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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1-Trichloroethane (Methyl chloroform) 1. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.2'.5'-Tetrachlorobiphenyl (PCB 49) 2.6'-Hexabromodiphenyl ether (BDE 154) 2.4'-Tetrabromodiphenyl ether (BDE 66) 2.4-Dichlorobenzene (p-Dichlorobenzene.3.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5-Pentabromodiphenyl ether (BDE 99) 2.5'.6.5’.html.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.3.4'-Tribromodiphenyl ether (BDE 28) 2.3-Dichlorobenzene (m-Dichlorobenzene) 1.1.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2-Dichloropropane 2. Table 1.4’.1-Dichloroethane 1.2'.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.1.6-Pentabromodiphenyl ether (BDE 100) 2.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4.1.3-Tetramethylbutyl] phenol) Triclosan (2.1.5.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2'4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2. The process for selection is described at http://www.What’s New in this Report What’s New in this Report In this Fourth Report.2'3.4'.2'.3. Paradichlorobenzene) 1.5.2-Dichloroethane (Ethylene dichloride) 1. 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.cdc.4.4’.1-Dichloroethene (Vinylidene chloride) cis-1.4.4'.4.2.5'-Hexabromodiphenyl ether (BDE 153) 2. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.2-Dichloroethene trans-1.2'.2'. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.5'-Tetrachlorobiphenyl (PCB 44) 2.4'.3'.4.2-Dichlorobenzene (o-Dichlorobenzene) 1.4.2-Dichloroethene Dichloromethane (Methylene chloride) 1.4.4-Tribromodiphenyl ether (BDE 17) 2.3.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .5.4'-Tetrabromodiphenyl ether (BDE 47) 2.4'.4.2'.2'.2’.2'.6-Heptabromodiphenyl ether (BDE 183) 2.4.5.3’.2'.4.4.4'.4.gov/exposurereport/chemical_selection.

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

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

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

furans. Assigning a value of the LOD divided by 2 made little difference in geometric mean estimates. the maximum LOD value is provided in each data table and in Appendix D. 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. because this concentration determines the analytical sensitivity.” For most chemicals. which uses Taylor series linearization for variance estimation. LOD calculations were performed using the chemical concentration expressed per amount of lipid. For chemicals measured in urine. concentrations less than the individual LOD were assigned a value equal to the individual LOD divided by the square root of 2. each individual sample has its own LOD. In the lipid unadjusted 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. For chemicals measured in serum lipid. sex and race (e. Limit of detection: The limit of detection (LOD) is the level at which the measurement has a 95% probability of being greater than zero (Taylor. The 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.. For these chemicals. for proper interpretation of LODs in the data tables.. For the same chemical. One possible consequence is that results may be reported as “< LOD” in the 1999-2000 data but be reported as a concentration value above the LOD in 2001-2002 or 2003-2004 because the analytical method had improved. the LOD is constant for each individual specimen analyzed. the percentile estimate was not reported. a better ability to detect low levels). That is. PCBs. 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. Percentile estimates (see below) that are less than the LOD for the chemical analysis are reported as “< LOD. If the proportion of results below the LOD was greater than 40%. For chemicals that had individual sample LODs.1). 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 standard error was computed with SUDAAN’s Proc Descript (design=WR). 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). In the creatinine corrected tables. The LODs for each chemical and survey period are provided in each data table and collectively in Appendix D. because this concentration determines the analytical sensitivity. 75th. A higher sample volume results in a lower LOD (i. five results that all have a value of 90. Percentiles: Percentiles (50th. For example. Geometric mean and percentile calculations were performed separately for each of these concentrations. LOD calculations were performed using the chemical concentration expressed per volume of urine. a result for a geometric mean or percentile was reported as < LOD if the corresponding geometric mean or percentile was < LOD in the lipid adjusted table. the mean LOD was about 40-50% of the maximum LOD. 6 a conservative rule was used for reporting percentiles: if any individual sample LOD in the demographic group was above the percentile estimate.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. Geometric mean and percentile calculations were performed separately for each of these concentrations. Percentile estimates and 95% confidence interval estimates that are less than the limit of detection are indicated as <LOD in the data tables. 1987). 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).e. geometric means were not calculated. LOD values may change over time as a result of improvements to analytical methods. For this reason. in non-Hispanic white males 12-19 years old. The maximum LOD was the highest LOD among all the individual samples analyzed — typically. The same procedure for imputing values below the LOD in calculations of geometric means was used for chemicals with individual LODs for each sample. In the Third National Report on Human Exposure to Environmental Chemicals. 90th. weighted percentile estimates for 1999-2000 and 20012002 data were calculated using SAS Proc Univariate and a proportions estimation procedure. For this reason. and a few other pesticides. care must be taken to use the LOD that applies to the survey period. Since the Third Fourth National Report on Human Exposure to Environmental Chemicals . LOD results for chemicals measured in each data table and in Appendix D are in weight per amount of lipid. organochlorine pesticides. Thus.g. These analyses have an individual LOD for each sample. mostly because the sample volume used for analysis differed for each sample. For dioxins. A percentile estimate may fall on a value that is repeated multiple times in a particular demographic group defined by age. and 95th) are given to provide additional information about the shape of the distribution. if the 50th percentile for males was < LOD in the table using weight per volume of urine.

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). Taylor JK. we have improved the procedure for estimating percentiles to better handle this situation. This improved procedure makes each repeated value unique by adding a unique negligibly small number to each repeated value. Quality Assurance of Chemical Measurements. 1987. Therefore. Lewis Publishers. Appendix A gives the details of the new procedure for estimating percentiles.Data Sources and Data Analysis Report. Fourth National Report on Human Exposure to Environmental Chemicals 7 .

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

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

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

Recently.0-49.9 (54.2-118) 98.4 (53.8 (52. FDA.S.7) 54.9-61.9) 58.0 (53.6-75. gels.1-64. soil conditioners. Survey Geometric mean (95% conf. 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.5) 58.4) 57. Elimination occurs mainly in the urine as mercapturic acid conjugates.9-52.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.7-60.2) 57. see Data Analysis section) for Survey year 03-04 is 3.7 (65.1) 53.4) 100 (89.1-64.6-104) 82. Tareke et al. or to glutathione conjugates (Calleman et al. In the general population. Natural substances in the food are converted to acrylamide. interval) 61.2-114) 163 (147-191) 96.7-64.4) 57. 1990.4-60.0. People may be exposed to acrylamide from foods.1 (47.5-80.2-91.4-89.4 (54.6) 50.0-58. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. and in some cosmetics.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6-66.4 (59. acrylamide has produced upper airway irritation following inhalation of high levels.1-57.6-65.1) 101 (95.4 (54.6) 73.S.1 (52.5 (44.3-71.5 (52.9) 57. but can covalently bind to form adducts with proteins.9) 75. smoking.0) 57.4-83. drinking water. 217 million pounds of acrylamide were produced commercially in the U.0-108) 152 (139-175) 126 (111-142) 108 (86.6 (56. are heated at temperatures used for frying and baking. FAO/WHO.6 (81.4-76.9-105) 86.6) 90.2-59.5) 66. 2006.5 (79. 2005). 1994). Since acrylamide has limited volatility and high water solubility.9 (60. and cosmetics (NTP-CERHR.6-108) 61.0 (67.7) 75th 79. 2004.6-61. Fourth National Report on Human Exposure to Environmental Chemicals 11 . and from dermal contact with products that contain residual acrylamide. and binding agents.2-77.7) 96. 2005).1 (88. acrylamide is synthesized and used in the production of polyacrylamide polymer.1) 62.1) 55. but are generally above the U. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.2 (75.4-60. EPA.7 (55.7) 73.2) 57. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.5-85.1 (73. it was discovered that acrylamide is formed when starch-rich foods. EPA reference dose of 0. in permanent press fabrics.8 (81.1) 46. 2005.3) 70.0 (69. 2005). Acrylamide is not thought to accumulate in the body at environmental doses.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.S.8-57. pulp and paper production. and is either metabolized to the reactive epoxide.0 μg/kg for adults (FAO/ WHO.2 μg/kg/day (U. These estimated intakes are hundreds of times lower than occupational exposures..3 (55. In 1997.1 (83.2 (62.8-55.0 (57.6) 71.5 (74. and an average daily intake is estimated as 0. 2005).3-2.9 (69. glycidamide. Estimated intakes in children are about twice that of adults (DiNovi and Howard.7) 58.3) 86.1-61.S.3 (53. 2006). and well below doses known to cause nerve damage or carcinogenicity in animals. Polyacrylamides are useful water-compatible polymers used in water treatment.9) 63.6 (51. In humans. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.8 (91.7 (58. population from the National Health and Nutrition Examination Survey. Fennell et al. 2002). in some sealing grouts. (NTP-CERHR. Commercially.2-93. ocular and dermal irritation from direct contact with acrylamide containing materials.3) 63. the main source of exposure is from the diet.Acrylamide Acrylamide CAS No. widely distributed in tissues.4 (51.2-67. and in the synthesis or compounding of dye materials..0-66.S. Animal studies indicate that acrylamide is well absorbed. EPA. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. as an absorbent in disposable diapers.8 (57. 2004). such as potatoes and some grains.0) 85.7 (63. 2005).2 (58..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 61.7-64.2-70. mineral processing.

Vesper 2005) and smoking (Bergmark. 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. 2004).7-62. glycidamide (NTP-CERHR.4-98.6-90.9-138) 143 (130-159) 96.0.S. 2006. 2005).1-56.2-91.5 (56.Acrylamide occupational exposures.. 2005.4-103) 79.3) 59. Hagmar et al. Survey Geometric mean (95% conf. uterine.7 (87.2 (56.. 2006) have been demonstrated after acrylamide dosing. Mucci et al. IARC classifies acrylamide as probably carcinogenic to humans. 2005.int/ ipcs/food/jecfa/summaries/summary_report_64_final.3) 59.5 (42. and cancer (mammary.4 (57.5) 71..4) 83.9-76. 2003. and other sites) (FAO/WHO.3-78.8 (51. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. 2001). Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.. 2006).5) 87.1 (66.5-92. Glycidamide has been shown to react with DNA (Doerge et al.1) 56. 2005).6 (66.7 (57. 2005..5) 75th 85.4 (90. 2002. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.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. 2005. 1997. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2005) have been demonstrated in animals.7) 60.1 (57.S. Levels of AHA and GHA reported the NHANES 20032004 sample are generally similar to those seen in several previous studies of non-occupationally exposed subjects (Bergmark et al. 2005. Klaunig et al.1-70.1) 62.5 (59.2-90.. Schettgen et al.9 (58... Schettgen et al.1 (82. presynaptic nerve terminal binding (LoPachin. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. 2005) and sperm DNA adducts (Xie et al.0) 94.4 (51.7) 61. Acrylamide is clastogenic and can produce dominant lethal mutations.S. 2006).7) 74.5-64. 2005).. probably through its epoxide metabolite. 2005). and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. 2008).4) 53.0 (80.epa.5 (83.1) 60..6-64. Axonal degeneration.pdf.8-49. reproductive effects (reduced litter size..0 (75.3 (56.9) 75.4-59....9-78.8) 60.2 (63.4 (81.1) 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 59.3) 85.2-68. 2009). 2002.2) 55. 2005. scrotal.6 (90. Maniere et al.8) 45.7-86. thyroid.9) 65.4) 46.1 (70. although different analytic methods can affect results.0-62. male germinal cell injury. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.2) 87. adrenal.9) 87. interval) 59.8 (44.. In addition.3) 59. Rice. 2005. Additional information is available from U..who. fetal death. dominant lethality).2 (72.7) 90.1 (56. 2005.7 (84. After exposure ceases. and neuronal DNA reactivity (Doerge et al. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.9 (81.2) 65. respectively) are markers of integrated acrylamide exposure over the preceding few months. see Data Analysis section) for Survey year 03-04 is 4.8-61.4 (61. EPA.0 (70.0 (52. EPA at: http://www. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.S.9) 59.7 (61. 2008). 2004. EPA. Puppel et al.9-77.1-62. population from the National Health and Nutrition Examination Survey..6-62. U.5-94. altered gene expression in testicular tissues (Yang et al.. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. U.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.0-93. 2005. NTP-CERHR.3-101) 95.1-60.8-48. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).9 (57. 1997.4 (56. Puppel et al.9-62..7-64. AHA levels have been shown to increase with dietary intake (Hagmar et al..9-64.4-65.0) 118 (103-126) 121 (112-134) 113 (94.5-66.0-103) 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. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. Vesper et al. 2005.

Costa LG. Scand J Work Environ Health 2001. and Research Strategies. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Adv Exp Med Biol 2005. Duale N. 64th Meeting: Summary and Conclusions (FAO/WHO). In another study. 1999). Bridson WE. Toxicol Sci. Maniere I. 1994). Mechanisms of acrylamide induced rodent carcinogenesis.cfsan. Uncertainties. J Agric Food Chem 2008. Zhang S.Acrylamide In occupational settings. Tornqvist M.. McDaniel LP. Acrylamide intake through diet and human cancer risk. Chicago. 2001). Mutat Res 2005. Doerge DR. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Calleman CJ. Twaddle NC. Bruze M. Fennell TR.gov/chemicals/ acrylamide/Acrylamide_Monograph. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. July. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. gov/~dms/acrydata.85:447-459. Joint FAO/WHO Expert Committee on Food Additives. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. He F. 2001. Farmer PB. Hagmar L. Tian G.. Mutat Res 2005. Perez et al. Cheong HK. Guffroy M.561:49-62. Acrylamide neurotoxicity: neurological. Granath F. Rosen I. Food and Drug Administration (FDA).pdf.nih. Summer SCJ. Bjellaas T. 2004. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 2005. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Survey data on acrylamide in food: individual food products. Rome. CFSAN/Office of Plant and Dairy Foods. Malmberg B. da Costa GG. 2009 Jan 8.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Paulsson B. February. Italy. 2006. Kautiainen A. National Toxicology Program. smokers and nonsmokers. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose.126(2):361-371. Tornqvist M. Beland FA. Toxicol Appl Pharmacol 1993. Snyder RW. 2/3/09 Perez HL. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. 2/3/09 Klaunig JE. Chem Res Toxicol 1997 Jan. et al. Food Chem. Fennell TR. Axmon A. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. DiNovi M and Howard D. Illinois. et al.who. 054472.580(1-2):119-129.fda. Chem Res Toxicol 1990.580(1-2):157-165. Churchwell MI. 2/3/09 Hagmar L. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. 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. Hagmar et al. Mutat Res 2005. Metabolism and hemoglobin adduct formation of acrylamide in humans. et al. Laurentie M. 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. Aprea P. Wirfalt E.3:406-412. morphological and molecular endpoints in animal models. 1993. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.56. References Bergmark E.. Spicer R. Godard T. Yang JS. et al. Calleman CJ. Bergmark E. Bergmark E. Calleman CJ. Available at URL: http://www. Available at URL: http://www. Osterman-Golkar S.Toxicol Appl Pharmacol 1994. Magnusson AL. Doerge DR.. Human exposure and internal dose assessments of acrylamide in food. Toxicol 2005. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Churchwell MI. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake.120(1):45-54. Mucci LA. LoPachin RM.pdf.html#u1004. Alexander J. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. et al.niehs. Bergmark E. Nordander C. Wu Y.43:365–410. Andersen M. 8-17 February 2005. Haugen M. NIH Publication No. 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. smoking habits and gender. Kamendulis LM. Toxicol Sci 2005.27(4):219-226. Burgess J. Costa LG.. He F. [Epub ahead of print] Dybing E. Adv Exp Med Biol 2005. April 13-15. Available at URL: http://cerhr. Becher G.10(1):78-84.561:21-37.580(1-2):131-141. Wilson KM. 6013-6019. Paulsen JE. The Updated Exposure Assessment for Acrylamide.

Sun H. EPA).163(2):101-8.19(4):527-34. Environmental Protection Agency (U.epa. Tornqvist M.274(1):59-68. Int J Hyg Environ Health 2003. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Broding HC. Vesper HW.gov/iris/subst/0286. et al. a carcinogen formed in heated foodstuffs. et al. Meyers T. Meyers T. Xie Q. Lee MH.S.epa. Vesper HW. revised 1/3/06. Angerer J. Reprod Toxicol 2005.htm. Drexler H. Rydberg P.56(15):6046-53.Acrylamide glycidamide by gas chromatography-mass spectrometry. Analysis of acrylamide. Mutat Res 2005. Rice JM. Yang HJ. Ingham L. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Kutting B. U. J Agric Food Chem 2002.gov/chemfact/s_acryla. Int J Hyg Environ Health 2004.S. Toxicol Lett 2002.20(6):959-64. Toxicological effects of acrylamide on rat testicular gene expression profile. Ospina M. Han DU. J Agric Food Chem 2008. Licea-Perez H. Office of Pollution Prevention and Toxics. Gray JG. Adv Exp Med Biol 2005. Smith A. 2/3/09. Acrylamide. Washington (DC). 1994. Drexler H. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Hallmans G. Schettgen T. Available at URL: http://www. Ding X. EPA).561:89-96. Schettgen T.S. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Marko D. Environmental Protection Agency (U. Hemoglobin adducts of ethylene oxide. Chae C. Tjønneland A. Letzel S.txt. Angerer J. The carcinogenicity of acrylamide. Chemical Summary for Acrylamide. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Tareke E.134(1-3):65-70. Agudo A. September. Choi JH.S. Angerer J. Drexler H. U.580(1-2):71-80. Rapid Commun Mass Spectrom 2006. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Han CH. Eriksson S. Schettgen T. Anal Biochem 1999. Liu Y. Puppel N.50(17):4998-5006.206(1):9-14. Slimani N. Myers GL. Liu K. Ospina M. Integrated Risk Information System (IRIS). propylene oxide. Weiss T. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Mutat Res 2005 Feb 7. Rossbach B. Lee SH.207(6):531-9.580(1-2):3-20. Tjaden Z. Jin Y. Benetou V. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. 2/3/09 Vesper HW. Available at URL: http://www. Fueller F. Fu D. Karlsson P. Toxicol Lett 2006. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.

137-.30) 2.670) .70) 2.220) .120-.060-.997-3.23 (1.030-.020-.120 (.840) 3.726) .47-3.047-.660) .540 (.140 (.057-.40) .070) .17) .00) .49) 1.160 (.05.030 (.063) .080) < LOD .62) 2. maternal exposure during pregnancy can result in lower birth weight.175 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer. respectively.34 (1.073) < LOD . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease. DHHS.55-2.770) . Children exposed to ETS are at increased risk for sudden infant death syndrome.213) .180) . which may vary for some chemicals by year and by individual sample.070) .20) .480-.50 (1.85 (1.080 (.110) .49) 1. acute respiratory illness.040-.32-2.302) .11) .22) 2.066 (.110 (.050-.312) .310-1. and various other disorders (U.42 (1.054 (. 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.30) * .090-.060 (<LOD-.630 (. emphysema. Cigarettes contain about 1.39) 3.44) 2.S.145) . DHHS.310-1.570 (.260) 1.95) 1.20 (.79) 3.061) < LOD .43 (1.100-.00) 1.42-4.320) .63 (2.68) 2.55 (1.428-.040 (.120) .050) .580 (.39 (1.350-.088-.068) .201) .09-3.14) .50-4.92) 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 .850 (.220) .44 (2.062 (.14) .077) .Cotinine Cotinine CAS No.690 (.910-1.21 (.19-2.200) 1.621-1. 2006). see Data Analysis section) for Survey years 99-00.068) .500 (.54 (1.188) .071 (.154-.50) 3.35 (2.350-. cardiovascular disease.193) .071) .153-.066) .080-.030-.080-.44 (1.09-2.160) .77 (2.070) 75th . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.710 (.990 (.66) 1.111-.65 (1.077) .180) .167 (.S.81-2.280 (.053 (<LOD-.54 (1.230 (.180 (.130 (.900-1.630 (..84-3.180) .080 (.505 (.060-.730 (.160-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .216 (.108) * . Survey Geometric mean (95% conf.310) 90th 1.14-1.164 (.190-.820) .140-.086 (.S.131 (.19) .93) .01 (1.05) 1.160 (. ** In the 2001-2002 survey period.106-.087 (.180) .050 (<LOD-.059-.770-1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.104-.160 (.260-1.060 (. and 0.60-2.360) .110 (.058 (.17 (1.62 (2.20-2.12 (2.33-2.190-.142-.163 (.080-.220-.090-.040 (.09-3.350 (.740-1.76 (1. and 17% had an LOD of 0.120 (. 2004).87-3.080) < LOD < LOD .110 (.050 (<LOD-.052 (<LOD-. population from the National Health and Nutrition Examination Survey.110-.310) .28-1.580) .094) .600-1.38-2.15 (2.570-1.96-4.23-2. < LOD means less than the limit of detection.120 (.080-.076-.860 (.21-1.140-.030-.740-1.96) 2.540-.120 (.930 (.510 (.04 (1.308 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.89) 1.110-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .15) 2.180 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.02 (.12 (1.23 (.17 (.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.230) .48-2.20 (1.05 ng/mL.770) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.070-. ear problems.32-2.150) .66-3. 2004).53-4.110 (.015 ng/mL.950 (.5% nicotine by weight (Kozlowski et al.28) .32) 1.53 (1.44) 2.087-. 1998).052 (<LOD-.94) 1. and 03-04 are 0.50-1.164 (.050 (.620 (.059-.430-1.066-.88 (1.83-2.580-1.790) .12) 1.198) * .470-.043-.12-4.48-3.187) .26-1.99) 2.70-2.060 (<LOD-.115-.040 (.050) . Fourth National Report on Human Exposure to Environmental Chemicals 15 .533-.139) * .99) 2.210 (.130) .960-1.96 (1.070 (<LOD-.087) < LOD < LOD .19) 1.506 (.060 (.300) . stroke.77 (1.050 (<LOD-.197) .144 (.084) .124 (.090-.410) .110) .54) 1.240 (.68) . 83% of measurements had an LOD of 0.110 (.163) .88 (.630 (.234) .520 (.30) 2.01) 3.620-1.137 (.089) Age group 3-11 years 99-00 01-02** 03-04 .18-3.160) .180) .16) .23 (2.63-2.480-1.148-.150) .050 (<LOD-.060) .047-.920 (.190-.950-1.110-.370-.400-.140 (.21-1.57) 2. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. and exacerbated asthma (U.060-.68 (1.92 (1.040-.990) .625) .77 (1.120-.02) 1.015.45) 1.66 (1.20) 1.78) 2.75) 1.02) 1.120 (.075 (.800 (.126) .050-. acute respiratory infections.450-.

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

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

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

110 (.160) < LOD .130 (. DEET is not a developmental or reproductive toxicant in animals (U.270) 688 678 518 700 598 956 Limit of detection (LOD. DEET can be applied to clothing and the skin to repel biting insects.140-. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.220 (. 2003).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 .150) < LOD . DEET is not genotoxic.120-. Sudakin and Trevathan.130-.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.180) < LOD . 1998).140) < LOD .110 (<LOD-.110 (<LOD-.130-. DEET is not registered for use on agricultural commodities.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.130 (. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.S.130) < LOD . 2002). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140 (.epa.140) < LOD .gov/pesticides/.S. EPA. including seizures and encephalopathy.180 (. population from the National Health and Nutrition Examination Survey. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.180 (.140) < LOD .170 (. Neurological effects in humans. One survey detected DEET in 74% of sampled streams in the U.EPA. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Additional information is available from U. 2003).110-. < LOD means less than the limit of detection. and it has not been rated by IARC or NTP with respect to human carcinogenicity.120-.S.210 (. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.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 . have been reported as result of self-poisoning by ingestion or excessive dermal application.110 (. (Kolpin et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.100-. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby..N-Diethyl-meta-toluamide (DEET) N. 134-62-3 General Information N. 1995.100-. Its use is recommended for prevention of several vector-borne diseases.100 (<LOD-. There are over 225 insect repellents brands containing DEET.130) < LOD .EPA. and they range in concentration from 4% to 100%..130-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . (U.170 (. 1998).560) < LOD . but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. Fourth National Report on Human Exposure to Environmental Chemicals 19 .100-.EPA at: http://www. DEET has low acute toxicity.520) < LOD . which may vary for some chemicals by year and by individual sample.110 (.110-.100-.130-.110 (. 2002).S.190) < LOD .N-Diethyl-meta-toluamide (DEET) CAS No.100-. 2005).S.250) < LOD . Urinary N.180 (.100-.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . About 3-8% of dermally applied DEET is absorbed.449 and 0.1.. DEET is also used in combination with dermal sun screens (U.S.240) < LOD .N. After absorption.130 (.

500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.290-.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.370-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.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 . 2007).320 (. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.230) < LOD .170-.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 .410-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240) < LOD .240-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .390-.250 (.370) < LOD .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.280-1..N.350) < LOD .S.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.270 (.230-.350) < LOD .190 (.150) < LOD .270 (<LOD-.330 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.250) < LOD .640 (. 1992).190 (<LOD-.410 (.200 (.190 (.410 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.320) < LOD . Survey Geometric mean (95% conf.300 (.230-.350-.190-. 2005).S.490) < LOD .330 (.140-.280 (. 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.270) < LOD .270-.500 (.480 (.440) < LOD .93) < LOD .130 (<LOD-.250-.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 .. 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 . Urinary DEET levels as high as 5.630) < LOD . population from the National Health and Nutrition Examination Survey. representative subsamples from NHANES 2001-2002.150-. Urinary N. In this survey period.

and excretion of N. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. EPA. Diethyltoluamide (DEET).epa.S. pp.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.epa. Meyer MT.N-diethyl-mtoluamide following dermal application to human volunteers.S. 4/9/09 U. Bell JW.S. Osimitz TG. Centers for Disease Control and Prevention (CDC). N. Zaugg SD. Toxicity and Exposure Assessment in Children’s Health. Gabriel KL.EPA. Chemical Summary. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . hormones.N. Third National Report on Human Exposure to Environmental Chemicals.16(1):10-13.2:341352. DEET: a review and update of safety and risk in the general population. Absorption. DeBord KE. Smallwood AW. et al. Human exposures to N.N-Diethyl-meta-toluamide (DEET) References Arcury TA.S. Selim S. EPA 738-R98-010. 1-118.115(8):1254-1260. Environ Health Perspect 2007. Furlong ET. Reregistration Eligibility Decision (RED): DEET. Barr DB. September 1998.pdf. Sudakin DL. Chen H. Environmental Protection Agency (U. Environ Sci Technol 2002. Tapia J. Available at URL: http://www.36(6):1202-1211.S.41(6):831-839.S. Quandt SA. 2005 Kolpin DW. 1999-2000: a national reconnaissance.S. J Anal Toxicol 1992. and other organic wastewater contaminants in U. Trevathan WR. Veltri JC. J Toxicol Clin Toxicol 2003. Barber LB. metabolism. U. Int J Toxicol 2002. Environmental Protection Agency (U.EPA). streams. Available at URL: http://www. Thurman EM. U.gov/teach/chem_summ/ DEET_summary. Page BC.EPA).N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Fundam Appl Toxicol 1995. Lowry LK. 1993-1997. Schoenig GP. Grzywacz JG. Hartnagel RE Jr.gov/oppsrrd1/REDs/0002red.25:95-100. Atlanta (GA). 2005. Pharmaceuticals. pdf. Washington (DC): U.

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

Available at URL: http://ecb. bisphenol A glucuronide. 4. Imai H. Kim CS. Cohen JT.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt.137(3):353-362. September. Hlywka JJ.S.S.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Wong LY. Cunha G.113(4):391-395. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. J Am Dent Assoc 2006. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Zaugg SD. Research Triangle Park. Ikka T. Chem Res Toxicol 2001.gov/chemicals/bisphenol/bisphenol. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Szigeti-Buck. vom Saal FS.nih. Reprod Toxicol 2001. Exposure of the U. Bradley S. 2/4/09 European Commission. Ye X. Arakawa C.102(19):7014-7019. Kim YH. Fujii S. Toxicol Sci 2002. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. and other organic wastewater contaminants in U. Koh WS. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Gray GM. Endocrinology 2008. Lynch BS. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.. Thomas BF.Environmental Phenols References Akingbemi BT. Barber LB. Marr MC. August 2001. Barton L.149:988-994. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.S. Biochem Biophys Res Commun 2003. DirectorateGeneral Health and Consumer Protection. Kawamura N. Available at URL: http://ntp. niehs.145:592-603. European Commission. National Institutes of Health. 1999-2000: a national reconnaissance.jrc. Brine DR. et al. Pyo MY. Bisphenol A. Proc Natl Acad Sci USA 2005. National Toxicology Program. Reidy JA. Timms BG. Munro IC. Calafat AM. In vitro and in vivo interactions of bisphenol A and its metabolite.68(1):121-146. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).69(22):2611-2625. May 22. Nippon Eiseigaku Zasshi 2004. Environ Health Perspect 2005. Howdeshell KL. Kim JC. Environ Health Perspect 2008.pdf. Ema M. Furukawa M. Koulova AI. Kroes R. Kuklenyik Z. Twomey K. Reidy JA. Richter CA..pdf. Tyl RW. Rhomberg et al. 2002. Park S.nih. et al. Ispra. Sottas CM. Cha SW. McConnell EE. Calafat AM. NC. Haighton LA.780(2):365-370. Chung MK. MacLusky. and Hajszan. Ekong J.59(9):625-628.eu/ health/ph_risk/committees/sct/documents/out156_en.europa.59(4):403-408. C.gov/chemicals/bisphenol/BPAFinalEPVF112607. Joskow R. T. streams. Kolpin DW. Environ Sci Technol 2002. Department of Health and Human Services. Meyer MT. and Hardy MP. Serizawa S.Scientific Committee on Toxicity. Caudill SP. Thurman EM. Hughes C. November 26. Shin HC. Barr DB. Joint Research Centre Institute of Health and Consumer Protection.. Furlong ET. K.36(6):1202-1211. Doull J.nih. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy.10:875-921. 2008. Available at URL: http://ec. Belgium. Kiguchi M. Needham LL. Pharmaceuticals. Watanabe S. 2003. Brussels. hormones. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. et al.niehs. An evaluation of the possible carcinogenicity of bisphenol A to humans. N. Han SY. J Chromatogr B Analyt Technol Biomed Life Sci 2002. 32 Fourth National Report on Human Exposure to Environmental Chemicals . 2/4/09 Fujimaki K. Human Health. 5: 505-523.35(2 Pt 1):238-254. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Yoshinaga J.pdf . Leranth. Rat two-generation reproductive toxicity study of bisphenol A.pdf . Endocrinology 2004. Matthews JB. Myers CB.14(2):149-157. Keimowitz AR.J.pdf. Tsugane S. 2/4/09 Ouchi K. Needham LL. Barr JR. Italy. National Institute of Environmental Health Sciences.312(2):441-448.116(1):39-44. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Calafat AM. 2007. Hanaoka T. Available at URL: http://cerhr. Hum Ecol Risk Assess 2004. Harazono A. Han SS. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Klinefelter GR. 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. Gender differences in the levels of bisphenol A metabolites in urine. Available at URL: http://cerhr. Yang M. Rubin C. U. Hara K. Life Sci 2001. with estrogen receptors alpha and beta. Ecotoxicity and the Environment (CSTEE). Zacharewski TR. niehs. Watanabe C. Regul Toxicol Pharmacol 2002. Occup Environ Med 2002. Needham LL.

Chuang JC. Environ Res 2007. et al. Kim SY. III.40(7):905-12. Endocrinology 2006. Environ Health Perspect 2005. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Chem Res Toxicol 2002.15:12811287. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Jang JY. Nagel SC. bisphenol-A. Vom Saal FS. Biological monitoring of bisphenol a in a Korean population. Sheldon LS. Dekant W. Filser JG. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Csanady GA.147(6 Suppl):S56-69.103(1):9-20. Chang SS. Lordo RA. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Wilson NK.113(8):926-33. Large effects from small exposures.Environmental Phenols Volkel W. Kawamoto T. vom Saal FS. Arch Environ Contam Toxicol 2003. Witorsch RJ. Food Chem Toxicol 2002. Welshons WV. Colnot T. Yang M. An observational study of the potential exposures of preschool children to pentachlorophenol. and nonylphenol at home and daycare. Hughes C. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Morgan MK.44(4):546-51. Lee SM.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 2. Less frequently. impaired steroidogenesis. streams in 30 states (Kolpin et al. In the 1990s.900 (. and emulsifiers. Saito et al.80 (1.200-. 140-66-9 General Information 4-tert-Octyphenol.50) . 1995. < LOD means less than the limit of detection. pesticides.369 (.357 (.200-.30 (1..1.10-2. over 500.600-1. including 4-tert-octylphenol. In rats..20 (1.10 (.300 (<LOD-.90) 2.300 (<LOD-.500) 75th .10 (.60) 1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.20-2.500-1.900 (. through sewage.20) 2.10 (1. and was quickly eliminated from the blood (Certa et al..80) 2. 2003.20-2.60) 613 652 1092 Limit of detection (LOD. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.S. Survey Geometric mean (95% conf.g.00 (1.274-.600-1. 2002). textiles. leading to inhalation as another potential exposure route (Rudel et al.600) .300-. and through manufacturing waste streams (Warhurst.50-2.20-2.40) 2.00 (.300 (<LOD-. During the 1980s and 1990s.00) 1229 1288 03-04 03-04 03-04 * .300 (<LOD-..50) . and some of their degradation products are toxic to aquatic life.500) . and from contact with some personal care products and detergents. Disposition in humans has not been studied sufficiently. orally administered 4-tert-octylphenol was well absorbed.S.. The alkylphenols can bioaccumulate in some fish. industrial cleaners. The alkylphenol ethoxylates enter the environment through human use of products containing them. Several alkylphenols.300 (<LOD-.60-3.20) 314 715 1488 03-04 03-04 * * .40) 1. 1996).600) .40) 2.400 (. Indoor and to a lesser extent.20-2.500) .80 (1. altered estrus cycles and reproductive outcomes.20-2.3.40) * 03-04 03-04 03-04 .60-3.30 (.40) 1.497) * .40 (1.30) 1.50) 1. 4-octylphenol monoethoxylate was detected in 43..500-1. Katsuda et al.900 (. which are anionic surfactants used in detergents.30 (1.30) 90th 1.20) 1.70 (1.50) 1.700-1. population from the National Health and Nutrition Examination Survey. 34 Fourth National Report on Human Exposure to Environmental Chemicals . did not bioaccumulate. and to alkylphenoxycarboxylates..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 .5% of 139 U. and the polyethoxy chain may consist of up to 50 ethoxy units.600-1.268-. the various alkylphenols have also been used as emulsifiers and modifiers in paints.20-2. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. which may vary for some chemicals by year and by individual sample. 2006.60-3. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.10) 1.. Blake and Boockfor. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). 2000.500) .600) .80 (1. 2002).50-3. is used to manufacture alkylphenol ethoxylates.70 (1. Bian et al.400 (. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.900 (.30-2. Laws et al. and some personal care products.600-1.300-.00 (. testicular atrophy.50) 1.400) 1.70 (1.600-1.389 (.60-3.. have demonstrated estrogenic effects particularly when injected at high doses in animals.800-1.600) 1.70 (1.900 (. 1997. and impaired spermatogenesis (e. an alkylphenol.000 tons of alkylphenol ethoxylates were produced annually worldwide. Urinary 4-tert-Octylphenol (4-[1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. to shorter chain alkylphenol ethoxylates. 2004).60-3.30 (1.2. 2000.g.299-. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins..60) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. see Data Analysis section) for Survey year 03-04 is 0.400 (. fish) and drinking water.60-3.507) * < LOD .Environmental Phenols 4-tert-Octylphenol CAS No. altered neonatal sexual development.10) 2.500 (.90) 2.477) . In 1999-2000.50 (1. Ying et al.600-1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.30 (1.

Nagao et al.78) 1228 1286 03-04 03-04 03-04 * ..460 (.03-6.03 (1.00) 1.67-2.65-3.620) . Urinary 4-tert-Octylphenol (4-[1.630-1.03 (1.Environmental Phenols Myllymaki et al.380 (<LOD-.320 (<LOD-.890-2.00) 2.270 (.76 (2.400) .62 (1.08) 1.560) . representative subsample of NHANES 2003-2004.50 (2.00) 2.78) 3.470) 75th . 4-tert-Octylphenol is not considered directly genotoxic.59 (1. In a small number of adult Japanese volunteers.25) 90th 1..349) * < LOD .640-1. It is unclear if estrogenic or other effects occur in animals through oral dosing.85 (1.S.435 (. population from the National Health and Nutrition Examination Survey.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..170-. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.60 (1.20 (1.500-1.11) 1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al. IARC and NTP have not rated octylphenol.14) 314 713 1487 03-04 03-04 * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.00 (..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 .43) 1.40-4.300 (<LOD-.29) 2.54) * 03-04 03-04 03-04 . 2004. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.31 (1.68-2.550-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.59) 1. 2004). or their corresponding ethoxylates with respect to human carcinogenicity.43-3.276 (.17 (.730-1. Fourth National Report on Human Exposure to Environmental Chemicals 35 .10-2.270-.280-.370 (<LOD-.269 (.420) .05-2.910 (. nonylphenol.3.. 2000. Tyl et al.11-2.620-1.25) 2..337-.96-4.1.850 (.384) * .450) 1.02-4.770 (.43) 1. 2003.860 (.530) .199-. at lower or environmentally relevant doses (Blake et al.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.62 (1.73) 2.11) 2.610) .40 (1. 2001. Survey Geometric mean (95% conf.33) 3.81 (1.260 (<LOD-.22) . Kawaguchi et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.570) .160-.71) 2. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U. 2005.410 (.41) . 2001).207-.15) 1. Yoshida et al.06 (2. Sweeney et al. 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.64 (. Calafat et al.18-4.270 (.740 (.62) .740 (.00 (.450) .25-2. 1999).540-1.470-1.36-3.470-1.68) 2.31-2.53-3.S.78 (1.33 (2.

141(7):2667-2673. and sertoli cell number. Muller AM. Biol Reprod 1997. Zaugg SD. Katsuda S. Yoshimura Y. Blake CA. Song L. Bolt HM. Needham LL. Furlong ET. Izumi S. Kolpin DW. Reidy JA. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats.28(3):215-226. Nagao T. 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. Tyl RW.15(6):683-692. Taya K.116(1):39-44. J Chromatogr B Analyt Technol Biomed Life Sci 2004. polybrominated diphenyl ethers. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. and testosterone. Millette CF. Ono H. Boockfor FR. Seto H. et al. streams. Okada F. Roche JF.Environmental Phenols References Bian Q. Sweeney T.54(1):154-167. Kookana R. Certa H. Toxicol Appl Pharmacol 2005. Boockfor FR. and other endocrine-disrupting compounds in indoor air and dust.14(5):325-332. Korn LR. Xu L. et al. Saito Y. Available at URL: http:// www. Toppari J. Reprod Toxicol 2004.foe. Takai N. Toxicol Sci 2000. Indoor air pollution by alkylphenols in Tokyo. Ye X. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review.36(6):1202-1211. Environ Int 2002. Rudel RA. Inoue K. Wong LY. Wiegand HJ. Environ Sci Technol 2002. Brody JG.18(1):43-51.S. 2003.121(1):21-33. Horie M. Haavisto TE. Thurman EM. Takenaka A. and other organic wastewater contaminants in U. Watanabe G. Raychoudhury SS. Paranko J. 1999-2000: a national reconnaissance. Seely JC. Barber LB. Toxicokinetics of p-tert-octylphenol in male Wistar rats.44(8):1355-1361. Two-generation reproduction study with para-tert-octylphenol in rats. Nair-Menon JU. nonylphenol. Katsuda S.folliclestimulating hormone. Ferrell JM. Yoshida M. Regul Toxicol Pharmacol 1999. Warhurst AM. Food Chem Toxicol 2006. Maekawa A. Meyer MT. 1995.S. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Pharmaceuticals. Wang X. Indoor Air 2004. Makino T. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats.57(2):255-266. Usumi K. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Exposure of the U. Yoshimura S. Nicol L. Environ Sci Technol 2003. Toxicol Appl Pharmacol 2000. prolactin. hormones. Saito I.165(3):217-226. Onuki A. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. McCoy GL. Bodman GJ. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Sakui N. Camann DE. Laws SC. Watanabe G. Estrogenic activity of octylphenol.pdf. Myllymaki SA. Fedtke N. Qian J. Reprod Toxicol 2001. Williams B. Arch Toxicol 1996.799(1):119-125. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.71(1-2):112-122.30(2 Pt 1):81-95. Brooks AN. Carey SA. Maekawa A. Fail PA. Endocrinology 2000. Toxicol Lett 2001.37(20):4543-53. Myers CB.uk/resource/reports/ethoxylates_alkylphenols. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Cooper RL.207(1):59-68. Blake CA. Karjalainen M. Kawaguchi M. Kawaguchi M. Calafat AM. 2/4/09 Ying GG. Inoue K. testis size. Brine DR. Spengler JD. pesticides. Chen J. et al. Ito R. Phthalates. et al. Environ Health Perspect 2008. Taya K. bisphenol A and methoxychlor in rats. alkylphenols.co. Anal Chim Acta 486:41-50. Yoshida M. Nakagomi M. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Marr MC.

Triclosan formulations may rarely cause skin irritation.. and wound disinfection solutions. 2007).. It acts by inhibiting bacterial fatty acid synthesis. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. 1987). the median urinary triclosan level of 7.. 2007). Mezcua et al. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect.. and medical devices. Triclosan enters the aquatic environment mainly through residential wastewaters. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. 2007. General population exposure results from dermal and oral use of products containing triclosan. Triclosan is not considered teratogenic at maternally toxic doses. 2005. 2006).. acne medications.. Triclosan has a low bioaccumulation potential in fish. mouthwashes. 1976.S. Matsumura et al. streams sampled in 30 states (Kolpin et al. Triclosan can be absorbed across skin into the blood stream... it has low acute toxicity. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. young girls. 2002). representative subsample of NHANES 2003-2004.Environmental Phenols Triclosan CAS No. 2008 has shown higher levels during the third decade of life and among people with the highest household income. Triclosan has been added to soaps. 1988.2 µg/L was comparable to the median level (8. and has also been impregnated into some kitchen utensils. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. Fourth National Report on Human Exposure to Environmental Chemicals 37 . 2007.6% of 139 U. In animal studies.. In the body it is conjugated to glucuronides and sulfates (Bodey et al. Moss et al. 2000. Lyman and Furia. 2000).. In animal and human studies.. 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. a process that can result in the formation of small amounts of 2. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Calafat et al. It can be photochemically and biologically degraded. Calafat et al. Some reports show endocrine effects are observed in amphibians and fish (Foran et al.S. triclosan was found in 57. (Sandborgh-Englund et al.8-dichlorodibenzo-p-dioxin (Aranami et al. In a study of 90 U.. In a U. toys. In 1999-2000.. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. 2004). Biomonitoring Information Urinary triclosan levels reflect recent exposure.S. but not by race/ethnicity and sex. 1996. IARC and NTP do not have ratings with respect to human carcinogenicity. Veldhoen et al.. toothpastes..2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. 1969). 2008). deodorants.

6) 90th 212 (172-241) 03-04 03-04 03-04 9.9) 8.3) 6.4) 75th 43. interval) 12.90-10.5) 11.0-15.72-13.6 (9.60 (6.5-14.8-60.1-39.45-10.0) 65.7 (28.6-15.20-13.3 (8.3 (26.2-58.8-127) 37.7 (39.40-11.00 (4.6-20.82 (8.80 (5. see Data Analysis section) for Survey year 03-04 is 2.4) 51.9-236) 193 (90.4) 25.8) 14.3 (9.1 (15.2) 9.7) 123 (36.1) 11.9 (33.3 (11.1) 9.48-10.4.5) 66.0-19.1) 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 9.50-10.7 (11.4 (12.54 (8.8-112) 30.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.0 (34.93 (7.2 (25. Survey Geometric mean (95% conf.20-11.9-61.8-85.29-12.8) 7.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.0 (26.1) 9.7) 10.22-10. Survey Geometric mean (95% conf.8-63.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.89-11.6) 12.9) 75th 47.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.2 (37.3-35.9 (11.2 (11.0-213) 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 .5) 13.7 (14.2 (27.6 (12.1) 9.8 (21.7) 292 (151-432) 132 (78.4 (38.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.94 (7.0-15.Environmental Phenols Urinary Triclosan (2.32-14.1) 14.4) 73.4) 90th 249 (188-304) 03-04 03-04 03-04 8.2-46.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10-9.6 (30.92-12.2) 13.20 (7.9 (8.7 (9.6-14.6) 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 9.4) 357 (225-456) 203 (87.6-65.1 (45.S.6) 10.3-31. population from the National Health and Nutrition Examination Survey.2-58.S.5) 20.9) 7.9 (50.20 (7.10) 84.1) 13.1) 9.2-14.3) 47.4-19.0 (11.16 (6.4-18.5 (11.8) 9.86-12.4) 317 (231-433) 144 (96.4 (32.18 (5.30-14.3-15.4 (11.3) 10.5-86.6-111) 33.11-11.70-16.43-13.3.6-37.1 (8.6 (10.3-67.74 (5.0 (36. interval) 13.20-10.8) 116 (39.6) 39.0-73.1) 50.4.45-13.55 (4.45 (5.48 (8.40-17.21 (6.6-14.2 (10.2) 12.00-8.6) 31. Urinary Triclosan (2.50) 10.0) 9.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14. population from the National Health and Nutrition Examination Survey.2 (13.4) 7.1) 7.0) 49.38-18.60 (8.0 (8.9) 32.

Mar Environ Res 2000. Ekstrand J. Howes D. Hong HC. IMS Ind Med Surg 1969. Ye X. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Needham LL. Osachoff H. et al. Bhargava HN. Veldhoen N. Barber LB. Zaugg SD. Gomez MJ. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Toxicology of 2. Sandborgh-Englund G. Environ Health Perspect 2008.66:1052-1056.4.4’-trichloro-2’hydroxydiphenyl ether). Katsura E. Bodey GP. Triclosan: applications and safety. et al. Percutaneous penetration and dermal metabolism of triclosan (2. streams. Windham G. et al. Teitelbaum SL. Moss T. Meyer MT. Environ Health Perspect 2007. Aranami K. Pharmaceuticals. Fernandez-Alba AR. Matsumura N.80(3):217-227. Reidy JA. Gilbert RJ. Ogawa H. 4. Thurman EM. Odham G.38(4):361370.S. Aguera A. Am J Infect Control 1996.83(1):84. The oral retention and antiplaque efficacy of triclosan in human volunteers. Adolfsson-Erici M. 4’-trichloro-2’-hydroxydiphenyl ether.116(3):303-307. Arch Environ Contam Toxicol 1988. Evidence of 2. Mezcua M. J Toxicol Environ Health A 2006. and phenols in girls. Urinary concentrations of triclosan in the U. Biol Pharm Bull 2005. Nagao Y. Williams PE.50(1-5):153-156. Lyman FL. Developmental evaluation of a potential non-steroidal estrogen: triclosan.69(20):1861-1873. Chelimo C. Readman JW. Ebersole R. Ishibashi H. Wigmore H.23(5):579-583. Anal Chim Acta 1004. Foran CM. J Invest Dermatol 1976. et al. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Williams FM. Leonard PA. Okui T. Aquat Toxicol 2006.S.Environmental Phenols References Aiello AE. Wong LY.. Skirrow RC.45 Suppl 2:S137-S147.38(2):64-71.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Food Chem Toxicol 2000. Hirano M. Pinney SM. Furlong ET. 1999-2000: a national reconnaissance. and other organic wastewater contaminants in U. Kaneshima H.7/2. Hernando MD.115:116-121.67(4):532-537. Environ Sci Technol 2002. Ferrer I. Kanetoshi A.524:241-247. Wolff MS. Levy SB.28(9):1748-1751. Photolytic degradation of triclosan in freshwater and seawater. Erratum in: Aquat Toxicol 2007. Chemosphere 2007. Larson EL. Britton JA. Pharmacokinetics of triclosan following oral ingestion in humans. hormones. Clapson DJ. Bennett ER. Calafat AM. Pilot study of urinary biomarkers of phytoestrogens. population: 2003-2004.36(6):1202-1211. Br J Clin Pharmacol 1987. Kolpin DW. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development.24(3):209-218. Furia T. Fourth National Report on Human Exposure to Environmental Chemicals 39 .17(5):637-644. phthalates. Gunderson MP. Shiratsuchi H. Watanabe N. Benson WH.

plants. and dermal contact with PCP-treated products. and animals.680-1.30 (1. mollusicide.350-1. PCP is degraded by sunlight and metabolized rapidly by microorganisms.350-1.10) 1. After a single dose.10 (.50) 1.62 (. hypertension.73 (1. has been restricted.90) 2.350 (.350) < LOD .47-3.350-..350-.350) < LOD . ingestion of contaminated food or water.350 (.860-2. PCP cannot be used on wood in residential or agricultural buildings.350 (.350) < LOD . Acute.350-1.990-2.510-5.30 (.37) .350-.58-2. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. utility poles and fence posts). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350) < LOD .76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350-. the elimination half-life may be a week or more (Uhl et al. After absorption.78) 1.350) < LOD .350 (.00 (. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350) < LOD < LOD 75th . 1997). along with small amounts of tetrachlorohydroquinone and conjugates. Human exposure to PCP has become less common.70) 2.90) 1. General population exposure to PCP may occur by inhalation of contaminated air.350-2.390 (.37 (.350-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350-.33) .350) < LOD .350) < LOD .480-2. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.51) 1.76) 1. 1976. Effects including hyperthermia. other polychlorinated benzenes.350 (.350) < LOD .94 (1.32 (.350-.960) 1.350-.30 (.850-2.350-.67) 1.350-. and possibly of lindane (IPCS. Survey Geometric mean (95% conf.08-3.10 (<LOD-1.70) .58-2..350 (..30) . PCP is absorbed rapidly and well by all exposure routes.350) .650 (.500-2.650) 1.350-1.350-.09) . < LOD means less than the limit of detection.94 (1.33-2.350) < LOD .48 (. and it is used primarily as a preservative for wood to be used outdoors (e.350) < LOD .83 (2.510-3. To-Figueras et al. PCP is eliminated over a few days (Braun et al. which may vary for some chemicals by year and by individual sample.350-2. 1986).90 (1.770 (. Since 1984.350) < LOD . water and sediments because of the large amounts that were produced and used historically.590-1.65 (.60) 1.350-2.350-. Kohli et al. air.350 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350-. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.S. herbicide.04) 1. bactericide.42) 696 680 521 696 603 951 Limit of detection (LOD.350 (.350 (.350 (. and metabolic acidosis were observed in CAS No.530) 1.350 (.350-.76) ..91 (1.350-.40 (.60) 1.350-.350-.350-.01 (<LOD-1.350 (.350) < LOD . population from the National Health and Nutrition Examination Survey.54-2.75) 2.g.10) 1.350 (.350 (.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .00) 1. 40 Fourth National Report on Human Exposure to Environmental Chemicals .23 (. 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.18 (<LOD-1.350) < LOD . In the environment.350 (.350 (. algaecide and insecticide.350-.47-5.990 (<LOD-2.660 (.980 (.65 (.350-.S.10 (1.350-.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .00) 2.350 (.350) < LOD .350) < LOD .25 and 0.890 (. PCP use in the U. The parent compound and conjugates.350) < LOD .350) 90th .30) 1. PCP has been detected in soils.45-2. PCP is distributed to most tissues and is not extensively metabolized.350 (.350 (. 2002.350-.00) 1. so it is relatively non-persistent. 1979).98 (1..350 (.350-2.30) 1.350-. with repeated or chronic exposure.390 (. are eliminated in the urine.890-1.5.80) .64) 1.48-2.350 (.630 (.

850 (.S. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.75) 1. EPA has developed standards for PCP in drinking water and the environment. 2003).320 (.320) < LOD .800) < LOD 1.830) < LOD .67-3.500-.EPA.30) 1.94-3.S.580-.00-1. van Raaij et al.430-.26 (1. or skin absorption.950-1.78) 1.52 (1.19 (1.240-.25-1. population from the National Health and Nutrition Examination Survey.52) 1. More information about external exposure (i.220-.atsdr.760 (.490) < LOD . chronically administered high doses of PCP were hepatotoxic.00-1.950-1.51) 1.370 (.360-.220-.610 (. Death can result from seizures and cardiovascular collapse.52 (<LOD-1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .06) 1.79) 1.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .67 (1.48-2.Fungicides adults and children severely exposed to PCP through ingestion. children in the 1980’s. Pentachlorophenol is not mutagenic or teratogenic.300 (.67 (1.330-.84-4. environmental levels) and health effects is available from the U. Among adults in the NHANES 1999-2000 subsample.260 (.40) 1.25 (1.67 (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 (4.40) 1.30) 1.cdc.06-3.11) 2.920 (.epa.290) < LOD .. In a small sample of U.82) 1.56) 1.300 (.29-3. In NHANES 2001-2002 subsamples.83 (1.430) < LOD . inhalation. EPA at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06 (..500-1.560-.650) 90th 1.84) 1.30 (.21 (.40) 1.350) < LOD .25-2. 2000)..69 (1.320) < LOD < LOD 75th . The U.780-1. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al.25) 1.94 (1.21-2.6 and 14.26 (1.280) < LOD .gov/ pesticides/ and from ATSDR at: http://www.290-.95) 3. carcinogenic..25 (1.10 (1. In animals. 2003).40) 1.S.67 (1.560) < LOD .18 (1.360 (..25-2. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.310-.35) 1. 1991).09-1.700-2.e.19) 2.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1989).590) < LOD . 1989).19) 2.630 (. respectively) (Becker et al.html. Fourth National Report on Human Exposure to Environmental Chemicals 41 . 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.36) .75 (<LOD-2. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.30-2. Survey Geometric mean (95% conf.560) < LOD .67 (1.57 (1.900-1.S.380-.710-1.310) < LOD .35-2.00) 1.320) < LOD .250 (.13 (. and adversely affected thyroid function (U.40) 1.340-.16-1.780) < LOD .10-2.67-3.09 (<LOD-2.300 (. 2004.400 (.78) 1.730) < LOD .52 (<LOD-1.500 (.510-.S.35-2.55) 1.92) 1.910-1.0 mg/L.. 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.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. and the FDA has established a standard for bottled water. respectively) (Seifert et al. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.290-.470 (.18) .35) 1.270-.570 (.420) < LOD .9 mg/L.800-1.40-2.270-.67-2.57 (. 1995).990 (.510-.90) 1.16 (.19) 2.73 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.84 (1.82 (1.gov/ toxpro2..650 (.590-1. OSHA has established an occupational standard..34 (.650 (.08 and 5.440 (.94 (1.250 (.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .950-1.

Fast DM. Int J Hyg Environ Health 2003.71:99108. Krause C.54(3):203-208. 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. Environmental Protection Agency (U.4:289296. Blau GE. To T. Pentachlorophenol measurements in body fluids of people in log homes and workplaces.18:475-481. Notten WR. Otero R. 11/30/2004. Needham LL. Braun WH. 206:15-24.105(1):78-83. Cline RE. Helm D. Schlatter C. Sala M. urine.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 1989.10:552-65. Lindane. Engel R. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Rodamilans M. Needham LL. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Kaus S. Schmid P. Chenoweth MB. Bragt PC. 4/21/09 Kohli J. Toxicology 1991: 67(1):107-16. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. International Programme on Chemical Safety (IPCS).inchem. The metabolism of higher chlorinated benzene isomers. Phillips DL. Jones D. References Becker K. Shealy DB. Becker K.58:182-186. Seiwert M. Arch Toxicol 1986. htm. U. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Arch Environ Contam Toxicol 1989. Smith SJ.S. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Dev Toxicol Environ Sci 1979. Pharmacokinetics of pentachlorophenol in man. Schulz C. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. PCP: Human Risk Characterization [online]. Safe A. Pesticide residues in urine of adults living in the United States: reference range concentrations. Santiago-Silva M. Seifert B. Can J Biochem 1976. 4/21/09 van Raaij JA. Uhl S. 42 Fourth National Report on Human Exposure to Environmental Chemicals . r e g u l a t i o n s . Environ Health Perspect 1997.18(4):469-474.S. Bailey SL. hair. drinking water and indoor air. Available at URL: h t t p : / / w w w. Barrot C. J Expo Anal Environ Epidemiol 2000. Head SL. available at URL: http://www. To-Figueras J. van den Berg KJ. 2002. Hill RH Jr. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. et al. et al. EPA). Hill RH Jr. Baker S.org/documents/jmpr/jmpmono/2002pr08. Gregg M. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402. et al. Schulz C. Seiwert M. Seifert B. Environ Res 1995. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Hill RH. Holler JS. house dust.

20 (1. on ornamental plants and turfs.85) 2.60 (1.30) < LOD .508 (.28 (. sodium ortho-phenylphenate (SOPP).20-3.33 (.710-2. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.386-.740 (.90) 1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Both chemicals degrade within hours to weeks in the environment (U.490 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 43 .370-.600) < LOD 75th .950) < LOD .20 (. OPP is considered to be moderately toxic after acute oral doses in animal studies.410-.500-2.90 (1.50 (1.80-3.742) * . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.590-2.50 (1.600) < LOD 1.560-8.20) < LOD 1. Most agricultural food applications have been revoked. are antimicrobial agents used as bacteriostats.552 (.497 (.570 (.780) < LOD .370-. < LOD means less than the limit of detection. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.34) 1.03) 1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .790) 2.60-3. Both have been used in agriculture to control fungal and bacterial growth on stored crops.40 (.490 (<LOD-.466 (.40-5.3. and as a wood preservative.800-3.00) < LOD .20) 2.710) 3.S..85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .890 (.690) < LOD . General population exposure can occur via dermal.496 (. Survey Geometric mean (95% conf.621) * .76) 1.50 (1.550-1.600-1.22) 2.S.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .10) 1. it was used in home sanitizers for surfaces.07 (. 1998..3 and 0.480-1.80) 1.10) .88) 1.490 (<LOD-.17 (.770 (. however. 2002.470 (<LOD-.80) 1.389-.750-2.696) * .S.493 (. and sanitizers.50) < LOD .450 (<LOD-.640) < LOD .600) < LOD .350-1.610 (.600-1.10) 1.EPA..23) 695 680 520 695 603 953 Limit of detection (LOD.EPA.880-2. in paints.10) .570-2.890) 1.389-. formulate.638) * .09) 2. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.40-7.20) < LOD 2.50) < LOD .27 (. but OPP and SOPP are still used on pears and citrus (U.10 (1.90) .50) < LOD .630) < LOD .40-5.00 (1. SOPP is applied topically to the crop and then rinsed off. Cnubben et al.10) . OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. Workers who manufacture.520 (. 2006). OPP is still used as a disinfectant fungicide for industrial applications.90 (1.370-.61) 2.490 (<LOD-.690-1.30 (1.570-.632) Selected percentiles ( 95% confidence interval) Sample 95th 2. EPA.60-2.567 (.10-1. 1989). 2006).60 (1. population from the National Health and Nutrition Examination Survey.840-1.00 (1.850 (.50-3.450 (<LOD-. 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. and it has limited water solubility. 1998).860 (.10 (1.540-2.498 (. inhalational.30) < LOD 90th 1.22 (. fungicides.820 (.00 (1.00) .364-.490 (<LOD-.50) 1. Available evidence suggests that OPP does not accumulate in the body.830 (.580-1.02) 1.20-2. In the past.92 (.433-.890 (. 2006).624) * .670) 2.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .28-3.00-2. 2006).930 (.509 (.30) 1.20 (1. Timchalk et al.645) * . or 2-phenylphenol) and its water-soluble salt.60 (1.402-.600) < LOD .00) . which may vary for some chemicals by year and by individual sample.10-2.349-.760-2.600-1. OPP is volatile.19 (. or apply these chemicals may be more highly exposed than the general population.80 (2.970 (.390-.14 (<LOD-3.636) * .770 (.30-7. 90-43-7 General Information Ortho-phenylphenol (OPP.836) * . such as fruits and vegetables.50) .570 (.50-4.00 (1. whereas SOPP is not volatile and is more water soluble.Fungicides ortho-Phenylphenol CAS No. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.570-1.10) 2.610-1.90) 2.450 (<LOD-.50-2. Estimated human intakes have been below recommended intake limits (U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.420 (<LOD-.30-2. leaving the chemical residue OPP.30) < LOD 1. interval) .90) .S.40-2.

07) 2.EPA at: http:// www.09-3.93) .38) 2.38) 1.43) 3. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.460-.510 (<LOD-.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Ito et al.EPA 2006).470) < LOD .21-2.361-.670 (.epa..52 (.38-3. interval) .96 (1.33) 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 .11) < LOD 90th 1.21) 1..248-.78 (2.910-1.780 (. 44 Fourth National Report on Human Exposure to Environmental Chemicals .670) < LOD .640-1.EPA 2006). 2005). but no neurologic.11-1.S.gov/pesticides/. 2005.900-1.810) < LOD . 1986).18) 2.910 (.690 (..420 (<LOD-.32) 1.Fungicides anemia. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Additional information is available from U..84 (1. Nakagawa et al.950) < LOD .33) .38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .940-2.74 (1.810-1.0) 1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.08) 1. 1992.11) 4.89 (1.17) 2.880-1.59) .470 (<LOD-.455-.93) 1.320 (<LOD-.00 (.04-4.496 (.12-2.656) * . 2005).329-.980 (.69 (1.96 (1.09-6.410 (<LOD-.600-1.910 (<LOD-1.08-1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.25-6.20) < LOD 3.40-13. U.560-2.4) 3.00 (1.43-2.S. 2002.75 (1.670 (. less likely. U.666) * .81) 1. 2002.06 (1.06-4.17 (.29) 1. 1997..550-. or developmental toxicity was observed (Bomhard et al.385 (.11 (.508) * .08-2.800-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.568) * .270-. In high dose animal studies.58) 2.61 (2. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.301-. or.484) * .28 (2. Detectable levels were seen in over half the U.750-2. by possible genotoxic mechanisms (Hagiwara et al. Pathak and Roy.473) * .30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .980 (<LOD-1.S.27) < LOD .61 (.410 (<LOD-.96-4.01) 1. Biomonitoring Information Urinary OPP levels reflect recent exposure.970) 1. 1993.86 (1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.46) < LOD 1.21 (.09 (1. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.75 (1.550 (. 1999.S.91 (1.24-2.650-1.. leading to production of two metabolites.791) * .580-1.990) < LOD . CDC.860 (.33-2.380 (.550) < LOD .05-2. 2002).382 (. Bomhard et al.12) < LOD 1.403-. reproductive.11 (.750 (.440 (.62) .. population from the National Health and Nutrition Examination Survey.343 (. 1984.291-. Kwok et al.560) < LOD 75th .480-. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.750 (.570) < LOD 1.420 (<LOD-.47) .93) ..580) < LOD ..610) < LOD 1.510-.453 (.620-1. 1998.88-4.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.311-.64 (2.770-2.444 (. Zhao et al. Survey Geometric mean (95% conf.500) < LOD .514 (.31) < LOD ..28 (<LOD-4.353-.620-1.32) 3.02 (. Brusick.43-2.17 (.780-14.59) 1.53) 1.4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.61 (1.06-5. OPP was not found to be mutagenic.13) 1.24-2.26) 1.29) 1.93 (1. 1984.360 (<LOD-. Volunteers exposed to 0.840 (.96) 1.51-3. 1999. IARC has classified SOPP as a possible human carcinogen.900) < LOD .590) * .97 (2. Murata et al. and it has classified OPP as not classifiable with respect to human carcinogenicity. Smith et al.44 (1.860 (.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .S. 2000.43 (1.

Buchholz BA. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Timchalk C. March 1986. J Agric Food Chem 2006.45(5):460-481.286(2):309-319.epa. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Moldeus P. Xenobiotica 1998. Biochem Pharmacol 1992.703(12):97-104. 4/13/09 Onstot JD. EPA-560/5-89-003. J Chromatogr B Biomed Sci Appl 1997.20(5):851-857. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. J Agric Food Chem 2002. Environ Mol Mutagen 2005. Kwok ES. Richter M. Centers for Disease Control and Prevention (CDC). Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Sangha GK. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. et al. Fukushima S. Food Chem Toxicol 1984. Sangha G. Third National Report on Human Exposure to Environmental Chemicals.17(8):411-417. Environmental Protection Agency (U. Vogel JS.43(7):14311437. St John MK. 90-43-7) in Swiss CD-1 mice (dermal studies). Bromig KH. Regul Toxicol Pharmacol 2002. Cano M. rat and man. Christenson WR. Hum Exp Toxicol 1998. et al. Ito N. Eastmond DA. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Fukushima S. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Bartels MJ. Mutat Res 1993. Imaida K.nih. Moriya K. Crit Rev Toxicol 2002. National Toxicology Program (NTP). EPA). Available at URL: http://ntp. Smith RA. Turteltaub KW. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Narang A. Shirai T.niehs. Moore GA. Stanley JS. Tayama S.54(16):5731-5735.32(6):551-625. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Christenson WR. Identification of SARA compounds in adipose tissue. Shibata M. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Office of Toxic Substances.22(10):809-814. Toxicol Appl Pharmacol 1999. Cnubben NH. 2005.Fungicides References Appel KE.S. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Meuling WJ. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats.pdf. Hirose M. Arch Toxicol 2000. Coelhan M..35(2 Pt 1):198-208.50(11):3351-3358. Arnold LL.EPA).gov/ntp/htdocs/LT_ rpts/tr301. The carcinogenicity of the biocide ortho-phenylphenol. Ito N. Hagiwara A. Herbold BA. Bartels MJ. Gierthy J. U.150(2):402-413. McNett DA. van de Sandt JJ. Comparative metabolism of orthophenylphenol in mouse. Bormett GA. Roberts AL. Elliott GR. Leser KH. Atlanta (GA). EPA 739 R-06004. Eadon G.159(1):18-24.S. Freyberger A. Toxicol Appl Pharmacol 1998. Hagiwara A. Inoue S. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Hakkert BC.74(2):61-71.(56):399-407.gov/oppsrrd1/REDs/ phenylphenol_red.pdf. Zhao S. Carcinogenesis 1999. Brzak KA. Mendrala AL. Bartels MJ. U.28(6):579594. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Bomhard EM. Murata M. Selim S. Nakagawa Y. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Environmental Protection Agency (U.S. Timchalk C. Roy D. July 28. Brusick D. Drugs. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. IARC Sci Publ 1984.S. 1989. Glas K. Kawanishi S. 2006. Pathak DN. Brendler-Schwaab SY. Bartels MJ. Available at URL: http://www. 4/9/09.

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

It is absorbed by plants and inhibits plant protein synthesis.. mainly corn. 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. Acetochlor is moderately toxic to fish and honey bees.. 2000. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. 2000). this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. Hladik et al. nasal epithelia. People exposed to acetochlor will excrete acetochlor mercapturate in their urine. in some species and at doses above maximum tolerated doses.EPA 2000. 34256-82-1 General Information Acetochlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural crop land. Feng and Wratten. Acetochlor is microbiologically degraded.S. renal injury. but other pathways occur. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. 2006). Urinary acetochlor mercapturate levels of 0.. 2007). 2006). In animals.. 2000.S. 1996). and hydroxymethyl ethyl aniline (U. Additional information about external exposure (i.S.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kolpin et al. which are often more prevalent in the environment. but it has produced testicular atrophy.e. including one that produces 2-methyl-6ethylaniline and its reactive metabolite. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC..EPA. 2005). NTP and IARC do not have ratings regarding human carcinogenicity. remains in soils for up to 3 months.epa..Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. Fourth National Report on Human Exposure to Environmental Chemicals 47 . General population exposure to acetochlor may occur through diet or drinking water. However. 2000.0 μg/L (Curwin et al. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. and has been detected in watersheds of agricultural lands (Battaglin et al. 2005). 2006). 2-hydroxyethyl-6-methylaniline. animals have demonstrated tumors of the lung.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al.gov/ pesticides/.S. environmental levels) is available from U. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. however.EPA. 1998). and it is unlikely to be genotoxic at relevant doses (Ashby et al. the latter which may account for some observed effects (Coleman et al. a major pathway for acetochlor metabolism involves mercapturate conjugation.. Acetochlor is not mutagenic. and thyroid (U. CAS No. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8.S. 1994. Davison et al. EPA at: http://www.EPA.EPA considers acetochlor likely to be carcinogenic in humans. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. Acetochlor has low acute toxicity.. Jefferies et al. U. 2006). 2005.S. 1989. and neurologic movement abnormalities (U. Estimated human intakes of acetochlor have been below recommended limits (U.

< LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0. 48 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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.1. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor 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.S. 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. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.

et al. Hladik ML. Available at URL(non U. 1998. J Expo Sci Environ Epidemiol 2007. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. et al. Green T. Tinwell H.html. Environmental Protection Agency (U. Atlanta (GA). Furlong ET. Centers for Disease Control and Prevention (CDC). Larsen GL. Acetochlor (Harness) Pesticide Petition Filing 1/00. Volume 65. Battaglin WA. Environmental Protection Agency (U. EPA 738-R-00-009. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.S.Herbicides References Ashby J. Jefferies PR. EPA).24(10):1003-1012. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Environ Health Perspect 2000. Sci Total Environ 2000.15(6):500-508. Barr JR. Kolpin DW. Alavanja MC. Dialkylquinonimines validated as in vivo metabolites of alachlor. Thurman EM. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Hodgson E. Camann DE.248(2-3):115-122. Olsson AO. Burkhardt MR. imidazolinone. and metolachlor herbicides in rats. Andrews HF.39(17):6561-6574. Curwin BD. Barr DB. Wratten SJ.cornell. J Agri Food Chem 1989. Wilson AG. Kinney PL.15(9):702-735. Reynolds SJ.S. Federal Register: January 24. Quistad GB. Peter CJ. Barr DB.37(4):10881093. and other herbicides in rivers. epa. Linhart SM.S. 2005. 5/30/06 U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Hsiao JJ.111(5):749-756. Available at URL: http://www. Striley CA. 2000. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Rose RL.248(2-3):123-133. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Barr DB. reservoirs and ground water in the Midwestern United States. March 2006. sulfonamide. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Chem Res Toxicol 1998. Deddens JA. Sci Total Environ 2000. Third National Report on Human Exposure to Environmental Chemicals. 5/30/06. Linderman R. Davison KL. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Hines CJ. et al. pages 3682-3690.S. Casida JE. Environ Health Perspect 2003. Lefevre PA. Occurrence of sulfonylurea.108(12):1151-1157. acetochlor.gov/oppsrrd1/reregistration/REDs/acetochlor_tred.pdf.17(6):559-566. Whyatt RM. Comparative metabolism and elimination of acetanilide compounds by rat. Number 15. Kier L. Environ Sci Technol 2005.EPA): http://pmep. Coleman S. Sanderson WT. Roberts AL.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Hum Exp Toxicol 1996.S. J Expo Anal Environ Epidemiol 2005. Heederik D. Feil VJ. Xenobiotica 1994. Feng PCC. Ward EM.cce. Hein MJ. U. EPA).11(4):353359. Bravo R.

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

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

2/27/09 U. World Health Organization (WHO). Hladik ML.inchem. Third National Report on Human Exposure to Environmental Chemicals. Environ Sci Technol 2005. Thelin GP. Kinney PL. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Alachlor in Drinking-water. acetochlor. J Ag Food Chem 1995. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. 1997. March 2006.S. Background document for development of WHO Guidelines for Drinking-water Quality. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Linhart SM. Burkhardt MR.htm. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Martens MA. December 1998. Lau H. U.56(6):853-859. Reregistration Eligibility Decision (RED) Alachlor. 2007. reservoirs and ground water in the Midwestern United States. Driskell WJ. 1996. Barr DB. Circular 1291. Geological Survey (USGS). and metolachlor herbicides in rats. Biagini R. Available at URL: http://water. Chem Res Toxicol 1998. Hill RH Jr.pdf. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Sci Total Environ 2000. Feil VJ. Available at URL: http://www. Occurrence of sulfonylurea. Hsiao JJ. sulfonamide. Atlanta (GA). et al. Geneva. and other herbicides in rivers.S. Peter CJ. Bull Environ Contam Toxicol 1996. EPA).47(6):503-517. Casida JE. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Striley CA. 1992-2001.248(2-3):115-122. No. Comparative metabolism and elimination of acetanilide compounds by rat. Hines CJ. EPA 738R-98-020. Barr JR. Hum Exp Toxicol. Hull RD. Henningsen G.S. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor.usgs. Clark JM.111(5):749-756. Feng PCC. Centers for Disease Control and Prevention (CDC). Camann DE.org/documents/pds/pds/pest86_e. Tessier DM. Thurman EM.epa. Furlong ET. Erratum in: Life Sci 1989. 2003.248(2-3):123-133. Thake DC. Wratten SJ. Andrews HF. Dialkylquinonimines validated as in vivo metabolites of alachlor.S. Kolpin DW.18(6):363-391. Whyatt RM.39(17):6561-6574. 4/2/09 U. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Sci Total Environ 2000. Environ Health Perspect 2003. Hines CJ. Sacramento. who. 86. Kolpin DW. imidazolinone. Mutat Res. Sanderson WT. WHO/ FAO Data Sheets on Pesticides.395(2-3):159-171. Hill AB. Jefferies PR. Deddens JA. Xenobiotica 1994. Shoemaker DA.56(9):883-889. MacKenzie B. Available at URL: http://www.43(25):2087-94.Herbicides References Battaglin WA. 98-4245 (by Barbash JE. ALACHLOR. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Kimmel EC. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Larsen GL. Quistad GB.pdf.int/water_sanitation_health/dwq/chemicals/en/alachlor. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. 1999. Casida JE. Life Sci 1988. Brown KK. Shealy DB. Davison KL. Supplemental Technical Information (available on-line only). 1999. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Brown MA.php. Quistad GB. International Programme on Chemical Safety (IPCS). Wilson AG. et al. J Agri Food Chem 1989.43(9):2504-2512. Geological Survey (USGS).gov/oppsrrd1/ REDs/0063. Kier LD. 1998. 2005.11(4):353359.44(18):1325. Environmental Protection Agency (U. Heydens WF. World Health Organization.37(4):10881093. revised February 15. Roberts AL. Gilliom RJ). DNA adduct formation by alachlor metabolites. 2/27/09 Jefferies PR. Biagini RE. Ann Occup Hyg 2003. Am Ind Hyg Assoc J 1995. Available at URL: http:// www. Casida JE.24(10):1003-1012.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Tolos W. California.

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

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

82.. Vonk A. Blewett C. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Heederik D. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.html.. Third National Report on Human Exposure to Environmental Chemicals. Goodrow MH. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Cooper RL. Fleenor-Heyser DG.. Clayton CA.69(2):217-222. Ferrell JM. et al. Tapia J. urinary concentrations ranged from 5-1756 μg/L (Lucas et al.. 3/11/09 Laws SC. A risk assessment of atrazine use in California: human health and ecological aspects. Eldridge JC. Breckenridge CB.15(6):500-508. References Adgate JL. Wetzel LT. Proc Natl Acad Sci USA 2002. Deddens JA.. Moseman RF. Eldridge JC.htm. Toxicol Sci 2003. Chen H. Goldman JM.. Ferioli A. Available at URL: http://www. Lee M.61(4):331-355. Collins A. levels of atrazine mercapturate were generally not detectable (CDC. diamino-S-chlorotriazine and hydroxyatrazine. Reynolds SJ. Gillis JH. J Agric Food Chem 1982.99(8):5476-5480. Lioy PJ. Sanderson WT. Ann Occup Hyg 2003. Environ Health Perspect 2001. Barbieri F. Tyrey L. J Toxicol Environ Health 1994. Pfeifer KF. et al. Cooper RL.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Freeman NC. et al. ATRAZINE. Atlanta (GA). J Expo Anal Environ Epidemiol 2005. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.115(8):1254-1260. Stoker TE. 2007). Catenacci G.. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Hayes TB. The geometric mean of urinary atrazine mercapturate was 1. Seiber JN. Wetzel LT.47(6):503-517. 1996.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. 2005). Perry et al. Hermaphroditic. Extrom PC. 2001).cdc. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Maroni M. Toxicol Lett 1993. Biological monitoring of human exposure to atrazine. Simpkins JW. McElroy WK. Toxicol Sci 2000. Saiz SG.76(1):190-200. J Toxicol Environ Health 1994. WHO/ FAO Data Sheets on Pesticides. Stoker TE. Bersani M. Brown KK. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . In the NHANES 2001-2002 subsample.43(2):155-167. In a small number of field workers. et al. Centers for Disease Control and Prevention (CDC). Stuart AA. Grzywacz JG. Stoker TE.64(9):672-678. Schmid J. Gillis JH. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Agency for Toxic Substances and Disease Registry (ATSDR). 2001 [online]. 1993). Barr DB. Bradway DE. Environ Health Perspect 2007. Biagini RE. Toxicol Sci 2000. et al. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Mendoza M. 2003. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. International Programme on Chemical Safety (IPCS). Lucas AD.58(2):366-376.atsdr. 2000). Noriega N. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. 3/11/09 Arcury TA. Laws SC. Barr DB.109(6):583-590. World Health Organization. Barr DB. Curwin BD. Gammon DW.30(2):244-247. Available at URL: http:// www. Geneva. atrazine was detected in only four children (Arcury et al. Toxicological profile for atrazine. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.inchem. Eberly LE. 2005. Striley CA.org/documents/pds/pds/pest82_e. Carr WC Jr. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Jones AD. Hines CJ. Ferrell JM. et al.gov/toxprofiles/tp153. No. Steroids 1999. Pest Manag Sci 2005. Quandt SA.53(2):297-307. Stevens JT. Cooper RL. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Sanborn JR. In small studies of Maryland residents in 19951996 (MacIntosh et al. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hein MJ. Aldous CN. 2005). Shoemaker DA. 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. Cottica D.43(2):155-167. In a study of 60 farm worker children.

usgs. Stoker TE. Toxicol Sci 2002. Available at URL: http://water. Toxicology 1990. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Supplemental Technical Information (available on-line only). Kastl PE. Delzell E. Available at URL: http://www. Crit Rev Toxicol 1997.Herbicides development of a biomarker of exposure. Dagenhart D. March 2006. Langvardt PW. A longitudinal investigation of selected pesticide metabolites in urine. Laws SC.27(6):599612. Needham LL. MacIntosh DL. Circular 1291. Washington (DC). Tortorelli J. Toxicol Appl Pharmacol 2002. Office of Prevention. 6/1/09 U. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .10(7):479.S. J Toxicol Environ Health A 1999. 2007.pdf.56(2):69-109. Interim Reregistration Eligibility Decision For Atrazine. Environmental Protection Agency (U. Environmental Fate and Effects Division. Stevens JT.pdf. Dryzga MD. Wetzel L. Pesticides in the Nation’s Streams and Ground Water. Lansbergen GW. A review of epidemiologic studies of triazine herbicides and cancer. Sanderson JT. Guidici DL. Available at URL: http://www.S.67(2):198-206. J Expo Anal Environ Epidemiol 1999. Ryan PB. Wood C. 2003b. Stoker TE. Singzoni B.6(1):107-116. Timchalk C. A risk characterization for atrazine: oncogenicity profile. 1992-2001. Cooper RL.gov/oppsrrd1/REDs/ atrazine_ired. Sathiakumar N.58(1):50-59.S.9(5):494-501.S.S.182(1):44-54. Rayner JL. Breckenridge CB. Chem Res Toxicol 1993. Toxicol Appl Pharmacol 2004. Toxicol Sci 2000. Environmental Protection Agency (U. The Quality of Our Nation’s Waters. revised February 15. Guidici DL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Pesticides and Toxic Substances. May 2003a. 3/11/09 U.61(1):27-40. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Perry M.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Ann Epidemiol 2000.php. Cooper RL. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Osborne DW. van den Berg M. Fenton SE.epa. Case No. EPA Office of Pesticide Programs. 0062. White paper on potential developmental effects of atrazine on amphibians. Geological Survey (USGS). Laws SC. EPA). Boerma J. Christiani D. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.195(1):23-34.epa. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Hammerstrom KA. U. EPA).

4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. < LOD means less than the limit of detection.540-. myotonia. Human health effects from 2. nausea. and delayed Urinary 2.210-.S.440-1.740 (.310) < LOD . It is not well absorbed through the skin.2.EPA.40) 1. population from the National Health and Nutrition Examination Survey.250 (<LOD-..760 (. with a half-life of several days to several weeks.20 (.660) 1. renal and hepatic injury.4-Dichlorophenoxyacetic Acid CAS No. 2. Recent estimates of chronic intakes of 2. 2.4-D have been below recommended intake limits (U. these herbicides can enhance plant growth.810-1. 1989.250 (<LOD-. abdominal pain.490 (.4-D may occur during residential applications. General population exposure to 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. and aquatic environments. Similar to other chlorophenoxy herbicides.48) < LOD 1. 2. 2007).S.490) < LOD < LOD < LOD .610-.952 and 0.670-1.690 (.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .960-1.02-1. 94-75-7 General Information Widely used throughout the United States. 1977).66) < LOD 1.690-1.930-1.Herbicides 2. 2004). 2.21) 1. Survey Geometric mean (95% conf. the chlorophenoxy herbicide 2.400) < LOD .20 (<LOD-1.32 (1.420-. hypotension.27 (1.EPA.80) 1. but at higher levels they are herbicidal.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 . Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.16) < LOD .70) 1. and by consuming food or drinking water contaminated with 2. it acts as a plant growth hormone. by direct contact with agricultural and residential areas after applications.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. Fourth National Report on Human Exposure to Environmental Chemicals 57 . and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. MCPA. in 2001 (U.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.51 (1.910) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.S.4-D or exposed for prolonged periods.13) < LOD .05-2.320) 90th . agricultural.310 (. which may vary for some chemicals by year and by individual sample. At low levels. 1974.10 (<LOD-1.27-2.. Kohli et al.00-2.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.910) < LOD .03) 695 659 520 668 589 892 Limit of detection (LOD. dizziness.4-dichlorophenoxyacetic acid (2. It is rarely detected in ground waters (USGS.30 (<LOD-2.370-.24 (. and mecoprop).730 (.22) < LOD .560-.60) 1.260 (<LOD-.230 (<LOD-.420) < LOD .890) < LOD . 2005). It was first registered with U.230-.55 (1.43) 1..49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .EPA in 1948. It is poorly bound in soils.550-1.330 (.10) < LOD 1.210 (<LOD-.680-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.690 (.560-1. Sauerhoff et al. Once absorbed.10 (<LOD-1.27 (.350) < LOD < LOD < LOD .690 (.610 (. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.930 (.410) < LOD .07 (. 4-D.4-D) controls broadleaf weeds in residential.4-D can be applied either as an aqueous salt or as oil-soluble esters. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.4-D has low acute toxicity.890 (. As much as 62 million pounds of 2. headache.4-D is rapidly absorbed via oral and inhalation routes.08) < LOD .4-D were used in the U.

08 (.S.590 (<LOD-1.14 (.S. Knopp et al.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.08 (.7.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert..EPA.380-. Post-application levels in farmers and home gardeners were dependent on Urinary 2.340 (.720 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.270-.380 (<LOD-.380) < LOD .4-D does not have significant reproductive.4-D levels were detectable in less than a quarter of the individuals studied.480 (.620-.73) .4-D are eye irritants.590 (<LOD-1.330-.16) 1. Hill et al.560-.S.. Additional information is available from U. It is unclear whether these associations are related to the chlorophenoxy herbicides.890-1.17 (. Acute high doses administered to laboratory animals produced ataxia.. 2005. 2005). adrenals and gonads (NTP. 1980.S.890) < LOD 1. population from the National Health and Nutrition Examination Survey. myotonia.4-D reflect recent exposure. 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.820-1. or to contaminants in the herbicide formulations (specifically 2.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1985.EPA at: http://www.Herbicides neuropathy (Bradberry et al.24) 1.700 (.740 (. 2005). In previous samples of the U.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .930-1. 2002.660 (. IPCS.S. IPCS.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.27-1.610-.EPA.780-1.19) .490 (.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.. 2006. population (Hill et al. U. 2005).470) < LOD . liver.920) < LOD 1. U.660) < LOD .4-D production plant workers and a few forestry workers spraying 2. 2004). or teratogenic effects in chronic rodent studies (Charles et al.3.340-. CDC. Kolmodin-Hedman and Erne. 1996.05) .570) < LOD .520-.680) < LOD . 2005)..32 (<LOD-2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2001.380 (<LOD-.850) < LOD . 1994). 1995).35) < LOD ..980) < LOD 1. other exposures. 2. Survey Geometric mean (95% conf.56) .550-.670 (<LOD-1. 1996. Frank et al. eyes. 2005.410) < LOD < LOD < LOD .08 (.790) < LOD . 2005. 58 Fourth National Report on Human Exposure to Environmental Chemicals . 2. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.670 (.39) < LOD 1.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.560-.780 (.S... 1996. The acid and salt forms of 2. in small samples of children (Hill et al.390) < LOD < LOD < LOD .gov/pesticides/.EPA. 1992). 2000).790) 1.410) 90th . 2005.EPA 2005).350 (<LOD-. IOM.990-1. urinary 2. U. 2002. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270 (<LOD-. thyroid.810-1.670 (. Pearce and McLean. Kutz et al.13 (.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .780) .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 .S. and evidence of histological injury to the kidneys.13 (.. and of adults and children (Baker et al.580-. 1989).610-.410 (<LOD-.. Biomonitoring Information Urinary levels of 2. U. 2003. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.410) < LOD 1.41 (1.epa.810-1.640 (. Average post-application urinary levels of 2. 2. developmental. IPCS. Epidemiological studies have reported associations of several types of cancer. 1995.440 (.

htm. 2005 Charles JM.edu/catalog. Stephenson GR. 2005).10(6 Pt 2):789-798. and the use of protective clothing or equipment (Arbuckle et al.. Absorption and excretion of 2. Hill RH Jr. Tables.niehs. the number of acres to which it was applied (Curwin et al. References Arbuckle TE. Crit Rev Toxicol 2002.4. Baker BA. J Expo Anal Environ Epidemiol 2000. International Programme on Chemical Safety-INCHEM (IPCS). J Environ Sci Health B 1992.31 Suppl 1:90-97. Kolmodin-Hedman B. National Toxicology Program (NTP). Xenobiotica 1974. Scand J Work Environ Health 2005. van Ravenzwaay B. Review of 2.5-T). Head SL.15(6):500-508.gov/index. Available at URL: http://ntp.php?record_id=10603. Hill RH Jr. Carter-Pokras OD. Kohli JD.51(3):152-159. J Expo Anal Environ Epidemiol 2005 Nov. Harris SA. Cole DC. In farm families. et al. Environ Res 1995. Barr DB.nap.inchem. TOX-63 Peroxisone Project (2. Needham LL. Heederik D.31(2):121-125. Curwin BD.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 2.4-dichlorophenoxyacetic acid (2. Kutz FW. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Murphy RS. Finding a measurable amount of 2. Arnold EK. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Khanna RN. Selected pesticide residues and metabolites in urine from a survey of the U.60(1):121-131.. Bailey SL. Shealy DB.. J Toxicol Environ Health 1992.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. 914. Gupta BN. Assessment of exposure to 2.4-D): exposure and urinary excretion. 2006. Occup Environ Med 1994. Forestry workers involved in aerial application of 2.27(1):23-38. Ripley BD. Biomonitoring of herbicides in Ontario farm applicators.4-. geometric mean urinary levels of 2. Needham LL.4-D. Pesticide residues in urine of adults living in the United States: reference range concentrations. Harris et al. Philbert MA. Toxicol Sci 2001.4-D in urine does not mean that the level of the 2. Alexander BH. Chapman P. 2003.. Honeycutt R. TOX-63: TOXICITY REPORT CURVES.37(2):277-291. 1992). 2005. Exposure of homeowners and bystanders to 2. Arch Toxicol Suppl 1980.4-D were highest in the farmers who applied the 2.4:427-435.71(2):99-108. Developmental toxicity studies in rats and rabbits on 2. Biomonitoring for farm families in the farm family exposure study. 2005). Arch Environ Contam Toxicol 1985. Acquavella JF.4-Dichlorophenoxyacetic Acid). Arch Environ Contam Toxicol 1989.org/documents/jmpr/jmpmono/v96pr04. Ritter L. Available at URL: http:// www. Third National Report on Human Exposure to Environmental Chemicals. Cook BT. Frank R.4:97-100. Baker SE. Sircar KP. Baker S.4-D). Centers for Disease Control and Prevention (CDC). Tandon JS. Beasley VR.Herbicides the time since application. Dichlorophenoxyacetic acid.4 dichlorophenoxyacetic acid (2. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Available at URL: http:// www. general population. Holler JS. Fast DM. Wilson RD. Hanley TR Jr.31 Suppl 1:98-104. et al. Scand J Work Environ Health 2005. Driskell WJ. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.4-dichlorophenoxyacetic acid (2. Biomonitoring studies of 2. Solomon KR.S. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. 3/17/09 Institute of Medicine (IOM). Reynolds SJ. et al. Washington (DC): National Academies Press. Brody D. Atlanta (GA). 3/17/09 Knopp D. Survival and Growth Curves from NTP Toxicity Studies. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Sirons G J. Smith SJ.18(4):469-474. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. 2. To T. Erne K.4-D) epidemiology and toxicology.4-D will result in an adverse health effect. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.nih. Board on Health Promotion and Disease Prevention. Mandel JS.4-D than levels found in the general population. Mandel et al.32(4):233-257. Gregg M. Pesticides residues in food: 1996 evaluations Part II Toxicology.4-dichlorophenoxyacetic acid and its forms. Beeson MD. Hein MJ. Updated March 7. the amount of pesticide applied. Dhar MM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Barr DB. Vet Hum Toxicol 1989.4:318-321.4-dichlorophenoxyacetic acid in man.4-D and 2. Sanderson WT. Garabrant DH. Bus JS. Estimation of occupational exposure to phenoxy acids (2. Veterans and Agent Orange: update 2002. 2005. Campbell RA.

2. Environmental Protection Agency (U.pdf. March 2006. Available at URL: http://water. revised February 15. Braun WH. May. 3/17/09 U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Toxicology 1977.epa.S. The fate of 2. Available at URL: http://www. Circular 1291. June 2005. Environmental Protection Agency (U. Washington (DC): U. 2004. S. Supplemental Technical Information (available on-line only). 4/2/09 U. Pesticide industry sales and usage .S. The Quality of Our Nation’s Waters.epa. Available at URL: http://www.4-D) following oral administration to man.gov/oppsrrd1/ REDs/factsheets/24d_fs. 60 Fourth National Report on Human Exposure to Environmental Chemicals .EPA). 3/17/09.S. Pesticides in the Nation’s Streams and Ground Water. Geological Survey (USGS). EPA 738 F-05-002.htm.4-D RED Facts.2000 and 2001 market estimates.EPA. 2007.Herbicides Sauerhoff MW.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.S.4-dichlorophenoxyacetic acid (2.8:3-1U. Blau GE. Office of Prevention Pesticides and Toxic Substances. Gehring PJ.php.S.EPA).usgs. 1992-2001.

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

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

Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Reregistration Eligibility Decision (RED) Metolachlor. Peter CJ. Casida JE. Quistad GB.pdf. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Environmental Protection Agency (U.108(12):1151-1157.248(2-3):115-122.int/water_sanitation_health/dwq/chemicals/ metolachlor. Sanderson WT. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. J Agri Food Chem 1989. Barr DB. sulfonamide.html. Centers for Disease Control and Prevention (CDC). 2003. Sci Total Environ 2000. et al. Metolachlor in Drinkingwater. Environ Health Perspect 2003. Available at URL: http://www.S. acetochlor. Burkhardt MR. Background document for development of WHO Guidelines for Drinking-water Quality. Occurrence of sulfonylurea.41:3409-3414.248(2-3):123-133. Larsen GL. revised February 15. California.pdf. Feng PCC.S. Hodgson E. 1998. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.gov/nawqa/pnsp/pubs/files/051507. Furlong ET. and metolachlor herbicides in rats.S. 2007. J Expo Anal Environ Epidemiol 2005. reservoirs and ground water in the Midwestern United States.php. Kolpin DW. U. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. 2005. Heederik D. et al. World Health Organization (WHO). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. EPA). Sci Total Environ 2000. Hein MJ. Barr DB.15(6):500-508. 3/26/09 U. 6/1/09 Whyatt RM. Supplemental Technical Information (available on-line only). Available at URL: http://water. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. 4/2/09 U. Third National Report on Human Exposure to Environmental Chemicals. EPA 738R-95-006. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .usgs.111(5):749-756. Available at URL: http://water.39(17):6561-6574.gov/nawqa/ pnsp/pubs/wrir984245/text.Herbicides References Battaglin WA. Xenobiotica 1994.gov/oppsrrd1/ REDs/0001. Environ Health Perspect 2000.47(6):503-517.epa.37(4):10881093. usgs.S.ESTfeature_gilliom. Feil VJ. imidazolinone. Linderman R. Alavanja MC. Barr JR. 1999. Roberts AL. 98-4245 (by Barbash JE. Andrews HF. Gillion.who. 1992-2001.S. March 2006. Atlanta (GA).gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Curwin BD.pdf 3/30/09 Hines CJ. Gilliom RJ). Available at URL: http://www. April 1995. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.usgs. Thelin GP. Davison KL. Rose RL. Shoemaker DA. Sacramento. Thurman EM. Linhart SM. Brown KK. Comparative metabolism and elimination of acetanilide compounds by rat. R. Ann Occup Hyg 2003.11(4):353359. Reynolds SJ. Deddens JA. Dialkylquinonimines validated as in vivo metabolites of alachlor. Geological Survey (USGS). Environ Sci Technol 2007. Pesticides in U. Chem Res Toxicol 1998. Kolpin DW. Available at URL: http://water. Biagini RE. Ward EM. Environ Sci Technol 2005. Jefferies PR. Striley CA. Wratten SJ.24(10):1003-1012. Hsiao JJ. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Camann DE. and other herbicides in rivers. streams and groundwater. Circular 1291. Coleman S. Kinney PL. Geological Survey (USGS). Hladik ML.

.4.5-Trichlorophenoxyacetic acid (2.4. and concern about contamination with 2.S.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. renal and hepatic injury.4. 2. At low levels. dizziness. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. which may vary for some chemicals by year and by individual sample..5-T and 2. Given the commercial unavailability of 2.4. Ester forms of 2. 2.5-trichlorophenol and other degradates. ranging from several weeks to many months..4.. myotonia. Human health effects from 2.5-T use as a herbicide in 1985. 2007).4.5-T degrades to 2.4. 64 Fourth National Report on Human Exposure to Environmental Chemicals . 1974). < LOD means less than the limit of detection.4. hypotension. headache. nausea. The half-life of 2.g..5-T was once applied as either an aqueous salt or as an oil-soluble ester. 2. Nelson et al. Agent Orange). Kohli et al.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.4.5T is rapidly absorbed via oral and inhalation routes. Once absorbed into the body. it is not well absorbed through the skin. abdominal pain. 1989. but higher levels are herbicidal.Herbicides 2. Survey Geometric mean (95% conf. these herbicides can enhance plant growth.3. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Mohammad and St.5-T has been rarely detected in ground waters (USGS.7.4. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.5-T in soil varies with conditions. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.5-T is eliminated mostly unchanged in the urine. 2004).1. with an elimination half-life of approximately 19 hours (Arnold et al.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. the general population is unlikely to be exposed to it.4.4.2 and 0. 93-76-5 General Information 2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. and delayed neuropathy (Bradberry et al. Chlorophenoxy herbicides act as plant growth hormones. Epidemiological studies have reported associations of several types of cancer.5-Trichlorophenoxyacetic Acid CAS No.4.4. 1992). 1992.5-T.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. Although 2.4-D were used as defoliants in the Vietnam War (e.4. Omer. 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. 1986.5-T (Holson et al.4. 2.

S.5-T reflect recent exposure. population from the National Health and Nutrition Examination Survey. IOM.4.4. in which urinary levels of 2.4.4. Biomonitoring studies on 2. U. 1992). Additional information is available from U.EPA. 2004).5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4. Fourth National Report on Human Exposure to Environmental Chemicals 65 .5-T does not mean that the level will result in an adverse health effect..5-T itself is not mutagenic.EPA at: http://www. other exposures.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Pearce and McLean. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.S.5-T were generally below the limit of detection.3. Finding a measurable amount of 2. 2003. It is unclear whether these associations are related to the chlorophenoxy herbicides.gov/pesticides/. 1980).8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. 2002. 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. or to contaminants in the herbicide formulations (specifically 2.4. Urinary 2.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. 2005).4.5-T than levels found in the general population. urinary levels of 2.5-T also were below the limit of detection (Kutz et al.S. similar to results of NHANES II (19761980). Biomonitoring Information Urinary levels of 2.4.epa.Herbicides or contaminated herbicides. Mean urinary levels of 2. 2005.7. 1996. IPCS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Multireplicated dose-response studies with technical and analytical grades of 2. Estimation of occupational exposure to phenoxy acids (2.37(2):277-91. International Programme on Chemical Safety-INCHEM (IPCS). St Omer VE. Erne K. Gupta BN.epa. II. Vet Hum Toxicol 1989. 914. Third National Report on Human Exposure to Environmental Chemicals. Fundam Appl Toxicol 1992. Absorption and excretion of 2. Philbert MA. et al. Atlanta (GA). Holson JF.org/documents/jmpr/jmpmono/v96pr04.5-trichlorophenoxyacetic acid (2. Gaylor DW.23(2):65-73. Wolff GL. Mohammad FK.pdf. 2003. Office of Prevention Pesticides and Toxic Substances. Selected pesticide residues and metabolites in urine from a survey of the U.4-D/2. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Veterans and Agent Orange: update 2002. U. Sheehan DM. et al. Pesticides residues in food: 1996 evaluations Part II Toxicology. Murphy RS. Fundam Appl Toxicol 1992. Proudfoot AT. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Poisoning due to chlorophenoxy herbicides. Kolmodin-Hedman B.5-T). Bradberry SM. Washington (DC): National Academies Press. 2. Behavioral and developmental effects in rats following in utero exposure to 2. Board on Health Promotion and Disease Prevention. Vale JA.32(4):233-257. 2004. 2005.4. Garabrant DH.4.31(2):121-125. J Toxicol Environ Health 1992. Crit Rev Toxicol 2002. Developmental toxicity of 2. 210:250-255. Beasley VR.31 Suppl 1:1825. Holson JF.4-D and 2.4-D) epidemiology and toxicology.5-trichlorophenoxyacetic acid (2.5-trichlorophenoxy acetic acid in man.php?record_id=10603.inchem. general population. May. Tandon JS.EPA). Nelson CJ. Carter-Pokras OD. Khanna RN.19(2):286-297. 3/17/09 Kohli JD. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Arch Int Pharmacodyn Ther 1974.4:318-21.nap.edu/catalog. Developmental toxicity of 2.5-t mixture.htm. S. Pesticide industry sales and usage . Sircar KP. Dhar MM. Scand J Work Environ Health 2005. Dichlorophenoxyacetic acid.4. Review of 2. Toxicol Rev 2004.S.8(5):551-60. Available at URL: http:// www. Pearce N.4.4. discussion 5-7. Agricultural exposures and non-Hodgkin’s lymphoma. I. LaBorde JB. Kutz FW. Centers for Disease Control and Prevention (CDC).5-T in four-way outcross mice.EPA.2000 and 2001 market estimates. Available at URL: http://www. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Available at URL: http:// www. Cook BT. Gaines TB. 3/17/09 Institute of Medicine (IOM).4-.5-T).19(2):298-306.5-T).S.Herbicides References Arnold EK. Nelson CJ. McCallum WF. Environmental Protection Agency (U.S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Gaines TB. Neurobehav Toxicol Teratol 1986.4. Washington (DC): U. Brody D.4-dichlorophenoxyacetic acid (2.4. McLean D.4. LaBorde JB. Arch Toxicol Suppl 1980.

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

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

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

00 (8.8-17.50) 15.130 (.5 (16.30 (8.9 (13.108-.00-14.8-25.158) .120 (.2) 12.9 (12.101) .058) < LOD .0 (10.1) 10.0) 21.075) < LOD .1) < LOD 9.3-21.4) 539 456 484 487 980 885 Limits of detection (LOD.103 (.064) 90th . see Data Analysis section) for survey years 01-02 and 03-04 are 10.180) .3 (18. Survey years 01-02 03-04 Geometric mean (95% conf.9-22.088-.3 (14. < LOD means less than the limit of detection.062 (.8-17.062-.7 (15.160 (.062 (.054-.70 (7.080) .110) .8 (18.100 (.5-17.242) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.053 (<LOD-.109-.3 (18.112) 95th .089 (.110 (.7-19.8) 14.4) 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 8.124) .090 (.180) .8 (9.1) 14.113 (.4-17.070) .139 (.100-.1) 15.9 (14.102 (.117) < LOD .5 and 7.1) 13.170) .6-33.059 (.9 (12.S.4) 21.0 (10.109-.7) 15.054-.8 (11.1) 20.138) .1-19.5-15.073-.6-24.8-19.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .084-.138 (.147) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.100-.110) .160 (.8) < LOD 8.0) 19.5) 15.064 (.4) 14.0-25.140 (.109 (. population from the National Health and Nutrition Examination Survey.60-10.50 (8.80-9.4 (12.1-16.40-10.130) .8) 15.150 (.077 (.2) 11.2) 15.0-21.063-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (<LOD-10.1 (13.100-.090 (<LOD-.1) 15. which may vary for some chemicals by year and by individual sample.110 (.40-9.086-.112-.100) .116) .120-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 19.103 (.190) .083-.5) 19.6) 16.120 (.070-.6-24.2-15.4) 20.098 (.149) . 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.048 (<LOD-.070 (<LOD-.30 (8.6 (14.9 (13.150 (.130) .080 (.054-. Survey years 01-02 03-04 Geometric mean (95% conf.S.120) .140) .130) .110 (.6 (15.090-.0 (15.5 (<LOD-11.6) 9.3 (13.056-.90) 90th 15.090-.7-22.160) .0) < LOD 9.120 (.080-.9-38.10 (<LOD-16.139 (.1-24. population from the National Health and Nutrition Examination Survey.060) .077-.140-.130-.069) < LOD < LOD .096-.80-10.130-.9-23. 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 9.6 (15.1 (18.049-.100) .147 (.5-17. Fourth National Report on Human Exposure to Environmental Chemicals 79 .8.4) 19.4) 95th 20.1-18.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.8-24.130-.055 (.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.3 (19.4) < LOD < LOD 16.2) 14.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level. 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 .110-.090-.4 (12.5) 21.7 (14.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .093) .7 (<LOD-15.4-18.190) .0 (11.

inchem. Psychopharmacology (Berl) 1987.150:263-271. Ginsburg KS. 1992-2001. Eds.cdc. 4/21/09 Bates MN. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease.54:1431-1443. Turner W. and epidemiology in the United States. and lymphocyte sister chromatid exchange. Mumtaz MM. Pesticides in the Nation’s Stream and Ground Water. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Fernandez MG. Smith AG. No:429-436.14:95-102.64-65 Spec. 2 Classes of Pesticides. Narahashi T. Toxicological profile for aldrin/dieldrin [online]. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Exp Neurol 1998. PA. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. 2007 [online]. Int Arch Occup Environ Health 1994.gov/~dms/ pesrpts. Brock JW. Organochlorine exposure and risk of breast cancer. Grajewski B.org/documents/ehc/ ehc/ehc91. et al.103(Suppl 7):113-122. Stehr-Green. J Toxicol Environ Health. Available at URL: http://www. 4/21/09 Hoyer AP. 1989. August 2008.47:1059-1087. References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Jorgenson JL.cfsan. et al. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Part A 2000. Cancer Epidemiol Biomarkers Prev 2000. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.27:405-421. September 2002. Jorgensen T. Available at URL: http://www. Kanthasamy A.atsdr. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Song S. Basit A. 1991. Hartvig HB. Jr. Mink PJ. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Kanthasamy AG. Environmental Health Criteria 91. 15.gov/toxprofiles/ tp1. Mann D.352:1816-1820. Soto AM. New York. bioaccumulation. Needham LL. Tully DB. Toxicol Lett 1992. Revised Feb.gov/ circ/2005/1291/. Neurotoxicol 2005. Frey JM. Priestly BG. Chung KL. Cox. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Edwards JW. Food and Drug Administration (FDA). Chapin RE. Chemosphere 2004. Jr and Laws ER. David VL. Grandjean P. Corrigan FM.109(Supp1):113-139. Reprod Toxicol 2000. Environ Health Perspect 2001. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Roy ML. 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.html. VT. Andersen A.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Daniel SE. Chlorinated Hydrocarbon Insecticides. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Lancet 1998. Sonnenschein C.html.91(1):122-126. 6/1/09 Ward EM. pp. Serrano FO. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. In Hayes WJ. Sanchez-Ramos J. Buckland SJ. Handbook of Pesticide Toxicology. Li AA. Shore RF. International Programme on Chemical Safety (IPCS). Olea N. United States Geological Survey (USGS). Ellis H. Six high-priority organochlorine pesticides. 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. 80 Fourth National Report on Human Exposure to Environmental Chemicals . J Occup Environ Med 2005. Available at URL: http://pubs. Garrett N. Patterson DG Jr. either singly or in combination. Patterson DG Jr. McIntosh LJ.fda. Rosellini RA. Inc. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Facca A. are nonestrogenic in transfected HeLa cells. Academic Press.59:229-234. Schulte P.usgs.htm. plasma dieldrin. Aldrin and Dieldrin [online]. toxicology. Vol. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9:1357-1367. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health 1989.66(4):229-234. 731-915. Environ Health Perspect 1995. Wienburg CL.26:701-719. Available at URL: http://www. Anantharam V. Teta MJ. Kitzazwa M. Finley B. Carlson JN.

5) 9.10-18. 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.2-26.7) 9.4 (<LOD-12.7 (34.6) 8.1 (44.6) 49.3-49.5 (41. in addition to trace amounts of numerous other related compounds (ATSDR.1) * 11.5.30-11.6) 20. see Data Analysis section) for Survey years 99-00.5-40.4 (22.8-43.6 (9.9-21.1 (<LOD-12.0-67.1-15.8 (10.2 (41.7 (43.2-49. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.1-65.8 (17. from the early 1950’s until the mid-1980’s. and in soil.5 (33. 2007).1) 30.0-33.0) 75th 20.3-24.1-50.9 (15.5) 10.4 (30.90 (8.6) 9.5) 44.2) * 12.2-49.4-51.9) 11.63 (8.6 (25.1-25. Technical grade chlordane had contained 7% trans-nonachlor.0) 41.2) 33.3-45. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.5 (<LOD-12.7) 42. and dairy products are the usual sources of exposure to these chemicals in the general population.2) 22.8-33.0) 31.4) 39.0 (<LOD-12.6-53. Consequently. Fourth National Report on Human Exposure to Environmental Chemicals 81 .7-39.4) 18.8) 18.0 (26.4) 29.7-25.4) < LOD 11.4-21.9) 17. 1994.7 (34.7 (<LOD-32.9) 11.0) 37.2) 34.8-33.1) 22.0-25.2-21.20 (<LOD-11.4 (31.3 (20.5-65.5 (31.7) 35.8-61.6-24.3-32.8-42. Since 1992.5 (34.9) 36.2) 36.9 (36.9-40.5-38. and 03-04 are 14.7 (32.9 (26.8.5) 56.3 (21.1) < LOD < LOD < LOD < LOD < LOD 8.9) 47.0-18.2) < LOD 11.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9) 13.1 (<LOD-12.9-42. Survey Geometric mean (95% conf.3) 10.5-13.4) 37.36-11.1) 90th 34.9) 31.9 (17.0-13. heptachlor use has been limited to treatment of fire ants near power transformers.9) 39.9-38.9) 23.6 (16.9) 23. respectively.2) 46.5-41.3 (9.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.6 (9.1-25.5.8-23.3-45.0-12.3) 37.0-61.6-45.7-12.89-10.1) * 11.4 (10.10 (8.4) < LOD < LOD < LOD 23. and 7. 10.2 (9.2-56.8 (18.3) 18.6) < LOD 11.0 (37.10-11.7 (<LOD-13.5-47. 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.8) 27.6 (43.20-10.S.8 (42.9 (31.9 (26.5) < LOD < LOD 9.5-43.1-19.6) 23.9-21. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.8) 52.5) 38.37 (8.3-43. As a result of the manufacturing process.20-11. 2007).2-28.4-14.S.4 (35.5-32.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.7) 28. the technical grade product of each chemical contains 10%-20% of the other chemical.9 (11.2 (37.2 (28.7-70.1-51.0) 20.1 (11.5-42.6) 36.1 (27.2) 37.6-12.2) < LOD 11.9 (29.3 (28.2 (39.7) 19.74 (<LOD-10. < LOD means less than the limit of detection.6) 9. Chlordane is not currently produced or used in the U.9) 10.8) 53.3 (27.6-18.8 (10. 01-02. population from the National Health and Nutrition Examination Survey.7 (10.5) 21.5-44.7-14.1 (<LOD-12. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.6) 48. buildings. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.0) 21.69-10.S.1 (17. lawns.8 (17.7) 31.3) 18.0 (16.1 (16. 57-74-9 Heptachlor CAS No.3 (11.7 (42.2 (21. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.6) 48.Organochlorine Pesticides Chlordane CAS No. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.8) 44.4 (30.9 (18.1) 30.8 (40. 1994).9) 37.9 (11.3 (<LOD-19.6) 39.0 (20.8-31. foods high in fat such as meat.0 (32.8) 52.9 (15.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.3 (25.0) 27.1 (15.7 (19.4-40.7-56.3) 41.5 (8.5) < LOD < LOD < LOD < LOD 13.5) 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 * * * * 11.6) 11.1 (25.3 (26.7) 19.2 (10.1 (20.82-11.8-32. chlordane was used to kill termites and other insects on agricultural crops.7 (17.6-24.4) 12.9 (21.5) 37.3) 10.1 (40.4) 22. fish.70 (<LOD-10.8-73.2 (36. Until 1988.8-20.1) 16.4-45..

079) .070 (<LOD-. In laboratory animal studies.053-.223) .213) * .060 (<LOD-.270 (. OSHA has established occupational exposure criteria. 1991.300) .340) .204 (.057 (.370 (.092) .. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.087-. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.108-.070 (<LOD-.280-.057-.064) < LOD . The major metabolite of heptachlor is heptachlor epoxide.150) .106-.350 (. 1991).148-.210-.320) . and breast milk is a major excretion route in lactating women.510) .082 (.225 (.061-.077) .080) .090) .058-.210 (.136) .160) .220-.560) .S.070-.230 (.258 (.140-.140-.240-.Organochlorine Pesticides (Dallaire et al.070-. 2001.160 (.310) . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.310) .245-.280 (.300) .130) .115-.203-.048-.168-.057) * .220-.320 (.260-. and inhalation exposure. which is also persistent in the body (ATSDR. 1986). Takahashi et al.104-.290-.104) . IARC.287) .047 (<LOD-.269 (.290-.310) .100 (.300-.115 (.370 (.200-.068-.110-.070) < LOD < LOD < LOD < LOD < LOD .066-.380) .208 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. dermal.260 (.360) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .100 (<LOD-.270 (.149 (.373) .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.180) .069 (<LOD-.271 (.370 (.180) .067 (.063) * .170) .130 (. population from the National Health and Nutrition Examination Survey.280) .165-.240) . 1977b.207 (.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 * * * * .110 (<LOD-.148) .230-.200 (.077) .146) .112 (.190-.400) .260 (.280-.260 (.083) .150 (.075 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.170) .230-. 2006).440) .253-.083 (.066 (.330 (.290) .S.302) . to heptachlor.130-. Shindell and Ulrich.189 (. Rogan.216-.070-. Chlordane and heptachlor are absorbed after oral.073) < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.063 (.080 (.063 (.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .230-. Survey Geometric mean (95% conf. 1996.100-.240 (.250-.140 (.400) .270 (.250 (.280-..128 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.180-.315 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.190-.242-.130 (.058 (.063 (. Acute. 1977a. 2007.068) .056 (. 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.070 (<LOD-.170-.286 (.120-. 2002.077) .300 (.074-.126) .150-.066-.080) .258-.290-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.049 (<LOD-.310 (.170) .286 (. 1981). Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.290) .207) .130-. heptachlor.300) ..227) < LOD .120-. FDA established allowable residues of chlordane.320 (.062) < LOD .150 (.140 (.200-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.063) .068) 75th .050-. 1986).066 (<LOD-.063 (. Smith.063-.140) . and alterations in immune function of offspring.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .170) .320) .080) .133) 90th .055-. neonatal mortality.350 (.410) .080 (.126 (.320 (.058-.189-.450) .130 (.140 (. EPA has established environmental criteria for chlordane and heptachlor. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140 (.160) .091) . Le Marchand et al. 2007).130-.071 (.190-.210 (.130-.065-.050 (<LOD-.348) .250 (.070 (.246-.077) .120-.450) . The U.130-.070 (<LOD-.430) .320 (.100-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .150 (.090) .170) .053-.S. characterized by seizures and paralysis. and heptachlor epoxide in foods and bottled water.076) < LOD .119 (..090-.199-. and the U.240-.200-.160) .220 (.350) .120 (.430) .340) . Elimination of all these chemicals from the body occurs over months to years.231) .280 (.073 (.290 (.146) < LOD < LOD . chronic doses of heptachlor have produced liver enlargement and injury.079) < LOD < LOD < LOD .230 (.130) .180-.070) .310-.230) .

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

8 (18.0-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (11.0-17.5 (10.10-13. see Data Analysis section) for Survey years 99-00.3-18. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.2-27.5) < LOD 14.40) 15.5 (11. Survey Geometric mean (95% conf.9-25.3) 18.8 (13. 10. 84 Fourth National Report on Human Exposure to Environmental Chemicals .2-17.2 (18.50) < LOD < LOD < LOD 17.4 (15.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5.6 (8.0) 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.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 (11.2) 26.1 (16.3) 27.20 (<LOD-9.9-16.8) 15.2-27.S.9) 15.8-24.8 (<LOD-23.8) 13.2) 15.4 (<LOD-54. and 7.4 (11.6) 14.8) 19.4) 21.0-54.8) 14.0 (15.3) 18.3 (<LOD-25.5 (<LOD-32.6-17.5 (<LOD-21.3) 16. 01-02.1-38.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.1) 13.8-24.9-29.9 (12. and 03-04 are 14.2) 13.0-19.6 (<LOD-27.2 (<LOD-62.8) 14.8.6 (13.8 (18.90 (<LOD-9.8) 21.7-25.4 (<LOD-19.1) 20.6 (16.9-29.2) 20.6 (14. which may vary for some chemicals by year and by individual sample.1 (19. population from the National Health and Nutrition Examination Survey.8) 13.0-16.4) 18.9-23.6) < LOD < LOD < LOD 27.6 (11.6 (12. respectively.6) 13.9 (15.6.1) 23.3) 22.9) * * * 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 8.8) 16.3) 10.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8-46. < LOD means less than the limit of detection.8-23.6-21.5 (18.7 (10.8 (13.7-18.7 (16.6) 22.1-16.2-16.3) 18.1-15.2 (<LOD-16.3) 23.8-24.0) 13.8 (15.3 (13.6 (16.7-19.7 (13.5) 19.5 (11.2 (<LOD-25.8) 20.1-29.

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

1) 31.1 (47.8 (30.8) 80. population from the National Health and Nutrition Examination Survey.6 (56.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.9-58.1) 18.1-34.6-19.8-110) 59.1-126) 67.7-77.5) 14.2-37.8-90.2 (64.6) 10.8 (15.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.1) 14.3-57.6-22.6 (50.0) 18.5) 90th 55.9 (16.6-88.1) 17.6) 34.5) 36.9-45.2 (15.4) 59.0 (16.4) 19.1-34.10 (<LOD-11.3 (49.6-82.2-23.6 (52.8 (17.6-20.0) 33.8 (26.1-16.6) 25.7) 35.0 (15.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.2 (27.1-28.8) 47.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.3-39.8 (12.6) 54.8 (11.6 (32. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (25. 01-02.0 (14.86-13. < LOD means less than the limit of detection.0) 75th 31.7-38.8-67.0 (42.6-66.9) 51.0-23.0 (29.8-79.3 (16.9 (66.1) 17.9 (51.2) 20.1) 78.7) 17.8 (19.1) 32.6) 60.6 (57.4) 48.5) 77.1-55.0-93.1) 62.7-20.6) 56.2 (14.4) 55.8 (26.3) 30.4 (45.2 (26.8.0 (60.1-16.8 (13.0) 19.5 (15.5) 26.1 (41.1-20.9 (15.7 (35.4-36.9-35.0 (42.1 (17.4-22.9-69.8 (71.5 (44.9-22.6) 13. interval) 18.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.5) 14.9) 51.2 (14.3) 18.5.8 (42.3) 36.8 (28.1 (48.1) 17.0-38.9-64.1 (10.1-18.3 (56.4-23.7-34.7-113) 68.2 (7.7 (16.2-18.7 (18.8 (49.7) 15.7) 52.3) 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.5.3 (58.8-41.9-65.5 (13.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.7) 78.2-88.7) 73.0 (13.5) 35.8 (<LOD-20.5) 9.0-143) 112 (68.5 (45.7) 28.6) 84. see Data Analysis section) for Survey years 99-00.7-32.7-23.0) < LOD < LOD 8.9 (47.7-17.8-129) 74.5) 30.4) 16.0 (16. Survey Geometric mean (95% conf.5) 19.0 (62.7 (74.9-65.1) 17.4) 107 (84.9 (29.7 (13.9 (51.0 (15.0-59.4 (67.8) 19.7-35.4-52.1) 30.4 (12.2-17.7-29.8 (45.3-21.9) < LOD < LOD < LOD 20.7) 56.0-68.3) 19.7-22.7) 59.4-62. which may vary for some chemicals by year and by individual sample.8 (26.5 (15.6 (12.8) 51.2 (36.9 (36.0-23.9 (15.0-93.4 (11.7) 14.1) 17.0-113) 68.3) 25.0) 13.2) 19.9 (28.5-17.8-19.3) 15.5-19.3) 16.5-95.6 (<LOD-14.7 (59.0) 49. 86 Fourth National Report on Human Exposure to Environmental Chemicals .1) 78.5) 48.9) 14.9 (<LOD-14.8 (28.7 (11.1 (65.3-58.5) 20.0 (19.7-160) 86.8 (28.6-54.4-18.0-20.9-89.8-90.9-40.7 (28.9 (19.3 (14.3-86.9) 14.1) 16.7 (30.6) 82.3-74.0) 40. and 03-04 are 14.5) 22.8-16.3 (14.3-32.5-87.2 (19.2) 30.0 (13.2) 17.7-21.2 (59.2-18.4) 20.6 (56.1-22.5-20.5-69.4 (28.8-77.4 (16.8-16.5-36.1-51.6) 56.8-19.1 (22.7) 78.0-123) 74.3) 32.1) 17.1) 18.2) 34.4-35.6 (16.2-21.7 (59.7-18. 10.3) 18.3 (17.3-50.0 (48.8 (16.2 (60.S.6 (15.3) 32.2-16. respectively.4 (30.70 (<LOD-12.1) 17.0-37.3) 30.0-24.9-36.8-21.2) 59.9-20.0-22.3 (45.4-67.5) 78. and 7.5-111) 68.2) 39.2) < LOD 10.2 (25.8 (13.3-30.

080-.340-.370 (.112 (.490 (.497-.106 (.285-.240) .126) .190-.288 (.108 (.220 (.100-.390) .141) .400) .250) .100-.573 (.600) .069-.960) .089 (.461 (.150) .260) .171-. Survey Geometric mean (95% conf.055 (<LOD-.116 (.300-.180-.355 (.460) .120) .186 (.684) .210) .105 (.220 (.430-.390 (.091-.106 (.095-.220) .120) .395) .090) .324 (.490 (.122) .630) .640 (.160-.129) .100-.150) .930) .120 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .680) .079-.210 (.130 (.210-.060 (<LOD-.460) .110 (.690) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.093) .409-.279-.120-.340-.110 (.060-.120) .124) .071 (<LOD-.234) .310 (.109 (.220 (.130) .100 (.190-.119) < LOD < LOD < LOD .417 (.114) .220 (.096-.190-. interval) .111-.350-.127) < LOD < LOD .240 (.117) .490) .460-.087 (.141) .630) .098 (.410-.580 (.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .125 (.054-.191 (.190-.470-.270-.093-.134) .091) .420) .520) .430-.550 (.062 (.272-.211) 90th .580 (.470 (.097) .093-.260) .390) .590 (.470 (.210 (.090 (<LOD-.320-.120) .310-.220 (.250) .158-.280) .100-.340) .470-.210) .350 (.395-.090-.540) .085-. which may vary for some chemicals by year and by individual sample.220 (.370 (. population from the National Health and Nutrition Examination Survey.108) .135 (.490-.20) .559) .128 (.113) .400-.116-.068-.242) .240) .458 (.112 (.390 (.110 (.343 (.130 (.400 (.186-.210) .300) .630) .130) .093-.840) .161-.090-.520 (.651) .120-.119) Selected percentiles ( 95% confidence interval) Sample 95th .237) .131) .390-.082) .116) .414 (.760 (.190-.080-.130) .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 .145-.106 (.080-.830) .081 (.210 (.327 (.100 (.096-.177-.078 (.180-.830) .047-.111 (.085-.170 (.120 (.183 (.220 (.099-.190-.109 (.440) .230 (.069) .430-.600 (.690) .205 (.594) .420 (.237) .580 (.232) .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.078-.480) .080-.122) .240) .180-.090-.090-.500) .680 (.110 (.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-.330-.120 (.330 (.400-.081-.041 (<LOD-.470 (.317 (.120-.250) .060) .125) .288-.096) .210-.390 (.110-.400 (.061-.090-.090 (.440-.130) .080) .367) .310-.390 (.130) .202 (.113) < LOD .110 (.085-.090-.S.104 (.565) .103 (.380 (.286-.140) .103 (.130) .510 (.397-.450) .360-.510-.160 (.130) .099-.098 (.301-.220 (.240-.161) .371) .098) .098-.405) .410-1.108) 75th .310-.110 (.310-.360-.110) .079-.800) .080 (.520 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .104-.320-.290-.070 (.590) .084-.092 (.310) .092 (.094 (.173-.590 (.

Bioassay of heptachlor for possible carcinogenicity.372:20-31. Available at URL: http://www. Ayotte P. Takahashi W. Van Oostdam JC. Odland JO. Jr and Laws ER. Vol. Granath F. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. 9/25/07 International Programme in Chemical Safety (IPCS).niehs. 6/1/09 Rogan WJ. Lawrence River (Quebec. New York. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Toxicological profile for heptachlor and heptachlor epoxide [online]. Willman E. 2001. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Darnerud PO.inchem. Keller JA.html. International Agency for Research on Cancer (IARC) . Sci Tot Environ 2006. 1991 pp. A Report to the Hawaii Heptachlor Research and Education Foundation. Environ Res 2000. 2 Classes of Pesticides. 4/21/09 James RA.gov/toxprofiles/tp31. Muckle G. Jaraczewska K. Distribution of polychlorinated biphenyls. May 1994.html. Dewailly E. 79. Royce W. 1979-1980. Mortality of workers employed in the manufacture of chlordane: an update. Dendle WH. Tartter P.150:981-990. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. et al. Eds. 4/21/09 Baker DB. Laliberte C.8:1-123. Available at URL: http://www. et al. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Charles MJ.atsdr.nih.gov/ntp/ htdocs/LT_rpts/tr009.org/documents/iarc/ vol79/79-12.Summaries & Evaluations. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.org/ documents/cicads/cicads/cicad70. Bleiweiss IJ. Arch Environ Health.9:1-109. JAMA 1988. Circumpolar maternal blood contaminant survey. Available at URL: http://ntp. Concise International Chemical Assessment Document 70 Heptachlor [online]. et al.nih. Vol. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. 88 Fourth National Report on Human Exposure to Environmental Chemicals .html. Head SL.111:349355. Environ Health Perspect 2002.cdc.pdf.gov/ntp/ htdocs/LT_rpts/tr008. Hawaii Med J 1991. Available at URL: http://www. Bjerselius R. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor.110:617-624.330:55-70. maternal serum and milk from Wielkopolska region. Inc.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Berkowitz GS. Toxicological profile for chlordane [online]. In Hayes WJ. Shindell S and Ulrich S.50(3):108-118. Wolff MS. Siegel BZ. KalubaSkotarczak A. Brower S.htm. Jr. Glynn AW. Smith AG. Saidein D. Hertz-Picciotto I. Poland. Stehr-Green P. August 2007. Available at URL: http://www. Sci Total Environ 2004. Organochlorines in Swedish women: determinants of serum concentrations. Dewailly E. Chlordane and heptachlor [online]. Loo S. 1994-1997 organochlorine compounds. Canada). Wohlleb JC.org/site/foundation/ research/projects2. Kolonel LN. Takei G. Organochlorine exposures and breast cancer risk in New York City women. 2006.pdf. 731-915. 1993. Pollutants in breast milk. Atuma S. Available at URL: http://ntp. Senie R.htm. Hansen JC. Baker DB. Wong L. Barker J. Bull Environ Contam Toxicol 1981:27:506-511. 1963-1967.41:145–148. International Agency for Research on Cancer (IARC). Gilman A. Environ Health Perspect 2003. Arch Pediatr Adolesc Med 1996.atsdr. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Bioassay of chlordane for possible carcinogenicity.110(8):835-838. Environ Health Perspect 2002. 1986. Academic Press.28:497501.inchem. et al. 4/21/09 Dallaire F. Voorspoels S.heptachlor. 6/1/09 National Toxicology Program (NTP). Chashchin V. Handbook of Pesticide Toxicology. Organochloride pesticide residues in human milk in Hawaii. gov/toxprofiles/tp12. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Chlorinated Hydrocarbon Insecticides. Drews K. Available at URL: http://www.84:151-161. J Occup Med 1986.259(3):374-377. Aune M.niehs. LeMarchand L. National Toxicology Program (NTP).cdc. Lulek J. Covaci A.

9-34.S.2-95.8) 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. including 1.3) 22.50-11.6 (25.1) 31. food.2) < LOD < LOD 9.5-36. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. Gunderson. DDT usually refers to the technical product.3) 21.8.0-35.7 (15. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. and 7.5 (23.9) < LOD < LOD 9.9-28.4) < LOD < LOD < LOD 61.5) < LOD < LOD 9. It was produced and used in the U. 1991). depending on conditions. DDT is converted to DDE and several other metabolites.7 (19.4.9 (10.0 (21.1’-(2.6 (22.4) < LOD 17. and water. The biodegradation half-life of DDT in soil varies from 2 to 15 years.3) 28. resulting in fetal exposure. particularly meat. inhalation.9) 17.8-23.8-17. DDT is converted in the environment to other more stable chemical forms.p’-DDT (15%-21%). respectively.9) 14. and trace amounts of several related compounds.0 (18. DDT can be absorbed after ingestion.0 (10. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.6 (31.0-27. Fourth National Report on Human Exposure to Environmental Chemicals 89 .0) 19.1’-dichloro-(2.1-27. These chemicals are highly persistent in soil. It is still used in some countries.8) 15.7) < LOD 18. 2002.5) 25.p’-DDD (4% or less). population.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. sediments.0) 26. continues to be the primary source of DDT exposure.7-16.3 (<LOD-21. 1991).2-65.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.2 (11.0-155) 83.S. 17. after World War II until 1972.5-54.5 (14. 1988). 50-29-3 General Information Dichlorodiphenyltrichloroethane (DDT) has been used widely as a broad spectrum insecticide in agriculture and for control of vector-borne diseases. p.9 (10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-33.8-26.5 (23.0 (18.10 (<LOD-12.8-39.10-13. o.2) 30. see Data Analysis section) for Survey years 99-00.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.3 (<LOD-31.2 (<LOD-40.0) 20.4 (23.1 (<LOD-39.9 (10. which is a mixture containing p.1 (33.90 (<LOD-12.9) 29. air. population from the National Health and Nutrition Examination Survey. and 03-04 are 20.0-15.S. Smith. fish. 01-02.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.0-53. as well as in plant and animal tissues.3-590) 293 (104-541) 48.8) 36.1-71. and dairy products. In the body. particularly for endemic vector and malaria control.70 (8.00 (<LOD-10. Survey Geometric mean (95% conf.5 (15.2) 155 (59.3-236) 24.0-37. Both Serum p. Only a small proportion of DDT is metabolized and excreted (Smith.7) 12. DDT and DDE can cross the placenta.0) 40.1 (23.7.2-bis(p-chlorophenyl) ethane (DDD).8) 30. Food imported from countries that still use DDT may contain the chemical or its residues. when virtually all use of it was banned.9 (<LOD-20.3) 21.6 (9. or dermal exposure.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 10.1) 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. In the general U.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. although DDT and DDE intakes have decreased over time (FDA.5) 23. 2008.6 (<LOD-25.3-16.9 (21.p’-DDT (65%-80%). DDT was used at one time as a treatment for head and body lice.3 (27.

087 (.128 (. tremor. 2006)... 2000.62 (.105-. and o.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 . 2004.106) . 1956).051 (<LOD-. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. Gray et al.250 (.106-. and leukemia have also been inconclusive (ADSDR.189-. accidental exposures. Beard.078-. 2002.132-. overt signs of acute human toxicity include vomiting.400) . Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR.065-.078 (.063 (<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 . Jusko et al. dioxins and furans).140) . fertility.150) . Jusko et al.064 (. Longnecker et al.108 (. and duration of lactation. In laboratory animals. 2002. and seizures.313 (. Calle et al.230) .01) .071 (. 1997). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240) . Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.075) 1.160-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .180-.. Reproductive effects in humans affecting birth weight. Mariussen and Fonnum.130 (<LOD-.130-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.530 (. 90 Fourth National Report on Human Exposure to Environmental Chemicals .120 (<LOD-.250-1. 1996).g. which may vary for some chemicals by year and by individual sample. 2006).130 (<LOD-.Organochlorine Pesticides chemicals are excreted in breast milk.180 (. Survey Geometric mean (95% conf.530) .190 (. 1998).080-. 2006. and altered behavior after neonatal exposure (Eriksson and Talts.00) . other organochlorines.. polychlorinated biphenyls.570-4.240 (.095) < LOD . In high dose.170 (.112 (. 2006. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.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. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.107) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.140-. Hayes et al.290) ..084 (.203) .079) < LOD < LOD . Studies of DDT exposure and pancreatic cancer. resulting in exposure to nursing infants (Rogan.130 (<LOD-.071-.. 2001).. premature delivery.106) < LOD < LOD .180) .. Snedeker.086 (. Animal studies reported reduced fertility.150 (<LOD-..400 (.330-4.p’-DDD and p.074-.190 (.098-.146 (.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 .S.180 (.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .260) .26) 1.143) < LOD < LOD .146 (.059-. DDT may bind to estrogen receptors (Chen et al. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. reproductive organ abnormalities.170) .069) .220) .120-. A workplace standard for DDT has been established by Serum p. 2006).142 (. 2001).068-.061) < LOD < LOD < LOD .220) . 2002.420) .201 (.048 (<LOD-.150-. have not been consistently demonstrated (Beard. 2002.200 (. 2001). Gladen and Rogan.627) .34) .p’-DDE can produce anti-androgenic effects (Gray et al. 1995.114-. 2001).230) . population from the National Health and Nutrition Examination Survey. 2006.170-.343) < LOD .00 (.150 (<LOD-... lung cancer.180) .054-.190-1.150-.

so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. 2002. respectively.gov/ toxpro2. 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.e. More information about external exposure (i. respectively.S. EPA at: http://www. 1989).p’-DDT) as a possible human carcinogen.. Since the 1970’s. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. Compared to females in the NHANES 1999-2000 subsample. Link et al. Median DDE levels among a population-based sample of Swedish women in 19961997 were similar to females in the NHANES 1999-2000 subsample (Glynn et al.7-119) 113 (100-140) 93. see Data Analysis section) for Survey years 99-00..S. mean serum levels of DDT and DDE in the U. Heudorf et al. compared to levels observed in this Report (Anderson et al..0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD.Organochlorine Pesticides OSHA and a guidance established by ACGIH.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. 2003. IARC classifies DDT (p.gov/ pestcides/ and from ATSDR at: http://www.html.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. population declined by about fivefold to tenfold. 01-02. 1998. 2002. and 03-04 are 18.6. 1991). 8.. 2004). Biomonitoring Information DDE persists in the body longer than DDT. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. and 7.3. population from the National Health and Nutrition Examination Survey. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. 2003). 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.S. In a population-based sample of men and women from eastern Slovakia. Stehr-Green. NTP considers DDT as being reasonably anticipated to be a human carcinogen.. Smith.. Fourth National Report on Human Exposure to Environmental Chemicals 91 .epa.8. for males and females in the NHANES 19992000 subsample (Pavuk et al.. 2004). environmental levels) and health effects is available from the U..atsdr. In general.cdc. Declining DDE levels over time have also been observed in the German population. 2005).6 (81. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. Survey Geometric mean (95% conf.

24 (1.50 (2.43 (5.40-8.4) 13.90) 22.53 (2.3 (8.45 (1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.6) 9.22) .03-1.03-4.680-1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.62-6.9) 7.623 (.2) 26.870 (.40-4.6 (8.39 (3.51-49.53) 1.18) 1.01-15.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .456 (.02-8.32-9.7 (8.36 (3.72) 1.85-4.46 (1.97-4.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.7) 16.12 (.20 (. interval) 1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.57-2.9 (15.5) 16.51) 3.6) 9.. 2004). 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.06) 3.70) 1.01-11.57-13.57) 2.557) 1.43-8.9 (26.37-16.S.32 (1.36-2.17-3.51) 1.34-3.34) 2.31 (1.41 (1.36-11.93 (7.87 (5.75) 1..0 (9.0) 2.5) 5.9-38.25 (.8 (9.7-19.68) 2.18-4.4-19. High mean levels of whole blood DDT (about 3.43-4. Survey Geometric mean (95% conf.35) 1.63-15.11 (2.10) . In a subsample of NHANES II (19761980) participants.71) 32.31-12.16 (2.39-2.1 (9.49) 8.72) 1.76 (2.534-.47 (1.81-18.0 (12.01-1.p’-DDT.12-1.69 (.p’-DDT.91-2. 1991).7-48.24) 1.3-43.430-.70-3.8 (14.796 (.1 (8.965-1.83 (1.64-2.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.01-5.09-1.600) .7-20.6) 8.34 (7.63 (1.32) 1.37-10.7) 13.54-7.27-1.730) .84 (3.18-1.16-1.01-11.19-14.6 (7.07) 1.590 (.38 (1. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.80) 3.419-.3 (9.21) 90th 7.26-2.81 (7.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .25-14.82 (1.59 (1. considerably higher than levels in this Report (Smith.55 (2.52 (1.37 (1.820-1.6) 9.47) 3.01) 1.02) 1.48 (6.85-10. less than one percent had detectable serum levels of o.81 (1.59) 3.2 (19. 2001-2002 and 2003-2004 subsamples.58) 1.75 (8.56-2.25 (1.04 (6.4 (12.25-16.51 (1.00-1.61-2.76-3.54) 8.46-2.96) 1.24-17.07) 1.76) 1.10-1.38 (1.5) 10. population from the National Health and Nutrition Examination Survey.4) 9.90-8.18 (6.18-3.17 (3.46 (1.91 (6. serum levels of o.80) 1.49 (1.51-15.80 (2.49 (1.994-2. o.75) 6. Finding a measurable amount of p. or p.27) 3.3) 10.40-4.64) 3.8-90.14 (1.1) 40.9-17.32-1.43-4.07 (5.92 (3.66) 4.39-1.890-1. Serum p.Organochlorine Pesticides nearby agriculture (Botella et al.29 (1. 2005).88-35.23 (7..55-9.40 (3.05 (3.91-3.84-3.4 (8.57 (1. 309 versus 268 ng/g lipid.9) 5.1) 12.10-5.66) 3.37-1.99) 1.49 (6.5) 7.63 (6.59 (4.57 (3.8 (13.6 (17.34-11.69 (1.56) 2.30 (1.78 (4.860 ng/L) and DDE (about 14.56-6.10) 2.92) 1.4) 14.6) 12.34) 6.66-17.22 (7.13) 4.25) 8.2) 19.488-.36) 3.71 (6.39) 1.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.19) 4.04-1.01) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.80) 1.2-32.28) 1.01-1.2 (9.69 (2. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.68-4.33-1. In the NHANES 1999-2000.82) 1.12 (6.77 (1.25) 1.00) 7.77 (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.92 (3.52-6.71 (5.85 (1.45 (1.26 (1.6) 13..66) 1. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.6) 9.66-4.p’-DDT (Stehr-Green.26-10.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.05) 1.56-3.79) 4.1) 7.8) 15.13 (1.52 (3.75) 2.11-1.41-12.66-2.31-2.54 (1.81-5.37-4.58) 75th 3.30-1.6 (9.02 (2.68 (2.58) 1.50-17.53) 7.635) 1.2 (9.14-9.18-1.06) 1.p’-DDT were below the limits of detection.21) 3.71) 12.96) .14) 2.32 (1.57 (1.48-4.65 (1.76) 1.385-.516 (. 2004).75 (4.14) 2.69) 8.5) 22.520 (.00 (.963-1.88 (2.15-4.59) 6.36-1. 1971).66) 1.7) 9.51-8.32-1.57-3.44) 1.69) 4.26) 3.30-1.30 (1.726) .91) 3.87-16.3) 16.14-1.611-1.53-15.65) 1.59 (1.63 (1.22-1.646) .13-2.97 (3.8 (13.3) 13.6) 11.500-.2 (6. 1989).00 (6.81) 11.61 (1.561 (.60-13.

4.Organochlorine Pesticides Serum o.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. 17. see Data Analysis section) for Survey years 99-00. respectively. population from the National Health and Nutrition Examination Survey.7. 01-02. and 7.S. Fourth National Report on Human Exposure to Environmental Chemicals 93 . and 03-04 are 20.8.

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

Int J Hyg Environ Health 2003. Darnerud PO.html. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Chemosphere 2005.358:110-114. Jr. Effects of environmental antiandrogens on reproductive development in experimental animals. India. Zhou H. Chemosphere 2004. Organochlorines in Swedish women: determinants of serum concentrations. Cueto C.206:485-491.gov/~dms/ pesrpts.96:34-40. Lepom P. Sci Tot Environ 2006. DDT and human health. Davis MD. et al. Furr J. Hanrahan L. Link B. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Lancet 2001.17(6):692-700. Zoellner I. Neurotoxicol 2000. Swanson MK.71(6):1200-1209. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Eriksson P. Patterson DG Jr. Gabrio T. Barr DB.162:890-897. Maternal serum level of 1. Bjerselius R. Parks L. Kashyap R. Schulz C. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Hurd C. August 2008. Vorojeikina DP. et al. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Hayes WJ.355:7889. Environ Health Perspect 2004. Olson J. Katz SH. Seiwert M. Baker RJ. Heudorf U. Brock JW. Jusko TA. Brock JW. Environ Res 2004.155(4):313-322. Thun MJ. J Assoc Off Anal Chem 1988. FDA total diet study. Organochlorines and breast cancer risk. Granath F. et al. Arnold SF. et al.21(1-2)37-48. Lambright C. Kulkarni PK. Gunderson EL. Ellis H. Available at URL: http://www. Klebanoff MA. Longnecker MP. Environ Health Perspect 2003. Saiyed HN.205:297-308. Botella B. and HCB residues in human blood in Ahmedabad. Needham LL. Cerrillo I. hexachlorobenzene. et al. Henley SJ. Biomonitoring of persistent organochlorine pesticides.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Bates MN. DDE.7(3):248-264. Wolf CJ.gov/ toxprofiles/tp35. Falk C. Bhatnagar VK. et al. Piechotowski I. Zhou H. Garrett N. Zaidi SS. Ostby J.1-dichloro2. Levels of DDT. Food and Drug Administration (FDA). Vena JE. Biochem Pharmacol 1997.54:1431-1443.. and polythelia among male offspring. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Olson JR. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Gray LE Jr. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Available at URL: http://www. Kaus S. dietary intakes of pesticides.52:301-309.fda.85:504508.cfsan. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Charles MJ. Talts U.58:1185-1201. and DDD [online].106(5):279-289. Gladen BC. Krause C. and dichloro(diphenyl)ethylene (DDE). Buckland SJ. JAMA 1956. Angerer J. Needham LL. Bull Environ Contam Toxicol 2004.atsdr. Willman EJ. Rogan WJ. et al. Bloom MS. Klebanoff MA. 4/21/09 Gladen BC. and other chemicals. Atuma S. Am J Public Health 1995. et al. Drexler H. Koepsell TD. Needham LL. 4/21/09 Anderson HA. Notides AC. Frumkin H. Aune M. Hum Reprod Updat 2001. Burse VW. Durham WF. Gray KA. Exposure of women to organochlorine pesticides in Southern Spain. Longnecker MP. Toxicological profile for DDT. Calle EE.html. Herrman T. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Greenfield TA. Beard J. et al. lindane (g-HCH). HCH. Environ Health Perspect 1998.111:349355. Am J Epidemiol 2002.cdc. Int J Hyg Environ Health 2002. DDE and shortened duration of lactation in a northern Mexican town. Environ Res 2005. Maternal DDT exposures in relation to fetal and 5-year growth.97(2):178192. Rivas A.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Olea-Serrano MF. Paepke O.72:261265. April 1982 to 1984. CA Cancer J Clin 2002. Savitz DA. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings.112(17):1761-1767. Epidemiology 2006. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). dichlorodiphenyldichloroethylene. Hediger ML. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Chen CW. Jr. Klebanoff MA. FDA Pesticide Program Residue Monitoring 1993-2006 [online].53(8):1161-1172. hypospadias. selected elements. Moysich KB. Profiles of ortho-polychlorinated biphenyl congeners. Glynn AW. Becker K. Crespo J. The Great Lakes Consortium. Olea N. September 2002.

109:35-47.150:981-990. children and newborn infants. et al. and DDD in male rat liver and cultured rat hepatocytes.Organochlorine Pesticides Mariussen E. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Crit Rev Toxicol 2006.53:455-477. Rogan WJ. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Academic Press.20(2):186-193. Chemosphere 2004. J Toxicol Environ Health 1989. Handbook of Pesticide Toxicology. Smith AG. 1991 pp. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Cerhan JR. Pavuk M. Fonnum F. Chovancova J. Petrik J. Arch Pediatr Adolesc Med 1996. Snedeker SM. Lynch CF. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Comparative pharmacodynamics of CYP2B induction by DDT. PA. Pesticides and breast cancer risk: a review of DDT. Demographic and seasonal influences on human serum pesticide residue levels. Rey AA. In Hayes WJ. Pollutants in breast milk. et al. Inc. New York. 731-915. Fox S.54:1509-520. J Toxicol Environ Health Part A 1998.27:405-421. Deichmann WB. Nims R. Vol. DDE. Toxicol Appl Pharmacol 1971. Chlorinated Hydrocarbon Insecticides. Thomas PE. Eds. 2 Classes of Pesticides. Jones CR. and dieldrin. Schecter A. Astolfi E. DDE. Lubet R.36:253-589. Stehr-Green. Jr. Reddy AB. Environ Health Perspect 2001. Jr and Laws ER. Radomski JL.

S. 1991). or discarded. endrin is converted rapidly to its major metabolite. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.70) < 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 5.50) < LOD < LOD < LOD 5. Depending on soil conditions. Endrin does not accumulate in body tissues (IPCS. 1992). manufactured. or from contact with contaminated soils and sediments in areas where endrin was applied. inhalation or dermal exposure routes. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.09 and 7. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. 1996.40 (<LOD-6.10 (<LOD-5. An epidemic of acute endrin poisoning.S. IPCS.Organochlorine Pesticides Endrin CAS No..20 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. anti-12hydroxyendrin.. Over time.. 1979. 1992).S. 72-20-8 General Information Endrin. endrin can persist for years. Endrin is absorbed rapidly after ingestion.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. which may vary for some chemicals by year and by individual sample. At high doses. Endrin has been detected in soils. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. population from the National Health and Nutrition Examination Survey. and inflammation (Smith. 1992. endrin has been detected with declining frequency in U.. Survey Geometric mean (95% conf. is no longer manufactured in the U. Kavlock et al. Hepatic effects of endrin exposure have included necrosis.20 (<LOD-5. Ketoendrin is a major photodegradation product (IPCS.40-5.S. fatty infiltration. Smith. Because it is metabolized so rapidly. rodenticide and avicide. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 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. Endrin was not widely used as a termiticide. Endrin was used as an insecticide. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.10 (<LOD-5.50) < LOD 5. < LOD means less than the limit of detection.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. 1987). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1981). total diet surveys (FDA. All uses of the pesticide in the U. unless the dose is high and the exposure is very recent.8. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used.30 (<LOD-6. EPA. a stereoisomer of dieldrin.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. In the body. and occasionally at low levels in sediment and surface waters.S. 1992). 2008). unlike aldrin and dieldrin.60 (5. have been cancelled by the U. endrin usually is not detected in serum of exposed individuals.30) < LOD 5. 1991). endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.

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

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

4. 2005).0-25.3) 24.6 (21.7) < LOD < LOD 24.4 (18.3) < LOD < LOD 20.0 (25. Gunderson.6-33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3-26. and accumulates in fatty tissues where it persists for years.5-TCP) and 2.0-28.1-16.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. and 03-04 are 118.5) < LOD < LOD 18. EPA cancelled its use in 1984.0-19.4.1 (14.5 (13.5-33. and foods with a high fat content.4.9) < LOD < LOD 16.7-16.9) < LOD < LOD 28. 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.4) < LOD < LOD 23. air.6) < LOD < LOD 25. 2.0. Therefore.0) < LOD < LOD 15.4) < LOD < LOD 18. primarily as a fungicide and seed treatment until the U.8 (26. HCB is well absorbed after oral administration. HCB is slowly metabolized. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4 (22.3 (20.4) < LOD < LOD 19.3 (14. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. and has been detected in soil. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.0 (18.1 (14. < LOD means less than the limit of detection.2 (13..5-14.7) * * 14.S.8.0) < LOD < LOD 15.7 (15.7-26.4 (18.3 (22. 2008.4-16.9-20.4.6 (24.0) * * 15.1-20.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.2) < LOD < LOD 29.3) < LOD < LOD 29.6-44. 1988).7 (15.9 (23. and 7.6) < LOD < LOD 26.8) < LOD < LOD 27.0-16. which may vary for some chemicals by year and by individual sample.4) < LOD < LOD 14..4.0 (18.2-15. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. and elimination occurs by renal and fecal routes.S. Urinary metabolites include pentachlorophenol (PCP).1 (17.7 (19. 1976).5-15. particularly by consuming fish.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 * * 14.1 (13.5-trichlorophenol (2.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.9 (25. distributes widely throughout the body.2-15.2-31.2) < LOD < LOD 13.3 (16.7-16.. respectively.7 (27.6-trichlorophenol (2.3-22.9) < LOD < LOD 20.4 (11.9 (25.S.4) < LOD < LOD 33. 1997).. The general population may be exposed to HCB through diet.S.2 (17.Organochlorine Pesticides Hexachlorobenzene CAS No.8 (22. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. The FDA dietary surveys have shown that over time.1) * * 15.5 (14.2 (14.3 (12. Survey Geometric mean (95% conf.2 (14.3-20.9 (14. 01-02.6-32. see Data Analysis section) for Survey years 99-00.6) < LOD < LOD 14.6 (23.5-15.5-18. 31.1) < LOD < LOD 15. water.5 (13.7-21. or game taken from areas with HCB contamination.6) < LOD < LOD 24. population from the National Health and Nutrition Examination Survey. breast milk is an additional route of elimination in nursing women.8 (15.3) * * 15.9-30. Although it is not manufactured as an end-product in the U.3 (22.9) < LOD < LOD 19.9-17.6) < LOD < LOD 26.7-22. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.9-32.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.9-24.5-14.9-15.7-29.6-TCP) (To-Figueras et al.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6-19.9) < LOD < LOD 20. 2002).4) < LOD < LOD 22. and sediment (Barber et al.4-15.9) 19. wildfowl.8-15. HCB has been detected in fewer foods since the 1980s (FDA.2 (24.7-15.0 (14.6-26.9) < LOD < LOD 15.7-30. 100 Fourth National Report on Human Exposure to Environmental Chemicals .0) < LOD < LOD 24. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.

arthritis.098 (.078 (. Survey Geometric mean (95% conf.064 (. More information about external exposure (i. EPA at: http://www.196) < LOD < LOD .089-.html. IARC classifies hexachlorobenzene as possibly carcinogenic to humans. Biomonitoring Information Serum concentrations reflect the body burden of HCB.100) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 101 . 2002). population from the National Health and Nutrition Examination Survey.079 (.073-.083) < LOD < LOD .157-.111) < LOD < LOD .171 (.156 (.S.126) .062-.123 (..086-.095 (.gov/toxpro2.gov/pesticides/ and from ATSDR at: http://www. immunologic abnormalities.258) < LOD < LOD .095) * * .140 (.085-.115 (. 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.203) < LOD < LOD .087 (.147 (.163 (.109) * * .186 (.132) < LOD < LOD .113-.e.S.127-.088-.086-.123 (.173) < LOD < LOD .095 (. and the FDA has established a bottled water standard for HCB.102) < LOD < LOD . reproductive and developmental toxicities.176) < LOD < LOD .122) < LOD < LOD . which may vary for some chemicals by year and by individual sample.167 (.121 (.182 (.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.077-. With chronic exposure.157 (.099) < LOD < LOD .163) < LOD < LOD .135-.090-.118-.225 (.065 (.160 (.191 (.178-.118-.099) < LOD < LOD .091-.169-. and many died before 2 years of age (Peters et al.159-.174-.097) < LOD < LOD .118) < LOD < LOD . anorexia. thyromegaly.086) < LOD < LOD .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 * * .114-.099) < LOD < LOD . EPA has established a drinking water standard.090 (. Infants were exposed transplacentally and through breast milk.085) * * . 1982.155) < LOD < LOD .141) < LOD < LOD .147-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD . and liver and thyroid cancers (ATSDR.088-.cdc.104 (.082-. 1960).167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .095) < LOD < LOD 75th < LOD < LOD 90th * * .114-. Schmid.125 (.123 (.060-. 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.107) < LOD < LOD . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.092 (.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 * * .107-.atsdr.120 (.097) .129) < LOD < LOD .072-.163-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. In humans.069) < LOD < LOD .090 (. environmental levels) and health effects is available from the U.Organochlorine Pesticides chemical.143-.111-.092-. The U.081-.088-.097 (.102 (.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .190 (. and weakness.145-.089-.176-.090 (.094) < LOD < LOD .145-.203) < LOD < LOD .148-.092 (.epa.175) < LOD < LOD .094 (.081 (.095-. HCB interferes with normal heme synthesis. very high. acute doses produce central nervous system depression and seizures. as well as hypertrichosis. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.130) < LOD < LOD . ACGIH has developed workplace exposure limits for HCB. Chronic feeding studies in animals have demonstrated kidney injury.152) < LOD < LOD .069) * * . and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.092 (.179 (.. This condition.

Glynn et al. In Spain. Environ Health Perspect 2002. 2002) and among children (Link et al. Lackman. selected elements. HCB detection in serum also was proportional to age. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking.. 4/21/09 Glynn AW. 2002). FDA Pesticide Program Residue Monitoring 1993-2006 [online].. September 2002. 2005). declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Organochlorines in Swedish women: determinants of serum concentrations.fda. 102 Fourth National Report on Human Exposure to Environmental Chemicals . J Assoc Off Anal Chem 1988. Gocmen A. 2002. Sweetman AJ.cfsan. Biomonitoring of persistent organochlorine pesticides. Dallaire F. Lepom P. Biol Neonate 2002. Bertram et al. Over the past two decades. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Schulz C. Barr DB. References Agency for Toxic Substances and Disease Registry (ATSDR). Darnerud PO. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Kaus S.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples... et al. 1989). Ozalla D. Food and Drug Administration (FDA).. Schwartz JM. Sci Tot Environ 2005. Aune M. Canada). 2002. only 4. 1986. Can J Biochem 1976. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.58:1185-1201. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al.349:144. levels. et al. 2002. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Reference values updated. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Becker K. Chemosphere 2005.. In the 1976-1980 NHANES subsample.. Gabrio T. Eskenazi B. Bjerselius R. 2003). Hexachlorobenzene in the global environment: emissions. 2005). Zoellner I. Lecha M. Bertram HP.44 mg/L. FDA total diet study. Fenster L. Herrman T.71(6):1200-1209. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Bryan GT. Jones KC. As a result of the lower limit of detection in NHANES 2003-2004. et al. IARC Sci Publ 1986.111:349355. more HCB levels were quantified. Krause C. Granath F. April 1982 to 1984. 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. Otero R. Jones D. Santiago-Silva M. Muckle G.gov/ toxprofiles/tp90. distribution. Link B.. Toxicological profile for hexachlorobenzene update [online].gov/~dms/ pesrpts. Atuma S.17:388–399.77:173182. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Dogramaci I. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Arch Dermatol 1999. Bradman A. Kemper FH. 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. 2006). Environ Health Perspect 2003. Cripps DJ.html.html.54(3):203-208. 2005. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Safe A..110(8):835-838. Gunderson EL. but overall. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Arch Neurol 1982. and other chemicals. HCB levels were directly related to age.. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. 4/21/09 Barber JL. August 2008. The metabolism of higher chlorinated benzene isomers. Ayotte P. Laliberte C.205:297-308. van Wijk D.cdc. 1999). Lawrence River (Quebec.atsdr. trends and processes. Available at URL: http://www. J Exp Sci Environ Epidemiol 2007. Muller C. respectively. et al. Dewailly E. Holland NT.9% of participants had quantifiable levels (Stehr-Green. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Int J Hyg Environ Health 2002.39(12):744-749.135(4):400404. and the geometric mean concentration of HCB in whole blood was 0. Peters HA. however. Sala M. dietary intakes of pesticides. Bradman et al. Paepke O. Link et al. In a representative sample of the 1998 German adult population. 2002. Lackmann.. Kohli J.81(2):82-85. Herrero C. Lackmann GM. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Seiwert M. Piechotowski I.

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

1-27.7) 56. the U.1-36.9 (50.9) 17.60-13.0-34.7) 23.2) 9.8) < LOD 10.9-24.7 (35. HCH isomers.6-89. beta.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.0) 17.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.4-111) 84.6-20.8) 52.90-8.4 (52.2-67. see Data Analysis section) for survey years 99-00.0) 71.Organochlorine Pesticides Hexachlorocyclohexane CAS No.4) 901 1067 952 992 1224 1007 Females 11.3 (26. population from the National Health and Nutrition Examination Survey.1 (30.2 (18.3) 51.6-37.4) 10.4) 51.7-26.68 (<LOD-10.7-96.8) 12.9) 45.3) 14.3-38.3 (62.1-15. which may vary for some chemicals by year and by individual sample.4) < LOD 9. The other isomers can be formed during the synthesis of lindane.7) 32.8 (21.7) 10. exists in several isomeric forms. soil.0 (14.5 (24.3-85.9) 15.0 (19.3) 34.1 (9. Lindane has a half-life of about two weeks in soils and water.89 (<LOD-9. 608-73-1 beta-Hexachlorocyclohexane CAS No.4 (12. containing about 64% alpha and 10%-15% gamma isomers. commonly known as lindane.5) 11.9-178) 48. < LOD means less than the limit of detection.4 (11.4) 44.2 (50. 58-89-9 General Information Hexachlorocyclohexane (HCH).9 (9. In 2006.4) 27. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. water.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. See the section “What’s New” at the beginning of this Report for details.5 (43.7) 18. The gamma isomer.0 (35.2-20. 01-02.6-135) 69.0) 8.8 (23.1 (18.6) 16.0) 41.7 (13.0 (37.6 (22.61-12.3 (13.1) 12.2-55.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.7 (<LOD-16.80 (6.6 (17.9-21. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.0 (<LOD-12.2) 62. and 03-04 are 9. and have been used either as fungicides or to synthesize other chemicals.50) 8.2-98. **In survey period 2001-2002. formerly referred to as benzene hexachloride.9 (62.7-69.1-32.9 (11.7) 97.7-69.9 (32.7) 73.5 (8.8 (33.2) 142 (99.6 (10.7-166) 70.2 (9.2 (31.6) 35.6-42.0-111) 70.90) 7.0-23.8) 27.5 (11.8-54.1 (21.46-11.3 (42.9-51.8 (17.6 (33.6-47.4 (50. EPA cancelled agricultural uses of lindane (ATSDR.8 (32. and 7.0-20.1 (12.04-10.30-11.4 (16.2 (34.5528.7-96.8-87.70 (8.7 (25.6) 50.5) 40. It is no longer produced or sold in the U.8) * * * * * * 15. so they can accumulate in fatty tissues of animals.4) 11.8 (9.3 (42.9 (26. respectively.70 (6.3-56.36.S.66-12.80 (<LOD-14.1) 71.8-199) 134 (85.1 (9.1-16. including alpha.6 (16.0-70.7 (53.5) 14.8-68.7) 10.5-123) 49.4-50.4 (8. Technical grade HCH is a mixture of all four isomers.1) 13.8-19. HCH isomers are lipophilic.8.6-62.5 (14.5 (37.0) 7.1 (16. As pesticide applications of HCH were increasingly restricted or eliminated.2) 36.7 (30. 104 Fourth National Report on Human Exposure to Environmental Chemicals . 2005). each result has been multiplied by 1.0) 35.6) 653 758 589 1240 1533 1370 20 years and older 10. 2005).1-49.76.90-8.5 (16.9 (40.0 (33.1-32. 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.8 (10.7) 27.70-12.6) 36.4-45. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.5) 29.4-73.5) 67. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.6) 18. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.2 (29. gamma. However.7 (62.0-21.0-70.8) 39.3) 25.5) 90th 42.1 (11.1) 12.0 (8.2-22.6-18.6-14.8-16.2-52.6) 47.2-46.9-81.20-16.S.70-19.9 (30.3) 37.9-14.4) < LOD < LOD < LOD 46.5) 16.6 (40.2 (48. 6.4) 21.2-17.1-37.2-87.8) 7. particularly alpha and gamma have been detected widely in air.1) 31. environmental levels declined.8 (64.87 (9.9-56.8) 95th 68.7-20.S.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. 319-85-7 gamma-Hexachlorocyclohexane CAS No.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.56-12.2-42. interval) 9.5-29.1 (27.5) 22. and sediment as a result of historic production and use.7 (29.43 (<LOD-9.2) 13. and delta.9) 81.

060) . and nephropathy developed (IPCS. 1983). 1977).098 (.050-. Gunderson 1988).372 (.077) < LOD .290 (. paresthesias. The beta isomer accumulates in fatty tissues and is metabolized more slowly.280-.310) .073-.090 (. for lindane.460) .050-.056-.37) 1.580 (.139 (. the serum half-life was about 20 hours among children (Ginsburg et al.5528. resulting in a half-life of about seven years.070 (.210 (.173-.080 (.661) 901 1067 952 992 1224 1007 Females .320 (.214) .S.222 (.062 (. which may vary for some chemicals by year and by individual sample.103-.120) .120) . and seizures.290) .01 (.150-.057-.110) . probably by blocking inhibitory neurotransmitters in the central nervous system. tremors.250 (.050 (.05) .072 (.080-.S. enlarged livers.050-.160) .089) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .220) .280-.200-.077) < LOD .442) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .120-. ataxia.370-.680) .382-.620-1.057-.146-.091) .080-.110) .480) .220-.260-.050 (.380 (.050-.290 (.390-. Rogan. OSHA and ACGIH have established workplace standards and guidelines.340-. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.330 (.120-.290) .400) .287 (.814) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .065 (.191-.070 (.140) .100 (.064 (.350) .350 (.125) < LOD < LOD < LOD .160-. and FDA has established a bottled water standard and food residue tolerances for lindane. population from the National Health and Nutrition Examination Survey.048 (<LOD-.300-. each result has been multiplied by 1.330-.100-.600) . EPA has established a drinking water standard.050 (<LOD-.047-.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.360-.092 (. ingestion.103) 90th .064) .090-.390 (.100 (.220-. hepatic enzyme induction.090 (. 1971.250) .310) .710) .069) .319) .051-.100-.210) . U.570 (.230-. When animals were chronically fed lindane at high doses. Workers who directly handled HCH have complained of headache.Organochlorine Pesticides exposure to HCH is through the diet.221-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130 (.560) .050) .450) .190) .119) .240 (.305) .140 (.174) .840) .083) . 2002).420-..234 (.450 (. Distribution is mainly to fatty tissues.310 (.083 (.144 (.078 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.062 (.058 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 105 ..096) . HCH isomers are absorbed after inhalation.521 (.070-.059-. 1996. 1981). HCH crosses the placenta and is also excreted in breast milk (Radomski et al.191-.297-.220 (.410) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.175 (.260) .700) .065 (.150) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.067) .360 (.160 (.140) .100) .118-. **In survey period 2001-2002.260) .100) .360) .250 (.620) .410-.170-.067 (.140) .118 (.190) .100-.480 (.240-.281 (.081-.32) .340) ..470) .404) .501) .086) < LOD < LOD < LOD < LOD < LOD < LOD . interval) .150) . or dermal exposure. and memory loss (Nigam et al.110) .308-.120-.250-.400) .070) .124-.587) 653 758 589 1240 1533 1370 20 years and older .270 (..120 (.244-. respectively.080) .410 (.090 (.254) 95th .910 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.190-1.450-.690) .470 (.130) . 1986).216 (.170-. 2008.200 (.180-.167 (. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.S.051 (<LOD-.120 (.050 (<LOD-.580-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.250-.510) .480 (.290 (. After dermal application of lindane 1% lotion.057 (<LOD-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 . Saxena et al. 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.080 (..040-.150 (.103 (. See the section “What’s New” at the beginning of this Report for details.080-.331 (.294-.210 (.120 (. The U.210-.200-.412 (.131-.068-.460 (.410) .070-.089-.080) * * * * * * .070-.442 (.190-.056-.110-.560 (.130-.250 (.

< LOD means less than the limit of detection.. and 7. male sex.gov/toxpro2..5. In populationbased studies of New Zealand adults and German adults and children. Becker et al. respectively.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans.html.. Survey Geometric mean (95% conf. 2005. 106 Fourth National Report on Human Exposure to Environmental Chemicals . 2002). 2004) and India (Bhatnagar et al.S. and 03-04 are 14. respectively. EPA at: http://www. 1998. see Data Analysis section) for Survey years 99-00. In recent years. 2004). Bates et al. 1989). which may vary for some chemicals by year and by individual sample..atsdr. Sturgeon et al. 1991. Link et al.. 10. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. Stehr-Green.. In an earlier (1996-1997) sample of German children.. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. 2001-2002. Kutz et al. serum levels of lindane were generally below the limits of detection.gov/pesticides/ and from ATSDR at: http:// www. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. and a diet that includes meat (Becker et al. and 2003-2004.S.cdc. 2005. population from the National Health and Nutrition Examination Survey. the maximum and 95th percentile beta-HCH values.. older age. 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. 01-02. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998).. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers.8. environmental levels) and health effects is available from the U. Radomski et al. 1991. 2002. 1971. More information about external exposure (i.. aged 9-11 years.. 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. Biomonitoring Information Because of its longer half-life.. In NHANES 1999-2000.5. 1989.epa. Additional factors associated with higher beta-HCH levels include rural residence. Kutz et al. were similar to the 95th percentiles in this Report.e. 2004. Stehr-Green.

2005). Radomski et al. A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al. 2003). In a small study of adults who consumed sport fish from the Great Lakes. population from the National Health and Nutrition Examination Survey. 1998). 1986.. 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. 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). Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect... 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. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. 1971). respectively.. * 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.Organochlorine Pesticides 2001-2002 survey period (Link et al.S. Survey Geometric mean (95% conf. 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. 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.

August 2005.91:998-1000.inchem. 4/21/09 Kutz FW. Krause C.fda. Needham LL. Falk C.57(4):315-320.52(1):59-67. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Paepke O. et al. Radomski JL.gov/~dms/pesrpts. Bull Environ Contam Toxicol 2004. et al. Environ Res 2004. Rivas A. Raju GS. Arch Pediatr Adolesc Med 1996. Olson J. Gunderson EL. Bottimore DP. Burse VW. Saiyed HN. Available at URL: http://www. Zoellner I. International Programme on Chemical Safety (IPCS). India. et al. et al. Exposure of women to organochlorine pesticides in Southern Spain. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.58:1185-1201.96:34-4Food and Drug Administration (FDA).html.20(2):186-193. et al. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States).72:261265. Darnerud PO. Olea N. Int Arch Occup Environ Health 1986. Herrman T.120:1-82. Placental transfer of pesticides in humans. Bates MN.71(6):1200-1209. Brock JW. Metabolism of gammahexachlorocyclohexane in man. Atuma S. Saxena MC. Int Arch Occup Environ Health 1983. Lepom P. Heinrich R. Cancer Causes and Control 1998. Angerer J. Environ Health Perspect 2003.106(5):279-289.html. et al.atsdr.54:1431-1443. Levels of DDT. Lindane. Sturgeon SR.150:981-990. Kaus S. Bai KM. Cerrillo I. 4/21/09 Anderson HA. Brinton LA. Aune M. Chemosphere 2004. Reisch JS. Absorption of lindane (g benzene hexachloride) in infants and children. Nigam SK. April 1982 to 1984. Toxicological profile for hexachlorocyclohexanes update [online]. org/documents/jmpr/jmpmono/2002pr08. and other chemicals. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Rey AA. Garrett N. Demographic and seasonal influences on human serum pesticide residue levels. Schulz C. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Toxicol Appl Pharmacol 1971.205:297-308. Seiwert M.htm. Rothman N. J Pediatr 1977.48:127-134. Occupational exposure to hexachlorocyclohexane. Glynn AW. Patterson DG Jr. Visweswariah K. Rev Environ Contam Toxicol 1991. Olea-Serrano MF. Needham LL. available at URL: http://www. Link B. gov/toxprofiles/tp43.cdc. Maass R. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. VI. Available at URL: http://www. The Great Lakes Consortium. Hanrahan L.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Chemosphere 2005. Environ Health Perspect 1998. Biomonitoring of persistent organochlorine pesticides. 2002. Arch Toxicol 1981. Piechotowski I. Int J Hyg Environ Health 2002. Crespo J. PA. Pollutants in breast milk. FDA total diet study. Bhatnagar VK. children and newborn infants. Granath F. HCH. selected elements. Buckland SJ. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Lowry W. Bhargava AK. Astolfi E. Deichmann WB. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Karnik AB. Gabrio T. Zaidi SS.111:349355. Bjerselius R.9(4):417-424. Majumder SK. J Assoc Off Anal Chem 1988. dietary intakes of pesticides. Rogan WJ. Krishna Murti CR. J Toxicol Environ Health 1989. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Needham LL.27:405-421. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. 108 Fourth National Report on Human Exposure to Environmental Chemicals . August 2008. Ellis H. Kutty D. Siddiqui MKJ. and HCB residues in human blood in Ahmedabad. Kulkarni PK. Botella B. et al. Kashyap R. 4/21/09 Ginsburg CM. Stehr-Green. Organochlorines in Swedish women: determinants of serum concentrations. Becker K.cfsan. Potischman N. Wood PH.

animals.0 (<LOD-108) < LOD < LOD 50.6 (<LOD-23.0) * * * 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 19.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.4 (8.6) 9. or pesticide application. 1995).10-37. 1985. Mirex can cross the placenta and be excreted in breast milk. Formerly. resulting in exposure to newborns and nursing infants.2 (7.1 (8. water. sediments. Some states and the U.S.8 (<LOD-73..0 (12. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. Occupational exposure is limited to workers at sites where mirex contamination is present. aquatic organisms.0 (14.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.70 (<LOD-15.90-29.4) < LOD 63. 01-02. where it has a half-life of 12 years. Mirex is absorbed through the skin and from the gastrointestinal tract.S. where it was applied directly to soil and by aerial spraying. respectively.4) < LOD 15.S.7 (<LOD-47. 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. (Kutz et al. Mirex has been detected in air.7 (12.3 (15. and foods.6 (<LOD-31.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.7) < LOD 66.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD..2-230) 13.S. < LOD means less than the limit of detection.8) < LOD 15.5-82.10 (<LOD-15. it is a highly persistent chemical in the environment. and 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. disposal. 1991). Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. Fourth National Report on Human Exposure to Environmental Chemicals 109 . after which it is widely distributed in the body and stored in fat.8 (12.1 (13. see Data Analysis section) for Survey years 99-00.70-24. population from the National Health and Nutrition Examination Survey. soil.5 (9.6-305) 15.3) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.5 (<LOD-115) 153 (30. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.2) 51.6) < LOD < LOD < LOD < LOD 71.1 (<LOD-65. especially those from persons living in the southeastern U.5-425) 40.1) 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. which may vary for some chemicals by year and by individual sample.40 (<LOD-13.5 (<LOD-42.4-230) 18. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. Mirex binds strongly to soil. Mirex is not metabolized in the body. since 1977. 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. 10. and 03-04 are 14.3 (15.0-374) 11.70-40.S.5-291) 11. Survey Geometric mean (95% conf.Organochlorine Pesticides Mirex CAS No. 2385-85-5 General Information Mirex has not been produced or used in the U. In studies conducted in the 1970’s and 1980’s.6 (<LOD-108) 9. mirex was detected in human adipose samples.5.7) 8.3-225) 15.8.6.

106) < LOD .gov/toxpro2.310 (. and 2003-2004 subsamples. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.cdc.430 (. 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. 2001-2002.635) < LOD .. 7. 1991).256 (.79) . The U.080-1. The geometric mean mirex levels of the Inuit mothers were 8.470 (.08 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.053-.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. environmental levels) and health effects is available from the ATSDR at: http://www. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.7 ng/g of lipid.090 (<LOD-. 1995.089-.070-1.077 (<LOD-.052-.100 (<LOD-. as well as in a subsample of NHANES II (1976-1980) participants. EPA has established environmental standards for mirex. which may vary for some chemicals by year and by individual sample. 2004). In samples obtained between 1994 and 1997.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.140 (<LOD-.112 (.690) . Smith.S.470) . Biomonitoring Information In the NHANES 1999-2000.220 (<LOD-.108 (.S.100 (<LOD-.370 (.080-1.055-. 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.102) < LOD < LOD < LOD < LOD .8.079 (<LOD-.090-1.110 (<LOD-.090 (<LOD-.106 (.170-3.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . serum mirex levels were generally below the limits of detection (Stehr-Green. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .610) < LOD < LOD < LOD < LOD .064 (<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 . reproductive toxicity included decreased fertility and testicular damage.054 (<LOD-.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. 2005).79) ..062-.059 (<LOD-.92) . and 4.450) 1.37) .html.410 (. 110 Fourth National Report on Human Exposure to Environmental Chemicals .090-1.Organochlorine Pesticides exposures are unknown. In addition.090-1. IARC classifies mirex as possibly carcinogenic to humans. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.73) . More information about external exposure (i.268) < LOD . and NTP classifies mirex as reasonably anticipated to be a human carcinogen. 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.093 (. 1989).470) .e.02) .170) < LOD .41) .090 (<LOD-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . Laboratory animals fed high doses developed liver enlargement and liver tumors.510) < LOD < LOD .450 (.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 .220) .

Sci Total Environ 2004. August 1995.27:405-421. Academic Press. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. hexachlorobenzene. New York. In Hayes WJ. Van Oostdam JC. Available at URL: http://www. Rev Environ Contam Toxicol 1991. Stehr-Green. Jr and Laws ER. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.120:1-82. References Agency for Toxic Substances and Disease Registry (ATSDR). Leininger CC.15:385-394. Inc. Dewailly E. Hansen JC. et al. dichlorodiphenyldichloroethylene.Organochlorine Pesticides effect. 1991 pp. 1994-1997 organochlorine compounds. Kutz FW. 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. Kutz FW. Circumpolar maternal blood contaminant survey. The human body burden of mirex in the southeastern United States. 4/21/09 Bloom MS. Watts DL.atsdr. J Toxicol Environ Health 1985.html. Gilman A. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Vena JE. et al. Eds. Vol. Olson JR. Toxicological profile for mirex and chlordecone [online].97(2):178192.gov/toxprofiles/ tp66. Handbook of Pesticide Toxicology. PA. Carra JS. J Toxicol Environ Health 1989. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Chlorinated Hydrocarbon Insecticides. Wood PH. Profiles of ortho-polychlorinated biphenyl congeners. Bottimore DP. Odland JO. Chashchin V. Environ Res 2005. 2 Classes of Pesticides. Smith AG. Moysich KB. Strassman SC.cdc.330:55-70. Swanson MK. Demographic and seasonal influences on human serum pesticide residue levels. Stroup CR. Jr. 731-915.

0 (4.0) 2. other organochlorines.0) 14.20 (4. usually at herbicide production or waste incineration facilities.40) < LOD 6.50-25.03) 9.5-Trichlorophenol CAS No.50 (1.20) < LOD 1.30-27.7. < LOD means less than the limit of detection.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.40) < LOD 1.40 (1. 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.27) 696 661 521 696 603 939 Limit of detection (LOD.0) < LOD 11.6-Trichlorophenol CAS No.7) 24.900-2.00-8.60 (4. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.80 (1. population from the National Health and Nutrition Examination Survey.00 (2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.S.40 (.9 (<LOD-121) 9. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (4. Both chemicals have been detected in air. Formation of 2. recent sampling of U. including hexachlorobenzene and hexachlorocyclohexanes.80 (2.80-41.4.0) < LOD 11. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.30-3. 1999). 1999).60 (2.30) < LOD < LOD < LOD < LOD < LOD 1.3.30-27.0) 2.920-3.31 (<LOD-9.50 (2.0) 2. and sediments. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR. 95-95-4 2.4.0 (3.6-TCP). 2006).00-3.4.0 (3.50) < LOD 1.60-18.71 (<LOD-8. Survey Geometric mean (95% conf.4. Trichlorophenols are no longer manufactured commercially.40-18. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.40) < LOD 4.6-TCP were used as intermediates in the production of certain pesticides.40 (1..40 (2.30 (. public drinking water systems did not detect 2.950 (<LOD-1.90-33.980-3. EPA. surface water.0) < LOD 5.0) 2.980-3. may occur by inhalation or dermal routes.50 (.4.0) 2.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .40-11. are metabolites of several organochlorine chemicals.10-3.42 (<LOD-8.0) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1976).940-3.00 (3.40 (2.30-27.4.Organochlorine Pesticides 2.5-TCP) and 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.5-trichlorophenol.4.42 (<LOD-12.0 (8.4.71 (<LOD-8.0 (5.8) 21.9. hexachlorobenzene. and polychlorinated benzenes (Kohil et al. 2.5TCP and 2.20) < LOD 90th 5.0 (4. 2.4.20-71.40 (.30) < LOD 4.60) < LOD 8.4.4.6-trichlorophenol (2.40 (2.30-11.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.00-3.50-16.60 (. which may vary for some chemicals by year and by individual sample. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.19 (<LOD-6.50-63.5-trichlorophenol (2.S.30-40. however.20-36.72) < LOD 1. Such workers would probably Urinary 2.9 and 0. Exposure to trichlorophenols also may result from metabolism of lindane. soils.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.0) < LOD 5. 2.4.80) < LOD 1.63) 18.27) 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 1.40 (2. 112 Fourth National Report on Human Exposure to Environmental Chemicals . Occupational exposures.0) < LOD 5.6-TCP in any of the samples (U.S. Historically.20) < LOD 5.60-8.0) < LOD 21.0) 2.57 (<LOD-15.30-44.

44 (.24) < LOD 1. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.68-4. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.13-13. as being possibly carcinogenic to humans..1) 2.5-TCP or 2.17) 9.33) < LOD < LOD < LOD < LOD < LOD 2.00-29.05-17.4.44 (1.57 (<LOD-7.79-4.8) < LOD 9.16 (.00) < LOD 4.5-TCP nor 2.68 (<LOD-8.78) < LOD 1.64 (4.81 (<LOD-9. 1995) and up to 19 times higher than the 95th percentile value of 1.53-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.S.67 (1. urinary 2.9) 12. population from the National Health and Nutrition Examination Survey.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.43 (2.46 (1.gov/toxpro2.6) 4.15) < LOD 2.4.4.57 (<LOD-7.02) < LOD 7.920-2. furans.37-11.6-TCP levels at the 95th percentile were up to eight times higher than 3.4) 5. and other chlorinated compounds. Fourth National Report on Human Exposure to Environmental Chemicals 113 .820-2.Organochlorine Pesticides be exposed to mixtures of chlorophenols.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.4.4..86 (3. in addition to dioxins.4.8) 4. 1995) were similar.5-TCP and limited for 2.75 (3.31) < LOD 2.78 (3.9 (5.980 (<LOD-1.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . environmental levels) and health effects is available from ATSDR at: http://www. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. More information about external exposure (i. Among 6-11 year old children in NHANES 1999-2000.78-19.4.19-12.16) < LOD 90th 5.5) < LOD 12..0 mg/L.7 (4.4 (6.5) 11.4) < LOD 3.6-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.4) < LOD 3.20-6. 7.82 (<LOD-32.60-3.3 (5. the 95th percentile urinary 2.69-18.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.67 (1.cdc.4.36 (1. Laboratory animals chronically fed high doses of 2. 2004).6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.1 (<LOD-58.24) < LOD 6. leukemias.32) < LOD 4.e.19-4.05-8.27-17.83-12. Survey Geometric mean (95% conf.2) 2.6-TCP as reasonably anticipated to be a human carcinogen.html..6-TCP had increased rates of hepatic tumors.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). and lymphomas. Human health effects from 2. which includes trichlorophenols.2 (2. 1989).69 (2.29 (1. 1989).02-3. 2003.57 (3. In the same 2-6 year old children.4..28-25.4. Urinary 2.93-11.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2003). The 95th percentiles for 2..6) 4.4.4.00-19.49 (1. However.62-20. animals showed hepatocellular abnormalities.37) 16.8 (5.24 (3.55 (4.24) < LOD 5.5-TCP. the 95th percentile urinary 2.6) 4.24-11. NTP classifies 2.0) 7..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. 2003). recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.50) < LOD 2.53-3.73 (<LOD-8.75 (<LOD-6.47-8. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.95 (3.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2) < LOD 5.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.88-16. Neither 2.74) 11.6-TCP. IARC classifies combined exposures to polychlorophenols.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. Radon et al. At lower doses.90 (4.3 mg/L reported in German adults aged 18-69 years (Becker et al.43) < LOD 12..80 (1.atsdr.

Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.32-4.5-TCP and to the median 2.0-44.0-38.80-6.4.60 (3.54) 6.4.6-22.44) 75th 4.8) 32.5 mg/g creatinine) were similar to the limit of detection for 2.80 (2.4.60 (3.5-TCP level of 0.40) 2.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.0 (9.32) * 3.4. 2004).0) 7.95-6.33-4.60 (2.0) 15.30-2.78 (2. In harbor workers exposed to chlorophenol-contaminated river silt.85 (2.4.70) 5.70) 3.6-TCP level.0 (6.8) 18.30-33.9 (11.68 (<LOD-2.58 (1.6) 26.0 (14.70-3. which may vary for some chemicals by year and by individual sample.0-38.S.40 (2.0) 7.0) 10.52 (2.5-TCP (0.0 (13.67-12.40) 3. 1998).20) 4.63) 90th 15.6-TCP than are found in the general population.4.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.0 (14.0 (4.3) 23.80 (2.80 (3. for males in NHANES 19992002 (Agramunt et al.4.5-TCP and 2.40-14.58-3.32) 3.0 (15.6-19.3) 20.4.4 (17.76) 3.4.49 (6.00-4.60) < LOD 5.73-9.74 (2.70) 1.30-2.95 (4.10-3.3.4.7 mg/L.70) 5.09) 15.36 mg/g creatinine.40-2.65 (5.7 (9.26 (2.20 (3.0) 19.7-16.69 (3.24 (2.0) 13.48-26.50-5.0 (6.6) 21.10 (5.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.09-7..8-15.2) 25.4.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.0) 17. Mean values of 2.3) 37.0-68.25-11.70 (2.7 (13.0) 9. Urinary 2.59) 4.12) 2.79 (5. similar to the limit of detection for this Report (Anderson et al.89-6.4.87-14.5-TCP and 2.1) 16.9) 694 677 519 696 602 931 Limit of detection (LOD.10) 2.6-TCP (0.1 (8.00-21.60-3.45 (2.0) 11.40) 4.40) 2.55-3.4.50 (2.6TCP values.70-6. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 19.00 (1.5-TCP or 2.95) 3.0 (20.0 (8.4.80-20.60) 6.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3-17.06) * 2.4.80) 1.40-2.18-3.4.98-7.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0 (14.6-TCP in urine does not mean that the level of 2.4.7-3.00 (4.0) 10.85) * 3.20-23.7) 21.4. population from the National Health and Nutrition Examination Survey.92 (2.56 (3.02) 2. 0.0-18.72-10. Finding a measurable amount of 2.10-2.28) * 2.0) 14.7) 33.00 (2.23) 2.67) 4.47 (3.07 (<LOD-3.5-TCP or 2.36-5.0-37.9) 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 2.2-0. was about six times lower than the median urinary levels for males in this Report (Radon et al.2) 12.90 (3.4 (8.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.0) 9.6-17.57 (<LOD-2.0) 17.60-37.8-24.6-TCP exposure and health effects.70-6.70 (2.3 (11.53) 4.9) 13.75 (8.2 (14.30) 4.0) 13.0) 12.1 (10.46-3.08 (2.6 (12.36 (1.80-25.23-2.84) 2.3-26..90 (4.0 (7.04) 2. Biomonitoring data will also help scientists plan and conduct research about 2.40-7.40-4.4-17.0 (15.6 mg/g creatinine) and 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.31 (3. Survey Geometric mean (95% conf.0 (12.90-8.45) < LOD 11.40-32.20-3. Biomonitoring studies on levels of 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (8. interval) 2.0-54. < LOD means less than the limit of detection.98-11.0-41. 114 Fourth National Report on Human Exposure to Environmental Chemicals .01-6.23) 3. 1991).0 (16. respectively.91-4.0 (6.78 (2.52-3.8-13.45 (5.5-46.20 (3.4 (10.0) 14.40 (2.53) 2.10-3.45-9.0) 13.0-50.0) 11.30-11..99) 6.90) 2.0 (11.4 (9..60-21.0 and 1.8 (9.3 (11.0-43.4.89 (3.6 (11. 2003). Urinary 2.59-6. the median urinary 2.4.35-3.0) 6.10) 6.66 (8.6TCP causes an adverse health effect.31) * 2.1-25.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.0) 13.14 (2.74-3.9 (13.5-TCP or 2.28) 24.5-TCP or 2.20-6.0 (20.51-12.65) 15.80-7.

5) 11.94-13.0 (6.5) 11.22 (3.25-15.82) 2.89) 10.82 (8.9) 7.73) 5.87-6.32-19.1) 14.27-9.33 (1.53-11.22 (<LOD-2.88-7.23) 4.25-17.4) 4.77-4.24 (1.6) 13.30-2.15 (1.6 (22.06) 11.9-64.00 (3.S.22-9.17) 13.9) 19.25-2. population from the National Health and Nutrition Examination Survey.76) 2.38 (4.4 (12.56-5.63 (<LOD-2.41 (3.63-13.96) < LOD 4.56) < LOD 11.Organochlorine Pesticides Urinary 2.2 (8.26-13.87 (3.83-6.1) 11.01 (3.51-21.60-2.23 (1.33) * 2.82 (3.09-3.76-8.68) 2.83 (3.1 (13.9-29.43 (<LOD-2.58 (4.47-5.88) 1.60 (4.65-21.52 (3.8 (7.40 (2.9-34.22-2.8) 19.7-36.90 (1.6 (6.6) 8.35 (3.71 (3.25 (3.9-32.16-10.81-9.13 (1.90) 2.91 (3.19-5.9 (9.6) 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 2.2 (13.68) 2.56 (7.2) 19.06-2.11) 10.33 (7.51) 18.4) 8.17-4.04-16.6 (9.70-9.05 (6.0 (9.52 (5.26 (6.44 (3.83-5.59 (2.63 (2.52) 2.8) 21.00 (2.32 (2.54 (2.42 (2.82-2.5) 9.02) 3.49) 4.88 (2.53) * 2.6) 12.43-7.20-2.6 (12.76) 4.9 (9.42) 2.81) 2.0) 10.72-16.33-2.3) 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.46-14.1 (8.38-5.3 (9.5 (8.0) 8.8) 12.22 (1.4.41-6.52) 2.5) 12.53) 4.10-9.9) 8.9) 8.99-2.65) 18.65-2.79-17.29 (6.67-17.53 (3.5) 8.83-6.29-4.0 (11.18-4.6 (10.00) 4.48-2. Survey Geometric mean (95% conf.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.88) 4.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.75) 75th 4.17) 2.98) 10.18-2.72) 32.98 (1.02 (1.1-32.15 (6.7) 6.91-2.05 (3.88) 5.28-4.25 (3.38) 22.2 (12.7) 25.3-23.29-4.51 (2.87-7.8 (8.78) 90th 12.77) 2.89-2.4 (11.5 (7.88) 4.76) 1.40 (7.5-28.5 (10.95-2.55-2.88) * 2.73-22.6 (5. Fourth National Report on Human Exposure to Environmental Chemicals 115 .6-31.06) 4.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.78 (2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.91 (7.38 (2.4) 9.78) 2.63-15.21-11.65) 2.14-2.00) 4.13-6.04-2.87) * 2.10) 4.10 (6.2 (7.63) 4.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.7 (14.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.1-21.49-3.14-13.50 (2.6 (9.3-37.92) 4.63) * 4.87) 2.08-2.66-4.8) 11.50-8.62-15.43 (2. interval) 2.

Aitio A. Becker K. Schulz C. Jones D. Lindroos L. To T. Kaus S. Shealy DB. 206:15-24. 4/21/09 Agramunt MC. html. Int Arch Occup Environ Health 1991. Radon K. Poschadel B. 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]. Domingo A. The Great Lakes Consortium. December 2006 Draft.45:440-445. The metabolism of higher chlorinated benzene isomers. Falk C. Olson J. Needham LL.63:57-62. et al. Heinrich-Ramm R. Smith SJ. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Head SL. Luotamo M.epa. Anderson HA.54(3):203-208. Corbella J. Wegner R. Available at URL: http://www. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Burse VW.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Environ Health Perspect 1998.atsdr.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Chlorophenol exposure in harbor workers exposed to river silt aerosols. Environmental Protection Agency (U. Available at URL: http://www. U. Jarvisalo J. Safe A. et al. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. S. Arch Environ Contam Toxicol 1989. Toxicol Lett 2003. Gregg M. Can J Biochem 1976. Hill RH Jr.EPA).gov/toxprofiles/tp107. Szadkowski D. Baker S. Toxicological profile for chlorophenols [online].71:99108. Bailey SL. Kohli J. Urinary excretion of chlorinated phenols in saw-mill workers. et al. Fast DM. Hill RH Jr. Environ Res 1995. Hanrahan L. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. July 1999.pdf. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Int J Hyg Environ Health 2003.18(4):469-474.106(5):279-289. Domingo JL. Pesticide residues in urine of adults living in the United States: reference range concentrations.146:83-91. Needham LL. Holler JS. Baur X. Seiwert M.S.cdc. Am J Ind Med 2004. Seifert B. Pekari K.

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

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

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

Survey years 99-00 01-02 03-04 Geometric mean (95% conf.780) < LOD 3.70-23.0) 10.72) 5.80) .3-15.00-27. see Data Analysis section) for Survey years 99-00.8-32.8 (9.82-12.40-5.90) 2.61) 4.16 (2.5) 15.2 (9.5-16.36-4.954 (. 01-02.98-5.4 (7.13 (2.1) 10.758-1.S.17-3.40-14.860-2.34-7.7) 11.40-19.0) 10.599-1.79-7.80) 2.61 (3.19) 9.4) 20.0 (6.58 (3.530 (<LOD-2.1 (9.58 (2. and 0.1) 13.56-13.80-4.60) . 120 Fourth National Report on Human Exposure to Environmental Chemicals .00 (1.00 (5.0) 6.0-28.91) 4. and 03-04 are 0.12-19.29) * * 1.0 (6.39 (8.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.2 (11.970-2.0) 5.0 (4.9 (8.56 (6.80-22.48-7.83 (5.5) 20.0 (7.76 (2.40 (.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. which may vary for some chemicals by year and by individual sample.30 (2.85 (3.890 (<LOD-2.20 (.620-1.99 (5.20 (2.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.02-5.290 (<LOD-1.35-11.80) 2.08-2.32 (.54 (3.70) < LOD < LOD 75th 3.0) 10.45 (2.7 (12.33 (5.0 (7.8 (14.26-8.56 (4.0 (8.8) 7.3) 17.9) 14.0 (9.80) 2.98-12.490-2.90) 3.21) 9.81) 11.70-14.70-19.38-5.0 (12.63) 1.01) * * 1.7 (14.71-9.8 (12.10) < LOD .74 (8.30 (2.94) 3.2) 16.0 (5.55-8.50-36.47) * * 1.6) 18.5 (8.03 (.90 (1.39 (3.4) 17.2.70 (2.82) 10.60 (1.0 (8.2 (7.42) .717-1.00-12. 0.95) 5.08 (<LOD-2.67) 3.4) 18.00) 3.0) 7.840-1.757-2. population from the National Health and Nutrition Examination Survey.34-3.33-18.30-6.97) 90th 7.70-11.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.43-12.12) 4.21 (.60 (5. respectively.2 (14.30 (4.10 (.52-11.80) 11.58 (5.44-38.1.5-17.80 (4.6) 7.66) * * 1.20-30.00-27.4 (7.00-19.0) 20.0) 6.1) 95th 13.13 (2.00) 3.93 (4.13-2.11 (.44 (2.90-5.8) 7.73) * * .53) 4.81) 1. < LOD means less than the limit of detection.9) 8.32) 1.71 (2.89) 9.10 (.8 (8.79 (5.15-12.50 (4.00 (4.600 (<LOD-1.50 (.5 (11.50) 2.8) 19.3) 14.740-2.750-1.0) 15.0) 10.56 (1.10-7.70 (4.70) .2 (14.16) 4.93-24.42-3.0) 6.0 (8.02) 4.46) 10.0) 11.2 (7.08-15.60-11.20 (.10 (2.0) 10.0) 5.94) * * .26-6.10) < LOD < LOD 4.55-6.28) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-4.4 (9.2) 471 576 308 664 822 701 814 1122 922 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 11.2 (9.4 (9.0) 12.37 (3.2) 16.70) < LOD < LOD 1.81) 11.1-17.52) * * 1.27-3.15) 14.00-7.2-20.290 (<LOD-.86 (1.60-25.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.623-1.80) 4.52) 6.26 (5.51) 2.80 (2.2) 14.0 (7.60) < LOD < LOD 4.1 (10.700-1.68-7.74 (8.80) .1-23.670-1.0) 9.07-10.96-3.35-16.830 (<LOD-3.579-1.0-27.955 (.2.80) 3.57-7.0 (7. interval) 1.0 (9.97) 8.05-7.0) 11.47) 5.60-18.50 (2.80-24.10 (2.22 (.810-1.20 (.9-18.50-5.20 (.20-4.0) 5.30-4.14) * * .40-11.40-1.20-7.2 (7.0) 11.23-5.00-12.3) 16.44-3.981 (.86-15.04) < LOD 1.8) 11.35-12.27-15.40-16.

55-20.84 (5.45-5.98) 9.47) * * .75 (3.60) * * .66-34.11-6.00-17.80 (6.27) < LOD 2.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.883 (.03-6.47 (3.88-10.8) 12.92-2.06-2.04 (1.996 (.574-1.28-9.500-1.56) .75) 2.66 (1.2) 8.62-5.2) 95th 12.24-3.88 (5.35 (1.03 (2.13) 4.87-5.10 (3.34) * * .7 (8.28 (2.440 (<LOD-2.21-23.53) 9.82-14. interval) .28) 10.8 (10.830-1.5) 11.43) 2.5) 7.4) 4.8) 8.90-8.9) 11.07 (.81-5.36) * * 1.54-4.95 (3.633-1.80 (7.5-13.2) 5.00-19.1-15.43 (3.1) 4.76-4.61 (1.9 (9.1) 4.924 (.20-8.02 (2.92-5.40-12.93-5.4) 13.1 (8.83) 8.608-1.35) < LOD < LOD 3.67-19.75 (7.4 (9.03 (7.88-15.09 (.60-9.750 (<LOD-1.2 (10.67) 1.25) < LOD .9 (5.0) 7.23 (4.5-20.3) 16.860 (.870-2.50) 7.820 (.2) 7. population from the National Health and Nutrition Examination Survey.7) 5.02-14.25) 6.66 (2.54-2.82-6.37-3.3) 5.62) .23) 4.80 (2.67) 4.52) 4.9-28.40) 4.68) < LOD < LOD 3.61-29.75) 14.64-5.6) 11.1 (7.09-11.7) 12.2) 13.81 (1.18 (.87 (3.76) < LOD .57 (4.75-7.03) 2.773-1.57-10.34 (6.6) 13.39 (2.2) 5.95) 2.40-3.46-5.05 (1.2 (6.51-5.4) 4.02-2.89) * * 1.69) 2.40-28.6 (9.3) 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 1.15-10.05 (.28 (5.29 (2.2) 9.7) 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 .02 (7.68-4.43 (.620-1.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.19 (4.1 (9.1 (10.540-1.71) 10.03) 2.72) 11.0 (8.533-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.510-1.69-10.9) 12.41-12.28 (4.42) 12.9) 16.566-1.3) 15.84) 7.98-22.85) 2.780 (<LOD-1.40) < LOD < LOD 75th 2.5-16.09) 2.00) 8.5) 7.47 (3.10-13.82-26.00-13.37 (5.98-5.83 (7.54-11.41) .9 (9.56) 4.01-2.77 (6.45-11.47 (1.37-5.790 (.94 (2.3) 12.7) 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.47) 2.890 (<LOD-1.6) 9.920 (.71-2.932 (.94-9.29) * * .37) 9.74) 90th 7.S.5) 8.5-32.30) 2.42 (3.82-14.57) 4.2 (8.87 (1.93) 9.8) 16.38 (1.31-14.31 (3.94-23.54) .855 (.00 (4.710 (<LOD-1.4 (4.93-9.74) 4.60) 2.79-9.46) 2.53-11.78 (2.34 (6.90-5.900 (.7 (10.40-5.570-1.05) .98 (3.560-1.98) .30 (1.40 (3.1 (6.14 (3.960 (<LOD-2.56) 7.79-3.818 (.5 (4.00 (4.61-13.66 (5.58) * * 1.7) 18.430-1.89-3.69) 4. Fourth National Report on Human Exposure to Environmental Chemicals 121 .80) 9.549-1.85 (6.7 (9.53 (6.32-12.6) 8.5) 12.0) 6.04-6.38) .69 (4.44 (2.8) 6.650-1.61 (1.57 (6.6 (10.88) 2.94-10.34) < LOD < LOD .1 (11.41) Selected percentiles ( 95% confidence interval) Total * * 50th .73 (1.40-14.960 (.54-15.890 (<LOD-1.94 (4.45-5.66-15.8) 7.98) .94-22.26) * * .37 (4.56-13.

7) 15. 0.41) 3.4) 7.46-28.0 (5.20) 3.5) 21.29) < LOD < LOD < LOD < LOD 3.42 (1.92-17.7-21.S.90 (2.3) 22.9-14.70) 2.7-19.34 (6.3) 8.9) 16.39-13.66) 4.90 (6.41-5.3) 20.970 (<LOD-2.96) 3.49-4.7) 14.70-8.60 (2. population from the National Health and Nutrition Examination Survey.9 (7.0) 12.95 (2.00) < LOD .22 (6.0) 12.53 (3.0) 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 9.4) 11.18 (3.50) .0 (7.95-9.6) 11.00) 3.98-9.80) .20-18.3) 14.34-10.11-6.90-31.0 (9.80 (5.80-8.92) 9.15-6.34-5.10) 6.16-1.27) .35) 4.66-13.86-10.12 (4.8) 9.0) 14.0) 11.50) 5.34-3.35 (6.8-17.15-2.90 (1.9-15.5-26.24-5.10-4.0 (15.14 (6.20-8.3) 10.01 (2.74) * * * * * 1.0) 11.5 (8.30) 3.8-20.00-18.27) 9. < LOD means less than the limit of detection.00) 8.89 (2.90 (2.2) 14.0 (14.60 (5.0) 19. see Data Analysis section) for Survey years 99-00.680 (<LOD-1.59-3.28 (7.60 (6.70-9.9 (12.35-3.97-4.4 (10.90) 8.40 (2.0-33.7) 16.90-9.90 (6.45 (3.790 (<LOD-1.50) 3.0 (9.78) 5.00-4.5 (8.37 (3.10-15.80-14.670 (<LOD-1.0-29.30) 3.0 (8.00-9.80-21.62-17.67) 4.84-4. 01-02.90-15.00-16. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .3 (12.910 (<LOD-2.67-10.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.29-4.77-14.0) 23.46-4.47-6.580-2.1-23.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.88) 3.20) . which may vary for some chemicals by year and by individual sample. respectively.30) < LOD < LOD 4.0) 13.0 (10.90 (6.52 (6.20) 3.33-11.90-15.73) 7.40 (2.3 (7.7) 10.8 (12.10 (.20 (<LOD-2.72) 2.0) 9.89) 2.2 (9. and 03-04 are 0.20-4.00-4.1 (10.0) 6.82) 8.80 (2.6 (10.4 (14.70 (1.90 (5.50-4.88) 10.70-9.4-17.7 (11.70 (8.5) 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 * * * * * * .6-19.81-6.24 (2.8) 8.10 (<LOD-1. 122 Fourth National Report on Human Exposure to Environmental Chemicals .63-14.4 (10.9) 95th 14.5.8 (12.6) 14.5 (9.6 (10.3 (11.00) 3.99 (3.8-20.31-12.3 (9.80 (2.2 (7.22 (6.1 (10.0-19.61-32.51) < LOD 1.39 (5.0) 7.75 (3.22) 8.7) 22.670 (<LOD-1.80) 5.6-41. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.77-3.90 (6.00 (.80-4.27 (3.0-24.67) 3.50-5.06 (2.40) < LOD < LOD 75th 2.37) 2.17 (7.5.740 (<LOD-1.58.6) 18.8-21.04 (3.0) 9.670 (<LOD-1.31) 1.80-3.0) 14.670 (<LOD-1.30) 8.96) 90th 7.75 (2.9) 10.1) 11.650-1.7 (10.90) 4.70-5.10-10. and 0.80) .60) < LOD < LOD 2.3 (6.0 (10.0-24.27 (7.8) 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 1.64) 10.80-12.25 (2.30) < LOD < LOD .80-6.0) 13.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 18.58 (1.18) * * * * * * * * 1.61 (3.9-17.27) 4.31-7.95 (5.90 (2.00-18.6) 14.22-12.0 (13.00) 7.3 (9.

population from the National Health and Nutrition Examination Survey.11 (5.4) 9.2) 12.93 (2.04) 9.2-15.54 (7.91-9.55) 16.61 (2.2) 19.8) 16.77) 3.3-17.78 (4.530-1.6 (11.21-21.5 (8.14 (2.27) * * * * * * * * 1.2) 12.2) 10.01-5.4-16.590 (<LOD-.7 (10.71) < LOD < LOD 2.95) 90th 8.0 (8.71 (1.68-4.67 (1.42-19.38 (.38 (1.74-19.3) 9.2 (9.70-2.3-21.99) 2.89-3.28-12.2 (9.37-5.42) 7.95 (2.54-5.9) 16.85-17.5 (15.27) 5.82-8.3 (7.973 (.79-9.20-3.19) 3.45) 6.00) 8.6) 95th 16. Fourth National Report on Human Exposure to Environmental Chemicals 123 .89-3.43 (2.2) 8.12) < LOD < LOD 4.86 (3.4) 7.1 (8.25-9.15 (1.53-8.63 (2.80) 3.00 (5.7 (8.92 (5.29) 3.6 (13.S.11-3.4) 6.75-3.2) 16.3) 8.6) 7.77 (2.8) 14.41 (7.78-10.51-7.63 (6.8 (8.68-19.51-10.93-10.6 (11.28 (1.0 (11.34) < LOD < LOD < LOD < LOD 3.74-4.27-13.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.6 (13.85-8.28) 6.760 (<LOD-1.07 (5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33) 3.690 (.6) 13.5 (11.2) 15.4-18.00) 2.03 (2.7-23.950) .27) < LOD .39-17.0) 14.9 (9.9) 19.5) 10.3-17.33-10.94 (5.50-17.8) 11.95) 3.93 (<LOD-2.7 (10.6) 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 * * * * * * .67 (7.45) 3.21) * * * * * 1.4-16.3) 6.32-8.4) 15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.75-3.02-4.03) 3.16 (3.16-14. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .82-11.2-30.27) 1.86-3.81 (7.93 (6.9-25.64-11.15) < LOD < LOD 75th 2.72-4.1) 13.6) 14.30) 2.910 (<LOD-1.30) 8.25 (4.23-3.0-21.1) 10.5-17.5) 8.7) 12.30-5.78) 4.32) 2.05-3.06 (<LOD-1.0 (13.9 (9.55) .09-11.7) 9.890-2.00 (<LOD-1.3-34.5) 22.59-3.77 (2.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.3) 12.38 (2.4) 16.4-15.58 (4.6) 6.94-14.99 (4.89) 5.7) 14.7) 14.1) 20.620 (<LOD-.6) 12.07) 2.29 (2.1 (19.37) 3.97-4.810 (<LOD-1.36 (2.12 (7.96-11.47-9.850 (<LOD-1.83 (7.780-1.96-10.3-15.44-6.1 (13.07-3.88-7.79-6.89 (3.7-19.6 (12.07) 2.54) 9.92) 3.73 (5.4 (11.00 (2.38) 1.86) 9.5 (9.87 (3.30) 7.9 (9.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.5 (10.940) < LOD < LOD 1.69-11.52-3.06) .42) 8.7 (11.78 (6.72) 4.7) 15.2) 12.03 (6.6-19.89-13.91) 3.68) .89-10.5) 13.29-2.88 (1.9-17.0 (10.48 (2.00 (7.4) 7.00 (3.97) < LOD .0-19.4) 7.34-18.68-10.6 (10.18) 2.920 (<LOD-1.8 (10.00 (<LOD-1.50 (6.83 (6.89 (2.29 (5.55 (2.70-35.38-13.09-11.6) 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 * * * .

94) .58 (1.740-1.90-4.46) 1.10) 1.749 (.59-6.490 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.949) .50 (1.50) 1.20 (1. and 0.91) 2.380-.30) 2.620-1.01-1.710 (.17) 1.450 (<LOD-.800 (.540 (.73-5.47) 2.98) .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 * .38) 1.20) 1.585) * * .500 (<LOD-.89) 1.14-1.95 (2.790 (.23-3.690) .77-2.840 (.54 (2.670) .73 (1.29) 1.336-.350-.930) < LOD .00) 2.240 (<LOD-.550 (.20 (1.570-1.80) 3.59-2.600-.45 (1.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.03) 1.30-3.830 (.08 (2.09 (. see Data Analysis section) for Survey years 99-00.16) 1.960 (.780 (.60) 3.88) 1. which may vary for some chemicals by year and by individual sample.550 (.398-.74-5.60 (2.600-1.15) 2.S.457 (.590-.710) .77 (1.31) 2.210 (<LOD-.89) .201-.20-2.970) 1.83 (2.60) 2.98-3.390-.759) * .11-3.83 (2.690-1.20) 2.13) .453 (.39) 2.17) 1.600 (<LOD-.70 (1.94 (3.05-2.41 (2.570 (.49) .353-.96-3.64 (1.14 (1.50-2.50 (1.87-3.00) 1.86 (1.280-. population from the National Health and Nutrition Examination Survey.10) 3.592) * 50th .740 (.00-2.382-.700) .31) 95th 2.587) * * .820 (.20-3.74) 3.30 (1.467 (. interval) Selected percentiles ( 95% confidence interval) Total * .75-2.89-6.388-.16-3.960) 1.910-1.30-1.680-1.340-.30) 1.70 (1.63 (1.960-1.910) 1.460-. 01-02.25-1.90 (1.20) 3.700) .46 (1.592-.83) .390-.16) 2.657) * * .76 (1.36-4.850) < LOD .31-3.560-.09.940) < LOD .11-3.20-1.89) 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 * .30 (.80) 5.34) 2.90) 2.780 (.42-2.70-2.97 (2.970) .359-.570 (<LOD-.68-5.49) 2.20) 3.18 (.510 (.730) .90) 2.510 (<LOD-.720-1.45-4.41-5.73 (2. and 03-04 are 0.98 (2.80) 3.78) .30 (.76-6.710 (.46 (2.910 (.57 (2.17-4.96-5.990-1.680-1.10-1.80) 2.690-.90) 3.80) 3.27 (2.70 (1.27 (3.459 (.505 (.580-.20-2.04) 1.33-2.760 (.47 (1.750) 1.740-.46-3.95-5. < LOD means less than the limit of detection.31-3. 124 Fourth National Report on Human Exposure to Environmental Chemicals .50-2.35) 1.343 (.303-.57 (1.18 (1.570 (.820 (.160 (<LOD-.650-.690 (.15) 2.10) 1.10-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 0.22-3.22-2.960) .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 * .30) 4.10) 1.20 (2.95) 2.549 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.79) .570 (<LOD-.260 (<LOD-.55 (3.880) < LOD 75th .19-1.45 (2.61 (1.880 (.740 (.50 (1.32-1.980) 1.810) .930-1.440-.950) 90th 1.65 (2.26 (2.80 (2.32) 3.400) .2.01) .380) .05-3.32 (1.580-1.29-2.30) 4.584) .22-3.20) 2.1.69-4.570) * .30 (.13) 2.40 (1.60-4.880) < LOD .37-2.618) * .80) 2.22-8.425 (.592) * .960) .720 (.40 (1.750-1.75 (2.860) < LOD < LOD .70-7.83) 1.48 (2.54-2.86) 3.930) 1.780) .930 (. respectively.30-3.22 (1.21) 3.01-3.08 (2.449 (.20 (1.20) 1.00 (1.45 (1.54) .720-1.83) 2.34) 2.00-4.94 (2.50 (1.26) .597) * .380-.48 (1.79) .04) .350-.80 (1.50 (1.455 (.

84 (2.71) 2.89-3.460) .448 (.444-.64 (2.09) .38 (2.08-3.393 (.67 (1.300-.370-.98) 1.18-2.32 (.67-3.460 (.740) .73-3.55-3.67 (1.480) .92-8.490 (.440-1.50 (1.60) .11-2.285-.S.20-2.739) * .320-.310-.07) 5.760) < LOD 75th .49-4.08-3.320-.03-1.08-2.73 (2.43 (1.05) < LOD .32-1.840) 1.92) 3.66) .58-6.660-.870) .07-2.08) 1.310 (<LOD-.32) 5.305 (.377-.840) .790) .830 (.38 (1.510 (.400) .800) < LOD .08-2.88) .03-2.590-1.23) 3.403) .97 (1.28 (1.17-2.60 (2.08-3.75 (1.270-.920) .63 (1.02-3.710 (.65) 2.350) .460-1.700 (.81) 2.43) 1.47-4.22) .24) 4.16) 1.447 (.560-.22 (2.280 (<LOD-.61 (3.380-.23) 2.66 (2.22) 1.300 (<LOD-.645) .470) .22-2.00-3.97) 2.07 (.348-.99) 1.55 (1.412-.597) * .980-1.950-2.234 (.97) 1.62 (2.680 (.515) * * .540-.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.990-1.04) 95th 2.95) 1.730) .720 (.42-8.08) 2.72-4.05-2.06) 4.64 (2.77-3.30-2.71 (1.510 (.136-.700 (.80) 2.910) < LOD .75 (2.630) * .580) .05 (1.07-3.250 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 125 .70 (3.480-1.43) 2.485) * * .25-3.940-1.49 (1.04-1.750 (.67) 1.45 (2.23) 2.72 (2.90) 2.820) 1.550-.84-6.560 (.509 (.670 (.72) 1.77 (3. population from the National Health and Nutrition Examination Survey.53) .550-.880) 1.43) 2.253-.250 (<LOD-.57 (3.36) 3.16-2.520 (.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 * .87 (2.47 (1.380-1.02-6.590) * 50th .22-3.79) 1.69 (3.580 (.11 (.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .38-3.640 (.61-3.97 (1.52) 3.91 (1.310 (<LOD-.08-2.82) 2.750 (.20) 1.62 (1.42 (.31-1.640 (.58 (1.552 (.720-1.89 (1.61) 2.92 (1.33) .42) .335-.94) .800-1.14 (2.34 (1.44-2.75) 6.04-5.13 (1.11) 1.535 (.39 (1.380) .690) < LOD < LOD .16-1.19 (1.88 (1.470 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.57-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.510-.45 (1.00 (3.78) 3.07) 1.77-4.710 (.330-.23 (. interval) Selected percentiles ( 95% confidence interval) Total * .640 (.900) 1.400-1.550) .60) 1.41 (.05) 1.471-.20-7.930-1.42-6.52 (1.39) 2.07) 1.550-1.500-.700 (.270 (<LOD-.530 (.32) 1.50) 1.57-4.72 (1.99) 2.08 (2.05-4.368) * .688) * .67) .79 (1.710 (.270-.830) 90th 1.60 (1.23) 1.33 (1.08 (.32) 2.372 (.82 (2.390) .453 (.17) 2.17) 2.760) .75-3.820) .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.10) 2.00-1.230 (<LOD-.02-3.44) 2.29-4.70 (2.580-.08-3.180 (<LOD-.740) < LOD 1.69 (1.30) 3.58) 3.330 (<LOD-.560-.591 (.840) 1.07) 1.318-.06-2.790 (.71) .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 * .520-.850) 1.390-1.22-3.22) 4.742) * * .870 (.57 (1.76) 1.61-3.47 (1.590 (.

690-3.1 (22.70) 1.05) * 2.40-16.76 (2.20 (2.8) 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) 20.96) 5.0-41.0 (38.80-18.0 (37.8 (12.41 (1.6 (9.0 (38.70 (1.10 (1.10 (1.50 (2.10 (1.16) 2.4 (10.83 (3.91 (4.3 (12.93-3.1 (11.32 (2.0 (17.0-53.14) 5.5) 69.6) 52.26) 75th 11.5 (24.70 (.97) 6.0-110) 42.80) .8) 62.0 (20.80) 1.13) 12.53) * 2.92) * 2.0 (38.10 (7.05) 1.0 (38.31-6.99 (2.1 (10.3 (10. and 03-04 are 0.9 (19.70-17.64-8.79-2.30) 4.0 (11.4.6-54.44) Selected percentiles ( 95% confidence interval) Total * 2.45) 2.12) 1.46-6.8-21.50-2.9) 48.5-40. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 16.8 (12.80) < LOD 1.82 (1.0 (19.1-25.0) 20.86 (1.1) 95th 48.4-22.05-3.67 (1.0-50.0-52.21 (3.48-2.71 (4.04-8. respectively.60) < LOD 1.60 (2.48-2.0-110) 34.0-260) 34.0) 5.75-14.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.0) 17.0-47.2-27.2) 31.04) 3.10) 39.81-3.59 (1.470 (<LOD-1.40) < LOD 1.76 (2.44) 2.7) 47.78) 9.25-3.90 (1. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0) 15.0-43.9) 18.830-3.18) 14.0 (7.58-2.70) 5.53) 40.660-2.13 (1.30 (.11 (4.0) 4.8 (22.7) 20.19) 2.6 (26.02 (2.30) 11.1) 38.83-2.0 (20.92-5.07-5.9 (10.44-7.0 (6.8) 41. and 0.0 (8.85 (1.0 (33.8) 32.17-2.18.4-76.7-22.79 (1.74-2.77) 38.5.S.53 (1. < LOD means less than the limit of detection.48) 5.2-47.69) 2.2-26.58) 16.6 (15.41) 1.44) 3.0) 6.0 (21. 01-02.16) * 1.94 (1.40) 50th 2.10-13.20-4. interval) 1.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.0) 15.3 (14.88) 3.9 (19.7 (28.95 (5.71-2.3 (12.0) 28.88) 1.2-62. which may vary for some chemicals by year and by individual sample.81-2.0-62.35-6.70-6.530-4.61-2.2) 16.3 (23.23-2.1 (26.0) 19.9) 17.0) 30.0 (26.50-5.64-3.2 (12.54 (1.8) 39.18) 20.00 (.23) 9.1-19.600-2.5-45.66-5.78 (1. population from the National Health and Nutrition Examination Survey.610 (<LOD-1.0-58.5) 30. 0.2-39.72 (1.09 (4.0) 42.87-7.40) < LOD 2.42) 1.0) 32.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1) 140 (46.0 (13.43-7.6-27.0) 16.4 (15.52 (4.90-8.9 (23.29-9.29) 2.3) 38.13 (1.4) 19.2 (19.49-2.0-31.1) 18.0) 17.00-24.0 (40.41) 1.0-62.79 (2.1) 38.0 (38.3) 33.4 (19.46 (.41) 5.830-4.0-39.30-14.6 (11.2-27.63-6.0) 3.1-47.21 (4.2-80.0 (38.10 (1.0-69.0 (8.18) 6.7 (12.0-29. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 18.7-41.0-41.5-27.59 (1.0 (25.3) 31.00 (.1 (25.0-58.19-2.70 (7.6-45.70) 1.9-21.53) 1.1-46.9 (27.7 (12.46-2.26 (.1 (25.3) 28.77 (1.57-2.0 (24.0) 3.50-17.90 (1.0 (32.90) 11.61 (1.50-7.0) 28.45) 2.3) 26.0) 3.04 (<LOD-2.80-2.1-40.1-20.06) * 2.36-2.9-51.5-20.8 (26.0-53.33 (5.86-3.0) 45.9) 38.10) .06 (1.98) * 2.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.27-6.0) 8.0-41.83-2.12 (3.40-4.0-49.0 (38.98 (1.0 (8.80) 90th 38.10-4.5-74.57-2.2-33.41-4. see Data Analysis section) for Survey years 99-00.0-92.29-4.0) 4.0-39.70 (1.23-2.6-22.11) 2.20) 1.0) 31.54 (3.0-230) 35.0) 4.83 (1.0) 13.71) 5.65 (4.8-24.21 (1.3 (24.4) 38.85) * 2.50-20.0) 33.0) 3.

22 (.3 (10.71) 8.8) 3.76-2.36 (4.7 (11.68 (1. interval) 1.1 (39.2-34.2) 33.75 (1.56 (2.8-37.3) 13.860 (<LOD-1.9 (26.7) 66.58-2.91 (6.50-5.84-13.7-20.70-4.00-16.4 (11.51) .6 (24.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.7-43.6) 3.03) 1.3) 28.0) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70 (1.59-2.28) 1.59-15.4-67.7-38.88 (4.40 (5.0) 13.2 (16.41 (2.30) 28.7) 15.8-26.67 (1.07) 9.17) 2.6) 19.95) 90th 32.06) 1.7 (18.72) 2.48) 1.6) 3.19-14.0-40.64 (1.55 (2.1) 27.5 (13.56) 1.7) 61.43-2.6 (7.4 (9.6) 7.71-2.18) * 2.0-70.53) 1.11) < LOD 1.4-34.4 (5.0-71.24 (1.40-7.38 (3.0) 25.38) 5.5) 27. Fourth National Report on Human Exposure to Environmental Chemicals 127 .1 (12.6) 11.4 (21.28 (1.680-4.5 (17.5 (6.7 (24.2-47.5-36.8-34.1) 52.2-70.23) 37.6 (11.5 (8.1) 17.8) 23.2-28.9-95.40 (2.2 (15.9-41.95-16.03-2.94) 1.67-3.61-22.90 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.27-3.6) 23.45-1.9) 54.8-43.2) 41.9) 3.2 (9.6-51.23) < LOD 2.22 (2.36) 10.80 (1.5) 70.99-4.61 (1.7-109) 22.2) 36.S.22-2.83) .07-2.26-4.9 (39.38-5.19) 5.46-5.20) Selected percentiles ( 95% confidence interval) Total * 1.1) 15.9) 24.06) 75th 9.37 (1.0 (39.2) 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 2.19) 5.86) * 2.46-6.60) 4.35) .4-71.68) 47.4 (25.1 (33.33) 1.16-2.1) 25.33) < LOD 1.32 (3.79 (2.83 (.6-49.9) 12.27 (6.4 (19.9-18.75) * 1.3 (10.870-3.47 (1.7-47.2 (22.35 (2.47 (3.5 (41.43) * 2.66 (1.4-21.08 (1.00 (4.59-2.6 (27.19-6.39 (1.96) 2.52 (1.8) 31.00) 1.4-39.4) 14.1) 36.750 (<LOD-1.66) 8.8) 32.34) * 1.0 (32. population from the National Health and Nutrition Examination Survey.16 (1.19 (1.888-1.88 (1.52-4.02) 1.8-45.75 (1.54-2.36-13.5-97.1) 13.0) 3.890-4.9-36.7-37.79-17.7) 95th 51.1-60.4 (25.4 (12.8) 15.1-22.67 (1.16 (1.3 (8.17-3.01 (.5 (34.00) 6.47-17.9) 3.6-32.67-16.3-42.3-22.3 (9.69-18.02 (.15 (.0 (23.0) 48.4) 3.97 (1.8) 11.93) 5.11-2.0) 10.9-52.57) 4.32-3.0 (19.2 (8.61-2.58-17.670-1.2) 4.71 (1.62) 4.9) 24.95 (2.18) 3.1 (34.16 (1.2-38.870-3.37-2.0-118) 29.54-15.14 (.94) 19.7) 26.12) 3.18-1.46-22.3 (20.4) 12.0 (6.35) 1.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.3-19.5-43.26-2.62 (2.7) 23.0 (14.06) 1.1 (50.9 (13.9 (10.51) < LOD 1.75-6.94-20.27) 10.0) 47.23-1.08) 1.80-8.96-16.88 (1.44) 9.5-190) 30.7 (10.60 (.25-3.27) 50th 2.02) * 1.0) 30.1) 13.69-5.7-19.899-2.57 (6.12 (1.21 (4.46) 1.6-38.7) 30.870-3.20-5.7 (18.31) 2.82 (2.06-1.8 (7.1-63.2 (21.82) 1.07-2.43-12.50 (2.1) 27.9 (7.86) * 3.14-8.0 (17.66 (1.91-2.48 (4.1) 25.930 (<LOD-1.2) 13.9 (19.29-5.38-1.09 (5.95-16.5 (15.0 (23.4) 12.33-5.6) 112 (40.0 (25.7) 34.1 (25.5 (15.33) 2.63-5.45 (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.3-27.22-3.2) 13.88 (4.9-37.40-4.

160) .270 (.560 (.310) < LOD < LOD < LOD < LOD .05.160) .490 (.430 (.10) .10 (.830) < LOD .430-.230) .310) < LOD < LOD < LOD < LOD .830 (.650) .850) < LOD .660 (.730-.140-.090 (<LOD-.10) .720 (. see Data Analysis section) for Survey years 99-00.260 (.00) .190 (.820 (.140-.680) .540) Sample size 1949 2516 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .03) .990) .117 (.290 (<LOD-.550) .770 (.320-.230-.820 (.220 (.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.600 (.930 (.860) .100 (.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 .200) < LOD < LOD .620 (.162) * * * * * .120-.20) .290) < LOD < LOD < LOD < LOD 90th .370-.13) . which may vary for some chemicals by year and by individual sample.080 (<LOD-.300-1.640) .830 (.540) .140-.870) < LOD .990 (.090 (<LOD-.400-.630 (. population from the National Health and Nutrition Examination Survey. 128 Fourth National Report on Human Exposure to Environmental Chemicals .30) .410) < LOD < LOD < LOD < LOD .870 (.S.640-1.870 (.870 (.720-1.10) .310 (.320 (.830) .15) .470 (.540 (<LOD-.730) .180) .420-.310 (.680-1.380-.610-1.150 (<LOD-.700-1.090 (<LOD-.130) .110-.610 (.130-.390 (.650-1.099-.770) < LOD 95th . 0.760) < LOD .560 (.610-.850 (.370-.330-.30) .150) .130-.350) .42) . 01-02.700-1.090 (<LOD-.840) .440-1.360-.650-1.12 (.450 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .510-1.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.460 (.220 (<LOD-. and 0.530-.380-.640) .190 (.570) .360-.680 (.210 (.350) < LOD < LOD < LOD < LOD .610 (.650) .1.390) < LOD < LOD .780) < LOD 1.470-1.30) .130-.310-.410-.540) . < LOD means less than the limit of detection.410-.210 (.32) .130) .990) .160-.300-.630 (.120 (<LOD-. and 03-04 are 0.090 (<LOD-.1.170-.450 (.190 (.900 (.700-1.050-.280) < LOD < LOD < LOD < LOD .410-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.290) < LOD < LOD < LOD < LOD .720) . respectively.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 * * * * * * .171) * * .680-1.460-.870 (.084-.120-.240 (<LOD-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .60) 1.130 (.700-1.450 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.690-1.40) .42) .380-.860-1.080 (<LOD-.650 (.840) .140) .58) .740) < LOD .940 (.870 (.850 (.640 (.36) .090 (<LOD-.

580) .490-1.150-.03) .210 (.070 (<LOD-.670 (.660-1.610-1.700-1.580 (.600-1.120) .057-.360 (.24 (.110) .86) .700 (.260-.880-1.300-.700 (.14) 1.070 (<LOD-.20) 1.570 (.580 (.190 (.330-.850 (.111) * * * * * .440 (.670-1.090 (.140-.880 (.390-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.380-.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 .520-.450 (.080 (.270 (.650) < LOD .400 (<LOD-.58) 1.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .180-.300-.460 (. population from the National Health and Nutrition Examination Survey.170 (.670 (.140-.340-.860-2.230 (<LOD-.560 (.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.550 (.730) .02-1.12) < LOD .170) < LOD < LOD .380-.730) .86) .330 (.78) .410 (.870) .400) .110) .66) 1.300 (.280) < LOD < LOD < LOD < LOD .410-.510-.380-1.380-.720 (.570-.810 (.140) .500-1.080) .780 (.540 (.310) < LOD < LOD < LOD < LOD .540 (.02) .140-.380 (.080 (<LOD-.550 (.450) .190-.960) .03 (.360-.220) < LOD < LOD < LOD < LOD .084-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270) < LOD < LOD < LOD < LOD .290) < LOD < LOD < LOD < LOD 90th . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .120) .36 (1.890 (.580) < LOD .780) < LOD 1.01 (.67) .140-.740 (.700) .170 (.200 (.600) .090 (<LOD-.750) < LOD 95th .060-.330-.410) < LOD < LOD .09) .800-1.740) < LOD 1.650-1.03 (.03 (.860 (.116 (.330-.050 (<LOD-.070 (<LOD-.230) < LOD < LOD < LOD < LOD .990) .730 (.00) < LOD .S.110-.580-1.570-1.100 (<LOD-.200 (.110) .500) .860 (.940) .640-1.390-.110) .29 (.730) .990) .62) 1.540) .190 (.60) .360) < LOD < LOD < LOD < LOD .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .330 (.470 (<LOD-.440-1.19 (.38) 1.710-1.24) .370 (<LOD-.500 (<LOD-.940) .100-.161) * * .410 (.070 (<LOD-.720 (.970) .250-.320 (<LOD-.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .260) .43) .240-.220 (.230-.140-.360-.760) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410) . Fourth National Report on Human Exposure to Environmental Chemicals 129 .410-.

00 (1.480-.37) .59-5.730 (.00-17.0) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.97) 20.960 (. respectively.63) 32.770) 2.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .07 (3.1.67 (1.580 (.425-1.20-4.0-38.74) 5.0 (4.360-1.30 (.86) 4.80 (4.0 (3.960 (<LOD-1.40-8.52 (1.770 (<LOD-1.10-3.46 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 5.26 (2.00-17.0) 2.60) 1.890 (.51-8.07 (3. and 0.0) 2.76 (1.65) 1.99 (1.90-37.01) 5.48) 13.31-10.840 (.0 (6.190-1.30-7.690 (.0 (17.900 (. see Data Analysis section) for Survey years 99-00.20-17.0 (5.74 (3.30 (1.0 (7.32-9.0-40.1.30-3.0) 4.800) 90th 13.0) 2.170-1.32 (1.49) 17.70-3.28-9.94-8.36-3.70-30.0) 3.691 (.14-5.40) 1.87) 12.66) 4.35) 11.62) 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 * * * * * * .20) < LOD < LOD < LOD < LOD < LOD 1.07-3.40-4. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0-40.11) .0) 2.350-.90 (1.0 (13.640 (.0) 5.51 (2.90) .6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 01-02.53 (2.00) .28) 1.10-3.88-3.39 (2.36-3.30) .90) .83-3.0-38.05-3.50) 2. < LOD means less than the limit of detection.400-1.870) < LOD < LOD .28) .13 (3.05 (2.0 (5.18) 1.610 (.70) 2.14) 2.48 (2.830 (.67) .97) 20.90 (2.67 (2.90-9.35) 5.49 (1.94-3.0 (5. and 03-04 are 0.12-1.840-3.0 (4.800-4.30 (1.99) 19.0 (5.620-1.40) 2.3) 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 * * * * * * * * * .70-17.30 (2.00 (.0) 2.0 (17.38-3.0) 4.750-1.350-.40 (1.61 (1.850) 16.87) 5.30 (1.45 (2.10 (3.910) 2.24-7.83-3.90) .96 (1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.600 (.94 (1.0 (17.610) < LOD < LOD < LOD < LOD < LOD 2.0) 7.55-8.380-.43-4.00) 1.21) 3.14) .03 (.21-3.10 (.740 (.85-3.52 (1.07) 1.29-10.0) 5.0 (17.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.90-28.52) 5.800) 17.0 (5.53) 20.31) .0-38.82-4.63 (3.0-44.20 (1.840 (<LOD-1.70-50.35-10.42) 2.07-3.15) 19.11) 13.05 (3.510-.0) 5.640 (.70-7. which may vary for some chemicals by year and by individual sample.10 (3.62-8.6) 5.11 (1.370-.0 (16.720) 2.49 (1.07 (1.590 (.30) 95th 19.60) .00) .39) .10-9.0-39.20 (1.080-1.83) 2.42) .0) 2.33 (4. population from the National Health and Nutrition Examination Survey.47 (3.S.50) .68) 2.23-6.210-1.40-20.750-2.20-4.08.0) 4.110 (<LOD-.880) 5.250 (<LOD-. 0.330 (<LOD-1.12) * * * * * * * * .40 (1.0 (17.30-6.53-7.99) 11.40-7.260-.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.15) 14.0) 4.90-20.55-4.

830 (.770) .1 (7.07-21.32) 9.31-7.28-6.08) .18) 95th 21.580 (.390-.50 (4.620-3.25 (1.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .27 (2.600 (<LOD-1.650 (.51-44.57) 8.33-5.91-4.3) 2.2 (8.71 (2.360 (.86 (3.96) 2.690-5.64) 30.17 (1.69-7.780-4.40) 1.30 (4.5) 2.67) 2.15) 9.44) .55) 21.88-3.800-2.8) 7.02) .0) 4.670 (.370 (.8-33.79 (.2-38.0 (4.45 (1.51-4.33 (3.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.49-2.840-3.190-1.8) 1.560 (.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.00-19. population from the National Health and Nutrition Examination Survey.31-18.18) 1.80) 3.0 (9.96-25.660) < LOD < LOD .270 (<LOD-.47-10.55 (3.25-38.56) .1) 2.5 (9.13 (2.340-.62 (1.41) 18.64-4.580) 16.37) 4.07 (2.7) 6.88 (2.5-40.12-4.14-6.740-1.31) .940-4.970-3.500 (.75) 5.33 (1.4-34.47) .24) 3.7 (12.29 (4.82-11.66-47.21-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.150 (<LOD-.580) 1.85-3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.71 (.84) 9.56 (1.03) 16.57-40.05) .60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.22-27.14 (1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .630-1.77 (.260-.580-1.S.67-6.47) 5.1 (5.29-4.01 (1.8) 2.80 (.340 (.700) 6.474-1.7) 3.11) .23-7.53) 27.36 (.03) 2.83 (4.48-42.73 (4.320-1.8) 7.5) 2.90-6.33-3.47-10.17) 5.35 (.470 (.43) .4) 2.790 (.7 (6.7) 5.710 (<LOD-1.62-17.730-3.9) 6.41 (4.930) .830-3.89 (2.430) 1.59 (1.5 (11.55) 21.50) .91) 2.250 (<LOD-.96-8.540 (.3) 3.5) 7.820 (.890 (.98 (4.04 (1.8) 4.450 (.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 * * * * * * * * * .5 (8.02 (.270-.340-.92 (2.65 (2.40-2.86) .31) .370) < LOD < LOD < LOD < LOD < LOD 1.09-3.330-1.57 (.9 (11.38 (2.960 (.650) 90th 10.67 (2.06 (.340-.50 (2.04-16.48 (4.67) 1.11-5.748 (.44-11.9) 5.40 (.430 (<LOD-.39) 20.240-.7) 4.97) .40-12.57) 1.850-3.10-3.8) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.820) .310-.8 (20.10 (2.1) 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 * * * * * * .25-9.48-7.700) < LOD < LOD < LOD < LOD < LOD 1.02-4.88 (.590) 2.52 (.88) 17.12 (4.860-2.60 (1.370-1.540-1.00) .260-.85 (1.83-11.32-6.81-17.790) 11.50) 11.02 (1.22) 2.10) 2.56) 2.69) 2.53) .4 (4.18) * * * * * * * * .33-4.74 (2.

Fenske RA. Krieger RI. Hawk R. Mathieu L.59(1):217-228. Environ Health Perspect 2005. Charnley G. Barr DB. Seta N. Grzywacz JG. Regul Toxicol Pharmacol 2003.46(4):367-378.16(5):417-426. Hansen S. Heudorf U. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Urinary excretion of alkylphosphates in the general population (Italy). Young AD. Arcury TA. Demers P. Angerer J. Fenske RA. A clinical neurological.110(8):829-833. Sciarra G. Kipen H. Neuropsychological performance among agricultural pesticide applicators. Barr DB. Buchanan D. et al. Arch Environ Health 1998. Eaton DL. Chen W.38(1):91-97. Barr DB. Miller M. Engel LS. Environ Health Perspect 2003. Davis SW. Eskenazi B. Vaughan TL. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Keifer MC. Surveillance of occupational. Aprea C. Lu C. 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Lewis JA. Stokes L. Stephens R.20(2):115-22. Lancet. Rothlein J. Claypoole K. Pilkington A. et al. et al. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Bull Environ Contam Toxicol 1994. Thompson ML. Frasca G.338(8761):223-227.nap. Robson MG. Occup Environ Med 2001. S. The Pesticide Health Effects Study Group.2000 and 2001 market estimates. Arch Environ Health 1975.38(4):546-563. Office of Prevention Pesticides and Toxic Substances. Environ Health Perspect 2006. Scherer J.12(2):153-172. Saieva C. An epidemiological study of the relations between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy and neuropsychological abnormalities in sheep farmers and dippers. Phillips J. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Myers JE. Bravo R. Available at URL: http://www. National Research Council (NRC). Aprea C. Rodnitzky RL. Rohlman D. Prendergast MA. Lasarev M. et al. Gladstone EA. Neurotoxicology 2005. Wickremasinghe AR. Lambert WE. Chronic neurological sequelae to organophosphate pesticide poisoning. Pesticide industry sales and usage . Rothlein J. Fourth National Report on Human Exposure to Environmental Chemicals 133 .pdf. Occup Environ Med 1995. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Russo J. Mounce LM. J Occup Environ Med 2002. Effects of chronic. Buchanan D.44(4):352-357.345(8958):11351139. 2004. Jenkins B. Caltabiano LM. U. low-level organophosphate exposure on delayed recall. Lancet 1995. May. Rosenstock L. and cholinesterase status of date dusters and harvesters in California. Hansen S. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Terry AV Jr.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI.58(11):702710.332(1-3):71-80. metabolite clearance. Smit LA. Lu C. Calvert IA. Jamal GA. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Masala G.epa. Stark A. and spatial learning in monkeys and rats. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Effects of long-term organophosphate exposures on neurological symptoms. Levy LS. Malathion deposition. Bradman A. vibration sense and tremor among South African farm workers. Gillham R.edu/ openbook. Weisskopf C.26(2):199-209. Arch Environ Contam Toxicol 2000. Burcar PJ.php?record_id=2126&page=1. 4/7/09 Young JG. Environ Health Perspect 2005. Dinoff TM.84(5):731-736. Spurgeon A. Pesticides in the Diets of Infants and Children. Vitayavirasak B. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Berry H. Environmental Protection Agency (U. Daniell WE. Am J Public Health 1994. et al. Lasarev M. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Am J Ind Med 1987. Keifer M.S. Washington (DC). Kidd M. Heaton RK. 1991. Arch Environ Health 1988. Neurotoxicity among pesticide applicators exposed to organophosphates. et al. Ames RG. Chrislip D.114(5):691-696. Scand J Work Environ Health 1998. London L. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Int J Occup Environ Health 2006. 1/12/09 Peiris-John RJ. Seiber J.52(2):190-195. Eskenazi B. A behavioral evaluation of pest control workers with short-term. van der Hoek W. Salvini S. Visuthismajarn P. Narang A. McCauley L. Savage EP. McConnell R.S. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Ruberu DK.68(3):209-227 Maizlish N. Sci Total Environ 2004. EPA). Schenker M. Neurotoxicol Teratol 1998. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Hore P. Marshall E. discrimination. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Tumino R.12(2):134-141. Steenland K.52(10):648-653. Pedersen L. Keefe TJ. low-level exposure to the organophosphate diazinon. EPA. 1993 [online]. J Toxicol Environ Health A 2005. Available at URL: http://books. Beach J.113(4):504-508.43(1):38-45. Irish RM.30(2):98-103. Buccafusco JJ. National Academy of Sciences. Petchuay C. Takamiya K. Weerasekera G. Muniz J. Santana J. O’Malley M. Nell V.24(1):18-29. Johnson C. Barr DB. Muniz J. Samuels S. Washington (DC): U.

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

90-4.70-15.94 (4.39-2.67 (2.45 (1.40-13.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.40) 2.4 (8.53 (1.57 (2.20 (4.80) 1.46-2.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.91 (1.51-2.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.50 (2.86) 4.0) 6.0) 12.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.74-9.8) 10.30) 4.0) 14.0) 12.16) 2.95 (4.20) 4.90 (6.29-1.90) 7.27 (7.0) 11.71 (2. pre.0 (7.44-2.25) 3.47-13.7) 8.67 (1.59) 2.28) 2.20) 10.71 (1.22) 2.09 (3.20-14.5) 7.80-8.0) 15.50-2.47) 1.0 (7. dermal. 2007).20-11.20-16.72) 2.60-3. interval) 1.80 (7.31-2.47 (4. The general population may be exposed to chlorpyrifos via oral.5 (8.77-6.30-2.70 (1.51) 1.00) 3.32) 2.00) 2.0) 12. air.04-10.1-16.4 (9. Survey Geometric mean (95% conf.60-4.0 (7. staying bound to soil particles.00-24.20) 2.68 (7.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.0 (9.30) 5.9 (10. It also has been applied directly on animals to kill mites.80-10.50 (1.39) 4.80) 12.17 (1. Approximately 21-24 million pounds per year were used domestically from 1987-1998.3 (11.97) 2.0) 10.89 (2.95) 7.04-10.20-2.10) 6.22 (1.63 (1.99-4.50-4. 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. It has low leachability.90 (1.30 (2.S.20) 2.90 (2.0) 9.63 (2.78 (7.50-5.9 (7. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.S.19-3. USGS.71 (6.8) 9. Chlorpyrifos is degraded in agricultural soils with a half-life of several months. and on plants for days to several weeks. and dust.40 (5.70 (1.0) 10. in 142 urban homes and preschools in North Carolina.70-16.10 (5.0 (13.90-7.2 (10. Approximately 80.76 (1.79-2.50 (2. and sprayed to kill mosquitoes.76 (1. 2002).0) 12. 2005).19 (1.81-2.32-1.3 (10. 1999. chlorpyrifos was no longer registered for indoor residential uses in the United States.50-2.38 (3.50-4.25) 1.88 (1.0 (7.30-12. After 2001.55-5.28-3.90 (3.20-4.44-5.66-4.40-2.60-2.40-26.70-17.02 (7.59-2.97) 4.40-10.0) 7.24-1.26) 7.87-6.97) 2.9 (9.7) 13.77-15.89-2.6) 7.0) 8.20-3.61 (1.00-8.03) 1. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.0) 8.1) 5.02 (1.80) 4.3 (8.3) 8.0-28.EPA.5-24.31-2.40 (6.80 (1.44 (3.90) 3.20 (2.10-17.50 (1.EPA. and inhalation routes.29) 90th 7.66-15.30-1.90 (1. and is infrequently detected in ground water (IPCS.0) 12.77 (1.43-2.61-7.50-8.4-15.40) 9. Chlorpyrifos is Urinary 3.90-8. Fourth National Report on Human Exposure to Environmental Chemicals 135 .10 (4.4 and 0.70-5.05-5.4.15 (1.10 (1.34) 1.0) 18.50-14.80) 2.60-3.5.30-9.30 (4.37 (1.40 (5.84) 1.13 (1.7) 9.30-11.70-11.02) 1.60) 5. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.0 (7.30-5.77) 1.and post-construction structural applications for termite control were to be phased out by 2005 (U.9) 697 660 521 701 602 947 Limit of detection (LOD.51 (1.8-15.52-2.47-11. applied to structures to kill termites.10 (3. Exposure can also result from contact with contaminated surfaces. 5598-13-0 General Information The chemical 3.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.3) 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 1.0) 10.21) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.00) 1.13-3.50 (2. but can be detected in streams receiving runoff from application sites.60 (4.62-2.90-2.30 (2.37) 5.96) 3.64) 3.68-2. population from the National Health and Nutrition Examination Survey.43-2.97) 7.83) 1. 2002).7-23.24-3.35) 2. For instance.91) 16.47-9.52-12.98-15. Estimated intakes from diet and water have not exceeded recommended intake limits.60 (5.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.36 (4.09 (2.37 (4.92 (1.S.9) 11.61) 75th 3.000 pounds are used per year.74 (1.30) 4.0 (10.70) 1.97-7.10) 2.9-18.60 (2. 2921-88-2 Chlorpyrifos-methyl CAS No.35) 1.72-4.63 (8.67 (2.5..4 (10. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.01) 1.05) 1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.

neurotransmission.59) 3.80-6.99-8..42 (6.97 (2. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates. cholinergic effects.06-4.82 (3.20 (2.17-4. Ricceri et al.32) 1.58-5.60-3.96) 3.2 (7. Slotkin et al.51 (1.82 (2. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.6) 9.78 (1.07) 5.68) 1.62-7. and seizures. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.23) 14.44 (1. Based on animal data and human cholinesterase monitoring during occupational exposure. 2000).72-2.97 (3.70-4.22) 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 1.95 (3.01) 3.S.88 (1.09-2. interval) 1.06 (5.92-2.27-1.39-1.81) 2.82-4.0) 10.05-3.91) 10.88) 6.38) 3.50 (4.14) 1.66 (1.65-11.00-8..25-1.07) 1.85 (3.33) 2.71) 3.97-3.93) 2.44 (1.98 (6.91 (4.EPA.36) 1.. Howard et al.69 (1.91-4.09-3.85) 1.85) Selected percentiles ( 95% confidence interval) Sample 95th 8. 2005.63 (4.75) 6.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.93 (2.74) 1.43 (4.11 (2.42 (5.05-8.82) 8.95 (1. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.12-1.56) 5. resulting in excess acetylcholine at nerve terminals.76 (2.06 (1. 2006.43-10.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. Thus.05-4.46 (2.46 (1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.39 (2.28) 2.60 (1.1-21.56 (4. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.57-2.28) 2.01) 1.3) 8. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.85-4. Once absorbed.45-1.31) 1. Survey Geometric mean (95% conf.24) 75th 2.2) 6.86 (1.24) 5. 2006b). paralysis.89) 4.94-14. 1984).11) 7.21-6.92) 3.16) 6. 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.5) 5. TCPy is more persistent in the environment than chlorpyrifos itself (U.79-13. weakness.56 (1.80-11. Betancourt et al.55) 1.1 (7.88 (1.30-4.54) 5.45 (1.44 (6.11-9.05) 3.42-2.87-3.8) 9.16 (4.31-4.86 (1.64 (1.93 (4.59-2.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .48 (1.83) 1. and producing acute symptoms such as nausea.84-6.09 (1.55 (1.19) 6.22 (6.15 (4.83-11.03) 1.58 (4.31-1.33-7.6) 10.0) 16.76 (3.47 (1.65-15.88-10.58) 1.09-1.29 (3.58) 5.81 (3.1 (10.57) 2.40) 1.49-2. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.88-8.35) 1.91 (3.27-7.00 (7.47 (5.00) 1.56) 2.12-3.33 (5.39 (4. The metabolite TCPy does not inhibit acetylcholinesterase enzymes..02 (5.85 (2.75 (1. vomiting.02) 7.5 (6.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.19-1.21-1.57) 9.86 (3.4) 4.26-14.44 (5.62) 90th 5.66) 1.44-6.6-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. In pesticide applicators.73 (1.01) 3.3 (7.05-1.5.91-13.08) 6.93) 5..53-5.52 (5.49-2.940-1.90-9.0) 6.63 (5.47 (1.54 (2.17-4.57-2.80-4.71 (1. Roy et al.58 (1.30-1.11 (2.68) 6. population from the National Health and Nutrition Examination Survey. TCPy can also occur in the environment from the breakdown of the parent compounds.35-1..63-2.80) 3.20-1.24-24.25-11. Metabolic hydrolysis leads to the formation of TCPy. 2002).47-2.14-8.. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).0) 12. and other metabolites. 2005.72) 1.35) 2.99) 1.48 (2.49-2.23-1. 2006a. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.24-4. 2005.33 (1.49 (1.53 (2.33 (.64-7.92 (1.S.58 (1.85) 4.62) 1.41 (1.91) 1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.24 (1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.3) 9.24-1.24-5.97) 3.12) 1.91) 2.97) 3. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.19) 3. 2006.00-13.72) 2.98 (7.7) 7.19-2.25-12.22-6.88-9.91) 1..93 (1.44 (5.37 (1..77) 1.9 (12.34-1.3) 8.64-2.1-38.55 (4.88-8. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.22 (4.66-11.56-2. Urinary 3.39) 6.83-2.94-12.

S. Freeman NC. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. 1992. 2005).. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. 2005). Chlorpyrifos exposure and biological monitoring among manufacturing workers. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. 2005. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. Betta A. 2005. environmental levels) and health effects is available from ATSDR at: http://www. Haidar S. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.Reference values of urinary 3. CDC. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 2001) and Italy (Aprea et al. EPA at: http://www. Environ Health Perspect 2001. Burns CJ.113(8):1027-1031. Betancourt AM. Aprea C. In Iowa farm families using several different pesticides.. Albers JW. Levels of TCPy in the U.. U. 2004).e. 2005). In a probability-based sample of 102 Minnesota children aged 3-13 years. Perera et al.epa. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Whyatt et al. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. 2000). 2005).EPA. In Minnesota and South Carolina farmers who used chlorpyrifos. but levels were roughly four to six times higher than the geometric means in the U. Giordani B. et al. representative subsample of NHANES 19992000 (CDC. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Magnaghi S..63(3):218220.cdc. et al.. Slotkin TA. Seidler FJ. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.. 2003.5.. Garabrant D. the geometric mean urinary TCPy levels were similar in parents and children. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Toxicol Sci 2006. Lotti A. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. subsamples of NHANES 1999-2000 and 2001-2002 (CDC... Berent S. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.S. Of 482 pregnant women living in an agricultural community. 2005. 2006). Catenacci G. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. Aldridge JE..S. et al. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure.82(2):305-312. Clayton CA. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. population (CDC. Carr RL. Curwin et al.gov/toxpro2. Lioy PJ. 1999). MacIntosh et al.. Barr DB.atsdr..92(2):500-506. 2004).gov/pesticides/.Organophosphorus Insecticides: Specific Metabolites 2004. urinary TCPy levels in children were reported not to have increased (Hore et al.S. Occup Environ Med 2006. Environ Health Perspect 2005.. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. but not chlorpyrifos.. J AOAC Int 1999. Meyer A. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. 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. 2007). Burgess SC.S. 2001). Koch et al. Eberly LE. 2002).html and from U. 2005). Following crack-and-crevice application of chlorpyrifos in their homes. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Barisano A. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. 2005).109(6):583-590.. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Additional information about external exposure (i.

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Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Chrislip DW. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Hammerstrom KA. Roy TS. Howell RJ. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Mandel JS. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations.15(4):297-309. Toepel K. Toxicol Appl Pharmacol 2005. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Urinary pesticide concentrations among children. Ryde IT.niehs. Gurunathan S. Slotkin TA.111(2):201-205. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Third National Report on Human Exposure to Environmental Chemicals.204(2-3):175-180. Bradman A. Jones PA. Ryan PB. Edwards RD. Honeycutt R. Eskenazi B. Environmental Protection Agency (U. Environ Health Perspect 2006b. Nolan RJ. Acquavella JF. Scand J Work Environ Health 2005. Angerer J. Kinney P. et al.155(1):71-80.

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

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

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

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

1998). Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. Prior to 2000. diazinon was widely used in residential and garden application. in the past.49 (<LOD-2. Estimated intakes from diet and water do not exceed recommended intake limits (U. an organophosphorus insecticide that is used to control insects on nuts. Inhalational and dermal routes of exposure can be significant for pesticide applicators. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. and other metabolites.2 and 0. 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. Most granular formulations. vegetable. but is rapidly absorbed orally (IPCS. in some pest strips. fruits.45 (<LOD-3.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. It is also used for cattle ear tag applications to control flies and ticks and.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. Survey Geometric mean (95% conf. Diazinon is not well-absorbed through the skin.EPA.S. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon.7. Before these restrictions. population from the National Health and Nutrition Examination Survey. but these uses have been phased out. < LOD means less than the limit of detection. diazinon produced wild bird kills before use restrictions were in place.S. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004). 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. USGS. Once absorbed. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.EPA. and forage crops. and particularly when it was ingested in granular form. since 2004. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. which may vary for some chemicals by year and by individual sample. 2004). 2007). seed and foliar applications are planned to be phased out (U. as inferred Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine Metabolite of Diazinon Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1998. Fourth National Report on Human Exposure to Environmental Chemicals 143 .S. It is toxic to birds. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. diazinon cannot be sold for residential use. aerial.

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

Driskell WJ. Bouchard M. Banister E.org/documents/ehc/ehc/ehc198. Brunet RC. Kruse RL. Liu F. In 23 children.114(2):260-263. Third National Report on Human Exposure to Environmental Chemicals. Drobnis EZ. Sadowski MA. Available at URL: http://www.. Pesticides in the Nation’s Streams and Ground Water. May 2004. Carrier G.37(4):501-507. U.. Rajendra W. Environ Health Perspect 2003. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. 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. 1/14/09 U.S. International Programme on Chemical Safety-INCHEM (IPCS). Diazinon. Banister EW. Swan SH. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al.gov/ oppsrrd1/REDs/diazinon_ired.pdf. Drug Chem Toxicol 1986. Barr DB.S. 2007 [online]. Nguyen JV. Anal Bioanal Chem 2003. 2005. J Expo Anal Environ Epidemiol 2000.gov/circ/2005/1291/. 2006). Toxicol Lett 2002. Diazinon. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Semen quality in relation to biomarkers of pesticide exposure. The Quality of Our Nation’s Waters.9(2):117-131.usgs.epa. Barr DB. Oloffs PC. Environmental Health Criteria 198. Ann Occup Hyg 2006. In a small number of men visiting fertility clinics in Missouri and Minnesota. 2006).376(6):808-815. Irish R. Dumas P. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. March 2006. Baker SE. EPA 738-R-04-006.inchem. Effect of sublethal levels of diazinon: histopathology of liver. Centers for Disease Control and Prevention (CDC). Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Beeson MD.S.44(11):2243-2250. 1992-2001. revised February 15. Environ Health Perspect 2006. Oloffs PC. Needham LL. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Interim reregistration eligibility decision (IRED. Cocker J. Environmental Protection Agency (U. EPA). Bull Environ Contam Toxicol 1986. Mason HJ. Fenske RA. et al. Jones K. Swan et al. Barr DB. Study for Future Families Research Group. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Available at URL: http://www. 4/7/09 Lu C. In 54 Canadian greenhouse workers. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects.Organophosphorus Insecticides: Specific Metabolites 2005). Biochem Pharmacol 1992. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Toepel K. Barr DB. Pewnim T. Olsson AO.10(6 Pt 2):789-798. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 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. Atlanta (GA). Seifert J. Available at URL: http://pubs.50(5):505-515.htm. Noisel N.134(1-3):105-113. Bravo R. Redmon JB. Garfitt SJ. 1998.111(12):1478-1484. Geological Survey (USGS). References Anthony J.

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

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. but cholinesterase activity was not affected. and it is not considered an animal teratogen or a reproductive toxicant.. 2005). Additional information about external exposure (i.cdc.. Pluth et al. environmental levels) and health effects is available from ATSDR at: http://www. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 2003).0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Human studies of single oral doses between 0.. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.epa.EPA. Survey Geometric mean (95% conf..74 (<LOD-5.S. EPA at: http://www. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Flessel et al.S.. 2006). 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.. 2005).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. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure.. 1996. 2006). IARC considers malathion not classifiable as a human carcinogen. 1993. 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). Fourth National Report on Human Exposure to Environmental Chemicals 147 . 1990)..EPA. 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. CDC.. Lu et al. Toxicity from unprotected bystander exposure during applications is rare (U.. 1987.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions.gov/pesticides/. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 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.html and from U. Malathion itself has not been considered genotoxic (U.gov/toxpro2. representative subsample from NHANES 19992000 (Adgate. 2002. but isomalathion.atsdr. 2000). Thomas et al. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.5 and 5.S.S. Giri et al. 1999. 2001. 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. 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. 1999). Of 382 pregnant women living in an agricultural community.e. 2006). population from the National Health and Nutrition Examination Survey. 2005.

pdf. EPA). Bradman A. et al.S. Weltzien E. Jewell NP. Grether JK.56(10):2393-2399. Toepel K. Szyfter K. Environ Mol Mutagen 1993. and cholinesterase status of date dusters and harvesters in California.epa. Dumoulin MJ. Lu C. Harris JA.org/documents/jmpr/jmpmono/v2003pr06.77:1009-1010.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Irish R. Reregistration eligibility decision (RED) Malathion. Jaloszynski P. Griffith W. Clayton CA.74(2):following table of contents. Malathion (addendum). EPA 738-R06-030. et al. Hooper K. Arch Environ Contam Toxicol 2000. Albertini RJ. U.gov/circ/2005/1291/. Am J Public Health 1987.9(5):494-501.132(4):794-795. et al. Gosselin NH. Eskenazi B. Environ Health Perspect 2001. Neutra R. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. 6/1/09 U. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.38(4):546-553. International Programme on Chemical Safety-INCHEM (IPCS). Carrier G. Cancer Res 1996. Ryan PB. Erratum in: Toxicol Sci 2003 Aug. Barr DB. Flessel P. Bravo R. Hammerstrom KA. Environmental Protection Agency (U. J Expo Anal Environ Epidemiol 1999. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Toxicol Sci 2003 May. Prasad SB. Krieger RI.inchem. Goldhaber M. Available at URL: http://www. Barr DB. Thomas D. Lu C. Freeman NC. Rappaport E. Pesticides in the Nation’s Streams and Ground Water. Mutat Res 1999. Hertz-Picciotto I. O’Neill JP. 4/7/09 Kissel JC. Available at URL: http://pubs. Giri A. Dinoff TM. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.15(2):164-171. Giri S. Available at URL: http://www. March 2006. Environ Health Perspect 2004. Reproductive outcome in women exposed to malathion. Petitti D. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Environ Health Perspect 2006. revised February 15.114(2):260-263. Barr DB. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Trzeciak A. Atlanta (GA). Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.112(10):1116-1124. July 2006.109(6):583-590. Lioy PJ. Third National Report on Human Exposure to Environmental Chemicals. Eberly LE. metabolite clearance. Samuel O. Geological Survey (USGS).gov/oppsrrd1/REDs/ malathion_red. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. htm. 1992-2001. Mutat Res 2002. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Pluth JM. Sharma GD.73(1):182-94. Malathion deposition. Brunet RC. Am J Epidemiol 1990. Barr DB. Centers for Disease Control and Prevention (CDC). Bouchard M. Kedan G. MacIntosh DL.445(2):275-283. Nicklas JA. Needham LL. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Curl CL. Blasiak J.S. The Quality of Our Nation’s Waters.22(1):7-17.usgs.514(1-2):223231. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Harley K. J Expo Anal Environ Epidemiol 2005. 2005. Swan SH. 2007 [online]. Quintana PJ.S. Genetic toxicity of malathion: a review. A longitudinal investigation of selected pesticide metabolites in urine. Fenske RA.

32-1.37) 2.S.74) 5.12) < LOD < LOD 1.70) 2.05) 4. Fourth National Report on Human Exposure to Environmental Chemicals 149 . and eliminated rapidly from the body after absorption (Kramer et al.61) < LOD 1.28 (1.70-6.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .28 (1.40) 2.790 (<LOD-.11) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60-36.33) 2.20 (2.50) 3. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.80) 2.61) < LOD 1.0) 3.50) 2.990-1.18-3. ethyl parathion. 1977).49 (1.02-6.10-11. but by 2003. and aquatic invertebrates. In the 1990s.50) 3. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.300-.69 (2.00 (2.940 (<LOD-2.67) < LOD 1.37-4. Morgan et al.80 (2.46 (3.50 (1.10) 4.30-5.21 (2. 2000).41-4.32-1. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate..10 (<LOD-6.10 (3. more slowly absorbed through the skin.50 (1.40) 1.89 (2.EPA.70 (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 1.20 (<LOD-2.0) 2.30-3.48) 90th 2.36-1.0) 3.70 (3.19 (.57-4. first registered in 1948.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 2006).10-1.EPA.16) < LOD 1.70 (2.10) 22.0 (3.50-9.26 (1.860 (<LOD-1.01-4.770 (. Methyl parathion is not registered for residential use in the United States. peak domestic use was as high as 5-6 million pounds per year.28-4.67 (1.40) 4.72 (3. Both are toxic to birds.60 (4.92-2. pulmonary..02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .21-1.910) < LOD . 2007).58) 3.71 (3. 2003).50-14.850) < LOD .60-19.20-5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.45 (1.70 (<LOD-3.50 (2.33 (1.60-5.30-16. and oral routes can occur in pesticide and agricultural workers (Muttray et al.37-4.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.40-4.0) 3. Survey Geometric mean (95% conf. Many previous registered agricultural uses of methyl parathion have been cancelled (U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.57) 1.00) 3.298-00-0 Ethyl Parathion CAS No..01) 4.13-1.15-3. and of the chemical nitrobenzene.45) 5. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.70-6. Estimated intakes from diet and drinking water have been below recommended limits.09-1.40-3.85 (2. Increased risk of exposure via dermal.32-3. Once absorbed.01) 695 660 518 679 603 941 Limit of detection (LOD.80 (1.50) 1. and to a lesser extent.62 (1.22-3.11-4.79) 4.50 (2.60) 1.70 (2. Methyl Parathion. and has a short half-life in soils and on plants. 2002.20) 5. < LOD means less than the limit of detection.70-3. was once a restricted-use insecticide with limited applications on certain agricultural crops.47) 2.0) 4. on cereal grains.10 (3. population from the National Health and Nutrition Examination Survey.90 (1.70) 2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. with limited applications in agriculture.40-4.91-3. Methyl parathion has low water solubility.71 (2.37-2.92) 5. Ethyl parathion. Given its limited use.S.30 (2.32 (1.910) < LOD < LOD < LOD 1. It had been applied to cotton.27) 2.00 (2. all registered uses were voluntarily cancelled (U.730 (<LOD-.34 (3. binds tightly to soils resulting in low leachability.70-6.8 and 0.90-11.S.0) 3. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.70-3.50 (1. which may vary for some chemicals by year and by individual sample.70) 2.60-24. Methyl parathion use is highly restricted.700 (<LOD-.80 (2.90-9.910) < LOD < LOD .50 (1. methyl parathion was rapidly absorbed after ingestion.44) 2.66 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. fish.1. In animal studies.30 (1.40 (1. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.0) 3.69) 4.

45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.EPA considers methyl parathion unlikely to be carcinogenic to humans.680 (<LOD-1.71 (1.08) < LOD .57-7. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. cholinergic effects.540) < LOD .04 (2. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion. Additional information about external exposure (i.790-.95) 1.55) 2.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Thus.39) 1.98-7. 2003.26) 17. and seizures.20) 3.html and from U.21) 1.01 (.79) 1.80 (1.790-1.33-3.930 (.07 (1.31-3.16-4. does not inhibit acetylcholinesterase enzymes.89 (2. Zurich et al.35-3.60) 2.S. Survey Geometric mean (95% conf.30-1.epa.35-3.83 (1.70) 3.. 1990.14-3.82) < LOD . weakness. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.89 (2.17-4.7) 3.55 (<LOD-3.4 (3. Slotkin et al.37-1.90 (1.840 (. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.78 (2.730-1.970 (.05) 4.310-.11) 1.20) .79 (1.38-3.23) 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 . 2004).25) 1.23) 1.31) < LOD . Parathion and methyl parathion have high acute toxicity in animal testing. EPA at: http://www.cdc.870) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.87 (1. The metabolite.30) 3.11-4.77-7. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.48-4. Karanth and Pope et al.430 (. At high animal doses of methyl parathion.3) 2.76-14..atsdr. resulting in excess acetylcholine at nerve terminals. 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.88) 1.44-3. Methyl Parathion.800-1.640) < LOD < LOD 1.78-2.S. 1995).09) 2. 150 Fourth National Report on Human Exposure to Environmental Chemicals .56-2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).84) 3.60-2.44-3. gov/toxpro2. and other metabolites.980 (. teratogenic.15-10.97-10. 1995.940 (<LOD-1.92 (2.25 (2.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.690-1.950) < LOD .720-1. 2004).59 (1. U.67-2.82 (2.57) 6.91) 1. paralysis. Lores et al.10) 90th 2. Jaga and Dharmani.970 (.72-2. environmental levels) and health effects is available from ATSDR at: http://www.20 (3. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.08 (1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1978.500) < LOD < LOD . Orsorio et al.80 (1. population from the National Health and Nutrition Examination Survey.440 (<LOD-.720 (<LOD-.10 (1. 1991).60 (1.33-6.530) < LOD < LOD < LOD .04) 1.. accidental exposure. In addition to being a metabolite of methyl and ethyl parathion.67 (3.29 (2.94-4.370 (<LOD-.96 (1.26 (1. 2006.00 (1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .13-12.41-2.13) 4.39 (1.S. 2005. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.91 (1.01-3.2) 2. Methyl parathion is not considered genotoxic.07) 2.. In large doses.17) .61) 4. vomiting. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..29) 2. 2006.93 (2.43) 4.830-1.33-3. and producing acute symptoms such as nausea.94-47. WHO.78) 2. and unintentional acute or chronic high-level occupational exposure (Hill et al.2) 2.21-21.930 (.29) 1.9) 1.57-2.97 (2.880 (.08-3.97 (<LOD-4.96 (1. methyl parathion.73 (1. ethyl parathion.86 (2.15) 3.01 (2. but lists ethyl parathion as a possible human carcinogen.850-1. paranitrophenol.e.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD ...1) 2.78-2.00) 2.88 (1.71) 1.00 (1.400 (<LOD-. gov/pesticides/.

population (Olsson et al. et al.S. Pathak S. Environ Health Perspect 2002. Barr DB. 1995). Hetzler HL. and levels were similar or slightly lower that those in a small convenience sample of the U. 2005).. Rockhold RW. Pesticide residues in urine of adults living in the United States: reference range concentrations. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Toxicology 2005.. Hryhorczuk DO. ACGIH recommends a BEI of 0. Neurotoxicol Teratol 2003. Ashley DL. a range of values several hundred times higher than levels found in the U.56(7):449553. Lin LI. et al.org/documents/jmpr/jmpmono/v95pr14. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. J Biomed Sci 2002. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Bradway DE. Chicago area methyl parathion response. References Barr DB. Needham LL. Rubin et al. Laboratory investigation of a poisoning epidemic in Sierra Leone. In a study of workers who handle parathion. J Expo Anal Environ Epidemiol 2005.S. Costa LG. Griffith W.9:311-320. 1999). Kramer RE.21(1):5767.. Bailey SL. Biomonitoring studies of para-nitrophenol can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of parathion than are found in the general population. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Barr JR. Centers for Disease Control and Prevention (CDC). Kissel JC.33(5):270-276. J Anal Toxicol 1990.110 Suppl 6:1085-1091. Hill RH Jr. et al. Baker S. Parathion-Methyl (addendum). Hill RH Jr. Methyl parathion: an organophosphate insecticide not quite forgotten.. Eskenazi B.inchem. Kedan G. Clark JM. oral or dermal administration. Curl CL. Alley CC. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Wellman SE. Head SL. Slach EF.15(2):164-171. Hill et al. 2005. 2002. 2005).215(3):182-190. 2002). Turner WE. 2004). Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Third National Report on Human Exposure to Environmental Chemicals. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. Pesticide workers may have much higher levels following pesticide applications. McCann et al. Lewalter J. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Karanth S. Guizzetti M. Atlanta (GA). Environ Res 1995. Dharmani C.25(5):599-606. DiPietro E. Lores EM. Moomey CM. Harley K. et al. Rev Environ Health 2006. Leng G. Arch Environ Health 1978. Environ Health Perspect 2002. Gregg M. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Baker RC. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Barr DB.6(2-3):159-173. Morgan DP. Bradman A. 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. Jewell NP. Arch Environ Contam Toxicol 1977.. et al. Cline RE.112(10):1116-1124. Lu C. Giordano G. Role of individual susceptibility in risk assessment of pesticides. McCann KG. International Programme on Chemical Safety-INCHEM (IPCS). CDC.htm. Available at URL: http:// www. McClure PC. Occup Environ Med 1999. general population (CDC.110 Suppl 6:1075-1078. 2002. 2005. Runkle KD. Environ Health Perspect 2004. Shealy DB.5 mg (500 µg)/g creatinine for workers at the end of shift. 4/7/09 Jaga K.71:99108. and many residents were symptomatic (Barr et al. 1995. Barr DB.. 2005. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Weltzien E. Baker SE.. Moseman RF.14(4):213-216. Head SL. Pope C. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.

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

S. fish. cholinergic effects. (2003) detected 2-(diethylamino)6-methylpyrimidin-4-ol/one in 7. 2006). Fourth National Report on Human Exposure to Environmental Chemicals 153 . Olsson et al. and other metabolites. 29232-93-7 General Information The chemical 2-(diethylamino)-6-methylpyrimidin-4-ol/ one is a metabolite of the organophosphorus insecticide pirimiphos-methyl. The metabolite 2-(diethylamino)-6-methylpyrimidin-4-ol/one does not inhibit acetylcholinesterase enzymes. and seed. resulting in excess acetylcholine at nerve terminals. Additional information about pesticides is available from U. or reproductive toxicity (IPCS. teratogenic. Estimated intakes from diet and water have not exceeded recommended intake limits (U. Finding a measurable amount of 2-(diethylamino)-6methylpyrimidin-4-ol/one in urine does not mean that the level will result in an adverse health effect. pirimiphos-methyl and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. which are mainly excreted in the urine (IPCS. EPA at: http://www. In animal studies. U. Human health effects from pirimiphos-methyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses. Once absorbed. although the 95th percentile was characterized at 0.47 μg/L for the total population (CDC. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).Organophosphorus Insecticides: Specific Metabolites Pirimiphos-methyl CAS No. 1992). and producing acute symptoms such as nausea. or known to cause delayed neurotoxicity. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. It has a lesser use as a cattle ear tag application to control flies. In a nonrandom sample of 140 urine specimens obtained from adults and children in the United States. and it is not considered persistent. which has limited applications for control of beetles.S.EPA. sorghum.S. Pirimiphos-methyl is not considered mutagenic. vomiting. 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. Toxic effects below doses that cause inhibition of acetylcholinesterase are unknown. and aquatic invertebrates. In the general population.1% of the sampled population. 1992. weevils. Though considered moderately-to-highly toxic in birds. In addition to being a human metabolite of pirimiphos-methyl in the body. paralysis. and moths on stored grain products such as corn. phosphorothioates such as pirimiphos-methyl are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. Biomonitoring Information Urinary levels of 2-(diethylamino)-6-methylpyrimidin-4ol/one reflect recent exposure. 2005). infrequent dietary exposure to pirimiphos-methyl residues may occur from ingestion of food products containing stored corn or other treated grain (FDA. 2-(diethylamino)-6-methylpyrimidin-4-ol/one can also occur in the environment. 2003). weakness. Pirimiphos-methyl is not registered for residential use in the United States. In the U. Thus. 2006). most of the urinary measurements of 2-(diethylamino)-6-methylpyrimidin-4-ol/one were below the limit of detection. and seizures. pirimiphos-methyl is rapidly absorbed and metabolized to 12 metabolites.epa. the detection of 2-(diethylamino)-6-methylpyrimidin-4-ol/one may also reflect exposure to the environmental degradate. It easily hydrolyzes in the environment to 2-(diethylamino)-6-methylpyrimidine and other breakdown products. Pirimiphosmethyl has low acute toxicity in animal studies. occurrence of such toxicity is mitigated by its rapid degradation and its use in closed storage systems. Metabolic hydrolysis leads to the formation of 2-(diethylamino)-6methylpyrimidin-4-ol/one.EPA. subsample of NHANES 2001-2002.gov/pesticides/.S.

31) .S.210-.21) < LOD .700-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15) < LOD .07) .S.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .94) .210-1.27) . which may vary for some chemicals by year and by individual sample.410 (<LOD-1.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.2. < LOD means less than the limit of detection.500 (.200-.760 (<LOD-.250 (<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. interval) Selected percentiles ( 95% confidence interval) Sample 95th .740-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .610 (<LOD-1.820) < LOD < LOD .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.850 (. 154 Fourth National Report on Human Exposure to Environmental Chemicals .470 (.780 (.300-1.780 (<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 .680 (<LOD-.430 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.670 (<LOD-1.950) < LOD < LOD 1.840 (.64) .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.700-.580-1.17 (.55) . Survey Geometric mean (95% conf.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 .840) 669 687 929 Limit of detection (LOD.780 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.740 (.780 (<LOD-1.210 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

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

Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Elwan MA. Florio JC. cdc. Biochem Biophys Res Commun 1998. Chen JH. Int J Hyg Environ Health 2002. 2006. 2002). Zhao RC.. 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. Yang J. Okuno Y. Berger-Preiss E. In developing rodents.8(1):197-202. September 2003.211(3):188-197. Moniz et al. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. 2003. 2003. Kuhn K. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002.27(12):1273-1283.. Song L.. Lemonica IP. Ranft U. Idel H. Idel H. Eriksson and Fredriksson. Additional information about pesticides is available from U. 1999. 2002. Kang IH.23(6):665-673. Kamita Y.cdc. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Effects of prenatal exposure to deltamethrin on forced swimming behavior.gov/toxpro2. 2003.50(2):245-255. motor activity. Fourth National Report on Human Exposure to Environmental Chemicals 157 . EPA at: http://www. Thomson BM. Neurotoxicol Teratol 2005. 1991. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR.107(3):173-177. Kunimatsu et al. Ose K. Moniz AC. Elwan et al. Kim HS. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity.gov/pesticides/ and from ATSDR at: http://www.atsdr. 2005). 2006. Kunimatsu T. Neurosci Lett 2001. Neurotoxicol Teratol 2001. Yamada T. and permethrin) in the Hershberger and uterotrophic assays. Garey J. Xenobiotica 1997. Richardson JR. Kim et al. Caudle WM. 2004. fenvalerate. Bull Environ Contam Toxicol 1999. Miller GW. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.. et al..8(1):18-21. Hu JY. neurochemical changes in cholinergic.27(4):609-614. Adhami VM. epa.gov/toxprofiles/ tp155. Kim IY. Shafer. J Environ Monit 2006. et al. Go et al. 2003... Fredriksson A. Guillot TS. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Available from URL: http://www. Go V. salivation. In California. Estrogenicity of pyrethroid insecticide metabolites. Wolff MS. Agrawal AK. Bernardi MM. and seizures (ATSDR. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. 2001. Environ Health Perspect 1999. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Shin JH.62:101-108. Lazarini et al. et al. Hu et al. Toxicological profile for pyrethrins and pyrethroids. 2006). Lewalter J. Toxicol Appl Pharmacol 2006. bioallethrin and deltamethrin. Varoli FM. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. 2000. Cruz-Casallas PE.atsdr.. Leng G. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Regul Toxicol Pharmacol 2002. WHO. Kuhn KH. Wolff MS. and striatal dopamine levels in male and female rats. Spinosa HS. Soderlund et al. choreoathetosis. Kim TS.1/15/09 Aziz MH. Shaw IC. tremor. Garey J. Sunami O. Bernardi MM. McCarthy et al. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Leng G.. Lee SJ. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. 2002). 2005).html.108(1):78-85. Leng A. Abell AD. McCarthy AR. Lazarini CA.. 2005). Leng G.300(3):161-165.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Levsen K. References Agency for Toxic Substances and Disease Registry (ATSDR). Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Pogo BG. Pauluhn J. 2005).35(2 Pt 1):227-237.html. Neurotoxic effects of two different pyrethroids.. J Reprod Dev 2004. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Ray et al. et al. Wieseler B. Eriksson P. Garey and Wolff. dopaminergic. Wang SL. Shukla Y. hypersensitivity.205(6):459-472.S. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Toxicol Appl Pharmacol 1991.251(3):855-859. Salzgeber SA. Generally.. Sugiri D. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. 2001. 1998.. Seth PK. Pyrethroid pesticide-induced alterations in dopamine transporter function.

Marsh JR. Environmental Protection Agency (U. June 2006a. Permethrin. Sargent D.S. Laird WJ. 5/26/09 U. Spencer J. sumithrin synthetic pyrethroids for mosquito control. World Health Organization (WHO). Revised February 25.10.htm.S. 5/26/09 U. 5/26/09 Woollen BH. J Toxicol Clin Toxicol 2000.S. Mullin LS. Clark JM. synergies. and therapy. Pesticides in the Nation’s Streams and Ground Water. June 2006b. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.113(2):123-136. EPA). O’Malley M. 5/26/09 U. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Environmental Protection Agency (U. Forshaw PJ.who. Soderlund DM. 2007. Pesticide and Evaluation Scheme.38:95-101.gov/oppsrrd1/REDs/cypermethrin_red. resmethrin. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.S. Available at URL: http://www.Pyrethroid Pesticides Ray DE.186:57-72. pdf. EPA). Shafer TJ.S. Available at URL: http://www.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.epa. Environ Health Perspect 2005. U. EPA). Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Available at URL: http://pubs. 1992–2001. Safety of pyrethroids for public health use. 2005.S. Environmental Protection Agency (U. Toxicology 2002.epa.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.22(8):983-991. 19962002. Reregistration Eligibility Decision for Cypermethrin. et al.htm.171:3-59. Pyrethroid illnesses in California.gov/ circ/2005/1291/. March 2006. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .usgs.pdf. Rev Environ Contam Toxicol 2006. Piccirillo VJ.epa. Geological Survey (USGS). Lesser JE.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Meyer DA. Available at URL: http://www. Crofton KM. Available at URL: http://whqlibdoc.S. Sheets LP. Pyrethroid insecticides: poisoning syndromes. Xenobiotica 1992. April 2002.

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

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. < LOD means less than the limit of detection.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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.2. which may vary for some chemicals by year and by individual sample.2 and 0. 160 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.

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.S. Fourth National Report on Human Exposure to Environmental Chemicals 161 . 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. 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.

Angerer J. Int J Hyg Environ Health 2006. Idel H. Olsson AO.46(3):281-288. Drexler H. Angerer J. Int J Hyg Environ Health 2006. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Berger-Preiss E. Becker K. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Ranft U. Atlanta (GA).186:57-72. Arch Environ Contam Toxicol 2004.13(2):112-119. Krieger RI. et al. Sugiri D. Butte W. Spencer J.209(3):221-233. Centers for Disease Control and Prevention (CDC). Hadnagy W. O’Malley M. Kolossa-Gehring M. Int J Hyg Environ Health 2003.109(3):213-217.77(1):67-72.Pyrethroid Pesticides References Baker SE. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Pyrethroid illnesses in California. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. 162 Fourth National Report on Human Exposure to Environmental Chemicals . J Expo Anal Environ Epidemiol 2003. Rev Environ Contam Toxicol 2006. Third National Report on Human Exposure to Environmental Chemicals. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Environ Health Perspect 2001.206(2):85-92. Leng G. Bernard CE.209(3):293-299. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Ball M. 2005. Schulz C. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Heudorf U. Heudorf U. Angerer J. 19962002. Heudorf U. Williams RL. Barr DB. Hoppe HW. Int Arch Occup Environ Health 2004.

210) 90th . 1999).710-1.1 and 0.120-.220-.380-.920) 1.500 (.270 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.12 (.28) 671 680 518 701 591 957 Limit of detection (LOD.690) .870) 1.07 (.670-2.21) .150 (.680-3. The presence of cis-3-(2.68 (.24) 1. 1985.47 (.580) 1.680 (.670-1.or trans-3-(2.210) .250-.790-1.2-dichlorovinyl)- CAS No. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740 (. Cyfluthrin.380-.1.730 (.670 (.890 (.580-1. population from the National Health and Nutrition Examination Survey..900 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.510 (.460-1.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.44 (.740-2. Kuhn et al. Biomonitoring Information Urinary levels of cis. cis-cypermethrin.370-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. and ciscyfluthrin.460-. more of the trans-metabolite than Urinary cis-3-(2.890 (.490-1.180) .410) .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.770) .77 (. but it can also reflect exposure to cis-3-(2.790-1.740-1.68) .600 (.600) .11) .270 (.53) . and trans-cyfluthrin.10) size 1951 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.440 (.490-.200 (. 1999).600-1.730 (.880 (.380 (.270 (.630 (.280 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .770-1.630-.310) .50) .110-.550) .650-1.380) . cis-permethrin.490-1.380-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin. The chemical trans-3(2.2-dichlorovinyl)-2.43) . < LOD means less than the limit of detection.220-.220) .110 (<LOD-.490-. In the body.470 (.960 (.470-1.2-dichlorovinyl)-2.202 (.2dichlorovinyl)-2.180 (.300-.160 (.2dichlorovinyl)-2.340) . Kuhn et al. cis-3-(2.910-5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.280-. but can also reflect exposure to trans-3(2.2-dichlorovinyl)2.520) .300 (.270-.500 (.2-dichlorovinyl)-2.730 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .530 (.80) .68) .54) .200) .510 (.220-.670-1.68359-37-5 Cypermethrin Permethrin CAS No.820 (.250 (.120-. which may vary for some chemicals by year and by individual sample.630) .120-.32) .460 (. 52315-07-8 CAS No. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin. transcypermethrin and trans-cyfluthrin.420-.430-.780) .110-.155-.630) .160 (<LOD-.200-.140 (<LOD-.2-Dichlorovinyl)-2. Similarly.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.262) * * * < LOD < LOD . 1985.08) .15) .610) . trans-cypermethrin.330) .340) .740) 1. the presence of trans-3-(2.13 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .S.510 (.110-.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . ciscypermethrin and cis-cyfluthrin.300 (.and trans-isomers. Generally.35) 1.35) .950-2.300-.370 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.160 (.200-. trans-permethrin.200-.710) .350) .570-.570 (.340-.790 (.700) .220-.210-.850 (.200) < LOD < LOD < LOD . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U..200) .240) .170 (.230) .400-.790) .330 (.120-.260 (.610) .640 (.410) .240) .140 (.

2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.33) .370-.340-.680 (. In the same residents.270) .580-1. urinary levels of cis-3-(2.640-1.450-1.430 (.260 (.160 (<LOD-.300) . 2006) and 1177 urban adults and children (Heudorf et al.2-dichlorovinyl)-2.138 (.550) .550-1.67) .230 (.170 (. 2006).880) .11) .130-.700) ..260 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .600 (.780 (. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840 (.11) .410) .300 (. Lu et al.59) .200 (. 2004.390-. 2006. 2001.2dichlorovinyl)-2.and trans-3-(2.180-.260-.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.80) .340) .370-.080-.150-.560) 1.390 (.560) .2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al..170 (.260) .140-.360-1.830) .280 (.210-..350 (.340) . Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.500 (.290) .150-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .420 (.510-1..2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.900 (.450 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. 2006.240 (<LOD-.03) 1.270) . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.67 (.11 (. Schettgen et al.290 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.570) ..11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .300 (.190 (.250-.640-..530 (.2-dichlorovinyl)-2.230-.2dichlorovinyl)-2.440 (.380) . Cyfluthrin.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 .2-dimethylcyclopropane carboxylic acid did not increase.182) * * * < LOD < LOD .920 (. Other studies have provided evidence that urinary levels of cis.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.710 (. 2005).11) 1. 2001) showed urinary levels of cis.250) 90th .750 (.590 (.280-.. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al. median urinary levels of trans-3-(2.390-.220 (.270 (. population from the National Health and Nutrition Examination Survey.Pyrethroid Pesticides 2.250 (<LOD-.380-.250-.400-1.320-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.700-2.810 (. 2005).750-1. 2002).59) .150-.230-.120 (. the median and 95th percentile of urinary levels of cis-3-(2. In these volunteers.29 (.33 (.440-.450-..190) .37) . 2003).550 (. post- Urinary cis-3-(2.2-Dichlorovinyl)-2.250) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.400 (. In a study of volunteers.190) .800 (.200-.700) . Studies in Germany of 396 children and adolescents (Becker et al.250) .440 (.540) .and trans-3(2.710-3.. 2003).21) .840 (. 2006).470-1.320) .680-1..890) .260 (. 2005).170) < LOD < LOD < LOD .680-1.230-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.2-dichlorovinyl)-2.220) .430-1.780) 1. urinary trans-3-(2.380 (.220 (.440-.580) .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . 2005) In a small group of indoor pest-control operators.300) . Survey Geometric mean (95% conf. representative NHANES 2001-2002 subsample (CDC.31) .200-.270-.59 (1.890 (.250-.300-.690-1.290-.104-.350) .640 (.12-2.200) .14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. In a study of urban residents in Germany (Berger-Preiss et al.640-1.530 (.S.24) .370-.49) .S.550) .540 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin. 2002).590) .180 (.550-1.640) 1.540 (.430-..12 (.2-dichlorovinyl)-2. 2004).290) .

49-3.670) .16) 1.11-1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.03-1.2-dichlorovinyl)-2.95) 3.500-.63) 1.03-1.610) 1.69 (1.17-1.95) 2.4 and 0.550 (. however.07 (1. < LOD means less than the limit of detection.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .580 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.48) 4.68) 1.810-1.440 (<LOD-.750) .560 (.35) 1.54 (1.77) 1. The maximum post-application urinary levels.850-1.970 (.68-3. Fourth National Report on Human Exposure to Environmental Chemicals 165 .530) .55-4.97-11.23 (.Pyrethroid Pesticides application median urinary levels of summed cis.20 (.480-.11-2.09 (.20 (.520-.49-5.56 (1.4.830-1.560 (. population from the National Health and Nutrition Examination Survey.23) 2.60) .55-3.400-.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 .19 (2.87 (1.01) 4.42) 1.800-1.10) 2.26 (.700-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.410 (<LOD-.S.5) 2.13) .43) 2.01 (1.39-5.700) .68-2.and trans-3-(2.54) 4.91 (1.08) 1.680-1.410 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.or trans-3-(2.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .66) 691 680 518 690 595 954 Limit of detection (LOD.60-4.41-14.22 (1.27 (1.56) 2. 2005).420 (<LOD-.780 (.920-1.400 (<LOD-.14) 1.940 (. Survey Geometric mean (95% conf.40 (1.730) . were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.520) .840-1.14-6.84 (1.08-6.50 (1. which may vary for some chemicals by year and by individual sample.620) < LOD 2.570) 90th 1.56 (1.64-4. 2005).910-1.19 (3.08-4.63) 1.62 (1.470 (.68) 1.710 (. trans-Cypermethrin.39 (1.28 (1.20 (.760) .59 (1.410-.42 (2.25-3.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.660) 1.60) 1.7) 2. Finding a measurable amount of cis.37 (1.17 (. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.500) .68) 2.2-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.28 (2.12-6.17 (.2dichlorovinyl)-2.500 (.66) .76-3.77 (1.460-.14-2.410-.2-dichlorovinyl)-2.77) 2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.94 (1.2-Dichlorovinyl)-2.490 (<LOD-.19) 1.89 (2.910-1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.56) 2. Biomonitoring studies on urinary levels of cisor trans-3-(2.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .470 (<LOD-.69) 1. Urinary trans-3-(2.41 (1.560 (.820) .670) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.76-4.85) 4.25 (1.49-3.81) 2.90) 1.860) .490-1.07-3.460-.55-5.

33 (1.57 (1.86 (2.30-3.57) 3.07) 2.75 (1.880 (<LOD-1.30-6.900 (<LOD-1.700-.470-.700 (.00) 1.20 (1.07-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.440-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.37 (1.08 (.480-.65) 1.530 (.36) 2.720 (<LOD-. trans-Cypermethrin.730) .470 (.45-2.2-Dichlorovinyl)-2.47 (1.20-2.33-2.31) 1.660) .35) 1.60) 2.61) 1.850) .800-1.80) 1.55 (2.720-1.720-1.22-1.45 (1.Pyrethroid Pesticides Urinary trans-3-(2.580 (.87-8.87) 1.74) .74) 2.87-3.00) 1.07-1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .13) .22) 1.570 (<LOD-.35 (1.56 (1.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .34-4.15) 3.560 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.47-2.26 (1.67 (2.S.670) .91-11.850) 1.41) 1.16 (1.930-1.48-2.770) < LOD 2.07) 2.56-2.42 (.87 (1.00 (1.850-3.60) 2.880 (.60 (1.44) 2.520 (<LOD-.15-3.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .11) .87) 1. Survey Geometric mean (95% conf.89) 2.15-3.970 (.07-3.39) 1.55 (2.540) .19) .64 (1.81 (2.570 (.580) .33-1.610-.780) 90th 1.19 (1.28) 2.00-5.15) 2.42) 1.39 (1.570-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.55 (2.02-1.13) 1.36 (1.3) 2.48 (1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .34-3.800-1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.15-3.27-2.31 (.410-.65 (2.91) 1.27-2.500-.780 (<LOD-.740) .12-1.91 (1.760 (.31 (2.700 (.780) .640) .40-2.47-2.68) 3.750) .880-1.56-5.820-2.08 (.12 (.00) 5.22-2.29) 1.15 (1.70 (.98 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.530 (<LOD-. population from the National Health and Nutrition Examination Survey.

205(6):459-472. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Angerer J.209(3):293-299. Bull Environ Contam Toxicol 1999. Heudorf U. Kolossa-Gehring M.68(6):1160-1163. Centers for Disease Control and Prevention (CDC). Drexler H. Wieseler B. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Idel H. Lu C. Leng G. Idel H. Heudorf U. Environ Health Perspect 2001. Heudorf U. Leng G. Int J Hyg Environ Health 2003. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Levsen K. Angerer J. Angerer J. Ranft U. Sugiri D. Idel H. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.62:101-108. George DA. et al. Angerer J. Drexler H. Sugiri D. Schulz C.134(1-3):141-145. Ranft U. Leng G. Bravo R. Heudorf U. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Berger-Preiss E.206(2):85-92.Pyrethroid Pesticides References Becker K. Hoppe HW. Hardt J. Schettgen T. 2005. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int Arch Occup Environ Health 2004. Angerer J. Atlanta (GA).76(7):492-498.109(3):213-217.209(3):221-233. Bartell S. Butte W.114(9):14191423. Int Arch Occup Environ Health 2003. Seiwert M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Berger-Preiss E. Hadnagy W. Environ Health Perspect 2006. Int J Hyg Environ Health 2002. Biological monitoring of workers after the application of insecticidal pyrethroids. Ball M. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. Permethrin and its two metabolite residues in seven agricultural crops. Int J Hyg Environ Health 2006. J AOAC 1985.77(1):67-72. Pearson M. Int J Hyg Environ Health 2006. Kuhn K.

.2-dimethylcyclopropane carboxylic acid of 0. 2004). Deltamethrin can degrade to cis-3(2.. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2dimethylcyclopropane carboxylic acid formed in the environment.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.2-dibromovinyl)-2. 2005). Studies in Germany of 396 children and adolescents (Becker et al.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dibromovinyl)-2.2-dibromovinyl)-2. Following residential spraying with deltamethrin for malaria protection in Mexico. Outside the U.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. in detection of cis-3-(2.2-dibromovinyl)2. 2001.3-0. 2001) showed that urinary levels of cis-3-(2.2-dibromovinyl)-2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.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. Baker et al. 2006) and 1177 urban adults and children (Heudorf et al. (2004) reported a geometric mean concentration of cis-3(2. Urinary levels for adults and children in these studies were similar (Heudorf et al. 52918-63-5 General Information Cis-3-(2. in some situations replacing the use of DDT. 1990)..39 µg/L. deltamethrin has been used against mosquitoes that carry malaria. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 168 Fourth National Report on Human Exposure to Environmental Chemicals .Pyrethroid Pesticides Deltamethrin CAS No.5 μg/L) than the detection limit (0. 2005). 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.1 μg/L) for the NHANES 2001-2002 subsample (CDC. Finding a measurable amount of cis-3-(2. 2005). Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample..2-dibromovinyl)-2.. mean peak urinary levels of cis-3-(2. Thus. urinary levels of cis-3-(2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.

S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .Pyrethroid Pesticides Urinary cis-3-(2.2-Dibromovinyl)-2.1 and 0.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 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. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.1. Survey Geometric mean (95% conf.

population from the National Health and Nutrition Examination Survey.2-Dibromovinyl)-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. 170 Fourth National Report on Human Exposure to Environmental Chemicals . 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.Pyrethroid Pesticides Urinary cis-3-(2.

Torres-Dosal A. Angerer J. toxicokinetics. Lopez-Guzman OD. Angerer J. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Seiwert M. Centers for Disease Control and Prevention (CDC). [online] 1990. Angerer J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. International Programme On Chemical Safety (IPCS). et al. Environ Health Perspect 2001.org/documents/ehc/ehc/ ehc97. Environmental Health Criteria 97.77(1):67-72. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Ball M. and genotoxicity in exposed children.209(3):221-233. Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Hoppe HW. Int Arch Occup Environ Health 2004.inchem. Schulz C. et al. Atlanta (GA). Heudorf U. 5/26/09 Ortiz-Perez MD. Environ Health Perspect 2005. Int J Hyg Environ Health 2006.113(6):782-786.Pyrethroid Pesticides References Becker K. Int J Hyg Environ Health 2006. 2005. Batres LE. Carranza C. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Available at URL: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Kolossa-Gehring M.109(3):213-217. Butte W. Deltamethrin. Drexler H.209(3):293-299. Grimaldo M.htm. Heudorf U. Third National Report on Human Exposure to Environmental Chemicals.

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

273 (.362) .35) 2.570-1.04-5.78) 1.730 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .75 (1.750) .260 (.86 (1.328 (.265-.760 (.560-.41) 3.940) 1.12) 4.620-1.246-.76 (1.510-.49 (1.238-.340) 75th .39) 2.25 (2.92-3.352-.50 (2.78 (1.32 (1.360) .610) .430-.14-6.41-2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .230-.1) 3.190-.320) .370) .560-.27-11.640 (.990) .43) 3.290 (.1) 3.700-1.16) 1.490) .292 (.292-.230-.18 (2.56-5.840-1.450 (.83-11.750-1.510-.630) .200-.530-.42-2.710 (.267 (.270) .03 (3.680 (.21 (2.740 (.12 (.353 (.298 (.440) .740 (.13) .41-3.330) .25-7.190-.830-2.420) .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 .253-.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.230 (.960 (.230-.586) .45-5.233-.321 (.520 (. population from the National Health and Nutrition Examination Survey.311 (.49-2.590 (.230 (.427) .210-.90) 1.34 (2.48-2.49 (1.1.260 (.266-.62) 5.54) 1.384) .390) .250-.800 (.48-2. Survey Geometric mean (95% conf.530-.65-2.810) 1.260 (.34-6.288 (.340) .600 (.650 (.28) 1.26-2.373) .190-.41 (1.300 (.33 (1.434) .05) 1.277-.710 (. Deltamethrin.780) 4.260-.65 (1.49-2.220-.23 (2.570-.160-.35 (2.62-8.78) 1.330) .79) 3.300) .270 (.320) .227-.62-6.27-2.25-4.29-1.52-5. interval) .490-.46) 2.428-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.16-1.1 and 0.51-6.300 (.369) .406) .700 (.55 (1.89-71.271-.355) .315 (.160-.210-.250 (.64) 697 680 524 701 603 957 Limit of detection (LOD.S.325 (.340) 1.430-.417 (.81 (1.560-1.69) 3.276-.280 (.63 (3.454 (.26) 2.850) .72 (1.250 (.33 (2.288-.04) .830) 90th 1.320) .320 (.38 (2.25 (2.336 (.34) 8.820) .73) 1.52-4.507 (.870 (.33) .320) .35) 2.32-21.32 (2.595) .01 (1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.78) 6.820) .297 (.18 (1.670 (.300 (.250 (.27-2.53) 1.35) 1.13 (.60) .45 (2.800) 1.295) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .69 (1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.350-.550-.590-.02-6.364) .200-. Fourth National Report on Human Exposure to Environmental Chemicals 173 .71 (1.30 (1.53-3.180-.35 (1.226-.30 (.30) 3.1) 3.314 (.12) .46) .314) .44) 5.25-1.601) .200-.05) .470-.240 (.36) 1.93 (1.850) .247-.26) 2.38 (2.750) .8) 3.387) .190-.51-3.63-3.240 (.

35) 1.91-4.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.610 (.67 (1.280) .67) 1.37 (1.11 (.S.240-.190-.250 (.750-1.270 (.390-.13 (.55 (1.300-.400-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .730-1.720) 90th 1.261-.27) 1.720 (.200-.530-.270 (.580) .09) 3.200-.730) .274 (.43) 1.400-.270) .09-2.960-1.230) .178-.590) .224-.299-.330) 1.07-5.49-2.86 (1.95) 1.860-1.52) 2.240 (.54 (1.290) .321-.930) .173-.270-.227 (.677) .49) 1.230-.246 (.48 (1.480-.81 (1.226-.63) 1.72 (1.36 (1.63-3.22 (1.00) 5.387) .330) 75th .280 (.309) .590) .590-1.36-6.73) 1.03-1.02 (2. interval) .44) 2.75-8.440-.15-2.62) .440-.490 (.370-.41) 1. population from the National Health and Nutrition Examination Survey.420-.760) .53 (1.590) .410) .09-2.52 (1.311 (.400) .380-.49) 3.330) .272) .670) 3.00) 1.40 (1.810) 1.640 (.21-4.150-.328) .19) 2.240 (.02-1.440-.61-2.240-.25-2.96 (1.357) .278) .329) .309 (.10 (2.43 (2.67 (1.401) .51-7.0) 3.930) 1.00) 1.330 (.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 .446) .190-.73-4.210 (.04 (3.94 (1.55) 3.240 (. Survey Geometric mean (95% conf.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .37) 1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .316 (.35-3.550 (.700-1.437) .05-3.280 (.49 (1.60-4.200-.240 (.40) 2.490 (.238-.09 (.630) .74) 3.310) .378 (.362 (.91 (2.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.560 (.270) .03 (.90) 3.380 (.83 (1.240-.200-.250 (.510 (.13-1.240-.07) 2.62) 1.225-.91) 9.35) .370 (.32 (2.13-1.510 (.330) .88-5.550 (.19-6.320) .261 (.580 (.730) .460-.272 (.323 (.740) .480 (.43 (1.530-.229-.410-.540 (.280) .670) .335-.60) 1.210-.534) .25) 2.220 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .271-.06-3.275 (.41-4.510 (.312 (.11 (.423 (.860-1.274-.290-.460-.16-4.44 (1.860 (.264 (.253) .280-.190 (.372) .350 (.83) 1.230-.39) 1.84 (1.35 (1.17-1.570) .500) .216-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.650) .350) . Deltamethrin.202-.210 (.04 (.43-64.250) .300-.450 (.19 (2.25-5.91) .640 (.80) 4.234 (.21 (1.550 (.329) .280 (.64-5.290) .840-1.220-.160-.17 (.490-.

Berger-Preiss E. Ball M. Lapinski R.Pyrethroid Pesticides References Baker SE. Hardt J. Biological monitoring of workers after the application of insecticidal pyrethroids. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Idel H. Seiwert M. Grimaldo M. Pearson M. toxicokinetics. Environ Health Perspect 2003. Hadnagy W. Atlanta (GA). Ortiz-Perez MD. Sugiri D. 2005. Lopez-Guzman OD. Olsson AO. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. et al. et al. Leng G. Obel J. Environ Health Perspect 2006. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Leng G. Centers for Disease Control and Prevention (CDC). et al. Carranza C. Bartell S.206(2):85-92.113(6):782-786. Bravo R. urban cohort. Batres LE. Torres-Dosal A. Kolossa-Gehring M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int J Hyg Environ Health 2003. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Indoor pyrethroid exposure in homes with woollen textile floor coverings.114(9):14191423. Liu Z. Levsen K. Sugiri D.111(1):79-84. Int J Hyg Environ Health 2006. Ranft U. Barr DB. Godbold J. Angerer J. Becker K.76(7):492-498. Berkowitz GS. Int Arch Occup Environ Health 2003. Exposure to indoor pesticides during pregnancy in a multiethnic. Arch Environ Contam Toxicol 2004. Ranft U. and genotoxicity in exposed children. Int J Hyg Environ Health 2002. Lu C. Berger-Preiss E. Environ Health Perspect 2005. Angerer J. Idel H.205(6):459-472. Hoppe HW. Barr DB. Deych E.46(3):281-288. Third National Report on Human Exposure to Environmental Chemicals. Fourth National Report on Human Exposure to Environmental Chemicals 175 .209(3):221-233.

090 (<LOD-.300) .160 (. 01-02.190 (.370-.250-.122 (.370) .200-.169 (.390) .095 (.400 (.430 (. castings.117-.240 (.340 (.130 (.150 (.100) .250-.180 (. 0.220-.105 (.103) .360) .230-. Workplace exposures can occur at smelters.137) .200 (. coal-fired plants.320) Total .100-.160-.280) .170-.156-.170-.190) .200 (.320 (.123 (.140 (.460) .260) .070-.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 .180) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.090-.300-.134 (.070 (<LOD-.133) * .170-.130-. < LOD means less than the limit of detection.120-.180 (. and 03-04 are 0.128 (.220-.490) .390 (.260 (. and as a fire-retardant in textiles and plastics.099 (.130 (.150) 90th .109-.400 (.310) .710) .440 (.160-.160-.079-.130) .135) * .230) .087-.150 (.280-.110 (.180-.120 (. It is also used in paints. which may vary for some chemicals by year and by individual sample.120 (.280) .150-.180) .330) .Metals Antimony CAS No.093 (.350) .320-.120-.S.180 (.470) .390-.140) .220 (.130 (. The absorption.197) .310-.110-.164-. or other substances containing antimony is another means of exposure.220) .150 (.280) .240 (.178) .470 (.154) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .430 (.190) .200-.143 (.080-.410) .350 (. It is used in metal alloys.300) .440) .145) Selected percentiles ( 95% confidence interval) 50th . metal bearings.350 (.350-.130-.140-.120) .600) .280-.400-.460 (. fireworks.300) .130-.130 (.120-.240 (.320) 316 368 290 663 762 725 1297 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Stibine is a metal hydride form of antimony used in the semiconductor industry.420) .240) .200) .100-.161) .190 (.150-.320-.190-.210 (.120-.080) .350) .500) .200 (.130-. 0.400) .260 (.230) .350-.260-.120) .160 (.290-.190) .150) .140) .360-.460 (.088-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.110-.240-.150-.146 (. enamels.400 (.126-.360 (.220 (.240-.100 (.120-.150) . sheet and pipe metal.120-.154-.270 (.120-.130-.400) .250-.250 (.140 (. ceramics.175 (.310 (.130) .128 (.170-.200 (.120 (.160) .390) .230 (.200) .095-.260) .270) . water.220-.440) .160-.390-.090) 75th .130-.220) 95th .160 (.160) .190-.148-.390) . People are exposed to antimony primarily through food and.250 (. see Data Analysis section) for Survey years 99-00.250) .300-.176 (.131-.210) .280-.300 (.117-.310 (.290 (.130 (. Dermal contact with soil.157) .280-.210-.190 (.260-. to a lesser extent.500) .310) .210) .210) .320-.120 (.350-.136) * . storage batteries.490 (.560) .140) .470) .180 (.570) .310 (.130) < LOD .134-. ammunition.160) .330 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.270-.400) .330) .330) .240 (.210) .110-.090 (.290-.158 (.330-.310-.260 (.350) .390) .230 (.126 (.160) .270 (.410-.130 (.090-.170) .220) .132 (.130 (.170 (.070 (<LOD-. and 0.350 (.190) . solder.220-.04. from air and drinking water.170-.360) .230) . 7440-36-0 General Information Antimony is found in ores or other minerals.510) .200 (.210-.270 (.180-.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 .270) .320-.230-.115-.350 (.300 (.130 (.140) . Antimony enters the environment from natural sources and from its use in industry.120-.120) .108 (.150-. distribution.080) .132 (.350) . +3.340) .110-.100 (.207) .180-. and +5.137) .112-.220-.140 (.190 (.150) .280-.120) .260) .125 (.140) .115) .140 (. respectively.108-.190 (.180-.340 (.119) .200) . 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300-.330-. and excretion of antimony vary depending on its oxidation state.120-.360 (. interval) .07.098-.04.330 (.110) .144) .190-.190-.119-.330 (.200-.140) .280) .410) . and glass.160) .230-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications. population from the National Health and Nutrition Examination Survey.330) .280 (.180 (.250 (.280 (.190-.141-.080 (<LOD-.150-.230 (.530) .390-.230-.120 (.142 (.200) .320 (.200 (.210) .170 (.200-.130) .180 (.136-.320) .220) .230-.190) .180-. and pewter.250-.310 (.114) .220-.460 (.270 (.130-.210 (. and refuse incinerators that process or release antimony.154) .430 (.184) .350 (.145 (.240 (.160) .

119 (. 1988. and kidney have been demonstrated in high dose animal studies depending on the dose.414) .112 (.310 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.111 (.109 (.108 (. Histopathologic inflammatory and degenerative changes in the lung.400 (.192) .173 (.124 (. diarrhea.082 (<LOD-.263 (.425) .185-.298 (.173-.143 (.106-.143) .170 (.220) .122 (.122 (.167 (.103-.204-.124-.139 (.317) .286 (.146-.318-.333 (. Acute antimony poisoning may cause a metallic taste.075 (.178-.108-.228 (.127) .137 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.147) .135) .161) .145) .099-.081 (<LOD-.138-.245) .199-.248-.250-.126-.178 (.266 (.107-.195-.105-.173) .116 (.130) .203) .471) .265 (.163 (.127) .156-.317) .123) .267) .211) .080 (.352) .313-.265-.227-.115 (.126) . 1995).130 (.357-.127 (.333) 1132 1334 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .167-.741 (.175 (.188) .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 .193) .308-.485) .310) .096-.115 (.417) .104-.118 (.162-.217 (.430) .233) .127) .235-.181) .131) .191 (.257) . 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.176 (.130) .081) .207) .208 (.188-.144-.116-.103-.076-.132) .092-.187) .206-.167 (.082) .228 (.267-.135 (.135) .233-.153 (.131 (.114 (.120 (..179-.161) .069-.148-.095-.147-.338) .071-.241-.259 (.320 (.196 (. liver. skin.149-.128-.146-.134) .086 (.308) .321) .102-.061-.278) .200-.471 (.229-.276 (.138) * . and ulcers (Werrin.108-.138-.429 (.250 (.183) ..189 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.069-.173 (.185 (.230-.233 (. myocardium.164 (.236 (.114 (.120 (.343 (.068 (.195-. species.338 (.294) Total .159-.135 (.113-.124) .333-.250) .129) .119-.295 (.104-.080 (<LOD-.143) 90th .380 (.248) .225 (.480) . resulting in hemolysis with abdominal and back pain (Dernehl et al.098) .239-.139 (.315) .320) .224 (.111-.241-.244-.Metals than for trivalent compounds (Elinder and Friberg.098-.222 (.100 (.082) .120 (.250 (.193 (.261) .727) .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.120 (.192 (.140) < LOD .163 (.255-.106-.500) .228-.253 (.447 (.247) .181) .255) .226 (.098-.438) .112 (.075 (.109-.352 (.079 (<LOD-.148-.195 (.198) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.230) 95th .117-.121 (.113-.200-.129 (.333-.263-.149) .099-.277 (.364 (.238 (..181) .152) .077) .186) .121 (.138 (.092) .129 (.115 (.102-. Ming-Hsin et al.280-.373) .300 (.185 (.146-.112-. and gastrointestinal symptoms such as vomiting. 1962).338 (.085) .256 (.123 (.281-.153-.310) .288 (. 1986).148) * . and eyes. interval) .429) .115-.200) .364 (.089) .250-.143) Selected percentiles ( 95% confidence interval) 50th .741) .146) .225) .171) .159-.203) .132 (.320-.084) .133) .194-.333-1.405) .097-.130) .107-. 1986).267 (.200-.250-.385 (.125-.131-.159-.280 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.333 (.391) .115) .164-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.318-..124-..115-.143) . 1958) and occupational exposures (Briegner et al.164) .209) .278 (.333 (.140) .317) .238) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.238) .117-.135) .113) .205-.068-.086) 75th .095-.242-.152) .150-. 1973).108-.151) .087) .119-.114 (.107-.320 (. Inorganic antimony salts irritate the mucous membranes. and route of exposure (Elinder and Friberg.333) .213 (.268) .209) .150-.074 (.176 (. population from the National Health and Nutrition Examination Survey.271-.S.371 (.118 (.320-.127) .444) .269 (.272) .391) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.182 (.154-.136) . 1954).208-.417) .126 (.167 (.109 (.300) .176-.172-.192-.129) * . 1944).117-.333-.421) .121) .076-.214) .444) .300) .30) .156 (.160 (.078 (. abdominal pain.209 (.357) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .209-.125 (.253-.250-. 1953).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 .

Dezateux et al. and future strategies. Fuchs A. Cheng-Wei L. 1998) or compiled reference ranges (Hamilton et al. Liao Y-H. Semisch CW. Kiberd B. and a drinking water standard has been established by the U. respectively. Chin Med J 1958.48:93-97. Cullen A. 1990.76:432436. Pozzoli L. Trace element reference values in tissues from inhabitants of the European community I. Bailly R.. Kuo-Juie Y. Industrial antimony poisoning. et al. Costeloe K.76(2):103-115. Chest 1973. 1997). Sabbioni E. et al. Third National Report on Human Exposure to Environmental Chemicals. Rev Infect Dis 1988. Konings J. or exposure differences. Lauwerys R.. Wade A. Stone FD. 2nd ed. Review of elements in blood. Iavicoli et al. Biological monitoring of exposures to aluminum. Friberg L. Antimony. pp. Atlanta (GA). Arch Dis Child 1997. gallium.cdc. 1998). Apostoli P. In: Friberg L. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Paschal et al. 2005. 1987). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Matthews T. Lenert G. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. 1986. Sabbioni E. Ju-Sun P.16: 33-39. Chen J-R.106:33-39. Suchenwirth R. Yu H-S. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Wu M-T. Luedersdorf R. Piatnek DA. Weltle D. Vouk VB. Chemotherapy for leishmaniasis: Biochemical mechanisms.atsdr. J Occup Environ Med 2004. 26-42. EPA. J Clin Pathol 1998. Alimonti A. Dezateux C. Environ Health Perspect 1998. Delves HT. Industrial Medicine and Surgery (Dec. Dunkelberg.e. Petrucci F. Elinder CG. Arsine. clinical efficacy. 20012002. Pietra R.. Liao Y-H et al.. VI. Nau CA. O’Regan M.. even when exposure levels were below workplace air standards (Bailly et al. Mayer P. Industrial Medicine 1944. and antimony in optoelectronic industry workers. 1998. Van der Venne MT.64(2):182-185. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Ming-Hsin H. Gallorini M.51:238-240. 2002.html.. Information about external exposure (i. Br J Ind Med 1991. Shao-Chi C. Cordasco EM.. Handbook on the toxicology of metals.158:165-190. gov/toxpro2. Buchet JP. Caroli S. indium. Pilgrim L. arsenic. Iavicoli I. Yang C-Y. and hydrogen sulfide. Gebel TW. population. Ludersdorf et al. References Berman JD. 1994) have reported values slightly higher than those in this Report.10(3):560-586. HH. Carelli G. Pulmonary edema of environmental origin. Urinary antimony in infancy. Roland H.Metals to antimony have been established by OSHA and ACGIH. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000... Ho C-K. Leinemann M. stibine. Chia-Yu H. Bolten C. Stasney J. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Biological assessment of exposure to antimony and lead in the glass-producing industry. 1995. 2004.. Antimony trioxide is rated by IARC as a possible human carcinogen.46:931-936. Hamilton EI. Mahieu P. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. 1991. Earlier measurements in general populations (Minoia et al. Sci Total Environ 1994. and 2003-2004. Kentner et al. Schacke G. Int Arch Occup Environ Health 1995.13:361-362. Biomonitoring of a worker population exposed to low antimony trioxide levels. Centers for Disease Control and Prevention (CDC). Nordberg GF. plasma and urine and a critical evaluation of reference values for the United Kingdom population.67:119-123. 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.59:469-474. External and internal antimony exposure in starter battery production. et al. Dernehl CU.. Briegner H. Antimony in blood and urine of infants. eds. Delves HT. Skulsukai G. which may be due to methodologic. Kentner M.S. Minoia C. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Stocks J. Element reference values in tissues from inhabitants of the European community. J Trace Elem Med Biol 2002. Int Arch Occup Environ Health 1987.)1954. environmental levels) and health effects is available from ATSDR at: http://www. Schaller KH.521-523. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Mayne P. Stead FM. New York: Elsevier..

Renes LE.Metals in urine. Werrin M. Pirkle JL. Trace metals in urine of United States residents: reference range concentrations. blood. Chemical food poisoning. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Antimony poisoning in industry. Industrial Hygiene and Occupational Medicine 1953.76(1):53-59. Fourth National Report on Human Exposure to Environmental Chemicals 179 . and serum of Italian subjects. Sampson EJ. et al. Ting BG. Environ Res 1998. Morrow JC. Sci Total Environ 1990.99-108. Paschal DC. 27:38-45. Jackson RJ.95:89-105.

Although it is still widely used in the United States. grain. as alloy in metal bearings. semiconductors.000 metric tons annually.6) 11. arsenocholine. and as a cosmetic to lighten complexion. gaseous hydride manufactured in small quantities for use in the semiconductor industry.5) 95th 65.84) 8. Water sources contain mostly inorganic arsenate.3) 10.6 (13. Since the 1940s.90-8. Gallium.0 (14. and. it is found in over 200 crystalline or mineral forms.3-15.90-14. psoriasis. and in lead-acid storage battery grids. to a lesser extent.2-93.10-7.1) 1281 1276 03-04 03-04 03-04 9.7-83. In nature.5) 43.8) 29. aluminum. arsenic compounds.40) 7. lead. 2001). cancers.1) 15.2-20.34-9.5-19.0-60.50-14. and as homicidal poisons. Arsenic and its compounds have had many uses in the past and present as medicines.7) 24.2 (12.25-9.0 (11.00-9.80 (5. the smelting of copper. from coal burning.4) 60. and arsenosugars. sodium arsenite.97) 8.5 (34. Arsenic is measurable in most soils.8) 7.30) 17.4 (24. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.5 (23.8-61. population from the National Health and Nutrition Examination Survey. meats.90 (7.5 (40.74.10) 10.S. retaining walls. 2005).5) 66.70 (6.0 (22.70-9.7-95.2 (41.08 (5.3-19.77) 6. or rarely as elemental metalloids (yellow. 180 Fourth National Report on Human Exposure to Environmental Chemicals . Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.6-141) 53. and other metals. ocean and fresh waters. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. arsenic as elemental metalloids may be used in some ammunition.1-40. such as arsenopyrite (FeAsS) and realgar (As4S4).9) 21.30 (7. Also.9-34.4-65.02-8. +3 and +5).Metals Arsenic CAS No. and produce. interval) 8. mental disorders.13-8. lead hydrogen arsenate.29 (8.57) Selected percentiles ( 95% confidence interval) 50th 7.2 (13. see Data Analysis section) for Survey year 03-04 is 0. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.0 (43. Survey years 03-04 Geometric mean (95% conf.12 (6.80-9. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. black.10-10.6 (9.2-17.6 (32.70) 8.4) 13.9) 68. Arsenic trioxide is approved to treat acute promyelocytic leukemia. alloys.5-178) 46. arsenites.90-11.30 (6.5) 41.4 (26.6-43.6-35.90-8.8) 33. and foods. referred to as inorganic arsenic compounds.90-7. Arsenic trioxide (As2O3. to a lesser extent.8) 30.3) 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. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. trimethylarsine oxide. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (8. Various arsenic compounds were used in paint pigments and for tanning animal hides.8) 17. Before the 20th century. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. and play sets.1 (32.0-19. Arsine (AsH3) is a reactive.4) 40.00 (6. and arsenates (oxidation states of -3.6) 618 722 1074 Limit of detection (LOD.2 (51.2) 46. solders. particularly arsenic trioxide. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.27) 9.5-41.12-10.90 (7.2) 15.8 (48.4 (48. General population exposure to inorganic arsenic can occur through consumption of drinking water and.9-62.9 (8.4 (31.19-9.90 (5.8-77.8) 7.9-46.7) 90th 37. The United States no longer produces arsenic from mining but imports about 22.1) 290 725 1542 03-04 03-04 9.9 (17.34-10.84) 8.6 (15. In the last century. cacodylic acid.7 (11.4 (7.5 (36. and indium arsenides are used in the semiconductor industry.55 (7. though in some locations arsenite may be prevalent (WHO.10 (6.41 (7.2-61.1) 7. were used as treatments for syphilis.90) 75th 16.5-52. copper arsenates.50 (8.1 (38.80) 6.8) 34.1-18. and gray forms). pesticides. mostly for use in wood preservation (ATSDR.66-8.0 (15.7) 65.3-111) 78.5 (14.90) 16.

2001).4 (40. interval) 8. EPA. 2003.1) 7.25 (6. and some other seafood can contain organic forms of arsenic including arsenobetaine.93-8.4) 32.07-9. 2001).44) 6.51) 75th 14. Direct exposure to DMA and MMA may result from use of the two pesticides.2-46. Inorganic forms of arsenic demonstrate high acute toxicity.7-17.7-35. Extremely high groundwater arsenic levels. and arsenosugars.04 (5. dose level.18 (5.7 (9. and folate status (Chen et al.33 (6.33-10.0-38.7) 28.04) 7.1) 6.0-18.0 (17.06 (4. 2006.75) 13.. In aquatic sediments.g.66-8.99-9..23-7.1) 24. 2007.0) 1281 1276 03-04 03-04 03-04 8. arsenocholine. 2007.00 (6.30-9.32 (5. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.0) 42.7) 95th 50. organic arsenic can be converted back to methylated and inorganic arsenic.01) 7.50 (6.5) 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. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.5 (9.45) 5.9) 53.86-17. WHO.1 (11.8 (27.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .4 (12.3 (24.35) 7.2) 40.7-34.3) 9.0-69.8) 27. 2001).3-53.S.4 (11.47 (7. population from the National Health and Nutrition Examination Survey. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.13) 8.64 (7. 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.01) 11. Arsenate is reduced in the body to arsenite (oxidation state +3).96) 12. arsenic does not show biomagnification in the food chain (WHO.66-8. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. Smoking tobacco is also a source of inorganic arsenic.4-64.2) 90th 30.12-10. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.58-10.. 1988).8 (21.8-75.81-9.8-32.76 (6. kelp.8 (11.0) 12. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. cacodylic acid and monosodium methyl arsenate. Children may have additional exposures from ingestion of contaminated soils (e.8 (12.4 (42..5-17.24 (7. Fish. 2006.S.1) 58. shellfish. are used in enclosed ultraclean operations within the semiconductor industry.66 (7. have caused clinical arsenic poisoning. 2007.1) 8.25-9.3) 6. U.2 (12.31 (6.4 (24.2-15.4 (26.40) 8. 2001). arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.28-7. 2001).11 (5.6 (17. 2001). 2001). dust. 2001). inorganic arsenic is widely distributed within the body. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. so exposure to the general population is extremely limited. EPA’s maximum contaminant level (Hughes.3-64. but is poorly absorbed dermally (WHO.20-9. as observed in Bangladesh where millions of people have been exposed.93-9. 2001.10-8.4) 54.7 (11.59) Selected percentiles ( 95% confidence interval) 50th 7.47-6.3 (27.10-16.6 (35. age. Tseng.0) 26.44-11.9 (45.9) 13. mine tailings). though some reduction may occur in the gut prior to absorption.8 (20.. 2001.0) 33. Gamble et al.38-10.8) 22.S. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.6 (10.61 (7.5-120) 40.0) 14. WHO. and contact with CCA-preserved wood structures.7 (25.7-18. In aquatic organisms. NRC.7-188) 27.1-36.75 (5. trimethylarsine oxide (TMAO).0-26. Chowdhury et al.88 (5.6) 45.. After absorption.6-17.5) 17. selenium.88) 7.8-62. gallium arsenide and indium arsenide. 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.2) 15.41) 6.9-56. The semiconductor dopants.47 (6.3-41.1 (14. Steinmaus et al.3-62.0 (31. Though modest bioconcentration occurs in some aquatic life.5) 290 725 1542 03-04 03-04 8. Survey years 03-04 Geometric mean (95% conf.

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. 2001. lung. and childhood neurodevelopmental effects in observational human studies. 1998. population from the National Health and Nutrition Examination Survey. 2006. 2007). Acutely. and endothelial injury (Kumagai and Sumi. 2004).80) 1. 2001). 182 Fourth National Report on Human Exposure to Environmental Chemicals . hyperkeratosis. can cause peripheral sensorimotor neuropathies. see Data Analysis section) for Survey year 03-04 is 1. Chile). some of these effects may take years to develop. The organic forms of arsenic occurring in seafood have little known toxicity. 2001).. interference in signal transduction pathways.EPA.60) 1. Raml et al. fatty acid oxidation.. which can lead to dehydration and shock.S. Survey years 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004). 2001. Chronic arsenic exposure in humans is considered to be a cause of skin.. apoptosis. Taiwan. including drinking water sources with elevated arsenic levels (e.50) 1. leading to a decrease in adenosine triphosphate energy production.g. cytotoxicity. 2001). Studies of arsenic at levels typical of U. 2006) or when exposure occurs in smokers (Chen et al. Such actions may lead to decreased energy production. and by uncoupling oxidative phosphorylation (NRC. WHO. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.20 (<LOD-1. vomiting.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.60) 1. The U. and diarrhea. Bangladesh.. drinking water have not been associated with increased cancer rates (Schoen et al. 2006.S. Chronic human intake of arsenic at less than acutely toxic doses. 2000. noncirrhotic portal hypertension.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Cardiac arrhythmias. Arsenic has many actions demonstrated in cellular studies. arsenic trioxide) includes hemorrhagic gastritis with nausea.S.10 (<LOD-1. With chronic exposure. 2001).50) 621 725 1078 Limit of detection (LOD. and hyperpigmentation of the skin (NRC. 2004.20 (<LOD-1. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.10 (<LOD-1.0. Bredfeldt et al. NRC.. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. and bladder cancer (IARC.S.10 (<LOD-1. Cohen et al.20 (<LOD-1. including inhibition of numerous enzymes. NRC. WHO. hematocytopenias.20 (<LOD-1.EPA has established drinking water.. hypertension. Although arsenate is reduced in the body to arsenite.10 (<LOD-1. renal failure.. gluconeogenesis. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. Chronic elevated arsenic intakes have been associated with diabetes. increased oxidative stress.g.. and DNA repair inhibition (Cohen et al. and altered gene expression. 2007. and it also will inhibit succinate dehydrogenase. U. hepatotoxicity. but additional or confirmatory research is needed (Kapaj et al. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. cell transformations. Cellular glucose uptake.. WHO... substitution in phosphate metabolism. < LOD means less than the limit of detection. respectively. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. 2007. 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. food residue. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. peripheral vascular disease.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and production of glutathione may be affected as well. 2001).30) 1. 2006.10 (<LOD-1. 2001).Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. which may vary for some chemicals by year and by individual sample. WHO.

. 2004.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Compared with this Report. Pellizzari and Clayton 2006). 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Offergelt et al. population in NHANES 2003–2004 (Schulz et al.33 (<LOD-3. Valenzuela et al..69 (<LOD-3. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.. 2001). 1998.Metals compounds. 1999. Calderon et al. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. Josyula et al.. arsenic has been fetotoxic and teratogenic. 2003.61 (<LOD-3. 2007. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.. Shalat et al... 2006). population from the National Health and Nutrition Examination Survey. 2006).19) 3.S. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2001).. DMA produced bladder cancer in some chronic rat studies (Cohen et al.html.04 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 183 . Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. Pellizzari and Clayton. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. 2004...41) 3.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2006). 2000... 2007..cdc.00) 1. 2006.75 (<LOD-2. 1986). 2008. had decreased since the prior 1990– 1992 survey..89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1992. Meza et al.33 (<LOD-3. 2001). 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..70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 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. although urinary arsenic levels were not associated with CCA contact (Shalat et al. environmental levels) and health effects is available from ATSDR at: http://www.. 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. and were about two-fold lower than those for the U.S. Additional information about external exposure (i. Caldwell et al. 1999.. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. gov/toxpro2. WHO. but generally only at maternally toxic doses (WHO..18) 3. Shalat et al. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. Consequently. In a Nevada town where groundwater levels were naturally elevated. 2000)..80 (<LOD-4..e.. median urinary total arsenic levels in 4052 adults varied with seafood intake.S.atsdr. and the FDA has established a bottled drinking water standard. 2008). urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 2008). In the German Environmental Survey III of 1998. Vahter et al. 2006..50) 1.18 (<LOD-3. Survey years 03-04 Geometric mean (95% conf.75 (<LOD-2. 1999). In animal studies..S. population (Rubin et al. 2006). Pellizzari and Clayton. 2006. Levels of total urinary arsenic in the U.

2006).00-4. arsenite. 4.. 2008.10 (4. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. In the late 1980s. < LOD means less than the limit of detection.3 (21. In the residents of a Chilean town who consumed water with high levels of arsenic.700-1.19 (.70-21.20-190) 31.28) 1.e. Pellizzari and Clayton.83) Selected percentiles ( 95% confidence interval) 50th 1.5 (14.30) 10.20-3.05) < LOD .80 (4.5 (26.6 (25.45 (1.50) .8 (17.74 (1.8-50.. 2003). 2007). 2008). and TMAO.4. 2008.0) 4.Metals other areas of the world (Ahsan et al.900 (.6. geometric mean levels were about 70-fold higher than for the U.800) 1.70-21.20) 7.70 (3.6-44.50-6.62) 2.80-5.20 (4.90-29.7-22.900-1.500-1.20-25. Sun et al.. Aposhian et al.S. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. Caldwell et al. 2008). DMA and MMA compose most (about 75%) of the total arsenic species measured in urine..40-6. methylation capacity.68) .00-6.7 (21. dermal keratosis.. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.. Measurable organic arsenic species in this Report are three biologically generated environmental forms. and 0. 1985. MMA.g.0 (27. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.9-23.800 (.37 (1. respectively.3% of a representative sample of the U. Arsenate.3) 1284 1284 03-04 03-04 03-04 1. 2005.1-51.20 (.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. which may vary for some chemicals by year and by individual sample.40) 5. when seafood organic arsenic is subtracted).5) 29.S. 2008).7 (13. arsenocholine.S.. Blom et al... 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.70) 6.20) 3.8-40. 2005...700-1.4) 31.1-25.11-1..600 (.4) 23.4 (16. Chowdhury et al.8) 35. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and..00 (. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.800 (.31-1. The higher percentiles of total urinary arsenic levels in the U.00-1. population (Ahsan et al. Valenzuela et al. Some noncancer effects of arsenic (e.00 (1. Tseng et al.40) 75th 5. and two methylated metabolic products. 2007) with higher levels of arsenic in the drinking water. 2001).93) 1..30 (1.30) 2.10) 8.7) 15.43-1.9 (6.9 (7. population from the National Health and Nutrition Examination Survey..1) 45. These associations are stronger at higher urinary levels.3) 35. population (Sun et al. Also. 1990.66 (1.6 (11.00) 3.20 (2.17-1.400-.800-1.90-7. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. population in the NHANES 2003–2004 subsample. arsenobetaine. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.80) 1. 2000..2-38. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..10) 4.0-23.5) 32.S. and other factors such as nutrition. 1. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-35.80 (3. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. When seafood intake is avoided.50) 90th 16.9) 13.S. For residents of Inner Mongolia. Survey years 03-04 Geometric mean (95% conf.55 (1.3 (9.20) 18.30 (2.2 (6. China. with DMA.1-94.48-2.. vasospasm.00-12.800-4. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.0 (26. 2005.6 (13. population showed a higher contribution of arsenobetaine (Caldwell et al.8 (12. Individually measurable species resulting from inorganic arsenic exposure are arsenate. interval) 1. 2008). Caldwell et al. 2000.. and duration of exposure are also considered important.5) 292 728 1548 03-04 03-04 1. WHO. 2001. In most human studies. After recent seafood ingestion.8. arsenocholine.50) .1) 18.60) 1.0) 29. 1996. in NHEXAS 1995–1996.80 (.3-39.871-1.. Caldwell et al. DMA and MMA.7) 13. 2000.29 (1.70 (5. see Data Analysis section) for Survey year 03-04 is 0. Caceres et al.3) 95th 35.5) 621 725 1078 Limit of detection (LOD.40-7.60-3.6. and TMAO were detected in only 7.20 (1. arsenite. 184 Fourth National Report on Human Exposure to Environmental Chemicals .4-35.

1-18.8) 29..1) 26.29 (4. interval) 1.05 (.5) 17.15-1.93 (1.531 (.67) 1.Metals as with DMA.9 (25.S. In recent years.4) 292 728 1548 03-04 03-04 1.83) 8.30-1.44 (1.4) 32.7) 30.47 (2.91 (4.05) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70) 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.47 (1.4-21.11 (.64-29.88) 2.18-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.00 (3. not to imply a safety level for general population exposure.55) 1.901-2.25-7.1-36. 2001). which is below the ACGIH BEI (Caldwell et al.14 (1. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. Survey years 03-04 Geometric mean (95% conf.5 (18.68 (1.3) 1284 1284 03-04 03-04 03-04 1.19-2.28) 1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.58 (3. population for the sum of inorganic related species was 18.833-1. 2006. 2007).2 (12.15-4.7) 9.6) 19.79 (1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.88 (5.3) 95th 29.40) 1.00 (1.4-28. 1998.938-1.72) 12.37-2. 1986.9) 14.0 (9.53 (. 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.6-29. 1992.3-24.36) 2.6-46.21) 5.43) 75th 5.2 (12.13-39. Vahter et al. Caldwell et al.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 * * 1.786-1.50-15. WHO.32-7.1 (26.51) 5.. The 95th percentile of the U.612-1.400-.877 (..3 (10.7) 17.2 (13. Timber treatment workers had median urinary DMA levels that were about 15-fold higher than the general adult median levels reported in NHANES 2003–2004 (Morton et al.4-82.83) 2. 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.5-20.12) < LOD .9-18. 2001). 2003.82) Selected percentiles ( 95% confidence interval) 50th 1.40 (1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.16 (..43) 14. 2008). 2008).50-7.9) 32.91) 90th 16.5 (18.9 μg/L.4 (11.39-3.25 (. Offergelt et al.6 (9.78 (3.62-6.10 (.65 (1.54 (1. Information about the biological exposure indices is provided here for comparison.959-1.78-5.S.80) .29-14.6 (6.. Sun et al.9 (13.82) 4.4) 13.15-1. population from the National Health and Nutrition Examination Survey.0-36.67) 4.51-2.5) 26.909-1..2 (4.61-6.80-153) 17.45) 1.30) 1.6-32. 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.3 (10.638) 1.81 (4. Fourth National Report on Human Exposure to Environmental Chemicals 185 .4 (24..73-6.76-27..

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. Survey years 03-04 Geometric mean (95% conf.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.44) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.95 (<LOD-2.S. Fourth National Report on Human Exposure to Environmental Chemicals 187 .80) < LOD 621 725 1078 Limit of detection (LOD.08 (<LOD-4. population from the National Health and Nutrition Examination Survey.S.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 2.76) < 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. < 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.40 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 1.00 (<LOD-3. population from the National Health and Nutrition Examination Survey.00) 1.2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf.20 (<LOD-1.00 (<LOD-2.

17 (2.00 (6.0) 621 725 1078 Limit of detection (LOD.50-5.60-4.32 (8.00 (5.2) 10.67) 8.03-6.7) 13.94-3.00) 3.00-15.27 (2.45) 8.62) 4.34-4.80-5.00) 90th 11.00) 6.65-6.0) 292 728 1548 03-04 03-04 4.0 (10. Survey years 03-04 Geometric mean (95% conf.70-3.42) 3.00) 6.88 (4.0) 17.82-9.95 (4.28) 2.31) 4.5) 12.00-7.0) 9.06) 5.60-6. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic 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 1.0) 10.00-13.69-3.0-17.0-16.32-10.24-4.0-12.6) 292 728 1548 03-04 03-04 3.1-22.48 (3.73) 6.45 (8.44) 5.0 (9.14) 3.0 (9.05) 3.0 (14.00) 5.00) 6.34 (3.00 (4.00 (3.00 (7.11 (3.00-4.79 (3.94) 3.95-3.9) 5.34) 3.91) 75th 5.16-11.0) 11.13-4.50-15.00-7.48 (2.6) 1284 1284 03-04 03-04 03-04 4.0 (10.7) 12.57 (3.0 (8.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .29-4.0 (11.00) 6.90 (3.00-7.0 (13.00) 7.32 (4.00 (6.20-12.71 (4.52) 3. population from the National Health and Nutrition Examination Survey.8) 7.0 (13.80-3.70 (3.00 (3.69 (3.49) 10.08 (2.0-18.34-4.60-3.00-8.0) 17.24) 3. interval) 3.9) 12.20) 11.00-3.1-15.00-4.00 (7.61-11.12-4.59 (6.30) 3.78 (4.S.9 (11.0 (10.30 (7.00 (5. interval) 3.84-8.34 (3.65-8.0) 13.82) 3.8) 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 3.31-4.74 (2.57-5.0) 11.00-12.19) Selected percentiles ( 95% confidence interval) 50th 3.69 (3.20-4.18 (6.90) 2.10) 3.00-7.00 (3.16 (2.71-4.0) 9.7) 1284 1284 03-04 03-04 03-04 4.00 (3.17-4.38 (3.80-6.67) 9.78) 4.27-2.0-16.00-11.15) 4.46 (4.82-5.95-6. Survey years 03-04 Geometric mean (95% conf.27-5.3 (8.70) 5.0) 16.92) 3.05) 5.71 (3.98) 4.S.0) 95th 16.00) 4.70-12.00-4.00-15.00-11.45) 3.22) 4.44 (2.00-22.0-17.00-10.00 (5.0 (10.95-4.00) 4.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10) 6.00 (3.0) 14.12 (3.7.14) Selected percentiles ( 95% confidence interval) 50th 3.33) 3.85 (3.50 (4.0 (8.0 (9.0) 12.77 (3.81 (5.69-6.74) 90th 9.97-3.27 (3.3 (7.1-18.92-12.00-4.84-18.00) 9.25 (4.00-3.00 (6.03 (3.1 (8.5) 95th 13.0-25.72 (4.7 (10.3 (8.49-4.80 (4.16 (4.9) 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 Sample size 2568 03-04 03-04 03-04 4.00-11.0) 16.0 (12.00-5.86-7.00 (5.00) 3.09 (7.7-16.6-18. population from the National Health and Nutrition Examination Survey.4 (7.00 (5.00-4.00 (3.00) 75th 6.89 (3.0 (12.86-21.00-4.00-9.17-6.33-4.37 (3.55 (2.00) 12.6 (9.37 (2.73 (3.80) 7.00-12.0-19.90) 5.0) 9.80) 2.9) 13.5 (11.39-3.9 (7.05) 10.70-4.8) 7.0) 13.00-15.71) 3.60-7.61-16.11) 4.86 (2.

82-2.50 (2.00 (<LOD-1.43-3.85) 1.80-2.86 (2.77) 1.20 (1.30 (2.30-2.81) 1.30) 90th 1.10) 95th 2. Survey years 03-04 Geometric mean (95% conf.31-3.60) 2.00 (<LOD-1.05-1.86) 2. population from the National Health and Nutrition Examination Survey.17) 2.10 (1.93) .34) 2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.20) 2.16 (2.00) 1.10-1.36 (1.853-1.33 (1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.40) 1.80) 1.15-1.80-2.22) 3.90) 2.80) 1.80 (2.85) 2.30 (1.61) 2.40 (1.30) 2.37 (1.07 (1.50) 621 725 1077 Limit of detection (LOD.20 (1.60 (2.73-2.10 (1.23) 1.61-3. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.816 (<LOD-.50 (1.20 (1.80 (1.900-1.88-2.00-2.88 (1.40) 1.70-2.00) 2.63 (<LOD-1.60) 2.30 (1.00 (1.40-2.52 (2.20 (1.70-3.45) 3.84-3.50 (<LOD-1.18-1.00-2. see Data Analysis section) for Survey year 03-04 is 0.10 (.60-2.62) 2.985) 1.70) 2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.50 (1.00-4.10-1.10 (.35-3.31 (1.50) 1.50-2.30 (1.96-2.S.40-3.30) 1.20 (1.11-1.80 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-1.90) 2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .00 (2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample.57) 95th 2.90 (2.82-2.46-2.46 (1. population from the National Health and Nutrition Examination Survey.10 (<LOD-1.30-1.80 (1.20-1.53-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88 (1.07-3.00) 2.60) 1.S.70-2.30) 1.79) 2.00 (2.28 (1. < LOD means less than the limit of detection.40-3. Survey years 03-04 Geometric mean (95% conf.58) 2.00) 1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00-1.71-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07) 2.00) 1.10) 2.86 (2.86) 3.70-2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.9.10-3.28 (1.70-2.90) 1.40) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.40-2.40 (2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.22 (1.60 (1.20 (1.54) 90th 2.14-1.30-1.18-1.20-3.80 (1.33 (1.53 (1.36) 1.90 (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 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.S.0. population from the National Health and Nutrition Examination Survey. Urinary Trimethylarsine oxide (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Metals Urinary Trimethylarsine oxide Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. 190 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey year 03-04 is 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < 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.

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Smith AH. Environ Health Perspect 2006. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells. et al. 8/7/07 U. Nevada. et al.114(2):220-227. Meza MM.gov/iris/subst/0278. Vahter M. Chem Res Toxicol 2007. CruzGonzalez MB. Lu X. Gandolfi AJ. Available at URL: http://www. Buckley BT. Geneva 2001. Solo-Gabriele HM. pp. Schulz C. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Ochi T. Arsenic and Arsenic Compounds. Li B. Tseng CH. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Hoet P.epa. Yang MH. Liaw J.S. and metabolism of arsenic. Erratum in: Toxicol Appl Pharmacol 2006. Arsenic in drinking water-2001 update. Environ Health Perspect 2007. Lewis Publishers. Sci Total Environ 2006. Li L. Jhangri GS. Jin Y. Francesconi KA. Raml R. Boeckx M. Available at URL: http://www.114(8):1293-1296.S. Int Arch Occup Environ Health 1986. Wang Z. Sun X. von Ehrenstein O. January 2001 [online].115(4):648-652. urinary arsenic metabolites and human diseases: current perspective. et al. Tseng CH.25(1):1-22.htm. J Anal Toxicol 2006. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic.112(14):1375-1380. Br J Ind Med 1992. Conrad A. Black K. html. EPA). Fleming LE. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Available at URL: http://www. 3rd Ed.K. Zhang H. Nygren A. U. Huang YK. Int J Hyg Environ Health 2007. 2001. 8/7/07. Chung CJ. Marshall G. Genetic polymorphisms in MTHFR 677 and 1298. Kieszak SM. Morton J. GSTM1 and T1. Fok N. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Rahnster B. inorganic.115(1):151-157. Shalat SL.211(2):175. Huang YL. Lauwerys R. Kopplin MJ. Pellizzari ED. Nolinder P. Lauwerys RR. EPA).70(2):159-170. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley.113(3):250-254. Biggs ML. China. In:Industrial Chemical Exposure. World Health Organization (WHO). Kolossa-Gehring M. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Toxicol Appl Pharmacol 2007. Ferreccio C. Seiwert M.57(2):79-91. Burgess JL. J Toxicol Environ Health A 2007.49(6):387-393. Becker K. Seifert B. Boca Raton (FL). et al. Roels H. Environ Health Perspect 2005. et al. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals . Borja-Aburto VH.222(3):374-380. Washington (DC) National Academy Press. Environ Health Perspect 2007. Ibata K. Sun G. Environ Health Perspect 2006. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. Integrated Risk Information System. Kalman D. Goessler W. Friberg L. et al. Naranmandura H. 2nd ed. Rubin CS. et al. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood.org/documents/ehc/ ehc/ehc224.S. Garcia-Montalvo EA. Jimenez M.36-37. Clayton CA.gov/safewater/arsenic/regulations_factsheet. Arsenic. 2001. Jones RL. Arsenic on the hands of children after playing in playgrounds. Toxicol Appl Pharmacol 2005.S. Flanders WD. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Garcia-Vargas GG. Chen CJ. Yuan Y. Sonora. Mexico. Holmes AK. Environ Res 2004. Arsenic methylation. using a routine LC-ICP-MS method. Shipp M.96(2):119126. Li X. Arsenic exposure.htm. Valenzuela OL.20(8):1120-1125.210(3-4):271-297.Metals Kwon E. Xu Y. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS).inchem. Environmental Protection Agency (U. Rey OA. Steinmaus C.206(3):299-308. Buchet JP. EPA 815-F-00-015. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. Calderon-Aranda ES. 1998 [online]. Offergelt JA. Environmental Health Criteria 224. Arsenic. Suzuki KT. Environmental Protection Agency (U. Belson MG. Rumpler A.30(5):293-301. urinary arsenic speciation. National Research Council (NRC). Vahter M. Investigating childhood leukemia in Churchill County. Moore LE. A pilot study of children’s exposure to CCAtreated wood from playground equipment. Guidelines for Biological Monitoring. Arsenic in Drinking Water.367(1):80-88.epa. Mason H. Environ Health Perspect 2004. Fact Sheet: Drinking Water Standard for Arsenic.

20 (1.38 (1.80 (1.51) 1.61 (5.56 (2.47-1.50) 4.86-5.37) 1.66 (4.70) 3.39 (1.60-10. Small amounts of barium can be released into the air during mining and other industrial processes.20-1.40 (4.14-6.37) 5.35 (2.11-1.72) 75th 3.65-5.49 (1.31 (2.76-3.73-5. In nature.22) 6.10 (3.70-2.49-1.8 (6.52 (4.80 (2.70) 4.50 (6.46) 1. and 03-04 are 0. Barium compounds are also used commercially in paint.80 (1.44-2.87) 7.12 (2. fireworks.93-2.73 (5.95 (4. depilatories.80-7.12 (2.09 (1.10-4.26-1.37-8.54 (6. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).80-5.71-9.40-13.76-2.50 (4.30-2.40 (1.1) 9.70) 1. Barium salts have also been available as rodenticides.47-1.Metals Barium CAS No.87-9.51 (1.41) 1.88) 7. whereas others are practically insoluble (e.63 (1. such as brazil nuts.30-1.63) 1.15) 5.65) 1.34) 2.43) 2.36-1.00-3.61 (1.71) 95th 6.78-3.81-2.50 (4.90) 2.50 (5.54 (2.48 (6.71) 2.01 (4.36 (4.49) 11. 0.63) Total 1.75) 2.05% of the earth’s crust. tiles.80 (5. soluble forms of barium.30 (2.62 (1.15 (6.70 (1.50-6.24-1.80 (2.38) 8.24-1.87-14. Certain foods. see Data Analysis section) for Survey years 99-00.60 (1.31.00) 1.00) 6.60-6.95-6.73) 3.86 (4.94-6.15 (2.90-2.16 (1.74-3.68 (1. it combines with other chemicals such as sulfur or carbon and oxygen.43 (5.40 (1.00 (1.50) 2.57 (5.55-7.50-6.90) 1.15-11.00) 4.60) 3.78) 1.91 (2.29-5.36) 5.8) 9.44 (1.12-1.64-3.01-7.67) 6.76 (3.86) 6.56) 4.40 (5.15-1. In single dose animal studies. such as barium chloride.30) 4.54) 1.62) 1.11 (2.00-76.30) 8.37 (4.88 (5.10 (2.60) 1.78-2.49) 8.29) 5.20-6.18 (6.50-1. water. and 0.26) 5.87 (6.9) 5.04-2.10) 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. Workers employed by industries that make or use barium compounds can be exposed to barium dust.4) 7.41-3.60 (2.62) 1.20-1.36-1. bricks.54-8.87 (5.54) 1.48) 1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.15-1.05-2.46-1.53) 2.50 (1.35-1.28-1.80) 6.25 (1.65 (5.09 (2.77-3.08 (6.53-5.70-5.50 (1.35-4. 7440-39-3 Medically.88) 1.90 (1.00-8.49) 4.61 (2.88) 4.90) 2.40 (5.86 (4.86-4.34 (1.25-1.21 (1.50) 1.43 (1.08-8.20-1.54) 2.77) 1.10 (4.90-13.42 (1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .63) 1.48-4.38 (1.91) 6.16) 5.71 (2.32-1.26) 2.61 (3.4) 9.24 (4.82) 2.99 (4.2) 6. The general population can be exposed to low amounts of barium in air.06-1.69 (1.14-1.63 (2.52 (1.49-9.26-7.32) 8.30) 2.20 (3.12.47) 4. population from the National Health and Nutrition Examination Survey.38) 2.33 (1.20-8.70-8.30) 5.76) 1.11 (3.70) 7.57) 3.02 (7.90 (4.93 (4.60) 4. 01-02.07 (2.30-3.73 (6.98) 1.61 (1.00) 1.60) 1.39) 1. glass.27 (1.19-1.06-2.20-5.55-3.S.51) 7. respectively.40) 7.22-1.10-5.63 (8.62 (1.27) 2.35 (3.46) 1.12) 7.40) 3.35 (1.40) 7.18) 3.43 (1.30 (1.8) 5.80-3.48) 1.32-7.49) 2.22-1.20) 2.17-1.50 (1.30) 5.64 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.92) 2.90) 4.30 (5.21-8.14 (6.76-7.90 (6.54-1.80 (1.87-7.70) 1. 2001).56 (1.70) 5.56) 1. and food.30-1.03 (1.74) 3.65-8.30 (3.72) 4.40 (1.36 (1.50 (1.30-2.30) 3.70-2.65-1.43) 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 1.12) 6.74-2.40 (5.45 (1.50-1.48-4. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.59) 3.10) 3.35) 5.50 (4.4) 6.00 (2.54-1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60-2.90-9.64) 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 2.39 (1.30 (5.21-2.66) Selected percentiles ( 95% confidence interval) 50th 1.85) 1.91) 2.39) 4.70 (5.82) 1.20-8.51) 2.60-3.65) 1.15 (1.85 (2.82-6.50) 2.81-3.10) 5.g.53) 1.27 (1. and ceramics.60-6.59-11.43) 6. interval) 1.57-7.30-5.99-5.50 (2.61-8.20-1. Barium compounds are used by the oil and gas industries to make drilling muds.35-1.97 (1.34 (2.63 (5.75-3.56 (1.85) 1.71) 1.80) 1.30) 5.81-2.56 (6.96-2.21 (1.70-6.04-6.41-1.50 (3. barium sulfate and barium carbonate).20-8. are high in barium (Genter.73) 1.12.45) 7. Some barium salts are freely soluble in water.77 (3.78) 1.20 (4.93-8.80-2.87-3.19) 2. rubber.70-3.50 (1.11 (3.84) 5.18-1.28) 90th 5.31-2.72) 1.34 (1.65) 3.29-1.37-1.44-5..25-11.80) 7.39-1.

97-3. Wones et al.55-6.64) 7.23-1.52 (3.41) 5.27-3.96) 4.75) 2. Toxicity from soluble barium salts is rare. 2001).06) .24 (3.50 (4.86-7.80) 4.03-1.13-3.85-5.Metals was eliminated primarily in feces and to a lesser extent.18 (1.31-1.96-6. Following intravenous injection in animals.39 (2.25 (1.777-1.31 (4..96) 4.36-1.33 (1.38 (4.67-6.39 (2.47) 1.39) 4..74 (5. Chronic high doses in animals resulted in kidney damage (McCauley et al.0) 7.5) 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 1.89 (2. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.00 (3.68 (3.24-6.84-2.31) 5.34-3.8) 4.00) 1.01 (4.24-11.29 (3.76) 2.69 (5.04) 1. are not absorbed when administered.56-3.11) .58) 1.72) 4.45-1.00 (5.47) 4.24-1.62 (2.36 (5.34) 1.40 (1.10 (6.28-11. Symptoms following acute high dose include perioral paresthesias. hypertension.16-1.46) 3.51 (3.39-1.84 (3.49 (1.50) 1.81-7.43) 1.36-1.16) 11.58) 75th 2.37 (1. Perry et al.53) .48 (1.880-1.57) 2.832-1.47-8.60 (1.45 (3.34 (1. population from the National Health and Nutrition Examination Survey.34-1.00) 4.47 (5.71 (5.57-7.75) 1.62) 2.29-7.26-4.64 (1.26-1.09) 6.54 (2.01 (5. weakness. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.26) 4. The health effects of exposure to barium compounds depend on the dose.72) 6.03-1.24-1.10-2.73) 2.77) Total 1. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.19-1.00 (3.0) 5.55 (1.29 (1. interval) 1.36-2.46-22.00) 4.84) 2.38) 1.80-6.33) 6. in urine.84-5.39-1.86 (2.23-2.99 (2.40 (1.76 (2.29) 1.61 (4. Barium is not rated for human carcinogenicity.46) 2.80) 3.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .29-4.47) 1.44 (1.28-1.02) 4.03) 3.08-2.4 (5.26-1.59) 1.68) 1.35-1.59) 1.20-2.63) 1.53-21.45-1.64 (1.45) 1.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.55 (4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.18 (1.28-7.38 (4.37-2. NTP.59-7.77-5.56 (1.48-1.51) 4.28 (1.33 (1. and route of exposure.10-1.76 (4.96 (4. Insoluble barium salts.68) 3.33-4.915 (.59 (1.52-4.51) 4.20-8.38) 1.41) 4.81-6.02 (3.60 (2. 1990).46 (2..20) 4.99 (4.32) 2.24-3.42) 1.13-2.25-11.53 (2.56 (1.32 (2.45-8.703-1.38-7.32 (1.31-1.62 (1.73-2.27 (2.64 (1.26-1.00 (2.29-1.40 (1.42) 1.14-2.38-1.59) 2.58) 4. 1986).03) 2.31-1.76) 1.87) 1.921 (.29-4.06) 2.50) 1.32) 2.00-7.42 (4.55 (1.59 (1.52) 1.91-2.97 (4.55 (5.51 (1.79) 1.75) 1.20 (1.26-1.52) 7.68 (2.37 (1.23-5.92 (4.04) 5.02-5.3) 6.97-4.710-1.50) 2.76-3.754-1.22-1.881 (.963 (.54 (1.36 (3.24-6.22-2.38 (1.78 (2.57 (6.98 (2.64) 7.49-1.69-9.16 (1.75-22.39 (2.22-4.75-3.44-2. diarrhea.56) Selected percentiles ( 95% confidence interval) 50th 1.39 (3.32 (1.34-5.49-1.22-1.83) 3.38 (1.43-6.27-1.86) 5.96 (4.24) 3.83) 2.56) 4.51-3.82) 1.25) 4.10) 6.48) 2.01) 1.28-6.33-1.68-3.70) 1.96) 4.44-2.65 (2.4) 5.37-1.03) 1.73-4.11-2.60 (5.0) 6.3 (6.41 (1.2) 6.57-10.39-5. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.77) 1.19-2. and cardiac dysrhythmias.66 (1.92) 2.35-1.58 (2.36 (1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. water solubility.05-1.64 (1.36 (1.27) 7.29-3. 1994.68 (3.S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.62 (4.55) .10) 3.30 (1.35-3.24 (5.40-1.96) 7.21 (1.47) 10.77) 1.2 (3.89) 90th 4.47 (2.88 (2.19-1.65 (5.33 (5.54) 2.60 (2.52-10.46) 1.58 (4.04 (2. paralysis.52) 2.79-5.30 (1.41 (2.15-4. chemical form.63-4.48-3.38-5.75) 2.91) 2.08-1.45-6.48-5.88 (6. such as those used in medical radiographic procedures.28) 5.39-10.60 (1.19-1.48 (1.97 (5.33) 1.00) 6.54) 1.82) 1.00-1. a benign condition that may occur among barite ore miners.81-6.77) 5.49-1.12) 2.74) 1. 1989).72 (2.76 (3.91 (3.11) .97) 1.68-3.51) 6. 1985.61) 2.30) 2.38) 4.45) 95th 6.70) 4.90-2.74) 1.58-6.55-5.50) 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 1.36 (3.20-1. vomiting.02) .2) 5.41 (1.31 (1.45 (1.57-5.77) 1.891 (.37) 2. 1984.905 (.49 (1.48 (1.76) 2. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.70) 10.51 (1.99) 1.91 (3.

Pirkle JL. Pozzoli L. Powell C. and radium In: Bingham A. Weltle D. Available at URL: http://ntp. Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals 195 . Douglas BH.. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. 84-94. eds. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Zschiesche W. pp. Nordberg GF.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en.. New York: John Wiley & Sons. eds. 1989. calcium. Perry HM. Levy. Clin Chim Acta 2000. Sampson EJ. Gallorini M.html. Sabbioni E. blood. In: Inorganics in drinking water and cardiovascular disease. References Brenniman GR. 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. Stadler BL. Lack of effect of drinking water barium on cardiovascular risk factor. and 2003-2004 (CDC. Genter MB.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Howerton K.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. barium. Laurie RD.85:355-359. 2001-2002. 1990. p. Minoia C. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000.296(1-2):71-90.. and a drinking water standard has been established by U. Costa R.niehs. Jackson RJ. Magnesium. Biomonitoring Information Levels of urinary barium reflect recent exposure. Information about external exposure (i. Ting BG. et al. 1998). Inc. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). EPA. et al. Comparison of representative ranges based on U. p. Vouk VB. Environ Res 1998.gov/ntp/htdocs/LT_rpts/tr432. p. et al. Atlanta (GA). Trace metals in urine of United States residents: reference range concentrations.niehs. and serum of Italian subjects.95:89-105. National Toxicology Program (NTP). Int Arch Occup Environ Health 1992. Wones RG. 1984. environmental levels) and health effects is available from ATSDR at: http://www. Environ Health Perspect 1990.64(1):13-23. Cohressen B. 2nd Ed. Apostoli P. Barium. strontium. Exposure to soluble barium compounds: an interventional study in arc welders. Epidemiological study of barium in Illinois drinking water supplies. Paschal et al.e. Princeton (NJ): Princeton Scientific Publications. 1994. Investigations into the effect of drinking water barium on rats. 2001. 231-249.nih. 2005. Ash KO. 5th ed. Princeton NJ: Princeton Scientific Publications. Morrow JC. Reeves AL. 221-252 Komaromy-Hiller G. NTP. Kopp SJ. LA. Trace element reference values in tissues from inhabitants of the European community I.cdc. Frohman. patient population and literature reference intervals for urinary trace elements. McCauley PT.nih. Sci Total Environ 1990. Third National Report on Human Exposure to Environmental Chemicals.gov/toxpro2. et al. 1986.. 1985. Handbook on the Toxicology of Metals. Calabrese EJ. ed. 2005.S. In: Calabrese EJ. Patty’s toxicology.gov:8080/cs. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. [online]. Minoia et al.. Perry EF. Schaller KH.S. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. PS.html?charset=iso-88591&url=http%3A//ntp.197210.28(3):373-388. Advances in modern toxicology.atsdr.76(1):53-59.. J Toxicol Environ Health.. New York: Elsevier. 4/8/09 Paschal DC. Vol 2: Specific Metals. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Jr. Pietra R. the welders had no obvious adverse clinical effects (Zschiesche et al. ed. A study of 46 elements in urine.. In Friberg L. 1992). Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. 2000) to levels in NHANES 1999-2000 and 2001-2002.

7440-41-7 General Information Pure beryllium is a hard gray metal. which may vary for some chemicals by year and by individual sample. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. 0. or drinking water containing the metal. In studies of laboratory animals. 196 Fourth National Report on Human Exposure to Environmental Chemicals . and refined beryllium is used in mirrors and special metal alloys for the automobile. nuclear. beryllium is used in instruments. and 0. respectively. x-ray machines. and 03-04 are 0. and dental bridges. computer.S. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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 . soil. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. 01-02. population from the National Health and Nutrition Examination Survey.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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and can be found in mineral rocks. are mined for commercial recovery of beryllium. near some hazardous waste sites. Two types of minerals.140 (<LOD-. and machine-parts industries. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.130 (<LOD-.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. coal.Metals Beryllium CAS No. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.170) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and volcanic dust. bertrandite and beryl. Exposure to beryllium occurs mostly in the workplace.13. Beryllium compounds are commercially mined. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. the lightest of all metals. eating food. < LOD means less than the limit of detection.130 (<LOD-.13. aircraft. In medicine.13. and from breathing tobacco smoke. electrical. Low-level beryllium exposure in the general population can occur through breathing air. see Data Analysis section) for Survey years 99-00.

Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Fourth National Report on Human Exposure to Environmental Chemicals 197 .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 . The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. EPA.231 (<LOD-. Maier.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. respectively.346 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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.281 (<LOD-. 2002). Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. including contact dermatitis and subcutaneous nodules. which produces pneumonitis. or berylliosis. population from the National Health and Nutrition Examination Survey. IARC has classified beryllium as a human carcinogen.. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. 2003.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.S. * 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. Chronic beryllium disease. based upon excess lung and central nervous system cancers in studies of workers. 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 . is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. and drinking water and environmental standards have been established by U. Skin exposure can result in delayed hypersensitivity reactions. NTP considers beryllium to be a known human carcinogen. 1990).

Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. In other studies.org/documents/ehc/ehc/ ehc106. Morrow JC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. Given these results. Centers for Disease Control and Prevention (CDC).e..74:162-166. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. which approximate this Report’s limit of detection. et al. Third National Report on Human Exposure to Environmental Chemicals. International Programme on Chemical Safety (IPCS). Pozzoli L. Environmental Health Criteria. References Apostoli P. Comparison of representative ranges based on U.atsdr. Paschal et al. Andrew M. Biomonitoring studies on levels of beryllium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of beryllium than are found in the general population. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure.S. Apostoli P.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. 2001). Minoia C. Pietra R. Hamilton et al.158:165-190. Costa R. Schaller KH.23:827-839. 1990.296(1-2):71-90. Trace element reference values in tissues from inhabitants of the European community I. less than 0. 20012002.htm. Maier L. population were generally undetectable in NHANES 1999-2000. Paschal DC.157:388-398.gov/toxpro2.. patient population and literature reference intervals for urinary trace elements. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect.e. Am J Epidemiol 2003. Van der Venne MT.13 μg/L. Beryllium [online]. McCanlies EC.. Pirkle JL. and the fact that most NHANES participant levels were undetectable.76(1):53-59. Environ Res 1998. Sci Total Environ 1990. Howerton K. Hamilton EI. plasma and urine and a critical evaluation of reference values for the United Kingdom population. 3/27/08 Komaromy-Hiller G. et al. population are lower than levels in workers. 0.. Jackson RJ. 1998).S. VI.95:89-105. Ting BG. Gallorini M.12 to 0.1 μg/L).html. 2000. They reported urinary beryllium levels ranging from 0. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Kriess K. and serum of Italian subjects. it is likely that urinary beryllium levels in the U. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Sabbioni E. Minoia et al. and 2003-2004. blood.. Element reference values in tissues from inhabitants of the European community. Int Arch Occup Environ Health 2001. 106.Metals (i. 1990. Sabbioni E. Atlanta (GA) 2005. Sci Total Environ 1994. and the 95th percentile for males in NHANES 2001-2002.S. environmental levels) and health effects is available from ATSDR at: http://www.inchem. Trace metals in urine of United States residents: reference range concentrations. Sampson EJ. Clin Chim Acta 2000. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. HLA-DPB1 and chronic beryllium disease: a HuGE review. Clin Chest Med 2002. Levels of beryllium in urine for the U. A study of 46 elements in urine. Ash KO. Review of elements in blood. Genetic and exposure risks for chronic beryllium disease. Weston A.cdc.

as zinc sulfide) and to a lesser extent.600) 90th 1.400 (.20) .30-1.500-.00 (.300-.400) . plastic stabilizers.3. malleable. and 03-04 are 0.600) .400-.40 (1.00-1.60-1.300) 1.40 (1.400 (. The predominant commercial use of cadmium is in battery manufacturing.500) .600) .200-.30-1.00-1.368-.10 (1. Since 2001.10 (1.300 (<LOD-.500-.275-.40) 1.500 (.468 (.300 (.400) .300 (.600) .900-1.400) .331) .296-. Fourth National Report on Human Exposure to Environmental Chemicals 199 .300 (.300 (.600 (.600) .400-. EPA.60) 1.600 (.500-.500 (.600) .20) 1.300-.20) 1.60) 1.700) .900-1.403) . and incineration of municipal waste materials.30-1.700) .400) .600 (.00) .500-.425 (.300 (.400-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.600-.400-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400) < LOD .400) < LOD .300) .50-1.00 (.600 (.60) 1.50-1.10) 1.304-.300 (<LOD-.20) 95th 1.20 (.200 (<LOD-.40 (1.300) .500-.20-1.300-.00 (.40-1.500 (.300-.10) 1.40-1.40 (1.600 (.40) 1.20) 1.600 (.80 (1.600 (.255) .366) * * .400 (. or copper smelters (U.200-.00 (.300 (.200 (.300) 75th .300 (.3.40 (1.382 (.50 (1. cadmium use has declined in response to environmental concerns (http:// minerals. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00.266-.30 (1.20 (1.40 (1.30) .S.70) 1.412 (.Metals Cadmium CAS No.300-.300) .60 (1.900-1.gov/minerals/pubs/commodity/cadmium).300 (.500-. 7440-43-9 General Information Cadmium is a soft.00 (.500) .400-.400-.00 (.400 (.10 (.500 (.393 (.50) 1.20-1. respectively.00-1.378 (.400) .300-.500) .60) Total * .700-1.500 (.50-1.50 (1.400 (.500-.386-.600 (.30) 1.300-.400 (.300) .usgs.50) 1.337) .300 (.80) 1.333 (.70) 1.S.10) 1.900-1.70) 1.20) .200-.S.20) 1.283 (.400) .800-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil. Other uses include pigment production.200 (.90) 1.900-1.289-.40 (1.513) .300) .00 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (.400 (. < LOD means less than the limit of detection. lead. population from the National Health and Nutrition Examination Survey.00-1.304 (.80) 1.10 (1.600) .14.300 (.500-.400-.10) 1.500) .400 (.300 (.00 (.378-.70) 1.362-.500-.300) .421 (.00-1.700) .500-.300-.10 (1.600) .700 (.800-1.500-.20-1.300 (.313 (.00 (.800 (.30-1.300) .449) Selected percentiles ( 95% confidence interval) 50th .400) < LOD < LOD < LOD .500-.700) .500-.30) 1.216-.900-1.300-.600 (. U.400 (.300 (.300-.400 (.00-1.400) .400 (.200-.395 (.309-.300-.376-.470) * .20) 1.400-.367-.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 .600) .400) .10) 1.420 (.20) 1. which may vary for some chemicals by year and by individual sample.500-.900-1.600 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .400-.500 (.200) .10 (1.60 (1.200-.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 * * * * * * .326 (.00 (.600) .700) .400 (.600 (.400) .300-.441) * .300 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.452) .20-1.500) .10) 1.700) .500) .400 (.500-.500 (.400 (.400) .00) . Cadmium also may be emitted into the air from zinc.60 (1.900-1.00 (1. interval) .300) .900 (.403 (.60 (1.00-1.200) .300-.200 (<LOD-.300-.600) 1.300-.900 (.427) * .300-.20-1.300 (<LOD-.400) .300-.10 (1.359-.900-1.60 (1.20-1.20) 1.300-.700-1.300) .300 (<LOD-.600-1.700) .400) .600-. and 0.300) .50-1.500 (.600-.00-1.800) 1.700) 1. 01-02. 0.30-1.424) * .400-.50) 1.600 (.10 (1.800 (.600 (.700-1.300) .344) .00-1.304 (.300-.200 (.800) .400) < LOD .500) .460) .500-.10) 1.300-.500-.30) 1.500 (.300-.400-.50 (1.50 (1.300-. and nonferrous alloys.300) .300) .600 (.400 (.426-.800) . during refining of lead and copper from sulfide ore.400) .235 (.700) .361-.500-.10) 1.400 (.20) 1. coatings and plating.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 .900-1.20-1.00 (1.400) .

092) .700-.221 (.30-1.633-1.440-.394-.202 (.06) .400-.462 (. calcium.299) .175 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .255) .452 (.220-.17 (.354) .680 (.500) .38) 1.167-. 0.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.221) .919) . zinc.34) 1.240-.247) .510-.239 (.210 (..22 (1.126) . The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.436-. With chronic exposure.41 (.990) .963-1.148-.17 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.390-. potatoes.06-1.219 (.790 (.235) .28) 1.610) .875 (.440 (.748-1.810-1.426 (.551) .195-.290-. Diamond et al.257) .160-.200-.170 (.233) .980) .940-1..433-.220) .109-.559 (.540) .366-.539) .490) 1.065-.081) .237-.114-.179-.313) .440 (.077 (.507) .234 (.135-.390 (.510) .187 (. copper) and protein. population from the National Health and Nutrition Examination Survey.109 (.136) .061-.295) . To a lesser extent.713) .180 (.813 (.077 (.580) .06-1.38) . 2003).57) 1.766 (.476-.Metals 2000).308) .209 (.13 (.07-1.38) 1. see Data Analysis section) for Survey years 99-00. including many food crops such as cereal grains.25) 1.336) . however.74) 1. 2004a.190-. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg. Cadmium is absorbed via inhalation and ingestion.972 (.262) .858 (.189) .32 (1.733) .430-.52 (1.181 (.210 (.277 (.090) .281 (.165-.490) .456-.193 (.447 (.22 (.135 (.115-.229) .519) .918-1.09-1.198) .493-.243-.326) .177-.360) .83) 1.194-.241) .06.01-1.134) .148) .700-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.128 (.170-.714-1.238-.310 (.284) .06.351-.110-.184-.400-. Horiguchi et al.530) . 01-02.227 (.229) .980) .387) .839 (.388-.190-.229-.300) . Renal tubular and glomerular damage.210 (.800-.989-1.200 (.223 (.121 (.260 (.886) .200 (. drinking water is a source for cadmium intake.231) . rice.820) 1.160) .130 (.191-.157-.481) . and various seeds.20 (1.20) 1.140 (.191-.255) .519) .366-.306 (.350 (.206) .153-.170-.445 (.171-.13) .875) .458 (.47) 1.238) .260-.232) .12 (.753-.060-.393-.466 (.17 (.455 (.203 (.216 (.120 (.15) 1.196-.191 (.596) .330-.219 (.01) .329 (.700-.087-.623) .470-.255) .189-.980 (.282 (.302 (.492 (.211 (.219 (..310) .445 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.190-. 2003).843-1.72) 1.10 (1. For nonsmokers who are not exposed to cadmium in the workplace.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .327 (.210) .520-.500) 90th .25 (1.20-1.36) 1.818 (.265) .199 (. Cadmium in soil is absorbed by plants.890-1.545 (.20 (1.261-.220 (.265 (.13-1.479) .200-.733-.208-.061 (<LOD-.790 (.141 (.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 .100-.150) .480) .589 (.261-.226) .173) .112-.273 (.240) .246) .202-.860) 1.192-.20 (1.475 (.836-1.640) .090) . and 03-04 are 0.550 (.12-1.283 (..870) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.151-.220-. 2001).206 (.430) . interval) .817 (.15) .03) .04 (.806) .977) .741-1.300 (. wheat.067-.886-1.960) 1.26) 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.150-.633 (.214-.28-1. 1994).263) . and 0.253-. respectively.169-.848 (.249) . 2003.272-.498-.204 (.316 (.892 (.705-.390-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.880) .48 (1.01 (.362) .82) 1.730-.285-.192-.980-1.02-1.19) 1. Kikuchi et al.270 (.892-1.251) .412) .800 (.820-1.233) .51 (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 .230 (.189-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.320) .24) 1.067-.763-.855-1. ingestion through food is the largest source of exposure.279 (.289-.092 (. an inducible metal binding protein.107-.322 (.157) .203) .381-.38) .339) .607) .230) 75th .717-.980-1.211-..17) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.450 (.280 (.183-. 1999.551 (.193-. 2003).232 (..530 (.078 (.249-.260-.201 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.820 (.207-.270 (.372) .15 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals .222) .06.686-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein. The kidney is a critical target and shows the earliest sign of cadmium toxicity.43) 1.101) .257-.366) .160) .210 (.423-.890 (.817 (.** Survey Geometric mean (95% conf.160 (.04 (.210 (.482) . The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.175 (.210) .450 (.S.080 (.28 (1.230) .960 (.178-.

091 (.998) . can result from high dose chronic exposure.686 (.233 (.438-.166 (.204-.268 (.078 (.283 (.130-. 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.168-...084 (.196 (.297) .687-.806-1.789 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .538) .833-1.159 (.700) .223) .199-.176 (.423 (.240) .168 (. Staessen et al.296 (.719 (.560-.253 (.157-.150-.** Survey Geometric mean (95% conf.757) .225) .828) .208 (.181) .381-.09 (.481 (.221 (.222-.175 (. 2002.187) .293-.157-.123-.414 (.173-. 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. 2002.163 (.126 (.185) .146-.444-.075 (<LOD-.211 (.818) .767 (.158-. However. 1996.206-.919 (.220 (.691-.767) .074-.181 (.690 (.227-.304) .940-1.173 (.382-.716) .531 (.090 (.850) .678 (.263-.136-.382) . 2003. 1999).404) . Noonan et al.101) .927-1..630-.281) .063-.135) .404 (.434 (.865 (.690-.470) .156-.191-.614) .551) . During the 1950’s and 1960’s.199 (.215 (.421 (.663 (.12) 1.266-.607) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .674-1.979 (.282 (.876-1.446) . 2004).252 (..143-.696-.077-.247-.143-.192) .096) .10) 1.137 (.236-.856 (.440) .518) .261) .418-.917 (.536 (.311) .263 (.433-.239-.693 (.331 (.16) .187-.377-.941 (.154-.678-.418) .479 (.270 (.267 (.884) .144-.687 (.098) .304-.253) .432 (.261-.197-.316 (.181-.156) .241) .484 (.185 (.273 (.113-.131-.161-.645-.170 (.175-.288) .184-.250) .208-.754) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.288-.191 (.210 (.170-.533) .143) .156 (.245 (.112) . 2002.917) . 2000.07) .17) .182) .176 (.162 (.545) .826-1. Horiguchi et al.559-.647-.106) .083-.209) Selected percentiles ( 95% confidence interval) Sample 95th .235) .051-.501 (.289) .329 (.940 (.653) .795) 1.207) .16) 1.292) .985 (..335 (.183) .449) . 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.562-.093 (.426-.147 (.207-.792 (.415) .175 (. 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.490 (.00 (.667) .240) .219 (.267 (.666-.308 (.708-1. Fourth National Report on Human Exposure to Environmental Chemicals 201 .423-.181 (.205 (..769 (.716-.516-.440) .784) .779 (.107) .813-1.08) 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.431) .700 (.229) .08) .591 (.07 (.234) .622 (. 2004b).476) .325 (.757 (.163) .085 (.830-1.05) 1.183 (.300-.783) .256-.740 (.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 .727-.137-.091) .S.387-.950) .827) .830) .182) .261 (.212 (.352) .201-.321) .177) . 1999)..929) .02 (.318 (.906) .712 (.123-.725-1.688-.210 (.266) .184-.091 (.364) .075-.668-.154 (.491-.722-.507-.839) .398-.219 (.391-.184) .238) .414-.094) .178-.690-.191) . 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.438) 90th .182) .388-.340) .274) 1.202 (.962) .931 (..178) .338 (.200 (.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 .783 (.255-. most often a result of occupational exposure (Roels et al.242) .078-.308) .147-.280 (.470) .343-.38) .873 (.350) .086 (.288 (.06 (.541) .147-.122 (.00 (. At lower environmental exposures.148 (.159 (.226) 75th .171-.856) ..289) .189-.909-1.085-.140-.190 (.412 (.218) .813-.631) . 1999).097) .232) .136-.100 (. Jarup et al.071 (.194-.084-.850) .316) .168-. population from the National Health and Nutrition Examination Survey.718 (.650-.234 (.111-.067-.210) .729 (.140-.104) .387 (.232) . Olsson et al.473 (..247-.281) .247-.225) .228-.802 (.174-.617 (.336-.224 (.537-.190 (.216-.487 (.472) .500-.209) .13) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.278) .104) .234-.238-.826-1.441-.198) .818) .221-.303) .874-1. interval) .

EPA. 2002. Jarup et al. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Olsson et al... Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. 2004. Jin et al.. 2006. Wennberg et al.. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. Olsson et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Further research is needed to address the public health consequences of such exposure in the United States.1 mg/L (Alfven et al. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. Staessen et al. 2003. Ezaki et al. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. data (CDC.. 2003. Becker et al.. 2004. 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.cdc. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.S. 2006). 2003). 2004. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.. 2003. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . 2005.. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity... 2004).. respectively.S. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine).. Wilhelm et al. Noonan et al. 2006).gov/ toxpro2. Friedman et al. as may occur from welding cadmium-alloyed metals. 2006. 2000.... Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. Animal studies have demonstrated reproductive and teratogenic effects... 2004b).. Salpietro et al.. 2000. In the typical environmental exposure. Staessen et al. 2005). CDC. Ezaki et al. For NHANES 19992000... 1999.. Information about external exposure (i... 2002). 2000. Moriguchi et al. intermediate in former smokers and lower in never-smokers (Becker et al. maternal blood or maternal urine and birth weight (Nishijo et al. Becker et al. Jarup et al.. 2003. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Komaromy-Hiller et al. 2003. Mannino et al. Creatinine-corrected urine cadmium values in U. 2002) and length at birth (Nishijo et al.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. 2003. 1988).. 1999). 2005. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Horiguchi et al. 2002.atsdr. Acute and heavy exposure to airborne dusts and fumes. 2002. 2002.46 mg/gram of creatinine) (Ezaki et al. 2002. 2002). Olsson et al. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U.. approached these values associated with subclinical changes in renal function and bone mineral density..html. However. 2004b..e.. Cadmium can produce lung.. with peak values observed in the fifth to sixth decades (CDC. 1996. 2005. respectively. and drinking water and environmental standards have been established by U. potentially fatal pneumonitis (Fernandez et al. 2002)... 2002. Both IARC and NTP consider cadmium a human carcinogen. 1999). In postmenopausal women. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Staessen et al. 2005. 2002).. Horiguchi et al.. not to imply a safety level for general population exposure.. 2004.. two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1. Women had higher blood and urine cadmium levels compared to men of similar ages.. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. Becker et al. In adults aged 60 years and older.. Wennberg et al. 2000).S. 2002). 1996). Occupational standards are provided here for comparison only.26 and 3. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Zhang et al.. environmental levels) and health effects is available from ATSDR at: http://www.. Suwazono et al. has resulted in severe.

Persson B. 4/8/09 Alfven T. Jones RL.24:717-724.45:43-52. diabetes mellitus. 102:10581066. Mannino DM. Howerton K. Moriguchi J. Ye T.205:297-308. Lancet 1999. Machida M.66(Pt A):2141-2164. Ikeda Y. Becker K. J Toxicol Environ Health 2003. Wang H. Tsukahara T. Hellstrom L. Zhu G. Jin T. et al. Atlanta (GA). ShkiryakNizhnyk AZ. Palomar M. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Horiguchi H. Choudhury H. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Lepom P. Gadea E.110:699-702. Miyamoto K. Friedman LS. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Nerbrand C. Fayers PM.354:1508– 1513. Thorax 2004. Miyamoto K. Komaromy-Hiller G. Lukyanova EM. Occup Environ Med 2000.html.59:497]. Kikuchi Y. Nomiyama T. Fatal chemical pneumonitis due to cadmium fumes. 196:114-123. Cadmium fume inhalation and emphysema. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Sasaki S. Greves HM. References Akesson A. Environ Res 2004b. Serra J. Grubb A. Third National Report on Human Exposure to Environmental Chemicals. Uemura T. et al. Carlsson MD. Davison AG. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Bellerup P. Hotz P.000 women in the Japanese general population: a nationwide large-scale survey. Available at URL: http://www. Venables KM. Berglund M.296(1-2):71-90. Environ Res 2006. Environ Res 2004. Jarup L. Buchet JP. Toxicological profile for cadmium update. Machida M. Comprehensive study of the effects of age. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Darbyshire J. Toffoletto F. et al. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U.46:372-374. Becker K. Ash KO. Costa R. Ikeda Y. Sanz P. Vahter M. J Occup Health 2003.atsdr. 2005. Schulz C. Environ Health Perspect 2005. Krause C. Lundh T. et al. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Agency for Toxic Substances and Disease Registry (ATSDR). Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Kaus S. Int J Hyg Environ Health 2002. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers.S. Kumagai N.cdc.59:194-8.102:83-89.13(11):1627-1631. Environ Health Perspect 2002. Olfactory function in workers exposed to moderate airborne cadmium levels. Chislovska NV. Fukui Y. Environ Health Perspect 1994. Seiwert M. Moriguchi J. et al. Int Arch Occup Environ Health 2003. Kaus S.96:353-359. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. et al. Toxicol Lett 2004. Fernandez MA. Anthropometric. Savage-Brown A.1(8587):663-667. Horiguchi H. Centers for Disease Control and Prevention (CDC). German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. et al. Thayer WC. Mucha A. Jarup L. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Neurotoxicology 2003. iron deficiency. Clin Chim Acta 2000. 1999 [online]. Chiappino G. Consonni D. Furuki K. Ezaki T.gov/toxprofiles/tp5. Kundiev YT. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Elinder CG. et al. Ukai H. Furuki K. Oguma E. Pickering CA. Occup Med 1996. Schulz C. Diamond GL.57:668-672. Toxicol Appl Pharmacol 2004a. Lison D. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Akesson A. Tsukahara T. et al. Takebayashi T.95:20–31. Bernard A. Alfven T. Lancet 1988. Nordberg G. Seifert B.76:186-196. Bregante G.S. Lidfeldt J. Mascagni P. Taylor AJ. Ezaki T. Holguin F. 206:15-24.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. Stock AL. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. possibly better than b2microglobulin. Seiwert M. Oguma E. environmental. Lauwerys R. Fourth National Report on Human Exposure to Environmental Chemicals 203 . et al. Okamoto S. patient population and literature reference intervals for urinary trace elements. Comparison of representative ranges based on U.148(1-2):11-20. Bo M. Vahter M. Fukui Y. Nermell B. population. Sasaki S. Dekio F. Int J Hyg Environ Health 2003.

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16-6.20) 4.80-10.13-8.60) 7.07-11.05-5.62 (5.90-10.6) 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 4.73-11.49 (4.89) 5.3) 10.90 (6.54-11.60-7.00-9.70) 5.13 (8.08) 7.70 (6.7 (9.99-11.91-8.40-5.4 (9.34 (4.8 (11.5) 10.10 (6.09) 5.52-9. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.14.90-12. see Data Analysis section) for Survey years 99-00.68 (7.17) 4.35-5.40) 5.4) 10.9) 8. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.82) 5.42-7.10-9.71-9.2-12.1 (11. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.7 (10. Radioactive 137Cs has been used medically to treat cancer.40) 7.59 (5.38) 5.8-13.99-11.26 (3.64) 5.64 (4.27-5. although cesium was generally of low toxicity when given to animals.20 (4.64) 5. and 03-04 are 0.9 (11.9 (11.01) 7.70) 5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .79 (4.81) 4.2 (9.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.27) 4.3-15.5) 12.4) 11.95) 5.3-13.7) 11.0) 11.60-6.59) 7.6 (9. diarrhea.34) 9.63 (4.7 (10.68) 9.05) 5.89) 4.20-8.14.59-5.9 (10.03 (4.97-7.71 (4.1-12. 01-02.30) 7.2 (9.8 (10.98 (7.17-6.94 (4.56-11.64-5.30-5.61-6.80 (8.20-5.7 (10.25) 4. nausea.03 (4.37) 7.45-8.10 (6.5-14.0) 12.59-5.57-5.77 (4.7) 10.4) 12.26) 4.23-4.5 (10.6 (11.60-6.80-10.5) 9.25 (3.3 (8.80 (4.01-6.22-4.70 (4.1 (10.70-5.90 (4.2-13.90-10.14 (4.00) 4.9) Total 4.87 (4.7 (9.00) 7.0) 9.81 (4.9) 12.81) 9.92-13.13 (5. semiconductors.94) 4.07) 4.67 (4.50 (4.00-10.70) 7.80-11.53 (6. scintillation counters. Little is known about the health effects of this metal.05) 5.60 (7.70 (5.91 (7.50 (6.8) 12.00) 6.32) 4.50-7.89-5.1) 11.30-10.0) 12.55 (4.6 (9.97) 4. For absorbed cesium salts.80) 7.5-16.7 (8.72-7.84) 8.05-5.2-13.15-8.10-5.49 (5. However.17 (6.62) 4.90) 4.6 (9.3) 12.30 (6.99-6.86-11.3 (8.7) 10.7 (11.0 (9.04) 7.60 (8.59-5.3-13.81-14.70 (8.10 (8.90) 7.61) 7.87) 5.0) 10. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Most human exposure to cesium occurs through the diet. photographic emulsions.08-5.04 (4.20) 8.43 (5.74-5.4 (9.64-10.1) 10.71) 4.82-4.9 (10.2) 11.12-11.5 (8.52) 7.10-7.90) 5.60-5.20 (6.84-5.9 (11.76-6.74) Selected percentiles ( 95% confidence interval) 50th 4.4) 12.29 (4.45-5.20-4.2) 12.86 (7.24) 4. cesium hydroxide is corrosive and irritating at high concentrations.7 (9.0 (10.56 (4. and clay.84-9.47-4.72) 4.7) 11.36 (3.16-6.6 (9.97 (7.4) 9.54) 4.80-10.40-5.71-5.93 (4.60-7.77 (9.66 (7.7-14.70 (9.6) 10.55 (7.3) 10.10 (8.9) 11.6 (11.32-5. infrared lamps.22 (4.30) 5.20-7.33 (5.2.1 (9.50 (4.00-8. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 11.02 (4.8) 11.74 (4.84 (4.0-15.12-5.88 (8.50 (7.90) 5.36) 3.13 (7.80 (4.1-13.46) 7.8) 12.8 (10. and cardiac arrhythmia (ATSDR.56) 5.63) 6.40-11.00-8.50 (4.21 (4.56 (4.40-7.49) 75th 7.86-12.39-4.09-5.99) 7.1-12.49) 4.29) 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 4.0) 12.47-8.35 (4.90-12.39) 7.1) 9.01-8.87 (4.69-6.00 (7. 2004).4 (10.08 (6.80-6.10-8.50) 5. interval) 4.12 (4.87-7.70-8.70 (8.3) 10.S.2-13.27 (7.40) 5.2-14. and 0.96 (6.1) 9.80 (8.25-5.40-11.84) 5.0) 11.8) 9.44 (8.36 (6. and high-power gas-ion devices.08-5.3) 10.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90) 9.64) 4.80-13.8) 12.26-11.4) 10.60-12.31-8.12) 5.77-8.1) 11.55-11.4-13.50) 9.83-4.4) 95th 11.53-11.37) 5.5-13.81) 4.43-8.0-13.5-14.60) 7.70 (6.63-4.80 (8.21) 90th 9.20) 5.8) 9.94 (4. Whether cesium compounds are carcinogenic is unknown.95 (3. soil.62 (5.90-10.95-4.40-5. respectively.94-4.20) 7.00-4.80 (4.08 (7.77 (9.03-4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.98 (7.73-5. and as polymerization catalysts.23) 9.60) 5.33-5.Metals Cesium CAS No.9 (11.30 (6. population from the National Health and Nutrition Examination Survey.42) 7.71 (8.40-5.33 (6.71-8.40 (4.42) 6.99) 9. 0.83) 6.3) 9.6) 11.87 (4.90-8. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32 (3.26) 7.35 (4.

79) 6.36-6.13-9.3 (9.33 (5.06 (5.64 (4.51 (3.18-7.30) 10.25) 4.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.60 (3.74-11.87) 5.07) 8.51) 4.30-4.00-9.61 (7.21-5.6 (9.27-6.62) 5. Two small studies of European populations reported urinary cesium levels similar to U.74 (4.23 (7.83-7.76-9.48-6.84-7.47 (4.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.26 (4.93-7.30 (3.24 (3.99 (3.33-3.20-4.51 (4.07 (5.99-4.50 (7.05) 3.67) 5.77-5.16-8.10) 7.30 (7.18-6.68) 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.81 (4.88-4.40-5.83-6.99-9.17 (6.05-3.51 (7.47) 6.2) 11.0) Total 4.31-6.72) 4.35 (3.02 (5.58-5.38-12.84-9.97-4.17) 4.39) 5.35) 3.6) 6.48) 90th 7.08 (3.45-6.13-9.1) 11.83) 8.07) 8.7-12.00-5.9 (9.97) 8.24-4.S.63 (7.99-9.14-6.90-8.47) 6.15-11.77 (7.65-4.14) 4.58 (6.S.00 (8.37) 4.46-8.39) 8.6 (9.02-4.92 (5.48) 7. interval) 4.90-3.54 (4. population results shown in this Report (Alimonti et al.74 (5.24-10. 2004).85) 5.27 (8.98 (7.44-5.42 (5.57) 3.95) 8.33-8.05-4.45 (4.8) 6.18) 8.50) 4.21 (2.11 (5.74) 75th 5.59-8.26 (3.20) 5.94) 7.41) 9..95-12.46-4.08) 4.42 (4.31 (4..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 .78 (3.90-8.20-8.22-11.91-7.5) 7..93-9.54 (5.38) 10.47 (7.96-4.82-4.66 (5.86 (4.3) 11.04) 5.77) 4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.22 (3. population from the National Health and Nutrition Examination Survey.41) 4.96) 4.13 (3. Using clinically submitted specimens.28 (4.06) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.14 (6.70 (7.95) 10.46) 6.35 (4.68) 6.75 (6.88-10. (2000) found urinary cesium levels that were slightly lower than those reported for the U.73-4.91 (5.72 (4.17-4.10-4.55) 4.08) 3.16) 5.36-3.44 (4.58 (4.64) 4.29-3.73 (3.44) 3.28) 8.99) 4.95 (3.56-10.60-20.68) 4.5) 9.52-5.29-3.9) 10.82) 7.42-4.64) 5.87 (5.21-3.08 (6.07-4.35-11. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.8) 10.68-11.63) 6.20-4.96-4.05 (4.68 (4.75-11.85) 4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.28) 7.00-4.11 (5.30-4.98) 5.2 (8.12-6.66 (6.61-3.85-4.50) 4.91-6.14-7.31-4.7) 10.51 (3.64) 9.3) 9.3 (10.58) 8.91) 5.19-6.15) 95th 8.2 (8.70) 6.04-5.47) 7.50 (5.08 (5. population.70) 7.41 (5.37-3.10 (3.00-8.10 (3.91 (5.17) 9.79) 4.26-6.06 (3.27 (6.60-10.64 (8.4) 10.62-8.44-9.72-5.8) 5.03-6.30 (4.3 (8.28 (5.79 (5.21-4.91) 4.63-6.81 (4.43-11.50 (6.0 (7.35-7.43) 8.50-5.00-10.03) 6.75 (7.15-4. and were also roughly similar to those in this Report.30) 10.76-6.91) 5.43 (4.25) Selected percentiles ( 95% confidence interval) 50th 4.41-4.12) 3.29) 4.46 (7.16-8.90 (7.58) 3.56) 3.46 (8.95 (5. Minoia et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.13) 7.5 (9.96 (4.27) 4.38-7.60) 3.51 (4.53) 3.84-7.55-5.06) 5.43 (3.15 (7.41-7.77 (4.78) 4.33 (5.10 (5.98) 5.77 (6.54 (4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.78) 4.7) 10. 1990).08-3.71 (7.19-3.53) 6.5) 9.50) 8.20-4.91-9.79) 9.80) 6.3-15.22) 6.59) 4.50) 4.56) 4. 2005.36-10.74) 3.03-5.08) 4.S.01-8.27 (6.60 (5.18 (7. Komaromy-Hiller et al.09) 8.67 (6.31 (4.38 (3.65-3.44 (8.79-5.05) 6.09) 4.89-4.27-4.92) 3.95) 4.54 (3.34 (5.04-11.53 (6.42-4.87-4.00) 6.56) 4.40) 6.08-7.56 (4.03) 5.49) 3.29) 4.16-5.00-5.12 (3.84-11.14-4.04) 6.09 (4.55 (3.53 (4.43 (8.39 (5.63 (4.67 (5.66-6.3) 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 3.14) 4.47) 4.66 (5.43 (4.63-6.96) 4.65 (6.64-6.41 (8.05-3.84-9.97-5.43-6.9 (10.40) 7.71) 6.98 (6.78 (3.38 (3.63 (6.95-6.0) 7.42-6.41 (4.8 (9.94 (5.29) 5.

A study of 46 elements in urine.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Howerton K. blood.atsdr. Assessment of urinary metals following exposure to a large vegetative fire. Rapid Commun Mass Spectrom 2005. Sewell CM. Sabbioni E. Third National Report on Human Exposure to Environmental Chemicals. Clin Chim Acta 2000. Wolfe MI. Komaromy-Hiller G. Spezia S. Pozzoli L. Comparison of representative ranges based on U. Fourth National Report on Human Exposure to Environmental Chemicals 207 . and serum of Italian subjects. Sci Total Environ 1990.14:120-128.S. cesium. Minoia C. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. 2000. J Expo Anal Environ Epidemiol 2004.2004 [online]. Atlanta (GA) 2005. Voorhees RE. Wood CM.gov/toxprofiles/tp157. Mott JA. Gallorini M. Toxicological profile for cesium. Apostoli P. Mincione G. Pietra R. Centers for Disease Control and Prevention (CDC).html. et al. Ash KO. antimony and tungsten. Costa R.19:3131-3138. patient population and literature reference intervals for urinary trace elements.296(1-2):71-90. Gatti A. et al. Trace element reference values in tissues from inhabitants of the European community I. Forte G. et al. Paschal D. Available at URL: http://www.95:89-105. New Mexico.cdc. 4/8/09 Alimonti A. Ronchi P.

60 (1.410-.364-.410-.710 (.367 (.570 (. and 0.670 (.440-.550-.340-.590-.428-. and fertilizers.06 (.333-. 0.03) 1.810) .590-.890-1.640) .950-1.28 (1.950-1.Metals Cobalt CAS No.405-.480 (.520) .310 (.760 (.67) 1.07.16-1.590) .17 (1. seawater.390) .13) 1.564) .850) .460 (.520-.48) 1.350-.452 (.410 (. steel-belted radial tires.S.04-1.450) .348-.460 (.398 (.740-.460) .420 (.316 (.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 .490-.319) .81) 1.36) 1.33-1.359 (.81) 1.22) 1.334) .580 (.380 (.410 (.370-.740-.900-1.308-.461 (.940-1.285 (.14-1.560 (.519 (.05) 1.21) 1.291-.520 (.12) 1.515 (. 01-02.26-1.259-.450-.330-.810) .07.16 (1.750 (.710) 1.540-.06-1.750 (. respectively.620-.380 (.680 (.08.920-1.S.316-.23-2.830-1.880 (.430 (.487) .336-.620-.800) .490-.820 (.920) 1.670-.350-.480 (.68 (1.294 (.590 (.12) 1.373-.610 (.386) .800-.01 (.390-.53) 1.850-1.430) .420) .47 (1. Cobalt compounds are also used in manufacturing battery electrodes.700) .03 (.370) .00) . hard metal (alloys of cobalt and tungsten carbide).370-.427-.630 (.59 (1.750 (.424) .710) .380 (.06 (.550) 90th .33 (1.960-1.270-.16 (.313) .331-.45 (1.523) .360-.450) .04-1.430) .690-.330) .04) 1.430 (.890) 95th 1.65) 1.410 (.454 (.790 (.660) . blue-colored pigments.580 (.496) . Cobalt is used as a drying agent in paints.431) .04 (.680) .370 (.404) .379 (.09 (.14) .16 (1.450) .339 (.16-1.950 (.398) .460) . It is emitted into the environment from burning coal and oil and car and truck exhaust. population from the National Health and Nutrition Examination Survey.374 (.99) 1.870 (.660) .08-1.270-.320 (.670-.373) .388-.680) .840) .510) 1.07-1.343 (.410) .340-.430-.410 (.330 (.890-1.09 (.369 (.379 (.434 (.500 (.372) .620-.520 (.940-1.610) .900) .950 (. and inks.500) .520) .630-.980-1.610) . hard metal or in combination with other elements.890) .730) 1.790) .340) .47 (1.910-1.820 (.760) .47) 1. and soil.32 (1.73) 1.50 (1.650 (.650-.399) .32 (1.348-.75 (1.530) .460) .800-.338-. It is also a component of porcelain enamel applied to steel bathroom fixtures.850-1.650 (. diamond-polishing wheels.32) 1.570) . automobile airbags.900-1.19) .64) 1.340) .26) 1.570) .390 (.28-2.56) 1.660-.24 (.450) .414) .352 (.640) .870-1.810-.327-.890-1.350 (.540-.570-.860 (.600-.380-.360-.690 (.32) 1.583) .07-1.416) . Cobalt may be released into the systemic circulation of patients who receive joint prostheses that are Urinary Cobalt Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.670 (.690-.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 . Usual human exposure is from food sources.610-.25-1.463-.435 (.499 (.380-.01-1.17 (.900) .540-.394) . industry is imported or obtained by recycling scrap metal that contains cobalt.03-1.15-1.390 (. and kitchenware.630 (.880-1.410) .581) .870 (.600) .620) .03) .05 (.370-.92) 1.42) 1.393-. and in synthesizing polyester and other materials.08) .450-.05 (.20 (1.900) .03 (.355-.400-.350) 75th .410-.390 (.770) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .420) .340 (.940 (.44) 1.290-.26) Total .16) 1.580 (.930 (.950) . and 03-04 are 0.570-.26-2.17 (1.47) 1.15 (1. varnishes.01-2.37-1. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.790-.980) .530 (.930-1.410 (.16) 1. see Data Analysis section) for Survey years 99-00.375 (.470 (.02-1.740 (.28 (1.850) 1.32-2.750-.48) 1.333-.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 .310-.300 (.371 (. and magnetic recording media. The cobalt used in U.540-.550 (.543) .431) .417) .22-1.930) . shiny.350-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.28 (1.01 (.07 (.270-.09) .377-. interval) .700) .22 (1.460-.670 (.540) 1.50) 1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.502) . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.470) .46 (1.520-.680 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.820 (.04-1.17-1.300-.301 (. Cobalt compounds are used as catalysts in producing oil and gas.480-.39) 1.03) 1. Cobalt occurs naturally in airborne dust.280-.530-.360-.430 (. large appliances.418 (.600 (.24 (1.52 (1.23) .469-.520-.419) Selected percentiles ( 95% confidence interval) 50th .520 (.305-.640) .520-.29 (1.465) .520 (.

369 (.488) .533 (.938) .33) 1.268 (.239-.669) .952 (.600-.895-1.25 (.35) .662) .27) 1.760-1.632-.10) .833-1.247 (.355) .857-1.955) .16 (.331-.704-.279 (.444 (.215-.289) .306) 75th .29 (1.353-.898 (.626-. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.667-1.259-.932-1. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.616-.368) .647) .83) 1.640) .917) .679-.708) .419) . interval) .00 (.329-.879-1.683-.329 (.319-.523 (.17) .335 (.290 (.585) . and to a lesser extent.457-.554 (.975 (.286) .543) .15 (.534-.476-.04 (.402 (. refining or processing alloys.12-1.500 (.234 (.248-.243-.949) .360) .630-.804) 1.11-1.500-.609) .435-.599) .744) 1.353 (.393 (.02 (.615) .28) 1.861-1.582-.378-.750) .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 .29) . Smith et al. in the feces.983) .990) .301) .872 (.275-.630-.561) .534 (.505) .594) .29 (1.728) .733-1.60) 1. 1994).976 (.313 (.635 (.03 (.611) .27) 1.786-.S.313-.830 (.737 (.309) . Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).847) .327-. 1972). Survey years 99-00 01-02 03-04 Geometric mean (95% conf.362 (.644 (.280-.438) .57) 1.667-1.513-.29 (1.963-1.256-.757-1..433) .495 (.49) 1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.593) . 1972).608 (.44 (.14 (.911-1.462) .10) Total .290 (. Cobalt is absorbed by oral and pulmonary routes.391) Selected percentiles ( 95% confidence interval) 50th .707) .955) .378 (.842) .00) .449-.963) .550-.00 (. 1994.Metals fabricated from cobalt alloys (Lhotka et al.821-3.297) .35) 1.728 (.343-. 1979). an essential human nutrient.937 (.700 (.750-.513 (.278-.248-.50) 1.552 (.00 (.54) 1. or using diamond-polishing wheels that contain cobalt metal.294-.606 (.25 (. respectively.471 (.964 (.396) .352) .378-.581) .348) .394) .471-.426 (.850-1.12 (.281) .378-.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 .333-.723 (.361 (.361 (.523 (.442-.753) 1.04-1.400 (.314 (. Once absorbed and distributed in the body.700 (.327 (.781) 95th 1.547 (.349) .429) 1.848 (. A portion of cobalt retained for long periods is concentrated in the liver.425-.36) 1..257-.301-.638-1.328) .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 .673-.275-.469-.562) .824 (.851 (.06 (.861 (.467-.274-.452-.310) .346 (.33) .542 (.392 (.475 (.16 (.362-.481) 90th .435 (.960 (.251-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.479) .362) .829-1.30 (1.785) .00-1.365) .781-1.595) .388 (.313-.408 (.391 (.290 (.963-1.273 (.36) 1.16) .361-.487-.457) .296) .689 (.00) .900-1.313-.439) .990-1.792-1.19) .703-.461) .00 (.272-.333 (.500-.522) .407) .344-.300) .694) ..10 (.09) 1.634-.303-.963) . with pulmonary clearance half-lives of from one to two years (Hedge et al.60) 1.756 (.421) .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 .850 (.333-.363) .297-.316 (.323) .574-. population from the National Health and Nutrition Examination Survey.24) .386 (.727 (.257 (.304-.259 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.333-.821 (.326-. cobalt is excreted predominantly in the urine.611) .365-.425) .382-.463-.562) .304) .417 (.279) .380-.417) .929) .352 (.826-1.457 (.376 (.296-.537 (.23 (1.368 (.11-1.409) .50 (1.15) 1.407 (.829) .282 (.529 (.738 (.753-.298 (..343 (..293 (.983-1.838 (.393-.337 (.324) .334) .434-.471-.938-1.282-.777-.455 (.250) .388 (.598 (.50) 1.381) .563-.278 (.337) .387) .560-.368) .73) 1.324-. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.358 (.384) .487-.328 (.328 (.306 (.792 (.342-.548 (. Exposure in the workplace may come from electroplating.895-1.468) .55) .740-1..03-1. 2003).361-.302-.404-.844 (.449) .313-.479-.10-1.591 (.259) .277-.372) .660-.738 (.317 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.736-.774 (.352 (.29) 1.515 (.271 (.691 (. using hard metal cutting tools.313-.508-.339-.905) .554 (.237-. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.503-.16 (1.396) .513) .291 (.428-.

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

Wild P. Ichikawa Y. cobalt salts. Weber A. 1985. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Radulescu M. Tilley S. Daniel J. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.55(4):269-276. Romazini S. Zhuber K. Lison D. Occup Environ Med 1994. Am J Epidemiol 1998. Shirakawa T. Uitti J. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. et al. Bourne RB. et al. Pradhan C. Trace element reference values in tissues from inhabitants of the European Union. Sci Total Environ 1994. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Science 1988. Barnaby CF.50(9):835-842. et al. and cobalt metals. DeSantis V. Linna A. Mutat Res 2003. and hard metal dust.28(5):1121-1128. 2001. J Rheumatol 2001. Roto P. Heki S. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Pisati G. J Orthop Res 2003. Kiilunen M. Chest 1989. Alessandrelli M. salt. Falcone G. Swennen B. Stanescu D. McCalden RW. Vitali MT. Sabbioni E. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors.(1-3):133-139. Sci Total Environ 1994. Oksa P. Lisi P. Zobelein P. Hammon E. Bozec C. Cannon SR. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Jarvis JQ. Dunning SP. Sanghrajka AP. Molders J. Leghissa P. Smith T. Thabe H. J Bone Joint Surg Br 2006. Goldberg MA. Linnainmaa M. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades.58(10):631-634.22:359367. Hoher T. Unwin P. Sci Total Environ 1997. Meier R. J Bone Joint Surg Br 2005. Cobalt cardiomyopathy.242:1412-1415.45:246-247. Buchet JP. Occup Environ Med 2001. Int Arch Occup Environ Health 1997.44:124-132. et al. Lauwerys R. Buchet JP. X. Respiratory health of cobalt production workers. Biological monitoring of workers exposed to cobalt metal. Epidemiological survey of workers exposed to cobalt oxides.157:117121. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Lison D.406:282-296. Moulin JJ. Arch Intern Med 1990. 3rd ed. oxides. Salvatori S. Weyher I.533:135-152. Clin Orthop Relat Res 2003. Rorabeck CH. Blunn G. Mosconi G.204:147-160. Zweymuller K. Lung cancer risk in hard-metal workers. Szekeres T. Health Phys 1979.216:253-270. A report of two cases from mineral assay laboratories and a review of the literature. Industrial Chemical Exposure: Guidelines for Biological Monitoring. MacDonald SJ. Am J Ind Med 2003. et al. White MA. Edmonds CJ. Contact Dermatitis 2003. Fujimura N. Steffan I. Schank M.69(3):193-200. Kriss JP. et al. Absorption and retention of cobalt in man by whole-body counting.51(7):447450. Peltier A. Iavicoli I. Dickel H.48:172-173.148:241-248. Occupationallyinduced “isolated cobalt sensitization. Lison D. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Health Phys 1972. McMinn DJ. J Occup Med 1992. Kusaka Y. Bunn HF. The release of metals from metal-onmetal surface arthroplasty of the hip. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Dunstan E. Lhotka C.” Contact Dermatitis 2001. Br J Ind Med 1993.20(1):25-31.36:732-734.150(1-3):167-171. Meyer zum Buschenfelde K-H. Zedda S. Thakker DM. De Boeck M. Schaller KH. Sabbioni E. Palmroos P. Gross RT.150:177-183. Hoet P. Lauwerys RB. Ghat IS.88(4):443448. Robinson C. Salama A. Outcome of occupational asthma due to cobalt hypersensitivity. Laippala P. Kuska Y. Lauwerys R. Angerer J. Hedge AG. Cresti R. Swennen B. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.150. Goto S. Cobalt and antimony: genotoxicity and carcinogenicity. Kirsch-Volders M. Chess DG. Kato M. Kraus T. Thomassen H. Kristiansen J. Long-term clearance of inhaled 60Co.Metals effects of cobalt. Co-sensitivity between cobalt and other transition metals.21(2):189-195.34:620-626. a study of 13 elements in blood and urine of a United Kingdom population. Int Arch Occup Environ Health. Sci Total Environ 1998. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Christensen JM. Schramel P. Bacis M. Sabbioni E. Boca Raton (FL): Lewis Publishers. Carnes WH. Goto S. Ziaee H.95:29-37. Lasfargues G. Diepgen TL. J Trace Elem Med Biol 2006. Iversen BS. HoffmannB.87(5):628-631. Cleland D.

0.10 (2.40-1.20) 4.80) 3.40 (2.28.10-1.50-1.986) .20 (2.60 (1. Before the 1980’s.70-5.12-1.50-1.40-3.37-1.10 (1.70 (1.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.30 (4.20 (1.90 (2.90) 3.62) 1.40 (3.60) 3. and for radiation shielding. blue-gray metal that occurs naturally in soils and rocks.36-1.10) 3. population was aerosolized lead emitted from combustion engines that used leaded gasoline.80 (1.70) 3.30-2.90 (1.50 (2.80 (5.S.19 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20) 1.10-4.30) 95th 5.80 (1.g.90) 1.10-2.00-4.60) 5.60 (1.52 (1.65 (1.10 (3.90 (3.30) 2.69 (1.10) 1.60) 3.40-3.30-6.10) 4.09) 1.80-2.00-4. leaded glass.23 (1.90-2.30-2.20) 3.43-1.50-1. In the past.50 (1.10-3.90-4.40) 2.55-1.20) 3. antique-molded or cast ornaments.70-6. ceramic glazes.50) 4.80-3.10 (1.10-3.80 (1.00-1.70 (1.60-1.66) 1.50) 2.80 (2.20) 3.50-2. 01-02.10-6. such as lead phosphate and tetraethyl lead.50) 7.40 (2.40-1.55 (1.30) 5.90) 3.30 (2.17) .90 (1.90-2.900 (.45 (1.87 (1.30-4.20 (3.90) 1.36) 1.10-3.70) 2.40 (4.50) 1.00) 4.10-1.52-1.40 (1.20 (3.50 (2.10) 5. interval) 1.00) 2.80) 1.90) 2.90) 1.70) 1.20) 2.20-2.70 (5.81) 1.31) 1.50) 3.80 (4.50) 2.40) 2.60) 1.60 (3.00-6.00 (5.60-1.60-3.60) 2.60) 3.60 (2.00 (4.60) 2.20 (3.3.60-2.43 (1.00) 1.10 (2.50-2.60 (1.3.50 (2.900 (.80) 1.00-4.52-1.50-6.60 (2.60-1.40-4.50) 1.10 (1.30-2.90) 2.80 (1.60) 1.50-1.60) 5.86) 1.00 (4.68-1.25 (1.80 (2.71-1.37 (1.80-3.30-5.20) 4.50 (2.00) 2.60) 1.30-1.30 (2.70) 4.50) 5.20-4.89) 1.80-4.10) 2.80 (1.90) 5.20 (1. Elemental lead can be combined with other elements to form inorganic and organic compounds. the main source of lead exposure for the general U.10-6.878-1.02) 1.20-1.50-5.77 (1.20) 3.60 (4.20 (4.00 (2.37 (1.50) 75th 2.87) 1.70 (3.91) 1.30 (1.50-3.48) 1.90-4.60) 4.70) 1.00-5. and 03-04 are 0. bronze).95) 1.70) 4.56 (1.60) 4.70-2.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.30 (2.00) 6.90-6.00) 4.00-2.10-8.40) 1.50 (4.00) 3.50) 1.50) 1.60 (3.43) 1.50) 5.60 (3.90 (3.40) 5.43 (1.20 (1.80) 2.36-1.39-1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.90-4. solders.10) 2.40-6.60 (2.50-2.40 (1.50-1. Lead is most often mined from ores or recycled from scrap metal or batteries.51) 1.30 (2.10-2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70 (3.10-2.30-1.96-2.30 (1.60) 4.20 (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 2.40-5.60-1.900-1.34-1.80) 2.50 (3.70-1.90-3.20 (3.80 (2.75 (1.S.90-4.10-2.50 (1.75) 1.10) 3.90-2.50 (1.43) 1. malleable.50 (2. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.90 (3.40-1.50 (1.50-4. Since lead has been eliminated from gasoline.60-4.30 (2.70) 1.60) 2.10-1.20-3. Lead has a variety of uses in manufacturing: storage batteries.40-6. ammunition.20 (1.10-2.70 (2.60) 2.60) 4.00) 1.40 (1.800-1.70) 1.00) 2.00) 1.30-1.39) 1. metal alloys (e.70 (1.10 (4.50-5.69) 1. 212 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00.70) 1.70 (2.20-1.40-1.49-1.83 (1.55-1.20) 5.75-1.30 (3.70 (1.53) 1.40) Total 1.14-1.00) 5.30 (1.20-6.30) 2.20 (3.10) 1.80) 1.30-1.62 (1.80 (5. population from the National Health and Nutrition Examination Survey.22 (1.60 (1.60 (2.14-1.60 (2.10 (2.90) 2.78 (1.70-4.80) 1.942 (.32-1.90) 2.40 (1.50 (4.50 (3.70-1. respectively.60-4.60 (1. and 0.70) 4.00) . brass.10-4. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.50) 4.04-1.899-.40) 2.60 (3.40) 1.50-4.80-3.30) 2.30-2.60 (2.80-4.60) 1.00) 3. Lead was used in plumbing for centuries and may still be present.00) 1.00) 2.50-2.00 (6.946 (. dense.69) 1.70-2.00) 1.30 (4.90 (3.62-1. plastics.40) 3.69 (1.20-3.20-3.00-1.60) 2.90 (2.20 (2.50-3.80 (4.80) 1.40-2.80 (3.20) .01 (1.80-4.10) 1.30 (4.10-3.90) 2.20-3.40) 2.70-1.20) 90th 3.60-2.40 (5.14-1.60 (1.46 (1.30 (2.45-1.40-2.00 (1.70-2.30-1.32-1.30-1.Metals Lead CAS No.80-5.80) 2.30 (1.25 (1.40-2.70 (2.80-3.40) 1.72) Selected percentiles ( 95% confidence interval) 50th 1.60-6.00 (1.90 (3.25) 1.30) 1.66 (1.90-2.70) 4.40-1.20 (3. 7439-92-1 General Information Elemental lead is a soft.80 (1.70) 3.60) 3.20-2.40) 4.60 (1.93-2.80) 2.40-3.20 (3.40-1.70-3.10-2.60) 1.00 (3.75-2.90 (4.30 (2.10) 3.51 (1.70) 3.

718) .573 (.935) 1.70 (2.80) 3.757-.40 (2.14 (1.30-2.S.90) 2.80-2.10-1.605) .82 (1.30) 2.90) 1.30) 1.20) .20 (1.620) 1.90-2.70) 3.00 (1.33 (2.27 (1.10) 2.940 (.708-. 01-02.90 (1.04 (.90 (2.10) .90-2.60-2.553-.60 (1.923 (.600-.59) 1.564 (.40) 3.710-.10) 2.00 (2.17 (1.80) 2.10 (1.604 (.700 (.30 (3.20-2.20-1.701) .31 (1. Approximately half of the absorbed lead may be incorporated into bone.815 (. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.828) Selected percentiles ( 95% confidence interval) 50th . In the blood.04) 2.40-1. see Data Analysis section) for Survey years 99-00.04 (.06) .50-2.40 (2.560-.18-1.78-2.10 (.40) 1.50 (1.75) 4.30) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.800) .900-1.40 (2.66 (2.30) .00-2.636 (.60 (2.610 (.22) 1.80-3.729-.27) 1.900 (.900) .49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .800-1.60-2.766 (.91) 2.700 (.558 (.630 (.30 (1.50) 1.915-1.50-2.90-3.20 (2.80) 1.700) 1.910-.628) 1.90 (2.20 (3. 2007.60-3.40) 2.21 (2.20) .70) 3.20 (1.00) .10 (1.32 (1.650) 1. older plumbing systems with leaded pipes or lead soldered connections.900) .600) .700-.78-2.10 (.90-4.70 (2..800-1.800) .50) 3.20-1.1.70 (2.556-.80) 2.02 (.700-.10-3.625-.29) 2.970-1.00) .30-1.40) 1.1.40) 2. 0.900) .72) 1.11 (1. However.955-1.30-1.833-1.600-.700 (. lead-containing folk remedies and cosmetics.900-1.50) 2.800-.480-.40-2.641-.40) 2.13-3. pewter utensils and drinking vessels.20 (1.70 (1.920 (.20) .700 (.90-2.80 (1.800 (.20) . imported children’s trinkets and toys.60 (1.10-1.833 (. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.960-1.20-2.680) .674) 1.820-1.990) 2.80) 3. 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.900 (.591 (.00-2.52 (1.00-2.50-3.506-.600 (.80) 2.690) 75th 1.800 (.808 (.40) 2.600-.20 (1.30) 1.800 (.10) .52-1.540-.500-.49 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.710-1.66 (2.40 (1.86) 1. CDC. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.535-.41) 2.785) .33. lead-based painted surfaces undergoing renovation or demolition.960-1..60-3. stained glass framing.749) .50 (1.20 (2.20) 1.12) 90th 2.651) .90-2.941) .700-1.90) 2.600-. or water contaminated by mining or smelting operations.86) 95th 2. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.589-.44-2.Metals occupational (e.10-1.680-.700 (.89) 2.82 (2.50) 2. and 03-04 are 0.07 (.738) .640 (.10-1. population from the National Health and Nutrition Examination Survey.62) Total . Fourth National Report on Human Exposure to Environmental Chemicals 213 .620 (.30-1.848 (.900) .986) .640-.33-2.70 (2.50 (2.862) .30 (2.40 (2.70-2.86-2.50-1.50 (2.40-1.60) 2.00 (1.62-4. dust.03 (1.753 (.660) .810-1.13) .40 (1.90 (1.24-1.773) .526-.80) 2.857) .50) 1.700-.90 (2.59-2.613) .625 (.14-1.10-3.80) 1. bullet fragments retained in human tissue.60-1.80) 1.10) 1. or after soluble lead compounds are ingested.00 (.10-1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.840 (.20 (1.70) 2.14 (1.09) 1.40) 1.680-. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.80) 2.30) 1.745-.800) .20-1.850 (.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 1.731 (.00-1.659 (.695 (.642 (.97) 4.11) 2.661-.40) 1.40-1.700-.900 (. battery and radiator manufacturing) and recreational sources.10 (1. 1991).40 (1.671-.700-.07-1.23) .40-5.20 (2.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30) 1.04) .700) .990) 1.60 (1.30-5.40 (1.700 (. interval) .90) 2.677 (.752 (.40-1.60 (1.78-2.00) .600) .70-3.30-3.80 (1.40-3.595-.30) 1.920 (.800-.800) .822-1.52-1.02) 1.00) .80 (2.960 (.579-.86 (1.730 (.00-1.00 (1.75) 3.931) .691-.90-3. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. 2000).10-3.570-.35 (.795 (.540 (.900) .90 (1. and 0.31-3.40 (1.800 (.50 (2.580-.g.03-2.900) .30) 2.818) .04-2.616) . lead-contaminated dust in indoor firing ranges.19 (1.80-2.10 (.70) 1.00) 2.64) 2.00 (1.30-1.20) 1.20) 1.10 (1.00-1.29 (2.800) .900-1.637-.40) 1.70) 1.20 (1.73 (1.688 (.00) 1.600-.790 (.10-5.70) 1.00) 2. and contact with soil.50) 1.23-4.579-.572-.30) 2.600 (.590 (.900-1. respectively.50-2.

11 (.66) 2.979 (.00) . abdominal pain.53) 1.33 (1.08-2.51 (1.35) 2.957-1.679-.963-1. Lead can cross the placenta and enter the developing fetal brain.11 (1.408-.648 (.15-2.755 (.72) . 1996).14) 1.10) 1.688) .914 (.65-2.44) 1.69 (1.15-2.11-1.43) 1.12) 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .603-.03) 2.23 (1.701) .25-1.594-.79 (1.20) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .0) 3.22-1.870 (.52) 1.828) .625 (.02) 1.709 (.496 (.698) .50-2.51) 1.79) 2.03) 2.85) 1.918-1.605-.64) 95th 2.37-1.997-1.667-. encephalopathy.77) 2. population from the National Health and Nutrition Examination Survey.33) 1.633 (.41 (1.712 (.02-1.938-1.914-1.887 (.583-.432 (.638 (.933-1.670) 1.790) .64 (1.621 (.722 (. In 1991.492-.753) . Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.64-2.18 (1.926 (. Approximately 70% of lead excretion occurs via the urine. and nails (Leggett.88) 2.22) 1.618 (.893) .655) 75th 1.559-. 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.05 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.88-2.09-1.97) 1.Metals 90% of the body lead burden in most adults.20) .940 (.03) .38 (2.639 (.64) 2.612-.62-3.400) .37-1. The toxic effects of lead result from its interference with the physiologic actions of calcium.06) . and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.07 (.17 (.03) 90th 1.18) 2.594-.380-.920-1.09-1.53-1.645-.25-1.725) .702) .31 (2.33) 2.62-1.48 (1.00 (1.720 (.659-.933) . 1991.571-.838) .71-2.828-1.796-1.22) 1. seizures.592-.67-4. CDC. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.63) 4.47 (2.56-2.88) 2. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.83 (2.990 (.43-1.645-.03 (.40-1.671 (.698) .992-1.700-.96 (1. zinc.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 .710) .10 (1.85-2.46 (2.696 (.55 (1.677-.781-1. 1993). Staessen et al.10 (.551-.85 (1.655-.59-3. through the inhibition of certain enzymes.06 (.981-1.28-1.14 (1.05 (1.622 (.50-2.50) 1.742) .11 (.641 (.667-. 2003.20) .08) .43 (2.97 (1.49 (1.88 (1.635 (. and through binding to ion channels and regulatory proteins.569 (.. Large amounts of lead in the body can cause anemia.541-.746) . O’Flaherty.607-.72-2.918 (.677 (.03-2.586-.615 (.679) 1.28) 2.609 (.615 (..655) .702) .812-1.992-1.20-3. 2004.01) . BLLs and associated toxic effects differ in children and adults.535) . For instance.588-.658 (.12-1.529-.39-1.03) .03) 1.09-1.98) 2.603-.03 (1.85-2.623 (.988-1.43) 2.676) .404 (.11) .649 (.26) 2.94-2.01 (.758) .601-.52 (1.683-.17-1.977) 1.652 (.83) 1.15) 1.800-.681-.11 (1.721 (..428) .05-1.742) Selected percentiles ( 95% confidence interval) 50th .623 (. scant amounts are lost through sweat.24 (1.73-2.793-1.342-.579-.38 (2.461) .58) 1.62-2. The skeleton acts as a storage depot.739) .26) Total .79) 1.708 (. Nash et al.43 (1.508) . 1995).71 (1.56-3.55 (1.657) 1.632 (.03) 1.720 (.975-1.603 (.988 (.862-.92) 2.588-.639 (.604-.765) .375 (.61) 1.68 (1.78 (2.617-.841-1.08) . Schwartz.50 (1.44 (1. 2007).19-5.593 (. kidney injury.34-1.03 (.73) 2.571-.639 (.938 (.962 (.383-.38 (2.404 (.31 (1.07-1.47) 1.882-1.78-4.971 (. based on prospective population studies.04-3.06 (1.27 (1.702-.851) .15) 1.810 (.673) . with lesser amounts eliminated via the feces.75 (2.763) . Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.703) .66 (1.33-1.608-.18) 1.404-.61) 1.56 (1.18) 1.03 (.36-2.00 (1.608 (.681-.917-1.66 (1.693 (.701 (.22-2.469 (.28) .61) 1.639) .61) 3.00 (. with a half-life of years to decades.87) 1.46 (1.946-1.853-1.19) 1.914 (.731-.50-2.22) .05-1.15-3.31) 1.04) 2.06) 1.722 (.74 (1.72-2.97) 1.75-2.70 (1.47 (1.734) .94 (1.86 (1. hair.45 (1.730) 1.644 (. 1993.561-.89-5.07) .587-.725) .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 1.50-1.09) 1.56) 3.29 (1.898) .667) .718) .18) .00 (1.62) 2.63) 1.686) .682) .41) . and paralysis.41-1.97-18.31) 1.98-2. 1995.460-.510-. and iron.98 (1.644) .S.65 (1.677) .606-.82) 1.774 (. interval) .436) .31 (1.44 (1.876-1.718) 1.707 (.89-2.11) 1.654) .668-.61) 1.900 (.88) 1.

Payton et al.6% in NHANES 1988-1991 to 1. and peripheral neuropathy generally occurring at much higher levels (e.. particularly in the skeleton. 1996. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al.S. 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. The Adult Blood Lead Epidemiology and Surveillance program has tracked BLLs reported by states for mostly for occupational but also for non-occupational exposure in U. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 1999). seizures.07 µg/dL (Becker et al...e. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. 2003.Metals µg/dL or higher as the level of concern in children. At low environmental exposures. Telisman et al. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. Muntner et al. lead in women may be associated with hypertension during pregnancy. almost double the geometric mean of 1. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.. In NHANES 1999-2002 in children 1-5 years old.4% of children had BLLs of 10µg/dL or higher (CDC.3 million children tested had BLLs of 10 mg/dL or higher (http://www. 2002.xls). subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. and low family income (CDC. 2005b. urban residence.. 2006). 2009). A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. which is an 84% decline.S. 2006). A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. Urine levels may reflect recently absorbed lead. 2000). 1987. Both drinking water and ambient air standards for lead have been established by the U.S. Korrick et al. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 1998). 2003.. IARC considers inorganic lead compounds probable human carcinogens. 1991. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. the geometric mean BLL was 3. and spontaneous abortion (Baghurst et al.. Surveillance data reported by U. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.. Information about external exposure (i.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2003). 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. with overt encephalopathy.. 1996. Overall.. residing in housing built before the 1950’s. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.7 µg/dL and 4..5 per 100.75 µg/dL in U. including minority race or ethnicity. approximately 11. 2005b). For example... 1996.000 adults.gov/toxpro2...S..g. 2007).0 µg/dL in females (Soldin et al.. BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist. Schwartz et al. the prevalence rate has declined annually since 1994 (CDC. higher than 100-200 µg/dL). A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 2003.. Schwartz. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.html. 1999). adult residents. Borja-Aburto et al. However.S. BLLs reflect both recent intake and equilibration with stored lead in other tissues. respectively. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. may alter sperm morphology. adults in the 19992000 NHANES sample (Apostoli et al. 2002). High dose occupational lead exposure.6%) were lower than those from NHANES 1991-1994. Data submitted through state public health programs from 2006 showed that 1. 2000).. Fourth National Report on Human Exposure to Environmental Chemicals 215 . and decrease fertility (Alexander et al. Pirkle et al. 2005a). 1984. when the geometric mean BLL was 2. environmental levels) and health effects is available from ATSDR at: http://www. premature delivery.. both the geometric mean (1.cdc. 1994). and organic lead compounds not classifiable with respect to human carcinogenicity. The U. 2002a). In occupationally exposed adults.cdc.S..4% in NHANES 1999-2004.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. usually with BLLs greater than 40 mg/dL.atsdr. adults in the 1999-2000 NHANES sample. EPA.2 µg/dL in males and 3.21% of approximately 3. reduce sperm count. 1995. 2001). Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.. Lanphear et al. CDC.. Bellinger 2005. Staessen et al. More recently.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. Jones et al.

Available at URL: http://www. Centers for Disease Control and Prevention (CDC). Environ Res 2000. Speizer FE. Blood lead reference values: the results of an Italian polycentric study. Int J Hyg Environ Health 2002. Blood lead levels measured prospectively and risk of spontaneous abortion. Rojas LM. IARC Monogr Eval Carcinog Risks Hum 2006.gov/toxprofiles/tp13. References Agency for Toxic Substances and Disease Registry (ATSDR). The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.cdc. CDC.205:297-308. Neri A. Becker K. N Engl J Med 2003. Ganzi A. Schulz C. 2005. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Age-specific kinetic model of lead metal in humans. Payton M. Dietrich K. Weiss ST. Environ Health Perspect 1993. gov/mmwr/preview/mmwrhtml/mm5420a5. Am J Public Health 1999. Kaus S. Ewers TG. Cory-Slechta DA. Pediatrics 2009.150(6):590-597.cdc. Korrick SA.htm. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Farias P.348:15171526. Korrick S. Third National Report on Human Exposure to Environmental Chemicals. Hu H. Blanco J. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Checkoway H.cdc. Hänninen H. Meyer PA. Leggett RW. Acquisition and retention of lead by young children. Mantere P. Adult blood lead epidemiology and surveillance—United States. 1999-2002. Jacobson SW. 2005b.gov/mmwr/preview/mmwrhtml/ mm5532a2. Lepom P.275:1177-1181. Bavazzano P. McMichael AJ. et al. Ronchi L. Rotnitzky A. doi:10. MMWR Morb Mortal Wkly Rep 2005a. 4/14/09 Alexander BH.55(32):876-879. Toxicological profile for lead. Lead.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. Aug 2007 [online]. Caldwell KL. Muller CH. Baghurst PA. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.275(15):1171-1176. 4/14/09 Centers for Disease Control and Prevention (CDC). Kuehnemann TJ. Vimpani FB. Hu H. Bellinger D. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Available from URL: http://www.gov/nceh/lead/publications/ books/plpyc/contents. Atlanta. Hu H. Sci Total Environ 2002.89:330-335.atsdr. Pediatrics 2004. Batuman V. Angle CR. Atlanta (GA).54(20):513-516.53:411-416.cdc. et al. Scand J Work Environ Health 1984. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Neurodevelopmental effects of postnatal lead exposure at very low levels.htm. Jones RL. Kim R. Ga.htm. Sparrow D. 2002 [online]. Auinger P. Cox C. Public Health Rep 2000. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Canfield RL. Rotnitzky A. Aro A. Sparrow D.26:359-371. Stanek KL. van Netten C. Coresh J. Wigg NR. Am J Epidemiol 1999. Luukkonen R. Bellinger D. Blood lead levels—United States.113(4):1016-1022. Reese YR. et al. Neurotoxicol 1987. JAMA 1996. Roberts RR. Brody DJ. Hernberg S. Available at URL: http://www. Occup Environ Med 1996. JAMA 1996. Hunter DJ. Homa DM.82:60-80. et al.87:1-471. Jusko TA.10:43-50. Managing Elevated Blood Lead Levels Among Young Children.8(3):395-401. Weiss ST. Seiwert M. Rios C. 4/14/09 Centers for Disease Control and Prevention (CDC). Neurotoxicol Teratol 2004. Cox C. Inorganic and Organic Lead Compounds. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 2003-2004. Preventing Lead Poisoning in Young Children. Vupputyuri S.1542/peds:2007-3608. Pirkle JL.287:1-11. Atlanta (GA). Muntner P. Kaufman JD. Lanphear BP. Robertson EF. Birth Defects Research (Part A). Hertz-Picciotto I. Available at URL: http://www.123:e376-e385. 1988-2004. Baj A.htm.73:409-420. Semen quality of men employed at a lead smelter. 1991 [online]. The relationship of bone and blood lead to hypertension. Borja-Aburto VH. 4/14/09 Centers for Disease Control and Prevention (CDC). Lead and hypertension in a sample of middle-aged women. et al. 4/14/09 Centers for Disease Control and Prevention (CDC).html. Apostoli P.115:521-529. Chiodo LM. Manton WI. Teratogen update: lead and pregnancy.cdc. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Krause C. Available at URL: http://www.101(7):598-616. MMWR Morb Mortal Wkly Rep 2006.gov/nceh/lead/ CaseManagement/caseManage_main. Wager C. Lanphear BP. Henderson CR. Jacobson JL.

JAMA 2003. Fourth National Report on Human Exposure to Environmental Chemicals 217 .106:745-750.9:303-327. Amery A. IV. Low-level lead exposure and renal function in the Normative Aging Study.289(12):1523-1531. Sherwin R. J Hum Hypertens 1995. Flegal AR. Lustberg M. blood pressure. Environ Health Perspect 1996. Wilhelm M.S. Rubin R. Kaufmann R. stable lead isotopes to determine release of lead from the skeleton. Am J Epidemiol 1994. Clin Chim Acta 2003. Lee SS. Kidney Int 2003. Blood lead concentrations in children: new ranges. Payton M. Magder L.140:821-829. Cvitkovic P. Blood lead. Telisman S. dimercaptosuccinic acidchelatable lead. and hypertension in perimenopausal and postmenopausal women. Association of blood lead. Gavella M. et al.327:109-113. Paschal DC. Toxicol Appl Pharmacol 1993. Brody DJ. blood pressure and cardiovascular disease in men. Osterloh JD. Hu H.63:1044-1050. et al. Gunter EW. Lauwerys RR. Am J Epidemiol 2001. 50:31-37. Int J Hyg Environ Health 2006. lead. cadmium. Lee BK. O’Flaherty EJ. cadmium. Environ Health Perspect 1998. Hwang KY. Sparrow D. Hickman T. Kinetics of lead disposition in humans.Metals results from NHANES III. Schwenk M. Soldin OP. and copper in men. Hanak B. Stewar WF. Staessen JA. Kaufmann RB. Rocic B. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Soldin SJ. and tibia lead with neurobehavioral test scores in South Korean lead workers.209:301305. population to lead: 1991-1994. Weiss ST. Roels H. Pirkle JL. Arch Environ Health 1995. Pizent A. Schwartz J.104(1):60-66. Nash D. zinc. Environ Health Perspect 2000. Lead. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Exposure of the U. Revised and new reference values for arsenic. Smith DR.108(1):45-53. Jurasovic J. Use of endogenous. Schulz D. Physiologically based models for bone-seeking elements.153(5):453464. Lee GS.118:16-29. Schwartz BS. Low-level lead exposure and blood pressure.

753-1. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.300-. electrical lamps. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.60 (1.40 (3.800-1.703-.30 (1. interval) ..00-5. 2002).800-1. Accidental spills of elemental mercury.30-6.S.600 (.400-.S.927) .500-.40 (4. 1993).800-1.30) 4132 4241 03-04 03-04 03-04 . mercuric chloride). IARC.900) 1. 1980.800-1.90) 90th 3.700-.860-1.419 (.800 (. inorganic. thermometers.814 (.776 (. thimerosal.574) .655-.900) .50) 2. and organic forms.60-6. Kingman et al. population from the National Health and Nutrition Examination Survey.50-3.80 (3.781 (.60) 2085 2293 3478 Limit of detection (LOD.00 (2.60 (2.40 (4.20) 2.20-4. Apart from methyl mercury. such as chlorine (e.400-.30-4. and dental amalgam. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.40 (3.700 (.800 (.00 (.Metals Mercury CAS No.40-2. to form inorganic mercury compounds or salts. may contain inorganic mercury.797 (.00) 1.700-.372) .80) 1.484) ..40) 1.900 (. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. solid-waste incineration.30) 3.70 (1. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. Survey years 03-04 Geometric mean (95% conf. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.50) 5.700) .90-3.60-6.00) 1.30) 5. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.40-2.70 (3. sphygmomanometers and barometers.400 (.90 (1. merbromin).800-1.70-2.. The kinetics of the different forms of mercury vary considerably. predominantly from fish and other seafood.70 (4.70 (1. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).12) . Woods et al.00) .60-3. synthetic organomercury compounds were once used in pharmaceutical applications. Also.90 (4.50-2.60-2.40) 3. Elemental mercury is a shiny.80 (1.. 1999 .600) 1.20 (2. Some cosmetic skin creams from countries other than the U.877 (.300 (.500 (.800 (.80 (1.500-. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.30) 3.700-.700) .00 (.60-5.700-. The ingestion of methyl mercury.418-. Atmospheric elemental mercury can be deposited on land and water. or oxygen.00 (1. and is distributed to most tissues. an organic form of mercury. with the highest concentrations occurring in the kidneys (Barregard et al.00 (.00-1.500 (.30-2. which create an episodic potential for volatization and inhalation of mercury vapor.00 (2.. phenylmercuric acetate) or topical antiseptics (e. constitutes the main source of dietary mercury exposure in the general population.472-.900) 1.500) . 1994.00) 4. Poorly absorbed from the gastrointestinal tract.70) 911 856 2081 4525 03-04 03-04 .10) .979 (.90) 3.80) 3.50) 1.919) .689-.60) 1. sulfur. which can bioaccumulate in aquatic and terrestrial food chains.20-4.. Hursh et al.30-5.00 (. and mining and smelting. 218 Fourth National Report on Human Exposure to Environmental Chemicals .40-1.02) .40-1.50) 4..30 (2.50-1.. elemental mercury is absorbed mainly by inhaling volatilized vapor. 1998.800 (.900) 1. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).714-.10-3..00 (2.g.490 (.60 (1.672) .563 (.g.326 (. see Data Analysis section) for Survey year 03-04 is 0.50) 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 .30) 1. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.g.300) .90 (1. In addition.2.90) 95th 4.886) .903) Selected percentiles ( 95% confidence interval) 50th .40-3.363-.g.00) 3.285-.900) 75th 1.80 (1.80) 4. have often required public health intervention (Zeitz et al. and mercury compounds are still used as preservatives (e.60) 1.20-3. After elemental mercury is absorbed.30) 1. Other major uses include electrical equipment (e. thermostats and switches).700-. 2007). Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.

395) . Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.50) 3.700 (.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 .800-1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. 1992 and 1999.30-11..700 (.30 (1.90) 90th 1.70) 1.700 (.00) 6. 1975.268-.800-1. 1991..50 (1.70-3..20) .70-3.80 (3. 1998).300) .871-1.475) .10-3.600) .70 (1. 1992.20-2.50) 95th 2.40-2..40 (1.60 (1.700-1.10 (.200-.40) 1. interval) Selected percentiles (95% confidence interval) 50th .. Excretion occurs by renal and fecal routes.30) 3.50-2.10) 1.738-.307 (.269-.900-1.00) 2.0) 4.20-11. and a useful marker of exposure in epidemiologic studies (Grandjean et al..70-6.60) 2.50 (2.10) . Vimy et al. thereafter.14 and 0. 2004.50) 1.369) 1.374) . 2003).500 (.700 (.00-2. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.200-.30-4. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .27) .900 (.300) .200 (.500-.. 1990).800) 1.90) 2. 2003).700-.00) 7.00) 1.30-6.300) .300) .20) . After exposure to elemental mercury.318 (.10 (3.800) .30-6.940) Race/ethnicity (females.825-1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.40) 5.. 1995.00-2.800) 1. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.377) .300 (.30-6. Vahter et al.60) 1.407) .14.800) .300 (.500-.70-5. 1999).00-2.00) .Metals the tissues to mercurous and mercuric inorganic forms.. for both acute and chronic exposures. 2005)..01) .02 (.265-.10) .90 (3.3) 4.70) 4.90 (4.90) 3. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.200-. 1992).500-.29) .300) .20) 1.919) . population.800 (.30 (1.500-1.50) 1. 1993).80-3.30-4.90) 5.30-3. 1996).00 (2.00 (1.10 (5.70-5.60 (1..30-2..400-.30) 1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith. 1999-2002.06 (.60) 1.30 (.00-1.00 (3..00 (2.90 (1.80) 1. Methyl mercury enters the brain and other tissues (Vahter et al.00) 4.60 (3. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.343 (..299-.700-1. Fourth National Report on Human Exposure to Environmental Chemicals 219 .7) 4..200-.S.20 (2.541-.. 1969. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.50-3.329 (.700) 2.200-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80) 579 527 370 436 588 806 Limit of detection (LOD.30-5.73) 1. 1998).667 (.20-3. 1994). 1984.70 (1.200 (.500-.900-1.90 (4.00) 1.256-. Sandborgh-Englund et al.30) 1. McDowell et al.900 (. Jonsson et al.944 (. 1973). Suzuki et al..00-3.300 (.40) 2.200-.30 (1.300) .70 (1..00 (2.726-1.60 (2. 1971)..900 (.20 (.500-.600 (. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.23) . 1994. 1996.20-3. National Health and Nutrition Examination Survey.10 (1. 1993).600) ..90) 2. Geometric mean Survey years (95% conf. 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.300 (.20-3.697-. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.664-1.06-1.70) 4.297-. the transfer Total Blood Mercury−1999-2002 Geometric mean and selected percentiles of blood concentrations (in µg/L) for males and females aged 1 to 5 years and females aged 16 to 49 years in the U.40-2.90 (1.700-.10-1.10 (1.60 (1. a measure of accumulated dose (Cernichiari et al. Smith and Farris.50-12.833 (. with most elimination occurring through in the feces (Sherlock et al.. Myers et al.800-1.500 (.820 (.40-1.00-6.50) 2. Miettinen et al.800 (.800 (.824) 1.10 (1. Methyl mercury is incorporated into growing hair. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.35 (1.60 (3.40 (1.60) 3.80 (1. 1994) and then undergoes slow dealkylation to inorganic mercury.317 (.10 (..377 (.800) 75th . Smith et al.

42.600) .600-.600 (..800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500) .600 (. 2000. 1996). and neurocognitive and behavioral disturbances.600) . altered physical growth.600-. see Data Analysis section) for Survey year 03-04 is 0..800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. Smith et al. which may vary for some chemicals by year and by individual sample.500-. Once absorbed.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . causing parasthesias.600) .. In recent epidemiologic studies. 2004. 2002.. Drexler and Schaller. 2003). dysarthria... cerebellar ataxia.S. 1998.600 (. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. hearing impairment.600) . and progressive constriction of the visual fields.600-.500-. 1983). dysarthria.600 (. Bellinger et al. Sakamoto et al. 2005. and pinkish discoloration of the hands and feet (Tunnessen et al. < LOD means less than the limit of detection.600 (. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury..700 (.600) .700-.600 (. Factor-Litvak et al.. 1995.700 (. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. 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. 2004.500-.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 ..600-.700-. 1995. and cerebral palsy (NRC. 2006.500-. 1963). Acute. 2000.800) .600) . ataxia. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.500-. 220 Fourth National Report on Human Exposure to Environmental Chemicals . Inorganic mercury exposure usually occurs by ingestion.500 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.500-. and sleep disturbance (Bidstrup et al.700-. irritability.Metals may be more efficient for inorganic mercury (Grandjean et al. Rice. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.500 (<LOD-. 1970.700) 2007 2240 3406 Limit of detection (LOD.700) . gingivitis.700 (. pain in the extremities. 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. 2004). The constellation of findings may include anorexia. overt signs and symptoms of chronic inhalation may include tremor.700 (. depression. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Sakamoto et al.500-. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.600 (. Smith et al. hypertension.600) .700 (..600) . population from the National Health and Nutrition Examination Survey. Rissanen et al. insomnia.. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.500 (.. At levels below those that cause acute lung injury.700 (. typically after a latent period of weeks to months. Salonen et al. 1993). Vupputuri et al. DeRouen et al. 1951.800) .500-. the existence of a causal relation is unresolved (Chan and Egeland. 2004). anorexia. Stern 2005. 1987). interval) Selected percentiles ( 95% confidence interval) Sample 95th . particularly irritability... 2005).600) . 2006. limb deformities. maculopapular rash. fatigue.. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. Oskarsson et al. Overt poisoning from methyl mercury primarily affects the central nervous system.600 (...500-. short-term memory loss. 2000).500 (<LOD-. sensory impairments. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..

840-1. population from the National Health and Nutrition Examination Survey.gov/mercury and from ATSDR at: http:// www.42) 95th 3.960 (. 2001.430 (.430 (.770-1. and increased slightly in non-Hispanic white children (Caldwell.840) 1.940 (.34-3.atsdr.416 (. 2006).700-1. Benes et al.05) 1. 2009).360 (.408) .08 (1.492) Selected percentiles ( 95% confidence interval) 50th .254 (. 2004.88 (1.330 (. Biomonitoring Information In the general population. interval) .330-. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.350-.441 (.213-.76-3.534) . 2009). Survey years 03-04 Geometric mean (95% conf.97) 2.13-2.396-. total blood mercury geometric mean levels in females aged 16-49 years did not change. Sanzo et al. the total blood mercury concentration is due mostly to the dietary intake of organic forms. environmental levels) and health effects is available from the U.58 µg/L for 4645 adults.420 (. Kingman et al.05) 3. average age 33 years.460 (.78 µg/L for adults and 0.555) . In NHANES 19992002. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women. 2003). see Data Analysis section) for Survey year 03-04 is 0. Fourth National Report on Human Exposure to Environmental Chemicals 221 . adult women in several ethnic subgroups (Hightower et al.99-6.549) . 2001.18) 2.76-4.77-2.S.8 years. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. Over the NHANES 1999-2006 survey periods.68 (2. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. 2002). 758 children. who participated in a 1998 representative population survey (Becker et al. Schober et al.433 (.24 (2.495 (.330-.66) 3.530) .00) 1. Grandjean et al.52) 2.700 (. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.413-. and the age-related changes differed across the groups (Caldwell et al.870-1. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.gov/toxprofiles.28) 1. During the same survey periods. range 40 years to 78 years) had an average total blood mercury concentration of 2.463) .. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.340-.360-.290-.. EPA..90) 2..9 years).530) .509) .840-1.480) 75th 1.39-3. 2000). 1998).509) .55 µg/L. From 1996 through 1998.89) 3.93 (1.447 (.01 (.31) 1266 1272 03-04 03-04 03-04 .430) .. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.31) 2.476 (.S. 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.14-2.e. However. the median concentration of blood mercury was 0.67-2.29) 1.406-.85-2.19 (2. These distinctions can help interpret mercury blood levels in people.358 (.60) 619 713 1066 Limit of detection (LOD..07 (. average age 9. slightly higher total blood mercury levels were found in U.63-2.530-.250) .20 (1. 1997.78-2.cdc.370) ..26 (1.16 (..160-.46 µg/L for children.313-.382-.33 (2.23) 2..890 (..410-. In Germany the geometric mean for blood mercury was 0.88-3.08 (1..54 (2.30) 3.76-3.67-3.442-.09 (2.24) 1.96 (1. military veterans (mean age 52.304) .60-2.. particularly methyl mercury.200 (.930-1.405-. 1998). IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.46) 3.23) .61) 1.96 (1.400 (.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 .14.60 (1.S. et al..12 (. Among the three racial/ethnic groups.16 (1. A cohort of 1127 U.570) .360-. EPA at: http://www.S.Metals standard for inorganic mercury has been established by U.00 (. 2003). Information about external exposure (i. aged 18 to 69 years.420 (.870-1.580) . total blood mercury increased with age.520) .03-4.88) 287 722 1529 03-04 03-04 .610-1.280-. Total blood mercury levels increase with greater fish consumption (Dewailly et al.460) .. 1995.14) 90th 2.480 (.epa.65) 1.19 (1.S. Mahaffey et al.330-.440 (.

Urine mercury and the number of dental amalgams were correlated.301-.400) .40-1.00) 90th 1.11) 1.62 (1.32-2.875-1.54 (2.51-2.498) 75th .35 (1.11-2.309-.306 (.545 (..990) . mean urinary mercury was 3. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.535) 1.79) 1.1 µg/L for each surface with a dental amalgam (Kingman et al..S.447-.87) 2.486) Selected percentiles ( 95% confidence interval) 50th .23-2.652) .463 (.12-3.S.537) .696 (.67 (1.07) 1.447 (.362 (.S.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals . 2009). the urine mercury increased by approximately 0. 2002) adult population surveys were similar to those in a U.88-2.347) .768 (.588) . et al. 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. 2006).64-2. Langworth et al.365 (.16) 1.476 (.13-2. reversible increase in urinary N-acetyl-glucosaminidase.87 (1. 2006.06 (.11) 2. and Italian (Apostoli et al.276 (.32 (1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.297 (. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..800-1.455-.217 (.18-1.85) 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 . Department of Health and Human Services noted that several studies have observed a modest.. women of childbearing age have generally been much lower than these levels (CDC.208-. DeRouen et al.404-.86) 95th 2.39) 1. 2003).275) . Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population.88-2.78-4.88 (1. Czech (Benes et al.455) .289) . interval) . Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.. Urinary mercury levels in recent German (Becker et al.00 (.400-.65 (1. and on average.368) . 2005).28 (.599) .21) 1. military veterans with dental amalgams. 1992).376-.472-..06 (.784) 1.391) .196-.13 (1.30) 1.67 (1.964-1. Survey years 03-04 Geometric mean (95% conf.03) 2..667-1.443 (.333-.417) .385-.30) 2.63) 1. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.616) .391-.77 (2.785-1.1 µg/L.587 (.255 (.. not to imply a safety level for general population exposure. population from the National Health and Nutrition Examination Survey.56) 1266 1271 03-04 03-04 03-04 . 1988.619-. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.79 (1.04-3.40 (1. An expert-panel report recently prepared for the U.392-.566) .532 (.630) .41-2. Information about the biological exposure indices is provided here for comparison.76 (1.280-. a biomarker of perturbation in renal tubular function.S. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.09) 1.46-2.246-..225-.Metals 2000).365 (.44) 1.265-.343 (.455-.31 (1.384 (. 2009).969-1. 1998). et al.620-..01) 2.480) .508 (. 2002).61) 1.525 (.714-1.358) .909 (.522-.307-.485 (. In the study of U. Levels in U.S.970 (.00) 286 722 1529 03-04 03-04 .687) .464 (.25 (.

579-.95 (2.10-4.42-3.44) 3.65) 1.62 (1.709) 75th 1.600 (.565 (.520-.32 (1.723 (.721 (.724 (.85-3. 16-49 years) 99-00 01-02 .85) 4.42) 2.68 (3. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.686) .70 (2.27-1.99) 1.27 (2.09-1.522 (.54) 595 531 381 442 594 826 Limit of detection (LOD.07) 1.41 (2.540 (.68) 3.45-3.520-.790) .13-4.03 (.582-.83-3.742-1.38) 4.53-3.657 (.76 (1.07-5.610-.966) .14-2.39-3.41 (1.24) 6.18 (3.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.508-.99 (3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.37) 1.831) .98 (5.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.05 (2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .81-6.3) 5.809) .502-.14) 3.426-.910) .810) .04-1.79) 3.21 (1. Geometric mean (95% conf.45 (1.410-.850-1.00) 2.92) 3.00 (3. 1999-2002.47) 1.15-1.99-2.710) 1.710 (.41 (1.45) 2.870) .706 (.59-5.69 (1.50-4.557-.48 (2.22 (.30 (2.62 (4.710 (.560 (.526-.05 (3.578-.35 (1.04-10.94) 1.655 (.35) .833) .631-.685 (.420-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .14-1.92) 4.32) 2.92) 2.91-7.55-3.22-3.23-1.62 (3.56 (1.909-1.13 (2.61-6.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .636-.77) 1.25) 2.624-.832-1.81 (3.77) 2.46 (1.540-. population.30 (2.553-.72) 1.580-.03 (.15 (2.580 (.97) 2.605-. National Health and Nutrition Examination Survey.616-.68-3.774) .16) 5.699) 1.569-.28 (1. 16-49 years) 99-00 01-02 .606 (.772 (.665) .622-.596 (.387-. interval) Selected percentiles (95% confidence interval) 50th .560-. interval) Selected percentiles (95% confidence interval) Survey years 50th .79) 1.656-.691) .84 (2.00 (2.89 (2.97) 2.637) .31-1.03) 1.09-1.84 (2.76-5.639 (.799) .27 (1.23-1.99 (2.930) .16-5.51) .709) . 1999-2002.501-.56) 3.615 (.97) 2.50 (2.664) .892) .61) 1.50 (1.620 (.41-6.650) 1.475-.S.14.18) 3.670) 75th 1.97 (1. National Health and Nutrition Examination Survey.06 (.76) 2.21 (2.14 and 0.21-3. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.91 (2. population.450-.69-3.42) 90th 2.07-2.17) 95th 5.32-3.Metals Urinary Mercury−Females Aged 16-49 Years Old.46-4.516 (.831) .03-2.744) 1.824) .43-1.806) .719 (.45) 95th 3.S.500-.30-2.45) 2.846) .592 (.87-4.650 (.52) 3.31 (1.658 (.37 (1.57-4.650 (.55) 90th 3.47) 1.65-4.45-2.56) 4.30 (1.760 (.46) 3.740 (.632 (.24-1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for females aged 16 to 49 years in the U.51 (3.10-2. Geometric mean Survey years (95% conf.

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Guo S. Osterloh J. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Takahashi Y. Langolf GD. Longnecker MP. Goldberg J. Smith JC.4(5):981-988. The hair-organ relationship in mercury concentration in contemporary Japanese.289(13):1667-1674.31:687-700. Bolger PM. Lind B. Smith PJ. Schober SE. Zeitz P. 1999-2000. Amiano P. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Vimy MJ. Hum Toxicol 1984. Am Ind Hyg Assoc J 1970. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Daniels JL. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Am J Physiol 1990. Imai H.97(2):195-200. JAMA 2003. Most B. Smith RG. Hall LL. 226 Fourth National Report on Human Exposure to Environmental Chemicals .110:129-132. Turner MD. Suzuki T. Dorronsoro M. et al. Sandler DP. Orr MF. Stern AH. Burbacher T. Amurrio A. Kaye WE. Arch Environ Health 1993.37:245-252. Azpiri MA. Vahter M. Environ Health Perspect 2002.258(4 Pt 2):R939-945.98(1):133-142. et al. Topping G. Farris FF. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vupputuri S.48(4):221229. Toxicol Appl Pharmacol 1994. Sherlock J. Effects of exposure to mercury in the manufacture of chlorine.2:117-131. Smith JC. et al. Environ Res 2005. Vorwald AJ. DeRouen TA. Br J Ind Med 1983. Jones RL. Methyl mercury pharmacokinetics in man: a reevaluation. Environ Health Perspect 2003. Leroux BG. Woods JS.124:221-229. McMahon KJ. Smith AE. Toxicol Appl Pharmacol 1996.111(12):1465-1470. Mooney TF. Martin MD. Lorscheider FL.79:786789. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment.128(2):25125-25126. Fisher HL. Acrodynia: exposure to mercury from fluorescent light bulbs. Hislop D. Allen PV. Mottet NK.Metals Sanzo JM. Tunnessen WW. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Environ Res 2005. McDowell M. Patil LS. Toxicol Appl Pharmacol 1994. Hongo T. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Stern AH. Baser M. Aguinagalde FX. Sinks TH. Public Health Nutr 2001. The contribution of dental amalgam to urinary mercury excretion in children. Pediatrics 1987. The kinetics of intravenously administered methyl mercury in man. Yoshinaga J. Newton G. Shen DD. Friberg L. Effects of occupational exposure to elemental mercury on short term memory. Whittle K.40:413-419. Environ Health Perspect 2007. Blood mercury levels in US children and women of childbearing age.115(10):1527-1531. Leitao JG. Matsuo N. Bernardo MF. Nakazawa M. 1993-1998.

and 03-04 are 0.3-91.3 (38.6 (52.3-75. semiconductor and battery industries have begun to use molybdenum.0-100) 63. which exert homeostatic regulation over molybdenum balance.2-59.2 (49.6-82.7 (51.2) 41.3) 65.4-61.7) 45.0 (41.0) 62.0-56.9-55.5-52.7-39.5-66.6) 53.4 (48.6) 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. 1997).2 (83.9 (33. 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. urinary excretion over six days CAS No.8 (42.9-83.3-115) 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.9-82.8 (67. More recently.6 (55.8-90.4) 41.9 (32.5-91.3 (47. 01-02.9 (73. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.5 (67. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (38. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.8) 40. 2001).3 (71.0) 60.5 (49.7-50. and xanthine oxidase (Kisker et al.8) 44.9) 67.7-73.2 (38..8.S.7-41.4) 42.0-71.0) 84.9 (37.0-77.5-68.7-122) 93.8-106) 88.5-41.7) 78.2) 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 (98.1-52.7 (71.Metals Molybdenum or ore deposits. WHO.3 (37.3 (79.0 (42.5) 80.0 (43.6-42.6) Selected percentiles ( 95% confidence interval) 50th 50.6-55.0 (46. and paints.1) 57.8.2) 53.2 (69.2-59.3 (53.7 (50.8 (85.1 (34.3) 85.8 (82.5-65.8) 46. 1996).9 (78.4) 45.0 (48.6 (55.7) 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. interval) 45.3) 37.7-47. hydrogenation catalysts.5) 44. population from the National Health and Nutrition Examination survey.9) 34.2 (63.8-108) 87.7) 51.3 (55.5.0-38.3 (84.0-110) 90.2 (40.8) 75.2 (55.5-46.6 (40.2) 52.9-56.7 (58.4-52.7-68.7 (44.6) 51.2) 37.8) 39.9 (44.4 (48. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.8-46.9-109) 97.4) 76.2) 40.5 (74.6-58. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.3-44.6-72.3) 54.7-92.6-96.1) 126 (106-147) 109 (94.4-75.6 (73.4 (79.2 (56. 2001.0) 55.3-108) 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 47.8) 48. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.7-60.7 (73. Fourth National Report on Human Exposure to Environmental Chemicals 227 . 7439-98-7 General Information Elemental molybdenum is a silver-white.1) 60.2 (49.1-88.5 (41.4 (72.1-48.2-79.2-53.0) 54.2-37.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.6) 71.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.2-91.1-63. see Data Analysis section) for survey years 99-00.1-52. lubricants.9-85.7-84.7) 75th 84.7-96.6 (43.3) 41.3 (46.1-55.0-62.5 (37.5) 47.1-59.1-51.1) 59.1) 35. Excretion occurs predominantly via the kidneys.5) 85.7-51.0-53.9 (52.9 (40.0-65.8-94.6) 93.9 (34.2 (61. and 1.7) 57. Compounds of molybdenum are also used as corrosion inhibitors.0 (76. inks.1-44.3-47.6) 71.0) 45.5) 60.0) 97. chemical reagents in hospital laboratories.7 (36.9) 62.7) 77.3 (55.1 (91. 0.5-52.7-91.7) 78.0 (81.0) 39.2-70.5 (48.5 (41. respectively.0-85.5-124) 108 (92.7) 46.5 (43.5 (81.3 (73.7-105) 69. aldehyde dehydrogenase.4) 56.1) 46. At a daily oral molybdenum dose of 24 µg.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.5) 80.4-82.4) 49.4 (34. In humans.6-46.2) 79.8-49.1) 82.6-62.0 (42. and in pigments for ceramics.3 (64.7) 86.4) 52.7 (45.0-101) 82.6 (40.2-42.9-55.7 (37.4 (80.3) 83.3) 47.1 (71.2) 48. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.

8-46.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.0) 36.9 mg/kg/day and established a tolerable upper intake level of 0.1 (44.1-43.4) 61.5-50.5 (35.3 (51.7-120) 87.8-52.8) 38.2) 42.7 (77.7-38.2) 39.8-66.8-84.9) 44.5-119) 90.5 (41.2-49.9 (39.4) 40.5 (79. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.3) 64.2 (33.1-79. 1995). interval) 43.7-100) 77.9 (64.3 (71.6) 39.0-133) 119 (88.4) 89.3-45.9-118) 91.3-59.8) 39.1) 101 (83.4 (44.4-107) 85.8 (75.9 (79.1-39.1-81.2-96.0-46.3 (37.5) 90th 108 (97.1-34. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6-61.1-45.9) 92.9 (64.1) 43.8) 71.2 (43.9 (73.8) 45.4-106) 85.9-87.3) 61. Molybdenum is generally considered to be of low human toxicity.4 (67..8 (57.2 (36.4) 116 (101-126) 104 (88.3-56.7-62.5 (50.8) 61.0-46.1) 56.1-40.7) 42.3 (58.8 (90.9) 40.9-41.1) 37.4-120) 101 (84.3-46.1-43.6-61.3) 41.7-44.1-109) 89.3) 43.1 (54.0 (58.9 (49.8-118) 81.9 (36.5 (65. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.9-61.9) 41.6) 43.9-45.7 (66.1 (40.6-63.2) 42.0) 53.3 (36.4) 48.Metals was 18% of the ingested dose. respectively.2) 39.7) 112 (95.5 (39.5 (37.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.2) 37.5 (38.1) 65.0-120) 85.5) 72. and urinary levels reflect intake from all sources.3 (71.0 (74.4-39.2 (52.9 (40.4-76. urinary excretion over six days rose to 50% and 67%.5-62.9) 31.2 (69.1 (49. of the ingested dose (Turnlund et al.4 (37. U.6) 48. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-112) 78.0) 44.5 (34.9-68.5-35.2-47.9-96.1-100) 86.6 (71.1 (37.7-137) 129 (109-155) 112 (97. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.5 (40.5) 60.2-103) 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. Biomonitoring Information Molybdenum is an essential element for health.9-71.8-42.4) 122 (107-133) 109 (99.2-46.1 (38.3-141) 109 (81.6 (59.6-78.9-42. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.7) 62.8) 38.7-52..5) 63.03 mg/kg/day in humans (IOM.5-69.9 (39.5 (37.2) 38. 1961.5) 71.2-96. 1997)..4-185) 106 (94.2 (40.2 (50.8) 37.2-121) 107 (92.5-99.1 (33.5-70.1 (39.6 (36.5 (54.6-63. 1993).5 (39.0) 72.4 (78.5 (83.5-45.5 (36.6 (38.0-41.8 (36. but available epidemiologic data are scant.4 (40.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.4) 58. 2001).3 (83.7) 45.8 (37.5 (41.8-47.5-97.4 (53.1-41.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.1 (42. In industry.3-43.6 (36.0) 33.5 (78.9) 79.4-41.7-93.2 (40.0) 62.7-43.6 (42.4-42.3-68.5 (80.1-67. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.3) 57.4-66.0) 39.0-56.2-40.0) 38.3) 37.3-44.2) 58.1) 37.1 (30.4) 60.5-92.3) 44.5-46.8 (56.0-38.5-44.2 (37.2-80.0 (80.8-65.9-40.1-127) 90.9-45.3-52.9-117) 57. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.8) 79. and clinical or epidemiologic evidence of adverse effects is limited.5) 73. population from the National Health and Nutrition Examination survey.7 (75.7) 41.4 (55.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .5 (59.6) 36.5 (40.2 (73.1) 40.7 (30.2) 37.1-38.4) 47.3) 56.7) 75th 63. 1999).6-41. at daily oral doses of 95 µg and 428 µg.3-115) 98.8-47.2-41.3 (55.5 (65.7) 57.2 (57.7-40.0) 88. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 85.2-65.6-76.3 (36.4 (59.8) 62.6) 39.4 (56.1 (38.1-39.3 (37.0) 39.6-45.2) 43. Based on studies finding adverse reproductive effects in rats and mice.3 (53.5 (35.2) 55.0-103) 103 (90.1 (82.4) 44.6-88.4) 77.5-60.6) Selected percentiles ( 95% confidence interval) 50th 41.6 (57. EPA.3) 40.S.7) 53.2 (40.9 (35.0 (35.8-67.7) 115 (93.5-48.S.

National Toxicology Program (NTP). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Available at URL: http://ntp. Shmavonyan DM. Schindelin H. edu/openbook. X. Yarovaya GA. Rees DC. Sabbioni E. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. White MA. 2005. Weyler JJ. vanadium. Dietary reference intakes for vitamin A. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Sci Total Environ 1998. Aprea C. iodine. In: Trace elements in human nutrition and health. boron. Keyes WR. Vermeire PA. EPA). Minoia et al. Environmental Protection Agency (U. manganese. Food and Nutrition Board. A study of 13 elements in blood and urine of a United Kingdom population. Washington. Available at URL: http://www.niehs. Molybdenum 1993 [online]. 2001). Ronchi A. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Van Meerbeeck JP.22(3):179-191. Occup Environ Med 1999. Schaub J. Turnlund JR. Zhurnal Obshchey Biologii 1961. copper. silicon. Peiffer GL. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.. Turci R. 4/14/09 Sievers E. Institute of Medicine (IOM). Analyst 1998. 4/14/09 Iversen BS. Kisker C. Christensen JM. 144-154. Rapid Comm Mass Spectrom 2002. Am J Clin Nutr 1995.gov/index. Ann Rev Biochem 1997. Available at URL: http://books.nap.htm. Gatti A. Minoia C. Molybdenum absorption. pp. 56:322-327. Geneva: WHO. and zinc: a report of the Panel on Micronutrients.epa.php?record_id=10026&page=420. World Health Organization (WHO). Fourth National Report on Human Exposure to Environmental Chemicals 229 . Sabbioni E. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. 1998. Molybdenum. Occupational risk factors of lung cancer: a hospital based case-control study. Molybdenum in infancy: methodical investigation of urinary excretion. chromium. 16:1313-1319. Menne C. TR-462. 1996.Metals in urine for the U. nickel. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum.15(2-3):149-154. excretion. 4/14/09 White MA.62(4):790-796.nih. J Trace Elem Med Biol 2001. 1998). Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No.gov/iris/ subst/0425.216:253-270. et al. White and Sabbioni. iron. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. 2001. van Sprundel MP. Sciarra G. pp.. Third National Report on Human Exposure to Environmental Chemicals. References Centers for Disease Control and Prevention (CDC). Trace element reference values in tissues from inhabitants of the European Union.123(1):81-85. Droste JHJ.S.S.66:233-267. molybdenum. vitamin K. (DC): National Academy Press. 420-441.. 2005). Atlanta (GA). U. Koval’skiy GA. Kristiansen J. Schleyerbach U. Molybdenum-cofactorcontaining enzymes: structure and mechanism. arsenic. 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. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. 2002.

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

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

Influences on human internal exposure to environmental platinum..55(2):138-140. Schierl. Nickel. et al. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Biomonitoring Information Urinary platinum levels reflect recent exposure. 2003. Levels of platinum in urine for the U.htm.inchem. Allergy and histamine release due to some platinum salts. Stilianakis NI. 2004. Ewers U. Crocker W. 2001). ruthenium. Analyst 1998. Schierl R.. Saindelle A. 2000. Ruff F: Histamine release by sodium cholorplatinate. 3/31/08 Moore W Jr. Pethran A. Pethran A. Hauff K. 206:15-24. population were below the limit of detection (0. Turfeld M. 5th ed. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Petrucci F. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Carelli G. Biomonitoring of traffic police officers exposed to airborne platinum. Occup Environ Med 1998. Part 1: monitoring of urinary concentrations. 2003. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Senofonte O.. Seiwert M.005 µg/L (Iavicoli et al. 1991 [online].9:152-158. International Programme on Chemical Safety (IPCS). Jankofsky M. Pethran et al. Nowak D. Gieler U. Boos KS. Alimonti A. et al. eds. New York: John Wiley & Sons. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Powell CH. Available at URL: http://www.. palladium.4(1):27-36. Arch Environ Health 2001. Cohrssen B. van de Weyer C. Urinary excretion of platinum from platinum-industry workers. Iavicoli I. Uptake of antineoplastic agents in pharmacy and hospital personnel.org/documents/ehc/ehc/ehc125. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Neuendorf J. Herr CE. Thornton I. Hall L. Environ Res 1975a.61(7):636-9.207(1):69-73. pp. J Expo Anal Environ Epidemiol 2003. Urinary platinum levels associated with dental gold alloys. Hysell D. and gold excretion of patients after insertion of noble-metal dental alloys. Platinum concentrations in urban road dust and soil. Huber R. Environ Health Perspect 1975b. Kuster W. In: Bingham E. rhodium. Schulz C. Fries HG.04 µg/L) in this Report..org/documents/ehc/ehc/ ehc125. 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. Ensslin AS. Seifert B. Kazantzis G.70(3):205-208. Parrot JL. and platinum. Gromiec JP.10:63-71. 289-380.htm. Schierl et al. Wilhelm et al. Campbell K.. 2003). Wilhelm M. Farago ME.. Schierl R. References Becker K.13(1):24-30. Raab W. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure..01 µg/L (Becker et al. Kulka U. Kelly J. Int Arch Occup Environ Health 1997. 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. Herr et al.56(3):283-286. 2004) or less than 0. Int J Hyg Environ Health 2004. Br J Pharmacol 1969.. 2004). Biomarkers 1999. Ruff F: Platinum and platinosis.. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.35:313-321. Bocca B. osmium. 1998). 1998). Moore W Jr. Schierl R.19:685-691. Kaus S. Patty’s Toxicology. Herr et al. 1997. Czerczak S. Platinum. Schierl R. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.76(1):5-10.123(3):451-454. 2003. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Arch Environ Health:1969.S. Begerow J. Occup Environ Med 2004.inchem. Environmental Health Criteria 125.. and in blood and urine in the United Kingdom. Angerer J. Hysell D.Metals the International Programme on Chemical Safety at http:// www. et al. Int Arch Occup Environ Health 2003. which elevate urinary platinum by five to twelve-fold (Begerow et al. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Schulz C. International Journal of Hygiene and Environmental Health 2003. Kavanagh P. Saindelle A. Duneman L:Long-term urinary platinum. Fruhmann G. Blanks R. Hebert R. 1999. Rommelt H. Several studies have shown that background concentrations in general populations were usually less than 0. palladium. Grimm CH.

260-.218) .220 (. representing distribution into other tissues.160 (.330) .201 (.280) . Thallium disappears from the blood with a half-life of several days.340-.135-.490) .250-.430 (.201 (.243) .390-.400-.154-.460 (.240-.340-.360 (.190 (.360-.350-.450 (.270-.400) .280 (.160 (.220 (.340 (.145-.179-.450 (.490) .400 (.200 (. 01-02.330-.260) .430) .370) .02.330) .160 (.350-.330-.320) .240) .290-.196) .190-.167-.400 (.490) .300-.330) .400) .400-.450 (.197 (.470 (.147-.220) .165 (.290 (.350-.150-.430 (.230-.180-.290 (.470) .420-.440-.200 (.270 (.171 (.190 (.260 (. In addition.280 (.160-.400 (.190 (.400 (. interval) .280-.190 (.420) .230-.156) .260-.440 (.420) .147-.170-.420-.390 (.S.450) .390) .470 (.220 (.170-.160 (. In the past.330-.156-.370 (.280) .270-.160 (.180-.178) .183) .260 (.270 (.147-.260-.440) .520 (. 2005).215) .350 (.172 (.200-.202 (.450 (.310) . thallium readily crosses the placenta and also distributes into breast milk.300) .250) .153-.230) .310 (.200) .430 (.170 (.300 (. In the United States.420-. 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. and 03-04 are 0.440 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.460) 336 362 290 697 746 725 1380 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .200) .690) .180 (.460-.180) .187-.173) .218) .470) .290) .340) .260 (.360-.170-.370 (.410-.400-.590) .420) .202 (. however.370-.440 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.420 (.520) .480) .400-.490 (.230-.250-.410 (.410 (.330) .300) .160-.430-.162-. and 0.390-.330-.260-.167 (.217) .400 (.220) . the latter being the current major industrial consumer of thallium in this country.300 (.145 (.160-.330-.290) .480) .390) .480) .370-.170-.185-.150-.430 (. respectively.149 (.250-.410 (.150-.184 (. 0.240) .145-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.133-.330-.440) .150-.520) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.250-.190 (.320) .173) .350 (.200-.410-.290) 90th .159 (.159 (.188) .134-.370 (.230) .173-.260-.270-.360-.200 (.290 (.370 (.630) .290) .370-.350-.560) .220) .400-.390-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.510) .02.200 (.250 (.02.450 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.320) .430-.180-.220 (.320 (.163) .390) .170-.172) .159 (.217 (.160-. From these and other sources.330-.240) .200-.250-.280 (.420) .500) .210 (.360-.410 (.270) .360 (.310 (.180 (.190 (.500 (.380 (.180-.270 (.550 (.360) .430) .230) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.370) .300) .370-.300 (.390) .170) .410 (.360 (.200) .370 (.157-.144 (.350-. it has not been specifically mined or refined in the United States since 1984.175) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .200) .170 (.250-..240-.210) .210-.183) .225) .590) .400) .290 (.158) .380 (.280-. Human health effects from thallium at low environmental CAS No.510 (.176 (.410 (.640) .350-.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 .150-.290-.480) .340) .137-.300) .202) .460) .290 (.320-.170) .206) .450 (.180 (.350) .380-.167-.192) Selected percentiles ( 95% confidence interval) 50th .450 (.220-.220) .440 (.170) .230) .400) .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 .182-.360-.480) .170-.Metals Thallium depilatory cosmetics.239) .196) .420-.210 (.200 (.150-.200) .177) .500) .181-.220) .197-.191 (.490) Total .270) .450 (.172 (.270 (.410) .290 (.380-.410-.340-.360 (.420) .156) .200) .400) 95th .280) .170-.185 (.520) .250 (.200-. thallium was obtained as a by-product of smelting other metals.420) .390-.250-.440) .410-.350) .160-.470) .220) .390 (.430-.148-.140-.240-.146 (.450 (.410-.310 (.230 (.500) .340-.200 (. population from the National Health and Nutrition Examination Survey.370 (.220 (. see Data Analysis section) for Survey years 99-00.370 (.380) .155 (.420) .290) .310-.410-.270 (.170 (.250-.180) 75th .

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

Pietra R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Schmidt M. 1998).. with concentrations ranging up to 76. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust.Metals (CDC. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al.48(4):375-389.95:89-105.35(1):4-9.gov/toxprofiles/tp54. Pirkle JL. White MA. Minoia C. Kramer U. Sabbioni E.216:253-270. White and Sabbioni. 1981. Paschal et al. Apostoli P. Trace element reference values in tissues from inhabitants of the European community I.. Int Arch Occup Environ Health 1980. blood. Centers for Disease Control and Prevention. Dolger R. Investigations of thallium-exposed workers in cement factories.5 μg/L. (1981) studied 1. Third National Report on Human Exposure to Environmental Chemicals. et al.cdc. Boisson P. 7/15/09 Blanchardon E. 1998. Challeton-de Vathaire C. Trace element reference values in tissues from inhabitants of the European Union. Marcus RL. A study of 46 elements in urine. Morrow JC. Schaller et al. Valentin H. 2005. et al. Schaller KH. Available at URL: http://www. X. Environ Res 1998. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Sabbioni E. Investigation of a working population exposed to thallium. Brockhaus et al. Raithel HJ. Sampson EJ.76(1):53-59. A study of 13 elements in blood and urine of a United Kingdom population. Gallorini M. Atlanta (GA). Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging.. Ewers U. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Minoia et al..113(1):47-53. and serum of Italian subjects. 2005. Pozzoli L. 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. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium.S. Buhlmeyer G.html.265 people living near a thallium-emitting cement plant in Germany. et al.1 mg/m3 (Marcus. Martin J-C. Brockhaus A. Jackson RJ. 1992 [online]. Int Arch Occup Environ Health 1981. Radiat Prot Dosim. J Soc Occup Med 1985. References Agency for Toxic Substances and Disease Registry (ATSDR). Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Wiegand H. Toxicological profile for thallium. 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. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Ting BG. Cassot G. Paschal DC. Soddemann H. Sci Total Environ 1990. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. 1985). Trace metals in urine of United States residents: reference range concentrations. Sci Total Environ 1998. 1980.47(3):223-231.atsdr. 2005) and are shown with results from NHANES 2003-2004 in this Report. Celier D. Manke G. 1990.

084 (.380-.062 (.250-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.084-.060-.240-.110 (.440) .220-.370-.390 (.310-.140 (.250) .132) . and 03-04 are 0.420-.430 (. mainly as scheelite (CaWO4).070-.060 (.130-.270 (.113 (.110 (.095-.410 (.550) .530 (.150) .140 (.090-.670) .120-.320 (.340) .096 (.310-.170) .123-.069-.090 (.110 (.060-.260-.S.110-.137 (.130) .510 (. Evidence is lacking for the carcinogenicity of tungsten.100) .260-.093 (.092) .120-.380-. see Data Analysis section) for Survey years 99-00. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.107 (. which are used in rock drills and metal-cutting tools.180) .070) .550) .090-. 01-02.550 (.190 (.950) .490 (.430 (.290) .640 (.080-.090 (.111-.060-.400-.320 (.560) . Occupational exposure is from dusts released during grinding or drilling of hard metals.650) .350) .340-.086 (.560 (.090-.100) .370 (.520) .270 (.340-.560) .04.400) .140-. which is used in the steel industry.190) .120) .170) . Little information is available on the toxicity of tungsten.120-.073-. interval) .110-.105) .160 (.270-.460 (.076 (.180 (.320) .088 (.280 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.300-.130 (.550) .116) .260 (.560) .230-.073 (.140 (.570 (.430) .082) .360-.100) .300 (.090) .270-.120) .230-.590) .070) .190 (.160-.130-.210 (.520) .064-.100-.090-.060-.410-.630) .430-.060 (.400 (.110-.120) .300 (.090-.160-.260) .230-.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 .110) .310-.180-.113 (.066-.170 (.100) Selected percentiles ( 95% confidence interval) 50th .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 .320-.122) .310 (. population from the National Health and Nutrition Examination Survey.200 (.120-.360 (.090 (.160) . and for producing ferrotungsten.091) .120) .500 (.250) .430-.070 (.088) .160 (.230-.220) .160-.130) .580) .500 (.180-.210 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).130-.250) .170-.330-.071-.101-.530 (.450-.Metals Tungsten CAS No.230) .180) .090) .620) .810) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-1.180-.097-.090-.330) .380-.113 (.070-.480) Total .180) .113 (.460 (.510-1.170 (.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 .360 (.084) .300) 95th .050-.400 (.210) .160 (.250) .260-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.330 (.105 (.065-.204) .280 (.100 (.050-.220) .140) 90th .120-.100 (.150 (.090-.070 (.062 (. respectively.082-.056-.360) .800) .080 (. 0.060-.070) .130) .093-.190-.095-.120-.290-.130 (.130-.068) .830) .082 (.150 (.071 (.460) .060 (.350) .080-.230 (.092 (.790) .310) .135) .300) .080) .080) .050-. Tungsten compounds are used as lubricating agents.330) .070-.050-.420-.210 (.510-.360-.470-.109) .130) .290-.081 (.104) .160 (.260 (.073) .160) . and 0.070) .070-.620) .370) .270-.060 (.560) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.460) .350) .126) .070 (.380-.080 (.470) .470 (.076 (.110) .180-.04.120) .140 (.160-.087) .101 (.200-.069) .380 (.120 (.570 (.00) .093) .190-.080 (.078-.250) .470) .400 (.180) .158 (.110 (.100-.150-.080 (.53) .210 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .080) .190-.100) .133) .370 (.090-.370-.530 (.350 (.190-.065 (.090) .370 (.100) .290) .096-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Tungsten is used mainly for producing hard metals.230) .210-.210 (.120) .130) .770 (.140-.082 (.100 (.270 (.060 (.490) .080-. and as catalysts in the petroleum industry.087-.220 (.240 (. bronzes in pigments.060-.073-.170) .310-.450 (.080 (.220) .092 (.330-.290-.110 (.180 (.300 (.090) .080) 75th .150 (.520) .400 (.070-.360 (.04.310-.100-.690) .060 (.056-.290 (.620 (.250) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.430 (.460 (.380) .160 (.250-.320-.280-.170) .151) .800) . filaments for incandescent lamps.500) .390) .074-.340-.470 (.100 (.077-.200) .058-.270-.380 (.

122-.098-.386) .222) .144 (.069 (.136 (.065-.063 (.091 (.209-.130-.085-.412 (.138) .267-.484) .079) .167-.069 (.073 (.098) . or exposure that a control group of non-metal workers had mean levels differences.056-.072 (.301) .081 (.092) .081-.144-.293 (.150-.151 (.436-1.083-.090-.100 (.216 (.392) .237) .075) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.284) .063-.299 (.484 (.091) .197) .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 . Patients with medically-inserted tungsten found at increased levels in drinking water.145 (.797) .148) .075 (.216-.283) .272-.094-.339 (.070 (.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 . 2003.197 (. 1998).062 (.154) .077) ..084) .302-. population.095-.359 (.150-.059-.089 (.465) .061-.315-.197) .121 (.727) .240-.116 (.091 (.079 (.054-.197-.078-.103-.347 (.136-.233-.093-.081 (.180-.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 .116-.104-.105 (.096) .339 (.201) .205-.071-.360 (.385 (.093) .333 (.143-. 2001-2002.439 (.410-. interval) .072-.258-.056-.211 (.331-.126-.086) .078) .333) .136-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.S.453) .109-.317 (.326) .148 (.063-.083) .065) .074-.261-.482 (.184 (.306) .155-.270 (.154) .308) .169) .067 (.634 (.218 (.215 (.079) .216 (.086-.287) .059 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.125 (.066 (.179-.136-.265 (.300-. 2005).353 (.079) .354-.383 (.098 (.164 (.208-.073 (.105 (.250 (.085) .150 (.146 (.167) .074-.122-.158) .555 (.080-.086) .133) .381) .088) .068 (.108) .179-.084 (. Nicolaou et al.094) .308) .087) .060 (.064-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.088) .168 (. 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.073 (.439 (.275 (.582) .109 (.057-.080-.253) 95th .201 (.176-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.065-.426) .098-. population from the National Health and Nutrition Examination Survey.301) .190) .375) .082) .063 (.063-.059-.216-.074) 75th .554) ..078 (.116) .146 (.081) .167) .333 (.065 (.358) .216-.086) .414) .255-.214-.222-.188-.301) .055-.333-. measure urinary tungsten.359 (.200-.133) 90th .341 (.094) .139 (.214) .199 (.059-.379 (. similar to those in this Report (Schramel et al.054-.121-.099-.181 (.279 (.279 (.431) . 1997).075) .217-.300 (.095) Selected percentiles ( 95% confidence interval) 50th .152-.049-.300-.071) .169 (.091) .111 (.124 (.215) .452-.158) .329 (.079 (.108-.058-. (1987) found possibly due to methodologic.064-.333) .133) .067-.161) .198) .174) .285) .120) .074 (.267) .880) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.165) .206-.120) .073 (.067 (.431) .077) .119-.353 (.237-.075-.198-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.317) .136-.153-.253 (.075 (..199 (.063-.364 (.317-.069-.071) .28) .089) .060-.079) .462) .203-.167-.187) .250-.107-.354) .143 (.431) .224) .080 (.439) Total .083) .070 (.278-.071 (.091) .333-.231 (.500) .S.186 (.426) .083 (.072-.158 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.237) .117) .065 (.294 (.131-.077-.075-.538) .106 (.436) .071 (.122 (.258 (.138 (.344-.090-. Using neutron activation analysis to 2000.176-.497 (.078 (.217-.465) .667 (.100) .158) .333 (.139-.340 (.066 (.S.117 (. 2001).084 (. and 2003-2004 (Paschal et al.157) .253-.333 (.071 (.083 (.077-.071) .130 (.085 (.084) .605) .231-.124-.279 (.082) .739) .061-.074) .459) .174 (.823) .170-.302-.057-.667) .100) .(Kraus et al.080 (.245-.286-.082 (. population (CDC.139) .138 (.255 (.119 (.146) .300) .098-.053-.068-.078) .060-.329-.250 (.200-.065-.061-.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 .087 (.255 (.153) .091) .125) .

62:380-384. Schramel P. Atlanta (GA). lead. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. 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. Angerer J. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. 238 Fourth National Report on Human Exposure to Environmental Chemicals . cadmium. Cancer Clusters. Nevada Exposure Asssessment. The determination of metals (antimony. Weber A. Paschal DC. Environ Res 1998. Morrow JC. Catheter Cardiovasc Interv 2004. References Bachthaler M.69(3):219-223. and hair (Bachthaler et al. Zobelein P. [online] 2003.(2):73-77. Seghizzi P. Occup Environ Med 2001. Churchill County (Fallon). Jackson RJ. 4/15/09 Centers for Disease Control and Prevention. Schramel P. Trace metals in urine of United States residents: reference range concentrations. Manke C. Cassina G. Ting BG. Lenhart M.58(10):631-634. Mosconi G. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Available at URL: http://www. Feuerbach S.. Paetzel C. 2004). Third National Report on Human Exposure to Environmental Chemicals. Angerer J. National Center for Environmental Health. Schaller KH. Centers for Disease Control and Prevention. Int Arch Occup Environ Health 1997. Sabioni E.gov/nceh/clusters/Fallon/study. Pietra R. Sampson EJ.htm. Nicolaou G. et al. J Trace Elem Electrolytes Health Dis 1987. mercury. tellurium. bismuth. platinum. 2005.Metals blood. thallium. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Wendler I. palladium. Pirkle JL.cdc. Link J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kraus T. urine.76(1):53-59.

021-.016) .009-.021 (.017-.051) .006-.037) Total .011) .022-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.012) .027) .054) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).018) . Uranium has many commercial uses. human exposure occurs primarily by inhaling dust and other small particles.018 (. 0.007 (.007-.006-.041 (.016 (.015 (.012) .017) .064 (.008 (.007) .027 (.012 (.011-.015 (.030 (.024-.023 (.006-. milling.008 (.006-.027-. Variable concentrations of uranium occur naturally in drinking water sources.023-.017-.046) .029-.014 (.035) .008 (.043) .008 (.008-.009 (.020-.008 (.023-.008-.018) . and 0.028-.027-.009) * .036 (.009) .038 (.008 (.009 (.018) .039) .008) .018 (.033 (.038) .021) .010-.007-.020 (.006 (.010 (.050) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.018) . In workplaces that involve uranium mining.009 (.158) .031 (.014 (.009 (.029-.010-.009) .065) .028-.069) .044 (.008 (.011-.009) .047 (.031 (.020-.045) .016) .72%).013 (. 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.009-.027-.026) .010) .009) . interval) .009) Selected percentiles ( 95% confidence interval) 50th .007 (.053) .026 (.054-.007 (.036) .026) .007-.035) .017-.035-.006-.023) . see Data Analysis section) for Survey years 99-00.062) .037) .025-.014 (.043 (.028 (.006-.011) .011) .019-.006-.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 .011) .009-.016) .011-.013) 90th .279) .040) .010 (.026) 95th .007-.017) .009) .008 (.007-.033) .027 (.010-.007-.005-.033-.022-.048 (.017-.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 .007 (.009 (.013 (.026-.021-.048) .022 (.007-.042) .008 (.018-. 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. population from the National Health and Nutrition Examination Survey.015) .034-.013-.004.007-.027 (.012 (.016-.012 (.031 (. respectively.073) . nuclear fuel.045) .015 (.036) .009-.013-.023 (.009-.010) * . including nuclear weapons.008 (.039) 1227 1335 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .010) .008-.009 (.031-.010 (.037) .011 (.012-.056) .009) .063) .010) * .006-.036 (.008-.022-.008-.007 (.014 (.010) .006-.049) .007-.008 (.056) . and 234U.030 (.010) .023-.015-.039) .020-.008 (.066) .046 (.009-.127) .013 (.034-.010-.007-.039-.026-.015 (.016-.017 (.007) 75th .088) . 235U (about 0.Metals Uranium CAS No.007-.019-.009) .011-.009-.026 (.040-.017) .007 (.032 (.006-.005.013 (.114 (.010 (.S. and 03-04 are 0.016) .034) .009-.010) .028 (.007-.004.011) .007-.012) .009) .021) .008) .007) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.007 (.010 (. Since the 1990’s.006 (.005-.009 (.012-.012-.014 (.012) .008) .067) .022) .011 (.024-.027) .009 (.052 (.037-.046-.007 (.008-.012 (.037) .050) .010) .020-.011) .012-.009) .021 (.008) .012-.031 (.023-.067) .009 (.016) .007) .023 (.013 (.037 (.036-.006 (.054) .010) .040-.016-.065) .023) .024 (.013 (.026 (.006-.019 (.036-.013 (.007-.007-.011-.009) .009-.010) .046 (.060 (.008) .009) .011) .014 (. and as an aid in electron microscopy and photography.009) .040 (.041 (.029 (.072) .017) . 01-02.005-. in some ceramics.046 (.008 (.008 (.011-.013-.008 (.012-.017) .007) .012 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .007-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.016) .042 (.008 (.012 (.019-.011-.049) .017 (.020) .006-.030 (.010-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.008-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.017-.008-.017-.006 (.027) .021 (.030) .013) .009) .007-.040 (.023) .053 (.006-.027 (.007 (.021) .027) .031 (.007) .030-.015) .028 (.009-.005-.005-. or processing.010-.007 (.046 (.055 (.007-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.020) .019-.008 (.009 (.007 (.040) .024-.020-.033 (. Thus.

059 (.025 (.013 (.037 (.006-.007) .018 (.074) .018-.031-. where limited absorption occurs (less than 5%).015) .007 (.006-.021 (.005 (.005-.013) .008) .011) .008 (.008) .010 (.015-.006 (. liver.039) .007-.009) .016) .025) 95th .016) .011-.010-.020-.028 (.007 (.006-.009) .006) .034 (.007 (.019-.015 (.007-.017-.014-.030 (.051) .050 (.022 (.018-.015) . After exposure to soluble uranium salts.012) .006-.008) .026 (. 0.022) .007 (.006-.014) 90th .010-.034-. Radiation risks from exposure to natural uranium are very low.027) .008) .013 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.019) .1%-6% of an ingested dose may be absorbed.026) .024) .007 (.012) .015-.009-.005-.058) .009 (.008 (.007 (.006 (.007-.019-.024) .016) .013-.010-.027-.024) .008-.011-.009 (.025-.016) .009) .010-.039) Total .011-.006-.011-.025-.008 (.058) . population from the National Health and Nutrition Examination Survey.019-.020-.011) * .029) .010) .014 (.035 (.053) .030) .015-.010 (.027-.006-.005 (.015 (.048) .009) Selected percentiles ( 95% confidence interval) 50th .012 (. In cases of retained DU shrapnel.010) * .017 (.014) .019 (.006) .016) .027-.006-.009) . Uranium is eliminated in feces and urine.006 (.012 (.006-.024-.051) .019) .015 (.029) .010-.007-.007-. with much slower elimination from bone.034 (.012 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.035 (.012 (.034) .009) .051) .007 (. 2003). 2005).044) .034 (.039) .033) .011-. the shrapnel acts as a source of chronic.016-.009-.028 (.017) .007-.038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .029 (. 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.007-.040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result.006-.011) .006-.010) .011 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.013 (.006-.042) .030-.028-.006-..008) 75th .009) . which can occur occasionally from high occupational exposure.270) .077) .007) . After long term or repeated exposure.011-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.034 (.042-.029 (.020-.054) .024) .013 (.012-.026 (.025-.006-.010-.007) .022-.010) .006-.007 (.008) .009 (.011-.013 (.006-.009) .021 (.030 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.004-. Depending upon the specific compound and solubility. 240 Fourth National Report on Human Exposure to Environmental Chemicals .007 (.017) .032) .040 (.012 (..006 (.005-.050) . low level exposure.013) .007 (.007 (.016-.026-.005-.005-.008) .015 (.017-. which represents distribution and excretion.014) .028) .029) .018-.007 (.007 (.033 (.006-.011-.005-.010-.063) .022-.014-.007 (.030 (.010 (.028) .016-.006-.008 (.006) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.016) .009) .020 (. Health effects from uranium exposure result from chemical toxicity to the kidney.007 (.009-.006-.007 (.067) .024 (.009-. Inhaled uranium-containing particles are retained in the lungs.005-.020) .100 (.013 (.015-.013 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.005 (.029 (.008) .013 (.039) .025 (.010-.008 (.011-.023-.041) 1227 1334 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .010 (.034-.012) .019 (.007 (.027 (.010-.015) .033 (.030) .008 (.006-.016) .007-.042) .021) .008 (.008-.009 (.008 (.034 (.009-.033 (.010-.014) .006) .027 (.020 (.006) .016-.022 (.013 (.026 (.015-.025-.008-.009) .027-.008) .031 (.146) .024 (.009 (.022 (.019 (.008 (.018-.053) .020 (.006-.014-.028) .012 (.010-.008-.050) .022-.006-.080) .005 (.021-.006-.007 (.010) .008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .017) .008-.032) .019-.024-.056) .011 (. kidneys.016 (.011) .006 (.017 (. After inhalation.021 (.033 (..018) .009) .014 (.007 (.012 (.028) .004-.027) .012-.008) .016) .013 (.Metals impact.017-.017-.008) .007 (.013) .009) . interval) . 1992).048) .018-.010) .041) .030-.027 (.006 (.010) .020-.009) * .024 (.029) .047) .021 (.008) .010 (.007 (.024) .043 (.045 (.008 (.007-.008-.061) .024-.006-.019-.051 (.015) .S.007-.009-.

(Kurttio et al. 1994.62:562-566. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. The U.atsdr. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 2003. the geometric mean urinary uranium concentration was 0... NRC.78:143-146.. Radiation protection dosimetry.html. 2004). Carmichael AJ. Hamilton MM. 2006). 1-49. the median urinary concentration was 0. 2004). Breitenstein BD. Drinking water and other environmental standards have been established by U. Sci Total Environ 1991. McDiarmid M. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Pillai KC. Boyd P. 2004).110 to 45 μg/L (Ejnik et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. in that the levels were below their respective detection limits (Byrne et al. 2006. 1978). Health Phys 1992.066 μg/g creatinine (Gwiazda et al. Guidebook for the treatment of accidental internal radionuclide contamination of workers. (May et al. environmental levels) and health effects is available from ATSDR at: http://www. urinary levels of uranium were as high as 9.S. although slightly increased during and after deployment. Dietz LA.. Dang HS.. In a study of 105 persons exposed to natural uranium in well water.S. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Ejnik JW.S. Pullat VR. soldiers evaluated before. Stradling GN.S. pp.078 μg/L (ranging up to 5. respectively. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. during. In 17 U.. A cohort of 46 U. IARC and NTP have no ratings for uranium human carcinogenicity. Horan P. Atlanta (GA). and 2003-2004 (Dang et al. Durakovic A.. In: Gerber GB. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Komaromy-Hiller et al.. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Thomas RG. 28 soldiers who may have been exposed to DU by inhalation.S.cdc. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.55 μg/L (median 0. Galletti.1996. 1991... Volf V. 2002. Squibb K.. or wound contamination. Benedik L. 2000). 2006). Mil Med 2003. Health Phys 2000. 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. population. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Six workers in a depleted uranium program showed concentrations of 0. 2001-2002. 2006).107:143-157. Metivier H. ingestion. had a mean urinary uranium concentration of 0..1992. Kent (England): Nuclear Technology Publishing. McDiarmid et al.162 μg/L) (Orloff et al. et al.. 2005. EPA.. Centers for Disease Control and Prevention (CDC). 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). Zimmerman I. 41 (1). In the same study. Hamilton et al.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Information about external exposure (i. 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. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. eds. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. with emphasis on quality control. References Bhattacharyya MH. 2002).168(8):600-605..gov/ toxpro2. Byrne AR. but in whom no shrapnel was embedded. Tolmachev et al. 1992. and no consistent effects on multiple endpoints of kidney function were found.61 μg/g creatinine. 2006). the median urinary uranium concentration was 2.011 μg/L (McDiarmid et al. Muggenburg BA. Uranium content of blood. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. 2000).S.e. Third National Report on Human Exposure to Environmental Chemicals.. Vol. Karpas et al.65 μg/L)..

81:45-51. Gucer P. Health Phys 1996. Radiat Environ Biophys 2005. Paschal DC. et al. Element reference values in tissues from inhabitants of the European community. Saha H. Tolmachev S. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Paretzke HG. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Roth P. Nuclear Regulatory Commission (NRC) Guide 8. May LM. McDiarmid M. Squibb K. Health Phys 2002. Saha H. Sampson EJ. NRC). Ting BG. Human exposure to uranium in groundwater. McDiarmid MA. Engelhardt SM. Karpas Z. Roiz J. Charp P. Kuwabara J.44:29-40. 242 Fourth National Report on Human Exposure to Environmental Chemicals .47(6):972-982. Andrews WS. Int Arch Occup Environ Health 2006. Karpas Z. July 1978. Costa R. McDiarmid MA. Metcalf S. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Salonen L. Sci Total Environ 1994. Lewis BM. Health Phys 2004. Komaromy-Hiller G. Environ Health Perspect 2002. Komulainen H. Noguchi H. D’Annibale L. Oeh U. Review of elements in blood. Englehardt SA. et al. rapid.71(6):879-85. Katorza E. Clin Chim Acta 2000. Environ Res 1999. Cordero S. Makelainen I. Jarrett JM. Hollriegl V. et al. Nuclear Regulatory Commission (U. Pinto V. Jackson RJ. Shelly T. Marko R. Kalinsky V. Kurttio P. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.110(4):337-342. Comparison of representative ranges based on U.91(2):144-153. concentration and daily excretion of uranium in urine of Japanese. Ough EA. Health Phys 2006. Bennett LG. Ejnik J.94:319-326.67(8-10):697-714. Mistry K. Hancock RG.158:165-190. Auvinen A. Lorber A. Wilson PD. et al. Am J Kidney Dis 2006. Heller J.S.22–Bioassay at uranium mills. Gwiazda RH. Kurttio P. Oliver M. Environ Res 2004. Uranium daily intake and urinary excretion: a preliminary study in Italy. VI.S.296(1-2):71-90. Pirkle JL. Kidney toxicity of ingested uranium from drinking water. Hamilton EI. Harmionen A. Biologic monitoring for urinary uranium in Gulf War I veterans. Washington (DC): NRC.S. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Howerton K. et al.S. Marino R. Auvinen A.87:51-56. Health Phys 2003. Orloff KG. Van der Venne MT. Smith D. Squibb K. Biokinetic modeling of uranium in man after injection and ingestion.85:228-235. Salonen L. Scott K. Ash KO.79(1):11-21. U. Cremisini C.82(4): 527-532. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. U. Wahl W. Renal effects of uranium in drinking water. Sabbioni E. J Toxicol Environ Health A 2004.86:12-18.Metals Galletti M. Li WB. Halicz L. Oberbroekling KJ. Uranium and thorium in urine of United States residents: reference range concentrations. Health Phys 2004. Kane R. patient population and literature reference intervals for urinary trace elements. et al. Pekkanen J. Inductively coupled plasma mass spectrometry as a simple.

80 (3.31) 2.10 (7.70-12.50-3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 9.62 (3.S.20 (7.09) 3.0 (11.93 (4.0) 13.80) 3.90-9.90-12.0-17. and electroplating.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0) 12.50) 11.50) 3. potassium.90 (3.05 and 0.10) 3.47-4. certain catalytic metals.93-4.0 (11. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0) 10.0) 13.79 (2.0) 9.10) 5. lettuce) can be the main sources of intake for humans (FDA.0-18.76) 4.0-14.02 (3. 2005).40-4.20 (4. In addition.32 (3.26 (2. 2007).20 (4.00) 4.0) 13.0) 11.01 (2.60 (4.90-9.46) 3.70 (3. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0-15.20-11.0 (8.50) 5. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.60-7.0-19.0) 9. Other manufactured uses include fireworks.70-3.08-3.0) 19.30-17.16) 3.0) 11.0-23.40-11.12) 3.0 (12.00) 7.80-12.0) 8.0) 95th 14.70 (3.0) 14.40-6. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0) 13.50-4.30 (2.10-11.70-5. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.40-5.0) 9.20-4. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0 (8.30-7.90-11. matches.40) 6.50 (3.50 (5.0 (11. fabric dyeing.44-4.0 (9.20-12.0) 9. Perchlorate was added to the U.40 (4. but has strong oxidant properties in the presence of concentrated acids.90-6.05.50-7.30) 6.40 (3.0-15.70-11.10-4.56) 3.40 (8.60) 8.30-19.0-17.90-10.20) 7.0) 16.88) 3.10-11.38) 5.35 (3.20-3.70-3.51 (3.30 (5.76 (3.66) 3.0) 14.50-4.10-7.0 (11.90 (5.40 (5.75 (3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .60) 3.50-11.80-4.80) 7.80-8.0) 10.87-3.80 (7.10-12.60) 5.90) 6.30) 6.50 (8.0 (9.39-4. and limited applications in pharmaceutics.Perchlorate Perchlorate (Urbansky. Perchlorate is stable under most environmental and physiological conditions.0 (8.10 (5.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.90 (2.0) 15.20) 3.0-18.81) Selected percentiles ( 95% confidence interval) 50th 3.90) 5.90 (5. 1998).40-4.0 (11.0 (10. Drinking water. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.S.00-6.60 (4.45-4.0) 9. and reducing agents.93-3.40 (3.0) 708 617 681 652 1228 1092 Limit of detection (LOD.70-7.00-6.00) 3.00) 5.0 (9.0 (11.0) 10.81-16.10) 12. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.10 (6. and certain plants with high water content (e.0) 13.68) 4.0 (11. 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.11) 4.84) 14.22 (2. leather tanning.40) 3.10 (6.70-6.10 (2.20) 4.0) 11.20 (6.54 (3.0 (8.60 (7. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.22-5.0 (11. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.0-17.75-3.30 (2.70-9.0) 13.80-15. It is normally found and produced as the anion of a sodium.0 (12.0 (11.0) 15.0) 13.40 (5.0 (8.40) 3.07-4.50) 5.5 hours and has a small estimated volume of distribution (Crump and Gibbs. interval) 3.0 (9.0 (13.70 (3.90 (5.40-13.0-29. population from the National Health and Nutrition Examination Survey. milk.90-3.30 (5.00-5.0 (12.11) 3..0) 14.80 (6.0 (12.03) 3.90 (4.21 (2. laboratory analysis.0 (9.10) 5.51 (3.19-4.20-4.80-4.50) 6.0-17.80-6.49-3. 2005).40 (4. or ammonium salt.30-6. 2002).70) 3.0 (11.0-18.19 (3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.65) 3.18-3.40) 90th 10.40-7.90-11.90-3.20 (2.05 (2.0) 8.20 (2.40 (5.40) 4.40) 2.89-3.20 (8.30-7.40) 3.20 (5. Survey years 01-02 03-04 Geometric mean (95% conf..0 (9.80 (3.67-5.0-20.S.74-3.g.10) 3.96 (3.80) 12.0 (9.0-17.0) 13.EPA.29-3.00) 3.60-6.80) 75th 6.0-17.

80-3.90-15.00) 3. nitrate.1-22.1-13.70 (4.71 (5.96) 2. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.S.60 (3. 2007).0 (9.20 (7.97-5.4 (10.30-5.0) 12. Lamm and Doemland.3) 8.0 (8.60-5.50 (6.g.EPA.4-16.90-11. levels and sufficient in most participants (Tellez et al.30 (5.6) 12.60) 3. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.22-4.04-3.0) 13. congenital hypothyroidism is a condition for which nearly all newborn blood is screened. Also.30) 3.46-4.61 (5.70-4.10 (4.00-2.43) 6.3-14.19-10.76 (3.20 (3.20) 8.41-9.59) 3.20-3.89 (2.56 (3.22-4.09) 3.22 (2.45) 3.10 (2.6) 20. 2002)..60-5. perchlorate is negative in most genotoxic assays (U.0) 9. NAS. 2002.60-15. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability. and the presence of other substances known to affect thyroid function (e.80-3.7 (11. 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.50-5.93-5.12 (6.44) 3.1) 8. Steinmaus et al.98) 3. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.22-6.10-3.00-3.29) 2.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.30 (3.15-12.50 (3.60-11.20) 3. interval) 3.EPA.61-5.90-9. In the U.34-3.93-7.50) 2. 2005.90-3.40-10.0) 6.0-14.30) 90th 9.00) 9.0-44. 1999.1 (8.93-8. During gestation and infancy.50) 2.4 (11.0) 9.74) 7.60-3.90-20.00-11.76-3.03 (2.16-3.50-9.40 (7.46 (3.05 (4.33-6.87) 2.70) 2.20-4. Li et al.93) 3.47) 2.80 (4.S.S. women with urinary levels of iodine less than 100 micrograms per day.50) 9. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.0) 12.70-3..00 (6.40) 5.86) 4.18-3..0) 13.30) 5.50) 95th 12.00 (2.64) 5.20-3.26 (3.S.90 (4.50) 5.10 (6.10-7.0) 4.50-3.80 (7. 2005)..19-6.1-16.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.24-2.53 (2.82 (5.36 (8. 2001.0-17. 2005).0) 7. 2005).4) 8.0) 12.77 (3.26) 4.10) 13. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.60-11. Lawrence et al.90) 5.25) 5.84) 2.20-10.60-8.81-3.20 (2. 2005. U.08) 3.66) 3.29-6. age. 2006.75) 3.87-3.87) 7.3) 11.02-4.72 (3..90-2.00) 4.60-6.10 (4.20 (6.0) 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 .4) 13.90 (7.3) 12.10) 4.2) 8. levels.09 (7. Greer et al.0) 11. although iodine intake was higher than U.40) 17.0) 12.58) 2. population from the National Health and Nutrition Examination Survey.0 (11.30-10.35) 3..0 (9.4 (8. 2002.83 (5.80) Selected percentiles ( 95% confidence interval) 50th 3.56-3.02) 3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses. gender.99 (5.37-13.61-10.35 (4.90 (2. chronicity of exposure.91) 4.99-3.1-14.70-15.5 (13. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.70-5.0 (10.70 (2.0 (9.60) 8. However.87 (5. Many factors may be important in consideration of perchlorate action on the thyroid: dose.39 (3.12-2. thiocyanate.25 (3.24 (4.Perchlorate inhibition (RUI). in a representative sample of U.70 (2.00 (4.0) 14.20 (4.0-14. up to 68% RUI has been demonstrated.46-13..42 (3.52 (8.50) 6.52-9.95 (2.S.04-3.54 (3.40 (4.89-3.35 (2.39) 2.45-2.60) 10.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.40 (3.54 (2.20-9.73) 3.0 (11.8 (11.6-17.0) 10. Survey years 01-02 03-04 Geometric mean (95% conf.90 (2.0 (8.30-5. 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. menopausal status.60-8.10 (1.51-4.10) 3.1 (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 3.30) 75th 5. 2000).08 (3.07 (2.33-12. medications).S.80 (7.4 (11.0 (11.21 (2.10) 6.93-5.0-19.2) 8.14 (2.S.40) 3.44-6.25) 5..40 (3.33 (7.37 (4..70) 10.39-4.5) 8.51 (3.87 (7.3 (10. 2003.25) 5.64-3. dietary iodine intake.30 (6.67) 5.32) 5.

EPA at: http://www. Lau EC.10(8):659-663. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Li Z. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. Environ Health Perspect 2007. Additional information about exposure and health effects is available from the U. Kelsh MA.114(12):1865-1871.46(5):509. et al. Page Last Updated: 05/28/2009. Lawrence J. Braverman LE. Washington (DC): National Academy Press. Jackson WA. Perchlorate Exposure of the US Population. Crump KS. Mauldin JP. Environ Health Perspect 2006. Goodman G. Lamm SH.41(5):409-411. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Greer SE. most of the population is considered to be below the U.11(3):295. Doemland M. Crump KS. Thyroid 2000. J Clin Endocrinol Metab 2005. et al. Braverman LE. Thyroid 2001.fda. epa.atsdr.S.html. J Occup Environ Med 2000.113(8):10011008. Perchlorate in the United States. May 2007. Dyke JV. Daaboul JJ.gov/toxpro2. Gibbs JP. Kirk AB. thiocyanate.gov/safewater/ccl/perchlorate/perchlorate. Pirkle JL. Osterloh JD. and environmental perchlorate exposure among residents of a Southern California community. National Research Council of the National Academies. Buffler PA. Rutherford GW. Barnard JC. Blount BC.17(4):400-407. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Steinmaus C. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect.html and from ATSDR at: http://www. 2001-2002. et al. Tellez RT. 2007). Lamm SH. EPA reference dose (Blount et al.S. Pirkle JL.. Food and Drug Administration (FDA). 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. Miller MD. Lamm SH. Environ Health Perspect 2005. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. J Expo Sci Environ Epidemiol 2007.. Benchmark calculations for perchlorate from three human cohorts. Cross M. Li FX. Pino S. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. 2005). and nitrate on thyroid function in workers exposed to perchlorate long-term. Erratum in: J Occup Environ Med 2004. The effect of perchlorate. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. He X. Skeels MR. Deyhle GM. Erratum in: Environ Health Perspect 2005. Landingham CB. Blount BC. Blount et al. Neonatal thyroxine level and perchlorate in drinking water. population.115(9):1333-1338. Valentin-Blasini L. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Chacon PM. Primary congenital hypothyroidism. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. National Academy of Sciences (NAS).cdc. CFSAN/Office of Plant & Dairy Foods. Dasgupta PK. Health Implications of Perchlorate Ingestion. References Blount BC. Valentin-Blasini L.90(2):700-706. Environ Health Perspect 2002. Analysis of relative source contributions to the food chain.S.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Abarca CR.113(11):A732.110(9):927-937.45(10):1116-1127. newborn thyroid function. 2005). Also. Low dose perchlorate (3 mg daily) and thyroid function. Osterloh JD. Magnani B. Lawrence JE. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Available at URL: http://www.40(21):6608-6614. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. et al. Caldwell KL. Byrd D. 2005. Pino S. (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. Braverman LE. 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.42(2):200-205. Howd R. Pleus RC. Sesser DE. J Occup Environ Med 2003. Environ Sci Technol 2006. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.htm. Richman K.. Lamm S. 6/2/09 Greer MA.

S. EPA). Urbansky TF.S. Revised 2/11/05.S. Thyroid 2005. Available from URL: http://cfpub. 1988. Environmental Protection Agency (U. Perchlorate as an environmental contaminant.9(3):187-192.1/15/06 U. Environ Sci Pollut Res Int 2002. Environmental Protection Agency (U.S. EPA/600/F-98/002 Washington (DC). cfm?substance_nmbr=1007.gov/iris/quickview. No. Drinking Water Contaminant Candidate List.epa.Perchlorate pregnancy and the neonatal period. Doc. Integrated Risk Information System (IRIS). EPA). U.15(9):963-975. 246 Fourth National Report on Human Exposure to Environmental Chemicals . Perchlorate.

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

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

. In such studies. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 1999. which may vary for some chemicals by year and by individual sample. 2003. monkeys.800 (. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. 2007).500) .S.400-1.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.500-1.500 (<LOD-1.00) . EPA. 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.500) 90th ..600 (. 2004).400 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0. PFOS. 1992. population from the National Health and Nutrition Examination Survey.00) ..500-1.. and there was no clear evidence of excess all-cause or diseasespecific mortality. 2003.400-1.10 (.00 (. Lau et al.400) . 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. the potential to estimate risks to humans from animal doses is uncertain.500-3. EPA.900 (.20) .800 (.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 .500-1. Kennedy et al.600-2. perfluorohexanesulfonate (PFHxS).600 (.400-.. and changes in thyroid hormone concentrations (Grasty et al.10) * 03-04 03-04 * * < LOD < LOD < LOD ... Olsen et al. At high but non-toxic maternal doses of PFOS.400 (<LOD-. 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.700) .80) 640 1454 03-04 03-04 * * < LOD < LOD .300 (<LOD-. Survey Geometric mean (95% conf. 2007b).. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.00) . 2007a. < LOD means less than the limit of detection. 2001.800 (.50) . A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.600 (..108 times higher than background serum levels in humans (Butenoff et al.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . or increased cancer rates (Alexander et al. 2003a). 2004a. 2003a.700 (.500) . Fei et al..500-1.. Olsen et al. 2003).. 2003).S.. interval) Selected percentiles ( 95% confidence interval) Sample 95th .. 2004)..S. 2004b)..800) 1.400-. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. and humans.3.900 (. 2005).500) . developmental and teratogenic effects were demonstrated in offspring. Thibodeaux et al.. 2003a.800) 1. In comparing three separate reports on adults.10) . Fourth National Report on Human Exposure to Environmental Chemicals 249 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. reproductive. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. development in offspring was stunted and hypothyroxinemia was observed. However.10) .300 (<LOD-. 2007a. Cook et al. PFOA. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. Animal studies of PFOS have demonstrated weight loss. 2003). 2007.80) 485 538 962 Limit of detection (LOD. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. U. PFOS. PFOA.900 (. 2007b.300 (<LOD-. 2003. 2005). possibly related to lung immaturity (Lau et al. 2004.400-1.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.S. elderly and children. population. 2003a). Olsen et al.. 2003a. hepatotoxicity. thyroidal).500 (. 2004.40) .500) .800 (..400 (<LOD-. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.300-1.400-1. U. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Harada et al.500-..500 (. At doses causing maternal toxicity.400-1.

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

500) 485 538 962 Limit of detection (LOD.400 (<LOD-. < LOD means less than the limit of detection.600) < LOD .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (<LOD-.0. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900) < LOD .400 (. Fourth National Report on Human Exposure to Environmental Chemicals 251 . Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.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 < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.400) . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.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 .400 (<LOD-.S. see Data Analysis section) for Survey year 03-04 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.300-.300 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (.500-. < LOD means less than the limit of detection.3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample.

40) 1.912-1.70 (1.697-1.60-2.30) 3.67-2.80) 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 1.90-19.900-1.42 (1.60-2. Survey Geometric mean (95% conf.72 (1.30 (2.10) 1053 1041 03-04 03-04 03-04 .984 (.90) 1.80-3.809) 1.50-6. see Data Analysis section) for Survey year 03-04 is 0. interval) .50 (6.10) 6.50 (2.40) 4.56-1.50-3.10) 1.70-2.10-9.14 (.10) 75th 1.80 (1.80-4.10) 4.50) 6.44 (2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.20) 1.1) 485 538 962 Limit of detection (LOD.90 (1.30-6.50 (4.60) 9.62-2.900-1.834-1.30 (1.900-1.10 (.60) 2.60-8.90 (4.40 (1.40 (1.50 (1.10) 5. 252 Fourth National Report on Human Exposure to Environmental Chemicals .93 (1.40 (1.10-9.30 (1.60-3.70) 3.3. population from the National Health and Nutrition Examination Survey.30-12.50 (1.00-8.1.826-1.30) 3.20 (6.30-2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.00) 3.00 (1.835-1.40-1.00-7.12) .10) 4.08) 2. see Data Analysis section) for Survey year 03-04 is 0.60-2.10 (.20) 485 538 962 Limit of detection (LOD.10 (4.20) 03-04 03-04 2.90) 1.00) 1.50 (1.51) 1.00 (2.03) 1.70-7.00-1.60) 3.70) 13.30 (6.0) 1053 1041 03-04 03-04 03-04 1.80-6.54) .30) .20) 1.30) 03-04 03-04 .87-2.90) 1.40-3.700 (.00 (.91) 2.30-9.40) 640 1454 03-04 03-04 1.80 (4.80-8.10 (1.50) 2.80) 90th 2.10 (4.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.70-5.20 (1.70-10.852 (.816-1.70 (2.04) . population from the National Health and Nutrition Examination Survey.S.50) 2.00-1.40) 2.40 (1.5) 8.689 (.90-10.6) 7.20-1.20 (1.0) 8.70) 1.40) .80-7.30) 3.00 (5. interval) 1.86 (1.17 (1.10) 1.80-4.60 (1.800-1.S.30 (2.80-2.90 (1.40) 640 1454 03-04 03-04 2.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.09 (.00 (1.16) .60-4.27) 1.90) 90th 5.90 (1.721-1.90) 3.10 (.900-1.60 (6.40) 1.77-2.30 (3.92 (1.01 (1.40-1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.90 (2.20-1.3 (9.30 (1.00) 2.30 (1.80-4.50 (1.80) 1.60 (1.90 (1.00 (1.900 (.60-7.50 (6.900-1.40 (2.20-1.70) 1.90) 8.20-1.20) 2.80-7.900 (.10) 8.00-6.20) .10) 75th 3.50 (4.80) 5.80) 4.72) 1.900) 1.700-1.80 (1.05-2.20 (1.966 (.80-8.80-12.20-3.70) 2.70) 2.900-1.17-1. Survey Geometric mean (95% conf.20 (6.00 (1.60 (1.600-.70-6.00) 1.70-2.20-2.963 (.60) 1.60-4.800 (.861 (.10-5.586-.90 (4.90-2.30 (7.60-3.10) 6.50-10.00 (.20 (1.5) 5.80-3.50-6.26) 2.73-2.

2 (16.7-53.6 (44.90 (7.3-61.1) 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.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.70-10.3 (35.70-5.80 (5.7-33.30-11.5 (28.S.2) 30.20-9.30) 7.30 (3.7-49.7 (43.0) 485 538 962 Limit of detection (LOD.00 (3.80-9.6) 21.40-6.7 (13.96 (3.90 (7.79) 4.5) 9.3 (17.70-7.95 (3.50-13.8-30.1) 57.7 (19.60 (4.30 (3.6) 18.40) 5.50-4.50 (4.3 (35.5) 57.21-3.7 (7. interval) 3.1-52.5) 19.4 (23.91) 3.8) 46.1-25.35) 3.7-23.20 (4.9 (13.30-6.5-33.5) 1053 1041 03-04 03-04 03-04 14. Survey Geometric mean (95% conf.5 (28.4) 640 1454 03-04 03-04 23.3) 28.8-22.90-4.4) 21.1.65-4.1-24.84-3.2-22.60) 03-04 03-04 3.1) 15.6 (19.90) 6.20) 5.9-38.0-20.60-14.70) 3.4) 20.80-4.80 (6.2) 45.S.90-12.3 (44.7-30.7-69.60 (7.4 (19.20) 7.20) 10. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.1 (19.2 (28.20-5.80) 8.5) 7.70-7.0-16.6) 9.5) 32.0 (27.0) 23.9) 9.8-22.30-3.3) 485 538 962 Limit of detection (LOD.60) 8.1-36.27) 4.40-17.60-9.11 (2.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.7 (43.8-81.20-4.99-3.6) 35.5-23.1 (24.6) 1053 1041 03-04 03-04 03-04 3.4) 75th 30.9 (17. interval) 20.60 (6.2-57.20 (4.30 (5.6 (35.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.2 (27.6-45.10 (3.90 (5.20) 7.8-78.80 (6.0) 36.9 (22.4 (17.0 (20.2 (21.60 (6.80 (7.10 (3.70 (3.50) 7.40 (6. see Data Analysis section) for Survey year 03-04 is 0.10-3.70 (5.40) 3.1-35.3 (28.4-17.6) 7.0) 03-04 03-04 19.0) 90th 41.70-9.6) 62.1-33.7) 39.89 (3.85-4.4.8) 32.40-6.40) 90th 7.60-13.50 (3.6-50.5) 18.40-14.67-4.47 (4.20) 4.6 (42.0) 21.60 (3. Survey Geometric mean (95% conf.00) 3.30-8.9-19.00 (5.60-6.40) 75th 5.9) 27.80-12.2) 640 1454 03-04 03-04 4.4) 56.10) 5.9-23. population from the National Health and Nutrition Examination Survey.53) 3. Fourth National Report on Human Exposure to Environmental Chemicals 253 .8) 27.8-22.0) 43.8 (37.9) 22.00 (5.70) 4.9 (19.07-4.5-62.0) 21.5) 8.47-4.30-5.9) 22.7 (35.30) 6.50-6.7 (35. see Data Analysis section) for Survey year 03-04 is 0.10 (6.70 (5.3) 42.37 (2. population from the National Health and Nutrition Examination Survey.5-21.0-70.50) 4.2 (18.3) 41.8 (34.70) 6.4-25.1 (23.6-24.90 (7.3-22.6) 42.40 (4.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.4 (28.8-35.60 (5.4 (19.40-10.4-42.82) 4.18 (3.8 (45.0-66.90-4.2) 30.20) 5.2 (19.

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 .4. see Data Analysis section) for Survey year 03-04 is 0. Survey Geometric mean (95% conf.200-.500) .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 .200-.300) . see Data Analysis section) for Survey year 03-04 is 0.200-.300 (.S. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.500) .300 (.300-.300 (. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300) . Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300) .300 (.S.300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300-.300 (.500) < LOD 485 538 962 Limit of detection (LOD.500) 485 538 962 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.300-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (. < LOD means less than the limit of detection.300 (.200-.300) . < LOD means less than the limit of detection.200-. * 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.300) .200-.200-.500) .2. 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.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.300) .200 (<LOD-.300) .300 (.400 (<LOD-.200-.200-.200-.

which may vary for some chemicals by year and by individual sample.800) . which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.900) 1.30 (1.600 (<LOD-1.600 (<LOD-1.10-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .10) * 03-04 03-04 * * < LOD < LOD .70) 1.90) .10 (1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (.900-1.40) 1.10-1.700) 90th 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-.10 (.30 (1. population from the National Health and Nutrition Examination Survey.S.60) 485 538 962 Limit of detection (LOD.600) .20 (1.900 (<LOD-1.80) 1.S.10-1.00) < LOD . < LOD means less than the limit of detection.00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.900-1.6.700 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700) .30) 1.300-2.00-1.20-1.30) 1.300 (<LOD-.50 (1.900) 485 538 962 Limit of detection (LOD.00 (.900) .20) 1. see Data Analysis section) for Survey year 03-04 is 0.50 (1.10-1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .700 (<LOD-.3.900-1.700 (<LOD-.800) . < LOD means less than the limit of detection.700 (<LOD-. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.800 (<LOD-.700 (<LOD-.600 (<LOD-1.00 (.300 (<LOD-1. Survey Geometric mean (95% conf.700 (<LOD-.400 (<LOD-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .900-1.900 (.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600 (<LOD-.700 (<LOD-2.30) .900-1. see Data Analysis section) for Survey year 03-04 is 0.900-1.80) 1.900-1.10 (.10) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) 1.30 (1.10) .40) < LOD < LOD .700) 1.10-1.10 (.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .60) 640 1454 03-04 03-04 * * < LOD < LOD .10) .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .400 (<LOD-. Survey Geometric mean (95% conf.700) 1.

Cook JC. Ingall GB. Chem Biol Interact 2000.Perfluorochemicals References Alexander BH. Characterization of risk for general population exposure to perfluorooctanoate. et al. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Kennedy GL Jr. Kannan K. Rogers JM. Needham LL.and perfluorinated acids. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Wong LY.S. Toxicol Appl Pharmacol 1990. Calafat AM. O’Connor JC. Environ Sci Technol 2004. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Polyfluoroalkyl chemicals in the U. et al.115(11):1670-1676. Environ Health Perspect 2007. Taniyasu S. Halden RU. Kawashima Y. Environ Health Perspect. et al. 256 Fourth National Report on Human Exposure to Environmental Chemicals .S. Reidy JA. Jarnberg U. Environ Health Perspect 2007. Frame SR. The influence of time. O’Connor JC. Kannan K. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Hurtt ME. Environ Sci Technol 2005. Inoue K. Mohotti KM. Kannan K. Biegel LB. Mandel JS. Olsen GW.63:490496. Bandai N. de Voogt P. Environ Sci Technol 2005. Needham LL.1968--2003. Environ Sci Technol 2005. Keller JM.113(2):209-217. Hekster FM. et al. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Olsen J. brominated. Laane RW. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Cook JC.39(23):9101-9108. Environmental and toxicity effects of perfluoroalkylated substances. Perkins RG. Kuklenyik Z.Koizumi A. Calafat AM. Katakura M.39(3):363-380. Harada K.34(4):351-384. Grey BE. Morikawa A. Caudill SP. Kamiyama S. Bookstaff RC. Reidy JA. and ex vivo studies. Regul Toxicol Pharmacol 2004. Yoshinaga T. Peterson RE. Kuklenyik Z. Olsen GW. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. The toxicology of perfluorooctanoate. Liu RC. J Environ Monit 2005. Koizumi A. Mandel JH. Hurtt ME. Wijeratna S. Reidy JA. et al. Chemosphere 2006b. Crit Rev Toxicol 2004. Loganathan BG.104(2):322-333.46(2):141-147. Chlorinated.38(17):4489-4495. Mabury SA. Guruge KS.39(23):9057-9063. Olsen GW. Taniyasu S.38(10):2857-2864.40:21282134. Falandysz J. Tully JS. Frame SR. Yoshinaga T.179:99-121.115(11):1677-1682. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Tully JS. Yamashita N. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Edwards EA.60(10):722729.7(4):371-377. Environ Sci Technol 2006a. Hurtt ME.115(11):1596-1602. Saito N. Toxicol Appl Pharmacol 1995. et al. Ye Y. Seacat AM. Corsolini S. Suzuki E. Gaylor DW.41:2237-2242. Dinglasan MJ.99(2):253-261. Watanabe T. Mandel JH. Calafat AM. Perfluorinated chemicals in selected residents of the American continent. Witter FR. Needham LL. and perfluorinated contaminants in livers of polar bears from Alaska. J Occup Health 2004. Grasty RC. Biegel LB. McLaughlin JK. Arendt MD. Kuklenyik Z. Moore JA. Day RD. Lau CS. Reidy JA. Kudo N. Toxicol Sci 2001.134(1):18-25. Environ Sci Technol 2004. Yun SH. Caudill SP. Evans TJ. Fluorotelomer alcohol biodegradation yields poly. Toxicol Appl Pharmacol 1992. Rodricks J. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Yamashita N.39(1):80-84. Environ Sci Technol 2007a. Burris JM. Occup Environ Med 2003. Needham LL. Kuklenyik Z. Harada K. Birth Defects Res B Dev Reprod Toxicol 2003. Apelberg BJ. Environ Res 2005. Herbstman JB. Moore RW. Holmstrom KE. Sasaki S. in vivo. Saito N. Fei C.68(6):465-471. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Butenhoff JL. Aguilar-Villalobos M. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Cook JC. Calafat AM. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Rev Environ Contam Toxicol 2003. Fillmann G.60(1):44-55. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Tarone RE. Butenhoff JL.124(2):119-132. 2007b. et al. Bignert A. Murray SM. Calafat AM. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Seneviratne HR. Kumar KS. Inoue K.

fish. Environ Sci Technol 2003. Prevedouros K. Zobel LR.68(1):249-264. Mandel JH. A global survey of perfluorinated acids in oceans.37(12):2634-2639. Grey BE. Church TR. Burris JM.111(16):1900) Olsen GW. et al. Toxicol Sci 2003. Peterson RE.S. Yamashita N. Yamashita N. Olsen GW. Hansen KJ. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Olsen GW. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. 2003a. Biol Pharm Bull 2003. Buck RC. Horii Y. Hansen KJ. II: postnatal evaluation. Stanton ME. Washington.68:105–111. Larson EB. Hansen KJ. Olsen GW. Taniyasu S. Burris JM. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Seymour C. Hanson RG.Perfluorochemicals Kudo N. Froehlich JW. et al. Grey BE. Helzlsouer KJ. Taniyasu S. Huang HY. Kannan K.54(11):1599-1611. Kannan K. Rogers JM. Cousins IT. Half-life of serum elimination of perfluoroo ctanesulfonate. Toxicol Sci 2002. Toxicol Sci 2003. Petrick G. I: maternal and prenatal evaluations. fast foods. Butenhoff JL. Butenhoff JL. Olsen GW. Burlew MM. Ehresman DJ. Mandel JH. Butenhoff JL. Biochim Biophys Acta 1993. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. and food items prepared in their packaging. Kawashima Y. Rogers JM. et al. Barbee BD.26(1):47-51.82(1):359. Mair DC. Church TR. (Erratum in: Environ Health Perspect. J Ag Food Chem 2007. Gamo T. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Olsen GW. Ehresman DJ. Bronson R. J Children’s Health 2004b. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Toxicol Appl Pharmacol 2004. 1/15/06 Vanden Heuvel JP. Hanson RG. Coordinate induction of acyl-CoA binding protein.113(5):539-545. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees.74(2):369-381. Miller JP. Available from URL: http://www. and perfluorooctanoate in retired fluorochemical production workers. Historical comparison of perfluorooctanesulfonate. Thomford PJ. perfluorooctanoate andother fluorochemicals in human blood. Lundberg JK.. Olsen GW. et al. van Belle G. et al. Environ Sci Technol 2006. U. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. (Erratum in: Toxicol Sci 2004.2(1):53-76. Butenhoff JL. Environmental Protection Agency (U. Burris JM. Horii Y. Mar Pollut Bull 2005. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. J Occup Environ Med 2003b. birds. Hanari N. Mandel JH.epa.45(3):260-270. Burris JM.51(8-12):658-668. Hansen KJ.40(1):32-44. Lau C. J Occup Environ Med 1999. Lundberg JK. Moisey J. Ellefson ME. 2007a. Nesbit DJ. fate and transport of perfluorocarboxylates.) Tittlemier SA. Burris JM. Butenhoff JL. Richards JH.55:3203-3210. Seacat AM. Environ Health Perspect 2003a. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Butenhoff JL. Sterchele PF. Chemosphere 2004a. Olsen GW. Reagen WK. Korzeniowski SH. Thibodeaux JR. Chemosphere 2007b. Hansen KJ.S. EPA). Sources. Thibodeaux JR.198(2):231-241. et al. Case MT. htm.1177(2):183-190. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Pepper K. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Mandel JH.74(2):382-392. The developmental toxicity of perfluoroalkyl acids and their derivatives. Environ Health Perspect.perfluorohexanesulfonate. Cao XL et al. Church TR.111(16):1892-1901. Lau C. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. fish. Seacat AM. Olsen GW.115(9):1298-1305. 2003. and humans from Japan.41(9):799-806.gov/opptintr/pfoa/pfoara. Environ Health Perspect 2005. Rogers JM.

Various phthalate esters have been measured in specific foods.. 1982. hair spray. Ingested phthalate diesters are initially hydrolyzed in the intestine to the corresponding monoesters.. indoor dust. water sources.. inflatable recreational toys. 1989). Harris et al. plastic raincoats. phthalates can be released into the environment during use or disposal of the product.. excreted in urine largely as glucuronide conjugates (Albro et al. 2002). The intravenous or parenteral exposure route can be important in patients undergoing medical procedures involving devices or materials containing phthalates. 1982. dietary sources have been considered as the major exposure route.. indoor and ambient air. shampoo. and teratogenicity. 2001.. For the general population. intravenous medical tubing. which are then absorbed (Albro et al. Phthalates have low acute animal toxicity. Human health effects from phthalates at low environmental doses or at biomonitored levels from low environmental exposures are unknown. such as plastic bags. Dirven et al..Phthalates Phthalates General Information Phthalates are industrial chemicals that are added to plastics to impart flexibility and resilience and are often referred to as plasticizers. blood product storage bags. and.. corresponding monoester metabolites. There are numerous products that contain phthalates: adhesives. In settings where workers may be exposed to higher air phthalate concentrations than the general population... Parks et al. Because they are not chemically bound to the plastics to which they are added. lotions. solvents.. to a lesser extent. Mortensen et al. 2001). deodorants. In vitro studies showed that certain phthalates can bind to estrogen receptors and may have weak estrogenic or anti-estrogenic activity (Coldham et al.. liver injury. The table shows the phthalate diesters. Zacharewski et al.. automotive plastics. 2003). detergents. 2004. some medical devices and pharmaceuticals. garden hoses. Pan et al. Absorbed monoester metabolites are usually oxidized in the body and. dermal contact with products that contain phthalates. but in vivo studies did not support phthalates having estrogenic effects (Milligan et al. such as soap. lubricating oils. liver cancer. several of the phthalates produced testicular injury. in humans... 1985. and sediments (Clark et al. Human milk can be a source of phthalate exposure for nursing infants (Calafat et al. not all phthalates Phthalates and Urinary Metabolites in this Report Phthalate name (CAS number) Benzylbutyl phthalate (85-68-7) Dibutyl phthalates (84-74-2) Dicyclohexyl phthalate (84-61-7) Diethyl phthalate (84-66-2) Di-2-ethylhexyl phthalate (117-81-7) Abbreviation BzBP DBP DCHP DEP DEHP Urinary metabolite (CAS number) Mono-benzyl phthalate (2528-16-7) (some mono-n-butyl phthalate) Mono-isobutyl phthalate Mono-n-butyl phthalate (131-70-4) Mono-cyclohexyl phthalate (7517-36-4) Mono-ethyl phthalate (2306-33-4) Mono-2-ethylhexyl phthalate (4376-20-9) Mono-(2-ethyl-5-hydroxyhexyl) phthalate Mono-(2-ethyl-5-oxohexyl) phthalate Mono-(2-ethyl-5-carboxypentyl) phthalate (40809-41-4) Mono-isononyl phthalate Mono-methyl phthalate (4376-18-5) Mono-(3-carboxypropyl) phthalate Mono-n-octyl phthalate (5393-19-1) Abbreviation MBzP MiBP MnBP MCHP MEP MEHP MEHHP MEOHP MECPP MiNP MMP MCPP MOP Di-isononyl phthalate (28553-12-0) Dimethyl phthalate (131-11-3) Di-n-octyl phthalate (117-84-0) DiNP DMP DOP 258 Fourth National Report on Human Exposure to Environmental Chemicals . urinary metabolite and air phthalate concentrations are roughly correlated (Liss et al. 2000. however. 2005). and personal-care products. inhalation. followed by inhaling indoor air. 1985. Jobling et al. and toys (ATSDR. and nail polish. In chronic rodent studies. Phthalates are metabolized and excreted quickly and do not accumulate in the body (Anderson et al. 1993). vinyl tiles and flooring. 1998. fragrances. Albro and Lavenhar. 1997. Phthalates are often used in polyvinyl chloride type plastics. 1995). 2003. People are exposed through ingestion. Phthalates are also used as solubilizing and stabilizing agents in other applications. 2003)... and other oxidized metabolites included in this Report. 2006).. 1998). but these effects either have not been demonstrated when tested in non-human primates or are yet to be studied. Okubo et al. Infants may have relatively greater exposures from ingesting indoor dust containing some phthalates (Clark et al. 1997. Nielsen et al.

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

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Rusyn I. Environ Health Perspect 2004. Meek MD. 112(5):A270]. Cunningham ML. Ostby JS. Orton TC. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.36:459-479. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Toxicol Sci 1998. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Parks LG.45:11-17.46:282-293. Barr DB. Fielden MR. Wu ZF.112(3):331-338. Environ Health Perspect 2006. Jackson SJ. Silva MJ. Batten PL. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver.Phthalates phthalate (DEHP): a cross-sectional study in China. Zacharewski TR. Crit Rev Toxicol 2006. Matthews JB.S. et al.114(11):1643-1648. Barlow NJ. Klinefelter GR. Rhodes C. Bratt H. Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 1982. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Lambright CR.58:339349. et al. Environ Health Perspect 1986. Clemons JH. Albro PW. et al. Reidy JA.65:299-308. Peck CC. Abbott BD. Pratt IA. Malek NA. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Toxicol Sci 2000. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Caudill SP. Hodge CC. Peters JM.

8-18.8-16.5) 15.4) 14.6-72.3-18.9-47. it can be released into the ambient air during use or disposal of the products.1) 29. and 0.8 (53.2 (19.6) 16.1) 13.4 (63.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.1 (20.6) 29.1 (19.5-62.6) 14.8 (86.2) 33.6-116) 122 (102-142) 101 (85.3-27.1) 67.3 (29.3-21.5) 23.1-116) 122 (93.8 (71.4-127) 80.6 (66.1) Selected percentiles ( 95% confidence interval) 50th 17.9) 49. 01-02. 2004.6) 95th 103 (94.2) 14.4 (29.9-14.4 (13.2) 13.1 (10.8 (38.3 (12..4) 35.7 (12.6-92. sealants.8 (71.8-64.9-62.1) 12.9) 43.0) 24.2) 14.7 (70.5) 15.5-36.3 (12.1 (13.2-17.3-88.7-16. interval) 15.8-17.5 (57.2) 69.4) 108 (96.6-18.5-25.8 (80.0-130) 101 (86.6 (12.4-62.9 (39. High dose BzBP and its monoester metabolites.6-17.7-82.5-41.S.6-132) 103 (84.3) 94.2 (19.4 (27.3-125) Total 15.6) 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 39.5 (27.9 (13.2-38.3) 63.4) 38.3) 15.1-38.4 (68.8 (28.2 (10.9) 14.7-13.9) 11.4) 12.2) 66.7-16.5-35.1-15. respectively.8-121) 79.2 (43. IARC considers BzBP not classifiable with respect to human carcinogenicity.2-183) 101 (78.3-74.4 (10.7 (13. BzBP can be released into the environment during its production and.3-82.2 (14.7 (82.7) 38.2) 78.6) 13.6) 50. particularly male animals (McKee et al.7 (80.3 (22.1 (14.2) 12.9 (22.3 (54.1.6) 37.0 (14.0 (23.7-170) 169 (134-198) 152 (99.0 (26.1) 14.4 (32. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives. because it is not bound to products in which it is incorporated.8 (50.2-33.6-39.5-14. 0.0) 90th 67.5-40.5-18.1-16. vinyl tile. 262 Fourth National Report on Human Exposure to Environmental Chemicals .5) 30.0 (11.6 (41.3-75.5) 16. see Data Analysis section) for Survey years 99-00.0) 34.9 (16.4) 33.7-58.1-16.3-34. car care products. Food crops take up BzBP. and 2003-2004 were generally similar those reported in U.4 (53.7-17.3 (13.8-16.3) 13.9-87.0 (27.8-72.4-120) 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 13.3 (12.2 (47.2) 17.6-38.2-116) 122 (102-143) 101 (84.5) 82.1) 68.5) 55.4-92.2) 22.8) 14.0) 32.9 (70.0-85.4) 65.4) 129 (98.3 (33.7) 40.8-14.2-20.5-33.2) 15.8 (30.S.9-28.0 (34.4) 51.5-145) 138 (106-241) 143 (127-179) 120 (99.9 (12.2) 32.9) 18.0 (30.7 (15. 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.5) 27. 2001-2002.6 (21.5-97.6 (13. 2000).2-115) 113 (91.9-190) 86.8-76.9 (28.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.6) 24.8-14.3-161) 99.0 (33.1-61.6 (13.1) 32.9 (11.2-19.0 (30.0) 23.7-25.4) 98.3.0 (20.Phthalates Benzylbutyl Phthalate CAS No.6 (13. residents (Blount et al.9-27.8) 33. and to a lesser extent.3 (44.8-48.6-79.9-30.1 (58.9 (12. and diet is the major source for general population exposure.3-12.6-43.6) 35.2-155) 91. NTPCERHR.6 (32.5-94.6 (13.5 (26.3) 37.4 (53. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6-29.8 (10.6) 25. 2000).0 (15.8) 24.4) 81.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7 (11.8-35.5 (76.0) 70.8-41.0 (12.2-31.4-15.0-106) 58.7-35.1 (13.8) 28.8-98.1-35. some personal care products.8 (14.4 (32.9) 13.4-25.4) 49.7-15.4-24.4 (10.3-91.1 (32.6) 14.0) 16.1-43.8.0 (15.3 (29.4 (31. can produce developmental and reproductive toxicity in rodents.7 (51.7-172) 103 (74.0) 20.3-43.6) 15.5) 65.5 (66.0 (55.9) 15. including MBzP.6 (53.5 (61.1-214) 166 (116-191) 145 (110-213) 88.9) 12.5 (55.4 (59.3-18.0 (43.8-13.6) 35.9) 14.7-16.1) 76.0) 33.0-26.6-150) 94.3 (30.1-90.6-92.3) 23.5 (13.3) 13.1-18.4) 80.4) 71.8-133) 89. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.2-16.9 (21.1-120) 52.2-40. population from the National Health and Nutrition Examination Survey.7-119) 99.6) 63.5 (67. and 03-04 are 0.2-39.9-16.8 (21.5 (47.4-16.3-130) 122 (88.1) 31.1-15.2-16.5-36.1 (14.0-55.6) 67.2 (25.3) 54.1 (55.4) 75th 35.8 (12.7) 23.4 (48.7-14.1-39.5-84.4) 35.7 (53.8) 63..8-17.2 (11. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.9-49.

4 (74.1) 39.7 (19.7 (59.9 (24.4 (34. and females compared to males (Silva et al. Weuve et al.4-102) 70.8-15.5-38.0 (12.1) 24.2) 11.4-116) 73. 2006).3 (15. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.9) 24.8 (13.5-16.4) 13.5-23.0 (38.Phthalates York City (Adibi et al.7 (55.4 (11.0 (41. 2005).8) 54.7 (11.5 (10.6) 75th 25.5 (42.4) 15.4) 21.1) 17.7 (38.7-90.5-99.3-38.5-57.5) 78. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.3 (24.7-29.8 (57.1 (19.6) 53.5-76.5 (12.8-64.7) 56.6-81.8) 46.4) 28.8) 11.9 (51.6-26.4-17.6 (15.6-12.6 (11.9 (54.69-11.1 (41.5-26.6 (36.4-142) 134 (116-176) 136 (85.1-29.73-12.8) 33.9) 12.5-61.9 (12.8) 108 (75.0) 12.3) 55.2-57.1 (18.4 (12.3-64.6-86.1-12.5) 23..4 (63.2) 15.7) 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 40.8-48.1-12.3) 90.8-13.1) 23.5) 10.0) 13.8) 24.6-116) 74.4-15.8-13.9) 12.1 (11.7 (11.8-14.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .4-42.7 (12.1 (21.6-20.0-109) 65. 2002).1 (23.6) 13. 2007). Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (13. Hauser et al.9 (55. Hoppin et al.8) 53.7-14.0) 49.3) 13.2) 67.7-12.4 (33.9-28.3 (60. In an annual sample of German university students. In NHANES 1999-2000.0 (13.4) 51.8) 71.0 (62.9-115) 57.1-35.1 (15.2-15.0) 60.1 (34.3) 37.5-29. 2002.8-14.5) 16.9 (29.4) 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 12.9) 100 (80.5-26.4 (69.8) 16.5-13.9-23.1 (14.4 (11.4 (13.0 (11.7) 38.7) 25.8 (46.7-61.1) 27. in men attending a Boston infertility clinic (Duty et al.0 (12.5) 95th 77.8-69.4 (26.3) 13.7-69. 2005.7 (13.0) 24.1 (25.9 (24.2-17.3 (39..6 (11.5 (49.4) 50.6) 58.0 (49.2) 32.0) 15.8-85.2-12.6 (30.9 (12.2-21.5) 20.3-16. 2004).7-31.5 (35.4-14.4-23.5) 46.2-13.1-79.1-120) 77.5-213) 49.8-80.0) 24.4) 44.2 (27. 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.4-93.6-13.7 (23.6-47.1 (53.0-26.8-39.0-27.0 (67.8) 33.8) 34.8-27.9-13.3) 29.3 (35.7-20. and in a small sample of German residents (Koch et al.2-26.8 (11.0-48.1 (13.6) 25.7) 46.1 (21.8 (64.9 (22. 2004.6) 12.6) 73.1) 80.7-14.1-58.5 (9. population from the National Health and Nutrition Examination Survey.6 (34.4) 13.9 (10.1-125) 86. 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 (43.3) 89.8) 26.4 (60.95-14.0-53.8) 13.7-15.8) 68..7-123) 77.3) 16.6 (11.9 (39.9) Total 14.9-14.4) 17.6 (24.6-99.4 (46.0 (41.9 (43.5) 41.3) 21.4 (25.8-15.4) 25.7-56.4-27. 2003).5-79.1 (21.3) 13.3-11.0-90.7 (21. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.8-16.5 (48.5 (10.5) 14.6 (30.7-19.1) 142 (99.8 (12.S. A small study of African-American women in Washington.5-58. 2003).2-78.4) 14.6) 38.4-79.4-19.0 (10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (46.9) 12.8-60.4) 12.9 (10.5-42..7 (18.8 (10.8) 56.0) Selected percentiles ( 95% confidence interval) 50th 13.4-14.7 (54.2-117) 95.8-173) 195 (121-305) 229 (99.5) 13.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.4 (10.6-15. adolescents compared with adults..4 (21.4) 90th 50.6) 30.3 (38.1) 35..8 (30.7) 11.3) 14.2-13.6 (19.1-27.8-34.9-104) 62.2 (40.3) 18.2-49.6 (57.0 (33.0-51.8-13.3-34.3-73.9 (15.4) 104 (89.2-15.9) 52.7-19.6 (22.4-18.2-51.3) 73.2 (41.6 (14.2 (69. interval) 14.8-42.1) 12.8) 15.6) 12.4-60.9-40.1 (9.9-13.3 (13.5-58.4-99.7 (11.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3) 12.2) 11.3) 67.2 (56.7 (14..0-15.9 (15.3 (12..2) 26.3) 36.5 (56.7) 19.8 (69.3) 14.8) 80.9-62.7-20.0) 11.8 (50.9-69..8 (49.9) 42.4 (11.9 (9.1-14.2) 12.4) 60.5) 17.1) 24.9) 64.6-40.5-31.6 (51.9-16.3 (23.7-397) 70.7 (13.7-15. in young Swedish men (Jonsson et al.1 (21. 2007). median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.5 (11.9) 11.2) 11.9-83.9) 11.4-90.8) 53.

Environ Health Perspect 2004.18(1):122. et al. McKee RH. 2005.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. et al. Third National Report on Human Exposure to Environmental Chemicals. Koch HM. Butala JH. Helm D. Available at URL: http://cerhr. Green RA. Hodge CC. Wiesmuller GA. Silva MJ. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Research Triangle Park (NC). Brock JW. et al. Hagmar L. Angerer J. Hum Reprod 2007. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.112(3):331-338. Jonsson BAG. Ryan L. Hilborn ED.nih. Malek NA. Environ Health Perspect 2006. Hauser R. Needham LL. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Blount BC. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Dobler L. Levels of seven urinary phthalate metabolites in a human reference population. Urinary phthalate metabolites and biomarkers of reproductive function in young men. et al. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Bull Environ Contam Toxicol 2002.S. et al. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Calafat AM. et al. Jacek R. Phthalate monoesters levels in the urine of young children. Baird DD. Caudill SP. 4/20/09 Silva MJ.108(10):979-982. Epidemiol 2005. Hu H. Int J Hyg Environ Health 2007. et al.Phthalates References Adibi JJ. Reprod Toxicol 2004. Urinary levels of seven phthalate metabolites in the U.16(4):487-493.niehs. Poland.93:177-185.25(2):293-302. Ryan L. Wittassek M. Hoppin JA. Brock JW. Needham LL. Singh NP. Perera FP. Sanchez GN. Richthoff J. Davis BJ. 112(5):A270].110(5):515-518.22(3):688-695. Duty S. Sampson EJ. Caudill SP. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Gans G.114(9):1424-1431. Environ Health Perspect 2000. Camann DE. Rylander L. Reproducibility of urinary phthalate metabolites in first morning urine samples. Environ Health Perspect 2002.68:309-314. Silva MJ. Rossbach B. Drexler H. NTP-CERHR. Prenatal exposures to phthalates among women in New York City and Krakow. David RM. Weuve J. 2000 [online]. Environ Health Perspect 2003. Atlanta (GA). Barr D. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Eckard R.210(3-4):319-333. Caudill SP. Schettler T.html. Barr DB. Pirkle JL. Jedrychowski W. Koch HM. Duty SM. Calafat AM. Brock JW. Meeker JD. J Androl 2004. Chen Z. Centers for Disease Control and Prevention (CDC).111(14):1719-1722. Environ Res 2003. Silva MJ. Silva MJ. Giwercman A. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Reidy JA.

80 (2.7 (9.50) 8..90-7. residents (Blount et al.6) 10.3-20.17 (2.3-24.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.30 (3.22) 3. interval) 2.00) 10.0) 20.19-3.40-3.0 and 0.10 (4.28-5.30-11.80 (5.63) 3.1-25.4) 22.5) 18.40-3.5 (17.0 (13.4 (20.6 (10.00) 4.5) 22.6 (10.3 (16. 2007).2 (11.67 (5.5) 18.7 (16.00-4.50) 90th 12.56 (5.00-11.50) 18.20 (6.66) 2. Studies of children found age-related differences in urine MBP levels.0) 12.3) 33.6) 26.6) 12.1-12.50-6.80-5. 2005).S.6) 16. OSHA has established a workplace air standard for external exposure to DBP.8) 21.02) 4.30-2.40-4. 2004. Biomonitoring Information Median concentrations reported in the NHANES 19992000.S.3 (19. Fourth National Report on Human Exposure to Environmental Chemicals 265 .0) 24.50) 7.90-4.90-2.40 (2.5-29.5) 14.6 (29. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.6-34.30) 10. 2005).10 (3..6-18.97) 4.1) 22.7) 18.20) 7.60-6.5-16.Phthalates Di-n-butyl Phthalate CAS No.4-12. 2000.10-2.0 (11.6) 17.70-4.20-9.5 (20.4) 12.40-17.30) 6.80-5.0-25.5) 23. CDC.8) 40.. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.82-3.70 (5. population from the National Health and Nutrition Examination Survey.0-18.24-8.9-14.96) 3.40 (3. in a small sample of pregnant women in New York City (Adibi et al.56) 3. When total DBP metabolites have been measured. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.00-9.5) 19.70) 3. and in a small sample of Japanese adults (Itoh et al.4) 5.5-24.30-13.40 (2.0 (19.10-9.43) 6.40 (7.30) 2.26 (2.3 (11. and also in some printing inks.6) 16.9-23.30 (1.37) 6.71 (2.59) 3.3 (13.0-14.0 (13.1) 16. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.20) 4.4 (14.7-18.7-31..7-20.7) 15.40-4.50 (3.20 (7.17) 4.40) 5.50-10.50-4.80 (3.00-6.50 (6.90 (3.6 (11.07 (3.9) 10.2-22.81 (3.6 (13.70-8. 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. Koch et al.5 (11.91) 4.55 (3.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.5-16.3 (18.7 (17.10) 9.68 (2.3 (16..55) 2.7 (7.6-20.10) 11.0) 9.2) 5.60 (4.40-9.2-33.49-2.5) 25.30) 10.20 (3. NTP-CERHR.3) 18.97-7.20-12.4-27.30-7.10) 8.5 (10.1-17. 2004.56-4.2-14. mostly as MnBP (Anderson et al. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.44-2.8) 677 652 703 699 1216 1088 Limit of detection (LOD.6-26.30) 5.33 (2.5) 12.84) 4.40 (6. 84-74-2 Di-isobutyl Phthalate CAS No. 2000).7) 7.30-3.80 (5.20-2.6 (9.40-12.0) 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 2.1-20.90 (4.56 (3.60 (5. Survey Geometric mean (95% conf.3-48.3 (13.8 (9.1) 25. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.9 (16. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity. 2003).90) 12.85-6.90 (4. in men attending a Boston infertility clinic (Duty et al.60 (8.50-2.20-6. pharmaceutical coatings.1 (8..40-5. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.80) 75th 5..6) 17. Following oral administration of DBP to humans.50) 2.30 (4.90-4.1 (13.3-30.22 (3. DBP can produce reproductive toxicity in male rodents (McKee et al.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.00) 7.9) 15.00 (7.90 (6. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.7 (17.7) 14.3-18.6 (13. and insecticides.11-3.60 (2.80 (2.72-3.5 (27.60) 3.7 (18.46-5.48 (2.20-12.00) 6..2 (12.0-38. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al. about 65% to 80% of a dose is eliminated in urine within 24 hours.97) 2. 2005).10) 3.3. 2005. Hauser et al.2 (8.3-43.0) 13.46 (2. they have been referred to as monobutyl phthalate (MBP).10-9.6 (14.50) 5.3-19.6-14.46) 2.7) 4. In addition. 2001).70) 5.73 (2.10) 2.10 (4.30-6.70 (2.9 (16.46 (3. 2003).70-4.7-31.00) 4.00 (5.30-6.6 (14..3) 3.00-6.73-5.

43) 3.6) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.8 (9. 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.44 (3.68) 3.7 (11.52) 3.08) 75th 4.73 (5.6) 11.99) 7.66) 2.6 (10.93-6.26-2.29-8.51) 2. 2006). up to four and 13 fold.00 (3.25) 5.18-10.0) 3.0) 7.57-4.47 (3.76-3.72) 5.1) 4.1 (10.2-13.6 (8.78-8.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.04) 7.75 (4.53-4.11) 5.03 (5.04-5.5) 15.6 (8.84 (8.78) 9.24) 3.18-4.97-2. interval) 2. An analysis of NHANES 2001-2002 showed similar age.32) 7.81) 9.88 (2.51) 5. 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.62-12.6 (15.61-3.0-18.1) 15.17 (2.6-19.47-5. population from the National Health and Nutrition Examination Survey.84 (4..81) 4.33-9.54 (4.15) 3.92 (7.0 (12.65 (4.65-11.9-16.13-6.5-19.1) 10.36-2.51) 15.1-25.79-6.34 (3.00-3.17-12.3) 13.58-4..85 (2.38 (6.76 (3.8 (10. to about two to fourfold higher (Fromme et al.8-36.69) 4.37) 3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.47-12.52-20.66) 10.3 (13. 2005).76-15.05) 2.81 (3.18 (1.89) 6.69) 6.13 (2.96 (3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.62 (6.31) 2.8-18. 2007).08-2.65-4.89 (3.74 (4.31 (7.11 (5.0) 11.82 (4.3) 13.54 (2.66) 4.4 (12.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.4-16.10-5.01-2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .0 (10.33) 3.8-13.2) 8.83 (2.1) 11.64-7.3) 28.64-10.39-3.20-2.95-3.0) 15.64-7.07-5.75 (6.52 (2.7-28. In an analysis of NHANES 1999-2000. 2002.21) 10.95) 2.95) 10.67-5.28 (4.5) 13.94) 6.18) 4.04) 3. Between 1998 and 2003. while MnBP declined (Wittassek et al.00-3.99-4.17) 90th 8.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.79-8.7 (9.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.36-7.3) 16.20 (2.02-10.43) 3.58-3.56-4.07 (2.1-24. ranging from more than one-tenth the NHANES median (Itoh et al.32 (7.98 (2.81 (6.56) 2.27-12.18) 3.53-5.11-2.14 (4..94-12.68) 5.86) 6..31) 2.1) 7.45) 3.1-12.9-26.18 (4. Weuve et al.53-3.72-7.4) 7.46) 3.43) 3.02 (7.9) 12.9 (15.03-7.59 (4.6-19.55-6.2 (11.46-11.41 (2.56) 5.76-3.21 (5.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.6 (9.86-4.80 (3.89-5.69-7.7) 3. Biomonitoring studies on levels of MnBP and MiBP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of dibutyl phthalates than are found in the general population. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.79 (4.4) 23. Survey Geometric mean (95% conf.20 (2.28-13. 2005).26 (2.3 (17.7 (21.4) 15.8-18.15-4.74-3.52-3. the students’ median values for MiBP levels remained relatively unchanged. 2004).69 (2.1 (11.20-3.56-15.35) 3..91-6.54) 2.8) 10.6) 13.7 (13.29-3.30) 2.22 (2.1) 13.80-3.00-7.38-10. Over this time.82) 4.9 (11.20 (7. 2004).09-2.66 (8.33 (3.S.0 (8.2-15.5 (11. 2007).39) 5.2) 24.6 (12.78) 8. than adults in NHANES subsamples during the same time period.9-40.31 (2.57 (3.80) 7.2 (10.3) 18.94 (5.42) 2.7) 19.and gender.33 (2.7) 11.7) 10.46 (2.30 (6.57 (3.1-15.9 (9.03-11.32 (3.19 (2.8 (8.2) 9..5 (9. respectively.. 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.20-4.68 (2.

9-87.0) 120 (98.0-26.8-22.0 (45.6-37.1-29.5) 95.9 (79.6-143) 127 (99.6) 35.2) 26.4 (25.7-53.8) 62.3 (30.1 (19.7) 52.7-42.1 (16.4 (35. and 0.1) 47.6-33.1) 23. and 03-04 are 0.2-87.8-119) 90.3 (42.7) 74. respectively.7-111) 64.5-42.8) 43.2 (25. referred to as monobutyl phthalate (MBP).9) 46.5-27.8-42. Fourth National Report on Human Exposure to Environmental Chemicals 267 .2 (74.1 (28.1 (17.4 (72.0 (31.5) 36.4-18.8-132) 95.4.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.9) 18.6) 21.6 (61.4-20.1 (19.0 (18.9) 26.4-26.1-75.7 (16.0 (20.0) 30.7-117) 118 (108-143) 93. 1.1) 23.4 (84.0-51.7-34.5) 65.5) 26.4 (23.5 (59.3 (17.1-92.8-123) 101 (90.8 (57.2) 20.1 (26.3-76.4-159) 107 (84.1-20.0-73.4) 59.9 (79.1 (58.4 (21.1 (51.9-53.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.3-24.7 (64.7-116) 95.6 (22.5-60.0 (72.9) 71.2 (78.9-28.3-136) 137 (107-162) 119 (90.1 (31.0-21.2-56.7) 124 (98.0 (15.3-85.3 (56. 01-02.7-121) 97.1-80.2-23.1) 23.6-29.3) 26.3) 19.7-92.9 (17.0 (30.0 (25.5) 17.5-121) 106 (94.9) 36.3 (60.4-31.8-25.8) 48.1 (62.2-63.1-27.3) 24.1-22.1) 31.1 (19.2-114) 73.1 (18.7 (22.3 (23.3-96.5) 31.7-42. *In the 1999-2000 survey period.9 (17.6-20.8-111) 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 23.5 (28.2-33.8) 58.6-49.1 (19.6) 39.2-21.2-24.5 (59.9) 75.7 (51.2 (20.2 (18.0) 21.0-24.5 (74.2 (17.6-113) 108 (90.0-32.9-101) 77.4-25.4 (35.6 (16.6-40.2) 38. Survey Geometric mean (95% conf.6 (48.1-51.2 (19.1) 25.7-106) 69.1) 46.2-32.0-19.6) 80.4-60.1 (21. see Data Analysis section) for survey years 99-00.3-60.3-67.5) 34.3) 23.7-127) 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 22.7-20.1 (54.3-79.2) 90th 98.7) 28.1 (34.2-93.2-22.8) 23.1) 36.6) 20.5) 24.9-22.2-159) 92.4 (36.3) 36.7-26.5-43. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3) 21.3 (30.5) 40.2 (21.0-58.6-36.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.0) 38.9-42.4 (35.4) 22.5) 19.4) 20.9 (20.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.4) 64.6-69.0) 31.3-40.5) 21.1-82.5-117) 95.7 (43.5-53.2) 62.8 (19.6-31.4 (35.1) 17.1-24.7-91.5 (30.3-145) 85.5) 47.4) 52.6) 71.1) 30.2 (21.6) 38.8-29.0) 20.6 (32.0-19.7 (19.S.7-24.6 (55.7 (33.4 (38.9-22.8) 75th 51.0) 117 (104-131) 112 (84.9) 29.3 (36.7 (18.6) 17.7 (70.2 (79.7-124) 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.2) 42.1) 19.7-34.6) 46.5) 37.9.9-79.5-47.7) 42.2-49.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7 (38.4-44.0 (17.6 (19.6-24.4 (19.0 (78.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.7 (24.2 (58.2) 32.6 (26.6 (90.3 (23.6-48.2 (75.5 (29.5) 36.2) 68.9-33.6 (44.0-24.1 (36.8) 19.5) 20.1.6 (65.3 (37. interval) 24.7) 92. population from the National Health and Nutrition Examination Survey.4 (71.1 (41.9) 21.3) 40.9-92.5-47.5-44.0 (36.9-114) 116 (97.1) 20.6-29.0) 84.3 (51.3-21.7 (18.7 (28.6-44.3) 18.4-42.5) 78.2 (59.0 (23.0) 27.5) 85.

4 (20.1 (34.7 (43.5-16.9-38.6 (27.6-74.0) 25.2-27.6-119) 63.1) 42.5) 134 (93.6) 64.7-21.3-81. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.9) 28.4 (50.4 (37.4 (47.4) 53.6-44.1 (29.8) 34.7-28.3 (16.0) 108 (71.9 (58.3 (46.2) 21.0 (16.0-47.4-65.1-83.0) 70.2 (19.7 (57.4 (31.0) 75.4-47.8 (13.2-22.9 (30.9 (56.1-32. 268 Fourth National Report on Human Exposure to Environmental Chemicals .5 (14.4-34.0-75.7 (60.6 (57.2-85.3 (21.7-20.6-19.4 (31.8-24.9-105) 85.6) 24.7-26.8 (33.4-164) 96.2-48.S.3-49.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.4-72.5 (81.8) 34.2-73.3) 19.0) 29.2) 65.6) 37.9) 52.7) 19.4 (50.4) 15.9 (19.4 (16.6-26.6-128) 96.2) 16.6) 14.0) 28.8 (16.8 (18.9 (30.8 (22.8 (65.3-71.7 (19.7 (12.8-24.3-26.2-28.3) 20.3-40.2) 159 (102-263) 147 (93.4) 15.6) 24.7 (28.0 (69.9 (16.6 (31.7 (14.4-76.5) 91.0 (52.3) 21.3 (60.7) 20.3 (52.8) 40.9-14.6-16.7-51.9) 24.2-22.2 (35.8 (25.1 (21.3-18.6) 39.7 (73.6-92.5-18.2 (83.5 (18.1) 20.8) 20.1 (46.6 (17.1) 20.2-86.1-128) 97.9 (30.3) 67.4-135) 71.2-61.5) 21.5-76.4-131) 81.4) 19.0-90.3-106) 74.2-179) 84.0 (18.8) 13.2-106) 64.3) 59.3-21.1-99.5-142) 81.8-23.6-24.7 (27.4-103) 117 (83.2) 31.0-17.6) 31.4 (68.6-44.8 (17.0) 81.0 (61.0 (71.1) 44.5) 90th 68.9-68.7-80.7-39.9-68.9) 19.4 (45.8-43.8) 23.7-23.0 (18.7-78.8-235) 137 (108-198) 88.8) 17.0 (19.7) 36.7-42.5-23.6-53.4 (53.9 (21.3 (69.9 (39.9) 30.6) 65.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.6 (19.0 (70.1-21.7 (81.0) 26.3) 33.9-34.0) 53.4 (56.4) 21.8) 20.6) 25.8) 28.1) 53.5-142) 89.5 (30.3-20.3) 19.2-18.0-19.4 (18. population from the National Health and Nutrition Examination Survey.1) 22.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.5-70.3 (17.1) 61.7 (16.1-99.7 (60.4 (17.3 (52.9) 20.9-56.6 (74.4) 62.8) 17.2 (38.0) 35.8) 22.6 (29.4-61.3 (17.4 (31.6-23.0) 19.8 (18.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.9) 91.5-64.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.4 (33.0) 59.3) 17.6) 34.1 (61.0 (15.1) 17.1) 50.9-70.2) 59.1 (15.7 (20.0 (50.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.6-155) 91.6-32.3 (71.5 (18.3 (42.5) 82.3-23.5-37.2 (16.3 (76.9) 39. Survey Geometric mean (95% conf.6 (25.6) 83.0 (34.0) 94.5-22.7-37.6) 23.9-36.3) 33.3-32.1) 21.8) 35.9) 14.6-27.0 (20.9) 62.8) 19.7 (54.5) 17.3 (55.3 (48.5-21.6-28.7-19.4 (16.5 (64.9 (64.8 (50.3) 52.0 (26.9 (37.8) 75th 38.5) 39.1-18.8 (18.9) 49.6) 38.0 (27.6 (41.0-113) 104 (83.2 (19.2) 74.0-92.4-24.5-15.4 (19.3-38.1 (56.0-60.1-23.4) 51.5-30.2-22.4 (17.5) 84.6 (61.6-50.9-49.3-39.8) 30.0-38.2-16.4) 20.8) 63.0) 55. interval) 22.4) 16.3 (19.6-23.3-21.0) 41.7) 42.9 (35.1 (32.6 (25.7-19.9 (73.0-41.6-43.3) 35.3-17.1-62.9-26.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9 (20.0 (43.3) 18.6) 18.3 (17.6 (72.3-78.2-21.5) 60.9-100) 86.4 (23.9 (35.4 (13.9-84.3 (24.5-41.5 (15.6-24.8-32.6-42.1) 35.1) 37.8) 17.3 (28.6-22.

Phthalate monoesters levels in the urine of young children. Needham LL. Caudill SP. Food Addit Contam 2001. Hu H. Eckard R. 112(5):A270]. Angerer J. Levels of seven urinary phthalate metabolites in a human reference population.gov/chemicals/ phthalates/dbp/dbp-eval.68:309-314. Scotter MJ. Anderson WA. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.22(3):688-695. Sampson EJ. Hauser R. Itoh H. Calafat AM. Wiesmuller GA. Wittassek M. et al. Reprod Toxicol 2004. McKee RH. Koch HM. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Silva MJ. Int J Hyg Environ Health 2007. Springall C.16(4):487-493. Angerer J.S. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Caudill SP. Brock JW.nih.112(3):331-338. Pirkle JL. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Schettler T.208:237-245. Epidemiol 2005. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Urinary levels of seven phthalate metabolites in the U. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Bolte G. Richthoff J.niehs. Duty S. Silva MJ. Int J Hyg Environ Health 2007. Ryan L. Meeker JD. Green RA. Ryan L. Environ Health Perspect 2003. Sanchez GN. Barr DB. Fromme H. Brock JW. Boehmer S. J Androl 2004. Chen Z. Rylander L. Jedrychowski W. Hilborn ED.210(3-4):319-33.108(10)979-982. Perera FP. Koch HM. Dobler L. Poland. Silva MJ. Yoshida K. Prenatal exposures to phthalates among women in New York City and Krakow. Masunaga S. Drexler H. Jonsson BAG. Caudill SP.18(1):122. 4/20/09 Silva MJ. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Castle L. Gans G. Duty SM. Research Triangle Park (NC). Available at URL: http://cerhr. Environ Res 2003.111(14):1719-1722. Drexler H. Atlanta (GA). Environ Health Perspect 2004. Third National Report on Human Exposure to Environmental Chemicals. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.Phthalates References Adibi JJ. NTP-CERHR. Butala JH. et al. David RM. Rossbach B. Bull Environ Contam Toxicol 2002. 2000 [online]. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Giwercman A. Hum Reprod 2007. Calafat AM. et al. Reidy JA. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. 2005. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.210:21-33. Centers for Disease Control and Prevention (CDC). Massey RC. Hodge CC. Int J Hyg Environ Health 2005. Singh NP. Malek NA. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Camann DE.114(9):1424-1431. Hagmar L. et al. Jacek R.html. Blount BC. et al. et al. Environ Health Perspect 2006. Barr D.18(12):10681074. Koch HM. et al. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Weuve J. Helm D.93:177-185.25(2):293-302. Needham LL. Environ Health Perspect 2000. Silva MJ.

only levels at or above the 90th percentile could be characterized. 0.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.400 (.300) < LOD .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.700) . which may vary for some chemicals by year and by individual sample.900-1.400 (.500 (.00 (<LOD-1.500) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400 (.400) < LOD < LOD .300-.600 (.50) .200-.10) . 270 Fourth National Report on Human Exposure to Environmental Chemicals .500 (.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) 1. including nitrocellulose.200-.300) < LOD .70) .00-3.400 (.500) . and polymers.500) .00 (<LOD-1.400 (<LOD-.300-.90) .3.300-.600) .500 (.500) 1.400) 1.10 (.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 .00 (<LOD-1.200-.300-. resins.300 (.300 (.200-. 01-02.500 (. Survey Geometric mean (95% conf.500-.50) .00) .200 (<LOD-.700) .400 (<LOD-. polyvinyl acetate.400-.80) . 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.400-.300-.300 (.10 (<LOD-2. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.500 (. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500) . and 0.600) .400 (.400) 1.300-.300-.300-.300-.20) .400-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400-.300-.400 (.600) .600) .400 (<LOD-.300 (.10 (<LOD-1.300 (<LOD-. < LOD means less than the limit of detection.400-. and 03-04 are 0.400-.600) < LOD . 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. population from the National Health and Nutrition Examination Survey.500) < LOD < LOD .200-. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.400 (<LOD-.500 (.300 (.700) .500 (.Phthalates Dicyclohexyl Phthalate CAS No. respectively.500 (.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .70 (1.400) < LOD 1.400-.70) . 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.00-2.300 (.S.500 (.9.500) 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 .500) .200-. and polyvinyl chloride. see Data Analysis section) for Survey years 99-00.500) < LOD 1.600) .500) < LOD < LOD .400 (.10 (<LOD-1. In this Report.300 (.70 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

610 (.630 (<LOD-.310) < LOD .480 (.670-1. population from the National Health and Nutrition Examination Survey.670 (<LOD-.350-.400-.770) < LOD 2.450 (.740) .530-1.660) < LOD < LOD .420-.940 (.290-.490) .380-.34) .770-1.12-1.06) .630 (<LOD-.690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.690-1.67 (1.800-1.06) .690) < LOD < LOD .530) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.36-1.82) .770-1.53) .05) .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.910 (.560) 1.260-.33 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.530-.530 (.240-.660) .00 (<LOD-3.16) .380 (.590 (<LOD-.54 (<LOD-2.82 (1.53) .33) .74) .510-.10) .11) .170-.18) .710) .390 (.500) 3.620) < LOD .510 (.500) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250 (.740) < LOD < LOD .420-.500 (.910 (.270) < LOD .470 (.400-.360-.220 (<LOD-.770 (.590 (.470) 3.500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 271 .500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .14 (<LOD-3.330 (.310-.22 (<LOD-1.00) .54-6.17) .830) 1.790-1.16 (<LOD-3.910 (.54) .690) < LOD 2.690 (.910 (.S.770-1.530) 1. Survey Geometric mean (95% conf.370 (<LOD-.44) .950 (.330 (.420-.43 (1.410 (.450 (.880 (.

7 (70. In contrast.3 (74. colognes. 01-02. Products that may contain DEP include perfumes. DC (Hoppin et al. particularly those containing fragrances. soaps. 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.3 (82.1 (71. 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.Phthalates Diethyl Phthalate CAS No. and also in men attending a Boston infertility clinic (Hauser et al.8-111) 85. and hand lotions. deodorants.4. 2002).5) 81. 2007).9 (61. shampoos. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.S.2..1-93. population from the National Health and Nutrition Examination Survey. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 272 Fourth National Report on Human Exposure to Environmental Chemicals .3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. 2003) and African-American women in Washington.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. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. respectively. see Data Analysis section) for Survey years 99-00.9-92. 0.7) 71.4 (62. and 03-04 are 1. interval) 179 (156-204) Selected percentiles ( 95% confidence interval) 50th 164 (136-201) 169 (141-194) 174 (151-208) 75th 454 (370-538) 465 (415-527) 502 (457-555) 90th 1260 (1010-1480) 1230 (1040-1440) 1380 (1170-1750) Total 178 (159-199) 193 (169-220) Sample size 2840 (2150-3770) 2536 2500 (1860-3220) 2782 2700 (2160-3310) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 91. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2001-2002..2-102) 95. and 0. Biomonitoring Information MEP levels in the NHANES 1999-2000.9.

with adjusted geometric mean levels of urinary MEP that increased with age (CDC. 2003) were slightly lower than levels found in NHANES 2001-2002.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. 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. Analysis of NHANES 2001-2002 showed similar findings.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 ..6 (77.5-113) 122 (93. Other population estimates also differed by sex and race ethnicity (Silva et al. population from the National Health and Nutrition Examination Survey.5-114) 101 (87.2 (66. 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. Median MEP levels found in a small sample of German residents (Koch et al.9-110) 96.7-110) 81. 2004).9 (82. This age-related trend is opposite the direction seen for other phthalates. 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.Phthalates 2002 (Brock et al. 2005)..6 (65.3-105) 87. 2002). In an analysis of NHANES 1999-2000. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups.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.

Reproducibility of urinary phthalate metabolites in first morning urine samples. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Ryan L. Atlanta (GA). Jacek R. Needham LL.112(3):331-338. Centers for Disease Control and Prevention (CDC).93:177-185. Perera FP. Duty S. Angerer J. 112(5):A270]. Brock JW. et al. Hilborn ED. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Meeker JD.111(14):1719-1722.68:309-314. Silva MJ. Singh NP. et al. Bull Environ Contam Toxicol 2002. Drexler H. et al. Hoppin JA. Malek NA. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Davis BJ. Environ Health Perspect 2004.22(3):688-695. Hum Reprod 2007. Jedrychowski W. Camann DE.110(5):515-518. 2005. Barr DB. Baird DD. Barr D. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hauser R. Prenatal exposures to phthalates among women in New York City and Krakow. Caudill SP.Phthalates References Adibi JJ. Silva MJ. Rossbach B. Reidy JA. Phthalate monoesters levels in the urine of young children. Environ Health Perspect 2002. Brock JW. Environ Res 2003. Caudill SP. Koch HM. Hodge CC. Urinary levels of seven phthalate metabolites in the U.S. Third National Report on Human Exposure to Environmental Chemicals. Silva MJ. Environ Health Perspect 2003. Poland.

6 (16.40 (6.9-26.8 (19.1-17.60) 7.7) 37.84) 3.10-5.5 (31.92-2.10 (2.7) 27.70-3. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.7) 19.10 (4. 1989.50-5.8 (17.50-6.0) 23.1982). After parenteral administration.50-3.40 (4.80 (8.5) 37. ATSDR.50-20. toys.86) 2.2 (31.3 (15.49 (3.9-55.27) 2.5 (30.9-29.6 (11.0 (14.77 (2.0-18.2-35. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).5 (18.70) 16.70 (7.40 (4.40) 75th 7.57-7.35) 4.0 (9.3) 28.5-41.70-2.24-4.0) 31.70-4.5 (11.6) 15.80-9.41 (3.3 (24.0) 11.40-11.40) 9.00) 3.00) 2.70-8.5) 43.00) 2.5 (20.50-14.5-27.4) 5.67-4. as glucuronide conjugates (Albro et al.5) 21.0 (19.00) 19.70 (2.92-2.8-36. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.83) 2.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.5-28.2-28.50 (3.89-3.50-8.4) 15. respectively.40) 8.80) 6.10) 2.2) 6.10 (6.2 (11.40-8.32 (3.21 (2.4-42. Albro and Lavenhar.50 (2.60) 10. and blood product storage and intravenous delivery systems.5 (24.80) 13.50-16.96-5. mainly polyvinyl chloride.9 (29.10-3.6-38.51) 4. packaging film.80 (2.30) 2.85 (3.20 (3.15 (1.50 (8.0) 23.6-23.5 (25.90 (4.40-8.60-11.3-25.10-11.00 (4.42-5.2) 29.00) 11.9) 13.3-26.75 (3.9 (16.75-4.5-17.4) 7.70 (1.80-5. 1.90-3.4) 20.82) 3.0 (18.9) 13.0-84.0-18.3 (11.9 (15.70-2.0) 39.90) 1.30-6.40) 4.20 (1.1-48.92) 4. and 0.00 (5.23 (2.85) 4.10) 3.56 (2.3-64.00-5.4-20.80-4.6) 9.7 (14.6) 14.07-4.96) 4. population from the National Health and Nutrition Examination Survey.20 (1.6-60.9 (17.10-4.9) 27.0-19.40-8.2-17.0.4-20.4-27.70-5.0) 23.68 (3.80-8.40) 4.93) 6.3 (19.40-9.19-3.8) 15.2) 42.50 (3.10-5.1) 22.2) 23.1 (11.6 (9.9-49.3-57.10) 8.27 (3.90 (1.37-4.44) 4.61 (3. and in humans.6 (41.9 (7.5-40.25-3. 2002.00) 1.60) 4.16 (2.9.20 (3.90-4.10-3.5) 19.9 (29.4 (16.5-28.70 (3.70) 2.86) 2.4) 22.0 (21.90) 4.1 (8.7) 6. Peck and Albro.10-5.7) 8.6) 95th 23.50-6.4-40.50-11.57 (3.40-1.70 (1.6-25.Phthalates Di-2-ethylhexyl Phthalate CAS No.80 (1.34 (2.7) 18.3) 13.5) 32.90) 7.40-9.60) 9.5-36.60 (5.0) 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 3.6 (12. and 03-04 are 1.70) 7.80 (4