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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cdc.4'-Tribromodiphenyl ether (BDE 28) 2.2'.4.2'.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4'.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4-Tribromodiphenyl ether (BDE 17) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.5'-Hexabromodiphenyl ether (BDE 153) 2.4.2’.2'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.3’.6.4.What’s New in this Report What’s New in this Report In this Fourth Report.4-Dichlorobenzene (p-Dichlorobenzene.2'.1-Dichloroethane 1.4.5-Pentabromodiphenyl ether (BDE 99) 2.5’.2'3.6'-Hexabromodiphenyl ether (BDE 154) 2.1.2-Dichloroethene Dichloromethane (Methylene chloride) 1.4'.3-Tetramethylbutyl] phenol) Triclosan (2.6-Heptabromodiphenyl ether (BDE 183) 2.2-Dichloroethane (Ethylene dichloride) 1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.3.3'.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4.5'-Tetrachlorobiphenyl (PCB 44) 2.5'.5.html.2-Dichloroethene trans-1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals. 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 (2.4.2'.4.4.6-Pentabromodiphenyl ether (BDE 100) 2.5.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4'.1-Trichloroethane (Methyl chloroform) 1.4'.4.4. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.3.1.5.4'-Tetrabromodiphenyl ether (BDE 66) 2.3.2'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.2'.4’.5'-Tetrachlorobiphenyl (PCB 49) 2.3. The process for selection is described at http://www.2.2'4.4'-Pentabromodiphenyl ether (BDE 85) 2.5.4. Table 1.4’.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2-Dichloropropane 2.2'.2'.4'.1.1-Dichloroethene (Vinylidene chloride) cis-1. Paradichlorobenzene) 1.4.3-Dichlorobenzene (m-Dichlorobenzene) 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.gov/exposurereport/chemical_selection.

the presence of an interference) that produced results of inadequate quality. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods.4-dichlorophenol and 2. 2001-2002. Data for other pesticides are included only for 1999-2000 and 2001-2002. urinary 2. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. Explanations for each change are provided in Appendix B. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. five results that all have the value 90.What’s Different in this Report What’s Different in this Report The Fourth Report uses a new procedure to estimate percentiles when the percentile estimate falls on a value that is repeated multiple times (e. 2003-2004) have been re-computed by use of this improved procedure.g..5-dichlorophenol for the 1999-2002 survey periods. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. and these data will be included in the next release of the Report. Details of this procedure are provided in Appendix A. Percentiles for all three NHANES survey periods (1999-2000.1).g..

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

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

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

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

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

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

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

1) 62.1 (73.2 (58. in some sealing grouts.8-57.0 (57. gels..2 μg/kg/day (U. smoking. acrylamide has produced upper airway irritation following inhalation of high levels.2-91. 2005).8 (91.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.6-65.6 (56.8 (81.5-80.1-61.3) 63.7 (65. see Data Analysis section) for Survey year 03-04 is 3. in permanent press fabrics.1 (47.6-75.0-49.S.2-118) 98.7) 54.3-71. and in some cosmetics. such as potatoes and some grains.4) 100 (89.4) 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 54.7) 75th 79.4 (59.7 (63.7) 58. Estimated intakes in children are about twice that of adults (DiNovi and Howard.0-58.5-85. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.7-60.3 (55.1-64.9) 63. and well below doses known to cause nerve damage or carcinogenicity in animals.2-114) 163 (147-191) 96. EPA.7-64.3 (53.9-105) 86.1) 101 (95.9 (60.2) 57. These estimated intakes are hundreds of times lower than occupational exposures.4-89. and from dermal contact with products that contain residual acrylamide.2-93. but are generally above the U.S.Acrylamide Acrylamide CAS No.7 (58.9 (54.6-108) 61.7-64.0-66.S.9) 58.2-77. and is either metabolized to the reactive epoxide. 2005.6) 90.4) 57. FDA.0. Fennell et al. and cosmetics (NTP-CERHR.2 (62. Animal studies indicate that acrylamide is well absorbed.9 (69..4-83. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. but can covalently bind to form adducts with proteins. In 1997.0 μg/kg for adults (FAO/ WHO. 2005). Natural substances in the food are converted to acrylamide. glycidamide. Polyacrylamides are useful water-compatible polymers used in water treatment.S. or to glutathione conjugates (Calleman et al.9) 75.9) 57.1 (88.2-67.8-55.6) 50.5) 58.5 (74. and in the synthesis or compounding of dye materials. Fourth National Report on Human Exposure to Environmental Chemicals 11 .7) 96.5 (44.9-61.5) 66.8 (52. and an average daily intake is estimated as 0.9-52.6) 73. 217 million pounds of acrylamide were produced commercially in the U.1 (83. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.S.5 (52.4-76. FAO/WHO.4-60. 2005).6) 71. widely distributed in tissues. pulp and paper production.0) 57.6 (51.1) 53. ocular and dermal irritation from direct contact with acrylamide containing materials. Elimination occurs mainly in the urine as mercapturic acid conjugates. as an absorbent in disposable diapers.4 (54. People may be exposed to acrylamide from foods. EPA reference dose of 0.3) 86. 2005). mineral processing.1) 46. 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. population from the National Health and Nutrition Examination Survey. Commercially. 2004).3-2.2 (75.0 (53. and binding agents. it was discovered that acrylamide is formed when starch-rich foods. Acrylamide is not thought to accumulate in the body at environmental doses.4 (54. 1990. Recently.5 (79.8 (57. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.6-66.2) 57.0 (69.0-108) 152 (139-175) 126 (111-142) 108 (86. In humans. soil conditioners. Since acrylamide has limited volatility and high water solubility.0) 85.4) 57. (NTP-CERHR. 2005).0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. Survey Geometric mean (95% conf. In the general population.4 (51. are heated at temperatures used for frying and baking.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 61.3) 70. acrylamide is synthesized and used in the production of polyacrylamide polymer. EPA.1) 55.6-104) 82. 2006).4 (53.4-60. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2004.0 (67.2-70. 2006.1-57. 2002). drinking water.6 (81.7) 73.1 (52.6-61.1-64. Tareke et al.7 (55. 1994).. interval) 61.2-59.

8-48..5 (42. 2009). male germinal cell injury.7) 90. 2005) have been demonstrated in animals. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.. 1997.4 (56.epa.3) 85.9 (81. 2003.6-64. Vesper 2005) and smoking (Bergmark. 2002..2-91.0 (70. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).9) 75. Mucci et al.4) 83. although different analytic methods can affect results.. scrotal. Puppel et al. most non-smokers had levels less than about 100 pmol/gram hemoglobin.1-62.7 (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. 2005.S. Axonal degeneration.5-66.. 2008).5-92. 2005.5 (83. Glycidamide has been shown to react with DNA (Doerge et al.1-70. population from the National Health and Nutrition Examination Survey.7 (84.0 (52.9-77. 2005.2-68.2 (56.0 (75..who. Schettgen et al.. thyroid.6-62. 2008).4 (57.1) 56. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.2 (72.5 (59. probably through its epoxide metabolite. Schettgen et al. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.5-64.S.8) 60. 2005. EPA. 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.4 (81. Puppel et al.7) 60.7-86. EPA..5 (56.3 (56.7) 74.9 (58.4-103) 79.7-64.5) 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.7-62.9) 65. U. 2005). U. altered gene expression in testicular tissues (Yang et al.9-78. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al..5) 71.4 (90. NTP-CERHR. 2006.0-103) 136 (123-148) 125 (116-135) 126 (119-135) 141 (126-157) 146 (123-169) 187 (169-204) 129 (111-141) 174 (157-197) 159 (143-175) 411 784 1931 2623 1529 3604 3674 03-04 03-04 03-04 64. 2005).4-98. dominant lethality).8) 45. Rice.1 (57.5-94. 2004).6-90. 2005.2-90. and neuronal DNA reactivity (Doerge et al. Maniere et al. 2005) and sperm DNA adducts (Xie et al. uterine..9) 59.int/ ipcs/food/jecfa/summaries/summary_report_64_final. and other sites) (FAO/WHO.5) 87.8-49..0-93.7) 61. 2006). 2002.4) 53.3) 59..8-61. Hagmar et al.7 (57. AHA levels have been shown to increase with dietary intake (Hagmar et al. Klaunig et al. 2005..pdf. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA..2) 55.4-65. 2005.3-78.7 (61.4-59. Vesper et al. respectively) are markers of integrated acrylamide exposure over the preceding few months.Acrylamide occupational exposures.4 (51.3-101) 95.3) 59. 1997.5) 75th 85. EPA at: http://www. 2004.0) 118 (103-126) 121 (112-134) 113 (94.0-62.2 (63. 2005. see Data Analysis section) for Survey year 03-04 is 4. 2006) have been demonstrated after acrylamide dosing.8 (44.3) 59.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.1 (82. Additional information is available from U. 2005.9-76.. Survey Geometric mean (95% conf. Acrylamide is clastogenic and can produce dominant lethal mutations. glycidamide (NTP-CERHR.9-62.6 (90.9-138) 143 (130-159) 96. 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..0 (80.0) 94.9 (57..4 (61.S. 2005).1 (66. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. adrenal. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2005).1 (70.1) 62. In addition. reproductive effects (reduced litter size.6 (66. 2006). 2005. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers..2) 87.S.9) 87.2) 65.4) 46.1) 60.. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.9-64.. 2001). 2005. IARC classifies acrylamide as probably carcinogenic to humans. and cancer (mammary. interval) 59.1-56.1 (56. presynaptic nerve terminal binding (LoPachin.1-60. After exposure ceases.8 (51.0. fetal death.

Costa LG. 054472. DiNovi M and Howard D. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Duale N. He F. Toxicol 2005. morphological and molecular endpoints in animal models. Rome. Calleman CJ. 2/3/09 Perez HL. 2001. Beland FA. Available at URL: http://www. Magnusson AL. The Updated Exposure Assessment for Acrylamide.. [Epub ahead of print] Dybing E. Wu Y. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Fennell TR. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.126(2):361-371.561:49-62. Toxicol Sci 2005. Acrylamide neurotoxicity: neurological. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al.56. Tian G.. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Twaddle NC. 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. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Biomonitoring studies of acrylamide or glycidamide hemoglobin adducts provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acrylamide than are found in the general population. Available at URL: http://www.10(1):78-84. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Mutat Res 2005. Nordander C. 2009 Jan 8.. July. Adv Exp Med Biol 2005. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. 1994). and Research Strategies. Hagmar L. et al. Chem Res Toxicol 1990. Spicer R. 2004 Acrylamide in Food Workshop: Update Scientific Issues. da Costa GG. Tornqvist M.120(1):45-54. Chicago.43:365–410. He F.niehs. Farmer PB. Metabolism and hemoglobin adduct formation of acrylamide in humans. Costa LG. 1999). April 13-15. Burgess J.. Uncertainties. Survey data on acrylamide in food: individual food products. In another study. Becher G. 2001). smoking habits and gender. et al. 2/3/09 Klaunig JE. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. McDaniel LP. Tornqvist M. CFSAN/Office of Plant and Dairy Foods. smokers and nonsmokers.27(4):219-226. Human exposure and internal dose assessments of acrylamide in food.who. Bergmark E. Haugen M.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Snyder RW. 64th Meeting: Summary and Conclusions (FAO/WHO). LoPachin RM. Bjellaas T. Paulsen JE. Mutat Res 2005. Malmberg B. et al. J Agric Food Chem 2008. Acrylamide intake through diet and human cancer risk. Kautiainen A. Bruze M. Calleman CJ.pdf.Toxicol Appl Pharmacol 1994. Zhang S. Adv Exp Med Biol 2005. Cheong HK. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Andersen M. 1993. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose.561:21-37. Doerge DR. Laurentie M. 2006. Food Chem. 2004.. Yang JS. Chem Res Toxicol 1997 Jan. Hagmar et al. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Rosen I. February. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Godard T. Maniere I. Summer SCJ. Granath F. 8-17 February 2005. Scand J Work Environ Health 2001. Toxicol Appl Pharmacol 1993. Calleman CJ. Bergmark E. 6013-6019. 2005. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake.580(1-2):119-129. Churchwell MI. gov/~dms/acrydata.Acrylamide In occupational settings. Mucci LA.pdf. Guffroy M.3:406-412. Perez et al. Doerge DR.html#u1004. Aprea P. Mechanisms of acrylamide induced rodent carcinogenesis.fda.nih. Mutat Res 2005. 2/3/09 Hagmar L. Churchwell MI. Food and Drug Administration (FDA).580(1-2):157-165. Osterman-Golkar S. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Joint FAO/WHO Expert Committee on Food Additives.85:447-459. Axmon A. Toxicol Sci. Paulsson B. Fennell TR. Italy.cfsan. Bridson WE.580(1-2):131-141. 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. National Toxicology Program. Illinois. Wilson KM. Kamendulis LM. Bergmark E. NIH Publication No. References Bergmark E.gov/chemicals/ acrylamide/Acrylamide_Monograph. Alexander J. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. et al. Available at URL: http://cerhr. et al. Wirfalt E.

50(17):4998-5006. Toxicol Lett 2006. Meyers T. Meyers T. Yang HJ. Marko D. Drexler H. EPA). Tjønneland A. 2/3/09. 2/3/09 Vesper HW. Rice JM. Rapid Commun Mass Spectrom 2006. Mutat Res 2005 Feb 7.580(1-2):71-80. Tornqvist M. Letzel S. Ingham L. Karlsson P. The carcinogenicity of acrylamide.epa.S. Acrylamide. Angerer J.56(15):6046-53. Schettgen T. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Anal Biochem 1999. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Ospina M. et al.206(1):9-14. Lee MH.S. Drexler H. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. EPA). Schettgen T. Environmental Protection Agency (U. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.S. Int J Hyg Environ Health 2004. September.gov/iris/subst/0286. Hallmans G.274(1):59-68.htm. Environmental Protection Agency (U. Sun H. U.561:89-96. a carcinogen formed in heated foodstuffs. Tjaden Z. J Agric Food Chem 2002. U. et al. Benetou V. Reprod Toxicol 2005. Drexler H. Fu D. Toxicol Lett 2002. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Angerer J. Angerer J.txt. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.Acrylamide glycidamide by gas chromatography-mass spectrometry. Han CH. Kutting B.20(6):959-64. Ding X. Available at URL: http://www. Schettgen T. Myers GL. Weiss T. Eriksson S.163(2):101-8. Agudo A. Mutat Res 2005. propylene oxide. Office of Pollution Prevention and Toxics.gov/chemfact/s_acryla. Liu K. Tareke E.207(6):531-9. Toxicological effects of acrylamide on rat testicular gene expression profile.epa. Chemical Summary for Acrylamide. revised 1/3/06. Rossbach B.134(1-3):65-70. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Vesper HW.19(4):527-34. Hemoglobin adducts of ethylene oxide. Xie Q. Gray JG. Han DU. Washington (DC). Available at URL: http://www. Ospina M. J Agric Food Chem 2008. Smith A. Rydberg P. 1994. Puppel N.580(1-2):3-20. Lee SH. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Vesper HW. Chae C. Slimani N. Jin Y. Fueller F. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Choi JH.S. Analysis of acrylamide. Liu Y. Integrated Risk Information System (IRIS). Licea-Perez H. Adv Exp Med Biol 2005. Int J Hyg Environ Health 2003. Broding HC.

63 (2.280 (.140 (.052 (<LOD-.770) .080) < LOD .39) 3.059-.66-3.120 (.050-.920 (.187) .70-2. which may vary for some chemicals by year and by individual sample.040 (.23 (2.96 (1.621-1.960-1.76 (1.090-.030-.030 (.990 (.01 (1.062 (.050 (<LOD-. see Data Analysis section) for Survey years 99-00.120 (.21-1.950-1.073) < LOD .16) .150) .312) .68) 2.110) .15) 2.480-1. Fourth National Report on Human Exposure to Environmental Chemicals 15 . acute respiratory infections.49) 1.740-1.260) 1.120 (.11) .180) .160) .00) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 1.14) .75) 1.19) 1.080 (. and 03-04 are 0.070) .44 (1.580-1.180 (.220) .480-.240 (.120) .070-.17) . and various other disorders (U.180) .630 (.030-. stroke.110-.050 (.200) 1.188) .55 (1.510 (.068) .180) .040 (.44) 2.160 (.104-.060-. 2004).163 (.840) 3.43 (1. Cigarettes contain about 1.770-1.148-.47-3. 1998).080-.30) * .210 (.050) .050-.660) .110 (.23 (1.066-.05 ng/mL.540-.130 (.12 (2.860 (.14-1. DHHS.350 (.140 (.160 (.48-3.28) .12 (1.99) 2.080) < LOD < LOD .28-1.57) 2.094) .62 (2. 83% of measurements had an LOD of 0. 2004).05.500 (.198) * .131 (.39 (1.213) .230 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer. and 17% had an LOD of 0.110 (.19) .740-1.726) .77 (1.320) .106-.066 (.93) . and 0.310-1.137-.090-.32) 1.050 (<LOD-.053 (<LOD-.020-.160-.30) 2.88 (1.071) .230) .077) .190-.070 (<LOD-.800 (.00) 1.570-1. population from the National Health and Nutrition Examination Survey.20-2.080-.30) 2.197) .22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .142-.65 (1.043-.193) .600-1.96-4.930 (.060) .260-1.154-.520 (.625) .080-.79) 3.53-4.400-.111-. respectively.63-2.45) 1.50 (1.060-.089) Age group 3-11 years 99-00 01-02** 03-04 .22) 2.308 (.49) 1.506 (.670) .137 (.44 (2.17 (.S.620 (.052 (<LOD-.047-.580) .080 (.78) 2.030-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.075 (.120 (.09-3.17 (1.81-2.21 (.540 (.220) .40) .086 (.66 (1.820) .42-4.50-1.900-1.410) .910-1.690 (.063) .140-.124 (.44) 2.060 (.120-.95) 1.163) .55-2. 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.990) .070) 75th .139) * .175 (.153-.04 (1.428-.015 ng/mL.087 (.160 (.115-.059-.14) .060 (<LOD-.040 (. maternal exposure during pregnancy can result in lower birth weight.087-.5% nicotine by weight (Kozlowski et al. 2006).83-2.350-.54 (1.20 (1.167 (.076-.92 (1.12) 1.997-3.85 (1.580 (.20) .12-4.180) .850 (. cardiovascular disease.S.01) 3.77 (1.066) .300) .23 (.160) . producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.620-1.088-.88 (.Cotinine Cotinine CAS No..09-3.070) .53 (1.68) .33-2. acute respiratory illness.02) 1.770) .505 (.50-4.057-. emphysema.77 (2.108) * . ** In the 2001-2002 survey period. 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.630 (.50) 3.220-.234) .180) .470-. Children exposed to ETS are at increased risk for sudden infant death syndrome.54 (1.630 (.360) .180 (.071 (.370-. DHHS. < LOD means less than the limit of detection.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .68 (1.87-3.02) 1.110-.02 (.450-. Survey Geometric mean (95% conf.310-1.140-.09-2. and exacerbated asthma (U.216 (.48-2.19-2.058 (.23-2.201) .34 (1.26-1.090-.570 (.061) < LOD .110-.790) .164 (.040-.050) .050 (<LOD-.100-.110 (.040-.84-3.21-1.350-.302) .145) .110) .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 .084) .35 (2.38-2.S.120 (.310) . ear problems.54) 1.080-.730 (.533-.060 (<LOD-.126) .710 (.050 (<LOD-.950 (.060-.054 (.068) .110 (.99) 2.144 (.060 (.130) .66) 1.190-.150) .15 (2.087) < LOD < LOD .120-.047-.110 (.015.310) 90th 1.62) 2.077) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.32-2.70) 2.89) 1. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.32-2.42 (1.94) 1.20 (.18-3.05) 1.190-.60-2.96) 2.49) 2241 1878 1707 1333 1602 1704 1950 2847 2500 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02** 03-04 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.430-1.164 (.

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

Environ Health Perspect 2006. Kozlowski LT. Tobacco Smoke. Giovino GA. Available at URL: http://www. 4/13/09 Iwase A. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Pickett MA. Benowitz NL. Coordinating Center for Health Promotion. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention. Bernert JT. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . iarc. JAMA 1996. Caudill SP. Metabolism and disposition kinetics of nicotine.S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.iarc.18:188-204. Schwartz SS.57(1):79115. Pechacek TF.S Department of Health and Human Services (U. Perez-Stable EJ. Benowitz NL. Sweeney CT. JAMA 1998.gov/ntp/roc/eleventh/profiles/ s176toba.niosh.gov/tcrb/monographs/10/. Mehta NY.7:369-375. Jacob P. 1991. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Brody DJ. 2004. J Pharmacol Exp Ther 1999. 1988-1991. Epidemiol Rev 1996. National Institute for Occupational Safety and Hygiene (NIOSH). DHHS). Giovino G.56:483-493. et al. 11th ed. Kira S.63:139-43. Tob Control 2006. Benowitz NL. 4/13/09 Perez-Stable EJ. Benowitz NL. BMJ 1975. Maurer KR. cigarette smokers: the Third National Health and Nutrition Examination Survey. Office on Smoking and Health [online] 2006. Nicotine metabolism and intake in black and white smokers. Pirkle JL. Smoking and Tobacco Control Monograph 10 [online]. Available at URL: http://monographs.15:302-307. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Bernert JT. Pharmacol Rev 2005. U.114(6):853-858. Jacob P III. 4/13/09 U.pdf.S Department of Health and Human Services (U. Jacob P III. Fong I. Turner DM. Tob Control 1998. International Agency for Research on Cancer. Pirkle JL.php. Houseman TH. Dollery CT.S. In Report on Carcinogens. Caraballo R.280:135-140. IARC Monogr Eval Carcinog Risks Hum. DHHS). Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. the United Kingdom.291(3):1196-1203.gov/library/ secondhandsmoke/. Soliman S. and the United States. Flegal KM.S. [online]. Richter PA. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. available at URL: http://mtn.S. Schober SE. Exposure of the U. Jacob III P.surgeongeneral. Int Arch Occup Environ Health 1991. Warner K. 4/13/09 International Agency for Research on Cancer. National Center for Chronic Disease Prevention and Health Promotion. Herrera B. Lewis PJ. Hukkanen J. Ethnic differences in N-glucuronidation of nicotine and cotinine. Curtin LR. Centers for Disease Control and Prevention. population to secondhand smoke: 1988-2002. Vogler GP. Cotinine as a biomarker of environmental tobacco smoke exposure. Modin G.280:152-156. 1999. Sosnoff CS.niehs.nih. Benowitz NL.cancer.php. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. 4/13/09 Centers for Disease Control and Prevention (CDC).275:1233-1240. Atlanta (GA): 2005. Available at URL: http:// cancercontrol. Herrera B. References Armitage AK. Department of Heath and Human Services.gov/eid/rmca/critdocs/ criteriadoc/33.S. Racial/ethnic differences in serum cotinine levels among adult U. Absorption and metabolism of nicotine from cigarettes. Respiratory nicotine absorption in non-smoking females during passive smoking.94(2):314-320. Am J Public Health 2004.pdf. Vol 38. 1988-1991. 4/13/09 National Cancer Institute (NCI). Jarvis MJ. Summary of Data Reported and Evaluation [online] 1986. Available at URL: http://monographs. Brody DJ. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.fr/ENG/Monographs/ allmonos90. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Aiba M. Clin Pharmacol Ther 1994. Pechacek TF. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Etzel RA. Strauss WJ.cdc. JAMA 1998. Trends in the exposure of nonsmokers in the U. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Available at URL: http://ntp. U. 1999-2002. Coordinating Center for Health Promotion. National Toxicology Program (NTP). June.fr/ENG/Monographs/allmonos90. et al.S.4:313-316. Vol 83. Summary of Data Reported and Evaluation [online] 2004. Tobacco Smoke and Involuntary Smoking. Department of Heath and Human Services.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. U. George CF. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Tobacco related exposures. Centers for Disease Control. Pollack HA. Mowery PD. IARC Monogr Eval Carcinog Risks Hum.S.

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

One survey detected DEET in 74% of sampled streams in the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.epa.560) < LOD . DEET can be applied to clothing and the skin to repel biting insects. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.120-.100-.220 (. 2003). (U.140) < LOD .S. DEET has low acute toxicity.110-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.140 (. Sudakin and Trevathan. and it has not been rated by IARC or NTP with respect to human carcinogenicity. After absorption.S.140) < LOD .110 (<LOD-.EPA at: http://www.S.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. (Kolpin et al. DEET is not registered for use on agricultural commodities.S. 1998).130 (.140) < LOD .130) < LOD .180 (.100-. Survey Geometric mean (95% conf.210 (.100-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/pesticides/. including seizures and encephalopathy..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 . About 3-8% of dermally applied DEET is absorbed. 2002).140-. Fourth National Report on Human Exposure to Environmental Chemicals 19 . Additional information is available from U. 2003).180 (.130-. and they range in concentration from 4% to 100%. 1995.100-..190) < LOD .100-.180) < LOD .130-. 2005).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 . Neurological effects in humans.100 (<LOD-. 2002).170 (.S.250) < LOD . DEET is not a developmental or reproductive toxicant in animals (U.N-Diethyl-meta-toluamide (DEET) N.120-.1. which may vary for some chemicals by year and by individual sample.110 (. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.150) < LOD . Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.110 (<LOD-.130 (.180 (.N-Diethyl-meta-toluamide (DEET) CAS No. DEET is also used in combination with dermal sun screens (U. There are over 225 insect repellents brands containing DEET.110 (.170 (.110 (. 134-62-3 General Information N. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.EPA.130-. 1998).100-. Its use is recommended for prevention of several vector-borne diseases.110-.S.160) < LOD .110 (.130-.270) 688 678 518 700 598 956 Limit of detection (LOD.140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130 (.N.EPA.449 and 0.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.240) < LOD .520) < LOD . population from the National Health and Nutrition Examination Survey. EPA. < LOD means less than the limit of detection. Urinary N. DEET is not genotoxic. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. have been reported as result of self-poisoning by ingestion or excessive dermal application. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.130) < LOD ..

500 (..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 . Urinary N. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.270-.280-1.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .240-.270 (<LOD-.190 (<LOD-.170-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.480 (.290-. Survey Geometric mean (95% conf.230-.250 (.190 (.250-.130 (<LOD-.150-.640 (.240) < LOD . 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.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.350) < LOD .440) < LOD .280 (.330 (.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 .190 (.350) < LOD .300 (. 2005).410 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.370) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .320 (.230) < LOD .320) < LOD .410-.S.140-.S.270) < LOD .190-. Urinary DEET levels as high as 5.330 (. population from the National Health and Nutrition Examination Survey.. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. representative subsamples from NHANES 2001-2002.150) < LOD .410 (.93) < LOD .630) < LOD .270 (.N.200 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.230-.370-. 2007).580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . In this survey period.490) < LOD . 1992).550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.350-.250) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.390-. 20 Fourth National Report on Human Exposure to Environmental Chemicals .

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

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

Myers CB.niehs. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Endocrinology 2008. 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. November 26. McConnell EE. et al.113(4):391-395. Toxicol Sci 2002.Environmental Phenols References Akingbemi BT. Needham LL.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Brine DR. Thurman EM.eu/ health/ph_risk/committees/sct/documents/out156_en.gov/chemicals/bisphenol/bisphenol. Hlywka JJ. Zacharewski TR. National Institutes of Health. Chem Res Toxicol 2001. Hughes C. Matthews JB. Regul Toxicol Pharmacol 2002. Needham LL. Marr MC.gov/chemicals/bisphenol/BPAFinalEPVF112607. Kolpin DW. Kim YH. Reprod Toxicol 2001. Timms BG. Watanabe S. Joint Research Centre Institute of Health and Consumer Protection. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Barr JR. Kawamura N. Twomey K. Furukawa M. 2002. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. bisphenol A glucuronide. vom Saal FS. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Pharmaceuticals.Scientific Committee on Toxicity.. Calafat AM.pdf . Barr DB.pdf.145:592-603. Klinefelter GR. Occup Environ Med 2002. Ikka T. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).149:988-994. Haighton LA. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. N. Watanabe C.S.780(2):365-370. Reidy JA. hormones. 4. 2/4/09 Fujimaki K. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Life Sci 2001. 5: 505-523.137(3):353-362. Hum Ecol Risk Assess 2004. Ema M. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Joskow R. Ispra.. Cha SW. U. Wong LY.pdf. Belgium.59(9):625-628.S. and Hardy MP. DirectorateGeneral Health and Consumer Protection. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Environ Health Perspect 2005. and other organic wastewater contaminants in U. Reidy JA. Department of Health and Human Services. 2007. Human Health.nih.14(2):149-157. Furlong ET. niehs. Imai H.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Han SS. 2/4/09 Ouchi K. Keimowitz AR. Available at URL: http://cerhr. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. streams. C. Kroes R. Chung MK.68(1):121-146.nih. Rubin C. Ye X.35(2 Pt 1):238-254. Koulova AI. August 2001. Gray GM. K. Research Triangle Park.europa.102(19):7014-7019. Endocrinology 2004. with estrogen receptors alpha and beta. Available at URL: http://ecb. National Toxicology Program.nih. Cunha G. 2003.S. T. Bradley S. Park S. Available at URL: http://ec. Caudill SP. Brussels. Ecotoxicity and the Environment (CSTEE). Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Hara K. Yoshinaga J. Environ Health Perspect 2008..116(1):39-44. Han SY.312(2):441-448. Biochem Biophys Res Commun 2003. Lynch BS. Kiguchi M. Sottas CM. Meyer MT. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Calafat AM. Exposure of the U. National Institute of Environmental Health Sciences. Hanaoka T. Available at URL: http://ntp. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Thomas BF.jrc. An evaluation of the possible carcinogenicity of bisphenol A to humans. Nippon Eiseigaku Zasshi 2004. Tsugane S. Shin HC. et al. Howdeshell KL. May 22. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. NC. Pyo MY. 2008. Yang M. Kim CS.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Leranth. 1999-2000: a national reconnaissance. Barton L. et al. Kuklenyik Z. Rhomberg et al. Barber LB. Available at URL: http://cerhr. Zaugg SD.69(22):2611-2625. Environ Sci Technol 2002. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Cohen JT. September. Kim JC. niehs. MacLusky. In vitro and in vivo interactions of bisphenol A and its metabolite. 2/4/09 European Commission. Needham LL. Szigeti-Buck. Gender differences in the levels of bisphenol A metabolites in urine. Proc Natl Acad Sci USA 2005. Harazono A. Bisphenol A. Fujii S. Calafat AM. Arakawa C. European Commission.J. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Richter CA. Serizawa S. and Hajszan. Ekong J. Tyl RW.36(6):1202-1211. J Am Dent Assoc 2006. Doull J.10:875-921. Munro IC.59(4):403-408.pdf . NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Rat two-generation reproductive toxicity study of bisphenol A. Italy. Koh WS.pdf.

Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Wilson NK. Environ Res 2007. Csanady GA. Welshons WV. Large effects from small exposures. III.Environmental Phenols Volkel W. Vom Saal FS. Nagel SC. Lordo RA.15:12811287. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Dekant W. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Yang M. Colnot T. Hughes C.103(1):9-20. Kim SY. Sheldon LS. et al.147(6 Suppl):S56-69.40(7):905-12. Chuang JC. Chem Res Toxicol 2002. Jang JY. Biological monitoring of bisphenol a in a Korean population. Chang SS. Environ Health Perspect 2005. Morgan MK. Food Chem Toxicol 2002.44(4):546-51. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Witorsch RJ. vom Saal FS. Endocrinology 2006. 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. Arch Environ Contam Toxicol 2003. and nonylphenol at home and daycare.113(8):926-33. bisphenol-A. Kawamoto T. Lee SM. Filser JG.

500) .50-3.g..200-.500) 75th .20) 1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.30 (1.300 (<LOD-.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.50) 1.50-2. Ying et al.30) 1. streams in 30 states (Kolpin et al.5% of 139 U. 2002).477) .70 (1.80 (1. to shorter chain alkylphenol ethoxylates.90) 2.900 (.60-3. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. which may vary for some chemicals by year and by individual sample.600-1.600) 1.500) .Environmental Phenols 4-tert-Octylphenol CAS No.00 (1.20-2.2. 2000.50) 1. textiles. an alkylphenol.600-1. altered neonatal sexual development. Blake and Boockfor.20-2.70 (1. 2002).900 (. 34 Fourth National Report on Human Exposure to Environmental Chemicals .300 (<LOD-.369 (.. and through manufacturing waste streams (Warhurst.20-2. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).60) 613 652 1092 Limit of detection (LOD.268-.30 (1.500 (.50) 1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.300 (<LOD-.30 (1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.274-.20) 314 715 1488 03-04 03-04 * * .10 (1. In rats. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.60-3. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.400 (.70 (1.600-1. and emulsifiers.40) 1. Laws et al.60-3.. Saito et al. orally administered 4-tert-octylphenol was well absorbed. Disposition in humans has not been studied sufficiently. including 4-tert-octylphenol.40 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1996). the various alkylphenols have also been used as emulsifiers and modifiers in paints. testicular atrophy. Less frequently. Indoor and to a lesser extent. The alkylphenol ethoxylates enter the environment through human use of products containing them.299-.400) 1. over 500. and some personal care products.10) 1.600-1.900 (..800-1. and the polyethoxy chain may consist of up to 50 ethoxy units. through sewage. which are anionic surfactants used in detergents. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.500-1.600-1.700-1. Bian et al. is used to manufacture alkylphenol ethoxylates.40) 1. < LOD means less than the limit of detection.90) 2.50 (1.400 (.600) .60) . did not bioaccumulate. pesticides.40) 2.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th . During the 1980s and 1990s.000 tons of alkylphenol ethoxylates were produced annually worldwide..80 (1.80 (1.200-.30 (. 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.00) 1229 1288 03-04 03-04 03-04 * . impaired steroidogenesis.1.30 (1.10 (.500) .60) 1.60-3.900 (. 2003. 2006. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.60-3.40) 2.507) * < LOD ..497) * . and to alkylphenoxycarboxylates.600) . Survey Geometric mean (95% conf.00 (. Several alkylphenols.30) 90th 1. 2004). population from the National Health and Nutrition Examination Survey.50) ..357 (. and some of their degradation products are toxic to aquatic life.20 (1.300 (<LOD-. Urinary 4-tert-Octylphenol (4-[1. have demonstrated estrogenic effects particularly when injected at high doses in animals. 1995.30-2.10) 2. In 1999-2000.20-2. 2000. see Data Analysis section) for Survey year 03-04 is 0.10 (.30) 2.3..20-2.20-2.60-3. 1997. 4-octylphenol monoethoxylate was detected in 43.300-. In the 1990s.70 (1. and was quickly eliminated from the blood (Certa et al.900 (. altered estrus cycles and reproductive outcomes. Katsuda et al. industrial cleaners.600) .500-1. leading to inhalation as another potential exposure route (Rudel et al. 140-66-9 General Information 4-tert-Octyphenol..300-.g.80) 2.400 (.600-1. fish) and drinking water. and impaired spermatogenesis (e.10-2.20) 2..00 (.S.389 (. The alkylphenols can bioaccumulate in some fish.50) .300 (<LOD-. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. and from contact with some personal care products and detergents.40) * 03-04 03-04 03-04 .

or their corresponding ethoxylates with respect to human carcinogenicity. Tyl et al. 2004.860 (.00) 1.570) .380 (<LOD-.03-6.36-3.850 (. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.65-3.25) 90th 1.530) . It is unclear if estrogenic or other effects occur in animals through oral dosing.62 (1.269 (. at lower or environmentally relevant doses (Blake et al. 1999).03 (1. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U. Yoshida et al.71) 2.890-2.500-1.620-1.199-.540-1..160-.207-.25) 2. Sweeney et al. Kawaguchi et al.03 (1.78) 1228 1286 03-04 03-04 03-04 * . In a small number of adult Japanese volunteers..640-1.02-4. IARC and NTP have not rated octylphenol.60 (1.550-1.96-4.43) 1.78 (1.. 2003. nonylphenol.460 (.43) 1.410 (. 4-tert-Octylphenol is not considered directly genotoxic..73) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.68) 2.68-2.53-3. 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. 2001. 2000..24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.22) . 2001).370 (<LOD-.S.280-.630-1.400) .33) 3.76 (2..435 (.730-1.59) 1.62) .00 (.14) 314 713 1487 03-04 03-04 * * .17 (.85 (1.41) .11) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.450) .15) 1.62 (1.06 (2. 2005.78) 3.470-1. Fourth National Report on Human Exposure to Environmental Chemicals 35 .31-2.43-3.81 (1.349) * < LOD .40 (1.10-2. Urinary 4-tert-Octylphenol (4-[1.29) 2. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.450) 1. Nagao et al.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.910 (.610) .470-1.Environmental Phenols Myllymaki et al. Survey Geometric mean (95% conf.740 (.11-2.260 (<LOD-.31 (1.64 (.25-2.770 (.270 (.67-2.384) * .337-.11) 1. population from the National Health and Nutrition Examination Survey.20 (1.620) .270-.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 .59 (1. representative subsample of NHANES 2003-2004.270 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740 (.560) .420) .300 (<LOD-.05-2.40-4. Calafat et al.3.470) 75th .1.S.18-4.170-. 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. 2004).33 (2.320 (<LOD-.08) 1.54) * 03-04 03-04 03-04 .276 (.50 (2.00 (.00) 2.00) 2.

Exposure of the U. pesticides.57(2):255-266. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Kolpin DW. et al. Horie M. Tyl RW. Blake CA. Brody JG. Roche JF. Environ Sci Technol 2003. and other organic wastewater contaminants in U. et al. Ito R. Xu L.141(7):2667-2673. Kookana R. Onuki A. Environ Sci Technol 2002.165(3):217-226.co.207(1):59-68. Phthalates. Yoshida M. Toxicol Appl Pharmacol 2005. Food Chem Toxicol 2006. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Wong LY. Muller AM. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Saito I. Toppari J. Nicol L. Indoor Air 2004. Needham LL. streams.36(6):1202-1211.folliclestimulating hormone. 1999-2000: a national reconnaissance. Saito Y.54(1):154-167. polybrominated diphenyl ethers. testis size. Qian J. Millette CF.18(1):43-51. Arch Toxicol 1996.14(5):325-332. Anal Chim Acta 486:41-50. et al.pdf. Haavisto TE. Reprod Toxicol 2001. bisphenol A and methoxychlor in rats. Katsuda S. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Yoshimura Y.Environmental Phenols References Bian Q. Myllymaki SA. Thurman EM. Endocrinology 2000. Nagao T. Yoshida M. Sakui N. hormones. Pharmaceuticals. Ye X. Environ Health Perspect 2008. Blake CA. Makino T. Barber LB. Watanabe G. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Maekawa A. Environ Int 2002. Karjalainen M. Kawaguchi M. J Chromatogr B Analyt Technol Biomed Life Sci 2004.S. and testosterone.uk/resource/reports/ethoxylates_alkylphenols. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Taya K. prolactin. Regul Toxicol Pharmacol 1999. Rudel RA. Cooper RL.121(1):21-33. Korn LR. Song L. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Izumi S. Takenaka A. McCoy GL. Paranko J. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. 1995. Wiegand HJ. Wang X. Two-generation reproduction study with para-tert-octylphenol in rats. Yoshimura S. Nair-Menon JU.116(1):39-44. Warhurst AM. Sweeney T. Williams B. Reprod Toxicol 2004. alkylphenols. Bolt HM. nonylphenol. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion.44(8):1355-1361. Myers CB. Toxicol Lett 2001.15(6):683-692. Katsuda S. Raychoudhury SS. Marr MC. Takai N. Certa H. Reidy JA. Toxicol Appl Pharmacol 2000. Carey SA.71(1-2):112-122. Fedtke N. Laws SC. Bodman GJ. Toxicol Sci 2000. 2/4/09 Ying GG. Chen J. Calafat AM. Seely JC. Boockfor FR. Boockfor FR.37(20):4543-53. Fail PA. and other endocrine-disrupting compounds in indoor air and dust. Usumi K. Okada F. Inoue K. Taya K. Indoor air pollution by alkylphenols in Tokyo.30(2 Pt 1):81-95.foe. and sertoli cell number. Camann DE. Zaugg SD. Biol Reprod 1997.799(1):119-125. 2003. et al.S. Meyer MT. Furlong ET. Brooks AN. Estrogenic activity of octylphenol. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Brine DR. Maekawa A. Available at URL: http:// www.28(3):215-226. Kawaguchi M. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Nakagomi M. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Inoue K. Ono H. 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. Spengler JD. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Seto H. Watanabe G. Ferrell JM.

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

1) 7.00-8.8) 9.4.3-35.4 (12.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.1-39.8-63.8-127) 37.50) 10.94 (7.2) 12.8) 14.0) 65.8-112) 30.1) 13.7 (28.86-12.20-13. population from the National Health and Nutrition Examination Survey.11-11.3) 47. Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.48 (8.21 (6.43-13.7) 10.10-9.1 (8.45-13.5) 20.9) 75th 47.4) 317 (231-433) 144 (96.60 (8.92-12. interval) 12.4) 7.4) 90th 249 (188-304) 03-04 03-04 03-04 8.72-13.4 (38.2 (25.Environmental Phenols Urinary Triclosan (2.2 (10.3 (9.4 (11.6) 10.6-65.0 (11.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.4) 75th 43.0 (8. population from the National Health and Nutrition Examination Survey.89-11.2 (13.9) 7.6-111) 33.5) 11.6-14.4.8) 7.20 (7.0-73.3) 6.10) 84.48-10.6) 12.54 (8.2 (11.9 (50.2-14.5) 66.4) 357 (225-456) 203 (87.60 (6.22-10.3) 10.1) 14.9 (11.8-60.7) 292 (151-432) 132 (78.8 (21.0) 9. see Data Analysis section) for Survey year 03-04 is 2.3-31.5-14.2-58.3 (8.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .2-58.6-20.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.82 (8.2) 13.30-14.6 (9.7 (14.2) 9.5-86.1) 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 9.6) 31.4) 73.2 (27.45 (5.8-85.1) 9.93 (7.4) 25.55 (4.3.74 (5.20 (7.0 (36.8) 116 (39.S.3-15.32-14.6-15.9 (8.4) 51.0) 49.6 (30.6) 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 9.70-16.80 (5.00 (4.9) 32.38-18.40-17.6 (10. interval) 13.9 (33.9-61.3 (26.0 (26.1 (15.29-12.6) 90th 212 (172-241) 03-04 03-04 03-04 9.20-11.45-10.7 (39. Urinary Triclosan (2.7) 123 (36.5 (11.2-46.7 (11.18 (5.0-15.3-67.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9-236) 193 (90.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.1 (45.4 (32.6-14.1) 9.6-37.3 (11.9) 8.90-10.6 (12.20-10.0 (34.0-15.S.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.2 (37.6) 39.1) 11.4-18.0-19.1) 9.7 (9.5) 13.4-19.1) 9.40-11.16 (6.1) 50.50-10.

Calafat AM. and other organic wastewater contaminants in U. streams.S. Bennett ER. Percutaneous penetration and dermal metabolism of triclosan (2.S. Wong LY. Arch Environ Contam Toxicol 1988. Gunderson MP. Sandborgh-Englund G. Erratum in: Aquat Toxicol 2007.4’-trichloro-2’hydroxydiphenyl ether). Teitelbaum SL. Thurman EM. Meyer MT. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Foran CM. Leonard PA. Mezcua M.7/2. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Howes D. Windham G. Needham LL. et al.83(1):84.67(4):532-537. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Aquat Toxicol 2006. Food Chem Toxicol 2000. Photolytic degradation of triclosan in freshwater and seawater. Hirano M.4.17(5):637-644. Chelimo C. Barber LB. Aguera A. Wigmore H.115:116-121. hormones.36(6):1202-1211. Zaugg SD. Ekstrand J. Moss T. et al. Am J Infect Control 1996. Evidence of 2. 1999-2000: a national reconnaissance. Kolpin DW. Britton JA.66:1052-1056. Urinary concentrations of triclosan in the U.28(9):1748-1751.Environmental Phenols References Aiello AE. and phenols in girls. Katsura E. Mar Environ Res 2000. Veldhoen N. IMS Ind Med Surg 1969. Wolff MS. population: 2003-2004. Gomez MJ. Kanetoshi A. 4. Larson EL. Br J Clin Pharmacol 1987. Furlong ET. 4’-trichloro-2’-hydroxydiphenyl ether. Williams PE. phthalates. Levy SB. J Invest Dermatol 1976.. Williams FM. Okui T. Hong HC. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Lyman FL.45 Suppl 2:S137-S147. Pinney SM.38(2):64-71. Pharmaceuticals. Environ Sci Technol 2002. Biol Pharm Bull 2005. Triclosan: applications and safety. Osachoff H.23(5):579-583. Ogawa H.524:241-247.116(3):303-307. Furia T. Environ Health Perspect 2008.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Ye X. Pharmacokinetics of triclosan following oral ingestion in humans. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Environ Health Perspect 2007. Ebersole R. Readman JW. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Hernando MD. Matsumura N. Odham G. Ishibashi H. Bhargava HN. The oral retention and antiplaque efficacy of triclosan in human volunteers. et al. Nagao Y.50(1-5):153-156. Gilbert RJ.80(3):217-227. Reidy JA.69(20):1861-1873. Shiratsuchi H. Toxicology of 2.24(3):209-218. Pilot study of urinary biomarkers of phytoestrogens. Clapson DJ. Bodey GP.38(4):361370. Kaneshima H. Aranami K. Fernandez-Alba AR. et al. J Toxicol Environ Health A 2006. Adolfsson-Erici M. Skirrow RC. Chemosphere 2007. Watanabe N. Anal Chim Acta 1004. Ferrer I. Benson WH.

PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350) < LOD .48-2.58-2.65 (. 1997).350) < LOD ..98 (1.660 (. has been restricted. Human exposure to PCP has become less common.350) < LOD . 1979).650) 1.51) 1. hypertension.630 (.350-.390 (.01 (<LOD-1.32 (.350-.590-1.990-2.30 (. PCP cannot be used on wood in residential or agricultural buildings.350 (.350-. 1976.10 (<LOD-1.350-.960) 1.80) . After absorption. mollusicide.33) . which may vary for some chemicals by year and by individual sample. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350) 90th .76) .350) < LOD .47-5.350 (. algaecide and insecticide.350 (.350-.00) 2.350 (.37) . 1986).350) < LOD < LOD 75th .10 (.350-.350-.350-.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. so it is relatively non-persistent.00) 1.350) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.00) 1.350) < LOD . air.350 (. General population exposure to PCP may occur by inhalation of contaminated air.350-.350-1.510-5.62 (.350 (.70) .350) < LOD .350-.40 (.350 (. and dermal contact with PCP-treated products.350-..67) 1.350-2. 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) < LOD .350-.990 (<LOD-2.350 (. and metabolic acidosis were observed in CAS No.350-. PCP is distributed to most tissues and is not extensively metabolized.350) < LOD . PCP is absorbed rapidly and well by all exposure routes.350-.350-2.10) 1. Effects including hyperthermia.10) 1.48 (. water and sediments because of the large amounts that were produced and used historically. plants.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .30) 1.91 (1.350 (.350-.30 (.500-2.42) 696 680 521 696 603 951 Limit of detection (LOD. ingestion of contaminated food or water.60) 1.350-.350 (.350-.00 (.23 (.650 (.350) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.850-2.350-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350 (.09) . The parent compound and conjugates.50) 1.860-2. other polychlorinated benzenes.g.510-3.47-3.5.350-1. are eliminated in the urine.350) < LOD .350 (.76) 1. and it is used primarily as a preservative for wood to be used outdoors (e.350-1. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. herbicide. utility poles and fence posts).. and possibly of lindane (IPCS. < LOD means less than the limit of detection.94 (1. along with small amounts of tetrachlorohydroquinone and conjugates.60) 1.10 (1.08-3.350 (.75) 2.04) 1.350-2.350 (. bactericide.45-2.770 (.90) 2.350-.350-1. 40 Fourth National Report on Human Exposure to Environmental Chemicals .890-1. 2002. 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.54-2.90) 1.94 (1.30) .350-.350 (. Kohli et al.30) 1.350 (.350) < LOD .42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .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 .65 (. and animals..58-2. PCP use in the U.350-2.37 (. the elimination half-life may be a week or more (Uhl et al.890 (.64) 1.350) < LOD . Since 1984.350) < LOD .390 (. population from the National Health and Nutrition Examination Survey.350 (.. with repeated or chronic exposure.18 (<LOD-1. To-Figueras et al.350) < LOD .480-2.33-2.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .70) 2.83 (2.S.350-.S.90 (1. Survey Geometric mean (95% conf. After a single dose.350) < LOD .530) 1.73 (1. PCP is degraded by sunlight and metabolized rapidly by microorganisms.78) 1. PCP is eliminated over a few days (Braun et al.350 (.30 (1.350 (. PCP has been detected in soils.350-. Acute.680-1.350 (. In the environment.980 (.350-2.350) < LOD .25 and 0.

710-1. EPA has developed standards for PCP in drinking water and the environment. and adversely affected thyroid function (U.800-1.gov/ pesticides/ and from ATSDR at: http://www..19 (1. 2003).280) < LOD .gov/ toxpro2.34 (.52 (<LOD-1.19) 2.35-2.56) 1.25-2.470 (.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.430-.510-.18) .360 (.94 (1.25-2.500-.500 (.19) 2. IARC has determined that pentachlorophenol is possibly carcinogenic to humans. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.67 (1.40-2. Among adults in the NHANES 1999-2000 subsample.21 (.560) < LOD ..26 (1.18 (1.35) 1.510-.360-. The U.270-.67-3. 1991).10-2.290) < LOD .40) 1.00-1.420) < LOD .430) < LOD .S.06) 1..13 (.350) < LOD .51) 1.830) < LOD . OSHA has established an occupational standard. 2000). More information about external exposure (i.950-1.380-.00) 1.490) < LOD .06 (.0 mg/L.300 (.320 (.310-.67 (1.67-2.S.82) 1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.36) .220-.08 and 5.75) 1.79) 1.650) 90th 1. children in the 1980’s.990 (.16 (.90) 1.95) 3.290-.84-4.330-.570 (.cdc.900-1.35-2.30) 1.67 (1..21-2.09-1.52) 1.92) 1.780) < LOD .e.630 (.atsdr.6 and 14.780-1.29-3.760 (.69 (1.320) < LOD < LOD 75th . the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.290-.73 (1.440 (.250 (.06-3. EPA at: http://www.580-.340-.16-1.700-2. chronically administered high doses of PCP were hepatotoxic. 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 (4.75 (<LOD-2. 1989).94 (1.67 (1. environmental levels) and health effects is available from the U.67 (1. van Raaij et al. population from the National Health and Nutrition Examination Survey..40) 1. respectively) (Seifert et al. inhalation.html.94-3. 2004..270-.26 (1.9 mg/L. In a small sample of U.57 (.240-. respectively) (Becker et al.320) < LOD .250 (.55) 1. and the FDA has established a standard for bottled water.650 (.11) 2.67-3.EPA.25 (1.260 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.30-2. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 2003). 1989). carcinogenic. Death can result from seizures and cardiovascular collapse.35) 1.52 (<LOD-1.500-1.S. 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.590-1. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al.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 .48-2.920 (.00-1.300 (.78) 1.25) 1.30) 1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .800) < LOD 1.25-1.25 (1..910-1.30 (. In NHANES 2001-2002 subsamples.Fungicides adults and children severely exposed to PCP through ingestion. Survey Geometric mean (95% conf.09 (<LOD-2.84) 1. 1995).57 (1. Pentachlorophenol is not mutagenic or teratogenic.52 (1.950-1.epa.650 (.84 (1.370 (.730) < LOD . or skin absorption.320) < LOD .310) < LOD .950-1. In animals.83 (1.300 (.400 (.78) 1.40) 1.19) 2.S.40) 1.590) < LOD .560) < LOD .10 (1.560-.S. Fourth National Report on Human Exposure to Environmental Chemicals 41 .220-.82 (1.610 (.850 (.40) 1..

References Becker K. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. drinking water and indoor air. Hill RH Jr. Pharmacokinetics of pentachlorophenol in man. To-Figueras J. htm. J Expo Anal Environ Epidemiol 2000. 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. Becker K. urine. Can J Biochem 1976. Environ Res 1995. Kaus S. Seiwert M. EPA).18(4):469-474. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect.inchem. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Needham LL. Schlatter C. et al.S.105(1):78-83. Schmid P. PCP: Human Risk Characterization [online]. Dev Toxicol Environ Sci 1979. Rodamilans M. Needham LL. Int J Hyg Environ Health 2003. Otero R. To T. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Phillips DL. Seifert B. Chenoweth MB. 4/21/09 Kohli J. Seiwert M. Arch Toxicol 1986. Bragt PC. Pesticide residues in urine of adults living in the United States: reference range concentrations. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Sala M. Schulz C. 11/30/2004. 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. International Programme on Chemical Safety (IPCS). Environmental Protection Agency (U. available at URL: http://www. Arch Environ Contam Toxicol 1989. Cline RE. et al. Arch Environ Contam Toxicol 1989. van den Berg KJ. Schulz C.S. Santiago-Silva M. 4/21/09 van Raaij JA. Barrot C.71:99108. Shealy DB. house dust. Holler JS. 2002. 206:15-24. Blau GE. Notten WR. Helm D. Available at URL: h t t p : / / w w w. Fast DM. Environ Health Perspect 1997. Hill RH Jr. Gregg M. hair.10:552-65. Smith SJ.18:475-481.54(3):203-208. Seifert B. Toxicology 1991: 67(1):107-16.4:289296. Head SL. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.58:182-186. r e g u l a t i o n s . Jones D. Krause C. et al.org/documents/jmpr/jmpmono/2002pr08. Hill RH. U. Lindane. Uhl S. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Engel R. Safe A. Baker S. Braun WH. Bailey SL. 42 Fourth National Report on Human Exposure to Environmental Chemicals .

S.386-.600-1.S.Fungicides ortho-Phenylphenol CAS No.10) 1.567 (. Most agricultural food applications have been revoked.02) 1.30) < LOD 1.600-1.80) 1.610-1.498 (. and sanitizers.60 (1.50 (1.00) < LOD .23) 695 680 520 695 603 953 Limit of detection (LOD.670) 2.85) 2.590-2.10) .28 (. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. or apply these chemicals may be more highly exposed than the general population.497 (. fungicides..636) * . In the past.493 (.638) * .600-1.970 (.890 (.508 (.570-2.50-4..80 (2.560-8.570 (.30) 1.390-.790) 2.3. and as a wood preservative.14 (<LOD-3.00 (1.80-3. leaving the chemical residue OPP.490 (<LOD-.50) < LOD .10) .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .490 (<LOD-.10 (1.90) .600) < LOD 75th . Estimated human intakes have been below recommended intake limits (U. 2006).710) 3.480-1. which may vary for some chemicals by year and by individual sample.880-2.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .550-1.30) < LOD 90th 1. Available evidence suggests that OPP does not accumulate in the body. on ornamental plants and turfs.410-. OPP is volatile.640) < LOD .07 (.10) 1.09) 2.740 (.00 (1.570-1.370-. < LOD means less than the limit of detection.EPA.50-3. General population exposure can occur via dermal..600) < LOD . Both chemicals degrade within hours to weeks in the environment (U.800-3.00) . whereas SOPP is not volatile and is more water soluble. OPP is still used as a disinfectant fungicide for industrial applications.92 (.50 (1. Fourth National Report on Human Exposure to Environmental Chemicals 43 . but OPP and SOPP are still used on pears and citrus (U.60 (1.50) < LOD .20 (1.22) 2. inhalational.22 (.30-7.490 (<LOD-.90 (1.349-.600) < LOD 1.860 (.33 (.621) * .402-.03) 1.552 (.600) < LOD .624) * .490 (<LOD-.890 (. Workers who manufacture.490 (<LOD-.28-3.466 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .389-. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.630) < LOD . 1998.40 (.470 (<LOD-.820 (.17 (.20 (.433-.930 (. and it has limited water solubility.890) 1.60-3. 1998).850 (.836) * . population from the National Health and Nutrition Examination Survey.750-2.10-1.40-2.540-2. OPP is considered to be moderately toxic after acute oral doses in animal studies.420 (<LOD-.370-. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.350-1.EPA.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . interval) .742) * .34) 1.580-1.50) < LOD .364-.690-1.50-2.90) .770 (.509 (.61) 2. 1989). SOPP is applied topically to the crop and then rinsed off. 2006).780) < LOD .30) < LOD .10) 2.19 (.20) < LOD 1.90) 2.20 (1. 2006).40-7.690) < LOD .10 (1.450 (<LOD-.30-2.830 (.610 (.27 (. formulate.10-2. or 2-phenylphenol) and its water-soluble salt.770 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.00-2.496 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops. 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. 2002. however.645) * .3 and 0. Cnubben et al.570-.20-2.30 (1.40-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.450 (<LOD-. in paints.370-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10) .570 (. Timchalk et al.20) 2.40-5. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.00 (1.696) * .760-2.00) . sodium ortho-phenylphenate (SOPP). 90-43-7 General Information Ortho-phenylphenol (OPP.00 (1. it was used in home sanitizers for surfaces. Survey Geometric mean (95% conf. EPA. are antimicrobial agents used as bacteriostats. 2006).500-2.80) 1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.90) 1.20-3.450 (<LOD-.50 (1.76) 1.60 (1.S.20) < LOD 2.60-2. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.710-2.S. such as fruits and vegetables.520 (.950) < LOD .389-.50) .840-1.88) 1.50) 1.90 (1.

64 (2.33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .93) .S.666) * .21) 1. and it has classified OPP as not classifiable with respect to human carcinogenicity.18) 2.440 (. Ito et al.24-2. population from the National Health and Nutrition Examination Survey.550) < LOD .670 (.514 (.89 (1.460-.560-2.0) 1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone..473) * . Biomonitoring Information Urinary OPP levels reflect recent exposure.750-2.24-2.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .08-2.21 (.33-2.46) < LOD 1..96) 1. CDC.84 (1.950) < LOD . 2000.380 (. 1999.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.800-1.590) * . leading to production of two metabolites.420 (<LOD-.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .61 (1.04-4.32) 1.791) * .74 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S..270-. Detectable levels were seen in over half the U.690 (.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.61 (2.610) < LOD 1.86 (1.361-.510-.31) < LOD . Smith et al..S.480-.09-3.33) . Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.38) 1.20) < LOD 3.600-1.329-.810) < LOD .810-1.910 (<LOD-1.311-.78 (2. Zhao et al.550-.12) < LOD 1.12-2. 1984.580-1. 2005.360 (<LOD-.28 (<LOD-4.52 (. 1997.96-4. 44 Fourth National Report on Human Exposure to Environmental Chemicals ..gov/pesticides/.51-3.860 (.560) < LOD 75th .496 (. 1984.Fungicides anemia.43-2.93) 1.900) < LOD .444 (. interval) .81) 1. U.75 (1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC. or. by possible genotoxic mechanisms (Hagiwara et al.990) < LOD . Kwok et al.01) 1..07) 2.. Survey Geometric mean (95% conf.69 (1.21-2.970) 1.38) 2. Brusick.S.09 (1. IARC has classified SOPP as a possible human carcinogen.91 (1.17 (.00 (1.980 (<LOD-1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. 1986).301-.26) 1.455-. Murata et al.11 (.06 (1.410 (<LOD-. 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.13) 1.550 (.53) 1.S.508) * . Bomhard et al.40-13.93) .510 (<LOD-. Nakagawa et al.97 (2.640-1.02 (.17) 2.940-2. 2005).EPA 2006).403-.780 (. 2005).420 (<LOD-.910 (.epa.43) 3.62) .59) 1. Pathak and Roy. reproductive.840 (.670 (.08) 1.750 (.. In high dose animal studies.780-14.59) . 2002. 2002).453 (.43-2. OPP was not found to be mutagenic.750 (.656) * .500) < LOD .29) 1.291-.38-3.910-1.880-1.4) 3.05-2.470 (<LOD-.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . less likely. 1993.320 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.570) < LOD 1.06-4.00 (.470) < LOD .EPA 2006).770-2.343 (.58) 2.32) 3. but no neurologic.25-6.248-.385 (. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.860 (. 1999.. 2002.29) 1.980 (.06-5. 1998.568) * .47) . Volunteers exposed to 0.580) < LOD .44 (1.EPA at: http:// www.484) * .11-1. U.75 (1.410 (<LOD-.620-1.93 (1.11 (.382 (.17 (.43 (1..11) 4.96 (1.27) < LOD . 1992.08-1.650-1.670) < LOD . or developmental toxicity was observed (Bomhard et al.353-.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Additional information is available from U.61 (.96 (1.900-1.88-4. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.620-1.09-6.11) < LOD 90th 1.28 (2.

NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Christenson WR. Bartels MJ.35(2 Pt 1):198-208.32(6):551-625. Hirose M. Drugs. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Cano M. Freyberger A. EPA). July 28.EPA). Arch Toxicol 2000. Regul Toxicol Pharmacol 2002.pdf. Environmental Protection Agency (U. Bartels MJ.niehs. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. National Toxicology Program (NTP).22(10):809-814. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Christenson WR. Turteltaub KW. Elliott GR. Hagiwara A. et al. Fourth National Report on Human Exposure to Environmental Chemicals 45 .S. Hum Exp Toxicol 1998. rat and man. Moore GA. Food Chem Toxicol 1984. Bartels MJ. 2005. Hagiwara A. Atlanta (GA). Vogel JS. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. U. March 1986. Shibata M. Narang A. Bromig KH. Identification of SARA compounds in adipose tissue. Herbold BA. Zhao S. van de Sandt JJ. Hakkert BC. Smith RA. Brusick D.gov/oppsrrd1/REDs/ phenylphenol_red. 4/9/09. IARC Sci Publ 1984. Glas K. Brzak KA. Mutat Res 1993. Carcinogenesis 1999. Sangha GK. Coelhan M. Environmental Protection Agency (U. Bormett GA. Shirai T.S. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Mendrala AL. Gierthy J. Centers for Disease Control and Prevention (CDC). Environ Mol Mutagen 2005. Moldeus P. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Available at URL: http://ntp.gov/ntp/htdocs/LT_ rpts/tr301. Timchalk C. Eadon G. et al.20(5):851-857. Timchalk C. Nakagawa Y.150(2):402-413.S. Brendler-Schwaab SY. Kwok ES. Roy D. Arnold LL. J Agric Food Chem 2002.17(8):411-417. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice.(56):399-407. Roberts AL. Tayama S. 4/13/09 Onstot JD.nih. Third National Report on Human Exposure to Environmental Chemicals. EPA-560/5-89-003. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol.epa. Stanley JS. Toxicol Appl Pharmacol 1998. 2006.74(2):61-71. Available at URL: http://www. J Agric Food Chem 2006. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Sangha G.703(12):97-104. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Imaida K. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Ito N. Leser KH. Comparative metabolism of orthophenylphenol in mouse. Murata M. U. Ito N. 1989. Cnubben NH.. Biochem Pharmacol 1992. J Chromatogr B Biomed Sci Appl 1997. Toxicol Appl Pharmacol 1999.159(1):18-24. Inoue S. Pathak DN.43(7):14311437. Bomhard EM. Fukushima S. Richter M. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.S.Fungicides References Appel KE. Xenobiotica 1998. The carcinogenicity of the biocide ortho-phenylphenol. Office of Toxic Substances. Crit Rev Toxicol 2002.54(16):5731-5735.286(2):309-319. Kawanishi S. Fukushima S.pdf.50(11):3351-3358. McNett DA. Moriya K.45(5):460-481. EPA 739 R-06004. Buchholz BA. Bartels MJ. Selim S. Meuling WJ. 90-43-7) in Swiss CD-1 mice (dermal studies).28(6):579594. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Eastmond DA. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. St John MK.

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

in some species and at doses above maximum tolerated doses. Kolpin et al. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Fourth National Report on Human Exposure to Environmental Chemicals 47 . the latter which may account for some observed effects (Coleman et al. Acetochlor is microbiologically degraded. NTP and IARC do not have ratings regarding human carcinogenicity. People exposed to acetochlor will excrete acetochlor mercapturate in their urine.. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. 2000.epa. however. remains in soils for up to 3 months. General population exposure to acetochlor may occur through diet or drinking water. 2005). 2-hydroxyethyl-6-methylaniline.. 2007).EPA. 2005... 2006). However.gov/ pesticides/.EPA considers acetochlor likely to be carcinogenic in humans.S. In animals.. 1989.0 μg/L (Curwin et al. and has been detected in watersheds of agricultural lands (Battaglin et al. EPA at: http://www. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. animals have demonstrated tumors of the lung. 2005). Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. Davison et al..S.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure.. It is absorbed by plants and inhibits plant protein synthesis. Urinary acetochlor mercapturate levels of 0.S. 2000. Hladik et al. 1996). Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Acetochlor is moderately toxic to fish and honey bees. but it has produced testicular atrophy.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. 2006). a major pathway for acetochlor metabolism involves mercapturate conjugation. nasal epithelia. and it is unlikely to be genotoxic at relevant doses (Ashby et al.. CAS No.. but other pathways occur. 1998).EPA 2000.EPA. 2006). Additional information about external exposure (i. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. renal injury. 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. U. and hydroxymethyl ethyl aniline (U.e. Acetochlor has low acute toxicity.S. 2006). Acetochlor is not mutagenic. environmental levels) is available from U. 2000). Jefferies et al. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. Feng and Wratten. mainly corn. 1994. Estimated human intakes of acetochlor have been below recommended limits (U.EPA. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. and thyroid (U. 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. which are often more prevalent in the environment.S. and neurologic movement abnormalities (U. 2000. including one that produces 2-methyl-6ethylaniline and its reactive metabolite..S.

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

Barr DB.248(2-3):115-122.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Dialkylquinonimines validated as in vivo metabolites of alachlor. EPA). Kinney PL. Volume 65. Thurman EM. Kolpin DW. Davison KL. Furlong ET. Number 15. et al. Hladik ML. Third National Report on Human Exposure to Environmental Chemicals.39(17):6561-6574.S. Hein MJ.108(12):1151-1157. Jefferies PR. Roberts AL. J Expo Anal Environ Epidemiol 2005.pdf. Camann DE. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Olsson AO. Quistad GB. 2000. imidazolinone. Lefevre PA. Chem Res Toxicol 1998. Sci Total Environ 2000. acetochlor.37(4):10881093. 5/30/06 U. J Expo Sci Environ Epidemiol 2007. Reynolds SJ. 2005. Green T. March 2006.24(10):1003-1012.17(6):559-566. Linhart SM. Environmental Protection Agency (U. Linderman R. Coleman S. Available at URL: http://www. Hodgson E. et al. Larsen GL. EPA 738-R-00-009. Atlanta (GA). epa. Feng PCC. Ward EM. Casida JE. Wilson AG. Tinwell H. Heederik D. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Andrews HF. and other herbicides in rivers. Wratten SJ.S. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Whyatt RM.S. U. pages 3682-3690. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.15(9):702-735. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Centers for Disease Control and Prevention (CDC).S.Herbicides References Ashby J. reservoirs and ground water in the Midwestern United States. Occurrence of sulfonylurea. Hum Exp Toxicol 1996. 5/30/06. Environmental Protection Agency (U.cce. Federal Register: January 24. Sanderson WT. Comparative metabolism and elimination of acetanilide compounds by rat. Barr JR.11(4):353359. Kier L. and metolachlor herbicides in rats. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes.S. Deddens JA. Curwin BD. Bravo R.111(5):749-756. Sci Total Environ 2000. EPA).html. Hsiao JJ.EPA): http://pmep. Alavanja MC. Xenobiotica 1994.248(2-3):123-133. Environ Health Perspect 2003. Barr DB.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Rose RL. Available at URL(non U. Burkhardt MR. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Feil VJ.cornell.15(6):500-508. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. et al. 1998. Peter CJ. sulfonamide. Environ Health Perspect 2000. Battaglin WA. J Agri Food Chem 1989. Environ Sci Technol 2005. Acetochlor (Harness) Pesticide Petition Filing 1/00. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Barr DB. Striley CA. Hines CJ.

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

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

et al. International Programme on Chemical Safety (IPCS). Gilliom RJ). Xenobiotica 1994. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. and metolachlor herbicides in rats. and other herbicides in rivers. DNA adduct formation by alachlor metabolites. Brown KK.epa. Geological Survey (USGS). Kier LD. Comparative metabolism and elimination of acetanilide compounds by rat. Hull RD. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Feng PCC. WHO/ FAO Data Sheets on Pesticides.pdf. Thake DC.Herbicides References Battaglin WA. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.43(9):2504-2512. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.248(2-3):115-122. Striley CA. Biagini RE. Lau H. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.18(6):363-391. Available at URL: http://www. 86.php. World Health Organization. EPA 738R-98-020. Centers for Disease Control and Prevention (CDC). Barr JR. Sacramento. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Brown MA. Casida JE. 1992-2001.395(2-3):159-171. Camann DE. Casida JE. Shoemaker DA. Dialkylquinonimines validated as in vivo metabolites of alachlor. Wilson AG. 2/27/09 Jefferies PR. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Peter CJ.pdf. Kolpin DW. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Kimmel EC. Hum Exp Toxicol. 1999.int/water_sanitation_health/dwq/chemicals/en/alachlor. reservoirs and ground water in the Midwestern United States. 2007. Shealy DB. 1999. World Health Organization (WHO). Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Am Ind Hyg Assoc J 1995. Hladik ML. Sanderson WT. Roberts AL. Hines CJ. Environmental Protection Agency (U.37(4):10881093. Barr DB. Life Sci 1988. 1996. Whyatt RM. Available at URL: http:// www. Chem Res Toxicol 1998. imidazolinone. December 1998. Andrews HF. Ann Occup Hyg 2003. Clark JM.inchem. Background document for development of WHO Guidelines for Drinking-water Quality. Erratum in: Life Sci 1989. Available at URL: http://water. Thelin GP. revised February 15. sulfonamide. who.S.org/documents/pds/pds/pest86_e.S. Bull Environ Contam Toxicol 1996.248(2-3):123-133. Kinney PL.111(5):749-756. 2/27/09 U.39(17):6561-6574.htm. J Agri Food Chem 1989.56(6):853-859. Third National Report on Human Exposure to Environmental Chemicals. Hill AB. No. ALACHLOR.11(4):353359. Kolpin DW. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Atlanta (GA). 4/2/09 U. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. MacKenzie B. J Ag Food Chem 1995. Sci Total Environ 2000. Wratten SJ. 2003. Tolos W. Feil VJ. March 2006.44(18):1325. U. Deddens JA. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Heydens WF. Geneva. Casida JE. Environ Sci Technol 2005. Occurrence of sulfonylurea.gov/oppsrrd1/ REDs/0063. Thurman EM. Martens MA. Henningsen G. Geological Survey (USGS). Circular 1291. Hill RH Jr. 1997. et al.24(10):1003-1012. Hines CJ. Available at URL: http://www. Hsiao JJ. Jefferies PR.usgs. California. 1998. 98-4245 (by Barbash JE. Environ Health Perspect 2003. acetochlor.56(9):883-889. Biagini R. Sci Total Environ 2000. Linhart SM. Quistad GB. Larsen GL.S. Supplemental Technical Information (available on-line only). Driskell WJ. Alachlor in Drinking-water. Reregistration Eligibility Decision (RED) Alachlor. Davison KL. EPA).47(6):503-517. Mutat Res. Burkhardt MR. Tessier DM.S.43(25):2087-94.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Furlong ET. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. 2005. Quistad GB.

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

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

Lioy PJ..atsdr.. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Barr DB. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Seiber JN. Clayton CA. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.30(2):244-247. A risk assessment of atrazine use in California: human health and ecological aspects. International Programme on Chemical Safety (IPCS). Aldous CN. Toxicol Lett 1993. 3/11/09 Arcury TA.99(8):5476-5480. 2003. J Toxicol Environ Health 1994. Blewett C.43(2):155-167. Eldridge JC. Cooper RL. Noriega N. 2000). Stevens JT. Atlanta (GA).inchem..org/documents/pds/pds/pest82_e. References Adgate JL. Stoker TE. Stoker TE. atrazine was detected in only four children (Arcury et al. et al. 3/11/09 Laws SC.. 2005. Curwin BD. 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. Jones AD. J Expo Anal Environ Epidemiol 2005. Hein MJ. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Gillis JH. Gillis JH. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. 2007). Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Chen H. ATRAZINE. Toxicological profile for atrazine. Sanderson WT. Gammon DW. Cooper RL. Toxicol Sci 2003.. Schmid J. Tapia J. J Agric Food Chem 1982. Centers for Disease Control and Prevention (CDC). Eldridge JC.. No. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Geneva.109(6):583-590. Simpkins JW. levels of atrazine mercapturate were generally not detectable (CDC. Catenacci G. Toxicol Sci 2000. In the NHANES 2001-2002 subsample. Deddens JA.html. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. J Toxicol Environ Health 1994. et al. Maroni M. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 2001 [online]. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Lee M. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Agency for Toxic Substances and Disease Registry (ATSDR). Wetzel LT. Stuart AA. Perry et al. et al. Eberly LE. World Health Organization. Moseman RF. Heederik D. Carr WC Jr. 82. Ferrell JM. Wetzel LT. Available at URL: http:// www. Sanborn JR. Goldman JM. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Striley CA. In a small number of field workers.43(2):155-167. Grzywacz JG. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.61(4):331-355. Vonk A. In small studies of Maryland residents in 19951996 (MacIntosh et al. Tyrey L. Extrom PC. Cottica D. 1993). Brown KK. Shoemaker DA. Quandt SA. Barbieri F.53(2):297-307. Cooper RL.64(9):672-678.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Barr DB.69(2):217-222. Environ Health Perspect 2001. Hayes TB. et al. Biological monitoring of human exposure to atrazine.htm. WHO/ FAO Data Sheets on Pesticides. Third National Report on Human Exposure to Environmental Chemicals. Ferioli A. diamino-S-chlorotriazine and hydroxyatrazine.. Ferrell JM. Fleenor-Heyser DG. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 .gov/toxprofiles/tp153. Lucas AD. Bersani M. Biagini RE. Reynolds SJ. In a study of 60 farm worker children. McElroy WK. Toxicol Sci 2000. Laws SC. et al.47(6):503-517.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.58(2):366-376. Pfeifer KF. 1996. 2001). Available at URL: http://www. Steroids 1999. Collins A.cdc. Goodrow MH. Bradway DE. 2005).15(6):500-508. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. 2005). Breckenridge CB. Pest Manag Sci 2005. The geometric mean of urinary atrazine mercapturate was 1. Barr DB. Stoker TE. Hines CJ. Environ Health Perspect 2007.76(1):190-200. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Ann Occup Hyg 2003. Proc Natl Acad Sci USA 2002. Hermaphroditic. Mendoza M.115(8):1254-1260. et al. Saiz SG. Freeman NC.

The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Available at URL: http://water. Wood C. A risk characterization for atrazine: oncogenicity profile.10(7):479. Boerma J. revised February 15. A longitudinal investigation of selected pesticide metabolites in urine. EPA). Dryzga MD. Hammerstrom KA. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Pesticides and Toxic Substances. Pesticides in the Nation’s Streams and Ground Water.Herbicides development of a biomarker of exposure. Office of Prevention. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Environmental Fate and Effects Division. 3/11/09 U. U. Lansbergen GW. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Ann Epidemiol 2000. J Toxicol Environ Health A 1999. March 2006. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Toxicol Appl Pharmacol 2004.61(1):27-40. Kastl PE.S. Singzoni B. Ryan PB. Available at URL: http://www. Needham LL.67(2):198-206. Wetzel L. Osborne DW.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Stoker TE. A review of epidemiologic studies of triazine herbicides and cancer. Stevens JT. Circular 1291.195(1):23-34. Guidici DL.epa.pdf. EPA). Toxicol Sci 2000. Dagenhart D. 2003b. Christiani D. J Expo Anal Environ Epidemiol 1999. May 2003a.9(5):494-501. Available at URL: http://www.27(6):599612. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Sanderson JT.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Cooper RL. Perry M. Supplemental Technical Information (available on-line only). Toxicology 1990. Cooper RL. EPA Office of Pesticide Programs. Toxicol Appl Pharmacol 2002.S.182(1):44-54. Geological Survey (USGS). Fenton SE. 2007. White paper on potential developmental effects of atrazine on amphibians. Crit Rev Toxicol 1997.php. MacIntosh DL. Timchalk C. Sathiakumar N. Guidici DL.58(1):50-59. Laws SC. The Quality of Our Nation’s Waters.usgs. Rayner JL. Laws SC. Langvardt PW. Stoker TE. Washington (DC). Environmental Protection Agency (U. 6/1/09 U. 0062.S.56(2):69-109. Delzell E.gov/oppsrrd1/REDs/ atrazine_ired. Interim Reregistration Eligibility Decision For Atrazine. 1992-2001.6(1):107-116. Breckenridge CB.S. Environmental Protection Agency (U. Chem Res Toxicol 1993. Case No.S. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Tortorelli J. van den Berg M.pdf.epa. Toxicol Sci 2002.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. It was first registered with U. Survey Geometric mean (95% conf. 2.10 (<LOD-1.4-D has low acute toxicity.60) 1.03) 695 659 520 668 589 892 Limit of detection (LOD. myotonia. Recent estimates of chronic intakes of 2.910) 1.32 (1..310) < LOD .S.43) 1.02-1. < LOD means less than the limit of detection.420) < LOD . dizziness.07 (. these herbicides can enhance plant growth.S.560-1. 2.20 (<LOD-1. As much as 62 million pounds of 2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.690 (.27 (.Herbicides 2. MCPA.550-1. 2004).350) < LOD < LOD < LOD . 1974. 2.EPA.2.21) 1.10) < LOD 1.10 (<LOD-1.4-Dichlorophenoxyacetic Acid CAS No.S.00-2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.48) < LOD 1.230-. but at higher levels they are herbicidal.260 (<LOD-.30 (<LOD-2.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.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 .730 (. with a half-life of several days to several weeks. 1989.4-D have been below recommended intake limits (U.910) < LOD . and delayed Urinary 2.370-.210 (<LOD-.690-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.27-2.230 (<LOD-.55 (1. General population exposure to 2.24 (.EPA in 1948.952 and 0.930 (. and by consuming food or drinking water contaminated with 2. 2007).4-dichlorophenoxyacetic acid (2. At low levels.560-. Similar to other chlorophenoxy herbicides.22) < LOD . Human health effects from 2. abdominal pain.740 (.320) 90th . Kohli et al.330 (.490) < LOD < LOD < LOD .410) < LOD .51 (1. it acts as a plant growth hormone.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .960-1.4-D or exposed for prolonged periods.690 (. agricultural.890) < LOD .S.40) 1.16) < LOD .440-1.610 (.690 (. population from the National Health and Nutrition Examination Survey.EPA.4-D may occur during residential applications.400) < LOD .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .13) < LOD . Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.80) 1.930-1.08) < LOD .660) 1.610-.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Sauerhoff et al..05-2. It is not well absorbed through the skin. nausea.760 (.890 (. 94-75-7 General Information Widely used throughout the United States. and aquatic environments. renal and hepatic injury. 4-D.4-D) controls broadleaf weeds in residential.S.27 (1. in 2001 (U.250 (<LOD-.210-. by direct contact with agricultural and residential areas after applications. 2.490 (. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.310 (.670-1.680-1. and mecoprop).66) < LOD 1.540-.250 (<LOD-.420-.810-1.70) 1. Fourth National Report on Human Exposure to Environmental Chemicals 57 . 2005). hypotension.4-D can be applied either as an aqueous salt or as oil-soluble esters.20 (. 1977). It is rarely detected in ground waters (USGS. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.4-D is rapidly absorbed via oral and inhalation routes. which may vary for some chemicals by year and by individual sample. the chlorophenoxy herbicide 2. headache. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Once absorbed.4-D were used in the U.. It is poorly bound in soils.

. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.13 (.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .340 (. Post-application levels in farmers and home gardeners were dependent on Urinary 2. other exposures. 2005.73) . 2.29) 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. 2006. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.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.660) < LOD . 2000).850) < LOD .270 (<LOD-.810-1.640 (.930-1.620-. 1992).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 ..550-. 1995. Survey Geometric mean (95% conf. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.700 (. Acute high doses administered to laboratory animals produced ataxia. 1995).32 (<LOD-2. adrenals and gonads (NTP. U.16) 1. 2003.780-1.35) < LOD .S.680) < LOD .Herbicides neuropathy (Bradberry et al. eyes. Frank et al.780) .epa.EPA 2005).890-1.350 (<LOD-.19) .40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.4-D production plant workers and a few forestry workers spraying 2.720 (.EPA. 2.380-.920) < LOD 1.EPA.820-1.610-.4-D reflect recent exposure.. 2. Knopp et al.24) 1. population (Hill et al.410) < LOD < LOD < LOD . myotonia.670 (.610-.08 (. 2002. CDC. 2005.S. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.390) < LOD < LOD < LOD . Kutz et al.S.17 (. The acid and salt forms of 2..660 (.S. 1996. U.05) . population from the National Health and Nutrition Examination Survey. Kolmodin-Hedman and Erne. 1994).8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 2005).380 (<LOD-. or to contaminants in the herbicide formulations (specifically 2.560-.440 (.gov/pesticides/.470) < LOD .08 (.27-1.13 (. 2004). 2005).08 (. U.780 (. Epidemiological studies have reported associations of several types of cancer.890) < LOD 1.560-.590 (<LOD-1.790) 1.56) . 1989).380) < LOD .4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.810-1. 2005). thyroid. 1996..41 (1. IOM.S.670 (<LOD-1.330-.4-D levels were detectable in less than a quarter of the individuals studied.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2005).4-D are eye irritants. IPCS.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.480 (. 2005. Hill et al.980) < LOD 1.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. IPCS.7.410) 90th . or teratogenic effects in chronic rodent studies (Charles et al.580-...S. U.EPA at: http://www.. 2001.590 (<LOD-1.990-1.4-D does not have significant reproductive.S.410 (<LOD-.39) < LOD 1..670 (. IPCS.380 (<LOD-. 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.340-. Average post-application urinary levels of 2.570) < LOD . Biomonitoring Information Urinary levels of 2. and evidence of histological injury to the kidneys.410) < LOD 1. liver. urinary 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1985. 1980. Pearce and McLean. Additional information is available from U. 2005. It is unclear whether these associations are related to the chlorophenoxy herbicides. in small samples of children (Hill et al.14 (.790) < LOD .490 (. developmental.520-. 2002. 1996.3.. In previous samples of the U.270-.EPA. 58 Fourth National Report on Human Exposure to Environmental Chemicals .740 (.

4:318-321. Smith SJ. Sirons G J. Selected pesticide residues and metabolites in urine from a survey of the U. van Ravenzwaay B. Harris et al. Tables. Frank R. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Finding a measurable amount of 2. Acquavella JF. Updated March 7. Garabrant DH. Scand J Work Environ Health 2005.4:97-100.php?record_id=10603. Bailey SL. To T.org/documents/jmpr/jmpmono/v96pr04.4-dichlorophenoxyacetic acid in man. TOX-63 Peroxisone Project (2. J Toxicol Environ Health 1992. Arch Environ Contam Toxicol 1985. J Expo Anal Environ Epidemiol 2000. the number of acres to which it was applied (Curwin et al. Tandon JS.4 dichlorophenoxyacetic acid (2. Pesticides residues in food: 1996 evaluations Part II Toxicology.Herbicides the time since application.31 Suppl 1:90-97.15(6):500-508.4-D and 2.gov/index. 2005.32(4):233-257. Chapman P. J Expo Anal Environ Epidemiol 2005 Nov. 2005). Atlanta (GA). Head SL.nih.31(2):121-125. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ritter L. Occup Environ Med 1994. Biomonitoring for farm families in the farm family exposure study. Hein MJ. et al. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. geometric mean urinary levels of 2. Dichlorophenoxyacetic acid. Ripley BD. Sanderson WT. and the use of protective clothing or equipment (Arbuckle et al. Khanna RN. Environ Res 1995. Baker S.4-dichlorophenoxyacetic acid and its forms. Third National Report on Human Exposure to Environmental Chemicals. Hill RH Jr. Erne K. Shealy DB. Kutz FW. Arnold EK. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Brody D. Philbert MA. Stephenson GR. Sircar KP.nap. Vet Hum Toxicol 1989.10(6 Pt 2):789-798.4-D in urine does not mean that the level of the 2.4-D) epidemiology and toxicology. Carter-Pokras OD. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Biomonitoring studies of 2. TOX-63: TOXICITY REPORT CURVES. Honeycutt R. Hanley TR Jr. Gupta BN. Scand J Work Environ Health 2005. Beeson MD. Baker SE.S.. Gregg M. 2003. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Centers for Disease Control and Prevention (CDC). et al. Board on Health Promotion and Disease Prevention.4-D than levels found in the general population. Mandel JS. 2005. Available at URL: http:// www. Reynolds SJ. Hill RH Jr. the amount of pesticide applied. Kolmodin-Hedman B.4-dichlorophenoxyacetic acid (2.4-Dichlorophenoxyacetic Acid). National Toxicology Program (NTP).4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Absorption and excretion of 2. Murphy RS. Arch Environ Contam Toxicol 1989.51(3):152-159.htm.4-D). Washington (DC): National Academies Press.4-D will result in an adverse health effect. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.37(2):277-291.4:427-435.71(2):99-108. Solomon KR. Biomonitoring of herbicides in Ontario farm applicators. 1992). References Arbuckle TE. Wilson RD. Campbell RA. Holler JS. Arch Toxicol Suppl 1980.inchem. Available at URL: http://ntp. 914. Baker BA. Dhar MM.4-D): exposure and urinary excretion. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Needham LL. Cole DC. 3/17/09 Institute of Medicine (IOM). Mandel et al. Assessment of exposure to 2. Needham LL. Toxicol Sci 2001. Estimation of occupational exposure to phenoxy acids (2. Curwin BD. general population.. 2.5-T).edu/catalog. Heederik 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. Developmental toxicity studies in rats and rabbits on 2. Barr DB. Harris SA.niehs. Xenobiotica 1974.4-.. In farm families.60(1):121-131. Bus JS. 2005 Charles JM. Fast DM. International Programme on Chemical Safety-INCHEM (IPCS). Alexander BH. J Environ Sci Health B 1992.4-dichlorophenoxyacetic acid (2. 2005). Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Veterans and Agent Orange: update 2002.4. Available at URL: http:// www. Crit Rev Toxicol 2002.18(4):469-474. 3/17/09 Knopp D. 2006. Review of 2. Beasley VR. Cook BT. Survival and Growth Curves from NTP Toxicity Studies.. et al. Exposure of homeowners and bystanders to 2.4-D. Forestry workers involved in aerial application of 2. Kohli JD.31 Suppl 1:98-104. Barr DB. Driskell WJ. Pesticide residues in urine of adults living in the United States: reference range concentrations.4-D were highest in the farmers who applied the 2.27(1):23-38.

Blau GE. 3/17/09. gov/oppbead1/pestsales/01pestsales/market_estimates2001. The Quality of Our Nation’s Waters.S.S.S. Available at URL: http://water.4-D) following oral administration to man. May.8:3-1U. Available at URL: http://www.usgs.EPA). Washington (DC): U. EPA 738 F-05-002.S.Herbicides Sauerhoff MW. Available at URL: http://www.EPA.S. revised February 15.2000 and 2001 market estimates. Circular 1291. Office of Prevention Pesticides and Toxic Substances.EPA).epa. 60 Fourth National Report on Human Exposure to Environmental Chemicals . Braun WH.htm. 1992-2001. Geological Survey (USGS).php. Environmental Protection Agency (U. S. 4/2/09 U. 2004.gov/oppsrrd1/ REDs/factsheets/24d_fs. 3/17/09 U.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.4-D RED Facts. Supplemental Technical Information (available on-line only). Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water. The fate of 2. 2007. 2.pdf. Gehring PJ.epa. Toxicology 1977. June 2005.4-dichlorophenoxyacetic acid (2. Pesticide industry sales and usage . March 2006.

(2003) showed that 2.. though the 95th percentile for males was 0.S. and convulsions were observed at lethal doses in animal studies. 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.S. EPA.EPA. The geometric mean metolachlor mercapturate was 4. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. including corn.. metolachlor was quickly absorbed after dermal or oral doses. Feng and Wratten. It is absorbed by plants and inhibits plant protein synthesis. 1995. WHO. Metolachlor is well absorbed dermally. formulators.. 1994. EPA at: http://www.Herbicides Metolachlor available from U. mercapturate conjugates were the predominant metabolites. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. 1989.EPA considers metolachlor to be a possible human carcinogen. and it was not mutagenic in mammalian cells (U.S. U. whereas 60% of applicators had detectable amounts. and field workers may have significant exposures via this route. 2007.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine.. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. 1995). Estimated human intakes have been below recommended limits (U. metolachlor levels in water have exceeded lifetime human health advisory levels (U. NTP and IARC do not have ratings regarding human carcinogenicity. Davison et al. 2000.EPA. 2003). soybeans. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. General population exposure may occur through the consumption of contaminated food or drinking water. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment.S. and on non-crop land for general weed control. 2003). 1995). 1999.gov/pesticides/. 1995).S. In animal studies. lacrimation. and eliminated in urine and feces over two to three days (WHO. in both ground and surface waters (Battaglin et al.epa. Fourth National Report on Human Exposure to Environmental Chemicals 61 .7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al.. Gilliom. Biomonitoring Information CAS No. 2005). 1998).. Salivation. Jefferies et al. 2003). 2000. Metolachlor has low potential for acute toxicity (U. Kolpin et al. Biomonitoring studies on levels of metolachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels metolachlor than are found in the general population. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. so applicators. Metolachlor has a soil half-life of a few weeks to three months and is degraded microbiologically and photochemically to at least five different products.200 μg/L (CDC. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. 2005. sorghum and other crops. USGS. 2007. Hines et al. Hladik et al.. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land.EPA. WHO. Occasionally in the past. In animals.S. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2005).

Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Survey Geometric mean (95% conf.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.440 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0. 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 . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.200 (<LOD-.200 (<LOD-.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. 62 Fourth National Report on Human Exposure to Environmental Chemicals .240) 679 701 957 Limit of detection (LOD. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.670 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 .

24(10):1003-1012. 2007.47(6):503-517.pdf. Biagini RE. Barr DB. Thurman EM. EPA).108(12):1151-1157. 2003. and metolachlor herbicides in rats. Quistad GB. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. 2005. Wratten SJ. Kolpin DW. Davison KL. Rose RL. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . EPA 738R-95-006. Available at URL: http://water. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Thelin GP.S.pdf. 1992-2001. Circular 1291. R. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. et al. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Chem Res Toxicol 1998. Background document for development of WHO Guidelines for Drinking-water Quality. Comparative metabolism and elimination of acetanilide compounds by rat. Supplemental Technical Information (available on-line only). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Curwin BD. Reynolds SJ. Feng PCC. Burkhardt MR. Occurrence of sulfonylurea. 98-4245 (by Barbash JE.248(2-3):115-122. Peter CJ. 4/2/09 U. Hodgson E. J Expo Anal Environ Epidemiol 2005. Environ Health Perspect 2003. Ann Occup Hyg 2003. March 2006.ESTfeature_gilliom.111(5):749-756. Striley CA. Metolachlor in Drinkingwater. 3/26/09 U.41:3409-3414. Heederik D.php. Coleman S. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Hsiao JJ.usgs.39(17):6561-6574. streams and groundwater. sulfonamide. Sanderson WT. 6/1/09 Whyatt RM. Gilliom RJ). usgs. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www. Linderman R. Andrews HF. Kinney PL.S.248(2-3):123-133. Geological Survey (USGS). Deddens JA. acetochlor.who. Roberts AL. Gillion. Centers for Disease Control and Prevention (CDC).epa. Xenobiotica 1994.gov/oppsrrd1/ REDs/0001.gov/nawqa/pnsp/pubs/files/051507. and other herbicides in rivers. Barr DB. Kolpin DW. Sacramento.usgs. Environ Sci Technol 2005. Shoemaker DA.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Alavanja MC. Hein MJ. Sci Total Environ 2000.S. Geological Survey (USGS).37(4):10881093. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.S. Atlanta (GA). et al. Environ Sci Technol 2007. J Agri Food Chem 1989.pdf 3/30/09 Hines CJ. Available at URL: http://www.html. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Linhart SM. Available at URL: http://water. Furlong ET. Larsen GL. Brown KK. Reregistration Eligibility Decision (RED) Metolachlor. Pesticides in U. World Health Organization (WHO). 1998. Environ Health Perspect 2000.gov/nawqa/ pnsp/pubs/wrir984245/text. California. Dialkylquinonimines validated as in vivo metabolites of alachlor.S. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. reservoirs and ground water in the Midwestern United States. imidazolinone. 1999. U. Ward EM.15(6):500-508.int/water_sanitation_health/dwq/chemicals/ metolachlor. Environmental Protection Agency (U. Sci Total Environ 2000. Available at URL: http://water. Hladik ML. Casida JE. Feil VJ. April 1995. Camann DE.Herbicides References Battaglin WA. Barr JR.11(4):353359. Jefferies PR. revised February 15.

7. the general population is unlikely to be exposed to it. population from the National Health and Nutrition Examination Survey. Once absorbed into the body. Human health effects from 2.4. At low levels. and delayed neuropathy (Bradberry et al.g.5-Trichlorophenoxyacetic Acid CAS No.2 and 0. these herbicides can enhance plant growth.4. Nelson et al. Kohli et al.4. 2004).. Given the commercial unavailability of 2.5-Trichlorophenoxyacetic acid (2.5-T has been rarely detected in ground waters (USGS. Omer. 1989.. 1992.. 64 Fourth National Report on Human Exposure to Environmental Chemicals . Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.4.4. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.4.5-T was once applied as either an aqueous salt or as an oil-soluble ester.Herbicides 2.5-T degrades to 2. dizziness.4. 93-76-5 General Information 2.5-trichlorophenol and other degradates.5-T. Agent Orange).1.4.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. 1992). which may vary for some chemicals by year and by individual sample. Epidemiological studies have reported associations of several types of cancer.4. 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4-D were used as defoliants in the Vietnam War (e. and concern about contamination with 2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2. but higher levels are herbicidal. myotonia.5-T in soil varies with conditions..5-T is eliminated mostly unchanged in the urine.. Mohammad and St. renal and hepatic injury.. nausea.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.5-T and 2. 1974). Chlorophenoxy herbicides act as plant growth hormones. The half-life of 2. Ester forms of 2. < LOD means less than the limit of detection. 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. 2007). Although 2.5T is rapidly absorbed via oral and inhalation routes. 1986. abdominal pain.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. hypotension.5-T use as a herbicide in 1985.4.4.4. 2.3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. with an elimination half-life of approximately 19 hours (Arnold et al. 2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.5-T (Holson et al.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. it is not well absorbed through the skin. headache.4. ranging from several weeks to many months.4.S.4.4.

Pearce and McLean. 2002.5-T also were below the limit of detection (Kutz et al.7. 1980).5-T were generally below the limit of detection.S. IOM.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. Finding a measurable amount of 2.4. 1996.S.4. or to contaminants in the herbicide formulations (specifically 2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.5-T itself is not mutagenic.4. 2.5-T reflect recent exposure.epa.4. IPCS. other exposures.Herbicides or contaminated herbicides.EPA.4.gov/pesticides/.EPA at: http://www.4. similar to results of NHANES II (19761980). 2004). 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 2005. 1992).3.4. It is unclear whether these associations are related to the chlorophenoxy herbicides. Biomonitoring Information Urinary levels of 2.. Biomonitoring studies on 2. Additional information is available from U.5-T than levels found in the general population.S. urinary levels of 2. Survey Geometric mean (95% conf.5-T does not mean that the level will result in an adverse health effect. Mean urinary levels of 2. U. Fourth National Report on Human Exposure to Environmental Chemicals 65 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. population from the National Health and Nutrition Examination Survey.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. in which urinary levels of 2.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Urinary 2.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.4. 2005).4.

5-T). LaBorde JB.19(2):286-297. Erne K.5-T).4:318-21. Vale JA.4.32(4):233-257. Gaines TB. Brody D. LaBorde JB. Board on Health Promotion and Disease Prevention. Atlanta (GA). Dichlorophenoxyacetic acid. Nelson CJ.edu/catalog. U.31 Suppl 1:1825. Centers for Disease Control and Prevention (CDC). Bradberry SM.4. Mohammad FK.htm.4-D/2.pdf.5-T in four-way outcross mice. Environmental Protection Agency (U.4. Vet Hum Toxicol 1989. Agricultural exposures and non-Hodgkin’s lymphoma. Developmental toxicity of 2. 3/17/09 Kohli JD. Gaylor DW.org/documents/jmpr/jmpmono/v96pr04. Veterans and Agent Orange: update 2002. Poisoning due to chlorophenoxy herbicides. Developmental toxicity of 2. Gupta BN.php?record_id=10603. 2. Washington (DC): U. et al. Review of 2. Proudfoot AT. Pearce N. 3/17/09 Institute of Medicine (IOM). Pesticide industry sales and usage .S. Holson JF.4-D and 2. gov/oppbead1/pestsales/01pestsales/market_estimates2001.nap.19(2):298-306. Selected pesticide residues and metabolites in urine from a survey of the U.4-. Garabrant DH.EPA).5-trichlorophenoxyacetic acid (2. Wolff GL.4. 2003. 210:250-255. Fundam Appl Toxicol 1992.4. Holson JF. International Programme on Chemical Safety-INCHEM (IPCS). 2005. Tandon JS. Fundam Appl Toxicol 1992. Khanna RN.31(2):121-125. Pesticides residues in food: 1996 evaluations Part II Toxicology.37(2):277-91. Available at URL: http:// www.4-D) epidemiology and toxicology. Gaines TB.4. Estimation of occupational exposure to phenoxy acids (2.S. Available at URL: http://www. S. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Philbert MA. II. Cook BT.5-t mixture. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. general population.5-trichlorophenoxy acetic acid in man.5-trichlorophenoxyacetic acid (2. McLean D. Toxicol Rev 2004. McCallum WF.2000 and 2001 market estimates. Arch Toxicol Suppl 1980. Absorption and excretion of 2. Crit Rev Toxicol 2002.Herbicides References Arnold EK. et al.4. Available at URL: http:// www. J Toxicol Environ Health 1992. Nelson CJ. St Omer VE. Beasley VR.8(5):551-60. Scand J Work Environ Health 2005. 914. May.epa. Office of Prevention Pesticides and Toxic Substances. Kutz FW. Carter-Pokras OD. Behavioral and developmental effects in rats following in utero exposure to 2. Sircar KP. 2004. Kolmodin-Hedman B.EPA.4. Dhar MM. Arch Int Pharmacodyn Ther 1974. Multireplicated dose-response studies with technical and analytical grades of 2. discussion 5-7. I. Third National Report on Human Exposure to Environmental Chemicals.inchem. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .S. Murphy RS. Washington (DC): National Academies Press. Sheehan DM.5-T). The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Neurobehav Toxicol Teratol 1986.4-dichlorophenoxyacetic acid (2.23(2):65-73.

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

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

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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

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

098 (.070-.160) .158) .80-9.8) < LOD 8.056-.S.080 (.130-.062-.8 (9.116) .140 (.069) < LOD < LOD .110-.1-24.103 (.4-17.2) 12.100 (.170) .090-.130-.138 (.138) .140) .060) .080) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .117) < LOD .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 .090-.124) .120-.1) < LOD 9.6 (14.075) < LOD .120 (.0 (11.5) 19.50) 15.100-.0-21.180) .7-22.3 (13.120) .6) 9.093) .9-22.062 (.1-16.150 (.60-10.8-24. which may vary for some chemicals by year and by individual sample.070) .3 (18.80 (<LOD-10.110) . < LOD means less than the limit of detection.180) .0 (10.4) 20.6) 16.6-33.130) .100) . Fourth National Report on Human Exposure to Environmental Chemicals 79 .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 8.5 (<LOD-11.110 (.90) 90th 15.00-14.080-. Survey years 01-02 03-04 Geometric mean (95% conf.7-19.9-38. population from the National Health and Nutrition Examination Survey.063-. 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 9.7) 15.8) 14.4-18.150 (.110) .140-.7 (15.00 (8. 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.30 (8.090 (.102 (.2) 14.5-17.4) 539 456 484 487 980 885 Limits of detection (LOD.3 (14.5) 21.9 (13.084-.4) < LOD < LOD 16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-25.130) .120 (.113 (.049-.077-.4) 19.103 (.4) 21.2) 15.109-.0-25.0) 19.3 (19.8-17. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .077 (.058) < LOD .130-.8) 15.1) 13.055 (.1-19.083-.110 (.109 (.090 (<LOD-.100) .064) 90th .101) .242) .6) 19.054-.054-.70 (7.5 (16.8-19.112-.1) 20.5 and 7.190) .1) 14.064 (.1) 15.9 (12.9 (12.6 (15.160 (.0) 21.40-9.112) 95th .4) 95th 20.088-.100-.5) 15.147 (.160 (.0) < LOD 9.4) 14.4 (12.100-.0 (10. see Data Analysis section) for survey years 01-02 and 03-04 are 10.073-.S.6 (15.7 (<LOD-15.10 (<LOD-16.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.6-24.108-.5-15.062 (.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.30 (8.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level. population from the National Health and Nutrition Examination Survey.5-17.089 (.3-21.7 (14.9 (14.3 (18.8 (11.9-23.090-.096-.2-15.110 (. Survey years 01-02 03-04 Geometric mean (95% conf.149) .070 (<LOD-.Organochlorine Pesticides Serum Dieldrin (lipid adjusted) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0 (15.8 (18.8-17.053 (<LOD-. which may vary for some chemicals by year and by individual sample.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .120 (.054-.1) 15.40-10.1 (13.9 (13.190) .50 (8.109-.8.048 (<LOD-.086-.139 (.6-24.1) 10.130) .130 (.059 (.1-18.1 (18.139 (.80-10.2) 11.4 (12.

1989. Available at URL: http://www. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Demographic and seasonal influences on human serum pesticide residue levels.htm. Wienburg CL. Available at URL: http://www. 15.fda. either singly or in combination.gov/toxprofiles/ tp1. bioaccumulation. Jr. References Agency for Toxic Substances and Disease Registry (ATSDR).109(Supp1):113-139. Mink PJ.atsdr. Anantharam V.14:95-102. 4/21/09 Bates MN. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Int Arch Occup Environ Health 1994. In Hayes WJ. Mann D. Schulte P. Daniel SE. Fernandez MG. Environ Health Perspect 1995.org/documents/ehc/ ehc/ehc91.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Reprod Toxicol 2000.cfsan. Teta MJ. Neurotoxicol 2005. Corrigan FM.54:1431-1443. Garrett N.html. 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. Sanchez-Ramos J.gov/~dms/ pesrpts. David VL.usgs. Vol. Exp Neurol 1998. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Kitzazwa M. September 2002. No:429-436. 2007 [online]. Stehr-Green.103(Suppl 7):113-122.59:229-234. PA. 731-915. are nonestrogenic in transfected HeLa cells. Andersen A. Hartvig HB. Food and Drug Administration (FDA). Li AA. Cancer Epidemiol Biomarkers Prev 2000. Revised Feb. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Patterson DG Jr. International Programme on Chemical Safety (IPCS). Song S.64-65 Spec. 4/21/09 Hoyer AP. Available at URL: http://www. 2 Classes of Pesticides. 1991. Finley B. Sonnenschein C.66(4):229-234. Cox. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Toxicological profile for aldrin/dieldrin [online].inchem. Academic Press. Chung KL. Chapin RE. Grandjean P. Soto AM. Kanthasamy A. New York. Smith AG. Environmental Health Criteria 91. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.26:701-719. Priestly BG.47:1059-1087. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. 4/21/09 Jorgenson JL. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. toxicology.27:405-421. Tully DB. Pesticides in the Nation’s Stream and Ground Water. Six high-priority organochlorine pesticides. FDA Pesticide Program Residue Monitoring 1993-2006 [online].gov/ circ/2005/1291/. 1992-2001. Patterson DG Jr. Available at URL: http://pubs. Organochlorine insecticides in substantia nigra in Parkinson’s disease. United States Geological Survey (USGS). Mumtaz MM. Eds. Inc. Toxicol Lett 1992. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Jorgensen T. Environ Health Perspect 2001. Organochlorine exposure and risk of breast cancer. Rosellini RA. Serrano FO. et al.352:1816-1820. McIntosh LJ. Turner W. 6/1/09 Ward EM. Jr and Laws ER. VT. Facca A. Olea N. Lancet 1998. 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. Ellis H. Narahashi T.150:263-271. Handbook of Pesticide Toxicology. plasma dieldrin.cdc. Brock JW. Part A 2000. Buckland SJ. Basit A. J Occup Environ Med 2005. J Toxicol Environ Health. et al. Kanthasamy AG. Chlorinated Hydrocarbon Insecticides. Frey JM. and lymphocyte sister chromatid exchange. Grajewski B. August 2008. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Carlson JN. pp. Shore RF. Edwards JW. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Psychopharmacology (Berl) 1987. J Toxicol Environ Health 1989. Ginsburg KS.html. Chemosphere 2004. Needham LL.91(1):122-126.9:1357-1367. and epidemiology in the United States. Aldrin and Dieldrin [online]. Roy ML.

5 (<LOD-12.5-40.8) 52.30-11.1) < LOD < LOD < LOD < LOD < LOD 8.10-18.74 (<LOD-10.4) 12.0) 41.6 (25.8) 52. see Data Analysis section) for Survey years 99-00.9 (11.9 (31. buildings.5.3 (26.5-41.6) 39.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-38. 2007).36-11.9 (21.70 (<LOD-10.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.8-20.1 (27.5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.0-25. and 03-04 are 14.1 (40.5 (41.5 (33.4) 18.7 (<LOD-13.9) 23.8.7-14.0) 21.9) 11.6) 9.1 (11.3 (21.10-11.8-33. in addition to trace amounts of numerous other related compounds (ATSDR.7) 42. from the early 1950’s until the mid-1980’s.3 (20.1 (20.7-25.2-49.0 (<LOD-12.8 (18.9) 10.9-21.0 (20.. Technical grade chlordane had contained 7% trans-nonachlor.S.Organochlorine Pesticides Chlordane CAS No.2 (10.8 (10.1-51.3-24.7 (34.0-18.3-49. 2007).7-12.5) < LOD < LOD 9.1 (17.5-65.1 (<LOD-12.8 (17.8-42.0-12. Since 1992.2) 46.9) 23.8-43.6) 48. 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.0) 20.5-32.1-25.7-70.2) 37.3 (25.4 (10.1) 16.3-32.8-61.10 (8.7 (17.6 (43. Fourth National Report on Human Exposure to Environmental Chemicals 81 .3-45.4) 22. chlordane was used to kill termites and other insects on agricultural crops.2-56.0 (37.5) 10.3 (11.3 (<LOD-19.4) < LOD 11.1) 30. Chlordane is not currently produced or used in the U. 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.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.6-24.9 (18.3 (9.5) < LOD < LOD < LOD < LOD 13.5) 9.2) 34.6-45.82-11.6-53. 1994).20-11.4 (30. < LOD means less than the limit of detection. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.1-15.9 (29.8-23.1-19. foods high in fat such as meat.3-45.7 (10.9) 13.5-47.8 (17.8-73.9 (36.7 (19.4-51.1 (15.5 (31. As a result of the manufacturing process.2-28.9) 11.8 (10.7 (<LOD-32.7 (34.9) 36.4-14. Survey Geometric mean (95% conf.1) * 11.7) 28. the technical grade product of each chemical contains 10%-20% of the other chemical.6) < LOD 11. and dairy products are the usual sources of exposure to these chemicals in the general population.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12. fish.4) < LOD < LOD < LOD 23.8-33.90 (8.2) < LOD 11.37 (8. lawns. 1994.20-10.7) 19.1-65.9-40.1 (<LOD-12.2) 22.6-18.2 (9.0) 31.S.4 (30.0-67.7) 19.9) 39.5) 37.5-43.5) 56.0) 37.2 (21.8) 53.2-21.9 (15.7-39.6) 8.6) 20.2 (36.4-45.9) 37.4 (22.5) 44.3) 18.1 (16.4) 37.2-49.6) 36.3) 10.7 (32.3 (28.5) 21.2 (41.1) * 11. 01-02.3) 18.0 (32.1) 22.9 (17.1-25. which may vary for some chemicals by year and by individual sample.2) 36.8 (40.4) 29. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.8 (42.7) 9.2 (39.1) 90th 34.9 (15.7 (43.4-40.6-24.5-38.4 (<LOD-12.0-13.9) 31.0 (16.7-56.1-50.69-10.6) 49.9 (26.4-21.4 (31.2-26. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 30.63 (8.3 (27.5-44.4 (35.3) 37. Consequently.0) 27. and 7.8) 18.0 (26. and in soil.8) 27.6) 48.9 (26.3) 41. heptachlor use has been limited to treatment of fire ants near power transformers. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk. Until 1988. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.6 (16.6) 23.9 (11.89-10.0-61. 57-74-9 Heptachlor CAS No.9) 47.0-33.7) 35.2) < LOD 11.1 (<LOD-12.8-32.0) 75th 20.2 (28.5) 38. population from the National Health and Nutrition Examination Survey.9-42.6 (9.6) 11.8-31.5-13.7) 31.S. 10.4) 39.9) 17.5 (34. respectively.2) * 12. 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.1 (25.8) 44.1 (44.7 (42.2 (37.5 (8.20 (<LOD-11.9-21.3) 10.6) 9.3-43.5-42.2) 33.6-12.6 (9.

213) * .320) .063) .150) .120-.050 (<LOD-.146) < LOD < LOD .079) . Chlordane and heptachlor are absorbed after oral.140 (.280 (.180-.Organochlorine Pesticides (Dallaire et al. 1991).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. Chlordane is metabolized primarily to oxychlordane and to a lesser extent. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.053-.250 (.100 (.280-.216-.115 (.068) 75th .150 (.048-.300) .400) .300) .083) .270 (. 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.253-.210 (.320 (.069 (<LOD-.120-.075 (.076) < LOD . and the U. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.126 (.070 (<LOD-.066-.080) .070-.073) < LOD < LOD < LOD < LOD .190-.430) .230-.058-.286 (.310) .126) .100-.160 (.207) . and heptachlor epoxide in foods and bottled water.090) .204 (..170-.320 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . dermal.049 (<LOD-. 1977b.373) . 1986).290 (.190-.140 (.130-.068) .140-.290) .104) .290-.148-.070 (<LOD-.073 (.119 (.068-.150-.104-.130-.245-.080) .S.189-.077) .280-.070) .165-.240-.160) .140 (.160) .100-.130) .260 (. Acute.063 (.067 (.170) .120-.S.230-.120 (. heptachlor.240) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .280 (. 1991.150 (.250-. Rogan.055-.130-.310) . 2007.130-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .350 (. neonatal mortality.053-.200-. Survey Geometric mean (95% conf. Shindell and Ulrich.149 (.140) . 2006).220-.070-.133) 90th .S.260 (.063 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .400) .130-.189 (.230-.330 (.170) .227) < LOD .220 (.230 (.258-.148) .057) * .300) .258 (.070 (<LOD-.300-.063) * . and breast milk is a major excretion route in lactating women.047 (<LOD-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.063 (.410) . IARC.130) . 1981). The U.315 (.450) .370 (.057-. characterized by seizures and paralysis.200-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.170) .180) . Elimination of all these chemicals from the body occurs over months to years.190-.450) .340) .150 (.080 (.199-.061-.079) < LOD < LOD < LOD .240-.115-.260-.066 (<LOD-.310 (. Smith.430) .250 (.130 (.370 (.440) .200 (. 2002.077) .310) .083 (. 2007). FDA established allowable residues of chlordane.310-.271 (.270 (.210-.070 (<LOD-.270 (.065-.130 (.110-.348) .180-.220-.077) .092) . 1986). which may vary for some chemicals by year and by individual sample.320) .302) .112 (.128 (.300 (.240 (.208 (.200-.063 (.223) .280) .180) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.320 (.360) .290-. Takahashi et al.242-.286 (.070 (.090) .290) .231) .066 (.058-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .203-.146) .064) < LOD .370 (.130 (.380) .108-.070) < LOD < LOD < LOD < LOD < LOD .320 (.246-.062) < LOD .058 (.110 (<LOD-. to heptachlor.090-.269 (.087-.100 (<LOD-. chronic doses of heptachlor have produced liver enlargement and injury..560) .300) . EPA has established environmental criteria for chlordane and heptachlor.136) . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.077) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140 (.510) .350 (. 2001.140-.082 (.260 (.080) ..225 (.074-.066-.210 (.340) .168-. 1977a.070-.080 (. Le Marchand et al. OSHA has established occupational exposure criteria.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 * * * * . 1996. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and inhalation exposure.207 (.106-.063-.091) .350) . In laboratory animal studies.071 (.057 (.170) .290-.056 (..230) .287) . and alterations in immune function of offspring. population from the National Health and Nutrition Examination Survey.280-.170) .060 (<LOD-.050-.160) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. which is also persistent in the body (ATSDR.230 (. The major metabolite of heptachlor is heptachlor epoxide.

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

7 (10.1-38. and 03-04 are 14.3 (13.6 (16.6) 22.0) 13.4 (11.2) 20.0) 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 13.8.3) 22.5 (18.5 (11. 01-02.7-18. 84 Fourth National Report on Human Exposure to Environmental Chemicals .8) 14.1-16.9) * * * 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.S.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.1-15.6 (16.1) 23.8-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-25.8) 13. population from the National Health and Nutrition Examination Survey.5 (<LOD-32.3) 18.4) 18.9-29.5 (10.2 (<LOD-62.3) 18.6 (14.8) 19.0 (11.8 (18.4 (<LOD-19.2-17.10-13.20 (<LOD-9.2) 15.4 (<LOD-54.8-23.8) 13.6-17.6) 14.8 (<LOD-23.6-21.6 (<LOD-27.90 (<LOD-9.2) 13.3) 23.2-16.1-29.0-17.4) 21.4 (15.0-17.9-29.40) 15.6 (11.0-19.5.6 (13.8-24.2 (18.5 (11.6 (8.8) 21.8-24.9 (15.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. see Data Analysis section) for Survey years 99-00.0-16.1) 20.3-18.1) 13.50) < LOD < LOD < LOD 17.0 (15.3) 10. 10.8) 20.6) 13.8 (15.9-23.2 (<LOD-16.9-16.3) 27.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.9) 15.0-54.1 (19.7 (16.4 (11.2-27.7-25.8 (18.6) < LOD < LOD < LOD 27.8) 14.1 (16.5) < LOD 14.3 (<LOD-25.8-46.8) 15. Survey Geometric mean (95% conf.3) 16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.6.2) 26.2 (<LOD-25.8) 19.5 (<LOD-21.2-27.5) 19.3) 18. which may vary for some chemicals by year and by individual sample.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 7.8 (13.6 (12. respectively.7-19.9 (12.8 (13. < LOD means less than the limit of detection.8) 16. and 7.7 (13.

200) .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.200 (.240) .120 (.130 (.087 (.100 (.180 (.130-.100-.113-.140) .180) .126 (.110-.055 (<LOD-.150 (<LOD-.108-.310) .120) .063) < LOD < LOD < 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 .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 .120-.090-.170) .111) .130) .130) .098 (.170 (<LOD-.057 (<LOD-.S.135 (.150 (.100 (.220) . population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.170 (.110) .173) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-.130-.082-.130 (<LOD-.067-.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .116) < LOD < LOD < LOD .090-.170) .077-.094 (.070-.104) .120) .100 (<LOD-.063) .101 (.310) .097) < LOD .096 (.117) . * 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 .190) .190) .135 (.110 (.108) .110 (<LOD-.140-.110) .076-.180 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 85 .100-.120 (<LOD-.170) .180) .090-.090-.150 (.128 (.113) .101 (.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.170 (.111-.053-.180) .190 (.380) .071-.094 (.133 (.077-.149) . Survey Geometric mean (95% conf.090 (<LOD-.170 (.180) .130-.140) .106-.100 (.090-.107-.270) .200) .090 (.130-.110 (<LOD-.120 (<LOD-.110-.100 (.074-.069 (.157) .190) .110 (.

3) 25.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.9-65.6-54.6) 10.1-28.8-19.8 (15.5) 19.7-77.0-23.6 (57.8 (16.0-68.1-126) 67.2) 34.1 (17.7) 56.9) 14.8 (28.1-16.7) 15.8-90.5-36.4-67.3-39.0-24.8-79. population from the National Health and Nutrition Examination Survey.4 (30.6) 56.6 (56.8 (30.9) 51.6-66.8-21.5-19.0-93.7) 73.8 (71.6 (15.8 (11.5-95.1) 78.7) 17.1 (10.5) 36.4-35.5) 78.9) 14.5) 90th 55.9-40.9 (66.3) 36.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.2 (60.0) 75th 31.1 (65.9-65.6 (50.0 (16.6-22.2) 59.5-111) 68.1 (48.5) 14.0 (16.5 (45.2 (19.7) 78.9 (19.2-18.0 (48. 86 Fourth National Report on Human Exposure to Environmental Chemicals .3 (58.9 (29.7 (13.0) < LOD < LOD 8.1) 14.4 (11.1-20.2 (25.0-22.0-93.3-74.1) 31.4) 48.5) 35.1) 18.8 (17.9-89.0) 40.7 (59.9-45.7-17.7) 59.8-90.0 (15.1 (41.6 (16.5 (13.8-41.1-34.0 (62.8 (19.4-23.0 (60.3) 30.3 (14.2 (7.6) 84.6 (56.8) 47.7-34.9-36.1-34.3) 32.3) 16.6) 56.0-23.3-21.4) 19.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.3 (45.7 (30.0 (14.5-17.5) 9.3 (17.3-32.8 (26.2 (64.9 (15.3 (56.7 (28.6) 54.3) 32.6 (12.7-20.9-20.9) 51.4 (12.7 (11.2 (59.8 (28.1) 16.4-52.7-38.0 (13. 01-02.2 (14.0 (42. and 7.6) 82.7-21.1 (22.5 (44.4 (67.6 (<LOD-14.3 (49.5) 30.7 (35.8) 80.1) 30.2-16.6) 13.4-22.7) 14.8 (45.5) 22.1-18.1) 78.3-58.2) 17.4-18.1) 62.3-57.4-62.8 (42.0 (13.8 (<LOD-20.6 (52.5-20.9-64.5) 48. < LOD means less than the limit of detection.1) 18.1) 17.7) 35.9 (47.5.3) 18.6-82.0-20.8-19.2) 30.8 (13.7-22.7-35.2-18.8-77.0-143) 112 (68.8) 19.0) 13.8-16.7-29.5-69.4 (16.5-87.7-160) 86.1) 17.2 (26. which may vary for some chemicals by year and by individual sample.0 (42.5 (15.2) 20. Survey Geometric mean (95% conf.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.86-13.8 (26.3-50.5) 14.3 (16.0 (29.2-88.5 (25.2 (36.9 (51.2) < LOD 10.2-21. interval) 18.0-59.9 (16.4 (28.9-22.1 (47.1) 17.2 (15.8-67. 10.7-113) 68.0-38.3 (14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 20.5) 77.1) 17.8 (26.4) 55.5) 20.4-36.8-129) 74.7 (18.5) 26.8.4) 107 (84.2) 19.1-51.1-55.0-123) 74.7-18.7) 78.0) 18.6-19.1-16.1-22.0) 49.7-32.2 (27.7-23.3-30.3) 18.9 (28.3-86.7) 28. see Data Analysis section) for Survey years 99-00.0-113) 68.3) 15.6) 60.1) 32.9-69.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11. and 03-04 are 14.4) 59.S.8-16.3) 30.4 (45.0-37.6) 25.8 (13.8-110) 59.1) 17.6-88.3) 19.8) 51.70 (<LOD-12.6 (32.6-20.9) < LOD < LOD < LOD 20.2-37.0) 33.4) 16.2-17.7 (59.5.0) 19.1) 17.9 (51.9 (15.2) 39.8 (12.2 (14.7 (16.8 (28.9-35.9 (36.10 (<LOD-11.6) 34.1) 17. respectively.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.0 (15.8 (49.9-58.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.9 (<LOD-14.5 (15.7) 52.0 (19.2-23.7 (74.

210-.124) .186-.350-.220 (.470 (.460) .520 (.470-.330-.210-.093) .220 (.041 (<LOD-.111 (.099-.120 (.630) .098 (.080-.390 (.830) .340-.100 (.395) .240) .630) .370 (.310-.400 (.237) .106 (.090-.089 (.186 (.414 (.069) .080-.210 (.150) .520 (.047-.320-.680) .081 (.091) .651) .390-.490-.510 (.108) .130) .122) .190-.060-.098-.100-.120 (.220 (.071 (<LOD-.202 (.680 (.177-.350 (.190-.103 (.594) .410-.108 (.140) .092 (.081-.109 (.110 (.440-.085-.490 (.240) .205 (.095-.105 (.110 (.119) < LOD < LOD < LOD .085-.068-.130) .220 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .S.090) .270-.170 (.141) .130 (.060 (<LOD-.130 (.220 (.190-.099-.301-.450) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .090-.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.690) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-.405) .100 (.250) .355 (.630) .093-.260) .135 (.590) .106 (.097) .310-.410-1.096) .122) .460-.070 (.104 (.061-.240) .090 (.103 (.094 (.470-.460) .409-.211) 90th .160-.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 .573 (.130) . interval) .079-.327 (.131) .360-.497-.240-.129) .125) .161) .520) .060) .960) .300) .324 (.084-.113) .390) .540) .080) .116) .840) .098 (.090-.310-.110 (.286-.390 (.590 (.510-.340-.390) .237) .117) .480) .183 (.180-.116-.240 (.120) .690) .210 (.600 (.100-.390 (.440) .087 (.110 (. Survey Geometric mean (95% conf.500) .191 (.760 (.300-.288 (.310 (.371) .161-.220 (.127) < LOD < LOD .430-.173-.110-.112 (.128 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .290-.080-.130) .420) .640 (.092 (.430-.090-.800) .343 (.190-.093-.20) .130) .430-.100-.490) .093-.232) .190-.130) .100-.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.078 (.220 (.242) .260) .080-.080 (.113) < LOD .390 (.395-.120) .054-.210 (.280) .470 (.417 (.085-.111-.230 (.078-.116 (.684) .134) .114) .126) .210) .150) .288-.320-.055 (<LOD-.090 (<LOD-.120) .400 (.096-.220 (.079-.234) .380 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .600) .830) .098) .110) .180-.062 (.130) .559) .069-.091-.210) .397-.190-.930) .108) 75th .330-.220) .110 (.112 (.580 (.580 (.272-.580 (.210) .285-.400) .120 (.090-.104-.317 (.090-.160 (.370 (.458 (.109 (.120-.400-.310) .110 (.250) .340) .330 (.470 (.565) .250) .145-.400-.367) .590 (.420 (.096-.125 (.550 (.106 (.171-. population from the National Health and Nutrition Examination Survey.310-.180-.360-.082) .120) .120-.119) Selected percentiles ( 95% confidence interval) Sample 95th .490 (.158-. which may vary for some chemicals by year and by individual sample.279-.141) .461 (.

259(3):374-377.gov/ntp/ htdocs/LT_rpts/tr008. Jr and Laws ER. Smith AG.110(8):835-838. Lulek J. Circumpolar maternal blood contaminant survey. et al. Natl Cancer Inst Carcinog Tech Rep Ser 1977b.nih. et al. et al. Wolff MS. Dewailly E. Environ Res 2000.niehs. Head SL. International Agency for Research on Cancer (IARC). Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Vol. 2006. 6/1/09 National Toxicology Program (NTP).Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).41:145–148. Covaci A.28:497501. KalubaSkotarczak A.htm.atsdr. Stehr-Green P. Saidein D. 88 Fourth National Report on Human Exposure to Environmental Chemicals . New York.heptachlor. Distribution of polychlorinated biphenyls. Available at URL: http://ntp. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Hertz-Picciotto I.org/ documents/cicads/cicads/cicad70.9:1-109. Tartter P. Canada).html. Aune M.gov/toxprofiles/tp31. Eds. 4/21/09 James RA. Bull Environ Contam Toxicol 1981:27:506-511.atsdr. Charles MJ. Keller JA. Lawrence River (Quebec. National Toxicology Program (NTP). 1994-1997 organochlorine compounds. Bjerselius R. Hawaii Med J 1991. May 1994. Organochlorines in Swedish women: determinants of serum concentrations. Sci Tot Environ 2006. Handbook of Pesticide Toxicology. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.html. 4/21/09 Dallaire F. 1979-1980.nih. Chlorinated Hydrocarbon Insecticides. Arch Environ Health. et al.372:20-31. Wohlleb JC. Environ Health Perspect 2003. Berkowitz GS.cdc. In Hayes WJ. Pollutants in breast milk. Organochloride pesticide residues in human milk in Hawaii. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Muckle G. Available at URL: http://www. Available at URL: http://www. Available at URL: http://www. Sci Total Environ 2004. Granath F. Wong L.niehs.111:349355. Dendle WH.inchem.150:981-990. Mortality of workers employed in the manufacture of chlordane: an update.htm. Jr. Baker DB. 1986. Willman E. gov/toxprofiles/tp12.8:1-123.50(3):108-118. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. maternal serum and milk from Wielkopolska region. J Occup Med 1986. Shindell S and Ulrich S. Organochlorine exposures and breast cancer risk in New York City women.84:151-161. Laliberte C. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. LeMarchand L. Academic Press. JAMA 1988. Ayotte P. August 2007.110:617-624. Chashchin V. 1963-1967. Available at URL: http://www. Takahashi W.org/site/foundation/ research/projects2. 1991 pp. 4/21/09 Baker DB. Drews K. Van Oostdam JC. A Report to the Hawaii Heptachlor Research and Education Foundation. 9/25/07 International Programme in Chemical Safety (IPCS). Available at URL: http://ntp. Environ Health Perspect 2002.330:55-70.inchem.html. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR).cdc. Loo S. 2 Classes of Pesticides. Toxicological profile for heptachlor and heptachlor epoxide [online]. Toxicological profile for chlordane [online]. Darnerud PO. Kolonel LN. Royce W. Chlordane and heptachlor [online]. Bioassay of heptachlor for possible carcinogenicity. Inc. Senie R. Atuma S. 2001. Concise International Chemical Assessment Document 70 Heptachlor [online]. Takei G. Barker J.gov/ntp/ htdocs/LT_rpts/tr009. International Agency for Research on Cancer (IARC) . Brower S. Environ Health Perspect 2002. 1993. Gilman A. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Bioassay of chlordane for possible carcinogenicity. Arch Pediatr Adolesc Med 1996.Summaries & Evaluations. Voorspoels S. Vol. Dewailly E. Available at URL: http://www. Jaraczewska K.org/documents/iarc/ vol79/79-12. Bleiweiss IJ. 79.pdf. Siegel BZ. Odland JO. Poland. 6/1/09 Rogan WJ.pdf. Hansen JC. Glynn AW. 731-915.

0 (18.5 (23.S.1 (33.9 (<LOD-20.0-53.1) 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. and 03-04 are 20.3) 28. Gunderson.5) < LOD < LOD 9.9 (10. DDT was used at one time as a treatment for head and body lice.0-37.1) 31. DDT is converted in the environment to other more stable chemical forms.0) 20. and water.2) 30.9-28.0) 26.7 (19. after World War II until 1972.5) 25.2 (<LOD-40. air.3) 21. p. sediments.9 (10. DDT is converted to DDE and several other metabolites.3-16.5 (14. In the body.S. 1991).8) 15.6 (31.p’-DDT (15%-21%). 17.8-23.8-17.0 (10. fish. Survey Geometric mean (95% conf. inhalation. DDT and DDE can cross the placenta.0) 19. see Data Analysis section) for Survey years 99-00.5-54. as well as in plant and animal tissues. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.5 (23.8) 36. resulting in fetal exposure.7 (15. population.2) < LOD < LOD 9.2-bis(p-chlorophenyl) ethane (DDD). It was produced and used in the U.00 (<LOD-10. 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.p’-DDT (65%-80%).7) 12.10-13. The biodegradation half-life of DDT in soil varies from 2 to 15 years.1 (<LOD-39. DDT usually refers to the technical product.8.4. particularly for endemic vector and malaria control. Fourth National Report on Human Exposure to Environmental Chemicals 89 .70 (8.3 (27.p’-DDD (4% or less).8-26.4) < LOD 17.0-15.S.5-36.6 (<LOD-25.0-27. DDT can be absorbed after ingestion.3) 21. including 1.7) < LOD 18.5 (15.4 (23. and dairy products. and 7. or dermal exposure. 1991). population from the National Health and Nutrition Examination Survey.6 (9.7.1 (23. 2008.1-71.6 (22.3 (<LOD-31. < LOD means less than the limit of detection.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.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. Only a small proportion of DDT is metabolized and excreted (Smith.5) 23.2-95.1’-dichloro-(2.10 (<LOD-12.9-34. In the general U.2-65. which may vary for some chemicals by year and by individual sample. Both Serum p. respectively.7-16.7) 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 10.6-33. o.90 (<LOD-12.0 (21.3) 22.9) 29.50-11. Food imported from countries that still use DDT may contain the chemical or its residues. These chemicals are highly persistent in soil.0-155) 83.8) 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 8.0 (18. continues to be the primary source of DDT exposure. Smith.9) < LOD < LOD 9.2 (11. 2002.1-27.3-590) 293 (104-541) 48.1’-(2.3 (<LOD-21. although DDT and DDE intakes have decreased over time (FDA.8) 30.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.3-236) 24.6 (25.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9 (10.4) < LOD < LOD < LOD 61.8-39. food.0) 40.9) 17. depending on conditions.0-35. 1988).9 (21. 01-02. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. particularly meat. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. when virtually all use of it was banned. It is still used in some countries. which is a mixture containing p.2) 155 (59.9) 14. and trace amounts of several related compounds.

570-4.627) .201 (. fertility. dioxins and furans). interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2001).220) .114-. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.189-. 2000.079) < LOD < LOD .128 (. 1956). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.068-.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. 90 Fourth National Report on Human Exposure to Environmental Chemicals .150 (<LOD-. Survey Geometric mean (95% conf.120 (<LOD-.26) 1.190 (.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * ..140) . 2006.203) .. 2004.400 (. resulting in exposure to nursing infants (Rogan. 2006).150-.120-. Gladen and Rogan.180-.061) < LOD < LOD < LOD . both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.190 (.146 (. 2001). overt signs of acute human toxicity include vomiting.S.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 ..130-. 2002.080-.054-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.063 (<LOD-.290) .230) .075) 1. and altered behavior after neonatal exposure (Eriksson and Talts.146 (. have not been consistently demonstrated (Beard.170) . tremor.071-.240) . Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. Jusko et al.051 (<LOD-.048 (<LOD-.240 (..34) . and leukemia have also been inconclusive (ADSDR. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. Reproductive effects in humans affecting birth weight.530 (. Beard.170 (. In laboratory animals. Snedeker. Studies of DDT exposure and pancreatic cancer.530) .132-. DDT may bind to estrogen receptors (Chen et al.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 .160-.420) . Jusko et al. 2001).. which may vary for some chemicals by year and by individual sample.g.00) . 2001). Mariussen and Fonnum.078-.098-.106) . Animal studies reported reduced fertility. A workplace standard for DDT has been established by Serum p.106) < LOD < LOD .01) .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 .130 (<LOD-.130 (<LOD-.095) < LOD .059-. 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.Organochlorine Pesticides chemicals are excreted in breast milk. and duration of lactation. other organochlorines. polychlorinated biphenyls.62 (.086 (. 1998).105-.180 (.00 (. Hayes et al. 2002. 1996).220) . lung cancer.. In high dose.330-4.180) . 2002..084 (.106-.180 (.260) . premature delivery. 2006.250-1.064 (.p’-DDD and p. Longnecker et al. 2006)..180) .343) < LOD .400) . accidental exposures..071 (.190-1. reproductive organ abnormalities.112 (.143) < LOD < LOD . 1997).074-. and seizures. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995.142 (.. Calle et al. 2006.108 (.087 (.230) .200 (..069) .065-.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.130 (<LOD-. 2006).. 2002.p’-DDE can produce anti-androgenic effects (Gray et al. population from the National Health and Nutrition Examination Survey. Gray et al.150 (<LOD-.150) . and o.140-.250 (.313 (.150-.170-.078 (.

the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. In general. In a population-based sample of men and women from eastern Slovakia.S.. 8.. 1989). 2003.e. interval) 260 (226-298) Selected percentiles ( 95% confidence interval) Sample 95th 1830 (1410-2300) 2320 (1830-2780) 1860 (1400-2380) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 226 (184-278) 251 (228-278) 203 (163-275) 75th 537 (476-631) 598 (521-699) 509 (376-655) 90th 1150 (976-1350) 1410 (1210-1500) 1170 (836-1570) 295 (267-327) 238 (195-292) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 118 (102-135) 124 (106-146) 105 (84. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. 2003). for males and females in the NHANES 19992000 subsample (Pavuk et al. environmental levels) and health effects is available from the U. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. IARC classifies DDT (p. 2004).7-119) 113 (100-140) 93. Survey Geometric mean (95% conf. Biomonitoring Information DDE persists in the body longer than DDT.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. respectively. 1998.6.epa.8.html. More information about external exposure (i. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. 01-02.p’-DDT) as a possible human carcinogen.Organochlorine Pesticides OSHA and a guidance established by ACGIH. and 7. mean serum levels of DDT and DDE in the U.6 (81. Heudorf et al. population from the National Health and Nutrition Examination Survey. Stehr-Green. 2004).. NTP considers DDT as being reasonably anticipated to be a human carcinogen. 2002.S...cdc. Since the 1970’s.. 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.gov/ toxpro2. 2002. Compared to females in the NHANES 1999-2000 subsample.3. population declined by about fivefold to tenfold.gov/ pestcides/ and from ATSDR at: http://www. and 03-04 are 18. Declining DDE levels over time have also been observed in the German population..atsdr.0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD. Smith.S. compared to levels observed in this Report (Anderson et al. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. 2005). Fourth National Report on Human Exposure to Environmental Chemicals 91 . respectively. Link et al.. EPA at: http://www. see Data Analysis section) for Survey years 99-00. 1991).7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.

2) 19.8 (13.51) 3.66) 3.7) 16.76 (2.59) 3.25) 1.2 (19.02-8.33-1.21) 90th 7.6) 9.890-1.6) 12.57-3.7-19.12 (6.730) .38 (1. population from the National Health and Nutrition Examination Survey. High mean levels of whole blood DDT (about 3.4) 14.39 (3.39-2.81) 11.23 (7.0) 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 .59 (1.19-14.01-15.15-4.47) 3.01) 1.87-16.01-1.46 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.10-5.18-1. 2004).6) 9. serum levels of o.50 (2.14) 2.963-1.9-38. less than one percent had detectable serum levels of o.43-4.13 (1.30 (1.9) 7.01-11.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.18-3.69) 8.55 (2.1) 7.385-.90) 22.68) 2.34) 2.58) 1.44) 1.18 (6..6) 9. or p.57 (1.63 (6.2) 26.61 (1.11-1.8) 15.28) 1.63 (1.54) 8.07) 1.32-1.534-.07) 1.06) 3. 1971).66-17.85 (1.36 (3.25) 8.63 (1.55-9.32-1.81 (1.611-1.22-1.57) 2.9-17.85-10.77 (1.58) 75th 3.85-4.30 (1.59 (4.66) 1.0 (9.8 (9.7-48.6 (8.78 (4.16 (2.1) 40.64) 3.59) 6.2 (9.S.6 (17.43-4.00-1.3 (9.36-11.97-4.47 (1.63-15.13) 4.54 (1.92 (3.82) 1.65) 1.76) 1.91 (6. o.488-.03-1.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .97 (3.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.34-11.49 (6.p’-DDT.36) 3.18-4.99) 1.34-3.0 (12.590 (.600) .3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.5) 7.57 (3.18) 1.05) 1.22 (7.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.00 (.81-18.00 (6.24) 1.3) 16.92) 1.51 (1.61-2.68 (2.93 (7.45 (1.680-1.5) 10.56-2.83 (1.5) 16.10) .9) 5.p’-DDT (Stehr-Green.40 (3.49 (1.6) 8.40-8.21) 3.49 (1.96) 1.69 (2.18-1.10) 2.456 (.91-3.27-1.88 (2.96) .70-3.25-14.965-1.81 (7.59 (1.76-3.36-1.419-.01-1. 1989).76) 1.32) 1.39-1.57-2.77 (1.32 (1.20 (.4) 9.726) .65 (1.30-1. 2004).09-1.52 (3.02 (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.40-4.37-16.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.25-16.34) 6.32-9.50-17.12-1.40-4.45 (1.75) 6.72) 1.04 (6.48-4.71) 12.56) 2.7) 13.66) 4.53-15.8-90.516 (.06) 1..26 (1.48 (6.14) 2.5) 22. In a subsample of NHANES II (19761980) participants.796 (. In the NHANES 1999-2000. 1991).00) 7.90-8. 2001-2002 and 2003-2004 subsamples.80) 1.41 (1.7-20.14 (1.71 (6.80 (2.26-2.46 (1.66-4.51-8.24 (1.37 (1.69 (1.01-5.46-2.05 (3.62-6.57 (1.994-2.6) 13.80) 1.04-1.31-12.71) 32.75) 1.2-32.68-4. considerably higher than levels in this Report (Smith.70) 1.13-2.4 (12.91) 3.79) 4.1 (9.80) 3.25 (1..56-6.87 (5.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.69) 4.53) 7.870 (.25 (.84 (3.75) 2.557) 1.520 (.820-1.51-15.8 (14.91-2.6 (7.37-1.6) 11.5) 5.3) 13.9 (26. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.500-.12 (.53) 1.26) 3. Finding a measurable amount of p.16-1.17-3.56-3.36-2.03-4.7) 9..39) 1.3) 10.72) 1.30-1.38 (1.6 (9.58) 1.p’-DDT.37-4.2 (9.52 (1. 309 versus 268 ng/g lipid.29 (1.49) 8.p’-DDT were below the limits of detection.7 (8.92 (3.4-19. 2005).14-1.64-2.22) .82 (1.51) 1.07 (5.4 (8.1) 12.561 (. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.31-2.860 ng/L) and DDE (about 14.8 (13.14-9.17 (3.34 (7.26-10.75 (8.88-35.4) 13.51-49. interval) 1.43 (5.6) 9.37-10.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.430-.66) 1.0) 2.01) 1.1 (8.635) 1.52-6.75 (4.71 (5.35) 1.41-12. Serum p.31 (1.84-3.54-7.32 (1.01-11.81-5.24-17.27) 3.10-1.623 (.Organochlorine Pesticides nearby agriculture (Botella et al.43-8.19) 4.3 (8.66-2.60-13.9 (15. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.69 (. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.646) .02) 1. Survey Geometric mean (95% conf.3-43.53 (2.11 (2.2 (6.57-13.

population from the National Health and Nutrition Examination Survey.4.8.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. respectively. 17. and 7. which may vary for some chemicals by year and by individual sample. 01-02. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organochlorine Pesticides Serum o. Survey Geometric mean (95% conf. 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. and 03-04 are 20. Fourth National Report on Human Exposure to Environmental Chemicals 93 .7.S. see Data Analysis section) for Survey years 99-00. < LOD means less than the limit of detection.

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

Available at URL: http://www.7(3):248-264. J Assoc Off Anal Chem 1988. DDT and human health. Henley SJ. et al. Bloom MS. Levels of DDT.206:485-491. Jr. Brock JW.112(17):1761-1767. CA Cancer J Clin 2002.21(1-2)37-48. Hurd C.155(4):313-322. India. April 1982 to 1984. Kashyap R. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.162:890-897. Chen CW. Needham LL. Patterson DG Jr. Vorojeikina DP. Gunderson EL. FDA total diet study. Biomonitoring of persistent organochlorine pesticides. Lepom P.205:297-308. Frumkin H. Am J Public Health 1995. Burse VW. Falk C. hexachlorobenzene. Environ Res 2005.gov/ toxprofiles/tp35. Neurotoxicol 2000. et al. Kaus S. Bates MN. Gabrio T. Bhatnagar VK.96:34-40. Zaidi SS. et al. Gray LE Jr. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Becker K.html. Botella B. Furr J. Durham WF. Gladen BC.html. Saiyed HN. DDE. Hanrahan L. Hayes WJ. Atuma S. Klebanoff MA. et al. Biochem Pharmacol 1997. and polythelia among male offspring. Barr DB. Needham LL. Toxicological profile for DDT. 4/21/09 Anderson HA. The effect of known repeated oral doses of chlorophenothane (DDT) in man. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.fda. Ostby J. Cerrillo I. August 2008. Available at URL: http://www.111:349355. Gray KA. dietary intakes of pesticides. Garrett N. Rivas A. Greenfield TA.52:301-309. Epidemiology 2006.1-dichloro2. Food and Drug Administration (FDA). Angerer J. et al. Longnecker MP.71(6):1200-1209. and dichloro(diphenyl)ethylene (DDE). and DDD [online]. Notides AC. The Great Lakes Consortium. lindane (g-HCH). et al. Zhou H.106(5):279-289. Piechotowski I. Katz SH. JAMA 1956. Environ Health Perspect 1998. Lancet 2001. Krause C. and HCB residues in human blood in Ahmedabad.358:110-114. Paepke O.355:7889. Olea N. Calle EE.85:504508. Longnecker MP.cdc. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Brock JW. Zoellner I. Olea-Serrano MF.97(2):178192. September 2002. Seiwert M. Moysich KB. Chemosphere 2004. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Int J Hyg Environ Health 2002. Aune M. Lambright C. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Hediger ML. Willman EJ. Bjerselius R. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Organochlorines and breast cancer risk. Maternal DDT exposures in relation to fetal and 5-year growth. Exposure of women to organochlorine pesticides in Southern Spain. Arnold SF. Koepsell TD.atsdr. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Beard J. Davis MD. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Swanson MK. Crespo J. Baker RJ. Environ Res 2004. hypospadias. Granath F. et al. Darnerud PO. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Kulkarni PK. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT).58:1185-1201. 4/21/09 Gladen BC. dichlorodiphenyldichloroethylene..cfsan. Bull Environ Contam Toxicol 2004. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Environ Health Perspect 2003. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. et al. Chemosphere 2005. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Olson J. Charles MJ. Profiles of ortho-polychlorinated biphenyl congeners. Olson JR. et al. Hum Reprod Updat 2001. Organochlorines in Swedish women: determinants of serum concentrations. Schulz C. Jr. HCH. and other chemicals. Maternal serum level of 1. Sci Tot Environ 2006. Klebanoff MA. Int J Hyg Environ Health 2003. selected elements.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism.17(6):692-700. Am J Epidemiol 2002.72:261265. Savitz DA. Thun MJ. Heudorf U. Parks L. Environ Health Perspect 2004. Talts U. Eriksson P. Glynn AW.gov/~dms/ pesrpts. DDE and shortened duration of lactation in a northern Mexican town. Klebanoff MA. Rogan WJ.53(8):1161-1172. Zhou H. Link B. Needham LL.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Ellis H. Herrman T. Buckland SJ. Cueto C. Effects of environmental antiandrogens on reproductive development in experimental animals. Drexler H.54:1431-1443. Jusko TA. Vena JE. Wolf CJ.

54:1509-520. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Chemosphere 2004. Jr. Demographic and seasonal influences on human serum pesticide residue levels. 96 Fourth National Report on Human Exposure to Environmental Chemicals . 2 Classes of Pesticides. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Stehr-Green. Comparative pharmacodynamics of CYP2B induction by DDT. et al. Thomas PE. Lubet R. Toxicol Appl Pharmacol 1971. J Toxicol Environ Health Part A 1998. 731-915. Handbook of Pesticide Toxicology. Astolfi E. Eds.27:405-421.36:253-589. children and newborn infants.150:981-990. Pollutants in breast milk. Jr and Laws ER. DDE. Pavuk M. Lynch CF. J Toxicol Environ Health 1989. Chlorinated Hydrocarbon Insecticides. Snedeker SM.20(2):186-193. Schecter A. DDE. Cerhan JR. PA. and DDD in male rat liver and cultured rat hepatocytes. Crit Rev Toxicol 2006. Arch Pediatr Adolesc Med 1996. Reddy AB. New York.Organochlorine Pesticides Mariussen E. 1991 pp. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Deichmann WB. Rogan WJ. Chovancova J. Pesticides and breast cancer risk: a review of DDT. et al. and dieldrin. Fox S. Rey AA. Nims R. Vol. In Hayes WJ. Petrik J. Jones CR.109:35-47. Radomski JL. Environ Health Perspect 2001.53:455-477. Inc. Fonnum F. Academic Press. Smith AG.

30) < LOD 5. 72-20-8 General Information Endrin..10 (<LOD-5.20 (<LOD-5. Endrin does not accumulate in body tissues (IPCS.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. rodenticide and avicide. endrin usually is not detected in serum of exposed individuals. fatty infiltration. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. 2008).S. Kavlock et al. 1991)..40-5. population from the National Health and Nutrition Examination Survey. and inflammation (Smith.30 (<LOD-6. or discarded. Ketoendrin is a major photodegradation product (IPCS. Survey Geometric mean (95% conf. anti-12hydroxyendrin. 1981). EPA.S. unlike aldrin and dieldrin. is no longer manufactured in the U.S. which may vary for some chemicals by year and by individual sample. Endrin was used as an insecticide. 1992). largely the result of historical agricultural application or run off from contaminated soils (ATSDR. 1992). An epidemic of acute endrin poisoning. endrin can persist for years.20 (<LOD-5.S.. IPCS.60 (5. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 97 . unless the dose is high and the exposure is very recent. or from contact with contaminated soils and sediments in areas where endrin was applied. endrin has been detected with declining frequency in U.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. 1987). Because it is metabolized so rapidly. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.50) < LOD 5. 1992. total diet surveys (FDA.09 and 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organochlorine Pesticides Endrin CAS No. inhalation or dermal exposure routes. 1996.S. Endrin has been detected in soils. Smith. Endrin was not widely used as a termiticide. manufactured.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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. In the body. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. < LOD means less than the limit of detection. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.50) < LOD < LOD < LOD 5. 1992). characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.10 (<LOD-5. Endrin is absorbed rapidly after ingestion. 1991). Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.40 (<LOD-6. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. All uses of the pesticide in the U. 1979. Hepatic effects of endrin exposure have included necrosis. and occasionally at low levels in sediment and surface waters.8. Depending on soil conditions. Over time. have been cancelled by the U.. a stereoisomer of dieldrin. endrin is converted rapidly to its major metabolite.

with the highest value 6.24 ng/mL (about 6.. EPA has established environmental standards for endrin.gov/toxpro2.020 (<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 . In a small study of Spanish women hospitalized for elective surgery. which may vary for some chemicals by year and by individual sample. Ward et al. IARC has determined that endrin is not classifiable with regard to human carcinogenicity.020 (<LOD-. environmental levels) and health effects of endrin is available from ATSDR at: http://www.. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.Organochlorine Pesticides The U. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. serum levels of endrin were below the limit of detection..020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. 2000).020) < LOD .020 (<LOD-. This finding is consistent with other general population studies (Bates et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th .020 (<LOD-. endrin was detected in 9% of serum samples. Survey Geometric mean (95% conf. Workplace exposure standards for endrin have been established by OSHA.020 (<LOD-. 2004.cdc.S.S.atsdr.020) < LOD < LOD < LOD . Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.html.020 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.24 ng/g of serum) (Botella et al. 98 Fourth National Report on Human Exposure to Environmental Chemicals . 2004)..020-. and the FDA monitors foods for pesticide residues.020) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020) < LOD < 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 .e. Information about external exposure (i.020 (<LOD-. population from the National Health and Nutrition Examination Survey.

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

6-32.4.7) < LOD < LOD 24. population from the National Health and Nutrition Examination Survey. 1988). primarily as a fungicide and seed treatment until the U.3) * * 15. The general population may be exposed to HCB through diet. 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. which may vary for some chemicals by year and by individual sample.1 (14. 100 Fourth National Report on Human Exposure to Environmental Chemicals . HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. 01-02.7 (15.0 (25.6) < LOD < LOD 26.9 (25. wildfowl.6-TCP) (To-Figueras et al.5 (14. breast milk is an additional route of elimination in nursing women. and elimination occurs by renal and fecal routes.0-25.3 (22.7-26.4 (18.2 (13. 2002). and foods with a high fat content.9-15.7 (19.2 (14. The FDA dietary surveys have shown that over time.5-trichlorophenol (2.6) < LOD < LOD 25.7-29.6-26..6) < LOD < LOD 14.9-20.2-15. Survey Geometric mean (95% conf.1) * * 15. EPA cancelled its use in 1984.8-15.2) < LOD < LOD 13.6) < LOD < LOD 24.4.9-32.9-17.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-28. Gunderson. HCB is slowly metabolized.2-31.1 (17.3 (22. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.9 (14.8 (15.0) < LOD < LOD 15.9) < LOD < LOD 28.9) < LOD < LOD 20. HCB has been detected in fewer foods since the 1980s (FDA.0 (18.1-16.9-30.9) < LOD < LOD 16.3 (16.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.1 (14..8 (26.3 (20.4) < LOD < LOD 22.4 (22.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. 2005).3 (14. Urinary metabolites include pentachlorophenol (PCP). and 03-04 are 118.5 (13.4) < LOD < LOD 18.7-16.2 (24.0) * * 15.7-30. or game taken from areas with HCB contamination. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7-15.5-14.. air.4) < LOD < LOD 19.3) < LOD < LOD 29.4 (18. < LOD means less than the limit of detection.2-15.0) < LOD < LOD 15.8 (22.1 (13.6 (24.0-19.6) 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 sediment (Barber et al.5 (13. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. and accumulates in fatty tissues where it persists for years.4. distributes widely throughout the body.9-24.3-22.5) < LOD < LOD 18.3-20. 1976). 2008.7-22.8.0.Organochlorine Pesticides Hexachlorobenzene CAS No.8) < LOD < LOD 27.4) < LOD < LOD 33.9) 19.2 (17. 2.0 (18.2) < LOD < LOD 29.S.0-16.4-16.9 (25.6 (21.6-trichlorophenol (2.5-18.4-15..3-26.7 (27.4.S. and has been detected in soil. Although it is not manufactured as an end-product in the U.5-15.5-33.S.5-14.3 (12. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.6-33.6 (23. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.4) < LOD < LOD 14.7) 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 * * 16.9) < LOD < LOD 19. water.1-20. and 7. 1997).0) < LOD < LOD 24.2 (14. respectively.9) < LOD < LOD 15. particularly by consuming fish.7 (15. HCB is well absorbed after oral administration.7) * * 14.3) < LOD < LOD 20.0 (14.4) < LOD < LOD 23. 31.7-16.7-21.4.4 (11. see Data Analysis section) for Survey years 99-00.5-15.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.6-19.3) 24.6) < LOD < LOD 26.6-44.9 (23.5-TCP) and 2.1) < LOD < LOD 15.9) < LOD < LOD 20. Therefore.

cdc.174-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. reproductive and developmental toxicities.100) < LOD < LOD . HCB levels were generally below the limits of detection Serum Hexachlorobenzene (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.182 (.175) < LOD < LOD .130) < LOD < LOD .111-. and liver and thyroid cancers (ATSDR. Schmid.. immunologic abnormalities.088-.079 (.125 (.094 (.095) < LOD < LOD 75th < LOD < LOD 90th * * . Survey Geometric mean (95% conf.129) < LOD < LOD . acute doses produce central nervous system depression and seizures.118-.143-. anorexia.atsdr.132) < LOD < LOD .094) < LOD < LOD . EPA at: http://www. and many died before 2 years of age (Peters et al.095 (.090 (. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.145-.065 (.123 (. as well as hypertrichosis.191 (.090-.083) < LOD < LOD . In humans.122) < LOD < LOD .epa.099) < LOD < LOD . More information about external exposure (i. thyromegaly. The U.118) < LOD < LOD .069) < LOD < LOD .127-.095-.157-. 1960).141) < LOD < LOD .118-.113-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .092 (.102 (.081 (.114-.145-.171 (.126) .082-.090 (.090 (.092 (. With chronic exposure.135-. This condition.160 (.147-.179 (. 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.098 (.152) < LOD < LOD .064 (.097 (.115 (.120 (. HCB interferes with normal heme synthesis.196) < LOD < LOD .gov/toxpro2.089-.163) < LOD < LOD . arthritis. 2002).097) .157 (.072-.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . IARC classifies hexachlorobenzene as possibly carcinogenic to humans. EPA has established a drinking water standard.176) < LOD < LOD .060-.186 (.077-.173) < LOD < LOD .e.. environmental levels) and health effects is available from the U.190 (.069) * * .088-.225 (.088-.095) * * .S.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 * * .156 (.092-.155) < LOD < LOD .178-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.081-.163-.111) < LOD < LOD . and the FDA has established a bottled water standard for HCB.087 (.078 (.203) < LOD < LOD .095 (.140 (. which may vary for some chemicals by year and by individual sample.107) < LOD < LOD .167 (.159-. population from the National Health and Nutrition Examination Survey. very high. Infants were exposed transplacentally and through breast milk.099) < LOD < LOD .086) < LOD < LOD .169-.062-.123 (.226) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.123 (.107-.073-. Biomonitoring Information Serum concentrations reflect the body burden of HCB.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * . Fourth National Report on Human Exposure to Environmental Chemicals 101 .086-.S.099) < LOD < LOD .148-.S. Chronic feeding studies in animals have demonstrated kidney injury.html.121 (. ACGIH has developed workplace exposure limits for HCB.gov/pesticides/ and from ATSDR at: http://www. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.085) * * .085-.258) < LOD < LOD .109) * * .086-. and weakness.163 (.Organochlorine Pesticides chemical.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.176-.097) < LOD < LOD .092 (.147 (.104 (.102) < LOD < LOD .203) < LOD < LOD .091-. 1982.114-.089-.

. Link et al. levels. Schwartz JM. 2002. Can J Biochem 1976. HCB detection in serum also was proportional to age. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Becker K.111:349355. Gocmen A. 2002. Int J Hyg Environ Health 2002. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Bertram HP.. Jones D. HCB levels were directly related to age. Krause C. In the 1976-1980 NHANES subsample. Herrman T.. 4/21/09 Barber JL. van Wijk D. Laliberte C.gov/ toxprofiles/tp90.9% of participants had quantifiable levels (Stehr-Green. Atuma S.71(6):1200-1209. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. FDA total diet study. trends and processes. Over the past two decades. Otero R. Jones KC.. Lackmann. September 2002.. and other chemicals. Food and Drug Administration (FDA). Ozalla D. As a result of the lower limit of detection in NHANES 2003-2004. 1999). et al.135(4):400404. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. 2002). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.58:1185-1201. Arch Neurol 1982. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. and the geometric mean concentration of HCB in whole blood was 0. 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. however. Zoellner I..110(8):835-838. Fenster L. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. In a representative sample of the 1998 German adult population. Bradman A. Holland NT.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. The metabolism of higher chlorinated benzene isomers. Eskenazi B. selected elements. Bertram et al. Environ Health Perspect 2002. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. 2002. 2002. Herrero C. Ayotte P. but overall. Aune M. distribution.cfsan. 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. Dewailly E. 2003). Hexachlorobenzene in the global environment: emissions.. Organochlorines in Swedish women: determinants of serum concentrations. Sala M. Sci Tot Environ 2005. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Barr DB. Bjerselius R.205:297-308. Darnerud PO. 1989).. 2002) and among children (Link et al.html. Biomonitoring of persistent organochlorine pesticides. Bryan GT. Arch Dermatol 1999.44 mg/L. 2005). 2005. Muller C. et al. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Lawrence River (Quebec. Santiago-Silva M. Gabrio T. Muckle G. April 1982 to 1984. IARC Sci Publ 1986. Toxicological profile for hexachlorobenzene update [online]. Dogramaci I. Piechotowski I. Lepom P. Lecha M. Biol Neonate 2002. Schulz C. Peters HA.54(3):203-208.html. Link B. 2005). Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Safe A. Gunderson EL. 1986.17:388–399. Kemper FH. Available at URL: http://www. et al. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Seiwert M.. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. J Assoc Off Anal Chem 1988. Dallaire F. Available at URL: http://www. Cripps DJ.. 2006). Glynn et al. dietary intakes of pesticides.81(2):82-85. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Lackmann GM. Paepke O. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.gov/~dms/ pesrpts. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Health Perspect 2003. et al.fda.cdc. In Spain.atsdr. J Exp Sci Environ Epidemiol 2007. only 4.77:173182. Reference values updated.349:144. Lackman. Kohli J. more HCB levels were quantified. Chemosphere 2005. Kaus S. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Canada). Sweetman AJ.. Bradman et al. Granath F. August 2008. References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Glynn AW.39(12):744-749. respectively.

Sala M.27:405-421. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.263:397-398.105(1):78-83. J Toxicol Environ Health 1989.Organochlorine Pesticides Schmid R. Otero R. N Engl J Med 1960. Demographic and seasonal influences on human serum pesticide residue levels. Environ Health Perspect 1997. et al. To-Figueras J. Stehr-Green. Cutaneous porphyria in Turkey. Rodamilans M. Barrot C. Santiago-Silva M. Fourth National Report on Human Exposure to Environmental Chemicals 103 . PA.

9-14.1) 12.2 (50. However.5 (24.87 (9.5-29.9-21.8) 95th 68.2) 62.20-16. soil.0) 41.0-34. HCH isomers are lipophilic.0-23.7) 97.8-68.6 (10.7-96.4-73.6 (16.S.9 (9. Technical grade HCH is a mixture of all four isomers.9-24. The other isomers can be formed during the synthesis of lindane.4) 44.8.8 (64.1-16.8 (23.6) 35.7-69.2-20. 608-73-1 beta-Hexachlorocyclohexane CAS No.0) 35.9-81.8-16.8 (33. It is no longer produced or sold in the U.4-111) 84.7 (29.0) 7. gamma.S.7-69. beta. 319-85-7 gamma-Hexachlorocyclohexane CAS No.1 (30.8) < LOD 10.2-46.6) 16. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.9-56.4-45. particularly alpha and gamma have been detected widely in air.8 (32. In 2006.6) 653 758 589 1240 1533 1370 20 years and older 10.0-70.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.1 (9.6-47.3) 25.8-19. 01-02. population from the National Health and Nutrition Examination Survey.2-42.7 (62.6 (40. commonly known as lindane.5 (16. 6.66-12.8) * * * * * * 15.5 (8.1-32. **In survey period 2001-2002.1 (12.2) 142 (99.0) 17.1) 71.1-36.7) 56.0) 71. EPA cancelled agricultural uses of lindane (ATSDR.4) < LOD 9.4) < LOD < LOD < LOD 46.70-19.6) 18. interval) 9.5528.6) 50.4) 11. and 7.7) 23. < LOD means less than the limit of detection.30-11.3) 34.0 (33.8 (21.2-22.9-51.5) 22.2 (18.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.5-123) 49.3) 37.9 (30.3) 51.0 (<LOD-12.3 (42.60-13.9 (40.7) 18. 2005).6-89.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.7-26.50) 8. Lindane has a half-life of about two weeks in soils and water. HCH isomers.8-87.5) 14.7 (<LOD-16.2 (9.2) 9. 58-89-9 General Information Hexachlorocyclohexane (HCH).1 (9.7) 32.8-199) 134 (85.1) 31. exists in several isomeric forms.4 (50.0 (14.7 (53.8 (10.8) 39.2-17. The gamma isomer.0 (37.8) 52.6-18.4 (11.1-27.2-98.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. which may vary for some chemicals by year and by individual sample.0-70.7 (30.8 (17.9-178) 48. see Data Analysis section) for survey years 99-00.3 (62.8) 7.9 (62.3 (13.6-37. environmental levels declined.9 (32.6) 36.1-37.90) 7.3-56.1 (16. and 03-04 are 9.4 (12.S.6-62.80 (6.70 (8. See the section “What’s New” at the beginning of this Report for details.46-11.4) 51.5) 90th 42.5) 11.0-20.4-50.6 (17.6-14.61-12. including alpha.3 (26.9 (50.70-12.7) 27.8-54.0-111) 70. containing about 64% alpha and 10%-15% gamma isomers. formerly referred to as benzene hexachloride.5) 40.7 (35.4) 27.76.4) 21.7-166) 70.6 (33.2) 36.1) 13.6 (22.7) 73. 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.89 (<LOD-9.5 (43.9) 17.8) 12.9) 81.8) 27.2-87.1-49.90-8.0 (8.36. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-135) 69.2-67.2 (48.43 (<LOD-9.5 (14.1 (21.7-20. water.5) 16.4) 10.0) 8.1 (18. and delta. the U.1 (27.6-42.7-96.2-55.4) 901 1067 952 992 1224 1007 Females 11.1) 12.8 (9.1-32.9) 15.3-85. and have been used either as fungicides or to synthesize other chemicals. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.3 (42.0 (35.3-38.7 (13.7 (25.04-10. As pesticide applications of HCH were increasingly restricted or eliminated.2 (31.5 (37.9 (26.9 (11.70 (6. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.1 (11.2 (34.1-15. so they can accumulate in fatty tissues of animals.68 (<LOD-10.0 (19.9) 45.0-21.7) 10.5) 29.90-8. each result has been multiplied by 1.3) 14. and sediment as a result of historic production and use.2-52.6) 47.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.2 (29.4 (8.2) 13.6-20.4 (16. 2005).5 (11.7) 10.Organochlorine Pesticides Hexachlorocyclohexane CAS No.56-12.5) 67.80 (<LOD-14. 104 Fourth National Report on Human Exposure to Environmental Chemicals .4 (52.4) 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. respectively.

047-.070-.167 (.103 (.470) .120 (.410-.190) .050 (<LOD-.089-.690) .S.068-.173-.814) .390 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.308-.130-.070 (.450) . 2008. each result has been multiplied by 1.290 (.410) . 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.118 (.140) .480 (..200-.290) .080) * * * * * * .096) .080-.234 (.331 (.350) .180-.460 (.382-.200 (.580 (.083 (. 1977).139 (.086) < LOD < LOD < LOD < LOD < LOD < LOD . the serum half-life was about 20 hours among children (Ginsburg et al.250) .120 (.140) . and seizures. ingestion.100) .Organochlorine Pesticides exposure to HCH is through the diet.190-.372 (.062 (.S.092 (.350 (.050-. After dermal application of lindane 1% lotion.050-..360 (.110-.091) .100-.360-.048 (<LOD-. and nephropathy developed (IPCS.065 (.140 (.220 (.214) .710) .340) .103-.100 (. Rogan.131-.080 (.070-.050 (<LOD-.210-. for lindane.310) .090 (.050 (.067) .073-.. paresthesias.661) 901 1067 952 992 1224 1007 Females .290 (.400) .050 (.680) .080 (.118-.160-. See the section “What’s New” at the beginning of this Report for details.380 (.250-. probably by blocking inhibitory neurotransmitters in the central nervous system.390-.200-.056-.051-.069) ..521 (.330 (.450 (.37) 1.190-1. EPA has established a drinking water standard.560 (.190) .412 (. U.280-.254) 95th .175 (. population from the National Health and Nutrition Examination Survey.050) .100) .120-.210 (.078 (.250-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . When animals were chronically fed lindane at high doses.120-. 1971.290) .090 (.080-.057 (<LOD-.294-.570 (.244-. or dermal exposure.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .103) 90th .319) .360) .250 (.077) < LOD .081-.146-.098 (.5528.340-.330-.560) . Saxena et al.120-.160 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.080) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .700) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. 1986).220) .297-.404) .051 (<LOD-.057-.174) .580-1. resulting in a half-life of about seven years.250 (.501) . Distribution is mainly to fatty tissues.170-.320 (.150-.077) < LOD . enlarged livers.058 (<LOD-.100 (.067 (.01 (.420-.191-.160) .040-.600) .620-1.057-.150) . 1981).125) < LOD < LOD < LOD . ataxia.410) .150 (.260) .070) .090-. and FDA has established a bottled water standard and food residue tolerances for lindane. tremors.222 (.220-.221-. from 6% of samples in 1982-1984 to 2% in 1994 (FDA..S.210 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.442 (. 1983).080-.230-.100-.059-.240-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.050-.310 (.120) .281 (. respectively. **In survey period 2001-2002. The beta isomer accumulates in fatty tissues and is metabolized more slowly.480) . and memory loss (Nigam et al. HCH isomers are absorbed after inhalation.120 (. 2002). interval) .072 (.083) .070 (.210) .130 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .150) .310) .090 (.460) .100-.587) 653 758 589 1240 1533 1370 20 years and older .120) .250 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.110) .05) .110) .056-.260-. Workers who directly handled HCH have complained of headache.470 (.620) .287 (.840) .270 (.290 (.510) .280-.300-.260) .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.410 (.110) .240 (.450-.400) .124-.089) . 1996.130) .050-.305) . Gunderson 1988).060) .070-.064) . which may vary for some chemicals by year and by individual sample.064 (.216 (. OSHA and ACGIH have established workplace standards and guidelines. hepatic enzyme induction.065 (.220-.170-. The U.480 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.370-.191-.140) .32) .062 (.144 (.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 .910 (.119) .

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

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

Rey AA. et al. Environ Res 2004. Saiyed HN. Bai KM. et al.html. Zoellner I. dietary intakes of pesticides. gov/toxprofiles/tp43.205:297-308.48:127-134. Gunderson EL. Biomonitoring of persistent organochlorine pesticides. Available at URL: http://www. Ellis H. Rev Environ Contam Toxicol 1991. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Potischman N. Angerer J. et al. Rogan WJ. Brinton LA. Bull Environ Contam Toxicol 2004. Bjerselius R. J Pediatr 1977. available at URL: http://www.cfsan. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Visweswariah K. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.120:1-82. Kutty D.htm. Lepom P. Heinrich R.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Buckland SJ. et al.71(6):1200-1209. Seiwert M. Sturgeon SR.html. Needham LL. Atuma S. and other chemicals. Astolfi E. Available at URL: http://www. Kaus S.150:981-990. Rivas A. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Raju GS. Garrett N. Organochlorines in Swedish women: determinants of serum concentrations.9(4):417-424. Int Arch Occup Environ Health 1986. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Demographic and seasonal influences on human serum pesticide residue levels. Falk C. Bates MN. Link B. Arch Toxicol 1981. Cancer Causes and Control 1998. VI. Arch Pediatr Adolesc Med 1996. Nigam SK. Toxicological profile for hexachlorocyclohexanes update [online]. Chemosphere 2005. 4/21/09 Anderson HA. Placental transfer of pesticides in humans. Glynn AW. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Bottimore DP.58:1185-1201. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Needham LL.111:349355. Siddiqui MKJ. Levels of DDT. Olson J. et al. Zaidi SS. Exposure of women to organochlorine pesticides in Southern Spain. Patterson DG Jr. Majumder SK.72:261265.20(2):186-193. J Assoc Off Anal Chem 1988.atsdr. org/documents/jmpr/jmpmono/2002pr08. Rothman N. Karnik AB. Saxena MC. Krishna Murti CR. Herrman T. J Toxicol Environ Health 1989.91:998-1000. Wood PH. Environ Health Perspect 2003. Becker K. India. Maass R. HCH. Metabolism of gammahexachlorocyclohexane in man.106(5):279-289. et al. and HCB residues in human blood in Ahmedabad. Hanrahan L. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Chemosphere 2004. Kashyap R. Brock JW. Toxicol Appl Pharmacol 1971. Bhargava AK. 4/21/09 Ginsburg CM. Kulkarni PK. Absorption of lindane (g benzene hexachloride) in infants and children. Radomski JL.27:405-421. Int Arch Occup Environ Health 1983. Lowry W.57(4):315-320. August 2008. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Occupational exposure to hexachlorocyclohexane. Int J Hyg Environ Health 2002. April 1982 to 1984. The Great Lakes Consortium.cdc. Environ Health Perspect 1998. Granath F. Bhatnagar VK. 4/21/09 Kutz FW. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.inchem. Darnerud PO.gov/~dms/pesrpts. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Krause C. Piechotowski I. Burse VW. Schulz C. Olea-Serrano MF. Lindane. 2002. Olea N. Cerrillo I. children and newborn infants. PA.52(1):59-67.96:34-4Food and Drug Administration (FDA). Gabrio T. August 2005. Stehr-Green. et al. Needham LL.fda. selected elements. International Programme on Chemical Safety (IPCS).54:1431-1443. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Aune M. Deichmann WB. FDA total diet study. Botella B. Reisch JS. Paepke O. Pollutants in breast milk. Crespo J.

1995). 10. after which it is widely distributed in the body and stored in fat.8 (12. animals. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. Mirex is absorbed through the skin and from the gastrointestinal tract.6.5-291) 11.90-29.7 (<LOD-47.3 (15.70 (<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. soil. Mirex can cross the placenta and be excreted in breast milk. and foods. aquatic organisms. and 03-04 are 14. 01-02.0 (12.2) 51.7) < LOD 66. 1985. (Kutz et al.70-40.S.5 (<LOD-115) 153 (30. Fourth National Report on Human Exposure to Environmental Chemicals 109 .1 (8.6 (<LOD-108) 9. In studies conducted in the 1970’s and 1980’s. which may vary for some chemicals by year and by individual sample.5. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.Organochlorine Pesticides Mirex CAS No..5-82. 1991).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 16.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 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 13.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.1 (13.5 (<LOD-42.7) 8.40 (<LOD-13.10 (<LOD-15. water.4) < LOD 63. it is a highly persistent chemical in the environment.8 (<LOD-73.6 (<LOD-31. respectively. where it has a half-life of 12 years.1 (<LOD-65.8) < LOD 15.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Formerly.3 (15. 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. mirex was detected in human adipose samples.3-225) 15.. Mirex has been detected in air.5 (9.S.4 (8.6 (<LOD-23.5-425) 40.6-305) 15.0 (14.S. or pesticide application. and 7. 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. disposal. since 1977. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.4-230) 18. < LOD means less than the limit of detection.10-37.7 (12.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.8.2 (7. sediments.2-230) 13.S.0 (<LOD-108) < LOD < LOD 50. Occupational exposure is limited to workers at sites where mirex contamination is present. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.4) < LOD 15. Mirex binds strongly to soil. see Data Analysis section) for Survey years 99-00.S.6) < LOD < LOD < LOD < LOD 71. especially those from persons living in the southeastern U. Mirex is not metabolized in the body. resulting in exposure to newborns and nursing infants.0-374) 11. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Some states and the U.70-24.6) 9. where it was applied directly to soil and by aerial spraying. 2385-85-5 General Information Mirex has not been produced or used in the U.

110 Fourth National Report on Human Exposure to Environmental Chemicals .gov/toxpro2.e.02) .106) < LOD .090-1.690) .S. 2004).450) 1.064 (<LOD-. Smith.610) < LOD < LOD < LOD < LOD ..110 (<LOD-. reproductive toxicity included decreased fertility and testicular damage.106 (. The geometric mean mirex levels of the Inuit mothers were 8.79) .41) .8. The U. which may vary for some chemicals by year and by individual sample.7 ng/g of lipid.090 (<LOD-. population from the National Health and Nutrition Examination Survey.090-1.430 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.112 (.08 (.268) < LOD .79) .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 . and 2003-2004 subsamples. Laboratory animals fed high doses developed liver enlargement and liver tumors. interval) Selected percentiles ( 95% confidence interval) Sample 95th < 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.100 (<LOD-.077 (<LOD-. Biomonitoring Information In the NHANES 1999-2000.cdc.053-.090 (<LOD-.73) .170) < LOD .html. Survey Geometric mean (95% conf.470) .080-1.084) * * * 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 . 2001-2002. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.220) . 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.093 (.370 (.102) < LOD < LOD < LOD < LOD . 1989). 1995.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 7.37) .090 (<LOD-.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .059 (<LOD-. 2005). In samples obtained between 1994 and 1997.140 (<LOD-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.055-.080-1. EPA has established environmental standards for mirex. IARC classifies mirex as possibly carcinogenic to humans.089-. serum mirex levels were generally below the limits of detection (Stehr-Green.S.Organochlorine Pesticides exposures are unknown. 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.079 (<LOD-. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al. environmental levels) and health effects is available from the ATSDR at: http://www.170-3.. 1991).atsdr.052-.470 (.635) < LOD .054 (<LOD-.310 (.92) .510) < LOD < LOD . In addition.470) . and 4. More information about external exposure (i.062-.090-1.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . as well as in a subsample of NHANES II (1976-1980) participants. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. 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.108 (.220 (<LOD-.256 (.450 (.100 (<LOD-.410 (.070-1..

Available at URL: http://www. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Kutz FW.330:55-70. Stroup CR. Strassman SC. Wood PH. et al. dichlorodiphenyldichloroethylene.Organochlorine Pesticides effect. Leininger CC. Swanson MK. In Hayes WJ. Carra JS. 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. PA. Vol. Profiles of ortho-polychlorinated biphenyl congeners. Environ Res 2005. Moysich KB. Eds. References Agency for Toxic Substances and Disease Registry (ATSDR). Vena JE. Odland JO. Bottimore DP. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.atsdr. J Toxicol Environ Health 1985. J Toxicol Environ Health 1989. Watts DL. Jr and Laws ER.27:405-421.cdc.html. Hansen JC. New York. 731-915. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Toxicological profile for mirex and chlordecone [online].gov/toxprofiles/ tp66. Chlorinated Hydrocarbon Insecticides. August 1995. Gilman A. 1994-1997 organochlorine compounds. 4/21/09 Bloom MS. Olson JR. Van Oostdam JC. Sci Total Environ 2004. 2 Classes of Pesticides. Handbook of Pesticide Toxicology. Rev Environ Contam Toxicol 1991. Smith AG. 1991 pp. et al. hexachlorobenzene. Dewailly E. The human body burden of mirex in the southeastern United States. Stehr-Green. Circumpolar maternal blood contaminant survey. Jr. Kutz FW. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Chashchin V. Inc. Academic Press.15:385-394.97(2):178192.120:1-82.

40 (2.20-71. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (.50 (2.0 (4.0) < LOD 21.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.42 (<LOD-8.71 (<LOD-8. 2. public drinking water systems did not detect 2.4.63) 18.920-3.00-3.30) < LOD < LOD < LOD < LOD < LOD 1.10-3.7. which may vary for some chemicals by year and by individual sample. Historically. recent sampling of U.6-trichlorophenol (2.950 (<LOD-1.20) < LOD 90th 5.4.0) 2.00-3. 1976).71 (<LOD-8. Both chemicals have been detected in air.80 (2. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.940-3. Occupational exposures.5-trichlorophenol (2. Formation of 2.5TCP and 2.00-8.80) < LOD 1.6-TCP were used as intermediates in the production of certain pesticides.0) 2.20) < LOD 5.0) < LOD 5. EPA.6-TCP in any of the samples (U. Survey Geometric mean (95% conf.4. 2006).4.50-16.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .980-3.0 (5. 2.30 (. surface water.4.4.0 (3. 1999).0) 2.60-18.4.50-63.4.0) 2.0) 2. are metabolites of several organochlorine chemicals. hexachlorobenzene. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.0 (4.0) < LOD 5.0) < LOD 5.4. usually at herbicide production or waste incineration facilities.0) < LOD 11. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) 2.03) 9. Trichlorophenols are no longer manufactured commercially. and sediments.31 (<LOD-9.40 (2.30-27.4.40) < LOD 6. 112 Fourth National Report on Human Exposure to Environmental Chemicals .8) 21.20) < LOD 1..40 (1.40 (2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.9 and 0.30-40.50) < LOD 1.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.0) 14.60) < LOD 8.5-TCP) and 2.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.30) < LOD 4. soils.0 (3.0 (4.0) < LOD 11.00 (3.0) 5. Such workers would probably Urinary 2. population from the National Health and Nutrition Examination Survey.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.00 (2.60-8.9 (<LOD-121) 9.7) 24.40) < LOD 4.30-27.50-25.40) < LOD 1.19 (<LOD-6.57 (<LOD-15.60 (2. 95-95-4 2.9.20-36.30-11.80-41.3.30-3.20 (4. however.50 (1.6-TCP).S.60 (.40-18.980-3.Organochlorine Pesticides 2.90-33.S.40 (.6-Trichlorophenol CAS No.72) < LOD 1.40 (1.S.42 (<LOD-12. may occur by inhalation or dermal routes.0 (8. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.27) 696 661 521 696 603 939 Limit of detection (LOD.40 (2.4. < LOD means less than the limit of detection.5-Trichlorophenol CAS No.30-44. including hexachlorobenzene and hexachlorocyclohexanes.900-2. and polychlorinated benzenes (Kohil et al.30-27. other organochlorines.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.80 (1.5-trichlorophenol.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60 (4. Exposure to trichlorophenols also may result from metabolism of lindane. 1999).40-11. 2.50 (.

6-TCP as reasonably anticipated to be a human carcinogen.32) < LOD 4.html..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 1.37) 16.820-2.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .17) 9.75 (3.e.36 (1.0) 7.6-TCP had increased rates of hepatic tumors.27-17.82 (<LOD-32.4.2 (2.9) 12.62-20. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.44 (.19-4.5-TCP and limited for 2.. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.3 mg/L reported in German adults aged 18-69 years (Becker et al.81 (<LOD-9.0 mg/L.5) < LOD 12.7 (4.24-11.79-4.53-3. Laboratory animals chronically fed high doses of 2. Radon et al.9 (5.4. In the same 2-6 year old children.6) 4.28-25.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.6-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.05-17.5-TCP or 2. environmental levels) and health effects is available from ATSDR at: http://www.19-12. furans. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.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. 2003.8) < LOD 9.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.53-3. the 95th percentile urinary 2.6-TCP levels at the 95th percentile were up to eight times higher than 3.49 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.00-29. population from the National Health and Nutrition Examination Survey.6) 4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).1 (<LOD-58.57 (<LOD-7.4) 5..60-3.69-18.2) < LOD 5.5-TCP nor 2.24) < LOD 5.4.4.75 (<LOD-6.83-12.57 (<LOD-7. in addition to dioxins.50) < LOD 2.4.. However.47-8.00) < LOD 4.4) < LOD 3.68-4. NTP classifies 2..S.16 (.gov/toxpro2. Neither 2.44 (1.64 (4.37-11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. At lower doses.68 (<LOD-8.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.43) < LOD 12..24) < LOD 6. 2003). was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.20-6.00-19.24 (3.29 (1. the 95th percentile urinary 2.15) < LOD 2. and other chlorinated compounds.Organochlorine Pesticides be exposed to mixtures of chlorophenols.46 (1.4. Survey Geometric mean (95% conf. as being possibly carcinogenic to humans. leukemias.78) < LOD 1..4 (6.80 (1. which includes trichlorophenols.05-8.13-13.1) 2.920-2.57 (3. 1995) were similar.4.6) 4.3 (5.74) 11.5-TCP.4. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. More information about external exposure (i.02-3.55 (4.31) < LOD 2.4.90 (4.69 (2. The 95th percentiles for 2. Among 6-11 year old children in NHANES 1999-2000.. Human health effects from 2. animals showed hepatocellular abnormalities.93-11.4.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.73 (<LOD-8. Fourth National Report on Human Exposure to Environmental Chemicals 113 . 1989).95 (3.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2. 1995) and up to 19 times higher than the 95th percentile value of 1. urinary 2. 1989). and lymphomas.33) < LOD < LOD < LOD < LOD < LOD 2.980 (<LOD-1.4.88-16. 7.86 (3.67 (1.5) 11.2) 2.67 (1.02) < LOD 7.4.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.78 (3. IARC classifies combined exposures to polychlorophenols.atsdr.8 (5.4.4) < LOD 3.8) 4. 2004).43 (2.6-TCP. 2003). Urinary 2..cdc.78-19.16) < LOD 90th 5.

89-6.6-TCP than are found in the general population.80 (3.7) 21.95) 3.78 (2.40 (2. 0.2) 12.0) 14.36-5.10-3.95-6.0-43.01-6.0-38.70) 5.91-4.5-TCP or 2.0-41.40-2.54) 6. 1991).4 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-68.0 (12.4.85 (2.25-11.2-0.0) 19.87-14.40-2.8-13.0) 13.30-2.6TCP causes an adverse health effect.0-18. Survey Geometric mean (95% conf. Urinary 2.4.08 (2.4.52-3.70 (2.74-3.99) 6.0 (14.18-3.57 (<LOD-2.5-46.84) 2.3) 23. Urinary 2.8) 32.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.0 (15.6 mg/g creatinine) and 2.8-15.95 (4.23-2.7) 33.2 (14.80-6.4.60-3.0) 10.3.0) 9. 2003).6) 26.10) 2.58 (1.70 (2.10) 6.5-TCP (0.09-7.4 (10.0) 12.0) 17. population from the National Health and Nutrition Examination Survey.20-6.0) 19.18) Selected percentiles ( 95% confidence interval) Sample 95th 25..45 (2. Biomonitoring data will also help scientists plan and conduct research about 2.1) 16. was about six times lower than the median urinary levels for males in this Report (Radon et al.5-TCP or 2.0 (20.0) 13.4.0) 9.59) 4.6 (11..4.40) 3.47 (3.80-7.5-TCP and 2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.40) 4.07 (<LOD-3.0 (8.0) 6.00-4.0-44.32) 3.6TCP values.4.40-4.0) 10. similar to the limit of detection for this Report (Anderson et al.0-38.40-14.1 (10.70) 5.90 (4.85) * 3.60-21.70-3.7 (9.00 (4.0) 14.5-TCP and to the median 2..0 (15.90 (3.45-9.0 (14. In harbor workers exposed to chlorophenol-contaminated river silt.98-7.48-26.36 mg/g creatinine.70-6.23) 3.6 (12.0) 13.60) < LOD 5.90) 2.1-25.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.68 (<LOD-2.44) 75th 4. interval) 2.00-21.60 (3.28) 24. Biomonitoring studies on levels of 2.32) * 3.10 (5.52 (2.0 (20. for males in NHANES 19992002 (Agramunt et al.4.5-TCP or 2.00 (1.0) 17.6-TCP exposure and health effects.31) * 2.65 (5.0 (16.0-50.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.35-3.3) 20.9) 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 2.0 (13.4.4. the median urinary 2.60) 6.14 (2.7 mg/L.0 (9.40) 2.8 (9.31 (3.80 (2. Mean values of 2. 114 Fourth National Report on Human Exposure to Environmental Chemicals .33-4.45 (5.7 (13.0 (14.5-TCP level of 0.S.76) 3.9 (13.59-6.5 mg/g creatinine) were similar to the limit of detection for 2.5-TCP and 2.20-3.20 (3.2) 25.7-3.04) 2.0-54.00 (2.6) 21.90-8.0) 11.4.6-TCP (0.30) 4.78 (2.1 (8.5-TCP or 2.0) 7.60 (2. respectively. Finding a measurable amount of 2.23) 2.10-2.0) 13.09) 15.58-3.46-3.65) 15.51-12.12) 2.6-22.32-4.98-11.89 (3.40) 2.24 (2.4.4.0 (11.0 and 1.79 (5.63) 90th 15.45) < LOD 11. 1998).53) 4.4 (9.0) 11.67) 4.0 (6.4 (17.06) * 2.3) 37.30-11.50-5.60-37.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002..6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2. 2004).4-17.0) 15.56 (3.3 (11. < LOD means less than the limit of detection.7-16.53) 2.3 (11.10-3.8) 18.74 (2.0 (8. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.70) 1.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.6-19.4.4.70) 3. which may vary for some chemicals by year and by individual sample.8-24.6-17.6-TCP in urine does not mean that the level of 2.36 (1.80 (2.0-37.02) 2.80-20.20 (3.66 (8.60 (3.9) 13.0 (6.75 (8.20) 4.67-12.80) 1.26 (2.4.80-25.4.3-26.0) 7.55-3.73-9.70-6.50 (2.6-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.9 (11.6-TCP level.0 (7.28) * 2.40 (2.0 (6.30-33.40-7.4.40-32.3-17.9) 694 677 519 696 602 931 Limit of detection (LOD.72-10.20-23.0 (4.30-2.49 (6.4.4.69 (3.92 (2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.

9) 7.23 (1.20-2.9) 8.17-4.43 (<LOD-2.7) 6.00 (2.89-2.47-5.Organochlorine Pesticides Urinary 2.02 (1.49-3.50-8.06) 11.8) 19.14-2.87-7.05 (3.10-9.78) 90th 12.51 (2.6 (10.4 (11.33) * 2.4 (12.13 (1.83-6.10) 4.5-28.38) 22.5 (7.62-15.2 (13.53) * 2.65) 2.6 (5.63) 4.91 (3.9) 19.9 (9.11) 10.44 (3.5) 11.68) 2.72-16.82 (8.29-4.18-4.98 (1.88) 4.38 (2.83-5.02) 3.19-5.4) 9.79-17.67-17.0) 8.26-13.63) * 4.6 (9.87 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18-2.17) 2.4) 4.5) 11.9-32.63 (2.78) 2.52) 2.51-21.9 (9. Survey Geometric mean (95% conf.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 2.15 (6.0 (11.68) 2.7-36.38 (4.2 (8.91 (7.27-9.4) 8.88) * 2.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.6 (9.8 (7.15 (1.65-21.63-13.09-3. interval) 2.38-5.6) 12.33 (7.88) 4.16-10.98) 10.71 (3.3 (9.5) 8.81-9.40 (2.72) 32.52) 2.60-2.96) < LOD 4.52 (3.22-2.77) 2.50 (2.9-29.1-21.33-2.76) 1.17) 13.8 (8.66-4.33 (1.87-6.43-7.46-14.90) 2.48-2.82 (3.4.88 (2.1 (8.42 (2.53) 4.35 (3.6) 13.S.83 (3.49) 4.1) 14.99-2.25 (3.9-34.41-6.7) 25.63-15.88) 1.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.22 (1. Fourth National Report on Human Exposure to Environmental Chemicals 115 .8) 21.73-22.2 (12.43 (2.2 (7.63 (<LOD-2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.05 (6.88-7.04-2.06) 4.21-11.6 (12.25-17.55-2.10 (6.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.25-2.25 (3.32 (2.6 (22.23) 4.06-2.53-11.1) 11.41 (3.6-31.22 (3.40 (7.81) 2.76-8.0 (6.32-19.9) 8.7 (14.8) 12.00) 4.0) 10.22 (<LOD-2.29 (6.83-6.6 (6.3) 8.87) 2.00) 4.58 (4.56 (7.87) * 2.82-2.30-2.77-4.94-13.60 (4.26 (6.54 (2.3-23.0 (9.82) 2.22-9.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.52 (5.08-2.70-9.53 (3.01 (3.65) 18.91-2.73) 5.5 (8.28-4.5) 9.29-4.00 (3.51) 18.04-16.56-5.88) 5.76) 2.1-32.78 (2.42) 2.14-13.95-2.92) 4.3-37.1 (13.76) 4.65-2.13-6.56) < LOD 11.59 (2.5) 12.8) 11.89) 10. population from the National Health and Nutrition Examination Survey.6) 8.9-64.25-15.90 (1.24 (1.2) 19.5 (10.75) 75th 4.

S. Urinary excretion of chlorinated phenols in saw-mill workers.EPA). Jarvisalo J. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Hill RH Jr. Needham LL. The analysis of occurrence data from the first unregulated contaminant monitoring regulation (UCMR 1) in support of regulatory determinations for the second drinking water contaminant candidate list [online]. Luotamo M. December 2006 Draft. Head SL.106(5):279-289. Safe A. U. Fast DM. Seifert B. 4/21/09 Agramunt MC. Can J Biochem 1976. Wegner R.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). The Great Lakes Consortium. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.54(3):203-208. Kohli J.146:83-91. Lindroos L. Domingo JL. Aitio A. 206:15-24. Gregg M. Bailey SL. Anderson HA. Pekari K. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Environ Res 1995. Seiwert M. Environ Health Perspect 1998.epa. Arch Environ Contam Toxicol 1989. To T. Domingo A. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Holler JS. Falk C.18(4):469-474. Kaus S. Corbella J. Int J Hyg Environ Health 2003. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Toxicol Lett 2003. Olson J. July 1999. Schulz C.gov/toxprofiles/tp107. et al. Baur X. Needham LL.cdc. Toxicological profile for chlorophenols [online]. html. Poschadel B. Available at URL: http://www.atsdr. Int Arch Occup Environ Health 1991. Shealy DB. Baker S. et al. Jones D. Radon K.45:440-445. Burse VW.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. The metabolism of higher chlorinated benzene isomers. S. Environmental Protection Agency (U.pdf.71:99108.63:57-62. Smith SJ. Hanrahan L. Available at URL: http://www. Am J Ind Med 2004. Heinrich-Ramm R. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Szadkowski D. Hill RH Jr. et al. Becker K. Pesticide residues in urine of adults living in the United States: reference range concentrations.

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

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

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

2) 16.0 (7.0 (9.1-17.0) 11.70-23.1) 95th 13.10 (.5-17.3) 16.8) 11.13-2.80 (2.50 (.10 (2.0) 5.80-4.90 (1.20-4.35-16.5 (8.32) 1.43-12.34-3.67) 3.40-16.8 (14.70-19.740-2.10) < LOD .0) 10.38-5.0 (8. 01-02.56-13.80) 4.79 (5.20-30.0) 10.0) 6.623-1.08 (<LOD-2.44-38.00-19.290 (<LOD-1.71-9.33-18.04) < LOD 1.86-15.40 (.2.60) .53) 4.2 (11.63) 1.0) 12.36-4.1) 10.74 (8.700-1.981 (.S.98-12.81) 11.40-1.57-7.32 (.70) < LOD < LOD 75th 3.5-16.98-5.00-7.73) * * .05-7.47) * * 1. and 03-04 are 0.21 (.8) 7.00-12.23-5.03 (.58 (5.0 (6.26-6.15) 14.30 (2.50) 2.9) 14.7) 11.50 (4.1.4) 20.2) 16.20 (2.61) 4.79-7.94) * * .0 (6.2 (9.82) 10.0 (7.20 (.30-6.68-7.70 (2.830 (<LOD-3.20 (.80) 2.30 (4.0) 10.14) * * .51) 2.50-36.670-1.16) 4.40-14.750-1.00) 3.48-7.70-11.80) .56 (1.8 (12.89) 9.83 (5.970-2.08-2.10 (.52) 6.30-4.6) 18.45 (2.5) 15.35-12.0) 20.0) 11.71 (2.02-5.0 (7.40-19.12) 4.93-24.758-1.8-32.80 (4.02) 4.3) 17.3) 14.39 (3.0 (12.4) 17.600 (<LOD-1.72) 5.35-11.80-24.96-3.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.56 (4.29) * * 1.61 (3.8) 7.9) 8.8) 19.4 (9.20 (.0) 11. 0.00 (5.10 (2.08-15.70) .80-22. respectively.0 (8.810-1.0-28.26 (5.16 (2.19) 9.54 (3.8 (9.74 (8. and 0.40-11.60-18. 120 Fourth National Report on Human Exposure to Environmental Chemicals .81) 11.860-2.955 (.80) .0 (9.0) 5.4 (7. which may vary for some chemicals by year and by individual sample.80) 2.26-8. < LOD means less than the limit of detection.2 (14.2-20.90-4. population from the National Health and Nutrition Examination Survey.58 (2.780) < LOD 3.76 (2.80) 3.01) * * 1.99 (5.20 (.00 (4.13 (2.2.3-15.840-1.5) 20.50 (2.93 (4.2 (14.58 (3.5 (11. interval) 1.20-7.0 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6) 7.1-23.60) < LOD < LOD 4.66) * * 1.90) 3.42) .95) 5.0 (7.0) 11.2) 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 1.97) 8.00-27.17-3.10) < LOD < LOD 4.90-5.81) 1.00-27.70 (4.28) 1.0) 10.2 (7.890 (<LOD-2.27-15.2 (7.44-3.2) 14.00 (1.44 (2.91) 4.70) < LOD < LOD 1.954 (.579-1.34-7.82-12.0) 6. see Data Analysis section) for Survey years 99-00.9) 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 1.10-7.85 (3.0) 7.0 (4.80) 2.8 (8.4) 18.599-1.52) * * 1.47) 5.2 (9.56 (6.7 (12.0) 10.94) 3.55-8.290 (<LOD-.90) 2.13 (2.50-5.00) 3.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.490-2.30 (2.0-27.12-19.0) 15.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.620-1.7 (14.15-12.00-12.4 (9.757-2.530 (<LOD-2.37 (3.9 (8.1 (10.52-11.33 (5.27-3.21) 9.0 (8.60 (5.07-10.55-6.9-18.1 (9.40-5.11 (.70-14.60-25.717-1.4 (7.86 (1.42-3.1) 13.0) 6.60-11.0) 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 1.0) 9.39 (8.97) 90th 7.2 (7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 11.46) 10.60 (1.22 (.

7 (9.960 (.02 (2.05 (.03 (7.40) 4.883 (.85) 2.855 (.43) 2.25) 6.81 (1.1 (11.00) 8.80 (2.58) * * 1.68-4.5) 11.61-13.82-14.710 (<LOD-1.500-1.7) 18.608-1.6 (9.924 (.32-12.83 (7.750 (<LOD-1.996 (.76-4.8) 8.29) * * .83) 8.79-9.5 (4.5) 7.7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .8) 16.94-22.9) 16.3) 15.1 (8.820 (.46-5.28 (5.44 (2.50) 7.88) 2.78 (2.6) 8.34) < LOD < LOD .3) 16.71) 10.6) 13.45-5.07 (.40-3.00-19.36) * * 1.62) .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 1.56) 7.93-5.94 (4.75) 2.38) .75 (3.98) .932 (.25) < LOD .41) .0 (8.1 (10.54) .10 (3.8) 7.2 (8.61 (1.46) 2.900 (.57) 4.540-1.20-8.40-5.40 (3.28-9.41) Selected percentiles ( 95% confidence interval) Total * * 50th .92-5.60) * * .3) 12.66 (2.37-3.94-23.85 (6. Fourth National Report on Human Exposure to Environmental Chemicals 121 .06-2.960 (<LOD-2.37) 9.69) 4.9) 11.71-2.830-1.13) 4.570-1.4) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.23 (4.53-11.43 (.47 (3.41-12.93-9.30 (1.21-23.53) 9.2 (6.75 (7.37 (4.773-1.1 (7.88 (5.34 (6.05 (1.00-13.98) .51-5.430-1.53 (6.2) 7.03) 2.2) 5.54-2.02-14.89-3.19 (4.62-5.98-22.04-6.60) 2.2) 5.56) .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 1.40-14.2) 95th 12.2) 13.38 (1.79-3.52) 4.98) 9.0) 6.03 (2.4) 13.57-10.9 (5.95) 2.93) 9.95 (3.64-5.61 (1.7 (8.45-5.650-1.790 (.02 (7.4 (9.60-9.35 (1.05) .23) 4.8) 12.98-5.9) 12. interval) .87 (3.14 (3.69) 2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.860 (.1) 4.510-1.5-20.54-15.633-1.31 (3.74) 4.98 (3.47) * * .94-10.870-2.5) 7.890 (<LOD-1.6 (10.10-13.28 (2.818 (.1 (9.88-15.68) < LOD < LOD 3.47 (3.42) 12.5-13.80 (6.84) 7.56-13.28 (4.7) 12.54-11.11-6.61-29.67) 1.9 (9.89) * * 1.7) 5.09-11.66 (1.6) 9.75-7.57 (4.37 (5.26) * * .566-1.73 (1.66 (5.440 (<LOD-2.31-14.5) 12.4) 4. population from the National Health and Nutrition Examination Survey.9-28.82-26.30) 2.03-6.82-6.82-14.27) < LOD 2.18 (.8) 6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-15.76) < LOD .5-32.69 (4.87-5.67) 4.04 (1.80 (7.4 (4.34) * * .1 (6.45-11.42 (3.890 (<LOD-1.920 (.2) 8.40) < LOD < LOD 75th 2.55-20.39 (2.69-10.03) 2.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.47) 2.620-1.74) 90th 7.6) 11.66-34.9 (9.5-16.88-10.37-5.7 (10.24-3.09) 2.75) 14.0) 7.780 (<LOD-1.00-17.1) 4.72) 11.47 (1.57 (6.54-4.574-1.35) < LOD < LOD 3.77 (6.40-12.00 (4.533-1.80) 9.2) 9.3) 5.90-8.549-1.56) 4.40-28.66-15.94 (2.09 (.2 (10.43 (3.92-2.34 (6.84 (5.15-10.29 (2.67-19.02-2.5) 8.90-5.94-9.87 (1.00 (4.28) 10.01-2.81-5.560-1.8 (10.

90 (2.3) 20.3 (9.10-10.9) 9.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0 (9.70-5.16-1.5 (8.86-10.740 (<LOD-1.30) < LOD < LOD .910 (<LOD-2.20 (<LOD-2.0) 12.88) 10.20) 3.60 (5.28 (7.15-6.3 (6.6-41.37 (3.6) 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 * * * 1.78) 5.22) 8.90-31.30) 8.0) 11.90-15.64) 10.96) 90th 7.00) 3.80-6.39-13.75 (2.63-14.40 (2.0) 19.00) 3.24 (2.0) 9.34-3.580-2.0-24.7) 16.680 (<LOD-1.6) 18.7) 15.8) 8.2 (7.37) 2.9) 95th 14.80) .0) 14.0 (5.27) .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 1.4-17.40 (2.8-20. and 0.5) 21.8 (12.67) 3.0 (10.00 (.00-4.42 (1.97-4.0) 12.31-7.50) 3.70-9.95 (2. 122 Fourth National Report on Human Exposure to Environmental Chemicals .15-2.9-17.61 (3.4 (10.S.7) 10.4 (14.22-12. respectively.60 (6.66) 4.0 (14.51) < LOD 1.4) 11.10-15.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.92) 9.74) * * * * * 1.8 (12.73) 7.50-5.31) 1.5 (9.6) 14.81-6.90) 8.5.7-21.90 (6.00) 7.0) 12.6-19. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (10.77-14.0) 9.89) 2.66-13.50-4.59-3.35-3.40) < LOD < LOD 75th 2.34-5.95-9.70-9.0-19.11-6.99 (3.7) 22.0-33.39 (5.0) 14.80-21. < LOD means less than the limit of detection.0 (9.90 (2.4 (10.00-18.6 (10.7 (10.61-32.89 (2.0 (8.790 (<LOD-1.27 (3.49-4.92-17.30) < LOD < LOD 4.2 (9.2) 14.33-11.5-26.6 (10.58.5 (8.75 (3.0-29.0) 13. population from the National Health and Nutrition Examination Survey.67) 4.20) 3.9 (7.70-8.1-23.0) 7.90 (6.80 (5.3) 22.670 (<LOD-1.670 (<LOD-1.90 (6.80 (2.98-9.80) 5. which may vary for some chemicals by year and by individual sample.50) 5.90 (2.18) * * * * * * * * 1.24-5.80-14.0 (10.3) 8.70 (8.8-21.04 (3.00-18.6) 14.72) 2.970 (<LOD-2.6) 11.22 (6.27) 9.90-15.8) 9.53 (3.00-4.0 (7.00-16.90 (1.3 (11.80-12.18 (3.50) .88) 3.77-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 3.06 (2. 0.0) 11.10-4.90 (6. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .0 (15.52 (6.31-12.3 (7.0-24.29) < LOD < LOD < LOD < LOD 3.0) 23.14 (6.82) 8.9 (12.90) 4.70 (1.10 (<LOD-1.00-9.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 (13.0) 13.60) < LOD < LOD 2.22 (6.3 (9.7) 14.1) 11.62-17.25 (2.41) 3.00) 8.46-4.00) < LOD .58 (1.30) 3.3 (12.670 (<LOD-1.29-4.80) .8-17. see Data Analysis section) for Survey years 99-00.35 (6.46-28.8-20.90 (5.3) 10.20-4.0) 6.9-15.10 (.34 (6.96) 3.670 (<LOD-1.01 (2.84-4.45 (3.1 (10.20-8.27 (7.7 (11.34-10.80-4.650-1.9-14.7-19.35) 4.20-18.10) 6.80-3.67-10.80 (2.20) .47-6. and 03-04 are 0.5.9) 16.4) 7.3) 14.9) 10.60 (2.0) 18. 01-02.80-8.12 (4.27) 4.95 (5.90-9.41-5.70) 2.17 (7.

6 (12.890-2.25 (4.45) 6.72-4.4) 6.30-5.97-4.4) 15.6) 7.0 (11.30) 8.63 (6.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3-17.12 (7.55) 16.2) 10.02-4.5 (11.09-11.51-10.00 (3.50 (6.620 (<LOD-.6) 6.72) 4.780-1.7 (11. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7-23.92) 3.73 (5.4-15.5 (9.5) 8.1) 13.33) 3.03 (2.78 (4.5 (8.85-8.94-14.68-10.71) < LOD < LOD 2.6) 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 1.67 (7.21) * * * * * 1.82-8.5-17.8) 16.2) 12.77) 3.5 (15.1 (19.88-7.44-6.92 (5.8 (10.74-19.07 (5.75-3.07) 2.3-15.70-35.80) 3.0 (8.01-5.9) 16.2) 15.55) .690 (.86 (3.9-25.74-4.89 (2.2 (9.2 (9.6) 12.88 (1.2-30.54 (7.29 (5.6) 95th 16.1) 20.39-17.28) 6.05-3.00 (2.67 (1.47-9.38 (2.34) < LOD < LOD < LOD < LOD 3.00) 2.28 (1.19) 3.68-4.4) 16.30) 7.45) 3.5) 10.9 (9.93 (<LOD-2.41 (7.37-5.27) 5.21-21.6) 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 * * * * * * .38 (.03) 3.86-3.7-19.530-1.4) 7.25-9.99 (4.2) 19.29 (2.50-17.0) 14.11-3.94 (5.3) 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.8) 11.70-2.89-3.78 (6.53-8.04) 9.7) 9.32-8.810 (<LOD-1.71 (1.00 (<LOD-1.3-21.27) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 123 .00) 8.15) < LOD < LOD 75th 2.7) 12.06 (<LOD-1.95) 3.6 (11.79-9.37) 3.2) 8.7) 15.42-19.48 (2.7) 14.96-10.7 (10.0 (13.78) 4.920 (<LOD-1.7) 14.00 (<LOD-1.33-10.2) 12.6-19.6 (11.850 (<LOD-1.59-3.2-15.6) 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 * * * .61 (2.3) 12.11 (5.29-2.89-13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.75-3.68-19.16 (3.38-13.1 (13.4) 7.38 (1.4) 9.42) 7.95) 90th 8.9 (9.12) < LOD < LOD 4.4) 7.68) .6) 14.83 (7.86) 9.43 (2.79-6.00 (5.91) 3.32) 2.77 (2.973 (.29) 3.36 (2.54) 9.69-11.3-17.89 (3.6) 13.6 (13.93 (2. population from the National Health and Nutrition Examination Survey.3 (7.910 (<LOD-1.7 (10.38) 1.28-12.16-14.5 (10.51-7.23-3.07-3.940) < LOD < LOD 1.3) 6.95 (2.4-16.0-19.89) 5.4 (11.9) 19.34-18.96-11.1 (8.2) 12.87 (3.55 (2.91-9.1) 10.5) 22.89-3.590 (<LOD-.9-17.63 (2.0 (10.78-10.81 (7.7 (8.3) 8.9 (9.93 (6.0-21.30) 2.8) 14.S.4-16.5) 13.64-11.00 (7.93-10.8 (8.77 (2.83 (6.42) 8.85-17.97) < LOD .03 (6.27) 1.14 (2.27) * * * * * * * * 1.760 (<LOD-1.18) 2.15 (1.6 (13.09-11.20-3.99) 2.52-3.950) .3-34.07) 2.6 (10.89-10.54-5.82-11.06) .2) 16.58 (4.4-18.27-13.

94 (3.500 (<LOD-.20 (1.380-.467 (.20-3.27 (2.09 (.04) .690-1.42-2.850) < LOD .70 (1.36-4.80) 2.960) .860) < LOD < LOD .60-4.95) 2.597) * . which may vary for some chemicals by year and by individual sample.45 (1.S.01-3.98) .720-1.749 (.949) . respectively.388-.48 (1.32 (1.20) 1.830 (.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 * .16) 1.560-.88) 1.98 (2.343 (.22-8.980) 1.57 (2.710 (.79) .592) * 50th .54) .05-3.46 (1.580-.22 (1.10) 1.94) .960 (.353-.13) .359-.05-2.550 (.15) 2.47 (1.50 (1.880 (.650-.60) 2.570 (.620-1.32-1.21) 3.740-1.50 (1.76-6.780) .880) < LOD .11-3.49) . and 03-04 are 0.50 (1.46) 1.2.77 (1.453 (.48 (2.31-3.710) .240 (<LOD-.970) 1.400) .70 (1.20) 2. < LOD means less than the limit of detection.50-2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80) 3.78) .10) 3.33-2.910-1.65 (2.570 (.29-2.690 (.930) 1.40 (1.22-3.38) 1.55 (3.455 (.550 (.68-5.460-.303-.580-1.50 (1.1.380-.759) * .680-1.89) .54 (2.77-2.30 (.00) 2.20-2.340-.40 (1.18 (1.450 (<LOD-.592-.350-.01-1.60) 3.35) 1.70 (1.210 (<LOD-.750) 1. see Data Analysis section) for Survey years 99-00.22-3.30 (.32) 3.11-3.16-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (.760 (.570-1.27 (3.61 (1.20 (1.15) 2.30-1.20) 3.425 (.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.459 (.710 (.970) .00) 1. and 0.670) .13) 2.59-2.880) < LOD 75th .380) .70-2.74-5.41 (2.54-2.720 (.20) 1.585) * * .86 (1.03) 1.510 (.30 (.740-.86) 3.398-.720-1.00 (1.810) .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 * .490 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.89-6.20) 2.10-1.00-2.600-.98-3.657) * * .50 (1.940) < LOD .350-.80) 2.690) .59-6.20) 3.549 (.10) 1.80) 5.45 (2.590-. 124 Fourth National Report on Human Exposure to Environmental Chemicals .160 (<LOD-.26) .97 (2.18 (.700) .950) 90th 1.31) 95th 2.80 (2.83 (2.60 (2.00-4.26 (2.83) 2.449 (.20 (2.50-2.34) 2.587) * * .45-4.790 (.08 (2.960) . 0.30) 2.30-3.87-3.96-5.16) 2.260 (<LOD-.600 (<LOD-. 01-02.510 (<LOD-.73-5.960) 1.45 (1.90 (1.30) 1.20-1.29) 1.201-.57 (1.50) 1.584) .930-1.34) 2.64 (1.336-.680-1.20 (1.390-.31) 2.09.740 (.30) 4.25-1.90) 2.280-.41-5.690-.30-3.910) 1.17) 1.570) * .10-1.390-.94 (2.17-4.30) 4.14-1.570 (<LOD-.58 (1.90) 3.70-7.75-2.840 (.440-.31-3.79) .46-3.570 (<LOD-.505 (.780 (.23-3.90-4.76 (1.740 (.17) 1.80 (1.750-1.960-1.930) < LOD .820 (.80) 3. population from the National Health and Nutrition Examination Survey.700) .91) 2.83) 1.540 (.30 (1.04) 1.49) 2.910 (.75 (2.39) 2.96-3.20-2.46 (2.74) 3.22-2.19-1.592) * .600-1.990-1.730) .80) 3.47) 2.457 (.83 (2.37-2.14 (1.95-5.800 (.83) .618) * .930 (.73 (1.73 (2.08 (2.89) 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 * .382-.63 (1. interval) Selected percentiles ( 95% confidence interval) Total * .01) .69-4.89) 1.820 (.90) 2.95 (2.10) 1.

33 (1.740) .06) 4.71) 2.45 (2.180 (<LOD-.550-.65) 2.700 (.05-2.57 (3.412-.08-3.97 (1.990-1.43) 2.73-3.42 (.688) * .690) < LOD < LOD .11) 1.97) 2.99) 1.742) * * .880) 1.400-1.00 (3.60 (2.444-.67 (1.471-.520-.560-.82) 2.80) 471 575 296 664 821 689 814 1122 918 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .710 (.61) 2.67 (1.790) .52 (1.320-.285-.64 (2.50 (1.49-4.72) 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 * .710 (.61 (3.234 (.310-. population from the National Health and Nutrition Examination Survey.29-4.850) 1.750 (.460-1.84 (2.39) 2. interval) Selected percentiles ( 95% confidence interval) Total * .540-.870 (.900) 1.58-6.31-1.90) 2.07) 1.32 (.470) .67-3.30) 3.20-2. Fourth National Report on Human Exposure to Environmental Chemicals 125 .136-.47 (1.43 (1.03-1.393 (.32) 2.335-.485) * * .98) 1.250 (<LOD-.75) 6.23) 3.72-4.62 (2.97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.49 (1.88) .591 (.09) .60) .47-4.75-3.18-2.38 (2.550) .22 (2.750 (.69 (1.980-1.950-2.380-.05-4.75 (2.510 (.790 (.66) .07-2.330-.400) .10) 2.590 (.800) < LOD .07) 1.11 (.720 (.08 (2.08-2.79 (1.04-1.07 (.740) < LOD 1.280 (<LOD-.270 (<LOD-.840) 1.370-.700 (.92-8.580) .820) .88 (1.640 (.60 (1.509 (.00-3.42-6.510 (.552 (.72) 1.730) .590-1.330 (<LOD-.230 (<LOD-.372 (.19 (1.57 (1.08 (.310 (<LOD-.270-.250 (<LOD-.34 (1.95) 1.20-7.830) 90th 1.480-1.76) 1.700 (.380-1.22-3.33) .16-1.32-1.530 (.99) 2.08-3.41 (.91 (1.97) 1.760) < LOD 75th .71) .79) 1.300-.930-1.710 (.22) .05 (1.640 (.11-2.70 (3.448 (.07) 1.78) 3.318-.550-.348-.840) .447 (.23) 1.440-1.20) 1.75 (1.368) * .390-1.630) * .28 (1.660-.560 (.05) < LOD .62 (1.67) .640 (.670 (.460) .840) 1.72 (1.57-2.38 (1.820) 1.36) 3.23 (.870) .57-4.30-2.470 (<LOD-.305 (.42) .S.22) 4.590) * 50th .32) 1.39 (1.08) 2.52) 3.58 (1.453 (.02-3.270-.380) .63 (1.73 (2.43) 2.24) 4.82 (2.22) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.830 (.55-3.92) 3.98) 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 * .44-2.500-.32) 5.560-.08-3.84-6.760) .16) 1.720-1.55 (1.43) 1.680 (.69 (3.550-1.22-3.80) 2.89 (1.16-2.520 (.47 (1.515) * * .08) 1.597) * .81) 2.377-.300 (<LOD-.580 (.17) 2.17-2.02-6.25-3.23) 2.60) 1.03-2.07-3.510-.480) .910) < LOD .61-3.310 (<LOD-.45 (1.72 (2.04) 95th 2.645) .77-3.23) 2.13 (1.14 (2.38-3.77-4.05) 1.07) 5.920) .71 (1.97 (1.00-1.70 (2.04-5.350) .61-3.320-.87 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.940-1.02-3.77 (3.67) 1.89-3.08-2.490 (.535 (.94) .460 (.64 (2.17) 2.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.580-.06-2.08-3.253-.58) 3.53) .42-8.44) 2.66 (2.403) .800-1.92 (1.739) * .390) .08-2.22-2.50) 1.

4) 38.660-2.1 (11.0) 45.0-58.0-230) 35.6-22.2 (12.5-40.54 (3. 01-02.0) 18.0-53.46-2.66-5.83-2.1 (26.9 (10.0) 3.59 (1.1 (25. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.92) * 2.77 (1.0-29.3) 33.0) 28.12) 1. 0.49-2.10 (1.3 (14.88) 3.0-62.50-5.0) 6.0) 3.9-51.10-13.3 (12.21 (4.1) 95th 48.1 (10.4-76.14) 5.45) 2.83-2.86 (1.50-2.79-2.0-58.4 (15.75-14.27-6.64-3.26 (.2-33.0) 13.50-17.06) * 2.70-6.40) < LOD 1.80-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (22.1-19.10) .29-4.0 (40.5) 69.2-27.8 (12.85) * 2.8 (26.61 (1.71-2.20-4.44) 2.6 (11.1 (22.70) 1.0) 4.0) 15.0-62.21 (3.0 (37.88) 1.0 (38.31-6.95 (5. which may vary for some chemicals by year and by individual sample.40-4.80) .4.4 (10.8-24.40) 50th 2.91 (4.8) 39.8) 41.67 (1.5-20.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.470 (<LOD-1.30-14.10 (7.9 (27. < LOD means less than the limit of detection.77) 38.23-2. population from the National Health and Nutrition Examination Survey.6 (26.1-20.00 (.86-3.63-6.04 (<LOD-2.4 (19.5.5-27.48-2.78 (1.5-45.43-7.70) 1.2-39.58-2.16) 2.3) 26.0 (33.9) 18.90 (1.70 (.830-3.0 (20.0 (6.3 (24.8) 62.610 (<LOD-1.0-41.0-31.13 (1.4) 19.0-39.44) 3.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.1-40.06 (1.530-4.0) 19.0 (21.50 (2.33 (5.7-22.0) 17.6 (15.13) 12.0) 4.0 (25.41) 1.0) 31.10-4.10 (1.1-46.64-8.72 (1.0) 42.18) 6.0-50.81-2.0-53.0) 4.0) 20.41) 5.80) < LOD 1.48) 5.16) * 1.0 (24.46-6. and 03-04 are 0.12 (3.76 (2.20 (2.42) 1.80) 90th 38.0) 28.57-2.8 (12.90-8.0 (32.0 (38.1-47.05-3.0) 20.52 (4.87-7.97) 6.79 (2.0 (11.9 (19.1) 18.2-47.0 (20.0 (38.1-25.0 (13.6) 52.46 (.3) 28.65 (4.76 (2.35-6.690-3.0) 30.0) 3.0 (7.18) 14.70 (1.85 (1.32 (2.2-26.40) < LOD 2.9) 17.10) 39.21 (1.23-2.90 (1.26) 75th 11.7) 20.54 (1.98 (1.44-7.81-3.0-110) 42.19-2.40-16.2-27.50-7.0-41.41 (1.02 (2.1) 38.0) 17.S.9) 48.0 (8.9-21.1 (25.7 (28.53) 40.20) 1.0 (38.7 (12.70) 5.41-4.0) 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 2.53 (1.45) 2.0-69.0-110) 34.0 (17.30) 11.2) 16.71) 5.0 (19.4-22.0) 33. see Data Analysis section) for Survey years 99-00.6 (9.3) 31.0) 8.83 (3.10 (1.9 (23.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (26.44) Selected percentiles ( 95% confidence interval) Total * 2.00 (.18.70-17.8-21.36-2.3) 38.2) 31.74-2.1) 38.93-3.13 (1.11) 2.90) 11. interval) 1. and 0.0) 16.82 (1.0-92.71 (4.2-62.58) 16.6-45.80) 1.60 (2.69) 2.0-39.17-2.0) 15.41) 1.7) 47. 126 Fourth National Report on Human Exposure to Environmental Chemicals .78) 9.70 (7.3 (12.7-41.25-3.3 (23.0) 3.70 (1.99 (2.0-52.0) 5.57-2.29-9.79 (1.0-47.0 (38.0 (8.09 (4.9) 38.7 (12.0) 16.2-80.0-49.18) 20.11 (4.6-54.59 (1.53) 1.04-8.07-5.5) 30.0 (8.80-18.04) 3.96) 5.3 (10.10 (1.0-41.5 (24.830-4.48-2.61-2.6-27.50-20.2 (19.5-74.30) 4.53) * 2.29) 2.60) < LOD 1.0) 32.600-2.0-43.05) 1.1) 140 (46. respectively.8) 32.0 (38.83 (1.23) 9.0) 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 2.00-24.19) 2.98) * 2.92-5.05) * 2.94 (1.30 (.0-260) 34.0 (38.9 (19.

670-1.88 (1.54-15.44) 9.4 (25.40 (5.58-2.2) 33.16 (1.1) 52.35 (2.79-17.16 (1.00) 6.680-4.6-51.7 (10.4 (11.9 (10.9-37.02) 1.3 (10.66) 8.3 (9.0) 48.7 (18.3-22.59-2.48 (4.4) 14.1) 27.27) 50th 2.7-43.38 (3.6-49.4-34.19-14.6) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18) 3.7 (18.1-60.6) 11.2 (16.7) 61.1-22.1) 27.6 (27.6 (11.3 (8.40 (2.60) 4.1-63.94-20.69-5.870-3.48) 1.19 (1.03) 1.46-22.18) * 2.66 (1.0-70.4 (12.9 (19.2-28.46-6.7 (24.9-52.46-5.7) 15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (41.2) 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 2.16-2.20-5.870-3.16 (1.0 (14.23) < LOD 2.9 (26.6-32.6 (24.7) 34.19) 5.3 (20.71) 8.23) 37.6-38.01 (.6) 23.00) 1.2 (21.58-17.2 (22.61 (1.7) 30.8) 32.5 (15.4 (19.3-42.90 (.4 (9.7) 26.88 (4.86) * 2.61-22.33-5.08) 1.80 (1.4 (5.5-36.40-4.93) 5.08 (1.75) * 1.62 (2.0) 47.26-2.54-2.2 (9.1 (33.6) 19.70 (1.7) 95th 51.5) 27.50-5.57 (6.70-4.8 (7.3-19.36-13.07-2.21 (4.5 (6.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.1 (12.5 (17.82) 1.35) .69-18.27-3.0 (19.890-4.0 (23.99-4.3) 13.34) * 1.8-43.26-4.12) 3. interval) 1.6) 7.9) 3.37-2.33) 2.2-70.0) 13.41 (2.12 (1.8) 23.22-2.7-38.4-71.9 (39.7) 23.82 (2.4) 12.9) 24.83) .88 (4.27 (6.4-21.2) 671 678 497 509 694 578 595 947 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.1 (39.95 (2.79 (2.6) 3.9 (7.95-16.37 (1.56) 1.59-15.930 (<LOD-1.28) 1.51) < LOD 1.72) 2.1) 13.03-2.46) 1.60 (.94) 19.61-2.02 (.06-1.2-34.0-71.7 (11.22 (2.1) 17.2 (8.67-3.31) 2.06) 1.9) 3.83 (.0 (25.11) < LOD 1.5 (15.33) < LOD 1.2) 4.7-20.8-26.00 (4.17) 2.96) 2.9-18.75-6.0-118) 29.0-40.96-16.4) 12.29-5.36) 10.30) 28.39 (1.0 (23.33) 1.2-38.22-3.0 (6.8) 3.68) 47.14-8.19) 5.64 (1.67 (1.7-47.35) 1.5 (34.66 (1.2) 13.1) 15.4-39.67-16.38-1.06) 1.75 (1.43-2.43-12.18-1.45-1.27) 10.25-3.4 (25.68 (1.1) 13.870-3.750 (<LOD-1.3 (10.9-95.5-97.86) * 3.0) 10.0) 3.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.9) 54.84-13.06) 75th 9.36 (4.S.71 (1.1) 36. Fourth National Report on Human Exposure to Environmental Chemicals 127 .899-2.62) 4.38-5.32 (3.45 (1.32-3.860 (<LOD-1.38) 5.51) .6 (7.888-1.43) * 2.2) 41.95) 90th 32.94) 1.67 (1.5 (8.3) 28.50 (2.1) 25.9-36.2 (15.0) 30.1 (34.1) 25.0) 25. population from the National Health and Nutrition Examination Survey.8) 31.20) Selected percentiles ( 95% confidence interval) Total * 1.71-2.1 (50.47 (1.9-41.07-2.4 (21.7-109) 22.95-16.56 (2.55 (2.9 (13.0) 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 1.8) 11.22 (.59-2.2) 36.8) 15.75 (1.28 (1.9) 24.19-6.5-43.9) 12.09 (5.23-1.57) 4.11-2.53) 1.8-37.2) 13.7) 66.7-37.0 (32.17-3.8-34.5 (13.3-27.7-19.52 (1.91-2.4-67.5) 70.91 (6.40-7.0 (17.24 (1.5-190) 30.2-47.1 (25.14 (.4) 3.00-16.88 (1.52-4.63-5.47-17.80-8.15 (.47 (3.76-2.0 (39.8-45.97 (1.07) 9.6) 112 (40.02) * 1.

410-1.700-1.350) .850 (.660 (.090 (<LOD-.400-.090 (<LOD-.430 (.00) .650) .820 (. see Data Analysis section) for Survey years 99-00.990) .140) .15) .930 (.990 (.470-1.220 (<LOD-.100 (.650-1.300-.190 (.090 (<LOD-.380-.770) < LOD 95th .540 (<LOD-.130-.190 (.120-.220 (.450 (.700-1.270 (.260 (.10) .490 (.700-1. population from the National Health and Nutrition Examination Survey.03) .610-.150) .830) < LOD .310) < LOD < LOD < LOD < LOD .390 (.230) .990) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.760) < LOD .110-. < LOD means less than the limit of detection.780) < LOD 1.30) .730) .160-. respectively.320-.200) < LOD < LOD .140-.13) .099-.830 (.460-.540) .940 (.870) < LOD .310 (.680-1.620 (.080 (<LOD-.720) .650-1.850) < LOD .770 (.140-.360-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .080 (<LOD-.190 (.130) .720 (.550) .210 (.370-.160) .630 (.130) .650 (.470 (.610-1.160) .090 (<LOD-.090 (<LOD-.1.090 (<LOD-.600 (.360-.610 (.S.460 (.830) .12 (.870 (.680) .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 * * * * * * * * * .830 (.290) < LOD < LOD < LOD < LOD .300-1.380-.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 * * * * * * .410) < LOD < LOD < LOD < LOD .170-.370-. 0.530-.050-.560 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .820 (.084-.430-.690-1.180) .390) < LOD < LOD .560 (.20) .10 (.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.32) .870 (.870 (.900 (.240 (<LOD-.310 (.870 (. 01-02.860) .380-.840) .10) .310-.30) .640) .290) < LOD < LOD < LOD < LOD 90th . 128 Fourth National Report on Human Exposure to Environmental Chemicals .410-.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.42) .840) .130 (.640) .30) .680 (.130-.350) < LOD < LOD < LOD < LOD .58) .120 (<LOD-.450 (.330-.640-1.130-.210 (.860-1.36) .440-1.05. which may vary for some chemicals by year and by individual sample.700-1.610 (.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 .120-.162) * * * * * .650) .870 (.410-.10) .290 (<LOD-.850 (.720-1.510-1.171) * * .117 (.640 (.680-1.150 (<LOD-.280) < LOD < LOD < LOD < LOD .420-.740) < LOD . and 0.140-. and 03-04 are 0.1.630 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) .730-.450 (.42) .320 (.540) .60) 1.230-.570) .310) < LOD < LOD < LOD < LOD .

650-1.330-.580) .100 (<LOD-.100-.780) < LOD 1.890 (.360-.86) .43) .380-.330-.410) < LOD < LOD .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 * * * * * * * * * .550 (.380 (.080 (<LOD-.170 (.250-.810 (.390-.110) .161) * * .24 (.330 (.240-.084-.03 (.070 (<LOD-.750) < LOD 95th .111) * * * * * .670 (.700-1.02) .870) .58) 1.440-1.580 (.650) < LOD .120) .860 (.200 (.050 (<LOD-.550 (.450) .230 (<LOD-.510-.310) < LOD < LOD < LOD < LOD .860-2. population from the National Health and Nutrition Examination Survey.570-1.410-.370 (<LOD-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.190 (.800-1.360-.260) .850 (.410 (.540 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.580) < LOD .580-1.14) 1.990) .730) .19 (.140-.230-.610-1.760) .380-.470 (<LOD-.090 (<LOD-.570 (.710-1.86) .730) .01 (.180-.670 (.720 (.720 (.660-1.03 (.500-1.560 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .230) < LOD < LOD < LOD < LOD .600-1.360 (.410 (.940) .12) < LOD .570-.450 (.860 (.02-1.190-.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 .580 (.140-.110-.460 (.410-.320 (<LOD-.070 (<LOD-.640-1.62) 1.700 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.670-1.270 (.60) .170) < LOD < LOD .66) 1.380-.270) < LOD < LOD < LOD < LOD .24) .540) .990) .290) < LOD < LOD < LOD < LOD 90th .960) .29 (.410) .080) .116 (.S.700 (.210 (.057-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .110) .03) .730) .140) .38) 1.070 (<LOD-.740) < LOD 1.740 (.140-.080 (.00) < LOD .880-1.220) < LOD < LOD < LOD < LOD .150-.940) .340-.400) .200 (.540 (.280) < LOD < LOD < LOD < LOD .190 (.880 (.120) .060-.330-.36 (1.110) .260-.300-.700) .330 (.300 (.090 (.500 (<LOD-.520-.390-.380-1.500) .140-.730 (.170 (.970) .20) 1.360) < LOD < LOD < LOD < LOD .09) .03 (.070 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .220 (.400 (<LOD-.600) .78) .300-.140-.110) .67) .780 (.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.440 (.490-1.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .

28) .11 (1.0 (3.05-3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.43-4.0-38.35-10.35) 11.0) 4.30) .0) 2.47 (3.330 (<LOD-1.12) * * * * * * * * .730 (.0 (17. and 0.15) 19.20 (1.0 (17.750-1.0 (4.800) 17.210-1.770) 2. 0.0-39.67 (1.63 (3.30 (1.70) 2.00-17.640 (.85-3.07-3.50) .0-38. population from the National Health and Nutrition Examination Survey.0-44.51-8.97) 20.00 (1.425-1.52) 5.0) 5.0) 5.10-3.07 (3.830 (.90-28.10 (3.0-40.12-1.00) .11) 13.20-17.07 (1.0) 2.880) 5.00) 1.350-.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .0) 2.590 (.11) .00 (.26 (2.370-.31-10.350-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.14) .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.70-50.99) 11.0 (13.0 (5.20-4.39) .770 (<LOD-1.23-6. respectively. < LOD means less than the limit of detection.49) 17.0-40.30-3.15) 14.0) 4.42) .99) 19.0 (5.05 (3.10-3.49 (1.67 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.05 (2.0 (17.690 (.190-1.65) 1.74) 5.83-3.61 (1.850) 16.97) 20.0) 7.6) 5.94 (1.53-7.18) 1.0) 4.46 (1.0) 2.66) 4.0 (17.01) 5.840 (.1.30 (.28-9.07 (3.800) 90th 13.260-.52 (1.380-.39 (2.45 (2.35) 5.580 (.080-1.08.53) 20.94-3.40 (1.870) < LOD < LOD .110 (<LOD-.38-3.29-10. and 03-04 are 0.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.250 (<LOD-.40-20.1.63) 32.740 (.40-4.94-8.510-.67) .30-6.960 (.20) < LOD < LOD < LOD < LOD < LOD 1.40 (1.90-37.55-4.40-8.30 (1.20-4.10-9.62-8. which may vary for some chemicals by year and by individual sample.48) 13.0) 3.691 (.0 (4.40) 2.40-7.00) .610) < LOD < LOD < LOD < LOD < LOD 2.50) 2.00-17.0-38.48 (2.610 (.0) 2.360-1. 130 Fourth National Report on Human Exposure to Environmental Chemicals .13 (3.14) 2.960 (<LOD-1.40) 1.10 (3.0 (17.31) .840-3.0) 2.90 (2.86) 4.S.88-3.82-4.90 (1.90-9.30 (2.49 (1.21-3.59-5.36-3.53 (2.400-1.0 (5.0 (16.910) 2.80 (4.170-1.90) .0 (5.33 (4.20 (1.32 (1.07-3.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.87) 12.600 (.90-20.70-7.37) .0 (7.10 (.30 (1.0) 2.16) 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 .750-2.70-30.60) .90) .36-3.0) 5.800-4.76 (1.620-1.24-7.70-3.60) 1.720) 2.640 (.32-9.55-8. see Data Analysis section) for Survey years 99-00.99 (1.03 (.0) 4.840 (<LOD-1.0 (6.51 (2.28) 1.21) 3. 01-02.30-7.83) 2.900 (.890 (.0 (5.83-3.96 (1.74 (3.0) 5.90) .42) 2.68) 2.30) 95th 19.480-.70-17.14-5.07) 1.52 (1.87) 5.

55) 21.0 (9.33 (1.40 (.580) 1.47) .22-27.97) .13 (2.430) 1.700) < LOD < LOD < LOD < LOD < LOD 1.18) * * * * * * * * .430 (<LOD-.330-1.88-3.74 (2.340-.88) 17.80) 3.970-3.86 (3.790 (.96-25.84) 9.67-6.91-4.53) 27.04-16.83-11.940-4.28-6.25-9.17 (1.31-18.31) .8) 2.250 (<LOD-.580 (.47-10.80 (.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.5 (11.7) 6.38 (2.240-.340 (.580) 16.00) .64-4.5) 2.18) 95th 21.56) .370) < LOD < LOD < LOD < LOD < LOD 1.580-1.51-4.190-1.89 (2.18) 1.25 (1.92 (2.06 (.00-19.98 (4.71 (.67) 1.540 (.56 (1.560 (.25-38.86) .8) 2.10-3.470 (.02 (1.390-.790) 11.1 (7.12 (4.50) 11.08) .82-11.12-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.53) .60 (1.830 (.360 (.40) 1.7) 5.55 (3.9) 6.4 (4.1 (5.14-6.740-1.61) 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 .340-.11-5.270 (<LOD-.50 (4.32-6. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.96-8.850-3.7) 3.710 (<LOD-1.77 (.85-3.05) .48-7.S.450 (.670 (.69) 2.650 (.62-17.81-17.5) 2.8) 1.44) .748 (.44-11.14 (1. population from the National Health and Nutrition Examination Survey.35 (.150 (<LOD-.57 (.67) 2.8 (20.50 (2.8) 7.22) 2.47-10.83 (4.40-2.7 (12.630-1.800-2.03) 16.770) .29-4.1) 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.8) 4.8-33.39) 20.49-2.260-.10 (2.65 (2.88 (2.40-12.650) 90th 10.52 (.5 (8.7) 4.33-3.840-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8) 7.270-.50) .71 (2.31-7.88 (.57-40.56) 2.62 (1.03) 2.830-3.01 (1.960 (.75) 5.04 (1.690-5.320-1.57) 8.85 (1.540-1.24) 3.02 (.91) 2.890 (.48 (4.79 (.7 (6.4) 2.730-3.0 (4.43) .31) .17) 5.55) 21.48-42.41 (4.10) 2.860-2.07-21.5-40.59 (1.500 (.5) 7.2 (8.37) 4.41) 18.09-3.23-7.45 (1.51-44.47) 5.67 (2. Fourth National Report on Human Exposure to Environmental Chemicals 131 .32) 9.33-4.02-4.310-.4-34.474-1.0) 4.820) .600 (<LOD-1.620-3.15) 9.90-6.1) 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 * * * * * * .36 (.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 * * * * * * * * * .33-5.1) 2.340-.30 (4.780-4.590) 2.73 (4.700) 6.27 (2.11) .66-47.3) 2.96) 2.33 (3.5 (9.69-7.9 (11.64) 30.57) 1.29 (4.02) .820 (.07 (2.9) 5.930) .370-1.370 (.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.21-3.260-.3) 3.2-38.660) < LOD < LOD .

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Buchanan D. Narang A. Buccafusco JJ. 1991. Steenland K. EPA). Daniell WE.2000 and 2001 market estimates.113(4):504-508. Chrislip D. Masala G. Rodnitzky RL.58(11):702710. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Am J Ind Med 1987. Muniz J. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. 1993 [online]. Weerasekera G. J Toxicol Environ Health A 2005. Neurotoxicology 2005. Int J Occup Environ Health 2006. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Rothlein J. Claypoole K. London L. et al. low-level organophosphate exposure on delayed recall. Smit LA.20(2):115-22. Dinoff TM. The Pesticide Health Effects Study Group. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Lewis JA. Myers JE. Available at URL: http://books. Washington (DC). Environ Health Perspect 2006. Keifer M. Rohlman D. Bull Environ Contam Toxicol 1994. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Beach J. Seiber J. Jamal GA. Pesticides in the Diets of Infants and Children. Eskenazi B. Available at URL: http://www. 2004. Stark A. Terry AV Jr. discrimination. Jenkins B. Salvini S. Schenker M. Aprea C. Lu C.38(4):546-563. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Kidd M.pdf. Occup Environ Med 1995. Rosenstock L. Stokes L. Spurgeon A. Nell V. Scand J Work Environ Health 1998. Am J Public Health 1994. Hansen S. et al. McCauley L. A behavioral evaluation of pest control workers with short-term. Phillips J.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Neurotoxicol Teratol 1998. Saieva C. Chronic neurological sequelae to organophosphate pesticide poisoning. Samuels S.52(10):648-653.68(3):209-227 Maizlish N. Weisskopf C. metabolite clearance. et al. Office of Prevention Pesticides and Toxic Substances. vibration sense and tremor among South African farm workers. O’Malley M. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Lancet 1995. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Rothlein J. Marshall E. Berry H. Wickremasinghe AR. S.44(4):352-357. Occup Environ Med 2001. Calvert IA. low-level exposure to the organophosphate diazinon.114(5):691-696. Burcar PJ.345(8958):11351139. Barr DB.24(1):18-29. Keefe TJ.epa.43(1):38-45. Bravo R. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Lambert WE.php?record_id=2126&page=1. Savage EP. and spatial learning in monkeys and rats. National Academy of Sciences. Levy LS. Thompson ML. 1/12/09 Peiris-John RJ. Sci Total Environ 2004. Santana J. National Research Council (NRC). Effects of long-term organophosphate exposures on neurological symptoms. Visuthismajarn P. Malathion deposition.30(2):98-103. Lancet. Irish RM.26(2):199-209. Lasarev M. Hore P.12(2):153-172. Vitayavirasak B. Caltabiano LM. Heaton RK. Environ Health Perspect 2005. Environmental Protection Agency (U. Robson MG. Pedersen L. Russo J. Arch Environ Health 1975.52(2):190-195. and cholinesterase status of date dusters and harvesters in California.12(2):134-141. et al. Muniz J.84(5):731-736. Bradman A.338(8761):223-227. EPA.S. Ruberu DK. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. J Occup Environ Med 2002. Pilkington A. Ames RG. U. 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. Tumino R. Arch Environ Health 1988. Washington (DC): U. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Lasarev M.S. Takamiya K. van der Hoek W. Arch Environ Contam Toxicol 2000. Stephens R. Gladstone EA.nap. Mounce LM. Johnson C. Pesticide industry sales and usage . Effects of chronic. Prendergast MA. Petchuay C. 4/7/09 Young JG. Scherer J. Frasca G.332(1-3):71-80. et al. May. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Gillham R. McConnell R. Neurotoxicity among pesticide applicators exposed to organophosphates.edu/ openbook.

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

19-3. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.20-4.0) 10.70-17.50-2.90-2.63 (2.89 (2.37 (4.60-2.74-9. 2921-88-2 Chlorpyrifos-methyl CAS No.88 (1.0 (7.0 (10.39) 4.7) 9.74 (1.47-11.9) 697 660 521 701 602 947 Limit of detection (LOD.03) 1.20) 10. applied to structures to kill termites.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. 1999.0) 12.21) 3.0 (13.60 (4.71 (1. Exposure can also result from contact with contaminated surfaces.46-2.30-5.22 (1.10-17.50 (2.4 and 0.0 (7.30 (4.50-4.51-2. and sprayed to kill mosquitoes.90) 7.40 (6.62-2.43-2.40-13.2 (10.94 (4.77 (1.7) 13.70-11.80) 2.3 (8. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 135 .30) 5. staying bound to soil particles.70 (1.31-2.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04-10.5. and is infrequently detected in ground water (IPCS.52-2.20-16.0) 6. USGS.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 1.4 (8.27 (7.68-2.90 (6.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.20) 2.59-2.50 (2.64) 3.22) 2.39-2. dermal.60 (5.83) 1.80 (7. It also has been applied directly on animals to kill mites.90) 3.8) 10.3) 8.34) 1.30) 4.90-7.37 (1.61) 75th 3.20-14. and on plants for days to several weeks.16) 2.77) 1.77-15.7-23.3 (11.0) 8. For instance. pre. and inhalation routes.90 (2.80) 12.60-4.95 (4. 2002).9-18. air. 2007).00-24. but can be detected in streams receiving runoff from application sites.40 (5.15 (1. After 2001.9 (10.44-5. interval) 1.0) 14.68 (7.66-15.09 (3.29) 90th 7.50 (1.55-5.44 (3. 2005). Inhalational and dermal routes of exposure are important in pesticide formulators and applicators. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 10.72) 2.70-15. 5598-13-0 General Information The chemical 3.91) 16.35) 1. Approximately 80.19 (1.0) 10.57 (2.05-5. Estimated intakes from diet and water have not exceeded recommended intake limits.30) 4.10 (3.80) 4.0) 12.51) 1.10) 2.51 (1. and dust.31-2.97) 4.01) 1.0) 8.20-3.30-11.79-2.90 (3.13-3.40) 9.97) 7.70) 1.36 (4.0) 12.10 (4.3 (10.37) 5.40-10. Chlorpyrifos is Urinary 3.5) 7.28-3.S.90 (1.35) 2.59) 2.72-4.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.60 (2.87-6.5-24. It has low leachability.17 (1. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.0 (7.32) 2.29-1.0) 9.9 (9.S.78 (7.67 (1. in 142 urban homes and preschools in North Carolina.02 (1.80-10.30-9.77-6.EPA.98-15.50-4.8) 9.25) 3.45 (1.40) 2.4.25) 1.40 (5. The general population may be exposed to chlorpyrifos via oral.63 (8.70 (1.47 (4.90-4. Survey Geometric mean (95% conf. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.9 (7.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.0 (7.20 (2.20-11.47-13.40-2.0) 15.4 (9.000 pounds are used per year.99-4.30 (2.70-16.20) 2.97-7.00) 2.76 (1.0 (9.96) 3.6) 7.81-2.09 (2.9) 11.50-14.4 (10.89-2.20 (4.44-2.43-2.20-2.S.1-16.24-1.0-28.EPA.40-26.61-7.71 (6.0) 11.20) 4.90 (1.66-4.28) 2.30-1.52-12.32-1.38 (3.60-3.05) 1.50 (1.60) 5.47-9.00) 1.4-15.30-12.70-5.24-3.00) 3.97) 2.5 (8. chlorpyrifos was no longer registered for indoor residential uses in the United States.92 (1.0) 18.60-3.10) 6.7) 8.50 (2.95) 7.61 (1.02 (7.5.84) 1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.10 (5.26) 7. 2002).97) 2. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.00-8.1) 5.30 (2.0) 12.8-15.80-8.63 (1.71 (2.47) 1.53 (1.13 (1. 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.67 (2. Approximately 21-24 million pounds per year were used domestically from 1987-1998.50-8.0 (7. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.67 (2.and post-construction structural applications for termite control were to be phased out by 2005 (U.91 (1.50-5.80) 1.50-2. population from the National Health and Nutrition Examination Survey.0) 7.86) 4.90-8.02) 1.10 (1.76 (1.0) 12.04-10..30-2.80 (1.

vomiting.39 (2.91 (3.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.78 (1.6) 9.39 (4.29 (3.49-2.1 (7.42-2.88-8.42 (5. Thus.19) 3.47 (5.73 (1.07) 5.02) 7.14) 1..54 (2. population from the National Health and Nutrition Examination Survey.94-12.12-1.36) 1.63-2.82) 8..58) 1.56 (1.01) 3. weakness.88 (1.93 (1.91) 1.46 (2.09 (1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.0) 6.79-13.03) 1.8) 9.77) 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 (3.76 (2.56 (4.58) 5.21-6. 2005.60 (1.99-8.05) 3.3) 8.88) 6.44 (1.58 (4.91-4.16 (4.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.27-1.52 (5.19-2.28) 2.20 (2.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.43-10. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.46 (1.59) 3.45-1.82 (3. 2006.97) 3. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.97) 3.31) 1.24) 75th 2.85) 4.09-2.940-1.62) 90th 5. Urinary 3. Metabolic hydrolysis leads to the formation of TCPy.24-5.88-10. paralysis.39-1.17-4. 2006b). 2005.24-24.87-3.49-2.20-1.85) 1.35) 1. Howard et al.55) 1.44 (6. 2006a.24-4.5 (6.25-1.65-11.09-1.41 (1.49-2.26-14. In pesticide applicators.5. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.80) 3. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.0) 10.33-7.89) 4. cholinergic effects.49 (1.83) 1.90-9.68) 1.01) 1.1-21.11 (2.63 (5.48 (1.51 (1.91) 10.00-8.56) 2.62-7.1 (10.84-6. neurotransmission.68) 6.44 (5.33) 2.2) 6.82-4. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.75 (1.S.27-7.3) 9.92 (1.95 (1.64 (1.42 (6.47 (1.91) 1.05-4.2 (7.50 (4.40) 1.57) 2.62) 1. 2002). 1984). TCPy is more persistent in the environment than chlorpyrifos itself (U. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.44 (5.14-8. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.0) 12.94-14.91-13.58 (1.58 (1.80-11.33 (5. interval) 1.6) 10.98 (6..66-11. Slotkin et al.93 (2.15 (4.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.08) 6. and other metabolites.99) 1.80-4.66) 1.30-4.12-3. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.28) 2.24 (1.64-2.17-4.33 (.82 (2. TCPy can also occur in the environment from the breakdown of the parent compounds.91) 2.53-5.44-6.70-4. Survey Geometric mean (95% conf.63 (4. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals . In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.81 (3.21-1.86 (1.48 (2. 2006.86 (1. Based on animal data and human cholinesterase monitoring during occupational exposure. 2000). The metabolite TCPy does not inhibit acetylcholinesterase enzymes.05-1.55 (1. resulting in excess acetylcholine at nerve terminals.12) 1..4) 4.1-38. Roy et al.11 (2.31-4. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).83-11.45 (1.80-6.57-2.11-9.35) 2.47-2.56-2.57-2.88-9.7) 7.64-7.97 (2.93) 2.85-4.81) 2.3) 8.96) 3.54) 5..22) 1.71) 3.34-1.S.05-8. 2005...06 (1.25-11.16) 6.74) 1.23) 14.91 (4.98 (7.93) 5.32) 1.39) 6.57) 9. Once absorbed.5) 5.19-1.6-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.76 (3.31-1.69 (1.92) 3. and seizures.56) 5.02 (5.97-3.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.25-12.53 (2.19) 6.9 (12.75) 6.92-2.33 (1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis. Ricceri et al.93 (4.22 (6.43 (4.47 (1.72) 1.72) 2.59-2.60-3.11) 7.09-3.72-2.71 (1.00-13.00 (7..24-1.06-4.55 (4.88 (1.06 (5.00) 1.07) 1.35-1. Betancourt et al.24) 5.85 (2.22-6. and producing acute symptoms such as nausea.23-1.37 (1.44 (1.0) 16.22 (4.38) 3.97 (3.65-15.58-5. 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.66 (1.30-1.83-2.EPA.88-8.05-3.01) 3.86 (3.95 (3.3 (7.

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

EPA). Harley K. Environ Health Perspect 2006a. Seidler FJ. 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. Rick DL. Mandel JS. Morgan MK. Slotkin TA. Edwards RD. Weltzien E. Ryan PB. Lorenzini P. Camann D. Seidler FJ. Sharma V. 2005. Kinney P. Executive summary of safety and toxicity information. Slotkin TA. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. MacIntosh DL.6-trichloro 2-pyridinol in their everyday environments. Chuang JC.114(10):1542-1546. Capone F. Yang D. Urinary pesticide concentrations among children. Needham LL. Bennett DH. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Fortuna S. Steenland K. Roy TS.204(2-3):175-180. Ann Occup Hyg 2007. Howard AS. Nolan RJ.155(1):71-80. Freeman N. Bravo R. Neurologic function among termiticide applicators exposed to chlorpyrifos. Toxicol Appl Pharmacol 1984. Jett DA.niehs.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Kromhout H. Dick RB. 1999. 2921-882. Ryan L.93(1):105-113. Lu C.inchem. Chrislip DW. Heederik D. Environ Health Perspect 2003. 4/7/09 Perera FP. Exposures of preschool children to chlorpyrifos and its degradation product 3. Hammerstrom KA. Temporal variability of urinary levels of nonpersistent insecticides in adult men. A longitudinal investigation of selected pesticide metabolites in urine. Sheldon LS. Environ Health Perspect 2000. Acquavella JF. Cometa MF.112(10):1116-1124. Irish R. Shealy DB. Barr DB. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Freeman N. Eskenazi B. Baker BA. Jewell NP.113(2):211-219. Bravo R. 1992. Venerosi A. Honeycutt R. National Toxicology Program (NTP). Hein MJ. February 5. Toepel K. Bucelli R. 4/7/09 Koch HM. Lein PJ. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. gov/ntpweb/index. Meeker JD.15(3):271-281. Chlorpyrifos: pharmacokinetics in human volunteers.111(2):201-205. et al. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Environ Health Perspect 2006b. et al. Fenske RA. Robertson GL. Howell RJ. mothers and fathers living in farm and non-farm households in Iowa. Barr D. Herrick RF. Barr DB. Scand J Work Environ Health 2005. Bruun D. Baker S. Biomonitoring for farm families in the farm family exposure study. et al.5. Head SL. J Expo Anal Environ Epidemiol 1999. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Adgate JL.5. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Jones PA. Hore P.207(2):112-124. Lioy PJ. Ozkaynak H. et al. Third National Report on Human Exposure to Environmental Chemicals. International Programme on Chemical Safety-INCHEM (IPCS). Zhang J. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Angerer J.S. et al. Croghan CW.73:8-15. Gurunathan S.51(1):53-65. J Expo Anal Environ Epidemiol 2005. et al. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Pesticide residues in urine of adults living in the United States: reference range concentrations. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Saunders JH. Available at URL: http://www. Levin ED. Chapman P. Hardt J.108(4):293-300. Ryde IT. Gregg M. Environmental Health Criteria 198. Toxicol Appl Pharmacol 2005. et al. Slotkin TA. Atlanta (GA). House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.15(4):297-309.114(5):746-751. Barr DB. Robson M. Environ Health Perspect 2004. Striley C. Ricceri L. Alexander BH. Brain Res Dev Brain Res 2005. J Expo Anal Environ Epidemiol 2000. Environ Health Perspect 2005. Rauh V. Levin ED. J Expo Anal Environ Epidemiol 2005.org/documents/jmpr/jmpmono/ v99pr03. Toxicol Sci 2006. Hines CJ.S. Available at URL: http://ntp. Pellizzari E. Sanderson WT. Environ Health Perspect 2006. Tate CA.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Int J Hyg Environ Health 2001. et al. U.9(5):494-501.10(4):327-340. chlorpyrifos.114(2):260-263.nih.6-trichloro-2-pyridinol. Environ Res 1995. Bradman A. Seidler FJ. Tsai WY. Interim registration eligibility decision for chlorpyrifos. Hill RH Jr. Freshour NL. Wartenberg D. Chlorpyrifos.31 Suppl 1:98-104. Curwin BD. Environmental Protection Agency (U. et al.htm.71:99108. Reid TM. Bailey SL.

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

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

S.270) < LOD 659 701 920 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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 . which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.200 (<LOD-.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 141 . < LOD means less than the limit of detection.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. population from the National Health and Nutrition Examination Survey.670 (<LOD-1. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.380 (<LOD-.2.

A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www. EPA).S. Atlanta (GA). Nguyen JV.376(6):808-815. EPA 738-R-00-010.12(6):619-645. 2005.Organophosphorus Insecticides: Specific Metabolites References Astroff AB.epa. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.gov/oppsrrd1/ REDs/0018tred. Freshwater KJ.S. Environmental Protection Agency (U. U. Olsson AO. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Eigenberg DA. Anal Bioanal Chem 2003. Reprod Toxicol 1998. September 2000. Centers for Disease Control and Prevention (CDC).pdf. Sadowski MA.

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. Survey Geometric mean (95% conf. an organophosphorus insecticide that is used to control insects on nuts. USGS. Inhalational and dermal routes of exposure can be significant for pesticide applicators. Diazinon is not well-absorbed through the skin. in some pest strips.S. Estimated intakes from diet and water do not exceed recommended intake limits (U. Before these restrictions. diazinon produced wild bird kills before use restrictions were in place. but is rapidly absorbed orally (IPCS. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. 1998). and particularly when it was ingested in granular form.EPA. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. diazinon cannot be sold for residential use. 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. Once absorbed. and forage crops.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.7. vegetable.45 (<LOD-3.49 (<LOD-2. Most granular formulations. and other metabolites. fruits. < LOD means less than the limit of detection. 2007). in the past. Human exposure to diazinon from dietary sources is expected to be low due to its limited applications to food crops and due to its rapid degradation.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. aerial. It is toxic to birds.EPA.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. diazinon was widely used in residential and garden application. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). It is also used for cattle ear tag applications to control flies and ticks and. 2004). about 13 million pounds of diazinon were used annually on agricultural sites in the United States.S. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon.S. 1998. since 2004. seed and foliar applications are planned to be phased out (U. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. 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 1.2 and 0. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. Fourth National Report on Human Exposure to Environmental Chemicals 143 . Prior to 2000. 2004). but these uses have been phased out. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS.

In two nonrandom samples of United States adults and children.gov/toxpro2.72 (<LOD-4. In animals. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection.epa. 144 Fourth National Report on Human Exposure to Environmental Chemicals .76 (<LOD-3. 2003). In the U.. Olsson et al. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. and indoor applications have been documented. Diazinon has moderate acute toxicity in animal studies.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. respectively.atsdr.S. environmental levels) and health effects is available from ATSDR at: http://www. The U. At high doses. animal carcinogen. Diazinon is not considered to be a mutagen. 1986. Survey Geometric mean (95% conf.cdc. in the 2001-2002 subsample (CDC.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate..45 and 1. 1998). In addition to being a human metabolite of diazinon. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al.EPA considers diazinon unlikely to be carcinogenic in humans. 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. subsamples of NHANES 1999-2000 and 20012002. EPA at: http://www. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. 2002).49 μg/L. teratogen. Thus.. respectively (Baker et al. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2000. 1986 Rajendra et al. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Seifert and Pewnim. 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.. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.. weakness. agricultural.html and from U..e. Additional information about external exposure (i. or reproductive toxicant (IPCS. cholinergic effects. diazinon does not accumulate in tissues (IPCS. vomiting. resulting in excess acetylcholine at nerve terminals. 1992). paralysis.gov/pesticides/.S. and producing acute symptoms such as nausea. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.S. and seizures. 1998). Intoxications in humans from intentional overdose.

Available at URL: http://www. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Toepel K. revised February 15.44(11):2243-2250. Geological Survey (USGS). 1998. Baker SE. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. May 2004. Nguyen JV.. Barr DB. Ann Occup Hyg 2006. International Programme on Chemical Safety-INCHEM (IPCS). 4/7/09 Lu C. Effect of sublethal levels of diazinon: histopathology of liver. J Expo Anal Environ Epidemiol 2000. Sadowski MA. Seifert J. EPA). Liu F. Beeson MD. Rajendra W.9(2):117-131.inchem. Mason HJ. Barr DB. EPA 738-R-04-006. Swan SH. The Quality of Our Nation’s Waters. U. Driskell WJ. Diazinon. Drobnis EZ. 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. Dumas P. Environ Health Perspect 2003. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.114(2):260-263. Redmon JB. Study for Future Families Research Group. Pesticides in the Nation’s Streams and Ground Water. Carrier G. Semen quality in relation to biomarkers of pesticide exposure..134(1-3):105-113. 2005. Needham LL. Cocker J. Bull Environ Contam Toxicol 1986. References Anthony J. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Banister EW. Oloffs PC. Olsson AO. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. In a small number of men visiting fertility clinics in Missouri and Minnesota. Oloffs PC.50(5):505-515. Available at URL: http://www. Garfitt SJ. Toxicol Lett 2002. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Noisel N. 2006). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Available at URL: http://pubs. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Anal Bioanal Chem 2003. Fenske RA. Banister E.usgs. Brunet RC. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.org/documents/ehc/ehc/ehc198. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al.S. In 23 children. March 2006. 2006).epa.376(6):808-815. Atlanta (GA). Barr DB. Environ Health Perspect 2006.37(4):501-507. 2007 [online].10(6 Pt 2):789-798. In 54 Canadian greenhouse workers. Biochem Pharmacol 1992. Swan et al. Irish R.S.htm. Centers for Disease Control and Prevention (CDC). (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Bravo R. Jones K. Environmental Protection Agency (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.pdf. Bouchard M. Drug Chem Toxicol 1986.Organophosphorus Insecticides: Specific Metabolites 2005). Pewnim T. 1992-2001.S. Third National Report on Human Exposure to Environmental Chemicals.gov/circ/2005/1291/. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .gov/ oppsrrd1/REDs/diazinon_ired. Kruse RL. 1/14/09 U.111(12):1478-1484. Diazinon. Environmental Health Criteria 198. Barr DB. Interim reregistration eligibility decision (IRED.

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

Additional information about external exposure (i..S.74 (<LOD-5. 1990). 1987. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.EPA.. Malathion itself has not been considered genotoxic (U. 2000). 2006). Survey Geometric mean (95% conf. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. environmental levels) and health effects is available from ATSDR at: http://www. and it is not considered an animal teratogen or a reproductive toxicant. IARC considers malathion not classifiable as a human carcinogen. Human studies of single oral doses between 0. 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.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. The 95th percentile urinary levels of malathion dicarboxylic acid in both urban and nonurban Minnesota children aged 3-13 years (adjusted for sociodemographic variables) in 1997 were several-fold higher than the analytical detection limits reported for children aged 6-11 years in the U. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al.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. 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. EPA at: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 147 ..cdc.EPA.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Of 382 pregnant women living in an agricultural community. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Toxicity from unprotected bystander exposure during applications is rare (U.S. 2005. Pluth et al.. 2006). 2004). median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. Thomas et al. representative subsample from NHANES 19992000 (Adgate. population from the National Health and Nutrition Examination Survey.gov/pesticides/.e..S.. Giri et al.html and from U. Flessel et al. A study of agricultural workers reported preshift urinary levels of malathion dicarboxylic acid that were twofold to eightfold higher than detection limits in the NHANES 1999-2000 subsample (Krieger and Dinoff. 1999.atsdr. CDC.S. 2006).gov/toxpro2. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. 1993.5 and 5. 2003). Lu et al. 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. 1999). 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. but cholinesterase activity was not affected. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. 2001. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 1996. 2002. 2005).. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample...epa.. 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.S. but isomalathion..

Hammerstrom KA. Barr DB. Irish R. Brunet RC.74(2):following table of contents. htm.S. Barr DB. Available at URL: http://www. Giri S. Toxicol Sci 2003 May. Centers for Disease Control and Prevention (CDC). Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Malathion (addendum). 4/7/09 Kissel JC.109(6):583-590. Eskenazi B.pdf. Gosselin NH.73(1):182-94. International Programme on Chemical Safety-INCHEM (IPCS). Blasiak J. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Toepel K.epa.38(4):546-553. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 6/1/09 U. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Erratum in: Toxicol Sci 2003 Aug. Environmental Protection Agency (U. 2005. Carrier G. July 2006. Third National Report on Human Exposure to Environmental Chemicals. Pesticides in the Nation’s Streams and Ground Water. Fenske RA. Jaloszynski P. The Quality of Our Nation’s Waters. Genetic toxicity of malathion: a review. Petitti D. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Swan SH. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.445(2):275-283. Am J Epidemiol 1990. Geological Survey (USGS). Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Trzeciak A. Albertini RJ. Barr DB.112(10):1116-1124. Lu C. Reproductive outcome in women exposed to malathion. Environ Health Perspect 2004. revised February 15.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Griffith W. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . MacIntosh DL. Hertz-Picciotto I. Atlanta (GA). Needham LL.22(1):7-17. and cholinesterase status of date dusters and harvesters in California. Mutat Res 1999. Jewell NP. Arch Environ Contam Toxicol 2000. Available at URL: http://pubs. Sharma GD. Rappaport E. metabolite clearance. Harley K. Barr DB. Thomas D. Lu C. Samuel O.132(4):794-795. 2007 [online]. 1992-2001. Malathion deposition. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. EPA 738-R06-030.77:1009-1010. Weltzien E. Harris JA.15(2):164-171. Mutat Res 2002. Pluth JM. U. Hooper K. et al. Dinoff TM. Nicklas JA. Dumoulin MJ. Environ Health Perspect 2001. Bradman A. Goldhaber M. EPA). Environ Health Perspect 2006. Neutra R.usgs. Prasad SB. et al.inchem. et al.gov/oppsrrd1/REDs/ malathion_red. Am J Public Health 1987. Cancer Res 1996.gov/circ/2005/1291/.9(5):494-501.114(2):260-263. Grether JK. Ryan PB.org/documents/jmpr/jmpmono/v2003pr06.56(10):2393-2399. Eberly LE.S. Giri A. Freeman NC. Bouchard M. Krieger RI.514(1-2):223231. J Expo Anal Environ Epidemiol 2005. Reregistration eligibility decision (RED) Malathion. Kedan G. Szyfter K. Flessel P. J Expo Anal Environ Epidemiol 1999. Lioy PJ. Environ Mol Mutagen 1993. March 2006.S. Available at URL: http://www. A longitudinal investigation of selected pesticide metabolites in urine. Curl CL. Clayton CA. O’Neill JP. Bravo R. Quintana PJ.

850) < LOD .910) < LOD < LOD .. Fourth National Report on Human Exposure to Environmental Chemicals 149 .01) 4.15-3. Morgan et al.79) 4.11-4.32 (1.50 (1.16) < LOD 1.11) 2.0) 2.46 (3. and has a short half-life in soils and on plants.40) 2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.60 (4.12) < LOD < LOD 1.0) 4.80 (2.1.50 (2.50) 1. 1977).50) 3..60-24.00) 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 1.50-9.70 (<LOD-3.21 (2. with limited applications in agriculture.18-3. 2007).70 (2.71 (3.30-3.62 (1.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .36-1.28-4. 2000).44) 2.860 (<LOD-1.10 (3.EPA.40 (1. Increased risk of exposure via dermal.60-19. Methyl parathion has low water solubility.730 (<LOD-.300-.50 (2.80 (1. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.02-6.60-5.47) 2.10) 22.67 (1.32-1.40-4. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 1. first registered in 1948. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.92) 5.8 and 0. and to a lesser extent.70 (3. was once a restricted-use insecticide with limited applications on certain agricultural crops. Survey Geometric mean (95% conf.61) < LOD 1.70-6.EPA.66 (2.30-16.72 (3.45) 5. fish.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.0) 3. Ethyl parathion.13-1. Methyl parathion use is highly restricted.89 (2. peak domestic use was as high as 5-6 million pounds per year.. Estimated intakes from diet and drinking water have been below recommended limits. and oral routes can occur in pesticide and agricultural workers (Muttray et al.37-4.37) 2.57) 1.40-3.58) 3.40) 4. ethyl parathion. 2003).01-4. pulmonary.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .10 (<LOD-6. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. Many previous registered agricultural uses of methyl parathion have been cancelled (U.69 (2.50 (1.67) < LOD 1.910) < LOD < LOD < LOD 1.20) 5.790 (<LOD-. and aquatic invertebrates.50 (1.90 (1.20 (<LOD-2.298-00-0 Ethyl Parathion CAS No.33) 2. population from the National Health and Nutrition Examination Survey. 2002.0) 3.33 (1.940 (<LOD-2.22-3.32-1.09-1. but by 2003.0) 3.70) 2.91-3.70-6.50-14.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .71 (2. and of the chemical nitrobenzene.20-5.20 (2.37-2.01) 695 660 518 679 603 941 Limit of detection (LOD. Both are toxic to birds.80) 2.60-36.0 (3.0) 3.57-4. methyl parathion was rapidly absorbed after ingestion.910) < LOD .10 (3.70-6. It had been applied to cotton.40) 1.S.28 (1.21-1.90-9. Once absorbed.10-1.70) 2.50) 3.80 (2.770 (.90-11. which may vary for some chemicals by year and by individual sample. and eliminated rapidly from the body after absorption (Kramer et al. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.19 (. < LOD means less than the limit of detection. binds tightly to soils resulting in low leachability.05) 4.34 (3.45 (1.70-3.70) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In the 1990s. Given its limited use.49 (1.00 (2.69) 4.70 (2.32-3.50) 2. Methyl Parathion. 2006). all registered uses were voluntarily cancelled (U.S. Methyl parathion is not registered for residential use in the United States.26 (1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.27) 2. In animal studies. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40-4.28 (1.0) 3.74) 5.41-4. on cereal grains.70 (2. more slowly absorbed through the skin.70-3.990-1.85 (2.700 (<LOD-.S.30 (2.50 (1. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.30-5.48) 90th 2.30 (1.10) 4.61) < LOD 1.92-2.00) 3.00 (2.10-11.37-4.

but lists ethyl parathion as a possible human carcinogen. gov/toxpro2.05) 4. population from the National Health and Nutrition Examination Survey.44-3.950) < LOD .880 (.430 (. Methyl parathion is not considered genotoxic.cdc.930 (.400 (<LOD-. paranitrophenol. 150 Fourth National Report on Human Exposure to Environmental Chemicals .57-7.04 (2.11-4. Orsorio et al.21-21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Parathion and methyl parathion have high acute toxicity in animal testing.EPA considers methyl parathion unlikely to be carcinogenic to humans.21) 1..33-3.60-2.690-1.79 (1.08-3.23) 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 . U. 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..26) 17.25 (2.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.540) < LOD .790-1. Jaga and Dharmani.S.33-6. 2005.html and from U.970 (.20 (3.44-3.91) 1.78) 2.720 (<LOD-.08 (1.76-14.78-2. accidental exposure..31) < LOD .00 (1. weakness.10 (1.60) 2.80 (1. 1991).97 (2. 2006. Survey Geometric mean (95% conf..71 (1.93 (2.60 (1.91 (1.29) 1.98-7.39 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.94-47. In addition to being a metabolite of methyl and ethyl parathion.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . teratogenic.800-1.86 (2.00 (1.790-.35-3.38-3. 1995).S.15-10.67 (3.77-7.930 (. Thus. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.16-4.23) 1. does not inhibit acetylcholinesterase enzymes.29 (2.96 (1. environmental levels) and health effects is available from ATSDR at: http://www.55) 2.82) < LOD .20) .2) 2. methyl parathion.3) 2.840 (.720-1. The metabolite.94-4.80 (1..15) 3. and other metabolites.95) 1.Organophosphorus Insecticides: Specific Metabolites Metabolites”).00) 2.83 (1.14-3. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.48-4.870) < LOD . retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.04) 1.4 (3. gov/pesticides/.90 (1.730-1.530) < LOD < LOD < LOD . Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.640) < LOD < LOD 1.11) 1. WHO.2) 2.29) 2.09) 2.92 (2.70) 3.9) 1.41-2.17) . 1978.08) < LOD . para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.55 (<LOD-3. EPA at: http://www.89 (2.61) 4.. Slotkin et al.370 (<LOD-.01 (. 2003.88 (1.940 (<LOD-1. 2006. Zurich et al.57) 6.10) 90th 2. 2004).13-12.epa.440 (<LOD-. vomiting. and producing acute symptoms such as nausea..67-2.680 (<LOD-1. 1995.79) 1.13) 4.atsdr.78 (2.S.07) 2. ethyl parathion. cholinergic effects.88) 1. Additional information about external exposure (i.980 (.30) 3.25) 1.43) 4.96 (1.71) 1. and unintentional acute or chronic high-level occupational exposure (Hill et al.26 (1. 1990.97-10.89 (2. Methyl Parathion.850-1.72-2.310-.56-2. and seizures.39) 1.87 (1.20) 3.37-1.7) 3.07 (1.31-3.500) < LOD < LOD .33-3. resulting in excess acetylcholine at nerve terminals.01-3.35-3.59 (1.17-4. Lores et al.01 (2.73 (1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.97 (<LOD-4.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .e.30-1.78-2.970 (. paralysis. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. At high animal doses of methyl parathion.830-1. Karanth and Pope et al. 2004).84) 3. In large doses..1) 2. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.82 (2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.57-2.

J Expo Anal Environ Epidemiol 2005. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine.110 Suppl 6:1085-1091. et al. Harley K. Clark JM.S.71:99108. Barr DB. et al. J Biomed Sci 2002. Barr DB. Guizzetti M.. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 4/7/09 Jaga K. CDC.. Wellman SE. Laboratory investigation of a poisoning epidemic in Sierra Leone. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Ashley DL. Bradway DE. 2002). Costa LG. McCann KG. McClure PC. Baker RC. ACGIH recommends a BEI of 0. 2005. Leng G. Lewalter J.. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Morgan DP. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1995. Centers for Disease Control and Prevention (CDC). Pathak S. Environ Res 1995.110 Suppl 6:1075-1078. 2005. Lores EM. International Programme on Chemical Safety-INCHEM (IPCS). Chicago area methyl parathion response. Pesticide workers may have much higher levels following pesticide applications. Pope C. Kramer RE. Moomey CM. Rubin et al. Arch Environ Contam Toxicol 1977. Kissel JC. and levels were similar or slightly lower that those in a small convenience sample of the U. 2002. general population (CDC. Runkle KD. et al. a range of values several hundred times higher than levels found in the U. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.112(10):1116-1124. Toxicology 2005. Karanth S.5 mg (500 µg)/g creatinine for workers at the end of shift. Bradman A. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. 2004). 2005. Arch Environ Health 1978. Eskenazi B.33(5):270-276. population (Olsson et al. Hill RH Jr. Rev Environ Health 2006. Rockhold RW. DiPietro E.. Barr JR. Head SL. Baker S. Role of individual susceptibility in risk assessment of pesticides. Head SL. Needham LL.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.215(3):182-190.25(5):599-606. Moseman RF.14(4):213-216.21(1):5767. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Bailey SL. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Baker SE. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Turner WE.9:311-320. Griffith W. Methyl parathion: an organophosphate insecticide not quite forgotten.. McCann et al. Occup Environ Med 1999. Neurotoxicol Teratol 2003. Hryhorczuk DO.15(2):164-171. Third National Report on Human Exposure to Environmental Chemicals. Hill RH Jr. Gregg M. Barr DB.htm. 2005). Lin LI. Hetzler HL.S. Atlanta (GA). et al. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. J Anal Toxicol 1990. 2005). 2002. Parathion-Methyl (addendum).. Pesticide residues in urine of adults living in the United States: reference range concentrations. 1995). References Barr DB. Environ Health Perspect 2002. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Jewell NP.. et al. Lu C. Hill et al. and many residents were symptomatic (Barr et al. Environ Health Perspect 2002. Cline RE. 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. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Dharmani C. Kedan G.org/documents/jmpr/jmpmono/v95pr14. In a study of workers who handle parathion. 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. Environ Health Perspect 2004. Available at URL: http:// www. Weltzien E. Shealy DB. Slach EF. Giordano G. 1999). 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. Curl CL. oral or dermal administration. Alley CC. 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.56(7):449553.inchem.6(2-3):159-173.

Mengle DC. 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. Honegger P. Toxicol Lett 2006. Ames RG.S. 0153. Available at URL: http://www. Backer G. Facts. U. Slotkin TA. EPA).376(6):808-815. Olsson AO. Rosenberg J.04/106. gov/oppsrrd1/REDs/methylparathion_ired. Esteban E. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Appl Pharmacol 2004. EPA-738-FOO-009. External and internal exposure of wine growers spraying methyl parathion. Costa LG. Am J Ind Med 1991.pdf. Anal Bioanal Chem 2003. Available at URL: http://www. Available at URL: http://www. 2004. Hill RH Jr. Jung D. May 2003. Monnet-Tschudi F. 1992-2001. Methyl parathion in drinking water. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Environ Health Perspect 2002.E. Ryde IT.S. EPA). et al. Nguyen JV. The Quality of Our Nation’s Waters.162(2-3):219-224. Ethyl parathion. Sadowski MA.gov/circ/2005/1291/.110 Suppl 6:1047-1051. 2007 [online].gov/oppsrrd1/REDs/factsheets/0155fct. Letzel S.epa. Hill G. Geological Survey (USGS). Yacovac R.usgs. pdf. Environmental Protection Agency (U. Dunlop B. Case No. Available at URL: http://pubs.epa.20(4):533-546. 6/1/09 World Health Organization (WHO).S. 5/19/09 Zurich MG.Organophosphorus Insecticides: Specific Metabolites Muttray A. Pesticides in the Nation’s Streams and Ground Water. Rubin C. Investigation of a fatality among parathion applicators in California. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.D.S.114(10):1542-1546.201(2):97-104. revised February 15.S. March 2006. Schilter B. Osorio AM.who. WHO/SDE/WSH/03. Levin ED. Kieszak S. 1/14/09 U. Environmental Protection Agency (U. R. Barr DB. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Tate CA.int/water_sanitation_health/dwq/chemicals/ methylparathion.pdf. Environ Health Perspect 2006. 1995-1996. September 2000. Ohio. Seidler FJ. 1/12/07 U.

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

300-1.670 (<LOD-1. which may vary for some chemicals by year and by individual sample.780 (.700-1.580-1.94) .820) < LOD < LOD .250 (<LOD-. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 01-02 is 0.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th .200-.850 (.840) 669 687 929 Limit of detection (LOD.07) .780 (.210 (<LOD-.500 (.740 (.700-.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.780 (<LOD-1.610 (<LOD-1.680 (<LOD-.880) 567 810 1104 01-02 01-02 * * < 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 .950) < LOD < LOD 1. < LOD means less than the limit of detection.410 (<LOD-1.780 (<LOD-1.840 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210-.210-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals .760 (<LOD-.430 (<LOD-.55) .31) .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 .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .15) < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.740-1.27) .S.21) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.470 (. Survey Geometric mean (95% conf.17 (.64) .

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

WHO. 2003. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. agricultural fields. pyrethroid pesticides have less acute toxicity in animals and people.S. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U.. but may be poorly transferred across the placenta (ATSDR. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. by either ester hydrolysis or hydroxylation. They are also applied on livestock to control insects. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. 1992). followed by conjugation. resmethrin.S. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. Woollen et al. 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.. or carbamate pesticides. 2002). There are about 30 different pyrethroid pesticides in use. warehouses. Outside the U. 2002. In agriculture. 2005). 2005.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. 2006a. Compared with other classes of insecticides such as organochlorines. bind to soils. Soderlund et al. Certain pyrethroid insecticides (such as permethrin. pyrethroids are rapidly metabolized. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. 1997. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. organophosphorus. Unmetabolized pyrethroids have been measured in breast milk. and then eliminated over several days in urine and bile (Kuhn et al. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. 2006b).. animal facilities.. and synergists. cyfluthrin.EPA. Soderlund et al.. After absorption from inhalation or ingestion.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. This class of pesticides has low toxicity in birds and mammals. such as piperonyl butoxide.2-Dibromovinyl)-2. cypermethrin.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. in some situations replacing the use of DDT. so usage is restricted near water (U. 2007). Pyrethroid pesticides have low volatility. which are natural chemicals found in chrysanthemum flowers. but pyrethroids are highly toxic to fish and some aquatic invertebrates. Estimated intakes from diet and drinking water are below recommended limits. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. 2002). Generally. EPA.S... Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2003. 1999. 1992). Leng et al. and greenhouses. and deltamethrin have been used frequently on cotton. they are not persistent in the environment due to their rapid degradation within days to several months.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichlorovinyl)-2. solvent oils. and are rarely detected in ground waters (USGS.2-Dichlorovinyl)-2.. The table shows the urinary pyrethroid metabolites measured in this Report. They are ranked as having moderate acute oral toxicity. Pyrethroids are not well absorbed through the skin (ATSDR. and sumithrin) are also registered for use in mosquito-control programs in the United States. Woollen et al.

bioallethrin and deltamethrin. 2003. Leng G.107(3):173-177. 2005). Neurotoxicol Teratol 2001. Kuhn K.gov/toxpro2.html. Available from URL: http://www. Lewalter J. Chen JH. Go V. Bernardi MM. Garey J. motor activity. Leng G. Biochem Biophys Res Commun 1998. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Richardson JR. Pyrethroid pesticide-induced alterations in dopamine transporter function. Wolff MS. WHO. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. salivation. Sugiri D. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Idel H. cdc. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. 2006. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Yang J.gov/toxprofiles/ tp155. 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. 2006. et al. Toxicol Appl Pharmacol 2006.. 2001.. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. 1999.html. Ranft U. and permethrin) in the Hershberger and uterotrophic assays.cdc. et al. Int J Hyg Environ Health 2002. Estrogenicity of pyrethroid insecticide metabolites.. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO.S. et al. 2006). paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. tremor. 2005). Kim HS. Spinosa HS. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. and striatal dopamine levels in male and female rats.8(1):197-202. Wolff MS. Shaw IC. Moniz AC. In developing rodents. Salzgeber SA. September 2003.62:101-108. et al. Shin JH.205(6):459-472. J Reprod Dev 2004.. Eriksson and Fredriksson.251(3):855-859. hypersensitivity. Pauluhn J. Kuhn KH. Guillot TS.108(1):78-85. Neurosci Lett 2001. Wieseler B. Garey and Wolff. Seth PK. Moniz et al.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. References Agency for Toxic Substances and Disease Registry (ATSDR). Kunimatsu et al. epa. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Neurotoxic effects of two different pyrethroids. Berger-Preiss E.27(4):609-614. Neurotoxicol Teratol 2005. 2000. Adhami VM. Miller GW. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 2005). Hu JY.50(2):245-255.. Cruz-Casallas PE. Toxicol Appl Pharmacol 1991. 2001. Caudle WM. 2004. Yamada T. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Leng G. dopaminergic. EPA at: http://www. 2003. Ray et al. 2003. Idel H. Lazarini et al.27(12):1273-1283. In California. Pogo BG. Hu et al. Wang SL. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Sunami O. McCarthy AR. Toxicological profile for pyrethrins and pyrethroids... Elwan MA. neurochemical changes in cholinergic. Bull Environ Contam Toxicol 1999. Zhao RC. Generally. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. choreoathetosis. 1998. McCarthy et al. fenvalerate.23(6):665-673. Soderlund et al. Regul Toxicol Pharmacol 2002. Indoor pyrethroid exposure in homes with woollen textile floor coverings. J Environ Monit 2006.300(3):161-165.. 2002. Levsen K. Kunimatsu T. Go et al. Shukla Y. Song L. Kim TS. Additional information about pesticides is available from U. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. 2002). Kang IH. 2003. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Kim et al.atsdr. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring...gov/pesticides/ and from ATSDR at: http://www. Varoli FM.211(3):188-197. Lee SJ.atsdr. Fredriksson A.8(1):18-21.. 1991. Agrawal AK. Bernardi MM. Shafer. 2005). Abell AD. Ose K. Environ Health Perspect 1999. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Leng A. Okuno Y. Elwan et al..35(2 Pt 1):227-237. and seizures (ATSDR.. Kamita Y. Lemonica IP. Florio JC. Eriksson P. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Lazarini CA.1/15/09 Aziz MH. Garey J. Thomson BM. 2002). Kim IY. Xenobiotica 1997.

S. 1992–2001. Geological Survey (USGS).22(8):983-991.who. Available at URL: http://www. Available at URL: http://www. 5/26/09 U. sumithrin synthetic pyrethroids for mosquito control. Sargent D. Crofton KM. Soderlund DM.S.38:95-101. Pyrethroid insecticides: poisoning syndromes. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. et al. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://pubs.pdf. resmethrin. Shafer TJ.113(2):123-136. J Toxicol Clin Toxicol 2000.S. Safety of pyrethroids for public health use. June 2006a. World Health Organization (WHO).S. Available at URL: http://www. Available at URL: http://whqlibdoc. Xenobiotica 1992. Environmental Protection Agency (U. Revised February 25. Pyrethroid illnesses in California.S. Spencer J. EPA).Pyrethroid Pesticides Ray DE. EPA).gov/oppsrrd1/REDs/cypermethrin_red. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). April 2002. Pesticide and Evaluation Scheme. Clark JM.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. O’Malley M. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. 19962002. Mullin LS. Rev Environ Contam Toxicol 2006. 5/26/09 Woollen BH.epa.epa.epa.S. Laird WJ. U. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . pdf. Permethrin.usgs. Environmental Protection Agency (U. Sheets LP.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Environ Health Perspect 2005. 2005. synergies.171:3-59. 2007. Lesser JE.htm. Toxicology 2002. EPA). and therapy. Meyer DA.10. June 2006b.htm. Forshaw PJ. Environmental Protection Agency (U.S.gov/ circ/2005/1291/. Reregistration Eligibility Decision for Cypermethrin. Marsh JR. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.186:57-72. 5/26/09 U. Piccirillo VJ. March 2006. 5/26/09 U.

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

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

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

Spencer J. Arch Environ Contam Toxicol 2004. Drexler H. Berger-Preiss E. Leng G. Hoppe HW.77(1):67-72. Seiwert M. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Int J Hyg Environ Health 2003. Angerer J. Ball M. Butte W. Ranft U. Krieger RI. Angerer J. Int Arch Occup Environ Health 2004.206(2):85-92. Int J Hyg Environ Health 2006.13(2):112-119. Heudorf U. 2005. Sugiri D.186:57-72.46(3):281-288. et al. Heudorf U. 19962002. Olsson AO. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Atlanta (GA). Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Bernard CE. Schulz C. Pyrethroid illnesses in California. O’Malley M.209(3):221-233. J Expo Anal Environ Epidemiol 2003. Williams RL. Human exposure to indoor residential cyfluthrin residues during a structured activity program.Pyrethroid Pesticides References Baker SE. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Becker K. Hadnagy W. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Third National Report on Human Exposure to Environmental Chemicals. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Environ Health Perspect 2001. Int J Hyg Environ Health 2006. Rev Environ Contam Toxicol 2006.109(3):213-217.209(3):293-299. Angerer J. Barr DB. Heudorf U. Idel H. Kolossa-Gehring M. Centers for Disease Control and Prevention (CDC).

630) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.53) .44 (. population from the National Health and Nutrition Examination Survey.280-.80) .790) .410) .or trans-3-(2.300-.2-Dichlorovinyl)-2. more of the trans-metabolite than Urinary cis-3-(2.77 (.202 (. 1999). which may vary for some chemicals by year and by individual sample.470 (. the presence of trans-3-(2.520) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Cyfluthrin.600 (.670-1.68 (.160 (. Survey Geometric mean (95% conf.200) < LOD < LOD < LOD .68359-37-5 Cypermethrin Permethrin CAS No.710-1.68) .210) 90th .1 and 0.13 (.460 (.950-2.640 (..160 (<LOD-.2-dichlorovinyl)-2.300 (.670-2.330) .280 (.490-1.900 (.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.210-.220-.300-.12 (.890 (.S.870) 1.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .220-.230) .350) .15) .510 (.630) .550) .and trans-isomers.680 (.790 (.110-.380 (. cis-3-(2.200 (.790-1. cis-permethrin.770-1.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.510 (.910-5.180 (. and ciscyfluthrin. but it can also reflect exposure to cis-3-(2.670-1.600-1.730 (.35) .24) 1. Similarly.08) .270-.200-.240) . The chemical trans-3(2.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.380-.820 (.630 (.50) .500 (. Kuhn et al.270 (.160 (.890 (.120-.730 (.200-.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . trans-cypermethrin. Fourth National Report on Human Exposure to Environmental Chemicals 163 .155-.110-. In the body.380) .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 .2-dichlorovinyl)2.200) .740-2.32) .780) .140 (<LOD-. cis-cypermethrin.110 (<LOD-.420-.470-1. 1999).400-.490-.490-.310) .270 (.200) .120-.370-.610) . The presence of cis-3-(2.410) .920) 1.440 (. 52315-07-8 CAS No.600) .250 (.68) ..180) .220) .530 (.770) .850 (.2-dichlorovinyl)-2.210) .2-dichlorovinyl)- CAS No. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Kuhn et al.270 (.730 (. Generally.200-.2dichlorovinyl)-2.500 (.140 (.740-1.47 (.380-.740 (.43) .150 (.650-1.490-1.35) 1.340-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. and trans-cyfluthrin.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .2-dichlorovinyl)-2.1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.570 (.240) .220-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.580) 1.610) .21) .790-1. but can also reflect exposure to trans-3(2. 1985.740) 1. trans-permethrin.960 (.11) .54) .460-.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.460-1. ciscypermethrin and cis-cyfluthrin.110-.120-.680-3.120-.690) . 1985.28) 671 680 518 701 591 957 Limit of detection (LOD.710) . transcypermethrin and trans-cyfluthrin.630-. Biomonitoring Information Urinary levels of cis.340) .510 (.2dichlorovinyl)-2.580-1.700) .340) .07 (.262) * * * < LOD < LOD .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.570-.250-.370 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220-.330 (.170 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.380-.670 (. < LOD means less than the limit of detection.880 (.260 (.430-.300 (.

.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U..200 (.600 (.250) . In a study of urban residents in Germany (Berger-Preiss et al. 2005).130-.Pyrethroid Pesticides 2.260 (.890) .340-.640-1.470-1.080-.680-1.890 (. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. 2005). Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.250 (<LOD-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.and trans-3(2.710-3. 2005) In a small group of indoor pest-control operators.380 (.440 (.450 (.780 (.and trans-3-(2.340) .510-1.300 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.150-.250-.370-.360-1. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.540 (.. In these volunteers.150-.2-dimethylcyclopropane carboxylic acid did not increase.11) 1.190) .430-.170 (.250-.700) .430 (.380) .690-1.880) .400 (.550-1.03) 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 .150-.400-1. representative NHANES 2001-2002 subsample (CDC.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . post- Urinary cis-3-(2.340) .640) 1.280-.710 (.2-dichlorovinyl)-2.320) .270) .180-.180 (. 2002).550) . Cyfluthrin.590 (.830) .700) .260 (. 2006. 2005).300-. urinary levels of cis-3-(2.190 (.11) .67 (.290-.80) .2-Dichlorovinyl)-2. Studies in Germany of 396 children and adolescents (Becker et al.260 (.440-.390-.290) . In the same residents. 2002).21) .550) .520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .810 (.420 (. 2004.280 (.170) < LOD < LOD < LOD .540 (.900 (.260-.104-.160 (<LOD-.300 (.220) .300) .210-.250) 90th . population from the National Health and Nutrition Examination Survey.390 (. urinary trans-3-(2.2dichlorovinyl)-2.640 (.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.33) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In a study of volunteers.270-..230-.440 (.11) .. Schettgen et al.31) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al. Lu et al.750-1.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.290) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.59) .350) . the median and 95th percentile of urinary levels of cis-3-(2.450-1.2-dichlorovinyl)-2.59) .300) .560) .580) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.570) .270 (.29 (.270) .230-.430-1.410) .920 (.290 (. 2001) showed urinary levels of cis.680-1.640-.S. 2004).2dichlorovinyl)-2.780) 1.120 (. 2005).450-.67) .12-2.700-2..190) . 2006.320-.140-.840 (.138 (. 2006).800 (.370-.2-dichlorovinyl)-2.S.530 (.33 (.230-.680 (.440-.200-.260) .170 (.540) .59 (1.250) . 2001. 2006). median urinary levels of trans-3-(2.24) .550 (. Other studies have provided evidence that urinary levels of cis. 2006) and 1177 urban adults and children (Heudorf et al.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.590) .380-.220 (.49) .12 (.200-.200) .390-.530 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.560) 1.500 (.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.182) * * * < LOD < LOD .220 (...840 (..240 (<LOD-.580-1.230 (.. Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.250-. 164 Fourth National Report on Human Exposure to Environmental Chemicals .11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .640-1. 2003).750 (. 2003).370-.03) 1.37) .550-1.350 (.11 (.

460-.or trans-3-(2.40 (1. population from the National Health and Nutrition Examination Survey.560 (.20 (.910-1.940 (.28 (2.68) 1.08) 1.68) 2.60-4.660) 1.01) 4.68-3.500 (.670) .610) 1.680-1.43) 2.4. Finding a measurable amount of cis.54 (1.700-1.90) 1.860) .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 . 2005).410-.23) 2.410 (<LOD-.830-1.Pyrethroid Pesticides application median urinary levels of summed cis.11-2.25 (1.800-1.480-.66) 691 680 518 690 595 954 Limit of detection (LOD.730) .97-11.95) 3.76-3.66) .91 (1. < LOD means less than the limit of detection. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring studies on urinary levels of cisor trans-3-(2.780 (.S.09 (.63) 1.20 (.56 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.50 (1. Survey Geometric mean (95% conf. Urinary trans-3-(2.63) 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .520-. trans-Cypermethrin.56 (1.85) 4.69 (1.41-14.59 (1.81) 2.26 (.17 (.400 (<LOD-.14) 1.2dichlorovinyl)-2.410 (<LOD-.14-2.14-6.42 (2. The maximum post-application urinary levels. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08-6.28 (1.49-3.60) 1.410-.41 (1.69) 1.23 (.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .56) 2.77) 2. however.840-1. which may vary for some chemicals by year and by individual sample.68-2.620) < LOD 2.470 (.08-4. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.48) 4.820) .700) .13) .2-dichlorovinyl)-2.10) 2.39 (1.22 (1.25-3.420 (<LOD-.56) 2.76-4.49-3.87 (1.07-3.550 (.49-5.37 (1.54) 4.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.670) .11-1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.400-.55-3.12-6.94 (1.55-5.77) 1.5) 2.920-1.750) .07 (1.470 (<LOD-.35) 1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.16) 1.970 (.20 (.84 (1.55-4.68) 1.60) .460-.440 (<LOD-.710 (.560 (.570) 90th 1.530) .500-.560 (.810-1.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.17-1.27 (1.19 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.19 (3.910-1.and trans-3-(2.850-1.03-1.7) 2.39-5.01 (1.64-4.760) .2-Dichlorovinyl)-2.62 (1. 2005).77 (1.580 (.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .490 (<LOD-.500) .17 (.03-1.520) .2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.490-1.89 (2. Fourth National Report on Human Exposure to Environmental Chemicals 165 .42) 1.4 and 0.95) 2.19) 1.2-dichlorovinyl)-2.

86 (2.930-1.3) 2.740) . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.42 (.33-2.64 (1.900 (<LOD-1.720-1.40-2.15) 3.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-Dichlorovinyl)-2.60) 2.610-.07) 2.730) .31 (2.55 (2.70 (. population from the National Health and Nutrition Examination Survey.91-11.16 (1.98 (1. Survey Geometric mean (95% conf.15) 2.07-2.800-1.60 (1.12 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.00) 1.640) .00-5.36 (1.44) 2.22-1.07-1.880 (<LOD-1.13) 1.00 (1.56-5.67 (2.33-1.65 (2.S.19 (1.39 (1.15-3.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.880 (.41) 1.750) .11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .30-6.800-1.61) 1.07) 2.87) 1.11) .08 (. 166 Fourth National Report on Human Exposure to Environmental Chemicals .850) 1.55 (2.15-3.57 (1.850-3.91) 1.27-2.30-3.22) 1.780 (<LOD-.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 .81 (2.500-.660) .670) . trans-Cypermethrin.410-.20-2.89) 2.74) .780) 90th 1.33 (1.850) .560 (.87-8.530 (.540) .570 (.570-.470-.42) 1.39) 1.700 (.56 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.36) 2.15-3.47-2.820-2.440-.13) .74) 2.580) .08 (.68) 3.880-1.700 (.27-2.07-3.970 (.45-2.87-3.75 (1.470 (.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.56-2.29) 1.57) 3.12-1.26 (1.45 (1.48-2.55 (2.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.570 (<LOD-.37 (1.520 (<LOD-.47 (1.530 (<LOD-.20 (1.35 (1.34-3.80) 1.480-.02-1.65) 1.720-1.31) 1.91 (1.31 (.48 (1.35) 1.760 (.770) < LOD 2.580 (.Pyrethroid Pesticides Urinary trans-3-(2.87 (1.47-2.700-.720 (<LOD-.00) 1.28) 2.15 (1.780) .87) 1.60) 2.34-4.00) 5.19) .22-2.

114(9):14191423. Idel H. Environ Health Perspect 2006. Idel H. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Sugiri D.209(3):221-233. Schettgen T.205(6):459-472. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Int Arch Occup Environ Health 2003.68(6):1160-1163. Leng G. Ball M. Ranft U. J AOAC 1985. Drexler H. Levsen K. George DA. Berger-Preiss E. Heudorf U. Idel H.62:101-108. Barr DB. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides.209(3):293-299. Centers for Disease Control and Prevention (CDC). Leng G. Angerer J. Drexler H. Hardt J. Int J Hyg Environ Health 2002. Hadnagy W. Berger-Preiss E. Angerer J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Angerer J.134(1-3):141-145. Heudorf U. Bartell S. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Lu C. Butte W. Third National Report on Human Exposure to Environmental Chemicals. Angerer J. Int J Hyg Environ Health 2003. Schulz C. Kuhn K. Seiwert M. Wieseler B. Atlanta (GA). Heudorf U. Leng G. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Angerer J. Pearson M. Int Arch Occup Environ Health 2004. Heudorf U. Biological monitoring of workers after the application of insecticidal pyrethroids. et al. Ranft U. Angerer J.109(3):213-217.77(1):67-72. Sugiri D. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Environ Health Perspect 2001. 2005.76(7):492-498. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Hoppe HW. Permethrin and its two metabolite residues in seven agricultural crops. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Int J Hyg Environ Health 2006.206(2):85-92. Bravo R.Pyrethroid Pesticides References Becker K. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Bull Environ Contam Toxicol 1999. Int J Hyg Environ Health 2006. Kolossa-Gehring M.

2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. Deltamethrin can degrade to cis-3(2. Urinary levels for adults and children in these studies were similar (Heudorf et al. Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2. 2005).2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.. Outside the U. urinary levels of cis-3-(2..Pyrethroid Pesticides Deltamethrin CAS No..2-dibromovinyl)-2.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample.1 μg/L) for the NHANES 2001-2002 subsample (CDC. 2001. Finding a measurable amount of cis-3-(2. (2004) reported a geometric mean concentration of cis-3(2. in some situations replacing the use of DDT.. 52918-63-5 General Information Cis-3-(2. deltamethrin has been used against mosquitoes that carry malaria. 2005). Baker et al.2-dibromovinyl)-2.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2. 1990). 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Thus. 2005).2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dimethylcyclopropane carboxylic acid of 0.2dimethylcyclopropane carboxylic acid formed in the environment.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. 2006) and 1177 urban adults and children (Heudorf et al.S. mean peak urinary levels of cis-3-(2.2-dibromovinyl)2.3-0.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. Studies in Germany of 396 children and adolescents (Becker et al.2-dibromovinyl)-2.2-dibromovinyl)-2. 168 Fourth National Report on Human Exposure to Environmental Chemicals . Following residential spraying with deltamethrin for malaria protection in Mexico.5 μg/L) than the detection limit (0. in detection of cis-3-(2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. 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.39 µg/L.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects...

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

2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 170 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.Pyrethroid Pesticides Urinary cis-3-(2.2-Dibromovinyl)-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. 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.

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

2005). In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 52918-63-5 use and house dust levels (Lu et al. In one study of 145 urban residents in 80 private homes in Germany. 52645-53-1 Tralomethrin CAS No.. CDC. 2005. 2002..S. 68359-37-5 Cypermethrin Deltamethrin CAS No. Hardt and Angerer.. 2005). Following residential spraying with deltamethrin for malaria protection in Mexico.. In the New York City study. 2005). Saieva et al. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. 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. 2005. 2006. In a small group of indoor pest-control operators. CDC. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. 2003. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Fenpropathrin Permethrin CAS No. 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. 2006) showed that urinary levels of 3-phenoxybenzoic acid at the 95th percentile were similar to levels at the 95th percentile for children in the U. 2005). 2004). 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. A study of 396 German children (Becker et al. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. 2005). The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 2003. 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.. 39515-41-8 CAS No..Pyrethroid Pesticides Cyhalothrin CAS No. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. Baker et al. 2005). Becker et al. 2003).. 2005). Thus. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 2006).. CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides.52315-07-8 CAS No. 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 . the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. representative NHANES 2001-2002 subsample (CDC.

277-.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 .273 (.27-2.45-5.27-11.62-8.586) .595) .41 (1.510-.300 (.44) 5.32 (2.330) .1 and 0.41-3.16) 1.1) 3.32-21.450 (.280 (.700 (.14-6. Deltamethrin.560-1.30 (.04-5.336 (.200-.62) 5.210-.210-.34-6.250-.560-.850) .265-.253-.160-.93 (1.507 (.700-1.49-2.990) .620-1.53) 1.18 (2.54) 1.05) 1.230-.26) 2.374) 99-00 01-02 99-00 01-02 99-00 01-02 .250 (.36) 1.590-.S.190-.680 (.04) .35) 2.740 (.45 (2.26) 2.50 (2.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .51-3.180-.960 (.340) 75th .295) .63 (3.300 (.830) 90th 1.03 (3.32 (1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.42-2.530-.56-5.79) 3.325 (.427) .314) .190-.800 (.38 (2.270) .610) .35 (1.340) .27-2.49 (1.321 (.570-1.02-6.29-1.65-2.870 (.25 (2.352-.710 (.266-.48-2.25-7.33 (2.1.233-.520 (.362) .406) .35) 2. Fourth National Report on Human Exposure to Environmental Chemicals 173 .25-4.46) .320) .13) .530-.320) .369) .230-.298 (.34) 8.454 (.390) .320) .12) 4.260 (.820) .49 (1.387) .51-6.64) 697 680 524 701 603 957 Limit of detection (LOD.740 (.650 (.21 (2.230-.53-3.271-.73) 1.820) .276-.63-3.12) .160-.65 (1.230 (.830-2.250 (.46) 2.01 (1.810) 1.350-.1) 3.16-1.311 (.510-.76 (1.8) 3.780) 4.750) . interval) .550-.300 (.78) 1.78 (1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.246-.226-.238-.267 (.35 (2.417 (.940) 1.328 (.490) .370) .240 (.71 (1.33 (1.55 (1.297 (.364) .601) .34 (2.430-.330) .25-1.490-.60) .1) 3.345) Selected percentiles ( 95% confidence interval) Sample 95th 4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.62-6.260-.430-.353 (.630) .200-.41) 3.35) 1.83-11.570-.30) 3.434) .315 (.850) .288-.18 (1.52-4.640 (.33) .710 (.69) 3.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .230 (.300) . Survey Geometric mean (95% conf.590 (.560-.292-.190-.290 (.39) 2.240 (.28) 1.260 (.373) .227-.800) 1.25 (2.840-1.69 (1.12 (.360) .26-2.314 (.23 (2.52-5.43) 3.247-.340) 1.75 (1.49-2.760 (.200-.270 (.72 (1.220-.470-.78) 1.420) .750) .86 (1.750-1.288 (.428-.30 (1.41-2.260 (.13 (.81 (1.320) .730 (.90) 1.320 (.384) .440) .05) .89-71.190-.38 (2.292 (.48-2.78) 6.92-3.600 (. population from the National Health and Nutrition Examination Survey.670 (.355) .250 (.

43 (2.740) .49) 1.860-1.229-.225-.91 (2.362 (.290) .330) .00) 1.27) 1.329) .590) .460-.190-.261 (.48 (1.280) .311 (.278) .274-.09) 3.310) .25) 2.400-.510 (.750-1.390-.930) 1.240 (.43-64.72 (1.329) .530-.64-5.270) .61-2.35-3.25-5.357) .36 (1.11 (.590-1.52) 2.240-.480-.300-.238-.250 (.36-6.677) .440-.11 (.400-.03 (.490 (.88-5.37) 1.74) 3.62) .95) 1.316 (.35 (1.330 (.309 (.240 (.250 (.81 (1.590) .380-.290) .272) .510 (.21-4.240 (.350 (.73-4.810) 1.15-2.07) 2.25-2.300-.410) .274 (.220 (.253) .570) .91) .590) .19) 2.240 (.440-.90) 3.19 (2.160-.280) .43 (1.220-.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 .54 (1.270-.272 (.35) 1.400) .437) .202-.423 (.270) .84 (1.190 (.19-6.210-.580 (.630) .280-.73) 1.640 (.13-1.720) 90th 1.67) 1.67 (1.500) .200-.178-.280 (.63-3.39) 1.320) .670) 3.00) 5.370-.534) .150-.730) .670) .63) 1.440-.37 (1.530-.09-2.330) 1.02 (2.91-4.240-.264 (. interval) .60) 1.04 (3.280 (.309) .92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 . Deltamethrin.44 (1.378 (.640 (.200-.83 (1.04 (.960-1.02-1.13-1.230-.323 (.420-.67 (1.860 (.190-. Survey Geometric mean (95% conf.330) 75th .760) .13 (.226-.580) .52 (1.550 (.173-.540 (.230-.210 (.S.16-4.271-.299-.490 (.290-.49 (1.75-8.250) .246 (.275 (.650) .321-.370 (.234 (.200-.03-1.06-3.240-.51-7.510 (.21 (1.22 (1.216-.700-1.41) 1.335-.450 (.43) 1.330) .312 (.0) 3.55) 3.365) 99-00 01-02 99-00 01-02 99-00 01-02 .410-.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .200-.53 (1.09-2.460-.00) 1.860-1.94 (1.480 (.387) .610 (.490-.80) 4.328) .86 (1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.09 (.401) .41-4.730-1.49-2.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .32 (2.380 (.372) .40) 2.930) .44) 2.446) .55 (1.261-.96 (1.10 (2.560 (.230) .91) 9.840-1.40 (1.83) 1.35) .280 (.720 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.550 (.350) .60-4.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.240-.550 (.17-1.224-.17 (.07-5.227 (.05-3.49) 3. population from the National Health and Nutrition Examination Survey.210 (.730) .270 (.62) 1.270 (.

Angerer J. Batres LE. urban cohort. Lopez-Guzman OD. Bravo R.46(3):281-288. Sugiri D.Pyrethroid Pesticides References Baker SE.111(1):79-84. Environ Health Perspect 2003. Obel J. Carranza C. Angerer J. Int Arch Occup Environ Health 2003.113(6):782-786. 2005. Arch Environ Contam Toxicol 2004. Barr DB. Sugiri D. Levsen K. Third National Report on Human Exposure to Environmental Chemicals. Lu C. Ball M. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.114(9):14191423. Bartell S.206(2):85-92. Exposure to indoor pesticides during pregnancy in a multiethnic.209(3):221-233. Becker K. and genotoxicity in exposed children. Idel H. Ortiz-Perez MD. Ranft U. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. et al. Hardt J. Leng G. Centers for Disease Control and Prevention (CDC). Hadnagy W. Pearson M. Deych E. Torres-Dosal A. Environ Health Perspect 2005. Hoppe HW. Biological monitoring of workers after the application of insecticidal pyrethroids. Int J Hyg Environ Health 2002. et al. Grimaldo M. Berkowitz GS. Int J Hyg Environ Health 2003. Kolossa-Gehring M. Atlanta (GA). Olsson AO. Godbold J.205(6):459-472. Environ Health Perspect 2006. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Barr DB.76(7):492-498. Int J Hyg Environ Health 2006. Berger-Preiss E. Seiwert M. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. toxicokinetics. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Lapinski R. Berger-Preiss E. Liu Z. Ranft U. et al. Leng G. Idel H.

140 (. 01-02.350 (.148-.300) .190-.180) .160) .114) .130) .099 (.270) .154) .410) .131-.150 (.430 (.120) .260 (.Metals Antimony CAS No.250-.510) .280) .120-.280-.290-.350-.200 (.150 (.330) .126 (.310-.530) .200 (.200) .250-.150) .260) .250-.143 (. coal-fired plants.070 (<LOD-.210 (.360) .175 (.160) .180-.460) .330 (.128 (.320 (.330 (.120-.095 (.130 (.230) .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 .128 (.180-.330) .240-.190 (. The absorption.410) .390) .210) .156-. ammunition.160-.140) .360 (.400 (.240 (.110-.340 (.190) .120-.280 (.080-.710) .220-.220-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.146 (. to a lesser extent.270 (. Dermal contact with soil.160) .120-.125 (.310) .250-.260) .310 (.145 (.350 (.140) .180 (.136) * .320-.100-.180 (. 0.260 (.300 (.090-.178) .230) .240 (.120-.137) .260-.070 (<LOD-.190) .260-. metal bearings.330) .090 (.350 (.280-.270) .400 (.130 (.430 (.570) .160-.270 (.330) .240 (.260 (.160) .190-.410-.500) . 0.130-.117-.130 (.240 (.220-.230 (.126-.270 (.190 (.100 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .087-.170-. interval) .420) .157) . Antimony enters the environment from natural sources and from its use in industry.400) .170) .115-.210 (.160) .160 (.310 (.170 (.180-.330 (.120-.470) .350 (.150) 90th .210) .340) .360-.150-. water.110-.190 (.130-.270-.140) .350-.120 (.320) Total .230) .390-. and refuse incinerators that process or release antimony. Antimony can exist in one of four valences in its various chemical and physical forms: -3.210) .430 (. 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-.330-.120-.150-. Stibine is a metal hydride form of antimony used in the semiconductor industry.093 (.440) .109-.200 (.290-.280) .200-.460 (. and pewter.130 (.07.210) .320) . sheet and pipe metal. fireworks.390-.150) .120-.250 (.142 (.100) .400-.200 (.220-. from air and drinking water.500) . distribution. People are exposed to antimony primarily through food and. Workplace exposures can occur at smelters. solder.290 (.132 (.119-.240) . population from the National Health and Nutrition Examination Survey.350 (.197) .130-.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .190-.140) . It is used in metal alloys.115) .320-.120) .169 (.350) .180-.130-.250) .600) .280 (.150-.130) < LOD .130 (.079-.300-.130) .280) .207) .133) * .140) .360) . 7440-36-0 General Information Antimony is found in ores or other minerals.110 (.210-.350) .190 (.400) .130 (.470 (.300 (.080) . see Data Analysis section) for Survey years 99-00.160 (.170-.250 (. or other substances containing antimony is another means of exposure.150 (.250 (.400) .230 (.240-.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 .300-.134-.440) .220) .137) .160) .120) .200) .470) .184) .180 (.390) .460 (.088-.119) .310-.120 (.110-.108-.160-.120 (.490) .160-.230-.180 (.170 (.100 (.150-.140) .220-.230-.320 (.330-.560) . and glass.230-.090) 75th . It is also used in paints.160 (.310 (. and +5.110-.176 (.220 (.370) .190-.130-.141-.190) .220 (.390) .220-.134 (.070-.210) .200) .350-.135) * .180) . and 03-04 are 0.132 (.350) . and excretion of antimony vary depending on its oxidation state.120 (.260) .080 (<LOD-.130-.161) .120) .154) .270 (.105 (.220) .200 (.117-.110) .S.080) .154-.340 (.170-.090 (<LOD-.210-.200-.140 (.170-.370-.120-.200-.390-.320-.136-. < LOD means less than the limit of detection.350) .150-.490 (.098-.120 (.158 (.460 (.144) .095-.122 (.280-.180-.200-.108 (.390 (.310 (.190) .145) Selected percentiles ( 95% confidence interval) 50th .180 (.300) .200) .280-.200 (.130 (.112-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.230 (. enamels.230-.440 (.103) . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.220) 95th .04.140 (.123 (.130 (. and 0.090-.164-.280-. storage batteries. which may vary for some chemicals by year and by individual sample.320-. +3.240 (. respectively. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.360 (.140 (.280) .400 (.150) .230-.390) .190 (.180 (.04.300-.190-.300) . ceramics.130) . castings.170-. and as a fire-retardant in textiles and plastics.130-.140-.310) .220) .190) .

238 (.261) .135) .121 (.130) .121 (.255-.267-.338 (.086 (.136) .320 (..371 (.146-.069-.068 (.115 (.159-.075 (.263 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.308) .255) .061-.148-. 1995). 1986).480) .195 (.085) .228 (.120 (.095-.138-.098) .209 (.112-.178-.161) .417) .143) . and ulcers (Werrin.098-.152) .143) Selected percentiles ( 95% confidence interval) 50th .078 (.118 (.405) . species.204-. and eyes.176-.241-.471) .139 (.259 (. 1954).414) .191 (.156-.102-.100 (.206-.099-.185-.229-.391) .352) .298 (.338 (.179-.146-.357-. Inorganic antimony salts irritate the mucous membranes. abdominal pain.117-.153-.471 (.082) .082 (<LOD-. myocardium.164-.164) .300 (.149) .163 (.111-.203) . 1973).129 (.192 (.429 (.147) .741 (.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 .225 (.233) .321) .300) .438) .138 (.171) .124-.220) .143 (.280 (.076-. resulting in hemolysis with abdominal and back pain (Dernehl et al.217 (.109 (.123) .200) .120 (.127) .227-.129 (.167 (.214) .146-.108-.318-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.129) .082) .095-.135 (.268) . Acute antimony poisoning may cause a metallic taste.333-.104-.129) * .Metals than for trivalent compounds (Elinder and Friberg.120 (. diarrhea. 1944).143) 90th . and kidney have been demonstrated in high dose animal studies depending on the dose.150-.352 (.276 (.106-.225) .076-.113-. Ming-Hsin et al.278 (.447 (.317) .127) .131-.250 (.105-.244-.107-.126 (.103-.102-.189 (.114 (.127) .203) .069-.310) .135) . 1962).127 (.113-.238) .30) .181) .248) .333-.108-.081) .266 (.149-.250) .245) .192) ..239-.107-.112 (.117-. 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.131) .222 (.176 (.124 (.173) .248-.256 (.074 (.079 (<LOD-.173 (.182 (.200-.317) .133) .123 (.104-.265-.186) .151) .132 (.098-.236 (.084) .205-.116-.193 (.115 (.500) .135) .295 (.209) .192-.140) < LOD .209-..118 (.333 (.119-.333-1.338) .152) .109-.271-.400 (.178 (.114 (.391) .250-.230) 95th .193) .125 (.187) .097-.241-.242-.071-.162-.213 (.124) .172-.228-.265 (.224 (.485) .288 (.122 (. 1986).209) .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.333 (.364 (. liver.317) .121) .108 (.310) ..444) .087) .185 (.357) .211) .421) . and gastrointestinal symptoms such as vomiting.228 (.315) .075 (.195-.113) .145) .140) .144-.277 (.106-.200-.092) . and route of exposure (Elinder and Friberg.200-.281-. 1958) and occupational exposures (Briegner et al.385 (.122 (.159-.080 (.156 (.111 (.333) .128-.130 (.727) .267) .116 (.364 (.080 (<LOD-.119 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes. Fourth National Report on Human Exposure to Environmental Chemicals 177 .146) .130) . population from the National Health and Nutrition Examination Survey.253 (.125-.150-.112 (.086) 75th .175 (.164 (. interval) .257) .233-.247) .148-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.207) .115) .163 (.173-.114 (.117-. 1988.173 (.320) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.272) .310 (.115 (.139 (.181) .429) .148) * .159-.119-.120 (.154-.107-.108-.343 (.313-.280-.138-.130) .294) Total .124-.196 (.320-.134) .308-.250 (.250-.195-.068-.099-.380 (.430) .278) .183) .089) .286 (.425) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.127) . Histopathologic inflammatory and degenerative changes in the lung.081 (<LOD-.267 (.153 (.188) .208-.194-.143) .181) . skin.208 (.131 (.300) .226 (..333 (.318-.188-.115-.333-.115-.147-.S.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 .176 (.444) .320-.238) .230-.161) .417) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.135 (.320 (.170 (.160 (.137 (.741) .199-.092-.126) .126-.109 (.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 .132) .167-.138) * .253-.167 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.096-.198) .077) .185 (.373) . 1953).263-.269 (.250-.233 (.235-.103-.167 (.250-.

Delves HT. Fuchs A.. Antimony in blood and urine of infants. Suchenwirth R. Piatnek DA. J Occup Environ Med 2004. 1986.64(2):182-185. Pozzoli L. environmental levels) and health effects is available from ATSDR at: http://www. Hamilton EI. arsenic.76:432436. Schaller KH. Urinary antimony in infancy. Mahieu P. indium. Nau CA. 20012002. Third National Report on Human Exposure to Environmental Chemicals. Review of elements in blood. Biomonitoring of a worker population exposed to low antimony trioxide levels. Information about external exposure (i. and future strategies. Br J Ind Med 1991. J Trace Elem Med Biol 2002. 1995. Yu H-S. Nordberg GF. Petrucci F. Sabbioni E. Industrial antimony poisoning. Ho C-K. Atlanta (GA). Briegner H. Delves HT.. Element reference values in tissues from inhabitants of the European community. Stead FM. Chin Med J 1958. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Elinder CG. Earlier measurements in general populations (Minoia et al.158:165-190. Kentner et al. Stasney J. 1997).. Handbook on the toxicology of metals. Chen J-R.51:238-240. Shao-Chi C.59:469-474. et al. Dunkelberg. Cheng-Wei L. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Carelli G.. 2nd ed.48:93-97. Biological monitoring of exposures to aluminum. O’Regan M. Arsine. Stocks J.. Trace element reference values in tissues from inhabitants of the European community I. Int Arch Occup Environ Health 1987.. Luedersdorf R. Skulsukai G. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Buchet JP. Kiberd B.. Industrial Medicine 1944. Friberg L. 1987). Liao Y-H et al. Wu M-T. Minoia C. Iavicoli I. and 2003-2004. Gebel TW. which may be due to methodologic. VI. Lenert G. Alimonti A. Mayne P. Pietra R. clinical efficacy. 2002. gov/toxpro2. Dernehl CU. 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.html. and hydrogen sulfide.)1954. Kentner M. Lauwerys R. Konings J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. EPA. References Berman JD. Dezateux et al. or exposure differences. Cordasco EM.46:931-936. Matthews T. 1998.106:33-39. eds. Semisch CW. Vouk VB. Antimony. respectively. Leinemann M. population. Wade A. Cullen A. Sci Total Environ 1994. Caroli S. Chia-Yu H. Industrial Medicine and Surgery (Dec. Chemotherapy for leishmaniasis: Biochemical mechanisms. 26-42.e. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Centers for Disease Control and Prevention (CDC). Dezateux C.cdc. Kuo-Juie Y.67:119-123. 2005. Rev Infect Dis 1988. Ming-Hsin H. Environ Health Perspect 1998. Antimony trioxide is rated by IARC as a possible human carcinogen. stibine. and antimony in optoelectronic industry workers. 1991.Metals to antimony have been established by OSHA and ACGIH. Biological assessment of exposure to antimony and lead in the glass-producing industry.76(2):103-115. In: Friberg L. Schacke G. 1998) or compiled reference ranges (Hamilton et al. Int Arch Occup Environ Health 1995.S. Stone FD. Pilgrim L. Paschal et al. Pulmonary edema of environmental origin..10(3):560-586.. External and internal antimony exposure in starter battery production. Yang C-Y. Bailly R.521-523.. Iavicoli et al. Apostoli P. Costeloe K.16: 33-39. Van der Venne MT. J Clin Pathol 1998. Mayer P. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. 2004.13:361-362.. HH. 1990. Roland H. Arch Dis Child 1997. and a drinking water standard has been established by the U. 1994) have reported values slightly higher than those in this Report. Gallorini M.atsdr.. Biomonitoring Information Levels of urinary antimony reflect recent exposure. et al. Weltle D. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. plasma and urine and a critical evaluation of reference values for the United Kingdom population. pp. Liao Y-H. gallium. New York: Elsevier. Ju-Sun P. et al. Ludersdorf et al. 1998). even when exposure levels were below workplace air standards (Bailly et al. Bolten C. Sabbioni E. Chest 1973.

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

6-141) 53.6 (13. sodium arsenite.00 (6. population from the National Health and Nutrition Examination Survey.70-9. aluminum.4 (7. from coal burning.5) 66. and foods. and arsenates (oxidation states of -3.5-41.2-61.0 (15.2-20.90-11. arsenites. ocean and fresh waters. and indium arsenides are used in the semiconductor industry. Gallium.9) 21. Arsenic is measurable in most soils.10 (6.29 (8.90) 16.90-14. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. lead.6-35.90-7. to a lesser extent.2-93.97) 8.S.4 (31.8-61. Also.3-15.2) 15.8) 30.9-34.40) 7.8 (48. 2001). see Data Analysis section) for Survey year 03-04 is 0.6 (15. Survey years 03-04 Geometric mean (95% conf. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.90 (5.8) 7. Various arsenic compounds were used in paint pigments and for tanning animal hides.50-14. The United States no longer produces arsenic from mining but imports about 22.13-8.2 (41.12 (6.12-10. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. and other metals. or rarely as elemental metalloids (yellow.50 (8.5 (23. arsenic as elemental metalloids may be used in some ammunition. grain. trimethylarsine oxide. Arsine (AsH3) is a reactive. pesticides.80 (5.2 (13. referred to as inorganic arsenic compounds.8-77.7) 24.1 (32.4) 40.66-8.1-40. Arsenic and its compounds have had many uses in the past and present as medicines.1) 7.0 (22.1 (38. Arsenic trioxide (As2O3.80) 6. particularly arsenic trioxide.90-8.4 (26.27) 9. and in lead-acid storage battery grids. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80-9. as alloy in metal bearings.77) 6.19-9.3) 10.8) 17.30 (7.10-7.57) Selected percentiles ( 95% confidence interval) 50th 7.30) 17.2) 46.6) 618 722 1074 Limit of detection (LOD.90-8.5-178) 46.0-19.84) 8.2 (51. arsenic compounds.4) 60.90 (7.34-10.41 (7.02-8. cacodylic acid.5 (34. General population exposure to inorganic arsenic can occur through consumption of drinking water and.00-9.Metals Arsenic CAS No.10) 10. Arsenic trioxide is approved to treat acute promyelocytic leukemia.5 (36.3-19.3-111) 78. solders.5 (40. and as a cosmetic to lighten complexion. meats.6) 11. 2005).4 (24.4) 13.3) 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 7.84) 8. and arsenosugars. Although it is still widely used in the United States.6-43.90) 75th 16. copper arsenates.8) 7. gaseous hydride manufactured in small quantities for use in the semiconductor industry.1) 290 725 1542 03-04 03-04 9.30 (6. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.7) 65. Before the 20th century.08 (5. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. black.2-17.9-62. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.7-83. +3 and +5).5) 41. cancers. Water sources contain mostly inorganic arsenate.55 (7. Since the 1940s. and as homicidal poisons. 180 Fourth National Report on Human Exposure to Environmental Chemicals . mental disorders.9-46.9 (17. to a lesser extent. and gray forms). the smelting of copper. semiconductors. and produce.1) 15.0-60.7) 90th 37. psoriasis. and.8) 34.20 (8.74.34-9.8) 29. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.70) 8. it is found in over 200 crystalline or mineral forms. such as arsenopyrite (FeAsS) and realgar (As4S4).0 (43.5-52.1) 1281 1276 03-04 03-04 03-04 9.0 (14.8) 33. mostly for use in wood preservation (ATSDR.5) 95th 65. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.10-10.6 (9. retaining walls.5) 43. arsenocholine. In nature.2 (12. and play sets.0 (11.70 (6.000 metric tons annually.4-65. though in some locations arsenite may be prevalent (WHO. interval) 8.9 (8.90 (7. alloys.1-18. were used as treatments for syphilis.7-95.7 (11. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.25-9.5-19. lead hydrogen arsenate.5 (14.6 (32. In the last century.4 (48.9) 68.

8 (12. Inorganic forms of arsenic demonstrate high acute toxicity.41) 6. shellfish.0) 12.4) 54.13) 8.93-8.07-9.3-53.51) 75th 14.4 (42. EPA’s maximum contaminant level (Hughes. and folate status (Chen et al.0) 1281 1276 03-04 03-04 03-04 8. Tseng. and some other seafood can contain organic forms of arsenic including arsenobetaine. 1988).7) 28.9) 53.38-10. 2001).24 (7. 2001. have caused clinical arsenic poisoning.50 (6.04 (5. mine tailings). 2003. 2006. 2001).3-62.88 (5.18 (5. 2001.47 (7.8-62.45) 5.0) 42.7-34.01) 7.7-18.8 (11.7-17.1) 7. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.4 (11.1) 6.01) 11.5) 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 8.23-7.S.61 (7.1 (14.8 (27.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .8-32.8) 27.96) 12.9 (45. age. and contact with CCA-preserved wood structures. Smoking tobacco is also a source of inorganic arsenic. Arsenate is reduced in the body to arsenite (oxidation state +3).20-9. 2007.4) 32.88) 7.S.93-9. and arsenosugars. 2001). 2001). Though modest bioconcentration occurs in some aquatic life. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. Children may have additional exposures from ingestion of contaminated soils (e.8-75. but is poorly absorbed dermally (WHO. cacodylic acid and monosodium methyl arsenate.33 (6.58-10.0) 33. In aquatic organisms.S.2) 40. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.99-9.10-8. WHO.2) 15.28-7.66 (7.6 (17.3-41. Chowdhury et al.66-8.7 (9.06 (4.g.4-64..3 (27. U.76 (6. arsenic does not show biomagnification in the food chain (WHO.5) 17. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.3-64. After absorption.12-10.7-35.8) 22. 2001).5 (9. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.31 (6. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.7-188) 27.2-46. dose level.6 (10.9-56.0 (17.. The semiconductor dopants.00 (6. 2007.4 (40.75) 13. NRC.0 (31. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.0) 14. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.6-17.4 (24. 2006.44-11.32 (5.5) 290 725 1542 03-04 03-04 8.. trimethylarsine oxide (TMAO). 2001). Survey years 03-04 Geometric mean (95% conf.6 (35. gallium arsenide and indium arsenide. 2001).0) 26. Steinmaus et al.10-16.75 (5. kelp. Direct exposure to DMA and MMA may result from use of the two pesticides. arsenocholine. are used in enclosed ultraclean operations within the semiconductor industry. WHO.7 (25.1 (11.0-26. selenium.3 (24.25 (6.7 (11.0-38.3) 6.44) 6.9) 13.59) Selected percentiles ( 95% confidence interval) 50th 7.11 (5.25-9. 2007.1) 24. population from the National Health and Nutrition Examination Survey.2) 90th 30.30-9.47 (6.04) 7.5-120) 40.1-36.64 (7.35) 7..8 (20. though some reduction may occur in the gut prior to absorption. dust.2 (12. EPA.66-8. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.33-10.2-15. as observed in Bangladesh where millions of people have been exposed. Some studies suggest that variation in the degree of methylation among persons is related to the susceptibility of arsenicinduced disease and may involve consideration of genetic polymorphisms.3) 9.0-18. 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.8 (21. 2001).. so exposure to the general population is extremely limited.4 (26.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. inorganic arsenic is widely distributed within the body.. organic arsenic can be converted back to methylated and inorganic arsenic.6) 45.5-17.7) 95th 50.0-69.81-9. Fish.40) 8.4 (12.86-17. In aquatic sediments.1) 58. Gamble et al.47-6.1) 8. interval) 8. Extremely high groundwater arsenic levels.

vomiting. cell transformations. U. 2007. apoptosis. 2006.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. and diarrhea. food residue.. and endothelial injury (Kumagai and Sumi. 2001). it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways.10 (<LOD-1.80) 1. hyperkeratosis. 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. WHO.S. substitution in phosphate metabolism. lung.g. Acutely. renal failure. Cardiac arrhythmias. and by uncoupling oxidative phosphorylation (NRC. drinking water have not been associated with increased cancer rates (Schoen et al. Taiwan.60) 1. cytotoxicity. Cohen et al. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 2001).10 (<LOD-1. hepatotoxicity. 2007)... see Data Analysis section) for Survey year 03-04 is 1. fatty acid oxidation.10 (<LOD-1. Cellular glucose uptake. population from the National Health and Nutrition Examination Survey.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. NRC. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.S.30) 1.20 (<LOD-1. 2000. Studies of arsenic at levels typical of U. hematocytopenias. and production of glutathione may be affected as well..20 (<LOD-1. peripheral vascular disease.EPA has established drinking water. Survey years 03-04 Geometric mean (95% conf. Chronic arsenic exposure in humans is considered to be a cause of skin. 1998. and it also will inhibit succinate dehydrogenase.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. noncirrhotic portal hypertension. WHO. and altered gene expression. leading to a decrease in adenosine triphosphate energy production. 2007. Chile). Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 2001).20 (<LOD-1. 2006. and bladder cancer (IARC. and childhood neurodevelopmental effects in observational human studies... The U. Chronic human intake of arsenic at less than acutely toxic doses. 2001). arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. respectively.50) 621 725 1078 Limit of detection (LOD.50) 1.. can cause peripheral sensorimotor neuropathies. and hyperpigmentation of the skin (NRC. Although arsenate is reduced in the body to arsenite. With chronic exposure.. hypertension. Bredfeldt et al. 182 Fourth National Report on Human Exposure to Environmental Chemicals .. but additional or confirmatory research is needed (Kapaj et al.10 (<LOD-1. Raml et al. including drinking water sources with elevated arsenic levels (e. arsenic trioxide) includes hemorrhagic gastritis with nausea.20 (<LOD-1.10 (<LOD-1. 2001). < LOD means less than the limit of detection. some of these effects may take years to develop. 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. which may vary for some chemicals by year and by individual sample. The organic forms of arsenic occurring in seafood have little known toxicity.S. 2001). 2001. 2004. including inhibition of numerous enzymes. NRC. gluconeogenesis..0. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. 2006. Chronic elevated arsenic intakes have been associated with diabetes. Such actions may lead to decreased energy production. and DNA repair inhibition (Cohen et al. WHO. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.g.60) 1. 2001.S. 2004)..EPA. 2004). and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.. Arsenic has many actions demonstrated in cellular studies. increased oxidative stress.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. Bangladesh. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. WHO. which can lead to dehydration and shock. interference in signal transduction pathways. 2006) or when exposure occurs in smokers (Chen et al.

Though CCA-treated wood contains several thousand times more arsenic than untreated wood. Fourth National Report on Human Exposure to Environmental Chemicals 183 . Josyula et al. Urinary arsenic levels were a better predictor for risk of arsenical skin lesions than were arsenic levels in drinking water in Bangladesh (Ahsan et al. 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. Survey years 03-04 Geometric mean (95% conf. Shalat et al. 2001). 2006). but generally only at maternally toxic doses (WHO. Offergelt et al. Pellizzari and Clayton. 2004.. WHO. 2001). 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.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Levels of total urinary arsenic in the U. arsenic has been fetotoxic and teratogenic. 2008). 2001). Pellizzari and Clayton 2006). DMA produced bladder cancer in some chronic rat studies (Cohen et al.. 2007. 2006).41) 3.. Valenzuela et al.cdc. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Compared with this Report. had decreased since the prior 1990– 1992 survey...19) 3. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. and the FDA has established a bottled drinking water standard. Additional information about external exposure (i.18 (<LOD-3. In a Nevada town where groundwater levels were naturally elevated..50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Caldwell et al..80 (<LOD-4. and were about two-fold lower than those for the U. 2008).33 (<LOD-3. Consequently.33 (<LOD-3. In animal studies. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. 1999. population (Rubin et al..04 (<LOD-3.atsdr.75 (<LOD-2. gov/toxpro2.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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. Caldwell et al. 2003. 2006.Metals compounds.S.61 (<LOD-3. population from the National Health and Nutrition Examination Survey. Pellizzari and Clayton. In the German Environmental Survey III of 1998. 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.. Calderon et al..75 (<LOD-2..S. 2000). 2008.S. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 2006).... Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.. 1998.18) 3. 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).89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2..e. 2006. 2004.S. population in NHANES 2003–2004 (Schulz et al. Meza et al... median urinary total arsenic levels in 4052 adults varied with seafood intake. environmental levels) and health effects is available from ATSDR at: http://www.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Vahter et al.50) 1.00) 1. 2000. 1986).. 1992.html. 1999).. 2007. Shalat et al. although urinary arsenic levels were not associated with CCA contact (Shalat et al.69 (<LOD-3. 2006. 1999.

median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004..0 (27. population in the NHANES 2003–2004 subsample. when seafood organic arsenic is subtracted).20-25.6.800-4.00) 3. and TMAO.70-21.30) 10.10 (4..93) 1.. see Data Analysis section) for Survey year 03-04 is 0.1) 45.. Measurable organic arsenic species in this Report are three biologically generated environmental forms. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. These associations are stronger at higher urinary levels. dermal keratosis. interval) 1.3-39.00 (1. 2006).70-21. arsenite.3) 1284 1284 03-04 03-04 03-04 1. Chowdhury et al.5 (26.20-3. < LOD means less than the limit of detection.00-4. arsenocholine.83) Selected percentiles ( 95% confidence interval) 50th 1.28) 1.29 (1.37 (1.8 (12.20-190) 31.. Individually measurable species resulting from inorganic arsenic exposure are arsenate.20) 18.00-6.48-2. After recent seafood ingestion. vasospasm. 2003).4 (16.68) ..S. population (Ahsan et al.0) 4.1-25.. Some noncancer effects of arsenic (e.500-1.55 (1. and TMAO were detected in only 7.800 (. In most human studies.900-1.00-1. 2001). as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.4) 23. Arsenate. respectively..0 (26. The higher percentiles of total urinary arsenic levels in the U.S.S.00 (.62) 2.9 (6.60-3. 2001. 1990.. Survey years 03-04 Geometric mean (95% conf.40-7.7) 15..50) .6 (25. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.8-50..20 (.70 (3. 2000.50-6.4-35.80 (4.9) 13. methylation capacity. 2000. 2005.70 (5.3) 35.9-23.30 (2.700-1. In the residents of a Chilean town who consumed water with high levels of arsenic. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. which may vary for some chemicals by year and by individual sample.1-94.80 (.5) 29.6) 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 * * 1.20 (2.80) 1. Aposhian et al. Tseng et al. population from the National Health and Nutrition Examination Survey.0-23..S. 2008). 2008).45 (1.1) 18.20) 3.6.30) 2..5) 621 725 1078 Limit of detection (LOD.7-22.8.6 (13. China. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.31-1. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.5) 32. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3% of a representative sample of the U..700-1.. 2007) with higher levels of arsenic in the drinking water. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.e. In the late 1980s.3 (9. population showed a higher contribution of arsenobetaine (Caldwell et al.4) 31.19 (.3 (21. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. 4. MMA. 2008.800 (.6-44.50) 90th 16. and other factors such as nutrition.9 (7. For residents of Inner Mongolia. Caldwell et al. geometric mean levels were about 70-fold higher than for the U.g. 1. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. 1985. with DMA.2-35. Caldwell et al.8) 35.30 (1.3) 95th 35. Valenzuela et al.20 (1. Caceres et al.2-38. and duration of exposure are also considered important.90-29. 184 Fourth National Report on Human Exposure to Environmental Chemicals . 2000. 2008. When seafood intake is avoided.600 (.66 (1. and two methylated metabolic products. 2008). and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al..2 (6. 1996. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.5) 292 728 1548 03-04 03-04 1.40) 5. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.400-.7 (13.20) 7..Metals other areas of the world (Ahsan et al..74 (1. Caldwell et al. WHO.50) .7 (21.S.05) < LOD .800) 1. Pellizzari and Clayton.4.70) 6.8 (17.90-7.900 (.8-40.00-12.20 (4. arsenite. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.5 (14.11-1.40-6.43-1. arsenobetaine.40) 75th 5. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.17-1. Also.800-1.7) 13. population (Sun et al.6 (11. 2005.60) 1. and 0.10) 4.80-5. 2007).0) 29. 2008). 2005.10) 8.. DMA and MMA.80 (3.871-1. Blom et al.1-51. arsenocholine. Sun et al. in NHEXAS 1995–1996..

47 (1.13-39.70) 5.78-5.19-2.877 (..82) 4.4-28.43) 75th 5.00 (1.67) 1.2 (12. 1992.76-27.12) < LOD . 2006. 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. 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.7) 9.79 (1. Sun et al.531 (.51) 5. not to imply a safety level for general population exposure. Information about the biological exposure indices is provided here for comparison.9) 14.88 (5.. In recent years..83) 2.25-7.5) 26.3 (10.7) 30.40 (1.51-2.21) 5.00 (3.1) 26. 2001). Fourth National Report on Human Exposure to Environmental Chemicals 185 .18-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.82) Selected percentiles ( 95% confidence interval) 50th 1.0-36.14 (1. Studies of small groups of metal and sulfuric acid smelter workers with varying industrial hygiene conditions have reported urinary inorganic arsenic levels (arsenate + arsenite + DMA + MMA) ranging as high as several hundreds of μg/L during or after work exposure (Jakubowski et al. Caldwell et al.83) 8.9 (25.4) 32.32-7.55) 1.25 (.S.9-18. Offergelt et al.50-7.909-1.88) 2.3) 1284 1284 03-04 03-04 03-04 1.2 (4. interval) 1.37-2.61-6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6 (9.73-6.2 (13.9 (13.3 (10. 2008).80) .72) 12.28) 1.901-2.1-36.938-1. 2003.68 (1. 2001).44 (1...11 (.67) 4.5 (18.81 (4.786-1.6) 19.54 (1.64-29.6 (6..47 (2.30-1.612-1.36) 2. WHO.833-1.9 μg/L.7) 17.4-82.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.45) 1. 2008).53 (.2 (12. 2007).1-18.4 (11.93 (1..15-4.9) 32.4 (24.400-.3) 95th 29.5 (18.1 (26.3-24. population from the National Health and Nutrition Examination Survey.15-1. 1998.05) 1.5) 17. 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. Survey years 03-04 Geometric mean (95% conf.S.91) 90th 16.05 (.91 (4. 1986.6-32.6-46.80-153) 17. population for the sum of inorganic related species was 18.4-21.40) 1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.15-1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.0 (9. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.5-20.29-14.50-15. 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.4) 292 728 1548 03-04 03-04 1. The 95th percentile of the U.638) 1.58 (3.78 (3.16 (. which is below the ACGIH BEI (Caldwell et al.43) 14..959-1.4) 13.6-29.Metals as with DMA.8) 29.29 (4.4) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1.65 (1. Vahter et al.10 (.30) 1.39-3.62-6.

population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0. 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.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. 186 Fourth National Report on Human Exposure to Environmental Chemicals .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 < 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. Survey years 03-04 Geometric mean (95% conf.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.

00 (<LOD-2. which may vary for some chemicals by year and by individual sample.00 (<LOD-3.S.2.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.95 (<LOD-2.70) < 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. see Data Analysis section) for Survey year 03-04 is 1. < LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf.08 (<LOD-4.76) < 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 3.00) 1. Fourth National Report on Human Exposure to Environmental Chemicals 187 . 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. 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. Survey years 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.44) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (<LOD-1.40 (<LOD-1.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

00-4.0) 16.9) 11.46 (4.00-3.70-3.50 (4.0 (10.24-4.00-5.49) 10.29-4.0 (13. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (9.0-25.0) 292 728 1548 03-04 03-04 4.00) 75th 6.0) 9.80-6.73 (3.00-7.95 (4.50-5.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 17.0) 14.00 (7.27 (3.03 (3.0 (11.06) 5.4 (7.0) 621 725 1078 Limit of detection (LOD.78 (4.98) 4.15) 4. see Data Analysis section) for Survey year 03-04 is 1.49-4.00-9.22) 4.34) 3.00 (6.16 (2.00) 6.32 (4.73) 6.57 (3.44 (2.48 (2.9) 12.7-16.00-10.45) 8.05) 10.00-12.00 (5.86 (2.00 (3.39-3.0-17.16 (4.70-12.00-11.91) 75th 5.42) 3.00) 7.24) 3.34-4.0) 95th 16.1-18.00) 6.89 (3.10) 3.00-4.3 (8. interval) 3.00-7.80) 2.32 (8.00-15.00 (3.00-7.0-18.0 (10.00) 9.84-8.0-19.17 (2.86-21.7.1-22.05) 3.94-3.0) 11.70-4.27-2.31-4.48 (3.27-5.86-7.11 (3.9) 13.67) 8.00 (3.00) 3.00-4.20) 11.95-6.60-4.33) 3.94) 3.61-16.11) 4.09 (7.31) 4.70 (3.7 (10.0) 16.14) Selected percentiles ( 95% confidence interval) 50th 3.05) 5.20-12.0 (9.18 (6.7) 13.0-12.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .65-8.38 (3.0) 17.10) 6.72 (4.88 (4.0) 13.3 (7.00) 6.00-4. population from the National Health and Nutrition Examination Survey.00) 4.00 (3.45) 3.59 (6.9) 5.0 (10.00-15.00 (5.00) 12.71 (4.00-11.0) 12.S.00-8.8) 7.0 (13.37 (2.8) 7.0) 11.80-3.25 (4.84-18.0) 9.00) 90th 11.69 (3.00 (6.12 (3.34 (3.95-4.85 (3.55 (2.0-16.14) 3.1 (8.00) 4.16-11.0) 13.00-4.52) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.50-15.00 (7.03-6.00-22.0-16.74) 90th 9.00 (3.0 (12.0 (10.81 (5.9 (11.00) 5.34 (3.19) Selected percentiles ( 95% confidence interval) 50th 3.60-7.80-5.6) 292 728 1548 03-04 03-04 3.97-3.6) 1284 1284 03-04 03-04 03-04 4.6-18.12-4.82-5.0 (8.2) 10.17-6.00-4.00) 3.6 (9.71) 3.32-10.08 (2.80 (4.30 (7.82) 3.57-5.00-13.7) 12.33-4.74 (2.5) 95th 13.17-4.0) 10. Survey years 03-04 Geometric mean (95% conf.60-6.0 (8.00-7.00 (6.0) 9.28) 2.37 (3.00 (3.00-12.65-6.00-15.20-4.1-15.00) 6.13-4.9 (7.7) 1284 1284 03-04 03-04 03-04 4.62) 4.69-6.00 (5.00 (4.00 (5.60-3.69-3.80) 7.71 (3.5 (11.69 (3.82-9.67) 9.0-17.30) 3.0 (9.00-3.00-11. interval) 3.61-11.78) 4.70) 5. Survey years 03-04 Geometric mean (95% conf.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. population from the National Health and Nutrition Examination Survey.90) 5.92) 3.77 (3.92-12.95-3.44) 5.3 (8.27 (2.79 (3.45 (8.5) 12.S.90) 2.34-4.0 (14.0 (12.00 (5.71-4.90 (3.

90) 1.40) 1.10 (1.80-2.50-2.10 (<LOD-1.63 (<LOD-1.80 (1.00-2.22 (1.20 (1.30 (1.20) 2.80 (1.10) 95th 2.40) 2. population from the National Health and Nutrition Examination Survey.30-2.28 (1.90 (1.80 (1.853-1.37 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.46-2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.46 (1.77) 1.50) 621 725 1077 Limit of detection (LOD.85) 1.81) 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.20 (1.50 (1.30 (1.85) 2.33 (1.30) 1.20 (1.S.30) 90th 1.86 (2.36) 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.S.73-2.16 (2.50 (<LOD-1.70-2.20-3.18-1.58) 2.82-2.18-1.86 (2.31 (1.10 (.88-2.60-2.80) 1.70-2.33 (1.96-2.90) 2. see Data Analysis section) for Survey year 03-04 is 0.10) 2. which may vary for some chemicals by year and by individual sample.84-3.20-1.53 (1.53-2.30) 2.43-3.80 (2.900-1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.80-2.80 (1.00 (<LOD-1.14-1.28 (1.10-1.60) 2.816 (<LOD-.00-1.60 (1.15-1. Survey years 03-04 Geometric mean (95% conf.88 (1.00) 1.90) 2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.40-2.10 (.80) 1.36 (1.985) 1.05-1.00 (2.57) 95th 2.20 (1.70) 2.00 (<LOD-1.30) 1.23) 1.62) 2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40-3.00) 1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.79) 2.20 (1.10-1.07-3.17) 2.52 (2.31-3.34) 2.86) 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 . < LOD means less than the limit of detection.00-4.40-3.07) 2. Survey years 03-04 Geometric mean (95% conf.61-3.50) 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.30 (1.86) 3.70-3.00-1.30-1.45) 3.82-2.35-3.50 (1.71-2.11-1.40) 1.93) .00) 2.00 (2.70-2.20 (1.50 (2.10 (1.61) 2.00) 1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30-1.60 (2.00) 2.9. population from the National Health and Nutrition Examination Survey.00-2.88 (1.60) 2.40-2.30 (2.90 (2.40 (2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.00 (1.10-3.70-2.40 (1.22) 3.54) 90th 2.60) 1.07 (1.

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

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78) 1.30) 3.80) 6.94-6.36-1.55-3.81-2.29) 5.92) 2.82) 2.80 (1.81-2.63 (2.57) 3.20 (4.63) 1.50-6. rubber.41-1.21 (1.14-6.30-2.35-4.29-1.40 (1.59-11.g.55-7.11 (3.10-5.39) 1.25 (1. bricks.38 (1.30 (3.25-11.90) 4.56 (6.18-1.90 (1.40 (1.32) 8.61 (2.70) 5.73) 1.21-8.20-8.19) 2.36 (1.77-3.37) 5.35 (3.40 (5.87 (6.69 (1.43) 6. 2001).57-7.50 (4.99-5.60-10.70-3.50) 2.96-2.03 (1.20) 2.56) 1.65-8.80 (2.57 (5.11 (3.4) 6.65-5.90-9.25-1.60-2.00) 6.86 (4.07 (2.44-2.70 (1.30 (2.35 (1.78-2.70) 4.74-3. and 0.41-3.43 (5.71) 1. Certain foods.90) 2.22-1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.15-1.00) 4.70-2.61 (1.53-5.15 (2.50 (4.91) 6.70-8.71 (2.50 (2.44-5.28) 90th 5.47-1.11-1.98) 1.20-1.20-8. The general population can be exposed to low amounts of barium in air.8) 5.87-3.15-11.56 (1.00) 1.15-1.48-4.45 (1.38 (1.37) 1.49) 8.04-2.67) 6.00-8.16 (1.54) 1.87-7. water.54-8.93-8.73) 3.48 (6.4) 9. tiles. and food.85) 1.71) 95th 6.47) 4.81-3.00) 1.62) 1.87) 7.46-1.72) 75th 3. Workers employed by industries that make or use barium compounds can be exposed to barium dust.10 (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 2.46) 1.9) 5.30-3.59) 3.21 (1.88) 7.91 (2.90 (6.50 (1.73 (5.39) 4.12 (2.90) 1. are high in barium (Genter. population from the National Health and Nutrition Examination Survey.77 (3. such as barium chloride.10-4.68 (1.73-5.39-1.87-9.30-2.06-2.60) 1.14-1.40 (4.80 (5.27 (1.63) 1.76-7.30-1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .1) 9..70-5.74) 3. respectively. Barium salts have also been available as rodenticides.61 (5.35-1.32-7.50 (5.2) 6.09 (1.20-1.54-1.27) 2. fireworks.32-1.54 (6.65) 1.72) 4.18) 3.42 (1.84) 5.50-1.62) 1.51 (1.86) 6.65-1.48) 1.22-1.39 (1.15) 5.82-6.66) Selected percentiles ( 95% confidence interval) 50th 1.50) 1.43 (1.34) 2.62 (1.73 (6.49-9.70) 1.48) 1.37 (4.90-2.70-2.30) 2. 0.10) 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 1.36 (4.28-1.06-1.87 (5.45) 7. depilatories.20 (1.49) 2.64 (1.65 (5.60 (1.70 (5. soluble forms of barium.30 (5.10) 3.54-1.65) 1.47-1.40) 3.31.10) 5.00-3.37-1.99 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20-5.50 (4. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.02 (7.76-2.26) 5.38) 2. barium sulfate and barium carbonate).93-2.43 (1. Barium compounds are also used commercially in paint.20-6.52 (1.27 (1.80-7.40-13.91) 2.49) 11.16) 5.93 (4.63) Total 1. see Data Analysis section) for Survey years 99-00.30-5.51) 7.61 (3.19-1.78-3. such as brazil nuts.76) 1.60) 1. and ceramics.60-6.36-1.51) 2. it combines with other chemicals such as sulfur or carbon and oxygen.90) 2.00 (2.30-1.60-3.26-7.64-3.82) 1.76-3.34 (1.88 (5.80 (1.14 (6.39 (1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).43) 2.70) 1.78) 1.54) 2.35) 5.77) 1.54 (2.30) 5.70-6.88) 4.56 (2.50 (1.12) 6. Some barium salts are freely soluble in water.00 (1.86-4.41) 1. 7440-39-3 Medically.97 (1.80) 7.66 (4.09 (2.49-1.95 (4.40) 7.01 (4.26) 2.11 (2.30) 4.80-5.70) 7.50 (1.31 (2.71) 2.20-1. 01-02.50) 4. In single dose animal studies.30 (1.36) 5.40 (5.12.08 (6.74-2.61 (1.24-1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. whereas others are practically insoluble (e.54) 1.22) 6.30 (5.50 (3. Barium compounds are used by the oil and gas industries to make drilling muds.30) 5. glass.38) 8.62 (1.17-1.60 (2.15 (6.85) 1.40 (1.20-1.08-8.49 (1.24 (4.95-6.18 (6.S.35 (2.46) 1.20 (3.60) 3.04-6.51) 1.50 (1.29-5.31-2.65) 3.63 (5.70) 3.50 (1.12-1.21-2.71-9.90-13.56) 4.05-2.15 (1.87-14.30) 8.86 (4.60) 4.60-6.50-6.24-1.85 (2.8) 9.80-2.61-8.53) 2.44 (1.88) 1.35-1.52 (4. interval) 1.48-4.63 (8.12) 7.75) 2.12. Small amounts of barium can be released into the air during mining and other industrial processes.30) 5.76 (3.50-1.37-8. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80-3.63 (1.50) 2.4) 7.20-8.05% of the earth’s crust.8 (6.75-3.40 (5.00-76.33 (1.10 (4.26-1. In nature.34 (1.80 (1.53) 1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.Metals Barium CAS No.80 (2.01-7.86-5.49) 4. and 03-04 are 0.34 (2.90 (4.40) 7.12 (2.56 (1.10 (3.80) 1.72) 1.50 (6.

56) 4.52) 2.49-1.36-1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.50) 1.97-3.71 (5.62) 2. such as those used in medical radiographic procedures.37) 2.4) 5.65 (2.81-7. population from the National Health and Nutrition Examination Survey.24-3.68-3.46) 1.10 (6. 1994.59) 1.01) 1.00) 6.49 (1.2) 5.42) 1. Chronic high doses in animals resulted in kidney damage (McCauley et al.65 (5.51 (3. 1984.91 (3.33 (1.60 (1.06) .38 (4.76) 2.42) 1.10-2.01 (4.832-1.13-3.31-1.28-1.89 (2.881 (.00) 4.54) 2.48-1.44-2.49-1.76 (3.68-3.67-6.905 (.75-22.27 (2.24-11.59-7.03) 1.77) 5.22-4.24-6.25-11.10-1.74) 1.32) 2.28-7.00-7.47 (2.75) 1.84-2.04) 1.45) 95th 6.64 (1.61) 2.51 (1.29 (3.68 (3.8) 4. vomiting.91) 2.23-1.81-6.80) 3.62 (2.60 (2.24-6.27-3.64) 7. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.68) 1.49 (1.11-2.56-3.92) 2.77) Total 1.38-1.64) 7.25) 4. NTP.51 (1.64 (1.4 (5.45 (1.77) 1.99 (2.777-1.59) 2.33 (1.88 (6.32 (1.84 (3.31) 5.3) 6.03-1.48 (1. weakness.76) 2.98 (2.01 (5.11) .52) 7.46 (2.72) 6.48-5.27-1.48 (1.35-1.53 (2.59) 1.32 (1.70) 4.41) 5.52) 1.41 (1.29-4.44-2..79) 1.82) 1.96) 4.91 (3.03) 2.26-1.710-1.84-5.00 (3. Insoluble barium salts.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 .47) 4.30 (1.30) 2. Following intravenous injection in animals.2 (3.00-1.891 (.08-2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.34-1.68) 3.31 (4.34-3.33-1.35-1.39 (2.38 (4.76) 1.29-3.15-4.04) 5.36 (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.72 (2.06) 2.02 (3.55-6.2) 6.48-3.60 (1.52 (3.28 (1.43) 1.83) 3.26-1.53) .0) 7.33) 6.41) 4.02) .86-7.05-1.29 (1.96) 7.26-1. 1985.39-5.69-9.00) 1.20-2.0) 6.73-4.24 (3.31-1.43-6.84) 2.20 (1.0) 5.34 (1.86) 5.55) .68 (3.16-1.22-2.34-5.51-3.24 (5.03) 3.58 (2.69 (5.48 (1.26-4.02-5. Barium is not rated for human carcinogenicity. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.77) 1.92 (4.96-6.16 (1.59 (1.70) 10. 1986).28-11.754-1.38) 1.55 (4.29-7.97 (4.23-5.62 (4.38) 1.50 (4. Toxicity from soluble barium salts is rare.35-3. interval) 1.57 (6.33) 1.39-10.74) 1.74 (5.47) 1.22-1.00 (5.76 (4.03-1.39 (2.39-1.56 (1.19-1.39 (2.46) 2.55 (1.51) 6.57-5.32 (2.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2. Perry et al.45) 1.32) 2.963 (.39-1.63-4.00) 4.20-8.97-4.58 (4.11) .59 (1.60 (2.47) 10. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.22-1.39) 4.55-5.16) 11.42 (4.26) 4.81-6.19-1.33 (5.50) 2.78 (2.921 (.57-10.28-6.48) 2.10) 3. in urine.36 (5. and cardiac dysrhythmias.75) 2. are not absorbed when administered. chemical form.68 (2.703-1.77) 1.13-2.26-1.73-2.91-2.36-1.38) 4.52-10. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.40 (1.37 (1.63) 1.79-5.54) 1.18 (1.02) 4.46) 3.54 (1.46-22.12) 2.37-1.04 (2.51) 4.77-5.5) 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. 1990). Symptoms following acute high dose include perioral paresthesias.47) 1.S.75-3.96 (4.10) 6.. a benign condition that may occur among barite ore miners.45-1.40 (1.40 (1.36 (3.75) 2.60 (5.19-2.38 (1.51) 4.29-4.3 (6.09) 6.50) 1.49-1.97 (5.45-1.24-1.62 (1. Wones et al.56) Selected percentiles ( 95% confidence interval) 50th 1.97) 1.86 (2.99) 1.85-5. hypertension.00 (3.36 (1.21 (1.31-1.96) 4.39 (3.57-7.64 (1.56 (1.64 (1.31 (1.18 (1. 1989).45-8.55 (1.82) 1.99 (4.76-3. diarrhea.58) 1.58) 75th 2.66 (1.29) 1.20) 4.96) 4.73) 2.20-1.87) 1.38 (1.76 (2.23-2.44 (1. water solubility. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.45 (3.38-5.34) 1.30 (1.58) 4.37 (1.29-1. paralysis.37-2.90-2.24-1.38-7.41 (1.75) 1. and route of exposure. 2001). The health effects of exposure to barium compounds depend on the dose.14-2.55 (5.89) 90th 4.33-4.40-1.27) 7.47-8.25 (1..83) 2.45-6.80-6.52-4.00 (2.36-2.96 (4.36 (1.Metals was eliminated primarily in feces and to a lesser extent.47 (5.80) 4.08-1.57) 2.88 (2.880-1.19-1.70) 1.58-6.41 (2.61 (4.72) 4.915 (.28) 5.53-21.54 (2.24) 3.

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

< LOD means less than the limit of detection. and refined beryllium is used in mirrors and special metal alloys for the automobile. population from the National Health and Nutrition Examination Survey. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. coal.13. beryllium is used in instruments. In studies of laboratory animals. bertrandite and beryl. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. or drinking water containing the metal. respectively. the lightest of all metals. Low-level beryllium exposure in the general population can occur through breathing air. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.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 . nuclear. which may vary for some chemicals by year and by individual sample. soil. and 0.130 (<LOD-.Metals Beryllium CAS No. are mined for commercial recovery of beryllium. and volcanic dust. and machine-parts industries. Beryllium compounds are commercially mined. 7440-41-7 General Information Pure beryllium is a hard gray metal. and from breathing tobacco smoke. 0. near some hazardous waste sites. x-ray machines. eating food. electrical.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. aircraft. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.13. and dental bridges.S. 01-02. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.130 (<LOD-.13. Two types of minerals. In medicine. and can be found in mineral rocks. Exposure to beryllium occurs mostly in the workplace. 196 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and 03-04 are 0. computer. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.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 .140 (<LOD-. * 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.

346 (<LOD-. Chronic beryllium disease. based upon excess lung and central nervous system cancers in studies of workers.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. 2003.273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. IARC has classified beryllium as a human carcinogen. 1990). Skin exposure can result in delayed hypersensitivity reactions. population from the National Health and Nutrition Examination Survey. EPA. and drinking water and environmental standards have been established by U. S.. 2002). which produces pneumonitis. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. 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 . or berylliosis. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. NTP considers beryllium to be a known human carcinogen.281 (<LOD-. including contact dermatitis and subcutaneous nodules. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 . Fourth National Report on Human Exposure to Environmental Chemicals 197 . 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. Maier. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. respectively. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response.231 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Apostoli P. 2000. Paschal DC. environmental levels) and health effects is available from ATSDR at: http://www. Third National Report on Human Exposure to Environmental Chemicals. 3/27/08 Komaromy-Hiller G. and 2003-2004.inchem. Van der Venne MT.e..23:827-839. Ting BG. Gallorini M. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect.S. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. and the fact that most NHANES participant levels were undetectable. They reported urinary beryllium levels ranging from 0. 2001). McCanlies EC. International Programme on Chemical Safety (IPCS). population are lower than levels in workers.1 μg/L). and serum of Italian subjects. Sci Total Environ 1994. Kriess K. blood.12 to 0. Trace metals in urine of United States residents: reference range concentrations.e.296(1-2):71-90. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Howerton K.cdc.76(1):53-59. which approximate this Report’s limit of detection. In other studies. Pozzoli L. Environmental Health Criteria. 1990. Clin Chest Med 2002. Sci Total Environ 1990. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Genetic and exposure risks for chronic beryllium disease. Trace element reference values in tissues from inhabitants of the European community I. 106. it is likely that urinary beryllium levels in the U.95:89-105.Metals (i.S. population were generally undetectable in NHANES 1999-2000. Andrew M. 20012002. et al. HLA-DPB1 and chronic beryllium disease: a HuGE review. 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..gov/toxpro2. Element reference values in tissues from inhabitants of the European community. patient population and literature reference intervals for urinary trace elements. Beryllium [online].. Atlanta (GA) 2005. less than 0. Am J Epidemiol 2003. Ash KO. Jackson RJ. and the 95th percentile for males in NHANES 2001-2002. References Apostoli P. Morrow JC. 1998). Int Arch Occup Environ Health 2001.74:162-166. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Paschal et al. Environ Res 1998.atsdr. Sabbioni E. Sampson EJ. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Schaller KH.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. plasma and urine and a critical evaluation of reference values for the United Kingdom population.. Review of elements in blood. Hamilton EI. Levels of beryllium in urine for the U. Sabbioni E.html. Given these results. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.158:165-190. Maier L. Minoia et al. Available at URL: http://www. A study of 46 elements in urine. Pietra R. Minoia C. et al. Centers for Disease Control and Prevention (CDC). Costa R. Hamilton et al. 1990. VI. Pirkle JL. 0. Clin Chim Acta 2000. Comparison of representative ranges based on U.S.htm.13 μg/L. Weston A.157:388-398.org/documents/ehc/ehc/ ehc106..

441) * .S.400 (.00-1.400 (.10) 1.00 (.300) .400 (.500-.300-.400) . The predominant commercial use of cadmium is in battery manufacturing. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 1.600) .600) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .400) .400) .50 (1.10) 1.395 (.800 (.80) 1.300 (.600 (.300) .500-.700) 1.40 (1. 7440-43-9 General Information Cadmium is a soft.300-.20-1.600) 90th 1.400) .304-.300) 1.468 (.700-1.500) .200-.300) .400-.00 (.400 (.500 (.600 (.700) .700) .00-1.420 (.378-.30) 1.20-1.00-1.403) .216-.40 (1.300) .20 (.200) .289-.10 (1.30-1.500 (. < LOD means less than the limit of detection.50-1.900-1.20) .500-.900-1.Metals Cadmium CAS No.600) .800-1.400 (.500-.10 (. and 0.900-1.50-1.60 (1.275-.500-.20) 1.30 (1.600 (.10) 1.700) .513) .900-1.60 (1.300) .00 (1.600) 1.300-.300 (. and nonferrous alloys.300) . or copper smelters (U.300-.700 (.40 (1.200 (.00 (.70) 1.00-1.10 (1.366) * * .400-.50 (1.500-.500 (.200) .300-.3.400-.00 (.400) < LOD .200 (<LOD-.700) .400-.427) * .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 (.400) .20) 1.500-.300-.600 (.400 (.378 (.60) 1.600-.600) .300) .30-1.400 (.60) 1.600 (.60 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400-.60-1.40 (1.300-.300) . and 03-04 are 0.50) 1.400 (.400) .80 (1.500-.20-1.800-1.300-.00 (.00-1.30) 1.700-1.10) 1.300-.800 (.500 (.30) 1.400) .400-.460) .400-.470) * .300) .00 (.30-1.400 (.400-.600) .300-.50 (1.300 (<LOD-.90) 1.400) .300 (.20) 1.283 (.337) .368-.400) .300) .400 (.367-. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.376-.500-.400) .500) .20-1.386-.331) .20) 1.266-.500-. Cadmium also may be emitted into the air from zinc.700-1.500 (.10 (1.80) 1.30) .600 (.700) .10 (1.70) 1.40 (1.300-.344) .00-1.412 (.20-1.400 (.20) .400) .300-.500-. lead.300 (.60 (1.300 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.600) .300-.500-.300 (.359-.900-1.326 (.10 (1.00) .500) . respectively.900 (.300 (<LOD-.500) .20) 1. cadmium use has declined in response to environmental concerns (http:// minerals.30-1.00 (.400) < LOD .500-.10) 1.S.200-.14.400-.00 (.300-.313 (.60) 1.00-1.300-. interval) .300-.400) < LOD < LOD < LOD .70) 1.403 (. as zinc sulfide) and to a lesser extent.00 (.400-.10) 1.424) * .900-1.500) .900-1.900-1.600 (.400) < LOD .362-.40 (1.300-.50-1. plastic stabilizers.30-1.300 (.600-1.400 (.400) .400-.600 (.421 (. see Data Analysis section) for Survey years 99-00.50) 1.300 (.10 (1.333 (.500 (.300-.425 (.400 (.10) 1.200-.20) 1.452) .255) .500-.200 (.600-.300) 75th .300 (.200-.gov/minerals/pubs/commodity/cadmium).304 (.00-1.296-.300-.800) .300 (<LOD-.40-1. malleable. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.426-.500 (.50-1.600 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .449) Selected percentiles ( 95% confidence interval) 50th .20) 1.600 (.300-. coatings and plating.500 (.393 (.40 (1.600-.900-1.00 (1.600) .40) 1.900-1.00 (.200-.309-.300 (.20 (1. 01-02.00) .50) 1.600 (.200 (<LOD-.500) .500 (.700) . 0.400 (.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .700) .300 (<LOD-.10) 1.40) 1.900 (. EPA.800) 1.400) .500-.600) .10 (1. and incineration of municipal waste materials.300 (.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .20-1. population from the National Health and Nutrition Examination Survey.400 (.300 (. during refining of lead and copper from sulfide ore.500-.300) .00-1.60 (1.3.S.600) .40-1.235 (.300 (.300) .70) 1.200 (.300-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.700) .usgs.400) .800) .361-.400 (.20) 95th 1.500-.300 (.50 (1. Since 2001.382 (.300) . which may vary for some chemicals by year and by individual sample.500-.600 (. U.60) Total * .20-1.400 (.304 (.600 (.300-. Other uses include pigment production.500) .

193 (.101) .607) .060-. 2003). **All results are corrected for molybdenum oxide interference in the ICP-MS method.260-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.092) .980 (.790 (..452 (.277 (.203 (.13 (.191-. whose body burdens of cadmium can be approximately twice that of nonsmokers.381-.38) .393-.232) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.714-1.177-.194-.510) .855-1.313) .192-. Horiguchi et al. Cadmium is absorbed via inhalation and ingestion.06.150-. 1999.135 (.12 (.S. To a lesser extent.466 (.860) 1.28-1.19) 1. 2001).189-.198) .440 (.20) 1.800-.206) .01 (.255) .72) 1.519) .255) .817 (.220) .500) .390-.733) .219 (.817 (.15) 1.43) 1.270 (.221) . 2003.351-.01) .061 (<LOD-.980-1.326) .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 .148) .10 (1.284) .479) .210 (.22 (.181 (.114-.763-.283 (.06.589 (.820) 1.492 (. wheat. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.848 (.171-. For nonsmokers who are not exposed to cadmium in the workplace.700-.220 (. population from the National Health and Nutrition Examination Survey.220) Selected percentiles ( 95% confidence interval) Sample 95th 1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.238-.201 (.067-.. 200 Fourth National Report on Human Exposure to Environmental Chemicals .140 (.17 (.748-1. 2003).130 (.067-.686-.150) .231) .216 (..400-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .470-.300 (.220-.115-.48 (1. cadmium accumulates in the liver and kidneys where it is bound to metallothionein. 2003).251) ..112-.388-.34) 1.610) .229) . see Data Analysis section) for Survey years 99-00.980) .15 (.990) .766 (.211-.087-.481) .151-. 2004a.190-.28) 1.25 (1.230) .530) .387) .316 (. Diamond et al.551 (.20 (1.07-1.400-.121 (.183-.640) .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 .04 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.243-.963-1.233) .810-1.366-.229) .210) .30-1.25) 1.157-. The kidney is a critical target and shows the earliest sign of cadmium toxicity.260-.081) .839 (.520-.090) .366) .206 (.74) 1.240-.500) 90th .330-.329 (.426 (.623) .. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.680 (.210) . drinking water is a source for cadmium intake.227 (.980-1.196-.246) .843-1. zinc.17 (.241) .445 (.890 (.372) .200 (. calcium. interval) .175 (.247) . including many food crops such as cereal grains.232 (.299) .190-.078 (.160-.820 (.169-.41 (.12-1.080 (.362) .263) .265 (.128 (.430) .04 (.875) .208-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.226) .960 (.135-.462 (.445 (.977) .077 (.153-.06) .187 (.077 (.507) . potatoes.179-.83) 1.165-.482) .13-1.354) .713) . copper) and protein.219 (.262) .257-. 01-02.17 (.065-.22 (1.272-.20 (1.390 (.109-.530 (.175 (.184-.233) .433-.493-. 1994).180 (. and various seeds.700-. and 03-04 are 0.440-.38) 1.191 (.302 (.157) .989-1.230) 75th .265) .170 (.447 (.47) 1.249) .800 (.219 (.13) . Kikuchi et al.360) .136) .551) .327 (.540) .261-.339) .160) .580) .202 (.336) . 0.211 (.350 (.806) .195-.238) .06-1. rice.52 (1.741-1.199 (.633-1.120 (.285-.160 (.295) .940-1.28 (1.436-.237-. ingestion through food is the largest source of exposure.476-.559 (.255) .753-.38) .210 (.261-. and 0.717-.210 (.220-.222) .092 (.107-.214-.366-.880) .15) .257) .06-1.235) .818 (.193-.190-.207-.813 (.539) ..32 (1.633 (.892 (.322 (.300) .820-1.253-.204 (.192-.280 (.394-.519) .412) .202-.875 (.02-1.456-.270 (.160) .Metals 2000).919) .229-.100-.38) 1.282 (.210 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.20 (1.090) .200-.36) 1.134) .480) .490) 1.109 (.17) .170-.310) .239 (. Cadmium in soil is absorbed by plants.289-.455 (.279 (.510-.550 (.234 (.240) .170-.440 (.20-1.209 (.191-.210 (.230 (.09-1.173) .82) 1.148-. With chronic exposure.249-.430-.886-1.51 (1.320) .886) .200-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .836-1.545 (.450 (.061-.178-.260 (.730-.110-.223 (.733-.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.141 (.498-.490) .458 (.281 (.892-1. Inhalation of cigarette smoke is a predominant source of exposure in smokers.858 (.306 (.596) .308) .890-1.390-.972 (.423-.24) 1. respectively.790 (.167-.918-1.273 (.475 (.** Survey Geometric mean (95% conf. an inducible metal binding protein. however.06.980) .57) 1.705-.221 (.310 (.960) 1.200 (.203) .01-1.03) .189-. Renal tubular and glomerular damage.290-.700-.189) .450 (.870) .126) .

690-.08) .107) .678-. 2000.423 (.501 (.292) .07 (. 2002.757 (.273 (.156-.813-1. 1999).202 (.161-.431) . can result from high dose chronic exposure.783) . Noonan et al.197-.113-.663 (.607) .856) .316 (.236-.274) 1.404 (.311) .336-.168 (.308) .250) .304) .289) .147-.414 (. 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.144-.02 (.288 (.446) .255-.111-.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 .261 (.159 (.931 (.096) .177) .199-.647-.950) .175 (.382) .909-1.813-.381-.426-.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.261) .700 (.830) .09 (.094) .239-.300-.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 .874-1.267 (.708-1.226) 75th .238-.929) .767 (.919 (.340) ..143-.364) .163 (.181-.440) .232) .253 (.562-.828) .215 (.13) .263-.084 (.802 (.159 (.722-.343-..240) .666-.170-.173 (.147-.725-1.207) .266-.500-. At lower environmental exposures.136-.940-1.219 (.093 (.091) .201-.316) .281) ..329 (.278) .** Survey Geometric mean (95% conf.071 (.940 (.00 (.154-.668-..484 (.104) .472) .085-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan..757) .182) .873 (.818) . interval) .10) 1.12) 1.667) .126 (.148 (.181 (.168-.927-1.245 (. Jarup et al.051-. However.137 (.086 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.481 (.827) .184) .998) .476) .421 (.163) .533) .207-.631) .205 (.182) .112) .222-.091 (.147 (.234 (.220 (.101) .377-.253) .185) .288-.198) .325 (. 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.826-1.. Olsson et al.241) .137-.182) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.175-.181) .191 (.157-.07) .06 (.418-.210) .223) .185 (.16) .157-.178) .303) . 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.387-.173-.077-.247-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .075-.545) .289) . 2004b).170 (.423-.434 (. 1999).208 (. population from the National Health and Nutrition Examination Survey.221-. During the 1950’s and 1960’s.830-1.712 (.211 (.690 (.176 (.162 (.688-.876-1.063-.518) .388-.516-.614) .691-.S.196 (.200 (.106) .204-.268 (.387 (.171-.156 (.228-.650-.850) .941 (.130-.090 (.653) .487 (.283 (.199 (.335 (.17) .224 (.123-.100 (.415) .067-.350) .232) .767) .719 (.227-.693 (.441-.191) .209) Selected percentiles ( 95% confidence interval) Sample 95th .075 (<LOD-.143) .122 (.432 (.288) .470) .. 1999).962) .479 (.740 (.216-.296 (.536 (.331 (.192) .074-.674-1.084-.418) .716) .166 (.979 (.783 (.252 (.304-.267 (.233 (.645-..906) .085 (.078 (.856 (.175 (. most often a result of occupational exposure (Roels et al.449) .531 (. Horiguchi et al.218) .184-.806-1.391-.784) . 2002.630-.210 (.078-.191-.38) .05) 1.194-. 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.687 (.293-.206-.718 (.433-.617 (.150-.282 (. 2004)..209) .696-.382-.176 (.438) 90th .178-.318 (.242) .225) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .833-1.212 (.210 (.491-.140-.263 (.795) 1.181 (.559-.490 (.769 (.727-.537-.261-.398-.917 (. 2002.865 (.229) .238) . Staessen et al.470) .308 (.270 (.235) .097) .850) .219 (.266) .917) .338 (.183) .678 (.190 (.560-.234) .700) .146-.083-.189-.538) .622 (.135) .184-.104) .247-.321) .352) .985 (.686 (..16) 1.716-.187) .541) .884) .404) .190 (. 2003.131-.168-.818) .473 (.00 (.183 (.444-.225) .440) .438-.414-.221 (.123-.297) .507-.140-.591 (.839) .729 (.281) .754) .208-.234-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.779 (.136-.792 (.690-.240) .551) .280 (.156) . 1996.091 (.687-.826-1.098) . 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.789 (.174-.154 (.158-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .247-.143-.412 (.187-.256-.

Horiguchi et al. 2003. Staessen et al. 2004b. Jarup et al. 1996. 2003. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . Creatinine-corrected urine cadmium values in U. 2005. 2003).. Further research is needed to address the public health consequences of such exposure in the United States. EPA. intermediate in former smokers and lower in never-smokers (Becker et al. Noonan et al. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. Olsson et al. Becker et al. 2002) and length at birth (Nishijo et al. Suwazono et al. 2002.. Friedman et al. Horiguchi et al.atsdr. In the typical environmental exposure. respectively.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. Komaromy-Hiller et al.html. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Cadmium can produce lung.S. 2002. maternal blood or maternal urine and birth weight (Nishijo et al. Ezaki et al. Becker et al. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population.. 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. 2004..S.. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies.. Olsson et al. 2002. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Wennberg et al. respectively. 2002.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. CDC. Occupational standards are provided here for comparison only. Moriguchi et al.. 2005). Both IARC and NTP consider cadmium a human carcinogen.. 2005.. 2000).... potentially fatal pneumonitis (Fernandez et al. 2003.. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.e. 2000. 2004. 2000. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Ezaki et al. environmental levels) and health effects is available from ATSDR at: http://www.. Wilhelm et al.... 2005.... approached these values associated with subclinical changes in renal function and bone mineral density. 1988). 1999. 2003. Becker et al. as may occur from welding cadmium-alloyed metals. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. For NHANES 19992000. 1999). 2006.. 2002).S. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine). urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. 2004).. 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. Acute and heavy exposure to airborne dusts and fumes.. 2003. and drinking water and environmental standards have been established by U.. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. 2006). 2002). Wennberg et al. In postmenopausal women. 1996).cdc. Jin et al. However. 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.46 mg/gram of creatinine) (Ezaki et al. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Staessen et al. 2003. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. has resulted in severe..... 1999).. Jarup et al. 2002). Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al.. 2004.. 2002.1 mg/L (Alfven et al.. data (CDC.. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al.26 and 3.gov/ toxpro2. 2000. 2004b). Women had higher blood and urine cadmium levels compared to men of similar ages.. Staessen et al. 2002). 2006. Information about external exposure (i. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC... with peak values observed in the fifth to sixth decades (CDC. Salpietro et al... 2005.. Zhang et al. In adults aged 60 years and older. not to imply a safety level for general population exposure. 2004. Mannino et al. Animal studies have demonstrated reproductive and teratogenic effects. 2002). 2006). Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. Olsson et al.. 2002.

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0.13 (7.73-5.25 (3.9 (10.99) 7.17-6.30) 5.4) 9.50-7.43-8.90-10.22-4.1) 10.32 (3.7 (10.36) 3.00-10.9 (11.55 (7.70) 5.20) 5.37) 5.74) Selected percentiles ( 95% confidence interval) 50th 4.7) 11.50) 5.20) 7.05) 5.10 (8.90) 5.0 (10.32-5.6 (11.97) 4.40-7.70 (6.6 (9.68 (7.7) 10.03 (4.62 (5. population from the National Health and Nutrition Examination Survey.7 (8.76-6.94 (4.30 (6.00) 7.80 (8.80 (4.1 (11.20-8.81 (4.81) 4.09-5.49) 4.97 (7.9) 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 4.80) 7.20) 8.4 (10.9 (11.3-13.26-11.7 (9.08) 7.96 (6.84-5.32) 4.63) 6.0) 12.2 (9.4-13.61-6.66 (7.90) 7.56) 5.35 (4.14.04 (4.20-5.12 (4.59-5.68) 9.7-14.36 (6.8) 12.26) 7.14.30-5.7 (10.20 (6.60-12.89-5.35 (4.9 (10.5-13.01-6.89) 4.03 (4.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70-5.1) 11.40-5.71-8.42-7.6) 10.99-11.Metals Cesium CAS No.5-14. scintillation counters.00-8.62) 4.23) 9.54-11.4) 10.12) 5.5) 10.7 (11.8 (10.00-9. Most human exposure to cesium occurs through the diet.08 (7.86-12.67 (4.70) 5. and high-power gas-ion devices.59-5.63-4.13 (5.90) 9.43 (5.1-13.00-4.80-6.40) 7. For absorbed cesium salts.89) 5.5-16.6 (11.87 (4.46) 7.82) 5.83-4.64-5.71-5.87-7.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.90-10.64) 4.3) 10.59) 7.9) 8.90 (6.97-7.99) 9.60-5.50 (7.4 (9. see Data Analysis section) for Survey years 99-00.4) 12.31-8.16-6.3 (8.30 (6.90-12.94) 4. and as polymerization catalysts.6 (9.70 (4.80-10.2) 12.1 (10.40) 5.5 (8.8) 11.30) 7.70 (9.39) 7.13 (8.25-5.40-5. Radioactive 137Cs has been used medically to treat cancer.27 (7.99-11.86-11.12-5.2-13.90) 5.2-14.30-10.6 (9.52) 7.2-12.81) 4.24) 4.34 (4.16-6.3 (8.87) 5.91-8.9 (11.40-11.09) 5.8) 9.40-5.1 (9.80-13.64 (4.33-5.37) 7. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock. the body half-life is estimated to be 70-109 days based on 137Cs exposures. respectively.98 (7.08-5. infrared lamps.25) 4.80-10.55-11.2) 11.90 (4.4) 12.55 (4.92-13.10-9.70) 7.80 (8.71) 4.35-5.95) 5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .7 (9. However.0) 9.40-5.17) 4.84-9.53 (6.60-6.63 (4.26) 4.38) 5.47-8.29) 4.05-5. 2004).64) 5.90-8.90-12. although cesium was generally of low toxicity when given to animals. and 0.00-8.3) 9.13-8.8 (10. photographic emulsions.82-4.3-13.70 (8.2-13.69-6.8) 12.20-4.86 (7.10-5. semiconductors.02 (4.10 (8.3) 12.1) 9.0) 10.94 (4.70 (8.3) 10.95-4.33 (6.77-8.17 (6.60-6.27) 4.54) 4.00 (7.49 (5.6 (9. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.60-7.21) 90th 9. Whether cesium compounds are carcinogenic is unknown.53-11. nausea. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 11.80 (4.42) 6.4) 11.45-5.71-9.83) 6.5) 9.3-15. Little is known about the health effects of this metal.1) 9.90-10.9 (11. and cardiac arrhythmia (ATSDR.7) 10.20) 4.50) 9. 01-02.62 (5.8 (11. and clay.20-7.84 (4.95 (3.2 (9.20 (4.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.44 (8.72) 4.60) 7.59 (5.0-15.07) 4.01) 7.73-11.5-14.10-8.2-13.60) 5. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.80-10.05-5.79 (4. interval) 4.99-6.91 (7.60) 7.36 (3.60 (7.71 (8.80 (4.4) 95th 11.87 (4.98 (7.56-11.34) 9.10-7.03-4.39-4.49) 75th 7.23-4.0) 12.74-5.56 (4.80 (8.60 (8. and 03-04 are 0.1-12.8) 11.00) 4.22 (4.5 (10.05) 5.08 (6.70 (6.3) 10.10 (6.04) 7.84) 8.07-11.47-4.70-8.90) 4.8) 9.77 (9.12-11.87 (4.93 (4.9) 11.57-5.2.59-5.50 (4.9) 12.81-14. cesium hydroxide is corrosive and irritating at high concentrations.88 (8.8-13.27-5.29 (4.00) 6.01-8.50 (4.71 (4.1) 11.42) 7. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0 (9.5) 12.8) 12.52-9.56 (4.74 (4.45-8. soil.0) 11.0) 11.80-11.0-13.7 (9.49 (4.94-4.70 (5.77 (9.9) Total 4.S.10 (6.26 (3.50 (6.21 (4.4 (9.7 (10.14 (4.1-12.61) 7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.33 (5.81) 9.0) 12. diarrhea.3) 10.40-11.60-7.50 (4.40 (4.77 (4.08-5.84) 5.64-10.7) 11.72-7.40) 5.64) 5.4) 10.15-8.

17 (6.08 (5.68 (4.50 (7.79-5.73-4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.77) 4.36-3.53) 6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48-6.56) 4.25) 4. Using clinically submitted specimens.96-4.70 (7.31 (4.14-6.33 (5.44-9.88-10.75-11. 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.S.82) 7.5) 7.26 (4.12) 3. Two small studies of European populations reported urinary cesium levels similar to U.66-6.60-20.27-6.59-8.38 (3.91-7.08 (3.02 (5.14 (6.56-10.19-6.99-9.29-3.34 (5.43 (3.55) 4.38) 10.33-3.99) 4.17) 4.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.78 (3.22-11.51 (4.27 (8.64 (4.93-7.41-4.13) 7.63 (6.56) 4.55 (3.52-5.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .54 (4.05-4.04) 6.90-8.94 (5.47) 6.15-11.30 (3.00-8.84-7.96 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.79) 4.96) 4.12-6.28) 7.67 (5.97) 8.54 (3.06 (5.85) 4.97-5.14-7.81 (4.95) 10.91-9.2) 11.08-3.71 (7.99-4.64) 4.21 (2.84-9.27 (6.05-3.84-11.50) 4.8) 6.28 (4.43-6.9 (10.90-3.83) 8.78 (3.S.64-6.08-7.35) 3.S.33-8.97-4.3) 9.58) 3.46 (7.1) 11.08) 4.29-3.50 (5.14) 4.68-11.50) 4.16-8.90 (7.05-3.11 (5.51) 4.68) 3.43 (4.22) 6.07 (5.23 (7.41) 9.62) 5.42 (5.65-3.42 (4.0) Total 4.16-8.06) 4.30-4.61-3.91) 5.87) 5.30 (4.7) 10.3 (10.5) 9.74 (5.44 (4.91 (5.7) 10.43 (8.84-9.49) 3.39) 5.42-6.0 (7.75 (7.9 (9. (2000) found urinary cesium levels that were slightly lower than those reported for the U..20-4.2 (8.77 (7.35 (3.95-6.20-4.95-12.37-3.61 (7.47) 6.83-6.17-4.60 (3.15-4.39 (5. population.70) 7.75 (6.20-8.62-8.72-5.24-10.07) 8.21-5.38-7.72 (4.35-7. Minoia et al.95) 8.26 (3.92 (5.53 (6.6 (9.42-4.58 (6.85-4.65-4.05 (4.3 (8.21-3.15 (7.89-4.39) 8.46-8.63-6.77-5.60-10.09 (4.14-4.10 (5.64) 5.66 (6.06) 5.00-9..08) 4.27-4.26-6.28 (5.67 (6. and were also roughly similar to those in this Report. 2004).45 (4.85) 5.55-5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.22 (3.07) 8.50) 8.78) 4.0) 7. 1990).38-12.06 (3.05) 6.18-6.80) 6.43-11.29) 5.81 (4.57) 3.44 (8.43 (4.66 (5.48) 7.59) 4.47) 4.36-6.98 (6.95 (3.77 (4.40) 6.78) 4.10) 7.50-5.83-7.3-15.27) 4.28) 8.08) 3.11 (5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.09) 8.17) 9.94) 7.91-6.05) 3.46-4.8) 10.56) 3.20-4.16-5.47 (4.84-7.2 (8.00 (8.45-6.70) 6.18-7.35 (4.53) 3.64 (8.98 (7.74) 75th 5.31-4.13-9.73 (3.79 (5.79) 6.9) 10.30 (7.67) 5.63) 6.56 (4.48) 90th 7.00-4.03) 6.10 (3.31 (4. 2005.68) 4.90-8.01-8.99-9.76-9.86 (4. population from the National Health and Nutrition Examination Survey.87 (5.95 (5.21-4.92) 3.07-4.53 (4.04) 5.50) 4.24-4.51 (7.43) 8.76-6.37) 4.41 (8.40) 7.10 (3.74-11.95) 4.58 (4.3) 11.51 (3.00) 6.29) 4.7-12.30) 10.27 (6.50 (6. population results shown in this Report (Alimonti et al.54 (5.74) 3.96-4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.91) 4.44) 3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.98) 5.35-11.87-4.91 (5.63 (4.8 (9.10-4.60 (5.12 (3..96) 4.02-4.41-7.46) 6.65 (6.00-10.03) 5.25) Selected percentiles ( 95% confidence interval) 50th 4.15) 95th 8.18) 8.98) 5.8) 5.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.14) 4.18 (7.31-6.47 (7.79) 9.6 (9.20) 5.44-5.41 (4.74 (4.42-4.71) 6.66 (5.58-5.91) 5.5) 9.24 (3.46 (8.4) 10.5 (9.60) 3.93-9.08 (6.00-5.47) 7.36-10.00-5.41) 4.68) 6.64) 9.82-4.33 (5.13-9.63-6.3 (9.51 (3.13 (3.30-4.40-5.19-3.03-5.03-6.58) 8.30) 10.16) 5. Komaromy-Hiller et al.38 (3.88-4.54 (4.41 (5.99 (3.51 (4.6) 6.29) 4.77 (6.04-11.04-5.63 (7. interval) 4.09) 4.72) 4.

Trace element reference values in tissues from inhabitants of the European community I.19:3131-3138. Minoia C. Comparison of representative ranges based on U. 4/8/09 Alimonti A. Sci Total Environ 1990.14:120-128.S. Wood CM. Assessment of urinary metals following exposure to a large vegetative fire. Gatti A. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Mott JA. Forte G. Spezia S.atsdr. Ronchi P. Gallorini M. Ash KO. Available at URL: http://www.gov/toxprofiles/tp157. J Expo Anal Environ Epidemiol 2004. New Mexico. Atlanta (GA) 2005. and serum of Italian subjects.html. cesium. Sabbioni E. Sewell CM. Rapid Commun Mass Spectrom 2005. Clin Chim Acta 2000. Paschal D.296(1-2):71-90. et al. Mincione G. et al. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. A study of 46 elements in urine. Costa R. Third National Report on Human Exposure to Environmental Chemicals. Pietra R. Howerton K. Centers for Disease Control and Prevention (CDC). Pozzoli L. Toxicological profile for cesium. antimony and tungsten. 2000.95:89-105. blood. Apostoli P.cdc. Komaromy-Hiller G.2004 [online]. patient population and literature reference intervals for urinary trace elements. Voorhees RE. et al. Wolfe MI.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).

770) .800) .07.15-1.16) 1.450) .22-1.660) .50) 1.570-.28-2.450) .13) 1.610) .340-.03) 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 . interval) . and inks.600-.64) 1.313) .890-1.430 (.360-.650-.460) .583) .26-2.270-.12) 1.418 (.830-1.520 (.410-.03-1.860 (. and 03-04 are 0.S.590-.890-1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.17-1.32 (1.760 (.04-1. and in synthesizing polyester and other materials.03) . It is also a component of porcelain enamel applied to steel bathroom fixtures.350-.99) 1.430-.09 (.50 (1.336-.960-1.16-1.520 (.05 (.680 (.850) 1.520) .06 (.26) Total .870 (.523) .820 (.32 (1.420) .17 (1.620) .430) .810-.330) . varnishes.08.550 (.890-1.333-. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.550-.950 (.330-.319) .364-.496) . and 0.800-.377-.428-.470 (.660-.710 (.270-.81) 1.850) .32) 1.28 (1.388-.308-.750 (.454 (.46 (1.590 (.410 (.460-.610 (.01 (.19) .520-.03 (.590-.01 (.S.469-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.900-1.07-1.900) .900-1.47) 1.00) . hard metal or in combination with other elements. 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.620-. Usual human exposure is from food sources.380-.44) 1.398) .670 (.300-.630 (.410-.01-2.53) 1.340) .15 (1.515 (.690-.900) .590) .393-.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 .610-.880 (.316-.560 (.14) .870 (.343 (. blue-colored pigments. 208 Fourth National Report on Human Exposure to Environmental Chemicals .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 .373-.480 (.543) .300 (.620-.26) 1.17 (1.670 (.410 (.580 (.580 (.333-. and kitchenware.450) .410) .48) 1.03) 1. 0.350 (.39) 1.67) 1.32-2.33-1.470) .620-.880-1.339 (. large appliances.419) Selected percentiles ( 95% confidence interval) 50th . population from the National Health and Nutrition Examination Survey. respectively.24 (.540-.490-.370 (.12) 1. and soil.460) .06-1.410 (. 01-02.56) 1.461 (.68 (1.416) .500 (.350-.430 (.427-.502) .870-1.450-.04-1.340) .519 (. shiny.900) .430) .32) 1.07-1.431) .750 (.17 (.348-.26-1.750-.540) 1.410-.21) 1.390 (.09 (.394) .02-1.331-.25-1.680) .374 (.350-.430 (.04 (.950) .463-.22) 1.840) .414) .334) .301 (.04-1.36) 1.07.670-.47 (1.09) .940 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.710) . Cobalt compounds are also used in manufacturing battery electrodes.390 (.460) .480-.37-1.310 (.550) 90th .540-.01-1.530-. diamond-polishing wheels.405-.930) .520-.320 (.05 (.700) . Cobalt is used as a drying agent in paints.259-.570) .33 (1.290-.29 (1.23) .48) 1.330 (.750 (.790) .450-.660) .410 (.480 (.280-.630 (.398 (.20 (1.500) .410) .564) .285 (.520-.42) 1.399) .Metals Cobalt CAS No.820 (.460 (.570 (.370-.499 (.890) 95th 1.581) .690 (.08-1.610) .371 (.367 (.450) .04) 1.369 (. automobile airbags.350) 75th .920) 1.352 (. hard metal (alloys of cobalt and tungsten carbide).404) . industry is imported or obtained by recycling scrap metal that contains cobalt.359 (.930-1.920-1.59 (1.520 (. and fertilizers.790-.22 (1.640) .530) . The cobalt used in U.740-.930 (.510) 1.810) .370-. Cobalt occurs naturally in airborne dust.740-.23-2.379 (. Cobalt compounds are used as catalysts in producing oil and gas.570-.810) .294 (.420) . steel-belted radial tires.431) .60 (1.420 (. seawater.950 (.980) .47) 1.16 (1.487) .340-.580 (.06 (.710) 1.375 (.424) .14-1.630-.52 (1.92) 1.390-.373) .670-.73) 1.680) .380 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.47 (1.600) .327-.81) 1.980-1.540-.730) 1.28 (1.700) .490-.75 (1.16 (1.950-1.340 (.45 (1.390 (.650 (.07 (.760) .940-1.310-.65) 1.16 (.316 (. see Data Analysis section) for Survey years 99-00.386) .850-1.270-.348-.380-.640) .940-1.370) .08) .790 (.16-1.520) .530 (.465) .370-.360-.600 (.16) 1.434 (.05) 1.670 (.520 (.440-.452 (.305-. and magnetic recording media.28 (1.03 (.379 (.640) .520-.338-.740 (.570) .690-.650 (.417) .291-.360-.540-.355-.400-.850-1.820 (.460 (.910-1.380 (.890) .372) .24 (1.435 (.680 (.410 (.950-1.380 (.390) . It is emitted into the environment from burning coal and oil and car and truck exhaust.800-.

33) 1.10) ..898 (.15 (.786-.393-.296) .290 (.16 (.691 (.522) .16 (1.964 (.33) .455 (.278-.324-.548 (.326-.435-.19) .938-1.275-.632-.616-.895-1.838 (.738 (.301) .505) .29 (1.215-.960 (.313-.346 (.382-.00 (. in the feces.829) .273 (.274-.728 (.900-1.310) .316 (.513) .314 (.83) 1.298 (.669) .00 (.781-1..495 (.756 (.368 (..376 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.29) .335 (.393 (.290 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.368) .279) .550-.259) .469-.407 (.513 (.543) .611) .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 .929) .343 (.533 (.302-.425-.615) .667-1.280-. an essential human nutrient.679-.703-.328 (.955) .361-.348) .23 (1.396) .60) 1.932-1.309) .421) .826-1.259 (.728) .708) .500-.11-1.861 (.990-1.457 (. 2003).291 (.365) .750-.704-.327-.563-.55) .394) .449-.12 (.963-1. and to a lesser extent.352 (.476-.727 (.09) 1.03 (.361 (.04-1.13) 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 .744) 1.313-.402 (.339-.600-.534-.329-.337 (.467-.905) .00) .408 (.963) .833-1.611) .481) 90th .560-.248-.25 (.640) .35) .343-.29 (1.49) 1.647) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.368) .428-.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 .829-1.847) .850 (.471 (.04 (.361-.433) .362-.378 (.821-3.14 (.372) .342-.523 (.369 (.429) 1. 1994).Metals fabricated from cobalt alloys (Lhotka et al.10 (.523 (.27) 1.635 (.606 (.857-1.824 (.16) .388 (.00 (.804) 1.27) 1.329 (.542 (.753) 1.407) . with pulmonary clearance half-lives of from one to two years (Hedge et al. 1994.792-1.574-.738 (.508-.938) . interval) .391) Selected percentiles ( 95% confidence interval) 50th .323) .487-.358 (.417 (.386 (.00-1.449) .25 (.593) . 1972).306 (.792 (. Once absorbed and distributed in the body.286) .426 (.630-.488) .11-1.444 (.562) .503-.324) .425) .723 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).821 (.10) Total .24) . Smith et al.396) .313-.683-.15) 1. Exposure in the workplace may come from electroplating.30 (1.707) .248-.243-.360) .554 (..50 (1.850-1.28) 1.331-.594) .990) .733-1.239-. population from the National Health and Nutrition Examination Survey.737 (.16 (.963-1.975 (.247 (.419) .963) .06 (.277-.362) .250) .736-.02 (.333 (. respectively.599) .515 (.694) .313-.353 (.333-.387) .352) .363) .554 (.585) .333-.365-..303-.598 (. using hard metal cutting tools.638-1.381) .281) .271 (.626-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.471-.630-.73) 1.384) .355) .352 (.581) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700 (.591 (.439) .438) .256-.537 (.457-.304-.461) .378-.259-.278 (.10-1.757-1.955) .289) .457) .777-. cobalt is excreted predominantly in the urine.272-.29 (1. A portion of cobalt retained for long periods is concentrated in the liver. 1979).861-1. 1972).297) .471-.296-.400 (.487-.404-. Cobalt is absorbed by oral and pulmonary routes.313 (.634-.36) 1.353-.830 (.333-.689 (.609) .760-1.60) 1.306) 75th .17) .435 (.911-1.547 (.327 (.917) .952 (.301-.937 (.391 (.361 (.349) .388 (.275-.983-1.290 (.660-.234 (.452-.317 (.848 (.534 (.337) .667-1.479-.378-.872 (.983) . Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.895-1.297-.774 (.842) .644 (.500 (.257 (.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 .00) .562) .753-.44 (.257-.392 (.700 (.844 (.785) .319-.378-.57) 1.294-.50) 1.328 (.740-1.417) .582-.54) 1.781) 95th 1.462) .851 (.463-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.380-.500-.03-1.949) .595) .608 (.328) .442-.673-..279 (.513-.00 (.268 (.237-.409) .36) 1.282 (.344-.529 (.362 (.S.434-.300) .879-1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.561) .50) 1.552 (.334) .251-.12-1.29) 1.282-.313-.475 (.35) 1.468) . or using diamond-polishing wheels that contain cobalt metal.976 (.662) . refining or processing alloys.750) .293 (.479) .304) .

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

Industrial Chemical Exposure: Guidelines for Biological Monitoring. The release of metals from metal-onmetal surface arthroplasty of the hip. Science 1988. Int Arch Occup Environ Health 1997. Jarvis JQ. Szekeres T. Fujimura N. Peltier A. salt. Sci Total Environ 1994.150. Zweymuller K. Leghissa P. Palmroos P. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Bacis M.48:172-173. Kato M. Dunstan E. Angerer J.45:246-247. 3rd ed. Zedda S. et al. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Kraus T. J Rheumatol 2001. 2001. McMinn DJ. Kriss JP. Bourne RB. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. a study of 13 elements in blood and urine of a United Kingdom population. Unwin P. Mosconi G. Swennen B. Pisati G. Shirakawa T. Stanescu D. Rorabeck CH. Dunning SP. Kirsch-Volders M. Radulescu M.22:359367. Cleland D. Oksa P. Absorption and retention of cobalt in man by whole-body counting. et al. Health Phys 1979. Lauwerys R. Roto P. Bunn HF. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Cobalt cardiomyopathy. J Occup Med 1992. Linna A. Laippala P. J Bone Joint Surg Br 2006. Iavicoli I. Int Arch Occup Environ Health. Robinson C. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Sci Total Environ 1997. Vitali MT. Goto S. Steffan I. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Arch Intern Med 1990. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust.44:124-132. Contact Dermatitis 2003. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Blunn G. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Weyher I.95:29-37. Sci Total Environ 1994. Dickel H. J Trace Elem Med Biol 2006. Salvatori S. Edmonds CJ. and hard metal dust.87(5):628-631. Respiratory health of cobalt production workers. Lung cancer risk in hard-metal workers.242:1412-1415. Iversen BS. McCalden RW. Thabe H. Kusaka Y. Occupationallyinduced “isolated cobalt sensitization. Tilley S. Moulin JJ. Lison D.58(10):631-634. et al. Schramel P. Ghat IS. Long-term clearance of inhaled 60Co. Thomassen H. Weber A.204:147-160. Hoher T.406:282-296.533:135-152. Uitti J. J Bone Joint Surg Br 2005.20(1):25-31. Kuska Y. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Romazini S. White MA. Lison D. Bozec C. Epidemiological survey of workers exposed to cobalt oxides. Wild P. Sci Total Environ 1998. Am J Epidemiol 1998. Ziaee H.Metals effects of cobalt. Hoet P. oxides. Smith T. Carnes WH. Christensen JM. Kiilunen M.55(4):269-276. Pradhan C. Chest 1989.88(4):443448.148:241-248. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Sanghrajka AP.69(3):193-200. Swennen B. Daniel J. Boca Raton (FL): Lewis Publishers. Cresti R. Sabbioni E. Salama A. Clin Orthop Relat Res 2003. Mutat Res 2003.150(1-3):167-171.” Contact Dermatitis 2001. HoffmannB.51(7):447450. Sabbioni E. DeSantis V. Health Phys 1972. MacDonald SJ. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Meyer zum Buschenfelde K-H. Cobalt and antimony: genotoxicity and carcinogenicity. Linnainmaa M. Buchet JP. Occup Environ Med 2001. Br J Ind Med 1993.34:620-626. Diepgen TL. Kristiansen J. Alessandrelli M. Occup Environ Med 1994. Thakker DM. Lauwerys R. Lhotka C. Molders J. 1985. Chess DG. Lasfargues G.50(9):835-842. Zobelein P. Sabbioni E. Zhuber K. Hedge AG. Am J Ind Med 2003. Lison D. Ichikawa Y.(1-3):133-139. X.36:732-734. Gross RT. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Outcome of occupational asthma due to cobalt hypersensitivity. et al. et al. Heki S.157:117121. Lisi P. Buchet JP. De Boeck M. et al. Barnaby CF. Schank M. Schaller KH. Hammon E. and cobalt metals. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Meier R.150:177-183.21(2):189-195. Goldberg MA. Falcone G. Biological monitoring of workers exposed to cobalt metal. Co-sensitivity between cobalt and other transition metals.28(5):1121-1128. cobalt salts. A report of two cases from mineral assay laboratories and a review of the literature. Cannon SR. Trace element reference values in tissues from inhabitants of the European Union.216:253-270. Goto S. J Orthop Res 2003. Lauwerys RB.

30) 2.900 (.69 (1.10-2. antique-molded or cast ornaments.32-1.60-6.90) 2.45-1.50 (4.89) 1.10-8.66 (1.20 (1.30-2.20-1.20 (1.00 (6.70 (2.43 (1.70) 3.50 (3.20 (3.90 (3.32-1.80 (2.50) 5.00) 1.80 (4.40-1.75) 1.60-1. leaded glass. Lead has a variety of uses in manufacturing: storage batteries.30 (2.60) 1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.10-2.10-4.899-.70 (2.14-1.80 (1.00-4.90-4.3.70) 1.60-2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.30-1.60) 2.90 (1.10-1.50-5.90) 1.50 (2. brass.60) 1.90) 1.50) 5. such as lead phosphate and tetraethyl lead.50-1.30) 5. ammunition.10) 1.40-6.50 (3.80) 1.80) 2.20 (1.30 (4.90-2.00) 3.30 (1.70-5.30-1.40) 1.30 (4.40 (1. bronze).10-1.00) 1.10-1.50-1.60) 1.31) 1.80) 1.00 (1.80 (1.55-1.10) 3.80) 1.20) 4.50) 4.60) 2.70 (1.40 (2.40-5. 0.40-2.90-3.50-1.30 (1.20-2.80-2.60) 5.50-1. blue-gray metal that occurs naturally in soils and rocks.50 (2.60 (2.60 (1.25 (1.14-1.55 (1.60-4.80 (1.50 (1.10-3.80-4.10 (2. 01-02.43) 1.80-4.70-1.10-3.90-6.90-2.71-1.60) 4.50 (2.50-6.00) 1.00 (1.20-4.30-1.50 (1.43 (1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20-2.10 (2.40) 2.50) 2.40-4.30) 2.50) 3.20) 4.10) 2.900 (.12-1.70-3.00) 4.80-3.50-4.90) 2.20-3.60 (1.60 (1.40-1.40) 5.70) 1.20) 1.70) 3.34-1.90-2. respectively.80) 1.80 (4. Lead was used in plumbing for centuries and may still be present.30 (2. and 0.10) 1.50) 1.20-1. Elemental lead can be combined with other elements to form inorganic and organic compounds.00-2.65 (1.20-3.62) 1.30 (1.70) 4.00 (3.90) 3.50) 1.878-1.80 (1. metal alloys (e.50-2.90-2.20 (2.90 (3.10 (1.90 (2. interval) 1.51) 1. plastics.43-1.00-4.40) 2.00) 2.00) 6.10-3.10-2.60) 4.40 (2.60) 2.70 (1.09) 1.50) 7.70) 4.40 (1.30-5.00) 1.55-1.90) 5. Since lead has been eliminated from gasoline.93-2.20 (3.60 (1.75-1.90 (2.40) 3.60 (1.81) 1.40) 2.70 (1.00) 4.60) 2.80 (2.30 (2. Before the 1980’s.00 (4.96-2.62 (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. see Data Analysis section) for Survey years 99-00.20-6.g.60 (2.22 (1.10 (2.40) 1. Lead is most often mined from ores or recycled from scrap metal or batteries.80 (1.986) .40-6.30-2.30) 95th 5.90 (3.10-6.04-1.51 (1.90) 2.46 (1.30 (2.39) 1.Metals Lead CAS No.900-1.30-2. 212 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.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 2.00-4.70 (1.20) 3.80 (2.60-1.40 (3.50 (1.10) 1.37-1.60) 4.00) 1.70) 4.50-3.20 (3.40-1.30 (2.90) 2.20 (1.30) 2.20 (3.60 (1.50) 2.00-1.36-1.30-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.45 (1.50 (1.17) .60-3.60 (2.69 (1. In the past.50-2.01 (1.52-1.90-4.30) 1.942 (.40-2.30 (2.40) 2.80-5.60) 3.00) 2.52-1.70) 4.70-2.40-3.10 (4. and 03-04 are 0.30 (1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.70-2.10) 5.87) 1.20-3.10-2.30-1.60-1.00 (2.28.60 (4.60) 1.56 (1.20 (1.50-3.70-4.68-1.S.00-5.10-3.20) 3.83 (1.53) 1.80-3.72) Selected percentiles ( 95% confidence interval) 50th 1.60) 3.90 (1.80 (5.75-2.80) 1.62-1.10 (1.80-4.00) 5.36) 1.70-1.40-3.25) 1.30-2.80-3.20) 5.37 (1.80) 2.50-4.00 (5.78 (1.36-1.80) 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 1.00) 2.60 (2.60) 2.00) 2.19 (1.14-1.20) 90th 3.23 (1.30-4.80) 2.69) 1.90) 3.80 (3.60 (3.70) 3.40 (1. and for radiation shielding.70) 1.50-5.60) 3.10) 4.40) 1.20 (2.70) 1. ceramic glazes.40-3.40 (4.20 (3.40-1.40) 4.70-1.70-2.90-4.80 (5.77 (1.20 (3.20 (4.60) 5.10-2.10-4. solders.50-2.60 (3.39-1.10) 2.70 (5.87 (1.50 (4.40) Total 1.70 (3.00-6.75 (1.70) 2.30-1.86) 1.90 (4.50) 4.30-1.70) 1.90 (3.30 (2.30 (4.80) 3.91) 1.80 (1.60 (2.20) 3.40 (1.40-1.3.69) 1.66) 1.50-1.20) .60-1.40-2.10) 3.60 (3.80-3.70 (2.30 (3.10-2.50-2.40 (5.10-6.00) .60) 4.20) 3.70-6.10) 3.70 (3.50) 1.60 (2.49-1.52 (1.50) 75th 2.60-4.40-1.S.60) 1. 7439-92-1 General Information Elemental lead is a soft.43) 1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.95) 1.50 (2.48) 1.25 (1.60 (1. malleable.00) 3.00 (4.50) 1.90) 1.60-2.37 (1.00-1.60 (3. dense.20-3.02) 1.800-1.90) 2.90 (3. the main source of lead exposure for the general U.10 (3.80) 2.20 (3.20) 2.10 (1.946 (.90-4.50 (2.60) 3.

2000).40) 2.90 (1.06) .90-2.708-.651) .20 (1.00) .35 (.659 (.70 (1.00 (1.66 (2.40) 1.50-2.21 (2.10 (.90 (2.00 (2. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.20) .29 (2.640 (.31-3.44-2.50) 3.800-1.20-1.800) .900 (.745-.80) 2.600) .80) 1.808 (.75) 4.70-3.13) .50) 1.480-.628) 1.50 (2.00 (1.10 (.660) .579-.990) 1.86 (1.40-2. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.00-2.10-1.862) .40 (2.680-.66 (2.80-2.90) 2.80 (1.637-.690) 75th 1.620 (.30-3.30-5.40) 2.86) 95th 2.923 (.13-3. see Data Analysis section) for Survey years 99-00.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.920 (.86-2. dust.850 (.773) .970-1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20) 1.80) 2.915-1.14-1.10 (1.10-1.Metals occupational (e.40 (1.590 (. lead-based painted surfaces undergoing renovation or demolition.50 (2.30-1.00-1.52-1.40) 1.02 (. pewter utensils and drinking vessels.10-3.960-1.848 (.677 (.815 (.97) 4.90 (1.80) 2.822-1.642 (.00-1.59) 1.20-2.730 (.600-.900-1.800) .30) 1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al. battery and radiator manufacturing) and recreational sources.625-.833-1.50) 1.80) 2.766 (.00) .785) .50) 1.900-1.800-1.800 (. imported children’s trinkets and toys. 1991).50 (2.00-2.00 (.40-5.90-2.40-3.59-2.80) 1.20) .941) .86) 1.04) 2. population from the National Health and Nutrition Examination Survey.900) .30) 1.00) 2.790 (.20-1.23-4.70) 3.40 (2.70) 2.564 (.573 (.40) 3.661-.40) 2.50-2.820-1.556-.900) . lead-containing folk remedies and cosmetics. Fourth National Report on Human Exposure to Environmental Chemicals 213 .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 1.674) 1.800-.500-.30) 1.40 (2.14 (1.90-3.610 (.31 (1.90 (2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) .03-2.30) 2. bullet fragments retained in human tissue.10) .20 (1.620) 1.78-2.700 (.82 (1.955-1.30-1.605) .30-2.700-.20 (2.636 (.60-2.33 (2.80) 1.18-1.29) 2.00 (1.589-.70) 1.600) .11 (1.558 (.60-2.20 (1.535-.70 (2.700-1.640-.691-.700 (.62-4.10 (1.40) 1.60-3.00-1.70) 3.60 (2.30) .700 (.40-1.701) .82 (2.752 (.20 (1.02) 1.50-1.04 (. older plumbing systems with leaded pipes or lead soldered connections.20-1.12) 90th 2.90 (2.818) .90-3.50 (1. 01-02.20) 1.650) 1.19 (1. or after soluble lead compounds are ingested.506-.20 (2.00 (1.30-1.526-. 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.40 (1.07-1.40 (1.20 (1. stained glass framing.10) 2.40) 1.60 (1.10 (1. respectively.540 (.04 (.60-1.900 (.540-.22) 1.40 (1.560-.931) .731 (.710-.833 (.700) .753 (.33.89) 2.579-.800 (.700 (.680) .60-3. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.14 (1.50-3.40-1.80 (1.30 (3.700 (. CDC.70 (2.700-.04-2.800) .27 (1. and 03-04 are 0.10) .749) .90-2.90) 2.30 (1.50) 2.900 (.900) .10-3.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .671-.10-3.09) 1.64) 2.23) .30) 2.700-.595-..710-1.32 (1.40 (1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.604 (.20 (3.78-2.52 (1.935) 1.10 (.810-1.600-.80-2.80-3.72) 1.1.600-.40-1.700) 1. lead-contaminated dust in indoor firing ranges. 0.40) 1.00) . 2007.52-1.700-.828) Selected percentiles ( 95% confidence interval) 50th .800) .641-.49 (1.20 (1. Approximately half of the absorbed lead may be incorporated into bone.800 (.75) 3.07 (. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.90 (1.00) 1.20 (2.10-5.857) .570-.900) .940 (.70 (2.800 (.30) 2.50) 2.04) .900-1.600-.695 (.20-2.580-.60 (1.688 (. and contact with soil.03 (1.800) .840 (.10-1.27) 1.591 (.572-.41) 2.30) 1.900) .80) 2.30-1..91) 2.630 (.900-1.70-2.625 (.20) .680-.80 (2.700 (. or water contaminated by mining or smelting operations.986) .40) 2.00) 2.g.80) 3.24-1. However.78-2.90) 2.990) 2.50-2.10) 1.50 (1.700-.90-4.60) 2.S.80) 3.90-2.1.10-1.10) 2.600-. and 0.800-.920 (.960 (.10 (1.900) .17 (1.600 (.40 (2.613) .20) 1.60 (1.600 (.00-2.62) Total .553-. In the blood.960-1.70 (2.738) .729-.70) 1.30) 1.40-1.73 (1.910-.20) .00) .10-1.795 (.60 (1.757-.11) 2.70) 1.33-2.616) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30 (2.90) 1.718) .

979 (.838) . encephalopathy.71 (1.94 (1.98 (1.41) . 1995).957-1.59-3.78 (2.52 (1.623 (.64) 2.62-1.43) 2.606-.436) .82) 1. based on prospective population studies.15-2.765) .98-2.24 (1.03) 2.739) .853-1.37-1.62-2..43-1.607-.88-2.15-2.992-1.404-.649 (.43) 1.31 (1.68 (1.11) 1.561-.33) 2.639) .88) 2.657) 1.06 (1.725) .05 (.11 (.638 (.400) .461) .69 (1.71-2.10 (1.639 (.940 (.38 (2.645-.10) 1.755 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.659-.50-2.05-1.862-.33 (1.652 (.70 (1.383-.97) 1.79) 1.44 (1.45 (1.44 (1.85) 1.432 (.725) .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 .00) .571-.648 (.579-.20-3.851) .50-2.64-2.18 (1.621 (.971 (.15-3.00 (1.677-.03) 90th 1. kidney injury.40-1. Lead can cross the placenta and enter the developing fetal brain.65 (1.97-18.686) .37-1.47) 1.00 (.00 (1.718) .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 .707 (.18) 1.722 (.676) .85-2.20) .898) .428) .08) .03) 2.61) 1.632 (.88) 2.670) 1.56) 3.946-1.734) .15) 1.41-1.72-2.85 (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 .677 (.535) .608 (.75 (2.914-1. 1996). through the inhibition of certain enzymes.53-1.997-1.11-1.01 (.963-1.603-.810 (.900 (.603-.800-.03 (1.03) 1.667-.31) 1.677) .18) 2. Approximately 70% of lead excretion occurs via the urine.94-2.990 (.404 (. BLLs and associated toxic effects differ in children and adults.09-1.508) .696 (.917-1.38 (2.17-1.612-. For instance.09-1. O’Flaherty.11 (1.28) 2.693 (.658 (. Large amounts of lead in the body can cause anemia. and nails (Leggett.03) 1.38 (2.603 (. scant amounts are lost through sweat.89-5. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger. and paralysis.88) 1.77) 2.790) .594-. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.78-4.645-.92) 2.918-1.22-2.23 (1.679-.11 (1.51) 1.03 (.588-.615 (.730) 1.588-. 2007). 2004.41 (1. The toxic effects of lead result from its interference with the physiologic actions of calcium.841-1..559-.74 (1. interval) .03 (.702) .72-2.673) .380-.72) .11 (.586-.43 (1.625 (.22) .03) .73-2.36-2.529-.492-.828-1.633 (.681-.97 (1.28-1.48 (1.56 (1.09-1. and through binding to ion channels and regulatory proteins.975-1.85-2.34-1.05-1.07-1.496 (.742) .703) .710) .587-. Staessen et al.988-1.67-4.933-1.510-. population from the National Health and Nutrition Examination Survey. hair.83 (2.781-1.774 (.718) 1.19) 1.700-.758) .977) 1.79) 2.594-.623 (.18) .654) .98) 2.03-2. abdominal pain.681-.639 (.918 (.86 (1.583-.49 (1.44) 1.97) 1.79 (1.615 (.87) 1.608-.61) 1.22) 1.22-1.882-1.914 (. with lesser amounts eliminated via the feces.812-1.00 (1.720 (.569 (.53) 1.408-.73) 2.920-1.02) 1.06) .88 (1.742) Selected percentiles ( 95% confidence interval) 50th .601-.51 (1. with a half-life of years to decades. and iron.46 (2.66) 2.720 (.0) 3.14) 1.793-1.701 (.17 (.43 (2.655) .701) .938 (.62) 2.551-. seizures.58) 1.702) .05 (1.61) 3. 1993).56-3.26) Total .914 (.763) .893) .27 (1.541-.50 (1.07) .25-1.753) .722 (.667) .14 (1.46 (1.47 (1.08-2.731-.50-2.28) .796-1.64 (1.19-5.89-2.622 (.61) 1.609 (.09) 1.50) 1.83) 1.571-.47 (2.31 (1..342-.709 (.617-.644) .25-1.375 (.698) .592-.11) .64) 95th 2. Schwartz.S.63) 1.605-.66 (1.639 (. 2003.981-1.33) 1.708 (.04-3.06) 1.644 (.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.Metals 90% of the body lead burden in most adults.39-1.26) 2.655-.10 (.938-1.52) 1.618 (.635 (.63) 4. The skeleton acts as a storage depot.668-.828) .876-1.55 (1.07 (. Nash et al.926 (.22) 1.641 (. zinc.66 (1.31 (2. CDC. 1991. 1995.988 (.679) 1.721 (.02-1.65-2. In 1991.404 (.31) 1.56-2.698) .962 (.50-1.18) 1.04) 2.61) 1.870 (.08) .746) .29 (1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.03 (.593 (.35) 2. 1993. 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.683-.62-3.992-1.667-.655) 75th 1.33-1.933) .20) .702-.01) .06 (.688) .604-.460-.469 (.03) .682) .712 (.887 (.15) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.12-1.55 (1.96 (1.75-2.671 (.

2002a).S.6%) were lower than those from NHANES 1991-1994. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.. Pirkle et al. Jones et al. lead in women may be associated with hypertension during pregnancy. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.S. Both drinking water and ambient air standards for lead have been established by the U. Surveillance data reported by U.. 2002.4% of children had BLLs of 10µg/dL or higher (CDC. 1998). Muntner et al.. the prevalence rate has declined annually since 1994 (CDC.0 µg/dL in females (Soldin et al.. However. 2006). Lanphear et al. BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist. 1994). premature delivery. both the geometric mean (1. 1984. and decrease fertility (Alexander et al. 1999).S.. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. 1999). usually with BLLs greater than 40 mg/dL. Bellinger 2005. and organic lead compounds not classifiable with respect to human carcinogenicity. 1996.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample. In occupationally exposed adults.Metals µg/dL or higher as the level of concern in children. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. For example. 2003). approximately 11.cdc. EPA. Schwartz. seizures. residing in housing built before the 1950’s...e. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. Overall. Korrick et al. Staessen et al.S. In NHANES 1999-2002 in children 1-5 years old.gov/toxpro2. Information about external exposure (i. 2003. 2003. 1996. the geometric mean BLL was 3... BLLs reflect both recent intake and equilibration with stored lead in other tissues. higher than 100-200 µg/dL). Urine levels may reflect recently absorbed lead.3 million children tested had BLLs of 10 mg/dL or higher (http://www. though there is greater individual variation in urine lead than in blood and greater potential for contamination.7 µg/dL and 4.. adults in the 19992000 NHANES sample (Apostoli et al.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 1991. and low family income (CDC.cdc. High dose occupational lead exposure.07 µg/dL (Becker et al.g. 2001).. IARC considers inorganic lead compounds probable human carcinogens. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. with overt encephalopathy.S.21% of approximately 3.2 µg/dL in males and 3. At low environmental exposures. which is an 84% decline. respectively.. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.. 2005b. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. 2005b). when the geometric mean BLL was 2. particularly in the skeleton.S.html.6% in NHANES 1988-1991 to 1.. 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. Telisman et al. Schwartz et al. 2002).4% in NHANES 1999-2004.. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. urban residence. CDC. 2003. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. almost double the geometric mean of 1.000 adults. 1996.. 2000)...9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. The U.75 µg/dL in U. 1995.. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 2006). Fourth National Report on Human Exposure to Environmental Chemicals 215 . Borja-Aburto et al. and peripheral neuropathy generally occurring at much higher levels (e.5 per 100. 1987. adult residents.. Payton et al. may alter sperm morphology. including minority race or ethnicity. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. 2007). and spontaneous abortion (Baghurst et al.atsdr. 2009).. environmental levels) and health effects is available from ATSDR at: http://www. More recently.. reduce sperm count. Data submitted through state public health programs from 2006 showed that 1. 2000).xls). 2005a). A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 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. adults in the 1999-2000 NHANES sample.

doi:10. et al. Korrick S.82:60-80. Available from URL: http://www. Homa DM. Hertz-Picciotto I. Schulz C. Checkoway H. Sci Total Environ 2002.123:e376-e385. Hu H. Kim R. Jones RL. Bellinger D. Rotnitzky A.atsdr. Neurodevelopmental effects of postnatal lead exposure at very low levels.150(6):590-597. Blanco J. Farias P. Brody DJ. Acquisition and retention of lead by young children. Adult blood lead epidemiology and surveillance—United States. 2003-2004. 1988-2004. Payton M. Int J Hyg Environ Health 2002. Occup Environ Med 1996.348:15171526. Speizer FE. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas.101(7):598-616. Muntner P. Available at URL: http://www. Available at URL: http://www. Atlanta. Dietrich K. Centers for Disease Control and Prevention (CDC). Lead and hypertension in a sample of middle-aged women. Jacobson JL.htm. Chiodo LM. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. MMWR Morb Mortal Wkly Rep 2005a. Environ Res 2000. Hu H. 2005b. Available at URL: http://www. Seiwert M. Kaufman JD. Hernberg S. Blood lead levels—United States. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.gov/mmwr/preview/mmwrhtml/ mm5532a2. Ganzi A.cdc. van Netten C. Luukkonen R. Krause C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.1542/peds:2007-3608. Reese YR.10:43-50. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . 4/14/09 Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 1993. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.cdc. 1999-2002. Henderson CR. Ronchi L. Bavazzano P. Kuehnemann TJ. Caldwell KL.html.htm. IARC Monogr Eval Carcinog Risks Hum 2006. Stanek KL. Mantere P. Weiss ST.gov/nceh/lead/publications/ books/plpyc/contents. CDC. 4/14/09 Centers for Disease Control and Prevention (CDC). Birth Defects Research (Part A). Baj A.73:409-420. Batuman V. Rotnitzky A. 4/14/09 Centers for Disease Control and Prevention (CDC). Baghurst PA. Rojas LM. Auinger P. et al. Sparrow D. Korrick SA.54(20):513-516. Blood lead levels measured prospectively and risk of spontaneous abortion.gov/nceh/lead/ CaseManagement/caseManage_main.8(3):395-401. Pediatrics 2009. Wager C. Wigg NR. Scand J Work Environ Health 1984.275(15):1171-1176. Vupputyuri S.htm.cdc.cdc. 2005.26:359-371. Aro A. Bellinger D. Robertson EF. Atlanta (GA). Apostoli P. Hunter DJ. Public Health Rep 2000.55(32):876-879. The relationship of bone and blood lead to hypertension.87:1-471. Cox C. Lepom P. Available at URL: http://www. Aug 2007 [online]. Lead. Coresh J. Angle CR. Hänninen H. Cory-Slechta DA. Ewers TG. Jacobson SW. Jusko TA. JAMA 1996. Inorganic and Organic Lead Compounds. Atlanta (GA). Meyer PA. Rios C. Neri A. Pediatrics 2004. Roberts RR. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Age-specific kinetic model of lead metal in humans. gov/mmwr/preview/mmwrhtml/mm5420a5. et al. Neurotoxicol Teratol 2004.htm. Becker K. Manton WI. Am J Public Health 1999. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Borja-Aburto VH. Lanphear BP. Sparrow D. Managing Elevated Blood Lead Levels Among Young Children.115:521-529. Pirkle JL.53:411-416. Am J Epidemiol 1999. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Neurotoxicol 1987. Vimpani FB.gov/toxprofiles/tp13. 4/14/09 Centers for Disease Control and Prevention (CDC). 4/14/09 Alexander BH. Cox C. 2002 [online]. Preventing Lead Poisoning in Young Children. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Canfield RL.113(4):1016-1022.205:297-308.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. Ga.287:1-11. Muller CH.89:330-335. Weiss ST.275:1177-1181. Kaus S. References Agency for Toxic Substances and Disease Registry (ATSDR). MMWR Morb Mortal Wkly Rep 2006. JAMA 1996. Leggett RW. Lanphear BP.cdc. N Engl J Med 2003. Hu H. Toxicological profile for lead. et al. Semen quality of men employed at a lead smelter. Blood lead reference values: the results of an Italian polycentric study. Teratogen update: lead and pregnancy. 1991 [online]. McMichael AJ. et al.

Environ Health Perspect 1996. Physiologically based models for bone-seeking elements. Cvitkovic P. IV. Blood lead concentrations in children: new ranges. Sparrow D. Roels H. Soldin SJ. Rubin R. blood pressure and cardiovascular disease in men.106:745-750.209:301305. Hanak B. Brody DJ. O’Flaherty EJ.327:109-113. J Hum Hypertens 1995. Kaufmann R. Use of endogenous. Association of blood lead. cadmium. Toxicol Appl Pharmacol 1993. and tibia lead with neurobehavioral test scores in South Korean lead workers.118:16-29. Amery A. Smith DR. Semen quality and reproductive endocrine function in relation to biomarkers of lead. JAMA 2003. Hu H. Lauwerys RR. 50:31-37.108(1):45-53. Clin Chim Acta 2003. Exposure of the U. Low-level lead exposure and blood pressure. Telisman S. Lee SS. et al. Flegal AR. Nash D. Rocic B. Gunter EW. Kaufmann RB.140:821-829. Stewar WF. Staessen JA. Lee GS. and copper in men. Kidney Int 2003. stable lead isotopes to determine release of lead from the skeleton. blood pressure. Hwang KY. Gavella M. Wilhelm M. Hickman T.Metals results from NHANES III. cadmium.S. Payton M. dimercaptosuccinic acidchelatable lead. Schulz D. Environ Health Perspect 1998. and hypertension in perimenopausal and postmenopausal women. zinc. Am J Epidemiol 2001.63:1044-1050. Soldin OP. et al. Int J Hyg Environ Health 2006. Revised and new reference values for arsenic. Sherwin R. Lee BK.289(12):1523-1531. Paschal DC. Schwartz J. Pizent A. Lead. Schwenk M. Blood lead.9:303-327. population to lead: 1991-1994. Lustberg M. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Environ Health Perspect 2000. Kinetics of lead disposition in humans. Magder L. Am J Epidemiol 1994. Osterloh JD.104(1):60-66. Arch Environ Health 1995. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Jurasovic J. Low-level lead exposure and renal function in the Normative Aging Study. Weiss ST. Pirkle JL.153(5):453464. Schwartz BS. lead.

Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. 1993). have often required public health intervention (Zeitz et al.90 (1.02) .00 (.Metals Mercury CAS No.753-1.50-2.30) 1.60-2.700-..50) 2.00-5.800-1.00) 4.60 (2. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.40) 3. Accidental spills of elemental mercury.400-.50) 4.40 (4.860-1. or oxygen.00) 1.00 (2.800-1. 218 Fourth National Report on Human Exposure to Environmental Chemicals . and is distributed to most tissues.300) .00) . 2007).800-1.500-. predominantly from fish and other seafood.689-.700-.80 (3.700) .877 (. sulfur. and mercury compounds are still used as preservatives (e.60-6.00 (2.50) 1. see Data Analysis section) for Survey year 03-04 is 0.70 (1.60) 2085 2293 3478 Limit of detection (LOD. synthetic organomercury compounds were once used in pharmaceutical applications.919) .500 (.700-.900) 75th 1.672) .419 (.300-.797 (. constitutes the main source of dietary mercury exposure in the general population. merbromin). population from the National Health and Nutrition Examination Survey.800 (.S.80 (1.40-3. to form inorganic mercury compounds or salts.900 (. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.400-.g.500 (.800 (. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).703-.979 (. 1999 .600 (.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 . Elemental mercury is a shiny.70 (4.800-1.30-4.80) 1.30) 4132 4241 03-04 03-04 03-04 . and mining and smelting..20) 2.50-1.776 (.90 (4. 2002).326 (.800 (. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.60-3.60) 1.927) .781 (.g. interval) .g..40-2.285-.484) . In addition.30-5.500-.70-2. may contain inorganic mercury.00 (.574) . and organic forms. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.60-6. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. The ingestion of methyl mercury.300 (. elemental mercury is absorbed mainly by inhaling volatilized vapor. such as chlorine (e.563 (.363-. Survey years 03-04 Geometric mean (95% conf.90) 3.372) .90) 90th 3.40) 1.900) 1.600) 1. 1980.30) 3.714-.30 (2.418-. Woods et al.S. The kinetics of the different forms of mercury vary considerably.40 (3. thermostats and switches). IARC..00) 3.70 (3.10-3.800-1.655-.30) 3.90 (1.20-3.400 (. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.40 (4.490 (.30) 5.00-1.90) 95th 4. Poorly absorbed from the gastrointestinal tract. which can bioaccumulate in aquatic and terrestrial food chains.60-5..30 (1.30-2.. mercuric chloride).700-. sphygmomanometers and barometers. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).00 (.10) .700-. thimerosal. 1998. 1994.472-.90-3.40 (3.903) Selected percentiles ( 95% confidence interval) 50th .50) 5.70) 911 856 2081 4525 03-04 03-04 .80 (1.700) ..900) 1.60) 1.40-1.80) 3.20-4..20 (2.50-3.900) . Apart from methyl mercury.00 (.700 (.900) 1. which create an episodic potential for volatization and inhalation of mercury vapor. electrical lamps. solid-waste incineration. Also. Other major uses include electrical equipment (e. and dental amalgam.70 (1. with the highest concentrations occurring in the kidneys (Barregard et al.30) 1. Kingman et al.2.60 (1. After elemental mercury is absorbed.814 (.80) 4.00) 1. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.20-4. inorganic.500) .60 (1. thermometers.. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.80 (1.40-2. an organic form of mercury. Atmospheric elemental mercury can be deposited on land and water.g.800 (.00 (2. Hursh et al.886) . Some cosmetic skin creams from countries other than the U.40-1. phenylmercuric acetate) or topical antiseptics (e.00 (1.30-6.12) .

30 (.10 (.50) 1.919) .90) 90th 1.800 (.738-.700-.700 (. 1996).00 (1.30 (1.900-1. Fourth National Report on Human Exposure to Environmental Chemicals 219 .10 (.90) 5.300) .800 (.90) 2.800) 75th .06-1. 1971).00-2.30-6. thereafter.500-. Smith and Farris. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.20-3.900 (.00 (3.90) 2. Sandborgh-Englund et al. 2003).40) 5..700 (. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.50) 95th 2.726-1.20-3.90 (1.944 (..70-5.475) . 1992 and 1999.30 (1.871-1.40-2.800-1.30-2.35 (1.10 (1.500 (.70) 4..90 (4. 1994).10 (1. Miettinen et al. Vahter et al.80 (1..800) ...00-2. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.20-3.600) ..00-6.300) .700) 2.256-.50-2..407) . with most elimination occurring through in the feces (Sherlock et al.800-1.90) 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 .500-. 1999). Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.30-3.40 (1.299-.500-.268-.318 (.00) . 2004.30-11.00-1. Suzuki et al. 1973).60 (1. 1994.20) 1.70-5. Excretion occurs by renal and fecal routes.541-.377) .10-1.7) 4.200-.80) 1. Methyl mercury is incorporated into growing hair.700-1.00) 6.70) 1.80 (3. 2005).90) 3.Metals the tissues to mercurous and mercuric inorganic forms.20 (.697-.70 (1.300) .50) 2..500-1.317 (..200 (.300) .824) 1.369) 1..60 (1.70 (1.700-..664-1.30 (1. 1969.00-3. Vimy et al.800-1.60) 1.40-2. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.700 (.73) 1.20) .667 (.06 (. Myers et al.825-1..50-12. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.70-6.60 (1. population. 1990).500-.50 (1.600) . Jonsson et al.10 (5.10) .00) 1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.00) 1. 1993).60) 3.10-3.900 (.200-.30) 3.20-2. 1995.300 (.70-3.200-.600 (.700 (.940) Race/ethnicity (females.800) 1.00-2.90 (3.00 (2. 1984.90 (1.00) 7. McDowell et al.900-1.265-.20) .02 (. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.S.300) .30) 1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.30-4.60 (3. 1994) and then undergoes slow dealkylation to inorganic mercury.700-1. After exposure to elemental mercury. 1998).329 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.300 (.80) 579 527 370 436 588 806 Limit of detection (LOD.500 (.833 (.300) ..50) 3.30-6. 1991.70) 4. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .14.40-1..800) 1.30-6. 1998).00 (2.30-4.90 (4.50 (2.395) .10) .80-3.377 (.29) ...800 (.40) 1.200-.14 and 0.00 (2.269-.10 (1. 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. Geometric mean Survey years (95% conf.70 (1. 1999-2002. 1996.00) 2. interval) Selected percentiles (95% confidence interval) 50th .20 (2.00) 4.343 (. Smith et al.300 (.374) .0) 4.20-11.60 (3.. 1992)..200-.50) 1.. 2003).50-3.900 (. 1992.200 (.23) . The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al. for both acute and chronic exposures. National Health and Nutrition Examination Survey. and a useful marker of exposure in epidemiologic studies (Grandjean et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Methyl mercury enters the brain and other tissues (Vahter et al.307 (.60) 2..30-5.500-.40 (1.820 (.200-. 1993).01) . Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.800) .70-3.400-. a measure of accumulated dose (Cernichiari et al. 1975.27) .30) 1. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.60 (2.10 (3.40) 2. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.60) 1.297-.300 (.10) 1.3) 4..

S. 2000). 2000.500-. Bellinger et al. Rissanen et al. short-term memory loss. see Data Analysis section) for Survey year 03-04 is 0. Drexler and Schaller. altered physical growth. In recent epidemiologic studies.500 (.700-. overt signs and symptoms of chronic inhalation may include tremor. depression.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 .500-.700 (. gingivitis. fatigue. pain in the extremities.600-. limb deformities. 1963). Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 1996). anorexia. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. the existence of a causal relation is unresolved (Chan and Egeland. Once absorbed.. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 2004.. 2004). maculopapular rash. 2004). and neurocognitive and behavioral disturbances. 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.600-.600) . Acute.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . Factor-Litvak et al. 2006.600 (. and pinkish discoloration of the hands and feet (Tunnessen et al. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. which may vary for some chemicals by year and by individual sample. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. causing parasthesias.. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure..600 (.800) .. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease..600-. 1998. population from the National Health and Nutrition Examination Survey. cerebellar ataxia. hearing impairment.500-. The constellation of findings may include anorexia.500-. Vupputuri et al. Sakamoto et al..800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600 (. irritability. particularly irritability. dysarthria.700 (.Metals may be more efficient for inorganic mercury (Grandjean et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600 (. 1970.600) . Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600) . and progressive constriction of the visual fields. 2003).600) . Inorganic mercury exposure usually occurs by ingestion.600) .. sensory impairments.500 (.. 1995. At levels below those that cause acute lung injury. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.. Smith et al..500-. < LOD means less than the limit of detection. 2000.700-. typically after a latent period of weeks to months. 2005). 1995.500 (<LOD-.700-. Rice.700) .500-. 220 Fourth National Report on Human Exposure to Environmental Chemicals . dysarthria.600 (. 1983).600) . hypertension. 1993). DeRouen et al.500-. Overt poisoning from methyl mercury primarily affects the central nervous system. 2006. Sakamoto et al.600 (.... 1951. Oskarsson et al.700 (. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.700 (.. 2005. and sleep disturbance (Bidstrup et al. 2004. Smith et al. ataxia.700 (.. Salonen et al.500-. insomnia.500) .800) .500 (<LOD-.. and cerebral palsy (NRC.600 (.500-.600) .600 (.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600) . and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.600-. Stern 2005.700) 2007 2240 3406 Limit of detection (LOD.700 (.42. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2002.600) . Survey Geometric mean (95% conf.. 1987). Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.

420 (.67-3.405-.gov/mercury and from ATSDR at: http:// www.530-.534) .19 (2.420 (. adult women in several ethnic subgroups (Hightower et al.. 2006).76-3.250) .940 (. aged 18 to 69 years. Among the three racial/ethnic groups.530) .07 (. Sanzo et al. From 1996 through 1998.63-2. A cohort of 1127 U. the total blood mercury concentration is due mostly to the dietary intake of organic forms.840-1.870-1.65) 1.66) 3.33 (2...480) 75th 1.330-.55 µg/L. Information about external exposure (i.441 (.460 (.08 (1.16 (.960 (.580) . et al.304) . 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.08 (1.39-3. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. 2001. Mahaffey et al.05) 1. interval) .93 (1..555) .400 (.476 (.254 (. 2001..77-2. 1997.76-4.90) 2.509) .460) . Schober et al.26 (1. 2004.85-2.890 (.870-1. military veterans (mean age 52. population from the National Health and Nutrition Examination Survey.05) 3. and increased slightly in non-Hispanic white children (Caldwell..406-.930-1. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60 (1.46) 3.360-.96 (1.09 (2..610-1. Over the NHANES 1999-2006 survey periods. 2002). although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. 1998).382-. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.408) . During the same survey periods.S.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 .88) 287 722 1529 03-04 03-04 . Survey years 03-04 Geometric mean (95% conf. However.Metals standard for inorganic mercury has been established by U. average age 9.340-. particularly methyl mercury.46 µg/L for children. total blood mercury increased with age. Benes et al.e.440 (. 758 children.480 (.840-1. slightly higher total blood mercury levels were found in U.330-.9 years).509) .31) 2.700 (. These distinctions can help interpret mercury blood levels in people.360-.442-.01 (. range 40 years to 78 years) had an average total blood mercury concentration of 2.S.840) 1.24 (2. 2003).447 (.396-.29) 1. In Germany the geometric mean for blood mercury was 0.00) 1. Grandjean et al. Kingman et al..492) Selected percentiles ( 95% confidence interval) 50th .97) 2.280-. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. who participated in a 1998 representative population survey (Becker et al. 2000).12 (. 2009). environmental levels) and health effects is available from the U. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.S.14-2.89) 3.00 (.430) . total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.200 (.88 (1.epa.13-2.520) . and the age-related changes differed across the groups (Caldwell et al. 2009).34-3..330-.76-3.160-.78-2..96 (1.58 µg/L for 4645 adults. In NHANES 19992002..03-4.413-.358 (..88-3.S. EPA at: http://www. average age 33 years.570) .549) . EPA.18) 2.42) 95th 3.360 (..430 (. the median concentration of blood mercury was 0.. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.52) 2. total blood mercury geometric mean levels in females aged 16-49 years did not change.330 (.cdc.S. 2003).495 (.370) .290-.410-.14.350-.67-2. Fourth National Report on Human Exposure to Environmental Chemicals 221 .8 years. 1998).313-.99-6.60) 619 713 1066 Limit of detection (LOD.gov/toxprofiles.14) 90th 2. 1995.54 (2. see Data Analysis section) for Survey year 03-04 is 0.78 µg/L for adults and 0.16 (1.68 (2.30) 3.24) 1.20 (1.19 (1.770-1.atsdr.416 (. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.433 (.430 (. Biomonitoring Information In the general population.213-.463) . Total blood mercury levels increase with greater fish consumption (Dewailly et al.31) 1266 1272 03-04 03-04 03-04 .28) 1.530) .60-2.23) 2.61) 1.23) .

667-1.30) 1. the urine mercury increased by approximately 0. Langworth et al. Information about the biological exposure indices is provided here for comparison.21) 1..687) .620-.508 (.07) 1.566) . and on average.455-.275) . a biomarker of perturbation in renal tubular function. 2005). 1998).56) 1266 1271 03-04 03-04 03-04 .347) .01) 2. Department of Health and Human Services noted that several studies have observed a modest.11-2.85) 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 . 2006.463 (. and Italian (Apostoli et al. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.63) 1.54 (2.532 (.. not to imply a safety level for general population exposure.1 µg/L.32-2. military veterans with dental amalgams. et al.768 (.S.784) 1. Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al. 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.525 (.306 (.616) .587 (.Metals 2000).368) .522-.301-.696 (.1 µg/L for each surface with a dental amalgam (Kingman et al. 2009).964-1.. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.365 (. 2006).333-.13 (1.391) .307-.67 (1.447 (.970 (.309-.276 (.545 (.443 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.32 (1.39) 1.498) 75th .537) .30) 2. 1992).246-.455) .18-1.00) 286 722 1529 03-04 03-04 .217 (.35 (1.385-.343 (.40 (1.417) .714-1. An expert-panel report recently prepared for the U.44) 1.67 (1.909 (.79) 1.969-1.S.404-.51-2. 1988. In the study of U.785-1.40-1.77 (2.365 (. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.476 (. interval) . women of childbearing age have generally been much lower than these levels (CDC. DeRouen et al.. Survey years 03-04 Geometric mean (95% conf.87 (1.11) 1.88 (1. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.46-2. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. Levels in U.62 (1.06 (.400) .297 (.00) 90th 1. 2002) adult population surveys were similar to those in a U.16) 1.535) 1.391-.13-2.86) 95th 2.11) 2.03) 2.196-.225-.384 (.619-.64-2.09) 1..362 (.358) . population from the National Health and Nutrition Examination Survey.280-.265-.208-.480) . 2009)..289) . Urinary mercury levels in recent German (Becker et al.400-.00 (.87) 2.65 (1.875-1..12-3.652) .447-...79 (1.25 (.41-2.88-2. et al.485 (. Czech (Benes et al.28 (.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals . 2002).599) . Urine mercury and the number of dental amalgams were correlated.78-4. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L. mean urinary mercury was 3.255 (.630) .588) . Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.76 (1.S.464 (.392-.61) 1.800-1. reversible increase in urinary N-acetyl-glucosaminidase.376-.472-.455-.23-2.486) Selected percentiles ( 95% confidence interval) 50th ..06 (.990) .04-3.S.31 (1.88-2. 2003).S.

07) 1.540 (.580-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .799) .81-6.39-3.831) .31-1.806) .13-4.656-.744) 1.420-.3) 5.596 (.92) 3.99) 1.51 (3.S.723 (.81 (3.35) . Geometric mean Survey years (95% conf. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.47) 1.57-4.620 (.16) 5.740 (.91-7.04-1.42) 2.98 (5.930) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.Metals Urinary Mercury−Females Aged 16-49 Years Old.41 (2.810) .97 (1.03 (.97) 2.S.578-.520-.35 (1.45) 2.07-2.47) 1.06 (.665) .97) 2.48 (2.600 (.15-1.30 (2.03 (.592 (.565 (.724 (. 1999-2002.639 (. population.56) 3.77) 2.53-3.516 (.61) 1.850-1.43-1.670) 75th 1.83-3.76 (1.582-.92) 2.622-. interval) Selected percentiles (95% confidence interval) Survey years 50th .450-.23-1.615 (.721 (.45) 2.24-1.03) 1.50 (2.76) 2.14-2.772 (.65) 1.910) .70 (2.706 (.85) 4.99 (3. 1999-2002.50 (1.658 (. National Health and Nutrition Examination Survey.28 (1.650 (.664) .22-3.637) .710 (.636-.25) 2.605-.831) .742-1.10-4.426-.10-2.55-3.89 (2.41 (1.95 (2.540-.32-3.76-5.68) 3.91 (2.30 (2.62 (1.16-5.774) .00 (3.610-.87-4.42-3.691) .27 (1.79) 1.32 (1.14-1. population.500-.557-.21-3.00 (2.37) 1.05 (3.699) 1.45 (1.38) 4.833) .14.92) 4.69 (1.18) 3.502-.560 (.790) .760 (.824) .03-2.04-10.15 (2.655 (.650 (.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .966) .56) 4.46) 3.387-. interval) Selected percentiles (95% confidence interval) 50th .62 (4.475-.99 (2.14 and 0.59-5.410-.99-2.909-1.579-.30 (1.870) .631-.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.41-6.09-1. 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.45-2.05 (2.846) .21 (1.62 (3.606 (.45) 95th 3.09-1.526-.710 (.51) .41 (1.37 (1.56 (1.46 (1.17) 95th 5.560-.686) .27-1.616-.68-3.52) 3.522 (.94) 1.32) 2.892) .580 (.709) 75th 1.61-6.501-.50-4.18 (3.07-5.624-.69-3.520-.72) 1.79) 3.55) 90th 3. 16-49 years) 99-00 01-02 .23-1.00) 2.84 (2.657 (.809) .53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .14) 3.685 (.84 (2.710) 1.42) 90th 2.54) 595 531 381 442 594 826 Limit of detection (LOD.46-4.21 (2.650) 1.508-.77) 1.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.24) 6.85-3.13 (2.553-.832-1. Geometric mean (95% conf. 16-49 years) 99-00 01-02 .719 (.65-4.27 (2. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old. National Health and Nutrition Examination Survey.30-2.97) 2.45-3.632 (.68 (3.31 (1.44) 3.22 (.709) .569-.

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Toxicol Appl Pharmacol 1994. Lind B.110:129-132. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.111(12):1465-1470. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Orr MF. Public Health Nutr 2001. Smith AE. Yoshinaga J. Sandler DP. Environ Health Perspect 2007. Lorscheider FL. Farris FF. Goldberg J. Burbacher T. Effects of occupational exposure to elemental mercury on short term memory. Sinks TH. Turner MD. Arch Environ Health 1993. JAMA 2003. Vimy MJ. Smith JC. Amiano P. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Hum Toxicol 1984. Bernardo MF.128(2):25125-25126.79:786789. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Stern AH. Methyl mercury pharmacokinetics in man: a reevaluation.2:117-131. Aguinagalde FX.97(2):195-200. Zeitz P. Effects of exposure to mercury in the manufacture of chlorine. Most B. Environ Health Perspect 2003. 1993-1998. Kaye WE. et al. Leitao JG. McMahon KJ. Hall LL. Martin MD. Hongo T.289(13):1667-1674. The hair-organ relationship in mercury concentration in contemporary Japanese.31:687-700. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.40:413-419. Smith JC. Guo S. Daniels JL.98(1):133-142. Toxicol Appl Pharmacol 1994.115(10):1527-1531. Environ Health Perspect 2002. Allen PV. Azpiri MA. Vupputuri S. Dorronsoro M. Vorwald AJ. et al. Leroux BG.258(4 Pt 2):R939-945. Topping G. Environ Res 2005. Longnecker MP.4(5):981-988. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. The contribution of dental amalgam to urinary mercury excretion in children. Osterloh J. Whittle K. Am Ind Hyg Assoc J 1970. The kinetics of intravenously administered methyl mercury in man.37:245-252. Patil LS. Hislop D. Suzuki T. Bolger PM. Br J Ind Med 1983. Fisher HL. Baser M. Pediatrics 1987. Nakazawa M. Am J Physiol 1990. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain.Metals Sanzo JM. Friberg L. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Imai H. Environ Res 2005. Takahashi Y. Tunnessen WW. Shen DD. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. McDowell M. Smith PJ. Stern AH. Newton G. Acrodynia: exposure to mercury from fluorescent light bulbs. Jones RL. 1999-2000. Toxicol Appl Pharmacol 1996.48(4):221229. Mooney TF. Langolf GD. Vahter M. Sherlock J. Smith RG. Amurrio A. Mottet NK. et al. DeRouen TA. Schober SE. Blood mercury levels in US children and women of childbearing age. Matsuo N.124:221-229. Woods JS.

2 (56.5 (81. 0. interval) 45.5-124) 108 (92.5-46.0-77.6-42.3 (73.3 (38. population from the National Health and Nutrition Examination survey.7 (73.7 (37.2-79.7-51.8) 46.3) 54.4 (79. see Data Analysis section) for survey years 99-00. which exert homeostatic regulation over molybdenum balance. 01-02.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.1-52.7) 78. Fourth National Report on Human Exposure to Environmental Chemicals 227 .6-58.0 (43.9) 34.0-38.9-85.2-59.2 (49.0-85.1-55.5 (49.2 (63.7-91.1 (34.6-46.7) 75th 84.3) 47.1) 59. 7439-98-7 General Information Elemental molybdenum is a silver-white.0-62.6 (43.7 (58. aldehyde dehydrogenase.5-91.8-108) 87.0) 62.4 (48.2) 41.3) 65.0-65.3 (55.9 (52.9-56.3-44.7) 86.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.8) 40.5 (43.3 (84.1-48.4 (48.9-109) 97.0 (48.0) 60. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. chemical reagents in hospital laboratories.3 (37. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.2) 52.1) 57.3 (64. and 03-04 are 0.2) 79.9 (37.4) 42.7) 45. Compounds of molybdenum are also used as corrosion inhibitors.2 (55.3) 83.0 (42.3 (53.7-47.3) 41. 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.5. respectively.1-63.5-65.5-66.6-96.9-82.1) 35.8-94.5) 47.3-47. lubricants.9-83.3 (55.2-59.8-106) 88.9 (33.0-71.2-70. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5 (41. and paints.7-96.5) 60.8.7) 57.2 (69.5 (74.7) 46.6-55.5 (37.1) 82.3 (46.8 (42.0 (46.0) 54.7-68.3 (47.7 (36.8 (67.6) 53. 2001).4 (80.0 (76.8-46.6) 51.4-52.5) 80.7) 77.1 (38.0) 84.1 (71.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.6-82.4) 49.1) 60. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.9 (44.8) 44.6 (55.0-100) 63.9 (73.8) 39.4 (34.4-61.0-56.7 (50.6 (40.8 (85.6 (55.3) 37.7-41.7 (44. inks.7-73. More recently.5) 44.8) 75.1) 126 (106-147) 109 (94.3 (71.2 (40.0 (81. semiconductor and battery industries have begun to use molybdenum.2) 53.7-105) 69.1-51.2 (49.1 (91.6) 93.5-68.0-101) 82.6-72.9 (34.0-110) 90.9) 67.7 (71.6) Selected percentiles ( 95% confidence interval) 50th 50.3-108) 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 (40.7-92.5) 80. 1997).2-37. WHO.6 (52.4) 45.6-62. and xanthine oxidase (Kisker et al.3-91.1-52.2-53. 1996).5-52. At a daily oral molybdenum dose of 24 µg. and in pigments for ceramics.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.8) 48.8-90.7-50.3 (79.Metals Molybdenum or ore deposits.5 (67.7-84.8 (82.9 (32.8-49.1-59.4) 41.9 (78.5) 85. Excretion occurs predominantly via the kidneys.2) 40.4-75.5 (48.0 (42.9) 62.2 (38.2-42.4) 52.5-52. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2) 37.5 (41.7) 51.8.1-44.7-60.7-122) 93.3) 85.4 (72.6) 71.7 (51.7) 78.2 (61.0) 45.0 (41.6 (73.2-91.6) 71. 2001.7-39. In humans.2) 48.4) 56.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.2 (83. urinary excretion over six days CAS No. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 39. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.1) 46.4-82.3-75.9-55.0) 55.7 (45.4) 76.. and 1.2) 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 (98.0-53.S. hydrogenation catalysts.5-41.1-88.9 (40.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.9-55.0) 97.

2 (37.7-137) 129 (109-155) 112 (97.4-185) 106 (94.5 (50.9 (39.1-127) 90.5-119) 90.5 (40.7) 112 (95.9) 79.5) 90th 108 (97.4) 122 (107-133) 109 (99.5-60.2-40.0-120) 85.6-61.9 (36.7-40.2) 42.5-69.2 (57.5 (79.1-79.S.4 (37.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.6-88.8) 37.7-120) 87.5 (40. U.3 (37.0 (80.2-65.6-61.7) 42.9-41.1 (30.5 (36.8) 38.8-66.2-41.7) 45. Based on studies finding adverse reproductive effects in rats and mice.9 (39.4-41.8 (75.8-47.6-41. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al..3-59.3 (36.6 (59.2-49.4 (53.2) 38.0) 62.5-50.3) 64.1 (82.9) 44.7) 53.4-106) 85.0-46.3) 43.0-103) 103 (90.6 (38.4 (40.4) 61. at daily oral doses of 95 µg and 428 µg.1 (40.6-63.7-100) 77.8-84.6) 36.6) 43.3) 41.4 (55.5 (38.9 (73.3-43.6) Selected percentiles ( 95% confidence interval) 50th 41.6 (36.5-46.5-92.1-81.3-141) 109 (81.4) 89.0-56.2 (40.5 (41. 1995).1) 101 (83.8) 45.3 (58. 1997).2 (33. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 57.0) 39.1-38.2) 43.2 (40.1-100) 86.7-38.8-42.9) 92.7-43.5-62.3) 61. respectively.5 (35.5 (80.8) 71.2 (40.4-118) 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 .0) 36.7-62.8-52.3 (71.2-80.6-63.4 (59.2 (69.7) 75th 63. EPA.0-46.6) 39.8-46.9-87.9) 40.S.1-67.3 (37.2) 37.4-42.1) 40.0) 44. population from the National Health and Nutrition Examination survey.9-117) 57.8-47.1) 37.6 (42.3-102) 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 (65.9-61.1) 65.4-76.3) 44.1-40.8 (36.8) 62.4 (78.2-121) 107 (92.6-78.0-38.5) 72. 1961.9 (49.7 (66. but available epidemiologic data are scant.4) 40.5-70.4 (56.8 (57.3-46.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.9-71.2) 55. of the ingested dose (Turnlund et al. and urinary levels reflect intake from all sources.9 (79.7 (75.9-45.5 (41.8) 39. interval) 43.4) 58.9-40.0 (35.1-43.2) 58.7) 115 (93.3) 40.1 (39. 1993).1 (42.Metals was 18% of the ingested dose.1 (33.2 (73.6-76.5) 60.1-109) 89.3-68.0) 33.4-39.0-41.5 (34.1 (44.8-67.5-48.9-118) 91.4) 60.5-44.3-115) 98.4) 116 (101-126) 104 (88.2-46.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.8 (56. Molybdenum is generally considered to be of low human toxicity..2-47.1 (54.3 (51.1 (38.1 (37.0 (74.5 (65.4-107) 85.0-133) 119 (88.3) 57. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.4-66.7-52.3 (55. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.0) 88.6-45.8-118) 81.8) 79.3-56. Biomonitoring Information Molybdenum is an essential element for health.4) 48.5 (54.5-99. and clinical or epidemiologic evidence of adverse effects is limited.9-68.9) 31.2-96.9 (64.5 (39.9 (64.4) 47.4) 77.2 (36.3 (83.2-96.2) 37.1-43.1) 43.1-34.8) 38.7 (77.6 (71.2) 39.9 (35.0) 72.2 (52.3-45.8) 61.5-45.5 (59.9-96.1 (49.6) 39.7) 41.9-42.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.8-65.3 (71.7-44.7 (30. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.4-120) 101 (84.4) 44.3) 56.5-97. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9 mg/kg/day and established a tolerable upper intake level of 0.8 (37.5 (83.9-45.0) 38.5 (39.5) 73.1-112) 78.6 (57.7) 62. 1999).2 (50.9 (40. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.4 (67.2 (43.0) 53.5 (35.0) 39.3 (36. 2001).8 (90.2) 39.4 (44.. urinary excretion over six days rose to 50% and 67%. In industry.6 (36.5 (37.3-52.6) 48.1) 37.3 (53.1-45.5 (78.1-39.9) 41.1-41.3) 37.5) 71.3) 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 85.3-44.2) 42.1 (38.1) 56. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5) 63.5 (37.0 (58.03 mg/kg/day in humans (IOM.5-35.7-93.1-39.

Ann Rev Biochem 1997. White MA. iron. Gatti A. Occupational risk factors of lung cancer: a hospital based case-control study. Ronchi A. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. arsenic. Available at URL: http://www. White and Sabbioni. Schleyerbach U. 2005). 4/14/09 Iversen BS. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. TR-462. silicon. 1998). Keyes WR.123(1):81-85. Institute of Medicine (IOM). van Sprundel MP. Washington.62(4):790-796. (DC): National Academy Press. U. References Centers for Disease Control and Prevention (CDC). Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. edu/openbook. et al. Am J Clin Nutr 1995. vitamin K.gov/iris/ subst/0425. Molybdenum absorption.S. pp. Shmavonyan DM.22(3):179-191. Aprea C. Sciarra G.epa. and zinc: a report of the Panel on Micronutrients. Van Meerbeeck JP. manganese.216:253-270. excretion. Occup Environ Med 1999. Droste JHJ. EPA). Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Geneva: WHO. Vermeire PA. 2001). Kisker C. Zhurnal Obshchey Biologii 1961. vanadium. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Available at URL: http://ntp. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8.. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Rapid Comm Mass Spectrom 2002. Sabbioni E. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Menne C. Fourth National Report on Human Exposure to Environmental Chemicals 229 . molybdenum.nap. In: Trace elements in human nutrition and health. 420-441. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. National Toxicology Program (NTP). Atlanta (GA). Schindelin H. 2002.gov/index. Turci R.niehs. 1998. 4/14/09 Sievers E. World Health Organization (WHO). 1996.Metals in urine for the U. Available at URL: http://books. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. iodine. Kristiansen J.php?record_id=10026&page=420. Food and Nutrition Board. 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. boron. Environmental Protection Agency (U. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. X. Sci Total Environ 1998. Schaub J. Molybdenum.S. 16:1313-1319. Molybdenum in infancy: methodical investigation of urinary excretion. Trace element reference values in tissues from inhabitants of the European Union. 2001. Minoia et al. Turnlund JR.nih. 144-154. Sabbioni E.. Koval’skiy GA. pp.S. Christensen JM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. nickel. copper.htm. Third National Report on Human Exposure to Environmental Chemicals. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Yarovaya GA. 2005. Weyler JJ. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. 56:322-327. 4/14/09 White MA. Peiffer GL.66:233-267. Rees DC. chromium. J Trace Elem Med Biol 2001.15(2-3):149-154. A study of 13 elements in blood and urine of a United Kingdom population. Molybdenum 1993 [online].. Analyst 1998. Dietary reference intakes for vitamin A. Minoia C.

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

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

Ruff F: Histamine release by sodium cholorplatinate. Stilianakis NI.. Angerer J.4(1):27-36. Analyst 1998. Several studies have shown that background concentrations in general populations were usually less than 0. Kazantzis G. Ensslin AS. pp.55(2):138-140. Raab W. Saindelle A. Schulz C.56(3):283-286. 2003.htm. Occup Environ Med 1998. Schierl. 1997. Platinum. Urinary excretion of platinum from platinum-industry workers. Gromiec JP.04 µg/L) in this Report.13(1):24-30. Patty’s Toxicology.. Boos KS.005 µg/L (Iavicoli et al. 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. Hysell D. et al. International Journal of Hygiene and Environmental Health 2003. Wilhelm et al. and in blood and urine in the United Kingdom. et al. Herr et al. Nowak D. Seifert B. Urinary platinum levels associated with dental gold alloys. In: Bingham E. Biomonitoring Information Urinary platinum levels reflect recent exposure. Schierl et al. Huber R. palladium.35:313-321. Kelly J. Kulka U. Biomonitoring of traffic police officers exposed to airborne platinum. Saindelle A..70(3):205-208.10:63-71. Pethran A. Kavanagh P. Environ Health Perspect 1975b. which elevate urinary platinum by five to twelve-fold (Begerow et al. Rommelt H. New York: John Wiley & Sons. Levels of platinum in urine for the U.. Gieler U. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Int Arch Occup Environ Health 2003. ruthenium. International Programme on Chemical Safety (IPCS). Kaus S. Hysell D. 2004) or less than 0. Biomarkers 1999. osmium. 2004. 289-380. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Ruff F: Platinum and platinosis. Campbell K. Pethran A.61(7):636-9. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Br J Pharmacol 1969. 2004). rhodium. Duneman L:Long-term urinary platinum.. J Expo Anal Environ Epidemiol 2003. Alimonti A. Iavicoli I. 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. Pethran et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. population were below the limit of detection (0. Czerczak S. Occup Environ Med 2004. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Schierl R... Schierl R.htm.123(3):451-454.9:152-158. 1998). Jankofsky M.76(1):5-10. 1998).Metals the International Programme on Chemical Safety at http:// www. Environ Res 1975a. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 2000. Hauff K.19:685-691. Thornton I. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Int J Hyg Environ Health 2004. 206:15-24. Bocca B. Nickel.org/documents/ehc/ehc/ehc125. and gold excretion of patients after insertion of noble-metal dental alloys. et al. Platinum concentrations in urban road dust and soil. Parrot JL. Part 1: monitoring of urinary concentrations. 5th ed. Neuendorf J. References Becker K.. Herr et al. Int Arch Occup Environ Health 1997. Allergy and histamine release due to some platinum salts. Crocker W. Arch Environ Health:1969. Fries HG. Hebert R.org/documents/ehc/ehc/ ehc125. palladium. Ewers U. Powell CH. Influences on human internal exposure to environmental platinum. 2003). Petrucci F. Fruhmann G. 2003. et al. Moore W Jr.S. and platinum.inchem. Turfeld M. Cohrssen B. eds. Begerow J. Uptake of antineoplastic agents in pharmacy and hospital personnel. Environmental Health Criteria 125. 3/31/08 Moore W Jr. Arch Environ Health 2001. 2003.inchem. Herr CE. Senofonte O.01 µg/L (Becker et al..207(1):69-73. Wilhelm M. van de Weyer C. 1991 [online]. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.. 1999. Hall L. Seiwert M. Carelli G. Grimm CH. Farago ME. Schierl R. 2001). Schulz C. Kuster W.

155 (.185 (.400) .480) .260-.230-.218) .180 (.210 (.280 (.420) .410 (. In the United States.420) .360-.300 (. 0.280) .150-.400 (.280 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.350-.300) .330-.510 (.350-..218) .190 (.320) .370) .290) 90th .390) . see Data Analysis section) for Survey years 99-00.400 (.217 (.320-.172 (.180-.180-.160 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.430 (.420-.420) .410-.201 (.320) .370 (.290) .460 (.400 (.270 (.190-.360-.400) 95th .270-.148-.310) .180-.210 (.177) .250-.350 (.450 (.Metals Thallium depilatory cosmetics.185-.340-.410-.400-. In addition.490) .156) .340-.380 (.290 (.280) .440 (.173-.360 (.490) .500 (.330) .172) .440) .370-. 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. thallium was obtained as a by-product of smelting other metals.630) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.430) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400-.640) .200-.200) .450 (.192) Selected percentiles ( 95% confidence interval) 50th .160-.370) .470) .320) .410 (.410-.170-.340) .250-.160 (.160 (.146 (.390 (.201 (.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 .500) .260) .230) .243) .191 (.145-.220) .02.390-.330-.250-.380) .410 (.400-.330-.450 (.240) .150-.290 (.350-.310 (.230 (.210-.330) .310 (.470 (.260-.167 (.370 (.215) .182-.440 (.300) .147-.200 (. interval) .440) .137-.220 (.510) .250-.159 (.410 (.320 (.230) . Human health effects from thallium at low environmental CAS No.390) .260-.200-.350-.200) .230-.410 (. population from the National Health and Nutrition Examination Survey.240) .480) .154-.178) .163) .410) .250-.360 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.170) .180-.220) .220 (.350-.410-.350-.180) .400) .220) .145 (. From these and other sources.197-.170-.420 (.144 (.430-.150-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .270 (.158) . Thallium disappears from the blood with a half-life of several days.500) .S.240-.02.560) .270) .460-.360-.280-.400) .270-.159 (.450 (.300 (.450 (.380-.330-.300 (.390-.400) .360 (.430 (.230) .370 (.370 (.170-.290 (.197 (.160-.160-.690) .400 (.360-.230-.202) . respectively. and 03-04 are 0. 2005).165 (.184 (.280-.220) .260 (.450 (.179-.190 (.239) .170 (.360 (.140-.200) .196) .520) .290-.240) .300) .270-.350) .180 (.202 (.250) .440 (.400-.380 (.200) .170) .181-.135-.290 (.170 (.167-.170-.190 (.520) .430 (.200) .440-.290-.160 (.183) .410 (.470) .133-.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 .200 (. however.400 (.480) .180 (.420-.220-.170-.340-.190 (.290) .170-.157-.02.490) Total .390-.440 (.460) 336 362 290 697 746 725 1380 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .250 (.370-.470) .147-.220) .430) .390-. 01-02.170 (.167-.250 (.175) .340) .350 (.450) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.450 (.162-.173) .180) 75th .400-.410-.330-.225) .187-. In the past.160-.156-.430-. the latter being the current major industrial consumer of thallium in this country.490 (.590) .360-.450 (.280 (.160-.145-.310 (.370 (.480) . representing distribution into other tissues.200 (.280) .340-.490) .330) .134-. thallium readily crosses the placenta and also distributes into breast milk.200-.172 (.173) .250-.360) .270 (.217) .220 (.150-.390) .200 (.450 (.420) .430 (.500) .370 (.270 (.420-.200 (.171 (.200-.380-.220 (.170-.270) .330-.390 (.330) .370-.340 (.430-.147-.150-.590) .310-.260 (.370 (.480) .260-.250-.220) .230) .420) .300) .440) .290 (.470 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.202 (.550 (.410-.520) . it has not been specifically mined or refined in the United States since 1984.183) .520 (.240-.188) .370-.190 (.200 (.390) .300-.210) .290) .196) .420) .420) .260 (.176 (.160 (.290) .159 (.170) .206) .260-.190 (. and 0.200) .220 (.153-.150-.156) .250-.290 (.330-.240-.350) .460) .270 (.420-.149 (.

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

and serum of Italian subjects. Trace element reference values in tissues from inhabitants of the European Union. Martin J-C. Environ Res 1998. Radiat Prot Dosim. Apostoli P. White MA.216:253-270. References Agency for Toxic Substances and Disease Registry (ATSDR). X. Schaller KH. Jackson RJ. 7/15/09 Blanchardon E. Pietra R. 1998). Int Arch Occup Environ Health 1981. Investigations of thallium-exposed workers in cement factories. with concentrations ranging up to 76. Morrow JC. Marcus RL. 1998. Cassot G. Schaller et al. Trace metals in urine of United States residents: reference range concentrations..atsdr. Brockhaus A.113(1):47-53. Brockhaus et al. Wiegand H. Ting BG. Sampson EJ. Available at URL: http://www. Sci Total Environ 1990.html. Celier D.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. 1985). Minoia et al. 2005. (1981) studied 1. Trace element reference values in tissues from inhabitants of the European community I. 1992 [online]. Toxicological profile for thallium. White and Sabbioni. Pozzoli L.S. Paschal DC. Kramer U. 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. Sci Total Environ 1998. Fourth National Report on Human Exposure to Environmental Chemicals 235 . 2005) and are shown with results from NHANES 2003-2004 in this Report.95:89-105.. Buhlmeyer G. 1981.1 mg/m3 (Marcus. Sabbioni E. et al. et al. 1980. Investigation of a working population exposed to thallium. Raithel HJ. Minoia C. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Gallorini M. Third National Report on Human Exposure to Environmental Chemicals. et al.cdc.265 people living near a thallium-emitting cement plant in Germany. J Soc Occup Med 1985. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Boisson P. Pirkle JL. 1990. Challeton-de Vathaire C. Dolger R. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Paschal et al. Int Arch Occup Environ Health 1980. Manke G. Atlanta (GA).Metals (CDC. A study of 13 elements in blood and urine of a United Kingdom population.5 μg/L. Soddemann H.gov/toxprofiles/tp54.48(4):375-389.. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.35(1):4-9.76(1):53-59. A study of 46 elements in urine. Schmidt M. Sabbioni E. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Ewers U. Valentin H. blood. 2005. There was no increase in the prevalence of symptoms at levels less than 20 μg/L and only a slight increase in nonspecific symptoms greater than 20 μg/L. Centers for Disease Control and Prevention.47(3):223-231.

460 (.160 (.350) .250) .00) .090) .151) .097-.120 (.090-.220) .120-.100 (.350) .190 (.080) .060 (.100 (.430 (.200 (.240 (.470 (.070) .100-.087-.300) .300 (.670) .130-.340-.220) .126) .370 (.560) .300 (.250-.290 (.410 (.380) .260 (.105) .060 (.250-.090) .160-.04.130-.170) .058-.100 (.230) . bronzes in pigments.090-.770 (.220 (.120-.060 (.071 (.060-.360 (. and 03-04 are 0.150-.270-.430 (.290) .100) .056-.420-.580) .160 (.077-.390) .090 (.100) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.130) .310-.070 (.113 (.158 (.074-.110) .380-.100 (.100-.120) .080 (.080-.093) .330) .130-.070-.430-.140 (.130 (.530 (.090 (.340-.560) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.330-.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 .100-.050-.550) .060-.160 (.510-1.390 (.101 (.360 (.130 (.100) .130) .220) .270 (.084-.107 (.470) .090-.110-.340) .110 (.090-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.320 (.116) .062 (.060-.093-.070-.082 (.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 .160-.135) .620) .180) .310-. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.270 (.290-.080-. Tungsten is used mainly for producing hard metals.310-.370-. 236 Fourth National Report on Human Exposure to Environmental Chemicals .250) .090) .190-.460) .080) .510-.230-.190-.073 (.630) . and 0.250) . respectively.350 (.080 (.081 (.070) .065-.060-.620 (.070 (.460 (.160-.520) .120-.160) .120) .550) .073-.080-.620) .380 (.092) .800) . 01-02.490) .320) .069) .130) .520) .270-.140 (.230) .260-.070-.230-.280 (.400-.280-.260) . Tungsten compounds are used as lubricating agents.180-.084) .120-.380-.530 (.440) .590) .790) .180) .120) .170) .100) .111-.250) .310-.078-.300-.080 (.070-.150) .137 (. which is used in the steel industry.830) .150 (.096 (.190-.450 (.400) .090-.240-.220-.210-.950) .086 (.570 (. mainly as scheelite (CaWO4).330-.105 (.180-.060-.550 (.090-.130-.068) .082-.095-.330 (.140-.060 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.360-.400 (.170 (.150 (.096-.150 (.180) .410-. and as catalysts in the petroleum industry.120-. filaments for incandescent lamps.460) .400 (.070-.550) .190) .430) .123-. see Data Analysis section) for Survey years 99-00.092 (.100) .370 (.120) .380 (.170 (.Metals Tungsten CAS No.490 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.110-.065 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).050-.350) .560) .133) .160) .110 (.110 (.132) .800) . Occupational exposure is from dusts released during grinding or drilling of hard metals.380-.073) .100) Selected percentiles ( 95% confidence interval) 50th . Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.360) .290) .076 (.500 (.160-.310-.270-.04.260-.520) .230 (.130) .104) .690) .122) .076 (.310 (. which are used in rock drills and metal-cutting tools.290-.080) .320 (. Evidence is lacking for the carcinogenicity of tungsten.120) .073-.088 (.110 (.113 (.560 (.230-.S.260-.080 (. Little information is available on the toxicity of tungsten.109) .050-. 0.250) .430-.087) .250) .210) .280 (.180 (.180-.270 (.060-.140) 90th .320-.560) .360-.110 (.200) . interval) .160 (.062 (.430 (.090-.470 (.500 (.120) .310) .400 (.570 (.260 (.400 (.092 (.420-.04.810) .53) .200-.290-.090) .210 (.120-.140 (.300) 95th .160 (.130) .370 (.360 (.082) .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 .460 (.210 (.113 (.070) .110) .180-.090-.470) .210 (.090 (.069-.370) .093 (.210 (.084 (.060 (.088) .091) .170) .180) .370-.140-.270-. population from the National Health and Nutrition Examination Survey.320-.230-.330) .350-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.080) 75th .180 (.140 (.650) .071-.530 (.060 (.080 (.500) . and for producing ferrotungsten.204) .340-.380-.510 (.110-.450-.070) .190 (.066-.300 (.113 (.070 (.170) .064-.170-.480) Total .190-.640 (.470-.095-.082 (.050-.210 (.056-.101-.

823) .098-.439 (.198) .158) .184 (.073 (.107-.354-.255 (.158 (.215 (.216-.300) .136-.104-.136 (.293 (.075 (. interval) .216 (. 2001).063 (.206-.880) .161) .062 (.063-.078) .074) .285) .086) .465) .414) .083-.279 (. measure urinary tungsten.086) .333) .497 (.258 (.080-.(Kraus et al.060-.061-.233-.302-.333) .426) .080 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.385 (.086) .453) .299 (.091) .089 (.092) .079) .727) .329 (.153-.075) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.120) .217-.071) .122-.667 (.071-.105 (. 1998).341 (.167-.201 (.083) .439) Total .216-.217-.157) . population (CDC.169) .117) .070 (.058-.180-.077-.079 (.079) .231 (.339 (.150-. population from the National Health and Nutrition Examination Survey.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 .121-.069 (.209-.167) .119 (.108) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.333-. 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.109 (.083) .174 (.605) .133) 90th .179-.216-..344-.165) .068-.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 .484 (.301) .200-.300-. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure..119-.306) .340 (.275 (.222) .061-.056-.124 (.144 (.081-.224) .158) .059-.072 (.174) .079) .063-.075-.108-.462) .143 (.122-.283) .386) .065-.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 .059-.179-.S.739) .187) .063 (.286-.436) .211 (.333 (.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 .153) .379 (.069-.079 (.431) .333 (.091 (.205-.459) .103-.358) .139-.199 (.139) .412 (.056-.091) .065 (.075) . similar to those in this Report (Schramel et al.392) .302-.231-.237) .300-.284) .155-.136-.099-.301) .072-.278-.634 (.080-.063-.066 (.197-.100) .136-.500) .167) ..436-1.431) . Patients with medically-inserted tungsten found at increased levels in drinking water.059-.146 (.098-. or exposure that a control group of non-metal workers had mean levels differences.138) .375) .270 (.261-.070 (.133) .181 (.078-.084) .170-.555 (.197) . Using neutron activation analysis to 2000.064-.093-. 2003.272-.138 (.203-.255-.331-.085-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.066 (.353 (.353 (.426) .354) .090-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.154) .150-.098) .085 (.253 (.199 (.452-.383 (.148 (.200-.308) .116 (.054-.326) .148) .098-.333 (.146) .057-.053-.267) .081 (.063-.237-.465) .144-.081 (.095-.267-.317) .667) .347 (.121 (.084 (.075 (.109-.061-.077) .138 (.250-.214-.096) .279 (.072-.085) .093) .080 (.064-.073 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.265 (.082) .245-.333-.094) .218 (.060 (.164 (.075-.S.057-.105 (.188-.078 (. and 2003-2004 (Paschal et al.258-.146 (. population.054-. Nicolaou et al.065-.131-.126-.125 (.084) .078 (.151 (. 2005).190) .176-.431) .082) .197 (.067-.065-.150 (.168 (.152-.145 (.333 (.360 (.120) .073 (.154) .130 (.087 (.087) .094) .098 (.538) .069 (.100 (.091) .253-.106 (.074-.359 (.308) .125) . 1997).094-.077) .214) .067 (.158) .086-.S.240-.167-.124-.208-.068 (.083 (.300 (.084 (.049-.28) .250 (.482 (.122 (.287) .317-.090-.116-.055-.381) . (1987) found possibly due to methodologic.071) .091 (.081) .078) .065) .216 (.143-.089) .215) .116) .091) .059 (.329-.139 (.071 (.253) 95th .065 (.071 (.186 (.079) . 2001-2002.071 (.111 (.071) .133) .582) .067 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.255 (.364 (.301) .198-.060-.083 (.294 (.074-.074 (.074) 75th .095) Selected percentiles ( 95% confidence interval) 50th .317 (.554) .073 (.484) .176-.197) .088) .250 (.339 (.077-.088) .130-.797) .410-.237) .439 (.201) .117 (.082 (.169 (.222-.279 (.136-.359 (.315-.100) .

tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Angerer J. Nevada Exposure Asssessment. bismuth. Schramel P. Paschal DC.76(1):53-59. 2004). Zobelein P. Pietra R.htm. Wendler I. J Trace Elem Electrolytes Health Dis 1987. The determination of metals (antimony. References Bachthaler M. Sabioni E. Weber A. Cancer Clusters. Int Arch Occup Environ Health 1997. Centers for Disease Control and Prevention. et al. Ting BG. [online] 2003. lead. Paetzel C.69(3):219-223. mercury. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. cadmium. Schramel P. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Seghizzi P. and hair (Bachthaler et al. Jackson RJ.Metals blood. platinum.. National Center for Environmental Health. Schaller KH. Manke C. Lenhart M. Catheter Cardiovasc Interv 2004. tellurium. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Link J. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect.58(10):631-634. palladium. Trace metals in urine of United States residents: reference range concentrations.gov/nceh/clusters/Fallon/study. Cassina G. Third National Report on Human Exposure to Environmental Chemicals. Environ Res 1998.62:380-384. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Mosconi G. Biomonitoring studies on levels of tungsten provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of tungsten than are found in the general population.cdc. Atlanta (GA). Sampson EJ. 4/15/09 Centers for Disease Control and Prevention. thallium. Occup Environ Med 2001. Nicolaou G. Angerer J. Available at URL: http://www. Pirkle JL. Feuerbach S. urine. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Morrow JC.(2):73-77. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Churchill County (Fallon). Kraus T.

007 (.016) .008-.012 (.030-. 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.009) .007-.009) .007-.007-.012) .027 (. 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.007) 75th .008-.011) .021) .010-.012-.026) .279) .012 (.072) .046 (.014 (.047 (.011) .027-.007 (.012-.054-.008 (.008 (.048 (.020-.010 (.036 (.017) .010-.011-.023-.021-.049) .007 (.010) .010-.009-.050) .017-.158) .022 (.012) .S.053 (. in some ceramics.009 (.012-.011) .038 (.013 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.037) .048) .008 (.004.033 (.009-.009 (.010) .008 (.009-.051) .013) .053) .073) .011) .010-.72%).029-.026-.009) .009 (.007-.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .017 (.007 (.067) .033 (.037-.036-.016-. Uranium has many commercial uses.022-.036 (.014 (.028-. 01-02.027) .008) .056) .023 (.018) .007-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.021 (.Metals Uranium CAS No.009-.011-.012) .009) .005.006-.017) .011) .027 (.045) .050) .041 (.023) .007 (.024-.010 (.008 (.010 (.012-.018 (.012) .009 (.006-.009 (.027) .054) .054) .015 (.020-.012-.030 (.040 (.008 (.008-.009) Selected percentiles ( 95% confidence interval) 50th .036) . human exposure occurs primarily by inhaling dust and other small particles.023) .016-.007-.052 (.017) .009) * .021-.006-.012 (.007-.013) 90th .008-.006 (.026 (.009) .022-.031 (.011-.008 (.007-.065) .046 (.008) .024-.037 (.033-.009) .007-.006-.019-.008 (.013 (.033) .007-.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 .049) .008-.039) .007-.008-.062) .024-.010) .037) Total .017-.009 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.009 (.006-. Since the 1990’s.007) .027 (.040-.046 (. and 03-04 are 0.034) .014 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.020 (.008-.009 (.006-.011) .040-.065) .026) 95th .016) .009) .018) .006-.010-.030 (. Thus.026) .014 (.015) .012 (.007) .009-.008 (.114 (. milling. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).007 (.008) .043 (.011-. interval) .007-.020-.017) .010) .006 (.021) .017-.018) .041 (.013-.046) .027-.027 (.046 (.023-.027-.024 (.030) .006-.031 (.009) .038) .035) .005-.040) .042 (.021) . In workplaces that involve uranium mining. 0.037) .011 (.017) .011 (.034-.043) .040 (.017-.015 (.017 (.015-.016) .016) .044 (.020-.008 (.013 (.016) .007-.006-.017-.013 (.040) .010) * .035-.013 (.009) .007 (.031-.010-.011-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .023-.055 (.018) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.016) .007 (.031 (.008 (.008) .063) .029-.026 (.018 (. population from the National Health and Nutrition Examination Survey.006-.007) .014 (.010) .056) .067) .046-.010 (.021 (.013 (. or processing. nuclear fuel.009-.007-.010) * .026 (. and 234U.011-.066) .013 (.005-.029 (.014 (.023 (.034-.005-.016 (.009-.010) .011-.007-.008 (. see Data Analysis section) for Survey years 99-00. and as an aid in electron microscopy and photography.009) .013-.019 (.009) .023-.022-.028 (.020-.045) .012-.009-. including nuclear weapons.007 (.021 (.028 (.127) .007 (.023 (.027) .012 (.013-.032 (.005-.009 (.010) .017-.019-.006-. 235U (about 0.012 (.007) .069) . respectively.028 (.005-.009 (.010 (.015) .060 (.008) . Variable concentrations of uranium occur naturally in drinking water sources.018-.006-.006 (.010) .007 (.036) .016-.008 (.007) .028-.007-.006-.088) .009) .015 (.008 (.011) .039) . and 0.019-.004.020) .007-.008 (.042) .007-.009-.019-.031 (.009-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.037) .020) .026-.023) .022) .025-.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 .006 (.039-.036-.031 (.030 (.008 (.027) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.064 (.009) .008 (.008-.015 (.035) .

008-.028 (.037 (.007-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. where limited absorption occurs (less than 5%).011) .035 (.025) 95th .006) .018-.011-.009-.006-.006 (. the shrapnel acts as a source of chronic.005-.007 (.029 (.021 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. which can occur occasionally from high occupational exposure.005-.008 (.016) .018 (.028) .051) .030-.021-.009) .006) .005 (.016-.016) .008 (.013) .048) .077) .017 (.022 (.017-.008) .017) .007 (.034 (.007 (.026-.019 (.007-.020-.009 (.019-.028) .007-.028) .010) .022-.008) .007 (.013 (.015-.025 (. 0.033 (.024 (.009) * .009-.008 (..030) .008 (.007 (.007-.005 (.006 (. Radiation risks from exposure to natural uranium are very low.020-.015) .067) .008-.040 (.006-.007 (.016) .039) Total .058) .024-.006 (.011-.010-.030-.051) .025-.050) .024) .008-.005-.063) .012-.009) .006-.008 (.021 (.006) .011-.026 (.027-.042-.024-.007-.018-.270) .011 (.009) .007 (. 2005).009-.034-.012 (.020-.010-.008) .033 (.006-.015) ..034 (.015 (.019-.041) .028-.019-.027-.006-.028) .020) .022 (.007 (. kidneys.045 (.010-.006 (.027 (.010-.013 (.029) .007 (.013 (.008) .039) .034 (.006) .010 (.034-.006-.016) .008) .006-.020 (.015-.018) .146) .006-.015 (.011) * .009) .029) .007 (.006-.012-.010-.053) .009) .020 (. Health effects from uranium exposure result from chemical toxicity to the kidney.014) .011) .025-.006-.010) .050) .010-.027) .035 (.005-.016) .030 (.009) .027) .047) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.061) .012 (. 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-.034 (.010) .016-.004-. In cases of retained DU shrapnel.019) .025 (.005-.010 (.026 (.Metals impact.012 (.007) .007-.008) .007 (.007 (.006-.008) .015 (.022-.013) .019) .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 .S.007 (.006-.032) .050 (.016-.006-.010-. with much slower elimination from bone.008) .044) . After exposure to soluble uranium salts.026) .1%-6% of an ingested dose may be absorbed.013) .014 (.006-.011-.024) .010) .053) .006-.017-.015-.012) .029) .018-.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 .006 (.030 (.020-.017) .004-.022 (.024) .006-.009) .008-.007) .013 (.029) .017-.009) .027 (.034 (.009) .032) .012) .006-.009-.010) .008 (.019 (.007) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.013-.024) .022-.051 (.022) .014 (.011-.027-.014) 90th .014) .021) .007 (. 1992).008) .074) .007-.100 (.025-.010) * .011 (.012 (.006-.007 (.012 (.039) . which represents distribution and excretion.017) .027-.008 (.013 (.048) . After inhalation.059 (.080) .019-.056) .042) . interval) .010 (.014-.012 (.013 (. low level exposure. Uranium is eliminated in feces and urine. 240 Fourth National Report on Human Exposure to Environmental Chemicals .010-.016 (.011-.006-. After long term or repeated exposure.007-.005-.009-.028 (.009) Selected percentiles ( 95% confidence interval) 50th .033 (.024-.010-.006-.054) .010-.009 (.009 (.030 (.033 (.010-.029 (.006-.025-.008 (.011-.008 (.016) .007 (. Depending upon the specific compound and solubility.005 (.009) .017-.006-.013 (.011-.013 (.007 (.029 (. Inhaled uranium-containing particles are retained in the lungs.051) .015) .016) .021 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours. population from the National Health and Nutrition Examination Survey.009 (.043 (.018-.010 (.005 (.015-.014-.006) .014-.008) .014) .039) .008) 75th . 2003).027 (.011) .023-.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 .030) .024 (.024) .006-.019 (.011-.007-.009) .008) .010 (.009 (.031-.016) .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.006-.007 (.007-.020 (.009-.021 (.007 (.008 (.024 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract. the initial half-life of uranium is about 15 days (Bhattacharyya et al.019-.008-.015 (.013 (.058) ..012) .006 (.033) .026 (.010) .016-.013 (.042) .007 (. liver.034) .017 (.018-.015) .015-.031 (.005-.007 (.

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. 2004). Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. but in whom no shrapnel was embedded.S. 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.Metals injury associated with elevated urinary uranium levels (Kurttio et al. In a study of 105 persons exposed to natural uranium in well water.162 μg/L) (Orloff et al. Tolmachev et al. environmental levels) and health effects is available from ATSDR at: http://www. Pullat VR. 2002). respectively. 28 soldiers who may have been exposed to DU by inhalation.. Uranium content of blood. Third National Report on Human Exposure to Environmental Chemicals.. 2001-2002.S.. Hamilton et al..61 μg/g creatinine. 1992. pp.011 μg/L (McDiarmid et al. Drinking water and other environmental standards have been established by U. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Health Phys 2000.cdc.. In 17 U. IARC and NTP have no ratings for uranium human carcinogenicity. 1991. urinary levels of uranium were as high as 9. Ejnik JW. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Thomas RG. Zimmerman I. 2006)... Durakovic A. Fourth National Report on Human Exposure to Environmental Chemicals 241 . In the same study. Karpas et al. Volf V. Hamilton MM. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. et al. Kent (England): Nuclear Technology Publishing.S.S. Benedik L. during. or wound contamination...62:562-566.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. References Bhattacharyya MH. 2003.. Stradling GN. McDiarmid et al. The U. Atlanta (GA). and no consistent effects on multiple endpoints of kidney function were found. 41 (1). 2004).066 μg/g creatinine (Gwiazda et al. 2004). Muggenburg BA. Komaromy-Hiller et al. the median urinary uranium concentration was 2. Galletti. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.107:143-157.e. Boyd P. In: Gerber GB. 2002. although slightly increased during and after deployment. 2000). Metivier H. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 2005. 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. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. (Kurttio et al. Vol. Sci Total Environ 1991. the median urinary concentration was 0. Squibb K. EPA. 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. Centers for Disease Control and Prevention (CDC).078 μg/L (ranging up to 5.S. Guidebook for the treatment of accidental internal radionuclide contamination of workers. and 2003-2004 (Dang et al.168(8):600-605. Health Phys 1992. 2006). in that the levels were below their respective detection limits (Byrne et al... 2006). A cohort of 46 U. Radiation protection dosimetry.. Dang HS. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. 2004).html. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. 1994. with emphasis on quality control. Horan P. 1-49. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Information about external exposure (i.gov/ toxpro2. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Mil Med 2003. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. McDiarmid M. ingestion.1996.1992. (May et al.atsdr. Pillai KC. 1978). Six workers in a depleted uranium program showed concentrations of 0. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.78:143-146. the geometric mean urinary uranium concentration was 0.S.... 2000). Byrne AR. eds. 2006. soldiers evaluated before.110 to 45 μg/L (Ejnik et al. had a mean urinary uranium concentration of 0. NRC. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Dietz LA. Breitenstein BD. Carmichael AJ. 2006).. population.65 μg/L).55 μg/L (median 0.

Am J Kidney Dis 2006. Engelhardt SM.79(1):11-21. U. et al. Andrews WS. Jarrett JM. Health Phys 1996. patient population and literature reference intervals for urinary trace elements. Mistry K. Saha H. Jackson RJ.81:45-51. Sampson EJ. NRC). Paretzke HG. Ash KO. Lewis BM. Metcalf S. July 1978. Paschal DC. Li WB. Gwiazda RH. Komulainen H. Kuwabara J. May LM. Health Phys 2003. Squibb K.158:165-190. Sci Total Environ 1994. Cordero S. Komaromy-Hiller G. Makelainen I. Marko R. Kidney toxicity of ingested uranium from drinking water. Nuclear Regulatory Commission (U. Squibb K.71(6):879-85. Environ Res 1999. Costa R. Wahl W. Oliver M. Element reference values in tissues from inhabitants of the European community. et al.S. Washington (DC): NRC. Renal effects of uranium in drinking water. Orloff KG.S. Environ Health Perspect 2002. Hamilton EI. et al. Biokinetic modeling of uranium in man after injection and ingestion. Radiat Environ Biophys 2005. Saha H.85:228-235. Human exposure to uranium in groundwater. Van der Venne MT. Uranium daily intake and urinary excretion: a preliminary study in Italy. Nuclear Regulatory Commission (NRC) Guide 8. Review of elements in blood. Auvinen A. Heller J. Ting BG. et al. D’Annibale L. U. Pirkle JL. Auvinen A. Roiz J.Metals Galletti M. J Toxicol Environ Health A 2004.296(1-2):71-90. Roth P. Harmionen A.110(4):337-342. Englehardt SA. Halicz L. Noguchi H.67(8-10):697-714. Inductively coupled plasma mass spectrometry as a simple. Pekkanen J. Ough EA. Int Arch Occup Environ Health 2006.82(4): 527-532. Scott K. Cremisini C. Biologic monitoring for urinary uranium in Gulf War I veterans. McDiarmid MA. Wilson PD. Oberbroekling KJ. Lorber A. Hancock RG. Clin Chim Acta 2000. Karpas Z. et al.22–Bioassay at uranium mills. Bennett LG. Salonen L. Kalinsky V. McDiarmid MA. Katorza E.94:319-326. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.91(2):144-153. Charp P. Salonen L. Uranium and thorium in urine of United States residents: reference range concentrations. Environ Res 2004. Detection of depleted uranium in urine of veterans from the 1991 Gulf War.47(6):972-982. concentration and daily excretion of uranium in urine of Japanese. Health Phys 2006.87:51-56.44:29-40.86:12-18. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Marino R. Comparison of representative ranges based on U. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Shelly T. Ejnik J. Pinto V. Gucer P. Health Phys 2002. Sabbioni E. Kurttio P. Kane R. Smith D. VI. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Kurttio P. Health Phys 2004. Tolmachev S. Howerton K.S. Karpas Z. rapid. Oeh U. Hollriegl V.S. McDiarmid M. Health Phys 2004. et al. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium.

0 (12.10-11.07-4.70-12.10) 5.0) 13.0 (12. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.54 (3..20 (4. leather tanning.45-4.20) 3.40-5.39-4.30-19.0) 9.10 (2.08-3.60) 3.50) 6.30) 6.90-11.22 (2.0 (11.16) 3.0) 15.70-3.80 (3.40-6. Survey years 01-02 03-04 Geometric mean (95% conf.93-3.0) 19.00-6.0) 10. 2005).0) 9.0-17. In addition.62 (3.87-3.0) 8.20 (7.70-7.81-16. milk.90-11.60-6.80-8.0 (9.0 (11.90 (5.0-29. It is normally found and produced as the anion of a sodium.93-4.67-5.80 (6.20-3.80) 3.47-4.40-13.84) 14.68) 4.20 (6.90 (5.60) 5.70 (3.50-7.0-23. and electroplating.20-11.10 (7. and limited applications in pharmaceutics.40 (5.74-3.70 (3.0) 13.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.40 (4.0 (8.30 (2.0 (10.0 (11.0-17.09) 3.0) 9.0 (11.10-12.70 (3.0 (11.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.70-5.0-15.0) 16.0) 13. 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 (7.88) 3. and certain plants with high water content (e.0 (9.11) 4.0) 9. 1998).70-3. 2002). Perchlorate is stable under most environmental and physiological conditions.29-3.40) 2.0 (11.32 (3.0) 15. laboratory analysis.30 (5.03) 3.80-4.80 (3.0) 11.40) 3. Other manufactured uses include fireworks.0) 14. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0 (11.10) 3.10-11. population from the National Health and Nutrition Examination Survey.51 (3.89-3.90-12.19 (3.80) 12.00-6.20 (5.70-6.11) 3.00) 3. lettuce) can be the main sources of intake for humans (FDA.90) 5.0) 13.30 (5.50-4.10 (6.10) 5.26 (2.02 (3.10-7.50-4.21 (2.30-6. fabric dyeing.00) 4. 2005).80-15.0-17.0-18.0-14.50-3.20) 7.S.00-5.75-3.0 (12.0) 95th 14.90-3.10) 3.46) 3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0) 8.44-4. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0) 14.40 (4..0 (12.40) 4.0) 12.5 hours and has a small estimated volume of distribution (Crump and Gibbs. 2007).50 (8.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.30-7.0) 11.0) 10.0) 13.20 (4.0) 10.80) 7.40 (8. matches.0-17.Perchlorate Perchlorate (Urbansky.0 (9.80) 75th 6.40 (5.0 (9.90) 6.31) 2.0) 11.EPA.0 (9.90-3.70-9.20-4.90 (2.60 (4.50) 11.65) 3. certain catalytic metals.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0) 14.90-9.0) 13.0 (9.S.70-11. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.90 (4.80-6.60-7.0) 13.40 (3.00) 5.0 (11.0-20.30-17.10 (5.12) 3.0) 9.90-6.00) 3.20 (2.40) 3.35 (3.50) 5.20-12.20 (8.00) 7.g. 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. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.76 (3. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.20 (2.0 (8.51 (3.40) 3.60 (4.90-10. interval) 3.90 (5.10-4.0-19.90-9.10 (6.20) 4.38) 5.0-17.70) 3.49-3.19-4.0 (8.90 (3.0) 9.0-17.50-11. Drinking water.30) 6.40-11.40-7.22-5.0 (11.05 and 0.0 (8.0) 13.05 (2.0 (8.60 (7.40-4.56) 3.0-18.75 (3.50) 5.0 (11.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.81) Selected percentiles ( 95% confidence interval) 50th 3.18-3.50) 3.76) 4.40 (5.40) 90th 10.10) 12.20-4.80-4.96 (3. potassium.30-7.60) 8.05.93 (4. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.01 (2.0-18. or ammonium salt.80-12. but has strong oxidant properties in the presence of concentrated acids. Perchlorate was added to the U. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0 (13.40-4.40) 6.66) 3.S.30 (2. and reducing agents.40 (3.79 (2.50 (5.50 (3.0 (9.0-15.

60-15.70 (2.72 (3.90 (7.70-5.39-4. 2001.09 (7.00-2. 2002. chronicity of exposure.20) 3. women with urinary levels of iodine less than 100 micrograms per day.1-16.0) 9.0 (8.50-9..87-3.10-3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.3) 12.51-4.00-3. 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.66) 3.0) 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 .EPA.4) 13. U.00) 3.46 (3.03 (2.5) 8.0 (11. medications).60) 10. Li et al.87 (7.10 (1. and the presence of other substances known to affect thyroid function (e. thiocyanate. 2002).37 (4.30 (5.04-3.56-3.0) 11..87) 7. However.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.3 (10.70) 2.00 (4..99-3.60-3.18-3.22-4.50) 6.70-15.50 (6.46-4. menopausal status. 2006.4-16.0) 14.0) 6.29-6.91) 4.04-3.30-10.5 (13.80 (7.90 (2. age.0) 12.0) 12.60 (3..60-5.10 (4.3) 11.6) 20.10 (2.15-12.90-9.93-8..60) 3.22-4. Also..98) 3. 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.20 (7. although iodine intake was higher than U.30 (6.60-8.25 (3.19-10.33 (7.10 (4.0-14.20-3.35 (2.3) 8. Lawrence et al.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.08) 3.21 (2.90-20.90-11.52-9.90-3.90 (4.96) 2. up to 68% RUI has been demonstrated.EPA.30) 90th 9.S. 1999.67) 5. 2003.54 (3.70) 10.1 (11.50) 2.97-5.93-5.22-6.1-14.S.64) 5.44) 3.0) 9. dietary iodine intake.60-11.00-11.30) 5.86) 4. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.0-19..53 (2. 2000).35) 3.60-11.39) 2.0) 4.02-4.93) 3.2) 8.70 (2.25) 5.26 (3.46-13.40 (7.g.07 (2. 2002. 2005.61-5.33-6.47) 2.40) 17.30) 75th 5.0 (11.29) 2.36 (8.80 (7.6-17..90 (2.76 (3.70-4.4 (10.10) 3.60-6.60-8.10-7. interval) 3.20 (6.0) 7.20) 8.71 (5.0) 13.S.81-3.32) 5. levels and sufficient in most participants (Tellez et al. 2005).37-13.1) 8.70-3.34-3.0 (8.50 (3.61 (5.0-44.42 (3. NAS. In the U.59) 3. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al. 2007). gender.20-4.93-7.3-14.83 (5.30-5.60) 8.77 (3.52 (8.4 (11.75) 3.00) 9.40 (4. levels. Survey years 01-02 03-04 Geometric mean (95% conf.84) 2.0) 12.16-3.20-3.0 (9.24-2.0) 10.00) 4. nitrate.0 (9.6) 12.30 (3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability..2) 8.61-10.S.1 (8.50) 5.89-3.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.02) 3. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures.30-5.76-3.41-9.73) 3.7 (11.95 (2. Lamm and Doemland.12-2. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.39 (3.45) 3.30) 3.87) 2.35 (4.40-10.08 (3. Many factors may be important in consideration of perchlorate action on the thyroid: dose.S.4) 8. Greer et al.50) 95th 12.20-10.0 (11.10) 4. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.10) 13.50-5.40 (3. in a representative sample of U.90-15.87 (5.Perchlorate inhibition (RUI).50) 9.80 (4.0) 13.51 (3.19-6.25) 5.40 (3.90-2.12 (6. Steinmaus et al.99 (5. perchlorate is negative in most genotoxic assays (U.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 3.40) 3. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.82 (5.8 (11.00 (2. 2005).0-17.14 (2.40) 5.05 (4.20-9. population from the National Health and Nutrition Examination Survey.89 (2.1-13.10 (6.00 (6.4 (11. During gestation and infancy.93-5.43) 6.0-14.24 (4.56 (3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.1-22.20 (3.20 (2.90) 5. 2005.0) 12.58) 2.60-5.S.50) 2.80-3..4 (8.26) 4.S.80) Selected percentiles ( 95% confidence interval) 50th 3.09) 3.64-3.45-2.20 (4.70 (4.74) 7.22 (2.0 (10.54 (2.50-3.25) 5.80-3.10) 6.33-12. 2005).0 (9.44-6.

et al. Kelsh MA.41(5):409-411. et al.gov/safewater/ccl/perchlorate/perchlorate. Chacon PM. Sesser DE. Lamm S. 2005). Environ Health Perspect 2007. Environ Health Perspect 2002. newborn thyroid function. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Li FX. Blount BC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. References Blount BC.html. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Barnard JC. population.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Braverman LE. epa. Jackson WA. Benchmark calculations for perchlorate from three human cohorts. Environ Health Perspect 2006. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States.40(21):6608-6614. Cross M. Perchlorate in the United States. Deyhle GM. et al.htm. Osterloh JD. 2001-2002.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. 2005. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Howd R. Analysis of relative source contributions to the food chain. Thyroid 2001. Erratum in: J Occup Environ Med 2004. Lamm SH. Lawrence JE. Li Z. He X. Daaboul JJ.46(5):509. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Tellez RT. Richman K. 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. most of the population is considered to be below the U.. Thyroid 2000. Lawrence J. The effect of perchlorate. Pirkle JL.17(4):400-407.gov/toxpro2. Washington (DC): National Academy Press. 2007). Perchlorate Exposure of the US Population. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Environ Sci Technol 2006. Miller MD.42(2):200-205. Doemland M. Blount et al.45(10):1116-1127. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Caldwell KL. Environ Health Perspect 2005. Primary congenital hypothyroidism. Page Last Updated: 05/28/2009.114(12):1865-1871. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. EPA reference dose (Blount et al. Lau EC. Erratum in: Environ Health Perspect 2005.atsdr. Rutherford GW. Also. J Occup Environ Med 2003. National Academy of Sciences (NAS). et al. Low dose perchlorate (3 mg daily) and thyroid function.S. 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. Greer SE. Valentin-Blasini L.11(3):295. J Clin Endocrinol Metab 2005. Skeels MR. Pleus RC. Pino S. Osterloh JD. 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. Crump KS. Crump KS. Steinmaus C. CFSAN/Office of Plant & Dairy Foods. Neonatal thyroxine level and perchlorate in drinking water. Dyke JV.113(11):A732. Health Implications of Perchlorate Ingestion. Valentin-Blasini L. Mauldin JP.115(9):1333-1338. Landingham CB.10(8):659-663. Pirkle JL. National Research Council of the National Academies. Pino S. J Expo Sci Environ Epidemiol 2007.110(9):927-937. 6/2/09 Greer MA.cdc. thiocyanate. Additional information about exposure and health effects is available from the U.EPA at: http://www.S.S. Kirk AB. and environmental perchlorate exposure among residents of a Southern California community. Braverman LE. 2005). Byrd D. Food and Drug Administration (FDA). (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. and nitrate on thyroid function in workers exposed to perchlorate long-term. Abarca CR. J Occup Environ Med 2000..113(8):10011008. Buffler PA. Lamm SH. Gibbs JP. Blount BC.fda. Goodman G. Braverman LE. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Dasgupta PK. Lamm SH.. Magnani B.90(2):700-706.html and from ATSDR at: http://www. May 2007. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.

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

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

2000. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. 1995. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al.5 years and for PFOS.S. PFOA has been reported to cause liver. peroxisomal proliferation. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. thymus and spleen. 2005).. Taniyasu et al. endocrine and immune effects. 2007). in part. 2003.. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. All sources of human exposure are uncertain. or effects of other PFCs.. 2005. Excepting PFOS and PFOA.8 years (Olsen et al. 2004.. Some of the effects in animals may be mediated through peroxisomal proliferation. 2004. C7). Kannan et al. growth retardation and delayed sexual maturation (Kennedy et al. environmental fate. < LOD means less than the limit of detection. Prevedouros et al. Vanden Heuvel et al. but still can have long residence times in the body. Lau et al. 2003). 1993). 248 Fourth National Report on Human Exposure to Environmental Chemicals . For instance. The elimination half-life of PFOA in humans is roughly estimated to be 3.. 2004). may metabolize or degrade to PFOA (Dinglasan et al. human toxicokinetics. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al.. 2003).. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. kidney. Lau et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. Bookstaff et al.. 2002. population from the National Health and Nutrition Examination Survey. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. there is limited information on the sources. Unlike many organohalogen contaminant chemicals. 1990). U. 2004).. 2005). 2003a and 2004a). Olsen et al. 2005). Guruge et al.. It is unclear if environmentally degraded telomer products are a major source of other PFCs.. by high protein binding in plasma and other proteins. and β-oxidation of lipids (Kudo et al.... heptadecafluoro-1-decanol. the 8-2 telomer.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). 2005.4. 2007a). see Data Analysis section) for Survey year 03-04 is 0. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. in a wide variety of marine and land animals (Kannan et al.. environmental breakdown products of the telomers used to make fluoropolymers or the metabolic products of fluorochemicals in the body can produce PFCs that are measured human blood. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. and in human blood and semen (Calafat et al. 2006a.S. 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.. including immunologic effects and tumor induction. Survey Geometric mean (95% conf. but probably include dietary sources (Kannan et al.e. and in offspring... which may vary for some chemicals by year and by individual sample.. Tittlemier et al. C5. 2004.. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al.. EPA. pancreas.. PFOA is mostly excreted in the urine in animal studies.. 2006.. 2005. Keller et al. approximately 4. 2004. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. C6. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. The PFCs often measured in human serum are listed in the table. hepatotoxicity. In some cases.

600-2. Animal studies of PFOS have demonstrated weight loss. 2003a.. development in offspring was stunted and hypothyroxinemia was observed.800 (. Fourth National Report on Human Exposure to Environmental Chemicals 249 . Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00) .400 (<LOD-.80) 485 538 962 Limit of detection (LOD. 2004b). 2004).500-.00 (.400-1.40) .500) . 2004.900 (. Olsen et al.900 (. 2003. PFOS..500-1. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality... 2003.800) 1.500) 90th . monkeys. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.300 (<LOD-.500-1. population.500 (.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .00) . Olsen et al. 2007b).80) 640 1454 03-04 03-04 * * < LOD < LOD .Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. the potential to estimate risks to humans from animal doses is uncertain.500 (<LOD-1. reproductive.S.800 (.. and changes in thyroid hormone concentrations (Grasty et al.00) .. PFOS.. Harada et al. In such studies.700 (.300-1. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.. see Data Analysis section) for Survey year 03-04 is 0.. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.. or increased cancer rates (Alexander et al.400 (<LOD-. 2003a.S.500-3..400-1.10 (. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.500) .500 (. 2004.108 times higher than background serum levels in humans (Butenoff et al. hepatotoxicity. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.. U. < LOD means less than the limit of detection.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 . and there was no clear evidence of excess all-cause or diseasespecific mortality..S. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.400-. 2004a. 2007a.20) . However. perfluorohexanesulfonate (PFHxS). EPA. Cook et al. EPA. 2003). Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. 2003a).S. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. 2005). At high but non-toxic maternal doses of PFOS.400 (<LOD-.3.10) . Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. and humans. Kennedy et al. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al. 2003). Olsen et al. elderly and children. population from the National Health and Nutrition Examination Survey. At doses causing maternal toxicity... thyroidal)..800 (.700) . Survey Geometric mean (95% conf.800 (. 2003). 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.. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1992.600 (. 2001.400-1. 2004). U. possibly related to lung immaturity (Lau et al.400) . 2003a). 2007b.500) .300 (<LOD-. 2005).. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (. 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.. 2007.800) 1. Fei et al. PFOA.. 2007a. developmental and teratogenic effects were demonstrated in offspring.300 (<LOD-.50) . Lau et al. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.10) * 03-04 03-04 * * < LOD < LOD < LOD .600 (.400-.500) . PFOA.10) .900 (. Thibodeaux et al.500-1.500-1. In comparing three separate reports on adults.400-1.400-1. 2003a. which may vary for some chemicals by year and by individual sample.. 2007). 1999. 2003.

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

< 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. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 251 .500-.900) < LOD .400) . see Data Analysis section) for Survey year 03-04 is 1.500 (<LOD-.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.300-.600) < 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 .S.400 (<LOD-. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.S. 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.0.300 (<LOD-.400 (.300 (<LOD-. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. < LOD means less than the limit of detection.3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (.500) 485 538 962 Limit of detection (LOD.400 (<LOD-.

20-1. population from the National Health and Nutrition Examination Survey.30-6.10 (.20) 1.00 (1.56-1.10) 75th 3.600-.54) .700 (.44 (2.834-1.900-1.00) 1.50 (6.30) 3.40-1.00-8.20) 2. Survey Geometric mean (95% conf.809) 1.30-9.20 (6.10 (.90 (2. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10 (4.70-7.40-3.80 (1.60 (6.900) 1.14 (.90 (4.50-3.08) 2.70) 3.90 (1.966 (.10) 4.900-1. interval) 1.91) 2.00 (2.50 (1.16) . 252 Fourth National Report on Human Exposure to Environmental Chemicals .30 (1.80-4.40 (1.50 (1.30) 3.67-2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.86 (1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.90) 1.10-5.20) .90-10.90-19.60-3.5) 5.984 (.70) 1.40-1.30-2.70) 1.40 (1.10) 6.10 (1.40 (2.852 (.20 (1.70) 13.30) .70) 2.50-10.10) 1.00 (1.10-9.50-6.900-1.70-6.912-1.900 (.27) 1.80-8.70-10.30 (2.S.60-4.10) 5.20-1.80) 1.S.80-4.900-1.00 (.20 (1. see Data Analysis section) for Survey year 03-04 is 0.900 (.60) 9.721-1.09 (.50 (4.62-2.20 (6.586-.10 (4.93 (1.10-9.00-6.80 (4.60-2.70) 2.5) 8.40) 1.60) 3.00) 1.80) 4.20) 03-04 03-04 2.0) 8.60-3.70-5.30-12.50) 2.90) 3.80-12.20-2.72) 1.70 (2.90) 1.60-2.70-2.50 (4.40) 1.92 (1.12) .30 (1.60-2.73-2.30 (7.700-1.835-1.30 (1.00 (5.60) 2.900-1. interval) .20-3.10) 6.80-7.800-1.20 (1.816-1.0) 1053 1041 03-04 03-04 03-04 1.80-7.20-1.1) 485 538 962 Limit of detection (LOD.90 (1.10) 4.30 (1.1.60 (1.20-1.80-8.04) .80) 3. Survey Geometric mean (95% conf.30) 03-04 03-04 .10) 1.689 (.20) 485 538 962 Limit of detection (LOD.861 (.30 (6. population from the National Health and Nutrition Examination Survey.80 (1.900-1.3.70-2.00-1.20 (1.10) 75th 1.00) 3.60) 1.50 (1.90 (1.17-1.40 (1.40) 640 1454 03-04 03-04 1.50) 6.00) 2.10 (.60-7.80-6.40) .80-3.50) 2.60-8.90) 90th 5.51) 1.00-7.90-2.00 (.50 (2.80-2.826-1.00 (1.00-1.50 (6.963 (.90) 8.40) 640 1454 03-04 03-04 2.80-4.40 (1.60 (1.01 (1.30 (3.03) 1.6) 7.77-2.00 (1.30) 3.20) 1.800 (.60 (1.90 (4.90 (1.10) 8.10) 1053 1041 03-04 03-04 03-04 .90) 1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.26) 2.80-3. see Data Analysis section) for Survey year 03-04 is 0.87-2.05-2.42 (1.40) 4.72 (1.70 (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 1.40) 2.30 (2.50 (1.50-6.80) 5.80) 90th 2.17 (1.3 (9.60-4.697-1.

5) 19. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.3 (44.3 (35.60 (6.10-3.00) 3.70-7.6-45.20 (4.0 (27.1-36.1) 57.9 (19.70-10.70-5.60-13.4-42.8-22.7 (19.5-33.7-49.30-6.3) 28.80 (5.5-21.9) 22.21-3.2 (16.10) 5.84-3.7 (7.95 (3.60 (7.07-4.9-38.9 (22.80 (6.4) 640 1454 03-04 03-04 23.30-3. interval) 3.99-3.7 (35.0) 21.7 (35.65-4.2) 640 1454 03-04 03-04 4.60 (3.3 (28.50 (3.20) 10.5) 9.0 (20. Survey Geometric mean (95% conf.2 (27.4) 75th 30.20 (4.7 (13.4-17.0) 485 538 962 Limit of detection (LOD.1-24.3 (17.50-6.20) 7.2) 45.3 (35.20-4.8-81.6 (44.4) 20. Survey Geometric mean (95% conf.0-16.8 (34.9 (13.8-22.47-4.5) 32.20) 5.6) 62. population from the National Health and Nutrition Examination Survey.40-14.0-20.0) 23.47 (4.85-4.1 (24.3) 485 538 962 Limit of detection (LOD.80-4.70 (5.50) 4.4) 21.89 (3.9) 9.4 (28.70-7.8-30.4-25.80-12.20-5.80 (7.70) 6.9-23.67-4.6 (35.30-11.60 (4.3-22.40 (4.80 (6.37 (2.7 (43.6-24.20-9.82) 4.90 (7.90 (7.40-6. see Data Analysis section) for Survey year 03-04 is 0.79) 4.70-9.8 (45.40-17.50) 7.1.2-57.2 (18.9) 27.1-52.5) 57.4.7-53.40 (6.3-61.40) 3.5-62.60 (5.6) 21.10 (6.1 (19.90-4.0) 21.2-22.2 (21.9 (17.5) 1053 1041 03-04 03-04 03-04 14.35) 3.7 (43.6) 1053 1041 03-04 03-04 03-04 3.60) 03-04 03-04 3.3) 42.7-23.90 (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 21.80-9.5-23.4 (19.4 (19.30 (3.40) 5.0) 03-04 03-04 19.6) 9.30-8.8-22.1) 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.S.1-35.0) 43.40-10.7-69.9) 22.5) 18. population from the National Health and Nutrition Examination Survey.7-30.4 (23.1) 15.90) 6.90 (5.27) 4.11 (2.3) 41.18 (3.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.90-4.60 (6.5 (28.50 (4.0) 90th 41.6 (19.2) 30.30 (5.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) 7.4) 56.40) 90th 7.96 (3.6) 42.6) 7.6-50.8-78.70 (5.6) 18.20) 4.8 (37.40-6.2 (19.8) 32.50-4.30) 6.53) 3.4 (17.20) 5.0-66.30 (3.40) 75th 5.6 (42.0) 36.60-14. interval) 20.70) 4.8-35.7) 39.S.1-33.5 (28. see Data Analysis section) for Survey year 03-04 is 0.70 (3.2) 30.10 (3.30) 7.00 (5.60-6.80) 8.2 (28.0-70.9-19.30-5.1-25.8) 46.91) 3.5) 7.6) 35.00 (3.50-13.70) 3.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.7-33. Fourth National Report on Human Exposure to Environmental Chemicals 253 .60-9.5) 8.60) 8.1 (23.00 (5.10 (3.8) 27.90-12.

2.300-.300 (.500) . see Data Analysis section) for Survey year 03-04 is 0.200-.200-.S.200-.300) .300) .300) .200-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300 (. population from the National Health and Nutrition Examination Survey.300) .300 (.300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300 (. see Data Analysis section) for Survey year 03-04 is 0.300 (.300 (.300-.200-. which may vary for some chemicals by year and by individual sample.300) . Survey Geometric mean (95% conf.300 (.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) < LOD 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.500) .300 (.300) .300-.200-.200 (<LOD-.200-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) .200-.300 (.300 (.500) 485 538 962 Limit of detection (LOD.300) . which may vary for some chemicals by year and by individual sample.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.200-. 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 means less than the limit of detection.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.300 (.200-.4.300 (.300-. < LOD means less than the limit of detection. 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.400 (<LOD-.

900) 485 538 962 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th .10 (1.900-1.3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10) 1.00-1.S.90) .10) .10) 1.30 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (<LOD-.700 (<LOD-.900-1. see Data Analysis section) for Survey year 03-04 is 0. which may vary for some chemicals by year and by individual sample.00 (.20-1.900 (.800) .20) 1.500 (<LOD-.50 (1.30) 1.900-1.70) 1.700) .700) 1.10 (. Survey Geometric mean (95% conf.30) .600 (<LOD-.10-1.30 (1.900-1.400 (<LOD-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.10-1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .300 (<LOD-.900-1.00 (.10-1.900 (<LOD-1.600) .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.10 (. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.700 (<LOD-.60) 640 1454 03-04 03-04 * * < LOD < LOD .300-2.30 (1.600 (<LOD-1.700 (<LOD-2.400 (<LOD-.00) < LOD . Survey Geometric mean (95% conf. < LOD means less than the limit of detection.40) 1.800) .10) .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 .80) 1.700 (<LOD-.10-1.50 (1.10 (.10-1.20 (1. < LOD means less than the limit of detection.80) 1.30) 1.700 (<LOD-.700) 1.900) .300 (<LOD-1.800 (<LOD-.00 (.S.00 (. Fourth National Report on Human Exposure to Environmental Chemicals 255 .6.900-1. population from the National Health and Nutrition Examination Survey.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 .60) 485 538 962 Limit of detection (LOD.900) 1.900-1.700) 90th 1.600 (<LOD-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700 (<LOD-.40) < LOD < LOD .10) * 03-04 03-04 * * < LOD < LOD .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .600 (<LOD-1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.

Butenhoff JL. Keller JM. Wong LY. et al. Suzuki E. Mandel JS.Perfluorochemicals References Alexander BH. Loganathan BG.7(4):371-377. Butenhoff JL. Reidy JA. Holmstrom KE. Cook JC. Environ Sci Technol 2005. Needham LL.104(2):322-333. et al. Toxicol Appl Pharmacol 1995. Olsen J. Yamashita N. Reidy JA. Biegel LB. Crit Rev Toxicol 2004. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea.1968--2003.124(2):119-132. Rogers JM. Yun SH. Calafat AM. Birth Defects Res B Dev Reprod Toxicol 2003. Gaylor DW. Kudo N. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.and perfluorinated acids. Tully JS. Environ Sci Technol 2004.115(11):1670-1676. Jarnberg U. Koizumi A. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Guruge KS. Liu RC. Calafat AM. et al. Needham LL. Kumar KS. Day RD. Harada K. Inoue K. Needham LL. Bandai N. Olsen GW.99(2):253-261. Fluorotelomer alcohol biodegradation yields poly. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Harada K. Taniyasu S. Regul Toxicol Pharmacol 2004.60(10):722729. et al. Cook JC. Kannan K. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Environ Sci Technol 2005. Saito N. Hekster FM. Kuklenyik Z.39(1):80-84. Kamiyama S. 256 Fourth National Report on Human Exposure to Environmental Chemicals . O’Connor JC. Inoue K. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.38(17):4489-4495. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism.115(11):1596-1602. Calafat AM. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Fei C. in vivo. Olsen GW. et al. Peterson RE. Kuklenyik Z. Murray SM. et al. Arendt MD.68(6):465-471. Katakura M. Tarone RE.41:2237-2242. Caudill SP. Toxicol Appl Pharmacol 1992. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years.115(11):1677-1682. J Occup Health 2004.63:490496. Reidy JA. Polyfluoroalkyl chemicals in the U. The toxicology of perfluorooctanoate. McLaughlin JK. Edwards EA. Rodricks J. Hurtt ME. Mandel JH.39(23):9101-9108. Kuklenyik Z. Corsolini S.46(2):141-147. and ex vivo studies. Environmental and toxicity effects of perfluoroalkylated substances. Mandel JH.60(1):44-55. Mabury SA. Apelberg BJ. Yamashita N. The influence of time. Characterization of risk for general population exposure to perfluorooctanoate. Environ Sci Technol 2005. Fillmann G. Kennedy GL Jr. Bookstaff RC. Biegel LB. Perkins RG.39(23):9057-9063. Frame SR. Yoshinaga T. Chem Biol Interact 2000.S. Seacat AM. Aguilar-Villalobos M. Chemosphere 2006b.39(3):363-380. Falandysz J. Herbstman JB. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Environ Health Perspect 2007. Environ Res 2005. Taniyasu S. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Calafat AM. Bignert A. Laane RW. 2007b. Moore RW. Evans TJ. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Occup Environ Med 2003. Seneviratne HR. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Kuklenyik Z.Koizumi A. Perfluorinated chemicals in selected residents of the American continent. Kawashima Y. Mohotti KM. Dinglasan MJ. Environ Sci Technol 2007a.S. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Environ Health Perspect. Environ Sci Technol 2004. Hurtt ME. Kannan K. Toxicol Appl Pharmacol 1990. Grey BE. Reidy JA. Environ Sci Technol 2006a. Lau CS. Yoshinaga T. Watanabe T.38(10):2857-2864. J Environ Monit 2005. brominated. Ingall GB. Tully JS. Ye Y. Frame SR. Saito N. Olsen GW. Rev Environ Contam Toxicol 2003. Witter FR. Calafat AM. Environ Health Perspect 2007. Sasaki S. Halden RU.40:21282134. de Voogt P. O’Connor JC.113(2):209-217. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Burris JM. Kannan K. Chlorinated. Androgenic deficiency in male rats treated with perfluorodecanoic acid.34(4):351-384. Wijeratna S.179:99-121.134(1):18-25. et al. Grasty RC. Hurtt ME. Cook JC. Toxicol Sci 2001. Needham LL. Moore JA. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. and perfluorinated contaminants in livers of polar bears from Alaska. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Morikawa A. Caudill SP.

et al. Church TR. 2007a. Nesbit DJ. Hanson RG. Available from URL: http://www. Petrick G. Gamo T. Butenhoff JL.S. Burlew MM. Richards JH. U. Ehresman DJ. Buck RC. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. 2003.) Tittlemier SA. Horii Y. J Ag Food Chem 2007. Mandel JH. et al. J Occup Environ Med 1999. Moisey J. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Rogers JM. et al. Ellefson ME. Thibodeaux JR. Burris JM. Kannan K. fate and transport of perfluorocarboxylates. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Lundberg JK. Chemosphere 2004a.55:3203-3210. Case MT. Lundberg JK. Rogers JM. Environmental Protection Agency (U. Rogers JM. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Toxicol Sci 2003. Burris JM.epa. Helzlsouer KJ. 1/15/06 Vanden Heuvel JP. Butenhoff JL. Hansen KJ. 2003a. Sources. Butenhoff JL. Burris JM.198(2):231-241. Environ Health Perspect 2003a. Seacat AM. I: maternal and prenatal evaluations.113(5):539-545. Grey BE. Burris JM. Toxicol Appl Pharmacol 2004. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. J Children’s Health 2004b. and food items prepared in their packaging. Ehresman DJ.1177(2):183-190. Froehlich JW. birds. Mandel JH. Yamashita N. Biol Pharm Bull 2003. Cao XL et al. fish. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation.68:105–111. Mair DC.45(3):260-270.Perfluorochemicals Kudo N. Miller JP. et al. Seacat AM. Environ Health Perspect 2005. Reagen WK. Korzeniowski SH. Huang HY. Butenhoff JL. Historical comparison of perfluorooctanesulfonate. EPA). (Erratum in: Environ Health Perspect. Burris JM. Thibodeaux JR.26(1):47-51. J Occup Environ Med 2003b. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Taniyasu S. and humans from Japan. Seymour C. Olsen GW. Larson EB.51(8-12):658-668.111(16):1892-1901. Olsen GW.. A global survey of perfluorinated acids in oceans. Toxicol Sci 2002. Hansen KJ. Bronson R. Olsen GW. Peterson RE. Toxicol Sci 2003. Hansen KJ. Fourth National Report on Human Exposure to Environmental Chemicals 257 .115(9):1298-1305. htm.2(1):53-76. Barbee BD. Olsen GW. Thomford PJ. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. and perfluorooctanoate in retired fluorochemical production workers. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Butenhoff JL. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. et al. (Erratum in: Toxicol Sci 2004.41(9):799-806. Hanari N. Zobel LR.54(11):1599-1611. Lau C. Olsen GW. fish.S.40(1):32-44. Environ Health Perspect. Hanson RG.74(2):382-392. Butenhoff JL. Church TR. Coordinate induction of acyl-CoA binding protein. II: postnatal evaluation. Taniyasu S. Hansen KJ. The developmental toxicity of perfluoroalkyl acids and their derivatives. Olsen GW. et al. Sterchele PF. Pepper K. Mandel JH. Environ Sci Technol 2006. Lau C. Olsen GW. Yamashita N. Hansen KJ. Olsen GW. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water.68(1):249-264.74(2):369-381. Stanton ME. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Biochim Biophys Acta 1993. van Belle G. Environ Sci Technol 2003. Church TR. Chemosphere 2007b. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Half-life of serum elimination of perfluoroo ctanesulfonate. Prevedouros K. Grey BE. Mandel JH. perfluorooctanoate andother fluorochemicals in human blood.82(1):359.perfluorohexanesulfonate. Kawashima Y.gov/opptintr/pfoa/pfoara.111(16):1900) Olsen GW. Mar Pollut Bull 2005. Horii Y. Cousins IT. Kannan K. Washington.37(12):2634-2639. fast foods.

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

. phthalates produced anti-androgenic effects by reducing testosterone production and. 2001..cdc. 2001. Biomonitoring studies on levels of phthalate metabolites provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of phthalates than are found in the general population.. Environ Health Perspect 1982. 2006). 227-262. Clark K.. Vol. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. 2007). In Staples CA (ed). 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. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 1982). Needham LL. Springall C. testicular atrophy. McDonnell DP. 1985. Toxicological profile for di-n-butyl phthalate update [online]. 2004.niehs. pp.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. High doses of di2-ethylhexyl phthalate (DEHP). 2005. reducing estrogen production. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. J Chromatogr B 2004. and extent of metabolite conjugation to glucuronide (Albro et al. Lovekamp-Swan and Davis. 1982. Hauser et al. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. 2004.18(12):10681074.cdc.. ovarian abnormalities in the female animals (Jarfelt et al. and Sertoli cell abnormalities in the male animals and.html. interactions with macromolecules and species differences in metabolism of DEHP..cdc. However.e. 105:734-742. Kessler et al.3. Available at URL: http://www. Drug Metab Rev 1989. Corbett JT.. 2005).gov/toxprofiles/ tp135. and race/ethnicity (Silva et al. Dirven HA. 2004. 2002).. 2002.New York. Coldham NG. Dave M. but there are known species-related differences in the hydrolysis of diester phthalates.45:19-25. Peck and Albro. Food Addit Contam 2001. 2001). gender. Part Q: Phthalate Esters. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.. Environ Health Perspect 1997. which may be a pathway to the development of liver toxicity and cancers in these animals. Jordan S. 2004).html. Available at URL: http://www. at very high levels. Connor C. Scotter MJ. 2003. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 2004. In animals.21:13-34... Mackay D. 2000a. 2003.805:49-56.html).Phthalates and metabolites have been tested. variation also occurs in the same person during repetitive monitoring (Fromme et al. NTP-CERHR. These differences may contribute to species-specific differences in toxicity (ATSDR. van der Broek PH. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. Slakman AR. The Handbook of Environmental Chemistry. Massey RC. 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. efficiency of intestinal absorption. Herbert AR. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Evaluation of a recombinant yeast cell estrogen screening assay. Silvapathasundaram S.. Calafat AM. Schroeder JL. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites.gov/ toxprofiles/tp9. Hoppin et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Matthews HB. Jongeneelen FJ. Albro PW and Lavenhar SR.html. 2007. Pharmacokinetics.gov/toxpro2. Assessment of critical exposure pathways. Metabolism of di(2-ethylhexyl) phthalate. phthalates have been shown to induce peroxisomal proliferation in rodents.. Also. 2006). atsdr. Castle L. Population estimates of concentrations of specific phthalate metabolites may differ by age. Cousins IT. Anderson WA. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. Rhodes et al. 4/20/09 Albro PW. Information about external exposure (i. 2002). at higher doses. Toxicological profile for di(2-ethylhexyl)phthalate update [online]..atsdr. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Sauer MJ.. 2000c. Hauser et al. McKee et al. Silva MJ.atsdr. dibutyl phthalate (DBP).gov/ reports/index. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 .nih. 2000b. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Springer. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. 1986).

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because it is not bound to products in which it is incorporated.2 (19.4) 71. and 03-04 are 0.6) 24.1-39.3) 23.9 (70.6) 67.3-161) 99.3) 54.3 (22.2 (10.6-132) 103 (84.0-130) 101 (86.3-43.3-75.4 (63.2-155) 91.0) 32.5 (13.2) 14.8-98.4 (10.3-91.9 (12.6-92.2) 33.6-43.5-33.3 (29.9) 11.7) 38..1-15.2 (43.4) 129 (98.Phthalates Benzylbutyl Phthalate CAS No.0) 90th 67.5-36.1-18.4 (53.8-41.0 (15.1 (32.2) 13.1-61. respectively.6-39.5 (55.8 (71.1) 67.7 (51.1.0-85.6-79.1) 31.5 (76.1 (14.2) 66.4 (31. BzBP can be released into the environment during its production and.2) 78.0 (30.4 (59.8-13.9) 13.7-58. 262 Fourth National Report on Human Exposure to Environmental Chemicals . can produce developmental and reproductive toxicity in rodents.9-87.1-15.8-14.9 (22.8-16.3-34. 2004.0) 70.9) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8. IARC considers BzBP not classifiable with respect to human carcinogenicity.8 (30.7-16.8 (50.3 (30.4 (32.5-94.2-33.2) 17.S.4) 14.6-92.6 (32.9) 14.3) 63.5-40.3 (12. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.6 (13. and diet is the major source for general population exposure.1-214) 166 (116-191) 145 (110-213) 88.3 (54. 0.8-18.2-19.8-17.3) 13.8-48.6 (53.0 (27.7 (12.0 (34.1-16.2 (14.3.9-16.1 (58.7 (80.9-30.6-72.8-14.4 (29.4-92.5) 82.5-145) 138 (106-241) 143 (127-179) 120 (99.2-39.1-120) 52.4 (48.1) 14.7-13.2) 15.3 (33.6-38.9) 14.2) 32.7-35.3-18.1) 13.3 (12.7-170) 169 (134-198) 152 (99.5) 23. 01-02.6-18.4) 12.4) 75th 35.7-82. and 0.7 (70.0 (30.5 (47.8 (28.4 (68.5 (57.4) 51.4-24.1-116) 122 (93.1 (13.4-15.1) 29.7-119) 99.6) 25.6) 35.8 (38.8) 14.2) 12.5) 27.2 (11.8-72.4-127) 80.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (12.5-35.5-25.4) 49.7-16.6-150) 94.5) 16.6) 63.7 (82.1 (14.5-84.0) 34.9-27.7) 23.0-106) 58.6-116) 122 (102-142) 101 (85.S. some personal care products.6) 29.0 (11.8) 33.3) 15.3 (44.3-12. 2001-2002.3) 94.0 (15. 2000).3-18.0) 24.6 (21.7 (13.3-27.4) 38.7 (15.2-20.5 (26.3 (29.7) 40.9) 43.5) 30. population from the National Health and Nutrition Examination Survey.9-47.5-18.9) 49.3) 13.2-115) 113 (91.2-40.6) 14.1 (55.8 (10.7-15.6) 95th 103 (94.4-120) 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 13.4 (27. sealants.9 (21.4-25.8-64.8-76.6) 14.2-16.1 (13.4 (13.0 (20. NTPCERHR.9) 18.5) 15.8-16.4) 81.0-55.4 (53.2-31.0 (55.7-16.5 (27.6-17.1 (19.0 (14.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.3) 37.1-16.4) 35.8 (12.8 (86.5 (67.8-133) 89.0 (33.8 (53.1) 32.1) 76.4) 35. interval) 15.8) 63. it can be released into the ambient air during use or disposal of the products.5) 65.4) 33.5-97.5 (66.4) 80.3 (12.0) 20.4-16.9-14.5-62.7-172) 103 (74.2 (25. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine. residents (Blount et al.0) 33.6 (13. vinyl tile.1-43.9-62.6 (13.4-62.8) 28.6) 16.7-25.6-29.8 (21. Food crops take up BzBP.8 (14. and to a lesser extent.9) 15.0-26.9 (28.7 (11.3-21.9-49.6 (13.9-28.8) 24.6) 35.6 (66.9-190) 86. 2000).2-17.9 (39.7-14.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.1-90.5-14.3-88.8) 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 16.8 (71.6) 15.0 (12.2) 69.8-17.7 (53. 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. High dose BzBP and its monoester metabolites.2 (47.2-116) 122 (102-143) 101 (84.4) 98.5) 15.3-125) Total 15.2-38.1) 12.6) 13. particularly male animals (McKee et al.6) 50.4 (10.9 (12.1) Selected percentiles ( 95% confidence interval) 50th 17.9 (11. car care products.9 (13.1 (10.8-121) 79.6) 37.2) 14.2) 22.4) 65.1-35.5-41.0 (26.7-17.6) 13.1 (20.1) 68.8 (80. including MBzP.5-36.9 (16.4) 108 (96.2-16.5) 55.0) 16.2-183) 101 (78.0 (43.3-130) 122 (88.1-38.8-35.3 (13. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.5 (61.3-74.3-82. see Data Analysis section) for Survey years 99-00..6 (41.2 (19. and 2003-2004 were generally similar those reported in U.4 (32.0) 23.0 (23.

1 (15.2-13. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.6 (15.8) 24.0) 49.7-19.0-27. A small study of African-American women in Washington.9) 52.6 (22.4) 21.5 (11.9-115) 57.7 (54.3) 16.5) 41.6-86.5) 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 .4) 28.0) 24.7-19.0-53.7 (59.1) 142 (99.4 (60.8) 15.8-60.4 (13.8) 33.0 (67.9 (24.8 (13.7-31.6-40.7-56.6) 73.0 (38.9 (55.3 (13.6 (24.3) 13.2-57.0 (33.7) 46.1-35.4-99.0 (62..9-83. 2002).8-173) 195 (121-305) 229 (99.2-51.6 (11.8-14.8 (64.2-49.5-29.8) 68.0) 24. interval) 14.5-13.73-12.3 (24.4-79.8 (11.4) 50.6 (19.6) 53.. 2005.3 (39. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.5-23.2) 15.3) 21. In an annual sample of German university students. 2003).1) 17.4) 12.5-61.7 (11.9) 12.1 (9.2) 32.7-69.4 (11.6-15.8-27.1 (19.4) 17.5 (56.3 (60.3 (12.8 (30.8 (10.7) 25.1 (11.7) 11.1 (13.8 (46.7-61.69-11.4) 13.3) 37.4 (12. In NHANES 1999-2000.8-15.4-15.7 (55..9 (39. 2007).95-14.6-116) 74.5) 10.4 (63.0) 15.6-26.5-26.9-14.1) 12.7 (38.7-14.5) 14.8-42.9) 12.2) 67. and in a small sample of German residents (Koch et al.4 (33. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (49.6 (30..1-14.6) 12.7 (13.8) 108 (75.3) 14.3-34.0-109) 65.9-13.2-117) 95.2-13.1-79.7 (18.3 (23.3-38.3) 55.6-47.4-93.0 (41.9) 24.8 (50. in men attending a Boston infertility clinic (Duty et al.0 (12.6 (34.8) 13.4) 25.8) 54.1 (53. population from the National Health and Nutrition Examination Survey. adolescents compared with adults.3) 73.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.4-14.1 (21.4 (69.4) 15..8 (57.1) 35.5-76.6 (14.9) 11.4-14.7-15.8) 26.2-17.7 (21.1-27.5) 78.5) 95th 77.8-13.7-15.1 (13.0 (41.9 (10.9-62.1-120) 77.8) 16.8) 46.2 (27.8-48.4-42.8-69.7 (13.5 (48. Hauser et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-99.1) 23.4 (74.6 (57.5-16.1) 24.4-116) 73.2) 11.5 (35.5 (10. 2005).9-69.0 (13.4) 51.7 (11.6) 13.6-20.5) 16.8-16.2) 12.6) 12.4) 14.5-79.0-26.7-20.2 (69.7 (19.7 (14.8-64.1 (23.7 (12.7) 19.7) 56.7-12.4) 13.5) 17.2-78.4-90.4 (25.1 (21. 2004.9) Total 14.9-16.1 (41.7-29.9-40. 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.1 (43. in young Swedish men (Jonsson et al.0-15.0) 12.5-213) 49..8) 34.7-123) 77.6 (36.8 (12.2) 11.8-13.5 (12. 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.9) 42.9) 11.9 (9.9 (15.9) 64.2-15.4-23.2) 26.6-12.9-13.2-21. Weuve et al.1 (46.4) 44..1 (18.1-12.9 (10.8 (49.1-125) 86.0) 13.5-31.3) 89.4 (11.6-81.2 (40.4-19.2-12.6 (51.9 (22.7) 38.2) 11.3) 36. 2004).5 (42.5 (10.5) 46.8-14.9 (12.4) 90th 50.3) 90.0) Selected percentiles ( 95% confidence interval) 50th 13.4) 104 (89. Hoppin et al.1 (21.7 (11.0-48.6 (30.9 (24.7) 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 40.3 (38.8-39.1 (25.8) 53. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults..1-29.9 (54.5-42..Phthalates York City (Adibi et al.6 (11.8) 80.3) 13.9 (15.5-58.4-60. 2002. 2007).4 (26. 2006).0-51.3) 13.5) 13.6) 38.9-104) 62.4 (11.8-34.6) 58.9 (12.6 (11.6-99.4-142) 134 (116-176) 136 (85.S.8-85. 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.8 (69.0 (12.4 (46.4-17. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.5) 23.3-73.0 (11.3 (15.7-397) 70.3) 14.4 (34.5) 20.0) 11.8) 33.3) 67.5 (49.1 (14.6) 25.9 (51. and females compared to males (Silva et al.2 (56.1 (34.0-90.4) 60.9 (29.4-18.2-15.9) 12.1) 24.8-15. 2003).5-26.5-57.5 (9.8) 11.3) 12.3) 18.4-27.1-12.0 (10.7-14.5-38.9-23.6) 30.2-26.6-13.1) 39.1) 27.3 (35.8-80.9 (43.1) 80.8-13.4 (21.8) 53.6) 75th 25.2 (41.1 (21.4-102) 70.7-20.3) 29.1-58.5-58.7 (23.9) 100 (80.4) 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 12.3-64.4 (10.8) 71.8) 56..7-90.3-16.0) 60.9-28.3-11.

Richthoff J. Hum Reprod 2007. Urinary levels of seven phthalate metabolites in the U. David RM. Sampson EJ. Bull Environ Contam Toxicol 2002. Brock JW. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Silva MJ. et al. Baird DD. Wittassek M. et al.S.112(3):331-338.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Helm D. Poland. Giwercman A. Environ Health Perspect 2000. Brock JW. Eckard R.110(5):515-518. Silva MJ. Schettler T. Pirkle JL. Needham LL. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Chen Z. Phthalate monoesters levels in the urine of young children. Perera FP. Drexler H. Environ Health Perspect 2004.68:309-314. et al.html. Caudill SP. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Hilborn ED. 264 Fourth National Report on Human Exposure to Environmental Chemicals .111(14):1719-1722.210(3-4):319-333. Brock JW. Koch HM. Angerer J. Silva MJ. Third National Report on Human Exposure to Environmental Chemicals. Epidemiol 2005. Weuve J.108(10):979-982. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].22(3):688-695. Hu H. Available at URL: http://cerhr. Calafat AM.114(9):1424-1431. et al. Atlanta (GA). Camann DE. et al. Barr D. Int J Hyg Environ Health 2007. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Malek NA.niehs. et al. Jacek R. 2005. Environ Res 2003.16(4):487-493. Caudill SP. Calafat AM. Ryan L. J Androl 2004. Rylander L. 112(5):A270]. Caudill SP. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Levels of seven urinary phthalate metabolites in a human reference population. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. 4/20/09 Silva MJ. Sanchez GN. Jonsson BAG. Butala JH. Rossbach B. Environ Health Perspect 2006. Blount BC. Davis BJ. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Prenatal exposures to phthalates among women in New York City and Krakow. Environ Health Perspect 2003. Meeker JD. Green RA. Duty S. Reidy JA. Reproducibility of urinary phthalate metabolites in first morning urine samples. Hauser R. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.Phthalates References Adibi JJ. Environ Health Perspect 2002. Centers for Disease Control and Prevention (CDC). Silva MJ. Reprod Toxicol 2004. et al.nih. Ryan L. Research Triangle Park (NC). Wiesmuller GA. McKee RH. Jedrychowski W.93:177-185.18(1):122. Hagmar L. Hodge CC. Needham LL. Duty SM. Barr DB. NTP-CERHR. 2000 [online]. Singh NP. Koch HM. Gans G.25(2):293-302. Dobler L. Hoppin JA.

40-4.7-31. population from the National Health and Nutrition Examination Survey.10 (4.56-4.40 (3.90-4.40-4. mostly as MnBP (Anderson et al.40-3.00) 6.30) 10..8) 677 652 703 699 1216 1088 Limit of detection (LOD.5-29.4) 22.30 (3.40 (6.10-2. NTP-CERHR.1) 25.30-6. In addition.40 (2.6-20.49-2.33 (2.6 (9.68 (2. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.00-11.20 (6.7-20.3-43.0 and 0.3 (13. residents (Blount et al.40 (2. Hauser et al. about 65% to 80% of a dose is eliminated in urine within 24 hours.0) 20. 2003).0 (13.5 (27.22) 3.0 (13.5) 18.6-14.20-12.20 (3.3) 33.0) 9.46 (3.3-48.3 (19. 2005.10) 8. and insecticides.8) 40. see Data Analysis section) for Survey years 01-02 and 03-04 are 1. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.2-33.7) 4.8 (9.4-12.10) 2.6) 17.4) 12. 2004.60) 3. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.5) 22.10) 3.46 (2.96) 3.5) 14.70-8.40) 5.4) 5..7) 18.80 (2. 2003).50-2.00-6.6) 17.6 (13.00-4.5 (10.10 (4.30-11. Following oral administration of DBP to humans.97) 4.60 (4. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine..90 (6.00) 7.7-31. and also in some printing inks.46) 2.6) 10.9 (16.7 (17..50-10.10-9.40-17.40-5.37) 6.66) 2.30 (1.82-3. in men attending a Boston infertility clinic (Duty et al.. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.5-24.90 (3.81 (3.2) 5.6 (13.1) 22.50) 2. 2005).80-5.6 (14.40-9.0) 24.3-20.7) 15.20-2.6) 16.17 (2.9) 10.97-7. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.80 (5.5 (11.44-2.5 (20.28-5.91) 4.1-20.50-6.22 (3.6 (29.19-3.5) 18.9-14. 2004.3 (18.00-9.20-12.30) 6.50-4.90-7.30) 10. in a small sample of pregnant women in New York City (Adibi et al.30-13.5-16.30) 5.50 (6. pharmaceutical coatings.73 (2. and in a small sample of Japanese adults (Itoh et al.4 (20.1 (13. 84-74-2 Di-isobutyl Phthalate CAS No.10 (3.3-18.3) 3.2 (8.1-25.3-19.17) 4. Koch et al.00) 10..56 (3.8) 21. 2001).80 (2.1) 16.6) 26.6) 12.84) 4.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.S. 2007).S.1-12.1 (8.3 (13.25) 01-02 03-04 01-02 03-04 01-02 03-04 4..3) 18.0 (19.5 (17.00 (7.4-27.6-18. Studies of children found age-related differences in urine MBP levels.97) 2.10-9. Fourth National Report on Human Exposure to Environmental Chemicals 265 .5-16.40 (7.2 (12.56 (5.4 (14.55 (3.70-4.90 (4.6 (10.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.5) 23..40-12.70-4.48 (2.7 (16.50) 8.7 (9. CDC.85-6.80 (3.7 (7.20 (7. Biomonitoring Information Median concentrations reported in the NHANES 19992000.0-14.71 (2.50) 90th 12.3 (11. When total DBP metabolites have been measured.00) 4. 2000.60 (5.0) 13.40-3. they have been referred to as monobutyl phthalate (MBP).00-6.72-3.7 (18. 2005).73-5.56) 3. OSHA has established a workplace air standard for external exposure to DBP.6-34.0 (11.20) 4. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.9) 15.50) 7.00 (5.90) 12.30-3.70) 3.46-5.02) 4.10) 11.3 (16.6-26.20-9.20-6.70 (5.90 (4.55) 2.0-25.9-23.30-7. 2005).0-38.7-18.3 (16. interval) 2.30) 2.2 (11.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.26 (2.6 (11.90-2. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.80) 75th 5.6 (10.20) 7.9 (16.0) 12.80-5.60 (2.30-6.11-3.80 (5.7 (17. 2000).24-8.63) 3.10) 9.90-4.43) 6.60 (8.3.5) 12.7) 14.6) 16.2-14.50) 5. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-22.0) 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 2.5) 19.50 (3. Survey Geometric mean (95% conf.59) 3.00) 4.5) 25.1-17. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.30-2.7) 7.0-18.30 (4.Phthalates Di-n-butyl Phthalate CAS No.70 (2.60-6.67 (5.3-30. DBP can produce reproductive toxicity in male rodents (McKee et al.07 (3.70) 5..6 (14.3-24.50) 18.

58-3.46) 3.6-19.46 (2.8 (9.18) 4.69) 4.6) 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 2.3) 13.47 (3.78) 9.55-6.1-24. 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.53-4.33 (2.22 (2.20 (2.. 2004).57 (3.4) 23.2) 8. samples from German university students had consistently higher median urine levels of MnBP and MiBP.38 (6..31) 2.7) 3.08-2.9 (9.51) 2.91-6.15-4.7-28.7) 19.5) 15. up to four and 13 fold.74-3.11 (5.21 (5.43) 3.2-15.3 (17.93-6.86) 6.1-25.64-10.26-2.1) 13.7) 11.13 (2. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.36-7.76-3.75 (4.05) 2.97-2.8-18.9-40.66 (8. Survey Geometric mean (95% conf.53-3.37) 3.68 (2.65-11.19 (2.4) 7.2-13.69 (2.00-7.3) 18.09-2.2 (10.4 (12. to about two to fourfold higher (Fromme et al.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.18) 3.84 (4.56) 2.80 (3.01-2.8-18.1) 15.76-3.59 (4.6) 11.5 (11.78-8.30) 2.69-7.94) 6.79-8. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1) 11.and gender.75 (6. population from the National Health and Nutrition Examination Survey.9 (15.45) 3.64-7.81) 4.95) 2.47-12.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.1) 10.41 (2.98 (2.5) 13.20 (7.02-10. 2007).66) 4.6-19. Between 1998 and 2003.54 (4.17-12. 2005).1 (10.15) 3.46-11. while MnBP declined (Wittassek et al.81 (6.24) 3.99) 7.62-12.0-18.11-2.6 (8.25) 5.8) 10.8-13.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.66) 2.51) 5.1 (11.7 (9.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.32 (7.20-4.03-11.03-7.0) 15.31 (2.57 (3.74 (4.57-4.0) 11.29-3.94 (5.69) 6. 2002.8-36.4) 15. ranging from more than one-tenth the NHANES median (Itoh et al.99-4.00-3.1-12.29-8.20-2.61-3.04) 3.33 (3.18-10. 2007). 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. Weuve et al.56-15.62 (6.6 (9.42) 2.66) 10.18 (1.89 (3..34 (3.10-5.0) 3.3) 16.33) 3.56-4.52 (2.94-12.4-16.35) 3.56) 5.82) 4.88 (2.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.86-4.72-7. 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.9-26.04-5. An analysis of NHANES 2001-2002 showed similar age.52) 3.54) 2.72) 5.83 (2.07-5.1) 7. respectively. Over this time.64-7.67-5.26 (2.80-3.30 (6.52-20.21) 10.51) 15.65-4. 2004).1-15.5-19.8 (8.92 (7.36-2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.33-9. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.81) 9.52-3.6 (8.0 (10.43) 3.65 (4.28 (4.17) 90th 8.2) 9.0 (8.39) 5.27-12.9-16.7) 10.68) 5.6) 13. interval) 2.82 (4.38-10.11) 5.39-3.6 (12..17 (2.7 (21.1) 4.32 (3.7 (13.20-3.. 2006).3) 28.53-5.89-5.14 (4.28-13.9 (11.20 (2.44 (3.76 (3.79 (4.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals . the students’ median values for MiBP levels remained relatively unchanged.31 (7.2 (11.43) 3.31) 2.84 (8.95) 10.04) 7.00 (3.2) 24.9) 12.95-3.89) 6.6 (10. In an analysis of NHANES 1999-2000.58-4..00-3.S.79-6.68) 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.0) 7.6 (15.47-5.08) 75th 4.3) 13.85 (2.5 (9.78) 8.73 (5.03 (5.96 (3.18-4.80) 7. than adults in NHANES subsamples during the same time period.32) 7.3 (13.54 (2.0 (12.13-6.02 (7..07 (2.7 (11.81 (3.76-15.8 (10. 2005).18 (4.

1 (19.6-31.2 (78.6) 35.7-91.6-37.1) 19.0) 38.6-40.1-92.3) 19.4 (19.0) 21.1-22.7-20.6-69.1-29.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (22.7-42.S.3) 21.5 (59.1 (21.4-60.8-132) 95.8-119) 90.1 (34.0 (31.5) 21.3) 24.2) 32.1) 23.6 (48.4 (71.2 (21.4) 59.5-47.0) 30.8-22.0 (45.8-123) 101 (90. 01-02.6) 38.9) 21.7 (38.3-60.3 (56.4) 22.9 (79.4.9-92.2) 38.1-51.0 (20.3 (36.2 (59.2-23.7 (19.7) 28.9 (17.6) 46.3) 23.2 (18.1) 20.9 (17.1-82.0-21.8-29.9 (79.2-49.6) 71.5) 85.5-117) 95.7-26.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1) 23.7 (18. *In the 1999-2000 survey period.5) 20.4 (21.9-28.1 (19.7-117) 118 (108-143) 93.7 (33.7 (22.4-159) 107 (84.2-22. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2 (21.5) 24.6) 21.2-32.1.6) 17.9) 71.6-113) 108 (90.5) 37.7-42.6) 80.4) 20.1 (16.2) 20.7-34.4-42.4 (35.9-22.0-58.7-106) 69.0 (78.0) 27.2-87.4-31.8) 75th 51.5 (30.1-24.9) 36.6-24.3-40.8) 19.5) 47.6-20.4) 64.3-85.3 (37.2) 90th 98.7 (24.7-92.6-29.9-42.7-124) 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. see Data Analysis section) for survey years 99-00.6-143) 127 (99.1) 36. interval) 24.7 (43.0) 117 (104-131) 112 (84.7-116) 95.1 (62.1) 25. and 0.6 (61.6 (32.8-42.4 (23.0) 20.2 (58.2 (19.9) 18.6 (55.4 (35.9-101) 77.1 (36.6 (16.9) 46.7) 92.2) 26.9-33.1-27.1) 17.2-93.8 (19.9-87.0-19.1 (26.1 (54.2) 42.6 (26.7-34.5 (59.3) 18.5-53.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.5) 17.9-22.8-25.0-51.5) 65.4 (84.0) 84. Survey Geometric mean (95% conf.6-33.7 (28.4 (38.8 (57. population from the National Health and Nutrition Examination Survey.3 (51.4-25.0 (23.1) 46.6 (19.3-136) 137 (107-162) 119 (90.7 (16.5-44.5) 78.5-60.0-26.9.1 (17.3 (23.1 (19.1) 31.1 (51.8) 48. respectively.6 (44.6) 39.2-63.6-29.9) 26.8) 23.1-80.1 (31.3-145) 85.2-114) 73.9-79.0) 31.3 (23.7) 42.0 (18.1 (18.1) 30.2-21.5) 40.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.8) 58.4 (72.1 (19.0 (72.5-43.8-111) 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 23.4-26.3) 36.2) 68.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.3-76.7 (18.9-53.2 (74.5 (74.1) 47.1) 23.4-18.2 (25.9) 75.4 (36.0 (36.5-121) 106 (94.1-20.2 (79.2-56.7-24.6-44.5) 34.7) 124 (98.2 (75. referred to as monobutyl phthalate (MBP).5-42.0) 120 (98.0 (30.1 (41.3 (17.5) 36.1 (28.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.7) 74.7-111) 64. and 03-04 are 0.9) 29.3 (30.4 (35. Fourth National Report on Human Exposure to Environmental Chemicals 267 .7 (64.6) 20.3-21.3 (30.4 (25.3-24.2 (20.6-49.1-75.4) 52.0 (15.0-19.7-53.4-20.5 (29.0 (25.7 (70.3 (42.6 (90.0-24.1 (58.3 (60.6 (65.3-79.3-96.5) 26. 1.5) 19.5) 36.4-44.7-127) 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 22.5) 95.2-33.7-121) 97.5 (28.6-36.4 (35.9-114) 116 (97.0-32.9 (20.3) 40.7) 52.8) 43.2-24.6-48.2) 62.2 (17.7 (51.0-73.0-24.3-67.3) 26.5) 31.5-27.2-159) 92.8) 62.0 (17.5-47.

1-18.1) 50.8-235) 137 (108-198) 88.1) 37.0) 26.7-78.2) 159 (102-263) 147 (93.7-26.8) 40.0-19.0) 75.0-38.3 (52.3-20.6 (61.7 (60.0-17.1) 20.0) 28.6-155) 91.9) 24.6-92.0-75.0 (18.8) 63.7-37.7-19.9-56.8) 19.4) 16.4) 53.9-36.5 (14.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.3) 67.6-22.4 (31.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.6) 25.1-83.5) 90th 68.3 (69.2-61.3 (24.0 (15.6-32.8-24.4 (13.1-32. population from the National Health and Nutrition Examination Survey.6) 34.5-76.9 (39.0 (71.7-51.8 (50.4-76.3 (71.6 (27.9-38.8 (65.0 (20.6 (41.3-38.3 (42.2-18.1) 42.3 (52.2-27.9) 30.8) 20.5-30.6 (19.7) 36.7 (20.3 (19.6 (72.8 (13.4 (18.7 (14.8-23.2-73.0 (16.7 (19.4 (50.6-24.2-106) 64.5) 21.9-70.3) 20.3) 19.5-15.2) 21.3) 35.0-47.8) 34.9-84.6-53.4 (53.1) 53.4 (47.5 (18.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.1 (56.4-34.8 (18.3-21. interval) 22.9) 19. Survey Geometric mean (95% conf.6-23.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.4-164) 96.6-24.3 (76.3-106) 74.6 (25.6) 14.1 (32.6) 24.4-24.6 (31.3) 33.4 (45.9 (56.8) 22.9) 52.9 (73.0) 108 (71.1-62.5-22.7 (81.9) 39.2-22.3) 59.1 (34.6) 83.6-19.6-28.9 (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 17.5 (15.8-24.3-39.0 (27.2-22.5) 82.0-41.3-17.2-48.0 (50.9) 28.3-21.4 (31.6) 39.2) 74.0 (34.7-28.4) 19.1-128) 97.8 (25.5) 60.8 (18.9-14.1) 17.0) 29.9 (30.S.6-26.4-61.4) 15.8-32.6-27.7) 19.3 (17.5) 84.6-74.9) 62.8) 75th 38.4 (17.5-21.3-26.1 (21.6) 37.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.8) 34.6-44.9) 49.3) 19.4 (31.3 (21.2 (38.6) 64.3 (46.4-47.8 (22.9-49.0) 59.6) 18.0 (52.5) 91.5-70.7 (57.6) 65.4-131) 81.8) 13.4 (16.3-81.4-65.1) 61.8) 17.3 (28.0) 53.1) 21.7 (28.8) 20.4 (17.8) 35.3 (48.7 (27.1) 44.8) 17.9-100) 86.5 (18.1) 35.8) 23.0 (43.6) 24.2 (35.9 (16.6-16.0) 94. 268 Fourth National Report on Human Exposure to Environmental Chemicals .4) 15.4 (37.9) 20.0 (19.4 (19.4 (56.2-86.7-19.8) 30.9 (37.2 (19.2) 16.1 (29.6-119) 63.1-23.4) 20.2 (16.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.5) 17.5-64.0-60.5-41.6-128) 96.7 (54.9-68.4-135) 71.0) 81.6) 31.6 (25.9 (19.9 (58.7) 42.0) 41.0) 70.8) 17.7-21.3 (17.3 (55.6-44.7 (73.9) 14.3) 33.5 (64.4 (33.0) 35.9-68.8 (16.0 (69.2) 65.2-22.2 (19.1-99.2-85.0-113) 104 (83.7) 20.5-23.5 (30. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3 (60.6 (57.6-43.4-103) 117 (83.6) 23.2-21.7-23.5-16.9) 91.8) 28.9 (30.6) 38.9-26.3 (17.4 (68.4) 51.9 (21.1) 22.6 (74.7 (43.6-23.9 (30.2-179) 84.2) 59.5) 134 (93.7 (16.0 (61.4 (20.3-40.0) 55.4) 62.0 (26.1 (61.3-49.1 (15.6-50.2-16.0) 19.3) 17.0 (70.6-42.3) 21.3) 52.7-42.1-99.5-18.3-32.8 (18.6 (29.1) 20.9 (20.5 (81.7 (60.3) 18.4 (23.0-92.9 (35.6 (17.0-90.9 (64.8 (17.2) 31.2 (83.9-105) 85.1 (46.4 (50.2-28.3-18.4 (16.5-37.7 (12.4-72.5-142) 81.9-34.0 (18.5-142) 89.8 (33.1-21.3 (16.7-80.8-43.0) 25.3-71.3-23.7-39.7-20.5) 39.4) 21.3-78.

Koch HM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Meeker JD. Hauser R. Hum Reprod 2007. Silva MJ. NTP-CERHR.210:21-33. Caudill SP. et al.111(14):1719-1722.112(3):331-338. Jacek R. Perera FP.18(1):122.18(12):10681074. Bull Environ Contam Toxicol 2002. Hilborn ED. Barr DB. Caudill SP. 4/20/09 Silva MJ. Food Addit Contam 2001.210(3-4):319-33. Environ Health Perspect 2006. Atlanta (GA). et al. et al. Weuve J. Caudill SP. Research Triangle Park (NC). Environ Health Perspect 2000. et al.25(2):293-302. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Anderson WA.nih. Gans G.108(10)979-982. Wittassek M. Koch HM. Eckard R. Drexler H. Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals 269 . Int J Hyg Environ Health 2005. Third National Report on Human Exposure to Environmental Chemicals. Yoshida K. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Blount BC. 2000 [online]. Helm D. Hu H. Jonsson BAG. Butala JH. Springall C. Phthalate monoesters levels in the urine of young children. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Sampson EJ. Fromme H. Boehmer S. et al. Masunaga S. Barr D. Drexler H. Hodge CC. Koch HM. Brock JW. Angerer J. Rossbach B. Silva MJ. Richthoff J. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Environ Res 2003. Green RA. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Singh NP. Calafat AM. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. 2005. Itoh H. Silva MJ. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.22(3):688-695. Castle L. Prenatal exposures to phthalates among women in New York City and Krakow. Jedrychowski W. Angerer J. Epidemiol 2005. J Androl 2004. Hagmar L. Ryan L.html. Ryan L.niehs. Rylander L. Pirkle JL. Camann DE.gov/chemicals/ phthalates/dbp/dbp-eval. Int J Hyg Environ Health 2007. McKee RH.93:177-185. Chen Z. Wiesmuller GA.S. Sanchez GN. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Duty SM. Needham LL. Dobler L. Int J Hyg Environ Health 2007. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Environ Health Perspect 2003. David RM. Duty S. 112(5):A270]. Brock JW. Giwercman A.114(9):1424-1431. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.208:237-245.68:309-314. et al. Urinary levels of seven phthalate metabolites in the U. Scotter MJ. Massey RC.Phthalates References Adibi JJ. Calafat AM. Bolte G. et al. Malek NA. et al. Urinary phthalate metabolites and biomarkers of reproductive function in young men.16(4):487-493. Environ Health Perspect 2004. Silva MJ. Poland. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Reprod Toxicol 2004. Schettler T. Reidy JA. Needham LL. Levels of seven urinary phthalate metabolites in a human reference population. Available at URL: http://cerhr.

00 (<LOD-1. In this Report.300) < LOD .300-.200-.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300) 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 .200-.400 (.600) . population from the National Health and Nutrition Examination Survey.300 (<LOD-.500) < LOD 1.200-.80) . and 0.00 (<LOD-1.400-.600) .500 (.70) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. only levels at or above the 90th percentile could be characterized.600) .10 (<LOD-1. and 03-04 are 0. see Data Analysis section) for Survey years 99-00.300-.10 (<LOD-2.3.900-1.300-. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.600) .300 (.70 (1.S. < LOD means less than the limit of detection.400 (<LOD-.400 (<LOD-.00 (<LOD-1.500 (. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.500) 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 .700) .500) . 0.200-.9.400 (.500) 1. respectively.300-.400) 1. which may vary for some chemicals by year and by individual sample.20) .Phthalates Dicyclohexyl Phthalate CAS No.00-3.300-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. polyvinyl acetate.400 (.2.700) .300-. 01-02.300 (.300-. including nitrocellulose.00) .500 (.70) .300) < LOD . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.90) .500 (.400 (. 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.200 (<LOD-. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.400-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.500) < LOD < LOD .500 (.300 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and polyvinyl chloride.300-.500 (.500) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .400-.70 (1.400) < LOD < LOD .600 (.10) .400-.300 (.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600) < LOD .500-. and polymers.500 (.300-.600) . 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (.500) 1.300 (.400) 1.300 (.300 (.500) 1.500) .300-.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) < LOD < LOD .500 (. resins.700) .400 (<LOD-.400-.400-.200-.50) .400-.400 (.500) .400) < LOD 1.10 (.00-2.10 (<LOD-1.500 (.50) .

470 (.770 (.220 (<LOD-. population from the National Health and Nutrition Examination Survey.830) 1.500-.670 (<LOD-.950 (.490) .530-.16) .690) < LOD < LOD .410 (.05) .670-1.630 (<LOD-.510 (.18) .940 (.360-.450 (.330 (.400-.260-.00 (<LOD-3.33) .910 (.380 (.740) .530-1.660) .560) 1.290-.740) < LOD < LOD .34) .54) .370 (<LOD-.53) .06) .510-.44) .770-1. Survey Geometric mean (95% conf.33 (<LOD-3.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .500) 3.S.380-.530 (.06) .620) < LOD .790-1.420-.54-6. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.770-1.590 (<LOD-.420-.500 (.390 (.240-.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 1.690) < LOD 2.530) 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) 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 .470) 3.00) .310-. Fourth National Report on Human Exposure to Environmental Chemicals 271 .420-.610 (.910 (.690 (.22 (<LOD-1.480 (.53) .14 (<LOD-3.43 (1.590 (.710) .17) .660) < LOD < LOD .350-.400-.310) < LOD .67 (1.690-1.82 (1.250 (.16 (<LOD-3.530) 1.910 (.36-1.74) .450 (.170-.910 (.880 (.800-1.11) .770-1.54 (<LOD-2.270) < LOD .12-1.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.82) .330 (.630 (<LOD-.10) .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 .770) < LOD 2.

Survey years 99-00 01-02 03-04 Geometric mean (95% conf. In contrast. 0. 2001-2002. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.7) 71. and 03-04 are 1.1-93. DC (Hoppin et al.3 (74. 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.4 (62. 01-02.7 (70.4. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 2007).S..9. see Data Analysis section) for Survey years 99-00. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.3 (82.. 2003) and African-American women in Washington. and 0. Products that may contain DEP include perfumes.. soaps. 272 Fourth National Report on Human Exposure to Environmental Chemicals . deodorants.9-92. 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 91.3-103) 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. colognes. population from the National Health and Nutrition Examination Survey. 2002). Biomonitoring Information MEP levels in the NHANES 1999-2000.1 (71.2. shampoos. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. and hand lotions.8-111) 85.2-102) 95.5) 81.Phthalates Diethyl Phthalate CAS No. respectively. and also in men attending a Boston infertility clinic (Hauser et al.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. 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.9 (61. particularly those containing fragrances.

with adjusted geometric mean levels of urinary MEP that increased with age (CDC.6 (65.0 (66. This age-related trend is opposite the direction seen for other phthalates. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Analysis of NHANES 2001-2002 showed similar findings.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.S.2 (66..5-113) 122 (93. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6 (77.. 2002).3-105) 87.Phthalates 2002 (Brock et al. 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. 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. In an analysis of NHANES 1999-2000.0-156) 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 .. 2005). the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups.9 (82.5-114) 101 (87.9-110) 96.7-110) 81. 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. 2003) were slightly lower than levels found in NHANES 2001-2002. Other population estimates also differed by sex and race ethnicity (Silva et al. population from the National Health and Nutrition Examination Survey. 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. Median MEP levels found in a small sample of German residents (Koch et al.

Barr DB. Silva MJ. Hodge CC. et al. Koch HM. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.112(3):331-338. Environ Health Perspect 2003. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Phthalate monoesters levels in the urine of young children.111(14):1719-1722. Malek NA. Davis BJ. Centers for Disease Control and Prevention (CDC). Drexler H. Jacek R. Silva MJ. Baird DD. 112(5):A270].68:309-314. Camann DE. Brock JW. et al. Environ Res 2003.Phthalates References Adibi JJ. Meeker JD.S. Hum Reprod 2007. Environ Health Perspect 2004. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Reproducibility of urinary phthalate metabolites in first morning urine samples. Singh NP. Hoppin JA. Hilborn ED. Atlanta (GA). Ryan L.22(3):688-695. Reidy JA. Duty S. Poland. Brock JW. Hauser R.93:177-185. et al. Bull Environ Contam Toxicol 2002. Environ Health Perspect 2002. Barr D.110(5):515-518. Silva MJ. Caudill SP. Needham LL. Jedrychowski W. Prenatal exposures to phthalates among women in New York City and Krakow. Rossbach B. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Third National Report on Human Exposure to Environmental Chemicals. Urinary levels of seven phthalate metabolites in the U. Perera FP. Angerer J. 2005. Caudill SP.

27) 2.70 (8.51) 4.5 (31.1 (8.4-27.50-3.70) 7.3) 28.2) 6.42-5.5-36.80-4. packaging film.67-4.30 (3.5-17.90 (1.9) 18.2 (7.S.90) 7.9 (29.9-57.80 (8.5) 31.20 (3.00 (2.70-5.10-3.4) 13.49 (3.8 (19.00) 1.00) 2.40-8.1-48.54) 4.9 (17.40) 9.60) 4.1) 25.00) 11.50 (7.3) 52.41 (3.19-3.5 (12.10 (3.10-2.7) 22.21 (2.23) 3.40) 75th 7.9 (7.90) 1.77 (2. Fourth National Report on Human Exposure to Environmental Chemicals 275 .16-3.80 (4..75-4.50-6. and 03-04 are 1.0-18. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.6 (11.80-5.20 (3. 1982.5) 43.00) 2.40) 2.3 (10. Peck and Albro.60 (5.5 (18.7-18.3-49.3 (19.50 (3.0) 23.3-64.43 (3.5) 37.1982).8 (17.31-4.50 (3.10) 3.7-58.0 (18.40) 1. as glucuronide conjugates (Albro et al.30 (4.0 (19. mainly polyvinyl chloride.30-11.2-17.70 (3.90) 4.86) 2.70 (1.26-2.57-7.10) 2.90 (3.40) 11.5) 19.50-14.6 (9.10 (2.4-40.6 (20.20 (3.9 (29.16 (2.70 (7.84) 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 3.40-12.0-18.20 (1.96-5.86) 2.1) 29.6-23.1 (11.6-25.2-39.2 (31.1-27.84 (2.70-2.2) 23.30 (6.2.00) 9.30-13.50) 4.90) 4.1 (8.5 (12.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.0) 23.10-11. Following ingestion.9.40 (6.4) 22.9-26.6 (10.30-6. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.60) 7.41) 3.6-130) 31.6) 15.40) 8.35) 4.5 (12.60) 10.61 (3.0) 23.10) 3.63-4.9) 13.1-17.20 (4.40 (4.92-5.5-41.39) 3.93) 6.7) 8.50-5.60) 90th 14.5 (20.5-28.4) 15.5 (11.8 (19.00 (5.70-3.5 (18.12 (4.9 (13.00) 1.10-5.2-28.7) 27.56 (2.9) 15.69) Selected percentiles ( 95% confidence interval) 50th 3.00 (4.10 (4.7) 35.10) 3.4) 20.0 (13.50-3.68 (3.80-3.90-11. 1.6-60.50) 9. 2002.10 (5.80) 6.0-19.80 (8.6) 39.87-2.3-25.5) 23.0) Total 4.80-9.00-3.10 (3.70-4.50 (3.96) 4.50-11.7) 19.40) 4.9 (17.60-11.7) 6.10-4.5) 32.3 (15.2 (29. see Data Analysis section) for Survey years 99-00.0 (17.1) 22.82) 3.70 (5.2) 4.92-2.80 (1.00-3.60) 9.60-7.4) 7.50 (8.24-4.0.6) 9.92) 4.2 (11.9-48.0) 11.0 (14.60) 8.50 (2.6 (16.6 (12.8-50.70-2.0 (21.80-27.82 (3. population from the National Health and Nutrition Examination Survey. interval) 3. and blood product storage and intravenous delivery systems.70 (1.30 (7.23 (2.32 (3. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).7) 18.4) 22.9) 13.10-3.40 (2.5) 40.90-4.30) 2.00-4.6) 5.85) 4.4-20. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.7 (17.90) 4. After parenteral administration.35 (1.80-8.50-6.9) 5.92-2.6-28.83) 2.6 (41.7 (14.9-29.10) 2.10-5.40) 4.2) 42.3 (11.03-2.80) 9.3-57.57 (3.5-28.5-27. DEHP has been removed from or replaced in most toys and food packaging in the United States.80) 13.91-3.30-8.9 (15.07-4.40-8. Four meta