2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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4.2'.1.5’.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2'.5'-Hexabromodiphenyl ether (BDE 153) 2.3. Table 1.4'-Tribromodiphenyl ether (BDE 28) 2.2'.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .3'.4'.4'.4-Tribromodiphenyl ether (BDE 17) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.6'-Hexabromodiphenyl ether (BDE 154) 2.3.4.2'3.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4'.2-Dichloropropane 2.6-Heptabromodiphenyl ether (BDE 183) 2.2.4-Dichlorobenzene (p-Dichlorobenzene.4.2'.4. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4'.4. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.6'-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 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.1.2-Dichlorobenzene (o-Dichlorobenzene) 1.2-Trichloroethane Trichloroethene (Trichloroethylene) m. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.5'-Tetrachlorobiphenyl (PCB 49) 2.1-Dichloroethene (Vinylidene chloride) cis-1.4'-Pentabromodiphenyl ether (BDE 85) 2.4. The process for selection is described at http://www.2’.gov/exposurereport/chemical_selection.4.4'-Tetrabromodiphenyl ether (BDE 66) 2.What’s New in this Report What’s New in this Report In this Fourth Report.cdc.2'.2'.1-Dichloroethane 1.5'.6.3-Tetramethylbutyl] phenol) Triclosan (2.3.5.2'.4'.5.4’.1-Trichloroethane (Methyl chloroform) 1.5'-Tetrachlorobiphenyl (PCB 44) 2.4’.5.4.3-Dichlorobenzene (m-Dichlorobenzene) 1.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1. Paradichlorobenzene) 1.3’.4.3.2'.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.1.2'.2-Dichloroethane (Ethylene dichloride) 1.1.html.6-Pentabromodiphenyl ether (BDE 100) 2.2'4.2-Dichloroethene trans-1.4.5-Pentabromodiphenyl ether (BDE 99) 2.5.

1). 2003-2004 data for these other pesticides will be provided on this website as soon as they are available..g. 2001-2002. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. and these data will be included in the next release of the Report.. Percentiles for all three NHANES survey periods (1999-2000. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. five results that all have the value 90. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. the presence of an interference) that produced results of inadequate quality. Explanations for each change are provided in Appendix B.What’s Different in this Report What’s Different in this Report The Fourth Report uses a new procedure to estimate percentiles when the percentile estimate falls on a value that is repeated multiple times (e. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Data for other pesticides are included only for 1999-2000 and 2001-2002. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. urinary 2.4-dichlorophenol and 2.5-dichlorophenol for the 1999-2002 survey periods. Details of this procedure are provided in Appendix A. 2003-2004) have been re-computed by use of this improved procedure.g. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report.

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

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

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

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

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

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

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

9-52. Recently.4-60. glycidamide.1 (73.6) 90. 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.0-58.7-60.9 (69.3 (55. Commercially.0) 57. and in the synthesis or compounding of dye materials. 1994).6) 73. but can covalently bind to form adducts with proteins.5) 66.7) 58.5 (44. Since acrylamide has limited volatility and high water solubility. and cosmetics (NTP-CERHR.8-57.S.9 (54. and an average daily intake is estimated as 0. People may be exposed to acrylamide from foods.2 (62. smoking.2 (58. as an absorbent in disposable diapers.5 (52.3 (53. and in some cosmetics.9-105) 86. acrylamide is synthesized and used in the production of polyacrylamide polymer.S.2-91. 2006).4-89.4) 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. in some sealing grouts. and binding agents.4 (51.9) 57. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.3) 86. (NTP-CERHR.5-80.Acrylamide Acrylamide CAS No.7) 75th 79.9) 58.5-85.0 (53. 2004).3-2. In 1997.7-64.1-64.4) 100 (89. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. Estimated intakes in children are about twice that of adults (DiNovi and Howard.9 (60.1 (47.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.2-77.2 (75.1 (52.0 (57. 1990. are heated at temperatures used for frying and baking.8 (52. widely distributed in tissues. EPA.2) 57. or to glutathione conjugates (Calleman et al. gels.7 (58.1-64.7) 54. the main source of exposure is from the diet.6-65.8 (57.0-49. see Data Analysis section) for Survey year 03-04 is 3.4) 57..0 (67. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.1-61.2 μg/kg/day (U.0 (69.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61. 2005). Fennell et al.9) 63.6 (56. and from dermal contact with products that contain residual acrylamide. drinking water.4) 57.7 (65. ocular and dermal irritation from direct contact with acrylamide containing materials. EPA. Survey Geometric mean (95% conf.2) 57.8-55.4-60. Animal studies indicate that acrylamide is well absorbed. 2005). These estimated intakes are hundreds of times lower than occupational exposures.1) 101 (95.8 (91. in permanent press fabrics. In the general population. and well below doses known to cause nerve damage or carcinogenicity in animals.7) 73.6-108) 61.8 (81. 2006. Tareke et al.1 (88. Polyacrylamides are useful water-compatible polymers used in water treatment.7) 96. 2005).6-66. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.4 (54.2-70.3) 70.0 μg/kg for adults (FAO/ WHO. it was discovered that acrylamide is formed when starch-rich foods.4-76. and is either metabolized to the reactive epoxide.0.6 (81.. 2005. pulp and paper production. 2002).1) 53.4 (59.1-57.S.5 (74.0) 85. soil conditioners.6) 71. 2005).3) 63. such as potatoes and some grains. population from the National Health and Nutrition Examination Survey.1) 55.0-66. FDA.3-71.0-108) 152 (139-175) 126 (111-142) 108 (86.6-61.2-67.7 (55.1) 46. Elimination occurs mainly in the urine as mercapturic acid conjugates. but are generally above the U.2-59..S.6-104) 82.S.4-83.2-93.5 (79. 2004.1) 62.1 (83. EPA reference dose of 0.2-114) 163 (147-191) 96.5) 58.6-75. Natural substances in the food are converted to acrylamide. Acrylamide is not thought to accumulate in the body at environmental doses.7 (63. Fourth National Report on Human Exposure to Environmental Chemicals 11 .9-61.9) 75. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. 217 million pounds of acrylamide were produced commercially in the U. interval) 61.4 (54. In humans.4 (53. FAO/WHO. acrylamide has produced upper airway irritation following inhalation of high levels.6) 50. mineral processing.6 (51.7-64.2-118) 98. 2005).

gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 2005. 2005.0) 94.S.. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).5 (83.Acrylamide occupational exposures.0 (70.7) 74.4 (90.9) 59.9-64. Hagmar et al. 2005. Puppel et al.1) 60.3-101) 95. presynaptic nerve terminal binding (LoPachin.9-62. 2002.8-61.int/ ipcs/food/jecfa/summaries/summary_report_64_final. EPA at: http://www.4 (57.6-62. 2005.0-62.5-94.5) 87.7-86. 2005) have been demonstrated in animals.0 (52.1-60. 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.1 (82.. Puppel et al.8) 60. uterine...9-76.7 (61.1 (57.1) 56.1-62. In addition.. adrenal. and other sites) (FAO/WHO.5 (42..9 (58.. 2006) have been demonstrated after acrylamide dosing. 2005. After exposure ceases.3) 59. 12 Fourth National Report on Human Exposure to Environmental Chemicals ..4-103) 79.1 (66. interval) 59.9-138) 143 (130-159) 96. 2005.8 (51. 2005).3) 59.6-64. respectively) are markers of integrated acrylamide exposure over the preceding few months.. NTP-CERHR.9) 75. thyroid. 1997.2 (72.8-48. altered gene expression in testicular tissues (Yang et al. Axonal degeneration.0 (80. 2001)..S.4) 46. 2005).2-68. Klaunig et al.3-78. 2009).1 (56.4 (81.2-91. Maniere et al.9) 65.5-92.0.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.8-49.9) 87. U.7 (57.. and cancer (mammary. scrotal.4 (61.3 (56.1 (70.0 (75.5-64.. EPA. 2004).6 (90. and neuronal DNA reactivity (Doerge et al. Rice.5) 71. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. 2005.9 (81.3) 85.5 (56.S.. although different analytic methods can affect results.8 (44.7 (84.2) 55. 2005). and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.5 (59.6 (66. male germinal cell injury.4-59. 2008).2) 87. 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.7 (87. IARC classifies acrylamide as probably carcinogenic to humans. 2006. Vesper 2005) and smoking (Bergmark.S.2) 65. 2005. 2005).7) 90.epa..2 (56..1) 62. 2005.1-70. 1997.4 (51. most non-smokers had levels less than about 100 pmol/gram hemoglobin.4) 83. Glycidamide has been shown to react with DNA (Doerge et al. Schettgen et al.6-90.7-62..4-98. 2004..1-56.. 2002.0-103) 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. fetal death.2 (63. 2006). EPA.7) 60. dominant lethality). Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Vesper et al.9 (57.5) 118 (110-129) 121 (108-140) 136 (124-149) 152 (135-170) 159 (129-204) 172 (157-194) 1841 1954 3044 Limit of detection (LOD. Acrylamide is clastogenic and can produce dominant lethal mutations. 2005) and sperm DNA adducts (Xie et al..1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.5) 75th 85.who.0-93. probably through its epoxide metabolite.7-64. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. glycidamide (NTP-CERHR. 2003.3) 59.5-66. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. Mucci et al.4-65. see Data Analysis section) for Survey year 03-04 is 4.9-78.pdf. 2008). AHA levels have been shown to increase with dietary intake (Hagmar et al.2-90..7) 61. Schettgen et al. 2005. U. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. Additional information is available from U. 2006). reproductive effects (reduced litter size. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.4) 53. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.0) 118 (103-126) 121 (112-134) 113 (94.9-77. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.4 (56.8) 45. 2005.

Magnusson AL. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Chem Res Toxicol 1997 Jan. 1999). Survey data on acrylamide in food: individual food products. 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. Tornqvist M. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. 2001). Haugen M. morphological and molecular endpoints in animal models. Aprea P. Godard T.. Joint FAO/WHO Expert Committee on Food Additives. Uncertainties.561:21-37. Churchwell MI.niehs.561:49-62. et al. Farmer PB. Andersen M. DiNovi M and Howard D. 1993. 2006. Cheong HK.cfsan. Toxicol Appl Pharmacol 1993.. Bjellaas T. Tornqvist M. Perez et al. Fennell TR. smokers and nonsmokers. Toxicol Sci 2005. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Mucci LA. Paulsen JE. Axmon A. In another study. February. Mutat Res 2005. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Acrylamide neurotoxicity: neurological.pdf. Scand J Work Environ Health 2001. Bruze M. Human exposure and internal dose assessments of acrylamide in food. Burgess J. Granath F. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Kautiainen A. Doerge DR. Mechanisms of acrylamide induced rodent carcinogenesis. 2005. Kamendulis LM.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Calleman CJ. NIH Publication No.Toxicol Appl Pharmacol 1994. Spicer R. CFSAN/Office of Plant and Dairy Foods. Nordander C. Rome. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Hagmar et al. Doerge DR. Adv Exp Med Biol 2005. Twaddle NC. Fennell TR. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Yang JS. Costa LG. et al. Bridson WE.3:406-412. Guffroy M. Malmberg B. [Epub ahead of print] Dybing E. Food Chem. Tian G. Becher G. 2/3/09 Hagmar L.who. Summer SCJ. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 6013-6019. He F. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Italy. Calleman CJ. Adv Exp Med Biol 2005. gov/~dms/acrydata.120(1):45-54. Hagmar L. Duale N. Costa LG. LoPachin RM. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. 2001.. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.html#u1004. Chicago. 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. 2004. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Maniere I. Alexander J. Chem Res Toxicol 1990. 2/3/09 Klaunig JE. Food and Drug Administration (FDA). Available at URL: http://www. July. Toxicol 2005. Acrylamide intake through diet and human cancer risk.pdf. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 8-17 February 2005.126(2):361-371. Bergmark E. Available at URL: http://www. He F. Biomonitoring studies of acrylamide or glycidamide hemoglobin adducts provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acrylamide than are found in the general population. McDaniel LP.Acrylamide In occupational settings.580(1-2):131-141. da Costa GG. Laurentie M. Calleman CJ. References Bergmark E. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Zhang S. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Mutat Res 2005.85:447-459. 054472. Osterman-Golkar S. J Agric Food Chem 2008.. 2009 Jan 8. 1994). Illinois.nih. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Metabolism and hemoglobin adduct formation of acrylamide in humans.gov/chemicals/ acrylamide/Acrylamide_Monograph. Wirfalt E.43:365–410. Paulsson B. Churchwell MI.580(1-2):119-129. Beland FA. et al. Wu Y.580(1-2):157-165.10(1):78-84. April 13-15. Wilson KM. Rosen I. et al. et al..fda. smoking habits and gender. Toxicol Sci. Bergmark E.27(4):219-226. National Toxicology Program. 2/3/09 Perez HL. Available at URL: http://cerhr. Bergmark E. Snyder RW. and Research Strategies. 64th Meeting: Summary and Conclusions (FAO/WHO). Mutat Res 2005.56. 2004 Acrylamide in Food Workshop: Update Scientific Issues. The Updated Exposure Assessment for Acrylamide.

14 Fourth National Report on Human Exposure to Environmental Chemicals . Sun H. Lee MH. Lee SH. Chae C. U. Yang HJ.S. Int J Hyg Environ Health 2003.txt.htm. Smith A.207(6):531-9.274(1):59-68.56(15):6046-53. Rice JM. EPA).19(4):527-34.Acrylamide glycidamide by gas chromatography-mass spectrometry. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Tornqvist M. Adv Exp Med Biol 2005. Kutting B. Ingham L. The carcinogenicity of acrylamide.561:89-96. Han CH. Weiss T. Drexler H. Slimani N. Schettgen T. Gray JG.S. Drexler H.134(1-3):65-70. Rossbach B.206(1):9-14. Drexler H. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Environmental Protection Agency (U. Fueller F. Eriksson S. Rapid Commun Mass Spectrom 2006. Rydberg P.gov/chemfact/s_acryla. Myers GL. Karlsson P. Toxicological effects of acrylamide on rat testicular gene expression profile. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.S. Available at URL: http://www.163(2):101-8. Schettgen T. Meyers T.gov/iris/subst/0286. propylene oxide. 1994. Agudo A. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Han DU. U. Liu Y. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Washington (DC). a carcinogen formed in heated foodstuffs. Integrated Risk Information System (IRIS). Tjaden Z. Toxicol Lett 2006. et al. Letzel S. Fu D. Xie Q. 2/3/09. Hallmans G.S. Acrylamide. Jin Y.580(1-2):3-20. Meyers T. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Hemoglobin adducts of ethylene oxide. Mutat Res 2005 Feb 7. EPA). acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Angerer J. Office of Pollution Prevention and Toxics. Puppel N. Anal Biochem 1999.580(1-2):71-80. Marko D. September. Benetou V. Angerer J.50(17):4998-5006. Analysis of acrylamide. Vesper HW. Tjønneland A. Schettgen T. Toxicol Lett 2002. revised 1/3/06. Available at URL: http://www. Angerer J. et al. Ding X. Int J Hyg Environ Health 2004. Reprod Toxicol 2005.20(6):959-64. Licea-Perez H. Ospina M. Tareke E. J Agric Food Chem 2002.epa. Vesper HW. Chemical Summary for Acrylamide. Environmental Protection Agency (U. Liu K. 2/3/09 Vesper HW. Mutat Res 2005. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Choi JH. J Agric Food Chem 2008.epa. Ospina M. Broding HC.

02 (.770-1. 1998).071 (.26-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.164 (.35 (2.96) 2.19) 1..054 (.77 (1.312) .520 (.506 (.68) 2.070) 75th .21-1.050-.600-1.063) .83-2.070) .950 (.111-.570-1. maternal exposure during pregnancy can result in lower birth weight.920 (.63-2.188) .076-.130) .S.110 (.190-.15) 2.148-.075 (.21-1.310) .49) 1.120 (.78) 2.120 (. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.160 (.260-1.220-.43 (1.050 (<LOD-.057-.080 (.77 (1.030 (.047-.96 (1.38-2.62 (2.350-. Fourth National Report on Human Exposure to Environmental Chemicals 15 .28) . and 17% had an LOD of 0.052 (<LOD-.540-.62) 2.34 (1.153-.17 (1.197) .900-1.089) Age group 3-11 years 99-00 01-02** 03-04 .071) .54 (1.450-.14) . 2004).137-.44 (1.85 (1.160-.160) .533-.084) .30) * .060-.50-4.66 (1.120 (.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 .23 (2.088-.080-.20 (.230) .800 (.12-4. 2006).660) .120 (.106-.05) 1. ear problems.39) 3.066 (.308 (.16) .087-.770) .860 (.110 (.400-.480-.080-.160) .061) < LOD .68 (1.213) .S.92 (1.42-4.360) .234) .280 (.080) < LOD .087 (.020-.100-.12) 1.02) 1.630 (. and 0.110) .710 (.160 (.42 (1.23 (.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.53-4.030-.580-1.060 (<LOD-.040 (. see Data Analysis section) for Survey years 99-00.510 (.124 (.086 (.17 (.45) 1.043-.094) .126) .080 (.17) .740-1.88 (1.070 (<LOD-.200) 1.990 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.49) 1.180 (. < LOD means less than the limit of detection.350 (. 2004).997-3.54 (1.090-.110-.60-2.068) .65 (1.850 (.164 (. and various other disorders (U.187) .470-.09-3. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.110-.47-3.93) .Cotinine Cotinine CAS No.53 (1.04 (1.50-1.130 (.820) .14-1.190-.14) .240 (.625) .140-.120-.142-. ** In the 2001-2002 survey period.22) 2.95) 1.28-1.87-3.320) .058 (.160 (.180) .01 (1.040 (.150) .01) 3.620-1.480-1.201) .210 (.077) . Children exposed to ETS are at increased risk for sudden infant death syndrome.50) 3.55-2.50 (1.140-.00) .110 (.150) .050-.115-.410) .621-1.21 (.302) .080) < LOD < LOD .180 (.220) .33-2.726) .090-.910-1.110 (.12 (1.350-.053 (<LOD-. and 03-04 are 0.068) .02) 1.040-.060) .087) < LOD < LOD .00) 1.630 (.030-.050 (<LOD-.20-2.066) .70-2.070-.047-.060 (<LOD-.960-1.05.060 (.68) . stroke.216 (.062 (.730 (.059-.175 (.505 (.630 (.077) .740-1.015.110-.190-.030-.066-.39 (1.840) 3.77 (2.120-. Survey Geometric mean (95% conf.770) .23 (1.19-2.81-2.310-1.05 ng/mL. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.050 (<LOD-.44) 2.20 (1.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .180) .15 (2. 83% of measurements had an LOD of 0.163) . cardiovascular disease.20) 1.76 (1.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .57) 2.S.18-3.40) .670) .12 (2.990) .140 (.428-.54) 1.073) < LOD .050) .84-3.080-.23-2.310) 90th 1.430-1.070) .99) 2.154-.580) .44 (2.540 (.75) 1.88 (.89) 1.690 (.30) 2.110 (.63 (2. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. DHHS.99) 2.11) .570 (. and exacerbated asthma (U.580 (.167 (.30) 2.131 (.620 (.050 (<LOD-. acute respiratory infections. 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.060-.104-.060-.120) .66) 1.32-2. emphysema. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.48-2.500 (.059-.790) .930 (.260) 1.09-3.44) 2.120 (.96-4.09-2.040 (.230 (.015 ng/mL.180) .050 (.94) 1.163 (.180) .198) * .220) . which may vary for some chemicals by year and by individual sample. 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. population from the National Health and Nutrition Examination Survey.55 (1.140 (. Cigarettes contain about 1.48-3.145) .32) 1.180) .050) .370-. DHHS.950-1.144 (.090-.137 (.66-3.310-1.70) 2.32-2.110) .080-.040-.20) . acute respiratory illness. respectively.139) * .19) .060 (.052 (<LOD-.5% nicotine by weight (Kozlowski et al.79) 3.300) .193) .108) * .

1994). Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al. Cotinine. Hukkanen et al. Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al.3 to 30 µg/m3. variable changes in blood pressure and heart rate. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. 1998). Soliman et al. nausea. or chewing gum.. Perez-Stable et al.. The serum cotinine levels seen in the NHANES 20032004 appear approximately similar to levels seen in the previous survey period (NHANES 2001-2002) for the total population estimates. 2004).. 2005). 1999. Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. and peppers. seizures.. 1975. saliva. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005... NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration. html. 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. 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. or skin patches that contain nicotine. In homes with one or more smokers.nih.. Symptoms of 16 nicotine withdrawal include irritability. For an adult. tomatoes. Pirkle et al. 1991). Hukkanen et al. contains nicotine in larger amounts than other nicotine-containing plants. Wilson et al.. 2006). Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. which include potatoes. (CDC. salivation. mean air concentrations typically range from 2 to 14 µg/m3 (NTP. 1996). However. 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.Cotinine 1994. Cotinine can be measured in serum. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. 1996). The tobacco plant.. 2005). Children are primarily exposed to ETS by parents and caregivers who smoke. diarrhea. 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. a process involved in the development of addiction. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. urine. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . nicotine has a half-life in blood plasma of several hours (Benowitz. the primary metabolite of nicotine. nasal sprays. and hair. Once absorbed.. NCI. Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff. 2006). 2006.nida. 1999. diaphoresis. 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. and death. 2005)... craving. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. Nicotiana tabacum. cognitive and sleep disturbances. vomiting. 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. Over the previous decade. 2004). with heavy exposure to ETS producing levels in the 1–10 ng/mL range.. eggplants. non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al.. 2005. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al. chewing tobacco. The IARC and the NTP consider tobacco smoke to be a human carcinogen. More information about the effects of smoking and nicotine can be found at: http://www. Serum cotinine has been measured in many studies of nonsmoking populations. During each previous NHANES survey. 2005. Iwase et al. Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. 1998). with higher levels measured in restaurants and bars. Acute tobacco or nicotine intoxication can produce dizziness.. 1999). and increased appetite. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms.gov/researchreports/nicotine/nicotine. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans.

Department of Heath and Human Services. JAMA 1996. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.275:1233-1240. DHHS). Department of Heath and Human Services. Ethnic differences in N-glucuronidation of nicotine and cotinine. Benowitz NL. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .niehs. June. Curtin LR. Available at URL: http://www. National Institute for Occupational Safety and Hygiene (NIOSH). 4/13/09 Perez-Stable EJ. Nicotine metabolism and intake in black and white smokers. Pharmacol Rev 2005. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. the United Kingdom.S.fr/ENG/Monographs/allmonos90. Benowitz NL.7:369-375. Mehta NY. Aiba M. Respiratory nicotine absorption in non-smoking females during passive smoking. Warner K. George CF. Pollack HA. Tobacco Smoke.niosh. Schwartz SS.4:313-316. Centers for Disease Control and Prevention. Tobacco Smoke and Involuntary Smoking.gov/tcrb/monographs/10/. Metabolism of nicotine to cotinine studied by a dual stable isotope method. et al.pdf. 1991. Atlanta (GA): 2005. et al.php.iarc. Pechacek TF.php. 4/13/09 Iwase A. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Caraballo R. Office on Smoking and Health [online] 2006.fr/ENG/Monographs/ allmonos90. Turner DM.gov/ntp/roc/eleventh/profiles/ s176toba. Available at URL: http:// cancercontrol. and the United States. Sweeney CT. Coordinating Center for Health Promotion.280:152-156. Brody DJ. Bernert JT. Modin G. Richter PA. Fong I.18:188-204. Giovino G. Herrera B. Pirkle JL. 1988-1991. National Center for Chronic Disease Prevention and Health Promotion. Houseman TH. U.S Department of Health and Human Services (U. Perez-Stable EJ. 11th ed. Etzel RA.pdf. Vogler GP.S. Kozlowski LT. Smoking and Tobacco Control Monograph 10 [online]. Flegal KM. Third National Report on Human Exposure to Environmental Chemicals. Tobacco related exposures.surgeongeneral.S. Mowery PD. Available at URL: http://ntp. Clin Pharmacol Ther 1994. Schober SE. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Centers for Disease Control and Prevention. 1988-1991.S. Trends in the exposure of nonsmokers in the U. 1999-2002. Jacob P III. Am J Public Health 2004. Environ Health Perspect 2006. Lewis PJ. Summary of Data Reported and Evaluation [online] 2004. Kira S. Vol 83.gov/library/ secondhandsmoke/. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Vol 38. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Jarvis MJ. Dollery CT. U. Benowitz NL. 1999. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.56:483-493. available at URL: http://mtn.291(3):1196-1203. DHHS). Jacob P.63:139-43. 4/13/09 International Agency for Research on Cancer. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. References Armitage AK. IARC Monogr Eval Carcinog Risks Hum. Tob Control 2006.gov/eid/rmca/critdocs/ criteriadoc/33. IARC Monogr Eval Carcinog Risks Hum. 4/13/09 U. Available at URL: http://monographs. 4/13/09 Centers for Disease Control and Prevention (CDC).15:302-307.S Department of Health and Human Services (U. [online]. JAMA 1998. Centers for Disease Control. In Report on Carcinogens. Available at URL: http://monographs.S. Benowitz NL.cdc.S.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Benowitz NL. National Toxicology Program (NTP). Coordinating Center for Health Promotion. Pickett MA. Racial/ethnic differences in serum cotinine levels among adult U. Tob Control 1998. 4/13/09 National Cancer Institute (NCI). population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.114(6):853-858. 2004. J Pharmacol Exp Ther 1999. Exposure of the U. Absorption and metabolism of nicotine from cigarettes. JAMA 1998. Maurer KR. Cotinine as a biomarker of environmental tobacco smoke exposure. Summary of Data Reported and Evaluation [online] 1986. International Agency for Research on Cancer. BMJ 1975.94(2):314-320. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Jacob III P. Herrera B.nih. Pechacek TF. Pirkle JL. Bernert JT. iarc. Metabolism and disposition kinetics of nicotine. Hukkanen J. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.57(1):79115. U. Caudill SP. Brody DJ. Soliman S. Giovino GA. Strauss WJ. Int Arch Occup Environ Health 1991. population to secondhand smoke: 1988-2002. Epidemiol Rev 1996.cancer. Jacob P III.S. Sosnoff CS. cigarette smokers: the Third National Health and Nutrition Examination Survey.280:135-140.

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

1998). 2002). One survey detected DEET in 74% of sampled streams in the U. < LOD means less than the limit of detection.180 (.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. After absorption.. 2002). DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.130-. Survey Geometric mean (95% conf.100-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. DEET can be applied to clothing and the skin to repel biting insects. Neurological effects in humans.130 (..130) < LOD .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 .180 (.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th . Urinary N.180) < LOD . 2003).120-.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.110 (<LOD-.epa.gov/pesticides/.100-. EPA.S. 1995.100-..S. There are over 225 insect repellents brands containing DEET.120-.S. and it has not been rated by IARC or NTP with respect to human carcinogenicity.EPA at: http://www.100-.449 and 0.110 (.140 (. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.130-. (Kolpin et al.210 (.100-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. About 3-8% of dermally applied DEET is absorbed.160) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD.140) < LOD .520) < LOD .100-.S. DEET is not registered for use on agricultural commodities.130-.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .N.N-Diethyl-meta-toluamide (DEET) N.EPA. Sudakin and Trevathan.110 (.130-.240) < LOD . population from the National Health and Nutrition Examination Survey. (U.EPA.130) < LOD .180 (.170 (.190) < LOD . 1998). but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.110 (.140) < LOD . Its use is recommended for prevention of several vector-borne diseases. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.130 (.110 (<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 .1.220 (.560) < LOD . 134-62-3 General Information N. Additional information is available from U.110-. have been reported as result of self-poisoning by ingestion or excessive dermal application.110 (.S. 2003).170 (. including seizures and encephalopathy. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. DEET has low acute toxicity. DEET is not a developmental or reproductive toxicant in animals (U.140-.250) < LOD . which may vary for some chemicals by year and by individual sample.100 (<LOD-.130 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 .140) < LOD . and they range in concentration from 4% to 100%. DEET is also used in combination with dermal sun screens (U.N-Diethyl-meta-toluamide (DEET) CAS No.150) < LOD . DEET is not genotoxic.110-.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. 2005).

.S.410 (.250-.350) < LOD .320 (.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 .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.500 (.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.330 (.270 (.370-. 1992). Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.320) < LOD .410-.200 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.270) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. 20 Fourth National Report on Human Exposure to Environmental Chemicals .230) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170-.140-.190 (<LOD-.350-. 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.130 (<LOD-.500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th . Urinary N.190 (.410 (. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.640 (.N.300 (.390-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .190-.240-.230-.330 (.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .230-. Survey Geometric mean (95% conf..93) < LOD .240) < LOD .270 (<LOD-. population from the National Health and Nutrition Examination Survey.350) < LOD .290-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.190 (. In this survey period. 2007).150) < LOD .150-. Urinary DEET levels as high as 5.630) < LOD . 2005).490) < LOD .280 (.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 . representative subsamples from NHANES 2001-2002.280-1.250) < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.480 (.270-.370) < LOD .440) < LOD .250 (.

Gabriel KL. EPA. Fundam Appl Toxicol 1995.S. Bell JW. Washington (DC): U. Chen H. Zaugg SD. Human exposures to N. Available at URL: http://www.S. Pharmaceuticals. J Toxicol Clin Toxicol 2003. DEET: a review and update of safety and risk in the general population. September 1998. Atlanta (GA).gov/teach/chem_summ/ DEET_summary. EPA 738-R98-010. U. Barber LB. Environ Sci Technol 2002.pdf. Page BC.S. streams.16(1):10-13.EPA). Osimitz TG. Chemical Summary. Environmental Protection Agency (U. Hartnagel RE Jr. Third National Report on Human Exposure to Environmental Chemicals. 2005. Thurman EM. Selim S. Schoenig GP.gov/oppsrrd1/REDs/0002red. Reregistration Eligibility Decision (RED): DEET. 2005 Kolpin DW. Int J Toxicol 2002. pdf.N-diethyl-mtoluamide following dermal application to human volunteers.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Trevathan WR. Lowry LK. Toxicity and Exposure Assessment in Children’s Health.EPA. Absorption.N-Diethyl-meta-toluamide (DEET) References Arcury TA. Environmental Protection Agency (U.S.EPA).epa. and other organic wastewater contaminants in U.S. Grzywacz JG. Quandt SA. Barr DB. 1-118. Meyer MT. and excretion of N. Furlong ET. 1993-1997. hormones. Veltri JC.2:341352.41(6):831-839. 1999-2000: a national reconnaissance. U.36(6):1202-1211. Available at URL: http://www.epa. Smallwood AW.S.25:95-100. 4/9/09 U. J Anal Toxicol 1992.115(8):1254-1260. Diethyltoluamide (DEET). pp. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . DeBord KE. Sudakin DL.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography.N. metabolism.S. et al. Environ Health Perspect 2007. N. Centers for Disease Control and Prevention (CDC). Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Tapia J.

Disinfection By-Products (Trihalomethanes)

Disinfection By-Products (Trihalomethanes)
Bromodichloromethane CAS No. 75-27-4 Dibromochloromethane (Chlorodibromomethane) CAS No. 124-48-1 Tribromomethane (Bromoform) CAS No. 75-25-2 Trichloromethane (Chloroform) CAS No. 57-57-8 General Information Disinfection by-products (DBP) are a class of chemical by-products also referred to as trihalomethanes (THMs), formed when chlorine or bromine interacts with the natural organic materials found in water. DBPs also include other formed products, such as haloacetic acids, haloacetonitriles, haloketones, and chlorophenols. The composition and levels of specific DBPs are determined by water quality, water treatment conditions, and disinfectant type (IPCS, 2000). Primary sources of DBPs are chlorinated drinking water and recreational water bodies, such as swimming pools.

In drinking water, trichloromethane is the predominant DBP, usually found at much higher levels than bromodichloromethane; tribromomethane is the least abundant (Krasner et al., 1989). DBPs are volatile at room temperature and can be detected in ambient air during activities such as showering, bathing, dishwashing, and swimming (Backer, et al., 2000; Gordon et al., 2006). Trichloromethane has industrial applications and is used to produce refrigerants and feedstock. It may be released into the environment where chlorine-based chemicals are used for bleaching and disinfecting processes or disposed at hazardous waste sites (IPCS, 2004; LaRegina, et al. 1986). Tribromomethane has limited industrial uses, mainly in geological assaying, electronics manufacturing, and as a solvent in laboratory analyses (ATSDR, 2005). DBPs tend not to bioaccumulate in aquatic organisms or persist in open or surface waters or soils, but they can remain in water within closed pipe systems. Workplace exposure may occur during the production of trichloromethane or tribromomethane, or in workplaces where DBPs may be generated, such as pulp or paper manufacturing, swimming pools, and water treatment plants (IPCS, 2004). General population exposure to DBPs occurs primarily through ingesting chlorinated water and inhaling the water

Blood Bromodichloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 2.21 (1.65-2.97)

Selected percentiles
( 95% confidence interval)

50th 2.30 (1.56-3.21) 1.40 (1.10-1.90)

75th 4.63 (3.24-6.20) 3.40 (2.60-4.20)

90th 8.45 (5.86-12.0) 6.20 (5.30-7.00)

95th 12.0 (7.68-19.2) 9.50 (7.00-12.0)

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

1.50 (1.20-1.86)

Sample size 785 1322

01-02 03-04

2.21 (1.65-2.97) 1.50 (1.20-1.86)

2.30 (1.56-3.21) 1.40 (1.10-1.90)

4.63 (3.24-6.20) 3.40 (2.60-4.20)

8.45 (5.86-12.0) 6.20 (5.30-7.00)

12.0 (7.68-19.2) 9.50 (7.00-12.0)

785 1322

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

2.19 (1.60-3.00) 1.48 (1.18-1.85) 2.24 (1.66-3.01) 1.51 (1.21-1.90)

2.31 (1.63-3.21) 1.40 (.940-2.00) 2.28 (1.49-3.24) 1.50 (1.10-1.90)

4.64 (3.21-6.08) 3.40 (2.60-4.30) 4.63 (3.09-7.01) 3.30 (2.50-4.20)

7.96 (5.74-15.3) 6.60 (5.40-7.20) 8.62 (5.26-12.9) 6.10 (4.69-7.30)

13.0 (6.93-20.5) 11.0 (7.20-14.0) 11.1 (7.68-25.0) 7.80 (6.40-12.0)

382 650 403 672

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

3.28 (2.29-4.68) 1.65 (1.15-2.38) 2.32 (1.82-2.94) 1.56 (1.15-2.13) 2.02 (1.42-2.87) 1.42 (1.11-1.81)

3.32 (2.19-4.70) 1.60 (.820-2.80) 2.50 (1.56-3.55) 1.70 (1.10-2.20) 2.16 (1.36-3.09) 1.30 (.850-1.90)

6.81 (3.71-10.4) 3.50 (2.60-4.90) 4.57 (3.60-5.56) 2.90 (2.15-3.80) 4.34 (2.92-6.01) 3.30 (2.30-4.40)

10.8 (8.24-14.7) 7.30 (4.50-10.0) 8.69 (5.63-9.49) 5.10 (3.80-6.60) 7.33 (4.72-15.3) 6.20 (5.20-7.20)

14.7 (11.1-20.5) 10.0 (7.30-11.0) 10.0 (5.89-13.5) 6.60 (4.90-13.0) 11.1 (6.01-26.1) 9.80 (6.70-13.0)

227 244 130 290 365 684

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.233 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

22

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

vapor. Dermal absorption also may occur during bathing and swimming (ATSDR, 1997, 2005; Dick, et al., 1995; Leavens et al., 2007). Each of the DBPs is rapidly absorbed and distributed widely throughout the body. In animals, these chemicals undergo hepatic metabolism to reactive chemicals, which can bind to cell macromolecules and be toxic in large amounts (IPCS, 2000). Ultimately, DBPs are metabolized to carbon dioxide, which is eliminated in exhaled air within a few hours. Only a small amount of each DBP is eliminated unchanged in urine. Elimination halflives for these chemicals are less than four hours (ATSDR, 2005; Leavens et al., 2007). Human health effects from DBPs at low environmental doses or at biomonitored levels from low environmental exposures are unclear or unknown. Humans exposed to massive levels of trichloromethane or tribromomethane develop central nervous system depression and hepatotoxicity (ATSDR, 2005, 1997). Acute animal toxicity studies of each of these chemicals have found central nervous system depression, liver and renal damage or necrosis, and occasionally, cardiac depression and arrhythmias (IPCS, 2000). In studies of rodents chronically fed high doses of either trichloromethane or bromodichloromethane, carcinomas occurred in the liver and kidney; large intestine tumors and

polyps were also noted with bromodichloromethane (NCI, 1976; NTP, 1987). Chronic feeding studies in rodents with either dibromochloromethane or tribromomethane showed inconsistent evidence of carcinogenicity across species and genders. The DBPs did not produce reproductive or developmental effects in animals unless maternal toxicity was present, but bromodichloromethane altered sperm motility (IPCS, 2000). Numerous epidemiologic studies of the relationships between chlorinated water source and various cancers, adverse reproductive outcomes, and cardiovascular disease have been inconclusive (IPCS, 2000). IARC classified trichloromethane and bromodichloromethane as possible human carcinogens, and NTP determined that these chemicals are reasonably anticipated to be human carcinogens. However, IARC found dibromochloromethane and tribromomethane to be unclassifiable regarding human carcinogenicity. The U.S. EPA has established drinking water and environmental standards for “total THMs.” OSHA and ACGIH have established workplace standards and guidelines, respectively, for trichloromethane and tribromomethane. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at: http://www.atsdr.cdc.gov/toxpro2.html.

Blood Dibromochloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) .867 (.521-1.44)

Selected percentiles
( 95% confidence interval)

50th .780 (.340-1.90) < LOD

75th 2.61 (1.22-4.38) 1.30 (1.00-1.80)

90th 5.46 (3.53-9.71) 3.60 (2.70-4.80)

95th 8.96 (5.04-12.9) 7.20 (4.80-8.60)

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

*

Sample size 781 1333

01-02 03-04

.867 (.521-1.44) *

.780 (.340-1.90) < LOD

2.61 (1.22-4.38) 1.30 (1.00-1.80)

5.46 (3.53-9.71) 3.60 (2.70-4.80)

8.96 (5.04-12.9) 7.20 (4.80-8.60)

781 1333

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

.850 (.481-1.50) * .884 (.550-1.42) *

.730 (.300-2.25) < LOD .820 (.340-1.69) < LOD

2.66 (.960-4.38) 1.30 (1.00-1.90) 2.54 (1.37-4.31) 1.30 (1.00-1.80)

4.77 (3.33-9.20) 3.70 (2.70-5.70) 6.30 (3.28-10.1) 3.60 (2.50-4.80)

8.06 (4.31-14.6) 7.20 (5.20-8.60) 9.91 (5.02-13.0) 6.60 (3.80-9.20)

371 657 410 676

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

1.61 (.843-3.06) 1.20 (.963-1.50) 1.03 (.505-2.09) * .736 (.413-1.31) *

1.49 (.670-3.99) 1.10 (.810-1.40) .930 (.530-2.03) < LOD .640 (<LOD-1.93) < LOD

4.59 (1.93-8.89) 2.30 (1.50-4.10) 2.03 (.770-7.06) .970 (.650-1.60) 2.49 (.870-4.27) 1.30 (.950-1.80)

9.26 (5.21-12.1) 5.20 (3.80-6.90) 4.22 (2.01-10.5) 1.90 (1.20-3.20) 4.57 (3.00-7.12) 3.30 (2.50-4.60)

12.0 (9.63-16.1) 7.70 (5.20-11.0) 8.09 (2.80-16.5) 3.20 (1.80-5.20) 6.98 (4.27-11.1) 6.60 (3.70-9.20)

233 256 128 288 357 685

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.271 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

23

Disinfection By-Products (Trihalomethanes)

Biomonitoring Information Levels of blood DBPs reflect recent exposure. Geometric mean blood trichloromethane levels were 0.039 and 0.043 ng/mL among non-smoking and smoking adults, respectively, in a subsample of NHANES 1999-2000 participants (Lin et al., 2008), which were at least twice as high as comparable levels in NHANES 2001-2002 and 2003-2004. In a non-representative sample of NHANES III (1988-1994) participants, the geometric mean and median blood trichloromethane levels, respectively, were 0.043 and 0.023 mg/L (Churchill et al., 2001). Similar median blood trichloromethane levels were reported in smaller studies of U.S adults (Ashley et al., 2005; Backer et al., 2000; Buckley et al., 1997) and in this Report. Immediately following bathing or showering with chlorinated water, median blood levels of trichloromethane, dibromochloromethane, and bromodichloromethane can increase two to four times over baseline levels, and then return to baseline rapidly during the next one to two hours (Ashley et al., 2005; Backer et al., 2000). Finding a measurable amount of one or more of these THMs in blood does not mean that the level of THMs causes an adverse health effect. Biomonitoring studies of blood

THMs can provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of THMs than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Blood Tribromomethane (Bromoform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 1.57 (1.07-2.31)

Selected percentiles
( 95% confidence interval)

50th 1.39 (.960-2.02) < LOD

75th 2.78 (1.76-4.63) 1.80 (<LOD-2.80)

90th 6.05 (2.92-29.2) 3.74 (2.30-7.10)

95th 15.5 (3.68-85.4) 6.40 (3.60-14.0)

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

*

Sample size 774 1310

01-02 03-04

1.57 (1.07-2.31) *

1.39 (.960-2.02) < LOD

2.78 (1.76-4.63) 1.80 (<LOD-2.80)

6.05 (2.92-29.2) 3.74 (2.30-7.10)

15.5 (3.68-85.4) 6.40 (3.60-14.0)

774 1310

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

1.49 (.944-2.34) * 1.67 (1.17-2.39) *

1.29 (.850-1.98) < LOD 1.46 (1.05-2.21) < LOD

2.65 (1.49-5.05) 1.90 (<LOD-2.87) 2.86 (1.89-4.57) 1.72 (<LOD-2.65)

6.12 (2.26-33.9) 4.00 (2.40-6.80) 5.69 (3.30-27.5) 3.20 (1.93-7.70)

14.9 (2.79-69.9) 6.50 (4.00-13.0) 22.2 (5.09-49.6) 6.10 (3.10-31.0)

374 645 400 665

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

2.34 (1.15-4.77) * 1.51 (.857-2.67) * 1.47 (.980-2.22) *

1.66 (.990-3.38) 1.60 (<LOD-3.10) 1.47 (.780-3.15) < LOD 1.29 (.840-2.06) < LOD

4.03 (1.42-36.5) 3.30 (<LOD-9.40) 2.58 (1.39-4.64) 1.60 (<LOD-2.30) 2.58 (1.51-4.91) 1.70 (<LOD-2.90)

28.3 (4.39-49.2) 7.60 (3.60-14.0) 4.34 (2.57-8.48) 2.50 (1.80-3.20) 5.69 (2.84-21.2) 3.50 (2.00-7.70)

40.8 (31.5-57.9) 11.0 (5.60-210) 6.27 (3.28-15.2) 3.20 (2.40-6.10) 11.0 (3.30-69.9) 5.90 (3.30-21.0)

234 242 121 289 362 680

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.596 and 1.5. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

24

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

Blood Trichloromethane (Chloroform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 16.6 (13.0-21.1)

Selected percentiles
( 95% confidence interval)

50th 16.1 (11.9-22.2) 10.0 (8.50-13.0)

75th 31.7 (23.9-40.4) 20.0 (17.0-24.0)

90th 55.5 (44.5-68.6) 35.0 (29.0-40.0)

95th 72.1 (57.3-105) 50.0 (37.0-65.0)

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

10.2 (8.56-12.2)

Sample size 744 1222

01-02 03-04

16.6 (13.0-21.1) 10.2 (8.56-12.2)

16.1 (11.9-22.2) 10.0 (8.50-13.0)

31.7 (23.9-40.4) 20.0 (17.0-24.0)

55.5 (44.5-68.6) 35.0 (29.0-40.0)

72.1 (57.3-105) 50.0 (37.0-65.0)

744 1222

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

16.8 (12.0-23.5) 10.1 (8.43-12.1) 16.4 (13.4-20.1) 10.4 (8.41-12.7)

16.1 (11.0-24.8) 10.0 (7.90-14.0) 16.6 (12.0-21.5) 10.0 (8.40-13.0)

34.3 (22.4-48.7) 20.0 (17.0-25.0) 29.2 (24.0-36.5) 20.0 (16.0-23.9)

57.0 (39.9-76.4) 36.8 (29.0-49.0) 53.5 (38.4-68.9) 33.0 (26.0-40.0)

75.2 (54.5-156) 53.0 (36.8-69.0) 69.5 (53.3-104) 46.0 (35.0-65.0)

358 599 386 623

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

17.0 (10.5-27.6) 9.17 (7.45-11.3) 19.1 (12.9-28.1) 11.8 (9.54-14.6) 15.6 (12.0-20.2) 9.84 (8.09-12.0)

14.5 (10.0-32.7) 9.30 (7.60-11.0) 20.9 (9.28-37.4) 12.0 (8.90-15.0) 15.2 (11.2-20.5) 10.0 (8.10-13.0)

35.1 (18.6-57.6) 19.0 (15.0-24.0) 38.4 (27.7-46.0) 20.0 (15.0-30.0) 26.8 (20.4-39.5) 20.0 (16.0-23.0)

60.7 (41.5-100) 34.0 (24.0-44.4) 55.9 (45.5-69.8) 35.0 (28.0-59.0) 53.5 (35.3-72.1) 33.8 (27.0-40.0)

93.0 (49.7-243) 44.4 (30.0-59.0) 68.9 (51.9-74.0) 61.0 (34.0-100) 69.5 (53.5-105) 47.0 (35.0-67.0)

223 225 116 272 348 630

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 2.37 and 2.11. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

Fourth National Report on Human Exposure to Environmental Chemicals

25

Disinfection By-Products (Trihalomethanes)

References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for chloroform update. 1997 [online]. Available at URL: http://www.atsdr.cdc.gov/toxprofiles/tp6.html. 4/26/09 Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for bromoform and chlorodibromomethane. 2005 [online]. Available at URL: http://www.atsdr.cdc.gov/ toxprofiles/tp130.html. 4/26/09 Ashley DL, Blount BC, Singer PC, Depaz E, Wilkes C, Gordon S, et al. Changes in blood trihalomethanes concentrations resulting from differences in water quality and water use activities. Arch Environ Occup Health 2005;60(1):7-15. Backer LC, Ashley DL, Bonin MA, Cardinali FL, Kieszak SM, Wooten JV. Household exposures to drinking water disinfection by-products: whole blood trihalomethane levels. J Expo Anal Environ Epidemiol 2000;10(4):321-326. Buckley TJ, Liddle J, Ashley DL, Paschal DC, Burse VW, Needham LL. Environmental and biomarker measurements in nine homes in the lower Rio Grande Valley: multimedia results for pesticides, metals, PAHs and VOCs. Environ Int 1997;23(5):705732. Churchill JE, Ashley DL, Kaye WE. Recent chemical exposures and blood volatile organic compound levels in a large populationbased sample. Arch Environ Health 2001;56(2):157-166. Dick D, Ng KM, Sauder DN, Chu I. In vitro and in vivo percutaneous absorption of 14C-chloroform in humans. Hum Exp Toxicol 1995;14: 260-265. Gordon SM, Brinkman MC, Ashley DL, Blount BC, Lyu C, Masters J, Singer PC. Changes in breath trihalomethane levels resulting from household water-use activities. Environ Health Perspect 2006;114(4):514-521. International Programme on Chemical Safety (IPCS). Environmental Health Criteria 216. Disinfectants and Disinfectant By-Products. 2000 [online]. Available at URL: http://www. inchem.org/documents/ehc/ehc/ehc216.htm.4/26/09 International Programme on Chemical Safety (IPCS). Concise International Chemical Assessment Document 58. Chloroform. 2004 [online]. Available at URL: http://www.inchem.org/ documents/cicads/cicads/cicad58.htm. 4/26/09 Krasner SW, McGuire MJ, Jacaugelo JG, Patania NL, Reagan KM, Aieta EM. The occurrence of disinfection by-products in US drinking water. J Am Water Works Assoc 1989;81:41–53. LaRegina J, Bozzelli JW, Harkov R, Gianti S. Volatility organic compounds at hazardous waste sites and a sanitary landfill in New

Jersey. An up-to-date review of the present situation. Environ Prog 1986;5:18-27. Leavens TL, Blount BC, De Marini DM, Madden MC, Valentine JL, Case MW, et al. Disposition of bromodichloromethane in humans following oral and dermal exposure. Toxicol Sci 2007;99(2):432-445. Lin YS, Egeghy PP, Rappaport SM. Relationships between levels of volatile organic compounds in air and blood from the general population. J Expo Sci Environ Epidemiol 2008;18(4):421-9. National Cancer Institute (NCI). Report on the carcinogenesis bioassay of chloroform (CAS No. 67-66-3). National Cancer Institute Carcinogenesis Technical Report Series March 1, 1976. [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/htdocs/ LT_rpts/trChloroform.pdf. 4/26/09 National Toxicology Program (NTP). Carcinogenesis studies of bromodichloromethane (CAS No. 75-27-4) in F344/N rats and B6C31F mice (gavage studies). Technical Report Series No. 321. 1987 [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/ htdocs/LT_rpts/tr321.pdf. 4/26/09

26

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

Benzophenone-3
CAS No. 131-57-7 General Information Benzophenone-3 (2-hydroxy-4-methoxybenzophenone) occurs naturally in some flowering plants. It is commercially synthesized as a sunscreen for use in lotions, conditioners, and cosmetics. It is also used as a UV stabilizer in plastic surface coatings and polymers. Benzophenone-3 is a common ingredient in sun-blocking agents. People may be exposed through dermal application of sunscreens and cosmetic products. Small amounts of benzophenone-3 can be absorbed through human skin and excreted in the urine, mostly as a glucuronidated conjugate (Gonzalez et al., 2006; Gustavsson et al., 2002; Janjua et al., 2004; Ye et al., 2005). After dermal application of a 4% lotion over the entire body daily for 5 days, one study found that 1.2-8.7% of the applied benzophenone-3 amount was recovered in the urine (Gonzalez et al., 2006). Human health effects from benzophenone-3 at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Following dermal application, some cases of photoallergy or allergy to benzophenone-3 have been reported. Male reproductive toxicity has been inconsistently reported in chronic high dose animal studies (Daston et al., 1993; French, 1992). Benzophenone-3 has weak estrogenic activity or weak anti-androgenic activity (French, 1992; Schlecht et al., 2004; Schlumpf et al., 2001; Schreurs et al., 2005). No human hormonal changes were observed during four days of application of 10% benzophenone-3 lotion (Janjua et al., 2004). Benzophenone-3 is not considered mutagenic (Robison et al., 1994). IARC and NTP have no ratings as to human carcinogenicity of benzophenone-3. Biomonitoring Information Urinary benzophenone-3 levels include both conjugated and unconjugated forms and reflect recent exposure to the chemical. The NHANES 2003-2004 levels of urinary benzophenone-3 have been described by Calafat et al. (2008). The analysis showed that female participants had slightly higher urinary levels than males and that nonHispanic whites were more likely than non-Hispanic blacks to have levels above the 95th percentile of the overall population. In a study of 90 U.S. females aged 6-8 years, the median urinary benzophenone-3 level of 14.7 µg/L was comparable to the median level of children 6-11 years of age (17.2 µg/L) in the NHANES 2003-2004 subsample (Calafat

et al., 2008; Wolff et al., 2007). Total benzophenone-3 urinary concentrations were detectable in 90% of a small sample of adults in whom the values ranged up to 3000 μg/L (Ye et al., 2005). Following short-term application of 10% benzophenone-3 lotion, men and women had mean urinary levels of 140 and 60 μg/L, respectively (Janjua et al., 2004). Finding a measurable amount of benzophenone-3 in urine does not mean that the levels of benzophenone-3 cause an adverse health effect. Biomonitoring studies on levels of benzophenone-3 provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of benzophenone-3 than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Fourth National Report on Human Exposure to Environmental Chemicals

27

Environmental Phenols

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone)
Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.9 (18.1-28.9)

Selected percentiles
( 95% confidence interval)

Sample 95th 1040 (698-1390) size 2517

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

years 03-04

50th 18.1 (15.5-23.2)

75th 94.0 (67.5-123)

90th 370 (225-570)

03-04 03-04 03-04

21.2 (16.4-27.3) 22.9 (18.0-29.3) 23.1 (18.0-29.6)

17.2 (14.9-25.9) 20.1 (16.1-25.1) 18.1 (14.7-23.3)

66.7 (38.7-102) 67.1 (45.2-93.8) 109 (72.1-140)

158 (106-246) 170 (137-240) 450 (315-733)

246 (154-618) 407 (183-717) 1220 (769-1750)

314 715 1488

03-04 03-04

16.8 (13.2-21.3) 30.7 (23.7-39.8)

13.7 (11.4-16.8) 26.0 (20.2-34.1)

55.3 (33.2-86.6) 137 (106-172)

178 (134-324) 596 (403-769)

567 (238-1350) 1340 (776-1790)

1229 1288

03-04 03-04 03-04

16.5 (10.9-25.1) 12.8 (9.38-17.4) 27.7 (20.3-37.8)

11.9 (8.50-18.3) 10.2 (7.40-14.4) 24.4 (16.8-32.0)

45.5 (25.9-78.2) 34.3 (22.8-50.6) 121 (83.6-162)

178 (76.4-412) 127 (90.8-176) 507 (316-769)

412 (178-2180) 247 (143-499) 1340 (733-2070)

613 652 1092

Limit of detection (LOD, see Data Analysis section) for Survey year 03-04 is 0.3.

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) (creatinine corrected)
Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.2 (17.6-28.0)

Selected percentiles
( 95% confidence interval)

Sample 95th 1080 (686-1600) size 2514

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

years 03-04

50th 16.2 (12.7-21.6)

75th 82.0 (58.7-108)

90th 415 (283-577)

03-04 03-04 03-04

25.8 (19.5-34.1) 17.2 (13.7-21.5) 22.8 (17.8-29.1)

22.4 (14.4-33.7) 12.9 (10.4-16.5) 16.2 (12.7-21.9)

84.6 (41.0-131) 43.6 (29.5-57.7) 93.2 (66.0-130)

171 (132-365) 136 (91.7-239) 491 (361-700)

427 (171-710) 350 (173-646) 1330 (880-1880)

314 713 1487

03-04 03-04

13.6 (10.8-17.1) 35.5 (27.1-46.4)

10.3 (8.36-12.9) 28.2 (20.2-37.0)

40.0 (24.9-62.5) 144 (101-224)

169 (93.3-316) 686 (491-1130)

381 (229-685) 1850 (1220-2580)

1228 1286

03-04 03-04 03-04

15.1 (9.44-24.0) 8.78 (6.49-11.9) 28.3 (20.6-38.8)

11.1 (6.95-16.0) 6.80 (5.27-9.00) 22.0 (14.6-32.7)

40.7 (18.3-85.8) 19.7 (13.5-33.4) 116 (73.5-175)

158 (87.4-362) 79.8 (46.8-139) 510 (380-760)

595 (118-1860) 185 (79.8-536) 1330 (852-2410)

612 651 1091

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Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

References Calafat AM, Wong LY, Ye X, Reidy JA, Needham LL. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003--2004. Environ Health Perspect 2008;116(7):893-897. Daston GP, Gettings SD, Carlton BD, Chudkowski M, Davis RA, Kraus AL, et al. Assessment of the reproductive toxic potential of dermally applied 2-hydroxy-4-methoxybenzophenone to male B6C3F1 mice. Fundam Appl Toxicol 1993;20(1):120-124. French JE. NTP technical report on the toxicity studies of 2-hydroxy-4-methoxybenzophenone (CAS No. 131-57-7) Adminstered topically and in dosed feed to F344/N Rats and B6C3F1 mice. National Institutes of Health Publication No. 923344, October 1992 (also Toxic Rep Ser. 1992 Oct;21:1-E14). Gonzalez H, Farbrot A, Larko O, Wennberg AM. Percutaneous absorption of the sunscreen benzophenone-3 after repeated whole-body applications, with and without ultraviolet irradiation. Br J Dermatol 2006;154(2):337-340. Gustavsson Gonzalez H, Farbrot A, Larko O. Percutaneous absorption of benzophenone-3, a common component of topical sunscreens. Clin Exp Dermatol 2002;27(8):691-694. Janjua NR, Mogensen B, Andersson AM, Petersen JH, Henriksen M, Skakkebaek NE, et al. Systemic absorption of the sunscreens benzophenone-3, octyl methoxycinnamate, and 3-(4-methylbenzylidene) camphor after whole-body topical application and reproductive hormone levels in humans. J Invest Dermatol 2004;123(1):57-61. Okereke CS, Barat SA, Abdel-Rahman MS. Safety evaluation of benzophenone-3 after dermal administration in rats. Toxicol Lett 1995;80(1-3):61-67. Robison SH, Odio MR, Thompson ED, Aardema MJ, Kraus AL. Assessment of the in vivo genotoxicity of 2-hydroxy 4-methoxybenzophenone. Environ Mol Mutagen 1994;23(4):312317. Schlecht C, Klammer H, Jarry H, Wuttke W. Effects of estradiol, benzophenone-2 and benzophenone-3 on the expression pattern of the estrogen receptors (ER) alpha and beta, the estrogen receptorrelated receptor 1 (ERR1) and the aryl hydrocarbon receptor (AhR) in adult ovariectomized rats. Toxicology 2004;205(12):123-130. Schlumpf M, Cotton B, Conscience M, Haller V, Steinmann B, Lichtensteiger W. In vitro and in vivo estrogenicity of UV screens. Environ Health Perspect 2001;109(3):239-244. Erratum in: Environ Health Perspect 2001;109(11):A517. Schreurs RH, Sonneveld E, Jansen JH, Seinen W, van der Burg B. Interaction of polycyclic musks and UV filters with the estrogen

receptor (ER), androgen receptor (AR), and progesterone receptor (PR) in reporter gene bioassays. Toxicol Sci 2005;83(2):264-272. Ye X, Kuklenyik Z, Needham LL, Calafat AM. Quantification of urinary conjugates of bisphenol A, 2,5-dichlorophenol, and 2-hydroxy-4-methoxybenzophenone in humans by online solid phase extraction-high performance liquid chromatographytandem mass spectrometry. Anal Bioanal Chem 2005;383(4):638644.

Fourth National Report on Human Exposure to Environmental Chemicals

29

Environmental Phenols

Bisphenol A

CAS No. 80-05-7 General Information Bisphenol A is a phenolic chemical which has been used for over 50 years in the manufacture of polycarbonate plastics and epoxy resins; in thermal paper production; and as a polymerization inhibitor in the formation of some polyvinyl chloride plastics. Polycarbonates are used to make products such as compact discs, automobile parts, baby bottles, plastic dinnerware, eyeglass lenses, toys, and impact-resistant safety equipment. Epoxy resins containing bisphenol A are used in protective linings of some canned food containers, wine vat linings, epoxy resin-based paints, floorings, and some dental composites. In recent years, about 5-6 billion pounds of bisphenol were produced annually worldwide. Bisphenol A may enter the environment from industrial sources or from product leaching, disposal, and use. In 1999-2000, bisphenol A was detected in 41.2% of 139 U.S. streams in 30 states (Kolpin et al., 2002). Bisphenol A can be biodegraded and does not bioaccumulate significantly in aquatic organisms. Some invertebrates may be sensitive and show reproductive effects (European Commission, 2003).

component of total exposure estimates (Wilson et al., 2007. In animal and human studies, bisphenol A is well absorbed orally. In humans, little free bisphenol A circulates after oral absorption due to the high degree of glucuronidation by the liver. The glucuronidated bisphenol A is excreted in the urine within 24 hours with no evidence of accumulation (Volkel et al., 2002).

Human health effects from bisphenol A at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Occupational exposure of epoxy workers to bisphenol A dust may produce eye irritation and skin sensitization. In animal studies, bisphenol A has low acute toxicity. It is not considered a teratogen (Kim et al., 2001). Bisphenol A is rated as weakly estrogenic (Matthews et al., 2001). Some reproductive or developmental changes are observed at high doses in standard experimental animal studies (e.g., delayed vaginal opening and preputial separation) (Ema et al., 2001; Tyl et al., 2002; NTPCERHR, 2008). Reproductive and neurodevelopmental effects of bisphenol A at low doses in animals, including environmental doses potentially relevant to humans, have been the subject of ongoing scientific reviews and study (European Commission, 2002; Gray et al., 2004; NTP, 2001; NTP-CERHR, 2007 and 2008; vom Saal and Hughes, 2005 Welshons et al., 2006; Witorsch, 2002). Examples General population exposure to bisphenol A may occur of recent animal studies which suggest possible low dose through ingestion of foods in contact with bisphenol A effects include altered development of the fetal prostate containing materials. For small children, hand-to-mouth and mammary gland, inhibition of postnatal testosterone and direct oral contact with materials containing bisphenol production, and changes in neurodevelopment (Akingbemi A are possible. Exposure from indoor air is a small et al., 2004; Leranth et al., 2008; NTP-CERHR, 2007;

Urinary Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane)
Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 2.64 (2.38-2.94)

Selected percentiles
( 95% confidence interval)

Sample 95th 16.0 (14.4-17.2) size 2517

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

years 03-04

50th 2.80 (2.50-3.10)

75th 5.50 (5.00-6.20)

90th 10.6 (9.40-12.0)

03-04 03-04 03-04

3.55 (2.95-4.29) 3.74 (3.31-4.22) 2.41 (2.15-2.72)

3.80 (2.70-5.00) 4.30 (3.60-4.60) 2.60 (2.30-2.80)

6.90 (6.00-8.30) 7.80 (6.50-9.00) 5.10 (4.50-5.70)

12.6 (9.50-15.1) 13.5 (11.8-15.2) 9.50 (8.10-11.3)

16.0 (11.5-23.3) 16.5 (15.2-20.9) 15.2 (12.4-18.1)

314 715 1488

03-04 03-04

2.92 (2.63-3.24) 2.41 (2.11-2.75)

3.20 (2.70-3.60) 2.50 (2.20-2.80)

6.10 (5.40-6.60) 5.00 (4.20-6.20)

10.4 (9.50-11.6) 10.6 (8.70-12.5)

16.0 (12.7-17.6) 15.9 (13.5-20.1)

1229 1288

03-04 03-04 03-04

2.58 (2.15-3.08) 4.24 (3.73-4.82) 2.51 (2.26-2.79)

2.60 (2.10-3.20) 4.30 (3.80-5.10) 2.70 (2.50-3.00)

5.20 (4.40-6.50) 8.20 (7.10-9.80) 5.20 (4.70-5.80)

9.90 (7.30-13.9) 14.2 (11.7-16.9) 9.60 (8.30-10.9)

15.4 (10.2-19.7) 20.6 (14.9-25.2) 15.1 (12.6-16.7)

613 652 1092

Limit of detection (LOD, see Data Analysis section) for Survey year 03-04 is 0.4.

30

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

Timms et al., 2005). Bisphenol A is not considered mutagenic and is unlikely to be a carcinogen, although it may form DNA adducts in vitro and inhibit mitotic spindle activity (Haighton et al., 2002). IARC and NTP do not have ratings for bisphenol A with respect to human carcinogenicity. The epoxy resin oligomer, bisphenol A diglycidyl ether, has limited evidence of animal carcinogenicity and is not classifiable as a human carcinogen by IARC. Biomonitoring Information Urinary levels of bisphenol A include both conjugated and unconjugated forms and reflect recent exposure to the chemical. In the participants of NHANES 20032004, prevalent exposure to bisphenol A in the U.S. population was demonstrated with children, females, and lower income strata having slightly higher urinary levels (Calafat et al., 2008). This study confirmed levels seen in an earlier smaller sample of 394 U.S. residents (Calafat et al., 2005). Several previous small studies in Japanese pregnant women, Japanese university students, and Korean residents have found mean urinary bisphenol A levels to be similar or up to several times higher than those in the U.S. representative NHANES 2003-2004 subsample (Fujimaki et al., 2004; Kim et al., 2003; Ouchi and Watanabe, 2002), although one study of 73 Koreans found levels that averaged seven times higher than median levels in the NHANES 2003-2004 subsample (Yang et al., 2003; Calafat et al., 2008). Applications of certain dental sealants were shown to increase urinary levels of bisphenol A for 24

hours (Joskow et al., 2006). Hanaoka et al. (2002) studied workers with exposure to bisphenol A diglycidyl ether and found mean urinary levels of bisphenol A about double that of unexposed workers. Finding a measurable amount of bisphenol A in the urine does not mean that the levels of bisphenol A cause an adverse health effect. Biomonitoring studies on levels of bisphenol A provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of bisphenol A than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Urinary Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane) (creatinine corrected)
Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 2.58 (2.36-2.82)

Selected percentiles
( 95% confidence interval)

Sample 95th 11.2 (9.78-12.4) size 2514

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

years 03-04

50th 2.50 (2.31-2.80)

75th 4.29 (3.88-4.75)

90th 7.67 (6.62-8.66)

03-04 03-04 03-04

4.32 (3.63-5.14) 2.80 (2.52-3.11) 2.39 (2.17-2.64)

4.29 (3.63-5.23) 2.74 (2.35-3.22) 2.36 (2.15-2.59)

7.14 (5.83-9.56) 4.74 (4.21-5.09) 3.93 (3.44-4.33)

12.2 (9.84-14.8) 7.79 (6.41-8.87) 6.64 (5.97-7.74)

15.7 (12.2-23.2) 11.8 (8.05-14.2) 10.0 (9.01-11.4)

314 713 1487

03-04 03-04

2.38 (2.15-2.63) 2.78 (2.50-3.08)

2.31 (2.08-2.70) 2.68 (2.40-2.94)

4.19 (3.81-4.64) 4.41 (3.81-5.15)

7.10 (6.41-8.28) 7.93 (6.48-10.2)

9.94 (9.06-11.7) 12.4 (9.29-18.2)

1228 1286

03-04 03-04 03-04

2.34 (2.02-2.71) 2.92 (2.58-3.32) 2.58 (2.37-2.81)

2.38 (2.00-2.65) 2.95 (2.51-3.27) 2.55 (2.32-2.80)

3.85 (3.24-4.55) 4.90 (4.07-6.13) 4.30 (3.93-4.67)

7.09 (5.00-9.04) 8.64 (7.53-9.63) 7.58 (6.32-8.87)

10.9 (8.50-14.3) 11.9 (10.2-13.3) 11.0 (9.34-12.4)

612 651 1091

Fourth National Report on Human Exposure to Environmental Chemicals

31

Sottas CM. NC. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents.eu/ health/ph_risk/committees/sct/documents/out156_en. National Institutes of Health. Kroes R. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Needham LL.niehs. Hanaoka T. Gray GM. Leranth. Ye X. Ekong J. Brine DR. September. Research Triangle Park. Kim CS. Italy.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Kim YH. Twomey K. U.36(6):1202-1211. and Hardy MP. 1999-2000: a national reconnaissance. Cunha G. Fujii S. Marr MC. National Institute of Environmental Health Sciences.europa. Watanabe S. Shin HC. 2003. Pharmaceuticals. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Ikka T. Needham LL.312(2):441-448. 2007. Available at URL: http://cerhr. Szigeti-Buck. Regul Toxicol Pharmacol 2002. 32 Fourth National Report on Human Exposure to Environmental Chemicals .145:592-603. Myers CB. Barber LB. Koulova AI. Joskow R. 2008. DirectorateGeneral Health and Consumer Protection.nih. Zacharewski TR. Kawamura N. Rhomberg et al. Han SS.jrc. Gender differences in the levels of bisphenol A metabolites in urine. vom Saal FS. Barr JR. Calafat AM. with estrogen receptors alpha and beta. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Occup Environ Med 2002.102(19):7014-7019. MacLusky. Doull J. Ema M. Yang M. Cha SW. May 22.14(2):149-157.pdf. Life Sci 2001. Tyl RW. Tsugane S. Biochem Biophys Res Commun 2003. Matthews JB. hormones. Cohen JT. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Available at URL: http://ntp. European Commission. Kim JC. Barr DB. Kiguchi M. Chung MK. Environ Sci Technol 2002. T. Human Health. Timms BG. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. In vitro and in vivo interactions of bisphenol A and its metabolite. Toxicol Sci 2002. Bradley S.780(2):365-370. 2002. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Thomas BF. Barton L.S. Furlong ET. Wong LY. Needham LL. Meyer MT.137(3):353-362. et al. Proc Natl Acad Sci USA 2005. Munro IC. 2/4/09 Ouchi K. Arakawa C.59(9):625-628. Joint Research Centre Institute of Health and Consumer Protection. Kuklenyik Z. August 2001.35(2 Pt 1):238-254. Endocrinology 2008. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy.. Calafat AM. Watanabe C. 5: 505-523. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. An evaluation of the possible carcinogenicity of bisphenol A to humans. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). National Toxicology Program. Thurman EM. Brussels.149:988-994. N.. bisphenol A glucuronide. niehs. Park S. C. McConnell EE. Hara K. Kolpin DW. and Hajszan. Ispra. Environ Health Perspect 2008. Haighton LA.. Rubin C. Lynch BS.gov/chemicals/bisphenol/bisphenol. J Am Dent Assoc 2006. Reidy JA. Department of Health and Human Services. et al. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Nippon Eiseigaku Zasshi 2004. Reprod Toxicol 2001.59(4):403-408.pdf. Available at URL: http://cerhr. November 26.S.pdf .nih. Exposure of the U. Chem Res Toxicol 2001.69(22):2611-2625. 4. Howdeshell KL.116(1):39-44.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. et al. Available at URL: http://ecb.gov/chemicals/bisphenol/BPAFinalEPVF112607.Scientific Committee on Toxicity. Hlywka JJ. Serizawa S. Zaugg SD. Endocrinology 2004.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Harazono A. Environ Health Perspect 2005. Reidy JA. Ecotoxicity and the Environment (CSTEE). Furukawa M. Han SY. Hum Ecol Risk Assess 2004. 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.J. and other organic wastewater contaminants in U. 2/4/09 Fujimaki K.Environmental Phenols References Akingbemi BT. Rat two-generation reproductive toxicity study of bisphenol A. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Available at URL: http://ec. Imai H. Hughes C. Klinefelter GR.68(1):121-146. streams. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Caudill SP. Calafat AM. Keimowitz AR. Yoshinaga J.S. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Bisphenol A. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).10:875-921.pdf. niehs. 2/4/09 European Commission.nih. Richter CA. Belgium.pdf . Koh WS. Pyo MY.113(4):391-395. K.

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

140-66-9 General Information 4-tert-Octyphenol.60) 613 652 1092 Limit of detection (LOD.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.30 (1.50) 1.10 (1. 1995. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60-3.50 (1.299-. and emulsifiers. In the 1990s.500-1. impaired steroidogenesis. 2004). During the 1980s and 1990s.80) 2. see Data Analysis section) for Survey year 03-04 is 0..600-1. testicular atrophy.20) 2.30-2.300 (<LOD-. altered neonatal sexual development.20-2. 1997.600) 1..900 (. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.40) * 03-04 03-04 03-04 .500-1.500) 75th .500 (.600) .274-.600-1.10 (..g.5% of 139 U. 4-octylphenol monoethoxylate was detected in 43.000 tons of alkylphenol ethoxylates were produced annually worldwide. through sewage. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).... 2002). Indoor and to a lesser extent.10 (.90) 2. population from the National Health and Nutrition Examination Survey.00) 1229 1288 03-04 03-04 03-04 * . outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.500) .20-2.g.300 (<LOD-.300-. Bian et al.. Saito et al..60) .30) 1.600-1.10) 2. In rats.40) 1.20) 1.70 (1.700-1.2.. 2003.400 (.500) .497) * .60-3. orally administered 4-tert-octylphenol was well absorbed. and impaired spermatogenesis (e.70 (1.800-1.60-3.50-2.20-2.50) 1.200-.20-2. and the polyethoxy chain may consist of up to 50 ethoxy units.900 (.600) .00 (.30) 2. and was quickly eliminated from the blood (Certa et al.80 (1. leading to inhalation as another potential exposure route (Rudel et al. an alkylphenol.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.600) .50-3.300 (<LOD-. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.600-1. Survey Geometric mean (95% conf.20-2. 2000.300 (<LOD-. streams in 30 states (Kolpin et al.00 (1.500) . 1996). altered estrus cycles and reproductive outcomes.30 (1. Laws et al. 2002).70 (1. Several alkylphenols.40) 2. textiles. industrial cleaners.600-1.S. 2006. to shorter chain alkylphenol ethoxylates. pesticides. which are anionic surfactants used in detergents.30) 90th 1.357 (. is used to manufacture alkylphenol ethoxylates.900 (. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.40) 1.60-3. which may vary for some chemicals by year and by individual sample. and some personal care products.60-3. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.20 (1. and some of their degradation products are toxic to aquatic life.70 (1. and to alkylphenoxycarboxylates.20-2.30 (1.60-3.20) 314 715 1488 03-04 03-04 * * .400) 1. and through manufacturing waste streams (Warhurst.369 (.40 (1. including 4-tert-octylphenol. Blake and Boockfor.00 (.50) . In 1999-2000.20) 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 .S. did not bioaccumulate.50) .1.400 (.900 (.Environmental Phenols 4-tert-Octylphenol CAS No. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.900 (. 2000.80 (1.389 (.300 (<LOD-. Katsuda et al.477) .40) 2.80 (1.60) 1.90) 2.200-. Ying et al.300-.10-2.30 (. have demonstrated estrogenic effects particularly when injected at high doses in animals. The alkylphenol ethoxylates enter the environment through human use of products containing them.30 (1. Less frequently. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.10) 1. < LOD means less than the limit of detection.507) * < LOD . Urinary 4-tert-Octylphenol (4-[1. 34 Fourth National Report on Human Exposure to Environmental Chemicals . fish) and drinking water. and from contact with some personal care products and detergents. The alkylphenols can bioaccumulate in some fish. Disposition in humans has not been studied sufficiently. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. the various alkylphenols have also been used as emulsifiers and modifiers in paints.50) 1.400 (.268-.3. over 500.600-1. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.

530) .67-2. Tyl et al. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.03 (1.96-4.00) 1.570) .450) .890-2.410 (. 2003.85 (1.620-1..400) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. In a small number of adult Japanese volunteers.02-4.73) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.337-.68-2.3.11-2. 1999).270 (. 2001.S.770 (.320 (<LOD-.S.640-1.31-2. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.43) 1.270 (.03-6. 2001). Survey Geometric mean (95% conf.54) * 03-04 03-04 03-04 . 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.43-3.29) 2.78) 3.00 (.470-1.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .36-3.420) .62 (1.10-2.05-2.25) 90th 1.22) . 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.68) 2.550-1.33 (2. Fourth National Report on Human Exposure to Environmental Chemicals 35 . Kawaguchi et al.06 (2.71) 2. nonylphenol. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. at lower or environmentally relevant doses (Blake et al...435 (.910 (.31 (1. or their corresponding ethoxylates with respect to human carcinogenicity.00 (.43) 1. Yoshida et al.18-4.260 (<LOD-.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.276 (.25-2.610) .860 (.300 (<LOD-.78 (1.14) 314 713 1487 03-04 03-04 * * .380 (<LOD-.25) 2. Nagao et al.50 (2..470) 75th . Calafat et al. 2000.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.1.17 (. population from the National Health and Nutrition Examination Survey.11) 2.53-3.41) .620) .630-1.40 (1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.160-.270-.40-4.500-1. 2004.81 (1. representative subsample of NHANES 2003-2004.. 2005. It is unclear if estrogenic or other effects occur in animals through oral dosing.Environmental Phenols Myllymaki et al.540-1. 4-tert-Octylphenol is not considered directly genotoxic. 2004).65-3.76 (2.207-.20 (1.64 (.269 (.280-.00) 2.850 (..740 (.59) 1. Urinary 4-tert-Octylphenol (4-[1.370 (<LOD-.11) 1.62 (1.460 (.15) 1.78) 1228 1286 03-04 03-04 03-04 * .03 (1.384) * .560) .33) 3.59 (1.170-. Sweeney et al.199-.60 (1.450) 1.730-1.470-1.740 (.00) 2.08) 1. IARC and NTP have not rated octylphenol.62) .349) * < LOD .

Yoshida M. 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. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Two-generation reproduction study with para-tert-octylphenol in rats. Raychoudhury SS. Environ Sci Technol 2002. Bodman GJ. Thurman EM. Taya K. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental fate of alkylphenols and alkylphenol ethoxylates--a review.37(20):4543-53. Yoshimura S. Reprod Toxicol 2001. bisphenol A and methoxychlor in rats. Seely JC. and testosterone.54(1):154-167. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Carey SA. Wong LY. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Qian J. Watanabe G. Usumi K. 2003. Nicol L. Reprod Toxicol 2004. Watanabe G. polybrominated diphenyl ethers.co. Katsuda S. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Chen J. Izumi S. Inoue K. Bolt HM. Kolpin DW. Toxicol Sci 2000. Paranko J. 2/4/09 Ying GG. Camann DE. Inoue K. Xu L. Seto H. Anal Chim Acta 486:41-50.799(1):119-125. An environmental assessment of alkylphenol ethoxylates and alkylphenols.44(8):1355-1361. Takenaka A. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats.S. 1999-2000: a national reconnaissance.165(3):217-226. Sweeney T. Takai N.57(2):255-266. alkylphenols. Exposure of the U.uk/resource/reports/ethoxylates_alkylphenols. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Onuki A. Brine DR.121(1):21-33. Kookana R. Environ Sci Technol 2003.15(6):683-692. Kawaguchi M. prolactin. Reidy JA. Biol Reprod 1997. Myllymaki SA. Wiegand HJ. Blake CA. Roche JF. Marr MC. Makino T. Furlong ET. Phthalates.foe. Toxicol Appl Pharmacol 2000. Fail PA. Katsuda S. Saito I. and other organic wastewater contaminants in U. Brooks AN. streams.207(1):59-68. Environ Health Perspect 2008. Nakagomi M. Saito Y. et al. et al. Horie M. Haavisto TE. Williams B. Millette CF. Tyl RW. Wang X. Yoshida M.36(6):1202-1211. Nagao T. et al. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Brody JG. et al. Barber LB. Food Chem Toxicol 2006. Warhurst AM. Endocrinology 2000. Nair-Menon JU. Yoshimura Y. Taya K. pesticides.116(1):39-44.18(1):43-51. hormones. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Maekawa A. Toxicol Appl Pharmacol 2005. and other endocrine-disrupting compounds in indoor air and dust. Meyer MT. Ye X. Maekawa A. Fedtke N.30(2 Pt 1):81-95. Needham LL. Spengler JD. McCoy GL. Ferrell JM. Okada F. Cooper RL. and sertoli cell number. Environ Int 2002. Kawaguchi M. Arch Toxicol 1996. Korn LR. Regul Toxicol Pharmacol 1999. Certa H. Estrogenic activity of octylphenol.Environmental Phenols References Bian Q. Boockfor FR. Pharmaceuticals. Myers CB. Zaugg SD. Song L. Calafat AM.141(7):2667-2673. Blake CA. Boockfor FR. Available at URL: http:// www. 1995. Ito R.pdf. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Toxicokinetics of p-tert-octylphenol in male Wistar rats.28(3):215-226. testis size. Indoor air pollution by alkylphenols in Tokyo. Muller AM. Indoor Air 2004. Laws SC. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.folliclestimulating hormone.14(5):325-332. Sakui N.S. Ono H. Toppari J. Toxicol Lett 2001. Rudel RA.71(1-2):112-122. nonylphenol. Karjalainen M.

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

5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.2 (13.94 (7.50) 10.4) 25. population from the National Health and Nutrition Examination Survey.21 (6.6) 12.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.8 (21.4) 357 (225-456) 203 (87.4 (32.4) 7.20-11. Survey Geometric mean (95% conf.93 (7. population from the National Health and Nutrition Examination Survey.8) 7.9 (11.8-60.4.3-31.7) 292 (151-432) 132 (78.5) 13.2-58.3 (8.4-19.2-46.S.45 (5.0-15.1 (8.1) 50.0) 65.55 (4.29-12.0 (8. Survey Geometric mean (95% conf.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 .1) 9.4-18.54 (8.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.00 (4.3 (26.1) 14.1) 9.2) 13.90-10.2 (10.6-15.0-15.2 (27.9-61.6) 10.32-14.3) 6.4) 90th 249 (188-304) 03-04 03-04 03-04 8.7 (9.3) 47.38-18.6-20.1) 13.2 (25.45-10.4.70-16.2 (11.9) 8.50-10.5-86.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.1) 7.48-10.80 (5.7) 123 (36.9-236) 193 (90.82 (8.4) 73.5) 11.8) 14.0 (34.0) 49.S. Urinary Triclosan (2.9 (33.5-14.20 (7.8) 116 (39.0-73.43-13.0 (36.8-85.60 (8.6) 90th 212 (172-241) 03-04 03-04 03-04 9.92-12.0 (11.1) 9.2-14.6-111) 33.74 (5.22-10.20 (7.9) 32.18 (5.20-13.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.2 (37.4 (11.7 (11.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 39.11-11.3.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.3-67.9) 75th 47.7 (14.40-17.0) 9.10-9.6-65. see Data Analysis section) for Survey year 03-04 is 2.3-35.3 (11.7 (28.48 (8.3) 10.Environmental Phenols Urinary Triclosan (2. interval) 12.6 (9.00-8.1-39.7) 10.4) 317 (231-433) 144 (96.6 (12.5 (11.16 (6.6-14.9 (50.6) 31.10) 84. interval) 13.60 (6.6 (10.40-11.30-14.5) 20.3-15.1) 9.6-37.5) 66.4 (12.2) 9.89-11.9) 7.8-112) 30.1) 11.6-14.8) 9.2-58.8-63.7 (39.4) 51.45-13.3 (9.0 (26.86-12.1 (45.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.6 (30.2) 12.8-127) 37.4) 75th 43.1 (15.0-19.4 (38.9 (8.20-10.72-13.

Arch Environ Contam Toxicol 1988. Erratum in: Aquat Toxicol 2007.24(3):209-218. Benson WH. Chemosphere 2007. et al. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Photolytic degradation of triclosan in freshwater and seawater. Food Chem Toxicol 2000. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.7/2. hormones. Br J Clin Pharmacol 1987.83(1):84. Environ Health Perspect 2008. Biol Pharm Bull 2005. Nagao Y. Ye X. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Foran CM.4’-trichloro-2’hydroxydiphenyl ether). Reidy JA. Calafat AM. Aquat Toxicol 2006.Environmental Phenols References Aiello AE. et al.38(2):64-71.36(6):1202-1211. Windham G. J Invest Dermatol 1976.69(20):1861-1873. Needham LL. 4.S. Matsumura N. Osachoff H. Bodey GP. Adolfsson-Erici M.67(4):532-537. Sandborgh-Englund G. Williams FM. Williams PE. Meyer MT. Lyman FL. Percutaneous penetration and dermal metabolism of triclosan (2. Developmental evaluation of a potential non-steroidal estrogen: triclosan.115:116-121. et al.. J Toxicol Environ Health A 2006. Skirrow RC. Moss T. Environ Sci Technol 2002. Ogawa H. Pinney SM. Teitelbaum SL. Ferrer I. 4’-trichloro-2’-hydroxydiphenyl ether. Zaugg SD. Furia T. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Larson EL.80(3):217-227. Wigmore H. IMS Ind Med Surg 1969. Ebersole R. and phenols in girls. Ishibashi H. 1999-2000: a national reconnaissance. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Veldhoen N. Kaneshima H. Bennett ER.S. Evidence of 2.4. Odham G. Triclosan: applications and safety. population: 2003-2004. Hong HC. Aranami K. Am J Infect Control 1996. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Environ Health Perspect 2007. Toxicology of 2.28(9):1748-1751. Wolff MS. et al.524:241-247. Fernandez-Alba AR. streams. Pilot study of urinary biomarkers of phytoestrogens. Urinary concentrations of triclosan in the U. Watanabe N.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Gomez MJ. Kolpin DW.50(1-5):153-156. Hirano M. Mezcua M. Bhargava HN. Clapson DJ. Readman JW. Howes D.23(5):579-583. Hernando MD. Barber LB. Shiratsuchi H. Ekstrand J.17(5):637-644. Thurman EM.38(4):361370. Levy SB.66:1052-1056. Pharmacokinetics of triclosan following oral ingestion in humans. Katsura E. Furlong ET. Kanetoshi A. Pharmaceuticals. Gilbert RJ. Chelimo C. Okui T. Aguera A. Britton JA. and other organic wastewater contaminants in U. The oral retention and antiplaque efficacy of triclosan in human volunteers. Mar Environ Res 2000. Anal Chim Acta 1004. Gunderson MP. Wong LY. phthalates.116(3):303-307. Leonard PA.45 Suppl 2:S137-S147.

Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. utility poles and fence posts).73 (1. hypertension.90) 1.350 (. Since 1984.350 (. Survey Geometric mean (95% conf.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350) < LOD .350 (. 1997).590-1.350) < LOD .350-.23 (.37) .78) 1.350) < LOD .350-.94 (1.350 (. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.510-3.350-1.350-.680-1. algaecide and insecticide. and metabolic acidosis were observed in CAS No.42) 696 680 521 696 603 951 Limit of detection (LOD.67) 1.350-1.350-2.10) 1.350) < LOD . so it is relatively non-persistent. After absorption.18 (<LOD-1.350) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. and it is used primarily as a preservative for wood to be used outdoors (e. 1979).350-.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350-.00 (.390 (.350 (.30) 1. PCP is distributed to most tissues and is not extensively metabolized.76) 1.350 (. After a single dose.480-2.350 (.10) 1.350 (.350) < LOD .350-.350-.660 (.91 (1. water and sediments because of the large amounts that were produced and used historically. bactericide. are eliminated in the urine. and dermal contact with PCP-treated products.60) 1.350) < LOD .S.350 (. plants. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.990 (<LOD-2. 1986).64) 1.10 (.83 (2.S..90 (1. along with small amounts of tetrachlorohydroquinone and conjugates.350-2.90) 2.30 (. To-Figueras et al.630 (.510-5.350-.350 (. PCP has been detected in soils.390 (.01 (<LOD-1.32 (.98 (1.00) 1.350-.50) 1.48-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350-1.76) . ingestion of contaminated food or water.62 (.60) 1.350-2.00) 1.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th . General population exposure to PCP may occur by inhalation of contaminated air.33-2.350-.10 (<LOD-1.350-. 40 Fourth National Report on Human Exposure to Environmental Chemicals .04) 1.58-2.350) < LOD .650 (. the elimination half-life may be a week or more (Uhl et al.08-3.860-2.70) 2. Kohli et al.30) 1. herbicide.58-2.09) .75) 2.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .47-3.990-2.350) < LOD .350 (.350 (.350-1.350 (.g.80) .350-.350) < LOD .350) < LOD < LOD 75th .350 (. air. Acute.350) < LOD .350) 90th .350) < LOD . other polychlorinated benzenes.30 (1..53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . 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.37 (.65 (.350-2. population from the National Health and Nutrition Examination Survey.650) 1. 1976.51) 1.48 (. which may vary for some chemicals by year and by individual sample.00) 2.33) . < LOD means less than the limit of detection.350 (.350) < LOD .980 (. PCP is eliminated over a few days (Braun et al. Effects including hyperthermia.350 (.350-.350-.350) . Human exposure to PCP has become less common.350 (.350 (.770 (.350) < LOD .65 (.350-.350-.350-.350 (.94 (1.500-2.350-2. and animals. mollusicide.960) 1. The parent compound and conjugates..530) 1. PCP use in the U.70) .350) < LOD .890-1.25 and 0.30) .10 (1.890 (. PCP is absorbed rapidly and well by all exposure routes.45-2.350 (.850-2. with repeated or chronic exposure.5.350-.54-2.350-..350-.350 (.47-5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 2002. PCP is degraded by sunlight and metabolized rapidly by microorganisms. In the environment.40 (.350-.350-. and possibly of lindane (IPCS. has been restricted.30 (. PCP cannot be used on wood in residential or agricultural buildings. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350) < LOD .

780-1.34 (.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . OSHA has established an occupational standard.630 (.910-1.67 (1.320) < LOD < LOD 75th .800-1.350) < LOD .990 (.560) < LOD .67 (1.10-2. and adversely affected thyroid function (U.26 (1.06 (.94 (1.470 (.40) 1. Pentachlorophenol is not mutagenic or teratogenic.400 (.320 (.25-1.580-.09 (<LOD-2.epa.220-.340-.25-2.300 (.920 (.290) < LOD .57 (1.330-. 1989). 2004.html.25-2.25 (1.500-.gov/ pesticides/ and from ATSDR at: http://www. EPA at: http://www.82) 1. 2003).380-. 2000). the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. inhalation. 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.16-1.00-1.6 and 14.500 (.590) < LOD . 1989).67 (1.79) 1.700-2.83 (1.290-.760 (.92) 1.94 (1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al. 2003).950-1. and the FDA has established a standard for bottled water. 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.67 (1.S.250 (.11) 2.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.310-.e.21-2.40) 1..430-.52 (<LOD-1.30) 1..S.40) 1. In a small sample of U.48-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.260 (.360 (.cdc.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 .300 (.26 (1.35) 1.29-3.19) 2.52 (<LOD-1.250 (.510-. Death can result from seizures and cardiovascular collapse. 1995).S.S.67 (1. environmental levels) and health effects is available from the U.75 (<LOD-2.94-3. population from the National Health and Nutrition Examination Survey.84 (1..84) 1.500-1.atsdr.19 (1.40) 1.08 and 5. 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.67-3.13 (.51) 1.06-3.830) < LOD .69 (1.18 (1.35-2.9 mg/L.590-1.00) 1. Survey Geometric mean (95% conf..40) 1.300 (.320) < LOD .850 (.52) 1.18) .560-.360-..16 (.730) < LOD .800) < LOD 1. respectively) (Seifert et al.67-2.06) 1.900-1. Among adults in the NHANES 1999-2000 subsample.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .240-.35) 1.370 (.21 (.35-2.90) 1.00-1.19) 2. EPA has developed standards for PCP in drinking water and the environment. van Raaij et al.650 (.25) 1. chronically administered high doses of PCP were hepatotoxic.420) < LOD .780) < LOD .55) 1.82 (1.36) .55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .430) < LOD .950-1.95) 3.570 (.0 mg/L..25 (1.560) < LOD . respectively) (Becker et al.40-2. 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.10 (1.67-3.220-. or skin absorption.gov/ toxpro2.290-.490) < LOD .710-1. In NHANES 2001-2002 subsamples.440 (.84-4. More information about external exposure (i.510-.270-.270-.78) 1. children in the 1980’s.610 (.Fungicides adults and children severely exposed to PCP through ingestion.280) < LOD .52 (1.30-2.30) 1. carcinogenic. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.73 (1.650) 90th 1.EPA. 1991).75) 1. The U..30 (..56) 1. In animals. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.19) 2.650 (.950-1.09-1.320) < LOD .78) 1.310) < LOD .S.57 (. Fourth National Report on Human Exposure to Environmental Chemicals 41 .

Seiwert M. available at URL: http://www. Jones D.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Arch Environ Contam Toxicol 1989. Bailey SL. et al. Becker K. van den Berg KJ. PCP: Human Risk Characterization [online]. Otero R. EPA). 11/30/2004. Pharmacokinetics of pentachlorophenol in man. Shealy DB. Environmental Protection Agency (U. et al. Needham LL. Notten WR.inchem. et al. house dust.S. 42 Fourth National Report on Human Exposure to Environmental Chemicals . urine. Kaus S. Schulz C.4:289296. Blau GE. Needham LL. 4/21/09 Kohli J. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Head SL. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. 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. International Programme on Chemical Safety (IPCS). Gregg M.71:99108. Hill RH Jr. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Engel R. Dev Toxicol Environ Sci 1979.54(3):203-208. Toxicology 1991: 67(1):107-16. Schulz C.org/documents/jmpr/jmpmono/2002pr08. 206:15-24. Environ Health Perspect 1997. Smith SJ. Safe A. Baker S. Can J Biochem 1976. Available at URL: h t t p : / / w w w. Schmid P. Int J Hyg Environ Health 2003. Fast DM. U. Santiago-Silva M. 4/21/09 van Raaij JA. To T. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 2002.18(4):469-474. Schlatter C. Phillips DL. drinking water and indoor air. J Expo Anal Environ Epidemiol 2000. htm. Krause C. Seifert B.10:552-65. Pesticide residues in urine of adults living in the United States: reference range concentrations.58:182-186. Rodamilans M. Uhl S. Cline RE. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Environ Res 1995. To-Figueras J. 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. Seifert B.18:475-481. Barrot C. Hill RH.105(1):78-83. References Becker K. Bragt PC. Braun WH. Arch Environ Contam Toxicol 1989. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Sala M. The metabolism of higher chlorinated benzene isomers. Chenoweth MB. Seiwert M. Arch Toxicol 1986. Lindane. Helm D. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. hair. Holler JS. Hill RH Jr. r e g u l a t i o n s .S. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood.

890 (.970 (. SOPP is applied topically to the crop and then rinsed off.50) < LOD . Both chemicals degrade within hours to weeks in the environment (U. 1998.3 and 0.09) 2. fungicides.370-. 2006).389-.560-8.00 (1. Most agricultural food applications have been revoked.20 (. In the past.40-2. leaving the chemical residue OPP.370-.80) 1. Chronic dosing in animals resulted in such systemic effects as weight loss and Urinary ortho-Phenylphenol Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. on ornamental plants and turfs. and it has limited water solubility.27 (. OPP is still used as a disinfectant fungicide for industrial applications.570 (.90) .389-.621) * .830 (.390-.600-1. are antimicrobial agents used as bacteriostats.836) * .770 (.508 (.50) < LOD .600) < LOD . but OPP and SOPP are still used on pears and citrus (U.540-2.10-2.493 (.10) .40-5.490 (<LOD-.50) .90 (1.60 (1. 90-43-7 General Information Ortho-phenylphenol (OPP.90 (1.520 (.20-3. and sanitizers. in paints.670) 2.386-.645) * .90) .610 (.23) 695 680 520 695 603 953 Limit of detection (LOD.02) 1.636) * .950) < LOD .890 (.30) < LOD .470 (<LOD-.880-2.770 (.00 (1.480-1.88) 1.550-1.790) 2.85) 2.50-2.00) < LOD . and as a wood preservative.10 (1.30) < LOD 90th 1.EPA.20 (1.17 (.509 (.50 (1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.50-3.570-2.10) 1.3.402-.00 (1. or 2-phenylphenol) and its water-soluble salt.580-1.10) .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 . small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.630) < LOD . 1998).450 (<LOD-.Fungicides ortho-Phenylphenol CAS No.80-3.80) 1.60-3.50) 1. Fourth National Report on Human Exposure to Environmental Chemicals 43 .690-1.30-7. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.760-2.80 (2.800-3. General population exposure can occur via dermal.60 (1.710-2.690) < LOD . OPP is considered to be moderately toxic after acute oral doses in animal studies.00 (1. Timchalk et al. Estimated human intakes have been below recommended intake limits (U.490 (<LOD-.07 (..350-1.433-.22) 2.20 (1.640) < LOD .92 (.570-1. inhalational.40-7. interval) .19 (.490 (<LOD-.50 (1.28-3. Survey Geometric mean (95% conf.00) . population from the National Health and Nutrition Examination Survey. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.750-2.22 (.696) * . < LOD means less than the limit of detection. 2006). Both have been used in agriculture to control fungal and bacterial growth on stored crops.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.S. it was used in home sanitizers for surfaces.60 (1.50) < LOD .638) * .20) < LOD 1.364-.10) .40 (.76) 1. however.90) 2.420 (<LOD-.28 (.600-1.90) 1.600-1.61) 2.30) 1. whereas SOPP is not volatile and is more water soluble. EPA.466 (.10) 2. 2006).30-2.34) 1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.20-2.20) < LOD 2.S.EPA.349-. 2002.820 (. sodium ortho-phenylphenate (SOPP).410-.33 (.50 (1.600) < LOD .10) 1.00) .03) 1.610-1. OPP is volatile.710) 3.S.850 (.567 (.450 (<LOD-.570 (.552 (.60-2.20) 2. or apply these chemicals may be more highly exposed than the general population. Available evidence suggests that OPP does not accumulate in the body.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .30 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10-1. 2006).840-1.860 (.740 (.600) < LOD 1.490 (<LOD-.40-5.500-2.497 (.370-.780) < LOD .490 (<LOD-.S..14 (<LOD-3.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .450 (<LOD-.. 1989).590-2. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.496 (. such as fruits and vegetables.10 (1.570-. Workers who manufacture. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .30) < LOD 1.930 (.50-4. formulate.890) 1.624) * .742) * . Cnubben et al.00-2.498 (.600) < LOD 75th . which may vary for some chemicals by year and by individual sample.

by possible genotoxic mechanisms (Hagiwara et al. Smith et al.32) 3.17 (.403-.08) 1.500) < 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. reproductive.650-1.950) < LOD . 1999.420 (<LOD-. Brusick.508) * .96-4. 1997.750 (.gov/pesticides/. Murata et al.21 (.96 (1.510-.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .26) 1. 2000.11) < LOD 90th 1.74 (1.420 (<LOD-.18) 2.07) 2.329-.17) 2.epa.. In high dose animal studies.473) * . interval) .53) 1.61 (2.900) < LOD .484) * . U.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .00 (.52 (. 1993.84 (1.29) 1. 2002). IARC has classified SOPP as a possible human carcinogen.670 (. or developmental toxicity was observed (Bomhard et al.59) .860 (.750 (.514 (.88-4. less likely. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. and it has classified OPP as not classifiable with respect to human carcinogenicity.970) 1.97 (2. Additional information is available from U.24-2.EPA at: http:// www.05-2.440 (.28 (2. U.690 (.291-. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.656) * .51-3.38) 2.93) .410 (<LOD-.560) < LOD 75th .900-1.09-3.11 (.86 (1.590) * . population from the National Health and Nutrition Examination Survey.27) < LOD .620-1.21) 1.. 44 Fourth National Report on Human Exposure to Environmental Chemicals .780 (.02 (. 1998.S.840 (.470) < LOD .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.570) < LOD 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.670 (.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.EPA 2006).EPA 2006).496 (.01) 1.06-4. 1986).43-2.06-5. 1984. Ito et al.980 (.43 (1.32) 1.62) .89 (1.810-1.09 (1.353-..910-1.20) < LOD 3. Survey Geometric mean (95% conf. 2005.91 (1. Pathak and Roy.06 (1.343 (.780-14.320 (<LOD-.12-2.670) < LOD . or..44 (1. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.444 (.09-6.480-.43-2.550 (. OPP was not found to be mutagenic.910 (<LOD-1.24-2.S. 1984.75 (1.69 (1.301-.0) 1.360 (<LOD-.550-.43) 3. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. 2005)..550) < LOD .38) 1.Fungicides anemia. Kwok et al.61 (1.93 (1.385 (.311-.580-1. Zhao et al. 2005). Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. Nakagawa et al.93) .770-2..940-2.47) .11-1..560-2. 1992. 1999.64 (2.248-..00 (1.81) 1.17 (.12) < LOD 1.08-2.380 (.. Biomonitoring Information Urinary OPP levels reflect recent exposure.568) * .980 (<LOD-1.75 (1.21-2.460-.800-1. leading to production of two metabolites. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. 2002.791) * .96) 1.93) 1. Detectable levels were seen in over half the U.11) 4.58) 2.61 (.11 (.08-1. Volunteers exposed to 0.4) 3.510 (<LOD-.33-2.455-.410 (<LOD-.610) < LOD 1.453 (.25-6.640-1.470 (<LOD-.33) .31) < LOD .33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .13) 1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.78 (2. but no neurologic.860 (.04-4.S.750-2.620-1. Bomhard et al.666) * .28 (<LOD-4.40-13.810) < LOD .990) < LOD . CDC.46) < LOD 1.880-1..558) Selected percentiles ( 95% confidence interval) Sample 95th 2.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .38-3.600-1.361-.29) 1.580) < LOD .910 (.382 (. 2002.S.59) 1.270-.96 (1.

J Chromatogr B Biomed Sci Appl 1997.32(6):551-625. Bartels MJ. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. U. Bomhard EM. J Agric Food Chem 2002. Timchalk C. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Pathak DN.74(2):61-71. July 28. Sangha G. Fukushima S. Tayama S. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. van de Sandt JJ.286(2):309-319. food additives and natural products as promoters in rat urinary bladder carcinogenesis. 2006. Bormett GA. Coelhan M. Fourth National Report on Human Exposure to Environmental Chemicals 45 .gov/ntp/htdocs/LT_ rpts/tr301. EPA 739 R-06004. Hagiwara A. Fukushima S. Sangha GK. Xenobiotica 1998.20(5):851-857.45(5):460-481. Bartels MJ. Hagiwara A. Available at URL: http://www. Eastmond DA. Christenson WR. McNett DA.28(6):579594. The carcinogenicity of the biocide ortho-phenylphenol. 2005. Ito N. rat and man. Identification of SARA compounds in adipose tissue. Selim S. National Toxicology Program (NTP). Roy D. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Arch Toxicol 2000. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.S.Fungicides References Appel KE. Freyberger A.. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Mutat Res 1993. Eadon G. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Shirai T. Hirose M. Gierthy J. Murata M. Hum Exp Toxicol 1998. Shibata M. Christenson WR. Glas K. Leser KH. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Bromig KH. Toxicol Appl Pharmacol 1998. 1989. Stanley JS. Biochem Pharmacol 1992. Imaida K.gov/oppsrrd1/REDs/ phenylphenol_red. Smith RA. Mendrala AL. EPA-560/5-89-003.150(2):402-413.43(7):14311437.35(2 Pt 1):198-208. Vogel JS. EPA). Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Hakkert BC. Environ Mol Mutagen 2005.S. Richter M.159(1):18-24. Moriya K. March 1986.nih.pdf. 90-43-7) in Swiss CD-1 mice (dermal studies).S.niehs.(56):399-407. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Narang A. U. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). Carcinogenesis 1999. Bartels MJ. Brzak KA. Centers for Disease Control and Prevention (CDC). J Agric Food Chem 2006. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Brendler-Schwaab SY. Arnold LL. Moore GA. Nakagawa Y. Kawanishi S. Office of Toxic Substances. Cano M. Meuling WJ. Buchholz BA.50(11):3351-3358. et al. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Crit Rev Toxicol 2002. Zhao S. Drugs.54(16):5731-5735. Comparative metabolism of orthophenylphenol in mouse. Regul Toxicol Pharmacol 2002.epa. Inoue S. Ito N. Herbold BA. Kwok ES. 4/13/09 Onstot JD. Elliott GR. Environmental Protection Agency (U. et al.S. St John MK. Toxicol Appl Pharmacol 1999. Food Chem Toxicol 1984. 4/9/09.703(12):97-104. Turteltaub KW. IARC Sci Publ 1984.EPA). Environmental Protection Agency (U. Moldeus P. Available at URL: http://ntp. Cnubben NH. Bartels MJ.22(10):809-814. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Timchalk C.17(8):411-417. Brusick D. Roberts AL.pdf.

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

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

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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 01-02 is 0.S. 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.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1. 48 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. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. < LOD means less than the limit of detection.

sulfonamide. Whyatt RM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Olsson AO. Hladik ML. Deddens JA. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.111(5):749-756. EPA). Sci Total Environ 2000.108(12):1151-1157. EPA). pages 3682-3690.248(2-3):115-122. Environ Sci Technol 2005. Federal Register: January 24. Furlong ET. Feil VJ. Dialkylquinonimines validated as in vivo metabolites of alachlor. and metolachlor herbicides in rats. Barr DB.24(10):1003-1012. et al. J Expo Anal Environ Epidemiol 2005.pdf. Battaglin WA. epa. J Expo Sci Environ Epidemiol 2007. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Larsen GL. Ward EM. Environmental Protection Agency (U.15(6):500-508. reservoirs and ground water in the Midwestern United States. acetochlor. imidazolinone. Casida JE. Hodgson E. Volume 65. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.html. Barr JR. Barr DB. Jefferies PR. Burkhardt MR. Acetochlor (Harness) Pesticide Petition Filing 1/00. Centers for Disease Control and Prevention (CDC). Number 15. Thurman EM. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.S. Sanderson WT.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. 5/30/06. U. Kolpin DW.11(4):353359. Tinwell H.37(4):10881093. Alavanja MC. Atlanta (GA). Kier L. Wratten SJ.S. et al. Roberts AL.S. Green T.Herbicides References Ashby J. Linderman R. Environ Health Perspect 2003. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.15(9):702-735. Andrews HF.248(2-3):123-133. Feng PCC. Quistad GB. Environ Health Perspect 2000.S.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Lefevre PA. EPA 738-R-00-009. 5/30/06 U. Environmental Protection Agency (U. Linhart SM. Barr DB. Hein MJ. and other herbicides in rivers. Rose RL. Curwin BD. Davison KL.17(6):559-566. Hines CJ. Occurrence of sulfonylurea. Available at URL(non U. Hsiao JJ. Kinney PL. Chem Res Toxicol 1998. 1998. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.EPA): http://pmep. J Agri Food Chem 1989. Third National Report on Human Exposure to Environmental Chemicals. Reynolds SJ. Wilson AG.39(17):6561-6574. Available at URL: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 49 . March 2006. Camann DE. Striley CA. Bravo R. Heederik D. et al.S. Peter CJ.cce. Sci Total Environ 2000. Hum Exp Toxicol 1996. Comparative metabolism and elimination of acetanilide compounds by rat. 2005. Xenobiotica 1994. 2000. Coleman S.cornell.

U. 1997. and field workers. In animal studies. 1995). In chronic animal testing. Kolpin et al. WHO. 1999 and 2007. Estimated human intakes have been below recommended limits (U. Jefferies et al. mean values of urinary concentrations of alachlor metabolites. It is absorbed by plants and inhibits plant protein synthesis. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. 2005).. 1989. Hines et al. but not likely at low doses. 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. In a study of applicators and workers exposed to alachlor. the latter may account for some observed effects (Davison et al. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. 2005. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect.. Alachlor has a soil half-life of a few weeks. soybeans.. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Tessier and Clark.Herbicides Alachlor CAS No.. WHO. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. alachlor has demonstrated hepatotoxicity. IPCS.S. mercapturate conjugates were predominant metabolites. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. hemosiderosis. the dermal exposure route is potentially significant for applicators.. 2003). though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. 1996).2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. 2000.S. Hill et al. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al.S... alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. Alachlor itself is not considered mutagenic.gov/pesticides/.S. peanuts and other crops. 1996. 2003). stomach. but has not shown developmental or reproductive toxicity in mammalian systems (U. 1998. U.EPA.EPA. but another metabolic pathway can produce 2. Since the late 1980s alachlor use has been declining. 1998). U..S. formulators. as measured through conversion to deethylamine. In animals.EPA. 1998).EPA considers alachlor to be a probable human carcinogen at high doses. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. WHO. WHO. NTP and IARC do not have ratings regarding human carcinogenicity. (2003) showed that 2. including corn.EPA. 1994. 2000.1 to 1. corn cropland was treated with alachlor. Alachlor has low potential for acute toxicity. 1998). 1998. Feng and Wratten.EPA.. In 1993-1995.S.epa. and uveal degeneration. Hladik et al.S.6-diethylaniline and its reactive metabolite. 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. 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. 1999. U. USGS. Because it can be absorbed through skin. whereas 60% of applicators had detectable amounts.1 mg/L at various collection times (Sanderson et al. but shows little bioaccumulation. and on non-crop land for general weed control. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. about 20-25% of the U. 1996. 2003). ranged from 0. 50 Fourth National Report on Human Exposure to Environmental Chemicals .S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1995. 2003). 1998. EPA at: http://www. Additional information about is available from U.. 1988.

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

Heydens WF. Lau H.pdf. Circular 1291.43(25):2087-94. World Health Organization. Available at URL: http://www.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.S. and other herbicides in rivers. 2005. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Barr JR. Life Sci 1988. December 1998. Feil VJ.56(6):853-859. Quistad GB. 1999. et al. Xenobiotica 1994.Herbicides References Battaglin WA. who. 2/27/09 Jefferies PR. Biagini RE.htm. acetochlor. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Tessier DM. Casida JE. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Reregistration Eligibility Decision (RED) Alachlor. Gilliom RJ). Hladik ML. Camann DE.usgs. Brown MA. Kimmel EC. Shoemaker DA. Deddens JA. J Ag Food Chem 1995. Supplemental Technical Information (available on-line only). WHO/ FAO Data Sheets on Pesticides. Peter CJ. 2003. Andrews HF. revised February 15.int/water_sanitation_health/dwq/chemicals/en/alachlor. Hum Exp Toxicol. Shealy DB. Furlong ET. sulfonamide. Wratten SJ. Thelin GP. March 2006. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Barr DB. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor.43(9):2504-2512. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.gov/oppsrrd1/ REDs/0063. DNA adduct formation by alachlor metabolites.S. EPA). Sci Total Environ 2000. Kier LD. Environ Sci Technol 2005. 1996. Hill RH Jr. Clark JM. Hsiao JJ. 86.248(2-3):115-122.org/documents/pds/pds/pest86_e. Bull Environ Contam Toxicol 1996. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Sci Total Environ 2000. Occurrence of sulfonylurea. Mutat Res. Tolos W.18(6):363-391. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes.11(4):353359. Jefferies PR. Chem Res Toxicol 1998. Biagini R.44(18):1325.inchem. Available at URL: http://water. J Agri Food Chem 1989. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Kolpin DW.24(10):1003-1012.39(17):6561-6574. Hines CJ. Roberts AL. U. Henningsen G. Casida JE. Martens MA. imidazolinone. Sanderson WT. Background document for development of WHO Guidelines for Drinking-water Quality. Geological Survey (USGS).56(9):883-889. Geneva. Casida JE. Driskell WJ. California. Feng PCC. Striley CA. 1997. Burkhardt MR. Kolpin DW. Dialkylquinonimines validated as in vivo metabolites of alachlor. Kinney PL. Hill AB. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Available at URL: http:// www. Whyatt RM. 1998. 98-4245 (by Barbash JE. Sacramento. Geological Survey (USGS). Davison KL. Linhart SM. 2/27/09 U. Wilson AG.47(6):503-517. Hull RD. ALACHLOR. et al. No. Environ Health Perspect 2003.395(2-3):159-171.S. World Health Organization (WHO). Centers for Disease Control and Prevention (CDC).248(2-3):123-133. 2007. Comparative metabolism and elimination of acetanilide compounds by rat. EPA 738R-98-020. Environmental Protection Agency (U. Available at URL: http://www. Quistad GB. Third National Report on Human Exposure to Environmental Chemicals. Ann Occup Hyg 2003.pdf. Alachlor in Drinking-water. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.php. and metolachlor herbicides in rats. 1992-2001. Larsen GL. reservoirs and ground water in the Midwestern United States. 4/2/09 U. Erratum in: Life Sci 1989. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Atlanta (GA). International Programme on Chemical Safety (IPCS).epa.111(5):749-756. 1999.S. Hines CJ. Brown KK. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. MacKenzie B.37(4):10881093. Thurman EM. Am Ind Hyg Assoc J 1995. Thake DC.

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

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

Stuart AA. Cooper RL. Centers for Disease Control and Prevention (CDC). Wetzel LT. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 1996. Heederik D.76(1):190-200. Carr WC Jr. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. 2005.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. J Agric Food Chem 1982. Bersani M. Bradway DE. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Toxicol Lett 1993. Ann Occup Hyg 2003.58(2):366-376. Environ Health Perspect 2001. WHO/ FAO Data Sheets on Pesticides. World Health Organization. Eldridge JC. Toxicological profile for atrazine.atsdr.. Wetzel LT. Moseman RF. Agency for Toxic Substances and Disease Registry (ATSDR). Pest Manag Sci 2005. Grzywacz JG. Reynolds SJ. Gillis JH. Breckenridge CB. levels of atrazine mercapturate were generally not detectable (CDC.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Pfeifer KF. Striley CA. Barr DB. diamino-S-chlorotriazine and hydroxyatrazine. Toxicol Sci 2003.html. Lucas AD. Barr DB. 2001 [online]. Hein MJ. Laws SC. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Barr DB..99(8):5476-5480.htm. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. J Toxicol Environ Health 1994. Brown KK. Curwin BD. Biagini RE. In small studies of Maryland residents in 19951996 (MacIntosh et al. Stevens JT. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. et al. ATRAZINE. Cooper RL. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Gillis JH. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. 3/11/09 Arcury TA. Mendoza M. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Hines CJ. The geometric mean of urinary atrazine mercapturate was 1.gov/toxprofiles/tp153. Steroids 1999. et al.69(2):217-222.53(2):297-307. 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.. Environ Health Perspect 2007. Clayton CA. International Programme on Chemical Safety (IPCS). Quandt SA.. Aldous CN. McElroy WK. Sanborn JR. Ferrell JM. Toxicol Sci 2000. Seiber JN. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Hayes TB. Lee M. Biological monitoring of human exposure to atrazine. No. A risk assessment of atrazine use in California: human health and ecological aspects.47(6):503-517. Cooper RL. Eberly LE. Third National Report on Human Exposure to Environmental Chemicals. In a small number of field workers. Chen H. Catenacci G. Shoemaker DA. Barbieri F. Gammon DW.43(2):155-167. 2000). In a study of 60 farm worker children. Available at URL: http:// www. Toxicol Sci 2000..115(8):1254-1260. Sanderson WT. et al. 2007). 2001). 2003. References Adgate JL. J Toxicol Environ Health 1994. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Tapia J. Vonk A. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.30(2):244-247. Stoker TE.cdc. Deddens JA. Atlanta (GA). Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. In the NHANES 2001-2002 subsample. Saiz SG.109(6):583-590.inchem. et al. Fleenor-Heyser DG..43(2):155-167. Collins A. Ferioli A. Maroni M. 2005). 82. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Simpkins JW. Geneva. Stoker TE. Schmid J. Tyrey L. J Expo Anal Environ Epidemiol 2005.61(4):331-355. Lioy PJ. Eldridge JC. Stoker TE. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Noriega N. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. 3/11/09 Laws SC. Goodrow MH. Available at URL: http://www. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.. Blewett C. Proc Natl Acad Sci USA 2002. Ferrell JM. et al.64(9):672-678. Jones AD. atrazine was detected in only four children (Arcury et al. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Goldman JM. et al. Perry et al. Extrom PC. Freeman NC. 1993).15(6):500-508. Hermaphroditic. 2005).org/documents/pds/pds/pest82_e. Cottica D.

195(1):23-34.pdf. Singzoni B. 2007.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. White paper on potential developmental effects of atrazine on amphibians.pdf. Stoker TE. 6/1/09 U. Toxicology 1990.S. A review of epidemiologic studies of triazine herbicides and cancer. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.56(2):69-109. Sathiakumar N. Circular 1291. Environmental Protection Agency (U. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Timchalk C. Toxicol Sci 2002. Stevens JT. EPA). Pesticides and Toxic Substances. The Quality of Our Nation’s Waters. A risk characterization for atrazine: oncogenicity profile. A longitudinal investigation of selected pesticide metabolites in urine. Sanderson JT. revised February 15. Toxicol Appl Pharmacol 2004. Wetzel L. Hammerstrom KA. J Expo Anal Environ Epidemiol 1999. Lansbergen GW.gov/oppsrrd1/REDs/ atrazine_ired. van den Berg M. Ann Epidemiol 2000. Fenton SE. 3/11/09 U. Needham LL. Environmental Fate and Effects Division. Laws SC. Stoker TE. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. U. Interim Reregistration Eligibility Decision For Atrazine. Geological Survey (USGS). EPA Office of Pesticide Programs. Toxicol Sci 2000. Office of Prevention. MacIntosh DL. Washington (DC). Environmental Protection Agency (U. Toxicol Appl Pharmacol 2002.S. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Dryzga MD.usgs. Crit Rev Toxicol 1997. Wood C. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. March 2006.58(1):50-59. Guidici DL. Cooper RL.10(7):479. 0062. Supplemental Technical Information (available on-line only).epa.Herbicides development of a biomarker of exposure.S.9(5):494-501. Delzell E. Christiani D.S. Osborne DW. Cooper RL. Available at URL: http://water. Kastl PE.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.6(1):107-116. Case No.67(2):198-206. Dagenhart D.S. J Toxicol Environ Health A 1999. Perry M. Ryan PB. Chem Res Toxicol 1993. Boerma J. 1992-2001. Pesticides in the Nation’s Streams and Ground Water. Langvardt PW.php. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Laws SC. EPA). Rayner JL. Tortorelli J. Breckenridge CB.epa. 2003b. Guidici DL.182(1):44-54.27(6):599612. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Available at URL: http://www.61(1):27-40. Available at URL: http://www. May 2003a.

690 (. Human health effects from 2.4-D or exposed for prolonged periods.560-.S. 2005).27 (.4-D have been below recommended intake limits (U.66) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (<LOD-. with a half-life of several days to several weeks. At low levels. dizziness. Sauerhoff et al.43) 1.08) < LOD .370-. As much as 62 million pounds of 2.730 (. Kohli et al.320) 90th .410) < LOD . It is rarely detected in ground waters (USGS.Herbicides 2. but at higher levels they are herbicidal.07 (. It is not well absorbed through the skin.350) < LOD < LOD < LOD . General population exposure to 2. 1989.20 (.S.4-D has low acute toxicity. Similar to other chlorophenoxy herbicides.30 (<LOD-2. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. Once absorbed.952 and 0.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.210-.230 (<LOD-. 1977). Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.80) 1.4-dichlorophenoxyacetic acid (2..51 (1.560-1. 2. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 57 . 2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.S. 2007).21) 1.330 (.27 (1. It was first registered with U.4-D were used in the U.40) 1.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . and aquatic environments.660) 1. 1974.10 (<LOD-1.680-1. these herbicides can enhance plant growth. by direct contact with agricultural and residential areas after applications. Survey Geometric mean (95% conf.960-1. It is poorly bound in soils.24 (. the chlorophenoxy herbicide 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.610 (.230-. hypotension. nausea.48) < LOD 1.EPA in 1948. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. MCPA.400) < LOD .EPA. it acts as a plant growth hormone. population from the National Health and Nutrition Examination Survey. abdominal pain.10 (<LOD-1. headache.310) < LOD .4-D may occur during residential applications.910) 1.260 (<LOD-. in 2001 (U.490 (.760 (.250 (<LOD-.4-D can be applied either as an aqueous salt or as oil-soluble esters. myotonia.00-2.4-D is rapidly absorbed via oral and inhalation routes.420-. 2.930-1. 94-75-7 General Information Widely used throughout the United States.490) < LOD < LOD < LOD .S.16) < LOD .4-D) controls broadleaf weeds in residential. 2. and by consuming food or drinking water contaminated with 2.890) < LOD .420) < LOD . renal and hepatic injury.810-1.27-2.540-.740 (. agricultural.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250 (<LOD-.670-1..2. Recent estimates of chronic intakes of 2.930 (.310 (.03) 695 659 520 668 589 892 Limit of detection (LOD.4-Dichlorophenoxyacetic Acid CAS No.60) 1.32 (1.20 (<LOD-1.690 (. and mecoprop).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 .910) < LOD . < LOD means less than the limit of detection.690-1.EPA.13) < LOD .690 (. which may vary for some chemicals by year and by individual sample.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 4-D.55 (1.S.05-2.550-1.10) < LOD 1..440-1.70) 1.22) < LOD . and delayed Urinary 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.02-1.890 (.610-.

05) .340 (.S. 1996. 2. Post-application levels in farmers and home gardeners were dependent on Urinary 2. U. 1989). 2005.4-D in farmers were more than 25-fold higher than the 95th percentiles in the NHANES 1999-2000 and 2001-2002 subsamples (Arbuckle et al.780) .08 (.380 (<LOD-. U.560-.270-.930-1. U.73) .. or teratogenic effects in chronic rodent studies (Charles et al. liver. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.810-1.32 (<LOD-2. 2005. eyes.480 (.4-D reflect recent exposure.19) .790) < LOD . 1996. Survey Geometric mean (95% conf.410) 90th . population from the National Health and Nutrition Examination Survey. 2005).270 (<LOD-.980) < LOD 1. 2004).680) < LOD .13 (.4-D production plant workers and a few forestry workers spraying 2.41 (1.56) .560-. Epidemiological studies have reported associations of several types of cancer.4-D does not have significant reproductive.. In previous samples of the U. 2002.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.7.610-.670 (.590 (<LOD-1..410) < LOD 1. CDC. 1980.470) < LOD .620-.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.610-. IPCS. 2005).40) 695 659 520 667 589 892 < 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.590 (<LOD-1.08 (. Additional information is available from U.S.330-.4-D are eye irritants. Frank et al.S.700 (. 2005.340-. 2002. Average post-application urinary levels of 2. Pearce and McLean.4-D levels were detectable in less than a quarter of the individuals studied. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 1992).EPA 2005).920) < LOD 1.380-.550-.S.S.670 (<LOD-1.39) < LOD 1. IPCS. 1985.740 (. IOM.24) 1.440 (. 1994). IPCS. 2003.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Herbicides neuropathy (Bradberry et al. The acid and salt forms of 2.13 (.780-1.380) < LOD .08 (.27-1.16) 1.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .S. It is unclear whether these associations are related to the chlorophenoxy herbicides. Hill et al. 2006.660) < LOD . or to contaminants in the herbicide formulations (specifically 2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. and evidence of histological injury to the kidneys. 2005). Biomonitoring Information Urinary levels of 2.S.. Kutz et al. population (Hill et al.660 (. 2.. 2005. thyroid. Acute high doses administered to laboratory animals produced ataxia. 1995).890) < LOD 1.850) < LOD . 58 Fourth National Report on Human Exposure to Environmental Chemicals ..580-.890-1. Kolmodin-Hedman and Erne. urinary 2. Knopp et al.EPA at: http://www. adrenals and gonads (NTP.35) < LOD . 2001.380 (<LOD-.490 (..640 (.14 (.gov/pesticides/. 1996.820-1.. 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.EPA. myotonia.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 .780 (.520-.. 2005).390) < LOD < LOD < LOD . 2000).EPA. in small samples of children (Hill et al.810-1.17 (.410 (<LOD-.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert..4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1995. and of adults and children (Baker et al.670 (.350 (<LOD-.410) < LOD < LOD < LOD .720 (.990-1.570) < LOD .790) 1. other exposures.epa.3.EPA.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 2. developmental. U.

2006.nih.4-D). van Ravenzwaay B. Kolmodin-Hedman B. Fast DM.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. J Expo Anal Environ Epidemiol 2000. Beeson MD. general population.4-dichlorophenoxyacetic acid in man. 2005. Centers for Disease Control and Prevention (CDC). et al. Toxicol Sci 2001. Frank R. Finding a measurable amount of 2.php?record_id=10603..5-T).4-.31 Suppl 1:90-97. Ritter L. Xenobiotica 1974. Sirons G J. Brody D. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Beasley VR. Head SL. Needham LL. International Programme on Chemical Safety-INCHEM (IPCS).4:427-435. 914. Kutz FW. Holler JS. Arch Toxicol Suppl 1980.4-dichlorophenoxyacetic acid and its forms. Gregg M. Tables. Arnold EK.4-dichlorophenoxyacetic acid (2. Biomonitoring studies of 2.S. Carter-Pokras OD. Stephenson GR.nap. Chapman P. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Reynolds SJ. Bus JS. Cook BT.15(6):500-508. Available at URL: http:// www. TOX-63: TOXICITY REPORT CURVES. 2005. the amount of pesticide applied.37(2):277-291. Wilson RD. Acquavella JF. Kohli JD.niehs.4-dichlorophenoxyacetic acid (2. J Toxicol Environ Health 1992. Available at URL: http:// www.edu/catalog. 2.18(4):469-474. 2003. Environ Res 1995.31(2):121-125. Harris et al. 3/17/09 Knopp D.. Honeycutt R. Biomonitoring for farm families in the farm family exposure study. Cole DC. Gupta BN. Available at URL: http://ntp. Needham LL. geometric mean urinary levels of 2. Murphy RS. Arch Environ Contam Toxicol 1989. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Assessment of exposure to 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Driskell WJ.71(2):99-108. Selected pesticide residues and metabolites in urine from a survey of the U. Curwin BD.4:97-100. Sircar KP. Exposure of homeowners and bystanders to 2.htm.32(4):233-257. Hanley TR Jr.4-D) epidemiology and toxicology. Biomonitoring of herbicides in Ontario farm applicators. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Occup Environ Med 1994. the number of acres to which it was applied (Curwin et al. Scand J Work Environ Health 2005. Survival and Growth Curves from NTP Toxicity Studies. Absorption and excretion of 2. Ripley BD. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.31 Suppl 1:98-104. Barr DB. Scand J Work Environ Health 2005. Veterans and Agent Orange: update 2002. Estimation of occupational exposure to phenoxy acids (2. National Toxicology Program (NTP). Board on Health Promotion and Disease Prevention. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.60(1):121-131. Arch Environ Contam Toxicol 1985.4-D were highest in the farmers who applied the 2.Herbicides the time since application.4-D): exposure and urinary excretion. Updated March 7. Developmental toxicity studies in rats and rabbits on 2.10(6 Pt 2):789-798. Smith SJ. 1992).4-D. Baker BA. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.27(1):23-38. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Tandon JS.51(3):152-159. Barr DB. Hill RH Jr. Third National Report on Human Exposure to Environmental Chemicals. et al. Vet Hum Toxicol 1989.inchem. Harris SA. Mandel JS. Washington (DC): National Academies Press.4-D in urine does not mean that the level of the 2. Review of 2. Heederik D. Hill RH Jr.. J Expo Anal Environ Epidemiol 2005 Nov. Bailey SL.4-Dichlorophenoxyacetic Acid).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. Khanna RN. TOX-63 Peroxisone Project (2. Alexander BH. 2005). Mandel et al. Dichlorophenoxyacetic acid. To T.4-D will result in an adverse health effect. and the use of protective clothing or equipment (Arbuckle et al.4 dichlorophenoxyacetic acid (2. Solomon KR. Atlanta (GA). Pesticides residues in food: 1996 evaluations Part II Toxicology. In farm families. Baker S. Crit Rev Toxicol 2002. Dhar MM. Shealy DB.4:318-321. Forestry workers involved in aerial application of 2. Garabrant DH. Campbell RA. References Arbuckle TE. Philbert MA. Hein MJ. J Environ Sci Health B 1992. Baker SE. 2005 Charles JM. Erne K.4-D than levels found in the general population. 2005).4-D and 2. 3/17/09 Institute of Medicine (IOM). Sanderson WT.4.org/documents/jmpr/jmpmono/v96pr04. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children..gov/index.

Pesticide industry sales and usage .S.epa. 4/2/09 U. Washington (DC): U.php.gov/oppsrrd1/ REDs/factsheets/24d_fs. Office of Prevention Pesticides and Toxic Substances.EPA).4-D RED Facts. Available at URL: http://www. 3/17/09 U.htm. 2007. Circular 1291. 60 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental Protection Agency (U.4-dichlorophenoxyacetic acid (2. Braun WH. Available at URL: http://www.S.epa. 2. June 2005. EPA 738 F-05-002. Toxicology 1977.S.8:3-1U. 3/17/09. S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Gehring PJ. Available at URL: http://water. The fate of 2.2000 and 2001 market estimates. March 2006.usgs. Supplemental Technical Information (available on-line only).S.Herbicides Sauerhoff MW. Pesticides in the Nation’s Streams and Ground Water. Geological Survey (USGS).EPA). Environmental Protection Agency (U. Blau GE.pdf. revised February 15.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. May.EPA.S.4-D) following oral administration to man. 2004. The Quality of Our Nation’s Waters. 1992-2001.

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

which may vary for some chemicals by year and by individual sample.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.S.200 (<LOD-.S.240) 679 701 957 Limit of detection (LOD.200 (<LOD-. population from the National Health and Nutrition Examination Survey.440 (<LOD-. < LOD means less than the limit of detection. 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.670 (<LOD-.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 62 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

Heederik D. Hodgson E. Xenobiotica 1994. usgs. Deddens JA. U. Metolachlor in Drinkingwater. 1998.html. 1999. Environ Sci Technol 2005.S.248(2-3):115-122. Brown KK. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Thelin GP.24(10):1003-1012. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Rose RL. Andrews HF. Centers for Disease Control and Prevention (CDC). Feil VJ. Sanderson WT. J Agri Food Chem 1989. et al. Jefferies PR.gov/nawqa/pnsp/pubs/files/051507. Kolpin DW. Linhart SM. Available at URL: http://www. Wratten SJ. Hsiao JJ.who.usgs. Environ Health Perspect 2000. Burkhardt MR. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. and other herbicides in rivers. Available at URL: http://www.php. Furlong ET. March 2006. Third National Report on Human Exposure to Environmental Chemicals. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Peter CJ. imidazolinone. Kolpin DW.41:3409-3414. Casida JE. Barr JR. 3/26/09 U. Davison KL.gov/nawqa/ pnsp/pubs/wrir984245/text. Hladik ML. R. World Health Organization (WHO). Comparative metabolism and elimination of acetanilide compounds by rat.37(4):10881093.S. Circular 1291. reservoirs and ground water in the Midwestern United States.int/water_sanitation_health/dwq/chemicals/ metolachlor. Barr DB. Sci Total Environ 2000. Coleman S. acetochlor. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .ESTfeature_gilliom.S. Quistad GB. Ward EM. 98-4245 (by Barbash JE. Geological Survey (USGS). Pesticides in U. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. J Expo Anal Environ Epidemiol 2005. Sacramento.usgs. and metolachlor herbicides in rats. Curwin BD. Environmental Protection Agency (U. Atlanta (GA). Environ Health Perspect 2003.15(6):500-508.pdf 3/30/09 Hines CJ. April 1995. et al. Roberts AL. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Kinney PL. Available at URL: http://water. Supplemental Technical Information (available on-line only). Linderman R. EPA 738R-95-006. Shoemaker DA. Camann DE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Striley CA. revised February 15. Reregistration Eligibility Decision (RED) Metolachlor. Thurman EM. Available at URL: http://water.47(6):503-517. streams and groundwater. Chem Res Toxicol 1998. 2007.gov/oppsrrd1/ REDs/0001. Alavanja MC. 6/1/09 Whyatt RM. EPA).248(2-3):123-133.S. 1992-2001.S. California.39(17):6561-6574. 2003. Sci Total Environ 2000. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.epa. Biagini RE.11(4):353359. Dialkylquinonimines validated as in vivo metabolites of alachlor. Hein MJ. Ann Occup Hyg 2003. Background document for development of WHO Guidelines for Drinking-water Quality. Geological Survey (USGS).Herbicides References Battaglin WA. Feng PCC. Gilliom RJ). Gillion. 2005.111(5):749-756. Environ Sci Technol 2007. 4/2/09 U.108(12):1151-1157. Reynolds SJ.pdf. Available at URL: http://water. Occurrence of sulfonylurea. Barr DB. Larsen GL.pdf. sulfonamide.

5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. dizziness.4. Kohli et al.. Epidemiological studies have reported associations of several types of cancer. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.7. 1992). abdominal pain.5-Trichlorophenoxyacetic Acid CAS No.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Mohammad and St. ranging from several weeks to many months.4. hypotension.5-T is eliminated mostly unchanged in the urine. headache.3.5-T in soil varies with conditions. and concern about contamination with 2.4.5-T use as a herbicide in 1985.5T is rapidly absorbed via oral and inhalation routes.5-T. Agent Orange). At low levels.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 and 0.4-D were used as defoliants in the Vietnam War (e.4. nausea. but higher levels are herbicidal.4. 2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. which may vary for some chemicals by year and by individual sample.4. 2. population from the National Health and Nutrition Examination Survey.4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Chlorophenoxy herbicides act as plant growth hormones. 2004).1. Ester forms of 2. 1986. renal and hepatic injury. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.5-T degrades to 2.4..5-T has been rarely detected in ground waters (USGS. 2. Nelson et al. < LOD means less than the limit of detection. these herbicides can enhance plant growth.5-T (Holson et al. Although 2.4. myotonia. The half-life of 2.4. it is not well absorbed through the skin.Herbicides 2.4.. and delayed neuropathy (Bradberry et al.S.4. 1992.4.. Survey Geometric mean (95% conf.5-Trichlorophenoxyacetic acid (2. 2007).4.4. Once absorbed into the body. 93-76-5 General Information 2. Given the commercial unavailability of 2. 2.4. with an elimination half-life of approximately 19 hours (Arnold et al. Human health effects from 2. 1989. 1974).5-T and 2..g. the general population is unlikely to be exposed to it. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Omer.5-trichlorophenol and other degradates. 64 Fourth National Report on Human Exposure to Environmental Chemicals .

2005). In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004). Finding a measurable amount of 2.S. in which urinary levels of 2. 2003. or to contaminants in the herbicide formulations (specifically 2.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.5-T were generally below the limit of detection. 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.gov/pesticides/.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.4. population from the National Health and Nutrition Examination Survey.4.5-T also were below the limit of detection (Kutz et al. Additional information is available from U.EPA.epa. It is unclear whether these associations are related to the chlorophenoxy herbicides.4.5-T reflect recent exposure.EPA at: http://www.Herbicides or contaminated herbicides. urinary levels of 2.S. IOM.4. 1992).7. U. 2002.3.4.4.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. other exposures. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 1980). 2005. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Biomonitoring Information Urinary levels of 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1996.5-T itself is not mutagenic..5-T than levels found in the general population. Pearce and McLean.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. IPCS.5-T does not mean that the level will result in an adverse health effect.4. Survey Geometric mean (95% conf. Mean urinary levels of 2.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2. Biomonitoring studies on 2. Urinary 2. similar to results of NHANES II (19761980).4.4.

Developmental toxicity of 2.4. Available at URL: http://www.8(5):551-60. Pearce N. gov/oppbead1/pestsales/01pestsales/market_estimates2001.4. Available at URL: http:// www. Board on Health Promotion and Disease Prevention. Developmental toxicity of 2. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. general population.EPA). Kolmodin-Hedman B. Gaines TB. Neurobehav Toxicol Teratol 1986. LaBorde JB.inchem. Washington (DC): National Academies Press. Atlanta (GA). LaBorde JB. II. Available at URL: http:// www.org/documents/jmpr/jmpmono/v96pr04.epa. Cook BT. Tandon JS.EPA. Kutz FW. Office of Prevention Pesticides and Toxic Substances. Centers for Disease Control and Prevention (CDC). Washington (DC): U. I.5-trichlorophenoxyacetic acid (2.2000 and 2001 market estimates. Sircar KP. Gaylor DW. Dhar MM. Arch Toxicol Suppl 1980.5-T). Holson JF. 2004.4. Murphy RS. 3/17/09 Institute of Medicine (IOM). Review of 2. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .23(2):65-73.4-D and 2.4. Vale JA.S. Philbert MA. Proudfoot AT. Third National Report on Human Exposure to Environmental Chemicals. 2.nap.32(4):233-257. S. Gaines TB. Absorption and excretion of 2. Nelson CJ. Carter-Pokras OD. U.4. Khanna RN.php?record_id=10603.31 Suppl 1:1825. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.S.5-T in four-way outcross mice. Beasley VR. International Programme on Chemical Safety-INCHEM (IPCS). The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.5-T).4. Veterans and Agent Orange: update 2002. Arch Int Pharmacodyn Ther 1974. J Toxicol Environ Health 1992. Toxicol Rev 2004. Dichlorophenoxyacetic acid. Erne K. Agricultural exposures and non-Hodgkin’s lymphoma. Poisoning due to chlorophenoxy herbicides.edu/catalog.5-trichlorophenoxyacetic acid (2. 2005.4-dichlorophenoxyacetic acid (2. Multireplicated dose-response studies with technical and analytical grades of 2.S. Environmental Protection Agency (U. 2003.4-D) epidemiology and toxicology. 210:250-255.4-. Fundam Appl Toxicol 1992. Pesticide industry sales and usage . Crit Rev Toxicol 2002.4. Brody D. Nelson CJ. Garabrant DH. McCallum WF. St Omer VE.4:318-21. 3/17/09 Kohli JD. Mohammad FK.htm. discussion 5-7. Scand J Work Environ Health 2005.4-D/2. McLean D. et al. Vet Hum Toxicol 1989.19(2):298-306. May.Herbicides References Arnold EK. Estimation of occupational exposure to phenoxy acids (2.19(2):286-297. et al.5-t mixture.pdf.4.5-trichlorophenoxy acetic acid in man.31(2):121-125.5-T). Gupta BN. Selected pesticide residues and metabolites in urine from a survey of the U. Holson JF. Fundam Appl Toxicol 1992. Bradberry SM. 914. Wolff GL. Sheehan DM.37(2):277-91. Pesticides residues in food: 1996 evaluations Part II Toxicology. Behavioral and developmental effects in rats following in utero exposure to 2.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

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

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

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

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

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

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

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

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

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

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

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

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

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Organochlorine Pesticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

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

Dieldrin

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

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

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

Fourth National Report on Human Exposure to Environmental Chemicals

77

. 1987). similar to results in a subsample of NHANES II (19761980) (Stehr-Green. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al. nausea. but no estrogenic effect was noted in a study that used cultured cells (Tully et al.. population from the National Health and Nutrition Examination Survey. 2000).html. tremors. 1989). Information about external exposure (i. and seizures. 1998) and behavioral changes (Carlson and Rosellini. both aldrin and dieldrin caused liver enlargement and liver tumors. 2004). dieldrin at higher doses caused irritability.Organochlorine Pesticides twitching. The median level in pooled samples from New Zealand adults obtained in 1996-1997 was generally similar to the 90th percentile for adults in this Report (Bates et al. median levels of dieldrin were more than thirtyfold higher than the 95th percentile Serum Aldrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Kanthasamy et al. serum aldrin levels were below the limit of detection. vomiting. 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. 2000.S. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. When fed to experimental animals.S. In samples obtained between 1973 and 1991 from Norwegian women. In a study of pesticide applicators with occupational exposure to aldrin. EPA has established environmental standards for aldrin and dieldrin.. 78 Fourth National Report on Human Exposure to Environmental Chemicals ... The U. 1998). the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. 2005). 1995). OSHA has established workplace exposure standards for aldrin and dieldrin.. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.. 2005..cdc. in which only 10.gov/toxpro2. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. 2000). which may vary for some chemicals by year and by individual sample. and the FDA monitors foods for pesticide residues. 2004). When dieldrin was fed to pregnant rodents. 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.. seizures (Smith. Li et al. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al.. Serum dieldrin levels at the 95th percentile in NHANES 2001-2002 and 2003-2004 subsamples were approximately ten times lower than the corresponding percentile measured in NHANES II (1976-1980). 1991).. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989).atsdr.e. environmental levels) and health effects is available from ATSDR at: http://www. and occasionally.

9 (12.4) 19.3 (18.0 (11.160 (.1) < LOD 9.0) 21.4) < LOD < LOD 16.140-.054-.6 (15.147 (.1-24.086-.080) .102 (.100) .30 (8.1) 10.2) 11.1-19.080-.139 (.3 (18.4) 21.9-23.2) 15.190) .158) .4) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.3 (19.073-.2-15.8-17.5 and 7.098 (.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.116) .048 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .1) 20.100 (. population from the National Health and Nutrition Examination Survey.100-.4 (12.069) < LOD < LOD .9 (14.170) .202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .100) .130 (.1) 15.3 (13.6) 9.062-.5) 15.1) 15.80-10.130-.109-.60-10.5-15.054-.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.090-.110) .101) .4) 95th 20.90) 90th 15.8.6 (15.5-17.109 (. Survey years 01-02 03-04 Geometric mean (95% conf.180) .096-.S.130) .140) .0 (15.7 (<LOD-15.110 (.150 (.090-.160) .089 (.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.0-21.6) 19.103 (.1-18.6-33. which may vary for some chemicals by year and by individual sample.080 (.5) 21. 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 9.0 (10.138 (.138) .6-24.8 (9.093) .5 (16.059 (.5 (<LOD-11. Fourth National Report on Human Exposure to Environmental Chemicals 79 .077 (.7 (14.8) < LOD 8.075) < LOD .077-.150 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140 (.7) 15.147) 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 .120 (.2) 12.110-.053 (<LOD-.130-.0 (10.063-.100-.110 (.083-.4-17.084-.50 (8.103 (.9 (13.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .090 (. which may vary for some chemicals by year and by individual sample.1 (18.6-24.112) 95th .062 (.120 (.80-9.0-25.064 (.130) .9-22.9 (13.8 (18.130-.00-14.40-9.1) 14.120) .070) .149) .00 (8. population from the National Health and Nutrition Examination Survey.4) 14.7 (15.5-17.7-19.8-17.4) 539 456 484 487 980 885 Limits of detection (LOD.100-.060) .70 (7.80 (<LOD-10.4-18.1) 13.8-19. 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.090 (<LOD-.109-.1 (13.110) .070-.088-.160 (.3-21.0) < LOD 9.108-.064) 90th .0) 19.112-.180) .8) 15.058) < LOD .8-24.8) 14.6) 16.055 (.5) 19.049-.3 (14.120-.9-38.6 (14.130) .8 (11. Survey years 01-02 03-04 Geometric mean (95% conf.120 (.117) < LOD .30 (8.9 (12.10 (<LOD-16.110 (.054-.4) 20. < LOD means less than the limit of detection.062 (.124) .4 (12.1-16. see Data Analysis section) for survey years 01-02 and 03-04 are 10.7-22.2) 14.070 (<LOD-.242) .056-.40-10.113 (.139 (.S.190) .50) 15.8-25.090-.

Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Shore RF. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress.150:263-271.usgs. McIntosh LJ. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Wienburg CL. are nonestrogenic in transfected HeLa cells. Hartvig HB. Brock JW. bioaccumulation. Rosellini RA. 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. Cox. Mink PJ. Frey JM. 731-915. and lymphocyte sister chromatid exchange. Teta MJ. Chung KL.gov/ circ/2005/1291/. toxicology. Environmental Health Criteria 91. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. pp. plasma dieldrin. Mumtaz MM. VT.352:1816-1820. Andersen A.109(Supp1):113-139. Buckland SJ.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Available at URL: http://pubs. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. United States Geological Survey (USGS).gov/~dms/ pesrpts. 4/21/09 Bates MN. Revised Feb. Environ Health Perspect 2001.cfsan. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. International Programme on Chemical Safety (IPCS).54:1431-1443. Chlorinated Hydrocarbon Insecticides. and epidemiology in the United States. Toxicol Lett 1992. Serrano FO. Ginsburg KS. Finley B. Carlson JN. Vol. Stehr-Green. Priestly BG. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.fda. 1989. Part A 2000.91(1):122-126. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Jr and Laws ER. Pesticides in the Nation’s Stream and Ground Water. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Facca A. Available at URL: http://www. 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. Basit A. Aldrin and Dieldrin [online].html.gov/toxprofiles/ tp1.14:95-102.26:701-719. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Garrett N. Ellis H. Toxicological profile for aldrin/dieldrin [online]. Turner W. Eds.cdc. Neurotoxicol 2005. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lancet 1998. et al. PA. David VL. Daniel SE.org/documents/ehc/ ehc/ehc91.27:405-421. Olea N. Psychopharmacology (Berl) 1987. Soto AM.htm. 2 Classes of Pesticides. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Sanchez-Ramos J.9:1357-1367. Food and Drug Administration (FDA). Corrigan FM. J Toxicol Environ Health 1989. et al. Jr. 1991.64-65 Spec. Narahashi T. J Toxicol Environ Health. Kitzazwa M. September 2002. Exp Neurol 1998. Fernandez MG. August 2008. Inc. Patterson DG Jr. Grajewski B. Organochlorine exposure and risk of breast cancer. Six high-priority organochlorine pesticides. Chemosphere 2004. 80 Fourth National Report on Human Exposure to Environmental Chemicals .103(Suppl 7):113-122. Environ Health Perspect 1995. Patterson DG Jr. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Int Arch Occup Environ Health 1994. Grandjean P. Kanthasamy AG. 15.inchem. Li AA. Reprod Toxicol 2000. No:429-436. 1992-2001. Chapin RE.html.47:1059-1087. Demographic and seasonal influences on human serum pesticide residue levels.59:229-234. Kanthasamy A. 2007 [online]. Mann D.atsdr.66(4):229-234. Sonnenschein C. Roy ML. Jorgensen T. 4/21/09 Hoyer AP. Edwards JW. Needham LL. References Agency for Toxic Substances and Disease Registry (ATSDR). J Occup Environ Med 2005. Available at URL: http://www. Tully DB. Handbook of Pesticide Toxicology. Song S. In Hayes WJ. 6/1/09 Ward EM. Anantharam V. Schulte P. 4/21/09 Jorgenson JL. either singly or in combination. Academic Press. Available at URL: http://www. New York. Smith AG. Cancer Epidemiol Biomarkers Prev 2000.

01-02.6-12.2) 37.1-51.6) 20.7-12.1 (15.S.8 (17.8-20. Fourth National Report on Human Exposure to Environmental Chemicals 81 .8 (10.9 (36.1 (20.2 (28.8-42.8) 27.7-56. and dairy products are the usual sources of exposure to these chemicals in the general population.3 (28.20 (<LOD-11.3 (9.4-51.1-25.1) * 11.8 (42.7) 31.5) 10.0 (<LOD-12.2 (21. 2007).4) < LOD 11.6) 48.Organochlorine Pesticides Chlordane CAS No.2-49. and in soil.0 (20.4 (10.7 (32.6-45.3) 37.9 (11.5-38.30-11. 2007).6 (9. respectively.7-14.0) 37.S.1) 16.6) 39.7-70.2 (41.1 (27.5 (8.1) 90th 34. As a result of the manufacturing process.8-43.7 (34.9 (15.6) 8.9) 47.7 (17.74 (<LOD-10.4 (<LOD-12.3-45.6 (16.9) 23.3) 41.4-14.2) 46.7) 35.70 (<LOD-10. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.7) 28.9) 37.8-73.6 (43. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.8) 53.3 (25.5-32. and 7. 1994).7-39.1-19.8) 18.20-11.9 (17.1 (<LOD-12.9) 36.9-40.4) 12.2) * 12.4) 37.4-21.9) 17.0) 20.5-41.2-49. the technical grade product of each chemical contains 10%-20% of the other chemical. fish.10-11. foods high in fat such as meat. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.5) 9.0 (37.9 (29.6) 48.1 (16.3-45.0-33. 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.37 (8.6) 23. Since 1992. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.6) 49.5.0-61.6) 36.1-25.5) < LOD < LOD < LOD < LOD 13.7 (43.3 (27.1) 30. Consequently. Technical grade chlordane had contained 7% trans-nonachlor.3-24.7-25.4) 18.9-42.4) 29.9 (26.5 (31.0 (16.5 (<LOD-12.8-33.4 (30.2-56.1 (11. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.3-32.5) 44. lawns.2) < LOD 11.82-11.3 (20.6 (25.8) 44.8.6-18.8-23.69-10.7) 19.2-21. which may vary for some chemicals by year and by individual sample.0 (32.5) 56.9) 39. Chlordane is not currently produced or used in the U. heptachlor use has been limited to treatment of fire ants near power transformers..0-13.0) 41.0-18.8-61.5-13.7) 9.89-10.63 (8.9 (15. 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.1-65.3) 10.3) 18.8-33.7) 42.2 (39.1 (<LOD-12.9) 10.3-49.0) 27. 1994.90 (8. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.0-12.5) 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 * * * * 11.2-28.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.9) 11.4) < LOD < LOD < LOD 23.1 (40.5) < LOD < LOD 9.5) 37. 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.7 (34.0) 21.3 (21. buildings.5 (41.7 (<LOD-32.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5-47.9) 11.0 (26.3) 10.7 (19.5-44.4) 39.4 (35.3) 18.2) < LOD 11.1) 22.9 (31. Until 1988.5.7 (<LOD-13.5 (34.6) 11.0) 75th 20.2 (36.3 (26.5) 21.6 (9.6) 9.0) 31.6-53.9 (21.7 (10.1-50.8 (17.6) 9.4 (22.4) 22.2) 36.3 (<LOD-19.9 (26.1-15.5) 38.2 (37.2) 33.9-38.8 (18.9-21. chlordane was used to kill termites and other insects on agricultural crops.1) * 11. 10.1 (17.9) 13.9 (18.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.1 (<LOD-12.5-65.4-45. from the early 1950’s until the mid-1980’s.0-67.8) 52.9) 23.4 (30.2) 34.5-42.8 (40.5-40.1 (44.8-32.10 (8.0-25.3 (11. and 03-04 are 14.8-31.36-11.2) 22.9 (11.2-26.S. 57-74-9 Heptachlor CAS No.1) 30.8 (10.8) 52.1 (25. < 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.9) 31.4 (31. in addition to trace amounts of numerous other related compounds (ATSDR.6-24.5 (33.2 (9.7 (42.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.6) < LOD 11.1) < LOD < LOD < LOD < LOD < LOD 8.2 (10. see Data Analysis section) for Survey years 99-00.7) 19.3-43.10-18.20-10.6-24.9-21.4-40.5-43.

140 (.207 (.130) . dermal.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .066 (.168-.074-. 1981).056 (.230 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.140) .130-.063) * . neonatal mortality.280 (..083) .290-. OSHA has established occupational exposure criteria.063 (.302) .104) .310) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.090) .270 (. 2006).230-. heptachlor. Elimination of all these chemicals from the body occurs over months to years.300) .128 (. 1991..073 (.260 (. population from the National Health and Nutrition Examination Survey.146) .270 (.330 (.140 (. 2001.290-.070 (<LOD-.060 (<LOD-.130 (.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.130 (.070) .180-.063-.230-.210 (.410) .S. interval) Selected percentiles ( 95% confidence interval) Sample 95th .290 (.230-.300) .092) .246-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.049 (<LOD-.310) .066-.050-.240 (.055-.130-.160 (.110 (<LOD-.216-.100-.068-.083 (.063 (.073) < LOD < LOD < LOD < LOD .189-. Takahashi et al. which may vary for some chemicals by year and by individual sample. and the U.280-. 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.280-.370 (.119 (.115 (.170) . IARC.080) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.160) .380) .068) .150) .130-.203-.070 (<LOD-.066 (<LOD-.080) .057-.260 (.058-.148) .350) . Le Marchand et al.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .082 (.190-.242-.210-. FDA established allowable residues of chlordane.120-.070-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al. 1986).070 (<LOD-.160) .180) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.063) . and inhalation exposure.200-.070-.100-.340) .091) .160) .065-.300 (. 2007).190-.370 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .360) .310-.450) .286 (.146) < LOD < LOD .130-.258 (.213) * .104-. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.320 (.126 (.230) . 1991).290) .090) .245-.100 (.075 (.280 (.340) .076) < LOD .080) .286 (.320 (.170) . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.400) . EPA has established environmental criteria for chlordane and heptachlor.240-.140 (.077) .510) .068) 75th .077) .320 (.271 (. which is also persistent in the body (ATSDR. to heptachlor. and breast milk is a major excretion route in lactating women.120-.140-.240-. 2007.058 (. and alterations in immune function of offspring.062) < LOD . characterized by seizures and paralysis. 2002.220-.560) .170) .053-.150 (.061-.150 (.064) < LOD .430) . chronic doses of heptachlor have produced liver enlargement and injury.310 (. The major metabolite of heptachlor is heptachlor epoxide.300) . 1986).108-.140 (.070 (<LOD-.050 (<LOD-.115-.373) .130 (.207) .077) .170) .070-..350 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.320 (.080 (.069 (<LOD-.130) .048-.077) .180) . Chlordane and heptachlor are absorbed after oral.079) .300) .260 (.189 (.140-.100 (<LOD-.240) . Rogan.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.S.300-.120 (.231) .208 (..063 (.280-.126) .400) .210 (.430) .200-.148-.079) < LOD < LOD < LOD . 1977b.Organochlorine Pesticides (Dallaire et al.260-.190-.225 (.440) .223) .090-.136) .170-. Acute.070) < LOD < LOD < LOD < LOD < LOD .200-.106-.058-.320) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.165-.063 (.204 (.258-.070 (.133) 90th .047 (<LOD-.130-. Shindell and Ulrich.287) .S. In laboratory animal studies.253-. The U.290-.290) . and heptachlor epoxide in foods and bottled water.087-.270 (.053-.280) .250-.080 (.200 (.315 (.066-.350 (. Survey Geometric mean (95% conf.450) .320) .220 (.348) .120-.071 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .149 (.180-.057) * .150-.227) < LOD . 1977a.370 (.150 (.230 (.310) .250 (.250 (.220-.110-.269 (. Smith.199-.067 (.057 (.112 (.

respectively. Biomonitoring studies on levels of oxychlordane. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000. 1988). mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher.html.atsdr.org/documents/cicads/cicads/cicad70. or heptachlor epoxide in serum does not mean that the level of oxychlordane. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al.. transnonachlor. resulting in human exposure to heptachlor epoxide that was excreted into the milk. In the Hawaii episode. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries. transnonachlor.htm#ref. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high. trans-nonachlor. respectively..gov/toxpro2. 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.. inchem. than the 90th percentile values of NHANES 1999-2000 (Baker. Finding a measurable amount of oxychlordane. 2000). 2002). 2001-2002. 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...e.. from ATSDR at: http://www. A recent assessment of heptachlor is available at: http://www. Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 . A small sample of Polish women had mean levels of oxychlordane and trans-nonachlor that were about fivefold lower than in females in the NHANES 20012002 subsample (Jaraczweska et al. 2003). and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al.cdc. or heptachlor epoxide causes an adverse health effect. 2004). 1993). For the exposed persons drinking milk in the Arkansas episode. Levels of heptachlor epoxide among females in this Report were approximately one tenth of the corresponding 90th percentile for a cohort of pregnant women in California studied from 1963 to 1967 (James et al. environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects..Organochlorine Pesticides about external exposure (i. 2006). and heptachlor epoxide provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of heptachlor and chlordane than are found in the general population.

3) 22. and 03-04 are 14. respectively.6) 13.40) 15.8 (18.4 (<LOD-54.8 (<LOD-23.6 (11.2-27.7-18. and 7.2) 20.9 (15.8 (15.5) < LOD 14.8) 16.6-17.3-18.2) 15.3 (<LOD-25. which may vary for some chemicals by year and by individual sample.8) 15. see Data Analysis section) for Survey years 99-00.8) 21.2 (<LOD-25.8 (13.2) 13. < LOD means less than the limit of detection.9 (12.0) 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 13.5) 19.5 (11.8) 13.5 (<LOD-21.9-29.50) < LOD < LOD < LOD 17.8-24.6-21.9-23.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8) 19.4 (<LOD-19.8) 20.6 (8.9-29.1-29.5 (11.2-27.0-17. 01-02.8-46.7-25.10-13.3) 18.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90 (<LOD-9.5 (<LOD-32.0-17.1) 23.8 (13.5.6 (<LOD-27.20 (<LOD-9.7 (13.5 (18.6) < LOD < LOD < LOD 27.7-19.6 (16.1 (16.2) 26.0) 13.3) 18.3 (13.3) 27.1-15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4 (11.2-17.1-16.0-54.2 (18.2 (<LOD-16.8-24.7 (10.1 (19.0 (11.5) 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 7.5 (10.2 (<LOD-62. Survey Geometric mean (95% conf.4 (15.6.8-23.1-38.8-24. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.1) 20.8) 14.0-16. population from the National Health and Nutrition Examination Survey.9-25. 84 Fourth National Report on Human Exposure to Environmental Chemicals .4) 18.8) 13.6 (12.9-16.6) 22.4 (11.3) 23. 10.1) 13.3) 10.6 (14.S.8) 14.2-16.0-19.6 (16.8) 19.0 (15.6 (13.8 (18.9) 15.9) * * * 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 8.6) 14.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.3) 18.7 (16.8.4) 21.3) 16.

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

6-82. < LOD means less than the limit of detection.1-55.3-50.1-28.9-58.9 (15.2 (60.1-16.1 (10.10 (<LOD-11.5 (44.7-160) 86. interval) 18.0 (14.4-18.4) 59.7 (13.9) 51.7-77.7-32.3 (58.0) 40.0-113) 68.7) 17.S.8) 51.5 (13.9 (51.2 (27.4) 107 (84.2) 30.0 (29.3 (56.4-52.8 (16.3 (49.9) 14.7) 28.0) 75th 31.6) 84.8-77. 86 Fourth National Report on Human Exposure to Environmental Chemicals .1) 17.7) 78.2 (14.8-110) 59.4 (11.86-13. respectively.0-38.6 (<LOD-14.9-65.1-34.4 (12.1) 78.2) 17.9 (47.7) 59.0 (60.8 (49. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-64.8 (13.8) 47.7) 14.7-18.5) 19.4 (30. 01-02.4-35.3-21.1) 17.8-21.7-17.7 (28.2-18.8) 80.1-20. 10.9-69.2) 39.6) 25. population from the National Health and Nutrition Examination Survey.8 (26.6) 82.7-20.7) 52.1) 31.6) 13.1) 16.5) 77.1 (48.7 (11.8-16.4 (28.1-16.5-17.0-123) 74.3-39.5) 90th 55.5 (25.0) 49.7 (59.9-36.6) 54.8 (28.2 (7.6 (52.7-113) 68.9 (36.8 (28.1) 17. and 03-04 are 14.7) 35.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3) 30.5-20. Survey Geometric mean (95% conf.1) 78.0) < LOD < LOD 8.8 (30.8-19.6 (16.3-57.1) 30.5 (15.0-93.3) 19.7) 15.0) 13.5-87.8 (45.2 (25.1-51.1-22.9) 51.0-23.2) 59.0-68.1) 18.7-38.3 (17.8 (26.4-67.8-79.0 (15.1) 62.6 (15.5) 48.5) 9.2-23.9) < LOD < LOD < LOD 20.4-36.3-86.6 (50.0-59.0 (16.3-74.6 (56.0 (13.7-35.7) 78.3) 16.7 (59.7 (18.1 (41.4 (16.1) 14.1) 32.3) 36.6 (32.8 (42.0 (19.8 (13.1) 17.7-21.8 (12.0 (62.0 (15.0 (13.5) 20.0) 19.8-90.3) 25.6-54.1-34.2-18.0 (48.7 (16.6) 56.4-23.6 (56.0-143) 112 (68.2) 34.9 (29.5) 36.8 (11.9 (15.1 (17.8 (15.9 (<LOD-14.3 (14.2-88.8-16.2-17.3-30.8 (19.5) 35.4 (67.5) 26.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.2 (64.6-22.7 (74.3) 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.5.6) 34.5-95.1 (65.8-90.3 (45.1) 17.9-65.9-89.0-23.4) 48.5) 14.8-19.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.5 (15.8 (28.3) 18.9-22.3) 32.3) 30.3) 15.9 (51.9-35.2) < LOD 10.0-20.1-126) 67.7 (35.1) 17.6 (12.6) 56. see Data Analysis section) for Survey years 99-00.7-23.9 (28.8-41.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.3) 32.7) 56.9-40.7-34.2 (15.8-67.3-58.4) 20.4) 55.9) 14.0) 18.5-19.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.3-32.6 (57.0-24. and 7.5) 30.2 (59.5-36.6-20.5) 78.9 (16.3 (16.2) 19.3 (14.1 (47.5. which may vary for some chemicals by year and by individual sample.0) 33.6-66.4-22.6-19.9 (66.9 (19.7-22.0-37.1 (22.2-37.6) 60.8-129) 74.2-16.5) 22.8 (<LOD-20.4) 16.1-18.0 (42.0 (42.5) 14.5 (45.0-93.6-88.8.9-20.2 (36.7-29.8 (26.2-21.7 (30.4 (45.2) 20.3) 18.9-45.8) 19.70 (<LOD-12.2 (26.8 (17.2 (19.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.5-111) 68.5-69.1) 17.6) 10.1) 18.7) 73.0 (16.4) 19.4-62.8 (71.2 (14.0-22.

110 (.103 (.220 (.270-.350-.130) .310 (.210 (.490) .068-.091) .280) .360-. interval) .131) .460-.110 (.390 (.510 (. population from the National Health and Nutrition Examination Survey.317 (.390 (.20) .286-.370 (.085-.240) .310-.110 (.594) .430-.120-.497-.047-.100-.112 (.240 (.090-.062 (.130) .090-.250) .094 (.117) .099-.360-.232) .093-.110 (.112 (.096) .240) .125) .190-.120) .100-.060) .220 (.095-.460) .490 (.085-.390) .960) .080-.082) .110) .414 (.090 (.400 (.106 (.119) < LOD < LOD < LOD .126) .190-.520 (.395) .113) < LOD .103 (.060-. which may vary for some chemicals by year and by individual sample.327 (.340-.130) .124) .120-.220) .520) .458 (.830) .760 (.104 (.310-.220 (.180-.210 (.S.186-.092 (.630) .590) .150) .930) .141) .340) .150) .100-.079-.300-.220 (.069) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .400) .573 (.100 (.070 (.110-.096-.105 (.390-.093-.093) .081 (.080-.640 (.106 (.134) .210) .410-.090 (<LOD-.288-.630) .079-.170 (.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .120) .320-.060 (<LOD-.098-.113) .093-.440) .140) .210-.450) .440-.405) .111-.078-.100 (.380 (.400-.520 (.098 (.390 (.069-.130 (.145-.290-.114) .355 (.087 (.310-.100-.301-.108 (.160-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220 (.680 (.410-1.580 (.180-.127) < LOD < LOD .180-.500) .097) .190-.250) .400-.158-.161) .370 (.220 (.122) .116) .840) .171-.371) .110 (.310-.830) .098) .092 (.190-.279-.220 (.122) .540) .324 (.108) .071 (<LOD-.470 (.340-.600 (.234) .490 (.343 (.177-.205 (.120 (.099-.120) .510-.090) .367) .130) .109 (.106 (.210) .285-.395-.109 (.461 (.460) .680) .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.190-.098 (.081-.390 (.054-.104-.470 (.470-.191 (.330-.559) .120 (.470-.120-.130 (.220 (.096-.630) .130) .320-.125 (.288 (.250) .260) .080) .080-.090-.565) .230 (.108) 75th .130) .055 (<LOD-.116 (.130) .160 (.091-.240-.272-.041 (<LOD-.580 (.260) .590 (.128 (.350 (.430-.330-.550 (.417 (.420 (.400 (.580 (.800) .470 (.211) 90th .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .090-.420) .480) .110 (.080-.080 (.090-.085-.120) .183 (.120 (.129) .210) .190-.173-.409-.240) .119) Selected percentiles ( 95% confidence interval) Sample 95th .242) .135 (.210 (.237) .161-.090-.210-.690) .141) .310) .300) .397-.651) . Survey Geometric mean (95% conf.600) .202 (.684) .078 (.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 .690) .084-.186 (.237) .111 (.490-.590 (.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.330 (.390) .061-.116-.089 (.430-.

2001. Toxicological profile for heptachlor and heptachlor epoxide [online]. Arch Environ Health.330:55-70. 6/1/09 National Toxicology Program (NTP). Siegel BZ. Sci Tot Environ 2006. Senie R.150:981-990.org/site/foundation/ research/projects2. Environ Health Perspect 2002. 1994-1997 organochlorine compounds. Academic Press.cdc. Lulek J. Toxicological profile for chlordane [online]. J Occup Med 1986.cdc.gov/toxprofiles/tp31.htm. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Jr. 1993. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor.372:20-31. Takei G.28:497501. National Toxicology Program (NTP).nih. Willman E. Chashchin V. Berkowitz GS.heptachlor. Environ Res 2000. Keller JA. Loo S. 6/1/09 Rogan WJ. Stehr-Green P. Distribution of polychlorinated biphenyls. Baker DB. A Report to the Hawaii Heptachlor Research and Education Foundation. 9/25/07 International Programme in Chemical Safety (IPCS). In Hayes WJ. Takahashi W. Eds.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).84:151-161. New York. JAMA 1988. 731-915. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Aune M. Hansen JC. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. et al.pdf. Circumpolar maternal blood contaminant survey. Odland JO. Chlordane and heptachlor [online]. Available at URL: http://www. Covaci A. Barker J. 1991 pp. Brower S. 1979-1980. et al. Poland. Dewailly E. Royce W. Bull Environ Contam Toxicol 1981:27:506-511. Charles MJ. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Natl Cancer Inst Carcinog Tech Rep Ser 1977a. maternal serum and milk from Wielkopolska region. Sci Total Environ 2004. Ayotte P. Dewailly E. Available at URL: http://www. Environ Health Perspect 2003. Inc. Smith AG.htm. Available at URL: http://ntp. Hawaii Med J 1991.html. Atuma S. Bjerselius R. Available at URL: http://www. Head SL. Organochlorines in Swedish women: determinants of serum concentrations.html. Dendle WH. Wolff MS. Jr and Laws ER.atsdr. Chlorinated Hydrocarbon Insecticides. Jaraczewska K.110(8):835-838. Concise International Chemical Assessment Document 70 Heptachlor [online]. Drews K.gov/ntp/ htdocs/LT_rpts/tr008. Shindell S and Ulrich S. Bioassay of chlordane for possible carcinogenicity. Lawrence River (Quebec. et al. Voorspoels S. Available at URL: http://ntp. Granath F. Available at URL: http://www.50(3):108-118. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Darnerud PO. Pollutants in breast milk. Organochlorine exposures and breast cancer risk in New York City women.Summaries & Evaluations. Saidein D.110:617-624. Tartter P. 1986. Wohlleb JC. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort.atsdr. Organochloride pesticide residues in human milk in Hawaii. Kolonel LN. 1963-1967. Van Oostdam JC.org/documents/iarc/ vol79/79-12. Handbook of Pesticide Toxicology.111:349355.niehs. August 2007. 4/21/09 Dallaire F. 2006. Muckle G.org/ documents/cicads/cicads/cicad70. International Agency for Research on Cancer (IARC). 4/21/09 James RA.inchem. Bioassay of heptachlor for possible carcinogenicity. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.gov/ntp/ htdocs/LT_rpts/tr009. Hertz-Picciotto I. 4/21/09 Baker DB.niehs. Vol. Canada). May 1994. gov/toxprofiles/tp12. 2 Classes of Pesticides. et al.259(3):374-377.41:145–148. Wong L.nih. Bleiweiss IJ. International Agency for Research on Cancer (IARC) . Glynn AW. Arch Pediatr Adolesc Med 1996.inchem.pdf. KalubaSkotarczak A. Vol. Available at URL: http://www.9:1-109.html.8:1-123. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. 79. Mortality of workers employed in the manufacture of chlordane: an update. LeMarchand L. Environ Health Perspect 2002. Laliberte C. Gilman A.

5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.4) < LOD 17. and 7.2 (11. DDT was used at one time as a treatment for head and body lice.6 (25. particularly for endemic vector and malaria control.9 (<LOD-20. 2002.0-37.5 (14. or dermal exposure.1-27. 1988). DDT and DDE can cross the placenta. 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.7 (19. which may vary for some chemicals by year and by individual sample.S. Gunderson.0-35. o.0 (18. Both Serum p.3) 28. 2008. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.3) 21.1 (<LOD-39. fish.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.p’-DDT (65%-80%).9) 29.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.6-33.1 (33.8) 30. It was produced and used in the U.2-bis(p-chlorophenyl) ethane (DDD).90 (<LOD-12. respectively.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 10.9 (10.0 (10.6 (22.S.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. In the general U.10-13. depending on conditions. Only a small proportion of DDT is metabolized and excreted (Smith.3-16.3) 22.8-26. Fourth National Report on Human Exposure to Environmental Chemicals 89 . 1991).7 (15. It is still used in some countries. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. after World War II until 1972.3) 21.8) 36.1-71.5-36.2-65.7) < LOD 18. see Data Analysis section) for Survey years 99-00.9 (10.p’-DDT (15%-21%).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 8.5 (15.2) 30. including 1. DDT can be absorbed after ingestion.4 (23.0-15.5) < LOD < LOD 9.1 (23.5 (23.p’-DDD (4% or less).9) 14. as well as in plant and animal tissues.3 (<LOD-21. inhalation.6 (9.0-53.9) 17.0 (21.5-54.1’-(2. DDT usually refers to the technical product. food.1) 31.4.0-155) 83.2) < LOD < LOD 9.2-95. < LOD means less than the limit of detection.0) 20.3-236) 24.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.6 (<LOD-25.3-590) 293 (104-541) 48.3 (<LOD-31.0) 26.7) 12. DDT is converted in the environment to other more stable chemical forms.8-17. DDT is converted to DDE and several other metabolites.9 (21.9) < LOD < LOD 9. and 03-04 are 20. The biodegradation half-life of DDT in soil varies from 2 to 15 years.2) 155 (59. 1991). Survey Geometric mean (95% conf. and water. sediments. air.9-28.6 (31.S.0 (18. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.8-39.2 (<LOD-40.9-34. particularly meat.7. when virtually all use of it was banned. These chemicals are highly persistent in soil.5) 25. and dairy products.70 (8.1’-dichloro-(2. population from the National Health and Nutrition Examination Survey.10 (<LOD-12. p.5 (23.8.4) < LOD < LOD < LOD 61. Smith.0) 19. resulting in fetal exposure.9 (10. which is a mixture containing p.50-11.0) 40. Food imported from countries that still use DDT may contain the chemical or its residues. 01-02.8-23.5) 23.3 (27. 17. population. although DDT and DDE intakes have decreased over time (FDA.8) 15.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7-16.0-27. continues to be the primary source of DDT exposure. and trace amounts of several related compounds. In the body.00 (<LOD-10.

1996). resulting in exposure to nursing infants (Rogan. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. Beard.220) .114-..059-..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.051 (<LOD-.189) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .128 (. tremor. Survey Geometric mean (95% conf.068-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 2006.34) .203) . and altered behavior after neonatal exposure (Eriksson and Talts. accidental exposures.120-.330-4.180 (.079) < LOD < LOD . and o.180) .00 (. 2001).078 (.. 2002..130-.120 (<LOD-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. other organochlorines.250-1.106) < LOD < LOD .130 (<LOD-.240 (.. 1956).230) .075) 1.Organochlorine Pesticides chemicals are excreted in breast milk.400) .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 . 1998).400 (.201 (. 2001).150 (<LOD-. 2006).069) ... Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.071 (.048 (<LOD-.142 (.290) . Gray et al.26) 1. 2002.240) .200 (. In high dose.150-.530) .132-.105-. 2004.01) . premature delivery.190 (. 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.108 (.074-. Snedeker.130 (<LOD-. DDT may bind to estrogen receptors (Chen et al.00) .086 (.140-.146 (.62 (. A workplace standard for DDT has been established by Serum p.. 90 Fourth National Report on Human Exposure to Environmental Chemicals . Longnecker et al..146 (. fertility.180) . 2002. interval) Selected percentiles ( 95% confidence interval) Sample 95th . have not been consistently demonstrated (Beard.095) < LOD .189-.180 (.S. 2006.p’-DDD and p. 1997).065-. Animal studies reported reduced fertility.112 (.087 (. dioxins and furans).106-.061) < LOD < LOD < LOD .140) . 2002. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2006).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.084 (.064 (. 2000. which may vary for some chemicals by year and by individual sample.170 (. overt signs of acute human toxicity include vomiting. 2001).180-. Jusko et al.627) .054-.. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.190-1. 2001).106) .. Studies of DDT exposure and pancreatic cancer. Hayes et al.250 (.343) < LOD .190 (.p’-DDE can produce anti-androgenic effects (Gray et al. Gladen and Rogan.078-.530 (. Jusko et al.260) .160-.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 .150 (<LOD-.170) .230) .150-. reproductive organ abnormalities.080-.063 (<LOD-. lung cancer.220) .170-.098-. polychlorinated biphenyls. and leukemia have also been inconclusive (ADSDR.130 (<LOD-.420) .071-. Mariussen and Fonnum. population from the National Health and Nutrition Examination Survey.143) < LOD < LOD . and duration of lactation. In laboratory animals. Reproductive effects in humans affecting birth weight.g. 2006). and seizures. 2006.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . Calle et al.. 1995.150) .313 (.570-4.

.. and 7. and 03-04 are 18.S. Smith.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. 8. Biomonitoring Information DDE persists in the body longer than DDT. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.. mean serum levels of DDT and DDE in the U. 1989).6 (81.. population declined by about fivefold to tenfold. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. More information about external exposure (i...cdc. respectively. 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. 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. 2004). Survey Geometric mean (95% conf.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. environmental levels) and health effects is available from the U. EPA at: http://www. In a population-based sample of men and women from eastern Slovakia. Since the 1970’s. Compared to females in the NHANES 1999-2000 subsample. see Data Analysis section) for Survey years 99-00.6. population from the National Health and Nutrition Examination Survey. 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.p’-DDT) as a possible human carcinogen. 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. 2002. Declining DDE levels over time have also been observed in the German population. 01-02.S. Heudorf et al. 2005). Link et al.Organochlorine Pesticides OSHA and a guidance established by ACGIH. compared to levels observed in this Report (Anderson et al. for males and females in the NHANES 19992000 subsample (Pavuk et al. 2004). IARC classifies DDT (p.epa. Stehr-Green.gov/ toxpro2.. Fourth National Report on Human Exposure to Environmental Chemicals 91 .7-119) 113 (100-140) 93.0-114) 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. 2003. 1991). levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.gov/ pestcides/ and from ATSDR at: http://www.8.atsdr.e. 1998.html.. NTP considers DDT as being reasonably anticipated to be a human carcinogen. 2002.3.S. 2003). respectively. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.

25 (.05 (3.9 (26.45 (1.20 (.963-1.07) 1.32 (1.97-4.7-48.14) 2.419-.87-16.31-2.71) 32.49 (6.37-1.80) 1.2-32.43-8.57) 2.22 (7.52 (1. Serum p.78 (4.76) 1.01-1.17-3.623 (.7) 16.5) 16.46 (1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.30-1.6) 8.75 (4.37 (1.40-4.27) 3.Organochlorine Pesticides nearby agriculture (Botella et al.30 (1.561 (.456 (.36-2.p’-DDT.57-3.860 ng/L) and DDE (about 14.36-1.4) 13.590 (.12 (6.70-3.24 (1.9) 5.6) 13.0 (9.69 (.47 (1.38 (1.81-18.25-14.9 (15.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.77 (1.02 (2.1 (8.84-3.0 (12. 2004).2 (19.57 (1.75 (8.43 (5.83 (1.56) 2.41 (1.21) 90th 7.91 (6. 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.58) 75th 3. Survey Geometric mean (95% conf.6) 9.64) 3.9-17.17 (3.18-3.53) 7.516 (.14) 2. High mean levels of whole blood DDT (about 3.66) 1.385-.25) 8.10-1.64-2.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.32) 1.28) 1.33-1.S.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.48 (6.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 . or p.11-1.32-1..32 (1.91-3.0) 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 .18) 1.76-3.p’-DDT (Stehr-Green.06) 3.4-19.14 (1.26 (1.870 (.890-1.430-.35) 1.4 (12.68 (2.15-4. population from the National Health and Nutrition Examination Survey.25) 1.85 (1.80 (2.34 (7.3 (8.7-19.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.97 (3.96) 1.965-1.8-90.7) 9.47) 3.6 (17.12-1.48-4.04 (6.31-12.56-2.81 (1.26-2.534-.796 (.52 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.75) 6.63 (1.34-3.59 (1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.3 (9.25 (1.75) 1.8 (9.57 (1.10) 2.10-5.55-9.2 (9.70) 1.71 (6.63 (6.994-2.488-.01-11.72) 1.46 (1.07 (5.0) 2.18 (6.3-43.00) 7.44) 1.7 (8.40 (3.520 (.9) 7.p’-DDT.54 (1.66-2.34) 2.81 (7.69) 8.16-1.01-5.49 (1.2) 26. 2001-2002 and 2003-2004 subsamples.3) 10.54) 8.04-1.57-2.21) 3.14-9.13) 4.85-10.. 1971).02-8.51) 3.36-11.66) 3.6 (7.49) 8.4) 14.91) 3.00-1.65 (1.6) 12. 309 versus 268 ng/g lipid.53) 1.22) .6 (9.07) 1.37-16.57-13.4) 9.85-4.01) 1.60-13.34) 6.24) 1.50 (2.14-1.1) 12.600) .82 (1. 2005).40-4.66) 4.12 (.3) 16.59 (1.2) 19.18-1.66-4.71) 12.61 (1.81-5.09-1.57 (3.80) 1.56-6.55 (2.635) 1.59 (4.71 (5.49 (1.730) .82) 1.65) 1.84 (3.50-17.1) 40.77 (1.39-2.92 (3. less than one percent had detectable serum levels of o.500-.41-12.68) 2. interval) 1. o.76 (2. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.43-4.726) .92) 1. In the NHANES 1999-2000. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.32-9.63 (1.19) 4.68-4.54-7.92 (3.45 (1.59) 6.51 (1.6) 9.38 (1.37-4.2 (9..34-11.1 (9.59) 3.820-1.5) 5.52-6.51-8.69 (1.13 (1.72) 1.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.39 (3.6 (8.01) 1.8 (13.05) 1..1) 7. 1991).16 (2. Finding a measurable amount of p.30 (1.69) 4.9-38.90-8.81) 11.58) 1.557) 1.23 (7.58) 1.8) 15.7) 13.88 (2.18-4.90) 22.46-2.36 (3.24-17. considerably higher than levels in this Report (Smith.18-1.88-35.2 (6.76) 1.31 (1.680-1. serum levels of o.56-3.8 (14.66) 1.01-15.02) 1.22-1.39) 1.4 (8.19-14.75) 2.5) 22.63-15.32-1.43-4.646) .40-8.62-6.5) 7.96) .6) 11.87 (5.7-20.00 (.6) 9. 2004).80) 3.30-1.53 (2.51) 1.51-15.66-17. In a subsample of NHANES II (19761980) participants.6) 9.01-11.10) .53-15.00 (6.13-2.69 (2.29 (1.26) 3.03-1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.51-49.25-16.01-1.27-1.p’-DDT were below the limits of detection.99) 1.06) 1.91-2.79) 4.11 (2.611-1.93 (7.61-2.26-10.03-4. 1989).39-1.5) 10.8 (13.36) 3.37-10.3) 13.

S. see Data Analysis section) for Survey years 99-00. Survey Geometric mean (95% conf. and 03-04 are 20. 17. < LOD means less than the limit of detection.7. and 7.8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < 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.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.Organochlorine Pesticides Serum o. Fourth National Report on Human Exposure to Environmental Chemicals 93 . respectively. 01-02.4. population from the National Health and Nutrition Examination Survey.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.Organochlorine Pesticides Serum o. 94 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.S.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. which may vary for some chemicals by year and by individual sample.

Hayes WJ. Zhou H. Lambright C.58:1185-1201.97(2):178192. Int J Hyg Environ Health 2003. Moysich KB. Heudorf U. Wolf CJ. Klebanoff MA. Rogan WJ. Willman EJ. Effects of environmental antiandrogens on reproductive development in experimental animals.106(5):279-289. Fourth National Report on Human Exposure to Environmental Chemicals 95 .162:890-897.21(1-2)37-48. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Saiyed HN. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males.cfsan. Krause C. Brock JW.17(6):692-700. Hanrahan L. and HCB residues in human blood in Ahmedabad. et al. Am J Public Health 1995. and DDD [online]. Eriksson P. Neurotoxicol 2000. Cueto C. August 2008. 4/21/09 Anderson HA. et al. Olson JR. Longnecker MP. Organochlorines and breast cancer risk. September 2002. Frumkin H.7(3):248-264. Kaus S.112(17):1761-1767. hexachlorobenzene. Glynn AW. Garrett N. Jusko TA.71(6):1200-1209. Burse VW. Durham WF. Klebanoff MA. Bjerselius R. Available at URL: http://www. Environ Res 2004. dichlorodiphenyldichloroethylene. Thun MJ. DDT and human health. Talts U. Hediger ML.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Buckland SJ. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. selected elements. Needham LL. Botella B. Chemosphere 2004. et al.85:504508. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. and other chemicals.96:34-40. HCH. et al.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. The effect of known repeated oral doses of chlorophenothane (DDT) in man. et al. Drexler H. Chen CW.. et al. Notides AC. Biochem Pharmacol 1997.fda. Paepke O. Arnold SF. hypospadias.html. The Great Lakes Consortium. Beard J. Henley SJ. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Bull Environ Contam Toxicol 2004. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Jr. Kulkarni PK. Zoellner I.205:297-308. Sci Tot Environ 2006. Food and Drug Administration (FDA). dietary intakes of pesticides. Gray LE Jr. Ostby J. Needham LL. Longnecker MP.72:261265. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Epidemiology 2006. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Toxicological profile for DDT. et al. Brock JW. FDA total diet study. Vena JE. Bhatnagar VK. 4/21/09 Gladen BC.gov/~dms/ pesrpts. J Assoc Off Anal Chem 1988. Parks L. Hum Reprod Updat 2001. Gabrio T. Available at URL: http://www. Charles MJ. Olea N.atsdr. and dichloro(diphenyl)ethylene (DDE). India. Organochlorines in Swedish women: determinants of serum concentrations. Olson J.1-dichloro2. Patterson DG Jr. Ellis H. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Zhou H.52:301-309. Environ Health Perspect 2003. Crespo J. Lepom P. Herrman T. Klebanoff MA.html. Levels of DDT. April 1982 to 1984. Jr. Link B. Cerrillo I. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Maternal DDT exposures in relation to fetal and 5-year growth. Needham LL. Davis MD. CA Cancer J Clin 2002. Gladen BC. Kashyap R. Furr J. Lancet 2001. Darnerud PO. Olea-Serrano MF. et al. Environ Health Perspect 1998. et al. and polythelia among male offspring. Chemosphere 2005. DDE. Greenfield TA.gov/ toxprofiles/tp35. Seiwert M. Vorojeikina DP. Savitz DA. Biomonitoring of persistent organochlorine pesticides. Calle EE. Profiles of ortho-polychlorinated biphenyl congeners. Maternal serum level of 1. Angerer J. Aune M. Atuma S. Gunderson EL. Bates MN. Gray KA. Katz SH. Hurd C. Exposure of women to organochlorine pesticides in Southern Spain. Am J Epidemiol 2002. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.cdc. Rivas A.355:7889. DDE and shortened duration of lactation in a northern Mexican town. Swanson MK. Baker RJ. Becker K. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Barr DB. Bloom MS. Zaidi SS. Falk C.206:485-491. JAMA 1956.111:349355. Piechotowski I. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.54:1431-1443.53(8):1161-1172. lindane (g-HCH). Environ Res 2005.155(4):313-322. Granath F. Environ Health Perspect 2004. Schulz C. Int J Hyg Environ Health 2002. Koepsell TD.358:110-114.

Comparative pharmacodynamics of CYP2B induction by DDT.36:253-589. 731-915.109:35-47. Rey AA.Organochlorine Pesticides Mariussen E.53:455-477. Crit Rev Toxicol 2006. Pesticides and breast cancer risk: a review of DDT. Thomas PE. Lubet R. J Toxicol Environ Health 1989. Pollutants in breast milk. Handbook of Pesticide Toxicology. et al. Inc. Pavuk M. DDE. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Rogan WJ. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Smith AG. Jr and Laws ER. Reddy AB. Fox S.54:1509-520. children and newborn infants. and DDD in male rat liver and cultured rat hepatocytes. Arch Pediatr Adolesc Med 1996. Demographic and seasonal influences on human serum pesticide residue levels. 2 Classes of Pesticides. In Hayes WJ. 1991 pp. Deichmann WB. Jr. and dieldrin. New York. Chovancova J.20(2):186-193. Astolfi E. Jones CR. Academic Press. Snedeker SM. Chlorinated Hydrocarbon Insecticides. Chemosphere 2004. Schecter A. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Radomski JL. 96 Fourth National Report on Human Exposure to Environmental Chemicals .27:405-421. PA. Nims R. Lynch CF. Cerhan JR. Eds. Toxicol Appl Pharmacol 1971. Stehr-Green. DDE. Petrik J.150:981-990. Fonnum F. et al. J Toxicol Environ Health Part A 1998. Environ Health Perspect 2001. Vol.

Survey Geometric mean (95% conf.10 (<LOD-5. endrin has been detected with declining frequency in U. or discarded.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5..09 and 7. 1987). High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. At high doses. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.40 (<LOD-6.60 (5.50) < LOD < LOD < LOD 5. Because it is metabolized so rapidly. or from contact with contaminated soils and sediments in areas where endrin was applied. Depending on soil conditions. which may vary for some chemicals by year and by individual sample. 1981). largely the result of historical agricultural application or run off from contaminated soils (ATSDR. fatty infiltration. Endrin does not accumulate in body tissues (IPCS.S. is no longer manufactured in the U. rodenticide and avicide.S. 72-20-8 General Information Endrin. An epidemic of acute endrin poisoning. population from the National Health and Nutrition Examination Survey. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. 1992).8. EPA. manufactured. In the body. and inflammation (Smith. Ketoendrin is a major photodegradation product (IPCS.20 (<LOD-5. Smith. 1991).10 (<LOD-5. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.50) < LOD 5.20 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1991). 1992. endrin can persist for years. Over time. Endrin was not widely used as a termiticide. Kavlock et al. 1992).40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. < LOD means less than the limit of detection.40-5. 2008).30 (<LOD-6. have been cancelled by the U. 1992). see Data Analysis section) for Survey years 01-02 and 03-04 are 5. Endrin has been detected in soils. All uses of the pesticide in the U. total diet surveys (FDA. 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.. Fourth National Report on Human Exposure to Environmental Chemicals 97 .S.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. Endrin is absorbed rapidly after ingestion. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. anti-12hydroxyendrin.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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. endrin is converted rapidly to its major metabolite. unless the dose is high and the exposure is very recent. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) < LOD 5..Organochlorine Pesticides Endrin CAS No. 1979. and occasionally at low levels in sediment and surface waters. inhalation or dermal exposure routes. endrin usually is not detected in serum of exposed individuals.S. 1996. unlike aldrin and dieldrin. Endrin was used as an insecticide.S. a stereoisomer of dieldrin.. Hepatic effects of endrin exposure have included necrosis. IPCS.

020 (<LOD-.020) < LOD .html.020) < LOD < LOD < LOD .020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level.Organochlorine Pesticides The U.020) < LOD . Information about external exposure (i.S.020 (<LOD-. Workplace exposure standards for endrin have been established by OSHA.e. EPA has established environmental standards for endrin.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. In a small study of Spanish women hospitalized for elective surgery..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 .24 ng/g of serum) (Botella et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.020 (<LOD-.020-. 2004.020) < 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 . Ward et al. with the highest value 6..020 (.cdc. Survey Geometric mean (95% conf.atsdr. which may vary for some chemicals by year and by individual sample. serum levels of endrin were below the limit of detection. population from the National Health and Nutrition Examination Survey. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.24 ng/mL (about 6.020 (<LOD-.020 (<LOD-.020 (<LOD-. environmental levels) and health effects of endrin is available from ATSDR at: http://www. IARC has determined that endrin is not classifiable with regard to human carcinogenicity..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 .gov/toxpro2. and the FDA monitors foods for pesticide residues. 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. 2000). 98 Fourth National Report on Human Exposure to Environmental Chemicals . This finding is consistent with other general population studies (Bates et al. endrin was detected in 9% of serum samples. 2004)..

Hanisch RC. 4/21/09 International Programme on Chemical Safety (IPCS). Ward EM. Andersen A. 1991. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Perinatal toxicity of endrin in rodents.21:141-150. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Chernoff H. Convulsions caused by endrin poisoning in Pakistan. Inc. Available at URL: http://www. August 2008. Needham LL. et al.gov/toxprofiles/tp89. et al.html. Saleem M. Chernoff N. Frey JM. August 1996.9:1357-136. Eds.inchem. Fetotoxic effects of prenatal exposure in hamsters. Smith AG. Available at URL: http://www. I. Garrett N. 731-915. Botella B. Hardjotanojo W.org/documents/ehc/ehc/ ehc130. Olea-Serrano MF. Jr.htm. Rivas A. Cerrillo I. Environ Res 2004. Gray LE. No:429-436. Hanisch RC.gov/~dms/ pesrpts. Grajewski B. Gray J. Fetotoxic effects of prenatal exposure in rats and mice.54:1431-1443. 4/21/09 Kavlock RJ. Endrin [online]. 2 Classes of Pesticides. Kavlock RJ. Pediatrics 1987.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Cancer Epidemiol Biomarkers Prev 2000.96:34-40. 1992. 4/21/09 Bates MN. Available at URL: http://www. Buckland SJ. II. Ginsburg KS. Turner W. New York. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Schulte P. Gray LE. Rogers E. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Olea N. Toxicology 1979.79(6):928-934. Food and Drug Administration (FDA). Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Academic Press. Environmental Health Criteria 130. pp. Gray JA. Jr and Laws ER. Roy ML. Patterson DG Jr. Exposure of women to organochlorine pesticides in Southern Spain. Rowley DL.cfsan. Sokal D. Patterson DG Jr. et al. Rab MA.fda. Toxicology 1981. Ellis H. Chlorinated Hydrocarbon Insecticides. Vol. Whitehouse DA. Burse VW. Chemosphere 2004. Narahashi T.atsdr. Toxicological profile for endrin [online].13:155-165. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.html. Crespo J. In Hayes WJ. Perinatal toxicity of endrin in rodents. Liddle J.64-65 Spec. Handbook of Pesticide Toxicology.cdc. et al. Toxicol Lett 1992.

wildfowl. and has been detected in soil.2-31.6) < LOD < LOD 24.3 (20.5-trichlorophenol (2.4) < LOD < LOD 14.1 (17.8) < LOD < LOD 27. Gunderson.Organochlorine Pesticides Hexachlorobenzene CAS No.9) < LOD < LOD 28.2 (14.0-28.. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.5-33.6-26.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. 2005).7-15.7 (19.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1-16.6-32.7 (15. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.3) < LOD < LOD 20.0-16.9-24.7-22.7-26.5 (13.4) < LOD < LOD 23. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.9) < LOD < LOD 16.3-20.0-19. HCB is slowly metabolized.4.1) * * 15.1) < LOD < LOD 15. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.3 (12.8. 1976).5 (13. and accumulates in fatty tissues where it persists for years.5) < LOD < LOD 18. 100 Fourth National Report on Human Exposure to Environmental Chemicals .4) < LOD < LOD 19. 01-02. and foods with a high fat content.9) < LOD < LOD 19.9) < LOD < LOD 20.3) * * 15. respectively.8 (26.5 (14.4) < LOD < LOD 33.9-32. see Data Analysis section) for Survey years 99-00.4.6-19.6) 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. 2. HCB has been detected in fewer foods since the 1980s (FDA.0. and elimination occurs by renal and fecal routes. and 03-04 are 118.7-16.3-22.9 (14.4 (22.0 (18.4 (18.6) < LOD < LOD 25.7) * * 14..4. 2008.4-15.5-15. population from the National Health and Nutrition Examination Survey.8 (15.9) < LOD < LOD 20.4) < LOD < LOD 18.7) 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. and 7.6-trichlorophenol (2.7-21.4 (18.1 (13.5-14.6 (23.6) < LOD < LOD 26.0) * * 15. and sediment (Barber et al.4-16.3) < LOD < LOD 29.4 (11.0-25.2 (17.9) 19.1 (14.3) 24.5-TCP) and 2. particularly by consuming fish.6 (24.9-17.5-18.3 (22. The FDA dietary surveys have shown that over time.S.5-14.7) < LOD < LOD 24. Therefore.2) < LOD < LOD 13.9 (25. 1997). these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. 1988).6-33. air.9-20. which may vary for some chemicals by year and by individual sample.2-15.3 (14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 (13. 2002). or game taken from areas with HCB contamination.0 (18.4.9-30. 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. breast milk is an additional route of elimination in nursing women. Urinary metabolites include pentachlorophenol (PCP).8-15.8 (22.0 (14. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.3 (16.4.9 (25..8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.S.9-15. Survey Geometric mean (95% conf. distributes widely throughout the body.7-29. < LOD means less than the limit of detection.3 (22.2) < LOD < LOD 29. EPA cancelled its use in 1984.5-15. Although it is not manufactured as an end-product in the U. water.1-20. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.7 (15.7-30.6) < LOD < LOD 26.S.4) < LOD < LOD 22.2-15.1 (14.7 (27.6) < LOD < LOD 14.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.0) < LOD < LOD 24. The general population may be exposed to HCB through diet.6-TCP) (To-Figueras et al.3-26.7-16..9 (23.6-44.6 (21.S. primarily as a fungicide and seed treatment until the U.9) < LOD < LOD 15. 31.2 (24.0) < LOD < LOD 15.2 (14.0) < LOD < LOD 15. HCB is well absorbed after oral administration.0 (25.

104 (.111) < LOD < LOD .173) < LOD < LOD .125 (. With chronic exposure.073-.141) < LOD < LOD .191 (. immunologic abnormalities.132) < LOD < LOD .102) < LOD < LOD .095) * * . population from the National Health and Nutrition Examination Survey.095 (.081 (.090 (.127-.163-.095 (. EPA at: http://www. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.203) < LOD < LOD .113-. The U.097) .190 (.102 (. In humans.143-.gov/pesticides/ and from ATSDR at: http://www. Survey Geometric mean (95% conf.129) < LOD < LOD .088-.088-.140 (. Chronic feeding studies in animals have demonstrated kidney injury.174-.114-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.085) * * .145-.085-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.097) < LOD < LOD .090 (.114-..115 (.163 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.147-.086-.118-.099) < LOD < LOD .179 (.089-.109) * * .155) < LOD < LOD .cdc.086-.118) < LOD < LOD . and weakness.175) < LOD < LOD . acute doses produce central nervous system depression and seizures.095) < LOD < LOD 75th < LOD < LOD 90th * * .097 (. Biomonitoring Information Serum concentrations reflect the body burden of HCB.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . thyromegaly.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 * * .072-.079 (. 1982.090-.178-.078 (. and liver and thyroid cancers (ATSDR.094) < LOD < LOD .065 (.159-.088-.157-.S.147 (.atsdr. as well as hypertrichosis. Schmid.077-.089-.171 (.092 (. and many died before 2 years of age (Peters et al. ACGIH has developed workplace exposure limits for HCB.118-. EPA has established a drinking water standard.258) < LOD < LOD .e.121 (.203) < LOD < LOD . very high.090 (.186 (. reproductive and developmental toxicities. This condition.176-.145-.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .082-.099) < LOD < LOD .095-. HCB interferes with normal heme synthesis.091-.167 (.100) < LOD < LOD .Organochlorine Pesticides chemical.062-.163) < LOD < LOD . 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.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..086) < LOD < LOD . arthritis.069) * * .123 (. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.123 (.176) < LOD < LOD . More information about external exposure (i. Infants were exposed transplacentally and through breast milk.152) < LOD < LOD .196) < LOD < LOD .111-.069) < LOD < LOD .064 (.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 * * .225 (.169-.092 (.107-. 1960).gov/toxpro2. 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. and the FDA has established a bottled water standard for HCB. anorexia.083) < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .130) < LOD < LOD .081-.092-.135-. environmental levels) and health effects is available from the U.148-. which may vary for some chemicals by year and by individual sample.120 (.epa.160 (.094 (.123 (.182 (.156 (.107) < LOD < LOD . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.157 (.060-.087 (.098 (.092 (.099) < LOD < LOD .126) . 2002).122) < LOD < LOD .S. Fourth National Report on Human Exposure to Environmental Chemicals 101 .html.

HCB levels were directly related to age. Gocmen A. Safe A. Dewailly E. 1986. In a representative sample of the 1998 German adult population. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 2002. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. References Agency for Toxic Substances and Disease Registry (ATSDR).html. Schulz C. Arch Dermatol 1999. 2006). and the geometric mean concentration of HCB in whole blood was 0. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Lawrence River (Quebec..html. respectively.. Arch Neurol 1982. Lackman.9% of participants had quantifiable levels (Stehr-Green. however. Bjerselius R.. J Exp Sci Environ Epidemiol 2007. As a result of the lower limit of detection in NHANES 2003-2004. et al. Ozalla D. Available at URL: http://www.. April 1982 to 1984.. Herrman T. Otero R. dietary intakes of pesticides.135(4):400404. Piechotowski I. Available at URL: http://www. 1989). 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.. Becker K. Zoellner I. Kaus S. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. van Wijk D. 2005. Int J Hyg Environ Health 2002.58:1185-1201. Paepke O. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Dogramaci I. selected elements.81(2):82-85. Muckle G. more HCB levels were quantified. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Darnerud PO.54(3):203-208.fda.gov/ toxprofiles/tp90..gov/~dms/ pesrpts.. 1999). Dallaire F. only 4. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. September 2002. Link B. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Food and Drug Administration (FDA). HCB detection in serum also was proportional to age. Ayotte P. Eskenazi B. The metabolism of higher chlorinated benzene isomers. 4/21/09 Glynn AW. Lecha M. Bradman A. Environ Health Perspect 2002. Bradman et al. Kemper FH. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Sweetman AJ. Toxicological profile for hexachlorobenzene update [online]. Cripps DJ.. Gabrio T. Organochlorines in Swedish women: determinants of serum concentrations. Herrero C.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. J Assoc Off Anal Chem 1988. Seiwert M. and other chemicals. Canada). levels. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. 2002. Santiago-Silva M. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Peters HA. 2002.110(8):835-838. 2002. Biol Neonate 2002.cfsan. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. 2003). Aune M. et al.. et al.39(12):744-749. Kohli J. Barr DB. Reference values updated. Environ Health Perspect 2003. 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. In the 1976-1980 NHANES subsample. IARC Sci Publ 1986. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Bertram et al. Holland NT. 4/21/09 Barber JL. Glynn et al. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.44 mg/L. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Can J Biochem 1976. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Lackmann GM. Fenster L. Bryan GT. Atuma S. Krause C. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Schwartz JM. FDA total diet study. Lackmann. 2005). Chemosphere 2005. Biomonitoring of persistent organochlorine pesticides. 2002) and among children (Link et al. distribution. Gunderson EL. Lepom P. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. et al. Link et al. Sci Tot Environ 2005. Sala M. Over the past two decades. Jones D. 2002). lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002.205:297-308. Muller C. Jones KC. August 2008.77:173182. but overall. Laliberte C. In Spain. FDA Pesticide Program Residue Monitoring 1993-2006 [online].111:349355. 2005). Bertram HP.71(6):1200-1209.17:388–399.cdc. trends and processes.atsdr. Hexachlorobenzene in the global environment: emissions.349:144. Granath F.

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

7) 23.8 (23.1) 13.0 (37.60-13.1 (30.9 (32.6) 18.3) 37.5-123) 49.5) 29.7 (25.9 (40.90-8. < LOD means less than the limit of detection.70-12.6-89.5) 11.6) 35.4-73.1 (21.7 (53.0-111) 70.4) 901 1067 952 992 1224 1007 Females 11.5 (11.9) 45.4 (16.20-16. 319-85-7 gamma-Hexachlorocyclohexane CAS No.0-20. Technical grade HCH is a mixture of all four isomers.8-19. and 03-04 are 9.6 (33.7) 97.04-10.2 (48.2 (31.8 (32.8) 27.7 (30. HCH isomers are lipophilic.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19. The gamma isomer.1) 31. interval) 9.9-21.0 (8.50) 8. formerly referred to as benzene hexachloride. and sediment as a result of historic production and use.2 (18.8-87.6 (17.5 (24. including alpha.7) 32.8) * * * * * * 15.9-14. particularly alpha and gamma have been detected widely in air.2-46. see Data Analysis section) for survey years 99-00.6) 50.3-38.76.8) 52.70 (8. The other isomers can be formed during the synthesis of lindane.5) 90th 42.4) 11.7-26. gamma.6-135) 69.89 (<LOD-9.0) 17.4) 51.90-8.4-45.8-54.1 (18.6-18.1-32.36.8 (21.9 (9. See the section “What’s New” at the beginning of this Report for details.1 (27.6-20. 608-73-1 beta-Hexachlorocyclohexane CAS No.9) 15.80 (6.8 (10.5528. 2005).3 (42.5 (37.9) 81.4) < LOD < LOD < LOD 46. HCH isomers. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.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. each result has been multiplied by 1.3-85.4 (11.5) 14.7-96.7) 10.6 (40.0 (14.3 (26.4 (50.2-98.3 (13.9 (11.2-17.2-87. population from the National Health and Nutrition Examination Survey.6 (10. 58-89-9 General Information Hexachlorocyclohexane (HCH).3 (62.9 (50.0-70.2 (50.7) 27.7 (29.0) 7.S.1) 12.5 (8.0 (19. exists in several isomeric forms.56-12.3) 25.5) 22.43 (<LOD-9.1-49.2-67.7-69.8) < LOD 10.9 (30.3 (42.2) 62.3) 14.8 (33. 6. respectively.6) 36.3) 51.8) 39.1) 71.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.5) 67.7) 73.6) 47. containing about 64% alpha and 10%-15% gamma isomers.8) 95th 68.2-42.5) 16.46-11.1) 12.9) 17.4) 27. 104 Fourth National Report on Human Exposure to Environmental Chemicals .6-47.7) 18.2-20. and have been used either as fungicides or to synthesize other chemicals.8 (64.1 (12. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.2 (29.1-37.2-52.6-62.8-199) 134 (85.4) 21.0) 41. **In survey period 2001-2002.6) 16.70 (6.0-21.9-81. so they can accumulate in fatty tissues of animals.68 (<LOD-10.2 (34. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. commonly known as lindane.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.9-178) 48.1 (11.2) 13.90) 7. Lindane has a half-life of about two weeks in soils and water.4-50. soil.6-37. which may vary for some chemicals by year and by individual sample.7 (35.8 (9.7-166) 70.4) < LOD 9.9-51.0-34. environmental levels declined.2) 36.5 (16.87 (9.2 (9.4) 44.70-19.0 (35. In 2006.8) 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5) 40.Organochlorine Pesticides Hexachlorocyclohexane CAS No.6 (16.7 (62. 2005).1-36.0 (<LOD-12.61-12.9-56.5 (14. It is no longer produced or sold in the U.9 (62.80 (<LOD-14.6) 653 758 589 1240 1533 1370 20 years and older 10.7) 10. water.2) 9.7 (<LOD-16. 01-02.9-24.4) 10.0-23.0) 35.1-32.1-15.0) 8.4 (52.0) 71.0-70.1 (16.8 (17. the U.8-16.3) 34.5 (43.7-96.8-68. EPA cancelled agricultural uses of lindane (ATSDR.66-12.8.30-11.1 (9.2-22.2) 142 (99.7) 56.0 (33. and delta.1 (9. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR. beta.S.7 (13.3-56.6 (22.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.5-29.2-55. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.S.1-16.7-69.4-111) 84. and 7.4 (8.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.8) 12. However.6-14.1-27.4 (12. As pesticide applications of HCH were increasingly restricted or eliminated.9 (26.7-20.6-42.

372 (.057-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.100 (.060) . OSHA and ACGIH have established workplace standards and guidelines. hepatic enzyme induction. resulting in a half-life of about seven years.160 (.100) .37) 1.150 (.380 (.100-.450) .S.067) .240-. or dermal exposure.089) .480 (. 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.480 (.280-.040-.056-. and memory loss (Nigam et al.210-..190-. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.120) .510) .350) .080) .250) .S. After dermal application of lindane 1% lotion.400) .210) .110) .131-.281 (.290) . When animals were chronically fed lindane at high doses.103 (.305) . 1981).090 (.170-.080) * * * * * * . **In survey period 2001-2002.048 (<LOD-.050-.056-.200 (.Organochlorine Pesticides exposure to HCH is through the diet.190) .160) .096) . Saxena et al. population from the National Health and Nutrition Examination Survey.103) 90th .070-.220) .150) .173-.130-.065 (.300-.140) . and FDA has established a bottled water standard and food residue tolerances for lindane.090-.150) .270 (.260-. each result has been multiplied by 1. tremors.410-. and seizures.310) .070 (. Workers who directly handled HCH have complained of headache.139 (.. interval) .330-.050) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .083) .410 (.080 (.410) .501) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.230-.124-.100 (.222 (.710) .234 (.480) .470) . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.. ataxia.100) .120) .091) . respectively.294-.050 (.140) .118-.370-.404) .32) .320 (.167 (.119) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .244-.814) . 2008.319) .077) < LOD .690) . probably by blocking inhibitory neurotransmitters in the central nervous system.460 (. The U.620-1.100-.050-. Rogan.051-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.073-.090 (.460) .360) .297-. U.310) .190) .910 (.067 (. 1983).146-.103-.086) < LOD < LOD < LOD < LOD < LOD < LOD .01 (.191-.280-.250-.260) .065 (. which may vary for some chemicals by year and by individual sample. 1977).200-. for lindane. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.250-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .080 (.070) . See the section “What’s New” at the beginning of this Report for details. Gunderson 1988).350 (. The beta isomer accumulates in fatty tissues and is metabolized more slowly.050-.072 (.214) .390-.382-.098 (.360 (.250 (.340-.100-. HCH isomers are absorbed after inhalation. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.340) .092 (.047-.150-.390 (.450 (.240 (.120-.062 (.220 (.521 (.661) 901 1067 952 992 1224 1007 Females .130 (.310 (.070 (.064) .580-1.560 (.083 (. and nephropathy developed (IPCS..125) < LOD < LOD < LOD .144 (. EPA has established a drinking water standard.210 (.360-.110) .840) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.051 (<LOD-.331 (.450-.059-.260) .580 (.068-.400) . the serum half-life was about 20 hours among children (Ginsburg et al.057-.216 (.S.470 (.570 (.080-.620) .221-.220-.080-. paresthesias.077) < LOD .560) .191-.069) .600) .078 (.064 (.410) .120 (.587) 653 758 589 1240 1533 1370 20 years and older .130) . 1986).140 (. Distribution is mainly to fatty tissues.160-.180-.058 (<LOD-.090 (.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 .050 (<LOD-.330 (.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.05) .254) 95th .120 (.081-.050 (<LOD-.250 (.412 (.210 (.050-.120 (.290) . FDA pesticide monitoring program has shown a temporal decline in the detection of lindane. enlarged livers.308-. 2002)..700) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .140) .250 (.442 (.290 (.420-.062 (.680) .200-.290 (.110) .5528.070-.057 (<LOD-.050 (.175 (. 1971. 1996.170-.287 (.089-.120-. ingestion.174) .118 (.190-1.080-.290 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.120-.110-.220-.070-.

see Data Analysis section) for Survey years 99-00. 1991.atsdr. Additional factors associated with higher beta-HCH levels include rural residence. Survey Geometric mean (95% conf. 2005..S. population from the National Health and Nutrition Examination Survey. 10.. Biomonitoring Information Because of its longer half-life. Bates et al. and 2003-2004. Becker et al. More information about external exposure (i. 2002. 1998).. 1989.epa. 2004).e. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. 1991.8. environmental levels) and health effects is available from the U..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 1998.. and 03-04 are 14. 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. 01-02. 2004. 106 Fourth National Report on Human Exposure to Environmental Chemicals . were similar to the 95th percentiles in this Report. Stehr-Green.. 2004) and India (Bhatnagar et al. male sex.html. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. In recent years. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. Link et al. 2001-2002.S.cdc. respectively. Kutz 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. 2005. 2002). Stehr-Green. In an earlier (1996-1997) sample of German children. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. older age. < LOD means less than the limit of detection. respectively. serum levels of lindane were generally below the limits of detection. In NHANES 1999-2000. 1971.5. Kutz et al.. Radomski et al. aged 9-11 years.gov/toxpro2.. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al..5. which may vary for some chemicals by year and by individual sample. 1989).gov/pesticides/ and from ATSDR at: http:// www. EPA at: http://www. the maximum and 95th percentile beta-HCH values. In populationbased studies of New Zealand adults and German adults and children. Sturgeon et al. and a diet that includes meat (Becker et al.. and 7.

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. in this Report (Nigam et al.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Radomski et al. In a small study of adults who consumed sport fish from the Great Lakes. population from the National Health and Nutrition Examination Survey. 1971). Survey Geometric mean (95% conf. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. 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. 2003). the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson 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.. which may vary for some chemicals by year and by individual sample. respectively. 1986. 1998). 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.. 2005).. 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. Fourth National Report on Human Exposure to Environmental Chemicals 107 .. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

J Assoc Off Anal Chem 1988. Available at URL: http://www. Environ Res 2004. Lowry W. Krause C. Gunderson EL. Heinrich R. Rey AA.9(4):417-424. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Saxena MC. Karnik AB.54:1431-1443. Paepke O. Kutty D.htm. Visweswariah K. Botella B. Needham LL. Chemosphere 2004. PA. Rothman N. Cancer Causes and Control 1998. International Programme on Chemical Safety (IPCS). Lindane. August 2008. Demographic and seasonal influences on human serum pesticide residue levels. FDA total diet study. available at URL: http://www.58:1185-1201.48:127-134. Nigam SK. Reisch JS. Bjerselius R.gov/~dms/pesrpts. Stehr-Green. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. 4/21/09 Ginsburg CM. April 1982 to 1984. gov/toxprofiles/tp43.atsdr.72:261265. Becker K. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant.205:297-308. Rivas A. Arch Pediatr Adolesc Med 1996.cfsan. et al. Bull Environ Contam Toxicol 2004. Olson J. Zoellner I. HCH. Metabolism of gammahexachlorocyclohexane in man. Granath F. Crespo J. Garrett N. Gabrio T. Piechotowski I. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.111:349355. Brock JW. Bhatnagar VK. Rogan WJ. dietary intakes of pesticides. selected elements.27:405-421. Olea-Serrano MF. Seiwert M. Bottimore DP. Lepom P. Maass R. Biomonitoring of persistent organochlorine pesticides. Environ Health Perspect 2003.71(6):1200-1209. Pollutants in breast milk. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.html. August 2005. Link B.20(2):186-193. 2002. Int J Hyg Environ Health 2002. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Krishna Murti CR. children and newborn infants. India. J Toxicol Environ Health 1989. Siddiqui MKJ. et al. Wood PH. Sturgeon SR. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Int Arch Occup Environ Health 1983. Buckland SJ.fda.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). et al. and HCB residues in human blood in Ahmedabad. Radomski JL. Hanrahan L. Bai KM. Arch Toxicol 1981. Patterson DG Jr. Cerrillo I. Needham LL. Aune M. Brinton LA. Occupational exposure to hexachlorocyclohexane.120:1-82. et al. et al. org/documents/jmpr/jmpmono/2002pr08. Toxicol Appl Pharmacol 1971. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Olea N. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Placental transfer of pesticides in humans.96:34-4Food and Drug Administration (FDA). J Pediatr 1977. Zaidi SS.57(4):315-320. Environ Health Perspect 1998. Bhargava AK. et al. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 4/21/09 Kutz FW. Chemosphere 2005.html. Kashyap R.106(5):279-289. and other chemicals. VI. Herrman T. Potischman N. Rev Environ Contam Toxicol 1991. Levels of DDT. 4/21/09 Anderson HA. Darnerud PO. Int Arch Occup Environ Health 1986. Ellis H. Bates MN.cdc. Atuma S. Kaus S. Angerer J. Kulkarni PK. Glynn AW. Saiyed HN.150:981-990. Majumder SK. Exposure of women to organochlorine pesticides in Southern Spain.inchem. Falk C. Absorption of lindane (g benzene hexachloride) in infants and children. Deichmann WB.91:998-1000. Raju GS. Available at URL: http://www. Burse VW. Organochlorines in Swedish women: determinants of serum concentrations. Needham LL. Astolfi E.52(1):59-67. Toxicological profile for hexachlorocyclohexanes update [online]. Schulz C. The Great Lakes Consortium. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.

Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. sediments.S.8.70-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.1 (<LOD-65.0 (<LOD-108) < LOD < LOD 50. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.5-291) 11.6) 9.1) 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. Mirex binds strongly to soil. after which it is widely distributed in the body and stored in fat. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.0 (14. Formerly. where it has a half-life of 12 years.4 (8.70 (<LOD-15.3 (15.5 (9.1 (13. In studies conducted in the 1970’s and 1980’s. 2385-85-5 General Information Mirex has not been produced or used in the U.10 (<LOD-15. population from the National Health and Nutrition Examination Survey. it is a highly persistent chemical in the environment.6 (<LOD-108) 9.40 (<LOD-13. and 03-04 are 14. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. 1995). since 1977.S. especially those from persons living in the southeastern U. 10. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.8 (12. 1991). (Kutz et al.8 (<LOD-73. aquatic organisms. or pesticide application. 01-02. and 7.Organochlorine Pesticides Mirex CAS No.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.S. Mirex is absorbed through the skin and from the gastrointestinal tract.4) < LOD 63.0 (12. 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.70-40.10-37.6.0-374) 11. where it was applied directly to soil and by aerial spraying. Fourth National Report on Human Exposure to Environmental Chemicals 109 . Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4-230) 18.7) 8.7 (12.5. mirex was detected in human adipose samples.3-225) 15.6 (<LOD-23. Mirex can cross the placenta and be excreted in breast milk. 1985..6 (<LOD-31. animals. respectively.2-230) 13. see Data Analysis section) for Survey years 99-00. Occupational exposure is limited to workers at sites where mirex contamination is present. Some states and the U.3 (15.. Mirex is not metabolized in the body.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.4) < LOD 15. and foods.6) < LOD < LOD < LOD < LOD 71.2 (7.5 (<LOD-42.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.S.6-305) 15. disposal.5-425) 40.7 (<LOD-47.S. which may vary for some chemicals by year and by individual sample.90-29.8) < LOD 15.2) 51.5 (<LOD-115) 153 (30.3) 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. resulting in exposure to newborns and nursing infants. water. soil.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.1 (8. Mirex has been detected in air.7) < LOD 66.5-82.

112 (.atsdr.080-1.052-.92) .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.055-.090-1. Survey Geometric mean (95% conf.470) . 2001-2002.090-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .090 (<LOD-.610) < LOD < LOD < LOD < LOD .256 (. 1991). In samples obtained between 1994 and 1997.106) < LOD . 1989). and 4.170) < LOD .110 (<LOD-.79) .090 (<LOD-.090 (<LOD-.37) .cdc.100 (<LOD-. 2004). In addition.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.510) < LOD < LOD . Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions.02) .062-.053-.410 (. reproductive toxicity included decreased fertility and testicular damage.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 .106 (.089-.690) . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. 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. serum mirex levels were generally below the limits of detection (Stehr-Green.79) . as well as in a subsample of NHANES II (1976-1980) participants. Laboratory animals fed high doses developed liver enlargement and liver tumors.. 110 Fourth National Report on Human Exposure to Environmental Chemicals .090-1.077 (<LOD-.140 (<LOD-.054 (<LOD-. 7.8. and 2003-2004 subsamples.430 (.html.079 (<LOD-.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 .080-1. Smith.7 ng/g of lipid.Organochlorine Pesticides exposures are unknown.73) .450) 1. 2005).102) < LOD < LOD < LOD < LOD .170-3.059 (<LOD-. population from the National Health and Nutrition Examination Survey.470) .gov/toxpro2.100 (<LOD-..08 (.450 (.S.220 (<LOD-.. The U. Biomonitoring Information In the NHANES 1999-2000.41) . environmental levels) and health effects is available from the ATSDR at: http://www. The geometric mean mirex levels of the Inuit mothers were 8. More information about external exposure (i.470 (. EPA has established environmental standards for mirex.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.070-1.064 (<LOD-.S. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.e.635) < LOD .268) < LOD .370 (. IARC classifies mirex as possibly carcinogenic to humans. 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.220) . 1995.093 (.108 (.310 (. 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.

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

4.5-trichlorophenol (2. EPA.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) 2.40-11.00 (2. usually at herbicide production or waste incineration facilities.6-trichlorophenol (2.40 (1..5TCP and 2.3.30 (. 95-95-4 2.00-3.60 (4.50) < LOD 1.0) < LOD 21.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20) < LOD 90th 5.0) 2.20) < LOD 1.10-3.40 (2. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.0) 2.00 (3.80-41.0) < LOD 5.50-16.4. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. which may vary for some chemicals by year and by individual sample.40 (2.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50-25.50 (.0) < LOD 5.5-TCP) and 2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.63) 18.40) < LOD 1.0 (3. Trichlorophenols are no longer manufactured commercially.7) 24.20) < LOD 5.03) 9. are metabolites of several organochlorine chemicals.900-2.0) < LOD 11. 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 (3.42 (<LOD-12. Occupational exposures.50 (1. soils.4.S.5-trichlorophenol.00-8.60-18.6-TCP were used as intermediates in the production of certain pesticides.31 (<LOD-9. < LOD means less than the limit of detection. and polychlorinated benzenes (Kohil et al.0) 2.40 (.0) 14.90-33.72) < LOD 1.40-18. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. including hexachlorobenzene and hexachlorocyclohexanes.40) < LOD 4.71 (<LOD-8.30) < LOD 4. 1999). but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.6-TCP in any of the samples (U.4.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.0 (8. population from the National Health and Nutrition Examination Survey. surface water.20-71.4. may occur by inhalation or dermal routes.6-Trichlorophenol CAS No. public drinking water systems did not detect 2.Organochlorine Pesticides 2.9.30-27.0 (5.4.980-3.9 and 0.40 (1.0) < LOD 5. Both chemicals have been detected in air. Historically. 2.30) < LOD < LOD < LOD < LOD < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. recent sampling of U.57 (<LOD-15.30-3. Formation of 2.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1976).0) 2.40) < LOD 6.60 (.7.940-3.0 (4.80 (2.20 (4.40 (2. other organochlorines.20-36. 2.30-44.0) < LOD 11. hexachlorobenzene.5-Trichlorophenol CAS No.980-3.4.30-27.50 (2.0) 2.0 (4.0) 5.60 (2. 2.80) < LOD 1.60) < LOD 8.19 (<LOD-6. Survey Geometric mean (95% conf.0 (4. Such workers would probably Urinary 2.50-63.42 (<LOD-8.4.4.40 (.8) 21.S. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.30-11.6-TCP).27) 696 661 521 696 603 939 Limit of detection (LOD.00-3. however.S.4.4.920-3. and sediments.30-27.40 (2.950 (<LOD-1. Exposure to trichlorophenols also may result from metabolism of lindane.4. 112 Fourth National Report on Human Exposure to Environmental Chemicals .71 (<LOD-8.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.30-40.9 (<LOD-121) 9.60-8. 2006).80 (1. 1999).

4.53-3.47-8.1) 2. 1995) were similar.0 mg/L.8) 4.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.67 (1. urinary 2. as being possibly carcinogenic to humans. environmental levels) and health effects is available from ATSDR at: http://www.6-TCP had increased rates of hepatic tumors.53-3.29 (1.4.5-TCP or 2.0) 7.4.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .27-17. In the same 2-6 year old children.00-19.83-12.74) 11.75 (<LOD-6.73 (<LOD-8.4. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.5) < LOD 12.68-4. and lymphomas.15) < LOD 2.16) < LOD 90th 5..57 (<LOD-7. IARC classifies combined exposures to polychlorophenols.. the 95th percentile urinary 2..html. 2003).24-11.32) < LOD 4.4.7 (4.8) < LOD 9.4.9) 12.820-2.5-TCP and limited for 2.24) < LOD 5.24) < LOD 6. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al. animals showed hepatocellular abnormalities.81 (<LOD-9.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78 (3.gov/toxpro2.57 (3.75 (3.5-TCP.3 mg/L reported in German adults aged 18-69 years (Becker et al.78-19. Urinary 2. Neither 2.6) 4. Human health effects from 2..78) < LOD 1.24 (3.19-4.3 (5.24) < LOD 1.13-13.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.6-TCP.05-8.19-12. in addition to dioxins.6-TCP as reasonably anticipated to be a human carcinogen. However.2) 2. Survey Geometric mean (95% conf.64 (4.atsdr.6) 4.4) 5.8 (5.93-11.37) 16. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.46 (1.02-3.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-TCP nor 2. At lower doses.4) < LOD 3.1 (<LOD-58.31) < LOD 2. Fourth National Report on Human Exposure to Environmental Chemicals 113 . and other chlorinated compounds.33) < LOD < LOD < LOD < LOD < LOD 2.920-2. population from the National Health and Nutrition Examination Survey.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). The 95th percentiles for 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.36 (1.S.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. More information about external exposure (i. 7. NTP classifies 2.37-11. 1995) and up to 19 times higher than the 95th percentile value of 1.67 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003. which includes trichlorophenols.79-4.62-20.49 (1.6-TCP levels at the 95th percentile were up to eight times higher than 3. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2..20-6.4.cdc.88-16.00) < LOD 4.44 (1.4.Organochlorine Pesticides be exposed to mixtures of chlorophenols.02) < LOD 7.43) < LOD 12.e.86 (3.69 (2. 1989).82 (<LOD-32.00-29.16 (. furans.5) 11.4..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 2.60-3.2 (2. Radon et al. Laboratory animals chronically fed high doses of 2.4.95 (3.9 (5.6) 4.4.2) < LOD 5.44 (.50) < LOD 2.05-17.4) < LOD 3. Among 6-11 year old children in NHANES 1999-2000..11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 2004).4.68 (<LOD-8.43 (2.980 (<LOD-1.28-25.4 (6.80 (1. leukemias.69-18.90 (4. 1989).57 (<LOD-7..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.17) 9.4. the 95th percentile urinary 2.55 (4. 2003)..2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.

6TCP causes an adverse health effect.31) * 2.84) 2.0) 13.70-3.95) 3.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.08 (2.0 (9.0-50.67) 4.0 (6.55-3.53) 4.4.67-12. population from the National Health and Nutrition Examination Survey. Mean values of 2. In harbor workers exposed to chlorophenol-contaminated river silt.07 (<LOD-3.99) 6.4 (17.00 (2.49 (6.40) 2.9) 13.4 (10.0-18.00 (4.0 (11.0-68.8) 18.18-3.70 (2.24 (2.20-6.0-54.0-43.0) 10.0-38.89 (3.10-3.80-25.6) 21.90-8.80-20.63) 90th 15.36 (1.6 mg/g creatinine) and 2.S.79 (5.60 (3.60 (2.73-9.80-7. the median urinary 2.0 (14.80 (2.4. which may vary for some chemicals by year and by individual sample.5-TCP and to the median 2.0 (6.7 (13.7 (9.56 (3.5-TCP or 2.09-7.0 (4.0) 9.12) 2.6TCP values. Biomonitoring data will also help scientists plan and conduct research about 2.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.66 (8.8-24.74 (2.3) 20.7 mg/L.60-3.1 (8. Survey Geometric mean (95% conf.40-2.89-6.3.4 (8..45) < LOD 11.57 (<LOD-2.70) 1.47 (3.20 (3.5-TCP level of 0.70 (2.78 (2.91-4.30) 4.6-TCP in urine does not mean that the level of 2.3 (11..95-6. Finding a measurable amount of 2.90 (3.70) 5.0 (16.40) 3.4.45 (5.65 (5.70-6.0) 13.0) 19.30-2.2-0.0) 11.28) 24.40 (2.50-5. for males in NHANES 19992002 (Agramunt et al.69 (3.1-25.10) 6.40) 4.6-19.23) 3.87-14.33-4.01-6.10-3.40-4.7-16.98-7.40 (2.5-TCP and 2.74-3.20) 4.04) 2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.4. 1991).6-TCP (0.10 (5.3) 23.80) 1.45 (2.0 (14.50 (2.00-21.51-12.4.7) 33. < LOD means less than the limit of detection.70-6.6 (11..4.5-TCP or 2.90) 2.6) 26.60) 6.65) 15.0 (8.40-14. Urinary 2.8-13.98-11.52-3..6-22.30-33.10) 2. 2004).0 (7.2) 25. respectively.4 (9.0 (14.0) 14.0) 6.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.6-17.58-3.5-TCP and 2.0 (13.32-4.4.0) 19.40) 2.0-37.72-10.4.54) 6. 2003).92 (2.28) * 2.75 (8.4.30-11.0) 15.40-7.0 and 1.40-2.60 (3.1) 16.2) 12.02) 2. Biomonitoring studies on levels of 2.25-11.10-2.4.48-26.80 (3.0-38.0-41.6-TCP level.70) 3.0 (15. 0.4.59) 4.0) 7.95 (4.35-3.0) 13.80-6.40-32.44) 75th 4.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.58 (1.8 (9.9) 694 677 519 696 602 931 Limit of detection (LOD.7-3.8) 32.0) 17.06) * 2. similar to the limit of detection for this Report (Anderson et al.85 (2.23) 2.4.09) 15.60-37. Urinary 2.0 (20.0) 7.0) 17.9 (13.7) 21.8-15.85) * 3.90 (4.5-TCP or 2.9 (11.4.4.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.4.78 (2.5-46. interval) 2.0) 11.0) 13.60) < LOD 5.0-44.0 (20.20-3.20-23.3 (11.45-9.00 (1.3) 37.36-5.1 (10.0 (8.0 (15.5 mg/g creatinine) were similar to the limit of detection for 2.23-2.70) 5.36 mg/g creatinine.0 (6.5-TCP or 2.2 (14.4.60-21.00-4.14 (2.4-17.0 (12.4.4.4. 1998).0) 9.76) 3.0) 14.68 (<LOD-2.3-17.20 (3.32) 3.31 (3.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.52 (2.53) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.30-2.46-3.4. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.6 (12. 114 Fourth National Report on Human Exposure to Environmental Chemicals .3-26.6-TCP exposure and health effects.59-6.5-TCP (0.0) 12.80 (2.6-TCP than are found in the general population.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. was about six times lower than the median urinary levels for males in this Report (Radon et al.0) 10.26 (2.32) * 3.

4) 9.41 (3.29-4.88) * 2.41-6.65) 18.63) * 4.43-7.1) 14.52) 2.06) 11.14-13.52 (3.30-2.76-8.0 (11.48-2.29-4.47-5.49) 4.50 (2.9-64.89) 10.13-6.18-4.15 (1.9-29.87-6.53) * 2.Organochlorine Pesticides Urinary 2.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.53 (3.62-15.6 (5.88 (2.19-5.76) 4.78) 2.22-9.22-2.14-2.20-2.11) 10.04-16.33) * 2.22 (3.1) 11.68) 2.67-17.S.73-22.2 (7.40 (7.63 (<LOD-2.76) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.42 (2.21-11.05 (6.54 (2.6 (22.79-17.08-2.5) 12.2 (8.18-2.96) < LOD 4.88-7.89-2.0 (6.8) 11.81) Selected percentiles ( 95% confidence interval) Sample 95th 21. population from the National Health and Nutrition Examination Survey.33-2.91 (7.33 (1.8) 19.77) 2.1-32.94-13.5) 11.56 (7.9) 19.70-9.5 (8.6) 12. Fourth National Report on Human Exposure to Environmental Chemicals 115 .81) 2.06-2.95-2.88) 4.5) 11.51-21.78 (2.51 (2.1-21.25-2.77-4.28-4.72-16.33 (7.10) 4.4 (12.9-32.68) 2.53) 4.2) 19.99-2.9-34.3-37.25-15.6 (10.00) 4.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.3 (9.02 (1.7) 25.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.23) 4.63-15.02) 3.82) 2.6 (12.01 (3.6 (6.04-2.6) 8.10 (6.38 (4.4 (11.59 (2.5) 8.72) 32.05 (3.71 (3.65-21.73) 5.9) 7.3) 8.44 (3.22 (<LOD-2.17) 13.82-2.00) 4.16-10.23 (1.5) 9.25 (3.42) 2.43 (2.4) 8.32 (2.76) 2.53-11.87) 2.90) 2.38 (2.58 (4.13 (1.91 (3.91-2.52) 2.9 (9.9 (9.00 (2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.35 (3.5-28.8) 21.0) 8.24 (1.88) 4.25-17.26 (6.98 (1.17-4.27-9.17) 2.83-6.56-5.9) 8.82 (3.22 (1.63-13.5 (10.56) < LOD 11.65-2.55-2.25 (3.6 (9.8 (7.7) 6.63 (2.26-13.38) 22.09-3.87) * 2.6 (9.82 (8.40 (2.00 (3.9) 8.63) 4.32-19.0 (9.46-14.98) 10.8) 12.3-23.83 (3.5 (7.66-4.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.60-2.87 (3.10-9.8 (8. interval) 2.0) 10.7-36.88) 1.92) 4.50-8. Survey Geometric mean (95% conf.29 (6.75) 75th 4.2 (13.1 (13.1 (8.52 (5.65) 2.7 (14.83-6.6) 13.2 (12.60 (4.4) 4.83-5.78) 90th 12.6-31.81-9.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.51) 18.87-7.49-3.06) 4.43 (<LOD-2.90 (1.15 (6.88) 5.4.38-5.

The Great Lakes Consortium.pdf.71:99108. Kohli J. Needham LL. Fast DM. Available at URL: http://www. Toxicological profile for chlorophenols [online]. Luotamo M. To T.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.63:57-62. S. Seifert B. Schulz C. et al. Hill RH Jr. Environmental Protection Agency (U. Becker K. Hanrahan L. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.gov/toxprofiles/tp107. Seiwert M. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). html. Arch Environ Contam Toxicol 1989. Lindroos L.45:440-445. Wegner R. Corbella J. Int Arch Occup Environ Health 1991. Anderson HA. Radon K. Pesticide residues in urine of adults living in the United States: reference range concentrations. Bailey SL. Urinary excretion of chlorinated phenols in saw-mill workers. Burse VW. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.S. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Safe A. July 1999. Available at URL: http://www.54(3):203-208. Head SL.146:83-91. Am J Ind Med 2004. Falk C. December 2006 Draft. Jones D.18(4):469-474. Pekari K. Baker S. Environ Res 1995. Domingo JL. Needham LL. Poschadel B. Szadkowski D. Smith SJ. 4/21/09 Agramunt MC.epa. Int J Hyg Environ Health 2003.EPA). Olson J. Toxicol Lett 2003. Holler JS. Heinrich-Ramm R. Hill RH Jr. Shealy DB. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Can J Biochem 1976. 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].cdc.atsdr. Environ Health Perspect 1998. Aitio A. Domingo A. Gregg M. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Kaus S. The metabolism of higher chlorinated benzene isomers. et al. Jarvisalo J. U.106(5):279-289. Baur X. et al. 206:15-24.

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

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

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

80) 2.91) 4.757-2.10 (2.8) 19.00-12.750-1.40-14.27-15.00-27.740-2.3) 14.530 (<LOD-2.00 (5.56 (6.94) * * .0) 10. < LOD means less than the limit of detection.00) 3.00-7.4 (9.0 (8. 120 Fourth National Report on Human Exposure to Environmental Chemicals .20-4.10 (2.35-12.33-18.60) .74 (8.35-11.860-2.00-27.0-28.6) 18.99 (5.39 (8.700-1.80 (4.70) < LOD < LOD 75th 3.1 (10.19) 9.58 (2.56 (4.1.70) .0 (7.0) 10.60-11.74 (8.28) 1.70 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.04) < LOD 1. respectively.44 (2.46) 10.0) 6.3) 16.3) 17.08 (<LOD-2.30-4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4) 20.73) * * .90) 3.90-5.86-15.0 (9.02-5.758-1.2) 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 1.48-7.7 (14. interval) 1.2) 471 576 308 664 822 701 814 1122 922 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.50-5.68-7.12) 4.2 (9.42-3.2) 14.80) 2.93 (4.290 (<LOD-.80-22.95) 5.82-12.07-10.67) 3.13 (2.0) 6.0) 11.26-6.810-1.56 (1.5 (8.2 (11.0) 15.58 (3.0 (7.81) 11.50) 2.70) < LOD < LOD 1.05-7.94) 3.40-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-7.32 (.90) 2.08-15.47) * * 1.2-20.97) 90th 7.23-5.30 (2.8) 11.00-19.830 (<LOD-3.50 (4.56-13.61 (3.1 (9.0) 5.9) 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 1.35-16.15-12.20 (2.89) 9.40-1.20 (.55-6.81) 1.38-5.8) 7.1) 95th 13.670-1.10) < LOD .16 (2.0) 5.70-11.290 (<LOD-1.00) 3.890 (<LOD-2.0 (5.00 (4.53) 4.4) 17.0) 9.0 (8.5 (11.2) 16.47) 5.0 (6.98-5. see Data Analysis section) for Survey years 99-00.40-11.21) 9.70-14.57-7.54 (3.0) 10.52) 6.37 (3.9-18.44-38.33 (5.82) 10.72) 5.0) 5.2) 16.20 (.96-3.44-3. and 03-04 are 0.4 (7.29) * * 1.00 (1.85 (3.61) 4.34-3.9 (8.71 (2.5-17. population from the National Health and Nutrition Examination Survey.620-1.0) 10.80) .20-30.80-4.2 (14.7) 11.0 (6.954 (.1-23.8) 7.579-1.40-19.03 (.0) 20.20 (.15) 14.717-1.50-36.02) 4.981 (.00-12.0 (7.599-1.66) * * 1.36-4.0) 11.50 (2.4 (7.2.11 (.26 (5.2 (7.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.0-27.21 (.50 (.623-1.17-3.60-18.63) 1.80) 3.2 (14.0 (7.01) * * 1.40-16. 0. and 0.7 (12.9) 8.2.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40 (.2 (9.10) < LOD < LOD 4.5) 15.43-12.42) .2 (7.8 (12.52-11.55-8.0 (12.30 (4.840-1.60) < LOD < LOD 4.600 (<LOD-1. which may vary for some chemicals by year and by individual sample.0 (4.80) 11.34-7.10 (.0) 7.1) 10.90 (1.14) * * .0) 6.12-19.80) 2.90-4.780) < LOD 3.81) 11.0) 11.93-24. 01-02.26-8.51) 2.79-7.0) 11.3-15.8-32.4) 18.80 (2.39 (3.0) 10.8 (8.0 (9.79 (5.20 (.30 (2.16) 4.13 (2.71-9.5) 20.60 (1.490-2.6) 7.27-3.60-25.2 (7.1-17.8 (14.83 (5.9) 14.08-2.70 (4.86 (1.97) 8.20-7.30-6.32) 1.70-19.80) 4.0) 12.8 (9.22 (.0 (8.13-2.45 (2.76 (2.970-2.10 (.S.5-16.58 (5.60 (5.98-12.70-23.80-24.80) .955 (.1) 13.52) * * 1.4 (9.

36) * * 1.1) 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 1.860 (.35) < LOD < LOD 3.35 (1.00 (4.94-23.41) Selected percentiles ( 95% confidence interval) Total * * 50th .50) 7.5) 12.7 (8.80 (2.7) 5.2 (6.83 (7.47) * * .45-5.00 (4.9-28.40-5.1 (9.67) 1.8) 7.710 (<LOD-1.549-1.29) * * .74) 4.53) 9.40-28.01-2.98) .57-10.71-2.80) 9.8) 6.9) 16.98-22.0) 7.66-34.9 (9.38 (1.5) 8.855 (.75-7.29 (2.7 (9.39 (2.25) 6.1 (10. interval) .80 (6.60-9.1 (8.66-15.04 (1.57 (6.5 (4.32-12.18 (.13) 4.20-8.4) 13.41-12.98) 9.72) 11.66 (1.2) 5.8 (10.10 (3.54) .69) 4.3) 5.25) < LOD .2 (10.8) 16.87-5.93) 9.94-22.66 (2.79-3.570-1.40-14.02 (2.28-9.540-1.7) 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 .26) * * .88 (5.09) 2.69 (4.37 (4.46-5. population from the National Health and Nutrition Examination Survey.76) < LOD .2) 8.03) 2.82-14.883 (.650-1.8) 12.932 (.28 (4.633-1.85 (6.69) 2.47 (3.84) 7.533-1.773-1.62) .06-2.31-14.90-8.56) 7.37-3.68-4.790 (.94-9.54-2.89) * * 1.93-9.67-19.98) .92-5.64-5.92-2.890 (<LOD-1.2) 9.94 (4.98-5.95 (3.43 (.3) 12.3) 16.5-13.19 (4.920 (.90-5.8) 8.28 (2.30 (1.620-1.57) 4.44 (2.04-6.7 (10.87 (3.74) 90th 7.00-13.94-10.34) * * .5-20.75 (3.14 (3.5-32.88-10.37 (5.4 (4.924 (.56) 4.10-13.82-14.73 (1.54-15.43 (3.5) 7.45-11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.03-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.45-5.60) 2.34 (6.41) .566-1.87 (1.61-13.5) 7.43) 2.1-15.818 (.75) 2.03 (2.6 (10.960 (.0 (8.510-1.66 (5.77 (6.56-13.6 (9.11-6.94 (2.54-11.05) .56) .4) 4.500-1.40) < LOD < LOD 75th 2.6) 9.37) 9.67) 4.79-9.02-2.42) 12.42 (3.84 (5.7) 12.890 (<LOD-1.40-12.53 (6.03) 2.34 (6.900 (.78 (2.4 (9.9 (9.46) 2.75 (7.58) * * 1.02-14.54-4.83) 8.28) 10.89-3.40 (3.34) < LOD < LOD .9 (5.57 (4.82-6.2 (8.95) 2.24-3.61-29.7) 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.996 (.88) 2.75) 14.40-3.47 (3.560-1.61 (1.28 (5.02 (7.S.21-23.2) 95th 12.750 (<LOD-1.27) < LOD 2.00-19.82-26.52) 4.81 (1.53-11.55-20.6) 13.85) 2.60) * * .430-1.61 (1.31 (3.830-1.1) 4.2) 13.7) 18.03 (7.62-5.870-2.81-5.608-1.1 (11.71) 10.09-11.960 (<LOD-2.6) 11. Fourth National Report on Human Exposure to Environmental Chemicals 121 .76-4.88-15.23 (4.574-1.30) 2.9) 11.80 (7.3) 15.37-5.1 (7.07 (.15-10.0) 6.5) 11.05 (1.440 (<LOD-2.47) 2.820 (.93-5.1 (6.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.1) 4.780 (<LOD-1.09 (.00) 8.3) 952 1187 927 997 1332 1001 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.00-17.5-16.40) 4.51-5.98 (3.6) 8.2) 7.38) .2) 5.4) 4.05 (.9) 12.23) 4.47 (1.68) < LOD < LOD 3.69-10.

20) 3.39 (5.6) 14.18) * * * * * * * * 1.40 (2.10 (. 0.0-33.10) 6.95-9.4-17.27) 9.0) 9.31-7.8) 9.00-18.67) 4.8 (12.16-1.910 (<LOD-2.22) 8.7) 22.6) 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 * * * 1.37) 2.790 (<LOD-1.9 (7.98-9.4) 11.4 (14.30) < LOD < LOD 4.49-4.8 (12.0) 14.3) 20.30) 3. respectively.88) 10.90 (2.9-15.5.30) 3.31-12.10 (<LOD-1.58.7) 16.0 (5.70-9.3) 10.7-19.95 (2.60 (2.3 (7.35-3.70-9.46-4.1) 11.67) 3.3 (12. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.77-14.63-14.28 (7.64) 10.70 (1.22 (6.77-3.60 (6.20 (<LOD-2.10-15.5 (8.34 (6.30) 8.5-26.0 (14.80-21.80) .92) 9.00) 3.14 (6.00-4.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9) 16.8-20.12 (4.0) 12.42 (1.20-4.0) 9.06 (2.95 (5.59-3.34-3.6) 11.1 (10.74) * * * * * 1.0-24.70) 2.3 (11.90 (5.5 (9.3 (9.35) 4.89 (2.5) 21.70 (8.61-32.80 (5.58 (1.0-29.6-41.96) 90th 7.7) 10. and 0.27) 4.17 (7.3 (6.8) 8.40) < LOD < LOD 75th 2.75 (3.80) 5.31) 1.0) 23.82) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-21. 01-02.50) 3.80-4.51) < LOD 1.66-13.650-1.6) 14.90) 4.0 (10.670 (<LOD-1.67-10.70-5.6 (10.39-13.0 (9.7-21.90 (6.60) < LOD < LOD 2.970 (<LOD-2.90 (6.4 (10.0) 19. which may vary for some chemicals by year and by individual sample.00) 8.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.34-10.90-15.0) 7. and 03-04 are 0.33-11.01 (2.37 (3.70-8.8-20.0 (7.78) 5.34-5.00) < LOD .50-5.89) 2.9) 95th 14.53 (3.2 (9.8-17.6) 18.90 (6.00-4.0) 6.6 (10.00-18.50) .2 (7.81-6.90) 8.80-14.73) 7.0) 14.41-5.90 (2.86-10.24 (2.41) 3.20-8.1 (10.90-9.75 (2.60 (5.84-4.9-14.670 (<LOD-1.80-3.6-19.99 (3.3 (9.0 (8.4 (10.04 (3.80) .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. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .S.00-9.00) 7.29-4.90 (1.80-8.0 (13.00-16.740 (<LOD-1.10-10.5.9) 9.0 (15.3) 14.72) 2.96) 3.9 (12.27 (7.92-17.1-23.7) 14.10-4.2) 14.50-4.45 (3.0) 12.680 (<LOD-1.0) 12.15-2.15-6.670 (<LOD-1.20) 3.80 (2.22-12.90-31.61 (3.7 (11.7) 15.18 (3.0 (10.80-12.11-6.0) 11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.670 (<LOD-1.0 (9.30) < LOD < LOD .90-15.00 (.50) 5.22 (6.5 (8.0-24.90 (6.0) 13.66) 4.3) 8.90 (2.80 (2.3) 22.0) 13.62-17.9-17.00) 3.52 (6.0) 18.40 (2.20) .580-2.0) 11.27) . 122 Fourth National Report on Human Exposure to Environmental Chemicals .20-18.27 (3.24-5.35 (6.47-6.97-4.4) 7. see Data Analysis section) for Survey years 99-00.88) 3.25 (2.5) 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 * * * * * * .7 (10.9) 10.80-6.29) < LOD < LOD < LOD < LOD 3.0-19.46-28.

50 (6.4-16.97-4.38) 1.06) .7) 12.1 (19.5 (10.7 (11.6 (12.6) 13.0 (13.4-16.95) 90th 8.02-4.5-17.77 (2.16 (3.28) 6.79-6.590 (<LOD-.1 (13.00) 8.1) 20.42-19.18) 2. Fourth National Report on Human Exposure to Environmental Chemicals 123 .25-9.5) 22.89) 5.8) 16.3-34.910 (<LOD-1.93 (6.2) 12.55 (2.78 (6.6 (11.973 (.3-21.25 (4.7) 14.78 (4.3-17.6 (10.2) 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.86) 9.82-8.2 (9.12 (7.8 (10.2) 12.38 (.83 (7.810 (<LOD-1.33-10.39-17.6 (11.27) * * * * * * * * 1.7) 14.6) 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 * * * .8) 11.93-10.93 (2.14 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.43 (2.81 (7.5 (9. population from the National Health and Nutrition Examination Survey.4) 7.15 (1.28-12.9) 16.86 (3.48 (2.71) < LOD < LOD 2.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.11 (5.78) 4.89-10.12) < LOD < LOD 4.5) 8.94 (5.00 (<LOD-1.85-17.0 (11.9-25.69-11.75-3.3) 8.780-1.55) .34) < LOD < LOD < LOD < LOD 3.2) 19.00 (<LOD-1.74-19.37) 3.9 (9.2) 16.67 (1.2) 15.01-5.20-3.00) 2.07) 2.0) 14.6) 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 * * * * * * .3) 9.07 (5.87 (3.6) 7.7 (10.3-15.5 (11.73 (5.4) 7.64-11.27) 5.00 (7.9 (9.58 (4.61 (2.75-3.3) 12.30) 2.99 (4.0 (8.850 (<LOD-1.32-8.7 (10.89-13.44-6.38-13.68) .4) 7.59-3.92 (5.6) 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 1.55) 16.42) 7.74-4.940) < LOD < LOD 1.5 (8.53-8.950) .2) 12.760 (<LOD-1.2 (9.890-2.1) 13.72-4.00 (3.77 (2.7) 9.8 (8.47-9.29-2.89 (3.91-9.38 (2.03 (6.3) 6.54 (7.77) 3.70-2.70-35.530-1.2-30.4-15.30-5.80) 3.03) 3.0-21.28 (1.03 (2.9) 19.6) 6.68-4.36 (2.91) 3.5 (15.0 (10.6) 14.1 (8.67 (7.30) 7.2-15.4) 16.4-18.690 (.3-17.6-19.7 (8.620 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 8.78-10.50-17.51-10.09-11.54-5.94-14.09-11.68-10.88 (1.00 (2.54) 9.4 (11.11-3.5) 13.15) < LOD < LOD 75th 2.37-5.89-3.6) 12.95) 3.86-3.99) 2.5) 10.89-3.00 (5.29 (2.0-19.83 (6.9-17.51-7.04) 9.34-18.7) 15.97) < LOD .88-7.45) 3.82-11.33) 3.89 (2.16-14.23-3.27-13.95 (2.4) 9.63 (2.920 (<LOD-1.93 (<LOD-2.68-19.29) 3.52-3.2) 8.07) 2.6 (13.2) 10.27) 1.92) 3.63 (6.32) 2.7-23.27) < LOD .29 (5.79-9.72) 4.41 (7.71 (1.96-11.9 (9.6) 95th 16.6 (13.4) 15.21-21. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .S.07-3.38 (1.19) 3.3 (7.85-8.06 (<LOD-1.1) 10.05-3.42) 8.8) 14.45) 6.96-10.4) 6.21) * * * * * 1.7-19.

80 (2.94 (3.50 (1. respectively.18 (.75-2.760 (.240 (<LOD-.540 (.00) 2.940) < LOD .390-.780 (.79) .32-1.20 (2.54-2.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .S.60 (2.26) .94) .580-.450 (<LOD-.550 (.960) .618) * .20-2.740 (.00-4.350-.88) 1.37-2.49) 2.960-1.860) < LOD < LOD .42-2.32 (1.40 (1.46) 1.57 (1.780 (.600-1.30 (.949) . see Data Analysis section) for Survey years 99-00.60) 2.80) 5.17) 1.05-3.880) < LOD .46 (1.77 (1.570 (<LOD-.20) 1.750-1.457 (.388-.30 (1.45-4.350-.343 (.505 (. 01-02.21) 3.690-1.990-1.710 (.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.201-.47) 2.65 (2.74-5.55 (3.10-1.80) 2.740-1.17) 1.22 (1.80) 3. and 0.63 (1.382-.20-1.59-2.16-3.960) .87-3.670) .510 (.27 (2.30 (.910-1.29-2.15) 2.20) 3.97 (2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.08 (2.39) 2.749 (.584) .46 (2.592) * .41 (2.720-1.49) .16) 1.90-4.600 (<LOD-.75 (2.30) 2.950) 90th 1.690-.930 (.46-3.32) 3.570 (.20-2.73 (2.70-7.78) .13) .22-8.710) .510 (<LOD-.10-1.830 (.00 (1.45 (2.01) .31-3.810) .89-6.04) .08 (2.600-.780) .15) 2.970) .80) 3.10) 3.50-2.73-5.930-1.20) 3.620-1.970) 1.25-1.930) < LOD .45 (1.30-3.50 (1.29) 1.03) 1.400) .30) 1.38) 1.22-3.14 (1.570-1.98 (2.336-.449 (.160 (<LOD-.48 (1.54 (2.22-3.83) 2.490 (<LOD-.27 (3.20 (1.31-3.91) 2.96-5.17-4.50) 1.700) .95) 2.60) 3.440-.20-3.549 (.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 * .61 (1.592-.45 (1.95-5.90 (1.23-3.20) 1.10) 1.98-3.740-.690 (.455 (.10) 1.70 (1.390-.880) < LOD 75th .980) 1. 0.570) * .359-. which may vary for some chemicals by year and by individual sample.550 (.960) 1.86 (1.303-.11-3.680-1.74) 3.459 (.398-.89) .650-.570 (.79) .57 (2.30-1.48 (2.11-3. < LOD means less than the limit of detection.36-4.80) 3.13) 2.83 (2.592) * 50th .380-.560-. and 03-04 are 0.83) 1.880 (.30) 4.41-5.69-4.580-1.90) 2.50 (1.720-1.94 (2.657) * * .353-.1.60-4.20) 2. population from the National Health and Nutrition Examination Survey.83) .453 (.790 (.30-3.280-.850) < LOD .50 (1.50-2.35) 1.34) 2.680-1.840 (.59-6.2.16) 2.587) * * .800 (.80 (1.50 (1.10) 1.930) 1.467 (.83 (2.86) 3.20 (1.590-.910) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.750) 1.33-2.700) .31) 95th 2.76-6.09 (.380) .380-.70-2.340-.70 (1.260 (<LOD-. 124 Fourth National Report on Human Exposure to Environmental Chemicals .64 (1.34) 2. interval) Selected percentiles ( 95% confidence interval) Total * .820 (.710 (.01-1.54) .40 (1.98) .76 (1.04) 1.70 (1.22-2.20) 2.20 (1.73 (1.690) .730) .90) 2.910 (.19-1.720 (.58 (1.30) 4.820 (.759) * .31) 2.210 (<LOD-.05-2.26 (2.460-.740 (.01-3.585) * * .570 (<LOD-.425 (.89) 1.500 (<LOD-.47 (1.96-3.00) 1.80) 2.77-2.18 (1.09. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) 3.68-5.597) * .95 (2.14-1.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .00-2.30 (.960 (.

43) 2.800) < LOD .980-1.530 (.790) .05-2.08 (.390-1.17) 2.403) .471-.58-6.43) 1.55-3.320-.75) 6.14 (2.590-1.645) .348-.453 (.412-.940-1.07) 1.24) 4.30) 3.550) .830 (.08-3.04-1.38 (1.90) 2.07) 5.13 (1.270-.16) 1.740) < LOD 1.57 (1.77 (3.310 (<LOD-.77-4.47 (1.880) 1.03-1.64 (2.760) < LOD 75th .400) .61) 2.00 (3.690) < LOD < LOD .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.31-1.97) 1.370-.07 (.97) 2.560-.97 (1.660-.930-1.72) 1.09) .640 (.50) 1.28 (1.22) 1.08-3.820) 1.510-.22-3.485) * * .07) 1.08) 2.42) .22) 4.75 (1.950-2.91 (1.66 (2.71 (1.20-7.23) 2.95) 1.47-4.510 (.16-2.320-.520 (.17-2.368) * .460 (.04) 95th 2.07-3.08-2.32) 1.22) .08-3.440-1.840) 1.60) .710 (.17) 2.43 (1.305 (.680 (.97 (1.32) 5.30-2.310-.720-1.710 (.62 (1.02-3.66) .23 (.45 (2.20) 1.88) .350) .81) 2.62 (2.72 (2.23) 1.11 (.52) 3.82 (2.444-.25-3.34 (1.670 (.72 (1.590 (.790 (.540-.33 (1.270 (<LOD-.740) .67 (1.87 (2.69 (3.44) 2.580 (.16-1.42-8.850) 1.560-.580-.597) * .700 (.63 (1.250 (<LOD-.88 (1.82) 2.700 (.42-6.285-.32-1.688) * .870 (.70 (2.32 (.99) 1.739) * .64 (2.19 (1.390) .318-.08-2.990-1.720 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.61-3.253-.61 (3.07) 1.69 (1.552 (.700 (.60 (1.89 (1.79) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.910) < LOD .460-1.06) 4.99) 2.560 (.335-.310 (<LOD-.515) * * .380) .02-3.06-2.470 (<LOD-.89-3.300 (<LOD-.550-.742) * * .04-5.05) 1.S.22-2.820) .57-4.94) .07-2.78) 3.900) 1.67-3.270-.60 (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.75-3.750 (.234 (.77-3. population from the National Health and Nutrition Examination Survey.50 (1.730) .11) 1.61-3.73-3.500-.330-.22 (2.393 (.08 (2.41 (.509 (.800-1.11-2.580) .53) .870) .760) .08) 1.280 (<LOD-.49-4.36) 3.830) 90th 1.29-4.73 (2.250 (<LOD-.70 (3.377-.448 (.92-8.535 (.49 (1.372 (.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 * .44-2.33) .08-3.750 (. Fourth National Report on Human Exposure to Environmental Chemicals 125 .42 (.00-3.52 (1.10) 2.98) 1.47 (1.38-3.71) .38 (2.380-1.84-6.330 (<LOD-.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 * .136-.710 (.20-2.39) 2.03-2.480-1.92 (1.71) 2.05 (1.180 (<LOD-.02-6.640 (.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 * .57 (3.92) 3.67 (1.300-.520-.640 (.65) 2.23) 3.490 (.22-3.60) 1.57-2.76) 1.00-1.920) .400-1.32) 2.590) * 50th .67) .05-4.470) .18-2.23) 2.45 (1.460) .80) 2.55 (1.630) * .79 (1.05) < LOD .230 (<LOD-.84 (2.840) .39 (1.510 (.380-.550-.75 (2.550-1.58) 3.08-2.58 (1. interval) Selected percentiles ( 95% confidence interval) Total * .480) .447 (.72-4.67) 1.840) 1.591 (.43) 2.

9) 17.0-53.50-7.2-39.18) 6.04-8.8 (22.30-14.5) 30.0-230) 35.0 (7.0 (38.8 (26.1) 140 (46.0-69.3 (10.0) 4.10) 39.3 (14. which may vary for some chemicals by year and by individual sample.0-92.85) * 2.0-260) 34.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.17-2.18) 14.690-3.16) * 1.2-80.48) 5.31-6.40) 50th 2.20 (2.18.78) 9.41) 1.0-31.0 (37.0 (40.8) 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 1.0-41.70-17.02 (2.4) 19.83 (3.86-3.70) 1.6-54.29) 2.86 (1.80) 90th 38.470 (<LOD-1.11) 2.90 (1.0-43.2-33.1 (26.14) 5.0 (26.93-3.7 (28.5-27.05-3. and 03-04 are 0.10 (1.59 (1.9) 38.70 (.0-52.44) 3.0) 17.2-62.50-2.1-19.66-5.0 (13.0) 42.5-45.2 (12.0 (8.600-2.0) 3.0) 15.0 (38.1) 95th 48.29-4.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.61 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (.4 (10.0) 28.91 (4.8) 41.1) 18.98) * 2.50-5.05) * 2.8 (12.0) 16.46-6.0) 31.06) * 2.27-6.0 (38.1-47.11 (4.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.79 (2.76 (2.6 (11.0 (38.97) 6.0 (19.00 (.59 (1.98 (1.9) 18.64-3.53 (1.72 (1.30) 4.69) 2.33 (5.64-8.67 (1.50 (2.70 (1.83 (1.0) 45.0) 13.9-21.0-50.0-39.88) 3.1 (11.80-2.90-8.0 (25.77 (1.0) 33.7) 47.0) 19.0 (21.830-3.8) 32.0) 15.3 (12.19) 2.2 (19.0-41.04) 3.1-46.53) * 2.23) 9.23-2.13 (1.4.8-21.04 (<LOD-2.23-2.06 (1.40) < LOD 1.05) 1.44) Selected percentiles ( 95% confidence interval) Total * 2.7-22.88) 1.0-41.80) 1.96) 5.49-2.0 (33.78 (1.57-2.0 (32.0 (6.40-16.830-4.57-2. population from the National Health and Nutrition Examination Survey.25-3.16) 2.70 (7. respectively.1 (25.10-13.60) < LOD 1.6-22.6 (9.70-6.12 (3.8-24.3) 31.45) 2.79 (1.0-49.76 (2. interval) 1.40) < LOD 2.41) 5.48-2.85 (1.4-76.52 (4.70) 1.26 (.43-7.41) 1.0-58.2-26.9 (10.0) 30.07-5.2) 31.0-47.S.13 (1.0-62.0 (11.0) 8.46 (.2-47.58-2. < LOD means less than the limit of detection.5) 69.1 (22.12) 1.6-45.1-40.95 (5.10 (1.58) 16.75-14.35-6.48-2.5-20.0 (38.660-2.26) 75th 11.0) 16.79-2.2-27. and 0.5-74.0 (38.41 (1.44-7.13) 12.21 (4.83-2.2-27.5.0 (8.3) 33.0) 3.9 (23.8) 62.0) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7-41.71-2.0 (38.0-110) 42.87-7.8) 39.40-4.77) 38.71 (4.610 (<LOD-1.3 (12.3) 28. 0.1) 38.0 (20.83-2.92) * 2.92-5.1 (10.0 (17.44) 2.5 (24.70 (1.80) .10 (1.99 (2.6 (15.3 (24.10 (1.4 (19.0) 4.0) 5.1-20.90) 11.36-2.53) 1.6 (26.0-39.0) 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 2.21 (1.1 (25.81-3.0) 6.74-2.80-18.50-17. 01-02.2) 16.94 (1.46-2. 126 Fourth National Report on Human Exposure to Environmental Chemicals .20-4.0) 20.4) 38.00-24.63-6.0) 28.10) .09 (4.3 (23.82 (1.50-20.0 (8.9) 48.7) 20.54 (3.0) 20.0 (20.0-53.42) 1.4 (15.90 (1.0) 18.6) 52.0 (24.00 (.10 (7.71) 5.60 (2.19-2.61-2.0-110) 34.9-51.4-22.41-4.20) 1.0-58.18) 20.0-29.9 (27. see Data Analysis section) for Survey years 99-00.3) 38.0-62.8 (12.70) 5.3) 26.53) 40.7 (12.10-4.7 (12.30) 11.1) 38.1-25.0) 17.81-2.32 (2.54 (1.6-27.65 (4.45) 2.9 (19.29-9.0) 32.9 (19.5-40.0) 3.530-4.21 (3.80) < LOD 1.0) 3.

5-97.9 (10. interval) 1.46) 1.57 (6.37-2.63-5.4-71.45 (1.70-4.82 (2.2 (15.67-16.0-71.43-12.2 (8.01 (.4) 12.4 (9.46-22.890-4.11) < LOD 1.12 (1.12) 3.7) 26.870-3.7) 23.94) 19.1 (50.9) 54.54-2.96) 2.38-1.2 (16.7-38.1) 13.79 (2.46-6.9) 3.3-27.17-3.2-38.5 (15.80 (1.07-2.5) 70.43) * 2.1) 25.57) 4.6) 23.9) 12.20-5.46-5.9) 24.9-41.2-28.20) Selected percentiles ( 95% confidence interval) Total * 1.1 (12.26-2.00) 6.4) 12.39 (1.60) 4.7) 66.19-6.40 (2.4) 3.2) 36.2) 13.27) 10.69-5.5 (15.88 (1. population from the National Health and Nutrition Examination Survey.75-6.21 (4.2-70.8-45.56 (2.6 (7.95-16.4-21.31) 2.76-2.9) 3.7 (11.8) 32.93) 5.6) 112 (40.930 (<LOD-1.1-60.52 (1.1) 52.3) 28.54-15.44) 9.02) * 1.51) .84-13.50 (2.56) 1.67 (1.64 (1.0) 30.09 (5.94-20.17) 2.35) .3 (9.34) * 1.02) 1.8-26.4) 14.47 (1.88 (4.66 (1.5 (17.16 (1.8-43.7) 34. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 95th 51.3-42.75 (1.52-4.47 (3.67 (1.6 (11.22 (.7 (10.18) * 2.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.8-34.5-36.8) 31.03-2.33) 2.35) 1.2) 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.6-49.71-2.3 (8.2-34.4-67.86) * 3.7) 30.23-1.19 (1.38-5.06-1.1 (39.9-52.70 (1.8 (7.24 (1.0 (23.0) 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 1.59-2.16 (1.6-38.60 (.40-7.9 (19.0 (17.71) 8.1) 15.0 (19.1 (34.62 (2.2) 13.27 (6.19) 5.1 (33.6-51.36-13.1) 17.59-15.06) 1.58-2.7-43.22 (2.6 (27.0 (23.25-3.15 (.08 (1.61 (1.97 (1.83) .94) 1.4 (19.0 (39.79-17.3 (10.50-5.888-1.6 (24.750 (<LOD-1.75) * 1.0-118) 29.9) 24.18) 3. Fourth National Report on Human Exposure to Environmental Chemicals 127 .68 (1.27) 50th 2.22-2.0) 3.9-95.1) 13.07-2.0 (14.96-16.9-37.2) 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 1.9 (13.3-19.59-2.32-3.22-3.38) 5.7 (18.9 (7.72) 2.7-37.95-16.1-63.23) 37.9 (26.1) 27.870-3.14 (.18-1.66) 8.6) 19.1) 36.36) 10.670-1.91 (6.0 (6.07) 9.2) 33.680-4.2 (22.29-5.899-2.0-40.66 (1.7) 61.3-22.33) 1.37 (1.4 (21.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.5-190) 30.9 (39.69-18.1 (25.4 (12.5 (41.16 (1.30) 28.9-18.03) 1.86) * 2.0 (32.88 (4.68) 47.860 (<LOD-1.61-2.6) 11.61-22.8) 15.3) 13.41 (2.19) 5.47-17.7 (24.0) 10.1) 25.99-4.95) 90th 32.11-2.5) 27.95 (2.3 (10.8) 11.4 (11.6) 3.6-32.28) 1.0 (25.1-22.S.4-39.5 (34.7) 15.14-8.8) 23.5 (6.06) 1.75 (1.6) 3.88 (1.40 (5.3 (20.33-5.8) 3.58-17.7-109) 22.43-2.4 (25.82) 1.00-16.7 (18.51) < LOD 1.53) 1.80-8.62) 4.28 (1.27-3.91-2.83 (.16-2.0) 25.40-4.32 (3.2) 4.0-70.06) 75th 9.0) 47.38 (3.0) 13.7-20.33) < LOD 1.90 (.71 (1.870-3.0) 48.9-36.7-19.08) 1.5-43.2) 41.02 (.8-37.26-4.45-1.23) < LOD 2.00 (4.6) 7.36 (4.5 (13.48 (4.2 (21.55 (2.4 (25.00) 1.4-34.35 (2.1) 27.2 (9.5 (8.4 (5.67-3.19-14.48) 1.2-47.7-47.

260 (.162) * * * * * .270 (.390) < LOD < LOD .30) .130-.540) Sample size 1949 2516 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .820 (.470-1.610-.680 (.210 (.690-1.720-1.380-.990) .540) .600 (. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00.650) .120 (<LOD-.40) .630 (.360-.310 (.840) .450 (.560 (.10) .380-.640) .160) .610 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .300-.870 (.560 (.830 (.460-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.330-.360-.42) .160) .470 (.370-.099-.870) < LOD .13) .990 (.410-1.60) 1.620 (.410) < LOD < LOD < LOD < LOD .180) .640 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.640) .090 (<LOD-.440-1.300-1.310) < LOD < LOD < LOD < LOD .850) < LOD .410-.940 (.870 (. and 03-04 are 0.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.350) .630 (.090 (<LOD-.830) .840) .10 (.230-.610-1.32) . and 0.00) .280) < LOD < LOD < LOD < LOD .390 (. which may vary for some chemicals by year and by individual sample. 01-02.140) .1.42) .460 (.760) < LOD .680-1.190 (.320 (.430-. 128 Fourth National Report on Human Exposure to Environmental Chemicals .650-1.S.860) .130 (.430 (.990) .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-.830) < LOD .130) .700-1. respectively.230) .740) < LOD .30) .730-.05.650 (.160-.090 (<LOD-.870 (.490 (.850 (.860-1.1.650) .450 (.420-.20) .720) .130) .36) . 0.150 (<LOD-.15) .240 (<LOD-.140-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .650-1.084-.450 (.310 (.117 (.900 (.10) .350) < LOD < LOD < LOD < LOD .930 (.220 (.130-.290) < LOD < LOD < LOD < LOD .850 (.090 (<LOD-.171) * * .30) .050-.410-.120-.210 (.12 (.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.680) .200) < LOD < LOD .570) .310-.540 (<LOD-.310) < LOD < LOD < LOD < LOD .130-.190 (.700-1.870 (.680-1.660 (.320-.640-1.530-.820 (.770) < LOD 95th .290 (<LOD-.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 * * * * * * .190 (.080 (<LOD-.140-.830 (.870 (.58) .510-1.730) .400-.720 (.700-1.380-.100 (.080 (<LOD-.150) .170-.03) .290) < LOD < LOD < LOD < LOD 90th .540) .220 (<LOD-.090 (<LOD-. < LOD means less than the limit of detection.770 (.090 (<LOD-.550) .140-.370-.110-.700-1.10) .780) < LOD 1.

300 (.670-1.460 (.340-.360-.190 (.700 (.280) < LOD < LOD < LOD < LOD .780 (.62) 1.720 (.140-.220) < LOD < LOD < LOD < LOD .170) < LOD < LOD .330-.450 (.230 (<LOD-.090 (.36 (1.760) .380-.260) .070 (<LOD-.550 (.02-1.400) .360) < LOD < LOD < LOD < LOD .600-1.380 (.58) 1.600) .730) .111) * * * * * .860 (.570 (.120) .01 (.860 (.60) .100-.03 (.170 (.640-1.410) .330 (.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .670 (.140) .440 (.810 (.66) 1.070 (<LOD-.190 (.450) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.960) .500 (<LOD-.43) .380-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.03 (.67) .140-.220 (.320 (<LOD-.440-1.050 (<LOD-.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.870) .700-1.170 (.580) .710-1.410) < LOD < LOD .570-1.140-.110) .780) < LOD 1.500-1.370 (<LOD-.270) < LOD < LOD < LOD < LOD .380-.161) * * .880 (.110-.78) .12) < LOD .330 (.890 (.070 (<LOD-.270 (.700 (.03 (.520-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th . Fourth National Report on Human Exposure to Environmental Chemicals 129 .730 (.210 (.470 (<LOD-.120) .180-.970) .400 (<LOD-.060-.660-1.410-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .720 (.20) 1.410-.070 (<LOD-.080) .250-.29 (.057-.110) .360 (.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 .410 (.490-1.610-1. population from the National Health and Nutrition Examination Survey.580-1.860-2.200 (.080 (.240-.86) .310) < LOD < LOD < LOD < LOD .080 (<LOD-.330-.580) < LOD .540 (.14) 1.290) < LOD < LOD < LOD < LOD 90th .570-.300-.500) .650-1.330-.00) < LOD .560 (.580 (.880-1.750) < LOD 95th .24) .260-.940) .19 (.110) .740 (.S.990) .86) .38) 1.300-.730) .03) .410 (.940) .800-1.140-.740) < LOD 1.850 (.730) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.670 (.990) .24 (.580 (.550 (.09) .360-.084-.540) .100 (<LOD-.150-.140-.510-.230) < LOD < LOD < LOD < LOD .230-.540 (.02) .390-.090 (<LOD-.110) .700) .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 * * * * * * .650) < LOD .380-1.116 (.390-.190-.200 (.

24-7.40-7.39) .62-8.70-3. respectively.0 (5.400-1.0) 3.0) 2.76 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.42) .0-40.00 (.510-.07-3.20-17.260-.05 (2.07 (3.70-17. and 03-04 are 0.90-28.61 (1.00) 1.1.67 (1.14) 2.28) .55-8.0 (17.30 (.28) 1.0-38.90 (1.20 (1.70) 2.74 (3.800) 17.480-.0-44.11) 13.83) 2.90) .0) 2.38-3.20) < LOD < LOD < LOD < LOD < LOD 1.42) 2.00 (1.32-9.94-3.50) 2.0 (16.380-.39 (2.48) 13.21) 3.20 (1.600 (.99) 19.80 (4.110 (<LOD-.36-3.47 (3.800) 90th 13.88-3.720) 2.1.35) 11.12) * * * * * * * * .0 (17.40-4.910) 2.30 (2.94 (1.16) 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 .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 * * * * * * * * * .82-4.62) 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 * * * * * * .880) 5.31-10. 0.6) 5.43-4.750-1.0) 2.620-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.580 (.26 (2.15) 14.32 (1.94-8.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.05 (3.0) 7.0) 5.68) 2.45 (2.55-4.60) 1.350-.0) 2.51-8.28-9.770) 2.66) 4.40-20.96 (1.70-50.52) 5.0) 4.23-6.30-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-38.50) .30-7.350-.97) 20.0) 2.0 (6.48 (2.49 (1.53 (2.330 (<LOD-1.14-5. 01-02.90-9.0 (5.10 (3.S.750-2.87) 12.190-1.87) 5.85-3.830 (.90-20.18) 1.59-5.0-39.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.07 (3.610) < LOD < LOD < LOD < LOD < LOD 2.360-1.51 (2.30 (1.53) 20.49 (1.63 (3.0 (4.770 (<LOD-1.11) .14) .870) < LOD < LOD . < LOD means less than the limit of detection.0) 5.730 (.840-3.31) .740 (.90-37.00-17.640 (.0) 4.10-9. population from the National Health and Nutrition Examination Survey.99) 11. 130 Fourth National Report on Human Exposure to Environmental Chemicals .40 (1.0) 2.0 (5.11 (1.10-3.30) 95th 19.36-3.00-17. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.07 (1.30) .0) 2.0 (5.49) 17.67) .35-10.840 (.960 (<LOD-1. which may vary for some chemicals by year and by individual sample.0-40.53-7.90 (2.691 (.250 (<LOD-.080-1.370-. see Data Analysis section) for Survey years 99-00.0 (5.0 (3.30 (1.40-8.0) 5.15) 19.0-38. and 0.20-4.960 (.52 (1.83-3.40) 1.0 (17.05-3.10 (.0 (17.74) 5.07) 1.0 (4.99 (1.840 (<LOD-1.0 (7.07-3.70-7.20-4.08.60) .52 (1.10 (3.67 (2.800-4.610 (.35) 5.03 (.65) 1.30-3.12-1.0 (17.0) 5.86) 4.590 (.890 (.0) 4.0) 4.0 (13.30 (1.33 (4.29-10.40 (1.900 (.46 (1.63) 32.10-3.90) .90) .21-3.01) 5.425-1.70-30.640 (.83-3.97) 20.13 (3.170-1.40) 2.00) .210-1.00) .850) 16.690 (.37) .

population from the National Health and Nutrition Examination Survey.83-11.96) 2.8 (20.7) 5.960 (.57 (.47) 5.370 (.03) 2.67) 1.14-6.40-12.32-6.80 (.33-4.33 (3.49-2.150 (<LOD-.88-3.260-.390-.51-4.580) 1.71 (2.450 (.37) 4.96-8.33-5.360 (.930) .2-38.44-11.700) < LOD < LOD < LOD < LOD < LOD 1.850-3.40-2.57) 8.71 (.75) 5.52 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.S.62 (1.430 (<LOD-.7 (6.33-3.0 (4.620-3.340 (.5 (11.710 (<LOD-1.09-3.770) .96-25.8) 4.56 (1.77 (.2 (8.85-3.00-19.600 (<LOD-1.53) 27.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.47-10.4 (4.11-5.370) < LOD < LOD < LOD < LOD < LOD 1.50) .03) 16.98 (4.190-1.830 (.65 (2.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.57-40.800-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.17) 5.430) 1.41) 18.340-.83 (4.24) 3.740-1.80) 3.8) 7.64) 30.48-42.18) 1.8) 2.25 (1.62-17.05) .66-47.89 (2.56) 2.650 (.830-3.14 (1.13 (2.69-7.31-7.55) 21.17 (1.630-1.39) 20.860-2.8-33.07 (2.60 (1.31) .9 (11.8) 7.55) 21.970-3.33 (1.790) 11.940-4.340-.45 (1.22) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.670 (.91-4.40 (.10 (2.560 (.11) .8) 2.1) 2.50 (2.780-4.55 (3.540-1.23-7.5 (8.1 (5.5) 7.01 (1.86) .500 (.67) 2.240-.04 (1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .4) 2.730-3.540 (.31-18.67-6.10) 2.59 (1.32) 9.1 (7.25-38.9) 6.07-21.91) 2.790 (.88 (.64-4.02-4.82-11.92 (2.30 (4.29-4.3) 2.270-.35 (.25-9.79 (.85 (1.270 (<LOD-.8) 1.48-7.700) 6.86 (3.38 (2.250 (<LOD-.88) 17.69) 2.41 (4.5 (9.1) 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 * * * * * * .81-17.48 (4.7) 4.53) .36 (.44) .02 (1.820 (.29 (4.840-3.02) .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 * * * * * * * * * .580) 16.31) .580 (.22-27.74 (2.88 (2.73 (4.47) .340-.7) 3.12 (4.310-.27 (2.1) 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.28-6.47-10.21-3.748 (.90-6.02 (.50) 11.43) .474-1.56) .580-1.590) 2.06 (.7) 6.61) 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 .320-1.470 (.51-44.08) .5) 2.330-1.890 (.5-40.370-1.5) 2.0) 4.7 (12.50 (4.00) .04-16.820) .97) .40) 1.15) 9.0 (9.260-.18) 95th 21.10-3.4-34.3) 3.84) 9.9) 5.12-4.67 (2.690-5.650) 90th 10.57) 1.18) * * * * * * * * .660) < LOD < LOD .

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Visuthismajarn P. Int J Occup Environ Health 2006. Russo J. Bull Environ Contam Toxicol 1994.12(2):153-172. Thompson ML.edu/ openbook. Sci Total Environ 2004. Berry H. 1993 [online]. Eskenazi B. Office of Prevention Pesticides and Toxic Substances. Barr DB. Jenkins B. Masala G. Gladstone EA. Environ Health Perspect 2005.12(2):134-141. Terry AV Jr. Weisskopf C.26(2):199-209. Beach J.84(5):731-736. Muniz J. Pesticide industry sales and usage . and cholinesterase status of date dusters and harvesters in California. discrimination. Scherer J. Caltabiano LM. Santana J. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. O’Malley M. National Research Council (NRC). Phillips J.24(1):18-29. Am J Public Health 1994. Smit LA. Prendergast MA. Occup Environ Med 2001. low-level organophosphate exposure on delayed recall. Lewis JA. Keifer M. Muniz J. Lasarev M. Myers JE. Stokes L. Mounce LM.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Malathion deposition. Aprea C. et al. Ruberu DK. Am J Ind Med 1987. J Occup Environ Med 2002. Pesticides in the Diets of Infants and Children. Calvert IA. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. EPA. Petchuay C. et al.52(2):190-195. Washington (DC): U.20(2):115-22. Narang A. Burcar PJ.43(1):38-45. and spatial learning in monkeys and rats. Available at URL: http://www. A behavioral evaluation of pest control workers with short-term. Bravo R. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Environ Health Perspect 2006. Saieva C. Hansen S. Lasarev M. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand.epa. Vitayavirasak B. Keefe TJ. Lambert WE.S. National Academy of Sciences.S.38(4):546-563. Daniell WE. Neurotoxicity among pesticide applicators exposed to organophosphates. Johnson C. Bradman A. Pedersen L.332(1-3):71-80. Washington (DC). Chronic neurological sequelae of acute organophosphate pesticide poisoning. et al. Neurotoxicol Teratol 1998.44(4):352-357. Robson MG. low-level exposure to the organophosphate diazinon. Rodnitzky RL. Schenker M.php?record_id=2126&page=1. Arch Environ Contam Toxicol 2000. Arch Environ Health 1975. 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. vibration sense and tremor among South African farm workers. Pilkington A. Nell V. Lancet 1995.30(2):98-103. Arch Environ Health 1988.58(11):702710. Takamiya K. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Scand J Work Environ Health 1998. London L. Gillham R. 4/7/09 Young JG. Lu C. Kidd M. Chronic neurological sequelae to organophosphate pesticide poisoning. Jamal GA. Steenland K. Rothlein J. May. McCauley L.nap. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Hore P. Effects of chronic. Available at URL: http://books. Frasca G. Savage EP. Stephens R. Samuels S. Effects of long-term organophosphate exposures on neurological symptoms. metabolite clearance. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Spurgeon A. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. S. Wickremasinghe AR. Salvini S.345(8958):11351139.338(8761):223-227. Irish RM. The Pesticide Health Effects Study Group.114(5):691-696. Weerasekera G. Buccafusco JJ. J Toxicol Environ Health A 2005. Occup Environ Med 1995. Claypoole K. EPA). 1991.68(3):209-227 Maizlish N. Rohlman D. Marshall E. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Levy LS. Rothlein J.113(4):504-508. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Seiber J. U. van der Hoek W. 1/12/09 Peiris-John RJ. Rosenstock L.2000 and 2001 market estimates. Stark A. Dinoff TM. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. et al.pdf. 2004. Neurotoxicology 2005. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). McConnell R. et al. Lancet. Buchanan D. Tumino R. Heaton RK. Environmental Protection Agency (U.52(10):648-653. Ames RG. Chrislip D.

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.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 . For example. malathion is metabolized to malathion dicarboxylic acid.5. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. In addition to reflecting exposure to the parent insecticide. parathion and methyl parathion are metabolized to para-nitrophenol.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3. For general information about the organophosphorus class of insecticides. the level may reflect exposure to the environmental degradation products of these pesticides. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.

Estimated intakes from diet and water have not exceeded recommended intake limits.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 1.52-2.90-8. in 142 urban homes and preschools in North Carolina.80) 4. and on plants for days to several weeks.71 (2.47 (4.66-4.20) 2.66-15.15 (1.0) 10.28-3.60) 5.26) 7.20-16.80) 1.59-2.51 (1.0) 7. population from the National Health and Nutrition Examination Survey.4.4 and 0.0 (13. 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.37 (1.95) 7. Fourth National Report on Human Exposure to Environmental Chemicals 135 .22 (1. The general population may be exposed to chlorpyrifos via oral.60 (2.0) 18. and inhalation routes.77 (1.62-2.16) 2.8) 10.98-15.and post-construction structural applications for termite control were to be phased out by 2005 (U.10 (4.5-24.90-2.70-17.5) 7.9-18.74 (1.28) 2.46-2.80-10.96) 3.70-5.4 (8. It has low leachability.0) 10.31-2.43-2.00) 1. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.91) 16.95 (4.09 (2.0 (9.70 (1.30) 5.44-2. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.90 (6.20-2. and dust.80-8.30-9.35) 1.0) 15.67 (2.25) 3.92 (1.53 (1. interval) 1.EPA.9 (10.61) 75th 3. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 11.80 (1.97-7.50-4.20-11.99-4.74-9.67 (2.60-4.19 (1..10) 2.S.50-14.90 (1.0) 8.03) 1. but can be detected in streams receiving runoff from application sites.30) 4.9) 11.90) 7.10 (5.94 (4. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.67 (1.0) 12.40-10.4 (9.59) 2.34) 1.90-7.8) 9.89 (2.50-2.10) 6.60-3.77-15. and sprayed to kill mosquitoes.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.24-1.0) 8. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.3 (10.02 (7.20) 2.25) 1.0-28.20) 4. After 2001.76 (1.71 (1.10 (1.60 (5.0) 9.63 (1.5.80) 2.35) 2.21) 3.50-5.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.40-2.6) 7.0) 12.9) 697 660 521 701 602 947 Limit of detection (LOD.90 (2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.70-11.9 (7.0 (7.7) 13.20-3.90-4.37) 5.55-5.80) 12.2 (10. Chlorpyrifos is Urinary 3.02 (1.83) 1.45 (1.4 (10.70) 1.19-3.50-4. pre.01) 1.77) 1.04-10.39) 4.40-26.90 (3.0) 12.24-3.4-15.04-10.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.00) 3.90) 3.86) 4.57 (2.5 (8.90 (1.20 (2.97) 7.20-4.71 (6.61 (1.3) 8.10-17. air.64) 3.50 (1.84) 1.76 (1.60-3.05) 1.68-2.81-2.29-1.30 (4. Approximately 80.51) 1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.0 (7. chlorpyrifos was no longer registered for indoor residential uses in the United States.50 (2.40 (6.8-15.13 (1. applied to structures to kill termites.S.27 (7.36 (4. dermal.0) 6. 5598-13-0 General Information The chemical 3.7) 9.1) 5.50 (2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration. 2921-88-2 Chlorpyrifos-methyl CAS No. 2007). 2002). Exposure can also result from contact with contaminated surfaces.20) 10.7-23.0) 12.30-2.0 (7. USGS.44 (3.EPA.97) 2.30-12.77-6.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.63 (2.22) 2.32) 2. 2005).79-2.17 (1.47-9.31-2.44-5.50 (2. Approximately 21-24 million pounds per year were used domestically from 1987-1998.S.52-12.0 (10.3 (11.29) 90th 7.0) 14.97) 4.50-8.30 (2.51-2.40 (5. For instance.0 (7.50-2.72-4.40) 2.68 (7.88 (1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.02) 1.72) 2.30 (2.40) 9.0 (7.97) 2.87-6.91 (1.20-14. and is infrequently detected in ground water (IPCS.63 (8.43-2.40-13.47) 1. staying bound to soil particles.05-5.60 (4.50 (1. 2002).6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40 (5.30-11.00-24.3 (8.80 (7.70 (1. Survey Geometric mean (95% conf.13-3.39-2.47-11. It also has been applied directly on animals to kill mites.00) 2.000 pounds are used per year.9 (9.30-1.37 (4.20 (4.10 (3.60-2.0) 10.32-1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.61-7.78 (7. 1999.38 (3.0) 12.00-8.30) 4.70-15.5.30-5.47-13.7) 8.1-16.70-16.89-2.09 (3.

62) 1.72) 2.91) 1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.33 (1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.97 (3.31) 1.83-11.88 (1.1-38.88-9.58) 1.56-2.42 (5.56 (4..80-6.21-6.6) 10. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.82 (2.23) 14.. 2006a.53 (2.79-13.7) 7.39) 6.24) 5.0) 6.02 (5.27-1.57) 9. Survey Geometric mean (95% conf.82-4.91) 1.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.83-2.12-1.5. Ricceri et al.98 (7.28) 2.1-21.58) 5. 2005.07) 1.37 (1. population from the National Health and Nutrition Examination Survey.47-2.1 (10.62-7.55 (4.12) 1.00-8.98 (6.93) 5.0) 12..88-10.33 (5.14-8.S. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.38) 3.58 (4.8) 9.. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.85 (2.76 (2. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.15 (4. cholinergic effects.0) 10.35) 2.44 (5..44-6.43 (4.71 (1.93 (2.43-10.73 (1.85-4.39 (4. Based on animal data and human cholinesterase monitoring during occupational exposure. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.19-2.50 (4.33) 2. 2002).49-2. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.2) 6.69 (1. 2005.9 (12.42 (6.54) 5.5 (6.05-8.5) 5.92 (1.81 (3. and other metabolites.55) 1.24-4.58 (1. Roy et al. and producing acute symptoms such as nausea.80) 3. 2006.91) 10.48 (1.45 (1. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. 2006b).64-7.90-9.47 (5.93) 2.49-2.47 (1.68) 6.97 (2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.64 (1.49-2.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .95 (3. 2006.64-2. 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.91 (4.29 (3.S.32) 1.80-4.60 (1.33 (.07) 5.88) 6. 2005.24 (1.06-4.40) 1.53-5.01) 3.35-1.94-14.25-12.16) 6.00-13.39-1.97-3. Urinary 3.02) 7.55 (1.77) 1.57-2.85) 4.88-8.93 (1.44 (1.2 (7.95 (1..44 (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 1.05-4. Howard et al.75) 6.86 (1. neurotransmission.05-3.01) 1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body. vomiting.63 (5.12-3.87-3.86 (1. interval) 1. paralysis. Thus.3) 9.30-1.06 (5.3) 8.63 (4.16 (4.89) 4.05) 3.39 (2.72-2.36) 1.25-1.56) 5.54 (2. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.60-3. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.44 (6.08) 6.03) 1.21-1.85 (3.75 (1.22 (4.09-3.62) 90th 5.99) 1. TCPy is more persistent in the environment than chlorpyrifos itself (U.17-4.44 (5.83) 1.11 (2.24) 75th 2.3) 8.20 (2.22-6. Betancourt et al.57) 2. and seizures.65-15.01) 3.25-11.91-13.14) 1.41 (1.59) 3. Once absorbed.27-7.97) 3.85) 1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.56) 2.28) 2.42-2.00 (7.22 (6.09-2.92-2.56 (1.51 (1. weakness.66 (1.24-24.49 (1.80-11..19) 3.91 (3.09 (1. Metabolic hydrolysis leads to the formation of TCPy.22) 1.20-1.45-1.76 (3.72) 1.17-4.09-1. 1984). Slotkin et al.88-8.46 (2.91) 2.34-1.31-4.78 (1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 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.91-4.26-14.33-7.74) 1.82) 8.05-1.11 (2.68) 1. In pesticide applicators.59-2.23-1.71) 3.3 (7.88 (1. 2000).58 (1.19) 6.940-1.93 (4.70-4.06 (1.97) 3.81) 2.30-4.86 (3.46 (1.65-11.0) 16.EPA.4) 4.66) 1.92) 3.35) 1.57-2.96) 3.19-1.63-2.94-12.82 (3.6) 9.47 (1.99-8.24-1.84-6.66-11. TCPy can also occur in the environment from the breakdown of the parent compounds.52 (5.11-9..58-5.24-5. resulting in excess acetylcholine at nerve terminals.1 (7.48 (2..00) 1.31-1.11) 7.

Organophosphorus Insecticides: Specific Metabolites 2004. Magnaghi S. 2007). Curwin et al. Lotti A. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Perera et al. but levels were roughly four to six times higher than the geometric means in the U. 1992.. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. representative subsample of NHANES 19992000 (CDC.. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Albers JW. population (CDC. 2005. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Burns CJ. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. 2005. 2005)... 1999). MacIntosh et al.113(8):1027-1031... Burgess SC.Reference values of urinary 3.. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Lioy PJ.... (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. et al. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. 2005). Berent S.html and from U. 2005). et al. Slotkin TA. 2005).S. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. 2001). 2003.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study).atsdr. Catenacci G. Environ Health Perspect 2001. Aldridge JE.gov/pesticides/. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Koch et al. Meyer A. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. J AOAC Int 1999. 2004). Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.109(6):583-590. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Following crack-and-crevice application of chlorpyrifos in their homes.gov/toxpro2.5. urinary TCPy levels in children were reported not to have increased (Hore et al. Occup Environ Med 2006.. References Adgate JL. 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. but not chlorpyrifos. EPA at: http://www.S..82(2):305-312. 2005). CDC. In Iowa farm families using several different pesticides. Chlorpyrifos exposure and biological monitoring among manufacturing workers. Environ Health Perspect 2005. Clayton CA. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Aprea C. the geometric mean urinary TCPy levels were similar in parents and children. 2002). Additional information about external exposure (i. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Of 482 pregnant women living in an agricultural community. Giordani B.. Levels of TCPy in the U. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. Freeman NC. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. 2000).S. Eberly LE. Garabrant D. In a probability-based sample of 102 Minnesota children aged 3-13 years. Carr RL.EPA. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. In Minnesota and South Carolina farmers who used chlorpyrifos. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos.. environmental levels) and health effects is available from ATSDR at: http://www.cdc. 2005). Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. 2006). suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. 2004). Barisano A. Betancourt AM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Betta A.S.92(2):500-506.63(3):218220. 2001) and Italy (Aprea et al.S. Barr DB. U. Haidar S. Whyatt et al. Fourth National Report on Human Exposure to Environmental Chemicals 137 . median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. Seidler FJ. Toxicol Sci 2006..e. 2005. et al. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.epa..

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Pellizzari E. EPA). Honeycutt R. Urinary pesticide concentrations among children. Neurologic function among termiticide applicators exposed to chlorpyrifos. et al. Hardt J. Lorenzini P. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Bucelli R.nih. J Expo Anal Environ Epidemiol 2000. Rauh V. Steenland K. Environmental Protection Agency (U. Baker S.51(1):53-65. Adgate JL. Saunders JH.5. Reid TM. Available at URL: http://ntp. 2005. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Hill RH Jr. U. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Jones PA. Hore P.204(2-3):175-180. Croghan CW.112(10):1116-1124. Barr DB. Chlorpyrifos: pharmacokinetics in human volunteers. Seidler FJ. Yang D.73:8-15.114(10):1542-1546. Lioy PJ.9(5):494-501. Toepel K. Seidler FJ. Sheldon LS. J Expo Anal Environ Epidemiol 2005. Shealy DB. Pesticide residues in urine of adults living in the United States: reference range concentrations. Gregg M. Seidler FJ. Brain Res Dev Brain Res 2005. A longitudinal investigation of selected pesticide metabolites in urine. Needham LL.

gov/ oppsrrd1/REDs/chlorpyrifos_ired. 2007 [online]. Available at URL: http://www. Andrews HF. 1992-2001.gov/circ/2005/1291/. Available at URL: http://pubs. revised February 15.111(5):749-56. Geological Survey (USGS). Environ Health Perspect 2003. Barr JR. 1/14/09 U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.epa. Barr DB. 6/1/09 Whyatt RM. The Quality of Our Nation’s Waters. Kinney PL.Organophosphorus Insecticides: Specific Metabolites 01-007.usgs. Pesticides in the Nation’s Streams and Ground Water. March 2006.pdf. Camann DE. et al. Fourth National Report on Human Exposure to Environmental Chemicals 139 . February 2002.S.

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

* 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.270) < LOD 659 701 920 Limit of detection (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 . Survey Geometric mean (95% conf.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0.200 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection.200 (<LOD-.S. Fourth National Report on Human Exposure to Environmental Chemicals 141 .S. 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.2. 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 . which may vary for some chemicals by year and by individual sample. 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.380 (<LOD-.670 (<LOD-1. Survey Geometric mean (95% conf.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 .

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

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

animal carcinogen. diazinon does not accumulate in tissues (IPCS.html and from U. and indoor applications have been documented. and producing acute symptoms such as nausea. vomiting.S. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. The U. Diazinon is not considered to be a mutagen. 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.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. 2000. In the U.cdc.49 μg/L. resulting in excess acetylcholine at nerve terminals. Intoxications in humans from intentional overdose. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.EPA considers diazinon unlikely to be carcinogenic in humans. Seifert and Pewnim. Thus. and seizures.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.e.epa.atsdr. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. Diazinon has moderate acute toxicity in animal studies.gov/toxpro2. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. 1998).Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. 1992). Additional information about external exposure (i. population from the National Health and Nutrition Examination Survey. respectively (Baker et al.. 1986 Rajendra et al. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. subsamples of NHANES 1999-2000 and 20012002. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.45 and 1.S. weakness.. EPA at: http://www. teratogen. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. In animals. 1998).. Survey Geometric mean (95% conf. 2003). In two nonrandom samples of United States adults and children. Olsson et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. in the 2001-2002 subsample (CDC. environmental levels) and health effects is available from ATSDR at: http://www.gov/pesticides/.S. agricultural.. 144 Fourth National Report on Human Exposure to Environmental Chemicals . At high doses.S.76 (<LOD-3. respectively. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 2002). or reproductive toxicant (IPCS. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. paralysis.72 (<LOD-4. cholinergic effects. 1986.

Needham LL. Effect of sublethal levels of diazinon: histopathology of liver. Available at URL: http://www. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .epa..gov/ oppsrrd1/REDs/diazinon_ired. Swan et al. J Expo Anal Environ Epidemiol 2000. 2006).org/documents/ehc/ehc/ehc198. In 23 children. Banister EW. Sadowski MA. Liu F. 4/7/09 Lu C. Dumas P. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Barr DB. Olsson AO. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Fenske RA. 2006). Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. 2007 [online].9(2):117-131. Third National Report on Human Exposure to Environmental Chemicals. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Toepel K.S. Barr DB. Baker SE. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environmental Health Criteria 198. 2005. Rajendra W. Available at URL: http://pubs. Available at URL: http://www. Driskell WJ.htm. Biomonitoring studies of 2-isopropyl-4-methyl-6-hydroxypyrimidine provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of diazinon than are found in the general population. International Programme on Chemical Safety-INCHEM (IPCS). The Quality of Our Nation’s Waters.Organophosphorus Insecticides: Specific Metabolites 2005). Jones K. Redmon JB. Drug Chem Toxicol 1986. Bull Environ Contam Toxicol 1986. EPA 738-R-04-006. Oloffs PC.50(5):505-515. Nguyen JV. Environ Health Perspect 2006. Kruse RL. Geological Survey (USGS). Brunet RC.inchem. Interim reregistration eligibility decision (IRED. References Anthony J. Environ Health Perspect 2003.S. Beeson MD. Bouchard M. Noisel N. Semen quality in relation to biomarkers of pesticide exposure. Barr DB.37(4):501-507. Biochem Pharmacol 1992. Carrier G. Seifert J. Swan SH. Irish R. March 2006.44(11):2243-2250. In a small number of men visiting fertility clinics in Missouri and Minnesota. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Bravo R. Mason HJ. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects.111(12):1478-1484. Environmental Protection Agency (U. Banister E. Cocker J.376(6):808-815. Centers for Disease Control and Prevention (CDC). Diazinon. Pesticides in the Nation’s Streams and Ground Water. revised February 15. Anal Bioanal Chem 2003.S. Atlanta (GA).134(1-3):105-113. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.10(6 Pt 2):789-798.usgs. May 2004.114(2):260-263. Diazinon.gov/circ/2005/1291/. U. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. In 54 Canadian greenhouse workers. 1998. Drobnis EZ. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. EPA). Oloffs PC. 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. 1992-2001. 1/14/09 U. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Study for Future Families Research Group. Pewnim T. Garfitt SJ. Ann Occup Hyg 2006. Toxicol Lett 2002. Barr DB..

the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate. and in government programs such as the USDA’s Boll Weevil Eradication Program. in fruit fly control. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion.S. and other metabolites. and producing acute symptoms such as nausea. and plants.S. resulting in excess acetylcholine at nerve terminals. 2003).Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. which may vary for some chemicals by year and by individual sample. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. vomiting. Malathion is infrequently detected in groundwater sampling (USGS. It has a short halflife in soils and water and is not considered persistent in the environment. < LOD means less than the limit of detection. Once they are absorbed. Most of the estimated 15 million pounds used annually are applied to cotton (U. depending on the species. When malathion is used on food or feed crops. malathion has low acute toxicity.64. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff. Malathion is slowly absorbed through the skin. Pesticide applicators and agricultural workers can have higher exposures via dermal. usually only a small fraction of the crop is treated. shrubs. In addition to being a metabolite of malathion. which is an organophosphorus insecticide that is used on a wide variety of agricultural crops. weakness. Survey Geometric mean (95% conf. but is more rapidly and efficiently absorbed via ingestion.EPA.80 (<LOD-5. Compared with other organophosphorus insecticides. population from the National Health and Nutrition Examination Survey.. 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. 146 Fourth National Report on Human Exposure to Environmental Chemicals . It is registered for use in public health mosquito control. At high doses. inhalational.EPA. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al.5%) to kill body lice. It is moderately to highly toxic to fish. or oral routes (U. Metabolism of malathion leads to the formation of malathion monocarboxylic acid. 2006). Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Limited general population exposure occurs through the diet. as well as lawns. 2006). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. paralysis. 2007). Estimated intakes for the general population have not exceeded recommended intake limits. 2000). Malathion is also used medically in lotion form (0. 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. phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide. and seizures. see Data Analysis section) for Survey year 99-00 is 2. Thus. malathion dicarboxylic acid. gardens. ornamental trees. cholinergic effects.S.50) < LOD < LOD 453 660 807 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 937 983 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 680 498 580 Limit of detection (LOD. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

A longitudinal investigation of selected pesticide metabolites in urine. Lu C.38(4):546-553. Toxicol Sci 2003 May. Krieger RI. Barr DB.S.gov/circ/2005/1291/. 2007 [online]. Rappaport E. Mutat Res 1999.22(1):7-17.445(2):275-283. MacIntosh DL. Environ Health Perspect 2006. Curl CL. Barr DB. Malathion deposition. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.56(10):2393-2399.132(4):794-795. et al. Harley K. Lu C. July 2006. Atlanta (GA).Organophosphorus Insecticides: Specific Metabolites References Adgate JL. et al.112(10):1116-1124.73(1):182-94. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Am J Public Health 1987. Bravo R. Environ Health Perspect 2004. Dumoulin MJ. Albertini RJ. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo.inchem. Weltzien E. Sharma GD. J Expo Anal Environ Epidemiol 1999. Irish R. Carrier G. Brunet RC. Flessel P.74(2):following table of contents. Needham LL. 4/7/09 Kissel JC. Giri S. Dinoff TM.epa. Clayton CA. Erratum in: Toxicol Sci 2003 Aug. 2005. Ryan PB. Hammerstrom KA. Lioy PJ. Barr DB.usgs. Pluth JM. Thomas D. and cholinesterase status of date dusters and harvesters in California. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. International Programme on Chemical Safety-INCHEM (IPCS). Available at URL: http://www. metabolite clearance. Toepel K. March 2006. Harris JA. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. 6/1/09 U. Nicklas JA.S. Trzeciak A. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.gov/oppsrrd1/REDs/ malathion_red. Quintana PJ. U. Third National Report on Human Exposure to Environmental Chemicals. Arch Environ Contam Toxicol 2000. Genetic toxicity of malathion: a review. Environmental Protection Agency (U. Blasiak J. Eberly LE. Malathion (addendum). Freeman NC. J Expo Anal Environ Epidemiol 2005. revised February 15. Available at URL: http://pubs. Jaloszynski P. O’Neill JP. Goldhaber M. Grether JK. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Hertz-Picciotto I. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .org/documents/jmpr/jmpmono/v2003pr06. Jewell NP.S. 1992-2001. Swan SH. Giri A. Am J Epidemiol 1990.109(6):583-590. Reproductive outcome in women exposed to malathion. The Quality of Our Nation’s Waters. Environ Mol Mutagen 1993. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Neutra R. Petitti D. EPA). Szyfter K.9(5):494-501. Gosselin NH. Samuel O. Eskenazi B. Pesticides in the Nation’s Streams and Ground Water. Geological Survey (USGS). EPA 738-R06-030. Cancer Res 1996.pdf. Hooper K.15(2):164-171. et al. Environ Health Perspect 2001. Bouchard M. Barr DB. Centers for Disease Control and Prevention (CDC).77:1009-1010. Griffith W. Mutat Res 2002. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.114(2):260-263. Kedan G. Bradman A. Reregistration eligibility decision (RED) Malathion. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Available at URL: http://www. htm. Prasad SB. Fenske RA.514(1-2):223231.

S. and aquatic invertebrates.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .940 (<LOD-2. first registered in 1948.50) 1. 1977).40-4.30 (2. Methyl Parathion.30 (1.50) 3.21-1.10-1.70 (3.22-3. all registered uses were voluntarily cancelled (U.01-4.66 (2.90-11.60-5.71 (2.0) 3. In the 1990s. Given its limited use. and eliminated rapidly from the body after absorption (Kramer et al.790 (<LOD-.21 (2.46 (3.50 (1.70) 2.00 (2.69 (2.770 (.37-2.20 (2. more slowly absorbed through the skin.S.05) 4.50-9. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.70 (<LOD-3.28-4.10 (<LOD-6.70 (2.80 (2. Once absorbed.32-1.50 (1.00) 3.71 (3. Methyl parathion is not registered for residential use in the United States.33 (1. fish.730 (<LOD-. 2000).0) 2.40) 4.32-1. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.33) 2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.67 (1.58) 3.0) 3.92-2.49 (1.70) 2.70) 2.40-4.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .28 (1. and has a short half-life in soils and on plants.1. Many previous registered agricultural uses of methyl parathion have been cancelled (U. Increased risk of exposure via dermal. Survey Geometric mean (95% conf.32-3.09-1.990-1.19 (.00 (2. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.0 (3.EPA. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) 2.00) 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 1.80 (1.70-3.0) 3. ethyl parathion. Ethyl parathion. and oral routes can occur in pesticide and agricultural workers (Muttray et al. and of the chemical nitrobenzene. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300-. was once a restricted-use insecticide with limited applications on certain agricultural crops.50 (2. but by 2003. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low..28 (1.40 (1. Estimated intakes from diet and drinking water have been below recommended limits.74) 5. methyl parathion was rapidly absorbed after ingestion.910) < LOD < LOD < LOD 1.69) 4.30-3.32 (1.60) 1.40) 1.13-1.72 (3.70-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.298-00-0 Ethyl Parathion CAS No. < LOD means less than the limit of detection. peak domestic use was as high as 5-6 million pounds per year.910) < LOD < LOD .10-11. Both are toxic to birds.80) 2.30-16.47) 2.15-3.700 (<LOD-. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.37-4.70-6.70-6. 2002.50-14.67) < LOD 1.16) < LOD 1.70-6.860 (<LOD-1.61) < LOD 1.34 (3. binds tightly to soils resulting in low leachability. 2006).12) < LOD < LOD 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. pulmonary.11) 2.50 (2.79) 4.18-3.70 (2.85 (2.26 (1.10 (3.60 (4. which may vary for some chemicals by year and by individual sample.40-3.57-4.60-24. 2003).S.850) < LOD .0) 3.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .41-4.11-4. In animal studies.60-36.30-5.01) 695 660 518 679 603 941 Limit of detection (LOD.91-3.20) 5.. It had been applied to cotton.57) 1.. and to a lesser extent.27) 2.10) 4.92) 5.EPA.10) 22.37) 2. Methyl parathion use is highly restricted. Fourth National Report on Human Exposure to Environmental Chemicals 149 .02-6.40) 2. 2007).20 (<LOD-2.61) < LOD 1. on cereal grains.0) 3.45 (1. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.48) 90th 2.01) 4. Morgan et al.80 (2.62 (1.44) 2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. with limited applications in agriculture.50 (1.910) < LOD .50 (1.90 (1.89 (2.8 and 0. Methyl parathion has low water solubility.60-19.36-1.70 (2.45) 5. population from the National Health and Nutrition Examination Survey.20-5.0) 4.37-4.10 (3.50) 3.90-9.

20 (3.4 (3. Methyl parathion is not considered genotoxic. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.04) 1.33-3.790-. cholinergic effects.80 (1.880 (.70) 3. 2005. 2003.730-1.26) 17.00) 2.97 (<LOD-4.77-7. 2004).07) 2.29) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.680 (<LOD-1.530) < LOD < LOD < LOD .76-14. gov/toxpro2.72-2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.29) 2.930 (.3) 2.88 (1.79 (1. resulting in excess acetylcholine at nerve terminals.67-2.400 (<LOD-. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.86 (2.25) 1.98-7. Methyl Parathion.720 (<LOD-.08) < LOD . IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. Orsorio et al.EPA considers methyl parathion unlikely to be carcinogenic to humans.60) 2.9) 1.91 (1.78 (2.35-3.S. 1978. At high animal doses of methyl parathion.87 (1. WHO.17-4.73 (1. methyl parathion.89 (2.33-3. U.67 (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 .970 (. 1991).30) 3.11) 1.7) 3. Lores et al.29 (2. accidental exposure.30-1.01 (. Thus.97-10. 1990.20) .26 (1. 150 Fourth National Report on Human Exposure to Environmental Chemicals .640) < LOD < LOD 1. and producing acute symptoms such as nausea.01 (2.23) 1.440 (<LOD-. vomiting.370 (<LOD-.57) 6. In addition to being a metabolite of methyl and ethyl parathion. and seizures.17) .790-1.79) 1.14-3. The metabolite. weakness.05) 4. but lists ethyl parathion as a possible human carcinogen.82) < LOD .720-1.83 (1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . EPA at: http://www. population from the National Health and Nutrition Examination Survey.39 (1.84) 3.95) 1.56-2. Additional information about external exposure (i.39) 1.93 (2.21) 1.55 (<LOD-3.89 (2. and other metabolites. 2006.310-. In large doses.atsdr.31) < LOD .94-4.840 (.830-1.43) 4.20) 3. paranitrophenol.S.94-47.35-3.08 (1.930 (.. environmental levels) and health effects is available from ATSDR at: http://www.540) < LOD .430 (...16-4.60 (1.57-7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.44-3.78) 2.13-12.41-2.78-2.92 (2.html and from U. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.90 (1. does not inhibit acetylcholinesterase enzymes.10) 90th 2.96 (1. 1995). 1995.88) 1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.33-6.60-2. paralysis.59 (1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.2) 2.690-1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.940 (<LOD-1. Slotkin et al.980 (.21-21.07 (1.96 (1.38-3.09) 2.800-1.57-2.82 (2..03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .78-2.15-10.15) 3. and unintentional acute or chronic high-level occupational exposure (Hill et al. teratogenic.10 (1.97 (2.61) 4... Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.71) 1..2) 2.. 2004).48-4.epa.08-3. 2006.80 (1. ethyl parathion.55) 2. Zurich et al. gov/pesticides/. Karanth and Pope et al. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.25 (2. 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.Organophosphorus Insecticides: Specific Metabolites Metabolites”).44-3.00 (1.31-3.37-1.11-4.950) < LOD .01-3.1) 2.e.S.71 (1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.970 (.91) 1.00 (1.870) < LOD .13) 4.850-1.cdc.04 (2. Parathion and methyl parathion have high acute toxicity in animal testing. Jaga and Dharmani.500) < LOD < LOD .

Pesticide workers may have much higher levels following pesticide applications. Kissel JC.25(5):599-606. 2005). Giordano G. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation.215(3):182-190. Laboratory investigation of a poisoning epidemic in Sierra Leone. Wellman SE. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Cline RE. Eskenazi B. et al. et al. Environ Res 1995.. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Third National Report on Human Exposure to Environmental Chemicals. and levels were similar or slightly lower that those in a small convenience sample of the U. oral or dermal administration.112(10):1116-1124. Lin LI..71:99108. Barr JR. Bradman A. Harley K.33(5):270-276. In a study of workers who handle parathion. 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. Ashley DL. and many residents were symptomatic (Barr et al. International Programme on Chemical Safety-INCHEM (IPCS). 2005). Head SL. 1995. Runkle KD. Karanth S. Rev Environ Health 2006.. Baker S.9:311-320. Role of individual susceptibility in risk assessment of pesticides. Atlanta (GA). 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. Dharmani C. McCann et al. 2005. 2002). Turner WE. Neurotoxicol Teratol 2003. Barr DB.6(2-3):159-173.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. a range of values several hundred times higher than levels found in the U. Leng G. Barr DB. 2002. Gregg M. 4/7/09 Jaga K.S. Griffith W.110 Suppl 6:1085-1091. Barr DB. Costa LG. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicology 2005. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Environ Health Perspect 2002. Environ Health Perspect 2002. Pathak S. et al. Kramer RE. Hill et al. 2005. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect.14(4):213-216. Morgan DP.org/documents/jmpr/jmpmono/v95pr14. J Biomed Sci 2002. 2005. J Anal Toxicol 1990. Chicago area methyl parathion response.S. Environ Health Perspect 2004. Curl CL. Centers for Disease Control and Prevention (CDC). et al. Clark JM. Hill RH Jr. DiPietro E. Bradway DE. 1995). McCann KG. Moseman RF. Arch Environ Contam Toxicol 1977. Weltzien E. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Pesticide residues in urine of adults living in the United States: reference range concentrations. 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.21(1):5767. Hryhorczuk DO. Hetzler HL. 1999). Rockhold RW. Arch Environ Health 1978.inchem. Baker SE. Kedan G. Bailey SL.110 Suppl 6:1075-1078. Alley CC. Slach EF.. CDC. Methyl parathion: an organophosphate insecticide not quite forgotten. Hill RH Jr. 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..5 mg (500 µg)/g creatinine for workers at the end of shift... J Expo Anal Environ Epidemiol 2005. Lewalter J. References Barr DB. Moomey CM. general population (CDC.15(2):164-171.htm. Baker RC. ACGIH recommends a BEI of 0. Lu C. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Parathion-Methyl (addendum). Head SL. population (Olsson et al. 2002. Guizzetti M. Jewell NP. McClure PC. 2004). Occup Environ Med 1999. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Lores EM. Needham LL. Shealy DB.56(7):449553. Pope C. Rubin et al. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Available at URL: http:// www.

110 Suppl 6:1047-1051.Organophosphorus Insecticides: Specific Metabolites Muttray A.usgs.20(4):533-546.04/106. Geological Survey (USGS). Backer G. 2007 [online]. 1992-2001. Osorio AM. March 2006. WHO/SDE/WSH/03.S. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Toxicol Lett 2006. Ohio. Case No. Tate CA. 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. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.E.201(2):97-104. Environmental Protection Agency (U.S. Investigation of a fatality among parathion applicators in California. Monnet-Tschudi F. 6/1/09 World Health Organization (WHO).S. R. Ryde IT. Methyl parathion in drinking water. Schilter B. Available at URL: http://www. Yacovac R. Costa LG. Kieszak S.376(6):808-815. Available at URL: http://www. 152 Fourth National Report on Human Exposure to Environmental Chemicals . External and internal exposure of wine growers spraying methyl parathion.who. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 0153.pdf. U. Environ Health Perspect 2002. Nguyen JV. 1995-1996. Mengle DC. Available at URL: http://www.epa. Interim reregistration eligibility decision (IRED) for Methyl Parathion.S. Barr DB. Pesticides in the Nation’s Streams and Ground Water. Environ Health Perspect 2006. revised February 15. Hill RH Jr. EPA-738-FOO-009. The Quality of Our Nation’s Waters. et al.pdf. September 2000. Dunlop B. Sadowski MA. Letzel S. 2004. pdf. 1/14/09 U.114(10):1542-1546.gov/circ/2005/1291/. EPA).162(2-3):219-224. Toxicol Appl Pharmacol 2004. 5/19/09 Zurich MG.int/water_sanitation_health/dwq/chemicals/ methylparathion. Levin ED. gov/oppsrrd1/REDs/methylparathion_ired.epa. Jung D.D. Rosenberg J. Rubin C. Anal Bioanal Chem 2003. Honegger P. May 2003. Olsson AO. Ethyl parathion. Esteban E. Ames RG. Available at URL: http://pubs. 1/12/07 U.gov/oppsrrd1/REDs/factsheets/0155fct.S. Hill G. Am J Ind Med 1991. Seidler FJ. Environmental Protection Agency (U. EPA). Facts. Slotkin TA.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .210-.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. < LOD means less than the limit of detection.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 .07) .500 (.S.760 (<LOD-.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.850 (.740-1. see Data Analysis section) for Survey year 01-02 is 0.470 (.780 (<LOD-1. population from the National Health and Nutrition Examination Survey.55) . Survey Geometric mean (95% conf.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th . Survey Geometric mean (95% conf.300-1. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.680 (<LOD-.430 (<LOD-.820) < LOD < LOD .15) < LOD .17 (.950) < LOD < LOD 1.700-. 154 Fourth National Report on Human Exposure to Environmental Chemicals .780 (<LOD-1.930) 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 .21) < LOD .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .580-1.840) 669 687 929 Limit of detection (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.94) .740 (.780 (.700-1.410 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .250 (<LOD-.31) .64) .200-.210-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (.210 (<LOD-.S.670 (<LOD-1.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .27) .610 (<LOD-1.840 (.2.

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

and deltamethrin have been used frequently on cotton. pyrethroids are rapidly metabolized. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. cyfluthrin.EPA.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. Woollen et al. pyrethroid pesticides have less acute toxicity in animals and people. cypermethrin. 2002). About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. 1992). and greenhouses. Soderlund et al. Outside the U.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .. and sumithrin) are also registered for use in mosquito-control programs in the United States. they are not persistent in the environment due to their rapid degradation within days to several months. so usage is restricted near water (U. After absorption from inhalation or ingestion.. WHO. solvent oils. 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. EPA. warehouses.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. Compared with other classes of insecticides such as organochlorines. 2003. or carbamate pesticides.2-Dichlorovinyl)-2..S. 1999.2-Dichlorovinyl)-2. 2006a. 1997. 2005). and then eliminated over several days in urine and bile (Kuhn et al. Soderlund et al. Pyrethroids are not well absorbed through the skin (ATSDR. followed by conjugation. 2005. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. bind to soils. 2002.. They are ranked as having moderate acute oral toxicity. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. which are natural chemicals found in chrysanthemum flowers. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. 2002). This class of pesticides has low toxicity in birds and mammals. and synergists. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. There are about 30 different pyrethroid pesticides in use. but pyrethroids are highly toxic to fish and some aquatic invertebrates.S. organophosphorus. Woollen et al. Pyrethroid pesticides have low volatility. 2006b). agricultural fields. but may be poorly transferred across the placenta (ATSDR. Generally.. They are also applied on livestock to control insects.. resmethrin. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. Estimated intakes from diet and drinking water are below recommended limits. The table shows the urinary pyrethroid metabolites measured in this Report.S. such as piperonyl butoxide. Unmetabolized pyrethroids have been measured in breast milk. animal facilities.. Certain pyrethroid insecticides (such as permethrin. 1992). in some situations replacing the use of DDT. In agriculture. Leng et al. 2007). 2003. and are rarely detected in ground waters (USGS.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins.2-Dibromovinyl)-2. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. by either ester hydrolysis or hydroxylation..

Wieseler B. Wang SL. Berger-Preiss E. Leng A. et al. Ranft U. Ose K.atsdr. and striatal dopamine levels in male and female rats. 2005). In developing rodents. J Environ Monit 2006. 1991. 2005). 1998. Zhao RC. salivation. Kunimatsu T..gov/toxpro2. Garey J. Pauluhn J. Spinosa HS. Kamita Y. Garey J.211(3):188-197. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Bernardi MM.. Neurotoxicol Teratol 2001. Leng G. Lewalter J. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Florio JC. Soderlund et al. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Generally. Leng G. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Moniz AC. et al. 2002). Adhami VM. 2006. Seth PK. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Regul Toxicol Pharmacol 2002. 2001. Elwan et al. Neurotoxic effects of two different pyrethroids. 2003. Bull Environ Contam Toxicol 1999. Kang IH. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Idel H. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. McCarthy et al.108(1):78-85. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. on immature and adult mice: changes in behavioral and muscarinic receptor variables. fenvalerate. 2005).50(2):245-255.23(6):665-673. Pyrethroid pesticide-induced alterations in dopamine transporter function. Wolff MS. Available from URL: http://www.cdc. Caudle WM. 2001. 2006. Miller GW. Sugiri D. Lemonica IP.107(3):173-177.251(3):855-859. 2003. Shin JH. 1999. Fredriksson A. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.. Kim TS. Bernardi MM. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. September 2003. Kim HS. bioallethrin and deltamethrin. Pogo BG. Wolff MS. Toxicological profile for pyrethrins and pyrethroids. Eriksson P. McCarthy AR. Varoli FM. Kunimatsu et al.62:101-108. In California.. Neurotoxicol Teratol 2005. Garey and Wolff. Lee SJ... Shafer. Cruz-Casallas PE. 2002)..Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Sunami O. Estrogenic and antiprogestagenic activities of pyrethroid insecticides.. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Chen JH. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity.S..35(2 Pt 1):227-237. Toxicol Appl Pharmacol 2006. 2005). and seizures (ATSDR. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.gov/pesticides/ and from ATSDR at: http://www. Toxicol Appl Pharmacol 1991.. 2004. Kim IY.html. Moniz et al. Neurosci Lett 2001.8(1):18-21. EPA at: http://www. Thomson BM. dopaminergic. cdc. Yang J. Ray et al.8(1):197-202. Hu et al. Lazarini CA. 2000. choreoathetosis. Agrawal AK. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. neurochemical changes in cholinergic. et al. Song L..1/15/09 Aziz MH. Kim et al. Environ Health Perspect 1999. Eriksson and Fredriksson. Kuhn KH.atsdr.. Abell AD. and permethrin) in the Hershberger and uterotrophic assays. Xenobiotica 1997. Shukla Y. et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Go et al. Estrogenicity of pyrethroid insecticide metabolites. Kuhn K. J Reprod Dev 2004.gov/toxprofiles/ tp155. WHO. Biochem Biophys Res Commun 1998.205(6):459-472. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Salzgeber SA.300(3):161-165. Hu JY. Okuno Y. Idel H. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Go V.27(4):609-614. Elwan MA. Richardson JR. 2006). 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. 2003. Guillot TS. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. 2002. tremor. Levsen K.27(12):1273-1283.html. Lazarini et al. Leng G. Fourth National Report on Human Exposure to Environmental Chemicals 157 . motor activity.. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. epa. 2003. Int J Hyg Environ Health 2002. Additional information about pesticides is available from U. hypersensitivity. Yamada T. Shaw IC.

et al. 5/26/09 U. 19962002. June 2006a. Geological Survey (USGS).htm. Sheets LP. 1992–2001. Available at URL: http://www. Laird WJ. Clark JM.113(2):123-136. Available at URL: http://whqlibdoc. Meyer DA. sumithrin synthetic pyrethroids for mosquito control. O’Malley M. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Sargent D. and therapy.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.S. Spencer J.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. J Toxicol Clin Toxicol 2000. June 2006b.186:57-72. 5/26/09 U. Lesser JE.gov/ circ/2005/1291/. Crofton KM. Reregistration Eligibility Decision for Cypermethrin. Toxicology 2002. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. pdf. EPA).S.38:95-101.epa. Environmental Protection Agency (U.S.who. Pyrethroid illnesses in California. Marsh JR. March 2006. Pyrethroid insecticides: poisoning syndromes.S. synergies. Pesticides in the Nation’s Streams and Ground Water. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Safety of pyrethroids for public health use. 2005. Permethrin.usgs.epa. 2007.S.pdf. World Health Organization (WHO). Rev Environ Contam Toxicol 2006. Environmental Protection Agency (U.htm.gov/oppsrrd1/REDs/cypermethrin_red. Piccirillo VJ.171:3-59.22(8):983-991. Pesticide and Evaluation Scheme. April 2002. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Xenobiotica 1992. Available at URL: http://www. 5/26/09 Woollen BH.S. Environmental Protection Agency (U.epa. U. resmethrin. Available at URL: http://www.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.10. Shafer TJ. Environ Health Perspect 2005. EPA). Mullin LS. Forshaw PJ. Available at URL: http://pubs. Revised February 25.S. 5/26/09 U. Soderlund DM.Pyrethroid Pesticides Ray DE. EPA).

2 μg/L) in the U. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. most of which were dermal and respiratory irritations (Spencer and O’Malley.. 2003).S... Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate.. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. Leng et al. Thus.Pyrethroid Pesticides Cyfluthrin CAS No. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. 2005). but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. 2003). Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. Studies in Germany of 396 children and adolescents (Becker et al. 2001. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. representative 2001-2002 NHANES subsample (CDC.S. 2006). the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. Cyfluthrin is rapidly metabolized and eliminated from the body. Urinary levels for adults and children in these studies were similar (Heudorf et al. Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al. 2003).. representative subsample in NHANES 2001-2002 (CDC.95 µg/L. 2004).. 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. 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. Baker et al. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). In an analysis of 217 urine specimens from a nonrandom sample of United States residents.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. 2005). Fourth National Report on Human Exposure to Environmental Chemicals 159 .. 2005. Following an indoor application exposure. 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. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin.

< LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.S.2.2 and 0. 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.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 160 Fourth National Report on Human Exposure to Environmental Chemicals .

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

Berger-Preiss E. Angerer J. Arch Environ Contam Toxicol 2004.186:57-72. Angerer J. Schulz C. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Seiwert M. Hadnagy W. Becker K. Olsson AO. 2005. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Barr DB. Pyrethroid illnesses in California. 19962002. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2003.Pyrethroid Pesticides References Baker SE. Int Arch Occup Environ Health 2004. Int J Hyg Environ Health 2006. O’Malley M.109(3):213-217. Williams RL. Leng G. Butte W. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.206(2):85-92. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.13(2):112-119. Drexler H. Heudorf U. Centers for Disease Control and Prevention (CDC). Ball M. Ranft U. Sugiri D. Int J Hyg Environ Health 2006.77(1):67-72. Atlanta (GA). Environ Health Perspect 2001. Heudorf U. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Idel H. Third National Report on Human Exposure to Environmental Chemicals. Kolossa-Gehring M. J Expo Anal Environ Epidemiol 2003. Krieger RI. Spencer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Rev Environ Contam Toxicol 2006.209(3):221-233.46(3):281-288. et al. Bernard CE. Hoppe HW.209(3):293-299. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Angerer J.

690) .170 (.680 (.110-. cis-permethrin.2-dichlorovinyl)- CAS No. cis-3-(2.S.570-.460 (.68) .262) * * * < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.15) .950-2.410) . The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.07 (.53) .2-dichlorovinyl)-2.300-.330) ..260 (.870) 1.300 (. 1985.630) .890 (.370-.400-.680-3.580) 1.202 (.670 (.630) .490-1. Similarly. which may vary for some chemicals by year and by individual sample.210) 90th .470 (. < LOD means less than the limit of detection.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin. the presence of trans-3-(2.600) .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * . and trans-cyfluthrin.580-1. 1999). The chemical trans-3(2.650-1.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.220-. Cyfluthrin.600-1.500 (.160 (<LOD-. Biomonitoring Information Urinary levels of cis.640 (.380-.2dichlorovinyl)-2.35) 1.630 (.340-. cis-cypermethrin. transcypermethrin and trans-cyfluthrin.50) .43) .440 (. but it can also reflect exposure to cis-3-(2.900 (.790) .380-.470-1.or trans-3-(2.140 (.180) .380) .520) .280 (. more of the trans-metabolite than Urinary cis-3-(2.670-1.220-.1.200 (. trans-cypermethrin.110-.2-Dichlorovinyl)-2.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.120-.510 (.220-.430-.600 (.200-.510 (.340) .420-.230) .730 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .200-.330 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.250 (.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .340) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.460-.220) .380 (.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.670-2.24) 1.730 (. Kuhn et al.2dichlorovinyl)-2.490-1. and ciscyfluthrin. population from the National Health and Nutrition Examination Survey.410) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.44 (.670-1.490-.120-.280-.370 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.110 (<LOD-.380-.910-5.200) .700) .850 (. 1999).35) .68359-37-5 Cypermethrin Permethrin CAS No. 52315-07-8 CAS No.270-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. but can also reflect exposure to trans-3(2.155-.68) .960 (.08) .770-1.710-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.12 (.160 (.200-.880 (.210) .110-. Kuhn et al.220-.770) .2-dichlorovinyl)-2.11) .47 (.240) .740-2.2-dichlorovinyl)-2.32) . trans-permethrin..730 (.and trans-isomers.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740-1.200) .630-.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .210-.500 (.250-.150 (.820 (.180 (.300 (.270 (.1 and 0.460-1. Survey Geometric mean (95% conf.610) .710) . ciscypermethrin and cis-cyfluthrin.270 (.240) .780) .920) 1.120-.310) .610) .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 .77 (.790-1.80) .140 (<LOD-.28) 671 680 518 701 591 957 Limit of detection (LOD.740) 1.120-.530 (.790 (. Generally.2-dichlorovinyl)2.510 (.740 (.550) .890 (.13 (.570 (.200) < LOD < LOD < LOD .68 (. 1985.54) .350) .160 (.270 (.21) . The presence of cis-3-(2.490-.790-1. In the body.

2004).640-1.59 (1.190 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.280-.350) .230-.2-Dichlorovinyl)-2.590) . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.21) ..690-1.230-.170) < LOD < LOD < LOD .640-. urinary trans-3-(2.600 (.700) . 2006. In a study of urban residents in Germany (Berger-Preiss et al. 2006.2dichlorovinyl)-2.680-1.340) .580) ..680 (.290-.340-.700-2.380) .530 (.700) . population from the National Health and Nutrition Examination Survey.80) ..59) .250 (<LOD-.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.190) .810 (.33 (. 2006). 2005).440 (.380 (.560) 1. Lu et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.560) .160 (<LOD-.29 (.200-.2-dichlorovinyl)-2.2-dichlorovinyl)-2.390-.. In a study of volunteers.840 (.11) .350 (.150-.420 (.250-.220) .750-1.12 (.550) .590 (.440 (.67 (. Studies in Germany of 396 children and adolescents (Becker et al.200-.220 (. 2004.640 (. 2001) showed urinary levels of cis.440-.2-dichlorovinyl)-2. 2002).250-.300 (. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.260-.12-2.300 (.150-.430 (..2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.33) .710 (.550 (.320-.220 (. 2001.510-1.450 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .67) .11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .11) 1.450-. In these volunteers.S. Schettgen et al.830) .370-.680-1.890) .2-dimethylcyclopropane carboxylic acid did not increase.. 2003).320) .750 (.530 (.200 (.230-.780) 1.900 (.104-.24) . 2005).270 (.550-1.11 (.290) .880) . representative NHANES 2001-2002 subsample (CDC.182) * * * < LOD < LOD . median urinary levels of trans-3-(2. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Cyfluthrin.S.540 (.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 . Survey Geometric mean (95% conf. the median and 95th percentile of urinary levels of cis-3-(2. post- Urinary cis-3-(2. 2005)..390-.300-.49) .380-. urinary levels of cis-3-(2.2dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC. 2006) and 1177 urban adults and children (Heudorf et al.920 (.180 (.550-1.and trans-3-(2.2-dichlorovinyl)-2.580-1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.130-.and trans-3(2.570) .540 (.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .170 (.170 (.890 (.270) . Other studies have provided evidence that urinary levels of cis.180-.250) 90th .290) .140-.280 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.37) . 2002). the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. 2005) In a small group of indoor pest-control operators.270-.370-.190) .780 (.440-.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. In the same residents.260 (.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.500 (..2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.360-1..080-.540) .250) .250-. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.Pyrethroid Pesticides 2.470-1.300) .270) .340) . 2005).640-1.430-.120 (. 2006).31) .200) .710-3.450-1.250) .410) .11) .430-1..2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.138 (.400 (.300) .03) 1..210-.230 (.260 (.550) .240 (<LOD-. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al. 2003).290 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .840 (.150-.370-.400-1.59) .800 (.390 (.640) 1.260) .260 (.

89 (2.64-4.4 and 0.49-3.01 (1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .81) 2.17 (.460-.500 (. trans-Cypermethrin.620) < LOD 2.07 (1.7) 2.03-1.68-2.55-4.77) 2. 2005).55-5.77) 1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.410-.19) 1.410 (<LOD-.28 (1.68) 1.14-6.660) 1.12-6.800-1.20 (.27 (1.60) .48) 4.39-5.780 (.23) 2.07-3.700-1.95) 2.94 (1.19 (2.400-.08-6. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. Fourth National Report on Human Exposure to Environmental Chemicals 165 .28 (2.700) .420 (<LOD-.68-3.570) 90th 1.25 (1.820) .500) .20 (.2-dichlorovinyl)-2.560 (.66) .42 (2.43) 2.580 (.37 (1.840-1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .470 (<LOD-.62 (1.55-3.440 (<LOD-.Pyrethroid Pesticides application median urinary levels of summed cis.63) 1.13) .850-1.08-4.40 (1.56) 2.4.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .17-1.84 (1.490 (<LOD-.56 (1.69 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.76-3. Urinary trans-3-(2.5) 2. The maximum post-application urinary levels.S.530) .and trans-3-(2.41 (1.97-11.39 (1.95) 3.14-2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.760) .14) 1.830-1. Biomonitoring studies on urinary levels of cisor trans-3-(2.2dichlorovinyl)-2.91 (1. however.920-1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.550 (.610) 1.63) 1.730) .60) 1.11-2. Survey Geometric mean (95% conf.60-4.50 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.970 (.41-14.810-1.25-3.23 (.670) .750) .16) 1.69) 1.400 (<LOD-.66) 691 680 518 690 595 954 Limit of detection (LOD.670) .87 (1.26 (.08) 1.2-Dichlorovinyl)-2.470 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.56 (1. 2005).940 (.2-dichlorovinyl)-2.520) .76-4.49-3.710 (.54) 4.49-5.03-1.09 (.17 (.56) 2.59 (1.460-.10) 2.500-.11-1.35) 1.520-.90) 1.68) 2. population from the National Health and Nutrition Examination Survey.860) .22 (1.85) 4.490-1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.20 (.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 .68) 1. Finding a measurable amount of cis.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.42) 1.410-.560 (.560 (.680-1.910-1. < LOD means less than the limit of detection.01) 4.54 (1.19 (3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.77 (1.410 (<LOD-.480-.or trans-3-(2. which may vary for some chemicals by year and by individual sample.910-1.

15-3.730) .08 (.30-6.00 (1.880 (.Pyrethroid Pesticides Urinary trans-3-(2.34-4.670) .57) 3.70 (.80) 1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . trans-Cypermethrin.65 (2.750) .40-2.13) 1.33-2.98 (1.27-2.87-3.560 (.61) 1.880 (<LOD-1.15 (1.470-.770) < LOD 2.87 (1.570 (.74) .07) 2.91-11.42 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.55 (2.56-5.20-2.850-3.44) 2.440-.850) 1.41) 1.91) 1.22-2.89) 2.36) 2.27-2.530 (<LOD-.56-2.850) . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.42) 1.580 (.31 (2.60 (1.780) 90th 1.33 (1.800-1.720-1.30-3.20 (1.81 (2.74) 2.720 (<LOD-.02-1.07-1.87) 1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.S.660) .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 .34-3.56 (1.480-.500-.570-.00) 5.720-1.16 (1.31) 1.15-3.37 (1.530 (.3) 2.00-5.22) 1.610-.640) .55 (2.22-1.33-1.28) 2.35 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11) .970 (.700-.64 (1.55 (2.07) 2.820-2.47-2.410-.39) 1.15) 3.00) 1.570 (<LOD-.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00) 1.540) .15-3.760 (.930-1.580) . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.60) 2.35) 1.36 (1.700 (.31 (.07-2.48-2.13) .57 (1.470 (.880-1.67 (2.700 (.780) .900 (<LOD-1.12-1.780 (<LOD-.19) .800-1.12 (.75 (1.26 (1.29) 1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .19 (1.2-Dichlorovinyl)-2.60) 2.87) 1.07-3.740) .47-2.68) 3.08 (.45 (1.45-2.39 (1.91 (1.87-8.86 (2.520 (<LOD-.15) 2.47 (1.65) 1.48 (1.

Pearson M. Int J Hyg Environ Health 2002. Bull Environ Contam Toxicol 1999. Bravo R. Kolossa-Gehring M. George DA. Hadnagy W. Angerer J.62:101-108. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.77(1):67-72. Atlanta (GA). Leng G. Int Arch Occup Environ Health 2003. Levsen K. Idel H. Biological monitoring of workers after the application of insecticidal pyrethroids. Berger-Preiss E. Centers for Disease Control and Prevention (CDC). Drexler H. Berger-Preiss E. Leng G. Int J Hyg Environ Health 2003.Pyrethroid Pesticides References Becker K. Schulz C. Angerer J. Butte W. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.76(7):492-498. Ranft U. Int J Hyg Environ Health 2006.134(1-3):141-145. Sugiri D. Angerer J. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Ranft U. Heudorf U.109(3):213-217. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Leng G. Permethrin and its two metabolite residues in seven agricultural crops. Environ Health Perspect 2001. Angerer J.206(2):85-92. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Ball M. Int J Hyg Environ Health 2006. Heudorf U. Int Arch Occup Environ Health 2004. Bartell S. 2005. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Heudorf U.68(6):1160-1163.209(3):293-299. Kuhn K. Barr DB. Third National Report on Human Exposure to Environmental Chemicals.205(6):459-472. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.209(3):221-233. Hardt J. J AOAC 1985. Seiwert M. Lu C. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Drexler H. Wieseler B. Heudorf U.114(9):14191423. Idel H. Environ Health Perspect 2006. Hoppe HW. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Idel H. Sugiri D. Schettgen T. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. et al.

urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dimethylcyclopropane carboxylic acid of 0.2-dibromovinyl)-2. (2004) reported a geometric mean concentration of cis-3(2. Thus. Finding a measurable amount of cis-3-(2. Deltamethrin can degrade to cis-3(2. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dibromovinyl)-2.2-dibromovinyl)-2. in detection of cis-3-(2. 2004). Outside the U.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.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.2dimethylcyclopropane carboxylic acid formed in the environment.2-dibromovinyl)-2.S... Baker et al. 2005). The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. deltamethrin has been used against mosquitoes that carry malaria. 2001.. 2006) and 1177 urban adults and children (Heudorf et al.2-dibromovinyl)-2.5 μg/L) than the detection limit (0. Urinary levels for adults and children in these studies were similar (Heudorf et al.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. Studies in Germany of 396 children and adolescents (Becker et al..3-0. Biomonitoring Information Urinary levels of cis-3-(2.39 µg/L. 168 Fourth National Report on Human Exposure to Environmental Chemicals . In the NHANES 2001-2002 subsample.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dibromovinyl)2. 2005).. 1990)..2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2.2-dibromovinyl)-2. 2005). 52918-63-5 General Information Cis-3-(2.2-dibromovinyl)-2.2-dibromovinyl)-2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Pyrethroid Pesticides Deltamethrin CAS No. in some situations replacing the use of DDT. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. mean peak urinary levels of cis-3-(2.

Pyrethroid Pesticides Urinary cis-3-(2. * 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.1.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-Dibromovinyl)-2. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf.S. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD.

population from the National Health and Nutrition Examination Survey. 170 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dibromovinyl)-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 830 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 700 527 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf.S.Pyrethroid Pesticides Urinary cis-3-(2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. representative NHANES 2001-2002 subsample (CDC. 2005)... 68359-37-5 Cypermethrin Deltamethrin CAS No. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 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. Hardt and Angerer. Becker et al. 2005. 2005)... 2002. 2005). 2005). (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. 2003. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides.. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 2006). In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 2006. 52918-63-5 use and house dust levels (Lu et al. 2003.. Following residential spraying with deltamethrin for malaria protection in Mexico.. 2005). Thus. 2003). median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . In one study of 145 urban residents in 80 private homes in Germany. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. CDC. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. Baker et al. urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al.Pyrethroid Pesticides Cyhalothrin CAS No. 39515-41-8 CAS No. In a small group of indoor pest-control operators. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 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. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect.S. Fenpropathrin Permethrin CAS No. 2005. CDC. In the New York City study. 2004). Saieva et al. 2005). CDC. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above.52315-07-8 CAS No. 2005). 52645-53-1 Tralomethrin CAS No. A study of 396 German children (Becker et al.

314) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.160-.35) 2.321 (.253-.52-4.417 (.32 (2.550-.41 (1.420) .227-.233-.30 (1.940) 1.64) 697 680 524 701 603 957 Limit of detection (LOD.65 (1.78) 1.230-.50 (2.490) .990) .530-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .45-5.1 and 0.250 (.01 (1.740 (.200-.90) 1.340) .270 (.62) 5.160-.700 (.680 (.390) .1) 3.76 (1.570-1.750-1. Deltamethrin.190-.28) 1.73) 1.450 (. population from the National Health and Nutrition Examination Survey.330) .63-3.02-6.470-.33 (1.353 (.362) .328 (.260-.700-1.13 (.260 (.34-6.69) 3.490-.21 (2.300 (.200-.850) .92-3.69 (1.240 (.38 (2.180-.520 (.81 (1.27-11.34) 8.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.48-2.430-.1.295) .740 (.434) .53-3.760 (.79) 3.298 (.840-1.374) 99-00 01-02 99-00 01-02 99-00 01-02 .336 (.800 (.595) .780) 4.430-.320) .83-11.350-.210-.78) 6.46) .65-2.750) .26-2.29-1.710 (.26) 2.53) 1.352-.49 (1.246-.601) .190-.560-1.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .250 (.8) 3.71 (1.830-2.290 (.44) 5.38 (2.62-6.34 (2.190-.292 (.26) 2.428-.311 (.51-3.43) 3.560-.590 (.72 (1.820) .78 (1.507 (.300 (.13) .93 (1.510-.670 (.570-.340) 75th .41-3.620-1.35 (2.320 (.280 (.369) .35) 1.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.S.12) .230-.18 (1.05) .78) 1.16-1.288 (.387) . interval) .03 (3.406) .710 (.41) 3.220-.325 (.510-.810) 1.260 (.240 (.360) .32-21.39) 2.230 (.266-.364) .270) .25-7.23 (2.830) 90th 1.12 (. Survey Geometric mean (95% conf.35) 2.41-2.49 (1.56-5.850) .730 (.49-2.320) .650 (.230-.30) 3.560-.271-.60) .55 (1. Fourth National Report on Human Exposure to Environmental Chemicals 173 .05) 1.250-.630) .33) .590-.200-.800) 1.300 (.610) .30 (.247-.62-8.300) .530-.1) 3.63 (3.454 (.18 (2.384) .330) .45 (2.89-71.320) .750) .230 (.600 (.820) .340) 1.260 (.35 (1.273 (.33 (2.25 (2.51-6.25-1.960 (.48-2.276-.42-2.25 (2.32 (1.315 (.267 (.75 (1.49-2.25-4.292-.586) .86 (1.46) 2.14-6.370) .12) 4.27-2.190-.288-.277-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.440) .870 (.250 (.297 (.355) .52-5.265-.54) 1.210-.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .373) .27-2.04) .427) .16) 1.1) 3.320) .04-5.238-.640 (.36) 1.226-.314 (.

36 (1.446) .312 (.240 (.328) .300-.700-1.261-.400-.216-.330) .264 (.250 (.750-1.534) .640 (.230-.280 (.00) 1.230) .380-.550 (.55) 3.13 (.330) 1.246 (.03-1. population from the National Health and Nutrition Examination Survey.225-.43 (2.330) 75th .04 (.460-.274-.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 .380 (.19 (2.55 (1.930) .309) .49-2.39) 1.67 (1.35-3.760) .37) 1.226-.190-.610 (.13-1.83 (1.210 (.80) 4.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .530-.63-3.229-.630) .930) 1.309 (.88-5.210 (.200-.860 (.650) .271-.590) .450 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.510 (.62) .860-1.440-.35) .40 (1.96 (1.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.730) .250 (.190 (.72 (1.357) .550 (.570) .670) .423 (.19) 2.03 (.150-.280) .400-.91 (2.350 (.67 (1.400) .590) .390-.460-.960-1.60-4.48 (1.173-.272) .372) .720) 90th 1.240-.560 (.540 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.62) 1.234 (.410-.17 (.41-4.0) 3.02 (2.36-6.200-.32 (2.25-2.27) 1.37 (1.240-.530-.300-.49) 1.590) .220-.329) .09) 3.329) .67) 1.11 (.677) .274 (.73-4.94 (1.91) 9.321-.290) .270-.64-5.280) .730-1.21-4.43-64.720 (.200-.280 (.510 (.07) 2.370 (.13-1.60) 1. Survey Geometric mean (95% conf.190-.378 (.299-.63) 1.90) 3.290-.240 (.21 (1.81 (1.40) 2.200-.240-.41) 1.272 (.840-1.25) 2.19-6.210-.49 (1.35 (1.670) 3.490-.316 (.401) .202-.07-5.09-2.550 (.53 (1.75-8. Deltamethrin.590-1.510 (.580) .370-.250) .15-2.25-5.480-.270) .16-4.52) 2.49) 3.335-.240 (.S.230-. interval) .43 (1.730) .278) .83) 1.275 (.280-.00) 1.09 (.440-.95) 1.10 (2.44 (1.00) 5.490 (.09-2.387) .178-.240-.290) .810) 1.440-.54 (1.160-.224-.220 (.227 (.320) .91-4.91) .74) 3.270 (.350) .330 (.310) .86 (1.35) 1.311 (.261 (.73) 1.410) .270) .92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .43) 1.580 (.22 (1.437) .860-1.480 (.84 (1.51-7.06-3.323 (.238-.44) 2.05-3.17-1.330) .740) .640 (.270 (.362 (.490 (.52 (1.365) 99-00 01-02 99-00 01-02 99-00 01-02 .253) .240 (.02-1.280 (.11 (.61-2.04 (3.420-.500) .

Leng G. Indoor pyrethroid exposure in homes with woollen textile floor coverings.46(3):281-288. Barr DB. urban cohort. Obel J. Angerer J. Hardt J. Pearson M. Ball M. Hadnagy W. Int J Hyg Environ Health 2002. Ortiz-Perez MD. Environ Health Perspect 2003. Lapinski R. Deych E. Batres LE. Int J Hyg Environ Health 2003. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.209(3):221-233. Torres-Dosal A. Berger-Preiss E. Leng G. Biological monitoring of workers after the application of insecticidal pyrethroids. Olsson AO. Grimaldo M.Pyrethroid Pesticides References Baker SE. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Exposure to indoor pesticides during pregnancy in a multiethnic.205(6):459-472. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Environ Health Perspect 2005.206(2):85-92. Arch Environ Contam Toxicol 2004. et al. Third National Report on Human Exposure to Environmental Chemicals. Ranft U. Int J Hyg Environ Health 2006. Godbold J. Atlanta (GA). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. and genotoxicity in exposed children. Lu C. et al. Berger-Preiss E. et al. 2005. Environ Health Perspect 2006. Levsen K. Bravo R. Centers for Disease Control and Prevention (CDC). Int Arch Occup Environ Health 2003.113(6):782-786. Carranza C.114(9):14191423.76(7):492-498. Angerer J. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Barr DB. Sugiri D. toxicokinetics. Berkowitz GS. Ranft U. Idel H. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Seiwert M. Lopez-Guzman OD. Kolossa-Gehring M. Liu Z. Hoppe HW.111(1):79-84. Bartell S. Becker K. Idel H. Sugiri D.

110-. interval) .260) .320-. 7440-36-0 General Information Antimony is found in ores or other minerals.160-.157) .470 (.190-.240-.200) .176 (.230) .370) .161) .210) .280-.169 (.350) .140 (.190) .07.146 (.270 (.150-.310) .190) .119-.133) * .140) .130 (. from air and drinking water.130-.390) .150) .210-.420) .108 (.230 (.240-.190 (.290 (.160) .430 (.400 (. Workplace exposures can occur at smelters. ceramics.140-.128 (.130-.210) .150 (.340 (.390-.126-.180 (.220) .270 (.150-.490) .230-.310-.460 (. to a lesser extent. 0.240) .140) .160) .130-.300-.125 (.250-.350-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140) .184) .260) .080) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.290-. sheet and pipe metal.120-.350) .170-.390-.112-.130 (.270 (.200 (.350 (.300 (.180-.390 (.390) .260-.090) 75th .330 (. and 03-04 are 0.400) .160-.230 (.114) .160) .105 (.230 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.110) .250) .S.180-.220-.190-.270 (.330 (.260) .220-.210 (.095-. solder.130 (.250 (.210) .120-. < LOD means less than the limit of detection.150-.117-.250 (.440) . storage batteries.103) .115-.100 (.280) .200-. see Data Analysis section) for Survey years 99-00.04.410) .110-.310 (.130) < LOD .154) . It is also used in paints.270-.180-.137) .120-.300-.080 (<LOD-.360) .220 (.220) .120 (.150) 90th .079-. and glass.350 (.270) .220-.120-. coal-fired plants.240 (.160 (.132 (.500) .250-.070-.115) .280) .200 (. and 0.119) .270) .390) . and excretion of antimony vary depending on its oxidation state.130 (.300) .180 (.260 (.160) .136) * . population from the National Health and Nutrition Examination Survey.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 .158 (.280-.099 (.310) .360) .210) .300) .330) .320-.080) . enamels. distribution. ammunition.150 (.070 (<LOD-.400 (.108-. +3.175 (.128 (.130 (.350-.134 (.200-.180) .140) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.330-.190) .460) .156-.144) .132 (.100) .140 (. Antimony enters the environment from natural sources and from its use in industry.140 (.130 (.120 (.080-.120-. People are exposed to antimony primarily through food and.190 (.560) .110-.120) .330) . or other substances containing antimony is another means of exposure.280) . Antimony can exist in one of four valences in its various chemical and physical forms: -3. 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.210-.240 (. respectively.250 (.190 (.117-.154-.Metals Antimony CAS No.230-.220-.170 (.154) . Stibine is a metal hydride form of antimony used in the semiconductor industry.200 (.220) .126 (. The absorption.100-.134-.440 (.130) .350 (.230) .123 (.330) 1132 1335 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .240 (.360 (.430 (.460 (.330) .170-.110 (.340) .320-. fireworks.410-.210) .280) .180-.207) .135) * .330-.04.180 (.090 (.145) Selected percentiles ( 95% confidence interval) 50th .470) .190-.090 (<LOD-.280-.180-.210 (.190-.160 (.200) .220 (.190) . 0.300-.230) .390) .200-.440) .130-.220-.260-. It is used in metal alloys.330 (.230-.250-. and refuse incinerators that process or release antimony.240 (.164-.310-.148-.280 (.120-.230-.400-.122 (.280-.095 (.130) .130-.090-. castings.120-.130-.120) .130 (. and pewter.230-.170-.600) .390-.141-.320) .160 (.130-. and as a fire-retardant in textiles and plastics.340 (.300) .200 (.170-.170) .160) .350) .220-.180 (.120) .170 (.143 (.350-.510) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.200 (.300 (.370-.109-.098-.120 (. water.130 (.220) 95th .320-.280 (.470) .150-.190-.200 (.131-.410) .093 (.280-.120) .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 .137) .320) Total . metal bearings.710) .150-.180) .350) .090-.170-.110-.350 (.160-.100 (.140) .330) .240 (.260 (.180 (.260 (. Dermal contact with soil.130) .430 (.140 (.180 (.070 (<LOD-.310 (.160) .190) .200-.290-.100-.120-.160-.490 (.190 (.250-.530) . and +5.460 (. which may vary for some chemicals by year and by individual sample.310 (.120 (. 01-02. 176 Fourth National Report on Human Exposure to Environmental Chemicals .197) .190 (.150) .360-.360 (.350 (.400) .140) .120-.145 (.120 (.142 (.400) .310 (.400 (.200) .087-.150) .150 (.500) .178) .088-.200) .570) .320 (.320 (.136-.

1953).310) .135 (.117-.236 (.220) .146) .130) .100 (.106-.117-.224 (. 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.153 (.147-.080 (.250) .238 (.130) .143) .256 (.182 (.129 (.338) . 1944).172-.170 (.080 (<LOD-.380 (. population from the National Health and Nutrition Examination Survey.205-.099-.485) .149-.109 (.113-.188) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.373) .129 (.417) .176-.228-.241-.278) .186) .209) . and gastrointestinal symptoms such as vomiting.267-.357) .124-.069-.113-.156 (.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 .198) .084) .183) .238) .139 (.148-.116-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.417) .203) .300) .096-.308) .112 (.152) .233 (.130 (.087) .102-.095-.146-.152) .173) .313-..250-.107-.118 (.195-.122 (.338 (.092) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.181) .149) .081 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .176 (.430) .214) .077) .103-.113) .272) .120 (.115 (.444) .333-1.176 (.118 (.160 (.131-.429) .228 (.162-.173 (.121 (.171) .143 (.727) .114 (.185-.150-.208-.421) .245) .294) Total .226 (.108-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.222 (. abdominal pain.357-.317) .352 (.343 (.132) .193 (.098-.148-.200-.255) .108 (.145) .425) .107-.391) .352) .175 (.189 (.250 (.364 (.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 .317) .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 .161) .209 (.181) .098-.082) .109-. Inorganic antimony salts irritate the mucous membranes.143) .131 (.086 (.209-.129) .320 (.257) .241-. diarrhea.106-.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.150-.115-.115) .092-.444) .144-.075 (.213 (.295 (. 1986).179-.105-.135) .281-.250-.112 (.267 (.138-.235-.134) .204-.253-.333-.187) .161) .192-.318-.229-.333) .230-. 1954).123 (..120 (. Acute antimony poisoning may cause a metallic taste. and eyes.193) .127) .123) .069-.259 (. 1995).085) .120 (.127) .115 (. and ulcers (Werrin.068-.082) .253 (.074 (.286 (.111 (.112-.143) 90th .114 (.265 (.128-.288 (.127 (.167 (.111-.121) .196 (.195-.269 (.480) .199-.225 (.217 (.081) .116 (.391) .317) .244-.159-.097-.267) .333-.178-.156-. and kidney have been demonstrated in high dose animal studies depending on the dose.143) Selected percentiles ( 95% confidence interval) 50th .061-.30) .136) .209) . species.239-. 1986).208 (.108-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.321) .125 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.164 (.163 (. 1973).227-.146-.225) .338 (..126 (.167 (.255-.099-. and route of exposure (Elinder and Friberg.135) .Metals than for trivalent compounds (Elinder and Friberg.121 (.268) ..250-.140) .185 (.119 (.471) .263 (.200-.191 (.385 (.192 (.164) .108-.300) .238) .075 (.405) . myocardium.126) .414) .233) .115 (.127) .250 (.276 (.089) .741) .S.211) .188-.280-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.247) .086) 75th .315) .167-.140) < LOD .164-.438) .078 (.104-.308-.320) .122 (.248) .265-. interval) .153-.103-.076-. 1958) and occupational exposures (Briegner et al.364 (.181) .130) . skin.138 (.119-.076-.. 1988.139 (.320-.167 (.098) .120 (.242-.228 (.127) .192) .500) .206-.119-.132 (.146-.131) .173-.200-.135 (.320-.400 (.371 (. 1962).271-.207) . resulting in hemolysis with abdominal and back pain (Dernehl et al.280 (.263-.109 (. Histopathologic inflammatory and degenerative changes in the lung.102-.261) .195 (.429 (.185 (.117-.159-.173 (.138-.079 (<LOD-.154-.233-.230) 95th . Ming-Hsin et al.300 (.114 (.125-.178 (.115-.133) .095-.447 (.194-.200) .310) .107-.277 (.068 (.333 (.129) * .741 (.135) .137 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.124-.298 (.248-.266 (.126-.320 (.471 (.333-.333 (.159-.203) .124 (.278 (.310 (.124) .104-. liver.163 (.082 (<LOD-.250-.333 (.138) * .071-.148) * .147) .151) .318-.

Atlanta (GA). which may be due to methodologic.e. Skulsukai G. Chia-Yu H. Sci Total Environ 1994. Buchet JP. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000.46:931-936.. Liao Y-H et al. Earlier measurements in general populations (Minoia et al. eds. Chemotherapy for leishmaniasis: Biochemical mechanisms. Wade A. Suchenwirth R. Industrial Medicine and Surgery (Dec. Stone FD. gov/toxpro2.521-523. Biological assessment of exposure to antimony and lead in the glass-producing industry. Petrucci F. 1986. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . In: Friberg L. Sabbioni E. 1990. Alimonti A. Piatnek DA. Carelli G. Dunkelberg. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Centers for Disease Control and Prevention (CDC). Ludersdorf et al. Paschal et al. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. EPA.atsdr. Bailly R. Iavicoli et al. Yang C-Y. Pulmonary edema of environmental origin.cdc.10(3):560-586.. Gallorini M. Kiberd B.html.. indium. 26-42.76(2):103-115.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Clin Pathol 1998... Caroli S. and future strategies. Kuo-Juie Y.S. Industrial antimony poisoning. Stocks J. Delves HT. 1991. References Berman JD. Elinder CG.16: 33-39. 2004. et al. Ming-Hsin H. Pilgrim L. Yu H-S. 1997). 1995. Costeloe K. Mahieu P. Chin Med J 1958. Br J Ind Med 1991. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Leinemann M. Sabbioni E.. 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. Schacke G.76:432436. stibine. Antimony trioxide is rated by IARC as a possible human carcinogen. Ho C-K.13:361-362. Arsine. Lauwerys R. Weltle D. Environ Health Perspect 1998. Rev Infect Dis 1988. Biological monitoring of exposures to aluminum. respectively. clinical efficacy. 2005. Fuchs A. Cordasco EM. Stasney J. Pozzoli L.. Chest 1973. Int Arch Occup Environ Health 1987. Trace element reference values in tissues from inhabitants of the European community I. Handbook on the toxicology of metals.. Pietra R. pp. 20012002. and hydrogen sulfide. Friberg L. Review of elements in blood. even when exposure levels were below workplace air standards (Bailly et al. J Trace Elem Med Biol 2002. Konings J.51:238-240. 1998) or compiled reference ranges (Hamilton et al. Apostoli P. arsenic. O’Regan M. Dezateux C. External and internal antimony exposure in starter battery production. VI. Kentner et al. and a drinking water standard has been established by the U. Luedersdorf R. Arch Dis Child 1997. Antimony. Biomonitoring of a worker population exposed to low antimony trioxide levels. HH. Wu M-T. Gebel TW. Third National Report on Human Exposure to Environmental Chemicals.59:469-474.158:165-190.67:119-123. Antimony in blood and urine of infants. Schaller KH. Minoia C. Dernehl CU. Chen J-R. Industrial Medicine 1944. Mayer P. J Occup Environ Med 2004. Hamilton EI. Mayne P. gallium. Information about external exposure (i. Vouk VB. New York: Elsevier. 1994) have reported values slightly higher than those in this Report. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect.48:93-97.64(2):182-185. population. Liao Y-H.Metals to antimony have been established by OSHA and ACGIH. Int Arch Occup Environ Health 1995.. environmental levels) and health effects is available from ATSDR at: http://www. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Iavicoli I.)1954. Ju-Sun P. Urinary antimony in infancy. 1987).. or exposure differences. Bolten C. 2002. 1998). Nordberg GF. Cheng-Wei L. Kentner M.. et al. Briegner H. 2nd ed. Lenert G. Dezateux et al. Nau CA. Roland H. Van der Venne MT. Semisch CW.106:33-39. and 2003-2004. Stead FM. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. and antimony in optoelectronic industry workers. et al. Cullen A. Element reference values in tissues from inhabitants of the European community. Shao-Chi C. Matthews T. Delves HT. 1998.

Quarterly Bulletin of the Association of Food and Drug Officials 1962. Trace metals in urine of United States residents: reference range concentrations. and serum of Italian subjects. Chemical food poisoning. Sci Total Environ 1990. Environ Res 1998.95:89-105. Renes LE. Paschal DC.76(1):53-59. Sampson EJ.Metals in urine. Industrial Hygiene and Occupational Medicine 1953. et al. Morrow JC. 27:38-45. Ting BG. Fourth National Report on Human Exposure to Environmental Chemicals 179 .99-108. Werrin M. blood. Antimony poisoning in industry. Jackson RJ. Pirkle JL.

In nature.10 (6. lead.27) 9. Arsenic is measurable in most soils.1) 7.40) 7. and as a cosmetic to lighten complexion. sodium arsenite.5) 66.70) 8.3) 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 7.90-8. Since the 1940s.6 (13. 180 Fourth National Report on Human Exposure to Environmental Chemicals .90) 16.90-7. Before the 20th century. Arsine (AsH3) is a reactive.5 (34.5-41.5-52.90) 75th 16.4 (24.2) 15.80) 6. gaseous hydride manufactured in small quantities for use in the semiconductor industry. arsenocholine. psoriasis.4 (26. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.1-40. ocean and fresh waters.77) 6. aluminum.2-61. The United States no longer produces arsenic from mining but imports about 22. Arsenic trioxide (As2O3. to a lesser extent.0-19.8 (48. or rarely as elemental metalloids (yellow. such as arsenopyrite (FeAsS) and realgar (As4S4).3) 10. semiconductors.7) 90th 37. cacodylic acid. arsenites.5) 43. particularly arsenic trioxide.97) 8.9) 68.2) 46.Metals Arsenic CAS No. Arsenic trioxide is approved to treat acute promyelocytic leukemia.0 (43.6) 618 722 1074 Limit of detection (LOD. and other metals.9-34.30 (7.2 (12.2-17. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.9-62. and in lead-acid storage battery grids. and.1 (38. copper arsenates. alloys. the smelting of copper.66-8.41 (7.2-20.6-35.80 (5. black. Water sources contain mostly inorganic arsenate. 2001). In the last century.29 (8. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. pesticides. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. Survey years 03-04 Geometric mean (95% conf. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.7-95.5) 41.7) 24.00-9.2 (13.4-65. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.12 (6.5 (14. mental disorders.00 (6.1) 290 725 1542 03-04 03-04 9.S.4 (48.5 (36. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.90 (5.0 (14.7-83. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. arsenic as elemental metalloids may be used in some ammunition.3-111) 78.6) 11.7 (11.10-7. Also. interval) 8. though in some locations arsenite may be prevalent (WHO.8) 7. solders.5) 95th 65.4) 13.02-8.8-61.000 metric tons annually.9 (8.84) 8.1) 15. Various arsenic compounds were used in paint pigments and for tanning animal hides. referred to as inorganic arsenic compounds.8) 30. Gallium.5 (40.6-43.5 (23. to a lesser extent. and indium arsenides are used in the semiconductor industry.30 (6.2 (51.0 (22. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.6 (9. and produce. and gray forms).0 (15. and as homicidal poisons.2 (41.0 (11.57) Selected percentiles ( 95% confidence interval) 50th 7.9-46.30) 17.50 (8.55 (7.10) 10. were used as treatments for syphilis.25-9.9) 21. meats.70 (6.3-19.8) 29. from coal burning.13-8. and arsenates (oxidation states of -3.80-9. trimethylarsine oxide. cancers. Arsenic and its compounds have had many uses in the past and present as medicines.8) 33.8) 34.50-14. and arsenosugars.6 (32.12-10. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.1-18.0-60.5-19. General population exposure to inorganic arsenic can occur through consumption of drinking water and.6-141) 53.5-178) 46.74.6 (15.8) 17.90 (7. grain.7) 65. Although it is still widely used in the United States. and foods. it is found in over 200 crystalline or mineral forms.90 (7.4) 40.08 (5.1 (32. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.84) 8. +3 and +5). arsenic compounds.70-9.10-10. retaining walls.4 (31. 2005).90-14.4 (7.1) 1281 1276 03-04 03-04 03-04 9.4) 60. mostly for use in wood preservation (ATSDR.90-11.19-9.9 (17.90-8.3-15.8) 7. as alloy in metal bearings.20 (8.8-77.34-10.34-9. and play sets. lead hydrogen arsenate.2-93.

S.2 (12. Tseng.1-36. In aquatic organisms.8 (12.5-120) 40.0) 42.04 (5.4) 54.9) 13. Steinmaus et al. population from the National Health and Nutrition Examination Survey.8 (11. inorganic arsenic is widely distributed within the body. 2007.88 (5.9) 53.8) 27. 2001). 2007.2) 15.4 (24.1) 6.33-10. 2007. Chowdhury et al.45) 5.20-9.7) 95th 50.07-9.1) 58. EPA’s maximum contaminant level (Hughes.0 (31.7) 28.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .47 (6.7-18.4) 32.0) 26.81-9. 2001).8 (27. 2001. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.25-9.13) 8. arsenic does not show biomagnification in the food chain (WHO.44) 6. and folate status (Chen et al.1 (14. 2001. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.6 (10.0) 1281 1276 03-04 03-04 03-04 8.4-64.0-38.8-75. 2001).93-9.7-35..28-7.5-17.41) 6.88) 7. In aquatic sediments.. age. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.7-34.4 (40. Smoking tobacco is also a source of inorganic arsenic.76 (6.0-69.3-53.4 (26.0 (17. 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.24 (7. are used in enclosed ultraclean operations within the semiconductor industry.5) 17.30-9.S. Inorganic forms of arsenic demonstrate high acute toxicity.61 (7.58-10.3-64.01) 7.44-11.3-62. NRC.3 (24..00 (6. arsenocholine. trimethylarsine oxide (TMAO).96) 12. 2003. The semiconductor dopants. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.18 (5.5) 290 725 1542 03-04 03-04 8.6 (17.38-10.1 (11. dust.11 (5.75 (5. organic arsenic can be converted back to methylated and inorganic arsenic.2) 40.01) 11.66-8.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.99-9.7 (11.50 (6. 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.40) 8. selenium.6-17.3) 6. 2001). and contact with CCA-preserved wood structures.4 (12.75) 13.66 (7. Extremely high groundwater arsenic levels. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.12-10.5) 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. as observed in Bangladesh where millions of people have been exposed.. EPA. 2001). 2001).2) 90th 30.7-17. Survey years 03-04 Geometric mean (95% conf.7-188) 27.9 (45. 2006. Direct exposure to DMA and MMA may result from use of the two pesticides.3-41.86-17.8-62. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. 2001).6) 45.g. so exposure to the general population is extremely limited. and some other seafood can contain organic forms of arsenic including arsenobetaine. but is poorly absorbed dermally (WHO..9-56.2-15. Children may have additional exposures from ingestion of contaminated soils (e.10-8.35) 7. dose level. U. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.8-32. 1988).33 (6.23-7. WHO. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.3) 9.1) 7.93-8.47-6.66-8. have caused clinical arsenic poisoning. Fish. and arsenosugars.31 (6.3 (27.8 (20. gallium arsenide and indium arsenide.8 (21. mine tailings).7 (9.06 (4.64 (7. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.4 (11. shellfish. WHO.0-18. interval) 8.59) Selected percentiles ( 95% confidence interval) 50th 7.10-16.04) 7.0) 33. Though modest bioconcentration occurs in some aquatic life.7 (25.1) 8.0) 14. After absorption.8) 22.0-26.1) 24.51) 75th 14.2-46.4 (42.47 (7. cacodylic acid and monosodium methyl arsenate. though some reduction may occur in the gut prior to absorption.32 (5. kelp.25 (6. Gamble et al. Arsenate is reduced in the body to arsenite (oxidation state +3).0) 12.6 (35. 2006. 2001).S..5 (9.

60) 1. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways.. NRC.0. and it also will inhibit succinate dehydrogenase. 2006) or when exposure occurs in smokers (Chen et al. cytotoxicity. and DNA repair inhibition (Cohen et al. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.20 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 1. 2006. substitution in phosphate metabolism.S. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. but additional or confirmatory research is needed (Kapaj et al.S. 2001. can cause peripheral sensorimotor neuropathies. Arsenic has many actions demonstrated in cellular studies. Studies of arsenic at levels typical of U. and endothelial injury (Kumagai and Sumi. Raml et al. fatty acid oxidation.g. hematocytopenias. interference in signal transduction pathways.50) 621 725 1078 Limit of detection (LOD. 2004).Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. vomiting. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. 2007.20 (<LOD-1. 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. food residue. 2001).60) 1. hypertension. 2004.10 (<LOD-1.10 (<LOD-1. drinking water have not been associated with increased cancer rates (Schoen et al. gluconeogenesis.30) 1.80) 1. Although arsenate is reduced in the body to arsenite. WHO. Chile).EPA has established drinking water. and production of glutathione may be affected as well. 2007. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 2001). WHO. hepatotoxicity. 2006.10 (<LOD-1. U. apoptosis. leading to a decrease in adenosine triphosphate energy production.20 (<LOD-1. arsenic trioxide) includes hemorrhagic gastritis with nausea. 2001. and altered gene expression. The organic forms of arsenic occurring in seafood have little known toxicity. 2001).50) 1. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. which may vary for some chemicals by year and by individual sample.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and childhood neurodevelopmental effects in observational human studies. peripheral vascular disease. 182 Fourth National Report on Human Exposure to Environmental Chemicals .. noncirrhotic portal hypertension. lung. Bangladesh. renal failure. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. Bredfeldt et al. < LOD means less than the limit of detection.20 (<LOD-1. Taiwan. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. including inhibition of numerous enzymes. Cardiac arrhythmias.. 2001). respectively. and by uncoupling oxidative phosphorylation (NRC. 2004). and hyperpigmentation of the skin (NRC. some of these effects may take years to develop... population from the National Health and Nutrition Examination Survey. 2006.. 2007). and diarrhea. Such actions may lead to decreased energy production. which can lead to dehydration and shock.. With chronic exposure. 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.S. 1998. hyperkeratosis. Cellular glucose uptake. Chronic human intake of arsenic at less than acutely toxic doses.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. increased oxidative stress.S.10 (<LOD-1. 2001)... NRC. Cohen et al. Chronic elevated arsenic intakes have been associated with diabetes..50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. cell transformations. 2001). Laboratory studies using inorganic arsenic have shown chromosomal aberrations. including drinking water sources with elevated arsenic levels (e... WHO. Survey years 03-04 Geometric mean (95% conf. The U. 2000.10 (<LOD-1. WHO. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. Chronic arsenic exposure in humans is considered to be a cause of skin. Acutely.EPA.g. and bladder cancer (IARC.

higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. gov/toxpro2..S. Additional information about external exposure (i.S. Shalat et al.69 (<LOD-3. 1999). Levels of total urinary arsenic in the U... although urinary arsenic levels were not associated with CCA contact (Shalat et al. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 2006. 1998. In a Nevada town where groundwater levels were naturally elevated.cdc. WHO.Metals compounds.. median urinary total arsenic levels in 4052 adults varied with seafood intake... Caldwell et al.. Pellizzari and Clayton 2006). Shalat et al. had decreased since the prior 1990– 1992 survey.75 (<LOD-2. arsenic has been fetotoxic and teratogenic.html..70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.. 1992. environmental levels) and health effects is available from ATSDR at: http://www. Vahter et al. 2008). 2008. 2006. Pellizzari and Clayton. Valenzuela et al. Compared with this Report.. Meza et al... 2007. In the German Environmental Survey III of 1998. 1999. 2001).. but generally only at maternally toxic doses (WHO. hand washings from children playing on CCA-treated wood compared to children playing on non-CCA-treated wood playground equipment were slightly to fivefold higher (Kwon et al. Pellizzari and Clayton. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf. 2000. and the FDA has established a bottled drinking water standard..75 (<LOD-2. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 1999.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Offergelt et al. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al. 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. population (Rubin et al.18 (<LOD-3. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.19) 3. 2004.41) 3.33 (<LOD-3.. 2006). the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. 2006). 2004..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2001).00) 1.80 (<LOD-4.. 2001).33 (<LOD-3. DMA produced bladder cancer in some chronic rat studies (Cohen et al. 2006). 2006...S.S.18) 3.04 (<LOD-3. Caldwell et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Josyula et al.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. and were about two-fold lower than those for the U. In animal studies. Consequently. 2007.61 (<LOD-3. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.50) 1. 2008). 2003. 2006). population in NHANES 2003–2004 (Schulz et al. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.e. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2000). 1986).atsdr.. 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... Though CCA-treated wood contains several thousand times more arsenic than untreated wood. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. Calderon 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.

Caldwell et al.4-35. 2008. 2007). 2000.. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.31-1. 2008).20) 3. arsenite.20-3. arsenite.74 (1.9) 13. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. population (Ahsan et al.6 (13.. 1990.8 (12.g.Metals other areas of the world (Ahsan et al. population from the National Health and Nutrition Examination Survey.10 (4.5 (26. MMA.871-1.400-.600 (.8-50. 2008).80-5. Sun et al. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.9 (7.00-1.7 (13.68) .80 (4.48-2... in NHEXAS 1995–1996.90-29. see Data Analysis section) for Survey year 03-04 is 0.1-51. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.S.6.S.e. 4. Survey years 03-04 Geometric mean (95% conf.2 (6..6 (25.3 (9. Blom et al. 1996.70 (3.1-25.3 (21..66 (1.. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. and other factors such as nutrition.3) 95th 35.6-44. Chowdhury et al... Caldwell et al.00) 3.20-25.. interval) 1.05) < LOD . After recent seafood ingestion. 2003).37 (1.50) 90th 16.6 (11. and 0.S. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. < LOD means less than the limit of detection. and TMAO were detected in only 7. 2000. dermal keratosis. and TMAO.500-1..80) 1. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.10) 4.62) 2.30) 2.00 (. and duration of exposure are also considered important. and two methylated metabolic products.11-1. Also.8) 35.20-190) 31. 2000.0 (26.0 (27.55 (1. 2006).00-12. 184 Fourth National Report on Human Exposure to Environmental Chemicals . Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. 2001.800 (.70-21.9 (6. 2005.S. Arsenate. Pellizzari and Clayton.900 (. When seafood intake is avoided.0) 29.19 (. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. DMA and MMA. 2008).800) 1.7) 15.40) 75th 5. population showed a higher contribution of arsenobetaine (Caldwell et al. Some noncancer effects of arsenic (e. 1985.S.70 (5.8 (17.3) 1284 1284 03-04 03-04 03-04 1.70) 6.5) 621 725 1078 Limit of detection (LOD. 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. In the late 1980s.9-23.6.40-6.800-4.1) 45. 2005.700-1.90-7.5) 292 728 1548 03-04 03-04 1. when seafood organic arsenic is subtracted). In the residents of a Chilean town who consumed water with high levels of arsenic..70-21. In most human studies.4) 31.1) 18. 2007) with higher levels of arsenic in the drinking water. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.43-1.50-6..2-35. 2008.29 (1.5 (14.3% of a representative sample of the U.45 (1. Individually measurable species resulting from inorganic arsenic exposure are arsenate.80 (.30) 10.4) 23.7-22.20 (. vasospasm.0) 4.7 (21.700-1.8-40.5) 32.3-39.93) 1.00-4.50) . Valenzuela et al. 2001). geometric mean levels were about 70-fold higher than for the U.00 (1. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level..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 * * 1.83) Selected percentiles ( 95% confidence interval) 50th 1. China.2-38. Caldwell et al.40) 5.60) 1. The higher percentiles of total urinary arsenic levels in the U. These associations are stronger at higher urinary levels. arsenocholine.20 (1. Aposhian et al.800 (.20) 7.20) 18.. arsenobetaine.4. 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. Measurable organic arsenic species in this Report are three biologically generated environmental forms.800-1.. 1. methylation capacity. with DMA. WHO. 2005.4 (16.900-1. For residents of Inner Mongolia.50) .30 (2..7) 13.80 (3. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.20 (2. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. respectively.20 (4. 2008)..3) 35. Tseng et al.17-1.30 (1.40-7.00-6. arsenocholine. population (Sun et al.5) 29. Caceres et al.60-3. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i..28) 1. population in the NHANES 2003–2004 subsample.1-94..10) 8.8.0-23.

64-29.91 (4. 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.82) Selected percentiles ( 95% confidence interval) 50th 1. Vahter et al.43) 14.83) 2.5 (18.638) 1.19-2.58 (3.833-1. Information about the biological exposure indices is provided here for comparison.2 (4.91) 90th 16.05 (. 1992.2 (12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.55) 1.47 (1.50-7.Metals as with DMA. 2008).14 (1. population for the sum of inorganic related species was 18.4 (11.4) 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 * * 1.28) 1...72) 12.13-39.29 (4.00 (3. 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.6 (6. Offergelt et al. Sun et al.81 (4.6-29.30-1.6 (9. 2001). Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. 2007).37-2. Caldwell et al. 1986.93 (1.400-.4) 292 728 1548 03-04 03-04 1.80-153) 17.7) 17.40 (1.S. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6-32.7) 30. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3-24.1-18.80) .4) 32.44 (1.32-7.82) 4.78-5.25-7.1-36.45) 1.2 (12. population from the National Health and Nutrition Examination Survey.9-18.877 (.00 (1.53 (.5) 17.18-1.9 (13.15-1.4-82.51) 5.88) 2.16 (.531 (.15-1.8) 29.. The 95th percentile of the U.78 (3.2 (13. 2008).65 (1.79 (1. WHO.1 (26.612-1. not to imply a safety level for general population exposure.10 (. 2003. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.62-6.6-46.4) 13.15-4. 1998.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.43) 75th 5.88 (5. 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.40) 1. 2006.50-15.S.. 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.786-1. 2001). Fourth National Report on Human Exposure to Environmental Chemicals 185 ..05) 1.4-21.9 μg/L.6) 19..3) 1284 1284 03-04 03-04 03-04 1.83) 8.76-27.3) 95th 29.4-28.70) 5.54 (1. which is below the ACGIH BEI (Caldwell et al.68 (1.3 (10..9) 14.3 (10.67) 1. interval) 1.30) 1.938-1.73-6.47 (2.4 (24..36) 2. In recent years.5) 26.39-3.51-2.61-6.0-36.11 (.1) 26.7) 9. 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.21) 5.5 (18.25 (.29-14.959-1. Survey years 03-04 Geometric mean (95% conf.9 (25.901-2.5-20.67) 4.9) 32.0 (9.12) < LOD .909-1.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.29) < LOD 621 725 1078 < 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.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.44) 2. < LOD means less than the limit of detection. see Data Analysis section) for Survey year 03-04 is 1.40 (<LOD-1. population from the National Health and Nutrition Examination Survey.00 (<LOD-3.95 (<LOD-2. Fourth National Report on Human Exposure to Environmental Chemicals 187 . 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.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 1.2.00 (<LOD-2.20 (<LOD-1.S.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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.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. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80) < LOD 621 725 1078 Limit of detection (LOD.08 (<LOD-4. Survey years 03-04 Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.

00-11.0) 292 728 1548 03-04 03-04 4.34 (3.20) 11.00-15.50-15.08 (2.00 (6.0 (9. population from the National Health and Nutrition Examination Survey.69-6.03 (3.7-16.31-4.80) 2.90) 2.71) 3.70 (3.46 (4.73) 6.30 (7.0 (9.00-4.31) 4.00-7.00 (3.70) 5.00 (3.85 (3.0 (14.0) 13.0-16.77 (3.32 (4.14) Selected percentiles ( 95% confidence interval) 50th 3. 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 3.78) 4.0) 12.0 (10.60-4. see Data Analysis section) for Survey year 03-04 is 1.00 (6.0 (13.00) 75th 6.16 (4.91) 75th 5.6) 292 728 1548 03-04 03-04 3.0 (8. population from the National Health and Nutrition Examination Survey.0) 9.17-6.69-3.0 (10.8) 7.80) 7.00-15.9) 13.94-3.37 (2.00 (5.78 (4.13-4.50-5.27 (3.18 (6.00-4.88 (4.1-15.0 (10.00) 6.38 (3.37 (3.12 (3.7) 1284 1284 03-04 03-04 03-04 4.45) 8.00-4.00) 6.00) 6.00 (5.00-7.0 (11.0) 13.3 (8.0) 11.0) 9.45 (8.6 (9.5) 12.48 (3.45) 3.67) 9.84-18.00) 5.00) 4.90 (3.86-21.00-12.0-17.32 (8.8) 7.65-6.67) 8.3 (8.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.80-6.5) 95th 13.90) 5.86 (2.27-2.28) 2.39-3.61-16.0-17.72 (4. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.34-4.00-8.00) 3.0 (12.24-4.22) 4.6) 1284 1284 03-04 03-04 03-04 4.1 (8.0 (12.S.92) 3. interval) 3.11) 4.0) 10.0 (9.00 (3.70-4.70-3.0) 9.49-4.10) 6.48 (2.80-5.70-12.71-4.20-4.42) 3.95 (4.0-16.95-3.80-3.06) 5.00) 7.05) 5.95-6.7.00-11.34 (3.0) 14.00 (3.00-3.10) 3.00-5.00-10.0) 621 725 1078 Limit of detection (LOD.55 (2.20-12.33) 3.34) 3.52) 3.62) 4.00-4.00 (3.61-11.86-7.00-9.6-18.00-4.80 (4.33-4.27 (2.74 (2.11 (3.0 (8.14) 3.7) 12.0-12.50 (4.9) 11.00) 9.00) 6.00 (6.82-5.71 (3.84-8.00-11.00) 3.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .00 (5.81 (5.95-4.32-10.00 (4.16 (2.89 (3.59 (6.65-8.0 (13.49) 10.29-4.44) 5.44 (2.00 (7.0 (10.00-4.0) 17.7) 13.82) 3.03-6.00-3.15) 4.4 (7.9 (11.60-6.2) 10.0) 17.00 (5.00) 12.12-4.00 (5.24) 3.16-11.05) 3.69 (3.27-5.0) 16.17-4.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.57 (3.3 (7.9) 5.82-9.73 (3.30) 3. Survey years 03-04 Geometric mean (95% conf.9) 12. interval) 3.00-12.60-7.19) Selected percentiles ( 95% confidence interval) 50th 3.00-7.34-4.0-25.00) 4.00 (7.74) 90th 9.00) 90th 11.1-22.60-3.S.05) 10.69 (3.71 (4.57-5.17 (2.00-7.09 (7.0) 95th 16.00-13.98) 4.00 (3.0-19.9 (7.0) 16.00-15.7 (10.92-12.1-18.00-22.5 (11.79 (3.25 (4.97-3.94) 3.0-18.0) 11.

30-1.70-2.80 (1.17) 2.35-3.31-3.88 (1.50) 621 725 1077 Limit of detection (LOD.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.30 (1.00 (1.82-2.22) 3.10-1.80-2.14-1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.86 (2.33 (1.07-3.90) 2.00-2.50 (1.20 (1.31 (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 1.816 (<LOD-.60) 2.40 (2.60) 1.61) 2.60-2.70-2.40-3.20 (1.00 (2.50 (1. Survey years 03-04 Geometric mean (95% conf.90 (2.50 (2. see Data Analysis section) for Survey year 03-04 is 0.07 (1.900-1. Survey years 03-04 Geometric mean (95% conf.10) 2.11-1.53-2.30 (1.30-2.30 (1.28 (1.80 (1.96-2.46 (1.86) 3.20 (1.30) 1.61-3.80) 1.00 (2.985) 1.30) 2.07) 2.45) 3.S.10-1.77) 1.9.81) 1.10-3.10 (<LOD-1.70-3.20-3.40) 1.40) 1.40) 2.50 (<LOD-1.20-1.52 (2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .79) 2.57) 95th 2.86) 2.62) 2.80 (2. population from the National Health and Nutrition Examination Survey.00) 1.60 (2.20) 2.73-2.58) 2.63 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.53 (1.33 (1.90) 2.10 (.40-2.18-1.00 (<LOD-1.36) 1.88-2.85) 1.54) 90th 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.23) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-2.80 (1.20 (1.00) 1.40-2.10 (1.18-1.34) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.93) .30 (2.00-1.S.30-1.30) 1.05-1.15-1.20 (1.50-2.90) 1.36 (1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.50) 1.86 (2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10 (1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.70-2.37 (1. population from the National Health and Nutrition Examination Survey.40-3.00) 2.60 (1.00-4.80 (1.80-2.30) 90th 1.88 (1.85) 2.40 (1.00-1.90 (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.16 (2.853-1.10 (.00-2.43-3.80) 1. which may vary for some chemicals by year and by individual sample.84-3.82-2.10) 95th 2.46-2.70) 2.00) 1.22 (1. < LOD means less than the limit of detection.28 (1.20 (1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.71-2.60) 2.00 (<LOD-1.00) 2.

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

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14-6.12-1.50) 4.55-7.21 (1.00-8.66) Selected percentiles ( 95% confidence interval) 50th 1.76) 1.29) 5. The general population can be exposed to low amounts of barium in air.65-5.33 (1.86 (4. interval) 1. population from the National Health and Nutrition Examination Survey.32) 8.63 (8.70-2.65) 3.30) 5.46) 1.30-3.63 (1.48) 1.40 (5.39 (1.61 (1.00-76.54-1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).35 (1.9) 5.50 (3.65) 1.31. it combines with other chemicals such as sulfur or carbon and oxygen.39) 1.00-3.54 (6.73 (6.26-1.06-1.26) 5.50 (1. depilatories.69 (1.16 (1.61 (3.88) 1.53) 2.56) 4.82-6.70) 7.12 (2.70) 1.12) 6.43 (1.39 (1.74-3.70) 4.82) 1.48-4. and ceramics.90) 4.81-3.20-1.45) 7.35-4.30 (2.90 (6.99-5. see Data Analysis section) for Survey years 99-00.60) 1. 7440-39-3 Medically.50) 2.57) 3.80 (2.62 (1.78-3.90 (4.50) 2.20) 2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.08-8.00) 1.41) 1.35 (2.12.41-3.50 (1..12.37) 5.60 (1.81-2.78) 1.40 (5.49 (1.63) 1.65-1.49) 11. 2001).29-1.60-6.15 (1.39) 4.60) 1.87 (6.10 (2.54 (2.18) 3.49-1.76-2.46-1.61-8.70-6.50 (4.30-2.38 (1.35-1.67) 6.49) 2.54) 1.11 (3.20-1.71 (2.11 (2.63 (2.99 (4.09 (1.78) 1.00 (1.64) 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 2.04-6.50) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.88 (5. water.56 (2. tiles.43 (1.76 (3.50 (5. 01-02. 0.28-1.90) 2.44-2.80-7.10) 3.44 (1.61 (2.86-4. Workers employed by industries that make or use barium compounds can be exposed to barium dust.21-8.82) 2.37) 1.54-8.35-1.50 (4.78-2.74) 3.40) 7.25-11.32-1.20-5.31-2.30-5.20-1.8) 9.90) 2.80-3.88) 7.50 (6.49) 4.80 (5.26) 2.22) 6.54) 1.50 (4.72) 75th 3.53-5.85 (2.20 (1.90-2. Barium compounds are used by the oil and gas industries to make drilling muds.59-11.91) 6.10-4.20-1. Barium salts have also been available as rodenticides.63) 1.42 (1.60) 3.40 (1.51) 7.30) 5.50-6.24-1.31 (2.8 (6.56) 1.70) 3. In single dose animal studies.4) 7.50-1.4) 9.60) 4.26-7.75-3.35) 5.10 (3.54) 2.08 (6.14-1.25 (1.36-1.94-6.71) 95th 6. Fourth National Report on Human Exposure to Environmental Chemicals 193 .91 (2. are high in barium (Genter.27 (1. In nature.64 (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 1.65-8.61 (5.71) 1.30) 2.66 (4.34 (1.00) 6.10-5.54-1. bricks.21 (1.Metals Barium CAS No.87-3.34) 2.21-2.51) 2.07 (2.77 (3.77-3.15-1.50 (2.90-13.24 (4.22-1. and 0.24-1.32-7.30-2.61 (1.50 (1.62) 1.60-10.50-1.43 (5.49) 8.70) 1.86) 6.38) 2.37-1.98) 1.03 (1.28) 90th 5.80 (1.70-2.30 (1.74-2.44-5.72) 1.30 (5. Some barium salts are freely soluble in water.20-8.80-2.86-5.50 (1. respectively.43) 2. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.40 (5.01 (4. Certain foods. Barium compounds are also used commercially in paint. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.57 (5.34 (2.06-2.70-8.35 (3.50 (1.93-8.95-6.8) 5.30) 4. and food.20-6.19) 2.88) 4.70) 5. such as barium chloride.80) 6.01-7.17-1.12) 7.10) 5.36-1.95 (4.10 (4.00) 1. fireworks.50-6.64-3.46) 1.90 (1.15 (2.27 (1.70-5.48) 1.15 (6.04-2.30) 3.37 (4.27) 2.87-9.51 (1.05% of the earth’s crust.63 (5.62 (1.60-6. and 03-04 are 0.1) 9. Small amounts of barium can be released into the air during mining and other industrial processes.12 (2.30-1. barium sulfate and barium carbonate). such as brazil nuts.g.62) 1.05-2.36) 5.77) 1.76-3.47-1.34 (1.47) 4.36 (4.49-9.59) 3.87-14.52 (1.71) 2.90) 1.73) 1.16) 5.84) 5.29-5.40-13.18-1.92) 2.48-4.09 (2.56 (1.68 (1. glass.22-1.70 (1.40 (1.73) 3.85) 1.80) 1.75) 2.30) 8.19-1.52 (4.65 (5.11-1.86 (4.38) 8.60-3.4) 6.81-2.80 (1.56 (6. whereas others are practically insoluble (e.56 (1.00) 4.41-1.30-1.40) 7.30 (3.65) 1.60-2.93-2.40) 3.45 (1.36 (1.76-7.90-9.87-7.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30 (5.80) 7.20 (3.00 (2.73 (5.40 (1.63) Total 1.60 (2.85) 1.15-11.48 (6.72) 4.25-1.87) 7.70 (5.80 (2.87 (5.91) 2.30) 5.71-9.39-1.80 (1.40 (4.51) 1.20-8.80-5.70-3.57-7.2) 6.14 (6. soluble forms of barium.S.18 (6.47-1.02 (7.15-1.37-8.20 (4.97 (1.20-8.93 (4.38 (1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.96-2.43) 6.53) 1.73-5.55-3.11 (3.15) 5. rubber.

30 (1. a benign condition that may occur among barite ore miners. The health effects of exposure to barium compounds depend on the dose.65 (5.27) 7.29 (3. in urine.36 (3.47 (2.68 (2.59 (1.21 (1.76) 2.00 (3.43) 1. 1986).72) 6.18 (1.00 (3.77) 1.68 (3.96) 4.38-5.68) 3.36-1.710-1. vomiting.16 (1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.52-10.777-1.74) 1.40 (1.3 (6.48 (1.72) 4.59) 2.12) 2.22-2.18 (1.60 (5.46 (2.00-7.10) 6.33) 6. Wones et al.67-6. population from the National Health and Nutrition Examination Survey.33-1.64 (1.69-9.36 (5.27-1..51 (3.20-8.34 (1.26) 4.53) .36-2.58 (2.82) 1.45-1.49 (1.98 (2.51-3.33 (1.55 (5. paralysis.23-1.55-6.11) . 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.S.91-2.86) 5.79-5.84-5.921 (.50 (4.36 (3.39) 4. 1985.96) 4.74 (5.02-5.31-1.60 (2.56 (1.99 (2.52) 1.56-3.57-7.64) 7.45) 1.32) 2.74) 1. 1990). water solubility.59) 1.81-6.10-1.60 (2.84-2.76 (4.20 (1.68 (3. such as those used in medical radiographic procedures.59) 1.66 (1.39-10.52) 7.57-10.14-2.47) 4.01 (5.963 (.10 (6.75) 1.73-2.97-4.65 (2.55-5.96 (4.880-1.34-1.77-5.35-1.24-6.91 (3.53-21.29 (1.84 (3.70) 4.99) 1.70) 10.75) 2.62 (4.48-1.40-1.45-6.64 (1.76 (2.46) 3.76) 1.45-8.50) 1.59-7.29-1. 1984.00-1.02 (3.00) 1.47) 10.96) 7.26-1.33) 1.58) 1.45) 95th 6.49-1.31 (1.68-3.51) 6. 2001).61) 2.64 (1.08-2.52 (3.24-3.02) .77) 5.37) 2.19-1.89) 90th 4.22-1.00) 4.48) 2.57) 2.45 (3.88 (2.88 (6. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.39 (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. Following intravenous injection in animals.61 (4.0) 5. and route of exposure.11) .76 (3..53 (2.48-5.81-7.16) 11.37-1.43-6.44-2.54 (1.51 (1.60 (1.03-1.28) 5.77) Total 1.38 (4.08-1.06) .24-11.85-5.10) 3.29-4.2 (3.41 (1. Insoluble barium salts.2) 6. 1994.26-1.00) 4.24) 3.83) 3.38 (4.832-1.51 (1.52) 2.50) 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 1.76) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. chemical form.0) 6.47) 1.50) 1. hypertension.34) 1.34-3.04) 5.75-3.25) 4.54) 2.13-3.41) 5.26-1.19-1.48 (1.02) 4.42) 1.38 (1.49-1. interval) 1.47) 1.45-1.58) 75th 2. Toxicity from soluble barium salts is rare. Perry et al.59 (1.97-3.22-1.28-11.881 (. Barium is not rated for human carcinogenicity.47-8.31-1.29-3.82) 1.87) 1.16-1. Chronic high doses in animals resulted in kidney damage (McCauley et al.01 (4.56) 4.96 (4.30 (1.42) 1.00 (2.31 (4.54 (2.75) 2.44-2.58) 4.33 (5.2) 5.69 (5.44 (1..56 (1.19-1.24 (5.62 (1.0) 7.97) 1.42 (4.04) 1.31-1.92) 2.57 (6. diarrhea.27 (2.33-4.33 (1.38) 4.20-1.55 (1.63-4.86-7.01) 1.891 (.03) 2.47 (5.22-4.58 (4.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .78 (2.29-4.39 (2.28 (1.77) 1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13-2.24-6.46) 2.03) 1.55 (4.26-1.38 (1.68-3.48-3.52-4.81-6.754-1.96) 4.23-2.26-4.28-6.75-22.35-3.36-1.62 (2.11-2.5) 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 1.46-22.71 (5.20) 4.48 (1.68) 1. NTP.79) 1.25 (1.39-1.80-6.86 (2.55) . and cardiac dysrhythmias.05-1.29) 1.83) 2.99 (4.38) 1.63) 1.38) 1.36 (1.32 (1.03-1.70) 1.32 (1.46) 1. Symptoms following acute high dose include perioral paresthesias.41) 4.41 (2.37 (1.38-1.75) 1.55 (1.60 (1.00) 6.72 (2.84) 2.15-4.51) 4.64) 7.28-7.80) 4.Metals was eliminated primarily in feces and to a lesser extent.32) 2.04 (2. 1989).905 (.57-5.96-6.36 (1.37-2.49 (1.27-3.49-1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.64 (1.24 (3.58-6.76-3.62) 2.40 (1.4) 5.24-1. are not absorbed when administered.51) 4.25-11.39-1.91) 2.39 (2.29-7.3) 6.28-1. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.703-1.97 (4.38-7.4 (5.30) 2.80) 3.56) Selected percentiles ( 95% confidence interval) 50th 1.09) 6.06) 2.31) 5.45 (1.97 (5.00 (5. weakness.19-2.39-5.41 (1.915 (.23-5.77) 1.50) 2.39 (3.40 (1.92 (4.20-2.90-2.24-1.73) 2.35-1.10-2. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.37 (1.89 (2.03) 3.91 (3.8) 4.73-4.34-5.32 (2.54) 1.

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

eating food. Two types of minerals. Low-level beryllium exposure in the general population can occur through breathing air. are mined for commercial recovery of beryllium.13. electrical. and can be found in mineral rocks.130 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 196 Fourth National Report on Human Exposure to Environmental Chemicals . inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. and dental bridges. computer. 01-02. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. < LOD means less than the limit of detection. the lightest of all metals. 7440-41-7 General Information Pure beryllium is a hard gray metal.13. beryllium is used in instruments. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air.13.130 (<LOD-.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 . respectively.140 (<LOD-. population from the National Health and Nutrition Examination Survey. In medicine. and machine-parts industries. or drinking water containing the metal. Beryllium compounds are commercially mined. nuclear. x-ray machines. and refined beryllium is used in mirrors and special metal alloys for the automobile.Metals Beryllium CAS No. and 03-04 are 0. which may vary for some chemicals by year and by individual sample. and 0. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. coal.S. aircraft. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. near some hazardous waste sites. and volcanic dust. 0. In studies of laboratory animals. Exposure to beryllium occurs mostly in the workplace. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.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. soil. and from breathing tobacco smoke. bertrandite and beryl.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 . see Data Analysis section) for Survey years 99-00.

The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure.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 . IARC has classified beryllium as a human carcinogen. Maier. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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 . 2002). EPA. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . S.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. Chronic beryllium disease. and drinking water and environmental standards have been established by U. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al.346 (<LOD-.281 (<LOD-. population from the National Health and Nutrition Examination Survey. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response.S. or berylliosis. Skin exposure can result in delayed hypersensitivity reactions. based upon excess lung and central nervous system cancers in studies of workers. NTP considers beryllium to be a known human carcinogen. 2003. which produces pneumonitis. 1990). respectively.. Fourth National Report on Human Exposure to Environmental Chemicals 197 .231 (<LOD-. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. including contact dermatitis and subcutaneous nodules.

Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. 2001). Centers for Disease Control and Prevention (CDC).296(1-2):71-90.e. blood.. 2000. Weston A. Clin Chim Acta 2000... 1990. Maier L. Clin Chest Med 2002. Paschal DC.157:388-398.htm. Available at URL: http://www.12 to 0.95:89-105. VI.html. Morrow JC. Environ Res 1998. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. et al.org/documents/ehc/ehc/ ehc106. population are lower than levels in workers. 3/27/08 Komaromy-Hiller G. environmental levels) and health effects is available from ATSDR at: http://www. Schaller KH.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Costa R.13 μg/L. Trace element reference values in tissues from inhabitants of the European community I. International Programme on Chemical Safety (IPCS). Jackson RJ. and the 95th percentile for males in NHANES 2001-2002. Howerton K. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures.atsdr. Trace metals in urine of United States residents: reference range concentrations. and serum of Italian subjects. Am J Epidemiol 2003.Metals (i. Minoia et al. McCanlies EC. Andrew M. Element reference values in tissues from inhabitants of the European community.S. Pirkle JL. 1990. Sci Total Environ 1994. which approximate this Report’s limit of detection.158:165-190. Pietra R. 1998). (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i.e. 0. Levels of beryllium in urine for the U. Hamilton EI. 20012002. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Given these results. plasma and urine and a critical evaluation of reference values for the United Kingdom population.1 μg/L).S. Int Arch Occup Environ Health 2001. Sampson EJ. They reported urinary beryllium levels ranging from 0. Comparison of representative ranges based on U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.74:162-166. A study of 46 elements in urine. and 2003-2004. Genetic and exposure risks for chronic beryllium disease. In other studies.inchem. Hamilton et al. Pozzoli L. Ash KO. it is likely that urinary beryllium levels in the U. 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.cdc. Ting BG.. less than 0. Sci Total Environ 1990. et al. HLA-DPB1 and chronic beryllium disease: a HuGE review. Minoia C.76(1):53-59. References Apostoli P.gov/toxpro2. Beryllium [online]. Sabbioni E.. Paschal et al. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Third National Report on Human Exposure to Environmental Chemicals.23:827-839. Atlanta (GA) 2005. Kriess K. and the fact that most NHANES participant levels were undetectable. Van der Venne MT. Review of elements in blood. Sabbioni E. Apostoli P. Gallorini M. 106. patient population and literature reference intervals for urinary trace elements. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.S. population were generally undetectable in NHANES 1999-2000. Environmental Health Criteria.

800-1. Fourth National Report on Human Exposure to Environmental Chemicals 199 . cadmium use has declined in response to environmental concerns (http:// minerals.361-. and 03-04 are 0.500-.700) .600) 90th 1.00-1.400 (.10) 1.00-1.70) 1.400) .600 (.600 (.600 (.300-.344) .00-1.40 (1.304 (.S.500-.20-1.382 (.900-1.200 (.500-.400) .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10 (1. 01-02.300) .900 (.00 (.400-.10) 1.400) < LOD .50 (1.70) 1.400-.600 (.30) 1.900-1.400-.600 (.200) .425 (.300 (<LOD-.400-.900-1. 0.50) 1.50 (1.283 (.500-.50) 1.449) Selected percentiles ( 95% confidence interval) 50th .300) .400 (.usgs.500-.300) .333 (.60 (1.00-1.300-.00-1.400 (.3.30-1.500) .00 (.10 (1.200) .40-1.300-.300 (.400 (.20) 1.20) 1.30 (1.400) .420 (.200-.300) .400) .10) 1. respectively.300-.513) .400-.500) .400 (.60 (1.60) Total * .800 (.395 (.10 (1.20-1.50 (1.500 (.200 (<LOD-.378-.00-1.500) .300) .400-.60 (1.14.400-.300 (<LOD-.00 (.800) .40 (1.600 (.600) . 7440-43-9 General Information Cadmium is a soft.400) .300 (<LOD-.313 (.300-.20) .300 (.500-.500-.500 (.10 (1.400) < LOD < LOD < LOD .20) 1.289-.326 (. plastic stabilizers.427) * .500-.400 (.600) 1. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.00 (.80) 1.400 (.300) .600 (.400 (.386-.700) .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 . population from the National Health and Nutrition Examination Survey.500-.300 (. interval) .400) . < LOD means less than the limit of detection.300 (<LOD-. which may vary for some chemicals by year and by individual sample.20-1.309-.275-. The predominant commercial use of cadmium is in battery manufacturing.300 (.300) .600) .398) < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00.300-.500-.30-1.900-1.362-.10 (1.400-.20) 95th 1.80 (1.500-.300-. EPA.400 (.400 (.900-1.900 (. and incineration of municipal waste materials.00-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-1.40 (1.400) .30-1. Other uses include pigment production.367-.10) 1.500 (.300-.412 (.400-.300 (.460) .800 (.300) .300 (.400 (.00 (.20) 1.600 (.600-.266-.300-. during refining of lead and copper from sulfide ore.304 (.00) .300-.600) .900-1.300) .500-.500-.403 (.500) .10) 1.600 (.40-1.500-.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .900-1. Since 2001.700) .300 (.441) * .600 (.400 (.600 (.216-.366) * * .3.900-1.304-.500 (. malleable.50 (1.200 (. Cadmium also may be emitted into the air from zinc.600-.600) . lead.700) .80) 1.700) .403) .00 (1.393 (.500) .600-.600 (.40 (1.300 (.70) 1.40 (1.20) 1.800) 1.20-1.10 (1.Metals Cadmium CAS No.359-.300 (. or copper smelters (U.60) 1.500 (.20) .600) .00 (.600) .900-1.400) .00 (.255) .30-1.50) 1.424) * .50-1.400) .400) .700-1.300 (.gov/minerals/pubs/commodity/cadmium). Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.30) 1.700 (.500 (.50-1.500 (. as zinc sulfide) and to a lesser extent.300-.600-1.400 (. coatings and plating.400) .200 (<LOD-.426-.50-1.400-.40) 1.200-.500 (.30) .700) .421 (.600) .40 (1.300-.10 (1.20) 1.600) .700) .400-.S.300-.500) .00-1.30-1.400 (.00 (.60-1.500-. U.70) 1.20 (1.500-.700-1.300 (.200-.800-1.10) 1.40) 1.600 (.900-1.300-.300-.60 (1.470) * .500) .337) . and nonferrous alloys.400) .700) 1.378 (.700) .300 (.200-.00 (.200 (.400) < LOD .300) .90) 1.300) .300 (.30) 1.S.452) .331) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.600) .500-.10) 1.00) .10) 1.20 (.20-1.400 (.500-.60) 1.400 (.800) .50-1.60) 1.300-.376-. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.300-.300 (.10 (.600 (.300-.300-.400) .00 (1.400 (.20-1.60 (1.300) 75th .400) < LOD .300) 1.500 (.300-.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 . and 0.235 (.368-.40 (1.300-.700-1.00 (.400) .468 (.300-.200-.300) .20) 1.20-1.300) .296-.20) 1.

078 (.134) .153-.596) .20) 1.289-.181 (.170-.980-1.733) .173) .960 (.216 (.219 (.870) .210 (.490) .510) .184-.136) .741-1.246) .447 (.13) .320) .220-.299) .400-.316 (.190-.607) .272-.980) .170-.240) .211 (.092) .38) .25) 1.25 (1.12 (.714-1.210) .229-..426 (.507) .848 (.445 (.680 (.372) .07-1.843-1.15) 1.388-.519) .207-.219 (.177-.206) .836-1.30-1.06) .880) .200-.061-.04 (.170 (. Diamond et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.221) .265) .22 (.265 (.100-. respectively.820 (.551) .15 (.067-.17 (.126) .633-1.530) .203) . drinking water is a source for cadmium intake. For nonsmokers who are not exposed to cadmium in the workplace.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.34) 1.247) ..210 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.977) .310) .220 (.551 (.860) 1.17 (.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.280 (.790 (. interval) .191 (.989-1.445 (.141 (.820) 1.790 (.559 (. and 0.121 (.081) .110-.539) .167-.230) 75th .260 (.806) .282 (.330-.700-.350 (.229) .366-.190-.165-.972 (.717-..210 (.200-.892-1.450 (.160 (.077 (. 01-02.239 (.327 (. With chronic exposure.839 (.500) 90th . 2003). however.458 (.090) . calcium.20 (1. 200 Fourth National Report on Human Exposure to Environmental Chemicals .610) .858 (.498-. and 03-04 are 0.226) .179-.107-.713) .20 (1.257-.200 (.06-1.37) 1121 1335 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 .339) .237-.151-.284) .589 (.233) .890 (.227 (.918-1.257) .390-.623) .060-. Cadmium is absorbed via inhalation and ingestion.12-1.231) .300 (.222) .169-.190-.090) .892 (.17 (.351-.249-.109 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120 (.238-.281 (.28) 1.436-. see Data Analysis section) for Survey years 99-00.766 (.214-.221 (.255) . including many food crops such as cereal grains.230 (.065-.220-.450 (.51 (1.83) 1.300) .270 (.366-.820-1.48 (1.748-1.412) .387) . Cadmium in soil is absorbed by plants.545 (. Renal tubular and glomerular damage. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.633 (.234 (.960) 1.230) .492 (.360) .180 (.510-.187 (.322 (.255) .171-.43) 1. Horiguchi et al.273 (.196-.160-.490) 1.32 (1. Kikuchi et al.493-.306 (.191-.128 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.210 (.481) .19) 1.150) .730-. whose body burdens of cadmium can be approximately twice that of nonsmokers.195-.130 (.135-.061 (<LOD-.390-. 2001).24) 1.261-.855-1.255) .160) .270 (.210 (.198) .262) .210) .336) .178-.47) 1. an inducible metal binding protein.077 (.189-.733-.550 (. 1994).440 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .219 (.10 (1.223 (.135 (.193-.519) . wheat..202-.112-.476-.875 (. 1999.52 (1.04 (.243-.456-.540) .480) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.810-1.400-.393-.38) .140 (.700-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.189-.06-1. 2003.38) 1.02-1.326) .Metals 2000).148-.440 (.067-.310 (.148) .886-1. rice.109-.251) .990) .175 (.09-1.430-.233) .800-. To a lesser extent.813 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .700-.875) .452 (.15) . The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.817 (.980) .01) .232 (.28-1.199 (. ingestion through food is the largest source of exposure.13-1.261-.232) .302 (.390 (.279 (.200 (.313) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.263) .** Survey Geometric mean (95% conf. Cadmium absorption may be increased with iron deficiency (Berglund et al.530 (.092 (.818 (.209 (.886) .394-.206 (.01 (.03) .980 (.466 (.41 (.S.22 (1.20-1.753-.241) .74) 1.249) . and various seeds.175 (.192-.204 (.686-.475 (.890-1.20 (1.482) .462 (. 2003).189) .800 (.366) .430) .208-.919) .201 (.193 (. potatoes.253-.260-.101) .470-.479) .080 (.157) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.220) .115-.17) .362) .157-. 0.329 (.763-.06. 2004a.295) .150-.38) 1. 2003).36) 1.06.260-.640) .203 (.423-.440-.381-.500) .285-.28 (1.940-1.194-.57) 1.160) .433-.580) .. copper) and protein.191-.817 (.211-.354) .01-1.283 (.963-1.. population from the National Health and Nutrition Examination Survey.520-.192-. zinc.114-.13 (.455 (.240-.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 .82) 1.980-1.235) .202 (.290-.087-.277 (.238) .72) 1.229) .705-.06.308) .183-.

802 (.S.653) .084-.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.239-.229) .123-.210 (.156-.161-.725-1.101) .329 (.538) .440) .176 (.268 (.135) .830) .063-.729 (.909-1.479 (.418) .077-.189-.415) .985 (.07) . 1999).184) .096) .545) .688-.178) .806-1.533) .38) .873 (.281) . 2000.708-1.700) .100 (.078 (.767 (.779 (.826-1.304-.678-.432 (.242) .197-.182) .757 (.687-.252 (.091 (.140-.136-.085 (.446) .16) .490 (.093 (.856 (.818) .783 (.769 (.674-1.219 (.941 (.204-.270 (.562-.686 (.917) .137-.075-.183 (..113-.352) .05) 1.198) .962) .377-.209) .950) .182) .131-.090 (.07 (.350) .067-.174-.690-.856) .622 (.767) .288) .143-.194-.. Olsson et al.06 (..297) .183) .071 (.234 (. 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.414-.289) .296 (.00 (.335 (.200 (.146-.184-.247-.219 (.650-.828) .278) .098) .541) .289) .850) .318 (.423-.267 (.979 (.700 (.874-1.190 (.16) 1.321) .293-.813-1.191 (.263 (.647-.078-.273 (.998) .316) . During the 1950’s and 1960’s.10) 1.481 (.631) .199 (.691-.404 (.09 (.839) .051-.206-.00 (.126 (.091 (.719 (.789 (. can result from high dose chronic exposure.223) . 2003.122 (.591 (.678 (.690-.617 (.444-.757) .331 (.236-.266-.813-. 2004b). most often a result of occupational exposure (Roels et al.783) .398-.876-1.940 (.191) .170 (.536 (.** Survey Geometric mean (95% conf.232) .308 (.382-.154 (.433-.091) .157-.434 (.245 (.470) .137 (. population from the National Health and Nutrition Examination Survey.250) .130-.222-.196 (.208 (.154-.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 ..185) .173-.192) .830-1.663 (.507-.112) .163 (.210) .111-.140-.147-..136-.150-.308) .176 (.940-1.14) 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 .171-. Fourth National Report on Human Exposure to Environmental Chemicals 201 ..440) .247-. 1999).238) .234-.693 (.253 (.074-.147 (.687 (.559-.792 (.537-.191-.263-.159 (.144-.311) .084 (.280 (.211 (..162 (.221-.123-.12) 1.240) .288-.666-.220 (.288 (.233 (.784) .645-.221 (.404) .238-.391-.216-.927-1.218) .722-.338 (.226) 75th .931 (.919 (.235) ..224 (.387-.227-. 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.441-. However.175-.181) .412 (. At lower environmental exposures.531 (.754) .210 (.225) .175 (.083-.228-.143-.181-.304) .173 (.184-.414 (.255-. 2002.187) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .283 (.387 (.300-.182) . 2004).340) .426-.336-.917 (.256-.086 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.551) .364) .158-.168-. 2002.501 (.02 (.850) .303) .716) .718 (. Noonan et al. 1999).418-.17) .094) .712 (.166 (.185 (.234) . interval) .143) .207) .421 (.476) .929) .668-.104) .431) .325 (.163) .484 (.104) .690 (.107) .207-.381-.282 (.382) .156 (. 2002.106) .516-.316 (.261) .177) .241) . 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.181 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.202 (.215 (.208-.13) .175 (.487 (..614) .500-.518) .212 (.740 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .696-.795) 1.827) .274) 1.865 (.449) .261-.833-1.343-.148 (.156) .085-.473 (.178-.716-.818) .884) .826-1.232) .906) .187-. 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.560-.438) 90th .727-.170-.199-.438-.470) .159 (.147-.261 (. older adults and postmenopausal women with Urinary Cadmium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.388-.181 (.472) ..423 (.607) .157-. 1996.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.253) .247-.209) Selected percentiles ( 95% confidence interval) Sample 95th .266) .168-. Horiguchi et al.075 (<LOD-. Jarup et al.168 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.08) .630-.267 (.667) .201-.281) .292) .240) . Staessen et al.097) .190 (.491-.225) .205 (.

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

Elinder CG. Comprehensive study of the effects of age. 206:15-24. 4/8/09 Alfven T. Moriguchi J. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers.102:83-89. Seiwert M. Mucha A. Komaromy-Hiller G. Kaus S. Serra J. Kumagai N. Palomar M.148(1-2):11-20. Centers for Disease Control and Prevention (CDC). Toxicological profile for cadmium update. iron deficiency. Venables KM. Anthropometric.59:194-8. Sanz P. et al. Lancet 1999. Bellerup P.45:43-52. Taylor AJ. Dekio F. Occup Med 1996. Toffoletto F. References Akesson A. Lauwerys R.atsdr. Miyamoto K. Ikeda Y. Atlanta (GA). Lundh T. Nerbrand C. Sasaki S. et al. Fatal chemical pneumonitis due to cadmium fumes.66(Pt A):2141-2164. Becker K. Environ Health Perspect 2005.gov/toxprofiles/tp5. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Oguma E. Kikuchi Y.95:20–31. 2005. Alfven T. Darbyshire J. Lukyanova EM. Miyamoto K. et al. Toxicol Lett 2004. Int J Hyg Environ Health 2002. Berglund M. Fukui Y. Nordberg G. Available at URL: http://www.96:353-359. Diamond GL. Jin T. J Toxicol Environ Health 2003. Machida M.46:372-374. Lidfeldt J.296(1-2):71-90. Ye T.76:186-196. Davison AG. Bregante G. Schulz C. Lancet 1988. Lepom P. et al. et al. Oguma E. population. Choudhury H. 1999 [online]. Persson B. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Zhu G. Horiguchi H. Ezaki T. Mascagni P. Nermell B. Hotz P. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Jarup L. Mannino DM. Consonni D. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. diabetes mellitus. Seifert B. et al.Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population. Kundiev YT. Fayers PM. Fernandez MA. Comparison of representative ranges based on U. Howerton K. Ukai H. Clin Chim Acta 2000.24:717-724.57:668-672. patient population and literature reference intervals for urinary trace elements. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. J Occup Health 2003. Furuki K. Gadea E. Third National Report on Human Exposure to Environmental Chemicals. Ikeda Y. Olfactory function in workers exposed to moderate airborne cadmium levels. Lison D. et al. Okamoto S.cdc. Costa R. Agency for Toxic Substances and Disease Registry (ATSDR). environmental. et al. Akesson A. Buchet JP. Kaus S. Int Arch Occup Environ Health 2003. Seiwert M. Wang H. Thorax 2004.205:297-308.13(11):1627-1631. Carlsson MD. Bo M. Environ Health Perspect 1994. Tsukahara T. Bernard A. Vahter M.S. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Moriguchi J. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Occup Environ Med 2000. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Vahter M. Takebayashi T. 102:10581066. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Ash KO. Uemura T. Toxicol Appl Pharmacol 2004a. Jones RL. Furuki K.html. Jarup L. Chiappino G. Krause C. Grubb A.354:1508– 1513.S. et al. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group.110:699-702. Environ Res 2006. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. possibly better than b2microglobulin. Environ Health Perspect 2002. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Cadmium fume inhalation and emphysema. Chislovska NV. Thayer WC. Machida M. Fukui Y. Becker K.000 women in the Japanese general population: a nationwide large-scale survey. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Neurotoxicology 2003. Schulz C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Stock AL.59:497]. Savage-Brown A.1(8587):663-667. Ezaki T. Holguin F. ShkiryakNizhnyk AZ. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Friedman LS. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Pickering CA. Environ Res 2004b. 196:114-123. Horiguchi H. Environ Res 2004. et al. Int J Hyg Environ Health 2003. et al. Nomiyama T. Tsukahara T. Greves HM. Hellstrom L. Sasaki S.

Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Jansson J-H. 2004. Biological monitoring of toxic metals. age. created 1992. Lancet 1999.html. Bruiglia S. Cadmium in blood and urine – impact of sex. 151-168. Oskarsson A. Saito S. Kuznetsova T. Occup Environ Med 2002.39:2507-2515. Int J Hyg Environ Health 2006. Hazard Summary. Ren Fail 1999. Roels HA.epa. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Vangronsveld J. Arch Environ Health. Tanebe K. Skerfving S. or cadmium in controlling occupational and environmental risks of nephrotoxicity. J Cardiovasc Risk 1996. Environ Res 2000. Nakagawa H. Roels H. Zhao YC. In: Clarkson TW. Okubo Y. United States Environmental Protection Agency (U. et al. Honda R. forearm bone density. Nordberg GF. Staessen JA. eds. pp. EPA). J Perinat Med 2002.353:1140-1144. et al. Gallmans G. Nakagawa H. Effects of exposure to low levels of environmental cadmium on renal biomarkers.100:330-338. Nakagawa H. et al. et al.84 (Section A):4455. Emelianov D. Olsson IM. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Thijs L. Schultz C. et al.110:151-155. Friberg L. Environ Health Perspect 2002. Wennberg M.59(1):22-25. Relationship between newborn size and mother’s blood cadmium levels.110:1185-1190.59:394-397. Staessen J. Tawara K. Japan. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Environmental exposure to cadmium. Liu QF.3:26-41. Hoet P. Noonan CW. Wilhelm M. Merlino MV. Schwenk M. Revised 2000 [online]. Honda R. Cadmium carcinogenesis. Zhu HD. Gangemi S. Nordberg GF. Tanebe K.30(5):395-399. Lison D. Stegmayr B. Available at URL: www. Mutat Res 2003. lead.Metals Nishijo M.533(12):107-120. Lauwerys R. Bensryd I.209:301305. Environ Health Perspect 2002. Sarasua SM. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Sager PR. Kathman SJ. J Environ Sci Health B 2004. Salpietro CD. cadmium. Kobayashi E. lead. Time trends in burdens of cadmium. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. 2000. Ottosson H. Buchet JP. lead. Environ Res 2006. Biological monitoring of cadmium. Wang JX. Ginucchio G. Zhang YL. Lijnen P. Minciullo PL. Roels HA. Lybarger JA. dietary intake. Suwazono Y.21(3-4):251-262. Nordberg M. and risk of fractures: prospective population study. 2001. Fan YG. Mueller PW. iron status. and mercury in the population of northern Sweden. Cadmium compounds. Kido T. Nishijo M. Nogawa K. Toyama. Usefulness of biomarkers of exposure to inorganic mercury. Lundh T. Bergdahl IA.S.gov/ttn/atw/ hlthef/cadmium. Revised and new reference values for arsenic. 4/8/09 Waalkes MP. Lundh T. Stelitano A. et al. New York: Plenum Press. Campagna D. and former smoking – association of renal effects.

08) 7.63 (4. 01-02.30) 7. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.56) 5.8 (10.86-11.12) 5.80 (8.20) 7.94 (4.2-14.17) 4.86 (7.77 (9. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.64-10.97-7.8-13.95) 5.00-9.34) 9.80-13.5-14.86-12.71-5.3-15.21 (4.12-5. and 03-04 are 0.49) 4.46) 7.54-11.90) 5.1) 9.20-7.50) 5.5-14. scintillation counters.4) 11.72) 4.1-12.80-11.4 (9.70 (6.45-8.0) 12.20 (4.6 (11.8 (11.60-12.S. and high-power gas-ion devices.0-13.77 (4.90-8.61-6.36 (6.84) 5.14.49) 75th 7.4) 10.7) 11.00 (7.22 (4.9 (10.10 (6.09) 5.60 (7.7 (9. nausea.4) 12.0) 12.27-5.98 (7.70 (6.0) 12.40-5.37) 7.0 (10.60) 7.04 (4.1) 11.80 (4.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.80 (8.60) 7.2-12.40) 7.59-5.52-9.90 (6.68 (7.80-10.17 (6.64-5.29) 4.05-5.03 (4.13 (5.1 (9.2 (9.7) 10.7 (9.93 (4. However.5) 12.8) 9.67 (4.45-5.81) 4.50) 9.1 (10.82-4.14 (4.90) 5.33-5.59) 7.35 (4.71-9.80-10.35 (4.80 (4.33 (6.20-4.84-5.39) 7.60-6.10-9.40-7.2-13.81 (4.17-6.7 (9.90-10.1 (11.66 (7.8) 12.83-4.80) 7.01) 7.81-14.07) 4.7) 10.64) 5.00-8. 2004).71-8.63) 6.02 (4.20) 5.3) 10.80-10.30 (6.16-6.43-8.32) 4.70 (9.34 (4.60-7.56 (4.42) 7.0 (9.7 (10.27 (7.37) 5.4 (10.89) 4.23-4. photographic emulsions.7 (8.84 (4. Whether cesium compounds are carcinogenic is unknown. see Data Analysis section) for Survey years 99-00.40-11.40-5.53 (6.83) 6.4 (9.40-5.04) 7.21) 90th 9.20-8.60) 5.99-6.9 (11.62) 4.50 (4.64 (4.42) 6.9) Total 4.35-5.3 (8.70-5.73-5. soil.8) 12.81) 4.0) 11.90-10.08 (6.20) 4.33 (5.2-13.20 (6.10-7.87 (4.3-13.6 (9.47-4.59-5.87 (4.98 (7.50 (4.99-11. and 0.4) 9.74) Selected percentiles ( 95% confidence interval) 50th 4.57-5.25 (3.03 (4.6) 10.5-16.3) 9.80 (8.8) 11.12 (4.1-13.99) 9.95-4.40) 5.54) 4.20) 8.60 (8. the body half-life is estimated to be 70-109 days based on 137Cs exposures.6 (9.2-13.59 (5.0-15.00-4.15-8.90) 7. 0.4-13. interval) 4.10 (8.25-5.64) 4.05) 5.84-9.55 (7. although cesium was generally of low toxicity when given to animals.10 (8.6 (11.70 (4.5 (10.05) 5.30-5.23) 9. cesium hydroxide is corrosive and irritating at high concentrations.80-6. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.74 (4.3) 12.30) 5.44 (8.12-11.99) 7.5 (8.9) 12. diarrhea.26-11.10-5.3 (8.82) 5.77 (9. and clay.70-8. and cardiac arrhythmia (ATSDR.2) 12.80 (4.26) 4.00) 7.60-6.3) 10.94-4.8) 9.36 (3. population from the National Health and Nutrition Examination Survey. semiconductors.Metals Cesium CAS No.7) 11.97) 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 4.13 (8.3) 10.08-5. and as polymerization catalysts.59-5.90 (4.90-12.70) 7.01-6.7 (11.00-10.84) 8.70) 5.79 (4.89-5.94 (4.7 (10.9) 11.91 (7.0) 11.50 (7.91-8.4) 12.31-8.90) 4.00) 4.30 (6.73-11.50 (6.90-12.88 (8.96 (6.8) 12. Most human exposure to cesium occurs through the diet.5) 10.10-8.97) 4.13-8.70 (8.40-5.6 (9.2 (9.60-5.69-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.03-4.00) 6.97 (7.40) 5.87 (4.26 (3.99-11.89) 5.56-11.9 (10.8) 11.43 (5.40-11.71) 4.87) 5.29 (4.76-6.26) 7.47-8.71 (8.22-4.50-7.71 (4.56 (4.39-4.63-4.4) 95th 11.1) 10.90) 9.08 (7.7-14.6 (9.30-10.25) 4.5) 9.49 (5.70) 5.38) 5.90-10.70 (5. For absorbed cesium salts.9) 8.60-7.14.92-13. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.6) 11.62 (5.7 (10.09-5.49 (4.50 (4.55 (4.27) 4.94) 4.1-12.20-5.5-13.2. infrared lamps.70 (8.32-5.08-5.00-8.8 (10.0) 10. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.62 (5.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.32 (3. Little is known about the health effects of this metal.77-8.64) 5.53-11.9 (11.68) 9.81) 9.95 (3.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.72-7. Fourth National Report on Human Exposure to Environmental Chemicals 205 .9 (11.1) 11.13 (7.1) 9.52) 7.61) 7.36) 3.10 (6.3) 10.3-13. respectively.87-7.4) 10.55-11.42-7.01-8.07-11. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.2) 11.74-5.9 (11.40 (4.16-6.0) 9.05-5.24) 4. Radioactive 137Cs has been used medically to treat cancer.

28 (5.24-4.08 (3.83-7.9 (9.9) 10.95) 8.53 (4.36-10.56) 4.79-5.36-3.98 (6.42-6.14-4.35 (4.30) 10.29) 4.08) 4.64 (8.38) 10.12-6.33 (5.14-7.50 (6.38 (3.54 (4.14 (6.27-6.91) 4.64-6.9 (10.96-4.28 (4.78 (3.64) 5.73 (3.05-4. Minoia et al.33-3.68) 3.3-15.80) 6.48) 7.39) 8.78) 4.13) 7.31 (4.33-8.18) 8.35-7.23 (7.83) 8.91 (5.50 (7.59-8.14) 4.63-6.37-3.96 (4.84-7.46-4.81 (4.95-6.42 (5.17) 4.91) 5.27 (8.16-8.58 (6. interval) 4.14-6.07) 8.42 (4.46-8.55-5.8 (9.3 (10.33 (5.72) 4.15-11.75 (6.05) 3.60 (5.56) 4.96) 4.66 (6.79) 9.58) 3. and were also roughly similar to those in this Report.59) 4.78 (3.55) 4.00 (8.63 (4..88-10.70) 7.48) 90th 7.72 (4.91) 5.72-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 10.03-5.55 (3.47 (7.82) 7.06) 4.50) 4.75-11.0) Total 4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 (9. Using clinically submitted specimens.27) 4.8) 10.56) 3.67 (5.71) 6.S.40) 7.58-5.30 (4.09) 4.53) 3.41 (8.10 (5.4) 10.10) 7.91 (5.44-9.67 (6.50) 8.10-4.51 (4.93-7.5) 9.87 (5.60 (3.71 (7. 1990).43) 8.20-8.90 (7.36-6.04) 5.3) 9.17 (6.43 (8.18 (7.06 (3.58 (4.15 (7.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.99 (3.78) 4.46 (7.88-4.73-4.54 (4.40-5.46 (8.03-6.79) 4.43 (4.98) 5.45-6.22-11.09) 8.12) 3.97-4.84-7.21-4.10 (3.49) 3.0) 7.50) 4.76-6.77-5.60) 3.00-8.42-4.66 (5.40) 6.07 (5.08 (6.35-11.92) 3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.98) 5.63) 6.75 (7.95-12.79) 6.20) 5.44 (4.51 (3.83-6.87-4.24 (3.99-9. population results shown in this Report (Alimonti et al.56 (4.19-3.74) 3.99) 4..96) 4.00-5.68) 6.95) 10.1) 11.03) 5.35 (3.20-4.92 (5.29) 5.8) 6.34 (5.37) 4.68-11.47) 4.60-10.64 (4.05) 6.03) 6.6) 6.79 (5.95) 4.38-12.20-4.02-4.24-10.50) 4.41 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5 (9.2 (8.43 (3.12 (3.66-6.08-7.04-11.5) 9.47) 7.54 (5.99-9.44 (8.22) 6.29-3.53 (6.S.00-5.93-9.27-4.58) 8.18-6.74 (4.17-4.50 (5.38-7.47) 6. Two small studies of European populations reported urinary cesium levels similar to U.15-4.90-8.62) 5.45 (4.17) 9.18-7.3) 11.44) 3.96-4.64) 4.19-6.84-9.90-3.3 (8.26 (4.74-11.14) 4.04) 6.31-6.81 (4.5) 7.85-4.01-8.99-4. 2005.10 (3.95 (5.S. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.00-4.11 (5. population from the National Health and Nutrition Examination Survey.48-6.87) 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 5.21-5.51 (3.74) 75th 5.25) 4.51 (7.77) 4.26-6.85) 4.7-12.2) 11.2 (8. (2000) found urinary cesium levels that were slightly lower than those reported for the U.16) 5.39) 5.30 (3.86 (4.30-4. 2004).05 (4.31 (4.11 (5.97-5.43-11.13 (3.77 (6.27 (6.66 (5.91-9.98 (7.30-4.47 (4.41) 9.22 (3.84-9. Komaromy-Hiller et al.50-5.09 (4.16-8.52-5.29-3.51) 4.89-4.6 (9.51 (4.42-4.65 (6.6 (9.25) Selected percentiles ( 95% confidence interval) 50th 4.56-10.63 (6.0 (7.05-3.68) 4.64) 9.43-6.65-4.87) 5.28) 7.26 (3.63-6.8) 5.91-7.27 (6.41-7.54 (3.68 (4.30) 10.35) 3.84-11.74 (5.43 (4.91-6.44-5.41) 4.28) 8.94 (5.00-9.95 (3.07-4.08) 4.76-9.08) 3.41 (5.31-4.07) 8.39 (5.61 (7.16-5.63 (7.13-9.13-9. population.47) 6.02 (5.62-8.7) 10.77 (4.06 (5.38 (3.67) 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 3.94) 7.97) 8.06) 5.61-3.05-3.20-4.21 (2.85) 5.57) 3.29) 4.60-20.08-3. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.08 (5.15) 95th 8..70) 6.04-5.46) 6.00-10.41-4.65-3.53) 6.70 (7.90-8.0) 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 .82-4.77 (7.21-3.3) 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 3.30 (7.00) 6.

Third National Report on Human Exposure to Environmental Chemicals. Voorhees RE.html. Ash KO. Apostoli P. Centers for Disease Control and Prevention (CDC). Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Howerton K. cesium. Pozzoli L. Costa R. Gatti A. Assessment of urinary metals following exposure to a large vegetative fire. patient population and literature reference intervals for urinary trace elements.14:120-128. Clin Chim Acta 2000.19:3131-3138.S. Gallorini M.2004 [online]. 2000.95:89-105. Available at URL: http://www. A study of 46 elements in urine. Mott JA. Comparison of representative ranges based on U. et al. Wood CM. Atlanta (GA) 2005.atsdr. Spezia S. et al. Sci Total Environ 1990. Komaromy-Hiller G. and serum of Italian subjects. Sewell CM. Minoia C. antimony and tungsten.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).cdc. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Trace element reference values in tissues from inhabitants of the European community I. Forte G. Sabbioni E. 4/8/09 Alimonti A.gov/toxprofiles/tp157. Pietra R. Ronchi P. et al. blood. Wolfe MI. Mincione G. New Mexico. Paschal D. J Expo Anal Environ Epidemiol 2004.296(1-2):71-90. Toxicological profile for cesium. Rapid Commun Mass Spectrom 2005.

499 (.520-.370) .800) .340 (.850-1.398) .920-1.900) .14) .810) .386) .313) .583) .850-1.259-.740 (.520 (.373-.880-1.28 (1.500 (.25-1.28-2.434 (.580 (.36) 1. and inks.515 (.610 (.530 (.810-.390 (.640) .14-1.23) .37-1.940-1.59 (1.16) 1.348-. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.367 (.820 (.03) 1.24 (1.S.450) .454 (.950-1.03 (.17 (.670-.920) 1.360-.28 (1.336-.810) . diamond-polishing wheels.600 (.00) .430) .750-.16-1.32-2.519 (.760 (.760) . varnishes. steel-belted radial tires.750 (.950 (.640) .81) 1.590-.327-. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.16) 1.16 (1.388-.710 (.550-.17 (1.410 (.330-.450) .418 (.520 (.394) .330) .32) 1.33-1.308-.600-.09) .350-.520 (.50 (1.15-1.564) .26) 1.05 (.26) Total .29 (1.99) 1.502) .740-. Usual human exposure is from food sources.470 (.04-1.47) 1.930 (.420) .410) .06 (.39) 1. It is also a component of porcelain enamel applied to steel bathroom fixtures.310-.620) .03-1.377-.410) . and magnetic recording media.294 (.81) 1.21) 1.540-.369 (.670-.300-.600) .01-2.340) .04 (.26-2.730) 1.650-. and 0.47 (1.316 (.980) .372) .469-.860 (.420) .12) 1.350) 75th .900) .580 (.480-.20 (1. and soil.790) . respectively.790 (.940-1.680) .355-.03 (.450) .460) .680 (. seawater.350-.430 (.334) . population from the National Health and Nutrition Examination Survey.450-. Cobalt compounds are also used in manufacturing battery electrodes.390 (.17 (1.48) 1.690-.350-.431) .930-1.373) .343 (.500) .03) 1.05 (. Cobalt occurs naturally in airborne dust.33 (1.460-.22) 1.840) .740-.291-.890-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.339 (.379 (.550 (.Metals Cobalt CAS No.05) 1.32) 1.431) .410 (.452 (.300 (. and 03-04 are 0.416) .460 (. industry is imported or obtained by recycling scrap metal that contains cobalt.26-1.08-1.290-.870 (.333-.390-.435 (.419) Selected percentiles ( 95% confidence interval) 50th .370-.410 (.04) 1.570 (.410-.424) .570-.280-.700) .870-1.340) . blue-colored pigments.910-1.343) 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 .64) 1.420 (.380 (.03) .270-.370-.630 (.520) .44) 1.405-.379 (.S.15 (1.414) .270-.380 (.22 (1.520) .338-.620-.399) .870 (.670 (.23-2.930) .285 (.364-.880 (.380-.417) .400-.750 (.820 (.520-.398 (.270-.680 (.560 (.620-.340-.73) 1.301 (. hard metal or in combination with other elements. shiny.340-.530-.410-.19) .540-.430 (.01-1.480 (.790-.690 (.330 (.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 .42) 1.68 (1.710) . large appliances.890) .581) .690-.450) .52 (1.890-1. Cobalt compounds are used as catalysts in producing oil and gas.570) .01 (.940 (.900-1.390 (.07-1.28 (1.47 (1.570-.09 (.550) 90th .46 (1.04-1. The cobalt used in U. 01-02.428-.410-.590) .890) 95th 1.09 (.32 (1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.680) .523) .590-. It is emitted into the environment from burning coal and oil and car and truck exhaust.487) .305-.352 (.830-1.14) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .520-.590 (. see Data Analysis section) for Survey years 99-00.670 (.570) .56) 1.465) .07.331-. 208 Fourth National Report on Human Exposure to Environmental Chemicals .319) .350 (.08) .06-1.08.310 (.24 (.461 (.45 (1.460) .13) 1.710) 1.660-.750 (.620-.540-. and in synthesizing polyester and other materials.700) .543) .610) .950-1.800-.380 (.460) .17-1.640) .610-.410 (.50) 1.800-.650 (.463-.950) . automobile airbags.07.440-.371 (.850) .960-1.16 (1.520 (.393-.16-1. and fertilizers.470) .60 (1.410 (.430 (.320 (.374 (.496) .75 (1.540-.32 (1.333-.430) .480 (. 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.67) 1.390) .540) 1.610) .520-.430-.630 (.580 (.92) 1.12) 1. and kitchenware.348-.490-.370 (.16 (.375 (.670 (.65) 1. Cobalt is used as a drying agent in paints.900-1.510) 1.850) 1.48) 1.04-1.770) .490-.450-.06 (.404) .07-1.359 (.660) .360-.47) 1. hard metal (alloys of cobalt and tungsten carbide).660) .980-1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.630-.820 (. interval) .07 (.460 (.380-.01 (.360-.53) 1.427-.890-1.650 (.316-. 0.950 (.900) .22-1.02-1.530) .370-.

409) . in the feces.15) 1.611) . 1994). Exposure in the workplace may come from electroplating.297-.830 (.243-.738 (.16 (.29) .444 (..513) ..737 (.476-. using hard metal cutting tools.990) . 1972).963) .333 (.937 (.335 (.376 (.534-.429) 1.278 (.12-1.599) .938) .457) .251-.326-.380-.609) .963) .842) .561) .848 (.872 (.368) .16) .271 (.879-1. with pulmonary clearance half-lives of from one to two years (Hedge et al.15 (.04 (.552 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.534 (.239-.28) 1.290 (.728 (.513 (.372) .691 (.10) Total .16 (.297) .316 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).333-.844 (..29 (1.33) 1.562) .16 (1.313-. an essential human nutrient.334) .781-1.660-.360) .976 (.426 (.296) .475 (.12 (. 1972).328) .457 (.606 (.60) 1.343-.634-.703-. and to a lesser extent.304) ..237-.738 (.00) .00 (.581) .256-.278-.560-.378-.352) .669) .847) .850-1.821-3.647) .298 (.826-1.449) .760-1.33) 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 .250) .750) .400 (.689 (.391 (.03-1.733-1.433) .955) .396) .608 (.500 (.25 (.500-.27) 1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.337) .314 (.728) .29) 1.35) .343 (.327-.905) .268 (.50) 1.471-.744) 1.296-. interval) .259 (.248-.425-.361-.626-.404-.328 (.300) .694) .829-1.11-1..515 (.286) .44 (.291 (.488) .963-1.421) .611) .310) .662) .362-.757-1.50) 1.342-. 1979).630-.547 (.774 (.513-.06 (.861-1.449-.895-1. cobalt is excreted predominantly in the urine.361-.949) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al. Once absorbed and distributed in the body.00 (.358 (.753-.279) .328 (.548 (.30 (1.60) 1.861 (.00 (.363) .368) . 1994.313-.593) .302-.282 (.554 (.277-.591 (.346 (.463-.S.289) .04-1.247 (.324) .00 (.960 (.309) .408 (.955) .632-.388 (.392 (.683-.487-.435 (.723 (.33) .667-1.543) .471-.361 (.293 (.542 (.582-.838 (.306 (.439) .495 (.630-.387) . or using diamond-polishing wheels that contain cobalt metal.10) .272-.804) 1.640) .54) 1.10) 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .14 (.736-.673-.339-.975 (.17) .407 (.365-.917) .900-1.369 (.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 .329-.595) .821 (.487-.257 (.25 (.259) .533 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.756 (.03 (.57) 1.55) .313-.384) .895-1. population from the National Health and Nutrition Examination Survey. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.10-1. refining or processing alloys.523 (.550-.378-.635 (.279 (.50 (1.467-.273 (.317 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.319-.785) .362 (. A portion of cobalt retained for long periods is concentrated in the liver.36) 1.306) 75th .329 (. respectively.313 (.644 (.503-.352 (.781) 95th 1.461) .537 (.00) .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 .386 (.435-.833-1.964 (.929) .708) .857-1.344-.275-.594) .393 (.667-1.829) .27) 1.505) .35) 1.10 (.331-.598 (.990-1.368 (.290 (.679-.323) .704-.Metals fabricated from cobalt alloys (Lhotka et al.248-.290 (.257-.786-.215-.274-.740-1.301) .442-.378-.428-.562) .434-.851 (.700 (.750-.407) .352 (.898 (.19) .348) .234 (.23 (1.419) .29 (1.638-1.417 (.391) Selected percentiles ( 95% confidence interval) 50th .563-.281) .24) .337 (.333-.468) .378 (.983) .388 (. Cobalt is absorbed by oral and pulmonary routes. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.707) .850 (.963-1.469-.36) 1.425) .523 (.554 (.824 (.457-.381) .294-.83) 1.574-.73) 1.911-1..362) .500-.313-.259-.275-.471 (.29 (1.393-.333-.529 (. 2003).280-.452-.481) 90th .615) .353 (.600-.479) .349) .753) 1.394) .327 (.49) 1.11-1.00-1.382-.983-1.932-1.09) 1.282-.365) .727 (.301-.508-.462) .438) .402 (.455 (.585) .616-.353-.417) .324-.02 (.700 (.522) .313-.777-.479-. Smith et al.952 (.396) .792-1.361 (.304-.938-1. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.355) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.792 (.303-.

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

J Trace Elem Med Biol 2006. Bourne RB. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Sci Total Environ 1997. Boca Raton (FL): Lewis Publishers. Lison D. et al.(1-3):133-139. Weber A. Am J Epidemiol 1998.55(4):269-276.150(1-3):167-171. Lauwerys R. Swennen B. Kirsch-Volders M. Int Arch Occup Environ Health 1997. Contact Dermatitis 2003. Health Phys 1972. Sci Total Environ 1994. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors.22:359367. Lison D. Thakker DM.204:147-160. Cresti R. and hard metal dust. 1985. Chess DG.” Contact Dermatitis 2001. Weyher I. Carnes WH. Zhuber K. White MA. Kraus T. Roto P. Buchet JP. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Dunning SP. Stanescu D. Moulin JJ. Steffan I. Alessandrelli M. Bunn HF.69(3):193-200. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Dickel H. Sanghrajka AP. Cleland D. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Thomassen H. Dunstan E. a study of 13 elements in blood and urine of a United Kingdom population. Linnainmaa M. Salvatori S. Lauwerys RB. Thabe H.148:241-248. Linna A. Buchet JP. Zedda S. Occupationallyinduced “isolated cobalt sensitization. Hoher T. The release of metals from metal-onmetal surface arthroplasty of the hip. Epidemiological survey of workers exposed to cobalt oxides.45:246-247.242:1412-1415. Kiilunen M. Mosconi G. Romazini S. Bozec C. Rorabeck CH. DeSantis V. Sabbioni E. Sci Total Environ 1994. A report of two cases from mineral assay laboratories and a review of the literature. Barnaby CF.150:177-183. Cobalt and antimony: genotoxicity and carcinogenicity. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Salama A. Kusaka Y. Br J Ind Med 1993. Goto S.58(10):631-634. Lasfargues G. Bacis M. Am J Ind Med 2003.48:172-173. J Bone Joint Surg Br 2005. Laippala P. X. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Iversen BS. Daniel J. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.406:282-296. Zweymuller K. Absorption and retention of cobalt in man by whole-body counting. Hammon E. et al.150. et al.51(7):447450. Clin Orthop Relat Res 2003. Palmroos P. Diepgen TL. Cobalt cardiomyopathy. De Boeck M. Lison D. Schaller KH. Goldberg MA.533:135-152. cobalt salts. Jarvis JQ.95:29-37. Meyer zum Buschenfelde K-H.21(2):189-195.157:117121.36:732-734. Schank M. MacDonald SJ. Zobelein P. Goto S. Szekeres T. Kuska Y. Pisati G. Science 1988. Peltier A. Iavicoli I. Hedge AG. HoffmannB. Smith T.87(5):628-631.88(4):443448. Lauwerys R. J Rheumatol 2001. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Tilley S. Health Phys 1979. Kristiansen J. J Occup Med 1992. Lung cancer risk in hard-metal workers.20(1):25-31. Swennen B. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Meier R. Unwin P. McMinn DJ. Outcome of occupational asthma due to cobalt hypersensitivity. Int Arch Occup Environ Health. Edmonds CJ. Leghissa P.216:253-270. Chest 1989. Mutat Res 2003. Sci Total Environ 1998. Trace element reference values in tissues from inhabitants of the European Union. et al.34:620-626. Radulescu M. Kato M.28(5):1121-1128. Angerer J. J Orthop Res 2003. Blunn G. Lhotka C. Long-term clearance of inhaled 60Co.Metals effects of cobalt. Schramel P. Wild P. Ichikawa Y. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Christensen JM. Robinson C. Oksa P. Cannon SR. Fourth National Report on Human Exposure to Environmental Chemicals 211 . 2001. salt.44:124-132. Molders J. Lisi P. McCalden RW. Pradhan C. Uitti J. Occup Environ Med 1994. Arch Intern Med 1990. Sabbioni E. Heki S. Falcone G. Ghat IS. J Bone Joint Surg Br 2006. 3rd ed. et al. Biological monitoring of workers exposed to cobalt metal. Occup Environ Med 2001. and cobalt metals. et al. Vitali MT.50(9):835-842. Hoet P. oxides. Respiratory health of cobalt production workers. Ziaee H. Fujimura N. Sabbioni E. Co-sensitivity between cobalt and other transition metals. Gross RT. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Shirakawa T. Kriss JP.

adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U. Lead has a variety of uses in manufacturing: storage batteries.00-6.80) 2.95) 1.90-4.80) 1.69 (1.90) 3.90) 2.70-5.80 (1.70) 4. solders.30 (2.70 (1.60-1.60-1.30-2.20) 3.60) 2.90 (3.60) 1. 7439-92-1 General Information Elemental lead is a soft.81) 1.62-1.70) 1.90-2.80 (5.40) 1.90) 5.70 (1.90 (4.90) 1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.60-6.899-.60) 1.69 (1.60-4.55 (1.53) 1.40 (1. brass.90-2.Metals Lead CAS No.80-2.40) 3.50-2.20 (3.65 (1. Since lead has been eliminated from gasoline.60) 4.60 (2.00) 3. 01-02.78 (1.50) 1. plastics.90 (3.S.40-1.36) 1.00 (4.00) 4.70) 4.40 (2.30 (1.20) 90th 3.70) 1.23 (1.20 (1.80 (1.40-1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70 (3.04-1.00-1.10-3.80) 2.20 (3.40-6.40-2.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2. malleable.56 (1.50-6.60 (1.00) 1.90-6.30) 1.50) 2.50) 75th 2.51 (1.60) 3.20) 3.60) 5. antique-molded or cast ornaments. leaded glass.10-3.39) 1.43 (1.60 (2.70 (1.80-4.80) 1. such as lead phosphate and tetraethyl lead.40) Total 1.00) .60-1.20 (4. 212 Fourth National Report on Human Exposure to Environmental Chemicals .30-2.20) 4.20) 5.50) 1.10-8.20-1.71-1.72) Selected percentiles ( 95% confidence interval) 50th 1.00-4.80 (4.62) 1.50 (4.60-3.00) 1.10-3.60-2.50-5.60 (1.40-6. Elemental lead can be combined with other elements to form inorganic and organic compounds.800-1.10-2.10-6.50 (1.40) 2.40-1.20) 3.50) 5. and for radiation shielding.70-2.30 (4.70) 3.50-3.70-2.80 (4. dense.60) 2.30-1.80-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20 (1.12-1.43) 1.40-2.60 (1. the main source of lead exposure for the general U.00) 1.75) 1.40) 2.40-3.90 (2.00 (5.60 (1.60) 4.90) 1.900-1. blue-gray metal that occurs naturally in soils and rocks.10) 3.90 (3.90) 2.22 (1.10-6.30) 5.55-1.30 (2.40-4.50) 1.10 (1.50) 1.10) 4.60 (1.40 (3.80 (1.52 (1.S.20-3. Before the 1980’s.37-1.00) 4.50-2.10-2.70) 3.20-2.96-2.70) 3.40) 5.60) 3.90) 2.80-3.3.10) 3.30-5.87) 1.20) .40 (1.30-2.60) 1.90) 3.20 (2.20 (1.60) 2.30) 2.50 (1.10 (4.80) 2.20 (3.90 (3.60 (2.40 (1.20-3.30 (2.10-1.60 (3.91) 1.25 (1.60 (2.90-3.70-2.75-1.43 (1.900 (.70-6.10 (2.52-1.00) 1.30-1.70-1.70 (1.70-1.80 (2.90) 2.49-1.986) .50 (2.52-1.50-2.80 (2.60-4.10) 2.90-4.60) 3.77 (1.55-1.00 (6.90-4.40) 1.75 (1.10) 1.51) 1.50-4.40-1.40-3.20 (1.37 (1.30 (4. population was aerosolized lead emitted from combustion engines that used leaded gasoline.93-2. ceramic glazes.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) 2.83 (1.60) 1.20 (2.28.00) 3.20 (3.68-1.50-1.10) 1.50-1.50 (2.14-1.80) 1.30 (1.946 (. metal alloys (e.942 (.09) 1.00 (2.46 (1. Lead is most often mined from ores or recycled from scrap metal or batteries.69) 1.00-4. lead was added to gasoline and residential paints and used in soldering the seams of food cans.80-3.80) 1.20-2.80) 1.25) 1.40) 2.60) 4. bronze).10-2.10 (2.43) 1.25 (1.30 (1.20) 1.00) 5.00) 6.50-1.48) 1.00) 1.900 (.90) 2.40-2.50 (3.20-3.31) 1.40) 2.50) 3.80 (3.20 (3.70) 4.10-4.00 (4.70-1.40-3.60) 2.00-1.66 (1.00-2.70 (2.50-1.30-1.40-1.70-4.50 (1.70) 1.69) 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 2.30-6.80) 2.60) 1.50-5.30 (2.20) 3.50) 4.50 (3.17) .01 (1.50) 4.20-4.878-1.10-4.20 (3.40) 4.14-1.60) 3.30) 2.30) 2.60 (4.10) 5.80 (1. respectively.45 (1.80 (1.30 (2.70 (5.30 (2.00) 2.10 (3.70 (2.50 (4.50) 2.60 (3.20 (3.02) 1.10 (1. ammunition.62 (1.60) 2.10-1.36-1.30-2.30-1.80 (5.80-4.3.20 (1.20) 4.80-3.50) 7.30-4.32-1.90 (2. and 0.32-1.00) 2.10-1.10-3.14-1.60-1.40 (1.45-1.37 (1.60 (2.60-2.70) 4.75-2.10-2.50-1.60 (1.10-2.40 (2.34-1.50-4.20) 2.10) 3.86) 1.36-1.30-1.70 (3.60) 5.00 (1.90-4.00-4.00-5.50-3.50 (1.90-2.19 (1.10) 1.50) 5.70) 1. Lead was used in plumbing for centuries and may still be present.87 (1.39-1.70-3.43-1. 0.30) 95th 5.90) 1.80-5.10) 2.70) 1.00) 2.50 (2.70) 2.30 (3.90-2.90 (1.40) 1.70 (2.60 (1.00 (3.89) 1.30 (1.60 (2.00 (1.90 (3.60) 4.20-1.66) 1.80-4.50-2.60 (3.30 (2. interval) 1.40-5.60 (3. and 03-04 are 0.20-6.40 (5.80 (1.50 (2.90 (1. population from the National Health and Nutrition Examination Survey.40 (4.80 (2.40-1.30-1.10-2.30 (4.10 (2.50 (2.g.10 (1. In the past.80) 3. see Data Analysis section) for Survey years 99-00.20-3.

22) 1.700 (.00 (1.600-.82 (2.589-. and contact with soil.70 (2.70) 2.900-1.900 (.900) .50 (1.70 (2. or after soluble lead compounds are ingested.40-1.560-.40) 2.64) 2.21 (2.00-2.90) 2.50) 1.60-3.00) .10) 1. respectively.955-1.Metals occupational (e.04 (.50 (2.680-.90 (2.970-1.660) .986) .50-2.52 (1. older plumbing systems with leaded pipes or lead soldered connections.40-3.800 (.20-1. CDC.40) 3.625 (.89) 2. population from the National Health and Nutrition Examination Survey.616) .20-1.52-1.41) 2.637-.628) 1.20 (1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.04) .20 (1.20 (1.40) 1.20 (2.80) 2.30 (1.773) .766 (.690) 75th 1.27) 1.90) 2.80) 3.20 (2.700-.60 (1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .833-1.40) 2.920 (. battery and radiator manufacturing) and recreational sources.50) 2.613) .30) 1.40) 1.90 (1.815 (.30) 1.580-.90-2.80) 1.10 (.50-3.931) .800) . Lead is absorbed into the body after fine lead particulates or fumes are inhaled.00) .650) 1.1.800 (.572-.40) 1.674) 1.50) 1.40 (2.60 (1.50-1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.00) .900) .915-1.920 (.600) .20-1.33.701) .10) 2. stained glass framing.960-1.60 (1.625-.700) 1.700 (.600-.04-2.73 (1.558 (.850 (.700-.535-.20) .553-.30 (3.40-1.72) 1.800-1.900-1.75) 3. In the blood.86-2. interval) .31-3.10-3.03 (1.10-1.900-1.70) 3.40 (2.800 (.659 (.745-.80 (2.70-3.70 (2.910-.80) 2.540 (.900) .90) 2. or water contaminated by mining or smelting operations.06) .700 (.900 (.10 (.17 (1.671-.78-2.710-1. 2000).10-1.40 (1.40 (2.800-1.677 (.14-1.00-1.10 (.695 (.800-.00 (2.90 (2.833 (.738) . Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.00-1.90-3.30) . imported children’s trinkets and toys.97) 4.708-.564 (.700 (.990) 2.785) .62) Total .59-2.S.718) .02) 1.680) .941) .60 (1.78-2.10-1.23-4.30 (2.35 (.80) 2.30-1. 2007.800) .80) 2.610 (.40) 1.27 (1.90-2.990) 1.700) .02 (.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.11 (1.700-.50 (1.12) 90th 2.90-2. and 03-04 are 0.848 (.20) .700 (.50 (2.30-1.00) .80) 1.90 (2.800 (.40-2.80) 1.30) 2.700-.30) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.30) 1.900 (.59) 1.960-1.62-4.600-.31 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60-3.32 (1.86) 95th 2.10 (1.30) 1.820-1.605) .900) .20) 1.691-.900-1.30-1.10-1.642 (.808 (.556-.730 (.641-.90-3.82 (1.86 (1.10) .590 (.11) 2.600 (.640 (.23) .10-3.60-2.66 (2.00-2. Approximately half of the absorbed lead may be incorporated into bone.00) 2.30) 1.604 (.540-.10-5.40-1.33 (2.66 (2.90) 1. lead-containing folk remedies and cosmetics.810-1. see Data Analysis section) for Survey years 99-00.800-.661-.700-.800) .630 (.10-3.00) 1.49 (1.80) 2.818) .10 (1.18-1.940 (.10-1.749) .70-2. pewter utensils and drinking vessels.13) .700 (.800) .600-.80 (1. 0.00-1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.620 (.00) 2.790 (.757-.700-1.03-2.80-3.50) 1.900) . lead-based painted surfaces undergoing renovation or demolition.573 (.90 (1.14 (1.30-5.857) .29 (2.40-1.10 (1.40 (1.680-.636 (.80 (1.78-2.753 (.600 (.40 (1.20 (1.822-1.10 (1.923 (.20 (3.20 (2.44-2. and 0.600) .752 (.570-.33-2.70 (2.52-1.480-.620) 1.70 (1.506-.80-2.20-2.80) 3.60-2.579-. lead-contaminated dust in indoor firing ranges.960 (.07 (.70) 1.07-1.86) 1.60-1.60 (2.29) 2.00 (.00 (1.651) .10) .900) .20 (1.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.20) .828) Selected percentiles ( 95% confidence interval) 50th .729-.04) 2.80-2.20 (1.g.90-2.00-2.70) 1..30) 2.40-5.40 (2.40) 1.00 (1.20) 1.00 (1.50) 3.30-1. 01-02.40 (1.20) .600-.800) .935) 1.90 (1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.13-3..840 (.10) 2.70) 3.640-.795 (.20) 1.90-4.1.60) 2.04 (.30-2. dust.50 (2.50-2. 1991).24-1.50-2.579-.40 (1.40) 2.688 (.862) .50) 2.20-2.526-. However.500-.91) 2.30) 2. bullet fragments retained in human tissue.30-3.75) 4.731 (.70) 1.14 (1.591 (.19 (1.710-.40) 2. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.09) 1.595-. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR. Fourth National Report on Human Exposure to Environmental Chemicals 213 .

670) 1.971 (.992-1.668-.914 (.79) 1.86 (1.28) 2. For instance.00 (1.914-1.588-.739) .50 (1.11 (.23 (1.65-2.47 (1.677 (. Lead can cross the placenta and enter the developing fetal brain. 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.608-. CDC.710) .46 (1.61) 1.698) .460-.52 (1.11) 1.09) 1.914 (.79 (1.586-.02-1.97 (1.88 (1.05 (1.673) .15-2.810 (.79) 2.593 (.19) 1.66) 2. zinc.428) .17 (.38 (2.71-2.607-. 2003.Metals 90% of the body lead burden in most adults.876-1.408-.S.29 (1.612-.853-1.07-1.83 (2.579-.22) 1.588-.03 (1.64) 95th 2.75-2.851) . abdominal pain.44 (1.828-1.58) 1.97) 1.83) 1. The skeleton acts as a storage depot.621 (. with a half-life of years to decades.742) .700-.82) 1.56) 3.00) . and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.62) 2.838) .43) 1.18 (1.03) 2. through the inhibition of certain enzymes.667-.712 (.35) 2.988-1.623 (.64) 2.605-.00 (1.681-.667-.529-.43-1.00 (1.492-.03) 2. hair.78-4.03) .734) .603-.41 (1.61) 1..73-2.03) 1.55 (1.03 (.926 (. scant amounts are lost through sweat.46 (2.679-.50-1.635 (.404 (.990 (.569 (.977) 1.702) .05 (.38 (2.657) 1..63) 1.594-.25-1.04-3. Large amounts of lead in the body can cause anemia.583-. In 1991.31 (1.22-1. BLLs and associated toxic effects differ in children and adults.43) 2. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.74 (1. population from the National Health and Nutrition Examination Survey.633 (.400) .03) 1.0) 3. 1995.606-.75 (2.18) .89-5.940 (.15-3.72-2.383-.40-1. 1993).632 (.50) 1.49 (1.01 (.48 (1.862-.28-1.742) Selected percentiles ( 95% confidence interval) 50th .841-1.41-1.25-1.662) 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 1.77) 2.96 (1.828) .45 (1. and through binding to ion channels and regulatory proteins. The toxic effects of lead result from its interference with the physiologic actions of calcium.03) 90th 1.997-1.667) .87) 1.26) 2.47 (2.882-1.404-.617-.22-2.623 (.693 (.39-1.09-1.50-2.587-.615 (.55 (1.56-2.15) 1.375 (.10) 1.97) 1.774 (.17-1. and iron.50-2. Nash et al.535) .27 (1.938 (.72) .592-.88) 1.63) 4. seizures.08-2.43 (2.644) .88-2. with lesser amounts eliminated via the feces.918 (.98-2.43 (1.66 (1. interval) .11 (1.963-1.85 (1.41) .655-.10 (.37-1.638 (. 1993.65 (1.15) 1.975-1.917-1.746) .639 (.20) .676) .22) 1.78 (2.615 (.701 (.887 (.31) 1.24 (1.92) 2.28) .696 (.731-.98) 2.342-.04) 2.609 (.69 (1.64 (1.601-.654) .33-1.496 (.61) 3. Schwartz.755 (.08) .644 (.559-.05-1.85) 1.510-.720 (.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 .44) 1.603-.957-1.625 (.03-2.26) Total .681-.11-1.571-.551-. based on prospective population studies.18) 2.404 (.10 (1.15-2.725) .88) 2.763) . and paralysis.781-1.37-1.20) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.59-3.22) .56-3.979 (.730) 1.962 (.06) .14 (1. Staessen et al.51) 1.677-.31 (1.992-1.758) .981-1.05-1.89-2.52) 1.50-2.44 (1.604-.508) .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 .02) 1.652 (.85-2.88) 2.594-.722 (.00 (.679) 1.94-2.61) 1.18) 1.622 (.720 (.718) 1.702-.708 (.682) .683-.11) .38 (2. Approximately 70% of lead excretion occurs via the urine.920-1.33) 1. kidney injury.608 (.933) .988 (.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 . Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.08) .19-5.571-.33 (1.71 (1.765) .31) 1.603 (.53) 1.98 (1.06 (1.718) .03 (.645-.722 (.698) .645-.725) .36-2.938-1.09-1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.639 (.432 (. O’Flaherty.62-2.793-1.53-1.702) .709 (.97-18.677) .64-2.659-.68 (1. 2004.790) .870 (.946-1.03 (.94 (1.649 (.658 (.61) 1..707 (.812-1. encephalopathy.898) .11 (. 2007).33) 2.03) .671 (.67-4.933-1.893) .07) .56 (1.796-1.47) 1.62-1. 1991.85-2.688) .31 (2.14) 1.641 (.07 (.18) 1.800-.461) .51 (1.900 (.380-.561-.20-3.34-1. 1996).918-1.09-1.436) .541-.753) .686) .01) .70 (1. 1995).639 (.703) .639) .469 (. and nails (Leggett.721 (.62-3.648 (.12-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.618 (.655) .06 (.66 (1.73) 2.72-2.06) 1.11 (1.655) 75th 1.701) .

adults in the 1999-2000 NHANES sample. premature delivery.S. 2003. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. Korrick et al. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Pirkle et al.S. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Staessen et al.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. 2002). Information about external exposure (i. Urine levels may reflect recently absorbed lead. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 2009). both the geometric mean (1. 1999). 2006). lead in women may be associated with hypertension during pregnancy. 1991. 1999). Telisman et al..e.7 µg/dL and 4. Both drinking water and ambient air standards for lead have been established by the U.4% of children had BLLs of 10µg/dL or higher (CDC.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. At low environmental exposures.. Schwartz et al... 2005a).000 adults. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. In occupationally exposed adults.. 2007). However.atsdr.Metals µg/dL or higher as the level of concern in children.gov/toxpro2.2 µg/dL in males and 3. the prevalence rate has declined annually since 1994 (CDC. respectively. 2005b. 1994). 2003. the geometric mean BLL was 3. High dose occupational lead exposure..9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2001).. which is an 84% decline. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. More recently.. and peripheral neuropathy generally occurring at much higher levels (e.. Overall.cdc. 1996. residing in housing built before the 1950’s. 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. Lanphear et al... In NHANES 1999-2002 in children 1-5 years old. Data submitted through state public health programs from 2006 showed that 1.S.. urban residence. and organic lead compounds not classifiable with respect to human carcinogenicity. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. and spontaneous abortion (Baghurst et al. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. 1987.S. Borja-Aburto et al. particularly in the skeleton.S. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. 1996. Muntner et al.cdc. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.. approximately 11. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. 2002.xls). The Adult Blood Lead Epidemiology and Surveillance program has tracked BLLs reported by states for mostly for occupational but also for non-occupational exposure in U. 2003.3 million children tested had BLLs of 10 mg/dL or higher (http://www. 2003). 1995. CDC. Fourth National Report on Human Exposure to Environmental Chemicals 215 . Bellinger 2005. almost double the geometric mean of 1. and low family income (CDC. 2002a). 2005b). environmental levels) and health effects is available from ATSDR at: http://www.5 per 100.g. For example.. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. usually with BLLs greater than 40 mg/dL. 2000)..21% of approximately 3. BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist. Surveillance data reported by U. when the geometric mean BLL was 2. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.. Jones et al. 1984. adult residents... Schwartz.. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. may alter sperm morphology.75 µg/dL in U. higher than 100-200 µg/dL). and decrease fertility (Alexander et al. 2006).6% in NHANES 1988-1991 to 1. The U.4% in NHANES 1999-2004. reduce sperm count..html. Payton et al. seizures.S. IARC considers inorganic lead compounds probable human carcinogens..0 µg/dL in females (Soldin et al.07 µg/dL (Becker et al. 1996. 1998). 2000). 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. with overt encephalopathy. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. including minority race or ethnicity...6%) were lower than those from NHANES 1991-1994. adults in the 19992000 NHANES sample (Apostoli et al. EPA.

Baj A. Auinger P. References Agency for Toxic Substances and Disease Registry (ATSDR). et al. gov/mmwr/preview/mmwrhtml/mm5420a5.115:521-529. Angle CR. Occup Environ Med 1996. Available at URL: http://www. Hunter DJ. Am J Public Health 1999. 2003-2004. Cory-Slechta DA. Environ Res 2000. Aro A.cdc. 4/14/09 Centers for Disease Control and Prevention (CDC). Ganzi A. Third National Report on Human Exposure to Environmental Chemicals. Acquisition and retention of lead by young children. Bavazzano P. Kim R. Toxicological profile for lead. 4/14/09 Alexander BH. 1988-2004. Reese YR. 2005b. Brody DJ. Jones RL. Becker K. Hänninen H. Adult blood lead epidemiology and surveillance—United States. Centers for Disease Control and Prevention (CDC). MMWR Morb Mortal Wkly Rep 2005a. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Hu H. Managing Elevated Blood Lead Levels Among Young Children. McMichael AJ.htm.123:e376-e385.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.275:1177-1181.348:15171526. JAMA 1996. et al. Checkoway H.htm. Mantere P. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Jacobson JL. Coresh J. Payton M. Lepom P. Available at URL: http://www. Speizer FE. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Hernberg S. Henderson CR. Seiwert M. Neri A. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.53:411-416. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lead.55(32):876-879. van Netten C. 4/14/09 Centers for Disease Control and Prevention (CDC). Public Health Rep 2000. Atlanta (GA). The relationship of bone and blood lead to hypertension. Sparrow D. N Engl J Med 2003. 4/14/09 Centers for Disease Control and Prevention (CDC). Borja-Aburto VH. Sci Total Environ 2002. Blanco J.gov/toxprofiles/tp13. Blood lead levels—United States. Canfield RL. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Neurodevelopmental effects of postnatal lead exposure at very low levels.html. Cox C. Hu H. Homa DM.26:359-371. Krause C. Pediatrics 2009.82:60-80. Jusko TA. Available at URL: http://www. Wigg NR. Neurotoxicol 1987. Robertson EF. Muller CH. CDC.275(15):1171-1176. Atlanta (GA). Hu H. Blood lead reference values: the results of an Italian polycentric study. Cox C.atsdr.gov/nceh/lead/ CaseManagement/caseManage_main. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. IARC Monogr Eval Carcinog Risks Hum 2006.87:1-471. Birth Defects Research (Part A).89:330-335. Lanphear BP.cdc. Bellinger D. Korrick SA. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . doi:10. Available from URL: http://www. Aug 2007 [online]. Rios C. Meyer PA.113(4):1016-1022. Semen quality of men employed at a lead smelter. Rotnitzky A. Kaus S. Ronchi L.htm. JAMA 1996. Environ Health Perspect 1993.htm. Manton WI. Lead and hypertension in a sample of middle-aged women. et al. 1999-2002. Rojas LM. Jacobson SW. Inorganic and Organic Lead Compounds.cdc. Bellinger D.cdc. Caldwell KL. Am J Epidemiol 1999.287:1-11. Chiodo LM. Kuehnemann TJ.205:297-308. Rotnitzky A.gov/nceh/lead/publications/ books/plpyc/contents. Vupputyuri S. Teratogen update: lead and pregnancy. MMWR Morb Mortal Wkly Rep 2006. Vimpani FB.cdc. Stanek KL. Age-specific kinetic model of lead metal in humans. Ewers TG.1542/peds:2007-3608. Available at URL: http://www. Int J Hyg Environ Health 2002. Weiss ST. Lanphear BP. Sparrow D.gov/mmwr/preview/mmwrhtml/ mm5532a2. et al. et al. Hertz-Picciotto I. Pirkle JL. Intellectual impairment in children with blood lead concentrations below 10 µg/dL.54(20):513-516. Kaufman JD. Roberts RR. Wager C. Batuman V. Preventing Lead Poisoning in Young Children.10:43-50. Atlanta. Dietrich K. Apostoli P. Baghurst PA. Scand J Work Environ Health 1984. Korrick S.101(7):598-616. Pediatrics 2004. Ga. Schulz C. 2002 [online]. 4/14/09 Centers for Disease Control and Prevention (CDC). Weiss ST. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study.73:409-420.150(6):590-597. Luukkonen R. 1991 [online]. Neurotoxicol Teratol 2004. Farias P. Blood lead levels measured prospectively and risk of spontaneous abortion. 2005. Leggett RW.8(3):395-401. Muntner P.

Low-level lead exposure and blood pressure. Staessen JA. Kaufmann R. Sparrow D. Soldin OP. and tibia lead with neurobehavioral test scores in South Korean lead workers. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Blood lead. and copper in men. J Hum Hypertens 1995. stable lead isotopes to determine release of lead from the skeleton. cadmium. Sherwin R.289(12):1523-1531. Payton M. Kinetics of lead disposition in humans. Exposure of the U. Roels H. Nash D. 50:31-37. Cvitkovic P.63:1044-1050. Clin Chim Acta 2003. Int J Hyg Environ Health 2006. Arch Environ Health 1995. et al. Jurasovic J. Lustberg M. Lee GS. dimercaptosuccinic acidchelatable lead.209:301305. Schwenk M.327:109-113. Gavella M. Blood lead concentrations in children: new ranges. Kidney Int 2003. Brody DJ. Environ Health Perspect 1996.104(1):60-66. Stewar WF.140:821-829. Pizent A. Hickman T. Magder L. O’Flaherty EJ. Low-level lead exposure and renal function in the Normative Aging Study.118:16-29. Soldin SJ. Kaufmann RB. Fourth National Report on Human Exposure to Environmental Chemicals 217 . blood pressure. Osterloh JD. Am J Epidemiol 2001. Schwartz J. Paschal DC. blood pressure and cardiovascular disease in men.Metals results from NHANES III. Lee BK. Lauwerys RR.S. and hypertension in perimenopausal and postmenopausal women. Toxicol Appl Pharmacol 1993. Flegal AR. Environ Health Perspect 1998. Revised and new reference values for arsenic. lead. Physiologically based models for bone-seeking elements. Pirkle JL. Use of endogenous. Telisman S. population to lead: 1991-1994. cadmium.9:303-327. Rocic B. Hanak B.153(5):453464. Wilhelm M. Hu H. Lead. Lee SS. Environ Health Perspect 2000. Rubin R. Schwartz BS. Smith DR. Am J Epidemiol 1994. Schulz D. Weiss ST. Amery A. Association of blood lead.106:745-750. zinc. Gunter EW. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. IV. JAMA 2003. et al.108(1):45-53. Hwang KY.

50) 5.800-1.60-3.20-4..90) 95th 4.2.30) 5. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.900) 1. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.90) 90th 3.50) 2.70) 911 856 2081 4525 03-04 03-04 ..900) 75th 1.714-. merbromin). Kingman et al.00 (.30-6.40 (4.672) . population from the National Health and Nutrition Examination Survey.700-.50-3. electrical lamps. and mercury compounds are still used as preservatives (e.689-. Elemental mercury is a shiny. thermostats and switches).285-. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.50) 4.80 (1.484) .60) 2085 2293 3478 Limit of detection (LOD.00) 1. Accidental spills of elemental mercury.563 (. Atmospheric elemental mercury can be deposited on land and water.900) .814 (.776 (. The ingestion of methyl mercury.60 (1. Some cosmetic skin creams from countries other than the U.20-3.300-.574) .418-. Woods et al.60) 1.300 (.00 (. 2002).90 (1. have often required public health intervention (Zeitz et al.40-1. 218 Fourth National Report on Human Exposure to Environmental Chemicals .472-.903) Selected percentiles ( 95% confidence interval) 50th .S.10-3..860-1.800-1.700-.753-1..g.500-. or oxygen. 1994.326 (.80 (3. Apart from methyl mercury.20-4.40 (3.00 (2. 2007). Also.900 (.30) 1.40-1.60-6. mercuric chloride). elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. Survey years 03-04 Geometric mean (95% conf.80) 4.797 (.800 (. IARC.781 (.12) .30) 3.90) 3.700-. see Data Analysis section) for Survey year 03-04 is 0.10) .00) 4. which create an episodic potential for volatization and inhalation of mercury vapor.800 (.490 (.Metals Mercury CAS No. Poorly absorbed from the gastrointestinal tract. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.500 (.800-1..00 (.40 (4.927) . Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.703-.00 (2.70 (3. sphygmomanometers and barometers.40-2.700) .S. phenylmercuric acetate) or topical antiseptics (e.300) .30-4.30-2. The kinetics of the different forms of mercury vary considerably.60-2.60-5. inorganic.400-.600 (.00 (.02) .. and is distributed to most tissues.20 (2.90-3. In addition.50) 1.80 (1.00-1. After elemental mercury is absorbed.800 (.363-. predominantly from fish and other seafood. and mining and smelting. Other major uses include electrical equipment (e. may contain inorganic mercury.30 (1. 1999 .877 (.30-5. and dental amalgam.400 (.g.30 (2. 1993).700 (. to form inorganic mercury compounds or salts. synthetic organomercury compounds were once used in pharmaceutical applications.80 (1. with the highest concentrations occurring in the kidneys (Barregard et al.80) 3.40) 1.655-..70 (1.419 (.40-3.00 (1.40) 3.70 (4.70-2.800-1.60) 1. which can bioaccumulate in aquatic and terrestrial food chains.50-2.700-. elemental mercury is absorbed mainly by inhaling volatilized vapor.60 (2.50-1.00 (2.g. 1980.800 (.00-5. 1998.40 (3.886) .80) 1.372) . Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).30) 4132 4241 03-04 03-04 03-04 .900) 1. interval) .900) 1.60 (1.400-.700) .90 (4.20) 2.600) 1.500 (. constitutes the main source of dietary mercury exposure in the general population.979 (.30) 3.919) .60-6.70 (1. thermometers. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach..00) 3.700-. such as chlorine (e.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 .800-1.30) 1. solid-waste incineration.500) .00) . and organic forms.. Hursh et al.90 (1. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. an organic form of mercury.g. sulfur. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).00) 1.500-.40-2. thimerosal.

50) 95th 2. 1969. Excretion occurs by renal and fecal routes.697-.300 (.90) 90th 1.944 (.30-6.10 (.800) .S.00-2.90 (3. 2003). and a useful marker of exposure in epidemiologic studies (Grandjean et al.200-.900 (.70-5.919) .726-1.20 (..600) .20) 1.317 (.01) . Vimy et al.70-6.60) 1. Jonsson et al.20) .369) 1.06-1. 1992).73) 1.00) 7. Smith and Farris. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.70) 1. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.500-.667 (.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 .30-2.30-6.30-6.200-.300) .60 (3.06 (.800-1.300) .70-3. 1973).500 (.00-6. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.407) .50) 1.70-3.00 (2.10 (.824) 1.10 (3. Vahter et al.299-. 1999-2002..700 (..800 (.800-1.377) .374) .297-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.300 (.30-4.395) .200-.40 (1.700-1.60 (1..343 (.70 (1.80-3.200 (.10 (5..02 (.20-2.500-. Methyl mercury is incorporated into growing hair.700 (.20-3. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al. 1984. with most elimination occurring through in the feces (Sherlock et al.. 1994) and then undergoes slow dealkylation to inorganic mercury.800) 1.800 (.700-.00 (2.664-1.Metals the tissues to mercurous and mercuric inorganic forms.90 (4.80 (1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.00-1.90) 5.541-.00-2.50-2.00) 6.900 (. National Health and Nutrition Examination Survey.700-.833 (. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.. 2004.30-5. population.300) .256-. 1991.318 (.900-1.7) 4. interval) Selected percentiles (95% confidence interval) 50th .90 (1.265-. Suzuki et al.90 (4.80) 1.30) 3.800) .35 (1. McDowell et al.200-.30-11. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.700 (.10-3.871-1.00 (1.329 (. 1994).800 (. 1998).300) .. Methyl mercury enters the brain and other tissues (Vahter et al.00) 4.20 (2.900 (. 1975.825-1.0) 4. 1999).90) 2.. a measure of accumulated dose (Cernichiari et al..700) 2..300) . Myers et al.50 (1.. Miettinen et al.307 (. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .60 (3.40) 5.60 (1.10 (1.300 (.200 (.60) 1.. 2003). 1998).80) 579 527 370 436 588 806 Limit of detection (LOD.30 (. Fourth National Report on Human Exposure to Environmental Chemicals 219 .269-.27) . The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.3) 4.820 (.475) . 1992. 1996)..10 (1.800) 1.300 (.40-1.00) 2.00 (2.10-1..500 (.400-.60) 2. 1992 and 1999.80 (3.300) . Sandborgh-Englund et al. 2005). Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith... 1993).200-. thereafter.940) Race/ethnicity (females.90 (1.800) 75th . 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.50) 3.14 and 0.900-1.30) 1. After exposure to elemental mercury. for both acute and chronic exposures.00-3.50) 1.70-5..90) 2.00) 1.30) 1.30-4.70 (1.50-12.500-.00 (3.40-2. 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.500-. 1995.600 (.500-. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. 1994.10) ..14.20) ..20-11.10) 1.200-.500-1.700-1.70) 4. Geometric mean Survey years (95% conf.70) 4.29) .40) 1.23) .70 (1. 1993).377 (.40 (1.50) 2.60 (2.700 (.30-3.50 (2.. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al. 1971)..20-3.600) .50-3.800-1.30 (1.30 (1.60 (1.40-2.20-3.00) 1.40) 2. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.10) .60) 3.10 (1.00) .90) 3. 1996.30 (1. Smith et al.268-.738-.00-2. 1990).

Smith et al. 2002. 1970. 1983). Survey Geometric mean (95% conf. the existence of a causal relation is unresolved (Chan and Egeland. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.600-.600) .600 (.600) . Overt poisoning from methyl mercury primarily affects the central nervous system.600 (. Inorganic mercury exposure usually occurs by ingestion.800) .. ataxia. 2005).700 (.. 1998. Stern 2005. anorexia. 1987).600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Metals may be more efficient for inorganic mercury (Grandjean et al. gingivitis..600-. 2000..800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . dysarthria. Oskarsson et al. Sakamoto et al.500 (<LOD-. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease..700) 2007 2240 3406 Limit of detection (LOD. 220 Fourth National Report on Human Exposure to Environmental Chemicals . limb deformities.500-. see Data Analysis section) for Survey year 03-04 is 0.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .S. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. and neurocognitive and behavioral disturbances. 2004. maculopapular rash. 1951.800) . short-term memory loss.500-. particularly irritability. population from the National Health and Nutrition Examination Survey.600) . 2000..700 (.700 (.500-. 1995.. interval) Selected percentiles ( 95% confidence interval) Sample 95th . altered physical growth. 2004).700 (. < LOD means less than the limit of detection. hypertension.500-.700-.600) .500-. Salonen et al. 1993).42. DeRouen et al. Rissanen et al. Acute.700-. irritability. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600-. which may vary for some chemicals by year and by individual sample. Bellinger et al.700 (.600 (. Rice. 2006.600) . Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.500 (.600-. sensory impairments. 2005.600 (. high-dose exposure to elemental mercury vapor may cause severe pneumonitis..600 (. Sakamoto et al. 2003). Smith et al.500-.600) . the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis...600 (. 2006..500 (<LOD-. typically after a latent period of weeks to months. and progressive constriction of the visual fields. fatigue.600 (. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and sleep disturbance (Bidstrup et al.600) .500 (...600) . Once absorbed. insomnia.700 (.700-. lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC.500-. 2004). In recent epidemiologic studies...700) . 1996). depression. Factor-Litvak et al.500-.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 . At levels below those that cause acute lung injury. Vupputuri et al. 1995. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. overt signs and symptoms of chronic inhalation may include tremor. and pinkish discoloration of the hands and feet (Tunnessen et al. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 1963). and cerebral palsy (NRC.. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.600 (. The constellation of findings may include anorexia.500-. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. cerebellar ataxia.500) . dysarthria. Drexler and Schaller. causing parasthesias.. pain in the extremities.600) . 2000).. 2004. hearing impairment.

400 (.05) 1.313-.14. Over the NHANES 1999-2006 survey periods.97) 2. et al.12 (.07 (. population from the National Health and Nutrition Examination Survey. However.52) 2.. particularly methyl mercury. 2002)..440 (. These distinctions can help interpret mercury blood levels in people.549) . and increased slightly in non-Hispanic white children (Caldwell.58 µg/L for 4645 adults. 1998).870-1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.S.890 (. 2003).76-3. who participated in a 1998 representative population survey (Becker et al.530) .93 (1.700 (.00 (.S. total blood mercury increased with age. 1998).358 (.520) .160-.16 (1.555) .433 (.492) Selected percentiles ( 95% confidence interval) 50th .54 (2. Grandjean et al.66) 3.46 µg/L for children.33 (2.463) .870-1.330-.60) 619 713 1066 Limit of detection (LOD.447 (.476 (. Survey years 03-04 Geometric mean (95% conf.420 (.78 µg/L for adults and 0.441 (.460 (.31) 1266 1272 03-04 03-04 03-04 .S. 2009).96 (1. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC.39-3.. Kingman et al. 2006). Mahaffey et al. During the same survey periods.13-2.88-3.77-2.cdc.. In NHANES 19992002.480) 75th 1.509) .30) 3.416 (.280-.410-.570) .610-1.19 (2. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.530) .42) 95th 3.8 years.78-2.24 (2.28) 1.304) .250) . Sanzo et al. interval) .63-2.55) 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 ..840-1.200 (.05) 3.08 (1..34-3. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.396-. average age 9. Among the three racial/ethnic groups.90) 2.442-. Benes et al.340-.29) 1.430 (. EPA at: http://www.406-.09 (2. aged 18 to 69 years.700-1.atsdr. adult women in several ethnic subgroups (Hightower et al. slightly higher total blood mercury levels were found in U.370) .Metals standard for inorganic mercury has been established by U. From 1996 through 1998.. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.67-2.88) 287 722 1529 03-04 03-04 .940 (. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.213-.89) 3.420 (.88 (1.18) 2.85-2. In Germany the geometric mean for blood mercury was 0.413-..330-.00) 1. 2000).9 years).408) . Schober et al. Information about external exposure (i. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.480 (.840) 1.. the total blood mercury concentration is due mostly to the dietary intake of organic forms.01 (.580) . see Data Analysis section) for Survey year 03-04 is 0. Fourth National Report on Human Exposure to Environmental Chemicals 221 . Biomonitoring Information In the general population. 2004..20 (1.14-2. and the age-related changes differed across the groups (Caldwell et al.495 (.S.19 (1.99-6.840-1.16 (.. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.290-.gov/toxprofiles.gov/mercury and from ATSDR at: http:// www.460) .23) 2.76-4.03-4.. 2001.530-.60-2.405-. average age 33 years.S. 2001.960 (. 2003). Total blood mercury levels increase with greater fish consumption (Dewailly et al. range 40 years to 78 years) had an average total blood mercury concentration of 2. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.930-1. 1995.55 µg/L. the median concentration of blood mercury was 0..534) .08 (1.46) 3.330-.e.350-. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.509) .382-.360-.96 (1. 758 children.31) 2.330 (.360-.23) . EPA.430 (.254 (.61) 1. military veterans (mean age 52.26 (1.14) 90th 2.360 (. 1997.epa.24) 1.60 (1. A cohort of 1127 U..65) 1.67-3.68 (2.76-3. total blood mercury geometric mean levels in females aged 16-49 years did not change. environmental levels) and health effects is available from the U.430) . 2009).770-1.

2006.498) 75th .41-2. et al.S.13 (1.51-2..11) 2.391-..365 (.40 (1.508 (. DeRouen et al.88-2.86) 95th 2. An expert-panel report recently prepared for the U.630) .12-3.67 (1.417) .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 .289) .455-.32-2.969-1.16) 1.391) . representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. not to imply a safety level for general population exposure.486) Selected percentiles ( 95% confidence interval) 50th .00) 90th 1.. 1998). Urine mercury and the number of dental amalgams were correlated.785-1.00) 286 722 1529 03-04 03-04 .S. a biomarker of perturbation in renal tubular function.455-. 1992).455) .217 (.61) 1.06 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.01) 2.362 (. 1988.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals . 2005).964-1.56) 1266 1271 03-04 03-04 03-04 .78-4. interval) ..88 (1. mean urinary mercury was 3.463 (.566) .246-.545 (.464 (. military veterans with dental amalgams. Survey years 03-04 Geometric mean (95% conf.784) 1.696 (.S.77 (2.06 (..667-1.196-.376-.67 (1.714-1.64-2.30) 2.S.275) .588) .31 (1.443 (.88-2.11-2.54 (2. Levels in U. 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.276 (.63) 1.265-. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. et al.07) 1.46-2.990) . 2006).21) 1.447-. 2003).365 (.S.62 (1.28 (.76 (1.347) .. 2002) adult population surveys were similar to those in a U. women of childbearing age have generally been much lower than these levels (CDC.480) . 2009).652) .616) .09) 1.309-.343 (. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.385-.307-.39) 1.970 (..358) . Langworth et al. and on average.392-..400-.333-. the urine mercury increased by approximately 0. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13-2.599) .1 µg/L for each surface with a dental amalgam (Kingman et al.11) 1.306 (.532 (. Urinary mercury levels in recent German (Becker et al. and Italian (Apostoli et al.447 (.225-.368) .. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.208-. 2002).404-.1 µg/L.472-.255 (.384 (.18-1.79) 1.537) .40-1.297 (.32 (1.525 (.03) 2.909 (.87) 2.35 (1.400) .620-.65 (1.522-.619-.280-. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.30) 1.800-1..87 (1. reversible increase in urinary N-acetyl-glucosaminidase.535) 1. Department of Health and Human Services noted that several studies have observed a modest.25 (.587 (.687) .768 (. In the study of U. population from the National Health and Nutrition Examination Survey.476 (.875-1.00 (. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. 2009).44) 1.04-3.23-2.79 (1.301-.485 (. Czech (Benes et al. Information about the biological exposure indices is provided here for comparison.Metals 2000). 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.

14-1.699) 1.00 (3.45) 95th 3.966) .55-3.565 (.24) 6.65) 1.774) .502-.831) .706 (.65-4.97) 2.664) .97) 2.475-.772 (.520-.622-.92) 2.47) 1.606 (.610-.665) .639 (.37) 1.41 (2. Geometric mean Survey years (95% conf.79) 3.00) 2.56) 4.45-2.27 (1.99-2.98 (5.95 (2.833) .832-1.99 (3. 16-49 years) 99-00 01-02 .48 (2. 1999-2002.15-1.99 (2. National Health and Nutrition Examination Survey.14) 3.54) 595 531 381 442 594 826 Limit of detection (LOD. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.569-.520-.596 (.624-. 16-49 years) 99-00 01-02 .50 (2.32 (1.91 (2.76 (1.09-1.32-3.44) 3.03 (.850-1.81-6.27-1.22 (.32) 2.670) 75th 1.799) .14 and 0. National Health and Nutrition Examination Survey.910) .Metals Urinary Mercury−Females Aged 16-49 Years Old.15 (2.31 (1.744) 1.05 (3.77) 1.631-.97) 2.846) .615 (.52) 3.686) .87-4.501-.03 (.68 (3.420-.500-.18) 3.710 (.909-1.724 (.410-.42) 90th 2.740 (.03-2.691) .51 (3.17) 95th 5.580 (.831) .92) 3.04-1.10-2.43-1.742-1.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .89 (2.57-4.721 (.35 (1.657 (.14.94) 1. 1999-2002.23-1.39-3.824) .790) .03) 1.620 (. interval) Selected percentiles (95% confidence interval) Survey years 50th .81 (3.656-.553-.00 (2.508-.28 (1.21 (1.579-.46-4.870) .16) 5.387-.92) 4.600 (.14-2. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.25) 2. Geometric mean (95% conf. 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.21-3.540-.809) .930) .450-.68) 3.605-.650 (.45) 2.85) 4.62 (1.41 (1.13-4.24-1.582-.516 (.76) 2.45) 2.45 (1.46 (1.62 (3.35) .99) 1.46) 3.30 (2. interval) Selected percentiles (95% confidence interval) 50th .38) 4.45-3.84 (2.21 (2.30-2.31-1.53-3.685 (.30 (1.37 (1.3) 5.05 (2.07-5.56) 3.62 (4.55) 90th 3.650) 1.760 (.61-6. population.637) .51) .18 (3.426-.655 (.710 (.S.06 (.22-3.70 (2.650 (.560-.69 (1.61) 1.560 (.892) .59-5.723 (.709) 75th 1.41-6.41 (1.522 (.578-.580-.719 (.10-4.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .83-3.76-5.42-3.04-10. population.557-.709) .30 (2.56 (1.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.592 (.50-4.69-3.09-1.50 (1.42) 2.540 (.47) 1.79) 1.616-.07-2.658 (.84 (2.72) 1.85-3.91-7.710) 1.16-5.97 (1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.07) 1.27 (2.636-.806) .810) .23-1.68-3.77) 2.632 (.526-.13 (2.S.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .

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40:413-419. Blood mercury levels in US children and women of childbearing age. Environ Health Perspect 2003. JAMA 2003. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Vorwald AJ. The hair-organ relationship in mercury concentration in contemporary Japanese. Stern AH. Sherlock J. Whittle K. Shen DD. Kaye WE. et al. Lorscheider FL. Smith JC. Tunnessen WW.124:221-229. McMahon KJ. Environ Res 2005. Environ Health Perspect 2007. Effects of exposure to mercury in the manufacture of chlorine. Burbacher T. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Lind B. Sinks TH. Schober SE. DeRouen TA. Suzuki T. Smith JC. Effects of occupational exposure to elemental mercury on short term memory. Takahashi Y. Hislop D. Farris FF. Goldberg J. Smith PJ. The kinetics of intravenously administered methyl mercury in man. Bolger PM. Zeitz P.128(2):25125-25126. Mooney TF. The contribution of dental amalgam to urinary mercury excretion in children. Methyl mercury pharmacokinetics in man: a reevaluation. Patil LS. Newton G. et al. Vahter M. Yoshinaga J.289(13):1667-1674. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Baser M. Hum Toxicol 1984. Aguinagalde FX. Am Ind Hyg Assoc J 1970. Smith AE. Martin MD. Woods JS. Dorronsoro M. Jones RL.79:786789. Vupputuri S. Leitao JG. 1993-1998.37:245-252. Allen PV. Fisher HL. Daniels JL. Longnecker MP. Nakazawa M. Pediatrics 1987. Toxicol Appl Pharmacol 1994. Br J Ind Med 1983. Toxicol Appl Pharmacol 1996. Langolf GD. Arch Environ Health 1993. Acrodynia: exposure to mercury from fluorescent light bulbs.110:129-132. Vimy MJ. Hall LL.4(5):981-988. Sandler DP. Bernardo MF. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Osterloh J. Orr MF. Am J Physiol 1990.111(12):1465-1470. 1999-2000.258(4 Pt 2):R939-945.2:117-131. McDowell M. Environ Health Perspect 2002. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Guo S. Amiano P. Environ Res 2005. Matsuo N. Turner MD. Hongo T. Leroux BG. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.97(2):195-200. Stern AH. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Smith RG.31:687-700.Metals Sanzo JM. Most B. Imai H.48(4):221229. Azpiri MA. Mottet NK. Toxicol Appl Pharmacol 1994. Amurrio A.98(1):133-142. Friberg L. Public Health Nutr 2001.115(10):1527-1531. Topping G. et al.

hydrogenation catalysts.1-59.9-55.2) 41.2 (63.7) 78.0) 60.0) 97. At a daily oral molybdenum dose of 24 µg.8) 46.5.4 (48.5-65.8.1-63. Compounds of molybdenum are also used as corrosion inhibitors.6-46.7) 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 78.2 (49.5 (67.9 (34.0) 84.5-41.6 (40.0 (43.8) 75.1) 57.4 (34.4) 42.4 (79.2 (55.1-52. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.8-94.5 (41. and paints.1 (38.1) 46.5-91.6-82.6) Selected percentiles ( 95% confidence interval) 50th 50.7) 45.1 (34.7-91. inks.5) 80.9-85.8-46.8 (42.1-51. aldehyde dehydrogenase.7) 77.8 (85.2) 37. and 03-04 are 0. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.7 (71.2 (38. see Data Analysis section) for survey years 99-00.3 (64.0-62.6 (43.0 (42.7-96.4-61.4-75.3) 47.9 (44.5-46.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-70.7 (37.3 (46. In humans. lubricants.3) 83.1 (71.7) 75th 84.0-38.5-124) 108 (92.1) 82.2 (56.3 (38.9 (37. 01-02.7) 51.0-56. 0.6-62.4 (80.3) 54.7-50.0) 39.1) 59.9) 34.5 (74.8-108) 87.6-72.3) 41.7) 78. and in pigments for ceramics.1-52.0 (42.4) 49.4) 52.5 (49. population from the National Health and Nutrition Examination survey.3 (73.3) 37.6) 93. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.6) 53.1-55.2 (69.7 (58.3-108) 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 47.9 (40.3-47.7-39.5 (48.3-91.0) 55.1-88.6) 71.9-82.6 (73.2 (49.2-37. semiconductor and battery industries have begun to use molybdenum.7) 46.7-105) 69.2) 79.6) 51. Fourth National Report on Human Exposure to Environmental Chemicals 227 . interval) 45.2-91.4 (72.3 (53.8-90.5-52.0 (41.5 (43.9 (33.Metals Molybdenum or ore deposits.2) 53.8) 40.3) 85. 1997).0-65.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.7-68.3) 65.6 (55.0-85.2-59.9 (32.7 (45.5-68.7-47.8 (82.5 (41.2-79.7-92.7-41.4-52.6-96.4) 76.6-111) 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 52.2) 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 (98.0-101) 82.0-71.8) 48.2-42.7 (51. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.6 (40.9 (73.7-60.4-82.6 (52.4) 56.1) 60.7) 86.9-109) 97.7-51.4) 41.9 (52.5 (37.3-44.5) 47.6) 71.5 (81.7 (36.3 (47.7-73.0 (81.6-58.0-77.3 (55.2-59.7-84.2) 48.2) 40. 2001).0) 54.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.1 (91.6-42. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.3 (71.5) 80.3 (37.9-55. 1996). 7439-98-7 General Information Elemental molybdenum is a silver-white.5) 44.5-52.0) 62. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9 (78.1) 126 (106-147) 109 (94.1-44. respectively.0 (76.8) 44.5-66. chemical reagents in hospital laboratories.5) 60. and xanthine oxidase (Kisker et al.7 (73.3-115) 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.6 (55.3 (84. WHO.5) 85.7-122) 93.7 (50.0 (48.8-49.9) 67. More recently. urinary excretion over six days CAS No.7 (44.S. which exert homeostatic regulation over molybdenum balance.7) 57.0-110) 90.0 (46.6-55.9-83.2 (83.1) 35.2) 52.4 (48.8.. Excretion occurs predominantly via the kidneys.0) 45.2-53.2 (40. 2001.9-56.8 (67.1-48.3-75.0-100) 63. and 1.8) 39.0-53.4) 45.3 (55.8-106) 88.3 (79.9) 62. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.2 (61.

5 (37.6) Selected percentiles ( 95% confidence interval) 50th 41.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.1-40.1) 37.5-44.0-56.2-65.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.5) 72.8-52.3-141) 109 (81.5 (38.7-120) 87.1) 37.1) 101 (83.9 (73.6 (36.2-96.5-50.2-40.5-45.4 (59.4) 44.9-71.4 (55.0-103) 103 (90.8) 45.9-117) 57.3) 64.8-46.8) 79.8-118) 81.8) 38.6 (38.0-41.6-41.8) 71.1 (38.6-63.5 (34.2 (40.1 (38.0 (80.1) 65.6-88.1 (44.3 (71.9 (36.4) 48.9-61.3) 43.6-63.4 (37.5 (50.1-112) 78.2-49.6) 39.4 (44.2 (57.7) 112 (95.1) 43.2-46.2-121) 107 (92.9 (39. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0. 1999).3) 44.4-76. population from the National Health and Nutrition Examination survey. 1961. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.5-70.3 (58.3 (55.1-109) 89.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .5 (40.5-119) 90. Based on studies finding adverse reproductive effects in rats and mice.9) 31.9) 92.4-42.3) 61. urinary excretion over six days rose to 50% and 67%.6-78.9 (40.7-38.5-99.1-39.5) 73. Molybdenum is generally considered to be of low human toxicity.7-44.7-62.9-40.5 (39.9) 44.1-100) 86.3-45.4-39.0) 38. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.7-137) 129 (109-155) 112 (97.2 (33. In industry.5 (41.2-80.5 (40.1-45.9 (64.2 (37.7-100) 77.7) 53.2) 43.2) 39.9 mg/kg/day and established a tolerable upper intake level of 0.1 (49.4-66.8 (90.1 (30.7 (75.5 (79.5 (65.4) 122 (107-133) 109 (99.2 (52.0-46.5 (35.9-118) 91.0 (74.5 (80.3-44.3-59. interval) 43.2 (73.3) 56.9 (49.6) 43.6 (57.0-38.5) 90th 108 (97.8 (56.5-97.3-115) 98.2-47. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0) 44. respectively..0) 88.8-65. 2001).6-61.Metals was 18% of the ingested dose.9) 79. and clinical or epidemiologic evidence of adverse effects is limited.6-61. U.7 (66.3 (37.0) 39.7-93.1 (82.7) 62.8) 37.2 (69.3) 41.2) 37.4) 77.2 (40.1-41.7) 75th 63.4) 89.8-47.0-46.6) 48.0) 33.9-42.1-67.3 (36.2) 42.1 (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 40.9-96. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4 (78.4-185) 106 (94.2) 42.. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.2-41.2 (50.S.5-48.6-76.9-45.5-69.S.6 (71.9-87.2-103) 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 42.0) 53.8-84.4-107) 85.8 (57.1) 40.3 (36.1 (37.6 (59.5 (59.7-52. 1995).3) 57.5-60.3-43.7 (77.5 (83.2) 39. of the ingested dose (Turnlund et al.4) 60.9-41.4-41.3 (53.5) 63.0 (35.6-45.7) 57.1-39.1) 56.5-62.8) 62.1-43.8-67.5 (54.9-68.0) 62. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.3 (51.8-42. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.8-66.4) 40.5 (35.4 (67.03 mg/kg/day in humans (IOM.3 (83.3-68.5 (36.5 (41.3) 40.4) 61.2 (40.2 (43.7-43.4-120) 101 (84.8 (75. 1993).3 (71.5 (78.6) 39.9 (79. at daily oral doses of 95 µg and 428 µg.0) 72.3-46.3) 37.8 (36. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. but available epidemiologic data are scant.7-40.9) 40.1 (39.4) 47.4 (56.1 (40.1-79.0) 39.0 (58.8) 39.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.1-127) 90.5 (37. 1997).5-35.7) 41.6) 36.5-46.9) 41.4) 58.9-45.2) 37.1 (33.9 (39.3 (37.8) 61.4 (53.0-120) 85.1-81.2-96.7 (30.5 (65.8) 38.3-56.9 (35.5) 71.0) 36.4) 116 (101-126) 104 (88.5) 60. EPA.2 (36.2) 38.1 (54.2) 58.8 (37.5-92. Biomonitoring Information Molybdenum is an essential element for health.9 (64..7) 42.4 (40.6 (42.8-47.1-43.5 (39.1-38.1-34.7) 45.7) 115 (93.2) 55. and urinary levels reflect intake from all sources.3-52.4-106) 85.6 (36.0-133) 119 (88.

copper. Shmavonyan DM. Atlanta (GA). Molybdenum 1993 [online]. Keyes WR. Geneva: WHO. Menne C. Gatti A. 56:322-327. Peiffer GL. 1996. Rapid Comm Mass Spectrom 2002. Van Meerbeeck JP. silicon. Christensen JM. 4/14/09 Iversen BS. Third National Report on Human Exposure to Environmental Chemicals.gov/iris/ subst/0425. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Rees DC. iodine. Koval’skiy GA. Kisker C. edu/openbook. Washington. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. chromium. Sabbioni E. Dietary reference intakes for vitamin A. iron. Vermeire PA. 2005. nickel. National Toxicology Program (NTP). 16:1313-1319. Ann Rev Biochem 1997. Occup Environ Med 1999. Minoia et al. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Yarovaya GA.nih. EPA). Ronchi A. molybdenum. Aprea C. Droste JHJ. Sci Total Environ 1998. Food and Nutrition Board.htm. Turnlund JR.66:233-267. 1998). Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. pp. van Sprundel MP.123(1):81-85.nap.S.epa. U.22(3):179-191. 2005). boron. Trace element reference values in tissues from inhabitants of the European Union. Sciarra G. (DC): National Academy Press. Institute of Medicine (IOM). Available at URL: http://www. 2002. Molybdenum-cofactorcontaining enzymes: structure and mechanism. A study of 13 elements in blood and urine of a United Kingdom population. White and Sabbioni. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Minoia C. Molybdenum. Weyler JJ. White MA.. Available at URL: http://books. 144-154. Molybdenum absorption. Am J Clin Nutr 1995. pp. Kristiansen J. manganese.. Zhurnal Obshchey Biologii 1961. vitamin K.216:253-270.62(4):790-796. Inductively coupled plasma mass spectrometric determination of molybdenum in urine.15(2-3):149-154. arsenic.niehs. World Health Organization (WHO).gov/index. Analyst 1998. Fourth National Report on Human Exposure to Environmental Chemicals 229 . vanadium.Metals in urine for the U. Schaub J. 4/14/09 White MA. References Centers for Disease Control and Prevention (CDC). 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. X. 4/14/09 Sievers E. 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. Schindelin H. Turci R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Available at URL: http://ntp..php?record_id=10026&page=420. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. and zinc: a report of the Panel on Micronutrients. Schleyerbach U. J Trace Elem Med Biol 2001. 2001. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. 1998. Environmental Protection Agency (U. In: Trace elements in human nutrition and health. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. excretion. 420-441. Molybdenum in infancy: methodical investigation of urinary excretion. Occupational risk factors of lung cancer: a hospital based case-control study. TR-462.S. et al. Sabbioni E. 2001). Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect.

jewelry. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. Important properties of platinum are resistance to corrosion. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. carboplatin) in the treatment of cancer. 1998). and 03-04 are 0.07. as oxidation catalysts in chemical manufacturing. which may vary for some chemicals by year and by individual sample.Metals Platinum CAS No. respectively. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. 230 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Platinum compounds are used in electrodes.S. thick-film circuits printed on ceramic substrates. however.04. strength at high temperatures. dental alloys. see Data Analysis section) for Survey years 99-00. and as drugs (e. and iron.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. and 0. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. copper.. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. 01-02. and high catalytic activity. 7440-06-4 General Information Platinum is a silver-gray. 0. cisplatin. < LOD means less than the limit of detection. 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.04. population from the National Health and Nutrition Examination Survey.

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

New York: John Wiley & Sons. Available at URL: http://www. Begerow J. 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. Seiwert M. palladium. 2004) or less than 0. 1991 [online]. 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. Hall L. Kazantzis G. 1998). Several studies have shown that background concentrations in general populations were usually less than 0. 2000. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. J Expo Anal Environ Epidemiol 2003. Crocker W. References Becker K. 1999. Patty’s Toxicology. 206:15-24.. Br J Pharmacol 1969. pp.04 µg/L) in this Report. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.htm..13(1):24-30. et al.123(3):451-454. Jankofsky M. Kuster W. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. 2004. Pethran A.005 µg/L (Iavicoli et al. Biomonitoring Information Urinary platinum levels reflect recent exposure. Herr CE. 2003.. Hysell D. Rommelt H. Pethran et al. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Nowak D.htm. Hysell D. Parrot JL. Int Arch Occup Environ Health 1997. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Petrucci F. Gromiec JP. Wilhelm et al. 2003). 1998). In: Bingham E. 2001). Boos KS. Czerczak S.55(2):138-140. Pethran A. Int Arch Occup Environ Health 2003. Powell CH. Schulz C. Analyst 1998.4(1):27-36. Hebert R. Arch Environ Health:1969. Urinary platinum levels associated with dental gold alloys. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Fries HG. Schierl R. Part 1: monitoring of urinary concentrations.01 µg/L (Becker et al.207(1):69-73. Iavicoli I. et al. Duneman L:Long-term urinary platinum. Biomarkers 1999. and platinum. Schierl. Turfeld M. Nickel. Ruff F: Platinum and platinosis.. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Herr et al. 5th ed.70(3):205-208. Wilhelm M. Carelli G..S. et al. Neuendorf J. Influences on human internal exposure to environmental platinum.10:63-71. Kulka U.Metals the International Programme on Chemical Safety at http:// www. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.56(3):283-286. Seifert B. Ewers U. Grimm CH. Schierl R. 2003.inchem.19:685-691. eds. Alimonti A. Saindelle A. Herr et al.org/documents/ehc/ehc/ ehc125. Huber R. Angerer J. 3/31/08 Moore W Jr.. osmium.35:313-321. rhodium. Moore W Jr. Uptake of antineoplastic agents in pharmacy and hospital personnel. Biomonitoring of traffic police officers exposed to airborne platinum. ruthenium.9:152-158. Farago ME. et al. 1997. van de Weyer C. 232 Fourth National Report on Human Exposure to Environmental Chemicals .org/documents/ehc/ehc/ehc125.61(7):636-9. Ruff F: Histamine release by sodium cholorplatinate. Occup Environ Med 2004. International Programme on Chemical Safety (IPCS).76(1):5-10. Kavanagh P.. 289-380. Bocca B. 2004). Levels of platinum in urine for the U.. Gieler U.. which elevate urinary platinum by five to twelve-fold (Begerow et al. Schierl R. Arch Environ Health 2001. Saindelle A. 2003. Int J Hyg Environ Health 2004. Raab W. Blanks R. Hauff K. and gold excretion of patients after insertion of noble-metal dental alloys. Cohrssen B.inchem. Thornton I. Stilianakis NI. Fruhmann G. Environ Health Perspect 1975b. Kaus S. Allergy and histamine release due to some platinum salts. Schierl R. Occup Environ Med 1998. Ensslin AS. palladium. Environmental Health Criteria 125. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kelly J.. and in blood and urine in the United Kingdom. International Journal of Hygiene and Environmental Health 2003. Campbell K. Environ Res 1975a. Senofonte O. Platinum. Schulz C.. Platinum concentrations in urban road dust and soil. Schierl et al. 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. Urinary excretion of platinum from platinum-industry workers.

370 (.190 (.430 (.218) .270-.440) .154-.171 (.430-.200-.520) .184 (.410) .160-.380 (.180-.170-.420) .390-.260-.200 (.320 (.420-.201 (.590) .440) .290) . thallium was obtained as a by-product of smelting other metals.290 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.590) .150-.200) .370 (.300 (.400 (.02.410-.340) . interval) .290 (.173-.162-.640) .430) .330-.220) .280) .170 (.220 (.520 (.420-.240) .330-.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 .410-.280) .250-.490 (.260-. In the past.172 (.200) .330-.230-.370 (.360 (.280 (.177) .145-.300 (.190 (.420 (.280 (.156) .300) .430-.170-.400) .220) .420) .250-.135-.370 (.170-.206) .320) .350-.230) .280 (.200 (.380-.200) .410 (.340-.430 (.510) . In the United States.340-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.440) .180 (.370 (.340-.360-.310 (.191 (.170 (.172 (.420) .160 (.330-.220) .182-.450 (.220 (.180-.270 (.196) .172) .145 (.240-.350-.390) .140-.300-.460-.350-.300) .160-.390) .183) . population from the National Health and Nutrition Examination Survey.420) .560) .260 (.165 (.350-.270) .320-.490) .149 (.200 (. Thallium disappears from the blood with a half-life of several days.410 (.400-.210-.160 (.240) . In addition.360-.410 (.150-.160 (.330) .290-.500) . 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.400 (. and 03-04 are 0.420) .155 (.218) .370) .360-. Human health effects from thallium at low environmental CAS No.470) .160 (.220 (.200 (.230) .290 (.201 (.220) .220-.156-.380) .197-.202) .239) .450) .270 (.170-.430 (.220 (.480) .200 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.390 (.202 (.159 (.210 (.270 (.400 (.200) .360 (.230) .170-.300 (.290-. the latter being the current major industrial consumer of thallium in this country.370 (.230-.190 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.460) .350) .250 (.179-.400) .400) .440 (.400 (.390-.183) .02.240-.210 (.188) .170) .470 (.450 (. however.260-.170) .420-.510 (.400-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.160-.330) .190 (.270 (.370-.450 (.330) .360-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.220) .200 (.250 (.400-.390 (.180 (.480) .217) .410-.360 (.500) .157-.370 (.160-.185-.280) .450 (.340) .520) .200) .170-.150-.410 (.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 .240-.400) .197 (.290) 90th .153-.480) .180) 75th .430 (.150-.250-.180-.440 (.190 (.250) .690) .410 (.310-.550 (.260-.360) .190-.330-.163) .150-.310) .290 (.185 (.420) .200-. 01-02.156) .170) .148-.300) .440-.250-.170-.260) .310 (.450 (.410-. thallium readily crosses the placenta and also distributes into breast milk.390-.470 (.360 (.440 (.202 (.370-.173) .196) .350-..490) .410-.160-.192) Selected percentiles ( 95% confidence interval) 50th .02.230) .360-. see Data Analysis section) for Survey years 99-00.250-.147-.210) .340-.200-. and 0.178) .159 (.370-.500 (.410 (.470) .243) .173) .137-.450 (.440 (.240) .S.450 (.350) .200-.350-. 2005).230-.500) .180-.217 (.460 (.400) 95th .260-.330) .390-. From these and other sources.220 (.145-.400-.480) .250-.290) .320) .215) .230 (.160 (.225) .350 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.167-.200) .144 (.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 .380-.490) .400 (.133-.176 (.450 (.420) .390) .147-.159 (.250-.134-.330-.270) .400-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .310 (.430-.180 (.300) .150-.167-.280-.147-.Metals Thallium depilatory cosmetics. it has not been specifically mined or refined in the United States since 1984.520) .290) .167 (.340 (. respectively.450 (.170 (.260 (.420-.330-.630) .370) .220) .350 (. 0.370-.187-.280-.410-.270-.430) .380 (.158) .270-.270 (.290 (.320) .490) Total .290 (.250-.470) .290) .146 (.390) .175) .181-. representing distribution into other tissues.180) .260 (.190 (.480) .

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

Celier D. Boisson P. Minoia et al. There was no increase in the prevalence of symptoms at levels less than 20 μg/L and only a slight increase in nonspecific symptoms greater than 20 μg/L..html. Ewers U. Third National Report on Human Exposure to Environmental Chemicals. White MA. 7/15/09 Blanchardon E.95:89-105. with concentrations ranging up to 76. 1992 [online]. Sabbioni E. Sampson EJ. Sabbioni E. 1998. Valentin H. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Schaller KH.. 2005. Available at URL: http://www. Sci Total Environ 1998. Toxicological profile for thallium. 2005) and are shown with results from NHANES 2003-2004 in this Report. Dolger R. et al. Schmidt M. 1981. 1980. Kramer U. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Wiegand H.cdc. Trace element reference values in tissues from inhabitants of the European Union.35(1):4-9. Minoia C. White and Sabbioni. Soddemann H. A study of 13 elements in blood and urine of a United Kingdom population. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. et al. X. Investigations of thallium-exposed workers in cement factories. Gallorini M.. Schaller et al. 1990. A study of 46 elements in urine. et al.atsdr. Ting BG. Morrow JC.47(3):223-231. Int Arch Occup Environ Health 1981. References Agency for Toxic Substances and Disease Registry (ATSDR).216:253-270. Pietra R. 2005. Marcus RL. Manke G.1 mg/m3 (Marcus. Pozzoli L. Investigation of a working population exposed to thallium. (1981) studied 1.113(1):47-53. J Soc Occup Med 1985.gov/toxprofiles/tp54. Apostoli P. Paschal et al. Buhlmeyer G. Cassot G. Paschal DC. Trace metals in urine of United States residents: reference range concentrations. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Radiat Prot Dosim..5 μg/L. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Brockhaus A. Brockhaus et al. Centers for Disease Control and Prevention. blood. Sci Total Environ 1990. and serum of Italian subjects. Raithel HJ. 1998). Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust.S. 1985). 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Jackson RJ.76(1):53-59.48(4):375-389. Pirkle JL.Metals (CDC. Trace element reference values in tissues from inhabitants of the European community I. Int Arch Occup Environ Health 1980. Challeton-de Vathaire C. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Martin J-C.265 people living near a thallium-emitting cement plant in Germany. Atlanta (GA). Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Environ Res 1998.

and as catalysts in the petroleum industry.084) .250) .050-.090-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).53) .510-1.430-.380 (.140-.080-.190-.460 (.330-.060 (.070-.630) .050-. interval) .390) .140 (.320-.330) .300 (.076 (.160 (.620 (.530 (.220) .Metals Tungsten CAS No.064-.170) .093 (.080 (.180-.620) .400-.130-.120-.450 (.113 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.830) .130-.400 (.210 (.290) .370-.260) .113 (.056-.260-.180) .122) .790) .080) . filaments for incandescent lamps.450-. Little information is available on the toxicity of tungsten.300-.160) .470) .086 (.460 (.290) .082-.560) .100) .130) .180 (.110 (.380-.180) .081 (.080 (.400 (.104) .170 (.088) .060-.420-.107 (. Evidence is lacking for the carcinogenicity of tungsten.120-.123-. respectively.350-1.073 (.080) 75th .068) .080 (.100) .500 (.430 (.130-.370-.120-.260 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.190-.110) .380-.400 (.109) .360) .110-.200 (.170 (.470) .120) .360 (.140-.056-.062 (.330) .135) .200-.360 (.300) .270-.04.180) .120 (.110 (.160 (.220) .490 (.090-.077-.170) .230-.069) .082 (.090-.290-.250-.340-.580) .810) .310-. Tungsten compounds are used as lubricating agents.090) .180) .080) .250-.490) .160 (.090 (.360-.093-.074-.096-.097-.260-.210-.084 (. and 03-04 are 0.310 (.090) .160 (.130) .380-.310) .310-.300) 95th .290-.087-.470 (.091) .110 (.120) .116) .220) .570 (.240 (.270-.770 (.380 (.096 (.550 (.070-.190 (.210 (.500) .111-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.113 (. bronzes in pigments.390 (. and 0.270-. and for producing ferrotungsten.590) .140) 90th .090) .500 (.060 (.076 (.200) .070 (.560) .220 (.350) .120) .370 (.410 (.270 (.100 (.170) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.060 (.078-.100 (.250) .180-.190-.120) .070-.100-.04.133) .160-.073-.510-.090-.250) .280 (.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 .290 (.950) .120) .800) .190-.070 (.690) .100) Selected percentiles ( 95% confidence interval) 50th . which is used in the steel industry.050-.260-.065 (.370 (.080-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.530 (.190) .460 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.060-.100-.380) . 01-02.470-.560 (.088 (.170-.110 (.095-.310-.430 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.100) .330-.080 (.350 (.100 (.092 (.082) .160-.180 (.050-.04.270 (.150 (.070) .137 (.670) .060-.210) .150 (.360 (.380-.071-.150-.100) .073) .230-.520) .370) . 236 Fourth National Report on Human Exposure to Environmental Chemicals .150 (.090-.420-.065-.310-.650) .310-.160-.300 (.460) .062 (.140 (.069-.150) .070) .093) .560) .073-.060 (. Tungsten is used mainly for producing hard metals.140 (.130 (.520) .360-.070) .080 (.060-.250) .090-.060-.070 (.126) .230 (.110-. mainly as scheelite (CaWO4).110-.430-.070-.230) .071 (.230-.260 (.470 (.220-.080-.060 (.130) .210 (.090 (.120) . 0.120-. see Data Analysis section) for Survey years 99-00.240-.230) .120-.570 (.410-.090-.400) .340-.250) .158 (.058-.070-.070) .530 (.370 (.130) .090 (.105 (.095-.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 .550) .092 (.080) .060-.640 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.270 (.300 (.082 (. which are used in rock drills and metal-cutting tools.S.560) .100-.113 (.060 (.180-.340) .440) .520) . and it has not been classified with respect to its carcinogenicity by either IARC or NTP.250) .101-.510 (.084-.151) .110) .320 (.130 (.340-.160-.105) .180-.160) .330 (.620) .190 (.320 (.270-.110 (.087) .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 .350) .130) .101 (.130-.160 (.290-.320) . population from the National Health and Nutrition Examination Survey.090) .400 (.550) .066-.100) .430) .280 (.092) .800) .320-.480) Total .210 (.120-.132) .280-.230-.090-.430 (.550) .140 (.460) .350) .204) .210 (.00) .170) .100 (.

339 (.436) .333 (.075 (.340 (.065 (.055-.116 (.131-.174) .136 (.301) .439) Total .109 (.077) .364 (.484) .253-.153-.064-.124-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.217-.199 (. interval) .108) .308) .091) .145 (.126-.187) .375) .151 (.667 (.197-.089) .080-.200-.087) .119 (.462) .122-.074-.165) .278-.106 (.086-. similar to those in this Report (Schramel et al.133) 90th .216-.317 (.054-.071 (.083) . 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.094) .168 (.136-.071) .079 (.279 (.333 (.253) 95th . population (CDC. 2005).286-.154) .331-.069 (.174 (.157) .167-.085-.797) . measure urinary tungsten.056-.081) .161) .070 (.179-.071) .081 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.049-.100) .100 (.136-.079) .186 (.121-.167) .169 (.064-.412 (.059-.359 (.634 (.279 (.086) .358) .179-.078) .459) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.079) .107-.360 (.085 (.054-.083 (.085) .198) .117 (.053-.347 (.065) .181 (.299 (.061-.379 (.146) .072-.265 (.190) .105 (..465) .453) .154) .152-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.091) .084 (.092) .386) .075) .326) .080-.063 (.077) .057-.082) .086) .086) .130-.090-.116-.203-.410-.283) .108-.354-.095-.083 (.139-.069 (.208-.073 (.058-.111 (.057-.300-.188-.100) .074) .070 (.497 (.109-.214-.237-.218 (.091 (.099-.482 (.150-.133) .144-.333-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.554) .287) .184 (.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 .125) .087 (.078) .133) .074) 75th .072-.211 (.170-.237) .069-.739) .089 (.164 (.279 (.167-.095) Selected percentiles ( 95% confidence interval) 50th .067-.090-.158) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.066 (.272-.143-.315-.333 (.216 (.116) .138 (.088) .300 (.308) .062 (.120) .431) .067 (.S.385 (.231 (.066 (.439 (.240-.136-.074-.059 (.300) .059-.431) .(Kraus et al.139) .465) .245-.071 (.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 .068 (. or exposure that a control group of non-metal workers had mean levels differences.339 (.080 (.071) .392) .198-.150-.255 (.306) .353 (.139 (.082 (.094) .484 (.201) .214) . 1998).063 (.222-.065-.317-.197) . population from the National Health and Nutrition Examination Survey.880) . Patients with medically-inserted tungsten found at increased levels in drinking water.098 (.075) .224) .329 (. Nicolaou et al.148 (.104-.098-.084) .231-.155-.082) .426) .199 (.217-.250 (.329-.302-.136-. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.250-.359 (.073 (.317) . Using neutron activation analysis to 2000.078-.426) .333-.354) .075-.301) .333) .077-.083) .103-.582) .197) .146 (.143 (.250 (.098) .294 (.067 (.333 (.079) .063-.258-.216 (.148) .215 (.122-.077-.093-.258 (.300-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.060 (.098-.079 (. and 2003-2004 (Paschal et al.605) . 2001).061-.222) .075-.436-1.056-.197 (.S.353 (.059-. (1987) found possibly due to methodologic.084 (.073 (..093) .060-.285) .255 (.667) .078 (.169) .431) .098-.063-.267) .144 (.074 (.084) .063-. 2001-2002.216-.167) .201 (.538) .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 .125 (.146 (.138) .381) .261-.075 (.091) .158 (.081-.117) .176-.088) .215) .500) .727) .452-.823) .063-.216-.255-.270 (.091 (.555 (.072 (.071-.119-.293 (.267-.344-.176-.S.150 (.081 (.071 (.065 (.158) .28) .153) .233-.083-.091) .180-.124 (.105 (.073 (.122 (.237) .078 (.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 . 1997).120) . population.130 (.341 (.253 (.439 (.414) .094-.284) .383 (.275 (.065-.200-. 2003.158) .061-.205-.301) .206-.096) .060-..079) .333) .080 (.138 (.209-.065-.121 (.302-.068-.

Weber A.htm. Schaller KH. Angerer J. Schramel P. References Bachthaler M. Nicolaou G.(2):73-77. urine.. Occup Environ Med 2001. Int Arch Occup Environ Health 1997. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Trace Elem Electrolytes Health Dis 1987. 238 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Schramel P. Paschal DC. Link J. Cassina G. Paetzel C.76(1):53-59. Sampson EJ. 2004).gov/nceh/clusters/Fallon/study. 4/15/09 Centers for Disease Control and Prevention.69(3):219-223. Pietra R. bismuth. platinum. 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. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Seghizzi P. Morrow JC. Wendler I. [online] 2003. The determination of metals (antimony.Metals blood. Atlanta (GA). Zobelein P. Sabioni E. palladium. Jackson RJ. Pirkle JL. Manke C. Feuerbach S. Angerer J. cadmium. Ting BG. National Center for Environmental Health. tellurium. mercury. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Environ Res 1998. Centers for Disease Control and Prevention.62:380-384. and hair (Bachthaler et al. Kraus T. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Lenhart M. Trace metals in urine of United States residents: reference range concentrations.cdc. Cancer Clusters. Available at URL: http://www. Catheter Cardiovasc Interv 2004.58(10):631-634. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. et al. lead. Churchill County (Fallon). Nevada Exposure Asssessment. thallium. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Mosconi G. Third National Report on Human Exposure to Environmental Chemicals.

018) .008-.073) .010 (.010) .005-.049) .035) .Metals Uranium CAS No.030 (.008) .012-.72%). human exposure occurs primarily by inhaling dust and other small particles.011) .014 (.010 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .019-.040) .046 (. 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.011-.028-.024 (.007-.009-.018 (.007-.007-.067) .007-.013-.016) .060 (.010) * .046 (.010) .009) .023) .016) .007-.005-.024-.017 (.006-.012 (.033-.030 (.006 (.008) .009 (.037) .009-.046-.009) .012 (.033) .015 (.067) .016-.008-.022-.037) .009 (.005-.007-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.012 (.010-.008 (.021) .006-.033 (.027) .007 (.009) .010) .011-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.036-.007 (.045) .013 (.008 (.054) .054) . see Data Analysis section) for Survey years 99-00.009) .018 (.006 (.021 (.042) .021 (.017-.010) * .007-.007-.007 (.009 (.009) .016-.020) .026) .037 (.008) .010) .011) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.046 (. and as an aid in electron microscopy and photography. 235U (about 0.010 (.031 (.006-.056) .027-. or processing.008 (.017) .007) .010 (.279) . nuclear fuel.012-.009) .027) .008-.008 (.011-.017 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.021 (.007 (.012) .009 (.014 (.014 (.013) .031 (.016) .036 (.020-.043) . and 03-04 are 0.020-.012) .009 (.007 (. in some ceramics.011) .006-.021-.008-.037-.042 (.011) .018) .023-.007 (.007-.028 (.008 (.051) .011) .008 (.040) . Variable concentrations of uranium occur naturally in drinking water sources.010-.023 (.050) .011-.016) .010) .010) .127) .007) .065) .013 (.088) . population from the National Health and Nutrition Examination Survey.039) .021-.114 (.008 (.009 (.009 (.053) .009-.056) .028 (.028-.013-.026 (.022-.007-.026 (.038 (.020-.023-. including nuclear weapons.007 (.009-.007-.004.039) .029-.012-.006 (.006-.025-.027) .009 (.015 (.007-.008 (.008 (.050) .023-.007 (.007 (.036) .027 (.038) .031-.033 (.026-.024-.006-.008) .013) 90th .026 (.008 (.054-.009-.008 (.011-.007-.012-.015-.040 (.020-.008-.017-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.039-.031 (.008-.009 (. respectively.008-.027 (. 01-02.022) .011 (.013 (. Since the 1990’s.018) .011-.013 (.029 (.013 (.063) .022 (.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 . milling. and 234U.009) .037) .018-.006-.007-.008-. In workplaces that involve uranium mining. Thus.023) .040-.009) Selected percentiles ( 95% confidence interval) 50th .006-.030) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.011 (.069) .008 (.017-.027) .012 (.004.029-.008 (.027-.024-.027 (.007-.010-.007-.026) 95th .052 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).006-.021) .012-.016) .011) .013 (.009-.055 (.036 (.062) .031 (.009) .007) .009) * .066) .013 (.032 (.005-.034) .014 (.008 (.045) .040-.012 (.019 (.158) .023) .012-.007-.009) . Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.026-.034-.009) .012) .027-.017) .015) .011-.037) Total .006 (.007-.020-.027 (.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 . and 0.009-.026) .009) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.010-.030 (.044 (.072) .047 (.020) .010) .009) .016-.015 (.005-.008 (.019-.048) .014 (.009-.010-.015) .053 (.035) .021) .018) .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 . 0.020 (.007 (.043 (.017-.017) .011) .010 (.009) .012) .041 (.007) .010) .046) .017) .035-.017) .013-.009-.017-.034-.010-.017-.006-.006-.006-.S.028 (.022-.016) .009 (.040 (.036-.031 (.023 (.015 (.007 (.019-.048 (.006-.012 (.005.065) .008 (.019-. interval) .036) .064 (. Uranium has many commercial uses.016 (.008) .041 (.049) .030-.009-.008 (.007) 75th .046 (.023-.023 (.007) .014 (.

034-.007 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.005 (.009) .011-.016) .056) .006-.006-. interval) .035 (.007 (.010) .007 (.025 (.018-.033 (.007-.011) * .008 (.024) .027) .051) . In cases of retained DU shrapnel.006 (.034 (.050) .011-.022 (.007) .051) .006-.015-.005 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.016-.006-. Radiation risks from exposure to natural uranium are very low.024-.021 (.016) .008-.008-.013 (.014) .010-.014 (.032) .010-.034 (. Uranium is eliminated in feces and urine.S.011-.013 (.022-.009-.006-.031 (.020 (.021 (.008 (.011) .039) . liver. 2005).010) .026) .270) .007 (.042) .015) .008 (.006 (.011) .028) .005-.008) .008) .010-.006-.007 (.019-.024 (.013 (.012 (.008 (.006-. kidneys.035 (.006-.054) .007 (.008) .042) ..006) .013) .015 (.007 (.010 (.007 (.014-.1%-6% of an ingested dose may be absorbed.024) .018) .031-.042-.033 (.007 (.008) .033 (.029 (.020-.006 (.009-.053) .017) .005 (.008 (.009 (.008) .014-.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 .021) .009) .010-.007) .008-.077) .013 (.014) .019) .008) .009) .034 (.034) .048) .010-.028-.010-. After exposure to soluble uranium salts.011 (.007-.028) .045 (.009) .026-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.007 (.016) .015) .015-.034 (.012 (.008) .004-. Health effects from uranium exposure result from chemical toxicity to the kidney.025 (.006-.025-.007 (.007 (.010) .025-. 0.008-.006) .007 (.008) .005-.006-.007 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .006 (.061) . 1992).010-.026 (.006) . 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.009) * .030 (.006-.010-.018-.010 (.013 (.012) .026 (.005-.027 (.016) .010 (.027 (.007 (.033 (.011-.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.021 (.009) . with much slower elimination from bone.080) .024-.020-.020-.027-.007 (.029 (.022) .010) .Metals impact.019 (.019-.010-.018-.051) .040 (.058) .039) .028 (.013 (.007-.019 (.008 (.014) 90th .050) .039) .013 (.015-.007-.006-.027-.009) .006-.010) .016) .030-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.006-.020) .012 (.009) .014 (.029) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.017-.006) .007-. population from the National Health and Nutrition Examination Survey.030) .039) Total .006) .030) .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 .019 (.009) .023-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.007-.017-.016-.008 (. where limited absorption occurs (less than 5%). Depending upon the specific compound and solubility.014-.017) .008) .028) .022-.007-.008) .009 (.032) .025) 95th .067) .044) .019-.016) .027 (.012 (.011 (.019-.007-.051 (.016) .018-.010 (.015-.006-. low level exposure.007-.020 (.007 (.011) .050 (.020 (.030-.006 (.022 (. After long term or repeated exposure.012-.007 (.016-.011-.004-.006-.017 (.012 (.018 (.011-.024) .006-.008-.024) .006-.026 (. 2003).006-.009 (.009) .018-.022 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.034-.027-.024 (.005-.010) * . which can occur occasionally from high occupational exposure.027) .028) .048) .009-.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 .015-.005-.024 (.063) .028 (.021 (.009-.009 (. which represents distribution and excretion.015) .013 (.022-.005-.014) .029) .025-.016) .058) .029) .030 (.005-.009) Selected percentiles ( 95% confidence interval) 50th .015 (.009-.017-.009) .010-.008 (..008) 75th .013) .074) .033) ..007-.009 (.012-.021-.012) .006-.008-.017) .013 (.007 (.009-.005 (.059 (.013 (.020-.015) .009) .024-.034 (.006-.030 (.010-.007) .025-.015 (.006-.043 (.010 (.012 (.006-.016-.047) . the shrapnel acts as a source of chronic.008) .013) .012) .007 (.015 (.006-.012 (.011-.016 (.019) .019-.011-.041) .027-.008 (. Inhaled uranium-containing particles are retained in the lungs.037 (.007 (.024) .017 (.011-.053) .100 (.010) .008 (.029) .029 (.006 (.013-. After inhalation.017-.146) .

soldiers evaluated before.atsdr. 1992. The U. In a study of 105 persons exposed to natural uranium in well water. 2003. Tolmachev et al. 28 soldiers who may have been exposed to DU by inhalation. (May et al..Metals injury associated with elevated urinary uranium levels (Kurttio et al.S. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.78:143-146.. Ejnik JW. 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. 2004). A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. although slightly increased during and after deployment. Atlanta (GA). Horan P. 2006. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. In the same study.S. 2002). NRC...S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. during. Vol.65 μg/L).html. 1-49. population. Metivier H. 2005. (Kurttio et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. 1991.. Pillai KC. Mil Med 2003.162 μg/L) (Orloff et al. and 2003-2004 (Dang et al. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. 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. and no consistent effects on multiple endpoints of kidney function were found. environmental levels) and health effects is available from ATSDR at: http://www. A cohort of 46 U. Muggenburg BA..e. had a mean urinary uranium concentration of 0. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.107:143-157.. with emphasis on quality control. Health Phys 2000..1996.. 2002. respectively. 1978).S. IARC and NTP have no ratings for uranium human carcinogenicity. Centers for Disease Control and Prevention (CDC).55 μg/L (median 0. 2004). 2000). Hamilton et al. Estimate of the time zero lung burden of depleted uranium in Persian Gulf War veterans by the 24-hour urinary excretion and exponential decay analysis.. 2006). pp.gov/ toxpro2.62:562-566. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 2001-2002. 2004). Sci Total Environ 1991.S. urinary levels of uranium were as high as 9. the median urinary uranium concentration was 2. ingestion. 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.. Six workers in a depleted uranium program showed concentrations of 0. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. McDiarmid et al. 2000). but in whom no shrapnel was embedded. Karpas et al. eds. 2006).. Fourth National Report on Human Exposure to Environmental Chemicals 241 ..011 μg/L (McDiarmid et al. Galletti. Guidebook for the treatment of accidental internal radionuclide contamination of workers. In 17 U. Komaromy-Hiller et al..61 μg/g creatinine. Dietz LA.. Uranium content of blood. or wound contamination. Byrne AR. 2004). Hamilton MM. Zimmerman I. Radiation protection dosimetry. 1994. et al. EPA. Squibb K. 41 (1). Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Stradling GN. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.S..1992. the median urinary concentration was 0. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure.168(8):600-605.. Pullat VR.078 μg/L (ranging up to 5. Volf V. 2006). Durakovic A. in that the levels were below their respective detection limits (Byrne et al. In: Gerber GB. References Bhattacharyya MH. Health Phys 1992. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Dang HS.. Benedik L. Carmichael AJ. the geometric mean urinary uranium concentration was 0. Information about external exposure (i.cdc. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. McDiarmid M.066 μg/g creatinine (Gwiazda et al. Drinking water and other environmental standards have been established by U. Thomas RG. Third National Report on Human Exposure to Environmental Chemicals. 2006). Breitenstein BD. Kent (England): Nuclear Technology Publishing. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.110 to 45 μg/L (Ejnik et al. Boyd P.

McDiarmid M. Marino R. concentration and daily excretion of uranium in urine of Japanese. July 1978. Sampson EJ. Roth P.S. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Review of elements in blood. Howerton K. Kane R.81:45-51. Washington (DC): NRC. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Uranium daily intake and urinary excretion: a preliminary study in Italy.S. Squibb K. Health Phys 2004. Noguchi H.67(8-10):697-714. Makelainen I. Scott K. Ash KO. et al. Harmionen A.71(6):879-85. Oliver M. Environ Health Perspect 2002. Charp P. May LM. Roiz J. Komaromy-Hiller G. Paretzke HG. Karpas Z. Oeh U. Nuclear Regulatory Commission (U. Jarrett JM. McDiarmid MA. D’Annibale L. Salonen L.S. Metcalf S. Shelly T. Ough EA.86:12-18. Engelhardt SM. Inductively coupled plasma mass spectrometry as a simple. Costa R. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.79(1):11-21. Kuwabara J.91(2):144-153. Van der Venne MT. et al. Ting BG. Mistry K. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Oberbroekling KJ. Salonen L. Pirkle JL. Cremisini C. Auvinen A. Bennett LG. Tolmachev S. Health Phys 2006. Hollriegl V. Radiat Environ Biophys 2005. Gucer P. patient population and literature reference intervals for urinary trace elements. et al. Heller J. Renal effects of uranium in drinking water. Cordero S. Biologic monitoring for urinary uranium in Gulf War I veterans. Hancock RG. U. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Uranium and thorium in urine of United States residents: reference range concentrations. Biokinetic modeling of uranium in man after injection and ingestion. Int Arch Occup Environ Health 2006. Orloff KG. Comparison of representative ranges based on U. NRC). Ejnik J. Smith D. Human exposure to uranium in groundwater. Health Phys 1996. Auvinen A.22–Bioassay at uranium mills.87:51-56. Health Phys 2002. Li WB. et al. Kidney toxicity of ingested uranium from drinking water. Katorza E. Gwiazda RH. U.82(4): 527-532.44:29-40. Nuclear Regulatory Commission (NRC) Guide 8. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Health Phys 2004. rapid. Hamilton EI. et al. Squibb K. et al. Wilson PD. Komulainen H.158:165-190. Am J Kidney Dis 2006. VI. Element reference values in tissues from inhabitants of the European community. Lewis BM. Halicz L. Sabbioni E.47(6):972-982. Pekkanen J.296(1-2):71-90. Wahl W.94:319-326.85:228-235. Environ Res 2004. Pinto V. McDiarmid MA. Kalinsky V. Andrews WS. Jackson RJ. Englehardt SA. Paschal DC. Lorber A.S.Metals Galletti M. J Toxicol Environ Health A 2004. Health Phys 2003. Environ Res 1999. Kurttio P. Saha H. Clin Chim Acta 2000. Kurttio P.110(4):337-342. Saha H. Sci Total Environ 1994. Marko R. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Karpas Z.

12) 3.96 (3.10 (6.0) 13. Other manufactured uses include fireworks. 2002).10 (6.0) 13. 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 (4.40 (4.00) 5.56) 3.0 (8.0-17.20 (8. leather tanning. potassium.0-20.50-4.40) 3. 2005).08-3.50-7.0) 19. and limited applications in pharmaceutics.0 (12.88) 3.10) 12.S.40) 3. 2007).70-9.68) 4.S. and electroplating.70-5.79 (2.60) 3.50-3.62 (3.0-18.40 (3.93 (4.89-3. Perchlorate is stable under most environmental and physiological conditions.90-10.11) 3.76) 4.50 (5.84) 14.70-3.07-4.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.20 (6.16) 3.0-17.49-3.31) 2.0 (13.20-4.00) 4.90-3.50) 5.18-3. 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 (8.60) 8.0) 11.20) 4.70 (3.0-23.0 (9.0 (11.40-4.10 (7.40-7.0 (9.29-3.0 (11.0-29.0) 13. and certain plants with high water content (e. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0) 10.22-5.20-3.80-4.60 (4.80 (3.40 (4.10 (2.90-3.80 (3.44-4.80) 7.60-7.50-4.70 (3.20 (4.0 (9.70-3.0) 8.0-18. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0 (11. 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.0) 14.10-12.45-4.80-12. It is normally found and produced as the anion of a sodium.0 (11.0 (10. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 10.0) 9.50-11.20) 3.20 (2.0-15.46) 3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.20 (5. fabric dyeing.19-4.70-6.10-7.51 (3.00-6.54 (3.40-11. lettuce) can be the main sources of intake for humans (FDA.40) 90th 10.60 (4.30 (5.40-5. certain catalytic metals.40 (5.30-7. Survey years 01-02 03-04 Geometric mean (95% conf.50) 6. 1998).66) 3.50) 5.30-17.02 (3.70-11.39-4.0) 10.90 (4.40 (5. milk.47-4.40) 2.81) Selected percentiles ( 95% confidence interval) 50th 3.74-3.0 (12.35 (3.03) 3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.80) 12. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.50) 11.90 (5.30-19.05 (2.90-6.0) 15.0) 11.0) 9.19 (3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.40-13.S.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.0) 15.0-17.10) 5.30 (2.0 (12.90 (5.10) 3.40) 3.20 (7.0) 11.11) 4.90-11.g.60 (7.80-8.70) 3. 2005).20 (2.90-9.80-6.40 (8. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.65) 3.10-11.0 (8.38) 5.30-6.0) 708 617 681 652 1228 1092 Limit of detection (LOD.50 (3.01 (2.50 (8.0) 9.30-7.0-17.0 (11.0 (11. but has strong oxidant properties in the presence of concentrated acids.0) 8.0 (11.0) 9.10-11.0) 95th 14.0 (9.05 and 0.09) 3.90 (3.70-7.70-12. or ammonium salt.75 (3.80) 75th 6.0-18.0) 9. and reducing agents.80 (7.0) 13.0 (8..80-4.51 (3.10) 3.0) 13.93-3.10) 5.0 (12.0-19. population from the National Health and Nutrition Examination Survey.90) 6.10 (5. In addition.00-5.87-3.00) 3..75-3. interval) 3. Drinking water.05.21 (2.00) 7. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.26 (2.60-6.00) 3.0 (11.22 (2.80 (6.30) 6.0-17.00-6.0 (9.20-11.0) 14.0 (9.10-4.40 (3.0-15.90-12.0) 9.0) 12. laboratory analysis.32 (3.70 (3. Perchlorate was added to the U.20-4.90-9.30 (2. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.93-4.67-5.40) 4.40-4.30) 6.0 (11.30 (5.0-14.0) 14.50) 3.90-11. matches.0) 16.40) 6.0 (11.20) 7.0) 13.0 (9.0 (8.80) 3.90 (5.80-15.0) 13.90 (2.Perchlorate Perchlorate (Urbansky.EPA.76 (3.40-6. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.90) 5.0-17.60) 5.81-16.20-12.0) 13.40 (5.

70 (4.0 (9. NAS.54 (3. Survey years 01-02 03-04 Geometric mean (95% conf.10-7.54 (2.05 (4.22-4.08 (3. 2000).S. Many factors may be important in consideration of perchlorate action on the thyroid: dose.60) 10. 2001.86) 4.3) 8.99 (5.S..10) 3.93-8.15-12.20 (4.46-13.51 (3. Greer et al.33-12..40 (3.20-3.0-14. dietary iodine intake.0 (11.24-2.61 (5.52 (8.83 (5.70 (2.1 (8.39 (3.0) 14.1 (11. In the U.60-11.90) 5.90-11.45-2.0 (9.70-5. Steinmaus et al.67) 5.20 (2.37-13. interval) 3.0) 4..00-11.18-3.60-8.50) 5.93-7.97-5.30-5.07 (2.80-3.84) 2.20 (6.25) 5.6) 12.44-6.93-5. 2002.50) 6.87-3.52-9..41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.26 (3..10 (1.0-19.93-5. medications).41-9.87 (5.00 (2.87 (7.60-6.30) 3.30) 75th 5.90 (7.0) 9. 2002)..00) 3.25) 5.1-16.1-22.90-9. During gestation and infancy.29) 2.76 (3.10) 13.30 (6. 2006.10 (4.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.30) 90th 9.40) 5.0) 9.80) Selected percentiles ( 95% confidence interval) 50th 3.39) 2.3) 11. in a representative sample of U.20-4.50-3.19-6. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.80 (4.70-3.g.08) 3.6) 20.96) 2.2) 8.10 (4. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.5 (13. Li et al. women with urinary levels of iodine less than 100 micrograms per day.02) 3.16-3. Lawrence et al. 2005).0 (8.0 (9.81-3.3) 12.6-17. 2007). population from the National Health and Nutrition Examination Survey.70-15.4) 13.71 (5.40 (3.98) 3.60-5.7 (11.70 (2.33-6.0) 10.0) 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 .60) 8.0 (11.1-13.0-17.40-10.99-3.59) 3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.40) 17.0-14.90 (4.53 (2.3 (10.50 (6.09) 3.10-3.4 (11.30-10.04-3.22-4.00) 9.S. 2002.0 (8.22-6.56-3.40 (7.0) 12.89-3.50) 2.20-9.73) 3.Perchlorate inhibition (RUI).80-3.87) 2. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U. Lamm and Doemland.20-10. 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. 2003.00-3.61-5.44) 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 3.40) 3. although iodine intake was higher than U.30) 5.0) 12..90 (2.00) 4.60-15.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.21 (2. chronicity of exposure.35 (2. gender.5) 8.20 (3. menopausal status.4 (11.30-5.39-4.60-3.47) 2. However.4 (10.32) 5.80 (7.36 (8.50) 9.10) 4.14 (2.0) 12.64) 5. up to 68% RUI has been demonstrated.77 (3. levels and sufficient in most participants (Tellez et al.60-11.58) 2.50 (3.60-5.93) 3.70-4.90-2.72 (3. thiocyanate.0) 12..29-6.2) 8.75) 3.74) 7.90-15. age.64-3.51-4.12 (6.0) 11.60 (3.50) 2.89 (2.0) 13.22 (2.95 (2.10) 6..90-3.0) 6.60-8.20) 8.12-2.1) 8.4 (8. and the presence of other substances known to affect thyroid function (e.1-14. 2005. 2005).30 (5.04-3. nitrate. perchlorate is negative in most genotoxic assays (U.26) 4.25 (3.70) 2.34-3.90 (2.20 (7. levels.8 (11.45) 3.0-44.4) 8.19-10.4-16.82 (5.50-5.EPA.42 (3.00 (4.20) 3.10 (6.91) 4.00 (6.09 (7.50) 95th 12. 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.20-3.80 (7. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.S.00-2.S.35) 3.61-10.03 (2.46-4..56 (3.0) 13.87) 7. 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.76-3. 1999.70) 10.46 (3.43) 6. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al. congenital hypothyroidism is a condition for which nearly all newborn blood is screened. Also.02-4. U. 2005.60) 3.24 (4.40 (4.3-14.S.35 (4.66) 3.30 (3.0 (10. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al. 2005).10 (2.90-20.25) 5.50-9.33 (7.EPA.0) 7.S.37 (4.

Thyroid 2000. Lau EC. Blount BC. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. population.fda. Lamm SH. Erratum in: J Occup Environ Med 2004. Available at URL: http://www. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Doemland M.40(21):6608-6614.. Low dose perchlorate (3 mg daily) and thyroid function. epa. Food and Drug Administration (FDA). Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Environ Health Perspect 2007. Tellez RT. Deyhle GM. Environ Health Perspect 2006. J Occup Environ Med 2003. and environmental perchlorate exposure among residents of a Southern California community. Greer SE. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.45(10):1116-1127. Skeels MR.42(2):200-205. Valentin-Blasini L. Chacon PM. J Occup Environ Med 2000. Pino S. Dyke JV. Magnani B.gov/safewater/ccl/perchlorate/perchlorate. thiocyanate. Crump KS. Braverman LE. Cross M. Rutherford GW.11(3):295.113(11):A732. Biomonitoring Information Urinary perchlorate levels reflect recent exposure..S.. 2005.S.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis.90(2):700-706. Analysis of relative source contributions to the food chain. Washington (DC): National Academy Press. Buffler PA. Neonatal thyroxine level and perchlorate in drinking water. Environ Sci Technol 2006. et al. 2007). Howd R. Environ Health Perspect 2005. Mauldin JP. Perchlorate in the United States. Lamm SH.110(9):927-937. 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.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. 6/2/09 Greer MA. Thyroid 2001. Valentin-Blasini L. Also. Osterloh JD. 2001-2002. Daaboul JJ. Gibbs JP. National Academy of Sciences (NAS). Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Environ Health Perspect 2002. Goodman G. Kelsh MA. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Pleus RC.113(8):10011008. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. The effect of perchlorate. Landingham CB. et al. Pirkle JL. National Research Council of the National Academies. Miller MD. Kirk AB. Byrd D. (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.htm. EPA reference dose (Blount et al. May 2007.114(12):1865-1871. Richman K. Jackson WA.10(8):659-663. Additional information about exposure and health effects is available from the U.46(5):509. Caldwell KL. Perchlorate Exposure of the US Population. Sesser DE.17(4):400-407. CFSAN/Office of Plant & Dairy Foods. Abarca CR.S. et al. Blount BC. 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. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lamm SH.atsdr.EPA at: http://www. Benchmark calculations for perchlorate from three human cohorts. Li FX. and nitrate on thyroid function in workers exposed to perchlorate long-term. Health Implications of Perchlorate Ingestion.41(5):409-411. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. He X.115(9):1333-1338. Lamm S. Page Last Updated: 05/28/2009. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Lawrence JE. Pirkle JL. Barnard JC. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. et al. Li Z. Dasgupta PK.gov/toxpro2. References Blount BC. 2005). Steinmaus C. J Expo Sci Environ Epidemiol 2007. Osterloh JD. Braverman LE. Erratum in: Environ Health Perspect 2005. most of the population is considered to be below the U. Blount et al. 2005). Crump KS.cdc. newborn thyroid function.html. Primary congenital hypothyroidism. Lawrence J. Pino S.html and from ATSDR at: http://www. Braverman LE. J Clin Endocrinol Metab 2005.

15(9):963-975. Thyroid 2005.gov/iris/quickview. Environmental Protection Agency (U.S. EPA).1/15/06 U.Perchlorate pregnancy and the neonatal period.S. No. 1988. Environ Sci Pollut Res Int 2002.9(3):187-192.epa.S. Revised 2/11/05. Perchlorate as an environmental contaminant. Urbansky TF. Available from URL: http://cfpub. Integrated Risk Information System (IRIS). EPA). Doc. cfm?substance_nmbr=1007. 246 Fourth National Report on Human Exposure to Environmental Chemicals . EPA/600/F-98/002 Washington (DC). Environmental Protection Agency (U. Drinking Water Contaminant Candidate List. Perchlorate.S. U.

such as perfluorochemical telomers. and insulation of electrical wire. chemical processing. chlorofluorocarbons and investigational blood substitutes. 2005. several pathways (during manufacturing) can lead to formation of PFOS or other sulfonyl-containing PFCs as residual contaminants in the final polymer products. Perfluorooctanoic acid (PFOA) has been manufactured since the 1950s.. There are many other fluorocarbon type chemicals which are not addressed here. end products. 2006). Other perfluoroalkyl carboxylates of various chain lengths were also formed in the process used prior to 2002.. PFOA is usually not a residual contaminant in non-stick surfaces made of polytetrafluoroethylene. fluoropolymer products are used in a wide range of industries including aerospace.. Perfluorooctanesulfonyl fluoride (POSF) was synthesized as a polymerization starting material. and fire protection.g. 2006). automotive. Global production that year for POSF materials was 3700 metric tons (Prevedouros et al. 2006). or form in the final product (e.. respectively. Because of their properties. fire retardant foam. The PFCs have limited water solubility. Discussed here are perfluoroalkyl acids. Perfluorohexane sulfonate (PFHxS) has also been used to synthesize the fluoropolymers used in firefighting foams and some carpet treatments. N-methylperfluorooctanesulfonamidoacetic acid (Me-PFOSA-AcOH) and N-ethylperfluorooctanesulfonamidoacetic acid (EtPFOSA-AcOH). furniture. POSF-based polymers have been used in a wide variety of products such as waterproofing. building/construction. may be markers of food or consumer exposures. perfluorooctane sulfonamide... MeFOSE and EtFOSE have been used in food packaging and textile treatments. and also as constituents of floor polish. current manufacturing Perfluorinated Chemicals in this Report practices reduce the formation of these by exclusively using fluorotelomers (Prevedouros et al. adhesives. amides. primarily as its ammonium salt. U. as a solubilization aid in the synthesis of polytetrafluoroethylene. some fish bioconcentrate Perfluorinated Compounds Serum Perfluorobutane Sulfonic Acid Serum Perfluorodecanoic Acid Serum Perfluorododecanoic Acid Serum Perfluoroheptanoic Acid Serum Perfluorohexane Sulfonic Acid Serum Perfluorononanoic Acid Serum Perfluorooctanoic Acid Serum Perfluorooctane Sulfonic Acid Serum Perfluorooctane Sulfonamide Serum 2-(N -Ethyl-Perfluorooctane sulfonamido) Acetic Acid Serum 2-(N -Methyl-perfluorooctane sulfonamido) Acetic Acid Serum Perfluoroundecanoic Acid CAS number 335-76-2 307-55-1 375-85-9 355-46-4 375-95-1 335-67-1 1763-23-1 754-91-6 2058-94-8 Abbreviation PFBuS PFDeA PFDoA PFHpA PFHxS PFNA PFOA PFOS PFOSA Et-PFOSA-AcOH Me-PFOSA-AcOH PFUA Fourth National Report on Human Exposure to Environmental Chemicals 247 . semiconductor. and alcohols which are by-products.g. PFOS) (Hekster et al. perfluorooctane sulfonate. However. PFOSA). manufacture of POSF-based products began ending in about 2000. finalized perfluorochemical polymer products. A major application of one important fluoropolymer. low volatility (as salts or ionized) and can remain in the environment and bioconcentrate in animals (e. In addition. EPA.. 2003). Worldwide annual production of PFOA was estimated to be 260 metric tons in 1999 (Prevedouros et al. Fluoropolymers have applications in waterproofing and protective coatings of clothes. and their oxidation products.g. electrical and electronics. Olsen et al. and textiles. Perfluorononanoic acid (PFNA) was an impurity in the process that produces PFOS. or form as degradation products during its reaction to create the intermediate reacting monomers. U.. Production rates and emission rates have fallen since 2002 after conversion to a new synthesis process. Other PFCs (including small amounts of PFOA) can also form as side-reaction by-products in the synthesis of POSF (e.S. N-methylperfluorooctanesulfonamidoethanol (MeFOSE) and N-ethylperfluorooctanesulfonamidoethanol (EtFOSE).S. and other products.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. has been the heat-resistant non-stick coatings used on cooking ware and other protected surfaces. 2003. or processing aids used in the synthesis of fluoropolymers. polytetrafluoroethylene. textiles.

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. Some of the effects in animals may be mediated through peroxisomal proliferation.. The PFCs often measured in human serum are listed in the table.. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. 2005). PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. 2004). 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. 2005. 2005). Lau et al. PFOA is mostly excreted in the urine in animal studies. but still can have long residence times in the body. in a wide variety of marine and land animals (Kannan et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. or effects of other PFCs. 2003). 2004.5 years and for PFOS. The elimination half-life of PFOA in humans is roughly estimated to be 3.. but probably include dietary sources (Kannan et al.. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. 2004. EPA. 2004).. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. It is unclear if environmentally degraded telomer products are a major source of other PFCs. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. Kannan et al.. Guruge et al. 2003.4. growth retardation and delayed sexual maturation (Kennedy et al. 2004. Olsen et al. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. < LOD means less than the limit of detection.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). Survey Geometric mean (95% conf. peroxisomal proliferation. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. 2005.e. may metabolize or degrade to PFOA (Dinglasan et al.. 2005. Unlike many organohalogen contaminant chemicals... and β-oxidation of lipids (Kudo et al. U. Keller et al. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. environmental fate. Vanden Heuvel et al. see Data Analysis section) for Survey year 03-04 is 0. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. PFOA has been reported to cause liver.. 248 Fourth National Report on Human Exposure to Environmental Chemicals .S. 2004. 1995.8 years (Olsen et al. including immunologic effects and tumor induction.. Taniyasu et al. 2003a and 2004a). endocrine and immune effects. there is limited information on the sources. 2005). C7).. 2006a. kidney. C6. approximately 4. heptadecafluoro-1-decanol. which may vary for some chemicals by year and by individual sample. 2003). 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. pancreas.. thymus and spleen.. and in offspring.... Tittlemier et al. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 2002. in part. and in human blood and semen (Calafat et al...... 1990). 2000. Prevedouros et al. by high protein binding in plasma and other proteins. Bookstaff et al.. 2007a). 2006. In some cases.. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. C5. human toxicokinetics. Excepting PFOS and PFOA.. the 8-2 telomer. population from the National Health and Nutrition Examination Survey. 1993). Lau et al. hepatotoxicity. For instance. All sources of human exposure are uncertain. 2007).

800 (..300 (<LOD-..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . and no substantial age trends were seen within adults ages 20-69 (Olsen et al.300 (<LOD-.400-1.50) .500-. 2003a).400-1. and changes in thyroid hormone concentrations (Grasty et al. 2007). 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.20) . At high but non-toxic maternal doses of PFOS..40) . Thibodeaux et al.3. or increased cancer rates (Alexander et al.. Fei et al.400-1. monkeys.500-1. PFOA. 2003a. 2007a. 2003).400-1. 2003). Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. EPA. perfluorohexanesulfonate (PFHxS).Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.500-1.900 (. 2005). Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. PFOS. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.900 (. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.. Fourth National Report on Human Exposure to Environmental Chemicals 249 . animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. the potential to estimate risks to humans from animal doses is uncertain..500) . 2001. 2004.500-3. development in offspring was stunted and hypothyroxinemia was observed. which may vary for some chemicals by year and by individual sample. 2003. 2004a.S.. and humans. U. 2004b).400 (<LOD-.500 (<LOD-1. 2004.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. U. < LOD means less than the limit of detection..500) . EPA. Harada et al.500) ...S. population.300 (<LOD-.800) 1..700 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result...500-1.. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.600 (. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.10) .108 times higher than background serum levels in humans (Butenoff et al.400 (<LOD-.80) 640 1454 03-04 03-04 * * < LOD < LOD . Survey Geometric mean (95% conf.400 (<LOD-.700) . 1992..S.800 (. 2005).300-1. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.400-. 2007a. Animal studies of PFOS have demonstrated weight loss. In comparing three separate reports on adults. see Data Analysis section) for Survey year 03-04 is 0.. elderly and children.500) . 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).. In such studies. 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. 2003. reproductive.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 . Lau et al. and there was no clear evidence of excess all-cause or diseasespecific mortality.800 (.600 (. 2007b).. thyroidal).500 (. population from the National Health and Nutrition Examination Survey. Cook et al. PFOS. 2007b. PFOA.400-. 2003a.800 (.400) . Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) .900 (.400-1.800) 1. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. hepatotoxicity. 2004). Olsen et al. Olsen et al.10) * 03-04 03-04 * * < LOD < LOD < LOD . However..00 (.500 (. At doses causing maternal toxicity. developmental and teratogenic effects were demonstrated in offspring. 2007. 2003a. 1999. 2004). and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 2003.10 (.. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Kennedy et al. Olsen et al.00) .80) 485 538 962 Limit of detection (LOD.. possibly related to lung immaturity (Lau et al.600 (.500-1.600-2.500) 90th .00) .00) . 2003a).

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

400) .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 251 . Survey Geometric mean (95% conf. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.3. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.300 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.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.300-.500 (<LOD-.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .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 .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .400 (.500-.900) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.600) < LOD .0. see Data Analysis section) for Survey year 03-04 is 1. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.S.500) 485 538 962 Limit of detection (LOD.600 (.400 (<LOD-.

50-3.50 (6.70) 1.50 (2.80) 90th 2.10 (4.809) 1.62-2.50 (1.60) 1.90-10.20 (1.70) 13.87-2.40 (2.00 (5.00-7.10) 1.60 (6.40 (1.30) 3. interval) .51) 1.92 (1.816-1.30 (6.30 (3.20) 1.700-1.30-12.12) .40) 640 1454 03-04 03-04 1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20-1.80-2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.30) .50-6.60-7.40) 1.50) 2.30 (1.20 (6.30 (1.44 (2.70 (2. interval) 1.20-1.90 (1.10) 1.20-2.50 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.27) 1.80 (1.20) 03-04 03-04 2.50 (6.70) 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. see Data Analysis section) for Survey year 03-04 is 0.10) 4.50-6.900-1.70 (1.60) 9.20-1.40 (1.00 (2.90 (4.80 (1.00 (.6) 7.60-8.30 (2.10 (4.00) 1.900-1.800 (.70) 3.60 (1.72 (1.50) 2.40) 640 1454 03-04 03-04 2.00 (1.60-2.697-1. population from the National Health and Nutrition Examination Survey.42 (1.586-.90 (1.04) .54) .20-3.70) 2.30 (1.20 (1.80-7.1.10) 75th 1.20 (1.50 (1.70-2.721-1.70-5.40) .689 (.05-2.984 (.80-6.16) .600-.60-3.80-4.90 (4.30-6.900-1.700 (.08) 2.1) 485 538 962 Limit of detection (LOD.90) 8.90-2.30) 3.20) .40) 1.40 (1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .3 (9.10 (1.10) 6.73-2.90-19.90) 1.10 (.80) 5.70) 2.5) 5.912-1.70-7.60-4.60 (1.5) 8.30) 03-04 03-04 .60 (1.90) 1.70-6.40) 4.60-2.80-8.826-1.80) 1.900-1.14 (.70-2.30 (2.80-3.77-2.80-7.90) 3.00 (1.10) 1053 1041 03-04 03-04 03-04 .10-9. Survey Geometric mean (95% conf.90 (1.900-1.852 (.10) 5.900 (.10) 4. Survey Geometric mean (95% conf.50 (4.17-1.20) 2.09 (.90) 90th 5.00-6.00-8.30) 3.93 (1. see Data Analysis section) for Survey year 03-04 is 0.40-3.20 (1.10-5.00) 3.80) 4.3.80 (4.900 (.00 (1.86 (1.90 (2.10) 75th 3.S.00) 2.91) 2.60) 2.S.10) 8.50 (4.0) 8.80-4.70-10.30 (7.40) 2.20-1.00-1.10) 6.01 (1.20) 485 538 962 Limit of detection (LOD.67-2.00 (1.40-1.10 (.10 (.60-3.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.20) 1.72) 1. population from the National Health and Nutrition Examination Survey.30-2.50) 6.40 (1.00) 1.03) 1.10-9.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.90) 1.834-1.966 (.00 (.17 (1.900-1.80-12.20 (6.80-3.90 (1.40-1.00-1.30-9.900) 1.60) 3.963 (.800-1.80-4.50 (1.26) 2.70) 1.60-2.80-8.60-4.80) 3.50-10.0) 1053 1041 03-04 03-04 03-04 1.56-1.861 (.835-1.30 (1.

8) 46.0) 90th 41.47 (4.60-14.5) 9.30-3.2) 30.2) 640 1454 03-04 03-04 4.50-4.5) 1053 1041 03-04 03-04 03-04 14.60 (4.3) 28. see Data Analysis section) for Survey year 03-04 is 0.8-22.90 (7.60 (6.1.30 (3.4) 20.70-9.8-30.1-24.5-23.80 (6.2 (27.90 (5.20) 7.4-25.3) 485 538 962 Limit of detection (LOD.60-13.6 (19.6) 1053 1041 03-04 03-04 03-04 3.7-30.4) 21.80-4.99-3.6 (35.S.6) 9.7 (13.9 (22.7-53.0 (20.60 (3.20 (4.80 (6.00 (5.7 (35.3 (35.2 (18. interval) 3.1 (19.S.4-17.10-3.0) 21.53) 3.7-49.0) 03-04 03-04 19.7-69.8-78.11 (2.20) 7.90-4.50) 7.1) 15. population from the National Health and Nutrition Examination Survey.4.9 (17.90-12.2 (28.0-66.5) 19.27) 4.80-12.10 (3.1) 57.2 (21.10 (3.4 (28.4) 75th 30.3 (35.30-11. Survey Geometric mean (95% conf.90 (7.20-9.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.79) 4.1-35.07-4.82) 4.60 (5.0-16.80) 8.5) 57.70 (5.8 (37.30) 6.60 (6.40-6.96 (3.5-21.0 (27.7-23.10) 5.21-3.8 (45.89 (3.9 (13.7-33.6) 35.3) 41.70) 6.10 (6.70) 4.35) 3.20-5.3 (17.90 (7.6) 62.60) 03-04 03-04 3.8) 27.8-22.5) 8.2 (19.30-5.1-36.70) 3.30-6.3-61.5) 7.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.9) 9.40) 75th 5.5 (28.40-6.7 (7.84-3.9-38.2) 30.5) 32.5-33.20) 5.90-4.9) 27.4 (17.0) 43.30) 7.4) 56.3) 42.9-19.3-22.18 (3.70-10.1 (24.6-50.0-70.1-33.3 (28.3 (44.6) 21.9 (19.20-4.8) 32.7 (43.0-20. Survey Geometric mean (95% conf.70-5.4) 640 1454 03-04 03-04 23.60-6.40-14.50-13.6-24.40 (4.0) 485 538 962 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 253 .47-4.40-10.5) 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 21.40-17.6) 18.6 (42.2-22.9-23.8-35.80-9.4 (23.50 (4.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (3.20) 10.7 (43.2) 45.6-45.7) 39.6 (44.50) 4.40) 90th 7.8-22.80 (5.6) 42.40 (6.1 (23.40) 5.65-4.6) 7.20) 4.60) 8.90) 6.50 (3.4 (19.2 (16.60 (7.0) 23. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30 (3. see Data Analysis section) for Survey year 03-04 is 0.91) 3.95 (3.5-62.70 (3.70 (5.7 (19.30-8.7 (35.80 (7. interval) 20.8-81.00) 3.50-6.85-4.5 (28.0) 21.60-9.70-7.30 (5. population from the National Health and Nutrition Examination Survey.00 (5.8 (34.70-7.1-52.37 (2.2-57.40) 3.20) 5.9) 22.4 (19.9) 22.5) 18.1) 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 4.20 (4.0) 36.67-4.4-42.1-25.

300 (.2.300) .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 . which may vary for some chemicals by year and by individual sample.300 (.200-.300 (.500) < LOD 485 538 962 Limit of detection (LOD.300) .300-. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.200-.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.200-. population from the National Health and Nutrition Examination Survey.500) .300 (.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.300 (.300 (. which may vary for some chemicals by year and by individual sample. 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.4.S. < LOD means less than the limit of detection.500) .200-.300) . Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th .200-.300 (.300 (.300 (.300 (.300) .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300) . population from the National Health and Nutrition Examination Survey.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300-.500) 485 538 962 Limit of detection (LOD.400 (<LOD-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.200 (<LOD-.300-.300) .200-.200-.200-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .S. Survey Geometric mean (95% conf.200-.300) .500) .300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .

10 (.20) 1.10-1. population from the National Health and Nutrition Examination Survey.00 (.60) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .400 (<LOD-.900) 485 538 962 Limit of detection (LOD.800 (<LOD-.300-2.30 (1.70) 1.30 (1.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900) .00 (.900) 1.900-1.700) .30) 1.700 (<LOD-.900-1.10 (.00 (.10) .700 (<LOD-.10-1.10) .300 (<LOD-1.30) 1.900-1.900 (<LOD-1.600 (<LOD-1.S.20 (1.800) .50 (1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700 (<LOD-.600 (<LOD-1.00-1.10-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 . which may vary for some chemicals by year and by individual sample.30) .30 (1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .80) 1.900-1. < LOD means less than the limit of detection.600 (<LOD-1. < LOD means less than the limit of detection.900-1.900 (.80) 1.700 (<LOD-2.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500 (<LOD-.600 (<LOD-.60) 640 1454 03-04 03-04 * * < LOD < LOD .10 (.6. 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.900-1.700) 1.700) 90th 1.10) 1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.00 (.300 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .10-1.10 (1. Survey Geometric mean (95% conf.700) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800) .400 (<LOD-1.700 (<LOD-.10-1.10) 1.S.10) * 03-04 03-04 * * < LOD < LOD .700 (<LOD-.90) .00) < LOD .40) < LOD < LOD .900-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .50 (1.3.40) 1. see Data Analysis section) for Survey year 03-04 is 0.600) .20-1.

Mabury SA. Olsen GW. Reidy JA. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Fei C. Environ Sci Technol 2004. The toxicology of perfluorooctanoate. Ingall GB. Calafat AM. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism.1968--2003. Koizumi A. Burris JM. Kudo N.40:21282134. Kannan K. Holmstrom KE. Evans TJ. Caudill SP. Halden RU.115(11):1677-1682. Tully JS. Yamashita N. Environmental and toxicity effects of perfluoroalkylated substances. de Voogt P. Rev Environ Contam Toxicol 2003.60(10):722729. Cook JC. Environ Health Perspect 2007. Taniyasu S. Fluorotelomer alcohol biodegradation yields poly. Herbstman JB. Calafat AM. Moore JA. O’Connor JC. Wijeratna S. Bookstaff RC. Kannan K. Lau CS.39(23):9057-9063. J Environ Monit 2005. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.134(1):18-25. Polyfluoroalkyl chemicals in the U.68(6):465-471. Yoshinaga T. Toxicol Appl Pharmacol 1990. McLaughlin JK.115(11):1670-1676. Needham LL. Yamashita N. Reidy JA. Environ Sci Technol 2004.34(4):351-384. Reidy JA. Murray SM. et al. Suzuki E. Kumar KS. Mandel JH. Frame SR. Grey BE. Edwards EA. et al. Saito N. Aguilar-Villalobos M.104(2):322-333. Occup Environ Med 2003. Yoshinaga T. Environ Sci Technol 2005. Tully JS. Toxicol Appl Pharmacol 1992. in vivo.39(1):80-84.39(3):363-380. O’Connor JC. Needham LL. Calafat AM. Kawashima Y. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Mandel JS. Peterson RE. J Occup Health 2004. Hekster FM. Mohotti KM. Perfluorinated chemicals in selected residents of the American continent. Kuklenyik Z. Saito N. Laane RW. Guruge KS. Moore RW. Wong LY. Olsen GW. Inoue K.41:2237-2242. Katakura M.S. Butenhoff JL. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea.and perfluorinated acids. Characterization of risk for general population exposure to perfluorooctanoate.38(17):4489-4495. Apelberg BJ. Environ Sci Technol 2005. et al. Falandysz J. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.39(23):9101-9108. Chemosphere 2006b. Taniyasu S. Watanabe T. Toxicol Appl Pharmacol 1995. Crit Rev Toxicol 2004. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka.S. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Needham LL. and perfluorinated contaminants in livers of polar bears from Alaska. Inoue K. Arendt MD. Environ Health Perspect. Corsolini S. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro.Perfluorochemicals References Alexander BH. Toxicol Sci 2001.46(2):141-147.113(2):209-217. Cook JC. Environ Sci Technol 2007a. Morikawa A. Chlorinated.99(2):253-261. Grasty RC. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Rogers JM. Rodricks J.115(11):1596-1602. Sasaki S. Kamiyama S. Yun SH. Ye Y. Fillmann G. et al. et al. Perkins RG. Kuklenyik Z. Environ Health Perspect 2007. et al. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. 2007b.Koizumi A.7(4):371-377. brominated. Kuklenyik Z. Witter FR. Jarnberg U. Day RD. Olsen J. Harada K. Environ Sci Technol 2005. Chem Biol Interact 2000. Kennedy GL Jr. Hurtt ME. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Regul Toxicol Pharmacol 2004. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Needham LL. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Frame SR. Caudill SP. Keller JM. Kannan K. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. and ex vivo studies. Calafat AM. Biegel LB. Loganathan BG. Gaylor DW. Tarone RE. Kuklenyik Z. Mandel JH. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Biegel LB.124(2):119-132. Seacat AM.63:490496. Bignert A.38(10):2857-2864. Bandai N. The influence of time. Environ Res 2005. Calafat AM. Olsen GW.60(1):44-55. et al. Liu RC. Hurtt ME. Butenhoff JL. Birth Defects Res B Dev Reprod Toxicol 2003. Reidy JA. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Environ Sci Technol 2006a. Harada K. Dinglasan MJ. Cook JC. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Hurtt ME. Seneviratne HR.179:99-121. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats.

Environ Health Perspect. Yamashita N. Butenhoff JL. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Olsen GW. Ehresman DJ.45(3):260-270.54(11):1599-1611.2(1):53-76. Moisey J.) Tittlemier SA.37(12):2634-2639.Perfluorochemicals Kudo N. Taniyasu S. J Children’s Health 2004b. Lundberg JK. Environ Health Perspect 2005. Cao XL et al. Cousins IT. J Occup Environ Med 2003b.55:3203-3210. Church TR. Toxicol Sci 2003.epa.82(1):359. Yamashita N. Olsen GW.perfluorohexanesulfonate. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Barbee BD. Olsen GW.198(2):231-241. Sterchele PF.S. Seacat AM. Environ Sci Technol 2006. (Erratum in: Toxicol Sci 2004. J Ag Food Chem 2007. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Mandel JH. Mandel JH. Mar Pollut Bull 2005. The developmental toxicity of perfluoroalkyl acids and their derivatives. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Pepper K.115(9):1298-1305.74(2):369-381. Half-life of serum elimination of perfluoroo ctanesulfonate. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. J Occup Environ Med 1999. Grey BE. U. Washington. Burris JM. Case MT. Horii Y. Nesbit DJ. Butenhoff JL. Burris JM. Prevedouros K. Butenhoff JL. htm. 2003a. Lau C. Zobel LR. Rogers JM. Larson EB. et al. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle.74(2):382-392. Burris JM. Mandel JH. Hansen KJ. Hansen KJ. Olsen GW. Kannan K. Fourth National Report on Human Exposure to Environmental Chemicals 257 . 2003. Hansen KJ. Historical comparison of perfluorooctanesulfonate. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Hanson RG. EPA). Environ Health Perspect 2003a.. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Gamo T. fish. Rogers JM. Reagen WK. Toxicol Appl Pharmacol 2004. Petrick G.111(16):1892-1901.68:105–111. Burlew MM.51(8-12):658-668.41(9):799-806. Olsen GW. Thomford PJ. Environ Sci Technol 2003. Lau C. Environmental Protection Agency (U. Korzeniowski SH. Grey BE. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Chemosphere 2007b.S. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Richards JH. Mair DC. Helzlsouer KJ. Kannan K. Ellefson ME. et al. and food items prepared in their packaging.26(1):47-51. 1/15/06 Vanden Heuvel JP.gov/opptintr/pfoa/pfoara. Hanari N. Taniyasu S. Huang HY. Butenhoff JL. van Belle G. Church TR. (Erratum in: Environ Health Perspect. and perfluorooctanoate in retired fluorochemical production workers. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Burris JM. Olsen GW. Rogers JM. fish. Mandel JH. Seymour C. and humans from Japan. II: postnatal evaluation. I: maternal and prenatal evaluations. fate and transport of perfluorocarboxylates. Thibodeaux JR. Toxicol Sci 2002. Available from URL: http://www. Church TR. Hansen KJ. Biol Pharm Bull 2003. et al. Froehlich JW. Hanson RG. Olsen GW. 2007a. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Butenhoff JL. Peterson RE.68(1):249-264. Butenhoff JL. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Buck RC. Biochim Biophys Acta 1993. Ehresman DJ. Kawashima Y. A global survey of perfluorinated acids in oceans. perfluorooctanoate andother fluorochemicals in human blood. birds.111(16):1900) Olsen GW. Miller JP. Bronson R. Lundberg JK. Toxicol Sci 2003. Hansen KJ. Seacat AM. et al. Stanton ME. Olsen GW. Burris JM. fast foods. et al.1177(2):183-190. Chemosphere 2004a.113(5):539-545. et al. Horii Y.40(1):32-44. Sources. Thibodeaux JR. Coordinate induction of acyl-CoA binding protein.

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

. Herbert AR. 2003. ovarian abnormalities in the female animals (Jarfelt et al. In animals. 2002. which may be a pathway to the development of liver toxicity and cancers in these animals. 2002). 2004.. and Sertoli cell abnormalities in the male animals and.. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. 105:734-742. atsdr. 1982.gov/toxpro2.. testicular atrophy. Silvapathasundaram S. In Staples CA (ed). A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Population estimates of concentrations of specific phthalate metabolites may differ by age. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. Corbett JT.. High doses of di2-ethylhexyl phthalate (DEHP).21:13-34. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Silva MJ. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 1982). Environ Health Perspect 1982.805:49-56. Slakman AR. 2004). Pharmacokinetics. 1985.html. Food Addit Contam 2001. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. Peck and Albro. These differences may contribute to species-specific differences in toxicity (ATSDR. 2007).. 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. Jordan S. 2004.45:19-25. Cousins IT. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . Calafat AM. Toxicological profile for di-n-butyl phthalate update [online]. Schroeder JL.. Metabolism of di(2-ethylhexyl) phthalate. The Handbook of Environmental Chemistry. 2004. 2001.cdc. but there are known species-related differences in the hydrolysis of diester phthalates. 2001). Also. Hauser et al.. at higher doses. reducing estrogen production.niehs. Kessler et al. McDonnell DP.gov/ reports/index. efficiency of intestinal absorption. Assessment of critical exposure pathways. Coldham NG. variation also occurs in the same person during repetitive monitoring (Fromme et al. However..cdc.nih. Hoppin et al. 4/20/09 Albro PW. Dave M.html).e. 2006). Drug Metab Rev 1989. 2007. Information about external exposure (i. 2006).. Hauser et al. Clark K. 2004.html. Available at URL: http://www.atsdr. Anderson WA.. References Agency for Toxic Substances and Disease Registry (ATSDR).. 1986). 2000c. 2000a. pp. Dirven HA.18(12):10681074.Phthalates and metabolites have been tested.html.. J Chromatogr B 2004. and extent of metabolite conjugation to glucuronide (Albro et al.atsdr. Jongeneelen FJ.New York. Scotter MJ. Sauer MJ. 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 1997. 2005). 2000b.gov/ toxprofiles/tp9. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Rhodes et al. Matthews HB. Mackay D. van der Broek PH.3. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. 2005. Available at URL: http://www. Massey RC. Castle L. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). 227-262. 2003. NTP-CERHR.. 2002). Part Q: Phthalate Esters. McKee et al. Toxicological profile for di(2-ethylhexyl)phthalate update [online].. Springer.. 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. at very high levels.gov/toxprofiles/ tp135. Springall C. phthalates have been shown to induce peroxisomal proliferation in rodents. Needham LL. Vol. 2001. phthalates produced anti-androgenic effects by reducing testosterone production and. and race/ethnicity (Silva et al. Connor C. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Evaluation of a recombinant yeast cell estrogen screening assay. interactions with macromolecules and species differences in metabolism of DEHP. Lovekamp-Swan and Davis. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. Albro PW and Lavenhar SR. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. dibutyl phthalate (DBP).cdc. gender.

Environ Health Perspect 2004. Rylander L. Borch J. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Environ Health Perspect 2003.111(2):139-145. Brock JW.Phthalates in human urine samples. Available at URL: http://cerhr. consumer milk. Stringer WT. Harris CA. Ladefoged O. Environ Health Perspect 1998. Butala JH. J Androl 2004. Jarfelt K. Parker MG. Filser J. Silva MJ. Research Triangle Park (NC).niehs. Int J Hyg Environ Health 2007. Jonsson BAG. Liss GM.nih.64(8):555-560. et al. Chahoud I. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. 6/2/09 NTP-CERHR. Chen Z.25(2):293-302. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. and infant formula by tandem mass spectrometry (LC-MS-MS). Hum Reprod 2007. Duty SM.112(17):1734-1740. gov/chemicals/dehp/dehp-eval. Davis BJ.210:21-33. Yoshimura M.gov/chemicals/dehp/dehp-eval. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int Arch Occup Environ Health 1993.46(11):643-647. Available at URL: http://cerhr. Available at URL: http://cerhr.110(5):515-518. Davis BJ.106(1):23-26. Sumpter JP. Suzuki T. Lovekamp-Swan T. 6/2/09 Okubo T. Epidemiol 2005. Environ Health Perspect 2002. Am Ind Hyg Assoc J 1985. Bolte G. Hauser R. Koch HM. Skakkebaek NE.19(4):505-515. Dalgaard M. Scand J Work Environ Health 1985. 2000c [online]. Albro PW. Biol Pharm Bull 2003. Hartle RW. Hagmar L.105:802-811. Kano K. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Kano I. Skerfving S. Duty S. Research Triangle Park (NC). Richthoff J. Research Triangle Park (NC).nih. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).195:142-153.26(8):1219-24. Mortensen GK. Zhang S. McKee RH.22(3):688-695. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). et al. Calafat AM. Pan G. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). 2006 [online]. Environ Health Perspect 1997. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Silva MJ. Hauser R.16(4):487-493. 6/2/09 NTP-CERHR. 2000a [online]. David RM. et al. The estrogenic activity of phthalate esters in vitro. Reynolds T.112(17):1740]. Gans G.html. Angerer J. Mechanisms of phthalate ester toxicity in the female reproductive system. Sumpter JP. Meeker JD. Toxicol Appl Pharmacol 2004. Anal Bioanal Chem 2005. Calafat AM. Main KM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Numtip W. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Jacobsen H. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Andersson A-M. Nielsen J. Brock JW. Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals .18(1):122.nih. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Reprod Toxicol 2004. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Csanády G. Grote K.nih. et al. White R. Drexler H.niehs. Boehmer S. Milligan SR. 6/2/09 NTP-CERHR. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Balasubramanian AV. Reproducibility of urinary phthalate metabolites in first morning urine samples.103:582-587.niehs. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Tsukino H.gov/chemicals/ phthalates/dbp/dbp-eval. Hass U.html. Giwercman A.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Jobling S. Singh NP. Meeker JD. Fromme H.11(5):381-387.html. Park S. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. 2000b [online]. Leffers H. Reprod Toxicol 2005.html. Henttu P. Ryan L. NTP-CERHR. Akesson B. Environ Health Perspect 1995. Determination of phthalate monoesters in human milk. Available at URL: http://cerhr. Ryan L. Baird DD. 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Urinary levels of seven phthalate metabolites in the U. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Caudill SP. Silva MJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Environ Health Perspect 1982. Clemons JH.S. Peck CC. Albro PW. Toxicol Sci 1998. Orton TC. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Environ Health Perspect 2004. Environ Health Perspect 1986. Cunningham ML. et al. et al. Toxicol Sci 2000. Barr DB. Reidy JA.65:299-308. Rusyn I.114(11):1643-1648.Phthalates phthalate (DEHP): a cross-sectional study in China. Pratt IA. Crit Rev Toxicol 2006. Batten PL. Lambright CR. Matthews JB. Ostby JS.36:459-479.58:339349. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Rhodes C.112(3):331-338. Wu ZF. Klinefelter GR. Zacharewski TR. Peters JM. et al. Malek NA. Fielden MR. Jackson SJ.45:11-17. Meek MD. Parks LG. 112(5):A270]. Hodge CC. Environ Health Perspect 2006. Bratt H.46:282-293. Abbott BD. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Barlow NJ.

0 (30.8-16.5) 16.4 (48..5 (26.8 (12.9 (22.5-40.9) 15.6) 35.3 (29.3 (33.3) 13.4 (27.7 (13.3) 13.9) 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 39.2-155) 91.5 (57.6-38.6-39.6 (12. some personal care products. including MBzP.1-18.3-130) 122 (88.0-85.8-16.0 (11.5 (67.5-25.0) 24.8) 28. interval) 15. see Data Analysis section) for Survey years 99-00. and to a lesser extent.0 (43.8 (38.0) 20.9 (70. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.5-94. and 0.6-72.6 (13.0 (34.4 (59.8-35.4) 75th 35.6 (53.6) 15.7-13.4 (53.8) 33.2) 69.1.7 (80.4-92.4 (13. car care products.5-36. can produce developmental and reproductive toxicity in rodents.0-130) 101 (86.9) 12.4) 38.3-34.6 (13.7 (15.1-43.3 (54.0) 16. vinyl tile.8-48. BzBP can be released into the environment during its production and.1-35.6-92.6-79.9 (39.6) 50.6 (41.2) 32.2) 13.4 (63.4) 49.3) 54.1-116) 122 (93.6) 95th 103 (94.6 (13.8-14.3 (12.4) 108 (96.1) 31.2-183) 101 (78.3-91.8-41.5-145) 138 (106-241) 143 (127-179) 120 (99.2 (19.3 (12.1) 29.3.0 (15.7-172) 103 (74.6) 25. 2000).4 (29.8 (53.3-161) 99.1 (14.0) 34.9) 43.1) 68.1) 76.9-30.9-62.4) 71.1-16.3 (22.8-72.1-214) 166 (116-191) 145 (110-213) 88.5 (13.8 (80.3) 15.1 (13.7 (53.5-36.6) 16.1 (55.9) 18.8-18.9 (11.5 (47.3 (44.3-88.3) 63.8 (14.5 (27.3-18.3-18.4) 98.8-133) 89.6 (32.4) 12.5-97. population from the National Health and Nutrition Examination Survey.7-16.6) 37.9) 11. 01-02.3 (29.1-120) 52.8 (86.2) 22.2-33.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.Phthalates Benzylbutyl Phthalate CAS No.8) 14.4-24. 2004.8 (71.6 (66.0) 33.9-16.3 (12.9 (13. 2001-2002.6-132) 103 (84. particularly male animals (McKee et al.3-82.7-16.4-16.5) 65.4-62.7 (70.5) 82.6) 13.8-17.1-15.9) 49.7 (51.7-119) 99.2-17.5-35.7 (11.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-49.9-14.9 (28.2-38.8-64.9) 14.7-58.1-39.6-92.4) 33.5) 55.4 (32.7-35.2-16.2) 14.8-14.4 (68.0 (15.5 (66.2) 33.1-61.6) 24. respectively.5-62.7-16. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.1 (32.7-15.0) 70.2 (14.1 (19.3) 37.4 (53.2) 14.1) 67.7 (82.6 (13.2-40.4-25.8-13.6-43.6-17.0 (26.3-12.2 (43.4-127) 80.5-41.1 (14.5) 30.0 (55.2) 12.7 (12.1-90.5) 23.5) 15.8 (50.4 (32.9) 13. High dose BzBP and its monoester metabolites.4) 35.2 (25.2-19.9 (21.8 (71.1) 12.2 (10.3-74.6-116) 122 (102-142) 101 (85.9-27.5 (55.7) 23.8-17.1 (20. Food crops take up BzBP.9 (12.3-125) Total 15. 0.8-98.2-39.6) 13.1 (58. 262 Fourth National Report on Human Exposure to Environmental Chemicals .8.1 (13.6 (21.5-14.0 (14.9) 14.4) 65.2 (11. it can be released into the ambient air during use or disposal of the products.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 16.7) 40.6-29.0 (12. and diet is the major source for general population exposure.9-87. sealants.7) 38.2) 78.5-18.0) 23.4) 51.9 (12.0-106) 58.2-31.4) 80.4 (10.5 (76.4-15.4 (10.1) Selected percentiles ( 95% confidence interval) 50th 17.6-150) 94.5-33.6-18. residents (Blount et al.3-43.0 (33.0 (20.6) 14.3-75.5) 27.1-15.4 (31.1) 14.7-14.4) 14. IARC considers BzBP not classifiable with respect to human carcinogenicity. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1-38.2) 66.0-55.3 (30.5-84.0) 32. 2000).1 (10.S.2-116) 122 (102-143) 101 (84.8 (10.3-21.4) 35.3-27.8) 63.2) 15.4) 81.9-28. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.8 (28..0) 90th 67.S. NTPCERHR.8-121) 79.2-20.2-115) 113 (91.1) 13.8) 24.1) 32.6) 67.2 (19.3 (13.1-16.9-47.9-190) 86. and 03-04 are 0.0 (27.0 (23.6) 29.8 (21.0-26. because it is not bound to products in which it is incorporated.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.8 (30.3) 94.5) 15.3) 23.7-17.6) 35.6) 63.8-76. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 2003-2004 were generally similar those reported in U.4) 129 (98.2) 17.5 (61.6) 14.9 (16.2-16.0 (30.7-170) 169 (134-198) 152 (99.7-82.2 (47.7-25.

2003).2-12.8 (46.8) 46.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.7 (21.8) 68.2-15.7-56.1 (21.2 (41.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.8-60.6) 75th 25. 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.1) 80.9-83. 2005.9) 12.3) 37.1 (19.6-12.3 (13. 2005).8 (12.6) 30.0) 49.1-35.4-15... adolescents compared with adults.3 (38.0 (33.1 (46.6-15.3) 21.3-64.9-62.4 (60.1 (25.1) 39. In NHANES 1999-2000.4-23.3) 55. 2007).7-12.9-40.5) 13.0) 13.9 (10.1 (9.4 (74.6-40.7-15.3) 12.4-14.0 (10.4-79.5-213) 49.0) 15.7-61.0 (13.3-34.1 (13. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.9) 12.0) 24.2-51.4 (12.3 (15.8-34.2-78.4 (11.0) 24. 2007).7-69.7 (55.2) 15.4) 25.5) 16.1-125) 86.7 (19.0) 60.2) 11.1-58.7 (38.9) 11.5-26.5 (56.3) 13.7) 56.2) 11.8-13.1) 23. In an annual sample of German university students.95-14.2) 11..9 (24..5) 20.0 (38.9) 11. Weuve et al.9 (54.7) 11.7-19.9 (15.6-116) 74.5 (10.8-13.6 (11.5) 95th 77.8) 71.6 (51. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. 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. 2002.8 (30.3) 14.2-21.3) 29.6) 53.0-27.9) 12.8) 16.4 (13..4 (10.8) 26.5) 41. 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.3 (39.7 (54. 2003).8 (57.8-64.1-27.6-20.8 (50.5-99.3) 14.8-48.6-26.4-90.4 (69.4 (34.4 (25.3) 73.73-12.1 (21.5-38. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.8) 53.0-109) 65.8-13.5) 17.7 (14.7-123) 77.5-42. in young Swedish men (Jonsson et al.1 (34.6 (22.5-58.5 (10.1-12.4) 44.0-48.8 (69.1 (53.4) 17.0 (11.4 (33.4 (46.8) 11.5-13.8 (64.9 (22.4-17.7) 25.6) 25. and in a small sample of German residents (Koch et al. interval) 14.3) 89.5 (49..2-13.8) 80.9) 24.6 (19.1-12.4-27.2 (27.6-81.8) 53. in men attending a Boston infertility clinic (Duty et al.6 (34.7-20..1) 27.5-79.6 (30.9-28.5-29.1 (41.9) 52.9 (43.8-14.6) 38.6) 73.8) 33.3 (60.4-116) 73.4-42.9) 42. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.8-39.2-17.0-51.7 (13. 2004).4-14.8) 15.4-18.6-86.8-173) 195 (121-305) 229 (99.7) 46.7-29. and females compared to males (Silva et al.4) 90th 50.1 (43.3-11.7 (18.1) 24.7) 19.8 (49. 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. 2002).5 (9.9 (9.6 (11.5-26.3-38.7 (12.0) Selected percentiles ( 95% confidence interval) 50th 13.9 (12.8) 34.9 (15.0 (67.0) 11. A small study of African-American women in Washington.2-57.4 (11. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.5) 10..4-93.1 (13.2) 26.4) 12.6 (15.4-102) 70..4) 60.5-58.7 (11.9-23.2) 12.3) 90.4 (21.4) 50.7 (11.6 (57.0 (41.9) Total 14.0) 12.6-47.2-26.9-14.3) 13.2-117) 95.5-57.1) 12.4 (63.8) 56.5) 14.5 (48.S.8) 24.4 (11.6 (30.8-16.9 (29.7-20.5) 46.9-115) 57.0-15.1-29.9 (51.8-42.8) 54.8) 13.4) 21.8-15.9) 100 (80.1-14.5 (35.8-85.2-15.5 (12.1 (18.9 (24.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.2) 67.8-69.5-16.7-19.0 (49.4) 28.0 (62.3 (35.7-14.9) 64.6-99.7-15.8) 33.6) 12.7 (11.1 (11.3) 13.3) 36.9-104) 62.3-73. population from the National Health and Nutrition Examination Survey.8-27.1 (21.6) 58.3 (23.4 (26.69-11.1 (21.2-49.5-76.1) 24.3-16.7-397) 70.5 (11.1-79.8 (11.5) 23. Hoppin et al.8 (10.8-15.7 (59.3) 67. 2004.9-13.1) 17.3 (24.4) 13.5-31.4-60.5) 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 .9-13.4-142) 134 (116-176) 136 (85.6) 13.0-90.9-16. 2006).0-26.3 (12.9 (39.5-23.4) 14.1 (23.7 (23.6 (11.8) 108 (75.1 (15.2-13.1-120) 77.0 (12.1 (14.8-80.0-53.7-31.4) 104 (89.6) 12.9 (12.1) 142 (99.6 (36.4-19.Phthalates York City (Adibi et al.9 (55.7) 38.4) 51.9-69.5) 78.7-14.5 (42.7 (13. Hauser et al.2 (40.4) 15.2 (69.3) 16.9 (10.7-90.8 (13.4) 13.5-61.6-13.1) 35.6 (14.0 (12.3) 18.2 (56.4-99.8-14.2) 32.0 (41.6 (24.

93:177-185.210(3-4):319-333. Gans G. Epidemiol 2005. Angerer J. Hoppin JA. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Helm D. Urinary levels of seven phthalate metabolites in the U. Eckard R.html. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Chen Z. Environ Health Perspect 2002. Hodge CC. 264 Fourth National Report on Human Exposure to Environmental Chemicals .111(14):1719-1722. Caudill SP.Phthalates References Adibi JJ. Richthoff J. Environ Health Perspect 2000. Brock JW. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Meeker JD. J Androl 2004. Weuve J. 2005.nih. NTP-CERHR. Needham LL. Sanchez GN. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Wiesmuller GA. et al. Urinary phthalate metabolites and biomarkers of reproductive function in young men. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Caudill SP. Sampson EJ. Drexler H. McKee RH. Hagmar L.68:309-314. Environ Health Perspect 2004.114(9):1424-1431. Jonsson BAG. et al. Int J Hyg Environ Health 2007.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. et al. Research Triangle Park (NC). Atlanta (GA). Calafat AM. Pirkle JL. et al. Camann DE. Hum Reprod 2007. Silva MJ. Barr D.112(3):331-338. et al.niehs. Rossbach B. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Koch HM. Levels of seven urinary phthalate metabolites in a human reference population. Jedrychowski W. Prenatal exposures to phthalates among women in New York City and Krakow. 2000 [online]. Perera FP. Third National Report on Human Exposure to Environmental Chemicals. Silva MJ. 4/20/09 Silva MJ. Phthalate monoesters levels in the urine of young children. Ryan L.18(1):122. Wittassek M. Malek NA. Davis BJ.110(5):515-518. David RM. Green RA.25(2):293-302. Butala JH. Reprod Toxicol 2004.108(10):979-982. Hu H. Duty S. Giwercman A. Reidy JA.22(3):688-695. Barr DB.16(4):487-493. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Jacek R. Available at URL: http://cerhr. Silva MJ. et al. Environ Res 2003. Koch HM. Silva MJ. Ryan L. Needham LL. Singh NP. Baird DD. Environ Health Perspect 2003. Calafat AM. Brock JW. Brock JW. Reproducibility of urinary phthalate metabolites in first morning urine samples. Bull Environ Contam Toxicol 2002. Environ Health Perspect 2006. Duty SM. Caudill SP. Centers for Disease Control and Prevention (CDC). Hilborn ED. Dobler L.S. Rylander L. Schettler T. Poland. et al. Blount BC. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). 112(5):A270]. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hauser R.

90 (4.60 (5.66) 2.1) 25.1) 16. DBP can produce reproductive toxicity in male rodents (McKee et al.60 (2.80-5. 2005).00 (5.85-6.2-22.90 (6.70 (5.60) 3.2 (11.02) 4.67 (5.44-2.90-7.50-2.5 (17. and in a small sample of Japanese adults (Itoh et al.56-4..30-7. 2000).72-3.80 (5.20 (3.30 (4.10-2.8) 21.5 (11. and also in some printing inks.50) 2. 2004.00-6.6 (13.10) 9.50) 5.5 (27.60 (4.0) 24.6 (10.4 (20. 2005).40-3.0) 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 2.00) 4.40) 5. In addition.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.97) 4. 2003). mostly as MnBP (Anderson et al.0-14.3-48. population from the National Health and Nutrition Examination Survey.3 (13.07 (3.00) 10.80 (3.1-17.7) 14. in men attending a Boston infertility clinic (Duty et al.3 (19.9 (16. 2003).40 (2.Phthalates Di-n-butyl Phthalate CAS No.70 (2.3) 33. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.20 (7.10) 3.50 (6.0-18.30-11.00) 4. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.5-16.20) 7.30-3.00) 6.0 and 0.90 (4.3 (16.73 (2.20-2.10) 11.70-8.5) 25.6-34. 2004.22) 3.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.50-4.46 (2.20-9. Biomonitoring Information Median concentrations reported in the NHANES 19992000.1 (13. interval) 2. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.6) 26.80 (2.3) 3. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.5) 23.40 (3. in a small sample of pregnant women in New York City (Adibi et al.50) 18.7 (17.7) 18.40-4.40-12.1-12.6 (9.5) 22.3-20.7-31.9) 10.3 (13.40-17.1 (8.00 (7.63) 3.56) 3.50) 8.00-9.50 (3.8 (9.4) 12.7 (18.82-3.40-9.17) 4.7 (9.9) 15.4) 22.56 (5.0) 12.10 (4.46 (3.70) 5.5) 18.6) 17.40 (2.10-9.91) 4.10) 2. Following oral administration of DBP to humans.70-4. 2007).50-10. they have been referred to as monobutyl phthalate (MBP).3-30.90) 12.80-5.6 (14.40 (6. NTP-CERHR.6 (10.0 (19. Fourth National Report on Human Exposure to Environmental Chemicals 265 .5-24.90-4.19-3.20-12.5) 14.6-14.0) 20.3-24.30) 2.30) 10...0 (13.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.59) 3.30-2.6 (13.26 (2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.3.40-4.00-6..2-33. Koch et al.30) 6. 2005).55) 2.2-14.46) 2.46-5.0 (11.6) 10.7 (17.00) 7.00-11...0 (13.4-27.9-23.0-38.90-4.6-26. When total DBP metabolites have been measured.9-14.60 (8. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity. 2000.1-20.30 (3.11-3. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.37) 6.24-8.60-6.7-31.30) 5.3-19.6-20.4-12.40 (7.17 (2.6) 17.33 (2.30) 10.6 (11.20) 4. 2001).22 (3. OSHA has established a workplace air standard for external exposure to DBP.6) 16.50) 90th 12.30 (1.S.7-18.40-3.71 (2.1) 22.3-18.5 (20.81 (3.3 (18.2 (12.1-25. residents (Blount et al.55 (3.90 (3.90-2.6 (29.5-16.43) 6.5) 18.80 (5.9 (16. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.80) 75th 5.3 (16.0) 13. CDC.S.73-5.4) 5.20-12.5) 12.3-43.3 (11. Studies of children found age-related differences in urine MBP levels. Hauser et al. about 65% to 80% of a dose is eliminated in urine within 24 hours.10) 8.50-6.7 (7.97-7. 84-74-2 Di-isobutyl Phthalate CAS No.28-5.30-6.6) 16..8) 40.80 (2.7) 15.50) 7.49-2.20-6. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.70) 3.0) 9.5-29.10-9.5 (10.7-20.8) 677 652 703 699 1216 1088 Limit of detection (LOD..96) 3.68 (2.10 (3.70-4.30-6.4 (14. and insecticides.. pharmaceutical coatings. Survey Geometric mean (95% conf.10 (4. 2005.7) 4.97) 2.30-13.48 (2.7) 7.6 (14.20 (6. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6-18.56 (3.2 (8.6) 12.5) 19.0-25.40-5.2) 5.7 (16. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.3) 18.84) 4.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.00-4.

6 (10.98 (2.4) 15.7 (13.88 (2.20-2.93-6.8 (9.1) 13.84 (8.86) 6.6 (12.41 (2.66) 4.7) 3.8-18.1) 15.1) 7.17 (2.84 (4.1-25.47 (3.6) 11.20 (2.65 (4.56) 5.6 (8.76 (3.3 (17.08-2.46) 3.82) 4.44 (3.74 (4.81 (3.79 (4.1-12.25) 5.80) 7.78-8. up to four and 13 fold.2) 9.18) 4.3 (13.0-18.00 (3.69) 4.0) 15.51) 2.0) 11.30) 2.20 (7.76-15.53-5.6-19.13-6.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.31 (2.66) 10.8 (8.08) 75th 4.81) 9.35) 3.86-4.6) 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 2.1) 11.67-5. Survey Geometric mean (95% conf.20 (2.72-7.58-4. 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.32) 7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31) 2.62 (6. Finding a measurable amount of MnBP or MiBP in urine does not mean that these levels or the parent compound cause an adverse health effect.7) 10.52-3.72) 5.38 (6.28 (4.79-8.54 (2.9) 12.92 (7. interval) 2..54 (4.20-3.3) 18.3) 13.34 (3.6 (15.03-7.68) 5.66) 2.52-20.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.37) 3.31 (7.95-3.64-7.26 (2.1 (10.6-19.97-2.5) 15. 2006).64-10.5) 13.27-12.4 (12..8-18.81) 4.76-3.1) 4.5 (11.43) 3.56-4.5 (9. the students’ median values for MiBP levels remained relatively unchanged.52) 3.6) 13.58-3.26-2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.36-2.42) 2.8-36.18 (1.18-10. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.69-7.53-3.04) 7.2) 24.9-16.7 (21. samples from German university students had consistently higher median urine levels of MnBP and MiBP. ranging from more than one-tenth the NHANES median (Itoh et al.33-9.7-28.75 (6.18 (4.3) 16. 2007).03 (5.33 (3.95) 10.0 (10.89-5. than adults in NHANES subsamples during the same time period.18-4.59 (4. to about two to fourfold higher (Fromme et al.7 (11.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .0) 3.2-13.5-19.94 (5.79-6.51) 5. 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.13 (2.9 (11..17-12.1-24.78) 9.3) 28. 2005).95) 2.30 (6.11) 5.78) 8.19 (2.54) 2.07-5.96 (3. An analysis of NHANES 2001-2002 showed similar age.53-4.8-13.S.80-3.4) 23.2 (11.0 (8.89) 6.2-15.55-6.9 (9.65-4..45) 3.39) 5.0) 7..1 (11. In an analysis of NHANES 1999-2000.33 (2.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.38-10..82 (4.00-3.18) 3. 2007).11 (5.02 (7.04-5.4) 7. 2004).7) 11. Between 1998 and 2003.22 (2.69) 6.39-3.99) 7.05) 2.00-3.43) 3.68) 3.29-8.04) 3.32 (7.15-4.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.7) 19.6 (9.01-2.74-3.32 (3.47-5.11-2..89 (3.99-4. 2004). 2002.75 (4.51) 15.83 (2.2 (10.91-6.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.1) 10.47-12.80 (3.9 (15.0 (12.56) 2.10-5.24) 3.07 (2.76-3.73 (5.81 (6. 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.57 (3.94-12. Weuve et al. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.69 (2.62-12.94) 6.68 (2.66 (8.65-11. Over this time.33) 3.36-7.8 (10.85 (2.2) 8.9-40.3) 13.4-16.21) 10.52 (2.1-15.46-11.00-7. respectively.15) 3.43) 3.9-26.57 (3. 2005).03-11. while MnBP declined (Wittassek et al.17) 90th 8.20-4.8) 10.09-2.02-10. population from the National Health and Nutrition Examination Survey.56-15.64-7.14 (4.61-3.46 (2.7 (9.31) 2.6 (8.28-13.29-3.and gender.57-4.21 (5.

4 (84.9) 75.7-24.2) 32.2 (78.8-25.5) 85.2-159) 92.5 (29.3 (17.1 (18.6 (22. population from the National Health and Nutrition Examination Survey.3) 24.2) 20. see Data Analysis section) for survey years 99-00.7-117) 118 (108-143) 93. Survey Geometric mean (95% conf.3 (30.5) 40.1-29.6) 17.5) 26.7) 74. Fourth National Report on Human Exposure to Environmental Chemicals 267 .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 22.1 (19.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5) 34.3-79.3-136) 137 (107-162) 119 (90.0-58.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.2 (21.2-114) 73.4-25.8) 62.5-53.5-47.9-114) 116 (97.5-47.8) 75th 51.5) 78.6-37.8 (57.0) 20.9 (17.3 (23.1) 31.1-92.1) 47.0 (20.0) 117 (104-131) 112 (84.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.1) 25.2-93.4) 64.1) 23.9-87.8) 58.5-43.1) 19.6-20.6 (32.2-87.1) 17.6) 39.0 (23.7-42.5-117) 95.5) 17.7 (38.0 (36.9-101) 77.5) 19.4 (35.9-42.5) 95.4 (23.2) 62.0) 84.9) 46.1 (62.5 (28. interval) 24.5 (30.7-34.3 (36.6) 21.6) 46.3) 23.1) 36.7-111) 64.9-22.7 (18.1) 30.0-73.1 (28.0) 31.4-159) 107 (84.3-96.8) 23. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2-63.5 (59.0 (45.9) 26.3 (42.7-42.9-22.8-42.6 (65.8-132) 95.0-32.4) 20.9-79.3-60.4 (72.1 (51.0 (25.8-22.2 (17.2) 38.2) 26.1) 20.2 (18.4 (25.3 (51.7 (28.6) 38.0-19.1-75.2-56.6-143) 127 (99.6-113) 108 (90.3-85.0 (17.0 (15.0) 21.8) 19.3) 26.2 (19.7 (19.6-29.0-51.1) 23.8-123) 101 (90.7 (33.5-121) 106 (94.5) 20.8) 48.1 (41.7 (51.6) 20.0) 120 (98.0 (30.1) 23.7-106) 69.1 (36.3-145) 85.7-53.4-20.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.7-26.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.5) 36.4 (35.8-29.2 (20.2-32.7-124) 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.4-44.7 (16.6-36.4-31.6-48.1.1 (21.6-69.3 (60.2-21.3) 21. *In the 1999-2000 survey period.3) 40.6 (16.4 (71.0-21.2-49.1-82.6 (26.9-28.6-31.7 (22.4 (35.2 (58.5) 24. referred to as monobutyl phthalate (MBP).1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.8 (19.4 (21.1 (19.3-40.4) 22.9-33.5) 31.3-21.0 (78.4 (35.5-60.1 (16.8) 43.2) 42.9) 36.2) 68.7 (70.1 (26.0-19.7-91.0) 38.0) 30.7) 28.1 (17.9-53.7-92.4 (38.5) 36.6 (61.6-33.5-27.3-67.0 (31.2-23.4.S.2 (79.9) 18.9 (20.4 (19.1 (58.9) 29.3-76.5) 21.1 (54.9-92.6-44.7 (43.6 (90.5 (74.5-42.5 (59.5) 47.0) 27.7 (64.7-20.5) 37.6-40.1-51.2) 90th 98.4-18.9) 71.2-33.1) 46.1 (34.1 (19.6-49.0-24.4) 59.9. 1.3 (23.3) 36.0 (18.3) 18.9 (17.2-24.0-24.1-27.9 (79.3 (37.8-111) 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 23.7 (24.6-29.7-121) 97.2 (25.7) 124 (98. and 03-04 are 0.6 (55.9) 21.9 (79.3-24.6) 35. and 0.0 (72.7) 42.1-24.8-119) 90.2 (74.6) 71.1-22.2 (75.7) 52.2 (59.4-26.5) 65. respectively.1 (31.7-116) 95.4-42.5-44.7) 92.6 (19.7 (18.4) 52.4-60.1-20.3 (30.3) 19. 01-02.6-24.1-80.1 (19.6 (48.6) 80.2-22.0-26.3 (56.7-34.6 (44.2 (21.4 (36.

1) 17.5-37.9 (56.6 (25.4-61.2 (83.6-23.1 (29.0 (16.6-28.0) 81.6-16.7-80.9-49.0-92.2-22.8) 17.8) 20.7-21.4) 15.1-99.8 (13.0) 28.6-42.8 (16.4-72.5) 134 (93.1) 21.4-76.9-26.0) 35.4 (17.8-24.4 (31.8 (33.3 (52.4 (23.0 (18.5 (15.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.4) 62.6-23.9-34.6-44.3 (16.3-81.2-21.8 (50.0-90.9 (39.6-43.9) 39.5-70.9 (20.7-39.2-22.1 (61.3 (76.2-61.4 (45.6-53.6) 23.3-17.6-26.3-21.1-99.7 (60.5) 39.3-32.2-18.3-38.5) 17.7 (28.0 (61.4-34.7 (20.5-76.4-164) 96.4) 15.0) 29. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0) 26.9) 14.7 (12.0-19.4 (20.8) 40.6) 38.3) 59.2-179) 84.6-74.7 (16.6-24.1 (34.4 (50.6) 64.3-23.0 (15.1-18.4 (50.3 (17.0 (34.1) 53.0) 94.7) 36.4 (31.4) 21.5 (64.2 (19.3) 17.7 (19.6-119) 63.1-23.5) 84.6) 14.1) 20.5-64.9 (30.5 (30.0 (50.8-43.4-131) 81.8) 28.9) 20.2) 59.2 (38.6 (57.7-37.4 (31.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.6 (72.5-142) 89.0 (69.5-142) 81.7-42.1-83.0) 53.5) 91.0-38.9) 52.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.1 (15.1) 44.9-56.6) 18.7-51.3) 20.3 (17.6) 24.6 (61.2) 21.1-62.9-68.9-100) 86.7-19.2-73.4 (16.3-71.6-19.3-18.4 (47.2) 65.2) 31.0-41.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.0 (52.9-105) 85.1) 42.0 (70.5) 82.9 (16.9 (58.8) 75th 38.0) 19.7 (81.3) 35.3) 67.4) 19.0) 41.6-92.0 (26.9 (37.3 (46.7) 42.2 (16.2) 16.3 (21.0) 59.0 (27.1) 22.4 (13.4) 16.9-84.3) 33.9 (35.5-21.7 (57.2 (35.6) 83.2-48.8-23.3 (71.0) 70.8) 35.5-16.0-75.6 (31.8) 13.2-106) 64.7 (14. Survey Geometric mean (95% conf.4-103) 117 (83.2) 74.3 (17.8-32.9) 28.4-65.8) 34.1 (56.2) 159 (102-263) 147 (93.8-235) 137 (108-198) 88.8-24.5-23.7) 20.9) 30.1-128) 97.4 (19.7-26.9) 24.4 (16.8) 23.2 (19.6 (29.4 (33.3 (48.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.3) 52.2-28.9-14.9-36.3 (42.8) 30.0 (43.0 (20.9 (73.6) 24.4 (37.4 (68. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.8 (25.7-28.3-40.3 (60.8) 17.0 (19.5-18.5) 21.5) 90th 68.1-21.8) 22.3 (69.3-78.6) 34.3-26.1) 37.9 (30.9 (64.S.3 (24.1 (46.7-19.6 (17.5 (18.6-128) 96.4 (53.3-49.0) 75.9 (19.1 (32.1 (21.6 (19.2-85.5-30.9 (21.6 (41.7 (43.5-15.9) 49.3-21.6-27.3-106) 74.9 (30.2-27.9) 62.7 (73.6 (74.4-135) 71.9 (35.3 (52.9) 19.5 (81.7-23.0 (71.3) 19.1) 20.0-17.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.0-60.8 (65.4 (17.4-24.9-38.8 (18.8) 17.6-32. population from the National Health and Nutrition Examination Survey.8 (18.1) 50.6) 65.8) 19.3) 21.0 (18.0) 55.5) 60.0) 25.3) 18.7) 19.0) 108 (71.5 (14.1) 61.6-44.6) 39.1) 35.6 (25.5-41.8 (22.3-39.8) 63.4) 20.5-22.7-20.6-155) 91.3 (28.5 (18.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.3-20.9) 91.8 (18.8 (17.2-16.1-32.7-78.3) 19.7 (60.6-22.7 (54. interval) 22.6-50.7 (27.0-113) 104 (83.6) 31.3) 33.2-86.3 (55.8) 34.4) 51.4-47.6) 37.3 (19.9-70.6) 25.0-47.4 (18.4) 53.2-22.8) 20.6-24.6 (27.4 (56.9-68.

Barr D. et al. Itoh H. Dobler L. Jonsson BAG. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. McKee RH. Camann DE. Eckard R. Atlanta (GA).68:309-314. Singh NP. Rylander L. Environ Health Perspect 2004. Bull Environ Contam Toxicol 2002. Malek NA. Perera FP. Wittassek M. Food Addit Contam 2001. Butala JH. Epidemiol 2005.111(14):1719-1722.18(12):10681074. Hauser R. Silva MJ. Drexler H. Caudill SP.208:237-245. Hum Reprod 2007. Silva MJ. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Koch HM. Brock JW. Schettler T. Centers for Disease Control and Prevention (CDC). Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Calafat AM. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). David RM. Sampson EJ. Research Triangle Park (NC).S. Needham LL. Yoshida K.nih. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Koch HM. Green RA. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Massey RC. Sanchez GN. Phthalate monoesters levels in the urine of young children. 2000 [online]. 112(5):A270]. Jedrychowski W. Hu H. Hilborn ED. Pirkle JL. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Springall C. Int J Hyg Environ Health 2005. Fromme H.niehs. Giwercman A. Silva MJ. et al. Hagmar L. Scotter MJ. Environ Health Perspect 2003. Richthoff J. Drexler H. Calafat AM. Blount BC.25(2):293-302. Masunaga S. Available at URL: http://cerhr. Bolte G. Meeker JD. et al.210:21-33.93:177-185.112(3):331-338. Castle L. Helm D. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Reidy JA. Anderson WA.16(4):487-493. Gans G. Levels of seven urinary phthalate metabolites in a human reference population. Brock JW. Chen Z. Int J Hyg Environ Health 2007. Duty SM. Third National Report on Human Exposure to Environmental Chemicals. Ryan L. 4/20/09 Silva MJ. Environ Health Perspect 2006.22(3):688-695. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Urinary levels of seven phthalate metabolites in the U. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. et al. Poland.108(10)979-982. Jacek R.html. Ryan L.Phthalates References Adibi JJ. Int J Hyg Environ Health 2007.114(9):1424-1431. Reprod Toxicol 2004. et al. NTP-CERHR. Rossbach B. et al. et al. Weuve J. Needham LL. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. J Androl 2004. Wiesmuller GA. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Koch HM. 2005. Caudill SP. Barr DB.210(3-4):319-33. Angerer J.18(1):122. Caudill SP. Boehmer S. Hodge CC. Prenatal exposures to phthalates among women in New York City and Krakow. Environ Health Perspect 2000. Duty S. Silva MJ. Angerer J. Environ Res 2003.gov/chemicals/ phthalates/dbp/dbp-eval.

00-3. and polyvinyl chloride.300) < LOD . and 03-04 are 0.50) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) .200-.300-.200-.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 . only levels at or above the 90th percentile could be characterized.400-. 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. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 . see Data Analysis section) for Survey years 99-00. respectively.400 (<LOD-.600) .500) < LOD < LOD .00 (<LOD-1.500) .500) < LOD 1.10 (<LOD-2.400 (<LOD-.400) < LOD 1.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300-.300 (.500) 1.400 (. and polymers.600 (.300-. 01-02.500 (. < LOD means less than the limit of detection. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.500) < LOD < LOD .9.400-.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 1.200-.600) .10) .600) .400-.00) .900-1.500 (.400-.200 (<LOD-.300-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 270 Fourth National Report on Human Exposure to Environmental Chemicals .300) < LOD .500 (.300 (<LOD-.2.200-.70) .500) 1. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.10 (<LOD-1.300 (.500-.70 (1.600) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10 (.300-.300 (.Phthalates Dicyclohexyl Phthalate CAS No.300 (.400-.20) .300-.400) 1.500) .S.400 (.300 (.300 (.400 (.700) . In this Report.700) .500 (. population from the National Health and Nutrition Examination Survey.00 (<LOD-1. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. and 0.3.600) < LOD .500 (.70) .400 (.300-. 0.00 (<LOD-1. resins.500 (.90) .80) .300-.300-.400) < LOD < LOD . polyvinyl acetate.500 (.600) .400 (.500) .400 (<LOD-.700) .500) .300 (. Survey Geometric mean (95% conf. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400-.500) 1.400 (. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.400 (<LOD-. including nitrocellulose.400 (.500 (.400-.70 (1.200-.10 (<LOD-1.00-2.400) 1.500 (.

480 (.17) .710) .400-.590 (.170-.18) .74) .500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .790-1.740) < LOD < LOD .530 (.16 (<LOD-3.910 (.82) .67 (1.630 (<LOD-.770) < LOD 2.330 (.82 (1.770 (.410 (.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.S.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 1.53) .950 (.400-.330 (.510 (.12-1.310-.11) .06) .470 (.500 (.740) .420-.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 .380 (.33) .560) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.420-.05) .670 (<LOD-.630 (<LOD-.54-6.260-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.54) .16) .910 (.830) 1.670-1.800-1.590 (<LOD-. Survey Geometric mean (95% conf.370 (<LOD-.450 (.350-.450 (.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.490) .240-.380-.530) 1.620) < LOD .530-.10) .53) .910 (.44) .610 (.06) .500-. population from the National Health and Nutrition Examination Survey.34) .690 (.36-1.690) < LOD < LOD .880 (.00 (<LOD-3.270) < LOD .43 (1.770-1.220 (<LOD-.390 (.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.910 (.770-1.290-.00) .250 (.33 (<LOD-3.940 (.510-.360-.420-.500) 3.770-1.22 (<LOD-1.14 (<LOD-3.690) < LOD 2. Fourth National Report on Human Exposure to Environmental Chemicals 271 .310) < LOD .690-1.660) .660) < LOD < LOD .54 (<LOD-2.530-1.

5) 81. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7) 71. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.1 (71. 272 Fourth National Report on Human Exposure to Environmental Chemicals .S.4. deodorants.3 (82.4 (62.9-92.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. In contrast. 2007). soaps.3 (74.1-93. DC (Hoppin et al.Phthalates Diethyl Phthalate CAS No. 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. Biomonitoring Information MEP levels in the NHANES 1999-2000. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2001-2002. and 03-04 are 1. particularly those containing fragrances. and 0.9. respectively.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.8-111) 85. 01-02. 0.9 (61. population from the National Health and Nutrition Examination Survey.2-102) 95. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. colognes.2. shampoos. Products that may contain DEP include perfumes. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine... see Data Analysis section) for Survey years 99-00.7 (70. and hand lotions.. 2003) and African-American women in Washington. 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. 2002). and also in men attending a Boston infertility clinic (Hauser et al.

2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-113) 122 (93.9 (82. 2002). This age-related trend is opposite the direction seen for other phthalates. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups.9-110) 96. 2003) were slightly lower than levels found in NHANES 2001-2002. 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.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6 (77. 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. In an analysis of NHANES 1999-2000.5-114) 101 (87. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.2 (66.0 (66. 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.Phthalates 2002 (Brock et al.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 . 2004).. Other population estimates also differed by sex and race ethnicity (Silva et al. Median MEP levels found in a small sample of German residents (Koch et al. population from the National Health and Nutrition Examination Survey.7-110) 81.6 (65.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.S..3-105) 87. Analysis of NHANES 2001-2002 showed similar findings.

DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Silva MJ. Ryan L. Urinary levels of seven phthalate metabolites in the U. Baird DD. Silva MJ. Duty S. Environ Health Perspect 2004. Camann DE.22(3):688-695. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2002. Jedrychowski W. Brock JW. Hoppin JA. Poland. et al. Third National Report on Human Exposure to Environmental Chemicals. Drexler H. Reproducibility of urinary phthalate metabolites in first morning urine samples. et al. Bull Environ Contam Toxicol 2002. Environ Health Perspect 2003. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Atlanta (GA). Barr DB. Needham LL.68:309-314. Koch HM. Rossbach B. Hilborn ED. Meeker JD.112(3):331-338.110(5):515-518.Phthalates References Adibi JJ. Hum Reprod 2007. Davis BJ. Jacek R. Caudill SP. Environ Res 2003. Reidy JA. 2005. Hauser R.S. Caudill SP. Silva MJ. Malek NA.93:177-185. Perera FP.111(14):1719-1722. Prenatal exposures to phthalates among women in New York City and Krakow. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Singh NP. Barr D. Brock JW. Hodge CC. Angerer J. Phthalate monoesters levels in the urine of young children. et al. 112(5):A270]. Centers for Disease Control and Prevention (CDC).

Concentrations in plastic materials may reach 40% by weight.4-53.00) 3.4-40.4-42.0 (21. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.50-16.5 (31.50 (3.70 (8.8) 17.3-64.30 (4.40-8.7) 19.9 (29.68 (3.0) 35.90) 4.10-11.67-4.31 (3.35) 4.5-36.5-40.7) 6.86) 2.10-5.3-26.5 (11. ATSDR.60) 3.60) 90th 14.5) 19.77 (2.50-2..41) 3.10 (4.30-6.50-5.7) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.16 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90) 4.3) 13.10-5.30-13.93) 6.50 (8.6-60.90-11.00) 2.40) 75th 7.80 (8.1) 25.40) 8.5) 31.61 (3.5-41.50-20. Peck and Albro.9-48.14 (1.70 (3.3-57.00) 9.9 (17. respectively.8 (17.1 (8. mainly polyvinyl chloride.1) 22.92) 4.9-49.70 (1.60) 8.51) 4.39) 3.50) 9.7) 27.6) 39.90 (3.92-5.20 (3.6-23.40-12.00 (2.0 (18.6) 5.10) 3.2 (10.80-4.2 (7.30-8.5 (18.44) 4.40-8.9) 18.70) 16.42-5.25-3.0-18.96) 4.5-27.6 (9.41 (3.0 (14.16-3.9.40) 4.3 (11.60 (5.9) 13.7) 8.80-3.56 (2.92-2. 2002.90 (1.91-3.80 (1.69) Selected percentiles ( 95% confidence interval) 50th 3.1-48.1) 29. After parenteral administration.31-4.2 (31.9) 15.70-6.10) 3.00-5.S. and in humans.3 (10.12 (4.80) 6.50-8.0 (19.0) Total 4.80-8.90-5.00 (5.57-7.50-14. Following ingestion.21 (2.0 (19.6) 15.0-29.6-25.00) 1.83) 2.0 (13.00-3.70) 7.50-3.85) 4.89-3.50 (2.00-4.70) 2.3 (24.1-27. 1.60-7.60) 9.9-26.98) 2.50) 4.10-5.5-17.9 (15.10 (3.3-25.0) 23.70 (5.60) 10.40 (4.30 (6.3) 52.82 (3.30-11.9 (29.19-3. as glucuronide conjugates (Albro et al.7 (14.70 (1. which is used for many consumer products.46) 3.90-4.4-20.37-4.5) 23.6-28.7-58.43 (3.9) 5. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.10) 4.4) 6.03-2.80 (8.84-4.0-18.2) 6.4) 22. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).0 (17.4) 15.00) 2.0) 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 3.20 (1.1 (11.50 (3.9 (26.20 (4.50-2. 01-02.8) 15.50-11.10-4.60) 4.20 (3.86) 2.49 (3.5-28.0 (9.1982).40) 2.21 (2.90) 4.2) 29.40-11.40-9.Phthalates Di-2-ethylhexyl Phthalate CAS No.70-5.0) 23.00) 5.00) 19.50-6.2 (29.50 (7. toys.10 (2.70 (3.50-5. see Data Analysis section) for Survey years 99-00.5 (12.5) 37.96-5.7) 22.8 (19.5) 21.6) 95th 23.2-39.10) 8.4 (21.42) 3.80-9. 1982.0 (16.50 (7.7