregg M. Khanna RN. Hanley TR Jr. Occup Environ Med 1994.4-D): exposure and urinary excretion. TOX-63: TOXICITY REPORT CURVES. Honeycutt R. National Toxicology Program (NTP).4-D were highest in the farmers who applied the 2. Board on Health Promotion and Disease Prevention. Baker S.4-. Arch Toxicol Suppl 1980. Garabrant DH. Arch Environ Contam Toxicol 1985. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.4-D than levels found in the general population.4-Dichlorophenoxyacetic Acid). Erne K. Barr DB. Campbell RA. Assessment of exposure to 2. Third National Report on Human Exposure to Environmental Chemicals. Harris et al.10(6 Pt 2):789-798.org/documents/jmpr/jmpmono/v96pr04.51(3):152-159. 914. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Sirons G J.4 dichlorophenoxyacetic acid (2. Biomonitoring studies of 2. Baker BA. Philbert MA. Centers for Disease Control and Prevention (CDC). J Expo Anal Environ Epidemiol 2000. Cole DC. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Fast DM. Cook BT.gov/index. Holler JS. Crit Rev Toxicol 2002.. the number of acres to which it was applied (Curwin et al.niehs. Finding a measurable amount of 2.4:318-321. Available at URL: http:// www. et al..4-dichlorophenoxyacetic acid (2. J Environ Sci Health B 1992. Head SL. Acquavella JF. Beasley VR. Kohli JD. Scand J Work Environ Health 2005.inchem. 2005).Herbicides the time since application. To T. Available at URL: http://ntp.S.27(1):23-38. References Arbuckle TE. Washington (DC): National Academies Press. TOX-63 Peroxisone Project (2.71(2):99-108. van Ravenzwaay B. 2. Stephenson GR.nih. Tables. general population. 2005 Charles JM. Sircar KP. Kolmodin-Hedman B. Curwin BD. Barr DB. the amount of pesticide applied. Mandel et al. Veterans and Agent Orange: update 2002. Toxicol Sci 2001. Available at URL: http:// www. et al. Needham LL. Harris SA. Pesticides residues in food: 1996 evaluations Part II Toxicology. Absorption and excretion of 2. 2003. J Toxicol Environ Health 1992. Gupta BN. Reynolds SJ. Shealy DB. Survival and Growth Curves from NTP Toxicity Studies. Updated March 7. 2005. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.4-dichlorophenoxyacetic acid and its forms. geometric mean urinary levels of 2.htm. Hill RH Jr.4-dichlorophenoxyacetic acid in man. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31(2):121-125.31 Suppl 1:90-97. Sanderson WT. 3/17/09 Institute of Medicine (IOM). and the use of protective clothing or equipment (Arbuckle et al. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 2005.. Selected pesticide residues and metabolites in urine from a survey of the U.4-D in urine does not mean that the level of the 2. Smith SJ. Solomon KR.edu/catalog. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.60(1):121-131. Chapman P. Exposure of homeowners and bystanders to 2.4-D and 2.4:427-435.32(4):233-257. Baker SE. Bus JS. 1992).4-D will result in an adverse health effect. Vet Hum Toxicol 1989. Kutz FW. Ripley BD. Heederik D. Carter-Pokras OD.. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Bailey SL. 2005). Murphy RS. 2006. Needham LL. Hill RH Jr.nap. et al. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.php?record_id=10603. Dichlorophenoxyacetic acid. Review of 2. Frank R. Tandon JS.31 Suppl 1:98-104.37(2):277-291. Environ Res 1995. J Expo Anal Environ Epidemiol 2005 Nov. Beeson MD. Biomonitoring for farm families in the farm family exposure study.4:97-100. Brody D. International Programme on Chemical Safety-INCHEM (IPCS). Dhar MM. Wilson RD.15(6):500-508. Mandel JS.4-dichlorophenoxyacetic acid (2. 3/17/09 Knopp D. Biomonitoring of herbicides in Ontario farm applicators. Hein MJ. Atlanta (GA).5-T). Arnold EK.4-D) epidemiology and toxicology.4.18(4):469-474. Ritter L.4-D).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. Arch Environ Contam Toxicol 1989. Estimation of occupational exposure to phenoxy acids (2.4-D. Scand J Work Environ Health 2005. Forestry workers involved in aerial application of 2. Pesticide residues in urine of adults living in the United States: reference range concentrations. Xenobiotica 1974.

Available at URL: http://www. S. 3/17/09 U.Herbicides Sauerhoff MW.4-D RED Facts. Available at URL: http://www. Geological Survey (USGS).S.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Supplemental Technical Information (available on-line only). Toxicology 1977. 4/2/09 U.EPA). 2. Circular 1291.php. Environmental Protection Agency (U. EPA 738 F-05-002.S. revised February 15. Blau GE. The Quality of Our Nation’s Waters.htm. 3/17/09. March 2006.8:3-1U.S. Washington (DC): U. May.epa. Pesticides in the Nation’s Streams and Ground Water.usgs.S. Environmental Protection Agency (U. Braun WH.EPA).S. 1992-2001. 2007. 60 Fourth National Report on Human Exposure to Environmental Chemicals . Gehring PJ. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 2004.gov/oppsrrd1/ REDs/factsheets/24d_fs.4-dichlorophenoxyacetic acid (2.2000 and 2001 market estimates. Office of Prevention Pesticides and Toxic Substances.epa. The fate of 2. Available at URL: http://water. June 2005.pdf.EPA.4-D) following oral administration to man. Pesticide industry sales and usage .

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

S. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. 62 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 01-02 is 0.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 .670 (<LOD-.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (<LOD-. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.240) 679 701 957 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .2.S.440 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

acetochlor.html. Linhart SM. Peter CJ. 2005. Hodgson E. Sacramento. revised February 15. Centers for Disease Control and Prevention (CDC). and metolachlor herbicides in rats. Shoemaker DA. Geological Survey (USGS).108(12):1151-1157. Kolpin DW. streams and groundwater. Coleman S.gov/nawqa/ pnsp/pubs/wrir984245/text.248(2-3):115-122. Reregistration Eligibility Decision (RED) Metolachlor. Dialkylquinonimines validated as in vivo metabolites of alachlor. Thelin GP. Circular 1291.php. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Roberts AL.S. Rose RL. Available at URL: http://water. California.S.usgs.S. Environ Sci Technol 2005. Davison KL. usgs.11(4):353359. Feil VJ. Casida JE. 4/2/09 U. World Health Organization (WHO). Gillion.pdf.41:3409-3414. reservoirs and ground water in the Midwestern United States. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Environ Health Perspect 2003. Biagini RE. J Expo Anal Environ Epidemiol 2005. Curwin BD. Chem Res Toxicol 1998.S. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.pdf 3/30/09 Hines CJ. Kolpin DW. Barr DB.47(6):503-517.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Camann DE.pdf. Hein MJ. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.int/water_sanitation_health/dwq/chemicals/ metolachlor.gov/oppsrrd1/ REDs/0001. Wratten SJ. Comparative metabolism and elimination of acetanilide compounds by rat.248(2-3):123-133. Hladik ML. 3/26/09 U.37(4):10881093. Xenobiotica 1994. Ann Occup Hyg 2003. Available at URL: http://www. Barr JR. Environ Sci Technol 2007. Available at URL: http://water.Herbicides References Battaglin WA.15(6):500-508. Larsen GL. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Gilliom RJ).111(5):749-756. 2003. Hsiao JJ. EPA 738R-95-006.who. Quistad GB. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Furlong ET. Jefferies PR. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Striley CA.S. 2007. Heederik D. Atlanta (GA). Burkhardt MR. Sci Total Environ 2000. J Agri Food Chem 1989. Occurrence of sulfonylurea. Available at URL: http://water. Supplemental Technical Information (available on-line only). Brown KK. Thurman EM. Kinney PL. R. Deddens JA. Pesticides in U.usgs.ESTfeature_gilliom. imidazolinone.39(17):6561-6574. EPA). 98-4245 (by Barbash JE. sulfonamide. Andrews HF. 6/1/09 Whyatt RM. Alavanja MC. 1998. Available at URL: http://www.gov/nawqa/pnsp/pubs/files/051507. March 2006.epa. Sanderson WT.24(10):1003-1012. Metolachlor in Drinkingwater. et al. and other herbicides in rivers. Ward EM. Third National Report on Human Exposure to Environmental Chemicals. U. Environ Health Perspect 2000. Geological Survey (USGS). Reynolds SJ. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Feng PCC. Background document for development of WHO Guidelines for Drinking-water Quality. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. et al. Linderman R. April 1995. 1999. Environmental Protection Agency (U. 1992-2001. Barr DB. Sci Total Environ 2000.

1986.4. the general population is unlikely to be exposed to it. which may vary for some chemicals by year and by individual sample. myotonia.1. 2004). Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. abdominal pain. 64 Fourth National Report on Human Exposure to Environmental Chemicals . Human health effects from 2.4. renal and hepatic injury. At low levels...5-trichlorophenol and other degradates.4. 2. and delayed neuropathy (Bradberry et al. Epidemiological studies have reported associations of several types of cancer.2 and 0. with an elimination half-life of approximately 19 hours (Arnold et al. hypotension.. Kohli et al.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.4. Omer.4. 1989. Survey Geometric mean (95% conf.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.5-T is eliminated mostly unchanged in the urine.4. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.4.5-T in soil varies with conditions.5-T has been rarely detected in ground waters (USGS.4. Chlorophenoxy herbicides act as plant growth hormones. Although 2.3.g. Given the commercial unavailability of 2.4. Once absorbed into the body. dizziness. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. these herbicides can enhance plant growth.5-T degrades to 2. population from the National Health and Nutrition Examination Survey. 2007). and concern about contamination with 2..4.4.4-D were used as defoliants in the Vietnam War (e. but higher levels are herbicidal.Herbicides 2. headache. ranging from several weeks to many months. 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.5-T use as a herbicide in 1985.5T is rapidly absorbed via oral and inhalation routes. Ester forms of 2. 93-76-5 General Information 2. < LOD means less than the limit of detection. Agent Orange).S.4.5-Trichlorophenoxyacetic acid (2.5-T (Holson et al.. 1974).5-T and 2.7.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. 2.4.5-Trichlorophenoxyacetic Acid CAS No.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. nausea. it is not well absorbed through the skin.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Mohammad and St. 1992. 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-T.. 1992). The half-life of 2. Nelson et al.

Biomonitoring Information Urinary levels of 2.7. 2.5-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 2.4.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Survey Geometric mean (95% conf.4.4. Pearce and McLean. Biomonitoring studies on 2. 2002. Urinary 2.5-T also were below the limit of detection (Kutz et al.5-T itself is not mutagenic.4. IOM.5-T were generally below the limit of detection.5-T does not mean that the level will result in an adverse health effect. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-T reflect recent exposure. 2005). 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Herbicides or contaminated herbicides.4. 2005.EPA.EPA at: http://www. other exposures.4.3.. Additional information is available from U. IPCS. Mean urinary levels of 2. U.epa.S. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.4. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.5-T than levels found in the general population. in which urinary levels of 2.gov/pesticides/. or to contaminants in the herbicide formulations (specifically 2.4. 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. It is unclear whether these associations are related to the chlorophenoxy herbicides. population from the National Health and Nutrition Examination Survey.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.S. 1996.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Finding a measurable amount of 2.4. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 65 . similar to results of NHANES II (19761980). urinary levels of 2. 1992).S. 1980).

4.4. Washington (DC): U. Selected pesticide residues and metabolites in urine from a survey of the U. Board on Health Promotion and Disease Prevention. Murphy RS. J Toxicol Environ Health 1992. International Programme on Chemical Safety-INCHEM (IPCS). Vale JA.S.htm.EPA. 2003. Beasley VR. Pesticide industry sales and usage . Behavioral and developmental effects in rats following in utero exposure to 2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Available at URL: http:// www.5-T).4. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.4-D) epidemiology and toxicology. Available at URL: http://www. Review of 2. Holson JF. 210:250-255.nap. Office of Prevention Pesticides and Toxic Substances. Garabrant DH. Proudfoot AT. Vet Hum Toxicol 1989. Brody D.5-trichlorophenoxy acetic acid in man. Gaylor DW.5-trichlorophenoxyacetic acid (2.31(2):121-125.5-T). LaBorde JB.4. Gaines TB. Neurobehav Toxicol Teratol 1986.37(2):277-91. Environmental Protection Agency (U. I.31 Suppl 1:1825. Available at URL: http:// www. Pesticides residues in food: 1996 evaluations Part II Toxicology. gov/oppbead1/pestsales/01pestsales/market_estimates2001. et al.4-D and 2.4-dichlorophenoxyacetic acid (2. Holson JF.EPA). St Omer VE. McLean D. 914. Dichlorophenoxyacetic acid. 2005.19(2):286-297. Crit Rev Toxicol 2002. Philbert MA.php?record_id=10603.5-t mixture.5-trichlorophenoxyacetic acid (2. Tandon JS. Khanna RN. Centers for Disease Control and Prevention (CDC). McCallum WF. 3/17/09 Kohli JD.S. Fundam Appl Toxicol 1992.4:318-21.4-D/2. Wolff GL.23(2):65-73.2000 and 2001 market estimates. Scand J Work Environ Health 2005.inchem. discussion 5-7. Erne K. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . 2004. II. general population. Toxicol Rev 2004.org/documents/jmpr/jmpmono/v96pr04.4. Carter-Pokras OD.edu/catalog.32(4):233-257. Arch Int Pharmacodyn Ther 1974. U.4. Sircar KP. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Veterans and Agent Orange: update 2002.Herbicides References Arnold EK.pdf. Third National Report on Human Exposure to Environmental Chemicals. et al.19(2):298-306.epa.4. Estimation of occupational exposure to phenoxy acids (2. Developmental toxicity of 2.5-T). Kolmodin-Hedman B.5-T in four-way outcross mice. 3/17/09 Institute of Medicine (IOM). Bradberry SM.8(5):551-60. S. 2. May. Developmental toxicity of 2. Nelson CJ. Arch Toxicol Suppl 1980. Multireplicated dose-response studies with technical and analytical grades of 2. Pearce N. Gaines TB. Kutz FW.4-. Gupta BN. Sheehan DM. Poisoning due to chlorophenoxy herbicides. Agricultural exposures and non-Hodgkin’s lymphoma.4. LaBorde JB. Atlanta (GA). Mohammad FK. Nelson CJ. Absorption and excretion of 2. Fundam Appl Toxicol 1992. Washington (DC): National Academies Press. Dhar MM.S. Cook BT.

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

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

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

0 (10.102 (.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .1) 14.9 (12.6) 19.1) 20.5-17.053 (<LOD-.120 (.147 (.054-.4-17.055 (.103 (.100) .5) 19.0-25.049-.100-. population from the National Health and Nutrition Examination Survey.8 (11.054-.3-21.060) .120 (.4) 95th 20.1 (18. 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.110) . Survey years 01-02 03-04 Geometric mean (95% conf.0 (10.150 (.2) 12.130-.8 (9.180) .110 (.3 (19. Fourth National Report on Human Exposure to Environmental Chemicals 79 .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.30 (8.147) 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 .190) .2) 11.062 (.110) .098 (.1-19.064 (.7-22.080 (.7 (<LOD-15.8-25.1) 15.9-23.158) .S.103 (.00 (8.1) 13.7 (14.90) 90th 15.1) < LOD 9.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.059 (.090-.140 (.190) .100 (.108-.S.30 (8.5 (16.0) 19.5-17.7-19.4) < LOD < LOD 16.8) < LOD 8.149) .4) 14.090 (<LOD-.1) 15.100) .4 (12.9 (14.8-24.4) 539 456 484 487 980 885 Limits of detection (LOD.101) .180) .130) .110-.077-.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 9.4-18.090-.100-.8-17.0) 21.7 (15.093) . which may vary for some chemicals by year and by individual sample.9-38.070) .5) 15. which may vary for some chemicals by year and by individual sample.8) 14.064) 90th .120-.160) .9-22.80-9.090 (.6 (14.5-15.130-.048 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110 (.6-24.140) .112-.8 (18.070 (<LOD-.70 (7.140-.0 (11.6-33.9 (13.1-16.160 (.083-.062 (.4) 19.242) .8) 15.6 (15.4) 21.130 (.160 (.088-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) .120) .069) < LOD < LOD .7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.40-10.2) 14.109-.084-.139 (.0 (15.054-.1 (13.4) 20.058) < LOD .8-19.5 and 7.6-24.110 (.089 (.50) 15.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) 15.109 (.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. < LOD means less than the limit of detection.50 (8.8.062-.80-10.6 (15.60-10.117) < LOD .10 (<LOD-16.100-.120 (.096-.138 (. 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 (12.40-9.130) .150 (.3 (13.1-24.124) .1-18.116) .6) 9.0) < LOD 9.075) < LOD .073-.5) 21.1) 10.139 (.113 (.063-.080) .3 (18.109-.130-.9 (13.6) 16.00-14.080-. Survey years 01-02 03-04 Geometric mean (95% conf.138) .112) 95th .2-15.5 (<LOD-11.056-.3 (18.130) .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for survey years 01-02 and 03-04 are 10.8-17.3 (14. population from the National Health and Nutrition Examination Survey.4 (12.2) 15.070-.0-21.086-.80 (<LOD-10.077 (.

Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Teta MJ. Priestly BG. Needham LL. plasma dieldrin. J Toxicol Environ Health. Facca A. Andersen A. Rosellini RA. Sanchez-Ramos J. September 2002. August 2008. toxicology.14:95-102. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. 1991. David VL. Jorgensen T. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Soto AM. Finley B. Jr and Laws ER. Available at URL: http://pubs. In Hayes WJ. Carlson JN. Ellis H. pp. Olea N. Academic Press.inchem. Kanthasamy AG. Part A 2000. 1992-2001. New York. et al. Psychopharmacology (Berl) 1987. Pesticides in the Nation’s Stream and Ground Water.html.cdc. PA. Toxicol Lett 1992. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. No:429-436. either singly or in combination.usgs. Jr. Serrano FO. Narahashi T. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Patterson DG Jr. Turner W. Corrigan FM. Exp Neurol 1998. Basit A. Available at URL: http://www. Mann D. 2 Classes of Pesticides. Tully DB.org/documents/ehc/ ehc/ehc91. Shore RF.109(Supp1):113-139. Li AA. Ginsburg KS. Lancet 1998. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. 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. Fernandez MG.59:229-234. VT. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Garrett N. Cox. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Chemosphere 2004. Schulte P. Mink PJ. Daniel SE. J Toxicol Environ Health 1989. J Occup Environ Med 2005.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). McIntosh LJ. Brock JW. United States Geological Survey (USGS). References Agency for Toxic Substances and Disease Registry (ATSDR). and epidemiology in the United States. Stehr-Green. 731-915. Chapin RE. 4/21/09 Jorgenson JL. International Programme on Chemical Safety (IPCS). Aldrin and Dieldrin [online]. Eds. Effect of occupational exposure to aldrin on urinary D-glucaric acid. 6/1/09 Ward EM. Handbook of Pesticide Toxicology. Grandjean P. Chung KL. Mumtaz MM. Vol.150:263-271. Kitzazwa M. Neurotoxicol 2005. 4/21/09 Hoyer AP. Cancer Epidemiol Biomarkers Prev 2000. FDA Pesticide Program Residue Monitoring 1993-2006 [online].103(Suppl 7):113-122. are nonestrogenic in transfected HeLa cells. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Available at URL: http://www. Environ Health Perspect 1995. Demographic and seasonal influences on human serum pesticide residue levels.66(4):229-234.91(1):122-126. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Grajewski B. et al.cfsan. Chlorinated Hydrocarbon Insecticides. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Sonnenschein C. Frey JM. Smith AG.html.9:1357-1367. 2007 [online]. 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. Wienburg CL.atsdr. Kanthasamy A.htm. Organochlorine insecticides in substantia nigra in Parkinson’s disease. bioaccumulation. Hartvig HB. and lymphocyte sister chromatid exchange. Revised Feb.54:1431-1443. Roy ML. Environmental Health Criteria 91.gov/toxprofiles/ tp1. Environ Health Perspect 2001. 15. 1989. Food and Drug Administration (FDA). Available at URL: http://www. 4/21/09 Bates MN. Six high-priority organochlorine pesticides. Toxicological profile for aldrin/dieldrin [online].47:1059-1087. Reprod Toxicol 2000. Buckland SJ.64-65 Spec. Patterson DG Jr.26:701-719. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.gov/~dms/ pesrpts.352:1816-1820. Organochlorine exposure and risk of breast cancer.27:405-421.fda. Song S. Anantharam V. Int Arch Occup Environ Health 1994.gov/ circ/2005/1291/. Edwards JW. Inc.

4-14.10-18. 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.10-11.4) < LOD < LOD < LOD 23.1 (25.5) < LOD < LOD 9.2-28.8-42.36-11.7-39.3 (27.4) 37.9) 11.1-25.5) 9.9) 36.8-32. 1994).5) < LOD < LOD < LOD < LOD 13.2) < LOD 11. from the early 1950’s until the mid-1980’s.8 (40.0) 31. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. chlordane was used to kill termites and other insects on agricultural crops.5) 56.8-61.8-20.3-43.6) 20.8-43.6) 48.7 (10. buildings. Technical grade chlordane had contained 7% trans-nonachlor.9) 37. 57-74-9 Heptachlor CAS No.2) * 12.4) 39.5-43.6) 8. 10.1) 30.7) 42. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.9 (26.S.9) 23.1) * 11.6 (9.20 (<LOD-11.8) 18.9 (15.3 (<LOD-19.3) 10.1 (40.3) 41.2-49.6-53.20-10. 2007).2-21.5) 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 * * * * 11.1) < LOD < LOD < LOD < LOD < LOD 8.1) 30.3-32.1-15.3 (25.5-40.70 (<LOD-10.5 (33.4) 12.8-31.3-45.8) 53.9) 10.5 (41.30-11. foods high in fat such as meat.9-21.6-45.9 (15.0) 37.1) * 11.7-70.2 (9.8 (10.5-65.5-41.0) 75th 20.89-10.4 (35.4 (22.3-45.0-61.0 (37.2) 22..6) 23.3-24.7 (34. see Data Analysis section) for Survey years 99-00.6-12.8 (10.9 (31.5-42.7 (34.2 (28.7 (17.8 (17.1) 22.7 (19.7 (<LOD-32.5-32.5.7) 28.0) 20.8) 52.4) < LOD 11.0-67.5 (34. population from the National Health and Nutrition Examination Survey.6) 36. heptachlor use has been limited to treatment of fire ants near power transformers.2) 46.5. and 7. 01-02.90 (8.6) 9.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.2) 33.8 (18.S. Until 1988.7 (43.8-33.5) 21.7 (32.5) 10.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.1-50.4) 29.0 (<LOD-12. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.5 (31.5-47.2) 37.6) 39.0-12.9) 47.2-26.3-49.0) 41. As a result of the manufacturing process.7-56.1 (<LOD-12. and in soil. in addition to trace amounts of numerous other related compounds (ATSDR.4-45.3) 18.9) 23.0-18.9 (29.7) 19.6) 49.3 (9.5) 44.0-13. fish.9 (26.1-51.1 (11.5-44.9) 39.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (20.2 (37.63 (8.74 (<LOD-10.8-23.2-49. which may vary for some chemicals by year and by individual sample. and 03-04 are 14.1 (<LOD-12.2 (39.4) 22.7) 35.9 (21. 2007).4-21.9-38.1) 90th 34.9-42.2 (36.4 (10. Fourth National Report on Human Exposure to Environmental Chemicals 81 .2) 36.9-21.9 (36.0 (26.2-56.4 (30.0 (32.4-40.6) < LOD 11.8) 52. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.1) 16.1 (20.6 (16.7) 19.3 (20.8) 27. 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. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.S.4-51. Chlordane is not currently produced or used in the U.0-25.3) 37.8 (17.1-19.3) 18.4 (31. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.6 (9.9 (11.3 (26.Organochlorine Pesticides Chlordane CAS No.1 (27.5-13.7 (42.9) 13. respectively.5 (8.1 (17.1-25.0-33.5 (<LOD-12.6-24.6) 48.9-40.7-14.9) 11.2) 34.20-11.2 (41.5-38.5) 37. 1994.0) 27.3) 10.0 (16.5) 38.7) 9.6 (43.8. the technical grade product of each chemical contains 10%-20% of the other chemical.37 (8.1-65.9 (17.7) 31.8-33.2 (10.69-10.9 (18.8 (42.6 (25.3 (11.6) 9.1 (44.6-24.7-12.6-18. Consequently.8-73.4 (30.10 (8.82-11.9) 31.7-25.1 (<LOD-12.2 (21.1 (16.0) 21.4 (<LOD-12. lawns. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.7 (<LOD-13.2) < LOD 11.6) 11.9 (11. and dairy products are the usual sources of exposure to these chemicals in the general population.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.3 (28.8) 44.3 (21. Since 1992. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4) 18.1 (15.9) 17.

130) .079) .170) .370 (.230-. which may vary for some chemicals by year and by individual sample.290) .190-.450) . 2007).115 (.230) .180) .080 (.300) .240-.067 (.290 (.310) .133) 90th .200 (.070 (<LOD-. 1986).110 (<LOD-.168-. Shindell and Ulrich.140-.200-..560) .115-.204 (.120-.058-.170-.064) < LOD .280 (. chronic doses of heptachlor have produced liver enlargement and injury. interval) Selected percentiles ( 95% confidence interval) Sample 95th . IARC.240) . 2002.220 (. and alterations in immune function of offspring.070 (<LOD-.213) * .073 (.410) .119 (.210-.070-.260 (.260 (.320 (.250-.245-.240-.242-.120 (.S.108-.350 (.350 (.128 (.150) .080) .165-.340) .230 (.199-.071 (.373) .190-.146) < LOD < LOD .160) .080) .070-.070) < LOD < LOD < LOD < LOD < LOD . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.320 (.063 (.253-.310) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.315 (.250 (.380) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.082 (.120-.130-.076) < LOD .075 (.310 (.250 (.207 (. and inhalation exposure.149 (.230-.100-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.270 (. 1981).287) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .056 (.160 (. heptachlor.258-.280-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.350) .286 (.063 (. to heptachlor.300 (. The U. neonatal mortality.090-. Le Marchand et al. 1996.112 (.370 (.430) .090) . and heptachlor epoxide in foods and bottled water.140-.070 (<LOD-.320 (.146) . Survey Geometric mean (95% conf.290-.087-. Chlordane and heptachlor are absorbed after oral.100 (.180-.092) .510) .140) .160) .210 (.. 1986).077) .062) < LOD .170) .290-.080) .070) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.106-.083) .049 (<LOD-.160) .. Takahashi et al. characterized by seizures and paralysis.286 (.240 (.130-.104) .104-.216-.130) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.066 (.258 (.230-.320 (.200-. which is also persistent in the body (ATSDR.100-.207) .150-.110-.430) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.066 (<LOD-.070 (.070-.310-.090) .126) .140 (.330 (.058 (.074-.189-. EPA has established environmental criteria for chlordane and heptachlor.370 (.073) < LOD < LOD < LOD < LOD .208 (.047 (<LOD-. Rogan.080 (.S.260 (.210 (.290-.Organochlorine Pesticides (Dallaire et al. 1977a.050 (<LOD-.130-.077) .220-.065-.246-. 82 Fourth National Report on Human Exposure to Environmental Chemicals .450) .057) * .400) .270 (.136) .120-.170) .280 (.280-.063 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.140 (.290) .269 (.130-.126 (.083 (.260-.079) < LOD < LOD < LOD .063) * .360) .300-.130 (.231) .170) .400) .227) < LOD .280-.130 (.077) .300) .048-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .440) .053-.100 (<LOD-. Elimination of all these chemicals from the body occurs over months to years.150 (.057 (.055-.S.130-.190-.077) .140 (.063-.320) . In laboratory animal studies.300) . 2007.150 (.070 (<LOD-.170) .348) .225 (.068) 75th . 1991.230 (.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 * * * * .063) .057-.200-. Acute. 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. 2001. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.091) .302) .280) .340) . FDA established allowable residues of chlordane.203-. 2006). dermal.060 (<LOD-.180) .130 (. 1991).068-.050-.189 (.066-. OSHA has established occupational exposure criteria.150 (.271 (.220-.148-.061-. and breast milk is a major excretion route in lactating women.148) . and the U.300) .058-.180-.320) .320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . population from the National Health and Nutrition Examination Survey.223) .310) .140 (. Smith.066-.. The major metabolite of heptachlor is heptachlor epoxide.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.053-.068) .270 (.063 (.069 (<LOD-. 1977b.

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

2-17.8-24.1) 20.5 (11.8) 13.6 (16.8 (<LOD-23.6) 13.8-24. respectively.2) 13.4 (<LOD-54.S.9-25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 26.8) 19.5) 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. Survey Geometric mean (95% conf.3-18.9-16.4 (<LOD-19.4) 18.2 (<LOD-25.4) 21.8) 14.0) 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 (13.0-16.6 (11.6 (8.8 (18.2) 20.8) 15.2 (<LOD-62.5 (18.0-19.9 (12.0-54.2-27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.3) 10.7 (10.4 (11. 01-02.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.9 (15.6-17.1-38.40) 15.5.3) 22.5 (<LOD-21.3) 18.5) 19.8-24.90 (<LOD-9.8 (15.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8 (18.8) 19.1) 13. which may vary for some chemicals by year and by individual sample.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.7-19.1-15.5 (10.5 (<LOD-32. and 03-04 are 14.6) 14.6.2-16.6 (13.3) 18.7-25.6 (14.9-29.50) < LOD < LOD < LOD 17.8 (13.8) 21.7 (13.6-21.0-17.4 (15.3) 18.7 (16.6 (16.6) < LOD < LOD < LOD 27.8. 84 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection.0-17.9-23. 10.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8) 14. population from the National Health and Nutrition Examination Survey.8-46.1) 23.3) 23.2 (18.2) 15.6 (<LOD-27.2-27.1 (16.8 (13. see Data Analysis section) for Survey years 99-00.1-16.3) 27.1-29.3) 16.4 (11.9-29.9) 15.8) 13.2 (<LOD-16.0 (11.0) 13.6) 22.20 (<LOD-9.8) 16. and 7.5) < LOD 14.8-23.6 (12.1 (19.3 (<LOD-25.10-13.7-18.0 (15.5 (11.8) 20.

117) .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.190) .130 (<LOD-.170) .130-.120 (<LOD-.087 (.149) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180) . which may vary for some chemicals by year and by individual sample.090 (<LOD-.096 (.130-.135 (.110-.074-.200 (.128 (.135 (.100-.120 (.067-.108) .170 (.098 (.150 (.094 (.180) .140-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .094 (.220) .090-.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .100 (.170 (.111) .113-.076-.240) .170) .110 (.310) .090-.106-.108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .140) .270) .110 (.063) .180 (<LOD-.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 .110) .130-.170 (<LOD-.110-.190 (.S.150 (.110) .111-.090 (.126 (.180 (. population from the National Health and Nutrition Examination Survey.071-.097) < LOD .104) .116) < LOD < LOD < LOD .180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.120 (<LOD-.120) .090-.107-.100 (.170 (.130-.100 (<LOD-.157) .090-.090-.108-.380) .140) .150 (<LOD-.190) . Survey Geometric mean (95% conf.110 (<LOD-.180) .057 (<LOD-.120-.082-.120) .310) .100-.053-.110 (<LOD-.130 (. Fourth National Report on Human Exposure to Environmental Chemicals 85 .090-.055 (<LOD-.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 (.063) < LOD < LOD < LOD .170) .077-.100 (.069 (.077-.100 (.133 (.180) .130) .113) .200) .200) .070-.101 (.130) .190) .

9 (15.1) 16.6) 13.4) 107 (84.6) 60.7-32.9) < LOD < LOD < LOD 20.4) 48.3) 16.3-58.7 (18.8 (28.0-23.0-20.4-23.1) 31.5-69.6) 56.8) 51.2) 17.6 (56. 01-02.7 (30.4) 55.0 (42.9-40.8-90.7-20.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.8 (15.3 (49.0) 33.7-160) 86.6 (57.6 (12.6-19.0-93.7) 73.8-79.7-29.1) 17.0 (16.9 (51.5-87.4-18.1-55.6 (<LOD-14.4) 20.5) 22.3 (17.8 (19.3) 15.6-20.1) 18.7) 78.9) 14.10 (<LOD-11.0 (13.5) 30.2 (7.3-39.4) 19.8 (17.5 (15.0 (13.1-51.3-57.3 (56.1) 17.0-68.7) 56.6 (52.5 (15.9 (51.8 (26.3) 32.8 (42.1) 32.7 (59.7-18.2 (64.6-82.9-89.0 (48.8 (13.1-22.6) 82.9 (47.0 (62.0) 49.8 (26.1) 17.8 (49.6) 10.0) 19.4) 59.8 (26.4 (45.9-35.1 (10.8 (12. 10.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3) 30.4-67.5) 14.7-34.2) 39.6 (50.9) 51.7 (16.3) 32.6-22.4-36.0 (15.5 (25.8-110) 59.5-17.0-93.8 (28.5) 35.8 (16.1-34.0-37.7) 59.1 (41.3) 18.2 (25.2 (27.7-21.0 (16.7-38.7 (11.5) 26.5-95.1) 78.0 (14.7) 78.2 (15.2-18.2 (60.70 (<LOD-12.0 (42.0-22.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.1 (17.8 (30.7-17. interval) 18.0) 75th 31.3-32.5-36.9-64.5.6) 56.7-77.2) < LOD 10. and 03-04 are 14.8-19.1-16.86-13.1-20.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.5) 90th 55.6) 25.5) 19.3-86.8-41.5 (44.3) 19.S. and 7.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.6-66.3) 25.3 (14.0 (29.8-129) 74.4 (30.9-20.9 (36.6 (32.9 (19.4-52.7-22.2 (19.2) 30.4 (28.0) 13. population from the National Health and Nutrition Examination Survey.9 (66.0-143) 112 (68.9 (15.2 (14.8-67.1-28.4) 16.8-21.4-22.7 (13.0) < LOD < LOD 8.8.5) 77.6) 54.8-19.2) 20.5) 36.1) 17.0) 18.8 (71.5-111) 68.1 (47.7) 52.2 (36.3) 36. which may vary for some chemicals by year and by individual sample.1) 30.0 (60.3) 30.9) 51. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (28.5.2) 19.6) 84.4 (67.5) 9.9 (<LOD-14.7) 17.9 (29.1 (48.2-88.2) 34.1-126) 67. respectively.8 (<LOD-20.0 (19.5) 14.9-45.8 (11.3 (45.6-88.3-21.7) 35.3-50.8) 80.2-17.7-113) 68.1) 14.4 (11.3 (16.8-77.3-30.8-16.4-62.1 (65.9-22.8) 19. Survey Geometric mean (95% conf.3 (58.1-16.9) 14.4 (16.9 (16.4-35.1) 17.9-69.9-36.3 (14.4 (12.1 (22.7 (35.9-65.2-37.7 (28.0-38.7) 15.6 (16.6 (15.3-74.2) 59.5) 20. < LOD means less than the limit of detection.2 (26.0-24.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.7-23.7 (59.0) 40.0-123) 74.6 (56.1-18.1) 17.2-23.5) 48.7-35.0-59.8) 47.6-54. 86 Fourth National Report on Human Exposure to Environmental Chemicals .5-20.1) 17.2-21.1-34.2 (59.8 (13.0-23.1) 78.5) 78.9 (28.1) 18.5 (45.2 (14.2-18.7) 28.0 (15.8-90.5 (13.0-113) 68.9-65.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.2-16.8 (45.5-19.1) 62.3) 18.7 (74.7) 14.6) 34.9-58.8-16. see Data Analysis section) for Survey years 99-00.

590 (.242) .460) .250) .190-.092 (.130) .470-.141) .500) .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 .106 (.370 (.120-.370 (.080-.830) .400 (.360-.090-.108) .220 (.079-.125 (.470 (.130) .111 (.220 (.150) .090-.110 (.110 (.470-.150) .090-.390) .397-.100-.210) .288-.250) .120-.127) < LOD < LOD .110 (.559) .300) .158-.098 (.110) .103 (.084-.680 (.270-.120) .090-.069) .340-.130 (.060) .390) .161) .430-.960) .279-.190-.320-.240) .240 (.470 (.220 (.600) .205 (.330-.630) .082) .085-.112 (.220 (.390 (.069-.230 (.096-.210) .104-.098-.330 (.130) .145-.310-.054-.340) .041 (<LOD-.400) .095-.497-.210 (. Survey Geometric mean (95% conf.171-.405) .343 (.131) .510-.409-.460) .630) .327 (.113) < LOD .080) .580 (.116 (.410-1.285-.300-.116-.440) .460-.232) .113) .800) .093-.061-.078-.S.355 (.110 (.490-.186 (.080-.320-.190-.119) < LOD < LOD < LOD .110-.324 (.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.098) .078 (.097) .109 (.090 (<LOD-.089 (.573 (.220 (.100 (.430-. Fourth National Report on Human Exposure to Environmental Chemicals 87 . interval) .090-.930) .420) .260) .105 (.830) .180-.094 (.091-.120-.280) .420 (.340-.106 (.177-.360-.310 (.400-.211) 90th .134) .092 (.099-.580 (.490) .114) .690) .109 (.098 (.310) .210 (.350-.210 (.087 (.390-.600 (.116) .684) .170 (.180-.240) .100 (.047-.122) .117) .081 (.128 (.480) .093-.390 (.461 (.130) .310-.091) .160 (.096-.120) .119) Selected percentiles ( 95% confidence interval) Sample 95th .240-.112 (.510 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .490 (.210) .237) .140) .470 (.310-.120) .450) .099-.210-.183 (.096) .130) .220 (.085-.350 (.191 (.190-.680) .760 (.590 (.161-.120) .190-.173-.371) .130) .090 (.520 (.186-.130) .129) .104 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .062 (.286-.840) .414 (.108) 75th .081-.400-.110 (.126) .630) .237) .190-.093-.120 (.111-.651) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.272-.317 (.310-.079-.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.120 (.090) .580 (.520) .135 (.540) .103 (.367) .590) .068-.260) .395-.220) .288 (.550 (.100-.410-.100-.234) .380 (.055 (<LOD-.122) .141) .690) .100-.090-.060 (<LOD-.210-.125) .085-.640 (.160-.290-.060-.520 (.120 (.108 (.330-.180-.20) . which may vary for some chemicals by year and by individual sample.250) .070 (.458 (.220 (. population from the National Health and Nutrition Examination Survey.220 (.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .390 (.417 (.080 (.080-.110 (.565) .106 (.080-.594) .490 (.071 (<LOD-.440-.240) .130 (.202 (.430-.124) .400 (.301-.390 (.395) .093) .

Royce W. Environ Res 2000. maternal serum and milk from Wielkopolska region. Circumpolar maternal blood contaminant survey. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Siegel BZ. 1986. et al.nih.pdf.atsdr. 1991 pp. Smith AG. Shindell S and Ulrich S. 2 Classes of Pesticides. Environ Health Perspect 2002. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.28:497501. 4/21/09 Baker DB. Bull Environ Contam Toxicol 1981:27:506-511. Concise International Chemical Assessment Document 70 Heptachlor [online].heptachlor. Loo S.niehs.org/ documents/cicads/cicads/cicad70. Senie R. International Agency for Research on Cancer (IARC) . Organochlorines in Swedish women: determinants of serum concentrations. Chashchin V. 88 Fourth National Report on Human Exposure to Environmental Chemicals . JAMA 1988. Charles MJ. Available at URL: http://ntp. Environ Health Perspect 2002. Eds. May 1994. Canada).110:617-624. Gilman A. Vol. Hawaii Med J 1991. Dendle WH. National Toxicology Program (NTP). Chlorinated Hydrocarbon Insecticides. Available at URL: http://www. Glynn AW. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. 731-915.110(8):835-838.330:55-70. Organochlorine exposures and breast cancer risk in New York City women.inchem. Bioassay of heptachlor for possible carcinogenicity. et al.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Head SL. International Agency for Research on Cancer (IARC).150:981-990. 79. Odland JO. Laliberte C. Van Oostdam JC. Poland. Stehr-Green P. Mortality of workers employed in the manufacture of chlordane: an update. Arch Pediatr Adolesc Med 1996. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Brower S.gov/ntp/ htdocs/LT_rpts/tr008. J Occup Med 1986. Available at URL: http://www. 6/1/09 Rogan WJ.inchem. Available at URL: http://www.50(3):108-118. 1994-1997 organochlorine compounds.gov/toxprofiles/tp31. Aune M. Bleiweiss IJ. Muckle G. A Report to the Hawaii Heptachlor Research and Education Foundation. Environ Health Perspect 2003. Takahashi W.84:151-161. August 2007. Saidein D. In Hayes WJ. Dewailly E. Distribution of polychlorinated biphenyls. Granath F. Available at URL: http://ntp. 4/21/09 Dallaire F.html. Willman E. Hertz-Picciotto I. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. New York. Lawrence River (Quebec.htm. LeMarchand L. Berkowitz GS. 1979-1980.atsdr. Available at URL: http://www.nih. Kolonel LN. Darnerud PO. et al. KalubaSkotarczak A. Vol. Organochloride pesticide residues in human milk in Hawaii. Barker J.9:1-109. Tartter P.372:20-31. 1993. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Arch Environ Health. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Wolff MS. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Covaci A. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Inc. Voorspoels S. 2006. Wong L. 9/25/07 International Programme in Chemical Safety (IPCS).htm. Atuma S. Bioassay of chlordane for possible carcinogenicity. Chlordane and heptachlor [online].41:145–148. gov/toxprofiles/tp12.8:1-123.111:349355.niehs. Lulek J. et al. Handbook of Pesticide Toxicology. 1963-1967. 4/21/09 James RA. Dewailly E. Takei G. Jr. 6/1/09 National Toxicology Program (NTP). Toxicological profile for heptachlor and heptachlor epoxide [online].gov/ntp/ htdocs/LT_rpts/tr009.cdc.cdc. 2001. Pollutants in breast milk.org/site/foundation/ research/projects2. Sci Tot Environ 2006. Jaraczewska K. Bjerselius R. Baker DB. Sci Total Environ 2004.org/documents/iarc/ vol79/79-12.259(3):374-377. Hansen JC.pdf.html. Academic Press.Summaries & Evaluations. Ayotte P. Jr and Laws ER.html. Available at URL: http://www. Drews K. Keller JA. Toxicological profile for chlordane [online]. Wohlleb JC.

inhalation.9) < LOD < LOD 9.9 (<LOD-20. population from the National Health and Nutrition Examination Survey.9 (21. 01-02.4) < LOD 17.7) < LOD 18.3 (<LOD-21.6 (22.7.0-15. Fourth National Report on Human Exposure to Environmental Chemicals 89 . particularly meat.0-53. including 1. and dairy products.8.8) 30.0 (10.3-590) 293 (104-541) 48.2) 155 (59.7-16. DDT usually refers to the technical product. It was produced and used in the U.5) 23.1 (23. DDT was used at one time as a treatment for head and body lice. sediments. respectively.4 (23.8-26.0 (18.3 (<LOD-31. and trace amounts of several related compounds. Smith.6 (25.2-65.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. although DDT and DDE intakes have decreased over time (FDA.70 (8. particularly for endemic vector and malaria control. The biodegradation half-life of DDT in soil varies from 2 to 15 years. DDT and DDE can cross the placenta.9) 17. Gunderson. Food imported from countries that still use DDT may contain the chemical or its residues. after World War II until 1972.1) 31.2) < LOD < LOD 9.5 (14. Survey Geometric mean (95% conf. as well as in plant and animal tissues. In the general U. p.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 12.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.S.9-34.0-27. food.1 (<LOD-39. which may vary for some chemicals by year and by individual sample. o. In the body.10 (<LOD-12.0 (21.3 (27.4) < LOD < LOD < LOD 61. Both Serum p.2-bis(p-chlorophenyl) ethane (DDD).p’-DDT (65%-80%).2-95.5-36. 1988). depending on conditions.3-16.S.3) 22.0) 26.S.3) 21. DDT can be absorbed after ingestion.p’-DDT (15%-21%).2 (<LOD-40.0-35.9 (10. air.50-11.0) 20.0) 40. when virtually all use of it was banned. and water.3-236) 24.1-27.8) 36.1-71. < LOD means less than the limit of detection.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. 1991).6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. see Data Analysis section) for Survey years 99-00.8-17. These chemicals are highly persistent in soil.1 (33. and 03-04 are 20.3) 28.6-33. which is a mixture containing p. population. or dermal exposure.9) 29. 50-29-3 General Information Dichlorodiphenyltrichloroethane (DDT) has been used widely as a broad spectrum insecticide in agriculture and for control of vector-borne diseases.9) 14. fish.10-13.8-39.00 (<LOD-10.0-37.5 (23.6 (31. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.5 (23.3) 21.p’-DDD (4% or less). resulting in fetal exposure.5) < LOD < LOD 9.6 (9.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.6 (<LOD-25.8) 15.1’-dichloro-(2. and 7.9 (10. DDT is converted to DDE and several other metabolites.0) 19.1’-(2. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.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 (15.7 (19. 17.8-23.90 (<LOD-12.0 (18.2) 30. 2008.7) 12. Only a small proportion of DDT is metabolized and excreted (Smith. It is still used in some countries.2 (11.5-54. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. continues to be the primary source of DDT exposure. 2002.7 (15.4.9-28. 1991).0-155) 83.9 (10.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.5) 25. DDT is converted in the environment to other more stable chemical forms.

132-. 2006). and leukemia have also been inconclusive (ADSDR.160-. 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.170 (.420) .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..130 (<LOD-. polychlorinated biphenyls. 2001).114-.150 (<LOD-.098-.086 (. Reproductive effects in humans affecting birth weight.108 (.051 (<LOD-.. Calle et al. 1997). Longnecker et al.064 (. 2001).130 (<LOD-.290) . and seizures..p’-DDD and p.. premature delivery.074-. 2004.059-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 1956).180) .061) < LOD < LOD < LOD .S. fertility. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.170-.180-. Studies of DDT exposure and pancreatic cancer.075) 1. In high dose.250 (.120 (<LOD-.150-.190-1. which may vary for some chemicals by year and by individual sample.00 (.071 (.01) . 2002..063 (<LOD-.343) < LOD . A workplace standard for DDT has been established by Serum p.078 (.048 (<LOD-. overt signs of acute human toxicity include vomiting.26) 1.068-.069) .240 (.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 . 1995. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. accidental exposures.530) . and altered behavior after neonatal exposure (Eriksson and Talts.180) .201 (. 2006. In laboratory animals.00) .112 (. Beard.120-.180 (. 2000.130-. 2002..240) .142 (.095) < LOD .190 (. Hayes et al.106) .203) .150) . other organochlorines.143) < LOD < LOD .105-.g. 90 Fourth National Report on Human Exposure to Environmental Chemicals . reproductive organ abnormalities. 2002. resulting in exposure to nursing infants (Rogan. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140-. Animal studies reported reduced fertility. and o.078-.34) .570-4.220) .313 (.146 (. 2001).400) ..230) . tremor. Mariussen and Fonnum.62 (. DDT may bind to estrogen receptors (Chen et al. 2001). lung cancer. interval) Selected percentiles ( 95% confidence interval) Sample 95th .079) < LOD < LOD .530 (. 2006.080-.170) .627) .400 (. Snedeker.128 (.130 (<LOD-.Organochlorine Pesticides chemicals are excreted in breast milk.071-. Gray et al.084 (. 1998).220) .140) . 2006.180 (. 2002.. Survey Geometric mean (95% conf.189-. have not been consistently demonstrated (Beard..065-.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150-. dioxins and furans). Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.150 (<LOD-.189) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .p’-DDE can produce anti-androgenic effects (Gray et al.106) < LOD < LOD .200 (.. Jusko et al..190 (. population from the National Health and Nutrition Examination Survey.054-. 2006). although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.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.250-1.330-4.146 (.087 (. Gladen and Rogan. 1996). and duration of lactation.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .230) .260) .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 . Jusko et al.106-. 2006).

html. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 2002. Declining DDE levels over time have also been observed in the German population.cdc. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. 2002. 1991). Survey Geometric mean (95% conf.. IARC classifies DDT (p. for males and females in the NHANES 19992000 subsample (Pavuk et al.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. 2003).epa. EPA at: http://www.3. respectively. population declined by about fivefold to tenfold. Link et al. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. 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. 2005). Smith. NTP considers DDT as being reasonably anticipated to be a human carcinogen. 8. 2003.. In general.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. 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.S. Compared to females in the NHANES 1999-2000 subsample..atsdr..gov/ toxpro2. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. Since the 1970’s. 2004). In a population-based sample of men and women from eastern Slovakia. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. 2004). respectively. More information about external exposure (i.8. Stehr-Green.p’-DDT) as a possible human carcinogen.. 1989). mean serum levels of DDT and DDE in the U.. see Data Analysis section) for Survey years 99-00.. Fourth National Report on Human Exposure to Environmental Chemicals 91 .gov/ pestcides/ and from ATSDR at: http://www. population from the National Health and Nutrition Examination Survey.e.p'-Dichlorodiphenyldichloroethene (DDE) (lipid adjusted) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.S.6. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.S. and 7.6 (81. Biomonitoring Information DDE persists in the body longer than DDT. 1998. and 03-04 are 18.Organochlorine Pesticides OSHA and a guidance established by ACGIH. environmental levels) and health effects is available from the U. 01-02.7-119) 113 (100-140) 93.. compared to levels observed in this Report (Anderson et al.

1989).83 (1.92 (3.796 (.01) 1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.3 (8. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.5) 16.18-1.62-6.26-2.77 (1.7) 9.63 (1.88-35.32 (1.81 (1.81-5.63-15.2) 19.870 (.31 (1.3) 10.56) 2.18-3.75) 6.40-8.43-4.84 (3.40-4.59 (1.36 (3.2 (6. High mean levels of whole blood DDT (about 3.15-4.01) 1.01-11.27) 3.06) 3.30 (1.13-2. 2005).66) 1.92) 1.45 (1. 2001-2002 and 2003-2004 subsamples.30-1.4) 9.7) 13.05 (3.76-3.994-2.53) 7.520 (.534-.8 (13.64) 3. considerably higher than levels in this Report (Smith.10) 2.7 (8. less than one percent had detectable serum levels of o.54 (1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al. Serum p.92 (3.39) 1.38 (1.39 (3.8 (9.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.1 (9.6) 9.516 (. Finding a measurable amount of p.7-19.53 (2.p’-DDT were below the limits of detection.726) .66-2.60-13.635) 1.90-8.07) 1. population from the National Health and Nutrition Examination Survey.56-2.36-2.4-19.6) 9.500-.51) 1.0 (12.43 (5.69 (1.69 (2.72) 1.965-1.32 (1.51-49.87-16.6 (7.24-17.1) 7.75) 1. 309 versus 268 ng/g lipid.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.51-8.14) 2.12 (6.58) 1.61-2.80) 1.p’-DDT.32-1.680-1.5) 22.8) 15.1 (8.0) 2. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.9 (15.646) .80) 1. serum levels of o.65 (1.04 (6.57 (1.69) 4.561 (.30-1.6 (9.38 (1.81 (7.47) 3.3) 16.32) 1.1) 40.6) 11.66-17.40 (3.84-3.26 (1.25-14.53) 1.29 (1.93 (7.52 (1.69 (.01-15.18-1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.91-2.91) 3.18) 1.90) 22.9) 7.50 (2.14-9.25 (1.57 (1.91 (6.43-4.32-1.70) 1.p’-DDT (Stehr-Green.49 (1.47 (1.6) 9.30 (1.51-15.71 (5.4 (8.97-4.80 (2.49 (6.25 (.54) 8.24) 1.51 (1.590 (.27-1.57) 2..490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.14) 2.36-1.0 (9.39-1.66) 1.6 (8.22-1.20 (.69) 8.9) 5.557) 1.58) 75th 3.57 (3.37-10.2-32.49 (1.13 (1.Organochlorine Pesticides nearby agriculture (Botella et al.21) 3.05) 1. 2004).31-12.488-.6) 8.730) . interval) 1..34 (7.01-11.88 (2.85 (1.14-1.6) 12.59) 3.09-1.51) 3.2 (9.76) 1. o.2 (19.22 (7.75 (4.8-90.68-4.385-.23 (7.02-8.00 (.6 (17.00-1.19-14.75 (8.1) 12.37-1.81-18.53-15.39-2.85-10.41-12.6) 9.36-11.56-3.63 (1.419-.03-4.11 (2.70-3.59 (4.80) 3.9 (26.45 (1.58) 1.37-16.96) .57-2.50-17. 2004).46 (1.44) 1.12-1.25-16.7-48.25) 8.71) 32. 1991).68 (2.77 (1.19) 4.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.9-17.66) 4.860 ng/L) and DDE (about 14.04-1.3 (9.52-6.31-2. In a subsample of NHANES II (19761980) participants.61 (1.4) 14.66) 3.36) 3.01-5.07 (5.71 (6.456 (.34-3.06) 1.28) 1.65) 1.00) 7.34) 2.79) 4.87 (5.9-38.10-5.07) 1.7) 16.3-43.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.49) 8.48 (6. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.16 (2.59 (1.600) .96) 1.5) 7.68) 2.11-1.56-6.55 (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.43-8.18 (6.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.91-3.4) 13.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .82 (1.32-9.46-2.8 (14.01-1.6) 13.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .26) 3.4 (12.76) 1. In the NHANES 1999-2000.5) 10.14 (1.37 (1.01-1.78 (4.41 (1.16-1..75) 2.66-4.54-7.52 (3.57-3.64-2.611-1.40-4.35) 1.S.34-11.59) 6.71) 12.48-4. Survey Geometric mean (95% conf.3) 13.10-1.00 (6.26-10.63 (6. 1971).18-4..34) 6.2) 26.97 (3.p’-DDT.820-1.17-3.21) 90th 7.25) 1.37-4.8 (13.81) 11.10) .963-1.22) .17 (3.5) 5.72) 1.24 (1.03-1.33-1.02) 1.623 (.430-.99) 1.76 (2.2 (9.7-20.02 (2.890-1.12 (.55-9.82) 1.85-4.57-13.46 (1. or p.13) 4.

17. and 03-04 are 20. < LOD means less than the limit of detection. and 7.S. 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. Survey Geometric mean (95% conf.8.7.Organochlorine Pesticides Serum o.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 93 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 01-02. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00.4.

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

et al. Katz SH.gov/ toxprofiles/tp35. Kaus S.358:110-114. et al.1-dichloro2. Lambright C. Notides AC. Needham LL. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Wolf CJ. Available at URL: http://www. Hediger ML. Vena JE. Effects of environmental antiandrogens on reproductive development in experimental animals. hexachlorobenzene. Crespo J. Baker RJ. Gabrio T.21(1-2)37-48. Beard J. Bloom MS.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Hayes WJ. et al. Needham LL. 4/21/09 Gladen BC.355:7889.7(3):248-264. Bull Environ Contam Toxicol 2004. Environ Health Perspect 2004. Longnecker MP.155(4):313-322. Zhou H.53(8):1161-1172. HCH. lindane (g-HCH). Heudorf U. JAMA 1956. Koepsell TD. Herrman T. Rogan WJ.17(6):692-700. Burse VW. Brock JW. Food and Drug Administration (FDA). Jr. Organochlorines and breast cancer risk. Barr DB. Sci Tot Environ 2006. Lancet 2001. Thun MJ. Maternal DDT exposures in relation to fetal and 5-year growth. Organochlorines in Swedish women: determinants of serum concentrations. Seiwert M. Levels of DDT. et al. Olea-Serrano MF. Brock JW. Arnold SF. Charles MJ. Exposure of women to organochlorine pesticides in Southern Spain. Greenfield TA. Willman EJ. Available at URL: http://www. Swanson MK.96:34-40. Atuma S. FDA total diet study. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Fourth National Report on Human Exposure to Environmental Chemicals 95 .cdc. Environ Health Perspect 1998. et al. dietary intakes of pesticides. Davis MD. Chemosphere 2004. et al. and HCB residues in human blood in Ahmedabad. dichlorodiphenyldichloroethylene. Bjerselius R. Darnerud PO.85:504508.112(17):1761-1767. Needham LL. Piechotowski I.71(6):1200-1209. Zoellner I. Klebanoff MA.fda. Link B. Neurotoxicol 2000.58:1185-1201. DDE and shortened duration of lactation in a northern Mexican town.html. Savitz DA. Epidemiology 2006. Kulkarni PK. Krause C.html. Klebanoff MA. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Int J Hyg Environ Health 2003. Buckland SJ. Botella B. Am J Epidemiol 2002. Vorojeikina DP. Int J Hyg Environ Health 2002. Zaidi SS. August 2008. Cueto C. Olson JR. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.atsdr. Maternal serum level of 1. Schulz C. Granath F.206:485-491. Drexler H. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Profiles of ortho-polychlorinated biphenyl congeners. Hurd C. Garrett N. Kashyap R. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). FDA Pesticide Program Residue Monitoring 1993-2006 [online]. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Environ Res 2004. Hum Reprod Updat 2001. Am J Public Health 1995. Paepke O. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Falk C. Ellis H. Longnecker MP. Patterson DG Jr.cfsan. Chen CW. Zhou H.106(5):279-289. Eriksson P.162:890-897. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells.205:297-308. DDE. et al. Gray LE Jr. Rivas A..52:301-309.72:261265. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Moysich KB. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Calle EE. CA Cancer J Clin 2002. Bates MN.111:349355. Frumkin H. Becker K. Olson J. Klebanoff MA. Ostby J. J Assoc Off Anal Chem 1988.gov/~dms/ pesrpts. Gladen BC. selected elements. Saiyed HN. April 1982 to 1984. et al. Environ Health Perspect 2003.54:1431-1443. Gunderson EL. DDT and human health. and polythelia among male offspring.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Parks L. Cerrillo I. and DDD [online].97(2):178192. 4/21/09 Anderson HA. Hanrahan L. India. Jusko TA. Biochem Pharmacol 1997. and dichloro(diphenyl)ethylene (DDE). Durham WF. September 2002. Aune M. Lepom P. Jr. et al. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. and other chemicals. Henley SJ. Glynn AW. Chemosphere 2005. Toxicological profile for DDT. Angerer J. Gray KA. hypospadias. Olea N. Bhatnagar VK. The Great Lakes Consortium. Talts U. Furr J. Biomonitoring of persistent organochlorine pesticides. Environ Res 2005.

27:405-421. Comparative pharmacodynamics of CYP2B induction by DDT. Lynch CF. and DDD in male rat liver and cultured rat hepatocytes. Chovancova J. Chemosphere 2004. J Toxicol Environ Health Part A 1998. Vol. Fox S.54:1509-520. Pollutants in breast milk. PA.Organochlorine Pesticides Mariussen E. Handbook of Pesticide Toxicology. Petrik J. Snedeker SM. et al. 731-915.36:253-589.109:35-47. Rey AA. Schecter A. Smith AG. Toxicol Appl Pharmacol 1971. Cerhan JR. In Hayes WJ. Jr and Laws ER. Nims R. Environ Health Perspect 2001. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Inc.20(2):186-193. Demographic and seasonal influences on human serum pesticide residue levels. Academic Press. Jr. and dieldrin.150:981-990. Crit Rev Toxicol 2006. Thomas PE. Arch Pediatr Adolesc Med 1996. DDE. Fonnum F. DDE. Stehr-Green. Jones CR. New York. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Pesticides and breast cancer risk: a review of DDT. Radomski JL. Astolfi E. J Toxicol Environ Health 1989. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. 96 Fourth National Report on Human Exposure to Environmental Chemicals . 2 Classes of Pesticides. Reddy AB. 1991 pp.53:455-477. children and newborn infants. Rogan WJ. Eds. Deichmann WB. Pavuk M. Lubet R. Chlorinated Hydrocarbon Insecticides. et al.

manufactured.S.10 (<LOD-5. EPA. 1987). Endrin does not accumulate in body tissues (IPCS.S. unless the dose is high and the exposure is very recent. Hepatic effects of endrin exposure have included necrosis. endrin usually is not detected in serum of exposed individuals. is no longer manufactured in the U.10 (<LOD-5. IPCS. or discarded. endrin can persist for years.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. 1992). 1979. At high doses. < LOD means less than the limit of detection.40 (<LOD-6. Depending on soil conditions. and occasionally at low levels in sediment and surface waters. Survey Geometric mean (95% conf. Because it is metabolized so rapidly.50) < LOD < LOD < LOD 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.60 (5.20 (<LOD-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.30 (<LOD-6. which may vary for some chemicals by year and by individual sample.40-5. Endrin was used as an insecticide. endrin has been detected with declining frequency in U. Over time.20 (<LOD-5. 1991). see Data Analysis section) for Survey years 01-02 and 03-04 are 5. total diet surveys (FDA. largely the result of historical agricultural application or run off from contaminated soils (ATSDR.Organochlorine Pesticides Endrin CAS No. 1992.40) < 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. Kavlock et al.. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. 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.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..S.30) < LOD 5. and inflammation (Smith. endrin is converted rapidly to its major metabolite.8. Fourth National Report on Human Exposure to Environmental Chemicals 97 . All uses of the pesticide in the U. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Endrin was not widely used as a termiticide. have been cancelled by the U. Ketoendrin is a major photodegradation product (IPCS.09 and 7.. 72-20-8 General Information Endrin. inhalation or dermal exposure routes. Endrin is absorbed rapidly after ingestion.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. 2008). In the body. fatty infiltration. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. An epidemic of acute endrin poisoning.S. population from the National Health and Nutrition Examination Survey. 1996. rodenticide and avicide. or from contact with contaminated soils and sediments in areas where endrin was applied. 1992).50) < LOD 5. 1992). Smith. 1991). Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. a stereoisomer of dieldrin. 1981). High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Endrin has been detected in soils.. anti-12hydroxyendrin. unlike aldrin and dieldrin.

020 (.020 (<LOD-. with the highest value 6.. Information about external exposure (i.020-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.020 (<LOD-. and the FDA monitors foods for pesticide residues. 2000).020 (<LOD-.html.cdc. Workplace exposure standards for endrin have been established by OSHA.S.24 ng/mL (about 6.gov/toxpro2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.atsdr. 98 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides The U.24 ng/g of serum) (Botella et al.S. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.020) < LOD .. environmental levels) and health effects of endrin is available from ATSDR at: http://www.020) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2004.020 (<LOD-. which may vary for some chemicals by year and by individual sample. 2004). This finding is consistent with other general population studies (Bates et al. Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population.020 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Ward et al.020 (<LOD-.020) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect. IARC has determined that endrin is not classifiable with regard to human carcinogenicity.. endrin was detected in 9% of serum samples. serum levels of endrin were below the limit of detection.020) < LOD < LOD < LOD . Survey Geometric mean (95% conf.020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020) < LOD . EPA has established environmental standards for endrin..e. In a small study of Spanish women hospitalized for elective surgery.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. population from the National Health and Nutrition Examination Survey.

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

9-30.7-21.6-32.5 (13.3) * * 15.6 (24.3 (22.3) < LOD < LOD 29.4) < LOD < LOD 33..0 (14.3 (16.3) 24.0 (18.2 (24.9) < LOD < LOD 20..7-22.1-16. 2008.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.8 (15.Organochlorine Pesticides Hexachlorobenzene CAS No.4-15.9) < LOD < LOD 15. or game taken from areas with HCB contamination.9-24. 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.0-25.4 (18. and foods with a high fat content.2 (14.S.9) < LOD < LOD 28. wildfowl. HCB is well absorbed after oral administration. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. 2005).0 (18.3 (22. 1976).8-15.0-19.5) < LOD < LOD 18. primarily as a fungicide and seed treatment until the U.4 (22. 1988).9 (25.4 (18.2 (17.0-16. 100 Fourth National Report on Human Exposure to Environmental Chemicals .4.S.7) * * 14.6) < LOD < LOD 26.6 (23. The FDA dietary surveys have shown that over time. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.4) < LOD < LOD 14.S.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.2-31. Although it is not manufactured as an end-product in the U.3 (14.0) < LOD < LOD 15.4 (11.2 (13.7-16. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.5-trichlorophenol (2.2-15.4. The general population may be exposed to HCB through diet. and elimination occurs by renal and fecal routes.5-14.0) < LOD < LOD 24. and accumulates in fatty tissues where it persists for years.4) < LOD < LOD 18.3 (12.7-26. Urinary metabolites include pentachlorophenol (PCP). 2.7 (19.2) < LOD < LOD 29.4) < LOD < LOD 22.1) < LOD < LOD 15.7 (27. HCB has been detected in fewer foods since the 1980s (FDA.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. and 7.0 (25. population from the National Health and Nutrition Examination Survey.0) * * 15. distributes widely throughout the body. breast milk is an additional route of elimination in nursing women.6 (21.6-33.1 (17.5-18.7) < LOD < LOD 24. air.4.4) < LOD < LOD 23.7-30.5-TCP) and 2.2 (14. Therefore. 2002).5 (13.6) < LOD < LOD 26.6-44.9 (25..7-29.9-32. < LOD means less than the limit of detection.8 (26.9 (14.2) < LOD < LOD 13. EPA cancelled its use in 1984. particularly by consuming fish.1 (13.5-14.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-17..1) * * 15.9) < LOD < LOD 16.4-16.1-20.3-22. and 03-04 are 118.6) < LOD < LOD 24.6) < LOD < LOD 25.2-15.0-28.4.9-15.0.3-26.7 (15.1 (14.S. 31.8 (22.5-15.9-20.8.9) 19.9) < LOD < LOD 19.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.7-16. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.6-TCP) (To-Figueras et al. respectively.7-15. HCB is slowly metabolized. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. Gunderson. see Data Analysis section) for Survey years 99-00. 1997).0) < LOD < LOD 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 * * 16.6-trichlorophenol (2. which may vary for some chemicals by year and by individual sample.5-33. and has been detected in soil.1 (14. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.3-20. 01-02.6) < LOD < LOD 14.9 (23.7 (15.6-19. and sediment (Barber et al.9) < LOD < LOD 20.5 (14.3 (20.3) < LOD < LOD 20.6-26. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. water.5-15.4) < LOD < LOD 19.8) < LOD < LOD 27.

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 * * .118-.175) < LOD < LOD . and weakness.182 (.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . arthritis. anorexia.087 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .121 (.123 (.095) < LOD < LOD 75th < LOD < LOD 90th * * . reproductive and developmental toxicities.088-. and many died before 2 years of age (Peters et al.082-.cdc. acute doses produce central nervous system depression and seizures.092 (. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.113-.203) < LOD < LOD .095-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.178-.072-.S. In humans.218) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.098 (.. EPA has established a drinking water standard.092 (.086-.111-.085-. and the FDA has established a bottled water standard for HCB.127-.099) < LOD < LOD .118-.125 (.167 (.157-.077-.Organochlorine Pesticides chemical. and liver and thyroid cancers (ATSDR..176) < LOD < LOD .130) < LOD < LOD . 1982. With chronic exposure.145-. Survey Geometric mean (95% conf.160 (.225 (.115 (.147-.091-.081-.135-. which may vary for some chemicals by year and by individual sample. ACGIH has developed workplace exposure limits for HCB.163) < LOD < LOD . Infants were exposed transplacentally and through breast milk. Fourth National Report on Human Exposure to Environmental Chemicals 101 .062-.095 (.203) < LOD < LOD .148-.190 (.083) < LOD < LOD .163 (.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 * * .092 (. environmental levels) and health effects is available from the U.094 (.gov/pesticides/ and from ATSDR at: http://www. thyromegaly.114-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda. population from the National Health and Nutrition Examination Survey.099) < LOD < LOD .176-.173) < LOD < LOD .064 (.152) < LOD < LOD .122) < LOD < LOD .078 (.132) < LOD < LOD .118) < LOD < LOD .090-.094) < LOD < LOD .100) < LOD < LOD .097 (.140 (.081 (.191 (. immunologic abnormalities.111) < LOD < LOD .092-.073-.086-.179 (.090 (.147 (. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.126) .atsdr.085) * * . Biomonitoring Information Serum concentrations reflect the body burden of HCB. very high. More information about external exposure (i.089-. Schmid.109) * * .S.S.114-.120 (.epa.069) * * .123 (. as well as hypertrichosis.102) < LOD < LOD .html.107-.099) < LOD < LOD .090 (.088-. 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.145-. This condition.065 (.129) < LOD < LOD .156 (.088-.e. 1960).196) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * . 2002).171 (.086) < LOD < LOD .174-.155) < LOD < LOD .079 (.143-.097) . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.104 (. EPA at: http://www. HCB interferes with normal heme synthesis. 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.163-.095 (.157 (.141) < LOD < LOD . and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.095) * * .097) < LOD < LOD .107) < LOD < LOD .090 (.089-.159-.186 (.060-.102 (.069) < LOD < LOD .169-. The U. Chronic feeding studies in animals have demonstrated kidney injury.gov/toxpro2.258) < LOD < LOD .123 (.

Chemosphere 2005. levels. Krause C.81(2):82-85.77:173182.111:349355. Holland NT.. trends and processes. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. April 1982 to 1984. Atuma S.17:388–399. Gunderson EL. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. 2005)..349:144. 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. Ozalla D. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene.110(8):835-838.fda. Jones KC. Zoellner I. Kemper FH. respectively. Arch Dermatol 1999. 1986. dietary intakes of pesticides.atsdr. Sci Tot Environ 2005. et al. Over the past two decades. Glynn et al. Piechotowski I. 1989). Environ Health Perspect 2003. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. 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. Seiwert M. Toxicological profile for hexachlorobenzene update [online]. Available at URL: http://www.. Safe A. Int J Hyg Environ Health 2002. Biol Neonate 2002.. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Dewailly E. References Agency for Toxic Substances and Disease Registry (ATSDR).58:1185-1201. J Assoc Off Anal Chem 1988. Biomonitoring of persistent organochlorine pesticides. In a representative sample of the 1998 German adult population. Bradman A. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.39(12):744-749. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al.cfsan. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. however. 1999). et al. Gabrio T. Santiago-Silva M. Ayotte P. The metabolism of higher chlorinated benzene isomers. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Link B. Lawrence River (Quebec. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Lackmann GM. Eskenazi B. and other chemicals. 2002. Herrero C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.html. As a result of the lower limit of detection in NHANES 2003-2004.71(6):1200-1209. Hexachlorobenzene in the global environment: emissions. Lecha M. August 2008.. 2002). Granath F. In Spain.. Bryan GT. 4/21/09 Glynn AW. HCB levels were directly related to age. FDA total diet study.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. et al. Schulz C. 2006). Canada). 2005. Muckle G.cdc. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Available at URL: http://www. In the 1976-1980 NHANES subsample.gov/~dms/ pesrpts. 2002) and among children (Link et al. J Exp Sci Environ Epidemiol 2007. Bjerselius R. van Wijk D. September 2002. Organochlorines in Swedish women: determinants of serum concentrations. Lackmann. Gocmen A. Food and Drug Administration (FDA). and the geometric mean concentration of HCB in whole blood was 0. Becker K.. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Herrman T. Reference values updated. Lackman. Darnerud PO. Cripps DJ. HCB detection in serum also was proportional to age.135(4):400404. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. only 4. Bertram HP. Can J Biochem 1976. Dallaire F. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Sweetman AJ.. 2002.html.9% of participants had quantifiable levels (Stehr-Green. Laliberte C. Peters HA.44 mg/L. Kaus S.. more HCB levels were quantified. 2002.205:297-308. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Paepke O. Kohli J. Dogramaci I. IARC Sci Publ 1986. Environ Health Perspect 2002. Schwartz JM. Barr DB. Link et al..54(3):203-208. selected elements. 2005). 2002. Bertram et al. but overall. 4/21/09 Barber JL.gov/ toxprofiles/tp90. Jones D. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Otero R. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Lepom P.. Fenster L. 2003). Muller C. Aune M. distribution. Sala M. Bradman et al. Arch Neurol 1982. et al.

Organochlorine Pesticides Schmid R. Santiago-Silva M. Fourth National Report on Human Exposure to Environmental Chemicals 103 . et al. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.263:397-398. Cutaneous porphyria in Turkey. PA.105(1):78-83. Rodamilans M. To-Figueras J. Otero R. Environ Health Perspect 1997. Stehr-Green.27:405-421. Demographic and seasonal influences on human serum pesticide residue levels. Sala M. Barrot C. J Toxicol Environ Health 1989. N Engl J Med 1960.

6) 16.4) 51.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.56-12.8 (21.5) 29. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. 319-85-7 gamma-Hexachlorocyclohexane CAS No. It is no longer produced or sold in the U. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.8) 39.0 (19.6-42. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.2 (29.6-18.2) 13.6-37.0 (14.60-13.8) 95th 68.50) 8.9) 45.1-37.6-89.8) 12.90-8.2-22.2-98.7 (29. 2005).1 (12.2 (50.1-36.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. 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.80 (<LOD-14.3 (62.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.6 (10. gamma.4) < LOD 9.0-70.3 (42.3) 37.0 (37.S.4) 27.6-135) 69.7 (13. water.1-27.9 (32.0-20.9-178) 48.7-69. the U.0-70.8 (32.2 (34.1) 13.4) 21.6 (22. 2005).89 (<LOD-9.1 (11.4) 10.1-15.3-56.5) 22.2 (18.4 (8.5-123) 49.9) 81.3) 14.7) 10.0-34. However.70-12.3 (13.30-11.7) 56.8-87.36.7-96.1) 12.5) 14.8) 7.8-199) 134 (85.80 (6.2) 62.04-10.1) 12. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.8 (9.4 (16.2-52.7-166) 70.6-47.8 (23.0 (<LOD-12.5) 67.3-85.5528.0) 35.4-50.8) 27.5) 40.4-111) 84.5-29. and 7.1-32. Lindane has a half-life of about two weeks in soils and water. and 03-04 are 9.3-38.0) 71.9 (9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 51. exists in several isomeric forms. 608-73-1 beta-Hexachlorocyclohexane CAS No.4 (50.2-17. < LOD means less than the limit of detection. beta.6) 653 758 589 1240 1533 1370 20 years and older 10.90-8.61-12.7) 23.6-14.1 (16.3) 25.8) * * * * * * 15. respectively.0) 17. particularly alpha and gamma have been detected widely in air.8-54.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.0) 7.7 (62.1 (9.1-32.2) 142 (99.9) 17.Organochlorine Pesticides Hexachlorocyclohexane CAS No.2-67.5 (24.8 (10.5 (37.70 (6.0 (8.1 (18.4) < LOD < LOD < LOD 46.70 (8.4 (12.6) 36.9 (40.7 (53.9-51. formerly referred to as benzene hexachloride.7 (<LOD-16.2 (31.2-20.6 (17.1 (27.0 (33. and have been used either as fungicides or to synthesize other chemicals.2) 9.4) 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 21.3 (26.8) 52.68 (<LOD-10.1-49.0-111) 70.5 (8. see Data Analysis section) for survey years 99-00.8-16.8-19. 104 Fourth National Report on Human Exposure to Environmental Chemicals .1 (30.43 (<LOD-9. interval) 9.8-68.2 (48.5 (14.1-16.4-45.1 (9.7 (25.9 (30.0-21. In 2006.9 (26.7-20.9 (62.90) 7. so they can accumulate in fatty tissues of animals.2 (9. Technical grade HCH is a mixture of all four isomers.8) < LOD 10.9-24.7 (30.9-81.1) 31.6 (33.4 (52. and delta. environmental levels declined. each result has been multiplied by 1. The gamma isomer.3 (42. 6.8 (33.7) 32. 01-02.6) 18.20-16.9) 15.46-11.1) 71. soil. HCH isomers are lipophilic. EPA cancelled agricultural uses of lindane (ATSDR.9-21.5 (16.4-73. including alpha.0 (35. The other isomers can be formed during the synthesis of lindane.76.9 (11.4) 44.1 (21.6) 47.3) 34.5 (43.0-23. and sediment as a result of historic production and use.0) 41.2-42.7 (35. **In survey period 2001-2002.8 (17.8.7) 97.4) 901 1067 952 992 1224 1007 Females 11.7) 73.2-46.7) 18. population from the National Health and Nutrition Examination Survey.6 (40. containing about 64% alpha and 10%-15% gamma isomers.6) 50.7-26.7) 27.70-19.6-20.5 (11. commonly known as lindane.8 (64.5) 11. HCH isomers.7-96.0) 8.5) 16.9-14.2-55.5) 90th 42.66-12.87 (9.9 (50.6 (16.7) 10.6-62.S.2) 36.6) 35.2-87.4) 11. which may vary for some chemicals by year and by individual sample. 58-89-9 General Information Hexachlorocyclohexane (HCH). See the section “What’s New” at the beginning of this Report for details.7-69.S.4 (11. As pesticide applications of HCH were increasingly restricted or eliminated.9-56.

050 (<LOD-.191-.068-.382-.300-.120-.090 (.110) .570 (.064 (.091) .330-.089-.250 (.680) .390-.064) .048 (<LOD-. See the section “What’s New” at the beginning of this Report for details.100-.080-. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.521 (. Rogan. respectively.100) .120) .290 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .290 (. hepatic enzyme induction. which may vary for some chemicals by year and by individual sample.080) .560 (.280-.910 (. After dermal application of lindane 1% lotion. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity..140) .173-.167 (.210) .01 (.480 (.100-.140 (.150) . U.067) .103 (.210 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Distribution is mainly to fatty tissues. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.480 (.501) .580-1.710) .110) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .294-.103) 90th .119) . 2008.140) .244-.150) .080 (.080) * * * * * * .221-.200 (.250-.072 (.081-.460) .620-1.120 (.370-.210-.200-. ingestion.077) < LOD .080-.340) .281 (.130-.120-. OSHA and ACGIH have established workplace standards and guidelines.290) .096) .174) .190-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.051 (<LOD-.200-.220-. Gunderson 1988). Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. ataxia.050-.080-. and seizures.120 (.240-.5528.170-. 1977)..250 (.150 (. **In survey period 2001-2002. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.580 (.100) . When animals were chronically fed lindane at high doses.330 (.077) < LOD .32) .050 (<LOD-.360 (.090-.250-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.065 (.620) .319) .331 (.287 (.216 (.310 (.400) .058 (<LOD-.37) 1.060) .420-.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.050 (.090 (. interval) .470 (.S..410) .600) .083) .350 (.210 (.100 (.234 (.190-1. tremors.Organochlorine Pesticides exposure to HCH is through the diet.260) .450-.050-.160-.073-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th ..190) .050 (.078 (.470) .098 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.118-.S.400) .051-.125) < LOD < LOD < LOD . each result has been multiplied by 1.270 (.110) .083 (.047-.130 (.100 (..070-.700) . for lindane.230-. resulting in a half-life of about seven years.410 (. 1981).310) .057 (<LOD-.056-. 2002).250) .118 (.120-.320 (.297-. Workers who directly handled HCH have complained of headache.057-.254) 95th .070 (.056-.560) .220 (.059-. or dermal exposure.814) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .450 (.092 (.05) . EPA has established a drinking water standard.460 (.170-. 1983).260) . population from the National Health and Nutrition Examination Survey.308-.450) . and memory loss (Nigam et al. Saxena et al.350) .290) .062 (. the serum half-life was about 20 hours among children (Ginsburg et al.050) . and FDA has established a bottled water standard and food residue tolerances for lindane.480) .057-.340-.103-. paresthesias.240 (. 1986).690) . 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.160 (.065 (.360) .220-.069) .146-.310) .280-. and nephropathy developed (IPCS.305) .510) .139 (.260-. 1996.160) .120) .130) .380 (.140) .086) < LOD < LOD < LOD < LOD < LOD < LOD .067 (.220) .124-.110-.070) .180-.050-.587) 653 758 589 1240 1533 1370 20 years and older .214) .S.090 (.410) .175 (.050-.360-.222 (.150-.404) . probably by blocking inhibitory neurotransmitters in the central nervous system.372 (.080 (.661) 901 1067 952 992 1224 1007 Females .840) .410-.070-.442 (.290 (.144 (. The beta isomer accumulates in fatty tissues and is metabolized more slowly.089) .070-. 1971. enlarged livers.062 (.250 (.131-.190) .040-. The U. HCH isomers are absorbed after inhalation. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.412 (.070 (.100-.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 .120 (.390 (.191-.

.html. environmental levels) and health effects is available from the U. 2005. In populationbased studies of New Zealand adults and German adults and children. EPA at: http://www.5.gov/toxpro2. 2004. the maximum and 95th percentile beta-HCH values. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. 1971.. Biomonitoring Information Because of its longer half-life. More information about external exposure (i. see Data Analysis section) for Survey years 99-00.8.e... aged 9-11 years.gov/pesticides/ and from ATSDR at: http:// www. and a diet that includes meat (Becker et al.. 1989). In recent years. and 7.S. 2001-2002. respectively.. Stehr-Green. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004). 1998. Radomski et al. In NHANES 1999-2000. 2004) and India (Bhatnagar et al.. Link et al. 2005. 1998).5. 2002). and 03-04 are 14. Becker et al.atsdr. male sex. Survey Geometric mean (95% conf. Additional factors associated with higher beta-HCH levels include rural residence. 01-02.. < LOD means less than the limit of detection. 10. In an earlier (1996-1997) sample of German children.. 2002. were similar to the 95th percentiles in this Report. which may vary for some chemicals by year and by individual sample. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. serum levels of lindane were generally below the limits of detection. 1991.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. population from the National Health and Nutrition Examination Survey. Kutz et al. older age... and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. and 2003-2004. respectively.epa. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. 1989. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. Bates et al.cdc. Stehr-Green. 106 Fourth National Report on Human Exposure to Environmental Chemicals .. Kutz et al. Sturgeon et al.S. 1991. 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. 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.

population from the National Health and Nutrition Examination Survey. 2003). Radomski et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 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). 1986. 1998)... Fourth National Report on Human Exposure to Environmental Chemicals 107 . 1971). respectively. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. Survey Geometric mean (95% conf. Serum gamma-Hexachlorocyclohexane (Lindane) (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. in this Report (Nigam et al.. 2005). In a small study of adults who consumed sport fish from the Great Lakes. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. which may vary for some chemicals by year and by individual sample. Biomonitoring studies on levels of HCH isomers provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of HCH isomers than are found in the general population.S. 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.. 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.Organochlorine Pesticides 2001-2002 survey period (Link et al.

Kulkarni PK. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Stehr-Green. Herrman T.150:981-990. et al. August 2008. Maass R. Bhargava AK. Granath F. Radomski JL. Zoellner I. Visweswariah K. Link B. et al. Deichmann WB. International Programme on Chemical Safety (IPCS).inchem. Cerrillo I. Raju GS. children and newborn infants. VI. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. dietary intakes of pesticides. FDA total diet study. Piechotowski I. Saiyed HN. Int Arch Occup Environ Health 1983.htm. Lindane. Placental transfer of pesticides in humans. and other chemicals.57(4):315-320. Krause C. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health 1989. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Becker K. Botella B. Burse VW. Environ Res 2004. J Assoc Off Anal Chem 1988. India. Int Arch Occup Environ Health 1986. Cancer Causes and Control 1998. August 2005. Paepke O. selected elements. Needham LL. Rev Environ Contam Toxicol 1991. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 2002. Occupational exposure to hexachlorocyclohexane.72:261265. available at URL: http://www. et al. Gabrio T. Nigam SK. Potischman N. Atuma S. Bai KM.52(1):59-67. Falk C. Pollutants in breast milk. Kutty D.20(2):186-193.111:349355. 4/21/09 Ginsburg CM.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Krishna Murti CR. Schulz C. Metabolism of gammahexachlorocyclohexane in man. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Olea N. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Biomonitoring of persistent organochlorine pesticides. PA. Bottimore DP.27:405-421.205:297-308. Reisch JS. Darnerud PO. Olson J. Angerer J. Wood PH. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Rey AA. Garrett N.html.html.9(4):417-424.gov/~dms/pesrpts.106(5):279-289. Sturgeon SR. Absorption of lindane (g benzene hexachloride) in infants and children. Arch Pediatr Adolesc Med 1996. Bjerselius R. Needham LL. Toxicol Appl Pharmacol 1971. Patterson DG Jr.cdc. Bates MN. Bhatnagar VK. Lowry W. Organochlorines in Swedish women: determinants of serum concentrations. April 1982 to 1984. et al. Exposure of women to organochlorine pesticides in Southern Spain. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.cfsan. Brinton LA. Available at URL: http://www. Rothman N. Chemosphere 2004.120:1-82. et al. Brock JW. and HCB residues in human blood in Ahmedabad. Lepom P. 4/21/09 Anderson HA. gov/toxprofiles/tp43. Rogan WJ.91:998-1000. Hanrahan L. Bull Environ Contam Toxicol 2004. Astolfi E. Kaus S. Saxena MC. Available at URL: http://www. Gunderson EL. Rivas A. Aune M. et al.atsdr. 4/21/09 Kutz FW.58:1185-1201. et al. Karnik AB. The Great Lakes Consortium. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.54:1431-1443. org/documents/jmpr/jmpmono/2002pr08. Chemosphere 2005. Environ Health Perspect 1998. Int J Hyg Environ Health 2002. J Pediatr 1977. Ellis H. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Kashyap R. Glynn AW. Majumder SK. Zaidi SS. Needham LL. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Olea-Serrano MF. Arch Toxicol 1981. Crespo J. Heinrich R. Siddiqui MKJ. Seiwert M. Toxicological profile for hexachlorocyclohexanes update [online].96:34-4Food and Drug Administration (FDA). Buckland SJ. Levels of DDT.48:127-134.71(6):1200-1209. HCH. Environ Health Perspect 2003.fda.

8) < LOD 15. 1995).3 (15.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.1) 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 16.1 (8. and 03-04 are 14. aquatic organisms.S. Mirex binds strongly to soil.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.5-425) 40.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.Organochlorine Pesticides Mirex CAS No.4 (8. animals.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Some states and the U.1 (13. In studies conducted in the 1970’s and 1980’s. since 1977.0 (12. mirex was detected in human adipose samples. Occupational exposure is limited to workers at sites where mirex contamination is present.2) 51. 1991).5 (<LOD-42.6 (<LOD-31.2-230) 13.10-37.0-374) 11.8. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. after which it is widely distributed in the body and stored in fat.3-225) 15.70-40.4) < LOD 63.8 (<LOD-73.S. or pesticide application.0 (14. where it was applied directly to soil and by aerial spraying. water. especially those from persons living in the southeastern U. (Kutz et al.7) 8. it is a highly persistent chemical in the environment.3 (15.5-291) 11.7 (<LOD-47.2 (7.70-24. 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. where it has a half-life of 12 years. resulting in exposure to newborns and nursing infants.7) < LOD 66. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.8 (12.1 (<LOD-65. disposal. Fourth National Report on Human Exposure to Environmental Chemicals 109 . Survey Geometric mean (95% conf.5 (9.5-82. Formerly.6) 9. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.6. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. see Data Analysis section) for Survey years 99-00.5 (<LOD-115) 153 (30. and foods.70 (<LOD-15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-305) 15.3) 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 13.7 (12. Mirex is not metabolized in the body.4-230) 18.5.40 (<LOD-13. 2385-85-5 General Information Mirex has not been produced or used in the U.S.10 (<LOD-15.4) < LOD 15.0) * * * 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. 01-02. which may vary for some chemicals by year and by individual sample. 1985.90-29. Mirex is absorbed through the skin and from the gastrointestinal tract. < LOD means less than the limit of detection. soil.. 10.6 (<LOD-23.0 (<LOD-108) < LOD < LOD 50. sediments. and 7. population from the National Health and Nutrition Examination Survey.. Mirex can cross the placenta and be excreted in breast milk.S.6) < LOD < LOD < LOD < LOD 71. respectively.S. Mirex has been detected in air. 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.6 (<LOD-108) 9. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.

The geometric mean mirex levels of the Inuit mothers were 8.7 ng/g of lipid.html. and 4. population from the National Health and Nutrition Examination Survey. Smith.090-1.059 (<LOD-. In addition. 1995.079 (<LOD-.170) < LOD .140 (<LOD-. More information about external exposure (i.220) .090-1.089-.79) .gov/toxpro2.090-1.79) .112 (.450) 1.106) < LOD .100 (<LOD-.690) .450 (.055-. and NTP classifies mirex as reasonably anticipated to be a human carcinogen. 1991).S.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .102) < LOD < LOD < LOD < LOD . The U.470) . Biomonitoring Information In the NHANES 1999-2000. reproductive toxicity included decreased fertility and testicular damage. 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. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.41) . IARC classifies mirex as possibly carcinogenic to humans.470) .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 . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.090 (<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.054 (<LOD-. Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al.100 (<LOD-.atsdr.170-3.cdc. 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.064 (<LOD-. serum mirex levels were generally below the limits of detection (Stehr-Green.053-. In samples obtained between 1994 and 1997. environmental levels) and health effects is available from the ATSDR at: http://www.090 (<LOD-.110 (<LOD-. which may vary for some chemicals by year and by individual sample.080-1.062-.Organochlorine Pesticides exposures are unknown. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .08 (.268) < LOD .8. Survey Geometric mean (95% conf.108 (.510) < LOD < LOD . Laboratory animals fed high doses developed liver enlargement and liver tumors..02) .093 (.106 (. 2004). 7.370 (. and 2003-2004 subsamples. EPA has established environmental standards for mirex.470 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .084) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .635) < LOD .610) < LOD < LOD < LOD < LOD .220 (<LOD-.430 (.92) .410 (..090 (<LOD-.S. 2005).080-1. 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.070-1..052-.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 .310 (.73) .37) . 1989).077 (<LOD-. 2001-2002. as well as in a subsample of NHANES II (1976-1980) participants.256 (.e. 110 Fourth National Report on Human Exposure to Environmental Chemicals .

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

Exposure to trichlorophenols also may result from metabolism of lindane.00 (2.0 (5.0) 14.27) 696 661 521 696 603 939 Limit of detection (LOD.50-25.20-71.6-TCP in any of the samples (U.950 (<LOD-1. however. are metabolites of several organochlorine chemicals.40) < LOD 1.60 (2.6-TCP were used as intermediates in the production of certain pesticides.40 (2.20) < LOD 5. 2.0) < LOD 11.3. Such workers would probably Urinary 2.5-Trichlorophenol CAS No.40 (1.80 (1.71 (<LOD-8.30-44.80) < LOD 1.42 (<LOD-12.30 (. including hexachlorobenzene and hexachlorocyclohexanes.6-trichlorophenol (2.10-3. < LOD means less than the limit of detection.71 (<LOD-8.4. 95-95-4 2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.0) < LOD 5.0) 2.60-18.0) 2. Historically. Formation of 2.0) 2. usually at herbicide production or waste incineration facilities.30-27..20-36.0) < LOD 5.40 (1.60) < LOD 8.57 (<LOD-15.0 (4. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR. Occupational exposures.80 (2.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1. surface water.30) < LOD 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.9.30) < LOD < LOD < LOD < LOD < LOD 1.40 (2. and polychlorinated benzenes (Kohil et al.30-27.5TCP and 2.4.60 (.S.0 (3.00-3.20) < LOD 1.19 (<LOD-6. and sediments. 1999).20) < LOD 90th 5. 2006).5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.42 (<LOD-8. 1976).40) < LOD 4. other organochlorines.30-3.4.7.980-3. EPA.40 (2. which may vary for some chemicals by year and by individual sample.0) < LOD 21.50-16.30-11.60-8.0) 5. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.0) 2.03) 9. 112 Fourth National Report on Human Exposure to Environmental Chemicals .4. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.63) 18. may occur by inhalation or dermal routes.72) < LOD 1.00-3.40) < LOD 6. Both chemicals have been detected in air.40 (2.9 (<LOD-121) 9.4.50-63. 2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.50 (1. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.20 (4.50 (2.5-TCP) and 2. soils.6-Trichlorophenol CAS No.60 (4.S. 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.940-3.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.0) 2.40-18. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.40-11.7) 24. public drinking water systems did not detect 2.980-3. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. 1999).900-2.0 (3.4.50) < LOD 1.8) 21.4. recent sampling of U.30-27.4.0 (4.0 (8.9 and 0.5-trichlorophenol (2.0) 2.00-8.920-3.0) < LOD 5.80-41. hexachlorobenzene.4.50 (.4. 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.90-33. population from the National Health and Nutrition Examination Survey.0) < LOD 11. Trichlorophenols are no longer manufactured commercially.30-40.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .S.31 (<LOD-9.4.00 (3.6-TCP).0 (4.5-trichlorophenol.Organochlorine Pesticides 2.40 (.40 (.

animals showed hepatocellular abnormalities.00-19.64 (4.44 (.4.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.2) < LOD 5.5-TCP. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.68 (<LOD-8.4.47-8.6-TCP as reasonably anticipated to be a human carcinogen.55 (4. NTP classifies 2. population from the National Health and Nutrition Examination Survey. At lower doses.20-6. More information about external exposure (i.19-4.Organochlorine Pesticides be exposed to mixtures of chlorophenols..37-11.11) 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 2.79-4.4.57 (<LOD-7.1 (<LOD-58.6) 4.78-19.6-TCP.24) < LOD 6. and lymphomas.19-12. the 95th percentile urinary 2..78) < LOD 1.3 mg/L reported in German adults aged 18-69 years (Becker et al. as being possibly carcinogenic to humans.920-2.6) 4.83-12. in addition to dioxins.0) 7.cdc.67 (1..4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. Human health effects from 2. Neither 2. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. However.78 (3.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.33) < LOD < LOD < LOD < LOD < LOD 2. urinary 2.e. 2004).00-29..00) < LOD 4.4) < LOD 3.29 (1.62-20.27-17.49 (1. Fourth National Report on Human Exposure to Environmental Chemicals 113 .4.5-TCP and limited for 2.8) < LOD 9.13-13.46 (1.gov/toxpro2.24) < LOD 5.57 (3. 1995) and up to 19 times higher than the 95th percentile value of 1.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.5) < LOD 12.43 (2.57 (<LOD-7. and other chlorinated compounds. 2003). 2003. The 95th percentiles for 2.31) < LOD 2.6) 4.50) < LOD 2. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. In the same 2-6 year old children.atsdr.68-4.44 (1.60-3.53-3.75 (3.1) 2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.24) < LOD 1.5-TCP nor 2. environmental levels) and health effects is available from ATSDR at: http://www. IARC classifies combined exposures to polychlorophenols.0 mg/L. furans.69-18.17) 9. leukemias.75 (<LOD-6.95 (3. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.93-11.02) < LOD 7.73 (<LOD-8.4.html.8) 4. which includes trichlorophenols.16 (.9 (5.5) 11.4) < LOD 3.. Urinary 2.88-16.2) 2.74) 11. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. the 95th percentile urinary 2.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.15) < LOD 2.82 (<LOD-32.5-TCP or 2.6-TCP had increased rates of hepatic tumors. 7.2 (2.4.81 (<LOD-9.4. 1995) were similar.4.S.980 (<LOD-1. Laboratory animals chronically fed high doses of 2.90 (4.9) 12.820-2.6-TCP levels at the 95th percentile were up to eight times higher than 3.4.37) 16.7 (4.24 (3.36 (1.32) < LOD 4.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.05-17.05-8.6-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.. 1989). Survey Geometric mean (95% conf.4.67 (1.02-3.4 (6.4..8 (5.4. Radon et al.43) < LOD 12.69 (2.86 (3...4) 5. 1989).2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.3 (5. 2003).28-25.53-3.80 (1.16) < LOD 90th 5.24-11. Among 6-11 year old children in NHANES 1999-2000.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).

23-2.20-23.0) 19.9) 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 2.63) 90th 15.6-TCP than are found in the general population.0 (11.6TCP values.6 mg/g creatinine) and 2.4.20 (3.7-3.65) 15.30-11. respectively.35-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 10. 1998).4.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.40 (2.6-17.5-46.5-TCP level of 0.4.60) < LOD 5.0) 13.S.4.28) * 2.70 (2. Survey Geometric mean (95% conf.30) 4.0 (15.6TCP causes an adverse health effect.4.69 (3.0 (20.30-2.70-6.49 (6.91-4.36 mg/g creatinine.0-38. Urinary 2.60 (2.6) 26..4 (8.0 (14.0 (6.00 (1.5-TCP (0.02) 2.80 (3.32) 3.4.10-3. 114 Fourth National Report on Human Exposure to Environmental Chemicals .0) 19.92 (2.32-4.32) * 3.47 (3.60-21.3) 23.0 (16.12) 2.48-26.0 (6.50-5.5-TCP or 2.98-7.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.89-6.65 (5.23) 3.40) 2.60 (3. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.1 (8.8-13. Mean values of 2.2 (14. Biomonitoring data will also help scientists plan and conduct research about 2. In harbor workers exposed to chlorophenol-contaminated river silt.7 mg/L.8) 32.0) 10.6) 21.4.4.7) 21..2-0.6-TCP exposure and health effects.8-15.1 (10.0) 12.5-TCP and 2.9 (13.14 (2.0) 13.5-TCP or 2.10 (5.25-11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 694 677 519 696 602 931 Limit of detection (LOD.0 (6.95 (4.0) 9.44) 75th 4.23) 2.4.5-TCP and to the median 2.0 (12.56 (3.0) 6.2) 25.4-17.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.08 (2.80-7.7 (13.20-6.0) 14.4.4.20-3.58 (1.85) * 3.0 (8.57 (<LOD-2.0 (4.0 (14.40-2.9 (11.6-TCP level.0) 14.0) 13.79 (5.00 (4.59-6.6 (12.18-3.28) 24.45-9.90 (3. for males in NHANES 19992002 (Agramunt et al.0 (8.24 (2.09-7. < LOD means less than the limit of detection.52 (2.70) 5.4 (10.40 (2.40-7.70-3.0 and 1.40-32.0-43.20) 4.78 (2.0-44.50 (2.67) 4.70 (2.06) * 2.9) 13.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.74-3.0) 9.40) 2.53) 2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.80-20.4.70) 1.85 (2.0-54.75 (8.0) 13.4.87-14.7-16.0-38.6-TCP in urine does not mean that the level of 2. 2003).40) 3.0) 7.1-25.0) 11.0) 7.70-6.36 (1.78 (2.36-5.90 (4.10-3.45 (5.7) 33.99) 6.46-3. similar to the limit of detection for this Report (Anderson et al. 2004).70) 3. the median urinary 2.0) 11.51-12.40-4.0 (7.4 (17. 0.40) 4.58-3.73-9.59) 4.70) 5.3-26.80-25.3.90-8.68 (<LOD-2.3) 20.0 (9. Finding a measurable amount of 2.01-6.0-37.5-TCP or 2.7 (9.80 (2.0 (13.8) 18. Urinary 2.31) * 2.8-24.00 (2.1) 16.00-21.40-2.0-41.95) 3.4.3) 37.6-19.0 (15.5 mg/g creatinine) were similar to the limit of detection for 2.0) 17.4.6-22.3-17.4.0-50.55-3.89 (3.10) 6.09) 15.4.76) 3.84) 2.40-14.0) 15.30-2.26 (2..07 (<LOD-3.60-37.98-11.0-68.52-3.20 (3.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2. 1991).4.3 (11. was about six times lower than the median urinary levels for males in this Report (Radon et al.6-TCP (0. Biomonitoring studies on levels of 2.45) < LOD 11.33-4.66 (8.2) 12.4.80 (2.60) 6.5-TCP or 2.60 (3.45 (2.0 (20.80-6.4 (9.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.30-33.80) 1. population from the National Health and Nutrition Examination Survey.90) 2.10) 2.10-2.6 (11.0-18.3 (11.74 (2.04) 2.60-3.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.67-12.0 (14..53) 4.5-TCP and 2.4.8 (9.31 (3.0) 17.54) 6.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.72-10. interval) 2.95-6. which may vary for some chemicals by year and by individual sample.00-4.

63-13.22 (<LOD-2.7 (14.05 (6.0) 8.27-9.9) 8.43 (<LOD-2.47-5.58 (4.2) 19.4) 4. Fourth National Report on Human Exposure to Environmental Chemicals 115 .2 (12.08-2.75) 75th 4.91 (3.72-16.98) 10.22-2.29-4.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.26-13.6 (12.6) 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 2.65-21.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5) 11.4) 9.53 (3.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.25-2.78) 90th 12.1 (13.14-13.98 (1.94-13.43-7.6 (9.32 (2.00 (3.60 (4.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.9-64.56 (7.18-4.15 (6.78 (2.1) 11.18-2.4 (12.53-11.38) 22.9) 8.9-34.3-37.53) 4.1) 14.82 (3.01 (3.87) * 2.56) < LOD 11.63) 4.91 (7.87-7.53) * 2.52) 2.89) 10.7) 25.96) < LOD 4.00 (2.63-15.62-15.02 (1.77) 2.25-15.76) 1.50 (2.8) 11.6) 12.7) 6.41-6.05 (3.22 (3.5 (7.20-2.7-36.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.66-4.9) 19.65) 18.83 (3.6 (22.26 (6.2 (8.10-9.6 (6.10) 4.06) 11.33 (7.68) 2.88) 4.88) * 2.88-7.16-10.10 (6.51-21.5 (10.9 (9.81-9.29 (6.40 (2.49) 4.6) 8.5-28.44 (3.82-2.32-19.9-29.38 (4.82 (8.76) 2.8) 21.5) 11.81) 2.14-2.91-2.92) 4.76-8.43 (2.1-32.15 (1.9-32.87) 2.25-17.95-2.51 (2.99-2. interval) 2.67-17.88) 5.11) 10.76) 4.40 (7.8) 19.S.29-4.87-6.22 (1.6-31.28-4.46-14.5) 12.06-2.89-2.13-6.56-5.6) 13.2 (7. Survey Geometric mean (95% conf.0) 10.00) 4.33-2.5 (8.83-5.83-6.70-9.17-4.33 (1.4 (11.77-4.3 (9.72) 32.49-3.00) 4.6 (9.9) 7.0 (6.90 (1.21-11.8) 12.30-2.42 (2.71 (3.04-16.4) 8.2 (13.55-2.90) 2.17) 2.63 (2.09-3.25 (3.52) 2.1 (8.78) 2.0 (9.9 (9.52 (5.41 (3.6 (10.79-17.82) 2.8 (7.48-2.1-21.5) 9.25 (3.8 (8.73) 5.19-5.13 (1.17) 13.51) 18.88) 4.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.33) * 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.23) 4.59 (2.54 (2.68) 2.24 (1.4.3-23.50-8.60-2.5) 8.73-22.22-9.0 (11.35 (3.88) 1.42) 2.38 (2.02) 3.Organochlorine Pesticides Urinary 2.04-2.23 (1.6 (5.63) * 4.06) 4.65-2.88 (2.83-6.3) 8.38-5. population from the National Health and Nutrition Examination Survey.87 (3.63 (<LOD-2.65) 2.52 (3.

July 1999. Hill RH Jr.cdc. Baker S. et al. Int J Hyg Environ Health 2003.146:83-91. 206:15-24. Needham LL. Luotamo M. Environmental Protection Agency (U. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995. et al. Bailey SL. U. Am J Ind Med 2004. Jones D. Aitio A.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Smith SJ. Available at URL: http://www. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Needham LL.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Seiwert M. Urinary excretion of chlorinated phenols in saw-mill workers. Heinrich-Ramm R. Available at URL: http://www. Wegner R. Kohli J. Environ Health Perspect 1998. Holler JS. 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].18(4):469-474. Toxicol Lett 2003. html. Domingo A. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Toxicological profile for chlorophenols [online]. Safe A. et al.54(3):203-208. Can J Biochem 1976. Fast DM. Schulz C. S. Burse VW. Anderson HA. Falk C. Arch Environ Contam Toxicol 1989. Radon K. December 2006 Draft. Shealy DB.S. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Domingo JL. The metabolism of higher chlorinated benzene isomers. Gregg M. Baur X. Lindroos L. Olson J.63:57-62. Seifert B. Kaus S. Poschadel B. To T. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.atsdr.71:99108. Hill RH Jr.45:440-445. Pekari K. Int Arch Occup Environ Health 1991.EPA). 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .106(5):279-289. Szadkowski D. 4/21/09 Agramunt MC. Hanrahan L.gov/toxprofiles/tp107. The Great Lakes Consortium.epa.pdf. Becker K. Corbella J. Head SL. Jarvisalo J.

and a low persistence in the environment. florists. chlorpyriphos) are initially metabolized to the more toxic “oxon” form.. In general. 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. In general. and manufacturers of these insecticides may have greater exposure than the general population. naled) are also registered for public health applications (e.g. widely varying degrees of soil leaching or runoff potential. moderate to high soil binding.g.S.Diethyldithiophosphate phosphate phosphate phosphate phosphate phosphate (813-79-5) (1112-38-5) (756-80-9) (598-02-7) (2465-65-8) (298-06-6) • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • Fourth National Report on Human Exposure to Environmental Chemicals 117 . 1993). less common routes include inhalation and dermal contact. Many states have programs to monitor Pesticide (CAS number) Azinphos methyl Chlorethoxyphos Chlorpyrifos Chlorpyrifos methyl Coumaphos Dichlorvos (DDVP) Diazinon Dicrotophos Dimethoate Disulfoton Ethion Fenitrothion Fenthion Isazaphos-methyl Malathion Methidathion Methyl parathion Naled Oxydemeton-methyl Parathion Phorate Phosmet Pirimiphos-methyl Sulfotepp Temephos Terbufos Tetrachlorvinphos Dimethyl. Certain organophosphorus insecticides (e. with usage declining 45% since 1980 (U. malathion. most residential uses have been phased out in the United States as a result of implementation of the Food Quality Protection Act of 1996. 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. pesticide applicators.. EPA. Most organophosphorus insecticides undergo hydrolysis with excretion of major hydrolytic metabolites in the urine. The thiophosphate type organophosphorus insecticides (e. Although organophosphorus insecticides are still used for insect control on many food crops.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Organophosphorus Insecticides: Dialkyl Phosphate Metabolites General Information Organophosphorus insecticides. slight to moderate water solubility. Approximately 40 organophosphorus insecticides in a wide variety of formulations are registered for use in the United States by the U. 2004). Mammalian elimination halflives can range from hours to weeks.DimethyldithioDiethylDiethylthio.. mosquito control) in the United States.Dimethylthio. Farm workers. gardeners. have accounted for a large share of all insecticides used in the United States. the various organophosphorus insecticides demonstrate low vapor pressures (with some exceptions). the organophosphorus insecticides have better gastrointestinal than dermal absorption. which are active against a broad spectrum of insects. EPA.g.S.

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

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

82-12.35-16.4) 17.66) * * 1.0) 10.0) 11.290 (<LOD-1.23-5.80) 2.4 (9.60 (1.27-3.53) 4.12-19. 0.35-12.5) 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-16.30-4.81) 1.8 (12.3-15.0) 15.4) 20.58 (5.S.91) 4.9) 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 1.10) < LOD .0 (7.44-3.90) 2.0 (7.39 (8.71-9.757-2.2.5-17.79 (5.40-5. respectively.51) 2.70 (2.2) 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 1.2 (7.0 (4.4 (7.4) 18.0) 5.20-4.7 (12.50-36.13 (2.50) 2.15) 14.79-7.8-32.98-12.70-11.30 (2.57-7.0) 11.1) 13.52) 6.6) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (4.0 (6.8 (8.71 (2.00) 3.55-8.20-7.290 (<LOD-.0) 6.8) 11.0-27.0) 10.90) 3.60 (5.1 (9. 120 Fourth National Report on Human Exposure to Environmental Chemicals .0 (8.0 (12.600 (<LOD-1. and 0.80-22.37 (3.0) 11.740-2. 01-02.82) 10.8) 19.44-38.27-15.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.39 (3.58 (3.9) 14.13 (2.13-2.21) 9.00-19.30-6.840-1.90 (1.16) 4.48-7.61) 4.94) 3.80) 4.2) 14.11 (.99 (5.90-5.5 (11.01) * * 1.63) 1.30 (2.20 (.623-1.00-27.02) 4.579-1.9) 8.42-3.86-15.5 (8.40-19.700-1.58 (2.45 (2.810-1.717-1.93-24.80) 2. which may vary for some chemicals by year and by individual sample.19) 9.7 (14.40-14.60-25.32) 1.20 (.490-2.4 (9.50-5.80) .04) < LOD 1.0-28.80 (2.7) 11.0 (8.0 (7.93 (4.2 (7.74 (8.80) 3.26 (5.0) 10.9-18.2 (9.70-19.0) 5.2.2 (9.620-1.80) .20-30.80) 11.07-10.80-4.1.38-5.60-18.96-3.2 (14.33 (5.0 (5.0) 5.2) 16.0) 7.0 (9. interval) 1.90-4.56-13.21 (.3) 16.0) 10.530 (<LOD-2.08 (<LOD-2.00 (1.03 (.599-1.2-20.0) 9.50 (4.44 (2.10) < LOD < LOD 4.00-27.67) 3.830 (<LOD-3.81) 11.40 (.890 (<LOD-2.26-8.55-6.10 (2.20 (2.36-4.3) 14.8 (14.3) 17.2) 16.30 (4.94) * * .60) .02-5.61 (3.08-15.10-7.2 (7.860-2.1) 10.6) 18.00-12.2 (11.98-5.95) 5.47) 5.2) 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 1.80-24.4 (7.70) < LOD < LOD 1.97) 8.08-2.1 (10.26-6.00) 3.955 (.0) 6.60-11.60) < LOD < LOD 4.34-7.10 (.70-14.40-11.43-12.981 (.72) 5.22 (.954 (.89) 9.40-1.46) 10.670-1.9 (8.0 (8.81) 11.0 (6.780) < LOD 3.0 (9.73) * * .50 (.970-2.35-11.00-12.40-16.20 (.10 (.17-3.0) 20.05-7.8) 7.85 (3.0) 12.70) < LOD < LOD 75th 3.33-18.70 (4.50 (2. see Data Analysis section) for Survey years 99-00.20 (.80 (4.86 (1.0) 11.47) * * 1.750-1.1) 95th 13.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (7.00 (5.0) 10.52) * * 1.56 (4.1-17.8) 7.32 (.2 (14.0) 6.70-23.10 (2.42) .68-7.1-23.97) 90th 7.8 (9.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.12) 4. and 03-04 are 0.00-7.56 (1.56 (6.54 (3.83 (5.28) 1.15-12.29) * * 1.34-3. population from the National Health and Nutrition Examination Survey.76 (2.14) * * .758-1.74 (8.52-11.16 (2. < LOD means less than the limit of detection.80) 2.70) .5) 20.

81-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.55-20.57) 4.7 (8.84) 7.71) 10.80) 9.4 (9.2) 8.02-2.36) * * 1.30) 2.94 (2.54-15.69) 2.66-15.23 (4.39 (2.81 (1.1 (10.43 (.608-1.750 (<LOD-1.95) 2.1 (7.8) 8.18 (.75) 2.6 (10.28 (4.85) 2.1-15.9 (5.07 (.1 (9.57 (4.45-5.89) * * 1.8) 6.82-14.76) < LOD .780 (<LOD-1.78 (2.79-9.87-5.90-8.13) 4.93-5.03 (2.47) * * .54) .2) 5.10 (3.820 (.37 (4.41) Selected percentiles ( 95% confidence interval) Total * * 50th .570-1.00) 8. Fourth National Report on Human Exposure to Environmental Chemicals 121 .29 (2.46) 2.27) < LOD 2.8) 7.03-6.560-1.870-2.32-12.67-19.42) 12.7) 18.6) 11.0) 6.67) 4.28-9.996 (.68) < LOD < LOD 3.06-2.00-19.7 (9.430-1.40-14.5-16.5-13.8) 16.84 (5.0 (8.28) 10.3) 15.40-28.20-8.10-13.88-15.03 (7.82-6.30 (1.80 (7.60) 2.85 (6.05 (.2 (8.98 (3.03) 2.94-10.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.960 (<LOD-2.04 (1.47 (1.43) 2.650-1.7 (10.88) 2.00 (4.1 (6.68-4.40-3.9-28.7) 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 .5-32.66 (1.5) 7.40) 4.2) 5.0) 7.53-11.94-22.82-14.25) < LOD .40) < LOD < LOD 75th 2.94 (4.8) 12.37-3.23) 4.4) 4.710 (<LOD-1.6) 13.3) 12.98-5.510-1.7) 12.31 (3.3) 5.42 (3.98) 9.53) 9.89-3.46-5.3) 16.8 (10.60) * * .54-11.9) 11.15-10.90-5.1) 4.S.29) * * .00-13.5) 11.41-12.72) 11.830-1.60-9.4) 4.2) 95th 12.1 (8.6) 8.34) < LOD < LOD .890 (<LOD-1.9) 16.960 (.00-17.51-5.28 (2.633-1.2 (6.45-11.2) 7.41) .1) 4.900 (.890 (<LOD-1.09 (.75) 14.40-12.98) .50) 7.44 (2.2) 13.56) 7.69 (4.35 (1.932 (.93) 9.09-11.860 (.6) 9.98-22.920 (.31-14.88-10.19 (4.5) 8.93-9.9 (9.1 (11.88 (5.69-10.11-6.7) 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.56) 4.76-4.94-9.74) 90th 7.05 (1.83 (7.80 (6.500-1.64-5.02-14. interval) .56-13.75-7.25) 6.66-34.47 (3.2) 9.5) 7.83) 8.98) .34) * * .14 (3.21-23.4) 13.855 (.2 (10.69) 4.38) .540-1.6 (9.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.74) 4.3) 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 1.37 (5.7) 5.566-1.54-4.62-5.87 (3.24-3.5 (4.773-1.71-2.75 (7.09) 2.5) 12.9 (9.620-1.440 (<LOD-2.61 (1.02 (2.574-1.79-3.61 (1.00 (4.5-20.62) .40-5.92-5.52) 4. population from the National Health and Nutrition Examination Survey.95 (3.58) * * 1.47 (3.56) .818 (.40 (3.04-6.57 (6.34 (6.57-10.61-29.92-2.03) 2.67) 1.26) * * .28 (5.66 (5.75 (3.9) 12.37) 9.883 (.77 (6.4 (4.34 (6.924 (.533-1.47) 2.45-5.94-23.61-13.549-1.73 (1.37-5.80 (2.43 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.53 (6.87 (1.66 (2.02 (7.82-26.54-2.05) .35) < LOD < LOD 3.790 (.01-2.38 (1.

3) 20.18 (3.0) 13.80-3.4 (14.81-6.39 (5.34-3.3) 14.1 (10.8 (12.00) 3.20-4.82) 8.90) 4.22 (6.61-32.0-24.5.3) 10.1 (10.66-13.20-18.67) 3.80) .67) 4.5 (8.70 (1.80-12.00) 7.67-10.80 (2.50-5.0) 11.00-4.670 (<LOD-1.49-4.80-21.27) .40 (2.15-2.88) 10.50-4.34 (6. and 0.70 (8.90 (2.20) 3.4) 7.740 (<LOD-1.63-14.8) 9.60 (6.80-8.40) < LOD < LOD 75th 2.6) 18.3) 22.970 (<LOD-2.92) 9.00-18.10 (<LOD-1.40 (2.34-5.5 (8.59-3.80-6.00-16.90-15.8) 8.89) 2.9-17.50) .95-9.0 (9.0-29.11-6.10-10.41) 3.6) 14.1) 11.75 (2.7 (10.680 (<LOD-1.27 (7.9) 16.51) < LOD 1.90 (6.6-19.46-4.4-17.75 (3.8-17.6) 11.37 (3.00 (.90 (6.0 (5.8-20.27) 4.24 (2.47-6.0) 11.3 (11.70-8.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.27 (3.73) 7.00-18.60 (2.30) 8.30) 3.80 (2.8 (12.90-15.77-14.61 (3.80-4.0-24.88) 3.80) 5.10-15.4 (10.9 (12.580-2.3 (6.80) .33-11.7) 15.0 (14.0) 6.17 (7.35) 4.10 (.60) < LOD < LOD 2.670 (<LOD-1.6) 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 * * * 1.8-20.6-41.5) 21.30) < LOD < LOD 4.6 (10. 0.8) 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 1.34-10.7) 10.0) 12.60 (5.46-28. 01-02.4) 11.74) * * * * * 1.72) 2.24-5.58.0 (10. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .910 (<LOD-2.00-4.15-6.9) 9.00) 8.3 (9.62-17.9 (7.80 (5. and 03-04 are 0.20) .3 (12.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.0 (13.97-4.16-1.0) 23.14 (6.00) < LOD .9-14.04 (3.52 (6.22-12.78) 5.30) 3.39-13.35-3.12 (4.89 (2.7) 22.41-5.90-9.90 (6.27) 9.0) 12.99 (3.84-4.22) 8.3 (9.58 (1.2) 14.10) 6.9) 95th 14.28 (7.0-19.53 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.98-9.95 (5.9) 10.7 (11.10-4.9-15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 18.3 (7.01 (2.86-10.20-8.2 (9.90 (6.50) 3.20) 3.90 (2.18) * * * * * * * * 1.670 (<LOD-1.20 (<LOD-2. 122 Fourth National Report on Human Exposure to Environmental Chemicals .S.70-9.70-9.0) 14.0) 12.30) < LOD < LOD .5-26.06 (2.37) 2.64) 10.670 (<LOD-1.70) 2.0 (9.22 (6.5.650-1.0 (8.90 (5.0) 19.0) 14.6) 14.50) 5.0-33.42 (1.66) 4.31) 1. which may vary for some chemicals by year and by individual sample.4 (10.0 (10.0 (15.7-19. < LOD means less than the limit of detection.35 (6.0) 9.7-21.92-17.2 (7.0) 9.90-31.3) 8.95 (2.1-23.790 (<LOD-1.29-4.0 (7. see Data Analysis section) for Survey years 99-00.0) 13.96) 3.7) 14.45 (3.5) 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 * * * * * * .8-21.90 (2.90 (1.29) < LOD < LOD < LOD < LOD 3.31-12. respectively.00) 3.31-7.0) 7.7) 16.25 (2.5 (9.90) 8.96) 90th 7.6 (10.70-5.00-9.80-14.77-3.

70-2.21-21.0 (11.19) 3.3-17.89-10.15) < LOD < LOD 75th 2.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .95) 3.02-4.2) 15.7) 14.3) 6.2) 12.88-7.6 (11.2) 10.85-8. population from the National Health and Nutrition Examination Survey.94-14.38 (1.95 (2.34) < LOD < LOD < LOD < LOD 3.41 (7.1) 20.530-1.3 (7.30-5.9-17.42) 7.63 (6.6) 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 1.973 (.29) 3.4) 15.8) 14.2-15.86 (3.79-6.3-15.6) 95th 16.45) 3.00) 2.00 (<LOD-1.72-4.87 (3.1 (13.89 (3.5 (15.5) 10.36 (2.6-19.5 (11.75-3.16 (3.09-11.2-30.78 (6.4-16.810 (<LOD-1.620 (<LOD-.74-4.5 (10.55) .0 (13.37-5.S.910 (<LOD-1.91-9.43 (2.85-17.7) 14.42-19.55 (2.63 (2.7 (8.920 (<LOD-1.71) < LOD < LOD 2.78) 4.37) 3.7) 12.50-17.9 (9.1) 10.6) 13.58 (4.54 (7.73 (5.00 (7.6) 14.4) 6.79-9.83 (6.92 (5.68-10.03) 3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.72) 4.07) 2.1 (8.12 (7.07 (5.4-16.54-5.32-8. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .32) 2.4) 7.55) 16.06 (<LOD-1.30) 7.760 (<LOD-1.89 (2.77 (2.27-13.3) 8.89-3.780-1.27) 5.03 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.92) 3.18) 2.89) 5.77 (2.07) 2.71 (1.06) .6) 7. Fourth National Report on Human Exposure to Environmental Chemicals 123 .77) 3.20-3.14 (2.51-10.4 (11.75-3.45) 6.4-18.940) < LOD < LOD 1.6) 12.0) 14.29 (5.94 (5.39-17.15 (1.05-3.3) 9.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00 (<LOD-1.59-3.0 (10.9 (9.78 (4.7 (11.2) 19.690 (.86) 9.70-35.53-8.5) 8.9) 19.590 (<LOD-.82-8.3) 12.09-11.7 (10.2 (9.28 (1.23-3.38 (.93 (6.950) .16-14.74-19.93 (2.1) 13.5) 22.6 (13.96-11.91) 3.48 (2.2) 8.54) 9.9) 16.7-19.11-3.00 (5.0 (8.30) 2.82-11.83 (7.8) 16.68) .2) 12.78-10.25-9.07-3.3-17.38-13.89-3.8) 11.7) 15.4) 7.86-3.96-10.5-17.51-7.9-25.97) < LOD .4) 9.42) 8.12) < LOD < LOD 4.93 (<LOD-2.1 (19.47-9.88 (1.6) 6.8 (8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8 (10.93-10.81 (7.33-10.2) 12.30) 8.6 (13.27) < LOD .5) 13.3-21.99 (4.00 (3.2) 16.27) * * * * * * * * 1.67 (1.5 (8.38) 1.03 (2.850 (<LOD-1.6 (11.29-2.25 (4.7-23.61 (2.04) 9.6 (12.7 (10.97-4.7) 9.95) 90th 8.64-11.0-21.4) 7.4) 16.89-13.6) 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 * * * .00) 8.0-19.38 (2.6 (10.9 (9.68-19.28-12.00 (2.68-4.34-18.5 (9.69-11.21) * * * * * 1.28) 6.29 (2.67 (7.44-6.890-2.52-3.2 (9.4-15.33) 3.27) 1.11 (5.01-5.3-34.50 (6.80) 3.99) 2.

49) .201-.710) .910 (.460-.45-4.33-2.18 (1.14 (1.340-.740-.750) 1.930 (.600 (<LOD-.580-.59-2.30) 2.380-.01-3.30-3.459 (.22-2.63 (1.34) 2.40 (1.22-8.560-.720-1.60) 2.14-1.50 (1.690 (.22-3.17) 1.970) 1.49) 2.650-.457 (.86) 3.08 (2.960 (.749 (.740 (.22 (1.880) < LOD 75th .83 (2.50 (1.11-3.280-.570 (<LOD-.17) 1.240 (<LOD-.820 (.98 (2.46 (2.46 (1.450 (<LOD-.16-3.57 (2.00) 2.800 (.80 (1.80) 2.29) 1.930-1.87-3.47 (1.16) 2.720 (.74-5. see Data Analysis section) for Survey years 99-00.27 (3.80) 2.17-4.10) 1.20) 2.55 (3.83 (2.09 (.50 (1.60-4.70 (1.353-.88) 1.31) 95th 2.359-.810) .80) 3.740-1.390-.11-3.86 (1.60) 3.47) 2.26 (2.960) .04) 1.303-.79) .46-3.95-5.96-3.510 (.15) 2.76 (1.31-3.260 (<LOD-.54 (2.09.570) * .95 (2.425 (.35) 1.600-1.20 (1.550 (.45 (2.38) 1.398-.780 (.160 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.336-.850) < LOD .S.40 (1.500 (<LOD-.10-1.20-2.343 (.73-5.540 (.20-1.592) * .41 (2.20) 3.388-.584) .70 (1.30 (1.740 (.700) . 0.390-. < LOD means less than the limit of detection.550 (.382-.980) 1. 01-02.91) 2.690) .34) 2.76-6.453 (.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.570 (.45 (1.00) 1.00 (1.455 (.70-7.570 (.59-6.20 (1.80 (2.780 (.380-.75-2.20 (2.449 (. 124 Fourth National Report on Human Exposure to Environmental Chemicals .68-5.01) .2.710 (.96-5.710 (.50) 1.10) 1.467 (.960) 1.80) 3.600-.89) 1.20) 1.760 (.20-3.16) 1.10) 3.58 (1.730) .350-.30 (.30) 4.30) 4.592) * 50th .98) .73 (1.20) 1.64 (1.380) .54-2.00-4.690-.90) 2.04) .26) .930) < LOD .20) 3.820 (. interval) Selected percentiles ( 95% confidence interval) Total * .94) .29-2.83) .13) .510 (<LOD-.505 (.89) .30-3.05-3.22-3.440-.860) < LOD < LOD .970) .03) 1.10) 1.585) * * .50 (1.759) * .790 (.41-5.77-2.27 (2. and 0.587) * * .670) .60 (2.930) 1.680-1.39) 2.78) 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 * .592-.90-4.618) * .00-2.95) 2.50-2.70 (1.1.73 (2.20-2.08 (2.48 (1. and 03-04 are 0.79) . respectively.990-1.700) .30 (.20 (1.45 (1.74) 3.83) 1.880 (.48 (2.680-1.880) < LOD .54) .30 (.70-2.720-1.78) 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 * .780) .46) 1.18 (.97 (2.90 (1.36-4.960) .77 (1.910-1.42-2. population from the National Health and Nutrition Examination Survey.32-1.570-1.30-1.80) 5.400) .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.940) < LOD .949) .65 (2.549 (.960-1.350-.50 (1.570 (<LOD-.19-1.89-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.83) 2.597) * .657) * * .32) 3.31-3.75 (2.78) .98-3.21) 3.32 (1.580-1.37-2.490 (<LOD-.69-4.05-2.15) 2.23-3.90) 3.94 (2.620-1.20) 2.830 (.61 (1.13) 2.80) 3.10-1.57 (1.950) 90th 1.590-.30) 1.840 (.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 * . which may vary for some chemicals by year and by individual sample.25-1.31) 2.210 (<LOD-.750-1.690-1.94 (3.90) 2.910) 1.01-1.50-2.

58-6.08-3. population from the National Health and Nutrition Examination Survey.710 (.22) .79 (1.552 (.00 (3.02-6.990-1.34 (1.97) 2.45 (1.460 (.510 (.42-8.03-2.44) 2.04-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.680 (.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.447 (.11-2.880) 1.940-1.335-.250 (<LOD-.750 (.45 (2.750 (.300 (<LOD-.136-.71) .49 (1.471-.75) 6.580 (.75 (2.41 (.22-3.22-2.500-.310 (<LOD-.57 (3.590) * 50th .67 (1.14 (2.60) .270 (<LOD-.30-2.50) 1.52 (1.57-2.39 (1.05-2.62 (1.820) 1.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .38 (2.88) .64 (2.390-1.00-3.660-.22 (2.597) * .700 (. Fourth National Report on Human Exposure to Environmental Chemicals 125 .84-6.440-1.60) 1.760) .04-1.07) 1.91 (1.67-3.24) 4.49-4.65) 2.270-.22) 4.80) 2.71 (1.515) * * .710 (.380-1.88 (1.688) * .06) 4.25-3.230 (<LOD-.47 (1.560-.310-.580-.64 (2.17-2.75-3.520 (.92-8.02-3.82 (2.380) .10) 2.790) .18-2.790 (.99) 1.590-1.448 (.60 (1.69 (3.08-3.11 (.380-.980-1.372 (.08-2.20-2.42-6.640 (.89-3.530 (.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 * .67) 1.840) 1.720 (.310 (<LOD-.94) .470 (<LOD-.930-1.250 (<LOD-.78) 3.99) 2.43) 2.62 (2.08 (.30) 3.480) .50 (1.285-.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. interval) Selected percentiles ( 95% confidence interval) Total * .580) .870) .66) .69 (1.460-1.89 (1.348-.77-3.08-3.06-2.11) 1.60 (2.742) * * .55 (1.460) .97 (1.95) 1.740) < LOD 1.81) 2.17) 2.830) 90th 1.61) 2.318-.05) 1.800) < LOD .42 (.42) .645) .470) .90) 2.23 (.630) * .950-2.330 (<LOD-.20) 1.330-.23) 2.31-1.16-1.670 (.180 (<LOD-.520-.840) .S.47 (1.377-.61 (3.535 (.72) 1.840) 1.52) 3.850) 1.19 (1.36) 3.70 (3.32) 1.910) < LOD .22) 1.490 (.550-.57-4.32) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.76) 1.453 (.08-2.23) 1.17) 2.412-.400) .870 (.739) * .58) 3.84 (2.72 (1.33) .47-4.16) 1.07-2.98) 1.77 (3.400-1.480-1.740) .08-2.368) * .08-3.00-1.38-3.05-4.07) 1.280 (<LOD-.07) 5.61-3.61-3.44-2.560 (.75 (1.550-1.591 (.32) 2.55-3.13 (1.07-3.02-3.690) < LOD < LOD .16-2.97) 1.72-4.253-.53) .350) .43) 1.403) .700 (.33 (1.09) .38 (1.05) < LOD .22-3.393 (.485) * * .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) 3.32 (.370-.640 (.58 (1.920) .510 (.760) < LOD 75th .830 (.07 (.320-.67) .560-.08 (2.08) 1.57 (1.270-.710 (.550-.28 (1.444-.320-.92) 3.03-1.700 (.234 (.77-4.05 (1.550) .63 (1.509 (.43 (1.20-7.390) .92 (1.72 (2.70 (2.73 (2.67 (1.730) .23) 2.79) 1.300-.39) 2.97 (1.73-3.720-1.32-1.08) 2.590 (.87 (2.540-.29-4.07) 1.43) 2.900) 1.66 (2.820) .640 (.04) 95th 2.800-1.305 (.82) 2.510-.71) 2.

83-2. respectively.88) 1.0) 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 2.30) 11.0) 17.0) 3.6-54.1 (25.90-8.76 (2.660-2.29-4.57-2.3) 33.70 (1.6 (15.8) 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 1.18) 6.27-6.0-58.0 (20.04-8.5-20.3) 38.78 (1.10 (1.5-40.0) 4.7 (12.19-2.43-7.0) 20.65 (4.0-49.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.1) 38.3 (12.00-24.10) .30) 4.53) 40.32 (2.4 (19.1 (11.6-27.0 (6.0-62.46-2.2) 16.75-14.21 (3.0 (13.4) 38.3 (23.0) 16.86 (1.9 (23.23-2.9-51.8) 41.20) 1.1-19.72 (1.0 (25.46 (.70 (7.0 (8.3 (14.18.6-22.00 (.87-7.0) 13.0 (38.44) 3.41-4.50-20.690-3.0-43.16) * 1.600-2.0) 4.13) 12.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4 (10.76 (2.8) 39.6 (26.31-6. population from the National Health and Nutrition Examination Survey.0) 28.3 (24.0) 15.7 (12.18) 20.470 (<LOD-1.9-21.0) 16.10 (1.8-24.0) 5.9 (10.06 (1.0-29.4 (15.S.10) 39.2-27.0) 42.83 (3.80) 90th 38.40-4.61-2.19) 2.79-2.0 (33.83 (1.30-14.48-2.1) 140 (46.8 (12.41 (1.95 (5.1 (25. and 03-04 are 0.0 (38.2-80.64-8.50-5.20-4.8 (26.4) 19.1) 95th 48.79 (2.79 (1.2-27.99 (2.7-41.10 (7.58-2.80) .45) 2.92) * 2.2-62.80-18.0-69.42) 1. and 0.70-6.02 (2.16) 2.05) 1.0) 18. 0.2-26.13 (1.96) 5.9 (19.80) < LOD 1.81-3.54 (3.7-22.18) 14.97) 6.2-39.7 (28.86-3.0 (32.40) < LOD 2.3) 28.0-39.82 (1.04 (<LOD-2.41) 1.70) 1.10 (1.90 (1.21 (1.8-21.1 (22.70) 1.54 (1.88) 3.2 (12.3 (12.09 (4.0-41.61 (1.98 (1.0) 3.6) 52.0-62.40-16.57-2.0) 32.50-17.0 (21.4-22.53) * 2.07-5.53 (1.0-47.74-2.0-41.2 (19.1) 18.1-20.530-4.04) 3.0 (38.70 (.0-110) 42.10 (1.0 (24.77) 38.21 (4.45) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.66-5.9 (27.70) 5.3) 31.60 (2.0 (19.5 (24.11) 2.12) 1.17-2.46-6.0-41.0 (38.0-92.35-6.29-9.0) 6.7) 47. which may vary for some chemicals by year and by individual sample.63-6.0 (7.25-3.0 (40.8) 32.70 (1.90) 11.85) * 2. see Data Analysis section) for Survey years 99-00.78) 9.06) * 2.44) 2.0) 15.9) 18.1 (10.77 (1.50 (2.2) 31.8) 62.6-45.0) 3.50-7.13 (1.14) 5.94 (1.70-17.33 (5.41) 5.0 (8.6 (11.44) Selected percentiles ( 95% confidence interval) Total * 2.1-25.52 (4.40) < LOD 1.85 (1.0-230) 35.0 (26.0-39.67 (1.2-33.0 (37.0) 8.40) 50th 2.5) 30.4-76.1 (26.1-46.64-3.9) 48.90 (1.5-45.0 (11.53) 1.69) 2.58) 16.9) 17. < LOD means less than the limit of detection.59 (1.71) 5.8 (12.3) 26.830-3.60) < LOD 1.2-47.9 (19.23) 9.0 (38.0-110) 34.71 (4.0-52.0 (38.05-3.5-74.830-4.29) 2.93-3.48) 5.26) 75th 11.0 (8.12 (3.48-2.0) 17.83-2.5) 69.0 (20.0) 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 2.91 (4.80-2.0-260) 34.0 (38.5-27.00 (.36-2.0-50.0) 30.0 (17.20 (2.8 (22.0) 45.80) 1.49-2.0) 33. 126 Fourth National Report on Human Exposure to Environmental Chemicals .4.0-53.0-53.41) 1.05) * 2.81-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 4.92-5.59 (1.1-40.50-2.11 (4.5.9) 38.0) 20.3 (10.1-47.26 (.0-58.0) 28.7) 20. 01-02.44-7.71-2.10-4.0) 3.1) 38.30 (.0) 19.23-2.98) * 2.0) 31.0-31. interval) 1.6 (9.610 (<LOD-1.10-13.

4) 14.37-2.80-8.1 (34.0) 10.22 (.38) 5.23) < LOD 2.7-38.43-12.870-3.16-2.9-37.930 (<LOD-1.1 (50.S.66 (1.7) 66.2) 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.3-22.0 (25.38-5.6 (11.70-4.68) 47.9) 12.56) 1.6) 3.11) < LOD 1.94-20.3) 28.2 (16.23-1.57 (6.95 (2.24 (1.4-21.80 (1.25-3.7 (10.45-1.9 (26.51) < LOD 1.0 (39.7-43.27) 10.8-34.18) * 2.66) 8.7 (18.59-2.35 (2.9-36.7) 23.3-27.66 (1.91 (6.19-14.0) 30.2) 36.5 (15.9-95.46-6.79-17.17-3.19) 5.28) 1.46-5.9-52.8) 11.99-4.95-16.6-32.27 (6.0-118) 29.9 (10.09 (5.7-37.14 (.06) 1.43) * 2.32-3.7 (11.55 (2.7) 61.2-38.2-70.52-4.9-41.62 (2.9 (19.82 (2.3) 13.88 (4.36) 10.48 (4.83 (.40-4.90 (.9) 3.17) 2.35) .1) 27.07) 9.33) 2.27) 50th 2.1) 17.58-17.94) 1.11-2.06-1.69-18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 13.38 (3.95) 90th 32.40 (5.61-2.00-16.88 (1.60 (.8) 3.4) 12.8) 32.1) 25.6 (7.4) 3.3 (10.71-2.31) 2.0) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.12) 3.51) .8-45.860 (<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 1.63-5.8-37.5 (13.9) 54.3-19.83) .03-2.82) 1.4 (5.22-2.5 (34.7 (18.94) 19.61-22.53) 1.5-97.5) 27.07-2.3 (20.4) 12.26-4.2 (21.870-3.07-2.750 (<LOD-1.75 (1.6 (27.7-47.2 (22.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.4 (25.39 (1.20) Selected percentiles ( 95% confidence interval) Total * 1.59-15.61 (1.56 (2.37 (1.1) 52.95-16.34) * 1.0-70.5) 70.4 (25.79 (2.2) 33.67 (1.870-3.16 (1.0 (19.6) 11.4 (9.91-2.46-22.0-71.26-2.4-71.58-2.7-109) 22.1) 36.45 (1.00) 1.30) 28.6) 23.14-8.680-4.6-49.84-13.67 (1.33-5.2) 13.19 (1.93) 5.88 (4.60) 4.890-4.2-34. interval) 1.8-26.9) 24.2-47. Fourth National Report on Human Exposure to Environmental Chemicals 127 .0 (17.5 (6.7-20.36-13.76-2.96-16.9 (7.1 (33.5-190) 30.22 (2.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.6 (24.2-28.02 (.86) * 3.27-3.01 (.8 (7.4 (21.16 (1.1) 15.5-43.2 (8.71) 8.32 (3.1) 13.9) 3.0) 25.22-3.1-60.06) 75th 9.2) 4.18) 3.3-42.0 (6.19) 5.7) 30.29-5.5-36.69-5.888-1.64 (1.6) 3.41 (2.0) 48.54-2.8-43.43-2.1-22.88 (1.4-39.97 (1.0 (32.03) 1.06) 1.47 (3.2 (15.5 (15.6-51. population from the National Health and Nutrition Examination Survey.4-67.1) 27.4 (12.16 (1.72) 2.12 (1.33) 1.47 (1.5 (17.7) 34.62) 4.68 (1.1 (25.02) 1.6) 7.3 (10.44) 9.4 (19.00 (4.9-18.71 (1.9 (13.1) 25.35) 1.48) 1.70 (1.6) 19.54-15.59-2.6) 112 (40.0 (23.46) 1.1) 13.86) * 2.899-2.19-6.9) 24.1-63.7) 26.50 (2.0 (14.50-5.5 (41.2) 41.2 (9.38-1.40 (2.40-7.2) 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 1.08) 1.0-40.75 (1.3 (8.52 (1.2) 13.9 (39.1 (39.7-19.18-1.0) 47.36 (4.47-17.1 (12.7) 95th 51.8) 31.15 (.33) < LOD 1.28 (1.75) * 1.75-6.4-34.00) 6.7 (24.23) 37.08 (1.8) 23.8) 15.0 (23.670-1.57) 4.02) * 1.67-3.20-5.67-16.96) 2.7) 15.6-38.21 (4.3 (9.4 (11.5 (8.

540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .450 (.930 (.160-.120-.630 (.20) .680-1.300-.390) < LOD < LOD .870 (.200) < LOD < LOD . 128 Fourth National Report on Human Exposure to Environmental Chemicals .190 (.100 (.820 (.770) < LOD 95th .150 (<LOD-.700-1.090 (<LOD-.640) .310 (.650) .350) .130-. 01-02.310 (.610 (.290) < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.430-.080 (<LOD-.440-1.090 (<LOD-.15) .650 (.360-.540) .650-1.490 (.130) .050-.550) .090 (<LOD-.10) .450 (.410-1.860-1.560 (.270 (.080 (<LOD-.00) .460-.370-.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 * * * * * * .240 (<LOD-.840) .171) * * .410-.470-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .280) < LOD < LOD < LOD < LOD .380-.380-.650) .730-.190 (.42) .210 (.640-1.900 (.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.830 (.290) < LOD < LOD < LOD < LOD 90th .310-.830) < LOD .620 (.870 (.990) .650-1.S.090 (<LOD-.350) < LOD < LOD < LOD < LOD .162) * * * * * .630 (.160) .530-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.090 (<LOD-.720) .830) .03) .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 * * * * * * * * * .090 (<LOD-.60) 1.470 (.860) .390 (.117 (.099-.770 (.1.10) .380-.850 (.610 (.130-. which may vary for some chemicals by year and by individual sample.130 (.30) .410-.300-1.36) .400-.610-1.05.870 (.780) < LOD 1.320 (.370-.410) < LOD < LOD < LOD < LOD .990) .120 (<LOD-.140) .820 (.10 (.540 (<LOD-.130-.870) < LOD .32) .140-.360-.330-.290 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) . see Data Analysis section) for Survey years 99-00.840) .150) .850 (.720 (.870 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.730) .830 (. respectively.220 (.180) .230) .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 .420-.230-.450 (.140-.460 (.700-1.510-1.310) < LOD < LOD < LOD < LOD .30) .570) .140-.190 (.220 (<LOD-.540) .310) < LOD < LOD < LOD < LOD .940 (. and 03-04 are 0.12 (.700-1.10) .700-1.260 (.1.610-.160) .120-.560 (.760) < LOD .680 (.210 (.084-. and 0.30) .430 (.720-1.170-. 0.640) .680-1.640 (.130) .58) .680) .660 (.42) .110-.320-.690-1.870 (.600 (.850) < LOD . population from the National Health and Nutrition Examination Survey.13) .990 (.740) < LOD .

290) < LOD < LOD < LOD < LOD 90th .050 (<LOD-.300-.070 (<LOD-.880-1.760) .410 (.250-.170) < LOD < LOD .01 (.440-1.450) .140-.116 (.580) .86) .780 (.410) .78) .500) .070 (<LOD-.450 (.140-.460 (.140-.310) < LOD < LOD < LOD < LOD .220) < LOD < LOD < LOD < LOD .58) 1.500 (<LOD-.03 (.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 .570 (.140) .940) .110-.190 (.330-.860-2.750) < LOD 95th .080 (<LOD-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .03 (.440 (.410-.090 (.170 (.380 (.660-1.570-.960) .270) < LOD < LOD < LOD < LOD .410 (.540 (.190-.161) * * .19 (.110) .12) < LOD .940) .880 (.670-1.500-1.150-.360-.550 (.400 (<LOD-.610-1.700 (.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 * * * * * * * * * .870) .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 * * * * * * .740) < LOD 1.180-.36 (1.300-.070 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.730 (.24 (.62) 1.990) .67) .810 (.720 (.070 (<LOD-.09) .110) .580 (.860 (.320 (<LOD-.200 (.580) < LOD .700 (.720 (.43) .140-.600-1.084-.490-1.20) 1.390-.120) .210 (.380-1.330 (.66) 1. Fourth National Report on Human Exposure to Environmental Chemicals 129 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190 (.S.14) 1.110) .330-.850 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.300 (.03 (.550 (.740 (.340-.380-.38) 1.270 (.990) .520-.650-1.170 (.110) .700) .86) .640-1.100 (<LOD-.710-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .360-.540 (.29 (.380-.670 (.360 (.860 (.080) .670 (.120) .080 (.220 (.650) < LOD .02-1.390-.24) .140-.230-.560 (.600) .470 (<LOD-.700-1.330-.580 (.240-.280) < LOD < LOD < LOD < LOD .400) .090 (<LOD-.100-.060-.410-.03) .780) < LOD 1.410) < LOD < LOD .370 (<LOD-.730) .60) .380-.970) .230) < LOD < LOD < LOD < LOD .890 (.111) * * * * * . population from the National Health and Nutrition Examination Survey.730) .200 (.057-.580-1.260-.230 (<LOD-.00) < 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.510-.260) .540) .730) .330 (.02) .360) < LOD < LOD < LOD < LOD .800-1.570-1.

60) .70-30.0) 5.10 (. 0.690 (.66) 4.29-10.840-3.0 (5.55-4.30 (2.70-3. respectively.600 (.50) 2.52 (1.30 (1.870) < LOD < LOD .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 * * * * * * * * * .360-1.80 (4.170-1.960 (.840 (.0) 2.40-7.87) 12.74 (3.0-38.33 (4.14) 2.00) .83-3.40) 2.0) 4.88-3.0 (17.36-3.67 (2.31-10.52) 5.60) 1.94 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.70) 2.23-6.52 (1.00 (1.49 (1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0 (6.07-3.86) 4.63 (3.32-9.40-20.00) .0) 5.30 (1.0) 7.31) .05-3.30-7.210-1.47 (3.35) 5.07 (3.00 (.20 (1.10-3.48) 13.59-5.800) 17.48 (2.750-1.49 (1.03 (.61 (1.24-7.770) 2.90-9.21-3.40-8.11) 13.15) 14.36-3. see Data Analysis section) for Survey years 99-00.43-4.720) 2.800-4.65) 1. which may vary for some chemicals by year and by individual sample.770 (<LOD-1.67 (1.05 (2.0) 4.70-50.30 (.20-4.90) .38-3.07 (1.53 (2.30) .900 (.400-1.260-.35) 11.1.83-3.76 (1.40) 1.11) .0 (16.425-1.30 (1.14) .0) 2.0) 2.480-.0-38.0) 5.0 (5.51-8.0 (4.39) .90-20.610 (.10 (3.0) 2.0 (17.0) 3.640 (.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .0) 2.55-8.63) 32.62-8.0) 4.350-.510-.10 (3.590 (.90 (2.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.42) 2. 01-02.0 (7.0-40.70-7.62) 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 * * * * * * .110 (<LOD-.6) 5.94-8.750-2.94-3.0 (13.11 (1.0-38.370-.890 (.40 (1.51 (2.30-3.880) 5.50) .70-17.90-37.32 (1.12) * * * * * * * * .850) 16.07) 1.90) .26 (2. < LOD means less than the limit of detection.0 (5.05 (3.0) 5.0 (5.830 (.20 (1.30-6.960 (<LOD-1.39 (2.49) 17.0 (3.74) 5.800) 90th 13.40 (1.37) .40-4.610) < LOD < LOD < LOD < LOD < LOD 2.67) .620-1.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.0-39.0 (5.15) 19.21) 3.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.18) 1.53) 20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190-1.1.99 (1.82-4.840 (<LOD-1.350-.S.00-17. and 03-04 are 0.250 (<LOD-.0 (17.330 (<LOD-1.0 (4.00-17.20-17.28) 1.45 (2.10-9.28-9.0) 2.10-3.96 (1.0) 2.07 (3.580 (.13 (3. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0-40.00) 1.99) 19. population from the National Health and Nutrition Examination Survey.640 (.910) 2.87) 5.90-28.30) 95th 19.35-10.730 (.740 (.46 (1.20-4.83) 2.12-1.53-7.0-44.0 (17.080-1.0 (17.20) < LOD < LOD < LOD < LOD < LOD 1.14-5.0) 4.97) 20.99) 11.07-3.691 (.08.90) .380-.85-3. and 0.01) 5.90 (1.28) .97) 20.42) .68) 2.

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 * * * * * * * * * .1) 2.250 (<LOD-.55 (3.62-17.30 (4.24) 3.3) 2.0 (9.88) 17.67) 1.8-33.17) 5.5) 2.2 (8.50 (4.33 (3.49-2.81-17.390-.370 (.86 (3.8) 4.770) .40-12.57) 1.580-1.540-1.620-3.21-3.580) 16.71 (.474-1.77 (.580) 1.780-4.25-9.69) 2.84) 9.53) 27.80) 3.86) .41 (4.00) .44-11.67-6.8) 2.14 (1.748 (.52 (.41) 18.10 (2.33-3.01 (1.53) .5 (8.18) 1.890 (.670 (.8 (20.64) 30.2-38.1) 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 * * * * * * .83 (4.260-.40-2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.7 (12.7) 5.04-16.740-1.57-40.730-3.35 (.320-1.50) .17 (1.79 (.27 (2.270-.600 (<LOD-1.370-1.64-4.270 (<LOD-.5 (9.5-40.67 (2.500 (.340-.1 (5.69-7.540 (.60 (1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .820 (.73 (4.9 (11.48-7.7 (6.8) 2.67) 2.850-3.830 (.02 (.56) .62 (1.38 (2.03) 16.190-1.0 (4.8) 7.28-6.43) .650) 90th 10. population from the National Health and Nutrition Examination Survey.12 (4.660) < LOD < LOD .22) 2.5) 2.430 (<LOD-.88 (2.13 (2.08) .02) .11-5.29-4.10) 2.7) 3.57 (.33-4.580 (.05) .32) 9.23-7.02 (1.47-10.3) 3.80 (.45 (1.33 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (11.07-21.40) 1.700) 6.240-.07 (2.29 (4.36 (.790) 11.4-34.57) 8.930) .11) .85 (1.96-25.47) .830-3.04 (1.7) 4.55) 21.06 (.820) .18) * * * * * * * * .25 (1.90-6.0) 4.09-3.310-.83-11.970-3.260-.89 (2.560 (.150 (<LOD-.31-7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.690-5.4 (4.88-3.33-5.25-38.98 (4.75) 5.940-4.22-27.340-.14-6.650 (.330-1.960 (.31) .15) 9.00-19.56) 2.59 (1.12-4.860-2.340-.700) < LOD < LOD < LOD < LOD < LOD 1.91-4.51-4.31) .48-42.9) 5.51-44.840-3.450 (.50 (2.39) 20.1 (7.S.8) 1.40 (.02-4.47) 5.32-6.82-11.340 (.88 (.360 (.710 (<LOD-1.4) 2.65 (2.55) 21.790 (.66-47.48 (4.9) 6.5) 7.37) 4.74 (2.97) .590) 2.470 (.630-1.10-3.7) 6.18) 95th 21.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.03) 2.430) 1.56 (1.800-2.50) 11.1) 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.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.91) 2.96-8.96) 2.44) .47-10.92 (2.85-3.8) 7.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .370) < LOD < LOD < LOD < LOD < LOD 1.71 (2.31-18.

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Smit LA. EPA).24(1):18-29. Visuthismajarn P. and cholinesterase status of date dusters and harvesters in California. Malathion deposition. discrimination. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.php?record_id=2126&page=1.345(8958):11351139. Pesticides in the Diets of Infants and Children. Washington (DC). Daniell WE. Masala G. Vitayavirasak B. Rohlman D. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Arch Environ Health 1988. McCauley L.332(1-3):71-80. J Toxicol Environ Health A 2005. Robson MG. EPA. Bull Environ Contam Toxicol 1994. Keifer M. Saieva C. Lambert WE. Caltabiano LM.44(4):352-357. et al. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Sci Total Environ 2004. 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. et al. Bravo R. National Research Council (NRC).Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI.epa. Am J Public Health 1994. Salvini S. Claypoole K. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Santana J. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.nap. Petchuay C. Rodnitzky RL. Hore P. Occup Environ Med 1995.52(2):190-195. Environmental Protection Agency (U. Seiber J. S. Thompson ML. 4/7/09 Young JG. Muniz J. Stark A.edu/ openbook. Scand J Work Environ Health 1998. Environ Health Perspect 2005. Spurgeon A. Washington (DC): U. et al. Beach J. Weerasekera G. Neurotoxicol Teratol 1998. Rothlein J. Marshall E. et al.S.43(1):38-45.pdf. vibration sense and tremor among South African farm workers.26(2):199-209. Muniz J. and spatial learning in monkeys and rats. Lasarev M.84(5):731-736.58(11):702710. Nell V. Arch Environ Health 1975. Kidd M. Occup Environ Med 2001. Narang A. van der Hoek W. Jamal GA. Burcar PJ. Office of Prevention Pesticides and Toxic Substances. Dinoff TM.38(4):546-563. 2004.338(8761):223-227. Johnson C. metabolite clearance. low-level exposure to the organophosphate diazinon. Lancet 1995. Effects of long-term organophosphate exposures on neurological symptoms. Stephens R. Am J Ind Med 1987. Environ Health Perspect 2006. Effects of chronic.S. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Hansen S. Rosenstock L. 1993 [online]. Int J Occup Environ Health 2006. May. Berry H. Ames RG. Pilkington A. 1/12/09 Peiris-John RJ. Levy LS.30(2):98-103. Phillips J. Heaton RK. low-level organophosphate exposure on delayed recall. Frasca G.12(2):134-141. Mounce LM. Chronic neurological sequelae of acute organophosphate pesticide poisoning.113(4):504-508. Samuels S. O’Malley M. Keefe TJ. London L. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. J Occup Environ Med 2002. Scherer J. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Lasarev M. Wickremasinghe AR. Gladstone EA. The Pesticide Health Effects Study Group. Buchanan D. Stokes L. Arch Environ Contam Toxicol 2000. Prendergast MA. Schenker M. A behavioral evaluation of pest control workers with short-term. Aprea C. Terry AV Jr. et al. Lancet. Steenland K. Ruberu DK. Available at URL: http://www. Irish RM. Savage EP. Jenkins B.52(10):648-653. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates.12(2):153-172. Weisskopf C. Myers JE.20(2):115-22.68(3):209-227 Maizlish N. Barr DB. Chronic central nervous system effects of acute organophosphate pesticide intoxication. 1991. Chrislip D. Takamiya K. Russo J. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Neurotoxicology 2005. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Pedersen L. Neurotoxicity among pesticide applicators exposed to organophosphates. Lu C. Chronic neurological sequelae to organophosphate pesticide poisoning. Bradman A. U. Buccafusco JJ. Eskenazi B. Pesticide industry sales and usage . Available at URL: http://books.114(5):691-696. Lewis JA. Tumino R.2000 and 2001 market estimates. Gillham R. National Academy of Sciences. McConnell R. Calvert IA. Rothlein J.

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

00) 2.70-11.90) 3.7) 8.40-2.50-5. pre. and on plants for days to several weeks.29-1.70-17.30 (4.61) 75th 3.30) 5.70) 1.0-28.61-7.97-7. USGS.30-12.66-4.25) 3.70-16.71 (6.47-11.25) 1.26) 7.90 (1.20) 10. 2002).0) 8.0 (7.94 (4.7) 9.67 (1.43-2.68-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.15 (1.0) 18.30) 4.77-15.28) 2. Estimated intakes from diet and water have not exceeded recommended intake limits. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50 (2.5-24.55-5.9 (9. Survey Geometric mean (95% conf.90-7.60-3.62-2.20) 2.20-11.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.34) 1.1) 5.74-9. Exposure can also result from contact with contaminated surfaces.10 (3.13-3.10) 6. 2002).9) 11.S.99-4.60 (5.8) 9.76 (1. 2921-88-2 Chlorpyrifos-methyl CAS No.30-5.0) 12. 5598-13-0 General Information The chemical 3.0) 10.50 (1.60 (2.4-15.47 (4.40 (5.80 (1.30-1.20-3.77-6.S.0) 9.45 (1.4 and 0.3 (10.80-8.97) 7. Approximately 21-24 million pounds per year were used domestically from 1987-1998.67 (2.76 (1.05-5.3) 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 1.9 (10.8-15.16) 2.39-2. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.72) 2.3 (8. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.90 (1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.71 (2.90 (3.61 (1.27 (7. For instance.00) 3.0 (9.30 (2.43-2.04-10.59) 2.0 (7.01) 1.8) 10.02 (1.40-10.52-2. in 142 urban homes and preschools in North Carolina.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.EPA.59-2.89 (2.30-2.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.000 pounds are used per year.00-8.38 (3. Fourth National Report on Human Exposure to Environmental Chemicals 135 .30-11.17 (1.90 (6.9 (7.67 (2.29) 90th 7.35) 2.02) 1.60-2.20-16. Approximately 80.22 (1.63 (8.78 (7.20-4.19 (1.20) 4.10-17.0) 10.66-15.30) 4.4 (8.44 (3.57 (2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.84) 1.31-2.20 (2.80) 1.S.0) 8. 1999.1-16.64) 3.90) 7. and is infrequently detected in ground water (IPCS.40) 9.04-10.09 (2.95) 7.5.9) 697 660 521 701 602 947 Limit of detection (LOD.60) 5.70-5. 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.21) 3. dermal.97) 2.63 (2.96) 3.0 (7.13 (1.0 (13.51-2.22) 2.91 (1.60-3.72-4.37) 5.0) 12. It has low leachability.97) 4.90-4.98-15.40 (6. applied to structures to kill termites.80) 12.36 (4.50 (2.35) 1.32-1. and inhalation routes..70 (1.30 (2.0) 12.3) 8.5 (8.63 (1.32) 2.90 (2.5.and post-construction structural applications for termite control were to be phased out by 2005 (U.40) 2.4 (10.20 (4.51) 1.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. interval) 1.50-2.24-1. staying bound to soil particles.44-5.37 (1. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.89-2.5) 7.20-2.50 (2.86) 4.91) 16.50-8.05) 1.0) 11. After 2001.92 (1.50 (1. air.02 (7. Chlorpyrifos is Urinary 3.30-9.0 (7.20-14.24-3.46-2. and dust.68 (7.7) 13.0) 14. The general population may be exposed to chlorpyrifos via oral. but can be detected in streams receiving runoff from application sites. 2005).50-14. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.0) 7.40-26.60 (4.44-2.97) 2.83) 1.88 (1.00-24.3 (11.53 (1.2 (10.0) 12.00) 1.10 (5.4.70-15. 2007).09 (3.50-4.87-6.7-23.77 (1.28-3.0) 15.37 (4.81-2.10 (4.50-4.50-2.0 (7.40-13.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.47-13.0) 12.52-12.20) 2.77) 1.47-9.71 (1. chlorpyrifos was no longer registered for indoor residential uses in the United States.0) 6.90-2.0 (10.40 (5.4 (9. It also has been applied directly on animals to kill mites.74 (1.79-2. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators. population from the National Health and Nutrition Examination Survey.19-3. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.31-2.80-10.90-8.80) 2.51 (1.80 (7.39) 4.9-18.0) 10.80) 4.47) 1.60-4.EPA.6) 7.10 (1.95 (4.03) 1.10) 2. and sprayed to kill mosquitoes.70 (1.

31-1.33 (5.63 (5.33-7.30-4.97 (3.90-9..88-9.57-2. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.30-1.57) 2.. Howard et al.16) 6.74) 1.44-6.20 (2.12-1. Metabolic hydrolysis leads to the formation of TCPy.98 (6.24 (1.35) 1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.24-5.48 (2. 2006b)..60-3.93) 2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al. interval) 1.59) 3.0) 10.87-3.940-1. weakness.95 (3.6) 10.95 (1.50 (4.34-1.19) 3.27-1. vomiting. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.85-4. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.75) 6.31) 1.08) 6.12) 1.25-11.16 (4.68) 1.45-1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.36) 1. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.46 (2.39-1.01) 3.91 (4.94-12.14-8. Roy et al. 2002).91) 2.91) 1.52 (5.EPA.22-6.. and seizures.64-7.09 (1.93 (2. 2005. TCPy can also occur in the environment from the breakdown of the parent compounds.54) 5.58) 1.63 (4.28) 2.80-6.86 (1.11 (2.42 (6.17-4.56 (4.39 (4.63-2.56) 2.49 (1.49-2. Thus.82 (2.3) 9. resulting in excess acetylcholine at nerve terminals. 2000).73 (1.94-14.88) 6.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.46 (1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.88 (1. Betancourt et al.23-1.42 (5.24-1.66 (1.11-9.53 (2.48 (1.64 (1.25-12.80-4.58) 5.97-3.66-11.25-1.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.85) 4.71 (1. 1984).5 (6.47-2.4) 4.55) 1.23) 14.62) 1.9 (12.15 (4.84-6.47 (1.3) 8.91) 1.22 (4.88-8. Based on animal data and human cholinesterase monitoring during occupational exposure.80-11.24-4.88 (1.05-3. 2006.57) 9.82-4.72) 1.57-2. cholinergic effects.83-11.33 (1.92-2.0) 12.06-4.24-24.97 (2.93 (1.28) 2.59-2.82) 8.81) 2.70-4.75 (1.44 (5.80) 3.58 (1. 2005.58-5.05-4. Once absorbed.11) 7. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.71) 3.72) 2.88-8.02) 7.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.51 (1.1-38..76 (3.55 (4. and other metabolites.53-5.38) 3.3 (7.05-8.17-4.24) 75th 2.19-1.12-3. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.00 (7.01) 1.35) 2..97) 3.91 (3.1-21.01) 3.06 (5. 2006. Survey Geometric mean (95% conf. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).45 (1.2) 6.83-2.41 (1..39 (2.92) 3.64-2.91) 10.82 (3.24) 5.85 (3.85 (2.65-11.42-2.47 (1.00-8.56) 5.S.33 (.5) 5.. and producing acute symptoms such as nausea.47 (5.40) 1.21-1.43-10.77) 1.79-13. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.49-2.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.20-1. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.69 (1.60 (1.44 (1.31-4.05) 3.44 (5.72-2.19-2. In pesticide applicators.07) 5.6) 9. population from the National Health and Nutrition Examination Survey.27-7.14) 1.91-4. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates. Urinary 3.98 (7. paralysis.88-10.1 (7.99-8.92 (1.85) 1.26-14.29 (3.91-13.58 (4.35-1. 2006a.78 (1.0) 6. neurotransmission. TCPy is more persistent in the environment than chlorpyrifos itself (U.09-3.21-6.66) 1.86 (1.00) 1.S.76 (2.39) 6.19) 6.56 (1.6-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.09-1..06 (1.58 (1. Slotkin et al.07) 1.55 (1.7) 7.43 (4. 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. 2005.3) 8.05-1.2 (7.68) 6. Ricceri et al.44 (1.62-7.96) 3.56-2.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.09-2.89) 4.93) 5.65-15.03) 1.97) 3.8) 9.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .37 (1.1 (10.49-2.54 (2.22 (6.99) 1.44 (6.0) 16.00-13.81 (3. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.32) 1.11 (2.02 (5.22) 1.93 (4.86 (3.5.33) 2.83) 1.62) 90th 5.

. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Lotti A.. Toxicol Sci 2006. et al.92(2):500-506..Organophosphorus Insecticides: Specific Metabolites 2004. CDC.gov/pesticides/. 2000). Betta A.S. In Minnesota and South Carolina farmers who used chlorpyrifos. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. 2005.atsdr. the geometric mean urinary TCPy levels were similar in parents and children. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure.S.113(8):1027-1031. 2004). 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Biomonitoring studies of TCPy provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of chlorpyrifos or chlorpyrifos-methyl than are found in the general population.. 2005.html and from U. Garabrant D. Burgess SC. et al. Chlorpyrifos exposure and biological monitoring among manufacturing workers..cdc. Following crack-and-crevice application of chlorpyrifos in their homes. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. 2004). population (CDC. Betancourt AM.82(2):305-312. 2005). Barr DB. Of 482 pregnant women living in an agricultural community.EPA.. Koch et al. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Aldridge JE. EPA at: http://www. 1992. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Berent S. representative subsample of NHANES 19992000 (CDC. 2005). J AOAC Int 1999.109(6):583-590. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. 2005). urinary TCPy levels in children were reported not to have increased (Hore et al. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.S. Environ Health Perspect 2001. 2001). 2005. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.S.S. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. 2005). Perera et al.. Eberly LE. 2001) and Italy (Aprea et al. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. Aprea C. 2006).. Slotkin TA. Environ Health Perspect 2005. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Clayton CA.. Seidler FJ.. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. MacIntosh et al. Lioy PJ.epa. Occup Environ Med 2006. et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Magnaghi S. 2005).. Curwin et al... In Iowa farm families using several different pesticides. Barisano A. In a probability-based sample of 102 Minnesota children aged 3-13 years.e. 2003. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Catenacci G. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. 2005). Freeman NC. Carr RL. environmental levels) and health effects is available from ATSDR at: http://www. Burns CJ.63(3):218220.. 1999). 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.. Levels of TCPy in the U. Albers JW. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. References Adgate JL. Additional information about external exposure (i.5. Whyatt et al.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Giordani B. U. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. but not chlorpyrifos. Haidar S. 2002).. Meyer A.gov/toxpro2. 2007).Reference values of urinary 3. but levels were roughly four to six times higher than the geometric means in the U.

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National Toxicology Program (NTP). 4/7/09 Koch HM. Baker BA. Fenske RA. Chrislip DW. Jett DA. Atlanta (GA). 1992. Morgan MK. Environmental Protection Agency (U.108(4):293-300.6-trichloro-2-pyridinol.6-trichloro 2-pyridinol in their everyday environments. Exposures of preschool children to chlorpyrifos and its degradation product 3. Venerosi A. Chapman P.S. Hill RH Jr. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice.111(2):201-205. mothers and fathers living in farm and non-farm households in Iowa. chlorpyrifos. Levin ED. Freshour NL. Honeycutt R. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Baker S. J Expo Anal Environ Epidemiol 2005. Croghan CW. Mandel JS. gov/ntpweb/index. Toxicol Sci 2006. Wartenberg D. Bailey SL. Urinary pesticide concentrations among children. Eskenazi B. Seidler FJ.31 Suppl 1:98-104. J Expo Anal Environ Epidemiol 1999. Tsai WY. Executive summary of safety and toxicity information. Reid TM.15(3):271-281. J Expo Anal Environ Epidemiol 2005. Environmental Health Criteria 198. Barr DB. MacIntosh DL. Roy TS.112(10):1116-1124.113(2):211-219.

Environ Health Perspect 2003. February 2002.epa. The Quality of Our Nation’s Waters. Available at URL: http://www. Camann DE. 1992-2001. Kinney PL. Pesticides in the Nation’s Streams and Ground Water. Geological Survey (USGS). et al. March 2006. Available at URL: http://pubs.gov/ oppsrrd1/REDs/chlorpyrifos_ired. 6/1/09 Whyatt RM. Fourth National Report on Human Exposure to Environmental Chemicals 139 .Organophosphorus Insecticides: Specific Metabolites 01-007.111(5):749-56. revised February 15. Barr DB. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.S.usgs. 1/14/09 U. Andrews HF.gov/circ/2005/1291/.pdf. Barr JR. 2007 [online].

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

which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.S. Fourth National Report on Human Exposure to Environmental Chemicals 141 . 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 .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (<LOD-.S. 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . 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-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.380 (<LOD-. < LOD means less than the limit of detection.670 (<LOD-1.270) < LOD 659 701 920 Limit of detection (LOD.2. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0.

Barr DB.gov/oppsrrd1/ REDs/0018tred.epa. U. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. September 2000.S. Olsson AO. Anal Bioanal Chem 2003. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals .S. Centers for Disease Control and Prevention (CDC). Sadowski MA.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. EPA 738-R-00-010. Third National Report on Human Exposure to Environmental Chemicals.pdf.12(6):619-645. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Atlanta (GA). A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Eigenberg DA. Reprod Toxicol 1998.376(6):808-815. Freshwater KJ. 2005. Environmental Protection Agency (U. Nguyen JV. EPA). Available at URL: http://www.

and particularly when it was ingested in granular form. diazinon was widely used in residential and garden application. Inhalational and dermal routes of exposure can be significant for pesticide applicators. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. an organophosphorus insecticide that is used to control insects on nuts. 2007).S. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. and forage crops. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Most granular formulations. 2004). Estimated intakes from diet and water do not exceed recommended intake limits (U. 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. 1998. but is rapidly absorbed orally (IPCS. Before these restrictions. aerial.49 (<LOD-2. Survey Geometric mean (95% conf.EPA. vegetable. Fourth National Report on Human Exposure to Environmental Chemicals 143 . seed and foliar applications are planned to be phased out (U.2 and 0. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 1998). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.S. in the past.S. fruits. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. Once absorbed. Diazinon is not well-absorbed through the skin. It is toxic to birds. population from the National Health and Nutrition Examination Survey. 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 1.11) < 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. and other metabolites. Prior to 2000. in some pest strips.EPA. diazinon cannot be sold for residential use. It is also used for cattle ear tag applications to control flies and ticks and. 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. 2004). but these uses have been phased out. diazinon produced wild bird kills before use restrictions were in place. since 2004. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. which may vary for some chemicals by year and by individual sample. USGS. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.45 (<LOD-3.7.

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

Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. In a small number of men visiting fertility clinics in Missouri and Minnesota. Drobnis EZ. Liu F.gov/circ/2005/1291/.111(12):1478-1484.44(11):2243-2250.S.htm. Toepel K. Anal Bioanal Chem 2003. Seifert J.9(2):117-131. 2006). Diazinon. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Jones K.Organophosphorus Insecticides: Specific Metabolites 2005).50(5):505-515. 1/14/09 U. 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.114(2):260-263. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Banister E. Drug Chem Toxicol 1986. EPA).usgs. 4/7/09 Lu C. Bouchard M.inchem. Available at URL: http://www. Biochem Pharmacol 1992. Study for Future Families Research Group. Needham LL. EPA 738-R-04-006.S. Nguyen JV. References Anthony J. Interim reregistration eligibility decision (IRED. Swan SH. Bull Environ Contam Toxicol 1986. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . 1992-2001. Oloffs PC. Environmental Health Criteria 198. Dumas P. U. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Garfitt SJ.org/documents/ehc/ehc/ehc198.S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Atlanta (GA). Bravo R. et al. Available at URL: http://pubs. Beeson MD. Barr DB. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Pesticides in the Nation’s Streams and Ground Water. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Third National Report on Human Exposure to Environmental Chemicals.gov/ oppsrrd1/REDs/diazinon_ired.. 2006). 1998.epa. Available at URL: http://www. Sadowski MA. Barr DB. Pewnim T.376(6):808-815. Diazinon. Geological Survey (USGS). The Quality of Our Nation’s Waters. J Expo Anal Environ Epidemiol 2000. Irish R. Toxicol Lett 2002. Centers for Disease Control and Prevention (CDC). Effect of sublethal levels of diazinon: histopathology of liver. 2005. International Programme on Chemical Safety-INCHEM (IPCS). Driskell WJ. Carrier G. Mason HJ.134(1-3):105-113. Olsson AO. Semen quality in relation to biomarkers of pesticide exposure. 2007 [online]. Brunet RC. Banister EW. Oloffs PC. In 54 Canadian greenhouse workers. Noisel N.37(4):501-507. Environmental Protection Agency (U. March 2006. Barr DB. Swan et al. Ann Occup Hyg 2006.10(6 Pt 2):789-798. Environ Health Perspect 2003. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Environ Health Perspect 2006.pdf. May 2004. Rajendra W. Baker SE.. In 23 children. Fenske RA. 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. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Cocker J. revised February 15. Barr DB. Kruse RL. Redmon JB. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

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

Fourth National Report on Human Exposure to Environmental Chemicals 147 . CDC. Biomonitoring studies of malathion dicarboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of malathion than are found in the general population.cdc. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al.S.atsdr. 2006). Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 2005). 2005. but isomalathion. 2000). 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al. 2003). 1987.. 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. Of 382 pregnant women living in an agricultural community. 1999). Malathion itself has not been considered genotoxic (U. 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. 2001.S. Lu et al..S. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.EPA.74 (<LOD-5. Additional information about external exposure (i. population from the National Health and Nutrition Examination Survey. and it is not considered an animal teratogen or a reproductive toxicant.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. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.5 and 5. 2004). 2002. 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.e. representative subsample from NHANES 19992000 (Adgate.. Giri et al. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al..html and from U. Flessel et al. 1990).gov/toxpro2... 2006).. 1993.. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. EPA at: http://www.. A study of 13 children from an agricultural region of Washington State reported median levels that were below the detection limit in the NHANES 1999-2000 subsample (Kissel et al. but cholinesterase activity was not affected. Toxicity from unprotected bystander exposure during applications is rare (U.S.. 1999. Thomas et al. 2006).EPA. environmental levels) and health effects is available from ATSDR at: http://www. 1996.gov/pesticides/.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Human studies of single oral doses between 0.epa. Survey Geometric mean (95% conf. IARC considers malathion not classifiable as a human carcinogen. Pluth et al.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. 2005)..

Neutra R.inchem.77:1009-1010. 2005. Ryan PB. Griffith W. Barr DB. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. The Quality of Our Nation’s Waters.74(2):following table of contents. Centers for Disease Control and Prevention (CDC). 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Gosselin NH. Lu C. Reproductive outcome in women exposed to malathion. Thomas D. Quintana PJ. Fenske RA. Flessel P. Hertz-Picciotto I. Curl CL. Grether JK.56(10):2393-2399. Am J Epidemiol 1990. revised February 15. Barr DB. metabolite clearance. Dinoff TM. Harley K. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.org/documents/jmpr/jmpmono/v2003pr06. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Lu C.132(4):794-795. Giri A. U. Available at URL: http://www.114(2):260-263. Kedan G. Barr DB. March 2006. 4/7/09 Kissel JC. Szyfter K. O’Neill JP. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Dumoulin MJ. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. July 2006. Rappaport E. Toxicol Sci 2003 May. Jewell NP.gov/circ/2005/1291/.109(6):583-590. Toepel K. Third National Report on Human Exposure to Environmental Chemicals. Reregistration eligibility decision (RED) Malathion. Eberly LE. A longitudinal investigation of selected pesticide metabolites in urine. 6/1/09 U. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.73(1):182-94. Lioy PJ.9(5):494-501. Needham LL. Pesticides in the Nation’s Streams and Ground Water. Samuel O. Goldhaber M. Blasiak J. et al. Sharma GD. htm. Genetic toxicity of malathion: a review.usgs. Clayton CA. et al. Harris JA. J Expo Anal Environ Epidemiol 1999. Irish R. Bouchard M. Eskenazi B. 2007 [online]. Freeman NC. Krieger RI.gov/oppsrrd1/REDs/ malathion_red. Atlanta (GA).S.445(2):275-283.epa. Bravo R. Environmental Protection Agency (U. 1992-2001. et al. Prasad SB. Nicklas JA. J Expo Anal Environ Epidemiol 2005. Malathion deposition. Environ Mol Mutagen 1993. and cholinesterase status of date dusters and harvesters in California. Mutat Res 2002. Pluth JM. Trzeciak A. Carrier G. Mutat Res 1999. Malathion (addendum). Erratum in: Toxicol Sci 2003 Aug. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Hooper K. Environ Health Perspect 2006. MacIntosh DL. Environ Health Perspect 2001. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. International Programme on Chemical Safety-INCHEM (IPCS). Swan SH. Barr DB. Available at URL: http://pubs.112(10):1116-1124.38(4):546-553. EPA).Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Hammerstrom KA. Albertini RJ. Brunet RC. Giri S. Weltzien E. Am J Public Health 1987.15(2):164-171. Jaloszynski P.S. Environ Health Perspect 2004.S. Cancer Res 1996. Bradman A.22(1):7-17. Arch Environ Contam Toxicol 2000.pdf. Available at URL: http://www. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Geological Survey (USGS). Petitti D. EPA 738-R06-030.514(1-2):223231.

phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.50 (1.10 (3. 2000). O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 149 .300-.0) 3.40) 4.910) < LOD .21-1.49 (1.11-4.8 and 0. binds tightly to soils resulting in low leachability.44) 2.10 (3.298-00-0 Ethyl Parathion CAS No. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.01) 695 660 518 679 603 941 Limit of detection (LOD.770 (.850) < LOD .80 (1.57) 1.09-1.33) 2. Morgan et al. < LOD means less than the limit of detection. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.50 (2. with limited applications in agriculture.47) 2.70-6.62 (1.30-5. Both are toxic to birds. Survey Geometric mean (95% conf.89 (2.71 (2.S. first registered in 1948.70 (2.37-4.27) 2. 2006).12) < LOD < LOD 1.32-1.40) 1.990-1.91-3.26 (1.01) 4.70 (<LOD-3.46 (3.80 (2.69 (2.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .50) 3.860 (<LOD-1.90-9. Methyl parathion is not registered for residential use in the United States.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.40-4.69) 4.50-14.0) 4. methyl parathion was rapidly absorbed after ingestion. Methyl Parathion.30 (1.01-4.20) 5.05) 4.92) 5.37-2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10-1.41-4. Once absorbed.80 (2.11) 2.18-3.50-9. all registered uses were voluntarily cancelled (U.S.0 (3.50) 1.EPA. Many previous registered agricultural uses of methyl parathion have been cancelled (U.15-3. was once a restricted-use insecticide with limited applications on certain agricultural crops. Ethyl parathion.0) 2. Methyl parathion has low water solubility.50 (1.70 (3.30-3. and has a short half-life in soils and on plants.40 (1.700 (<LOD-.37) 2. 2007).910) < LOD < LOD < LOD 1.45 (1.0) 3.60-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60-5. on cereal grains.70-6.61) < LOD 1. peak domestic use was as high as 5-6 million pounds per year.67 (1.66 (2.02-6.40-3.10) 22.70-3.30 (2.00 (2.58) 3. and of the chemical nitrobenzene. Methyl parathion use is highly restricted.32 (1.74) 5. Estimated intakes from diet and drinking water have been below recommended limits. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.28-4.28 (1.70) 2.60) 1.20 (<LOD-2. pulmonary.20-5.60-36.00) size 1989 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1. and eliminated rapidly from the body after absorption (Kramer et al.48) 90th 2.EPA.50) 2.0) 3.22-3.70 (2. and oral routes can occur in pesticide and agricultural workers (Muttray et al.50 (2.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . It had been applied to cotton. and aquatic invertebrates.32-3.36-1.79) 4.70-3..90 (1.70-6.20 (2.13-1.71 (3.19 (.0) 3. In the 1990s.60 (4.10) 4. 2002.50) 3. ethyl parathion.00 (2.80) 2.40-4.85 (2.72 (3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.70) 2. 2003).00) 3.92-2.730 (<LOD-.10-11.50 (1.34 (3. and to a lesser extent.. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60-19.28 (1.21 (2.S.16) < LOD 1.50 (1.0) 3.. Given its limited use.45) 5.70) 2.940 (<LOD-2. population from the National Health and Nutrition Examination Survey.32-1.90-11.33 (1.40) 2.37-4.790 (<LOD-.70 (2. more slowly absorbed through the skin.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.67) < LOD 1.57-4.1.10 (<LOD-6.61) < LOD 1. In animal studies. 1977). but by 2003.30-16. fish. Increased risk of exposure via dermal.910) < LOD < LOD .

41-2.930 (.31) < LOD .08 (1.4 (3.04) 1.73 (1. The metabolite.370 (<LOD-.76-14.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .880 (.2) 2.78 (2. gov/pesticides/.23) 1. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 2005.78-2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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 .800-1.43) 4. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.08) < LOD . Methyl parathion is not considered genotoxic..57-7.77-7.00 (1.430 (.e. Lores et al.04 (2..87 (1.44-3.930 (.79 (1. Parathion and methyl parathion have high acute toxicity in animal testing.15) 3.60) 2. 1990.71 (1. 2004).310-.91 (1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high animal doses of methyl parathion.S.10) 90th 2.07 (1. weakness. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. methyl parathion.01 (2. gov/toxpro2.2) 2.82) < LOD .93 (2..06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .15-10.61) 4.980 (.71) 1.950) < LOD . IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. 1991). and unintentional acute or chronic high-level occupational exposure (Hill et al.55 (<LOD-3.78) 2. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. U.720-1.94-47. 1978. teratogenic.S.1) 2.96 (1.72-2. 1995.31-3.940 (<LOD-1. WHO.720 (<LOD-.29) 2.9) 1.09) 2.37-1.07) 2.atsdr.30) 3. Methyl Parathion.16-4.55) 2.epa.97 (2.20 (3. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.3) 2.. In addition to being a metabolite of methyl and ethyl parathion.39) 1.850-1.39 (1. Jaga and Dharmani. In large doses.78-2.38-3.540) < LOD .67-2.640) < LOD < LOD 1..13-12. cholinergic effects. 2004). 1995).70) 3.90 (1.840 (. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.00) 2. ethyl parathion.33-3.88 (1.01 (.17-4. and seizures.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 150 Fourth National Report on Human Exposure to Environmental Chemicals .94-4.690-1. and producing acute symptoms such as nausea.29) 1.33-6.680 (<LOD-1. does not inhibit acetylcholinesterase enzymes.35-3.13) 4.05) 4.7) 3.95) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. paralysis.. 2006.25 (2.57-2.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .870) < LOD .500) < LOD < LOD .cdc. Zurich et al.08-3.21) 1.91) 1.970 (.96 (1.97-10.25) 1.400 (<LOD-.30-1. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.11) 1. paranitrophenol. accidental exposure.440 (<LOD-.830-1. environmental levels) and health effects is available from ATSDR at: http://www.89 (2. Slotkin et al.33-3.26) 17.20) .790-1.S. Orsorio et al.730-1.79) 1.11-4.14-3.530) < LOD < LOD < LOD .97 (<LOD-4.00 (1.790-.80 (1. 2003.86 (2.56-2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).98-7.67 (3. resulting in excess acetylcholine at nerve terminals.970 (.21-21. vomiting.83 (1. Survey Geometric mean (95% conf.82 (2.60 (1.48-4.92 (2.29 (2.57) 6. and other metabolites.html and from U. EPA at: http://www. Additional information about external exposure (i. 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.35-3.26 (1.89 (2.10 (1. but lists ethyl parathion as a possible human carcinogen.80 (1.88) 1.44-3.84) 3.60-2.59 (1.EPA considers methyl parathion unlikely to be carcinogenic to humans.20) 3. Thus.17) .. Karanth and Pope et al.. 2006.01-3.

Lewalter J. population (Olsson et al. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.. Environ Res 1995.110 Suppl 6:1075-1078.. Slach EF. Atlanta (GA). 2002. 2005. Gregg M. 2005. et al.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Needham LL. Wellman SE. Kissel JC. 2002. and levels were similar or slightly lower that those in a small convenience sample of the U. In a study of workers who handle parathion. Cline RE. 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. Arch Environ Contam Toxicol 1977. Costa LG. McCann KG. Laboratory investigation of a poisoning epidemic in Sierra Leone. Toxicology 2005. 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. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Environ Health Perspect 2002. Hill et al. Head SL. Bradman A. References Barr DB.htm. Alley CC. et al. Turner WE. Karanth S. Centers for Disease Control and Prevention (CDC).56(7):449553. Kedan G. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Role of individual susceptibility in risk assessment of pesticides. Environ Health Perspect 2002. Bailey SL. Rockhold RW. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Kramer RE. Hill RH Jr. Baker RC. Baker S. Available at URL: http:// www. 2005). McCann et al. 2004). Runkle KD. Morgan DP. Lin LI. 1995). McClure PC. Third National Report on Human Exposure to Environmental Chemicals.21(1):5767. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. International Programme on Chemical Safety-INCHEM (IPCS).inchem. 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.71:99108. Eskenazi B.110 Suppl 6:1085-1091. Head SL. Barr JR. Pope C. Occup Environ Med 1999. Barr DB. Baker SE. a range of values several hundred times higher than levels found in the U. and many residents were symptomatic (Barr et al. general population (CDC. Clark JM. DiPietro E. et al. 2002)..6(2-3):159-173. Pesticide residues in urine of adults living in the United States: reference range concentrations. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. 2005. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Hetzler HL. Curl CL. Weltzien E. Shealy DB. Jewell NP.. Pharmacokinetics of methyl parathion: a comparison following single intravenous. J Expo Anal Environ Epidemiol 2005. Arch Environ Health 1978.S. Griffith W. Barr DB. Bradway DE. Neurotoxicol Teratol 2003. Lores EM.5 mg (500 µg)/g creatinine for workers at the end of shift. Rubin et al. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Ashley DL. Parathion-Methyl (addendum). J Biomed Sci 2002. et al. Fourth National Report on Human Exposure to Environmental Chemicals 151 .S. ACGIH recommends a BEI of 0. Giordano G. 1999). Guizzetti M. oral or dermal administration. Harley K.9:311-320.14(4):213-216.. J Anal Toxicol 1990. Pesticide workers may have much higher levels following pesticide applications..112(10):1116-1124. et al.215(3):182-190. Leng G. Moseman RF. CDC. Dharmani C. Moomey CM. Barr DB. 4/7/09 Jaga K. 1995.. Rev Environ Health 2006. Methyl parathion: an organophosphate insecticide not quite forgotten.33(5):270-276. Chicago area methyl parathion response. Pathak S. 2005).org/documents/jmpr/jmpmono/v95pr14. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.15(2):164-171. Hill RH Jr. Environ Health Perspect 2004. Hryhorczuk DO. Lu C.25(5):599-606.

Osorio AM.S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Geological Survey (USGS). Pesticides in the Nation’s Streams and Ground Water. Environ Health Perspect 2006. Ames RG.D. Olsson AO. 2007 [online]. 1/12/07 U. September 2000. R. Toxicol Appl Pharmacol 2004.int/water_sanitation_health/dwq/chemicals/ methylparathion. Rosenberg J.110 Suppl 6:1047-1051.114(10):1542-1546. Hill RH Jr. May 2003. Investigation of a fatality among parathion applicators in California.epa. Seidler FJ. Available at URL: http://pubs. 0153. March 2006. Environ Health Perspect 2002.who.162(2-3):219-224. et al.usgs. Mengle DC. WHO/SDE/WSH/03.S. Esteban E. Costa LG.gov/oppsrrd1/REDs/factsheets/0155fct. Backer G.20(4):533-546. 1992-2001. 1995-1996. The Quality of Our Nation’s Waters. gov/oppsrrd1/REDs/methylparathion_ired. Am J Ind Med 1991. Rubin C.E. Dunlop B.pdf. Facts. Case No. Environmental Protection Agency (U.376(6):808-815. Nguyen JV.S. Barr DB. 2004. EPA). Toxicol Lett 2006.201(2):97-104. Slotkin TA. Yacovac R. 5/19/09 Zurich MG. Schilter B. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Methyl parathion in drinking water. Hill G. Levin ED.gov/circ/2005/1291/. U.pdf.Organophosphorus Insecticides: Specific Metabolites Muttray A. Kieszak S. Sadowski MA. 1/14/09 U.S.S. Honegger P. 6/1/09 World Health Organization (WHO). Letzel S.04/106. pdf. Available at URL: http://www. Available at URL: http://www. Ethyl parathion. Environmental Protection Agency (U.epa. Ohio. Monnet-Tschudi F. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www. Jung D. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. External and internal exposure of wine growers spraying methyl parathion. EPA). Anal Bioanal Chem 2003. revised February 15. Tate CA. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. EPA-738-FOO-009. Ryde IT. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.

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

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 (<LOD-.07) .700-1.31) .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .300-1.840 (.15) < LOD .680 (<LOD-.210-1.470 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .740 (.64) .17 (.610 (<LOD-1.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey.S. 154 Fourth National Report on Human Exposure to Environmental Chemicals .740-1. 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.210-. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.27) .21) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .500 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.55) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .94) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 01-02 is 0.840) 669 687 929 Limit of detection (LOD.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .780 (.670 (<LOD-1.780 (<LOD-1. < LOD means less than the limit of detection.850 (.760 (<LOD-. Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.820) < LOD < LOD .700-.950) < LOD < LOD 1.430 (<LOD-.200-.410 (<LOD-1.2.250 (<LOD-.780 (<LOD-1.580-1.780 (.S.

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

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

Leng A.. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Estrogenicity of pyrethroid insecticide metabolites. and striatal dopamine levels in male and female rats. Regul Toxicol Pharmacol 2002.. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Varoli FM. Wolff MS. 2003. Thomson BM. Chen JH.. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Ose K. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. 2002).8(1):197-202.251(3):855-859. Soderlund et al. et al.62:101-108. Garey J. 2000. Toxicological profile for pyrethrins and pyrethroids. Abell AD. 2003. Song L. Shafer.gov/pesticides/ and from ATSDR at: http://www. Bull Environ Contam Toxicol 1999. Cruz-Casallas PE. cdc. 2001. Shukla Y. Bernardi MM. Hu et al.. Zhao RC. Shin JH. Lee SJ.S. Lewalter J. Toxicol Appl Pharmacol 1991. 2002). Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. salivation. 2005). 1999.. WHO. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Leng G.300(3):161-165. choreoathetosis. Pauluhn J.. Seth PK. Elwan MA. Go V. Salzgeber SA.gov/toxprofiles/ tp155. 2006). Kunimatsu et al. 2001. neurochemical changes in cholinergic.. Neurotoxicol Teratol 2005. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Kamita Y.27(4):609-614. 2003. Wolff MS.. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.html. Toxicol Appl Pharmacol 2006. Sunami O. Available from URL: http://www. and seizures (ATSDR. Int J Hyg Environ Health 2002. Lemonica IP. Kim HS. Garey and Wolff. Hu JY. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.35(2 Pt 1):227-237.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. epa. Effects of prenatal exposure to deltamethrin on forced swimming behavior. September 2003.gov/toxpro2. Eriksson and Fredriksson. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. References Agency for Toxic Substances and Disease Registry (ATSDR). McCarthy et al. Eriksson P. 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. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation.50(2):245-255. 2003. Moniz et al. Lazarini et al.23(6):665-673.27(12):1273-1283. tremor. Kuhn K. Adhami VM. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Yang J. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid.atsdr. et al. J Reprod Dev 2004. on immature and adult mice: changes in behavioral and muscarinic receptor variables.205(6):459-472. 1998. Moniz AC. In California.211(3):188-197. Spinosa HS. and permethrin) in the Hershberger and uterotrophic assays. Berger-Preiss E. Sugiri D. 2005). Fredriksson A. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Miller GW. Pyrethroid pesticide-induced alterations in dopamine transporter function. Kang IH. Guillot TS. bioallethrin and deltamethrin. 1991.108(1):78-85.. Go et al. Richardson JR. Biochem Biophys Res Commun 1998. Garey J.8(1):18-21. Environ Health Perspect 1999. Kunimatsu T. 2002. et al. Neurosci Lett 2001. Leng G. In developing rodents.107(3):173-177. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Okuno Y.. Bernardi MM.1/15/09 Aziz MH. Lazarini CA. et al. Wang SL. EPA at: http://www. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.. Wieseler B. Ray et al. Yamada T. 2006. Neurotoxic effects of two different pyrethroids. Kuhn KH. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Kim IY. Kim TS. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides.html. 2006. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Pogo BG. Additional information about pesticides is available from U.atsdr. J Environ Monit 2006. McCarthy AR. Idel H. Generally. Caudle WM.cdc. hypersensitivity. dopaminergic. Idel H. Leng G. Levsen K. 2005). 2005).. Elwan et al. 2004. Kim et al. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. motor activity. Florio JC. Agrawal AK. fenvalerate. Ranft U.. Xenobiotica 1997. Neurotoxicol Teratol 2001. Shaw IC. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.

and therapy. June 2006b.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Reregistration Eligibility Decision for Cypermethrin.186:57-72.usgs. Piccirillo VJ. Available at URL: http://www.epa. 1992–2001. Available at URL: http://www. Xenobiotica 1992. synergies. Rev Environ Contam Toxicol 2006. March 2006. Environmental Protection Agency (U. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.S. et al. Mullin LS.38:95-101. Available at URL: http://whqlibdoc. Pesticides in the Nation’s Streams and Ground Water.epa. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. EPA).10. Pyrethroid insecticides: poisoning syndromes. pdf. World Health Organization (WHO). Available at URL: http://pubs. Sheets LP.S. Meyer DA. Geological Survey (USGS). O’Malley M. Safety of pyrethroids for public health use. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.S. Pesticide and Evaluation Scheme. Available at URL: http://www. U.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. sumithrin synthetic pyrethroids for mosquito control. Shafer TJ.who. resmethrin.epa.htm. Crofton KM. 2007.22(8):983-991. June 2006a.pdf. 2005.S. Lesser JE. 5/26/09 U. Forshaw PJ. 5/26/09 Woollen BH. J Toxicol Clin Toxicol 2000. Environ Health Perspect 2005. Soderlund DM. 19962002. 5/26/09 U.S. Spencer J.S. Revised February 25. April 2002.113(2):123-136.S.htm. Environmental Protection Agency (U. Clark JM. Pyrethroid illnesses in California. Laird WJ.Pyrethroid Pesticides Ray DE. EPA). Permethrin.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Sargent D. Marsh JR. Environmental Protection Agency (U. 5/26/09 U. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicology 2002.gov/oppsrrd1/REDs/cypermethrin_red.171:3-59. EPA).gov/ circ/2005/1291/.

but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC.S. 2004). 2006). Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. 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. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. 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.2 μg/L) in the U.95 µg/L.. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. 2001. 2003). (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Urinary levels for adults and children in these studies were similar (Heudorf et al. 2005). 2005).S. representative 2001-2002 NHANES subsample (CDC. 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.. 2005.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. 2006) and 1177 urban adults and children (Heudorf et al. Following an indoor application exposure. Leng et al.. Fourth National Report on Human Exposure to Environmental Chemicals 159 . Cyfluthrin is rapidly metabolized and eliminated from the body. 2003). 2003).. most of which were dermal and respiratory irritations (Spencer and O’Malley. Baker et al..Pyrethroid Pesticides Cyfluthrin CAS No.. Studies in Germany of 396 children and adolescents (Becker 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. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate.. Thus. representative subsample in NHANES 2001-2002 (CDC. Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.

which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 160 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.S.2 and 0. < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < 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.

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

Environ Health Perspect 2001. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Barr DB. Hoppe HW. Int J Hyg Environ Health 2003.77(1):67-72. Angerer J. Rev Environ Contam Toxicol 2006. Heudorf U.46(3):281-288.109(3):213-217. O’Malley M. Kolossa-Gehring M. Int J Hyg Environ Health 2006. Krieger RI. 2005. Spencer J.13(2):112-119. J Expo Anal Environ Epidemiol 2003. Berger-Preiss E. Int J Hyg Environ Health 2006. Schulz C. Int Arch Occup Environ Health 2004. Bernard CE. Angerer J. Centers for Disease Control and Prevention (CDC). Heudorf U. Idel H. Williams RL. 19962002. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Olsson AO. Ball M. Heudorf U. Arch Environ Contam Toxicol 2004.186:57-72. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Sugiri D. Atlanta (GA). Drexler H.209(3):221-233.206(2):85-92. et al. Butte W. Angerer J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Becker K. Leng G. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Hadnagy W.209(3):293-299. Angerer J. Seiwert M. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Third National Report on Human Exposure to Environmental Chemicals. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Ranft U.Pyrethroid Pesticides References Baker SE. Pyrethroid illnesses in California.

490-1. Cyfluthrin.or trans-3-(2.68359-37-5 Cypermethrin Permethrin CAS No. Biomonitoring Information Urinary levels of cis.120-.380-. cis-permethrin.210-.120-.640 (.32) .680-3.2dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .110-.610) . Kuhn et al. trans-cypermethrin.330) .250-.2-Dichlorovinyl)-2.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.460-.790) .500 (.780) . Similarly.220) .440 (.770) .730 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.110 (<LOD-.630) .870) 1.S.670-1. The presence of cis-3-(2.250 (.460-1.15) .07 (. ciscypermethrin and cis-cyfluthrin. 1999). Survey Geometric mean (95% conf. more of the trans-metabolite than Urinary cis-3-(2.740) 1. Kuhn et al.120-.530 (.790-1.670-2.670 (..570-.270-.210) .490-.490-.610) .240) .160 (<LOD-.430-.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. In the body.300 (.43) .310) .270 (.350) .and trans-isomers.300-.380-.550) .370 (.44 (.08) .150 (.200 (.47 (.630) .960 (.470-1.262) * * * < LOD < LOD .770-1.120-.160 (.13 (.1. Generally.200) .410) .170 (.210) 90th . and trans-cyfluthrin.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George. < LOD means less than the limit of detection. 1999).890 (.790-1.68) .910-5. the presence of trans-3-(2.330 (.340) .202 (.68) .580-1.630-.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 .600) .35) .630 (.2dichlorovinyl)-2.230) .300 (.580) 1.53) .160 (. trans-permethrin.140 (.1 and 0. 52315-07-8 CAS No.155-.50) .510 (.200) .11) .270 (.240) .180 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.380 (..470 (.28) 671 680 518 701 591 957 Limit of detection (LOD.110-.700) . The chemical trans-3(2. and ciscyfluthrin.270 (.68 (.140 (<LOD-.380) .280 (.790 (.680 (.740-2.54) .710-1.690) .200) < LOD < LOD < LOD .950-2.890 (.570 (.24) 1.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .110-.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.220-.35) 1.2-dichlorovinyl)2.710) .520) .900 (.420-.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . 1985.340-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.2-dichlorovinyl)-2.77 (.340) . but it can also reflect exposure to cis-3-(2. which may vary for some chemicals by year and by individual sample.740-1.370-.2-dichlorovinyl)-2.280-. cis-3-(2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.200-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.880 (.2-dichlorovinyl)-2.740 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.730 (.220-. population from the National Health and Nutrition Examination Survey.380-. transcypermethrin and trans-cyfluthrin.220-.650-1.400-.12 (.460 (.850 (.500 (.730 (.220-. Fourth National Report on Human Exposure to Environmental Chemicals 163 .410) .200-.820 (.300-.510 (. 1985.260 (.80) .200-. cis-cypermethrin. but can also reflect exposure to trans-3(2.600-1.920) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.21) .510 (.670-1.600 (.490-1.2-dichlorovinyl)- CAS No.

380) .440-.550-1.590 (.12 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.and trans-3(2.370-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .640-1. 2006) and 1177 urban adults and children (Heudorf et al.710-3.680-1. 2006. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC..and trans-3-(2. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.59) .250-.150-.500 (.780) 1.180 (.270-.2dichlorovinyl)-2.200 (.2-dichlorovinyl)-2.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.890 (.230-. In these volunteers.340-.2dichlorovinyl)-2.440 (.120 (.680-1.170 (.300 (.33) .800 (.190) . 2001) showed urinary levels of cis.130-.380 (.390 (.380-.S. 2006.300) .430-.450 (.810 (.360-1.280 (.49) . urinary levels of cis-3-(2.540 (.29 (. the median and 95th percentile of urinary levels of cis-3-(2.640 (.580-1.11) .340) .340) .270) .260-.230-. 2005).780 (.840 (.180-.Pyrethroid Pesticides 2.890) ..250-. 2005). 2006).2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.400 (.280-.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * . Studies in Germany of 396 children and adolescents (Becker et al. 2005). post- Urinary 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 .400-1.260 (.03) 1.290) . Schettgen et al.200) .510-1.200-.390-..2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin. 2005).250) .390-. 2002). 164 Fourth National Report on Human Exposure to Environmental Chemicals .750-1.440-..530 (.690-1.640) 1.S.830) .550) .560) 1.240 (<LOD-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.67) .290 (.700-2. In a study of urban residents in Germany (Berger-Preiss et al.210-.840 (.250-. population from the National Health and Nutrition Examination Survey.540 (.33 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. In a study of volunteers.12-2.2-dimethylcyclopropane carboxylic acid did not increase.290) .. 2003).570) .680 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.880) . Lu et al.320) ... Survey Geometric mean (95% conf.560) . 2002).550 (.900 (.320-.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.580) ..37) .260) .700) .550) .150-.300) .750 (. 2003). 2004.270) .59) .640-.450-.190 (.350) .21) .220 (.410) . 2005) In a small group of indoor pest-control operators..250 (<LOD-. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.270 (.250) 90th .370-.11) 1. In the same residents. median urinary levels of trans-3-(2. representative NHANES 2001-2002 subsample (CDC.470-1.640-1.300-.430-1.150-.250) .700) .440 (.350 (.540) .2-dichlorovinyl)-2.290-.430 (.370-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.230 (.2-Dichlorovinyl)-2.710 (. urinary trans-3-(2. 2001.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .140-.920 (.080-.170) < LOD < LOD < LOD .600 (.182) * * * < LOD < LOD .220) .190) . 2006).200-.450-1.104-.2-dichlorovinyl)-2.11 (.530 (.67 (.2-dichlorovinyl)-2. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. Other studies have provided evidence that urinary levels of cis.230-.590) .138 (..170 (.300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.160 (<LOD-.80) .24) .11) .260 (.31) . Cyfluthrin.260 (.550-1. 2004).420 (.59 (1..2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.220 (.

39 (1.680-1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.780 (.43) 2. The maximum post-application urinary levels.850-1.2-dichlorovinyl)-2.08) 1.25 (1.2-Dichlorovinyl)-2. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.60-4.77) 1.49-5.20 (.920-1.14-2.39-5.530) .19) 1.4.49-3.41-14.50 (1. however.17-1.910-1.01) 4.70) 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 .84 (1.560 (.and trans-3-(2.40 (1.S.410-.59 (1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.700-1.54) 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.820) .830-1.490-1.95) 2.500 (.Pyrethroid Pesticides application median urinary levels of summed cis.60) 1.91 (1.56) 2.08-6.60) .90) 1.62 (1.670) .860) .14) 1.97-11.5) 2.500) .940 (.490 (<LOD-.660) 1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.400-.81) 2.400 (<LOD-.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .01 (1.66) 691 680 518 690 595 954 Limit of detection (LOD.4 and 0. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.14-6.37 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.26 (.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .440 (<LOD-.560 (.480-. population from the National Health and Nutrition Examination Survey.or trans-3-(2. 2005).11-2.17 (.09 (.23 (.840-1.69 (1.41 (1.23) 2. Finding a measurable amount of cis.28 (1.910-1.410 (<LOD-. Urinary trans-3-(2.710 (.68) 1.760) .49-3.56 (1. trans-Cypermethrin.420 (<LOD-.620) < LOD 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08-4.95) 3.76-4.66) .87 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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.20 (.42) 1.85) 4.460-.68-3.63) 1.03-1.56) 2.69) 1.03-1.56 (1.7) 2.68-2.410-.35) 1. 2005). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.77 (1.470 (<LOD-.2dichlorovinyl)-2. Survey Geometric mean (95% conf.550 (.13) . < LOD means less than the limit of detection.610) 1.17 (.22 (1.42 (2.19 (3.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .55-4.560 (.520-.77) 2.500-.63) 1.76-3.410 (<LOD-.970 (.580 (.520) .28 (2. which may vary for some chemicals by year and by individual sample.20 (.07 (1.19 (2.64-4.470 (.27 (1.700) .2-dichlorovinyl)-2.570) 90th 1.54 (1.670) .55-3.810-1. Biomonitoring studies on urinary levels of cisor trans-3-(2.800-1.730) .68) 2.460-.68) 1.55-5.750) .12-6.07-3.25-3.89 (2.16) 1.10) 2. Fourth National Report on Human Exposure to Environmental Chemicals 165 .11-1.94 (1.48) 4.

500-.410-.900 (<LOD-1.91-11.91) 1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.02-1.570 (.08 (.S.60) 2.30-6.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.610-.41) 1.720-1.720-1.850) .15) 2.80) 1.39 (1.31 (2.29) 1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .530 (.42) 1.440-.33 (1.00) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33-2.850-3.880-1.00) 1.740) .34-3.15 (1.770) < LOD 2.44) 2.33-1.19) .26 (1.35) 1.480-.87 (1.87-3.31) 1.07-1.15-3.570 (<LOD-.37 (1.560 (.55 (2.08 (.75 (1.87) 1.930-1. population from the National Health and Nutrition Examination Survey.970 (.31 (.47 (1.580) .580 (.15-3.730) .45 (1.60 (1.65) 1.27-2.86 (2.07-3.19 (1.61) 1.07) 2.720 (<LOD-.780) 90th 1.12-1.760 (.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-Dichlorovinyl)-2.40-2.74) 2.750) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.470-.60) 2.42 (.670) .47-2.880 (.67 (2.3) 2.880 (<LOD-1.13) 1.820-2.27-2.20 (1.00) 5.55 (2.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .74) .700 (.65 (2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.540) .520 (<LOD-.98 (1.87-8. Survey Geometric mean (95% conf.45-2.22-1.570-.800-1.470 (.16 (1.47-2.70 (.780) .850) 1.22-2. trans-Cypermethrin.530 (<LOD-.15) 3.00-5.700 (.39) 1.34-4.28) 2.20-2.55 (2.36 (1.48-2.10) 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 .00 (1.64 (1.48 (1.91 (1.07) 2.Pyrethroid Pesticides Urinary trans-3-(2.660) .13) .57) 3.780 (<LOD-.68) 3.15-3.87) 1.11) .800-1.56 (1.35 (1.36) 2.07-2.700-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.22) 1.12 (.81 (2.56-2.56-5.640) .89) 2.57 (1.30-3.

Ball M. Idel H. Hoppe HW. Berger-Preiss E. Environ Health Perspect 2006. Angerer J. Heudorf U. J AOAC 1985. Sugiri D. Berger-Preiss E. Fourth National Report on Human Exposure to Environmental Chemicals 167 . 2005.109(3):213-217. Atlanta (GA). Int J Hyg Environ Health 2002.Pyrethroid Pesticides References Becker K. Biological monitoring of workers after the application of insecticidal pyrethroids. Lu C. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Barr DB. Angerer J. Kolossa-Gehring M. Seiwert M.206(2):85-92. Third National Report on Human Exposure to Environmental Chemicals.76(7):492-498.205(6):459-472.62:101-108. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Drexler H. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Ranft U. Angerer J. Sugiri D. Angerer J. Centers for Disease Control and Prevention (CDC). Angerer J. et al.134(1-3):141-145. Heudorf U. Hadnagy W. Leng G. Leng G. Bartell S.209(3):293-299. Kuhn K. Int J Hyg Environ Health 2003. Ranft U.77(1):67-72. George DA. Bull Environ Contam Toxicol 1999. Permethrin and its two metabolite residues in seven agricultural crops. Levsen K. Heudorf U. Schulz C. Hardt J. Leng G. Pearson M. Int Arch Occup Environ Health 2003. Wieseler B. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Int J Hyg Environ Health 2006. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.68(6):1160-1163. Idel H. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.114(9):14191423. Environ Health Perspect 2001. Int J Hyg Environ Health 2006. Idel H. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Drexler H. Butte W. Schettgen T. Heudorf U. Bravo R.209(3):221-233. Angerer J. Int Arch Occup Environ Health 2004.

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

< LOD means less than the limit of detection.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.2-Dibromovinyl)-2.1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 and 0.Pyrethroid Pesticides Urinary cis-3-(2. which may vary for some chemicals by year and by individual sample. 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. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 169 .

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

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

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

35) 2.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .870 (.160-.311 (.1) 3.25 (2.18 (2.780) 4.490-.03 (3.750) .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.62) 5.1.430-.434) .510-.78) 6.26) 2.355) .190-.507 (.210-.33 (1.470-.440) .52-4.46) .81 (1.750-1.300 (.62-8.53-3.1) 3.65-2.288 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.53) 1.56-5.600 (.86 (1.298 (.680 (.710 (.760 (. Deltamethrin.320) .570-1.292-.52-5.35) 1.560-.25-4.200-.227-.75 (1.430-.55 (1.48-2.271-.369) .49 (1.28) 1.60) .42-2.30 (.300) .8) 3.250 (.276-.253-.200-.417 (.49 (1.940) 1.14-6.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.730 (.325 (.230-.315 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .S.12 (.454 (.800 (.328 (.230 (.590 (.273 (.16) 1.960 (.700-1.314) .250-.89-71.295) .362) .226-.586) .238-.610) .280 (.51-6.640 (.18 (1.595) .450 (.51-3.12) 4.13 (.321 (.850) .46) 2.530-.230-.260 (.26) 2.35 (2.620-1.353 (.330) .49-2.1) 3.92-3.290 (.800) 1.246-.27-2.45 (2.570-.12) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.406) .390) .49-2.63 (3.34) 8.1 and 0.32-21.336 (.34-6.41) 3.50 (2.277-.240 (.601) .02-6.180-.490) .41-2.260-.78) 1.210-.39) 2.43) 3.350-.340) .220-.830-2.79) 3.78) 1.05) .69 (1.510-.373) .190-.93 (1.820) .230-.233-.340) 1.820) .250 (.267 (.23 (2.260 (.265-.200-.32 (2.16-1.190-.990) .320) .740 (.27-2.710 (.04-5.54) 1.330) .830) 90th 1.560-.374) 99-00 01-02 99-00 01-02 99-00 01-02 .360) .428-.810) 1.63-3.25 (2. population from the National Health and Nutrition Examination Survey.30 (1. interval) .750) .260 (.32 (1.230 (.72 (1.670 (.650 (.83-11.90) 1.25-7. Survey Geometric mean (95% conf.65 (1.35) 2.33) .01 (1.352-.250 (.270 (.64) 697 680 524 701 603 957 Limit of detection (LOD.740 (.320) .25-1.34 (2.297 (.288-.71 (1.33 (2.700 (.38 (2.300 (.340) 75th .320 (.13) .247-.04) .550-.69) 3.35 (1.520 (.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 .29-1.850) .38 (2.292 (.44) 5.320) .48-2.270) .26-2.27-11.364) .45-5. Fourth National Report on Human Exposure to Environmental Chemicals 173 .530-.73) 1.630) .05) 1.314 (.41 (1.370) .427) .62-6.21 (2.78 (1.41-3.266-.240 (.190-.560-1.384) .36) 1.420) .300 (.160-.590-.30) 3.76 (1.387) .840-1.

226-.350) .63-3.07-5.55 (1.75-8.49) 1.540 (.590) .570) .60) 1.760) .550 (.95) 1.230) .280) .264 (.677) .387) .350 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.35) 1.21-4.05-3.280 (.25-5.17 (.378 (.840-1.490 (.62) .43-64.21 (1.91-4.11 (.19 (2.240-.250 (.750-1.25-2.280) .500) .19-6.240 (.250 (.328) .67 (1.229-.80) 4.278) .700-1.00) 1.309 (.372) .25) 2.960-1.64-5.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.400-.00) 1.238-.94 (1.534) .330) .246 (.590) . Deltamethrin.400) .309) .275 (.253) .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 .330) 75th .730) .510 (.220-.91) .55) 3.250) .49 (1.810) 1.54 (1.225-.270 (.200-.560 (.480-.330 (.17-1.03-1. Survey Geometric mean (95% conf.11 (.200-.450 (.320) .200-.270 (.930) .280-.330) .240 (.40) 2.440-.280 (.160-.48 (1.83) 1.36-6.860 (.200-.190-.90) 3.510 (.446) .590-1.91) 9.43) 1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .410-.270) .63) 1.437) .06-3.52 (1.335-.37) 1.400-.230-.550 (.300-.390-.316 (.91 (2.67) 1.311 (.330) 1.490 (.202-.43 (2.49-2.35-3.190-.630) .261 (.550 (.401) .178-.09-2.290-.39) 1.490-.03 (.27) 1. population from the National Health and Nutrition Examination Survey.410) .423 (.440-.860-1.84 (1.530-.61-2.13-1.88-5.02 (2.09) 3.590) .04 (3.15-2.240 (.460-.329) .365) 99-00 01-02 99-00 01-02 99-00 01-02 .13 (.52) 2.380-.73) 1.19) 2.270-.230-.224-.272) .280 (.240 (.670) 3.740) .04 (.190 (.321-.32 (2.49) 3.07) 2.610 (.83 (1.362 (.310) .10 (2.227 (.640 (.35) .274 (.36 (1.370 (.650) .720 (.299-.329) .730) .580 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .210-.234 (.216-.440-.240-.240-.930) 1.40 (1.271-.640 (.261-.580) .240-.510 (.S.210 (.44) 2.73-4.86 (1.53 (1.220 (. interval) .72 (1.323 (.81 (1.41) 1.0) 3.62) 1.670) .09 (.860-1.22 (1.380 (.44 (1.460-.274-.730-1.13-1.150-.290) .43 (1.272 (.74) 3.02-1.16-4.67 (1.530-.300-.312 (.270) .35 (1.357) .09-2.41-4.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .51-7.00) 5.290) .370-.37 (1.210 (.60-4.720) 90th 1.480 (.420-.173-.96 (1.

Exposure to indoor pesticides during pregnancy in a multiethnic. Kolossa-Gehring M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Barr DB. Sugiri D. Angerer J.205(6):459-472.46(3):281-288. Levsen K. Pearson M. Arch Environ Contam Toxicol 2004. Ortiz-Perez MD.114(9):14191423. and genotoxicity in exposed children. Lu C. Angerer J. Olsson AO. Torres-Dosal A. Hardt J.206(2):85-92. Int J Hyg Environ Health 2003. Grimaldo M. Seiwert M. Bravo R. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Hoppe HW. Berkowitz GS. Environ Health Perspect 2003. toxicokinetics. Barr DB. et al.113(6):782-786. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Lapinski R. Lopez-Guzman OD. et al.209(3):221-233.111(1):79-84. Liu Z. Godbold J. Carranza C. Sugiri D. Deych E. Ranft U. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Batres LE. 2005. et al. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Int J Hyg Environ Health 2006. Berger-Preiss E. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Bartell S. Idel H. Leng G. Environ Health Perspect 2005. Ranft U. Ball M. Leng G. Biological monitoring of workers after the application of insecticidal pyrethroids. Centers for Disease Control and Prevention (CDC). Atlanta (GA). Idel H. urban cohort.76(7):492-498. Int J Hyg Environ Health 2002. Hadnagy W. Becker K. Berger-Preiss E.Pyrethroid Pesticides References Baker SE. Third National Report on Human Exposure to Environmental Chemicals. Obel J. Environ Health Perspect 2006. Int Arch Occup Environ Health 2003.

240 (.143 (.160) .150) . sheet and pipe metal.430 (.260 (.122 (.170-.230) .240-.250 (.178) .200 (. 0.390-.190-.220-.120) .110-.156-.120-.260) .095-.400 (.176 (.114) .400) . 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.100) .340 (.200) .120) .210) . and glass.220-.280) .190) .310 (.160 (.150) .300-.560) .132 (.134-.350 (. and as a fire-retardant in textiles and plastics.310 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.090 (.130-.190 (.420) .160 (.290-.120-.190) .350) .460 (.360) .410-.410) . 7440-36-0 General Information Antimony is found in ores or other minerals.490) .230-.130 (.190 (.200-.410) .180 (.190 (.220 (.190 (.110-.210) .180 (.200) .140 (.130 (.150 (.115-.300) .510) .160) .250-.130 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.150-.170) .320-.220-.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 .120 (.170-.110 (. see Data Analysis section) for Survey years 99-00.160) .330 (.130) .140) .180-.130 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.108-.160) .220-.184) .320) Total .150) .130-.200 (.390 (.600) .350) .110) .320-.230) .180 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .250) .220) .260) .190) .100 (.095 (.500) .090) 75th .180) .087-.280) .080) . distribution.350 (.160-.180 (.160-.140) .220-.320-.080-.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 .470 (.360 (.190) . coal-fired plants.390-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite. or other substances containing antimony is another means of exposure. and pewter.300) .250 (.137) .197) .140) . population from the National Health and Nutrition Examination Survey. to a lesser extent.109-. fireworks.260 (.180-.240 (. ceramics.230 (. 0.134 (.154) .088-.340) .125 (.140) . ammunition.270 (.310 (.430 (.330) .390-.170-.158 (.136) * .137) .230 (.290-.260-.280) .128 (. and 03-04 are 0.080 (<LOD-. from air and drinking water.160-.103) .120 (.070 (<LOD-.440) .120-. water.080) .240) .135) * .470) . and +5.400 (.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 .180 (.150) 90th . and excretion of antimony vary depending on its oxidation state.200 (.140 (.157) . and refuse incinerators that process or release antimony.154-.350-.400-.148-.126-.290 (.210) .360-.300) .350-.270-.119) . The absorption.200 (.140 (.130-.400) .390) .280-.470) .130) .710) .220 (.130-.320) .530) .200-. interval) .200) .310-.108 (.280 (. storage batteries.130 (.150 (. enamels. 01-02.200-.140 (.180-.220-.120) .230 (.320 (.130-.300-.126 (.093 (. and 0.350 (.230-.320-.310) .140) .120 (.350 (.280-. Stibine is a metal hydride form of antimony used in the semiconductor industry.310) .150-.120) .280-.112-. Dermal contact with soil.120-.270 (.170 (.100 (.500) .119-.440) .130) < LOD . Antimony enters the environment from natural sources and from its use in industry. solder.350) .115) .146 (.390) .390) .141-.117-.099 (.310 (. < LOD means less than the limit of detection.170 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.490 (.360) .070-.098-.180 (.150-. which may vary for some chemicals by year and by individual sample.150-.110-.180-.270 (.190-.07.Metals Antimony CAS No.120-.180) .300 (.370-.230-. It is used in metal alloys. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110-.164-.210-. respectively.154) .070 (<LOD-.130 (.130-.132 (.200) . +3.120-.460 (.280-. castings.160) .200 (.130 (.145) Selected percentiles ( 95% confidence interval) 50th .04.230) .460) .200-.330) .220) .S.460 (.320 (.260-.570) .240 (.260) .300 (.270) . metal bearings.170-.130 (. It is also used in paints.240-.100-.240 (.280) .190-.145 (.220) 95th .310-.123 (.360 (.200 (.370) .136-.300-.330-.190-.140-.170-.160-.230-.260 (.270 (.140) .150 (.440 (.079-.161) .210) .169 (.105 (.390) .340 (.175 (.180-.160) .130-.250-.240 (.120 (.250 (.330) .330 (.350 (.330) .190-.120-.133) * .142 (.117-.350) .190 (.120-. Workplace exposures can occur at smelters.04.130) .150-.250-.430 (.220) .100-.270) .128 (.280-.210 (.090 (<LOD-.120 (.131-.250-.207) .210 (.280 (.090-.230-.400 (.330 (.120-.160 (.210) .330-. People are exposed to antimony primarily through food and.400) .190) .350-.144) .210-.090-.

105-.115 (.115-.076-.121 (.278 (.181) .068 (.098) .069-.161) .178 (.333) .125 (.167-.308-.200-.140) .188) .310) .30) .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 .207) .156-.185 (.192 (.092) .S.200) . Ming-Hsin et al.333 (.357-.371 (.118 (.241-.235-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.195-.181) .271-.352) .278) . population from the National Health and Nutrition Examination Survey.241-.421) .352 (.122 (.135) .280 (.250 (. 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.321) .108-.149-.320-.102-.136) .143) .135) .138 (.146-.148-. 1986).112 (.121 (.170 (.134) .119 (.178-.075 (.109 (.317) .147-.173-.741 (.187) .089) . 1953).185 (.189 (.186) .173) .122 (.146-.277 (.227-.153-.076-.092-.179-.078 (.194-.109 (.139 (.086 (.255) .199-.268) .200-.099-.095-.267 (.500) .192-.103-. interval) .131-.162-.069-.238 (.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 . 1954).176 (.082) . and kidney have been demonstrated in high dose animal studies depending on the dose.333-.130 (.333-1. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.253 (. liver.080 (.106-.417) .116-. 1988.120 (.338 (.159-.245) .129) .265-.214) . diarrhea. Acute antimony poisoning may cause a metallic taste.220) .248) .317) .255-.126 (.364 (.266 (.120 (.248-.414) .485) .148-.113-.193) .117-. resulting in hemolysis with abdominal and back pain (Dernehl et al.173 (.123 (. myocardium.250-.250-.172-. 1944).087) .124-.300) .128-.373) .191 (.132 (.250-. abdominal pain.071-.145) .Metals than for trivalent compounds (Elinder and Friberg.320 (. Histopathologic inflammatory and degenerative changes in the lung.364 (.225) .247) .265 (.135) .438) .129 (.106-.118 (.295 (.357) .114 (.159-.444) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.144-.224 (.163 (.124 (.154-.160 (.269 (.129) * .195 (.114 (..320 (.146-.111 (.127) .097-.121) .298 (.150-.082 (<LOD-.135 (.143 (.137 (.127) .112-.233) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al. and route of exposure (Elinder and Friberg.447 (.338 (.391) .131) .203) .074 (.259 (.161) .107-.310) .193 (.138-..203) .163 (.103-. 1986).099-.238) .127) .152) .085) . and gastrointestinal symptoms such as vomiting.143) .167 (.209) .120 (.075 (.084) .108 (.230) 95th . skin.208 (.727) .318-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.286 (.200-.313-. 1958) and occupational exposures (Briegner et al.229-. and ulcers (Werrin.211) .444) .124-.130) .308) .108-.143) Selected percentiles ( 95% confidence interval) 50th .391) .150-.119-. and eyes.405) . species.226 (.272) .380 (.256 (.204-.181) .123) .127 (.120 (.343 (.112 (.115) .250 (.081 (<LOD-.257) .167 (.176-.108-.320-.116 (.164) .176 (.086) 75th .213 (.338) .310 (..281-.267-.164 (.253-.171) .425) .239-.233 (.471 (.126-.430) .228 (.222 (.333-.195-.209) .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 .139 (.429) .183) .124) .140) < LOD .079 (<LOD-.175 (.276 (.117-.080 (<LOD-.115 (.385 (.119-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.192) .280-.111-.236 (.115-.114 (.198) .182 (.185-. 1973).300 (.098-.100 (.095-.400 (.126) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .098-.250-.230-.061-.261) .130) .138-.143) 90th .146) .115 (.131 (.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.081) .263 (.263-.320) .741) .102-.242-.188-.113-.109-.173 (.153 (.250) .147) .209-.125-.196 (.117-.208-.318-.159-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.205-.133) .130) .151) .228 (.333 (.164-.167 (.471) .333 (.156 (.317) .113) ..300) .082) .149) .135 (.107-.129 (.294) Total .315) .138) * .480) .244-.068-.104-.148) * .429 (.132) .107-.238) .417) .288 (.077) . Inorganic antimony salts irritate the mucous membranes.096-.209 (.228-.267) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.127) . 1995).104-.333-..152) . 1962).217 (.225 (.233-.206-.

environmental levels) and health effects is available from ATSDR at: http://www. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. 2004. eds. Delves HT. Vouk VB. VI. References Berman JD. Ludersdorf et al. In: Friberg L.13:361-362. Chia-Yu H.. Friberg L. Antimony. Biological assessment of exposure to antimony and lead in the glass-producing industry. Alimonti A. External and internal antimony exposure in starter battery production. Biomonitoring of a worker population exposed to low antimony trioxide levels. 20012002.51:238-240. Wu M-T. 1991.e. 1998) or compiled reference ranges (Hamilton et al. J Trace Elem Med Biol 2002. Dezateux C. Ju-Sun P. Industrial Medicine and Surgery (Dec. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Pozzoli L. Leinemann M. Ho C-K. respectively. Environ Health Perspect 1998. Antimony in blood and urine of infants. Ming-Hsin H. stibine. Piatnek DA. Urinary antimony in infancy. HH. J Clin Pathol 1998. even when exposure levels were below workplace air standards (Bailly et al. 1990. gallium. Sabbioni E. arsenic. Pilgrim L. Dernehl CU. et al. 1998. Chemotherapy for leishmaniasis: Biochemical mechanisms. Industrial antimony poisoning. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Iavicoli I. Luedersdorf R.. Chin Med J 1958. Earlier measurements in general populations (Minoia et al. Cordasco EM. Gallorini M. Skulsukai G. Arch Dis Child 1997. and hydrogen sulfide. Carelli G. O’Regan M.S.76(2):103-115. Schaller KH.cdc.48:93-97. Wade A. Handbook on the toxicology of metals. Schacke G. Stone FD. Stead FM.. and a drinking water standard has been established by the U. Cheng-Wei L. gov/toxpro2. Atlanta (GA). 1995.521-523. Paschal et al. Trace element reference values in tissues from inhabitants of the European community I. Kiberd B. Fuchs A. Arsine. Liao Y-H et al.. Minoia C. Review of elements in blood. 1998). Lauwerys R. Lenert G.46:931-936.. Br J Ind Med 1991. Element reference values in tissues from inhabitants of the European community. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Kentner et al. Antimony trioxide is rated by IARC as a possible human carcinogen. Shao-Chi C. Costeloe K. Chest 1973.. Industrial Medicine 1944.67:119-123. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. or exposure differences. J Occup Environ Med 2004. 2002.. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . EPA. Sci Total Environ 1994. Delves HT. Sabbioni E. Petrucci F. and future strategies. Stasney J.. Bailly R. Van der Venne MT. Liao Y-H. Matthews T.76:432436. Mayer P. plasma and urine and a critical evaluation of reference values for the United Kingdom population. 1987). and antimony in optoelectronic industry workers. 2005.html. clinical efficacy. Nau CA. 1997). and 2003-2004.158:165-190.. Elinder CG.106:33-39. Gebel TW. Roland H. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Buchet JP. Third National Report on Human Exposure to Environmental Chemicals. Pietra R. Bolten C. Semisch CW. Briegner H. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Iavicoli et al. population. pp. et al. Kentner M. Apostoli P. Nordberg GF. Information about external exposure (i.59:469-474. 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. 1994) have reported values slightly higher than those in this Report. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Chen J-R. Weltle D. Centers for Disease Control and Prevention (CDC). Rev Infect Dis 1988. Yang C-Y.16: 33-39. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Pulmonary edema of environmental origin. 26-42.Metals to antimony have been established by OSHA and ACGIH. Mayne P.)1954. Dunkelberg. Mahieu P..atsdr. Suchenwirth R.64(2):182-185. Biological monitoring of exposures to aluminum. Stocks J. 1986. which may be due to methodologic. Caroli S. Dezateux et al. Int Arch Occup Environ Health 1995. Cullen A. indium.. Hamilton EI. Int Arch Occup Environ Health 1987. 2nd ed. et al.. Yu H-S. Konings J.10(3):560-586. New York: Elsevier. Kuo-Juie Y.

27:38-45. Renes LE. Jackson RJ. Pirkle JL. Trace metals in urine of United States residents: reference range concentrations.99-108.95:89-105.76(1):53-59.Metals in urine. Antimony poisoning in industry. Paschal DC. Industrial Hygiene and Occupational Medicine 1953. blood. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Ting BG. Sci Total Environ 1990. Chemical food poisoning. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Werrin M. Sampson EJ. Morrow JC. et al. Environ Res 1998. and serum of Italian subjects.

and in lead-acid storage battery grids. trimethylarsine oxide. The United States no longer produces arsenic from mining but imports about 22.55 (7. the smelting of copper.0-19.8) 34. and other metals.90 (7.3) 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. and as a cosmetic to lighten complexion. Arsenic is measurable in most soils.4-65.6 (15.90-11.5 (40. lead. to a lesser extent.8) 33. arsenic as elemental metalloids may be used in some ammunition.5) 66.9-46.7) 24.S. Water sources contain mostly inorganic arsenate.70-9.12-10.90-8. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. copper arsenates. Before the 20th century.6 (13.9) 68.34-9.1) 290 725 1542 03-04 03-04 9.4 (24.6-141) 53.4) 40. see Data Analysis section) for Survey year 03-04 is 0.00-9.4) 60. and play sets.90) 75th 16.57) Selected percentiles ( 95% confidence interval) 50th 7. from coal burning.90-7. Arsenic and its compounds have had many uses in the past and present as medicines.1) 15.0 (14.000 metric tons annually.0 (15. Arsine (AsH3) is a reactive. Since the 1940s.2 (12.50-14.2) 46.0 (43. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. cacodylic acid.4) 13. In nature.1-40.7) 65. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. grain.6) 11.70) 8. it is found in over 200 crystalline or mineral forms.50 (8. lead hydrogen arsenate. Gallium. and gray forms). and arsenosugars. interval) 8.5) 43.66-8.41 (7.34-10.8 (48.4 (26.4 (31. arsenocholine.2) 15.5) 95th 65. population from the National Health and Nutrition Examination Survey.9 (8.80-9. referred to as inorganic arsenic compounds.2 (51.5-52.80) 6.90 (5. 2005). and indium arsenides are used in the semiconductor industry. cancers.6) 618 722 1074 Limit of detection (LOD.1) 7. to a lesser extent.1) 1281 1276 03-04 03-04 03-04 9.0 (22.3-111) 78. 180 Fourth National Report on Human Exposure to Environmental Chemicals . +3 and +5). though in some locations arsenite may be prevalent (WHO.1-18. General population exposure to inorganic arsenic can occur through consumption of drinking water and.3-19.5) 41.90 (7.40) 7.7) 90th 37.90-8.30 (7. particularly arsenic trioxide. mental disorders.2-17. mostly for use in wood preservation (ATSDR.80 (5.9) 21. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.8) 29.2-20.8) 30. Although it is still widely used in the United States.6 (9. and. or rarely as elemental metalloids (yellow. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.27) 9. retaining walls. solders.02-8.10 (6.1 (32.5 (36. arsenic compounds.4 (48. psoriasis. as alloy in metal bearings.12 (6. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. Arsenic trioxide (As2O3.Metals Arsenic CAS No.5-41. such as arsenopyrite (FeAsS) and realgar (As4S4).3-15.20 (8. alloys.10-7. semiconductors.5 (34.5 (23.5-178) 46.2-93.13-8.00 (6.8-61. gaseous hydride manufactured in small quantities for use in the semiconductor industry. and arsenates (oxidation states of -3. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.4 (7.0 (11.84) 8.84) 8.30) 17.10) 10. were used as treatments for syphilis.5 (14.5-19.77) 6.97) 8.9-34.30 (6.3) 10.8-77. and produce.2-61. pesticides.74.29 (8. meats.9 (17. ocean and fresh waters. black.10-10.6-43. Arsenic trioxide is approved to treat acute promyelocytic leukemia. and foods. arsenites.8) 17.25-9.90-14. Survey years 03-04 Geometric mean (95% conf. sodium arsenite.9-62.2 (41.7 (11.0-60. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. In the last century. 2001). chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.19-9.90) 16.8) 7.6-35.7-83.7-95. Various arsenic compounds were used in paint pigments and for tanning animal hides.08 (5. and as homicidal poisons.70 (6.2 (13. aluminum.8) 7. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.6 (32. Also.1 (38.

2001.45) 5.4) 54.10-16. EPA’s maximum contaminant level (Hughes. In aquatic organisms. Smoking tobacco is also a source of inorganic arsenic.2) 40. population from the National Health and Nutrition Examination Survey.0) 1281 1276 03-04 03-04 03-04 8.. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. 2001).7-17. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.S.4) 32.3 (24.00 (6. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. 2006. and folate status (Chen et al.0) 33. gallium arsenide and indium arsenide.4-64. dose level.1-36. 2001. The semiconductor dopants.2) 90th 30.8 (11.4 (40.8 (27.0) 42.. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.3) 6. shellfish.1) 7.5) 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 (7.8-32.23-7.06 (4. kelp.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . 2001).4 (42. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. Inorganic forms of arsenic demonstrate high acute toxicity. 2007.12-10.47 (6. Tseng. cacodylic acid and monosodium methyl arsenate.20-9.1) 6.0-26.47-6. 2001).. 2007.50 (6.18 (5.44-11. Though modest bioconcentration occurs in some aquatic life.g.5) 17.8-62.35) 7.31 (6. dust. inorganic arsenic is widely distributed within the body.04 (5.93-9. 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. 2003.0 (31.8 (12.86-17..6) 45.66 (7.3-62. 1988). Gamble et al.10-8. The reduced form of MMA (oxidation state Urinary Total Arsenic (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. After absorption.44) 6. are used in enclosed ultraclean operations within the semiconductor industry. 2001).32 (5. though some reduction may occur in the gut prior to absorption.6-17. and arsenosugars.4 (11. Extremely high groundwater arsenic levels.0-38. 2001). mine tailings). 2001).81-9.01) 7.99-9. selenium.13) 8.S. NRC. EPA.7 (9. Children may have additional exposures from ingestion of contaminated soils (e.5-120) 40. WHO. Chowdhury et al.40) 8.25-9.6 (10.0) 12.9 (45.2 (12.2-15. arsenocholine. 2001).5 (9.3-41.3) 9.0-69. U.64 (7. WHO.7-188) 27.4 (12.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.25 (6.93-8.0-18. Steinmaus et al. Arsenate is reduced in the body to arsenite (oxidation state +3).9) 53.04) 7.8 (20.1 (11.33-10. as observed in Bangladesh where millions of people have been exposed.9-56.6 (17. 2006.0) 26.58-10. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.07-9. 2007.11 (5.7-18.51) 75th 14.38-10.4 (24.0 (17.2-46.1) 8.8 (21..0) 14.5-17. Direct exposure to DMA and MMA may result from use of the two pesticides. In aquatic sediments.96) 12. arsenic does not show biomagnification in the food chain (WHO.1) 58.7-34.8-75.66-8.47 (7. trimethylarsine oxide (TMAO).76 (6.88 (5. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.2) 15.4 (26.75) 13.7 (25.28-7. and some other seafood can contain organic forms of arsenic including arsenobetaine. Survey years 03-04 Geometric mean (95% conf. 2001).3 (27. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.7-35.9) 13.5) 290 725 1542 03-04 03-04 8. age.. so exposure to the general population is extremely limited. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.7) 28. organic arsenic can be converted back to methylated and inorganic arsenic.6 (35.S.88) 7. Fish.24 (7.01) 11.8) 22.59) Selected percentiles ( 95% confidence interval) 50th 7.30-9.33 (6. have caused clinical arsenic poisoning.7 (11.8) 27.41) 6.3-64.75 (5. but is poorly absorbed dermally (WHO.66-8.7) 95th 50.1 (14. and contact with CCA-preserved wood structures.1) 24.3-53. interval) 8.

2006.S. WHO.S. which can lead to dehydration and shock.60) 1. Cohen et al.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. and hyperpigmentation of the skin (NRC. NRC. population from the National Health and Nutrition Examination Survey. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. 2001. 2007. food residue.... 1998..20 (<LOD-1. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 2006.10 (<LOD-1. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. 2001). hepatotoxicity. Chronic arsenic exposure in humans is considered to be a cause of skin. can cause peripheral sensorimotor neuropathies. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. and endothelial injury (Kumagai and Sumi. drinking water have not been associated with increased cancer rates (Schoen et al. arsenic trioxide) includes hemorrhagic gastritis with nausea. 2001). 2001). 2006. Chronic elevated arsenic intakes have been associated with diabetes. Acutely.EPA.50) 621 725 1078 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. 2007. but additional or confirmatory research is needed (Kapaj et al. 2001).20 (<LOD-1. With chronic exposure. Studies of arsenic at levels typical of U.. 2006) or when exposure occurs in smokers (Chen et al.0. 2000.60) 1. including drinking water sources with elevated arsenic levels (e. gluconeogenesis. WHO. U. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.. hyperkeratosis..S.. 2004). 2001)..EPA has established drinking water. apoptosis. including inhibition of numerous enzymes.g. Although arsenate is reduced in the body to arsenite. fatty acid oxidation. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. and bladder cancer (IARC. substitution in phosphate metabolism. interference in signal transduction pathways. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. renal failure.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. lung. WHO. 2001).10 (<LOD-1. Survey years 03-04 Geometric mean (95% conf. hematocytopenias.50) 1. 2004. Bangladesh. The U... WHO. < LOD means less than the limit of detection. 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.20 (<LOD-1. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. 182 Fourth National Report on Human Exposure to Environmental Chemicals . Cellular glucose uptake. vomiting. some of these effects may take years to develop. see Data Analysis section) for Survey year 03-04 is 1. Chile).20 (<LOD-1. Arsenic has many actions demonstrated in cellular studies. increased oxidative stress.10 (<LOD-1.10 (<LOD-1. NRC. leading to a decrease in adenosine triphosphate energy production. Chronic human intake of arsenic at less than acutely toxic doses. respectively. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. and childhood neurodevelopmental effects in observational human studies. and diarrhea. Such actions may lead to decreased energy production. hypertension.30) 1. Cardiac arrhythmias.. and it also will inhibit succinate dehydrogenase. 2001. Raml et al. Bredfeldt et al.10 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. cell transformations. peripheral vascular disease. Taiwan.S.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 2007). and altered gene expression. The organic forms of arsenic occurring in seafood have little known toxicity. and production of glutathione may be affected as well. and DNA repair inhibition (Cohen et al. cytotoxicity. noncirrhotic portal hypertension. and by uncoupling oxidative phosphorylation (NRC.80) 1.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 2004).g.

1999). In animal studies. 1986).. DMA produced bladder cancer in some chronic rat studies (Cohen et al.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2007. 2006.00) 1. 1998. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.. 1999... 1992... 2001). WHO. Offergelt et al. 2000.S. 2004. gov/toxpro2. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. arsenic has been fetotoxic and teratogenic. Pellizzari and Clayton...41) 3. 2006).70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Calderon et al. Compared with this Report. Valenzuela et al. Pellizzari and Clayton 2006)... In a Nevada town where groundwater levels were naturally elevated.. 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. 2006).html..75 (<LOD-2. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.cdc.. Consequently.80 (<LOD-4.. 2006).S. 2000).S. Survey years 03-04 Geometric mean (95% conf. 2001). population in NHANES 2003–2004 (Schulz et al.. 2004. 2006. but generally only at maternally toxic doses (WHO. 2008. and the FDA has established a bottled drinking water standard. Vahter et al. Levels of total urinary arsenic in the U. Pellizzari and Clayton. environmental levels) and health effects is available from ATSDR at: http://www. Caldwell et al. 2006.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. In the German Environmental Survey III of 1998..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.. median urinary total arsenic levels in 4052 adults varied with seafood intake. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2003.18 (<LOD-3. 2008).. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2006).33 (<LOD-3.50) 1.04 (<LOD-3.19) 3. 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. Josyula et al. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.. 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. 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. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2001). IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.33 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. Fourth National Report on Human Exposure to Environmental Chemicals 183 . and were about two-fold lower than those for the U. although urinary arsenic levels were not associated with CCA contact (Shalat et al.. Caldwell et al.S. population from the National Health and Nutrition Examination Survey. Shalat et al.75 (<LOD-2.e..69 (<LOD-3. population (Rubin et al. Shalat et al. 2008).. 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. Meza et al.Metals compounds.atsdr.. had decreased since the prior 1990– 1992 survey. 2007. 1999.18) 3.61 (<LOD-3. Additional information about external exposure (i.

6.90-7.00-12. WHO. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.30 (2.10 (4.500-1.8 (12. 2007) with higher levels of arsenic in the drinking water. MMA. In the residents of a Chilean town who consumed water with high levels of arsenic.48-2. 1990.40) 5. China.400-.. In most human studies. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. 2005.800 (. The higher percentiles of total urinary arsenic levels in the U. and other factors such as nutrition. Measurable organic arsenic species in this Report are three biologically generated environmental forms.0 (26.66 (1.20 (4. 2008)..0) 29.1) 18. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1996. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.S.S. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. vasospasm.74 (1. Tseng et al.5) 32.20 (2.80-5. 184 Fourth National Report on Human Exposure to Environmental Chemicals .80 (4.20-3. population in the NHANES 2003–2004 subsample.10) 8.28) 1.70 (3. and duration of exposure are also considered important..50) . Blom et al.90-29. 2008).62) 2.4 (16.20) 7.20) 18.6 (25.8-50. 4. arsenite.6-44. Survey years 03-04 Geometric mean (95% conf.00 (1.3% of a representative sample of the U.7 (13. Some noncancer effects of arsenic (e.80) 1.9) 13.800-4.0) 4. and TMAO were detected in only 7.17-1.70-21.55 (1. when seafood organic arsenic is subtracted)..70) 6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-35. arsenobetaine.20-190) 31. interval) 1. Valenzuela et al.6 (11. 2005..0-23.6.29 (1.11-1..20 (. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.600 (.4) 31.. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.7 (21. Aposhian et al.9 (7.8 (17.40-6. and 0. population from the National Health and Nutrition Examination Survey.Metals other areas of the world (Ahsan et al..10) 4.5) 621 725 1078 Limit of detection (LOD.3) 35..70 (5.50-6.00-4.3) 1284 1284 03-04 03-04 03-04 1. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.50) . 2000.800 (..43-1. population showed a higher contribution of arsenobetaine (Caldwell et al.4-35.. For residents of Inner Mongolia.3 (21.4.7-22.3) 95th 35. 2005. 2008. see Data Analysis section) for Survey year 03-04 is 0. and two methylated metabolic products. and TMAO.60) 1.2-38.37 (1.50) 90th 16.1-25.800-1..30 (1. Individually measurable species resulting from inorganic arsenic exposure are arsenate.40) 75th 5. Caldwell et al.9 (6.5) 292 728 1548 03-04 03-04 1. 1.8) 35.00 (. geometric mean levels were about 70-fold higher than for the U.20) 3. methylation capacity.S.00-6.871-1.6 (13. arsenocholine. Sun et al.. dermal keratosis.68) . Pellizzari and Clayton.S.30) 10.900 (.2 (6. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.00) 3.g.8. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.900-1. arsenocholine. Caldwell et al. 2000.80 (3.60-3. When seafood intake is avoided. arsenite.20-25.800) 1. 2006).83) Selected percentiles ( 95% confidence interval) 50th 1. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. 2007).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 * * 1.3 (9. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.20 (1. in NHEXAS 1995–1996.93) 1.80 (.00-1. Also.8-40. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.1-51.40-7.4) 23. population (Sun et al. with DMA. population (Ahsan et al. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.... In the late 1980s. After recent seafood ingestion...1-94.5 (26. DMA and MMA. 1985.0 (27. These associations are stronger at higher urinary levels.e. 2001).7) 15.05) < LOD . Caceres et al. 2008.5 (14.5) 29.45 (1.31-1. Chowdhury et al. < LOD means less than the limit of detection.1) 45. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. Caldwell et al.700-1.700-1. 2008). 2008). 2003).9-23. 2001.S.7) 13.70-21.. respectively. 2000.3-39. Arsenate.30) 2. which may vary for some chemicals by year and by individual sample.19 (..

Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.61-6.938-1.8) 29. 2001).68 (1.1-36.1-18.6-32..51) 5.9 (13.9 (25.62-6. Sun et al.37-2.80-153) 17.18-1. 1998.11 (.786-1.9 μg/L.53 (.9) 14.400-.05 (.29-14. 2003.25 (.65 (1. 1992.3) 1284 1284 03-04 03-04 03-04 1.25-7.67) 4.64-29.. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-36.93 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.28) 1.12) < LOD .40 (1.6 (9.638) 1.44 (1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. 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. WHO. Vahter et al.10 (. Fourth National Report on Human Exposure to Environmental Chemicals 185 .82) 4. not to imply a safety level for general population exposure.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 * * 1.901-2. Offergelt et al.1) 26.9) 32.4) 292 728 1548 03-04 03-04 1.91 (4.0 (9.67) 1.5 (18.78-5.2 (13.16 (.3 (10.6 (6.05) 1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2007).4) 32.959-1. 2008)..29 (4.00 (3.. population from the National Health and Nutrition Examination Survey.47 (1.30) 1.00 (1.3-24.1 (26.79 (1.82) Selected percentiles ( 95% confidence interval) 50th 1.5-20.15-1. interval) 1.70) 5.43) 75th 5.2 (12..3 (10.6) 19.4-82.. 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.73-6.39-3.55) 1. 2001).88 (5.32-7.5) 26.877 (.7) 9.4-21.4) 13.50-15.13-39.47 (2.15-1. 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.15-4.6-29.58 (3.9-18.612-1.36) 2.7) 17. 1986. 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.83) 2. 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.5) 17. Information about the biological exposure indices is provided here for comparison.2 (12.40) 1.21) 5. which is below the ACGIH BEI (Caldwell et al.6-46.531 (.30-1.Metals as with DMA. Caldwell et al.50-7. 2008)..3) 95th 29.7) 30. population for the sum of inorganic related species was 18.78 (3. Survey years 03-04 Geometric mean (95% conf. In recent years.4-28.19-2.76-27.909-1.91) 90th 16.81 (4..72) 12.51-2. The 95th percentile of the U.83) 8.88) 2.S.4 (11.4 (24.43) 14.2 (4.14 (1.833-1.S.80) .5 (18. 2006.45) 1.54 (1.

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

Survey years 03-04 Geometric mean (95% conf.S.40 (<LOD-1.00 (<LOD-2. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.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.S.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 187 . Urinary Arsenous (III) Acid (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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08 (<LOD-4.00) 1.20 (<LOD-1.95 (<LOD-2. population from the National Health and Nutrition Examination Survey.2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 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.00 (<LOD-3. Survey years 03-04 Geometric mean (95% conf.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.44) 2.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

3 (8.1 (8.00 (3.00 (5.0) 292 728 1548 03-04 03-04 4.00 (6.97-3.45 (8.00-7.48 (2.78 (4.27 (3.67) 8.6 (9.27-5.31) 4. Survey years 03-04 Geometric mean (95% conf.0) 11.00-13.00-11.0 (10.0 (8.0) 17.38 (3.00 (5.65-6.37 (3.86-21. interval) 3.0 (11.90) 5.00-8.50-15.70-3.0) 9.34-4.00 (5.77 (3.0-12.70-12.37 (2.20) 11.15) 4.70-4.33-4.0) 13.10) 3.60-7.92) 3.00-7.79 (3.45) 3.00-10.7) 13.7 (10.9) 5.9 (7.11) 4.16 (4. interval) 3.7) 12.19) Selected percentiles ( 95% confidence interval) 50th 3.00) 4.05) 5.31-4.0 (14.00 (3.0) 12.55 (2.27-2.00) 90th 11.00-4.00-4.3 (7.74) 90th 9.05) 10.S.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.00 (5.49-4.80) 2.6) 292 728 1548 03-04 03-04 3.16 (2.98) 4.00 (4.71) 3.27 (2.82-5.0 (9.0-17.0 (12.95-6.S.24-4.03 (3.71-4.00) 6.32 (8.30 (7. population from the National Health and Nutrition Examination Survey.95 (4.80) 7.12 (3.5) 12.88 (4.00-7.0 (13.00-12.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.94-3.00) 3.6-18.0) 14.00-4.5) 95th 13.00 (3.34 (3.71 (4.44 (2.00 (5.00-11.48 (3.4 (7.00 (3.00) 9.00-22.00-4.44) 5.0-16.25 (4.00) 6.0-17.8) 7.80-3.00) 6.0) 95th 16.49) 10.22) 4.0 (10.00-7.10) 6.06) 5.60-4.57-5.03-6.00) 4.7.30) 3.90 (3.80 (4.00-3.61-11.0 (10.11 (3.84-8.67) 9. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.82) 3.62) 4.69-6.0-18. Survey years 03-04 Geometric mean (95% conf.00-5.1-18.00-9.82-9.34) 3.32 (4.92-12.0 (9.29-4. see Data Analysis section) for Survey year 03-04 is 1.16-11.00) 3.34-4.80-5.0 (13.6) 1284 1284 03-04 03-04 03-04 4.24) 3.00) 7.09 (7.57 (3.00-11.69-3.0) 13.20-12.00) 12.00-15.00 (3.50-5.78) 4.52) 3.0 (10.0-16.0-19.0) 16.86 (2.60-6.17-4.00 (7.39-3.69 (3.8) 7.90) 2.0 (12.14) 3.12-4.14) Selected percentiles ( 95% confidence interval) 50th 3.70 (3.84-18.00) 6.80-6.0) 621 725 1078 Limit of detection (LOD.0-25.0) 10.94) 3.33) 3.73) 6.72 (4.86-7.50 (4.00-4.65-8.59 (6.18 (6.00) 5.0) 17.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.91) 75th 5.61-16.0) 9.7) 1284 1284 03-04 03-04 03-04 4.7-16.00-15.2) 10.28) 2.74 (2.9) 12.89 (3.17-6.3 (8.60-3.00-3.45) 8.95-4.08 (2.00 (7.42) 3.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .00 (6.69 (3. population from the National Health and Nutrition Examination Survey.00 (6.17 (2.1-22.00-12.05) 3.00-4.0) 9.00-15.9) 13.0 (9.46 (4.00) 75th 6.32-10.85 (3.13-4.70) 5.34 (3.81 (5.71 (3.0) 11.20-4.0 (8.1-15.9 (11.95-3.73 (3.00 (3.0) 16.9) 11.5 (11.

40) 2.77) 1.22) 3.30-1.05-1.35-3.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.61) 2.10) 2.15-1.86) 3.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.88-2.85) 1.00) 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 1.14-1.81) 1.70-2.60) 2.18-1.30 (1.54) 90th 2.00-4.17) 2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.10-3.82-2.00) 1.43-3.36) 1.53 (1.50-2.50) 621 725 1077 Limit of detection (LOD.57) 95th 2.60 (1.20 (1.86 (2.853-1.70) 2.00) 1.07 (1.90 (2.34) 2.00 (2.20 (1.61-3. population from the National Health and Nutrition Examination Survey.31 (1. Survey years 03-04 Geometric mean (95% conf.73-2.52 (2.10 (.00-1.70-2.30 (1. population from the National Health and Nutrition Examination Survey.60) 1.22 (1.40 (1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.90) 2.90) 1.60) 2.00-1.80-2.50 (1.30) 1.30) 90th 1.40) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (1.07) 2.S.S.63 (<LOD-1.20) 2.80-2.45) 3.80 (1.28 (1. < LOD means less than the limit of detection.30 (1.80) 1.53-2.00) 1.37 (1.20 (1.985) 1.00 (<LOD-1.00-2.00 (<LOD-1.80 (2.33 (1.46 (1.90 (1.80) 1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9.50 (1.40 (2.816 (<LOD-.93) .30-2.82-2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.23) 1.90) 2. see Data Analysis section) for Survey year 03-04 is 0. Survey years 03-04 Geometric mean (95% conf.00 (2.00-2.07-3.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10 (1.86) 2.70-2.71-2.30) 2.79) 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .50 (2.86 (2.70-3.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.50) 1.40-3.28 (1.33 (1.20 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10) 95th 2.30 (2.70-2.88 (1. which may vary for some chemicals by year and by individual sample.40) 1.80 (1.84-3.40-2.96-2.900-1.50 (<LOD-1.11-1.46-2.20-3.30-1.36 (1.58) 2.40-3.62) 2.10 (.60-2.60 (2.30) 1.10-1.18-1.80 (1.10 (1.20 (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 1.85) 2.40-2.31-3.16 (2.88 (1.20 (1.20-1.10 (<LOD-1.80 (1.10-1.

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

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50 (1. it combines with other chemicals such as sulfur or carbon and oxygen.56) 1.50 (4.30) 4.24-1.15-1.S.9) 5.46) 1.82) 2.19-1.46) 1.09 (1.06-2.25 (1.44 (1.49) 8. barium sulfate and barium carbonate).26-1.40) 7.31 (2.17-1.57 (5.10-4.91 (2.64) 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 2.86 (4.80 (1.95-6.30 (5.75-3.80-3.21-2.71) 2.00 (1.65-1.41-3.80-5.57-7.54-1.87-14.29) 5.32) 8.30-3.00) 6.50) 2.03 (1.51 (1.53) 1.11 (3. respectively.10 (3.59) 3.70) 4.76-3.54) 1.99 (4. Workers employed by industries that make or use barium compounds can be exposed to barium dust.70-3.70) 3. and 0.51) 2.70-5.Metals Barium CAS No. Barium compounds are used by the oil and gas industries to make drilling muds.20) 2.16 (1.62 (1.80-7.86 (4.85) 1.21 (1.66 (4.09 (2.20 (4.05% of the earth’s crust.00) 1.25-11.00-3.65 (5.14-6.90 (1.80 (1.80-2.08 (6.88 (5.61-8.36-1.4) 7.70 (1.61 (1.30 (1.80) 6. In nature.12.92) 2.30) 5.60) 3.49) 4.16) 5.50) 2.49-1.22) 6.06-1.41-1. Some barium salts are freely soluble in water.65) 3.56 (1.51) 1.46-1. bricks.47) 4.4) 9.68 (1.15 (1.88) 4.00 (2.21 (1.80 (2. and food.08-8.70) 7. see Data Analysis section) for Survey years 99-00.18) 3.66) Selected percentiles ( 95% confidence interval) 50th 1.01-7.54) 2.10) 5.61 (3.04-2.87 (5.28-1.30-1.50 (1.65-5.37) 5.12 (2.30-2.43) 2. depilatories.12) 7.50 (1.32-7.69 (1.61 (5.8) 9.56) 4.14 (6.90-9. Certain foods. are high in barium (Genter.53) 2.43) 6.81-2.30-1.86) 6.20-1. population from the National Health and Nutrition Examination Survey.30) 5.15-1.60 (1.63) 1.60-10.40 (1.44-5.20-1.87-3.38 (1.40) 3.77-3. soluble forms of barium.80) 1.43 (5. such as barium chloride.12-1.20-6.48-4. 2001).43 (1.20-1. and ceramics. In single dose animal studies.56 (2. Fourth National Report on Human Exposure to Environmental Chemicals 193 .8) 5.20-1.87-9.53-5.50 (5.35 (3.00) 1.10 (2.01 (4.24-1.64-3.20-5.39) 1.63 (8.48) 1.73-5.29-5.10) 3.75) 2.73) 3.49) 2.24 (4.48) 1. fireworks.12 (2.37-1.72) 4.34 (1.40 (5. such as brazil nuts.54 (2.47-1. and 03-04 are 0.38) 8.91) 2.72) 75th 3.42 (1. tiles.61 (1.20-8.20 (3.50 (1.40 (5. Barium compounds are also used commercially in paint.27 (1.50-1.28) 90th 5. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).20-8.55-7.76-7.81-3.10) 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. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.85) 1.25-1.50 (1.38 (1.74-3.71) 95th 6. glass.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 1.70) 1.12) 6.65-8.50-6.73 (6.22-1.31-2.76) 1.71-9.77 (3.93-2.60) 1.8 (6.11-1.54-8.76 (3.39) 4.90) 1.34 (1.39-1.35 (1.00) 4.45 (1.65) 1.70) 5.35-1. 7440-39-3 Medically.87) 7. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50-1.81-2.67) 6.45) 7.71) 1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Small amounts of barium can be released into the air during mining and other industrial processes.88) 7.87 (6.34 (2.70) 1.02 (7.60-6.37-8.93-8.86-5.30) 5.4) 6.36-1.30 (3.60-2.54-1.33 (1.62) 1.36 (4.50 (6. Barium salts have also been available as rodenticides.18-1.18 (6.30) 2. water.48-4.50) 1.30) 8.86-4.04-6.87-7.11 (2.40 (1.72) 1.40-13. 01-02.54) 1.00-76.36 (1. whereas others are practically insoluble (e.76-2.10-5.56 (1.29-1.10 (4.37 (4.1) 9.21-8.26-7. The general population can be exposed to low amounts of barium in air.99-5.73) 1.85 (2.15 (2.15) 5. 0.70-6.78-2.65) 1.52 (1.20 (1.30 (2.94-6. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.41) 1.50 (2.11 (3.15-11.90-13.40 (5.90) 2.90-2.54 (6.64 (1.g.97 (1.60-3.73 (5.74) 3.71 (2.70 (5.63 (2.88) 1.60 (2.15 (6.51) 7.70-8.49) 11.48 (6.32-1.82) 1.30-2.82-6. interval) 1.80 (5.77) 1.52 (4.31.49-9.27) 2.96-2.40) 7.37) 1.26) 5.70-2.57) 3.74-2.27 (1.56 (6.50 (4.63 (5.26) 2.78-3.05-2.84) 5.62 (1.80) 7.50-6.36) 5.19) 2.14-1.60) 1.63) 1.35-4.50 (3.38) 2.30-5.90) 2.63) Total 1.44-2.22-1.60-6.2) 6.07 (2.47-1.55-3.70-2.30) 3.78) 1.60) 4.40 (4.78) 1.43 (1.91) 6.40 (1.62) 1..90 (4.35 (2.39 (1.95 (4.35-1.63 (1.93 (4.49 (1.61 (2. rubber.90 (6.35) 5.59-11.12.98) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00-8.80 (1.80 (2.20-8.90) 4.30 (5.50) 4.50 (4.34) 2.39 (1.

02-5.38) 4.30 (1.11-2.41) 5.47) 1.24-1.99 (2.80) 4.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.58) 75th 2.31-1.16-1.51) 4.60 (5.50) 1.81-6. vomiting.20) 4.31 (1.24 (3.51 (3.01 (4.40 (1.2) 6.78 (2..65 (2.98 (2.26-1.96) 4.86-7.00) 4.06) .24-3.57 (6.00) 6.52-4.29-4.52 (3.46) 3.777-1.22-2.32 (1.76-3.36 (1.68 (3.60 (1.38 (4.45-1. a benign condition that may occur among barite ore miners.80) 3.92) 2.74 (5.915 (.0) 6.22-1.00) 1.39) 4.58) 4.64) 7.59) 1.24) 3.41 (1.3) 6.10-2.46) 2.97-4.35-1.49 (1.64 (1.77) 1. Symptoms following acute high dose include perioral paresthesias.26-1.52) 1.96) 7. Toxicity from soluble barium salts is rare.52-10.70) 1.36-2.68 (2.84 (3.01 (5.59 (1. 1994.30) 2.26-1.64 (1.16 (1.62 (4.10) 6. paralysis.20-2. The health effects of exposure to barium compounds depend on the dose.27) 7. Insoluble barium salts.33) 6. diarrhea.51) 4.29-4.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .37 (1.73) 2.25-11.23-1.96-6. 1985.50) 1.47) 10.49-1.83) 3. hypertension.00) 4.64) 7.33 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter. and cardiac dysrhythmias.08-2.39-10.65 (5.905 (.89) 90th 4.55 (5.39-1.36 (5.68) 1. NTP.28-11.38 (4.04) 5.0) 7.33-4.03) 2.38-7.832-1.60 (2.84) 2.70) 10.56 (1.40 (1.46) 1.39 (3. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.56) Selected percentiles ( 95% confidence interval) 50th 1.891 (.48-3.710-1.59-7.19-1.881 (.03-1.74) 1.51 (1. are not absorbed when administered.45 (1.73-2. 1986).36 (3.39-1.60) 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 2.45 (3. 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.35-3.29-7.08-1.41) 4. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.55 (4.45-1.31 (4. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.58 (2.47) 4.72) 4.00 (3.02 (3.71 (5.69-9.38-1. Chronic high doses in animals resulted in kidney damage (McCauley et al.57-7.97-3.88 (6.72 (2.40-1.86) 5.00 (3.10-1.61) 2.57) 2.10 (6.66 (1. interval) 1.76 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.921 (.4 (5.54) 1.74) 1.03-1.18 (1.754-1.22-4.38) 1.13-2.19-1.29-1.55-5.28-7.48-1.41 (1.26) 4.52) 2.28 (1.20-1.24-11.84-2.56-3.31) 5.32 (2.89 (2.28-1.51-3.26-1.59 (1.91 (3.39-5.56) 4.60 (2.48 (1.50) 2.24-1.55-6.77) 1.22-1.75) 1.46-22.37) 2.48 (1. population from the National Health and Nutrition Examination Survey.00-1.33-1.77) 1.69 (5.60 (1.57-10.29) 1.18 (1.25) 4.14-2. 1990).34-1.02) 4.88 (2.51) 6.43-6.84-5.44 (1.43) 1.81-7.59) 1. Perry et al.48) 2.35-1.03) 1.62 (1.33 (1.52) 7.37 (1.75) 2.75) 1.12) 2.76) 1.36 (1. Following intravenous injection in animals.963 (.24-6.39 (2. Wones et al.49-1.36-1.05-1.58) 1.32 (1.33 (5.48-5.68-3.37-1.87) 1.70) 4.76 (2.32) 2.27-1.64 (1. water solubility.75) 2.28) 5.880-1.62 (2.38 (1.77) Total 1.2 (3.79) 1.72) 6. in urine.19-1.99 (4.83) 2.29 (1.11) .00 (5.3 (6.54) 2.82) 1. such as those used in medical radiographic procedures.29 (3.50 (4.63) 1.15-4.26-4. chemical form.97 (5.39 (2.96 (4.91-2.32) 2.38) 1.53 (2. weakness.19-2.45) 1.97) 1.48 (1. and route of exposure.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 1.23-2.55 (1.76) 2.75-3.Metals was eliminated primarily in feces and to a lesser extent.11) .31-1.42) 1..91) 2.38-5.82) 1.40 (1.703-1.03) 3.38 (1.85-5.75-22.00 (2.79-5.39 (2.76 (3.21 (1.54 (1.45) 95th 6.24 (5.16) 11.20 (1.20-8. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.58-6.01) 1.99) 1.56 (1.25 (1.51 (1. 2001).29-3.47) 1.73-4.45-8.49 (1.36 (3.S.53-21.28-6.47 (2.47 (5.47-8.91 (3.34 (1.44-2.53) .04 (2.96) 4.30 (1.92 (4.62) 2.54 (2.64 (1.57-5.34-5.37-2.96) 4.86 (2.76) 2.55) .36-1.63-4.33) 1.81-6.97 (4.44-2.61 (4.46 (2.90-2.42) 1.24-6.58 (4.2) 5.68) 3.77-5.10) 3.06) 2.80-6.31-1.27 (2.67-6.27-3.55 (1.45-6. 1984.02) .04) 1.0) 5.34) 1.4) 5. Barium is not rated for human carcinogenicity.23-5.59) 2..8) 4. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.77) 5.42 (4. 1989).41 (2.09) 6.68 (3.68-3.96 (4.00-7.49-1.13-3.34-3.

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

and volcanic dust. nuclear.Metals Beryllium CAS No. Low-level beryllium exposure in the general population can occur through breathing air.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 . 01-02.160) < 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. Beryllium compounds are commercially mined. and dental bridges.13. eating food. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.130 (<LOD-. 7440-41-7 General Information Pure beryllium is a hard gray metal. and refined beryllium is used in mirrors and special metal alloys for the automobile. and from breathing tobacco smoke. coal. Two types of minerals. and 03-04 are 0. x-ray machines. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 0. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. bertrandite and beryl. 0. electrical. 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 . In medicine. 196 Fourth National Report on Human Exposure to Environmental Chemicals .140 (<LOD-. population from the National Health and Nutrition Examination Survey. and can be found in mineral rocks. the lightest of all metals. < LOD means less than the limit of detection.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 . aircraft. or drinking water containing the metal. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. In studies of laboratory animals. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. respectively. near some hazardous waste sites.13. soil. are mined for commercial recovery of beryllium. Exposure to beryllium occurs mostly in the workplace. see Data Analysis section) for Survey years 99-00. beryllium is used in instruments. computer. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.13. which may vary for some chemicals by year and by individual sample. and machine-parts industries. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.S.130 (<LOD-.

interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . based upon excess lung and central nervous system cancers in studies of workers. population from the National Health and Nutrition Examination Survey. which produces pneumonitis. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Maier. or berylliosis. S. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. IARC has classified beryllium as a human carcinogen.S. respectively. EPA. and drinking water and environmental standards have been established by U. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. 2003. NTP considers beryllium to be a known human carcinogen. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. Chronic beryllium disease.281 (<LOD-. Skin exposure can result in delayed hypersensitivity reactions. 2002). 1990). Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. including contact dermatitis and subcutaneous nodules.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 .346 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 197 .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.231 (<LOD-.

Pirkle JL. Apostoli P. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Pozzoli L. Available at URL: http://www. population were generally undetectable in NHANES 1999-2000. Sci Total Environ 1994. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.13 μg/L. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Costa R. Int Arch Occup Environ Health 2001. Sabbioni E. They reported urinary beryllium levels ranging from 0. Minoia C.74:162-166.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.S. 3/27/08 Komaromy-Hiller G. Minoia et al.95:89-105. Centers for Disease Control and Prevention (CDC). patient population and literature reference intervals for urinary trace elements. Howerton K. McCanlies EC. population are lower than levels in workers. Levels of beryllium in urine for the U. blood.12 to 0. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. 1998). 106. References Apostoli P. Atlanta (GA) 2005.. 1990. Environ Res 1998.158:165-190. Element reference values in tissues from inhabitants of the European community.1 μg/L). Ash KO. Van der Venne MT. Clin Chim Acta 2000.S. et al. Genetic and exposure risks for chronic beryllium disease. Sabbioni E. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Trace element reference values in tissues from inhabitants of the European community I. Gallorini M. Environmental Health Criteria.e. Jackson RJ. 0. it is likely that urinary beryllium levels in the U. and 2003-2004. Third National Report on Human Exposure to Environmental Chemicals. 2001). and serum of Italian subjects. Clin Chest Med 2002.cdc. Hamilton et al. Hamilton EI.inchem.. Am J Epidemiol 2003. Trace metals in urine of United States residents: reference range concentrations..Metals (i. Paschal DC. 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.htm.org/documents/ehc/ehc/ ehc106. Weston A. Morrow JC. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. HLA-DPB1 and chronic beryllium disease: a HuGE review. and the fact that most NHANES participant levels were undetectable. 1990.. Beryllium [online].gov/toxpro2.atsdr.23:827-839. Ting BG. environmental levels) and health effects is available from ATSDR at: http://www.296(1-2):71-90. Sampson EJ. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. et al. VI. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. International Programme on Chemical Safety (IPCS). and the 95th percentile for males in NHANES 2001-2002. Schaller KH. less than 0. 20012002. A study of 46 elements in urine. Paschal et al.76(1):53-59. Pietra R. Sci Total Environ 1990. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Andrew M. Maier L. Kriess K.html. Review of elements in blood. Comparison of representative ranges based on U.S. In other studies.157:388-398. Given these results. which approximate this Report’s limit of detection. 2000.e.

400 (. plastic stabilizers.700) .500-.400 (.20) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400 (.00-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.337) .20) 1.427) * .376-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.200 (<LOD-.00-1.344) .500-.10 (1.300 (.800) .60 (1.10) 1.403) .00-1.420 (.400) .367-.400) . 7440-43-9 General Information Cadmium is a soft.500 (.50-1.60 (1.300 (.500 (.20 (1.441) * . lead.700) 1.500-.20) 1.30) 1.235 (.500 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .200-.900-1.400) .30-1.600) .00 (.412 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 0.400 (.400 (.30-1.900-1.90) 1.304 (.513) .50-1.00 (.30) 1.gov/minerals/pubs/commodity/cadmium). EPA.80 (1.10 (1.300) 75th .60) 1.30-1.00 (.00 (.300-.393 (.00-1.400-. 01-02.10) 1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .600 (.600 (.60) 1.500-.10) 1.500-.200 (.400-.300 (<LOD-.600-1.309-.216-.50 (1. Since 2001.20) 1.60) Total * .20) 1.70) 1.400) .331) .700) .900-1.800-1.30 (1.80) 1.50 (1.200) .300) .500) .500-.366) * * .700) .10 (1.283 (. and 03-04 are 0.usgs.300) .500-. and incineration of municipal waste materials.300-.300-.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 . < LOD means less than the limit of detection.40-1.10) 1.60-1.600 (.50) 1.500-.70) 1.275-.700-1.40 (1.00-1.395 (.300) .400) .300-.900 (.600 (.10 (1.500-. population from the National Health and Nutrition Examination Survey.400 (.00 (.400-.20) 95th 1. U.60 (1.300-.333 (.600-.S.600) .600 (.500 (.400-.600) .300-.500-.368-.20) .20-1.20-1. see Data Analysis section) for Survey years 99-00.300 (<LOD-.3.470) * .400 (.900-1.300-.300) 1.10) 1.300) .500) .600 (.70) 1.300-.00-1.400 (.900-1.300 (.289-.00) .500) .00-1.200-.304-.00 (.20-1.300-.359-. Other uses include pigment production.80) 1.500-. and nonferrous alloys.425 (.50 (1.400-.600) 1.700) .300) .40 (1.900-1.398) < LOD < LOD < LOD < LOD < LOD < LOD .300 (.400 (.304 (.255) .500-.400 (.300-.326 (.400) .300) .400) .50-1.468 (.70) 1.600) .10 (1.20) 1.296-.200 (.40 (1.600) .361-.378 (.40) 1.200 (<LOD-.300-.900-1.600 (.500 (.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 .800 (.800 (.300 (.313 (.300) .200-.400) .300-.300) .200-.400) .400-.400 (.30) .386-.20-1.700 (.300-.421 (.500-.300 (<LOD-.400) .60 (1.500 (.500-.10) 1.300 (.300-.500-.10) 1.50) 1.300 (<LOD-.600 (. malleable.30) 1.700-1.40 (1.30-1. or copper smelters (U.S.10 (1.400 (.300-.300 (.500) .400 (. cadmium use has declined in response to environmental concerns (http:// minerals. Cadmium also may be emitted into the air from zinc.14.300-.600-.600-.500-.600 (.500) .30-1.300-.00 (.400-.00 (1.40-1.40 (1.40) 1.20-1.400 (. during refining of lead and copper from sulfide ore.300 (.10 (.400-. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.400) .300) .400) < LOD .900-1.700) .900 (.500 (.300 (.449) Selected percentiles ( 95% confidence interval) 50th .600 (.200) .20) 1.300 (.700) .40 (1.403 (.600) 90th 1.500) . bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.266-.10 (1.300 (. which may vary for some chemicals by year and by individual sample. respectively.600 (.700-1.00-1.900-1.300-.424) * .300-.460) .500) .400) .60 (1.200-.00 (.800) 1.400-.50-1.378-.400 (.300) .200 (.362-.600 (.500-.400-.20 (.400-.400) .10) 1.300) .600 (.20) .600) .00 (1.300 (.20-1. interval) .300) . and 0.452) .60) 1.20-1.400) < LOD .900-1.400) .300) .700) . coatings and plating.20) 1. as zinc sulfide) and to a lesser extent.S.40 (1.500 (.00 (.700) .00) .300-.400 (.400) < LOD .300 (.00-1.600) .800) .600) .600) .800-1.300-.426-.300-.500-.00 (.3.Metals Cadmium CAS No.600 (.400 (.382 (.400) < LOD < LOD < LOD . The predominant commercial use of cadmium is in battery manufacturing.500 (.50 (1.300 (.50) 1.

respectively.57) 1.135-.820 (.20 (1.700-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. copper) and protein.481) .366) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.279 (.290-.310) .170 (. and 03-04 are 0.733) .170-.540) .423-.191-.20 (1. and various seeds.372) .623) .500) 90th . however.820-1.078 (.492 (.20-1.17 (.748-1.38) 1.539) .875 (.206 (.320) .74) 1.196-.810-1.440 (.077 (. an inducible metal binding protein.519) .19) 1.387) . rice.28 (1.235) .240-.187 (.890 (.192-. drinking water is a source for cadmium intake.203 (.157-.170-.32 (1.190-.247) .412) .067-.551) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .980) .204 (.241) .327 (.455 (.220-.173) .233) .282 (.10 (1.28) 1.210 (.200-.153-.980-1. 01-02.223 (. 2003).194-.28-1.175 (.388-.128 (. wheat.191-.843-1.507) .238-.251) .189-.02-1.360) .596) .510-.610) .141 (.990) .479) .109-.430-.221) .790 (.Metals 2000)..273 (.177-.150) .817 (.230) .589 (.181 (.25) 1.13-1.249) .38) .219 (.41 (.730-.065-.918-1.090) .980) .426 (.980 (.490) .167-.977) .202 (. see Data Analysis section) for Survey years 99-00.766 (.30-1.262) .490) 1.800-.281 (.01-1.733-.52 (1.092 (.980-1.15) 1.295) .13 (.700-.960) 1. Inhalation of cigarette smoke is a predominant source of exposure in smokers.284) .229) .165-.686-.450 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.886) .238) .237-.329 (.270 (. zinc.210) .470-.175 (.233) .210 (.210 (. population from the National Health and Nutrition Examination Survey. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.201 (.972 (.858 (.121 (.800 (.870) .171-.713) .366-.456-.366-.447 (.640) .S.092) .243-.100-.183-.195-.308) .34) 1.240) .07-1.989-1.790 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.13) .210 (.148) .253-.806) .350 (.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.559 (.545 (.390-.255) .207-.227 (.306 (.336) .04 (.151-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .393-.01 (.813 (.077 (.519) . Kikuchi et al.260-.15 (.211 (.115-.705-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1. To a lesser extent.. interval) .38) .963-1.430) .892-1.219 (.860) 1.452 (..107-. ingestion through food is the largest source of exposure.135 (.200 (.717-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.206) .255) .239 (.458 (.230) 75th .339) .255) .198) .753-.257-.193-.191 (.326) .178-.081) .445 (.299) .482) . including many food crops such as cereal grains.157) .03) .06.01) .462 (.090) .22 (.51 (1. For nonsmokers who are not exposed to cadmium in the workplace.257) .466 (. calcium. Renal tubular and glomerular damage.24) 1. potatoes.818 (.272-.855-1.510) .261-. 1999..229-. Cadmium in soil is absorbed by plants.229) .202-.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 .210 (.940-1.12 (.886-1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg. **All results are corrected for molybdenum oxide interference in the ICP-MS method.633 (.820) 1.15) .190-.087-.209 (.192-.285-.300 (.440 (.362) .280 (.351-.20 (1.080 (.232 (.83) 1.06.300) .09-1.310 (.82) 1.354) .763-.22 (1.836-1.390-.160-.211-.580) .230 (.741-1.260-.43) 1.892 (.** Survey Geometric mean (95% conf.919) .220) .270 (.226) .714-1.433-.114-. 2001).221 (.249-.283 (.381-. 2003. Cadmium absorption may be increased with iron deficiency (Berglund et al.219 (.316 (.12-1.38) 1.680 (.17 (.48 (1.110-.848 (.199 (.234 (.179-.. Horiguchi et al.160 (.189-.169-.214-.120 (. and 0.112-.302 (.232) .06-1.208-.246) .130 (.313) .216 (.550 (.498-.180 (. 0.700-.200-.480) .150-. whose body burdens of cadmium can be approximately twice that of nonsmokers.520-.220-.193 (.101) . 2004a.960 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.190-.210) .231) .875) .06-1.134) .203) .06) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.260 (.390 (.160) .72) 1.17) .17 (.400-. 1994).04 (.060-. 2003).263) . Diamond et al.551 (. 2003).394-.839 (.607) .880) .530 (.265 (.530) .277 (.148-.450 (.061 (<LOD-.633-1.330-.440-.222) . Cadmium is absorbed via inhalation and ingestion.25 (1.436-.06.220 (.140 (.061-.136) .067-.445 (.184-.400-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .20) 1.36) 1..265) .476-.47) 1. With chronic exposure.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 .500) .261-.322 (.109 (.817 (.189) .160) .126) .200 (.289-.475 (.890-1.493-.

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.185 (. interval) .518) .288) .909-1.647-.668-.184) .273 (.779 (.617 (.336-.927-1.210) .181 (.769 (.143) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.281) .144-.240) .507-.261) .232) .211 (.917 (..806-1.08) .10) 1.434 (.783 (.501 (.293-.146-. However.470) . population from the National Health and Nutrition Examination Survey.199-.085 (.839) .196 (.940-1.716-.183 (.215 (.185) .813-1.414 (.792 (.221 (.135) .176 (.364) .826-1.084 (.666-.280 (.181) .104) .190 (.210 (.252 (.240) .562-. 2004b).440) .288 (. 2002.191) .051-. Jarup et al.242) .856 (.253) .678-. 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. 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.288-.491-.917) .181-.140-.136-.686 (.07) .247-.. 2002.175 (.687 (.096) .247-.931 (.607) .182) .304-.329 (.767 (.228-. Noonan et al.192) .398-.614) .767) .267 (.316) .184-.278) .253 (.113-.446) .473 (.708-1.421 (.190 (.663 (.740 (.204-.147-.206-.123-.929) .074-. At lower environmental exposures.985 (.100 (.784) .219 (.828) .S.183) .426-. 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.00 (.075 (<LOD-.150-.350) .085-.304) .850) . 2004).876-1.256-.712 (.653) .757 (.168 (.308) .827) .321) .559-.591 (.123-.126 (.352) .200 (.551) .216-.077-. 2003..311) .263-.097) .818) .255-.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 .941 (.075-.187-.292) . 1996. 1999).091 (.173-.338 (. most often a result of occupational exposure (Roels et al.423-.205 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .267 (.220 (.318 (.178) .856) .238-. can result from high dose chronic exposure.067-.688-.194-.263 (.147-.438) 90th .830) .091) .316 (.112) .335 (.229) .168-. 2002.16) . 1999).500-.225) .090 (.202 (.696-.086 (.250) .404) .143-.308 (.171-.700 (.432 (.241) .645-.325 (.382-.223) .281) .444-.234 (.07 (.181 (.487 (.722-.238) .091 (.282 (.531 (.156 (.106) .098) .209) .476) .865 (.222-.234) .063-.159 (.02 (.813-..104) .300-.687-.191 (.136-.440) .297) .470) .418) .381-.391-.16) 1.131-.197-.481 (.691-.340) .690-.154 (..207-.387-.154-.170-.13) .078 (.789 (. 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.06 (.433-. During the 1950’s and 1960’s. Olsson et al.219 (.261-.516-.137 (.175 (.247-. Horiguchi et al.802 (.187) .234-.208-.266) .545) .184-.212 (.199 (.678 (.412 (.962) .236-.17) . 2000.156) .757) .226) 75th .979 (.210 (.719 (.690 (.130-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .163) .716) ..227-.331 (.690-..377-.270 (.536 (.404 (. 1999).174-.754) .071 (.418-.208 (. Staessen et al.874-1.537-.235) .650-.479 (.239-.693 (.833-1.157-.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 .147 (.387 (.266-.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.382) .630-.189-.163 (.873 (.224 (.201-.182) .729 (.093 (.830-1.111-.191-.441-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.38) .884) .175-.388-.718 (.176 (.232) .343-.156-.261 (.484 (.168-.170 (.818) .173 (.159 (.449) .162 (.725-1.268 (.795) 1.094) .415) .289) .538) .09 (.245 (.472) .161-.431) .700) .622 (.940 (.919 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .490 (.05) 1.274) 1.198) .783) .083-.225) .296 (.107) .560-.122 (.233 (.906) .438-.303) .950) .283 (.178-.182) .143-.289) .084-.414-.00 (.667) .218) .850) .631) .727-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate..12) 1.157-.140-.137-..158-.826-1.674-1.207) .541) .148 (.101) .533) .177) .166 (.** Survey Geometric mean (95% conf.209) Selected percentiles ( 95% confidence interval) Sample 95th .423 (..221-.998) .078-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.

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

Nermell B. Taylor AJ. Vahter M. Diamond GL. Furuki K. Horiguchi H. Ezaki T. Nerbrand C.S. Int J Hyg Environ Health 2002. diabetes mellitus. Ye T. Environ Res 2004.45:43-52. Ukai H. Toxicol Lett 2004. Hotz P.66(Pt A):2141-2164. Third National Report on Human Exposure to Environmental Chemicals. Mascagni P.59:497].html. Tsukahara T. Clin Chim Acta 2000. Sanz P. Lukyanova EM. Jones RL. References Akesson A. Kundiev YT. Kikuchi Y. Ash KO. Gadea E. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Uemura T. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Bo M. et al. Howerton K. Atlanta (GA). Olfactory function in workers exposed to moderate airborne cadmium levels. et al. Okamoto S. 206:15-24. Kaus S. Toffoletto F. Cadmium fume inhalation and emphysema. Zhu G. et al. Toxicological profile for cadmium update. Moriguchi J. Occup Med 1996. Alfven T. patient population and literature reference intervals for urinary trace elements. Friedman LS. Ikeda Y. Sasaki S. Anthropometric. Sasaki S. possibly better than b2microglobulin. Oguma E. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers.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. iron deficiency. Int Arch Occup Environ Health 2003. Seifert B. population. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Lison D.102:83-89. Greves HM. Davison AG.atsdr.57:668-672. Ezaki T. Wang H.000 women in the Japanese general population: a nationwide large-scale survey. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Lidfeldt J. Environ Health Perspect 1994. Becker K. Comprehensive study of the effects of age. et al. Jarup L. Dekio F. Comparison of representative ranges based on U. Environ Health Perspect 2002. et al. Mannino DM. Palomar M. Holguin F. Kaus S. Berglund M. Darbyshire J. Venables KM.110:699-702. et al. Fatal chemical pneumonitis due to cadmium fumes.13(11):1627-1631. Elinder CG. Oguma E. Occup Environ Med 2000. Krause C. Bellerup P. Buchet JP. Environ Res 2006. Fayers PM. et al. Becker K. Fernandez MA. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10.96:353-359.59:194-8. Takebayashi T.46:372-374. Lundh T. Miyamoto K. environmental. Schulz C. Int J Hyg Environ Health 2003. Environ Health Perspect 2005. 4/8/09 Alfven T. Thorax 2004. Nomiyama T. Komaromy-Hiller G. Lepom P. Grubb A. 102:10581066.1(8587):663-667.205:297-308. Environ Res 2004b. Agency for Toxic Substances and Disease Registry (ATSDR). Miyamoto K. Chiappino G. Schulz C. Bregante G. Choudhury H. Chislovska NV. Neurotoxicology 2003.24:717-724. Costa R.354:1508– 1513. Hellstrom L. Mucha A. Carlsson MD. Bernard A. Lancet 1988. Fukui Y.296(1-2):71-90. 196:114-123. Machida M. Available at URL: http://www. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Serra J. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Jarup L. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Kumagai N. Nordberg G. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Seiwert M.gov/toxprofiles/tp5. et al. et al.76:186-196. Moriguchi J. Jin T. Akesson A. Savage-Brown A. J Toxicol Environ Health 2003. Lancet 1999. Furuki K. Tsukahara T. Lauwerys R. et al. Toxicol Appl Pharmacol 2004a. Machida M. et al. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Horiguchi H. 2005. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria.S. Consonni D. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Persson B. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Thayer WC.cdc. Centers for Disease Control and Prevention (CDC).95:20–31. J Occup Health 2003. Seiwert M.148(1-2):11-20. Fukui Y. Pickering CA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. ShkiryakNizhnyk AZ. 1999 [online]. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Vahter M. Ikeda Y. Stock AL.

Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Nogawa K.gov/ttn/atw/ hlthef/cadmium. Nordberg GF. Nakagawa H. Kathman SJ. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China.html.110:1185-1190. Mutat Res 2003. Time trends in burdens of cadmium. Nordberg GF. Skerfving S. et al. lead.59:394-397. Buchet JP. Japan. eds. Minciullo PL. In: Clarkson TW. Cadmium in blood and urine – impact of sex. 4/8/09 Waalkes MP. et al. Environ Res 2000. Environ Res 2006. Lundh T. Effects of exposure to low levels of environmental cadmium on renal biomarkers. J Cardiovasc Risk 1996. New York: Plenum Press. Vangronsveld J. Lison D. Bergdahl IA.epa. Lancet 1999. Roels H. Roels HA. Lybarger JA. Available at URL: www. and former smoking – association of renal effects. Saito S. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Roels HA. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Lundh T. Nishijo M. et al. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. et al. Campagna D. Stelitano A. Gangemi S. Kobayashi E. Bensryd I. Zhao YC. Tanebe K. Friberg L.30(5):395-399. Staessen J. Int J Hyg Environ Health 2006. Emelianov D. Zhu HD.110:151-155. Oskarsson A. Staessen JA. 2004. Noonan CW. lead. Mueller PW. Toyama. Tawara K. Environ Health Perspect 2002. J Perinat Med 2002. Cadmium carcinogenesis. Cadmium compounds. Nordberg M. Occup Environ Med 2002. Hoet P. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Gallmans G. et al. 151-168. Ottosson H. Sarasua SM. 2000. created 1992. cadmium. EPA). iron status. 2001. Thijs L.100:330-338.353:1140-1144. Arch Environ Health. Revised 2000 [online]. Biological monitoring of cadmium. Kuznetsova T. pp. Lijnen P. Olsson IM.59(1):22-25. Honda R. Liu QF. Relationship between newborn size and mother’s blood cadmium levels. Biological monitoring of toxic metals. Stegmayr B. and mercury in the population of northern Sweden. et al. Fan YG.21(3-4):251-262. Salpietro CD. Jansson J-H. Lauwerys R.3:26-41. Honda R. Wilhelm M. Environmental exposure to cadmium. Merlino MV. Bruiglia S. Revised and new reference values for arsenic. Usefulness of biomarkers of exposure to inorganic mercury. Tanebe K.S. Wennberg M. Suwazono Y. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2002. Zhang YL. Kido T. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Wang JX.39:2507-2515. United States Environmental Protection Agency (U.Metals Nishijo M. lead.533(12):107-120.209:301305. Schwenk M. age. Schultz C. Okubo Y. dietary intake. Ginucchio G. Hazard Summary. J Environ Sci Health B 2004. Sager PR. Nakagawa H. Ren Fail 1999. and risk of fractures: prospective population study. forearm bone density. Nakagawa H.84 (Section A):4455.

60) 7. although cesium was generally of low toxicity when given to animals.90) 4. scintillation counters.7 (9.6) 11.97) 4.6 (9.14.80 (4.49) 75th 7.1) 9.71 (8.10-8.1-13.01) 7.17-6. population from the National Health and Nutrition Examination Survey.42-7.8) 9.3) 10.13-8.70 (6.9 (11.5-13. and 0.64) 4.8 (10.4) 10.9) 8.8) 11.90-10.33-5.07) 4.94) 4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.82-4.89) 5.60-5.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.27 (7.10-7.5) 10.00 (7.7 (11.20-7.20 (4.17) 4.10-5.30) 5.90-8.90 (6. 01-02.7 (10.3-15. Radioactive 137Cs has been used medically to treat cancer.64-5.70-5.95 (3.43-8.8) 12. Fourth National Report on Human Exposure to Environmental Chemicals 205 .60-12.34 (4.0) 11.81-14.32 (3.00-4.20-4. infrared lamps. and cardiac arrhythmia (ATSDR.7) 10. and high-power gas-ion devices.59-5.04) 7.80-10.4) 12.73-11.40-5.03 (4.99-6.30-5.90 (4. diarrhea.1) 10.7-14.6) 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. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.50 (4.84) 5.2-12.62 (5.08-5.9 (10.77-8.60) 7.21) 90th 9.40) 5.5) 9.80-6.20) 7.26) 4.30 (6.5-16.59) 7.7 (9.70 (6.74 (4.50 (4.71-8.49) 4.66 (7. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.71 (4.90-10.9 (11.03-4.82) 5.1-12.81) 4.59-5.6 (9.0 (10.61) 7.2 (9.70) 5. For absorbed cesium salts.Metals Cesium CAS No.8) 11.3-13.1) 9.35 (4.98 (7.07-11.57-5. However. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.9 (11.14 (4.76-6.31-8.02 (4.25-5.17 (6.55 (7.0-15.20) 8.2-13.86 (7.99) 7.68 (7.60-7.59-5.0 (9. interval) 4.3) 12.3) 10.14.26 (3.44 (8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and as polymerization catalysts.4) 10.21 (4.64) 5.80-10.70 (8.35-5.2-13. Whether cesium compounds are carcinogenic is unknown.90) 7.08-5.1 (10.77 (4.50) 9.01-6.27-5. and 03-04 are 0.29) 4.12-11.90) 5.70 (4.30 (6.97 (7.8-13.03 (4.00-9.89) 4.23-4.2-14.10 (8.60) 5.64) 5.9) Total 4.81) 4.88 (8.16-6.61-6.25) 4.20) 5.53 (6.42) 6.83-4.84) 8.70) 5.9) 11.45-5.40) 7.5-14.49 (4.89-5.86-11.71) 4.5 (10.68) 9.49 (5.63 (4.26) 7.7 (8.80 (4.91-8.80) 7.08) 7.80 (8.90) 5. see Data Analysis section) for Survey years 99-00.94-4.00-8.60 (8.09) 5.70-8.4 (9.91 (7.00) 6.74) Selected percentiles ( 95% confidence interval) 50th 4.9) 12.55-11.32-5.84-9.05-5.33 (5.0) 12.3) 10.40-5.47-8.8 (11.64-10.95) 5.25 (3.30) 7.7) 11.05-5.3 (8. semiconductors.4) 11.71-9.40-5.39) 7.1) 11.72) 4.80 (8.50 (6.00-10.67 (4. and clay.42) 7.38) 5.6 (9.2.5 (8.80-13.20) 4.22 (4.1 (9.53-11.2) 12.70 (8.40-11.95-4.09-5.62) 4.7) 10.94 (4.54) 4.9) 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 4.7 (9.87) 5.4) 95th 11.50 (7.S.93 (4.90-12.98 (7.15-8.84 (4.97-7.0) 9.54-11.59 (5.40) 5.36 (6.30-10.56 (4.01-8.70 (5.32) 4.9 (11. the body half-life is estimated to be 70-109 days based on 137Cs exposures.87 (4.2 (9.77 (9.27) 4.0-13.08 (7.35 (4.60 (7.79 (4.22-4. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.60-7.6 (11.8 (10.5-14.86-12.43 (5.45-8.1-12.36 (3.0) 12.05) 5.4 (9.12) 5.4-13.37) 5.10 (6.04 (4.7 (10. nausea.80 (8.23) 9. Little is known about the health effects of this metal.00) 7.52) 7.10 (6.39-4.05) 5.99) 9.64 (4.13 (7.63-4.60-6.52-9.50) 5.2) 11.3 (8.8) 12.99-11.56-11.90-12.99-11.55 (4.70 (9.77 (9.80-10. soil.00) 4.73-5.10 (8.10-9.70) 7.87 (4.00-8.7) 11.3) 9.87 (4.90-10.60-6.3-13.20 (6. respectively.5) 12.13 (8.63) 6.13 (5.40 (4.50 (4.7 (10.20-5.72-7.12 (4.47-4.4) 12.8) 12. 2004).1) 11.56 (4.81 (4. cesium hydroxide is corrosive and irritating at high concentrations.16-6.84-5.3) 10.8) 9.83) 6.80 (4.6 (11.87-7.20-8.0) 11.33 (6.0) 10.46) 7.92-13.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.24) 4. photographic emulsions.50-7.12-5.9 (10.26-11.6 (9. Most human exposure to cesium occurs through the diet.29 (4.40-7.08 (6.74-5.40-11.80-11.36) 3.62 (5.96 (6.6) 10.37) 7.0) 12.90) 9.69-6.34) 9.56) 5.4) 9.2-13. 0.1 (11.71-5. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.94 (4.40-5.81) 9.4 (10.

18 (7.51 (3.8) 6.56 (4.78 (3.47 (4.43 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.35 (4.64) 4.8) 10.87-4.39) 8.16-5.06 (5.43-11.88-10.48-6.00-8.84-9.44 (4.60 (3.31 (4.84-11.3 (8.02 (5.01-8.42-4.98 (7.17 (6.81 (4.00-5.12) 3.50) 4.08-7.08) 3.46 (8.3 (9.17-4.95) 10. and were also roughly similar to those in this Report.91) 5. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.8 (9.S.05) 6.50 (6.67) 5.08-3.50) 4.70) 6.2 (8.44 (8.33-8.35-11.51) 4. Komaromy-Hiller et al.12-6.44-5.90 (7.35 (3.51 (3.97-5.28 (5.09 (4.1) 11.07 (5.03-5.77 (4.99-9.31-4.25) 4.20-4.56) 4.27 (6.77) 4.06 (3.05-4.6 (9.60 (5.2 (8.42-4.51 (7.56) 4.64-6.22) 6.40) 7.50 (7.64 (8.02-4.43) 8.56-10.21-4.04-11.31-6.27) 4.68) 3.36-10.47) 6.30-4.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.15-11.59-8.29-3.0) 7.83-6.93-7.72-5.74) 75th 5.03) 5.38 (3.75 (6.99-9.15) 95th 8.60-10.20-8.91-9.05-3.24-4.85) 4.36-6.0) Total 4.58 (6.7-12.66 (5.38) 10.14-6.73 (3.4) 10.84-7.53 (6.47) 6.9 (10.26-6.91-7.95) 8.96-4.99 (3.18-6.97-4.75 (7.79) 6.68 (4.29) 4.87) 5.S.27-6.33-3.46-8.43 (4.34 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60-20.28) 7.07) 8.19-6.24-10.47) 4.8) 5.91) 4.72) 4.00 (8.00-4.41-7.59) 4.62-8.03) 6.55 (3.78) 4.30 (4.00-5.77-5.50 (5.99) 4.91-6.46) 6.41 (4.00-10.0 (7. population.16-8.08) 4.83-7.50-5.62) 5.44) 3.65-3.45-6.78) 4.53 (4.07) 8.94) 7.30) 10.91) 5.11 (5. 2005.20-4.51 (4.76-9.58 (4.13-9.56) 3.98 (6.13) 7.13-9.3) 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 3.29) 4.00) 6.27 (8.54 (4. interval) 4.88-4.91 (5.61 (7.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .90-8.68-11.70) 7.98) 5.47 (7.82-4.96) 4.51 (4.63 (4.5) 9.26 (3.60) 3.29-3. 1990).73-4.80) 6.06) 5.54 (5.03-6.99-4.06) 4.42 (4.45 (4. Using clinically submitted specimens.63 (6. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.41 (5.50) 4.2) 11.64 (4.90-3.37) 4.54 (3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.66 (5.46-4.6) 6.44-9.30) 10.39) 5.3 (10.75-11.15 (7.33 (5.63 (7.63-6.86 (4.96-4.20) 5.5) 7.00-9.85) 5.63-6.42-6.79) 4.19-3.72 (4.95) 4.87 (5.65-4.21-3.68) 6.39 (5.81 (4. Minoia et al.74 (5.5) 9.30 (7.71 (7.52-5. Two small studies of European populations reported urinary cesium levels similar to U.91 (5.13 (3.38 (3.58-5.89-4.22 (3.58) 3.12 (3.95-12.21 (2.3) 9.29) 5.82) 7.87) 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 (5.10-4.48) 7.04) 5.70 (7.96) 4.15-4.41 (8.18) 8.14) 4.40-5.43 (3.18-7..95-6.3) 11.98) 5.66-6.74-11.64) 5. population results shown in this Report (Alimonti et al.14-7.08 (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.5 (9.55-5.79) 9.67 (6.33 (5.08) 4.38-7.10 (3.83) 8.47) 7.07-4.57) 3.05-3.53) 3.90-8..9) 10.30 (3.11 (5.04-5.71) 6.53) 6.68) 4.84-7.76-6.46 (7.. population from the National Health and Nutrition Examination Survey.94 (5.79 (5.43 (8.65 (6.74) 3. 2004).05 (4.S.6 (9.24 (3.10) 7.77 (6.54 (4.25) Selected percentiles ( 95% confidence interval) 50th 4.41) 9.10 (3.95 (3.16-8.37-3.04) 6.97) 8.08 (3.28) 8.85-4.26 (4.14) 4.10 (5.40) 6.16) 5.35-7.21-5.9 (9.92 (5.48) 90th 7.09) 8.08 (6.50) 8.14 (6.23 (7.28 (4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.96 (4.41-4.43-6.36-3.64) 9.27-4.61-3.78 (3.67 (5.14-4.2) 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 3.20-4.92) 3.93-9.7) 10.77 (7.66 (6.17) 9.30-4.79-5.74 (4.58) 8.42 (5.38-12.27 (6.35) 3.05) 3.55) 4.84-9.09) 4.7) 10.17) 4.31 (4.41) 4.63) 6.3-15.49) 3.22-11.

Costa R. Spezia S. Howerton K. cesium. Ronchi P. et al.html. J Expo Anal Environ Epidemiol 2004. Clin Chim Acta 2000.296(1-2):71-90. Komaromy-Hiller G. Trace element reference values in tissues from inhabitants of the European community I. Available at URL: http://www. antimony and tungsten. Comparison of representative ranges based on U. Pietra R. Third National Report on Human Exposure to Environmental Chemicals. Sabbioni E.14:120-128. Rapid Commun Mass Spectrom 2005. Apostoli P. patient population and literature reference intervals for urinary trace elements. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. New Mexico. Mott JA.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). et al. 2000.cdc. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Toxicological profile for cesium.atsdr. and serum of Italian subjects. Sewell CM. 4/8/09 Alimonti A. Mincione G.2004 [online].S. Ash KO.19:3131-3138. Atlanta (GA) 2005. Pozzoli L. Gatti A.95:89-105. Paschal D. Assessment of urinary metals following exposure to a large vegetative fire. Wolfe MI.gov/toxprofiles/tp157. Sci Total Environ 1990. Centers for Disease Control and Prevention (CDC). et al. A study of 46 elements in urine. Wood CM. Forte G. Gallorini M. Minoia C. Voorhees RE. blood.

430-.419) Selected percentiles ( 95% confidence interval) 50th .920) 1.05 (.520 (.371 (.810-.790) .730) 1.460) .33 (1.331-.Metals Cobalt CAS No. Cobalt occurs naturally in airborne dust.463-.60 (1.860 (.427-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.03) 1.550) 90th .390 (.900) .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 .469-.600 (.870 (.300-.380 (.650 (.610-.550 (.06 (.430 (.16-1.09 (.32) 1.28 (1.355-.600) .410 (.15-1.359 (.540-.21) 1. 0.330 (.870-1.540-.17 (1.450) .880 (.640) .12) 1.291-.64) 1.800) .348-.370 (.36) 1.47) 1.294 (.16 (1.37-1.29 (1.340 (.310-.377-.900) .373-.520-.340-.710 (.950-1.44) 1.820 (.620-.570 (.14) .410) . and fertilizers.16 (.530-. see Data Analysis section) for Survey years 99-00. It is also a component of porcelain enamel applied to steel bathroom fixtures.92) 1.07 (.850) 1.343) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .405-.790 (.700) .50) 1.48) 1.417) . The cobalt used in U.22 (1.840) .68 (1.370-.390) .338-.22-1.32-2. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.308-.500 (.870 (.16-1.564) .581) .03-1.S.380 (.05) 1.630 (.890) . industry is imported or obtained by recycling scrap metal that contains cobalt. and in synthesizing polyester and other materials.960-1.03) .583) .590-. 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.670 (.42) 1.04) 1.33-1.590-.487) .343 (.450) .32 (1.930 (.16) 1.370-.26) Total .350-.460) .890-1.450-.316 (.04-1.270-.460) .S.820 (.48) 1.14) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .03 (.660) .67) 1.424) .340) .450-.360-.350 (.319) .680 (.560 (.06-1.410 (.08-1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.08) .650 (.04 (.47 (1.23) .379 (.56) 1. steel-belted radial tires.680) .690-.280-.09 (.414) .259-.680) .352 (.543) .900-1. and 03-04 are 0.900) .620) . population from the National Health and Nutrition Examination Survey.760 (.434 (.32) 1.452 (.461 (.710) 1.300 (.03 (.420 (.404) .640) .800-.770) .670 (.550-.740 (.570-.01 (.930) . Cobalt compounds are also used in manufacturing battery electrodes. and 0.610 (.99) 1.14-1.375 (.520 (.08.17 (.327-.390-.810) .580 (.440-.500) .22) 1.420) .330) .370) .750 (.520 (.850-1.530 (.460 (.372) .53) 1.370-. and inks.760) .65) 1.330-.01 (.570-.00) .690 (.17 (1.379 (.460-.270-.430 (.416) .339 (.01-2.380 (. blue-colored pigments.386) .490-.388-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.32 (1.830-1.75 (1.81) 1.28 (1.348-.520 (.07.580 (.670 (.394) .15 (1.350-.600-.334) .470) .810) .373) .16 (1.610) . varnishes.890) 95th 1.418 (. seawater.454 (.50 (1. hard metal (alloys of cobalt and tungsten carbide).285 (. and soil.950 (.940-1.431) .393-.369 (. respectively. It is emitted into the environment from burning coal and oil and car and truck exhaust.13) 1.523) .03) 1.09) .750 (.367 (.59 (1.45 (1.380-.650-. shiny.660) .450) .02-1.399) . Cobalt is used as a drying agent in paints.28-2.07.670-.47 (1.660-.340-.820 (. Usual human exposure is from food sources.750-.800-.470 (.428-.570) .73) 1.940 (.360-.390 (.950 (.305-.320 (.410 (. interval) . 01-02.910-1.410-.890-1.490-.480 (.710) .26-1.690-.950) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.515 (.740-. diamond-polishing wheels.460 (.480-.05 (. and magnetic recording media.540-.26) 1.880-1.25-1.480 (.270-.570) .431) .620-.26-2.420) .17-1.39) 1.430) .350) 75th .790-.630-.04-1.07-1.316-. large appliances.07-1.580 (.364-.900-1.520-.520-.400-.410) .333-.310 (.540-.410 (.350-.23-2.465) .980) .950-1.24 (1.850) .920-1.450) .530) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .410 (.496) .670-.01-1.360-.04-1.52 (1.290-.590 (.398) .340) .680 (. automobile airbags.610) .540) 1.301 (.520) .502) .590) .435 (.19) .16) 1.940-1.980-1. Cobalt compounds are used as catalysts in producing oil and gas.430) .06 (.12) 1.410-.740-.28 (1.313) .24 (.620-.890-1.640) .519 (.520-.430 (.336-.520) .47) 1.333-.750 (.390 (.46 (1.850-1.81) 1.499 (.374 (. hard metal or in combination with other elements.398 (.630 (.380-.510) 1.700) .410-.20 (1. and kitchenware.930-1.

16 (1.297) .333-.304-.479-. 1979).23 (1.306 (.60) 1.00 (.898 (.595) .54) 1.738 (.27) 1.905) .736-.442-.316 (.362) .323) .387) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.15) 1.673-.426 (.16) .289) . 1972). refining or processing alloys.469-.17) .700 (.964 (.476-.29 (1.833-1.251-.534 (.599) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.28) 1.19) .248-.282 (..382-.757-1.257-.353-.394) .388 (.317 (. cobalt is excreted predominantly in the urine.384) .990-1.278-.475 (.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 .937 (.777-.419) .495 (. 1972).542 (.708) .215-. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.49) 1.847) .738 (.12-1.952 (. 1994).756 (.753-.369 (. Cobalt is absorbed by oral and pulmonary routes.851 (.361-.378 (.616-.955) .313-.594) .30 (1.900-1.844 (.861-1.27) 1.29 (1.508-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.55) .10-1.368) .433) .36) 1.660-.29) 1.386 (.640) . Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).547 (.457-.503-.428-.344-.282-.286) .12 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.248-.895-1.06 (.543) .296-.275-.16 (. an essential human nutrient.439) .29) .632-.296) .700 (.02 (.333-.300) .10 (.449-.408 (.861 (.481) 90th .786-.449) .895-1.932-1.35) .333 (.821 (.963) .611) .635 (. in the feces.848 (.574-.334) .301-.983-1.563-.608 (.04-1.313-.372) .313-.259) .402 (.487-.429) 1.479) .703-.328 (.600-.879-1.00-1..744) 1.11-1.11-1.792-1.343 (.393 (.552 (.774 (.50) 1.554 (.25 (.417) .728 (.850-1.955) .271 (..362-. 2003).239-.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 .365) .740-1.391) Selected percentiles ( 95% confidence interval) 50th .237-.581) .529 (.435-.14 (.515 (.368 (.679-.949) .00) .290 (.457) .753) 1.327-. 1994.691 (.280-.487-.598 (.324) .378-.733-1.561) .609) .355) .83) 1.00 (.737 (.396) .353 (.279 (.328) .689 (.585) .327 (.975 (.468) ..438) .303-.611) . or using diamond-polishing wheels that contain cobalt metal.290 (.723 (.938) .259 (.04 (..361-.290 (.352) .850 (.275-.667-1.400 (.10) .626-.425-.259-.343-.339-.457 (.376 (.257 (.328 (.523 (.842) .727 (.234 (.33) .606 (.785) .500-.268 (.272-.329-.425) .335 (.750-.247 (.274-.615) .662) .388 (.15 (.929) .392 (.313-.33) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .361 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.368) .250) .513) .591 (.537 (.407 (.461) .417 (.667-1.309) ..314 (.333-.471-.911-1. Smith et al.647) .378-.593) .630-.435 (.331-.694) .313 (.365-.337 (.634-.669) .278 (.358 (.277-.471-.361 (.554 (.298 (.838 (.630-.Metals fabricated from cobalt alloys (Lhotka et al.500 (.60) 1.380-.393-.349) .522) .500-.329 (.638-1. interval) .24) .306) 75th . using hard metal cutting tools. population from the National Health and Nutrition Examination Survey.533 (.00) .03 (.804) 1.391 (.256-.830 (.302-.00 (.273 (.10) Total .297-.829-1.455 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.00 (.313-.821-3.452-.243-.488) .513 (.404-.324-.444 (.467-.644 (.352 (.S.35) 1. Exposure in the workplace may come from electroplating.25 (.293 (.50 (1.378-.337) .781) 95th 1.562) . A portion of cobalt retained for long periods is concentrated in the liver.963-1. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.57) 1.560-.505) .548 (.346 (.301) .917) .523 (.03-1. respectively.342-.319-.50) 1.938-1.781-1.44 (.294-.360) .990) .396) .983) .421) .16 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.304) .963) .36) 1.550-.73) 1. Once absorbed and distributed in the body.381) .750) .348) . and to a lesser extent.471 (.857-1.407) .534-.434-.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 .462) .09) 1.683-.513-.310) .279) .792 (.326-.826-1.291 (.704-.363) .960 (.562) .352 (.463-.760-1.872 (.29 (1.728) .707) .281) .976 (.409) .582-.963-1. with pulmonary clearance half-lives of from one to two years (Hedge et al.33) 1.824 (.362 (.829) .

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

Long-term clearance of inhaled 60Co. J Bone Joint Surg Br 2006. Kato M. Cresti R. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Kusaka Y. Int Arch Occup Environ Health. Blunn G. Dunstan E. Hammon E. Diepgen TL. A report of two cases from mineral assay laboratories and a review of the literature. Goto S. Linna A.34:620-626. salt.22:359367. Daniel J. Oksa P. Romazini S. J Orthop Res 2003. Buchet JP. Laippala P. Zweymuller K. Kraus T. Sabbioni E. Lung cancer risk in hard-metal workers. et al. Lasfargues G. Weber A. a study of 13 elements in blood and urine of a United Kingdom population. Lauwerys R. Br J Ind Med 1993. Kiilunen M. Respiratory health of cobalt production workers. Chest 1989. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Szekeres T. De Boeck M. Leghissa P. McCalden RW. Schank M. Buchet JP.36:732-734. Dunning SP. Lauwerys R. Unwin P. McMinn DJ. Thabe H. Linnainmaa M. Health Phys 1972.242:1412-1415. Thomassen H.216:253-270. MacDonald SJ. Chess DG. Hedge AG. 1985. et al. oxides. Pisati G. Hoet P.51(7):447450. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Am J Ind Med 2003. Stanescu D. Lison D. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein.69(3):193-200. Rorabeck CH. Peltier A. Lauwerys RB. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. X. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.Metals effects of cobalt. and hard metal dust. Schaller KH. Zobelein P. Sabbioni E. Carnes WH. Palmroos P.28(5):1121-1128.21(2):189-195. Mosconi G. and cobalt metals. Edmonds CJ. cobalt salts. Kuska Y. Sci Total Environ 1998.55(4):269-276. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Sanghrajka AP. Boca Raton (FL): Lewis Publishers. Absorption and retention of cobalt in man by whole-body counting.150:177-183. Falcone G. Iavicoli I. Dickel H.88(4):443448. Meier R. J Rheumatol 2001. Barnaby CF. Roto P. White MA. Meyer zum Buschenfelde K-H. 2001. Salvatori S. Occupationallyinduced “isolated cobalt sensitization.(1-3):133-139. Lison D. Angerer J. et al. Cleland D. Co-sensitivity between cobalt and other transition metals. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Heki S. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Wild P.204:147-160. Uitti J. Jarvis JQ. 3rd ed. Cobalt and antimony: genotoxicity and carcinogenicity. DeSantis V. Arch Intern Med 1990. Zedda S. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust.” Contact Dermatitis 2001.533:135-152. Schramel P. Shirakawa T.95:29-37. Outcome of occupational asthma due to cobalt hypersensitivity.45:246-247. Kirsch-Volders M. Sci Total Environ 1997. Occup Environ Med 2001. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Fujimura N.148:241-248. Smith T. Contact Dermatitis 2003. Goto S. Bunn HF. Salama A.157:117121. Bacis M. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Kriss JP. Science 1988. Gross RT. Kristiansen J. Robinson C. Clin Orthop Relat Res 2003. Sabbioni E. Thakker DM. Swennen B. Steffan I. HoffmannB. J Trace Elem Med Biol 2006.48:172-173. Lisi P.58(10):631-634. Bourne RB. Cannon SR. Radulescu M. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.150. Hoher T. et al. Goldberg MA.406:282-296.44:124-132. Health Phys 1979.50(9):835-842. J Occup Med 1992.20(1):25-31. Swennen B. Zhuber K. Molders J. Cobalt cardiomyopathy. The release of metals from metal-onmetal surface arthroplasty of the hip. Am J Epidemiol 1998. Mutat Res 2003. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. J Bone Joint Surg Br 2005. Iversen BS. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Sci Total Environ 1994. Occup Environ Med 1994. Ichikawa Y. Biological monitoring of workers exposed to cobalt metal. Ziaee H. Int Arch Occup Environ Health 1997. Trace element reference values in tissues from inhabitants of the European Union. Weyher I. Moulin JJ. Pradhan C.150(1-3):167-171.87(5):628-631. Lhotka C. Ghat IS. Christensen JM. Bozec C. Sci Total Environ 1994. Tilley S. Vitali MT. et al. Epidemiological survey of workers exposed to cobalt oxides. Lison D. Alessandrelli M. et al.

50-1.20 (3.60 (1.60) 3.00) 3.60 (3.10 (4.50) 5.40) 1.40) 1.40-1.00 (1.20) 3.10-1.90) 1.70) 3. ammunition.00) 4.80-3.14-1.30 (2.19 (1.90 (2.10-2.900 (.00) 1.50 (2.40 (5.43 (1.10 (3.10) 5.40-1. Before the 1980’s.g.14-1.23 (1.60 (3.60 (3. population from the National Health and Nutrition Examination Survey.70 (2.80-2. and 03-04 are 0.30 (3.90) 3. such as lead phosphate and tetraethyl lead.83 (1.30 (2.00) 2.48) 1.50-2.90) 2.40-6.90 (3.30-1.60) 3.68-1.70 (1.40) 2.40) 3.60) 1.10) 3.12-1.60 (2.30-1. 01-02.40 (3.00-5.90 (3. respectively.50-3.78 (1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.40) 2.40-2. solders.40) 5.80 (1.00) 1.90) 1.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.69 (1.10 (2.69) 1.90) 5.45-1.75) 1.90 (3.32-1.60) 1.50) 75th 2.900-1.90-2.43-1.50) 5.40-6.70) 4.22 (1.20-4.50 (3.30-2.30 (1.50-2.50 (1. lead was added to gasoline and residential paints and used in soldering the seams of food cans. interval) 1.70) 1.60-1.10 (1.60 (1.800-1.10) 1.09) 1.60 (1.20 (3.10 (1.20 (3.60-3.30) 1.50 (1.30-2.70 (5.00-1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .60) 4.17) .20) 3.60 (4.40) 4. Lead was used in plumbing for centuries and may still be present.40-1.50 (4.00-6.36-1.30-4.10) 4.20-2.10 (2.90-4.50) 1.30-6.80) 1.30 (2.60 (1.70) 1.10) 3.80 (1.30 (4.50 (1.10-1.20-3.04-1.90 (4.10) 2.30-1.20) 1.37-1.40-1.50-2.10-1.10) 2. Since lead has been eliminated from gasoline.31) 1. the main source of lead exposure for the general U.81) 1.30) 2.60-6.20 (3.37 (1.36-1.80 (5.00) 4.40-1.40) Total 1.20) 2. ceramic glazes.00-1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30-2.30-1.10-2.60) 1.20) 5.30-1.40) 2.70) 2.80) 1.89) 1.00 (1.90-4.70-4.70-1.00) 2.80 (2.45 (1.20 (1.30 (4.40 (4.20 (3.00 (4.50) 2.14-1.90 (3.00-4.60) 1.40) 1.20 (1. Elemental lead can be combined with other elements to form inorganic and organic compounds.899-.40 (1.66) 1.72) Selected percentiles ( 95% confidence interval) 50th 1.10-3.62-1.60) 1.50-2.40-5.10 (2.20-3.20 (4. 7439-92-1 General Information Elemental lead is a soft.70 (1.20-6.80-4. and 0.40-2.00) 1.52-1.86) 1.20-1.50-1.90-4.50 (3.60) 2.70) 1.60 (1.80-4.50) 1.00) 3.70-5.70-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20) 4.80 (4.50) 1.00) 5.90 (3.70 (2.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.10-8.80-5.60) 3.80-4.95) 1.80-3.53) 1.70-3.50 (2.60) 3.30 (2.96-2. brass.20 (3.60) 4.60-2.50) 2.50 (4.50) 1.90-2.S.80) 2. dense.40 (2.52 (1.70-1.70) 4.20-3.10-3.39-1.60) 2.37 (1.55-1.69) 1.80) 2.10-2.30-1.60) 4.10-3.70 (3.75 (1.30 (1.50 (2.40-3.20) 3.90 (1.20-1.71-1.60) 2.36) 1.80 (5.80) 1.70) 3.87) 1.90 (1.60 (1.90) 2.00) 2.75-1.20) 4.28.10-2.02) 1.40 (1.70 (3.60 (2.50-6.80 (3.60 (2.90-2.60 (2.40 (1.30 (2.00) .20 (1. malleable.50-1.80 (1.60 (2.70-2.70 (2.49-1.20) 90th 3.80 (1.30-2.50-5.10-6.60 (3.90) 2.20 (3.30-5.91) 1.32-1.Metals Lead CAS No.70) 4.60) 2.80 (1.75-2.20 (2.70) 1.40-3.70 (1.87 (1. see Data Analysis section) for Survey years 99-00.00 (3.946 (.69 (1.00-2.90-2.80) 2.30) 5.70) 4. bronze).70) 1.80 (2.50) 7.00 (6.77 (1.10-6.20-3.50 (2.52-1.40 (2.80) 3.10 (1.50 (2.25 (1.43) 1.50-5.70-2.60-4.20) .10) 1. Lead has a variety of uses in manufacturing: storage batteries.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 1.51 (1.00 (4.62) 1.50) 3.00-4.50 (1.66 (1.55-1.878-1.90) 2.50) 4.40-2. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.60-1.80 (4.20 (2. blue-gray metal that occurs naturally in soils and rocks.90 (2.S.90-6. In the past.40) 2.40-3.60) 5.93-2.60) 4.80-3.80) 1.60 (1.70 (1.00 (5.10-3.50-4.50-1.60-1.20-2. plastics.10-4.25 (1.00) 6.3. leaded glass.30 (1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.50-4.56 (1.90-3.51) 1.90) 2.50) 4.50-1.20 (1.30) 2.39) 1.30 (2.00-4.30) 95th 5.80 (2.30) 2.90) 1. 0. Lead is most often mined from ores or recycled from scrap metal or batteries.46 (1.60) 2.00) 1.70-2.20 (1.10-4.10) 3.62 (1.90-4.20) 3.30 (2.55 (1. antique-molded or cast ornaments.3.60 (2.30 (4.942 (. metal alloys (e.30 (1.80-3.70-6.40-1.60) 5.10-2.40-4.80) 2.70) 3.00) 2.00) 1.43 (1.80) 1.986) .80 (1.34-1.90) 3.10) 1.43) 1.65 (1.01 (1.40 (1.50-3.00 (2.10-2.60-2.60-4.60-1.900 (. and for radiation shielding.25) 1.

1.729-.Metals occupational (e.640 (.80-2.506-. 0.10 (1.640-.04 (.30-5.02) 1.795 (.50-3.970-1.90) 2.86-2.833-1.680-.50 (2.86) 95th 2.850 (.810-1.636 (.30-1.605) .10 (.900) .570-.90-2.828) Selected percentiles ( 95% confidence interval) 50th .800) .745-.10 (1.04 (.480-.50) 1.70-3.30) 1.680) 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 1.50-1.60 (1.773) .40 (2.00) .600-.955-1.800) .60) 2.40 (1.700 (.10-1.32 (1.20) .553-..700 (.690) 75th 1.80) 2.14 (1.00-2.785) .620) 1.800) .540-.70 (2.40 (2.556-.80) 3.600-.40) 1.50-2.60-3.90 (1.808 (.35 (.660) .30 (1.695 (.90-2.10 (.70 (2.40 (1.30-1.800-.40) 2.10-3.700-.23) .700-.862) .31 (1.700-1.900-1.600 (.20-1.52-1.86 (1.80-3.790 (..10) 1.564 (.78-2.10-5.00-1.50) 1.44-2.33.730 (.10-1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al. and 0.579-.30 (3.00-1. interval) . 1991).91) 2.14-1.90 (2.749) .17 (1.52 (1.30) 1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .800 (.20) 1.589-. and contact with soil.66 (2.20) 1.40) 3.20 (1.731 (. 2007.960-1.82 (2.30) .20-2.80 (1.40 (1.00 (.50 (1.04) .40) 1.600 (.923 (.40 (1.60-1.50 (2.900-1.80) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 213 .40 (2.572-.50) 2.30-1.30-2.00) .600) .766 (.90-3.80 (2.940 (.20) .738) .90-2.00 (1. 2000).00 (1.30) 2.800) . and 03-04 are 0.10 (.70) 3.20) . Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.40) 1.59) 1.900-1.935) 1.920 (.90) 1.800) .04-2. respectively.60 (1. imported children’s trinkets and toys.20 (1.941) .815 (.610 (.21 (2.90) 2.900-1.40) 2.40 (2.840 (.20 (2.80) 2.718) .680-.78-2.70) 1.600) . However.701) .800-1.10) .20-2.10-3.50) 2.915-1.900) .753 (.931) .00 (2.10) .920 (. or water contaminated by mining or smelting operations.07-1.40-1.637-.30) 1.40-1.29) 2.04) 2.70 (2.00) 2.18-1.50 (1.86) 1.700-.52-1.62-4. pewter utensils and drinking vessels.910-.659 (.526-.20 (2.62) Total .60 (1. or after soluble lead compounds are ingested.700 (. Approximately half of the absorbed lead may be incorporated into bone.41) 2.580-.822-1.07 (.590 (.20 (3.10 (1.82 (1.03 (1.800-1. population from the National Health and Nutrition Examination Survey.688 (.671-.674) 1.00) 2.625 (.628) 1.900) .80) 2.30) 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 1.30-1.00-2.10 (1.80 (1.20) 1.625-.90 (1.595-.00-2.818) . Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.09) 1.33 (2.680) .23-4.90-3.20 (1.500-.10-1. lead-based painted surfaces undergoing renovation or demolition.g.691-.72) 1.800-.90 (2.78-2.700 (.70) 3.20 (1.60 (1. 01-02.800 (.90-4.10-1.990) 2.11 (1.60 (2. see Data Analysis section) for Survey years 99-00.90-2.558 (.20 (1.60-3.960 (.616) .19 (1.591 (.50-2.40) 1.700 (.20 (2.710-.02 (.10) 2.708-.1.06) . lead-contaminated dust in indoor firing ranges.573 (.89) 2.604 (.80) 1.700-.13) .70) 1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.986) .700-.641-.60-2.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.S.30) 2.30) 2.857) .80-2.30) 1.97) 4.70-2.752 (.80) 2.757-.535-.600-.600-. bullet fragments retained in human tissue.800 (.642 (. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.80) 1.70) 1.833 (.30-3.27 (1.30 (2.11) 2.33-2.14 (1.613) .20 (1.40 (1.73 (1.20-1.00) 1.50) 1. CDC.900 (.49 (1.661-. In the blood.40-2.800 (.70 (2.40-5.650) 1.22) 1.00) . stained glass framing.31-3.960-1.10-3.64) 2.900) .24-1.70 (1.50) 3.75) 3.20) .651) .75) 4.900) .50 (2.710-1.00) .40-1.630 (.40-3. dust.12) 90th 2.90 (2.677 (.03-2.60-2.620 (.40) 1.30) 1. battery and radiator manufacturing) and recreational sources.13-3.700 (.00-1.900) .29 (2.848 (.560-.80) 2. lead-containing folk remedies and cosmetics.820-1.10-1.50-2.579-.990) 1.540 (.90) 2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.70) 2.80) 3.40) 2.40) 2.900 (. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.10) 2.27) 1.20-1.700) .59-2.00 (1.900 (.90 (1.66 (2.600-. older plumbing systems with leaded pipes or lead soldered connections.40-1.700) 1.00 (1.

14) 1.43 (1.09) 1.03 (.24 (1. 1993).19) 1.992-1.71-2.22) 1.03) 1.71 (1.971 (.938-1.708 (.06 (.731-.08) .73-2.812-1.722 (.461) .428) .621 (.02) 1.712 (.718) .33) 2.51) 1.50-1.893) .681-. 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.601-.645-.753) .400) .18) .02-1.61) 1.676) .07) .97-18. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.990 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al. BLLs and associated toxic effects differ in children and adults.608-.33) 1.609 (.460-.52 (1.22) .15-2.957-1.19-5.00 (1.679) 1.677-.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 .607-.75-2.655) 75th 1.77) 2.11) .22) 1.98) 2.06) .975-1.721 (.44 (1.623 (.679-.887 (.914 (.92) 2.41) .69 (1.29 (1.31) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.870 (.43-1.Metals 90% of the body lead burden in most adults.469 (.686) .38 (2.693 (.380-.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 1.15) 1.15-3.40-1.408-.00 (1.800-.612-.12-1.50-2. encephalopathy.27 (1.841-1.15-2.722 (.88) 2.31) 1. zinc.588-. 2004.938 (.709 (.85 (1.64 (1.97) 1.17 (.702) .603 (.03 (.559-.641 (.579-.78-4.79) 2. abdominal pain.655) .510-.702) . Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.09-1.541-.432 (.08-2. 2007).828) .946-1.20) .988 (.707 (. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.05-1.657) 1.838) .648 (.83 (2.342-. 1995).720 (.35) 2.05-1.997-1.917-1.56) 3.06) 1.853-1.04-3.667) .03) .62) 2. through the inhibition of certain enzymes.529-.11) 1.10 (1.639 (.09-1.03) .58) 1.70 (1.635 (.11 (.05 (.68 (1.404-.977) 1.47 (1.03-2. For instance.603-.26) 2.78 (2.64) 95th 2.683-.87) 1. 1995.569 (.03) 2.88-2.755 (. population from the National Health and Nutrition Examination Survey.720 (.97) 1.688) .72) .710) . Schwartz.64-2.98 (1.09-1.404 (.94-2.725) .22-2. with lesser amounts eliminated via the feces.39-1.61) 1.49 (1.98-2.56-3.758) .617-.593 (.914-1.56 (1. and paralysis.43 (2.763) .603-.668-..698) .696 (.72-2.67-4.933) .920-1. kidney injury.52) 1.633 (.940 (.963-1.47 (2.59-3.725) .45 (1.85-2.671 (. The skeleton acts as a storage depot.594-.88) 2.981-1.11 (1. 2003.86 (1.655-.65-2.926 (.41 (1.639 (.645-.658 (.730) 1.644) .53) 1.03 (.615 (.11 (1.492-.10 (.742) Selected percentiles ( 95% confidence interval) 50th .681-. seizures. CDC.649 (.28) 2.06 (1.79 (1.605-.89-5.41-1.10) 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 .53-1. O’Flaherty.89-2.66 (1.46 (1.74 (1.615 (.63) 1.31 (1.625 (.734) .739) .718) 1.07-1.08) .20) .933-1.43) 2.50-2.962 (.64) 2. and iron.07 (.702-.992-1.50 (1.594-.698) .828-1.765) .673) .38 (2.18) 2.851) .608 (.535) .00) .94 (1.18) 1.11 (.28-1.31 (2.36-2.659-..50-2.862-.592-.774 (.00 (. Staessen et al.62-1.0) 3.33 (1.72-2.43) 1.587-.18 (1.47) 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 .918 (.914 (.44 (1.639 (.01) .31 (1.793-1.63) 4.436) .790) .62-3.61) 1.654) .900 (.73) 2.561-.700-.383-.796-1.83) 1. Approximately 70% of lead excretion occurs via the urine.33-1. interval) .61) 1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.639) .03) 1.876-1.988-1.623 (.496 (.667-.04) 2.S.85-2.25-1.65 (1.701) .588-.26) Total . Large amounts of lead in the body can cause anemia.37-1.85) 1.55 (1.88 (1.979 (.34-1. Lead can cross the placenta and enter the developing fetal brain.810 (.632 (..18) 1.61) 3.670) 1.404 (.667-. based on prospective population studies.742) .15) 1.14 (1.606-.17-1. The toxic effects of lead result from its interference with the physiologic actions of calcium.622 (.11-1.56-2.01 (.00 (1.03) 2. with a half-life of years to decades.746) .682) .03 (1.701 (.88) 1.583-.62-2.96 (1.375 (. 1996).44) 1.38 (2.79) 1.82) 1.898) .55 (1.571-.677 (.604-.28) .05 (1. and nails (Leggett.50) 1.20-3. 1993.781-1. and through binding to ion channels and regulatory proteins. hair.703) .23 (1.618 (.97 (1. Nash et al. In 1991.75 (2.571-.10) 1.66 (1.677) . scant amounts are lost through sweat.66) 2.51 (1. 1991.551-.638 (.48 (1.22-1.25-1.586-.37-1.652 (.644 (.03) 90th 1.46 (2.508) .918-1.882-1.

adults in the 1999-2000 NHANES sample. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. However. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. and organic lead compounds not classifiable with respect to human carcinogenicity. 1998). BLLs reflect both recent intake and equilibration with stored lead in other tissues.75 µg/dL in U. 2000). residing in housing built before the 1950’s. reduce sperm count.0 µg/dL in females (Soldin et al. and decrease fertility (Alexander et al.cdc.gov/toxpro2. 2006). both the geometric mean (1. Telisman et al. The U. Payton et al. may alter sperm morphology. 2002a). 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.. Information about external exposure (i. In NHANES 1999-2002 in children 1-5 years old. 1991.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample.S.S.. which is an 84% decline. 2003. Korrick et al..6%) were lower than those from NHANES 1991-1994. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. Pirkle et al.S. Surveillance data reported by U. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. 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. 1999).. For example.. adult residents. seizures. 2007). including minority race or ethnicity. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.4% of children had BLLs of 10µg/dL or higher (CDC.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. Schwartz.. 2005b). Staessen et al.5 per 100. Schwartz et al.. High dose occupational lead exposure. 2005a).cdc. 2003). Borja-Aburto et al.g...S..S. 2009). 2002).2 µg/dL in males and 3. 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. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. Bellinger 2005.4% in NHANES 1999-2004. CDC. Jones et al. Data submitted through state public health programs from 2006 showed that 1. 2003.. environmental levels) and health effects is available from ATSDR at: http://www. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Lanphear et al...7 µg/dL and 4.. lead in women may be associated with hypertension during pregnancy.html.. the prevalence rate has declined annually since 1994 (CDC. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. 1994).6% in NHANES 1988-1991 to 1. Both drinking water and ambient air standards for lead have been established by the U. Muntner et al. 1995. 1996.000 adults. with overt encephalopathy... usually with BLLs greater than 40 mg/dL. the geometric mean BLL was 3. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. Fourth National Report on Human Exposure to Environmental Chemicals 215 .9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2001). At low environmental exposures. 2000). 2002.S. almost double the geometric mean of 1. EPA. and peripheral neuropathy generally occurring at much higher levels (e. and spontaneous abortion (Baghurst et al. 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. More recently.. Urine levels may reflect recently absorbed lead. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. particularly in the skeleton. respectively.e.atsdr. 1999). premature delivery. higher than 100-200 µg/dL). 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. 2006).07 µg/dL (Becker et al.. Overall.21% of approximately 3. and low family income (CDC. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. 1984. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. adults in the 19992000 NHANES sample (Apostoli et al.xls).Metals µg/dL or higher as the level of concern in children. 1996. 2005b.3 million children tested had BLLs of 10 mg/dL or higher (http://www. urban residence. when the geometric mean BLL was 2.. 1996. approximately 11. 1987.. though there is greater individual variation in urine lead than in blood and greater potential for contamination. In occupationally exposed adults.. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.. 2003. IARC considers inorganic lead compounds probable human carcinogens. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.

et al. Chiodo LM.gov/mmwr/preview/mmwrhtml/ mm5532a2. N Engl J Med 2003. Apostoli P. Available at URL: http://www. Lepom P. Caldwell KL. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Wager C. Bellinger D. Vupputyuri S. Brody DJ. gov/mmwr/preview/mmwrhtml/mm5420a5.123:e376-e385. Korrick S. Age-specific kinetic model of lead metal in humans. Blood lead levels—United States. Jacobson JL. JAMA 1996. 2002 [online]. Adult blood lead epidemiology and surveillance—United States. Cox C.html. Teratogen update: lead and pregnancy. Pirkle JL. Wigg NR. Managing Elevated Blood Lead Levels Among Young Children. 2003-2004. Batuman V.atsdr. doi:10.113(4):1016-1022. 2005. Hu H.htm.cdc.275:1177-1181. Kaus S.gov/nceh/lead/ CaseManagement/caseManage_main. Baghurst PA. Neurotoxicol Teratol 2004. Environ Res 2000. JAMA 1996.73:409-420. Hänninen H.htm.gov/nceh/lead/publications/ books/plpyc/contents. Environ Health Perspect 1993. Neri A. Rotnitzky A. Bavazzano P. References Agency for Toxic Substances and Disease Registry (ATSDR). Muller CH. Jusko TA. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. 4/14/09 Centers for Disease Control and Prevention (CDC). Atlanta (GA). 4/14/09 Alexander BH. Pediatrics 2009. The relationship of bone and blood lead to hypertension. Sparrow D.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. MMWR Morb Mortal Wkly Rep 2006. Centers for Disease Control and Prevention (CDC).53:411-416. Available at URL: http://www. Int J Hyg Environ Health 2002. Weiss ST.cdc. Roberts RR. Hertz-Picciotto I.101(7):598-616. Cory-Slechta DA. Canfield RL. van Netten C.82:60-80. Sparrow D. Third National Report on Human Exposure to Environmental Chemicals. Aro A. Hu H. 1991 [online]. Rojas LM. 4/14/09 Centers for Disease Control and Prevention (CDC). Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals .cdc. Angle CR.cdc. Aug 2007 [online]. Bellinger D. Rios C.htm. Am J Epidemiol 1999. Stanek KL. et al. Available at URL: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.87:1-471. et al. Krause C. Weiss ST. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.55(32):876-879. Pediatrics 2004. Occup Environ Med 1996. CDC. McMichael AJ. Coresh J. et al. Birth Defects Research (Part A). Available at URL: http://www.54(20):513-516. Blanco J. Rotnitzky A.115:521-529. Toxicological profile for lead. Neurotoxicol 1987. Ga.287:1-11. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Inorganic and Organic Lead Compounds. Meyer PA.205:297-308. Seiwert M. Manton WI. Blood lead reference values: the results of an Italian polycentric study.89:330-335. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. IARC Monogr Eval Carcinog Risks Hum 2006. Auinger P. Homa DM.275(15):1171-1176. Atlanta. Reese YR.gov/toxprofiles/tp13. Neurodevelopmental effects of postnatal lead exposure at very low levels.1542/peds:2007-3608.348:15171526. MMWR Morb Mortal Wkly Rep 2005a. Cox C. Jones RL. Lanphear BP. Scand J Work Environ Health 1984. Hernberg S. Kaufman JD.cdc. Muntner P. 4/14/09 Centers for Disease Control and Prevention (CDC). Korrick SA. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Schulz C.26:359-371. Lead. Kim R. Lanphear BP. Mantere P. 1988-2004. 1999-2002. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention.150(6):590-597. Semen quality of men employed at a lead smelter.10:43-50.8(3):395-401. Ewers TG. 2005b. Hunter DJ. Farias P. Sci Total Environ 2002. Robertson EF. Am J Public Health 1999. Vimpani FB. Dietrich K. Leggett RW. Ganzi A. Baj A. Jacobson SW. Borja-Aburto VH. Available from URL: http://www. Public Health Rep 2000. Luukkonen R. Preventing Lead Poisoning in Young Children. Hu H.htm. et al. Payton M. Kuehnemann TJ. Atlanta (GA). Becker K. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 4/14/09 Centers for Disease Control and Prevention (CDC). Ronchi L. Henderson CR. Lead and hypertension in a sample of middle-aged women. Checkoway H. Speizer FE. Blood lead levels measured prospectively and risk of spontaneous abortion. Acquisition and retention of lead by young children.

Gunter EW.Metals results from NHANES III. Am J Epidemiol 2001. Rocic B. Pirkle JL. Sparrow D. Staessen JA.140:821-829. cadmium. Amery A.S. O’Flaherty EJ. Int J Hyg Environ Health 2006. Low-level lead exposure and renal function in the Normative Aging Study. Environ Health Perspect 2000. Rubin R.9:303-327. Lead. Blood lead concentrations in children: new ranges. Hwang KY. Kidney Int 2003. JAMA 2003. Soldin OP.104(1):60-66. blood pressure. Toxicol Appl Pharmacol 1993.63:1044-1050. Sherwin R. population to lead: 1991-1994. Low-level lead exposure and blood pressure. Roels H. Wilhelm M. Gavella M. Lee GS. stable lead isotopes to determine release of lead from the skeleton. Use of endogenous. Environ Health Perspect 1996. Clin Chim Acta 2003. Brody DJ. Arch Environ Health 1995. IV. Magder L. Osterloh JD.106:745-750. J Hum Hypertens 1995. et al. Exposure of the U. Hu H. Kaufmann R. Smith DR. Flegal AR. zinc. Schulz D. et al. Stewar WF. and copper in men. Fourth National Report on Human Exposure to Environmental Chemicals 217 .327:109-113. Am J Epidemiol 1994. Schwartz J. Blood lead. cadmium. Environ Health Perspect 1998.108(1):45-53. Soldin SJ.118:16-29. Lauwerys RR. Payton M. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. 50:31-37. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Kaufmann RB. Schwenk M.289(12):1523-1531. blood pressure and cardiovascular disease in men. Hickman T. Jurasovic J. Nash D. Lee SS. Telisman S. Hanak B. Pizent A. Physiologically based models for bone-seeking elements. Cvitkovic P. Revised and new reference values for arsenic. Weiss ST. Schwartz BS. Paschal DC. Association of blood lead. dimercaptosuccinic acidchelatable lead. and tibia lead with neurobehavioral test scores in South Korean lead workers.153(5):453464.209:301305. Lee BK. Kinetics of lead disposition in humans. lead. Lustberg M. and hypertension in perimenopausal and postmenopausal women.

300) .30) 1.30-5.418-.500-. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.814 (.70 (1.574) .484) . Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).00 (.472-.800-1.900) 75th 1.90-3. The kinetics of the different forms of mercury vary considerably.300 (.80) 4. After elemental mercury is absorbed.. sulfur.700-. merbromin).800-1.30 (1. 1998.20) 2.60) 2085 2293 3478 Limit of detection (LOD. mercuric chloride). and mining and smelting. which can bioaccumulate in aquatic and terrestrial food chains.979 (. to form inorganic mercury compounds or salts. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.2.50) 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 mercury compounds are still used as preservatives (e. solid-waste incineration.50) 4.714-..00 (.30) 3.00 (.60-5. thermometers. and organic forms.563 (.877 (. interval) .700) . Also.900 (.900) 1.700-.30) 3.40) 3.Metals Mercury CAS No.10) . elemental mercury is absorbed mainly by inhaling volatilized vapor. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals..400 (.80 (1.50-3.919) .700 (.363-.g.00 (. Hursh et al. synthetic organomercury compounds were once used in pharmaceutical applications.700-.20 (2. Other major uses include electrical equipment (e.30-6.00 (2. 1993).30-2.20-3. inorganic. 218 Fourth National Report on Human Exposure to Environmental Chemicals .285-.40-2.70 (1.60-6. Apart from methyl mercury.80 (1.60 (1.500-.689-. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. population from the National Health and Nutrition Examination Survey.60) 1. phenylmercuric acetate) or topical antiseptics (e.60) 1.00) 4.g.800-1.00-1.40-3.60 (2.90 (4. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.40-2. and is distributed to most tissues.90 (1. which create an episodic potential for volatization and inhalation of mercury vapor.S.30) 5. Elemental mercury is a shiny. Kingman et al.776 (. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.900) . 1994.02) .700-.400-. thimerosal.927) .40-1.S. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.700) .00) .20-4.90) 3.40 (4.70 (4.90) 95th 4. may contain inorganic mercury.50) 1.30 (2.500) ..g.. with the highest concentrations occurring in the kidneys (Barregard et al.900) 1. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. In addition.12) .30) 1.60-3. electrical lamps. IARC.40 (3.800-1.490 (.800 (.80) 1.672) .781 (..80 (1. 1980.80 (3.00) 1.80) 3.00) 1. an organic form of mercury. Some cosmetic skin creams from countries other than the U.00 (2.903) Selected percentiles ( 95% confidence interval) 50th .70-2. thermostats and switches). 1999 .10-3. Survey years 03-04 Geometric mean (95% conf.50) 5. The ingestion of methyl mercury.500 (. have often required public health intervention (Zeitz et al. 2007).372) .900) 1.70) 911 856 2081 4525 03-04 03-04 . Poorly absorbed from the gastrointestinal tract.500 (.. and dental amalgam.700-. or oxygen. predominantly from fish and other seafood. Woods et al.. such as chlorine (e.40) 1. sphygmomanometers and barometers.800 (.g.50-2.860-1.326 (.600) 1.60-2. Atmospheric elemental mercury can be deposited on land and water.703-.30-4.600 (.50-1.90) 90th 3.655-.800 (.00 (2.90 (1.40 (3.800 (. 2002).886) . 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).400-. Accidental spills of elemental mercury.30) 4132 4241 03-04 03-04 03-04 .70 (3.300-.60-6. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.50) 2.00) 3.797 (.419 (.00 (1. constitutes the main source of dietary mercury exposure in the general population..753-1.40 (4.00-5.40-1.60 (1.20-4.800-1. see Data Analysis section) for Survey year 03-04 is 0.

70 (1.00-6.269-.297-. 1991.833 (.30 (. 1994). 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. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.30) 3.500-..00) 2. Suzuki et al.400-.70 (1. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.800-1.20-11.00-2. 1994) and then undergoes slow dealkylation to inorganic mercury. 1999).60 (1.10 (. Geometric mean Survey years (95% conf..940) Race/ethnicity (females.90 (1.00-2.900-1.600) .90) 2.343 (.60) 3.30-4. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.700-.90) 90th 1.40-1.738-.. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.7) 4.300 (. with most elimination occurring through in the feces (Sherlock et al.664-1. 1993). Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.80 (1. Smith et al.02 (.50-3.200-.300 (.70 (1.200 (..475) .50-12.00) .50) 95th 2.500-.Metals the tissues to mercurous and mercuric inorganic forms.10 (5.900 (.06 (.30 (1.200-.20) 1.10 (3. Jonsson et al.00 (2.20-3.300) .50) 1.395) .30) 1.. for both acute and chronic exposures.00) 1. a measure of accumulated dose (Cernichiari et al.50 (2.944 (.40) 5. McDowell et al.377) .50-2.500-.60) 2.900 (. 1995.40) 1.800) 1. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.60) 1.871-1..50 (1.820 (.300) .377 (.70-5.30-5. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.70-3. 1999-2002.70) 4.90) 5.300) ..90) 2.90 (1.14. 1993).30-11.50) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. 1990). Excretion occurs by renal and fecal routes. 1969.00 (2.800) 75th .90 (4.00) 6. 1973).70-6.300) .00-3.541-. 1992)..20) .10 (1..20 (2.70) 1.800 (.40-2.256-.700 (.06-1.10) 1.700-1.40-2.29) .20-3.27) .800 (.80-3..700-.10 (..200 (. and a useful marker of exposure in epidemiologic studies (Grandjean et al.700 (..200-.00) 7.30) 1. Myers et al... National Health and Nutrition Examination Survey.40 (1.825-1.268-.30-6.20-3.700-1.300) .60 (3.667 (. 1998).60) 1.90) 3...40 (1.20-2.329 (. Vahter et al. 1996.700 (.73) 1.369) 1. 1996).700) 2.30-3.00) 4.374) . Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.50) 3. 2005). After exposure to elemental mercury.824) 1.30 (1.10 (1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.800) . interval) Selected percentiles (95% confidence interval) 50th .30-4.318 (.500-.23) .10) .500 (.60 (3.307 (.800) 1.20 (.80 (3.10 (1. 1971).35 (1.00 (1. Sandborgh-Englund et al.90 (3.00 (3.900-1. Fourth National Report on Human Exposure to Environmental Chemicals 219 . thereafter.80) 1.10-1.300) .30-6.900 (.800) .3) 4. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.00-2. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .726-1. Methyl mercury enters the brain and other tissues (Vahter et al. 1975.265-.697-.60 (2..800 (.500-.30 (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 .70-3.600 (. 1992.299-.300 (. 1998).407) ..600) .50) 1. Methyl mercury is incorporated into growing hair. population.60 (1.200-..90 (4.. Miettinen et al.0) 4.10-3. 1994.S.500 (.14 and 0.317 (.30-6.800-1...70) 4.700 (. Smith and Farris. 1992 and 1999.70-5.200-.40) 2.20) .30-2.500-1. 2003).00 (2. 1984. Vimy et al.60 (1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.10) .00) 1. 2004.919) . 2003).800-1.01) .80) 579 527 370 436 588 806 Limit of detection (LOD.200-.300 (.

sensory impairments. 2002. altered physical growth. 1998.. 2005. Rice..600) .. hearing impairment.500-.700 (.700-.600) . population from the National Health and Nutrition Examination Survey.700-. which may vary for some chemicals by year and by individual sample. Smith et al. and neurocognitive and behavioral disturbances.500-. and sleep disturbance (Bidstrup et al.600) . fatigue. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700 (.600 (. 1951. Oskarsson et al. 1993). and pinkish discoloration of the hands and feet (Tunnessen et al. Acute. 2006.700 (..800) .. Once absorbed. The constellation of findings may include anorexia.600 (.. Overt poisoning from methyl mercury primarily affects the central nervous system.700 (.600 (.. 2004). insomnia. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.600 (. 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. Salonen et al.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500-. Sakamoto et al. 2004.600-. Factor-Litvak et al.500) . short-term memory loss. see Data Analysis section) for Survey year 03-04 is 0. gingivitis. overt signs and symptoms of chronic inhalation may include tremor. Inorganic mercury exposure usually occurs by ingestion.600) . In recent epidemiologic studies. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1995. 1970. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.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 . 1983). Drexler and Schaller..Metals may be more efficient for inorganic mercury (Grandjean et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. 2004.500 (. 2003). hypertension. depression..700-.S.700 (.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .700) 2007 2240 3406 Limit of detection (LOD. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. irritability.600 (. pain in the extremities.500-. 2005).. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. Sakamoto et al. dysarthria.600) .600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. particularly irritability.600-. 1987).600) .700 (. Stern 2005. ataxia..500-.600 (.500 (.42. Rissanen et al. 2000). Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 2006..600) . Bellinger et al.700) . the existence of a causal relation is unresolved (Chan and Egeland. Vupputuri et al. 2004). Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.500 (<LOD-. cerebellar ataxia.500 (<LOD-.. and progressive constriction of the visual fields. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. and cerebral palsy (NRC.500-.500-. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. causing parasthesias. dysarthria. 1996).. 2000. 2000.600) . limb deformities..500-. 1963). At levels below those that cause acute lung injury.500-.600) .600 (. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al..600-. Smith et al.. anorexia. DeRouen et al.600-. 220 Fourth National Report on Human Exposure to Environmental Chemicals . 1995.600 (. typically after a latent period of weeks to months. maculopapular rash.800) ..

8 years.60 (1.930-1.555) .441 (.382-.52) 2. 2002).24 (2. 1998). From 1996 through 1998.460 (..88-3.88) 287 722 1529 03-04 03-04 . 2009). EPA at: http://www.250) .14.S.360-. and increased slightly in non-Hispanic white children (Caldwell. range 40 years to 78 years) had an average total blood mercury concentration of 2.405-.24) 1.54 (2.12 (.480 (.509) . 2003). 2003). Biomonitoring Information In the general population.08 (1.cdc.08 (1.890 (.90) 2..960 (.76-3.840-1.epa.370) . see Data Analysis section) for Survey year 03-04 is 0.03-4. and the age-related changes differed across the groups (Caldwell et al. Mahaffey et al.78-2.20 (1.213-. Sanzo et al.360-.58 µg/L for 4645 adults.330-.340-.Metals standard for inorganic mercury has been established by U.520) . EPA.480) 75th 1. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC. During the same survey periods. However.S. Fourth National Report on Human Exposure to Environmental Chemicals 221 .280-. adult women in several ethnic subgroups (Hightower et al.76-3. interval) . 1995.60) 619 713 1066 Limit of detection (LOD. the median concentration of blood mercury was 0.e.31) 2..05) 1.63-2. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.97) 2. 1998). the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.430 (.360 (.460) . Total blood mercury levels increase with greater fish consumption (Dewailly et al.31) 1266 1272 03-04 03-04 03-04 .413-. 2001.. average age 9.. 2009).99-6. slightly higher total blood mercury levels were found in U.530-.700-1.55) 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 .18) 2.42) 95th 3.85-2. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. Kingman et al. 2001.30) 3. Among the three racial/ethnic groups.28) 1. 1997.. military veterans (mean age 52. 758 children. 2004.495 (.65) 1. environmental levels) and health effects is available from the U. average age 33 years.770-1.420 (.05) 3.304) . although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.430) . Information about external exposure (i. 2006). Benes et al.S.19 (1.420 (.700 (.534) . Schober et al. 2000). Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.61) 1. population from the National Health and Nutrition Examination Survey.gov/mercury and from ATSDR at: http:// www.870-1.S..580) ..00 (.610-1.416 (.870-1.gov/toxprofiles.01 (..200 (.. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.67-3.66) 3. aged 18 to 69 years.09 (2.00) 1..S. total blood mercury increased with age.96 (1.9 years). (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women. particularly methyl mercury.34-3.89) 3.509) .16 (1.290-.840) 1.440 (..07 (.570) .442-.88 (1.77-2.13-2. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.476 (. Over the NHANES 1999-2006 survey periods.19 (2. These distinctions can help interpret mercury blood levels in people.55 µg/L.313-. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.16 (.76-4. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. Grandjean et al.396-.46) 3.433 (. who participated in a 1998 representative population survey (Becker et al.160-.330-.23) 2.530) .39-3.60-2. Survey years 03-04 Geometric mean (95% conf. In Germany the geometric mean for blood mercury was 0. et al.68 (2.940 (. total blood mercury geometric mean levels in females aged 16-49 years did not change.350-.atsdr.254 (.840-1.530) .67-2.410-.430 (.330 (. In NHANES 19992002.492) Selected percentiles ( 95% confidence interval) 50th .400 (.46 µg/L for children.33 (2.14-2.93 (1.14) 90th 2.330-.358 (..26 (1.23) ..29) 1.447 (. A cohort of 1127 U.463) .96 (1.408) .549) .406-.78 µg/L for adults and 0. the total blood mercury concentration is due mostly to the dietary intake of organic forms.

970 (. 1992).00) 286 722 1529 03-04 03-04 .667-1.S.39) 1.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .S.275) . 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.969-1. not to imply a safety level for general population exposure. women of childbearing age have generally been much lower than these levels (CDC.32 (1. 2006. Urinary mercury levels in recent German (Becker 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 .25 (.347) .619-.03) 2.964-1.87) 2.486) Selected percentiles ( 95% confidence interval) 50th .196-.28 (.620-.455-.79) 1.265-.04-3.768 (..522-.280-. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.385-.362 (.464 (. 2006). the urine mercury increased by approximately 0.76 (1.476 (. 2002).535) 1.255 (..800-1.306 (.696 (.41-2..S.365 (. Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.537) . mean urinary mercury was 3. reversible increase in urinary N-acetyl-glucosaminidase. et al..Metals 2000). population from the National Health and Nutrition Examination Survey.785-1.67 (1.358) . a biomarker of perturbation in renal tubular function.276 (. In the study of U. 1988. military veterans with dental amalgams.875-1.65 (1.40 (1. Levels in U.18-1.87 (1.77 (2.990) .88 (1.S.30) 2.784) 1.297 (. 2009).35 (1.384 (. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.630) .67 (1.86) 95th 2.30) 1.88-2.21) 1. interval) .217 (.208-. 2005). An expert-panel report recently prepared for the U.391) .62 (1.587 (.333-.525 (.11-2.1 µg/L.54 (2.01) 2.404-. Urine mercury and the number of dental amalgams were correlated.588) .46-2.16) 1. Information about the biological exposure indices is provided here for comparison.343 (.472-..51-2.400-.447 (.498) 75th .391-.246-. DeRouen et al.00) 90th 1.32-2.566) .909 (.455-. Survey years 03-04 Geometric mean (95% conf.301-. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.40-1. Langworth et al. 2003).652) . and on average.480) ..225-.485 (.13-2.508 (.455) . and Italian (Apostoli et al. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.07) 1.289) .06 (.12-3. Department of Health and Human Services noted that several studies have observed a modest.11) 1.376-.79 (1.63) 1.13 (1.417) .365 (.S.392-.1 µg/L for each surface with a dental amalgam (Kingman et al.06 (..00 (.714-1.307-.23-2.545 (.463 (.309-.61) 1.368) .443 (. 1998).88-2.31 (1.400) . 2009).56) 1266 1271 03-04 03-04 03-04 .09) 1.11) 2. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell..78-4.447-.599) . et al..532 (.64-2.687) .616) . 2002) adult population surveys were similar to those in a U.44) 1.. Czech (Benes et al. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.

76 (1.00) 2.540 (.719 (.45) 2.810) .560 (.85) 4.04-10.06 (.31 (1.45-2.686) .38) 4.21-3.565 (.81-6.740 (.56 (1.824) . 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.520-.664) .475-.27-1.22 (.51 (3.10-2.32-3.650 (.68-3.580 (.35) .81 (3.62 (1.685 (.99 (2.540-.3) 5.68 (3.420-.24) 6.721 (.578-.45-3.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.09-1. 1999-2002.98 (5.46-4.30 (1.650 (. interval) Selected percentiles (95% confidence interval) 50th .50 (1.57-4.909-1.83-3.09-1.17) 95th 5.68) 3. population.47) 1.605-.84 (2.870) .426-.637) .892) .55) 90th 3.710) 1.742-1.18) 3.27 (2.744) 1.43-1.03) 1.806) .56) 4.724 (.59-5.610-.S.32) 2.91-7.502-.710 (.596 (.14 and 0.91 (2.522 (.14) 3.32 (1. population.97 (1.501-. Geometric mean (95% conf.10-4.450-. 16-49 years) 99-00 01-02 .39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.76-5.16-5.41 (2. Geometric mean Survey years (95% conf.15-1.616-.79) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.21 (2.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .850-1.16) 5. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.387-.799) .62 (4.23-1.25) 2.84 (2.97) 2.03-2. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.639 (.831) .579-.45) 95th 3.606 (.24-1.42) 2.580-.48 (2.65) 1.69 (1.910) .41-6.42-3.582-.05 (3.516 (.04-1.18 (3. National Health and Nutrition Examination Survey.14.94) 1.13 (2.92) 3.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .760 (.632 (.500-.809) .85-3.00 (2.410-.37 (1.99) 1.691) .21 (1.656-.51) .99-2.S.665) .30-2.77) 1.07-2.706 (.72) 1.622-. National Health and Nutrition Examination Survey.95 (2.30 (2.52) 3.615 (.92) 4.846) .55-3.97) 2.50 (2.54) 595 531 381 442 594 826 Limit of detection (LOD.774) .699) 1.03 (.28 (1.14-1.15 (2.636-.650) 1.44) 3.35 (1.41 (1.833) .723 (.Metals Urinary Mercury−Females Aged 16-49 Years Old.520-.07-5.831) .61) 1.930) .79) 3.39-3.658 (.77) 2.87-4.47) 1.37) 1.46 (1.61-6.655 (.69-3.05 (2.709) .30 (2.657 (.50-4.99 (3.27 (1.560-.45 (1.13-4.70 (2.07) 1.772 (.56) 3. interval) Selected percentiles (95% confidence interval) Survey years 50th .00 (3.709) 75th 1.23-1. 1999-2002.557-.22-3.710 (.508-.89 (2.670) 75th 1.31-1.592 (.62 (3.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .92) 2.966) .97) 2.569-. 16-49 years) 99-00 01-02 .03 (.45) 2.41 (1.14-2.620 (.553-.790) .526-.65-4.42) 90th 2.832-1.46) 3.624-.600 (.76) 2.631-.53-3.

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hydrogenation catalysts.7 (44.3 (46.6-42.5 (37.6-96.8 (67.0 (42.7-91.6 (55. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5-91.1-63.7 (58.4 (48. WHO.0-53.2) 52. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.0) 54.7-68.5) 47.2) 40.4) 42.8.8) 39.6 (73.1-88.9) 67.6 (55.S.1-55.0-110) 90.9 (33.7-84.7) 77.1-51.0 (41. 1996).8 (82.6-46.7 (37.3 (37.1) 59.3-75. which exert homeostatic regulation over molybdenum balance.4-61.2) 53.0 (81. 7439-98-7 General Information Elemental molybdenum is a silver-white.9 (44.Metals Molybdenum or ore deposits.9 (73.3 (47.5) 44.3 (71.0-65.7) 78.9-85.0-62.5) 80.3-115) 152 (120-217) 177 (142-207) 152 (141-169) 206 (150-274) 166 (147-170) 156 (135-175) 187 (146-223) 152 (134-180) 130 (119-142) 780 683 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.5 (41.8-108) 87.7 (51.0) 97.7-51.4-82.7 (50.4 (72.2 (61.7-96.6 (40. and 1.7) 86.3) 85.3) 37.7) 51. More recently.9 (32. see Data Analysis section) for survey years 99-00.1 (91.8-90.8.5-46.9 (34.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.3-44.2-59.2 (38.2 (69.0 (48.1-44.2 (55.7-50.2 (83.9-83.4) 45.2 (40.9-55. inks.7) 46. 2001.0) 62.9-56.5-68.6-82.0-101) 82. and 03-04 are 0.4) 76.2-91.3) 54.0) 84.0) 45.6 (52.0-38.5 (48.8-46.7-122) 93.9 (37. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.0 (42.6) 71.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (46. 1997).5) 80.3) 47.3 (55. interval) 45.7) 45.7-92.8 (42.8-49.7 (36.6) 71.5-52.8) 40..4 (48.7-60.1-52.5-65.2) 79.4-75.2-37.2-42. hard metal widely used to add strength and hardness and retard corrosion in metal alloys. urinary excretion over six days CAS No. In humans.4) 56.9-109) 97.7 (71.5) 85.2-79. chemical reagents in hospital laboratories.2-59.2 (63.1) 60.1-59.3 (53.3 (79.4) 41.5-41.7-39.3 (55.9-55. and in pigments for ceramics.0) 60.4 (79.4) 49. Excretion occurs predominantly via the kidneys.8-94.6) 53.5. At a daily oral molybdenum dose of 24 µg.5 (49.8 (85.1 (34. population from the National Health and Nutrition Examination survey.1 (71.2 (49.1) 82.2 (56. and xanthine oxidase (Kisker et al.6 (40.6) 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 (99.4) 52.0 (76. aldehyde dehydrogenase.0) 39. 2001).2 (49.7) 75th 84.9 (52.3-108) 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 47.6) 93.6-58.7-41.0-77.5-124) 108 (92.0-100) 63.0 (43.9) 34. 01-02.5 (74.7 (73.9-82.2-70.9 (40.1 (38.3) 65.2) 37.8) 75.1) 57.1-48.7-47. Compounds of molybdenum are also used as corrosion inhibitors.1) 35. Fourth National Report on Human Exposure to Environmental Chemicals 227 .6) 51.7-73.7) 78.0-85.0-56.8) 48.2) 48.6 (43.9) 62. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.2-53.8) 46.1-52.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.7) 57.5 (41.3 (73. respectively. and paints. semiconductor and battery industries have begun to use molybdenum.3 (84.5 (43.0-71.3-91.2) 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 (98.4-52.6) Selected percentiles ( 95% confidence interval) 50th 50.1) 46.3) 41.6-62.7-105) 69.4 (80.4 (34.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97. 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.3 (64.3) 83.6-55.5) 60.2) 41. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.0) 55. lubricants.5-66.3 (38.5 (67.3-47.1) 126 (106-147) 109 (94.7 (45.5 (81. 0.5-52.6-72.9 (78.8) 44.8-106) 88.

3-44.2-40.2 (40.9-87.0-120) 85.3-46.5 (35.3-115) 98.4 (37.6-61.9 (36.0-133) 119 (88.5) 72.0) 38.Metals was 18% of the ingested dose.3 (71.4-118) 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 .1) 56.9-71.7-44.3-68.2-96.9 (64.9 mg/kg/day and established a tolerable upper intake level of 0.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.8) 39..7-93.5 (40.7-40.3) 41.5) 71.9) 41.4) 122 (107-133) 109 (99.4) 77.8-67.4) 47.0) 39.9 (64.8) 45. 2001).9-96.7-52.2 (36.9) 92.6 (38.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.5 (37.1 (38.3 (53.7) 115 (93.2-103) 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 42.6-61.7) 41.0-46.6 (36.6) 36.4) 58.4-41.1-40.5 (41.7) 112 (95.7) 42.3) 64.1) 101 (83.1-81.4 (67.7) 57.8 (57.9-117) 57.3 (51.5 (80.0 (35.6-63.9 (79.1 (44.2) 58.2) 42.2-80. Based on studies finding adverse reproductive effects in rats and mice.5 (41.1) 37.2 (40.8 (37.9) 79.4-42.3-141) 109 (81.9-118) 91.3 (58.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5 (34.1-38.5 (39.4-106) 85.4 (53.8 (36.9-40. 1993).0) 62.0) 88.8-47.2) 39.6) 39.4-107) 85. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7 (77.5 (65. but available epidemiologic data are scant.2-46.2) 37. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.7-100) 77.5-69.7 (66.4-39.1 (54. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.3) 44. and urinary levels reflect intake from all sources.3-45. Molybdenum is generally considered to be of low human toxicity.9-45.1-79.5 (39.9-41. EPA.5-44.5 (36.2) 42.7-62.1 (30.4-66.2 (40.8) 61.9-68.5 (38.6 (57. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.5-48.5-92.1-127) 90.6-76.9 (39.8-65.1-100) 86.4) 61.1 (33.7) 45.9) 44.4) 44. population from the National Health and Nutrition Examination survey. U.2 (33.6-78.8-46.9 (39.3) 37.2 (57.2 (69.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42. urinary excretion over six days rose to 50% and 67%.7 (75. 1961.6-41..7) 53.5 (50.0-56.9-42.7-43.1 (49.3 (37.0-38.3) 56.9 (35.2-65.1) 43.1-39.5 (78.3 (37.2 (43.8-47.8 (90.8) 71.4-76.1-67.5) 60..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 (59.6-63.9) 31.4 (78. at daily oral doses of 95 µg and 428 µg.03 mg/kg/day in humans (IOM.3 (36.6) 48.6) 39.5-119) 90. and clinical or epidemiologic evidence of adverse effects is limited.9-45.5 (37.2 (52.8) 38.S.1-43.7-120) 87.6) Selected percentiles ( 95% confidence interval) 50th 41.2-49.5 (35.8 (75.5-60.8-66.0) 33.0 (80. 1997).1 (38.1) 65.9-61.5) 90th 108 (97.5 (54.6 (42.7) 75th 63. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 37.4) 40. Biomonitoring Information Molybdenum is an essential element for health.9) 40.5-35.1-39.2-96.8) 79.1 (37.0 (58. interval) 43.6 (59.3) 57.3-43.0-103) 103 (90.1 (82.4 (59.3 (71.8) 38.8-52.1-41.2-121) 107 (92.0-41.5 (83.9 (49.1-109) 89.4 (56. In industry.5-70.2) 43.0) 72.0-46.2) 38.5-97.0) 39.7) 62.4 (44.1 (39.6) 43.4-120) 101 (84.3 (83.5-99.2-47.6 (36.S.2 (73.0) 53.5 (40.1-45.6 (71. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.5 (79.1-43.4) 48.4-185) 106 (94.9 (73.0) 44.5) 73.4) 60.2) 55.0 (74.1 (40.1-112) 78.8-42.1-34.5) 63.8) 62.8) 37.8 (56. 1995).4 (55.5-50.5-46.3 (55.2) 39.2 (50.2-41.5 (65.7-38.0) 36.2 (37.4) 116 (101-126) 104 (88. of the ingested dose (Turnlund et al.6-45.5-45.8-118) 81.3) 40.8-84.9 (40.7 (30.6-88.7-137) 129 (109-155) 112 (97. 1999). the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.3-59.3 (36.3) 43.1) 37.4 (40.1) 40. respectively.1 (42.3) 61.4) 89. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3-56.5-62.3-52.

Ronchi A. van Sprundel MP. excretion. White MA. Turnlund JR.niehs. 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. Washington. Koval’skiy GA. Yarovaya GA. and zinc: a report of the Panel on Micronutrients. Gatti A. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Dietary reference intakes for vitamin A. Zhurnal Obshchey Biologii 1961. 4/14/09 White MA. iodine. 1998.216:253-270.. X.123(1):81-85. Van Meerbeeck JP. Trace element reference values in tissues from inhabitants of the European Union. Turci R. Molybdenum 1993 [online]. EPA). 1998). Available at URL: http://www. Available at URL: http://ntp. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. A study of 13 elements in blood and urine of a United Kingdom population. vitamin K.nap. Kristiansen J.15(2-3):149-154. Atlanta (GA). molybdenum. chromium. 2005). 2001). 144-154. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.gov/iris/ subst/0425. Ann Rev Biochem 1997. boron. 420-441. U. Rapid Comm Mass Spectrom 2002.66:233-267. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Sabbioni E. Schindelin H. iron. silicon. Schleyerbach U. 4/14/09 Sievers E.. Molybdenum.Metals in urine for the U. TR-462.22(3):179-191. Occupational risk factors of lung cancer: a hospital based case-control study. Am J Clin Nutr 1995. Sci Total Environ 1998. nickel. Kisker C. Environmental Protection Agency (U. 4/14/09 Iversen BS. (DC): National Academy Press. Rees DC. Menne C. 2001. pp. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. References Centers for Disease Control and Prevention (CDC). Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Molybdenum in infancy: methodical investigation of urinary excretion. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Molybdenum-cofactorcontaining enzymes: structure and mechanism.S. Geneva: WHO. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Molybdenum absorption. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Sabbioni E. 2002. Occup Environ Med 1999.htm. 2005. pp.. Shmavonyan DM. arsenic. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Available at URL: http://books. National Toxicology Program (NTP). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Peiffer GL. 1996. Vermeire PA. manganese.epa. In: Trace elements in human nutrition and health. Food and Nutrition Board. vanadium. Third National Report on Human Exposure to Environmental Chemicals. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. J Trace Elem Med Biol 2001. Minoia et al. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Weyler JJ. Analyst 1998. Keyes WR. et al.nih.php?record_id=10026&page=420. 16:1313-1319. Droste JHJ.gov/index.S.S.62(4):790-796. copper. Minoia C. Christensen JM. World Health Organization (WHO). Sciarra G. edu/openbook. 56:322-327. White and Sabbioni. Aprea C. Schaub J. Institute of Medicine (IOM).

Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. 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. see Data Analysis section) for Survey years 99-00. population from the National Health and Nutrition Examination Survey. carboplatin) in the treatment of cancer. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. strength at high temperatures. which may vary for some chemicals by year and by individual sample. as oxidation catalysts in chemical manufacturing. 230 Fourth National Report on Human Exposure to Environmental Chemicals . respectively. 7440-06-4 General Information Platinum is a silver-gray. jewelry. and high catalytic activity. 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. 1998). dental alloys.07.04. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Platinum compounds are used in electrodes. thick-film circuits printed on ceramic substrates. and 03-04 are 0. cisplatin. however. and iron.. Important properties of platinum are resistance to corrosion. < LOD means less than the limit of detection. and as drugs (e.04.S. copper.g. 0. and 0. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. 01-02. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.Metals Platinum CAS No. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.

oral).. Platinum metal and insoluble salts can produce eye irritation. Fourth National Report on Human Exposure to Environmental Chemicals 231 . Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al. The carcinogenicity of other platinum compounds remains uncertain. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. whereas soluble platinum compounds (e.e. inorganic salt. Toxicity is determined by the type of compound (e. Information about external exposure (i. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Platinum metal is biologically inert. * Not calculated: proportion of results below limit of detection was too high to provide a valid result...g. metallic. 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. population from the National Health and Nutrition Examination Survey. intravenous medicinal use. 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.. inhalational. cutaneous.g. or recommended for the metal form by NIOSH (Czerczak and Gromiec. 1975a. 1969... 2000). 1969). Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH.Metals doses or at biomonitored levels from low environmental exposures are unknown. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP. Saindelle et al. platinum metal and insoluble salts are very poorly absorbed (<1% of a dose) and cleared from the body within a week after a single dose.g. 1975b). When ingested or inhaled. 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. route of exposure (e. and duration of exposure.. or organometallic).S.

Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Nickel. Blanks R. Schierl R. 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.35:313-321. Crocker W. Part 1: monitoring of urinary concentrations.13(1):24-30. which elevate urinary platinum by five to twelve-fold (Begerow et al.01 µg/L (Becker et al. J Expo Anal Environ Epidemiol 2003. Neuendorf J. Iavicoli I. Ensslin AS. Uptake of antineoplastic agents in pharmacy and hospital personnel. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Kazantzis G. Pethran et al. Hysell D. 2003). Cohrssen B. Herr CE.htm. Begerow J. Kavanagh P. Hysell D. 2004) or less than 0. Rommelt H. Kulka U. Gieler U. and platinum. 1998). Occup Environ Med 1998. Levels of platinum in urine for the U. 3/31/08 Moore W Jr. Herr et al. Stilianakis NI. rhodium. Bocca B. Hebert R.56(3):283-286. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Ruff F: Histamine release by sodium cholorplatinate. Senofonte O. Ewers U. Environ Health Perspect 1975b. Seifert B. et al. Grimm CH. Kuster W. Saindelle A. Petrucci F. Schulz C. 1997.. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Arch Environ Health:1969.70(3):205-208. Schierl R. 1999. Carelli G. 2004). 1991 [online]. van de Weyer C. Int Arch Occup Environ Health 1997. Nowak D. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Wilhelm et al. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Environ Res 1975a. 2003.. Br J Pharmacol 1969.. Schierl. In: Bingham E. Schulz C. 2001). Environmental Health Criteria 125. 232 Fourth National Report on Human Exposure to Environmental Chemicals .10:63-71. and gold excretion of patients after insertion of noble-metal dental alloys. Fruhmann G. Powell CH.005 µg/L (Iavicoli et al. Int J Hyg Environ Health 2004. Platinum. Schierl R. Schierl et al. Arch Environ Health 2001. Patty’s Toxicology. 2003. Hall L. Available at URL: http://www. Kaus S. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Seiwert M. osmium. 206:15-24.Metals the International Programme on Chemical Safety at http:// www. Huber R. Allergy and histamine release due to some platinum salts. et al. 289-380. 2000..76(1):5-10. pp. eds. Farago ME. Alimonti A. Biomonitoring Information Urinary platinum levels reflect recent exposure. International Journal of Hygiene and Environmental Health 2003.123(3):451-454. ruthenium.. palladium. Czerczak S.S. Angerer J. 2004. Turfeld M. 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.. Biomarkers 1999.4(1):27-36. Moore W Jr.. and in blood and urine in the United Kingdom.61(7):636-9.207(1):69-73. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Ruff F: Platinum and platinosis. Several studies have shown that background concentrations in general populations were usually less than 0.inchem. Herr et al.. 5th ed.04 µg/L) in this Report. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. International Programme on Chemical Safety (IPCS).org/documents/ehc/ehc/ ehc125. Boos KS.55(2):138-140. Saindelle A. palladium. Raab W.inchem. Biomonitoring of traffic police officers exposed to airborne platinum. Duneman L:Long-term urinary platinum.19:685-691... Hauff K. Campbell K.htm. Wilhelm M. Platinum concentrations in urban road dust and soil.9:152-158. Analyst 1998. Int Arch Occup Environ Health 2003. New York: John Wiley & Sons. Pethran A. Pethran A. Occup Environ Med 2004. Influences on human internal exposure to environmental platinum. Urinary excretion of platinum from platinum-industry workers.. et al. Parrot JL. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al.org/documents/ehc/ehc/ehc125. Urinary platinum levels associated with dental gold alloys. Schierl R. population were below the limit of detection (0. Jankofsky M. References Becker K. Fries HG. Gromiec JP. 2003. Kelly J. et al. 1998). Thornton I.

190 (.330) .340-.590) . and 03-04 are 0.S.220 (.158) .370 (.400 (.590) .330-.390 (.420-.260 (.250) .240-.187-.156) .217 (.270 (. and 0.180 (.133-.560) .400-.190 (.170) . In the past.172) .134-.230) .300) .330) .400-.175) .440-.400 (.480) .410 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. representing distribution into other tissues.170-.185-.410 (.144 (.270-.440) .220-.320-.160 (.180-.510) .240) .350-.02.200) .400) .280 (.190 (.470 (.410-.370-.290 (.167-.340-.200) .188) .170 (.350) .300) .280) .300-.290) .290) 90th .260-.290-.430) .340) .410 (.196) . population from the National Health and Nutrition Examination Survey.156) .380) .320) .370) .172 (.270) .159 (.150-.270-.520) .310-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.218) .202 (.280 (.480) .480) .173) .520) .360 (.350-.420-.500) .260-.370-.181-.147-.230-.202 (.410-.380-.150-.230) .220) .390) .310 (.390 (.145-.270 (.220) .200 (.145 (.150-.300 (.02.250 (.350) .160 (.280) .165 (.460-.300) .156-.400) 95th .183) .430 (.350 (.170-.400-.340 (.500) .150-.159 (.290) .250-.140-.230-.180) 75th .450 (.Metals Thallium depilatory cosmetics.370-.200) .350-.360-.350 (.510 (. 01-02.170 (.690) .430) .200) .135-.450 (.170) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .390) .270 (.154-.300 (.520 (.410) .160-.450 (.170 (.230-.162-.192) Selected percentiles ( 95% confidence interval) 50th .250-.180 (.153-.210 (.470) .440 (.220 (.400) .177) .220) .220) .260-.160-.430-.430 (.160-.640) .330) .300 (. thallium readily crosses the placenta and also distributes into breast milk.250-.280) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.290) .183) .240-.260-.320 (.146 (.180 (.230) .360-.440 (.420 (.240-.270) .370 (.167 (. In addition.490) .420) . 2005).02.196) .420) .290) .210-.450 (.410 (.260 (.380 (.390) .215) .240) .149 (.330) .180-.360 (.202) .330-.390-.218) .190 (.190-.250-.450) .370 (.145-.390) .163) .170-.230 (.410-.170-.400) .330-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.470) .160 (.380-.200 (.490) .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 .270 (.243) .460 (.173) .430-.400 (.400-.470) .170-.159 (.330-.400 (.450 (.410-.230) .400-.250-.290-.380 (.420) .340) .290 (.370 (. 0.171 (.630) .400 (.330-.137-.200-.440) .360-.430-. however.450 (.147-.225) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.550 (.200 (.290 (.480) ..185 (.190 (.160-.290 (.330-. see Data Analysis section) for Survey years 99-00.350-.184 (. Thallium disappears from the blood with a half-life of several days.200) . it has not been specifically mined or refined in the United States since 1984.360 (.176 (.360) .410-.300) . thallium was obtained as a by-product of smelting other metals.197-.200-.172 (.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 .250 (.239) .470 (.250-.370-.330-.440 (.200 (.440 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.280 (.370) .420) .201 (.320) .157-.220 (.200) .240) .420) .210 (.160-.147-.206) .350-.450 (. the latter being the current major industrial consumer of thallium in this country. Human health effects from thallium at low environmental CAS No.500) .370 (.260) .200 (.270-.220 (.520) .191 (.480) .360-.220 (. respectively.280-.178) .210) .197 (.390-.148-.420-.155 (.170-.160 (.450 (.167-.320) .160 (.200-.420) .200 (.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 .173-. 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.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.410 (.410 (.490) .180-.290 (.430 (.400) .201 (.179-.310 (.390-.260 (.182-.290 (.350-.360-.450 (.180) .180-.220) .170) .190 (.420-.390-.500 (.360 (.250-.370 (.340-.440) .270 (.410-.430 (.220) .200-.310) . In the United States. interval) .260-.420) .250-. From these and other sources.370 (.460) .340-.490 (.490) Total .217) .280-.150-.310 (.170-.150-.

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

Sci Total Environ 1998. Pozzoli L. Investigation of a working population exposed to thallium. Int Arch Occup Environ Health 1981. Sabbioni E. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Centers for Disease Control and Prevention. White MA.113(1):47-53.95:89-105.5 μg/L.35(1):4-9. 7/15/09 Blanchardon E. A study of 13 elements in blood and urine of a United Kingdom population.265 people living near a thallium-emitting cement plant in Germany. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Available at URL: http://www. Brockhaus A. Kramer U. (1981) studied 1. et al. Buhlmeyer G. 2005. 1980.. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Raithel HJ. Paschal et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Manke G. Schaller et al. Trace metals in urine of United States residents: reference range concentrations.cdc. 1981. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Valentin H. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. White and Sabbioni. Challeton-de Vathaire C.48(4):375-389. Environ Res 1998.. 1992 [online]. Schmidt M. Atlanta (GA). Soddemann H. 1990. X. 1998. Minoia et al. Trace element reference values in tissues from inhabitants of the European community I. 1985). Sabbioni E.gov/toxprofiles/tp54. 2005) and are shown with results from NHANES 2003-2004 in this Report. Minoia C. Investigations of thallium-exposed workers in cement factories. and serum of Italian subjects. Celier D. 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. Cassot G.Metals (CDC.atsdr. Toxicological profile for thallium.S. J Soc Occup Med 1985.. et al. with concentrations ranging up to 76. 1998). References Agency for Toxic Substances and Disease Registry (ATSDR). 2005. Fourth National Report on Human Exposure to Environmental Chemicals 235 .html. Paschal DC.47(3):223-231. Sampson EJ. Martin J-C. 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. Third National Report on Human Exposure to Environmental Chemicals. Sci Total Environ 1990. A study of 46 elements in urine. Trace element reference values in tissues from inhabitants of the European Union. Ting BG. Gallorini M..76(1):53-59. Brockhaus et al. Dolger R. Boisson P. et al. Radiat Prot Dosim.216:253-270. Apostoli P. Ewers U. Pirkle JL. Schaller KH. Morrow JC.1 mg/m3 (Marcus. Wiegand H. Jackson RJ. Pietra R. Int Arch Occup Environ Health 1980. blood. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium.

100) Selected percentiles ( 95% confidence interval) 50th .084 (.390 (.120-.120) .073-.084) .095-.420-.151) .060 (.080-.620) .140 (.300 (.090-.140 (.180-.110 (.132) .520) .090) .060 (.093) .310-.150 (.091) .130) .310-.090-.330) .530 (.330) . bronzes in pigments.070 (.110 (. Evidence is lacking for the carcinogenicity of tungsten.380-.360 (.070-.450-.310-.065-.340) .070 (.460 (.640 (.080 (.260 (.090-.130-.050-.140 (. and for producing ferrotungsten.290) .082-.460 (.340-.050-.210 (.100-.360) .056-.190-.550) .460) .070-.400 (.120) .270-.080) .210 (.076 (.220-.140-.320-.080-. which is used in the steel industry.200-.090-.170) .290-.230-.170 (.160 (.101 (.130) .570 (.080) .160 (.170) .069) .560) .101-. respectively.080) .133) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).510 (.560 (.080-.200) .550) .360 (.620 (.056-.120-.300) .100 (.250-.135) .080 (.380-.180 (.123-.100) .410-.490 (.250) .060-.190-.086 (.210-.130-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.430-.460) .230-.082 (. Tungsten compounds are used as lubricating agents.190-.290 (. filaments for incandescent lamps.230 (.070) .420-.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 .310-.110 (.070-.400 (.160) .130-.430 (.460 (.060-.070 (.260-.490) .570 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.110-.340-.060-.270 (.150-.630) .370) .360-.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 . 0.093 (.130 (.090) .500 (.120) .105 (.450 (.100-.280-.160-.350) .500 (.580) .250) .280 (.300 (.180-.090 (.113 (.095-.430-.250-.550 (.120 (.04. see Data Analysis section) for Survey years 99-00.480) Total . Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.087) .160-.160-.590) .060-.126) .170 (.084-.800) .790) .210) .060-.390) .400 (.430 (.370 (.093-.330-.090-.380-.430 (.100 (.320 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.060-.810) .260 (.090 (.04.090-.670) .180 (.060 (.350) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.270-.380 (.470-.130) .530 (.120-.070-.510-1.050-.100 (.150) .410 (.097-.062 (.280 (.560) .100) .130) .270 (.370-.250) .260-.300-.122) . interval) .100) .210 (.130) .430) .190-.110) .140-.150 (. and as catalysts in the petroleum industry.550) .180) .150 (.560) .370-. which are used in rock drills and metal-cutting tools.240-.180-.076 (.058-.690) .370 (.770 (.530 (.440) .190) .190 (.270 (.073) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.120-.110-.204) .140) 90th .270-.380) . mainly as scheelite (CaWO4).290-.071-.130-.073-.100-.120-.090-.130 (. Little information is available on the toxicity of tungsten.090 (.160-.074-.092 (.220) .220 (.065 (.070-.160 (.S.116) . Occupational exposure is from dusts released during grinding or drilling of hard metals.350) .250) . 01-02. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.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 .100) .230) .062 (.330-.092 (.096 (.350-1.250) .290) .113 (.090) .270-.650) .400 (.370 (.180) .220) .310-.100 (.200 (.080 (.210 (.068) .120) .109) .096-.087-.060 (.470) . population from the National Health and Nutrition Examination Survey.078-. 236 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.470 (.400) .050-.300) 95th .160 (.073 (.340-.080 (.088 (.560) .210 (.04.110 (.060 (.320 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.137 (.088) . Tungsten is used mainly for producing hard metals.180-.070) .090-.082 (.230-.158 (.360-.066-.290-.120) .160 (.081 (.082) .310 (.120) .107 (.240 (.170) .070) . and 03-04 are 0.53) .190 (.520) .310) .950) .111-.230-.510-.800) .620) .350 (.360 (.064-.380 (.071 (.104) .250) .470 (.160) .00) . and 0.170) .070) .180) .077-.092) .110 (.113 (.380-.120-.520) .110) .260-.830) .110-.140 (.060 (.090) .080) 75th .400-.180) .113 (.260) .470) .100) .220) .320-.105) .Metals Tungsten CAS No.320) .500) .330 (.230) .080 (.069-.170-.

250 (.452-.062 (.069 (.103-.215) .245-.093-.091) .201 (.084 (.253-.216-.206-.109 (.315-.199 (.083 (.119-.078 (.255 (.078-.153-. 2005).067 (.072-.216 (.104-.070 (.155-.068 (.161) .136-.462) .333) .060-.283) .083) .216-.339 (.092) . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.071) .133) .217-.073 (.S.386) .169 (.067 (.333-.634 (.300-. 2001).197 (.180-.075 (.333 (.091) .056-.069-.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 .301) .215 (.261-.078) .073 (.255-.205-.105 (.095) Selected percentiles ( 95% confidence interval) 50th .410-.S.253 (.060 (.055-.301) .075) .333 (.098-.158) .079) .143 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.063 (.085) .107-.431) .061-.300 (.066 (.083 (.054-.329-.087) .179-.341 (.111 (.188-.211 (.414) .130 (.465) .139 (.197) .300-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.146) .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 .086-.333 (.065-.082) .077-.165) .167) .074 (.158 (.088) .075) .060-.072 (.065 (.199 (.080 (.150-.120) . 1997).164 (. 2001-2002.308) .065-.071 (.153) .426) . or exposure that a control group of non-metal workers had mean levels differences.203-.497 (.214) .059-.105 (. 2003.071) .074-.358) .081-.073 (..331-.412 (.065-.078) .158) .(Kraus et al.100) .300) .198) .108) .061-.154) .158) .293 (.130-. interval) .169) .218 (.117) .119 (.063-.146 (.063-.359 (.122 (.279 (.287) .250 (.131-.157) .360 (.167-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.272-.085 (.148) .064-.301) .121 (.439 (.294 (.308) .253) 95th .070 (.138 (.150 (.106 (.217-.267-.090-.181 (.121-.080-.302-.144-.080 (.426) .436) ..056-.080-.174) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.174 (.168 (.286-.554) .667 (. measure urinary tungsten.087 (.250-. Nicolaou et al.184 (.436-1.375) .582) .364 (.133) 90th .057-.214-.086) .279 (.237-.167-.299 (.139-.125 (.258-. population (CDC.075-.068-.465) .329 (.126-.154) .077) .179-. (1987) found possibly due to methodologic.151 (.431) .098-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.667) .279 (.067-.231 (.823) .340 (.317 (.072-.096) .381) .S.138 (.216 (.074) .059-.146 (.216-.058-.065 (.091) .061-.439) Total .222) .053-.880) .136-.359 (.089 (. Patients with medically-inserted tungsten found at increased levels in drinking water.431) .091) .482 (.094) . population.078 (.074-.739) .100) .255 (.079) .727) .339 (.125) .500) .120) .484) .176-.071 (.116 (.459) .075-.082 (.209-.064-.116-.379 (.133) .094-.347 (. 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.084) .091 (.065) .098) .136-.278-. Using neutron activation analysis to 2000.122-.190) .148 (.187) .079 (.086) .224) .150-.258 (.385 (.069 (.170-.124-.317-.200-.063-.344-.077) .117 (.079) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.049-. population from the National Health and Nutrition Examination Survey.083-.144 (.231-.333) .077-.116) .073 (.265 (.186 (.200-.090-.353 (.075 (.439 (.306) .538) .100 (.439) 790 679 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 237 .071) .167) .354-.066 (.085-.063-.201) .138) . and 2003-2004 (Paschal et al.208-. similar to those in this Report (Schramel et al.122-.275 (.198-.353 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.071-.082) .285) .453) .392) .089) .233-.284) .124 (.108-.084) .057-.383 (.302-.326) .091 (.098-.095-.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 .197-.484 (.222-.074) 75th .354) .081 (.079) .094) .237) .240-.081) .317) .084 (.797) .136 (.071 (.145 (.197) .267) .333 (.099-.152-.088) .143-.098 (..237) . 1998).059 (.176-.136-.333-.054-.081 (.605) .109-.555 (.079 (.063 (.083) .270 (.086) .059-.139) .093) .28) .

Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Manke C. 4/15/09 Centers for Disease Control and Prevention.Metals blood. Wendler I. Seghizzi P. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Feuerbach S. mercury. Ting BG. Third National Report on Human Exposure to Environmental Chemicals. Schaller KH.(2):73-77. Weber A. Zobelein P. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. cadmium. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. Environ Res 1998. 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. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. urine. J Trace Elem Electrolytes Health Dis 1987.69(3):219-223. The determination of metals (antimony. and hair (Bachthaler et al. Churchill County (Fallon). 238 Fourth National Report on Human Exposure to Environmental Chemicals . Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Int Arch Occup Environ Health 1997. Paetzel C. [online] 2003. bismuth. thallium. 2004). Centers for Disease Control and Prevention. Sabioni E.htm. Sampson EJ. Nicolaou G. Occup Environ Med 2001. tellurium. Cancer Clusters. References Bachthaler M. platinum. Lenhart M. National Center for Environmental Health. Morrow JC. et al.58(10):631-634. Link J. Cassina G.. Pietra R. Atlanta (GA). Paschal DC. Schramel P.76(1):53-59.cdc. Pirkle JL.62:380-384. 2005. lead. Kraus T. Catheter Cardiovasc Interv 2004. Nevada Exposure Asssessment. Mosconi G. Angerer J. Jackson RJ.gov/nceh/clusters/Fallon/study. palladium. Schramel P. Angerer J. Trace metals in urine of United States residents: reference range concentrations.

013 (.007-.009) .035-.030 (.037) .158) .008 (.030 (.033-.016) .019-.050) .008 (.007) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).008) .006-.012) .039) . and 234U.018) .012 (.035) .037-.010) .009-.007 (.008 (.036) .006-.008 (.045) .018) .012 (.009-. Since the 1990’s.020-.027) .007-.043 (.026 (.010) .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 .017) .024-.037) .011) .027-.009-.007 (.031-.022-. 235U (about 0.013 (.037) .040) .014 (.009) .007 (.009-.010 (.023 (.012-.022-.010-.063) .031 (. milling.009) .036-.005-.008 (. 0.009 (.038) .027-.073) . 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.008-.007) 75th .010) .008) .016) .054-.028 (.72%).012) .031 (.034-.017-.006-.018-.026-.011-.031 (.011 (.009) Selected percentiles ( 95% confidence interval) 50th .019-.010) .007-.056) .011) . human exposure occurs primarily by inhaling dust and other small particles.Metals Uranium CAS No.046) .009-.017) .007) .016-. respectively.014 (.021 (.029-.025-.008 (.041 (.008) .007-.013 (.007) .007-.017) .012-.036) .027 (.029 (.034) .009) .046 (.010-.012 (.011-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.014 (. 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.010-. including nuclear weapons.010) * .008-.009) .016) .007-.005-.009-.020) .017-. nuclear fuel.006 (.007 (.114 (.013-.009 (.011-.016) .006 (.046 (.024 (.028 (.006-.017 (.009-.015 (.052 (. or processing.009) .009) .017) .016-.010) .007-.033 (.017-.008) .033 (.279) .040-.051) .006-.008 (.006-.016-.010) .020-.047 (.011-.035) .065) .067) .009 (.011) .006-.039-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.019 (.027 (.010 (.013 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .023) .021 (.011-.009 (.042) .011 (.066) .015) .021-. and 0.012 (.042 (.008-.046-. population from the National Health and Nutrition Examination Survey.011) .056) .014 (.006-.069) .043) .006-.041 (.021) .015 (.011) .033) .022-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.006 (.007 (.013 (.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 .060 (.009 (.012-.037 (.010) .S.064 (.004.027) .015) .026) .009) .018) .038 (.008-.009-.021) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water. and 03-04 are 0.026 (.036 (.007 (.013 (.030 (.017-.009 (.016) .009) .006-.026 (.027-.053 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.010-.026-.009) .036 (.016 (.008 (.011) .012-.034-.027 (.007-.013) .006-.023) .012-. see Data Analysis section) for Survey years 99-00.010 (.007) .020-.027 (.037) Total .012 (.022) .011-.014 (.008-.018 (.008 (.005-.021) .010-.020-.049) .013 (.065) .012) .007-.007-.009 (.016) .017-.048 (.024-.018) .014 (.023-.008-.055 (.008 (.007-.040-.007 (.040 (.088) .017 (.023 (.031 (.054) .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 (.007-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.049) .040) .012-.008-.023-.023-.010-.046 (.007 (.007 (.008 (. 01-02.008 (.023) .012 (.020) .006 (.006-.008 (.017-.008-.026) 95th .028-.039) .017) . interval) .022 (.021-.067) .007-.013) 90th .013-.012) . and as an aid in electron microscopy and photography.009) * .009-. in some ceramics.053) .031 (.005-.010 (.006-.009 (.020 (.011-.030) .009 (.004.062) .010) * .013-.072) .010) .019-. Thus.008 (.009 (.027) .048) .010 (.019-.008 (.007) .009) . 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.023-.054) .009) .050) . In workplaces that involve uranium mining.015 (.127) .040 (.026) .020-.007-. Uranium has many commercial uses.007-.015 (.032 (.011) .044 (.009-.023 (.028 (.007 (.029-.007-.008) .045) .005-.027) .009) .046 (.007-.008 (.030-.018 (.024-. Variable concentrations of uranium occur naturally in drinking water sources.007-.028-.036-.021 (.015-.007 (.005.

022 (.006-.032) .010-.024) .007 (.028) .035 (.029) .048) .010-.008-.051 (.024 (.051) .011-.016) .020) .020-.021 (.026 (.014 (.012 (.039) Total .021 (.008) .011 (.025 (. Depending upon the specific compound and solubility.033 (.006-.034 (. with much slower elimination from bone.009) * .006-.009) .067) .027-. Inhaled uranium-containing particles are retained in the lungs.025-.014-.014) .008) .020-.018-.033) .030 (.035 (.010) * .024-.017) .006) .020 (.013 (.042-.047) .029 (.011) * .008 (.018-.013 (.013 (.031 (.011-.008-.008 (.015-.051) .016-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.013 (.010 (.006-.006-.006-.039) .009 (.015 (.024) .061) .016-.007 (.012-.026 (.008) .010 (. population from the National Health and Nutrition Examination Survey.009-.004-.006) .006-. In cases of retained DU shrapnel.039) .017-.012 (.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.040 (.013) .011-.006-.015) .009-.042) .019 (.009) .006-.009-.027 (.007 (.006) .030-.028) .028 (.033 (.008-.008 (.031-.006-.021) .004-.015 (.010-.007 (.007-.026) .019-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.019-.019-.010) .009) .005 (.007 (.029) .006) .029) .006-.058) .034 (. interval) .017-.009 (.017 (.027-.009 (.009 (. liver. the shrapnel acts as a source of chronic.025-.056) .007 (.006 (.007-.009) .146) . 2005).022-.008) .008 (.080) .010) . kidneys.030 (.033 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.016) .008-.020 (.034) .021 (..024 (.008) .007 (.017-.009) .012 (.009) .027-.009 (.008 (.006-.007) .006-.005 (.007 (.011-.007-.015 (.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-.007 (.054) .063) .010-. Radiation risks from exposure to natural uranium are very low.006-.012) .017 (.074) .005-.043 (.027) .015-.042) .018-.019 (.005-.010-.007 (.009) Selected percentiles ( 95% confidence interval) 50th .029 (.009) .011) .005 (. After long term or repeated exposure. 0.013 (.041) .007 (.034 (.029) .007) .033 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.012-.039) . 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) .007-.015-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.009-.014-.016) .011 (.025-.012 (.007 (.050 (.007 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .011-.020-.027 (.006 (.007 (.005-. Health effects from uranium exposure result from chemical toxicity to the kidney.008) .024-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.017-.026 (.014) .016-.016) . low level exposure.077) .024) .008 (.009) .011) .009) .007-.014) .009) .013 (.020-.020 (.032) .006-.015-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.023-.051) .016) .015 (.024) .014-.008-.019-.015) .007-. which can occur occasionally from high occupational exposure.014 (.053) .006-.006-.005-.021-.034-.008 (.037 (.007 (.007-.006-.008) 75th .050) .006 (.053) .022-.007-.030) .013 (.010) .007) .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 .019) .028) .028-.018-.005 (.015) . 1992).013 (. 2003).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 .044) .005-.010-.030-.059 (.006 (.013-.030) .100 (.006-.027) .045 (.019 (. where limited absorption occurs (less than 5%).1%-6% of an ingested dose may be absorbed.S.021 (.008 (.012) .018 (.034 (.012 (. Uranium is eliminated in feces and urine.006 (.010-. After exposure to soluble uranium salts.034 (.007 (.010-.016 (.048) .017) .007 (.013) .034-.012) .007 (..010 (.012 (.018) .270) .008 (.024-.019-.013 (.009-.010-.030 (.011-.016-.013) .010 (.009) .022 (.017) . which represents distribution and excretion.016) .007-.005-.016) .007 (.006-.014) 90th . After inhalation.022) .027-.010-.010) .024 (.008) .016) .015) .013 (.006-.006) .011-.022-.058) .005-.009-.025-.006-.011-..006-.011-.006 (.010 (.Metals impact.007 (.008) .024) .008) .025) 95th .026-.022 (.018-.007-.008-.008) .010) .012 (.011) .019) .025 (.028) .028 (.029 (.007 (.050) .010) .006-.008 (.015-.027 (.

. 2004).162 μg/L) (Orloff et al.S.. Hamilton MM. 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. Ejnik JW.Metals injury associated with elevated urinary uranium levels (Kurttio et al.078 μg/L (ranging up to 5. Uranium content of blood. NRC. 2000). Durakovic A. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Boyd P.1996. Dietz LA. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Atlanta (GA)...78:143-146. Breitenstein BD..066 μg/g creatinine (Gwiazda et al. In a study of 105 persons exposed to natural uranium in well water.. respectively. population. 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. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Karpas et al. Metivier H. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 2002). Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 2002. EPA. A cohort of 46 U.168(8):600-605.011 μg/L (McDiarmid et al. Sci Total Environ 1991. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. In the same study.61 μg/g creatinine. In: Gerber GB. ingestion. 2004). soldiers evaluated before. eds. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Six workers in a depleted uranium program showed concentrations of 0. Thomas RG. Horan P. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. In 17 U. IARC and NTP have no ratings for uranium human carcinogenicity. during. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU..65 μg/L). 1994. the geometric mean urinary uranium concentration was 0. References Bhattacharyya MH. 1991.S. and no consistent effects on multiple endpoints of kidney function were found.cdc.gov/ toxpro2. 2006). (Kurttio et al. 2004).html. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Hamilton et al. Komaromy-Hiller et al. 1992. Squibb K. Galletti. (May et al. The U. urinary levels of uranium were as high as 9.. Information about external exposure (i. Stradling GN. Drinking water and other environmental standards have been established by U. Dang HS. Muggenburg BA.. Mil Med 2003.atsdr. Zimmerman I. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. the median urinary concentration was 0. pp.S. or wound contamination. Kent (England): Nuclear Technology Publishing. Third National Report on Human Exposure to Environmental Chemicals. and 2003-2004 (Dang et al.110 to 45 μg/L (Ejnik et al.107:143-157. Carmichael AJ. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.. 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. the median urinary uranium concentration was 2. in that the levels were below their respective detection limits (Byrne et al. McDiarmid et al. with emphasis on quality control. but in whom no shrapnel was embedded.. had a mean urinary uranium concentration of 0. Health Phys 2000.. Benedik L.. Tolmachev et al. Byrne AR. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. 2000). Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. 1978).62:562-566. 2004). Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Pullat VR. et al. 1-49. Volf V. Health Phys 1992. Vol... 28 soldiers who may have been exposed to DU by inhalation. Radiation protection dosimetry.S. 2001-2002. 41 (1)... 2006). 2006. environmental levels) and health effects is available from ATSDR at: http://www.e.. although slightly increased during and after deployment. 2003. 2006).S. McDiarmid M. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Pillai KC.55 μg/L (median 0.1992. 2006). 2005. 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. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Centers for Disease Control and Prevention (CDC).S.

S.86:12-18. Sampson EJ.71(6):879-85. Biologic monitoring for urinary uranium in Gulf War I veterans. Clin Chim Acta 2000. Englehardt SA. Pirkle JL. Salonen L. Kurttio P. Squibb K. Smith D. Metcalf S. et al. et al. Mistry K. Van der Venne MT. Renal effects of uranium in drinking water.91(2):144-153. July 1978. Environ Res 2004.79(1):11-21. Hancock RG. Am J Kidney Dis 2006. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Uranium and thorium in urine of United States residents: reference range concentrations. Oliver M. Wilson PD. Saha H. Orloff KG. Howerton K. Scott K. Nuclear Regulatory Commission (U. Makelainen I. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Komulainen H. Kidney toxicity of ingested uranium from drinking water. Li WB.296(1-2):71-90. Saha H. Shelly T. Health Phys 2004. VI. Sci Total Environ 1994. Heller J. Human exposure to uranium in groundwater. Ash KO. Charp P. Pinto V. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium.82(4): 527-532. Harmionen A. Marino R. Auvinen A. Tolmachev S. Lorber A. Gucer P. Andrews WS.87:51-56. Karpas Z. Health Phys 1996. Ough EA. Squibb K. Environ Health Perspect 2002. McDiarmid M. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. D’Annibale L. Paschal DC. Bennett LG.67(8-10):697-714. Wahl W. Jackson RJ. May LM. Health Phys 2003.S. Gwiazda RH. Noguchi H. Environ Res 1999. Kane R. Engelhardt SM. Cremisini C. Int Arch Occup Environ Health 2006. Element reference values in tissues from inhabitants of the European community. et al. Salonen L. Ting BG. Jarrett JM.158:165-190.44:29-40. Karpas Z. Lewis BM. NRC).S. Paretzke HG. Inductively coupled plasma mass spectrometry as a simple. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Health Phys 2006. et al. Ejnik J. Oeh U. concentration and daily excretion of uranium in urine of Japanese. McDiarmid MA. Kuwabara J.94:319-326. U. Health Phys 2004. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Pekkanen J. rapid. Nuclear Regulatory Commission (NRC) Guide 8. Sabbioni E. Review of elements in blood. Oberbroekling KJ.22–Bioassay at uranium mills. Uranium daily intake and urinary excretion: a preliminary study in Italy. Katorza E. et al. McDiarmid MA. Roth P. Comparison of representative ranges based on U. Kalinsky V. et al. Kurttio P. Biokinetic modeling of uranium in man after injection and ingestion. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Marko R. J Toxicol Environ Health A 2004. Cordero S. Komaromy-Hiller G. Costa R. Hamilton EI. Roiz J.47(6):972-982.S. patient population and literature reference intervals for urinary trace elements. U. Washington (DC): NRC.81:45-51. Radiat Environ Biophys 2005. Halicz L. Health Phys 2002. Auvinen A.85:228-235. Hollriegl V.110(4):337-342.Metals Galletti M.

54 (3.39-4. population from the National Health and Nutrition Examination Survey.0) 14. and limited applications in pharmaceutics.S. lettuce) can be the main sources of intake for humans (FDA..0) 13.0) 9.0 (9.0-29.81) Selected percentiles ( 95% confidence interval) 50th 3.0 (11.21 (2.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.0 (9.03) 3.40) 3.30) 6.0-17.0) 10. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.50 (8.90-3.0 (10. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.90 (5.0 (8. Perchlorate is stable under most environmental and physiological conditions.20) 7.0-18.19 (3.0-17.0) 16. matches.50) 3.80) 7.93 (4.20 (2.67-5.40-4.0) 13. fabric dyeing.30 (2.10-11.47-4.0-15.0) 708 617 681 652 1228 1092 Limit of detection (LOD.10-12.0) 9.00-5.80) 3.30-6.S.51 (3.30 (5.5 hours and has a small estimated volume of distribution (Crump and Gibbs.00-6.0) 9.0) 14.20 (4. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.74-3. Survey years 01-02 03-04 Geometric mean (95% conf.50 (3.40 (5.10-11. and reducing agents.0) 13. interval) 3. In addition.50) 5. Perchlorate was added to the U.75 (3.40) 90th 10.0-18.0 (9.10-7.10-4.38) 5.0) 11.02 (3.10 (2.40 (3.22 (2.60 (4.70-12.0-14.0 (8.76) 4.0-15.80-4.50) 6.0-17.0 (11.80-12.0 (11.00) 5.16) 3.0) 9.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.30 (2.80-6.76 (3.90 (3.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.50) 11.31) 2.80 (3.60) 8.0-17.20 (4.0) 14.60-6.20 (5.90-10.70-3.00) 7.0-17.80 (7.20) 3.0 (11. 2005).0 (11.12) 3.50 (5. It is normally found and produced as the anion of a sodium.45-4.40 (4.40 (4.0 (11.0) 8.0) 9.0) 13.11) 4.20-12.60) 5.40) 6.40) 3.0) 13. 2007).0) 13.90-3.70-11.30 (5.0-19.46) 3. certain catalytic metals.20-11.90-6.10 (7.50-11.40 (5.0) 95th 14.90 (4. and electroplating.05 and 0.89-3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0 (9. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.10) 3.50-4.70-3.40 (3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.90 (2.70 (3. 2002).05 (2.40-7.10 (5.60-7.0) 10.10) 12. leather tanning.50-4. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.0 (8. or ammonium salt. 1998).62 (3.65) 3.32 (3.56) 3.88) 3.30-7.18-3.29-3.40-5.84) 14.50-7.80 (3.20) 4.70 (3.Perchlorate Perchlorate (Urbansky.93-4.40-13..0) 11.90) 5.26 (2.09) 3.90-11.40-6.50-3.20-3.0) 19.40) 4.EPA.00) 3.90) 6.50) 5.90 (5.0) 15.05. potassium.01 (2. Other manufactured uses include fireworks.60) 3.96 (3.10 (6.0 (12. 2005).80) 75th 6.75-3.0 (9. 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.80-8.90-12.87-3.35 (3.0) 9.90-9.44-4.70) 3.10) 5.70 (3.66) 3. and certain plants with high water content (e.60 (4. but has strong oxidant properties in the presence of concentrated acids.68) 4.0) 15.81-16.08-3.90 (5.22-5. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.70-7.40-4. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.60 (7.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.20-4.79 (2.S.70-5.0 (11.0 (12.0) 8.0) 10. 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.20-4.0-20.10 (6.19-4.49-3.40) 2.93-3.0 (12.20 (7.00) 4.40 (5.0 (11.0) 13.0) 12. laboratory analysis.70-6.0 (11. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.90-9.30-17.0) 13.g.30-7.0 (9.0 (13.51 (3.0 (11. milk.00-6.0) 11.10) 5.20 (8.20 (2.11) 3. Drinking water.0 (12.90-11.00) 3.80) 12.20 (6.70-9.0 (8.10) 3.40-11.0 (8.07-4.30-19.0 (9.80-4.30) 6.40 (8.80 (6.0-17.80-15.40) 3.0-18.0-23.

29) 2.12-2.61 (5. and the presence of other substances known to affect thyroid function (e.89-3.00-3.87) 7.60-6.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.20-3.56 (3. thiocyanate.0) 11. 2003. NAS.76-3.14 (2.90) 5.0 (8.80-3.10 (4.10) 6.45-2.50) 2.20-4.0-14.30-10.56-3.87-3.30) 5.40 (3.00-2.35 (4.76 (3.40 (3.50 (3. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.3) 8.44) 3.0 (9.58) 2.20 (4.10-3. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.40) 17.20) 3.0) 9.42 (3.12 (6.09) 3. Lamm and Doemland.40 (7.36 (8.00) 9.2) 8.0) 12.51 (3. However. perchlorate is negative in most genotoxic assays (U.80-3.33-6. 2005.00-11. population from the National Health and Nutrition Examination Survey.60-8.70-5.47) 2. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.0) 9.26) 4.10) 13.6-17.19-10.08 (3.4 (10.37 (4.39 (3.1-13. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.81-3. 2000).21 (2.26 (3. U.60-11.52-9. gender. 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.50) 2.39) 2. Li et al.S.10) 3. medications).80) Selected percentiles ( 95% confidence interval) 50th 3.22-4.60) 8.0) 4. Also. 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.4) 8.0-44.20-10. women with urinary levels of iodine less than 100 micrograms per day.20 (2.3-14.33-12.0-17.19-6. Many factors may be important in consideration of perchlorate action on the thyroid: dose.64-3.0 (10.25 (3.10 (6. menopausal status.02-4.3 (10.22 (2.97-5. age.80 (7.46-13. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.08) 3.S.91) 4.0-19.5) 8. In the U.46 (3. levels..61-5.66) 3. Steinmaus et al.20 (7.70 (2..70) 2. 2002).60) 10.60-5.0 (9. dietary iodine intake.87 (7.35 (2.99-3.0 (11.05 (4.50) 6.S. 1999.40-10.0) 6.20-9.00 (2.43) 6.54 (3.72 (3.0) 12..00) 3.35) 3. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.40) 3.50) 9.60-15.70-4.60 (3.1 (8.25) 5.86) 4.25) 5.20) 8.53 (2.70) 10.50 (6.3) 11..1 (11.0 (11.37-13.Perchlorate inhibition (RUI). but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al. 2002.87 (5.0 (8.1-16. During gestation and infancy. although iodine intake was higher than U.29-6.34-3. 2002.4-16.75) 3.70 (2.03 (2.60-11.54 (2. chronicity of exposure.84) 2.24 (4.67) 5.1-22. 2005).33 (7.2) 8.93-7.50-3. Lawrence et al. 2005).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 .52 (8.64) 5. 2006. nitrate.10 (2.30 (5. 2007).95 (2.EPA.4 (8.g.90 (4.0-14..93-8.30-5.25) 5.24-2. Survey years 01-02 03-04 Geometric mean (95% conf.5 (13.70-15.0) 10.41-9.93-5. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3. up to 68% RUI has been demonstrated.8 (11.00 (6..S.98) 3.00 (4..09 (7.6) 12.07 (2.30) 90th 9.30-5.S.3) 12.0) 7.51-4.50-5. 2005).0) 14.04-3.39-4.7 (11.32) 5..45) 3.02) 3.50) 95th 12.10 (4.20-3.20 (3.50) 5.73) 3.40) 5.S.90-3.90 (2.0) 13.44-6.90-2.04-3.4 (11.22-6. 2001. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.60-5.EPA.0 (11.70 (4.30 (6.59) 3.30 (3.99 (5.16-3.46-4.90 (7.18-3.80 (7.90 (2.87) 2.77 (3.10 (1.20 (6.4) 13.1-14.74) 7.61-10.90-11.6) 20.60-3.15-12. 2005. Greer et al. in a representative sample of U..30) 75th 5. interval) 3.70-3.10-7.90-20.40 (4.1) 8..10) 4.90-9.83 (5.0) 13.0) 12.4 (11.60) 3.80 (4.0) 12.93-5.50-9.S. levels and sufficient in most participants (Tellez et al.82 (5.89 (2.0 (9.60-8.71 (5.96) 2.90-15.22-4.0) 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 3.00) 4.30) 3.93) 3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.

Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.113(8):10011008. Lamm SH. Washington (DC): National Academy Press. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.46(5):509. Magnani B. Thyroid 2001. Richman K. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Daaboul JJ.S. Environ Sci Technol 2006. 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. Barnard JC. Perchlorate in the United States.114(12):1865-1871. Jackson WA. Environ Health Perspect 2006.atsdr. EPA reference dose (Blount et al. most of the population is considered to be below the U. Pirkle JL.. Primary congenital hypothyroidism. Thyroid 2000. J Occup Environ Med 2000. Erratum in: Environ Health Perspect 2005. Crump KS.gov/safewater/ccl/perchlorate/perchlorate. Also. epa.41(5):409-411. Environ Health Perspect 2002. J Occup Environ Med 2003. Benchmark calculations for perchlorate from three human cohorts.10(8):659-663. Li FX. Pino S. Analysis of relative source contributions to the food chain. Gibbs JP. Braverman LE. Greer SE.. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Additional information about exposure and health effects is available from the U. et al. Available at URL: http://www. Steinmaus C.S. Food and Drug Administration (FDA). Byrd D. Valentin-Blasini L.11(3):295. J Clin Endocrinol Metab 2005. Mauldin JP. 2005). Blount BC. May 2007. Lawrence JE. Li Z. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Sesser DE. National Academy of Sciences (NAS). population.115(9):1333-1338. Low dose perchlorate (3 mg daily) and thyroid function. Kirk AB. Braverman LE. 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. and environmental perchlorate exposure among residents of a Southern California community. 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. Pino S..html. Pirkle JL. Blount et al. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Environ Health Perspect 2007.S. Abarca CR. Erratum in: J Occup Environ Med 2004. Neonatal thyroxine level and perchlorate in drinking water. thiocyanate.html and from ATSDR at: http://www. newborn thyroid function. He X. Caldwell KL. 2007). Doemland M. Lamm SH. References Blount BC. The effect of short-term low-dose perchlorate on various aspects of thyroid function.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Landingham CB. 2001-2002.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Buffler PA. Osterloh JD. (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. et al. National Research Council of the National Academies. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States.40(21):6608-6614. Braverman LE. Lau EC. Environ Health Perspect 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.42(2):200-205.htm. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Lawrence J.EPA at: http://www.gov/toxpro2. Chacon PM. 2005.45(10):1116-1127. 2005).fda.17(4):400-407. Pleus RC. Dasgupta PK. Deyhle GM.113(11):A732. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Goodman G. The effect of perchlorate. et al. Rutherford GW.cdc. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Crump KS. and nitrate on thyroid function in workers exposed to perchlorate long-term. Dyke JV. 6/2/09 Greer MA.90(2):700-706. Osterloh JD. Blount BC. et al.110(9):927-937. Health Implications of Perchlorate Ingestion. Howd R. Tellez RT. Lamm S. Lamm SH. Cross M. Page Last Updated: 05/28/2009. Valentin-Blasini L. CFSAN/Office of Plant & Dairy Foods. J Expo Sci Environ Epidemiol 2007. Skeels MR. Miller MD. Kelsh MA. Perchlorate Exposure of the US Population.

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

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

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

Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. hepatotoxicity. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al..800 (. 2004.10) .300-1.700 (. 2001.300 (<LOD-. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. and there was no clear evidence of excess all-cause or diseasespecific mortality.10 (. 2003.00) . Olsen et al. perfluorohexanesulfonate (PFHxS)..800 (... developmental and teratogenic effects were demonstrated in offspring.. 2003a).400-1. 2004a. 2007b). EPA. 1992.400-1. 2003).80) 640 1454 03-04 03-04 * * < LOD < LOD . and humans.800) 1..40) . 2003a.20) . 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.400-. Fei et al.00) . and no substantial age trends were seen within adults ages 20-69 (Olsen et al.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .300 (<LOD-.S. 2007a.400-1.80) 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 . 2003).500-1. population from the National Health and Nutrition Examination Survey. Harada et al. and changes in thyroid hormone concentrations (Grasty et al. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. 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.300 (<LOD-... Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.600 (. 2003).00) . monkeys.50) . reproductive. PFOA. PFOS.00 (. or increased cancer rates (Alexander et al..500) . thyroidal). Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Kennedy et al. elderly and children. 2003. < LOD means less than the limit of detection. 2004b).. At high but non-toxic maternal doses of PFOS. 2003a..400) .S.600 (. Cook et al. 2005). Olsen et al. 2007a...800) 1. 2004)..400 (<LOD-.108 times higher than background serum levels in humans (Butenoff et al. U. PFOA.3. 2004.500-1.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. Fourth National Report on Human Exposure to Environmental Chemicals 249 . In such studies.500 (. Thibodeaux et al.400-1.400-. 2003.900 (.900 (.10) .500) . 2003a).700) . possibly related to lung immaturity (Lau et al.500) . EPA. 1999.500 (<LOD-1..500 (. At doses causing maternal toxicity.500) 90th .500-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.500-1. see Data Analysis section) for Survey year 03-04 is 0. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. population..500-1. 2004). U.900 (. However.800 (.400 (<LOD-. 2007. 2005). 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.600-2.80) 485 538 962 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th .. the potential to estimate risks to humans from animal doses is uncertain. 2007b.S. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. PFOS.800 (. In comparing three separate reports on adults. Lau et al.600 (.400 (<LOD-.500) . Olsen et al.400-1. development in offspring was stunted and hypothyroxinemia was observed.10) * 03-04 03-04 * * < LOD < LOD < LOD . Animal studies of PFOS have demonstrated weight loss. 2007). which may vary for some chemicals by year and by individual sample. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U..500-...S. 2003a.

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

Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.300 (<LOD-.400 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.600 (. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600) < LOD . which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1.400 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.400) .300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.900) < LOD .600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.500-.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.3. Fourth National Report on Human Exposure to Environmental Chemicals 251 .0.300 (<LOD-.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .500 (<LOD-. Survey Geometric mean (95% conf.500) 485 538 962 Limit of detection (LOD.400 (. < LOD means less than the limit of detection. < LOD means less than the limit of detection.

90 (1.80 (1.00) 1.1) 485 538 962 Limit of detection (LOD.40) 4.54) .00 (1.800 (.689 (.40-3.60-3.00) 2.697-1. population from the National Health and Nutrition Examination Survey.60-2.70) 1.70) 3.60-7.3 (9.50 (4.10 (.20-3.90-10.00 (5.40 (1.80-12.70-6.30-2.600-.900-1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.90) 90th 5.70-7.90 (1.963 (.70-2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.00 (.10) 6.30 (1.40) 2.586-.70) 2.20 (1. interval) 1.60-2.00-8.70) 2.56-1.30 (2.30) .30 (1.826-1.08) 2.900-1.10 (4.80) 90th 2.90 (4.30 (7. see Data Analysis section) for Survey year 03-04 is 0.900) 1.50-6.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.73-2.900-1.0) 1053 1041 03-04 03-04 03-04 1.80) 3.27) 1.60 (1.70-2.00-7.900-1.20-1.30) 3.20) 1.0) 8.16) .20 (6.80) 1.50 (1.90 (4.70 (1.50-3.60-4.30 (1.30) 3.30 (3.900 (.00-1.70) 13. population from the National Health and Nutrition Examination Survey.50 (1.809) 1.30 (1.90 (2.00 (2.77-2.20-1.80-2.40 (1.721-1.20) 03-04 03-04 2.40) 640 1454 03-04 03-04 1.70 (2. Survey Geometric mean (95% conf.30) 3.17-1.20) 1.80-8.60) 3.20-1.40 (1.20 (1.80-4.30 (2. 252 Fourth National Report on Human Exposure to Environmental Chemicals .40) 640 1454 03-04 03-04 2.20) 485 538 962 Limit of detection (LOD.90-2.60) 2.80-7.900-1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.50 (1.90) 1.80-3.51) 1.62-2.90) 8.10) 5.50 (1.05-2.26) 2.70-5.90) 1.20-2.700 (.44 (2.70-10.00) 3.10 (.10) 1.80-3.86 (1.40) 1.00 (.912-1.80-8.40 (2.50) 2.80-6.00 (1.60 (6.50 (4.60 (1.90 (1.17 (1.60 (1.10) 1.20 (6.835-1.6) 7.700-1.800-1. Survey Geometric mean (95% conf.80) 4.30) 03-04 03-04 .00 (1.90 (1.5) 5.10) 1053 1041 03-04 03-04 03-04 .966 (.09 (.10 (.90) 1.10) 8.12) .3.900-1.40 (1.984 (.20 (1.00-1.30-6.72) 1.04) .92 (1.00-6.00) 1.40-1.10) 6.80 (4.60-3.01 (1. see Data Analysis section) for Survey year 03-04 is 0.852 (.91) 2.60-8.10 (1.816-1.30-9.30-12.90-19.861 (.50 (2.50 (6.80-4.80-4.20-1.50) 6.10-9.900 (.S.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.10) 4.03) 1.42 (1.40) .67-2.40-1.834-1.14 (.70) 1.80 (1.80-7.60) 9.50 (6.20) 2.1.40) 1.00 (1. interval) .80) 5.10) 75th 3.S.50-10.10-5.20 (1.30 (6.60-4.50) 2.93 (1.60-2.10) 75th 1.90) 3.5) 8.20) .10 (4.10-9.60) 1.50-6.87-2.10) 4.72 (1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.

population from the National Health and Nutrition Examination Survey.10-3.0 (20.1 (19.70-10.2 (18.8 (37.60 (4.1) 57.9-38.80 (6.5-21.0) 21.0) 90th 41.50) 7.8) 46.70) 4.80-4.40-6.60 (3.2 (28.4) 56.90 (7.30-5.6) 35.3-22. Fourth National Report on Human Exposure to Environmental Chemicals 253 .10 (6.80) 8.4) 20.70-5.9) 22.60 (7.5) 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 21.30) 7.70-7. Survey Geometric mean (95% conf.2) 640 1454 03-04 03-04 4.0-20.9-19.30 (3.18 (3.90-4.8-22.5) 9.6-50.7 (35.90-4.8 (34.37 (2.7-23.7 (35.0) 485 538 962 Limit of detection (LOD.80-12.1) 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 4.2-22. interval) 20.3-61.8-35.95 (3.8-30.7-49.1) 15.70 (3.8-81.10) 5.0 (27.50 (4.60) 03-04 03-04 3.20) 7.10 (3.4 (28.80-9.4 (23.20) 5.5) 32.3 (17.1-24.60-14.9 (13.27) 4.10 (3.6 (19.6 (42.30-6.60 (6.79) 4.90 (7.1-36.40) 75th 5.60-13.5-62.0) 21.7 (13.5 (28.8-78.7 (19.30 (5.84-3.50-6.8) 27.9 (22.4 (17.3) 28.0) 03-04 03-04 19.1 (23.7 (43.3 (28.20 (4.5) 18.20) 10.9 (17.20 (4. interval) 3.7 (43.50-13.30-8.90 (7.11 (2.30-3.8) 32.4 (19.4-25.30-11.35) 3.5) 19.2 (16.1.9 (19.0) 23.60-6.0-66.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.5) 8.2 (27.90) 6.6-45.20-5.9) 22.2 (19.3) 42.67-4.20) 4. see Data Analysis section) for Survey year 03-04 is 0.70-9.1 (24.20) 7.4-42.4.9) 9.65-4.7-69.7-53.4) 75th 30.S.6) 42.70-7.90-12.50) 4.40-14.70) 6.6-24.2-57.0-70.00 (5.6) 62.S.8-22.60) 8.80 (6.40-6.6) 7.47-4.6) 9.40) 5.4) 640 1454 03-04 03-04 23. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.1-25.60 (5.99-3.4) 21.1-33.1-35.7 (7.20-4.4 (19.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.40) 90th 7. population from the National Health and Nutrition Examination Survey.6) 21.7-30.20) 5.70) 3.90 (5.0) 36.40-17.50-4.5) 7.6) 1053 1041 03-04 03-04 03-04 3.3) 485 538 962 Limit of detection (LOD.30) 6.5) 57.3 (35.5-23.60-9. Survey Geometric mean (95% conf.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.6 (44.40) 3.9) 27.0-16.6) 18.40-10.5-33.7) 39.8 (45.7-33.5 (28.96 (3.9-23. see Data Analysis section) for Survey year 03-04 is 0.30 (3.00) 3.91) 3.70 (5.40 (4.5) 1053 1041 03-04 03-04 03-04 14.50 (3.85-4.00 (5.60 (6.40 (6.3 (35.89 (3.8-22.4-17.0) 43.1-52.21-3.6 (35.2) 30.00 (3.53) 3.3) 41.70 (5.47 (4.82) 4.80 (5.2 (21.2) 30.2) 45.3 (44.80 (7.20-9.07-4.

200-.200-.300) .500) .300-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .500) .300-. < LOD means less than the limit of detection.2.300 (.200-.400 (<LOD-.300 (.200-.300) . < LOD means less than the limit of detection.300 (.300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .200 (<LOD-.300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.200-.300 (.500) < LOD 485 538 962 Limit of detection (LOD.200-.200-. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.300) . Survey Geometric mean (95% conf. 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 (.S.300) .300) .4.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .300 (.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) . see Data Analysis section) for Survey year 03-04 is 0.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) 485 538 962 Limit of detection (LOD.300 (.300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300 (. Survey Geometric mean (95% conf.200-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500) . population from the National Health and Nutrition Examination Survey.200-.300) .300 (.300-.200-.

30 (1. population from the National Health and Nutrition Examination Survey.00) < LOD .10-1.00 (.50 (1.20-1.10) .700 (<LOD-.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.00 (.600) .800) . Survey Geometric mean (95% conf.60) 640 1454 03-04 03-04 * * < LOD < LOD .10-1.900-1.600 (<LOD-.300 (<LOD-.30) 1.800) . < LOD means less than the limit of detection.70) 1.3.700 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.700) .50 (1.80) 1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20 (1.00-1.900-1.10 (.10-1. population from the National Health and Nutrition Examination Survey.700 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.900-1.10) * 03-04 03-04 * * < LOD < LOD .80) 1.900 (<LOD-1.30 (1.900) .00 (.10 (.400 (<LOD-.900-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .40) 1.6. * 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.900-1.700) 1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .S.600 (<LOD-1.300-2.500 (<LOD-.700 (<LOD-2.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.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .900) 1.900-1.700) 90th 1.20) 1.30) 1.40) < LOD < LOD .900-1. which may vary for some chemicals by year and by individual sample.600 (<LOD-1.90) .300 (<LOD-1.700 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.30 (1.600 (<LOD-1.S.400 (<LOD-1.00 (.10-1.900 (.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .10-1.10) . which may vary for some chemicals by year and by individual sample.700 (<LOD-.10 (. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th .800 (<LOD-.700 (<LOD-.900) 485 538 962 Limit of detection (LOD.10) 1.700) 1.30) .10) 1.60) 485 538 962 Limit of detection (LOD.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .10 (1.

Edwards EA. Kannan K. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. O’Connor JC. Kumar KS. Halden RU. Needham LL. Watanabe T. Dinglasan MJ. Olsen GW. Environ Health Perspect. Kannan K. Keller JM. and perfluorinated contaminants in livers of polar bears from Alaska. Biegel LB. et al. Occup Environ Med 2003. Harada K. Corsolini S. Tully JS.115(11):1670-1676. Katakura M. The toxicology of perfluorooctanoate. Yamashita N. Moore RW. and ex vivo studies. Environ Sci Technol 2005. Butenhoff JL. Falandysz J. Environ Sci Technol 2005. Mandel JH. Mandel JS. Morikawa A.179:99-121. Jarnberg U. Saito N. Taniyasu S. Environ Sci Technol 2004. et al. Cook JC. Reidy JA.7(4):371-377. Lau CS. Chlorinated. Mandel JH. et al. et al. Peterson RE. Moore JA. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Kuklenyik Z. Koizumi A. Wijeratna S. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Loganathan BG. Hurtt ME. Chem Biol Interact 2000. Toxicol Appl Pharmacol 1990. Toxicol Appl Pharmacol 1995. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Hurtt ME. Ingall GB. Bookstaff RC. Toxicol Appl Pharmacol 1992.115(11):1596-1602. Kuklenyik Z. Perfluorinated chemicals in selected residents of the American continent.39(23):9057-9063. Tarone RE.63:490496. Holmstrom KE.S. Reidy JA. 2007b. Needham LL. Olsen GW. Environ Res 2005. Hurtt ME. Wong LY. McLaughlin JK.Perfluorochemicals References Alexander BH. Butenhoff JL. de Voogt P. Biegel LB. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Tully JS. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro.113(2):209-217. Yamashita N. Regul Toxicol Pharmacol 2004. Inoue K. Fei C. Environ Health Perspect 2007. Reidy JA.39(1):80-84.38(10):2857-2864. Polyfluoroalkyl chemicals in the U. Frame SR. Needham LL. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Mohotti KM. Perkins RG. Harada K. Kuklenyik Z. Toxicol Sci 2001.104(2):322-333.Koizumi A. Kamiyama S.39(23):9101-9108. Day RD.41:2237-2242. Guruge KS. Rodricks J. Characterization of risk for general population exposure to perfluorooctanoate. Bandai N.68(6):465-471. Witter FR. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort.40:21282134.39(3):363-380. Birth Defects Res B Dev Reprod Toxicol 2003. Reidy JA. Fillmann G. The influence of time. Grasty RC. Grey BE. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Ye Y. Liu RC. in vivo. Kudo N.38(17):4489-4495. J Environ Monit 2005. Calafat AM. Olsen J. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Environ Sci Technol 2006a. Environmental and toxicity effects of perfluoroalkylated substances. Sasaki S. brominated. Yoshinaga T. Yun SH. Kannan K. Calafat AM. Caudill SP.46(2):141-147. Calafat AM.60(1):44-55.134(1):18-25. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Environ Sci Technol 2005. Calafat AM. Gaylor DW. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Mabury SA. Yoshinaga T.99(2):253-261. Saito N. O’Connor JC. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Chemosphere 2006b. Apelberg BJ. Herbstman JB. Bignert A. Rogers JM.S. Seneviratne HR. Evans TJ.34(4):351-384. Kennedy GL Jr. Kuklenyik Z. Arendt MD.124(2):119-132. Laane RW. Environ Sci Technol 2007a. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth.and perfluorinated acids. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Serum concentrations of 11 polyfluoroalkyl compounds in the U. et al.115(11):1677-1682. Olsen GW. et al. Inoue K. Environ Sci Technol 2004.60(10):722729. Rev Environ Contam Toxicol 2003. et al. Crit Rev Toxicol 2004. Seacat AM. Cook JC. Burris JM. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Suzuki E. Fluorotelomer alcohol biodegradation yields poly. Environ Health Perspect 2007. Cook JC. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Frame SR. Needham LL. Taniyasu S. Aguilar-Villalobos M. Calafat AM. Hekster FM.1968--2003. J Occup Health 2004. Kawashima Y. Murray SM. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Caudill SP.

Gamo T. Mandel JH. Hanson RG.2(1):53-76. Helzlsouer KJ.37(12):2634-2639.epa. Biol Pharm Bull 2003. Kannan K. Hanson RG. Reagen WK. Rogers JM. Huang HY. van Belle G. Case MT. Seacat AM. Barbee BD. Ehresman DJ. The developmental toxicity of perfluoroalkyl acids and their derivatives. Church TR.perfluorohexanesulfonate. Historical comparison of perfluorooctanesulfonate. Rogers JM. Taniyasu S. Butenhoff JL. II: postnatal evaluation. J Occup Environ Med 2003b. Nesbit DJ. J Ag Food Chem 2007. 2003a. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Yamashita N. Kawashima Y. Olsen GW. Butenhoff JL.41(9):799-806. and perfluorooctanoate in retired fluorochemical production workers. Seymour C. Chemosphere 2007b. et al.55:3203-3210. Burris JM. Sterchele PF. perfluorooctanoate andother fluorochemicals in human blood. Environ Sci Technol 2006. Olsen GW. Horii Y. Olsen GW. Biochim Biophys Acta 1993. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Hansen KJ. J Children’s Health 2004b. Thomford PJ. Environ Sci Technol 2003. 2003. Grey BE. Butenhoff JL. Olsen GW. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Environ Health Perspect 2003a.115(9):1298-1305. Sources.26(1):47-51. Church TR. Mandel JH. Lau C. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Hansen KJ. Hansen KJ. 1/15/06 Vanden Heuvel JP. Larson EB. Toxicol Sci 2003. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Hanari N. Toxicol Sci 2003. Seacat AM. Mandel JH. EPA). fate and transport of perfluorocarboxylates.1177(2):183-190. Ehresman DJ. Buck RC. Olsen GW. and food items prepared in their packaging.) Tittlemier SA. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Cousins IT. et al. Chemosphere 2004a. fish. Environ Health Perspect. Burris JM. U. Kannan K. Church TR.gov/opptintr/pfoa/pfoara. Available from URL: http://www. Prevedouros K. Thibodeaux JR. Rogers JM.Perfluorochemicals Kudo N. Yamashita N. Olsen GW. Olsen GW.S. Froehlich JW. Toxicol Appl Pharmacol 2004. et al. Environmental Protection Agency (U.51(8-12):658-668.S. Coordinate induction of acyl-CoA binding protein. Miller JP. Butenhoff JL. Lundberg JK. fish. Burris JM. Mar Pollut Bull 2005. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. fast foods. Stanton ME. Toxicol Sci 2002.45(3):260-270. Hansen KJ. Cao XL et al. Thibodeaux JR. (Erratum in: Toxicol Sci 2004.111(16):1892-1901.40(1):32-44. Olsen GW.. 2007a. and humans from Japan. htm. Washington. Pepper K. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Peterson RE. Burlew MM. birds. A global survey of perfluorinated acids in oceans. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.68(1):249-264. Mandel JH. Mair DC. I: maternal and prenatal evaluations. Grey BE. Petrick G. Burris JM. Burris JM. Richards JH.111(16):1900) Olsen GW. et al.68:105–111. Taniyasu S. Ellefson ME. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Lundberg JK. Zobel LR.74(2):369-381. Horii Y. Moisey J.198(2):231-241. Bronson R. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Lau C. Environ Health Perspect 2005. Butenhoff JL. (Erratum in: Environ Health Perspect.54(11):1599-1611.82(1):359.74(2):382-392. Half-life of serum elimination of perfluoroo ctanesulfonate. J Occup Environ Med 1999. et al. Butenhoff JL.113(5):539-545. Korzeniowski SH. et al. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Hansen KJ.

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

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

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Kalita JC.25(2):293-302. Silva MJ. Toxicol Appl Pharmacol 2004. Available at URL: http://cerhr. Henttu P. Environ Health Perspect 2003. Suzuki T. Hanaoka T. Yokoyama Y.niehs. Nielsen J. McKee RH. Koch HM. Skakkebaek NE. Jonsson BAG. Tsukino H.112(17):1734-1740.110(5):515-518. Silva MJ. Andersson A-M. Akesson B. Duty S. Angerer J. Csanády G. Milligan SR. Davis BJ. and infant formula by tandem mass spectrometry (LC-MS-MS). Hagmar L. Silva MJ. Reynolds T. The estrogenic activity of phthalate esters in vitro. White R. Int J Hyg Environ Health 2007.105:802-811. Biol Pharm Bull 2003. 6/2/09 NTP-CERHR. Borch J.111(2):139-145. Calafat AM.html. Kano I.nih. et al. Numtip W. Dalgaard M. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Available at URL: http://cerhr. Anal Bioanal Chem 2005. Brock JW.11(5):381-387. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets.26(8):1219-24. Chen Z.nih. Ryan L. gov/chemicals/dehp/dehp-eval. Butala JH.html. Filser J. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. et al. Mortensen GK. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Leffers H. Hass U. Hauser R. Research Triangle Park (NC). Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals . 2000c [online].gov/chemicals/dehp/dehp-eval. Parker MG.Phthalates in human urine samples. Environ Health Perspect 2004. Chahoud I. Fromme H. Balasubramanian AV. Hartle RW. Jacobsen H. 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Peters JM. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Cunningham ML. Meek MD. Toxicol Sci 2000. Rusyn I. Toxicol Sci 1998.112(3):331-338. Rhodes C. Environ Health Perspect 1982. Barlow NJ. Pratt IA. Malek NA.S. Environ Health Perspect 2006. Lambright CR. Silva MJ. Orton TC. Ostby JS. et al. Fielden MR. 112(5):A270]. Clemons JH. Abbott BD.46:282-293. Peck CC.65:299-308.45:11-17. Zacharewski TR. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Crit Rev Toxicol 2006.114(11):1643-1648. Barr DB. Environ Health Perspect 2004. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Jackson SJ. Klinefelter GR. et al. Albro PW. Urinary levels of seven phthalate metabolites in the U.36:459-479. Reidy JA. et al.Phthalates phthalate (DEHP): a cross-sectional study in China. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Hodge CC. Matthews JB. Wu ZF. Parks LG. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Batten PL. Environ Health Perspect 1986. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.58:339349. Bratt H. Caudill SP.

particularly male animals (McKee et al.2) 13.8-121) 79.9 (13.5 (26.6) 14.8 (10. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.7 (70.6-92.5 (66.9-190) 86.S.6-39.2-16.3 (54.2) 33.7-17.0 (15.3-161) 99.6) 24.4) 65.1 (58.0) 24. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-17.5-35.0 (30.3-88.8-14.3-34.2 (14.2-115) 113 (91. Food crops take up BzBP.3 (30.5 (47.1 (13.2-20.1) 12.0 (27.0 (15.8-18.3) 15.0 (33.1-43.6 (12.9 (11.1 (14.5) 82.7-15.8 (21.9 (39.5) 55.1-18.8-133) 89.6-72.3.5-97.5) 15.7-16.6 (13.3-18.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.6) 35.2-19.5) 15.4 (27.6-116) 122 (102-142) 101 (85.5 (67.7 (51.1 (20. and 0.2-40.2 (25.1-116) 122 (93.1.7-172) 103 (74.0 (30.8 (86. 01-02. respectively.2) 15.4-25.1-16.5 (55.8) 14..4-62.9-27.2 (19.3) 94. sealants.7-25.4 (32.1) 76.4) 108 (96.3-43.3-27.2-38.7 (12.0 (23.4 (10.2-16.8 (71.4) 129 (98.5 (76.2 (10.5) 65.0 (55. 2004.0-85.8.5-36. can produce developmental and reproductive toxicity in rodents.6 (13.0 (26.0-55.5-84.3 (12.2 (47.1-16.8-16.3 (12.4) 81.8-41.7-16.3-125) Total 15. because it is not bound to products in which it is incorporated.4-15.2) 78.4 (53.9) 11.0-130) 101 (86.9-47.3) 13. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.9-62.2 (19.6) 63.7 (82. NTPCERHR.8) 63.7) 23.2) 22.1-15.6) 50.6 (66.9-14.4 (32.4 (13.9 (12.3-18.7) 40.7 (11.0) 20.5-25.9-87.6) 67.7-170) 169 (134-198) 152 (99.9 (21.4) 49.3 (33.6-43.5-62.1) 31.9) 14.9) 18.4) 38.9-30.2) 14. it can be released into the ambient air during use or disposal of the products.3-82. including MBzP.4 (10.2) 17.6) 14.5 (27.6-18.8 (80.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.Phthalates Benzylbutyl Phthalate CAS No. 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.S. 0.1) Selected percentiles ( 95% confidence interval) 50th 17.4 (48.4 (63.8) 33.4) 75th 35.7-119) 99.0 (34.9-16.4-24.2 (43.6 (13.9 (28.8-76.6 (32.1 (13.8-16.5-14.3 (22.7 (13.6) 37. residents (Blount et al.6) 13.7-58.6) 16.0 (20.3) 63.7 (53.1) 29.7 (80.0) 70.0-26.5-145) 138 (106-241) 143 (127-179) 120 (99.4) 35.3 (44.9) 12.0 (11.1-90.5) 16.3 (12. 262 Fourth National Report on Human Exposure to Environmental Chemicals .4-16.0) 34.8 (14.7-82.0 (14.8-72.0) 33.6-17.2-17.4 (31.3 (13.4 (59.4 (68.2) 32. see Data Analysis section) for Survey years 99-00.9 (12.2 (11.5-40.1-39.8 (71..0-106) 58.2) 66.8-48.1 (55.8) 24.9-49. and 2003-2004 were generally similar those reported in U.4-92.5) 30.6-150) 94. and to a lesser extent.7-16.9) 43.0 (12. 2001-2002.3-130) 122 (88.6 (53.5 (13. some personal care products.5-33.1) 14.5) 27.3-75.4) 51.6 (21.9) 13.1-120) 52.6 (41.1 (32.4) 80.1 (19.4 (29.5) 23.8-98.6) 25. and diet is the major source for general population exposure.4) 12. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.3) 23.9) 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 39.5 (61.1-214) 166 (116-191) 145 (110-213) 88.8-17.8-14.4) 71.7-35.1) 68.9) 14.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1-61.2-183) 101 (78.1 (14.0) 16.4 (53.9 (70.3-91.6) 35.8-64. vinyl tile.6-79.0) 32. BzBP can be released into the environment during its production and. High dose BzBP and its monoester metabolites.2-155) 91. car care products.4) 98.7) 38.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.5-94.1) 67.6 (13.1-38.9) 15.1-15.7-13.8 (12.3 (29.9) 49.7-14.0) 23.3-12.6) 29.5-36.3) 54.8 (28. population from the National Health and Nutrition Examination Survey.8-13.7 (15.5 (57.3-21.2-116) 122 (102-143) 101 (84.8 (38. 2000).6) 95th 103 (94.4-127) 80.1-35.2-33.8-35.8 (30.1 (10.2) 69.9 (22.9 (16.6) 13.3) 13. interval) 15.6-92.4) 33.0 (43. and 03-04 are 0.5-18. 2000).2-39.3-74.2) 12.2) 14.8 (50.6) 15.6-38.4) 14.8 (53.3) 37.5-41.1) 13.0) 90th 67.6-132) 103 (84. IARC considers BzBP not classifiable with respect to human carcinogenicity.1) 32.3 (29.9-28.8) 28.4) 35.2-31.6-29.

8-15.9 (9.7 (38.8-34.6 (22. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.2) 15.3 (35..8) 24.1 (21.5) 23.7) 56.8-69. and in a small sample of German residents (Koch et al.0-26.4) 12.4) 25.5-99.9 (15.1) 24.1 (21.6-13.8-39.5-23.3-73. adolescents compared with adults.7-90.9) 11.1) 23.7 (54.4-42. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.0 (41.0-90.7 (11.0) 24.6) 12.4) 104 (89.6-26.2-49.8) 11.4 (33. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.2) 12.1) 27.3 (13.5) 46.5) 10.8-48.6-116) 74.4 (74.7-15.4-79. 2004).2) 32.9) 42.7 (21.7 (18.5-38. 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. In an annual sample of German university students.9 (10.9 (12.8) 68.0-53.4 (21.3) 90.3) 14. 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.7-19.4-15.5) 17.8-85.3) 36.7-20.0-15.6) 75th 25.73-12.4 (11.0 (41.1) 35.5) 20.8 (11.1 (13.Phthalates York City (Adibi et al.8-42.4 (11.5-61.9) 12.1-29.1) 80.3 (23.2 (40.5) 95th 77.8-14.4 (60.7) 19.1-12.7) 25.4-14..2) 11.2) 11.1-58. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3-64.8-64.7-19. 2007).6) 58.1) 142 (99. Weuve et al.1 (34.1 (41.3-11.3) 13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9 (24.0 (33.4-102) 70.4) 13.1-35.9-23.1-120) 77.3-34.0-48.5-79.4 (12.8) 13.2-78.2-17.0) 49.7 (13.6) 30.4-19.4) 44.8) 53.4) 90th 50. A small study of African-American women in Washington. 2003).9) 11. 2006).8) 71.6 (11.9-62.4 (26.7) 46.4 (10. 2003).0) 60.8) 53.9 (24. 2002).8 (10.3 (24.7) 38.S.4 (34.7-69.3) 13.3) 89.7 (23.2-117) 95. population from the National Health and Nutrition Examination Survey.7-397) 70.3) 16.1 (23.7) 11.6 (30.6 (11.5 (49.2-13.4 (69. in young Swedish men (Jonsson et al.4 (25.4) 50.2-15..3) 37. Hauser et al.7-29.5-26.7 (55.3 (38.8) 26.5) 14.8) 46.1-79.5 (42.0 (12.9 (15.9 (12.7-31.1 (14.9) Total 14.3 (15.6) 53.9-104) 62.5-57.4-60.7-15.7-12.4-93.6 (19.9) 100 (80.9 (43.8 (30.9 (22.1-12.5-213) 49. in men attending a Boston infertility clinic (Duty et al.8-13.0) Selected percentiles ( 95% confidence interval) 50th 13.5 (35.8) 56. Hoppin et al.0 (11.9-40.5 (10.2-12.7 (59.4-23.0 (12.8-15.6 (36.6-81.9-115) 57.5) 13.3) 13.5-13.5 (48.0-51.2 (41.8) 33.8 (69.3-16.2 (69.1 (21.5-58.7 (11.1 (15.4 (11.1 (46.2) 26.4) 14.9 (55.8) 54.3) 14. 2005).6 (30.9 (51.8) 33.8) 34.7 (12.9-13.0) 13.4) 15.5-31.1 (18.6) 13.9 (39.3-38.5) 16.4) 51.8 (64.1 (21.3) 21.8) 16.1 (43.95-14. 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.2) 11.3) 55.1 (19.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.6 (51.4) 13.4-14.1) 24.5) 78.4) 17.0) 24.6) 12.8) 80.5 (10.9-16.9-14.6 (11.3) 67.0 (38.9) 24.6 (24.4 (63.5 (11.9-28.1 (25.8 (50.4-116) 73.3) 12. 2002.1 (13.9-69. 2004.0) 15.8-13.4 (13.. 2005. and females compared to males (Silva et al.3 (39.9-13.2-57.69-11.2-26.0 (62.4-90.4) 28.5) 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 .7 (13.9) 12.8-173) 195 (121-305) 229 (99.8 (13.6-20.5-58.5 (56.5-29.9 (54.6 (15.4) 21.1-125) 86.5) 41.0) 12.0 (10.9 (29.8 (57.8-14.1 (11.1) 39.4-27.2-21.7 (11.2) 67.5 (12.6) 73..9) 64.8-80.0 (67.6-15.6 (57.4) 60.8-60.5-42.4-17.3 (12. 2007).1) 12.0-27.4 (46.2 (56.2 (27..9) 52.8 (49.8) 108 (75..6) 25.1 (9.0-109) 65.9) 12.7-56.6-40.0) 11.9-83.8 (46.1) 17.5-16.8-13.3 (60. interval) 14.1 (53.3) 18.8) 15.7-14.9 (10.5-76.3) 29.2-51.2) 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 (12..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 12.7-20.4-18.8-16.6-86.0 (13. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC..6-99.8-27.5-26.7-14.5 (9.6-47.4-99.0 (49.7 (14.7-123) 77.4-142) 134 (116-176) 136 (85.6 (34.1-14.1-27.3) 73.6 (14.6-12.7 (19. In NHANES 1999-2000.2-15.6) 38.7-61.2-13.

Helm D. Environ Health Perspect 2003. Reidy JA. Angerer J. Davis BJ. Rossbach B. et al. Available at URL: http://cerhr. Blount BC. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Butala JH.niehs. Koch HM. Int J Hyg Environ Health 2007. Brock JW. Rylander L. Bull Environ Contam Toxicol 2002. Barr DB. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Caudill SP. Ryan L. Urinary levels of seven phthalate metabolites in the U. Hoppin JA. Duty S. Epidemiol 2005. Prenatal exposures to phthalates among women in New York City and Krakow. Needham LL. J Androl 2004. Richthoff J.Phthalates References Adibi JJ. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Calafat AM. David RM. Hilborn ED. Barr D.93:177-185. et al. Hauser R. Sanchez GN.112(3):331-338. Hodge CC. et al. Koch HM.114(9):1424-1431. 2000 [online]. NTP-CERHR. Wittassek M. Jedrychowski W. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Reprod Toxicol 2004. Research Triangle Park (NC). Jacek R.16(4):487-493. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].22(3):688-695.110(5):515-518. Poland. Hu H. 112(5):A270]. Silva MJ. Environ Health Perspect 2002. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.108(10):979-982. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.25(2):293-302. Hum Reprod 2007. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 2000. Brock JW. Environ Health Perspect 2006.S. Sampson EJ. et al. 4/20/09 Silva MJ. Levels of seven urinary phthalate metabolites in a human reference population.68:309-314. Caudill SP. Wiesmuller GA. et al. Silva MJ. Duty SM. et al. Calafat AM. Eckard R. Dobler L. Urinary phthalate metabolites and biomarkers of reproductive function in young men. et al.nih. 2005. Environ Res 2003.210(3-4):319-333. Chen Z. Jonsson BAG. Ryan L. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Giwercman A. Phthalate monoesters levels in the urine of young children. Reproducibility of urinary phthalate metabolites in first morning urine samples. Perera FP. Third National Report on Human Exposure to Environmental Chemicals. Meeker JD. Green RA. Malek NA. Weuve J. Atlanta (GA). Schettler T. Silva MJ. Drexler H. Brock JW. Silva MJ. Baird DD. Caudill SP.18(1):122. Needham LL. 264 Fourth National Report on Human Exposure to Environmental Chemicals .111(14):1719-1722. Environ Health Perspect 2004. Centers for Disease Control and Prevention (CDC). Pirkle JL. Gans G. Hagmar L. Singh NP. McKee RH. Camann DE.html.

00-11.20-12.80) 75th 5.5-16.10) 3.20-2.90 (4.70) 5..10-2.70 (2.46 (2.50) 2.96) 3.0) 20. 2003).1-12. 2001).7 (18.50 (6.2 (8.50) 8..48 (2.5 (10.5) 14.6 (13.6 (10.50-10.00-9.60 (8.60 (5.30) 5.10-9..30-3.90-2.6-18.00) 10. and also in some printing inks.90-4. Following oral administration of DBP to humans.6 (29.00-6.7-20.20-12.37) 6.80 (2.72-3.50-4.70) 3.6) 12.07 (3.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.1) 22.30-6.3-43.40 (3.40-12.40-5.5 (11.10) 2.40 (2. mostly as MnBP (Anderson et al. 2005).70 (5.10) 11.70-4. 2003). 2004. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. 2005).4) 5.0-18.2-33.S. Fourth National Report on Human Exposure to Environmental Chemicals 265 . 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.30) 6.20 (3.3-24.30) 10. 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.97-7..10 (4. 2007).3 (16.0) 12.40-9.0 and 0.3 (13.10) 8.46 (3.00) 6.46-5.3-19. 2005.30-7.85-6.. about 65% to 80% of a dose is eliminated in urine within 24 hours. Survey Geometric mean (95% conf.0-38.3) 18.0-25.6-26.3-18.90-7.24-8.50) 18.7 (16.26 (2.1) 16. pharmaceutical coatings.73 (2.60 (4.0 (13.6 (13... and in a small sample of Japanese adults (Itoh et al.8 (9. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.5-16.17) 4. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.56 (3.3 (16.6 (14. they have been referred to as monobutyl phthalate (MBP). interval) 2.10) 9.6) 16.50) 5. Hauser et al.4) 12.50-6.1-25.3 (19.4-27.9) 10.7-31.00) 4. Biomonitoring Information Median concentrations reported in the NHANES 19992000. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al. Koch et al.20-6.10 (4.20) 7.40 (2.7) 14.55 (3.30-13.60) 3.40) 5. DBP can produce reproductive toxicity in male rodents (McKee et al. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.82-3.9) 15. 84-74-2 Di-isobutyl Phthalate CAS No.40-4.30-2.49-2.73-5.0 (11.6 (11.44-2.5 (20.2 (12.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.55) 2.68 (2.30 (3.S.2 (11.Phthalates Di-n-butyl Phthalate CAS No. residents (Blount et al. In addition.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. 2000.3-48. 2000).91) 4.40-4.40-17.17 (2.1-17.40-3.0) 9.80-5.6-20.1 (8.5) 23.9-14.66) 2.97) 4.2) 5.90) 12.0 (13.97) 2.80-5. CDC.1-20.00-6. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.80 (3.6) 16.20 (6.7 (9.7) 4.80 (5.02) 4.50) 7. Studies of children found age-related differences in urine MBP levels.5 (17.8) 677 652 703 699 1216 1088 Limit of detection (LOD.90 (4.81 (3.40 (7.0-14.59) 3.3-20.00 (5. and insecticides.11-3.30 (4.2-14.30) 10.6-14.5) 18.70-4.50-2.3) 33.6) 26.7 (7.1 (13.25) 01-02 03-04 01-02 03-04 01-02 03-04 4. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.7-31.6 (10.0 (19.1) 25..40-3. 2004.40 (6.5 (27.56 (5. in a small sample of pregnant women in New York City (Adibi et al.90-4.8) 21. population from the National Health and Nutrition Examination Survey.00 (7.7-18.7 (17.90 (6.46) 2.9-23.4) 22.3 (11.00) 4.30) 2. OSHA has established a workplace air standard for external exposure to DBP.00) 7. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.6 (14.28-5.5) 25.5-24.33 (2. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.4-12.3-30.60-6.70-8.43) 6.7) 18.6) 17.30-11.6) 17. NTP-CERHR.20-9.67 (5.50) 90th 12.3 (18.8) 40.9 (16.60 (2.10-9.20 (7.3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.5) 19.5) 22.2-22.4 (14.80 (5.4 (20.80 (2.0) 13.6) 10.56) 3.20) 4.22) 3.84) 4.5-29. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.9 (16.63) 3.56-4.10 (3.7) 15.6 (9.19-3.50 (3.00-4. When total DBP metabolites have been measured. 2005).5) 12..6-34.90 (3.3 (13.3) 3. in men attending a Boston infertility clinic (Duty et al.71 (2.5) 18.0) 24.22 (3.30-6.7) 7.7 (17.30 (1.

56) 5.19 (2.9 (11.32 (7.31 (7.5 (11.1) 4. samples from German university students had consistently higher median urine levels of MnBP and MiBP. 2004).9-40.1) 7.69) 6.31) 2.0) 3.66) 2.5) 13.65 (4.18-4.95-3.52-3.8 (10.94 (5.93-6.2) 24.0-18.86) 6.1 (11.26-2.91-6. 2002.4) 23.33 (3.98 (2.94) 6.11) 5.3) 13.7 (13.56-15.7 (21.82 (4.75 (4.65-4.80-3.6) 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 2.05) 2.47 (3. 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.9-16.7 (9.2 (11.07 (2.08-2.13-6.6 (8.18) 3..66 (8...46) 3.37) 3.43) 3.0) 7.8-18.53-5.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.03-11.31 (2.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.61-3.43) 3. to about two to fourfold higher (Fromme et al.81) 4. An analysis of NHANES 2001-2002 showed similar age. 2007). respectively.54) 2.4) 15.7-28.74-3.29-3.62 (6.95) 10.38-10.83 (2.30 (6.1) 15.00 (3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.68) 5.88 (2.1-12.18-10.28-13.11 (5. interval) 2.8) 10.0 (8.21) 10.89 (3.34 (3.1-15.3) 18.76 (3. 2006).7) 19.00-3. 2007).8 (9.79 (4.78-8.35) 3.6 (10.56-4.14 (4.69-7.79-6. 2005).99) 7.55-6.3 (13.97-2.25) 5.53-4.15-4.01-2.57 (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.64-7.47-12.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.44 (3.1) 13.84 (8.08) 75th 4.52-20.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.9-26.3) 13.32) 7.00-3.47-5..6 (8.6 (15. Weuve et al.38 (6.79-8.39) 5.1 (10. Between 1998 and 2003.58-4.02-10.15) 3.81 (3.4-16.66) 4.36-7.17 (2.3) 16.0 (10.20-4.26 (2.69 (2.11-2.36-2.76-3.64-7.1) 11.72-7.66) 10.03 (5.1-24.4 (12.7) 11.8-36.68) 3.89) 6.41 (2.03-7.99-4.2-15.33 (2.43) 3.62-12.85 (2. the students’ median values for MiBP levels remained relatively unchanged.51) 5.46 (2.64-10.58-3.7 (11.92 (7. Survey Geometric mean (95% conf.78) 8.3) 28.2) 8.7) 10.52) 3.00-7. 2004).29-8.S.86-4.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.10-5.28 (4.33) 3.46-11. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples. than adults in NHANES subsamples during the same time period.95) 2.96 (3.94-12.74 (4. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.20 (2.6 (9.78) 9.42) 2..04) 7. ranging from more than one-tenth the NHANES median (Itoh et al.1) 10.80 (3.20-2.81 (6.82) 4.09-2. 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.76-15.30) 2.17-12.17) 90th 8.1-25.56) 2.24) 3. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80) 7.0 (12.54 (4..6 (12.2-13.2 (10.21 (5.51) 2.73 (5.5 (9.72) 5.3 (17.4) 7.2) 9. Over this time.22 (2. 2005).8-18.6) 11.7) 3.04) 3.65-11.13 (2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .68 (2.27-12.04-5.39-3. up to four and 13 fold.84 (4.0) 15.. In an analysis of NHANES 1999-2000.18 (4.52 (2.07-5.02 (7.57-4.9 (15.and gender.57 (3.33-9.9) 12.9 (9.67-5.45) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.81) 9.8-13.6) 13.6-19.89-5.59 (4.18 (1.51) 15.6-19.8 (8.31) 2.0) 11.69) 4.20 (7.75 (6.54 (2.20 (2.18) 4.53-3.20-3.5-19.76-3. while MnBP declined (Wittassek et al.5) 15. population from the National Health and Nutrition Examination Survey.32 (3.

6 (19.7-53.1 (58.9 (17.6 (16.4-44.4) 64.7 (18.2-24.4-18.2) 26.6 (22.1) 23. respectively.3-67.1-80.6-48.8) 58.2 (17.5-47.7-127) 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 22.3 (60.2-21.1 (36.0) 38.5-43.1 (19. 01-02.1 (34.1) 47.1-27.0 (17.4 (35.2) 38.5-60. and 0.4 (84.8) 43.0) 20.2 (59.2-33.0 (20.0 (31.5) 20.4-31.1) 30.4-42.7-111) 64.7-117) 118 (108-143) 93.9 (79.2 (79.4) 52.5 (59.1 (19.5) 40.4 (35.7-26.4.3 (36.3 (23.7 (18.3 (42.3-40.7 (22.2 (20.3) 19.5 (28.2) 62.9-53.4 (38.5-53.5) 36.6-20.1) 17.6) 39.4 (21.5 (59.0-24. Fourth National Report on Human Exposure to Environmental Chemicals 267 .2 (18.2 (21.7) 28.7-124) 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.0) 31.1) 46.6) 20.4-26.6 (55.1) 31.7 (24.8-111) 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 23.9) 26.3) 40.1-22.6 (44.5) 47.4 (25.8-25.2 (19.9-22.6 (48.3-21.2 (25.5) 85.1 (18.7) 124 (98.7-34.8-132) 95.0-51.5) 95.2-23.7 (38.7 (64. and 03-04 are 0.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.1 (31.1) 20.7) 42.9-114) 116 (97.7 (33.0) 27.2-32. 1.2 (74.5) 21.2) 90th 98.6-24.7-24.6) 46.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.5) 19.3-24.2-87.0 (45.6 (61.6-37.2-159) 92.8) 48.9 (20.7) 74.0-26.1 (21.6-33.9 (17.1) 25.4 (72.4 (35.4 (35.4 (71.4 (23. interval) 24.5-44.2) 68.6-143) 127 (99.1 (17.9) 71.3) 21. Survey Geometric mean (95% conf.5) 65.3) 24.9) 18.3) 26.5) 26.1 (62.3 (30.5-121) 106 (94.0 (36.3) 18.3-60.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.3-76.9) 21.5) 36.1-29.0-21.3-85.0-19.2-49.2-93.1) 19.3-96.7-92.6-69.4-25.4) 20.1) 23.7 (70.9-22.1.3 (30.3) 23.6) 17.2-22.9-79.3 (51.9) 29.1) 36.1 (16.1-24.7-42.0 (18.8-22.0 (78.2-63.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.6) 21.7) 52.6) 71.1-51.6 (90.8) 62.7 (51.9-101) 77.7-34.6 (32.9-28.3-136) 137 (107-162) 119 (90.1 (19.0 (25.3-79.4-60.6-40.1 (19.1-82.4 (36.4-159) 107 (84.9) 75. *In the 1999-2000 survey period.7) 92.0) 84.0 (15.5) 37.1 (51.5) 34.8 (57.4) 22.9) 46.S.1 (28.2 (75.0 (30.0-24.9) 36.0-58.9 (79.5) 31.1 (54.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.7-106) 69.2 (78.7-20.1 (41.6-31.4-20.5) 24.2 (58.9-33.8) 75th 51.5 (29.1 (26.6) 80.9-87.7-91.3 (56.1-20.0) 30.6) 35.2-114) 73.7 (43.0-73. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.0) 117 (104-131) 112 (84.5-47.5) 78.5 (30.1-92.9-92.6-36.2-56.7 (19.5-42.3 (23.7 (16.8-29.8-123) 101 (90.2) 42.5) 17.7-42. population from the National Health and Nutrition Examination Survey.1) 23.7 (28.8 (19.6-29.0) 120 (98.9.2) 20.0-19.3-145) 85.0) 21.5 (74.3 (17.3) 36. referred to as monobutyl phthalate (MBP). see Data Analysis section) for survey years 99-00.6-29.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.2) 32.6-113) 108 (90.7-116) 95.6 (26.8) 23.5-27.4) 59.6-49.0-32.3 (37.0 (72.9-42.6-44.6 (65.8-119) 90.6) 38.0 (23.8-42.4 (19.8) 19.5-117) 95.2 (21.1-75.7-121) 97.

0) 25.6-22.5-16.8 (22.3) 59.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.0-47.1 (56.7-20.3-18.2-22.0-19.1) 37.2-21.3) 67.9 (64.6) 34.0 (20.6-44.8 (33.4 (31.2-73.4 (17.3-26.8-23.4 (18.8-24.9 (20.7 (54.3) 20.5-142) 81.7 (28.0 (71.7) 20.3) 18.7-39.3 (42.2 (19.0-41.2-28.3 (48.5 (14.6 (25.0) 29.0 (70.5-37.3 (16.0 (50.3-81.6 (74.7 (20. interval) 22.9 (58.8) 23.5) 82.0) 108 (71.0 (43.7) 42.5-41.8) 35.3-114) 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 17.3-32.3 (17.4 (50.0-75.6-23.6-43.2-179) 84.6-28.9 (35.6 (19.2 (16.2-106) 64.7 (60.7 (60.8-43.9) 24.6-128) 96.3-106) 74.6-16.9) 28.5-23.8) 63.7 (43.5) 91.6) 39.6-119) 63.4 (17.4 (16.6) 25.4 (47.1) 21.0) 26.7-51.3) 19.5) 17.8 (13.9 (73.7-37.4) 21.1 (21.0) 81.0 (61.1 (46.7-19.6-155) 91.3 (24.8) 19.3) 35.1) 44.6-42.2) 59.1) 17.1 (34.0-38.6) 64.3-78.2-22.9-68.2) 21.3 (19. population from the National Health and Nutrition Examination Survey.2) 31.0) 28.9) 30.9 (35.5) 134 (93.6) 24.9 (30.3) 21.8) 13.4 (16.S.2-61.3-40.3-21.4 (31.8 (18.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.0) 55.4 (45.8) 75th 38.4 (50.9) 39.2) 16. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1) 53.7 (12.4-34.2-86.6) 14.6-50.7 (27.9-14.3 (71.8) 34.7 (14.5-21.3 (52.5-22.9-84.4 (56.0) 59.7-19.7-80.1) 20.1) 42.4) 15.6) 31.3 (17.7 (16.0 (18.5-142) 89.8 (17.7 (19.8 (65.9 (21.7 (81.6-24.9) 91.7-21.1-83.4 (33.3-20.0-17.6) 37.6 (72.6-27.4) 62.4) 15.1) 61.5-30.4 (68.4) 53.7-23.1) 22.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.0 (52.4-164) 96.3-23.6) 83.3 (69. Survey Geometric mean (95% conf.5) 21.3 (55.4) 51.0 (15.2 (19.9-68.8 (25.8-235) 137 (108-198) 88.0 (19.1) 50.3) 52.3 (52.0 (26.3-21.8) 40.4 (53.8 (16.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9-34.7 (73.9-100) 86.7) 36.6-44.4-24.4 (23.8-24.6-23.4-61.0) 53.0-92.4-135) 71.1-32.5 (64.2) 74.4-65.3 (76.2) 159 (102-263) 147 (93.3 (21.5-18.9 (39.8 (18.4) 16.5 (18.0 (18.9) 52.0 (16.9-105) 85.1) 20.9 (30.8) 30.1 (29.0) 94.3-38.9 (37.9-26.6 (41.9 (16.3-17.5) 90th 68.9-56.3-71.2-18.6 (57.8 (50.7-42.3 (60.9) 49.4) 20.5-64.9) 20.4-103) 117 (83.5 (15.6 (31.8) 17.5 (30.7-78.6-92.4) 19.8) 20.2-16.1-23.1 (32.3-39.4 (37.1-18.6) 24.5) 60.3) 17.6-32.0-113) 104 (83.1) 35.1-21.6-53.2) 65.0 (27.4-47.6 (61.0-90.7) 19.5-76.8) 22.6) 18.8) 17.5) 39.5-70.3 (28.8) 28.7-28.5-15.9 (56.2 (38.4 (13.5 (18.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.6 (17.9-70.1-128) 97.9) 62.9-38.3) 33.9) 19.4-76.1 (15.1-99.0) 19.2 (83.4-72.2 (35.0 (69.0) 35.3-49.5 (81.0) 75.9 (30.6 (29.6-19.3 (17.9 (19.4 (20.6) 23.0) 41.5) 84.6-24.0) 70.8) 17.1 (61.6 (27.6-26.3) 33.7 (57.9-36.2-48. 268 Fourth National Report on Human Exposure to Environmental Chemicals .1-62.3 (46.6) 65.0 (34.9-49.8-32.2-22.6) 38.8) 20.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.8 (18.4-131) 81.2-27.4 (31.2-85.0-60.4 (19.6 (25.9) 14.1-99.6-74.3) 19.8) 34.7-26.

Jacek R. Meeker JD. Fromme H. Int J Hyg Environ Health 2007. NTP-CERHR. et al.108(10)979-982. Eckard R. Barr DB. Needham LL. Ryan L.22(3):688-695.18(1):122.18(12):10681074.112(3):331-338. Hum Reprod 2007. Rylander L. Boehmer S. Perera FP.93:177-185. Bull Environ Contam Toxicol 2002. Jedrychowski W. Calafat AM.114(9):1424-1431. Centers for Disease Control and Prevention (CDC). Duty SM. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.208:237-245.210(3-4):319-33. Brock JW. Third National Report on Human Exposure to Environmental Chemicals. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Pirkle JL. Environ Health Perspect 2003. Helm D. Weuve J. Urinary levels of seven phthalate metabolites in the U.html. Itoh H. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. et al. Springall C. Green RA. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Available at URL: http://cerhr.nih. Sampson EJ. Food Addit Contam 2001. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.gov/chemicals/ phthalates/dbp/dbp-eval. Drexler H. Koch HM. Silva MJ.16(4):487-493. Anderson WA.Phthalates References Adibi JJ. David RM. Environ Health Perspect 2006. Rossbach B.210:21-33. Massey RC. Duty S.68:309-314. Butala JH. Epidemiol 2005. Ryan L. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].111(14):1719-1722. et al. J Androl 2004. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Research Triangle Park (NC). Giwercman A. Singh NP. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Int J Hyg Environ Health 2005.niehs. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Koch HM. Scotter MJ. Environ Res 2003.25(2):293-302. Hauser R. Calafat AM. Jonsson BAG. Schettler T. Koch HM. Silva MJ. Angerer J. Masunaga S. Brock JW. Needham LL. 2000 [online]. Silva MJ. Phthalate monoesters levels in the urine of young children. 112(5):A270]. Malek NA. Dobler L. Silva MJ. 4/20/09 Silva MJ. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Environ Health Perspect 2004. Gans G. Yoshida K. Prenatal exposures to phthalates among women in New York City and Krakow. Barr D. et al. Int J Hyg Environ Health 2007. Richthoff J. Environ Health Perspect 2000. et al. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Sanchez GN. Angerer J. Atlanta (GA). A biomarker approach to measuring human dietary exposure to certain phthalate diesters. McKee RH. Blount BC. Poland. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Caudill SP. Wiesmuller GA. Castle L. Reidy JA. Drexler H. Hilborn ED.S. Reprod Toxicol 2004. 2005. Chen Z. Hagmar L. et al. Hu H. et al. Bolte G. Wittassek M. Caudill SP. Caudill SP. Levels of seven urinary phthalate metabolites in a human reference population. et al. Camann DE. Hodge CC.

600) .90) .700) .300 (. 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 (<LOD-.00) . and 0.300-.500 (.70) .300) < LOD .400) 1. which may vary for some chemicals by year and by individual sample.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300 (.70 (1. 01-02. < LOD means less than the limit of detection.10) .00 (<LOD-1.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.300 (.300-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400-.500 (.400 (.300-.200-.80) . and 03-04 are 0.500) < LOD < LOD .600) . and polymers.300-.2.70 (1. only levels at or above the 90th percentile could be characterized.700) .200-.600) . including nitrocellulose. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.300-.400 (.50) .500 (. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.300-. 0.500 (.400 (.300-.500 (.500) < LOD < LOD . resins.400 (.10 (<LOD-1. see Data Analysis section) for Survey years 99-00. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.600) .70) .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 (.500) 1.300 (<LOD-.500 (.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.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 .10 (<LOD-1.300 (.200 (<LOD-.400-.400 (.00 (<LOD-1.00-2.400-. polyvinyl acetate.400-.00 (<LOD-1.200-.200-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.3. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.400 (. Survey Geometric mean (95% conf. 270 Fourth National Report on Human Exposure to Environmental Chemicals . respectively.Phthalates Dicyclohexyl Phthalate CAS No.400) < LOD < LOD .200-.500) .400-.10 (<LOD-2.50) . population from the National Health and Nutrition Examination Survey.500 (.700) .500) .900-1. In this Report.500) 1.300 (.9.500 (.400) < LOD 1.400-.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-.400-.600 (.500) .200-.300-.500) .500) 1.500 (. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population. and polyvinyl chloride.300-.10 (.20) .500-.400 (<LOD-.00-3.400) 1.300 (.600) < LOD .600) .500) < LOD 1.300) < LOD .300-.

54) .17) .05) .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.500 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .770 (.770) < LOD 2.940 (.54-6.690) < LOD 2.330 (.33 (<LOD-3.22 (<LOD-1.82) .420-.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 .250 (.18) .630 (<LOD-.670 (<LOD-.690) < LOD < LOD .690-1.400-.290-.660) . population from the National Health and Nutrition Examination Survey.00) .420-.11) .690 (.880 (.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.530-.310-.380 (.53) .33) .770-1.740) < LOD < LOD .00 (<LOD-3.12-1.43 (1.360-.530-1.450 (.400-.82 (1.06) .74) .220 (<LOD-.490) .910 (.530) 1.370 (<LOD-.420-.380-.910 (.54 (<LOD-2.950 (.610 (.770-1.260-.310) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.240-.560) 1.670-1.740) .830) 1.470 (.S.16 (<LOD-3.06) . Fourth National Report on Human Exposure to Environmental Chemicals 271 .510-.500) 3.790-1.270) < LOD .34) .770-1. Survey Geometric mean (95% conf.170-.800-1.480 (.910 (.350-.630 (<LOD-.67 (1.44) .390 (.590 (.660) < LOD < LOD .16) .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 1.710) .530 (.36-1.500-.330 (.410 (.53) .510 (.590 (<LOD-.14 (<LOD-3.910 (.470) 3.10) .450 (.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 .

In contrast. 2001-2002. shampoos.4 (62. 2002). Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. 0.5) 81. population from the National Health and Nutrition Examination Survey.2.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. deodorants. and 0. 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.9. and also in men attending a Boston infertility clinic (Hauser et al. 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.7 (70. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.8-111) 85. 2003) and African-American women in Washington. Biomonitoring Information MEP levels in the NHANES 1999-2000.1-93..S. particularly those containing fragrances.3 (82. respectively. Products that may contain DEP include perfumes.2-102) 95.. and hand lotions. and 03-04 are 1. 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.. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.9 (61. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 2007).4.9-92.7) 71.3 (74.3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (256-350) 357 (290-407) 306 (253-414) 134 (108-157) 147 (119-177) 148 (125-175) 441 (390-541) 530 (444-660) 597 (523-688) 789 (635-949) 853 (709-1090) 948 (769-1150) 367 (287-482) 413 (366-451) 418 (366-477) 1280 (851-1510) 1490 (1050-2110) 1640 (1320-2180) 1890 (1410-2270) 2160 (1620-2470) 2500 (1840-2980) 986 (798-1340) 1020 (905-1230) 1210 (954-1480) 1720 (1460-2130) 2630 (1540-4460) 3050 (2230-4300) 3610 (2130-4640) 3540 (2810-5070) 4370 (2780-5910) 2470 (1590-3880) 2320 (1560-2720) 2250 (1590-3290) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1 (71.Phthalates Diethyl Phthalate CAS No. DC (Hoppin et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. soaps. 01-02. 272 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00. colognes.

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.5-113) 122 (93.0-156) 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 .6 (65. Survey years 99-00 01-02 03-04 Geometric mean (95% conf..3-105) 87.. 2002).9-110) 96. 2005).6 (77.5-114) 101 (87. 2003) were slightly lower than levels found in NHANES 2001-2002.. Other population estimates also differed by sex and race ethnicity (Silva et al. This age-related trend is opposite the direction seen for other phthalates. Median MEP levels found in a small sample of German residents (Koch et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. population from the National Health and Nutrition Examination Survey.0 (66.9 (82. In an analysis of NHANES 1999-2000. 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. 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.S. 2004). 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.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.2 (66.7-110) 81.Phthalates 2002 (Brock et al.

Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.Phthalates References Adibi JJ. Duty S. Environ Res 2003. Hum Reprod 2007.68:309-314. Reproducibility of urinary phthalate metabolites in first morning urine samples. Third National Report on Human Exposure to Environmental Chemicals. 2005. et al. Reidy JA. Needham LL. Meeker JD. Ryan L.22(3):688-695. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 2004. et al.111(14):1719-1722. Centers for Disease Control and Prevention (CDC). Barr DB. Hodge CC. Brock JW. Bull Environ Contam Toxicol 2002. Singh NP. Hauser R.93:177-185.S. Jacek R. et al. Silva MJ.110(5):515-518. Jedrychowski W. Brock JW.112(3):331-338. Camann DE. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 2002. Environ Health Perspect 2003. Malek NA. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hilborn ED. Baird DD. Caudill SP. Rossbach B. Caudill SP. Phthalate monoesters levels in the urine of young children. 112(5):A270]. Prenatal exposures to phthalates among women in New York City and Krakow. Barr D. Perera FP. Atlanta (GA). Davis BJ. Poland. Angerer J. Silva MJ. Drexler H. Silva MJ. Hoppin JA. Koch HM.

9-26.70 (2.80 (2.90) 4.41) 3.5) 40.2-39.60-11.2) 6.7) 22.00) 11. ATSDR.80) 6.54) 4.90-3.20 (3.82 (3.7) 6.70 (5.2 (31.8-47.4-20.40-12.26-2.1) 29.0 (9.2-28..Phthalates Di-2-ethylhexyl Phthalate CAS No.27 (3.70) 16.30-8.4-40.3-64.20 (4.68 (3.0) 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 3.10) 3.25-3.56 (2.30) 2.5) 37.60) 10.10-3.31-4.2 (7.50 (3.5 (18.40) 11.30-11.7 (17.12 (4.2) 23.2 (29.23) 3.50-2.60) 4.20 (3.9-19.5 (25.6-25.70-4.9-48.40 (4.63-4. 1.93) 6.0-19.00-5.3-26.7-18.40) 4. Fourth National Report on Human Exposure to Environmental Chemicals 275 .50-6.37-4.S. mainly polyvinyl chloride.5 (18. interval) 3.5-36.10 (5.84) 3.40 (6.5-41.00 (2.40-8.9-55.7) 35.1 (8. After parenteral administration.6-60.40) 1.10-5. Albro and Lavenhar.50) 9.9 (7.8 (17. 2002. 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.60-7.6-28.32 (3.8) 15. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.50 (3.8 (19.75-4.60) 90th 14.6) 15.00) 3.0 (16.10) 3.0) 23.0 (13.43 (3.39) 3.5) 43.6) 14.00) 5.40) 75th 7.86) 2.96) 4.80 (1.40-9.5-40.80) 9.50-2.10 (3.9 (26.4) 6.00) 9.00) 2.4) 15.40-9.10 (4.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (3.50 (2.6-130) 31.50) 4.7-58.2) 42.0-18.4-42.50 (7.8 (19.0 (17.50-8.5) 31. population from the National Health and Nutrition Examination Survey.90) 4. and in humans.4-53.98) 2.6 (12.50-6.6 (16.2-17.67-4.9-28. and blood product storage and intravenous delivery systems.0.5 (12.60) 4.60) 7. 1989.80-5.70-6. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.92-2.6) 14.4-27.5 (12.40 (2.1-17.96-5. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP). respectively.61 (3.9 (13.6 (20.2 (10. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.70-2.90) 3.7) 27.30 (6. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).3-49.9 (15.0 (18.42) 3.5 (24.80-4.9 (29.44) 4.6 (41.10-11.9) 18.40 (4.7) 19.35) 4.21 (2.10-5.10-4.03-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.85 (3.4) 20.87-2.6) 9. 01-02.40-1. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.5) 23.16 (2.46) 3.50-11.50 (8.6) 95th 23.0) 23.5 (11.7) 8.90-5.16-3. DEHP has been removed f