2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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4'-Tetrabromodiphenyl ether (BDE 47) 2.3-Dichlorobenzene (m-Dichlorobenzene) 1.4.3'.4.2'.4.5'-Tetrachlorobiphenyl (PCB 49) 2. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4-Tribromodiphenyl ether (BDE 17) 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4'.2'.4'-Pentabromodiphenyl ether (BDE 85) 2. Table 1.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[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 (2.2-Trichloroethane Trichloroethene (Trichloroethylene) m.5.1.4’.2-Dichloroethane (Ethylene dichloride) 1.4.2’.6.5'.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2-Dichlorobenzene (o-Dichlorobenzene) 1.1.6'-Hexabromodiphenyl ether (BDE 154) 2.2-Dichloropropane 2.2'.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.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .1-Trichloroethane (Methyl chloroform) 1.2'3.5.1-Dichloroethane 1.5.4.4.4.2'.2-Dichloroethene Dichloromethane (Methylene chloride) 1.cdc. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4.2'.3’.5'-Tetrachlorobiphenyl (PCB 44) 2.2'.6-Heptabromodiphenyl ether (BDE 183) 2.5.2'.html.2'.1. Paradichlorobenzene) 1. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.1-Dichloroethene (Vinylidene chloride) cis-1.4-Dichlorobenzene (p-Dichlorobenzene.1.2'4.3-Tetramethylbutyl] phenol) Triclosan (2.4.5-Pentabromodiphenyl ether (BDE 99) 2.3.What’s New in this Report What’s New in this Report In this Fourth Report.4'.4'.4'-Tetrabromodiphenyl ether (BDE 66) 2.3.4.2. The process for selection is described at http://www.5'-Hexabromodiphenyl ether (BDE 153) 2.3.4'.2-Dichloroethene trans-1.4’.4.4'-Tribromodiphenyl ether (BDE 28) 2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2'.5’.4'.3.gov/exposurereport/chemical_selection.6-Pentabromodiphenyl ether (BDE 100) 2.4.

five results that all have the value 90. Explanations for each change are provided in Appendix B.. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.. Percentiles for all three NHANES survey periods (1999-2000. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. the presence of an interference) that produced results of inadequate quality. Data for other pesticides are included only for 1999-2000 and 2001-2002.4-dichlorophenol and 2. and these data will be included in the next release of the Report. 2001-2002. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. urinary 2. Details of this procedure are provided in Appendix A.1). 2003-2004) have been re-computed by use of this improved procedure.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. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.g.g. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Fourth National Report on Human Exposure to Environmental Chemicals 3 .5-dichlorophenol for the 1999-2002 survey periods.

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

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

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

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

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

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

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

0-49. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. People may be exposed to acrylamide from foods.2-93.5 (79.2-118) 98. Fennell et al.5 (44.8-57.S.1) 62. mineral processing.0 (57.3-2.S.8 (81.8 (57. and an average daily intake is estimated as 0.4-89. and from dermal contact with products that contain residual acrylamide. 2005). Animal studies indicate that acrylamide is well absorbed.2-70.0) 85.5) 58.1 (52.7) 96.6) 71. as an absorbent in disposable diapers. are heated at temperatures used for frying and baking.7-64.6-104) 82. 2005).5-80.4) 100 (89. 2005).1-57. or to glutathione conjugates (Calleman et al. Elimination occurs mainly in the urine as mercapturic acid conjugates.3) 70. pulp and paper production. 1990.4 (54.. FAO/WHO.1 (88. Tareke et al.7) 73.1 (83. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. In humans. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.2-77. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.9 (60.2-67.. glycidamide.6 (56.9-105) 86.4) 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. ocular and dermal irritation from direct contact with acrylamide containing materials. Recently.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.3) 86.7-60.6) 90. Acrylamide is not thought to accumulate in the body at environmental doses.5-85.0 μg/kg for adults (FAO/ WHO.7) 58.2) 57.4 (54.5 (52. in permanent press fabrics. 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.. 2002).4 (53. (NTP-CERHR.5) 66.0.0 (53. and cosmetics (NTP-CERHR.2 (75. such as potatoes and some grains. in some sealing grouts.6-108) 61.4) 57. smoking.6 (51.2-114) 163 (147-191) 96. and is either metabolized to the reactive epoxide.4-60. 2004.2) 57. Fourth National Report on Human Exposure to Environmental Chemicals 11 . 2004).7-64.0-58.3 (53. but are generally above the U. These estimated intakes are hundreds of times lower than occupational exposures. Natural substances in the food are converted to acrylamide.9) 57.S. acrylamide is synthesized and used in the production of polyacrylamide polymer.3 (55.0-66. 2005.1 (47.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.3) 63.8-55. the main source of exposure is from the diet. but can covalently bind to form adducts with proteins.9) 75. and in the synthesis or compounding of dye materials.9) 58.4-76.7) 54.5 (74. 217 million pounds of acrylamide were produced commercially in the U. EPA reference dose of 0.7 (58.2 (58. and well below doses known to cause nerve damage or carcinogenicity in animals. Survey Geometric mean (95% conf.1-61.S.9-61. 2005).9-52.9 (69.1) 46. FDA. soil conditioners.6-65.4 (59. 2006). In 1997.6) 73.9) 63.8 (91. gels.1-64.1) 101 (95.1-64.2-91.4-83. EPA.7 (55.1) 53.0 (67.6 (81.6) 50.2 (62. Polyacrylamides are useful water-compatible polymers used in water treatment.7) 75th 79. see Data Analysis section) for Survey year 03-04 is 3. Since acrylamide has limited volatility and high water solubility.3-71.Acrylamide Acrylamide CAS No.2 μg/kg/day (U. widely distributed in tissues.1) 55. it was discovered that acrylamide is formed when starch-rich foods. and in some cosmetics.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. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. acrylamide has produced upper airway irritation following inhalation of high levels. population from the National Health and Nutrition Examination Survey.6-61.0 (69.7 (65.9 (54. 1994). interval) 61.4) 57.4 (51. Commercially. EPA.1 (73.0-108) 152 (139-175) 126 (111-142) 108 (86.6-66. 2006.0) 57. Estimated intakes in children are about twice that of adults (DiNovi and Howard.S. and binding agents.4-60.8 (52. In the general population.2-59. drinking water. 2005).7 (63.6-75.

5) 71.0 (75..5 (83.7-86. 2005. glycidamide (NTP-CERHR. 1997. thyroid. In addition. 2005. EPA.4) 53. 2005.7) 74..1-60. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. and neuronal DNA reactivity (Doerge et al.9) 65. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.3) 85. dominant lethality).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. 1997.6 (90. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U..pdf..5) 87.8 (51.5-94.. see Data Analysis section) for Survey year 03-04 is 4. Glycidamide has been shown to react with DNA (Doerge et al. and other sites) (FAO/WHO. scrotal.7) 60. Klaunig et al.1) 56.5 (42.3 (56.9 (57. 2002.1) 60. 2001).8-61. altered gene expression in testicular tissues (Yang et al.2 (72.2-91. presynaptic nerve terminal binding (LoPachin. Vesper 2005) and smoking (Bergmark.4-65.1-56. 2004). 12 Fourth National Report on Human Exposure to Environmental Chemicals .. population from the National Health and Nutrition Examination Survey. probably through its epoxide metabolite.4 (56. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.. and cancer (mammary. 2005) have been demonstrated in animals. Mucci et al. Hagmar et al.9) 75.6-62. Survey Geometric mean (95% conf. 2005).. 2005.1-70.9-77. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al.5) 75th 85.0-62.9) 59.4 (61. Rice.7 (87.8 (44. Acrylamide is clastogenic and can produce dominant lethal mutations.9 (58.3) 59. AHA levels have been shown to increase with dietary intake (Hagmar et al. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. 2005. 2008). 2002. Vesper et al.5-64. Maniere et al.7 (61. 2006). EPA.. After exposure ceases.4-59.9-62.4-98.0 (70..S. 2006.4-103) 79.6 (66. 2005) and sperm DNA adducts (Xie et al.1 (56.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.5-66.4 (57.3) 59.9-76.7 (84.0-93.2) 55.2 (63.1 (66. reproductive effects (reduced litter size.3-78.7 (57. 2005. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.7-64.2 (56. 2005. Puppel et al.2) 65.epa.S. male germinal cell injury.8-48.7) 61.0) 118 (103-126) 121 (112-134) 113 (94.. NTP-CERHR.3) 59.0 (52..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. uterine.who. 2005). 2005.9-64. respectively) are markers of integrated acrylamide exposure over the preceding few months.0 (80.1-62. EPA at: http://www. interval) 59. 2009).9) 87. 2005.1 (57.2-90. IARC classifies acrylamide as probably carcinogenic to humans..6-64.2-68. 2003.1 (82.0) 94.6-90.int/ ipcs/food/jecfa/summaries/summary_report_64_final.4) 46.8) 45. 2006) have been demonstrated after acrylamide dosing. 2008).. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.4 (81.5-92. 2005.9 (81. Schettgen et al. adrenal.4) 83.S. Schettgen et al.0..2) 87. Additional information is available from U.7) 90.9-78. fetal death. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. 2005).1) 62. Axonal degeneration.4 (90.1 (70.9-138) 143 (130-159) 96...8) 60. 2006). Animal studies have shown that acrylamide can cause nerve damage (neuropathy). U. 2005.5 (56.S..Acrylamide occupational exposures. although different analytic methods can affect results. Puppel et al.7-62. most non-smokers had levels less than about 100 pmol/gram hemoglobin.. 2004. U. 2005)..5 (59.4 (51.1) 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 59.3-101) 95. 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.8-49.

Godard T. Kamendulis LM. Granath F. Haugen M. Magnusson AL. 2001). National Toxicology Program. Bergmark E. Churchwell MI. Acrylamide neurotoxicity: neurological. The Updated Exposure Assessment for Acrylamide.. Toxicol 2005. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Cheong HK. Bergmark E. Becher G. Bridson WE. Beland FA. Costa LG. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Adv Exp Med Biol 2005. et al.27(4):219-226. NIH Publication No. smoking habits and gender. Chem Res Toxicol 1990. Paulsson B. July. Osterman-Golkar S. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . et al.. April 13-15. Summer SCJ. morphological and molecular endpoints in animal models. 2/3/09 Hagmar L. Duale N.. Twaddle NC.120(1):45-54. Maniere I. LoPachin RM.who. J Agric Food Chem 2008. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Available at URL: http://www. Wilson KM. Farmer PB. 1993. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Available at URL: http://www. Illinois. Malmberg B.43:365–410. Calleman CJ. Doerge DR. Food Chem.85:447-459. Human exposure and internal dose assessments of acrylamide in food.Acrylamide In occupational settings. In another study. Alexander J. 2/3/09 Klaunig JE.niehs. Uncertainties. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Calleman CJ.561:49-62. Rome. He F. February.fda. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Tornqvist M. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Rosen I. Costa LG. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Paulsen JE. 2005.pdf. Italy. Scand J Work Environ Health 2001.. Food and Drug Administration (FDA). Aprea P. Metabolism and hemoglobin adduct formation of acrylamide in humans. Snyder RW. Bjellaas T. Chem Res Toxicol 1997 Jan. DiNovi M and Howard D. He F. [Epub ahead of print] Dybing E. et al.580(1-2):157-165. Andersen M. 2009 Jan 8. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Bergmark E. Wu Y. Churchwell MI. Yang JS.56. Mutat Res 2005. Tian G. Burgess J. Wirfalt E. Acrylamide intake through diet and human cancer risk. 8-17 February 2005. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Guffroy M. Axmon A. 054472. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. 2006. Survey data on acrylamide in food: individual food products.580(1-2):131-141. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. McDaniel LP.cfsan. Mutat Res 2005.nih. 1999). and Research Strategies. Mutat Res 2005. Toxicol Sci 2005. Doerge DR. Hagmar et al. 2001. Zhang S. Toxicol Appl Pharmacol 1993. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1994). Laurentie M. 6013-6019. Perez et al. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. smokers and nonsmokers. Kautiainen A. Tornqvist M. da Costa GG.Toxicol Appl Pharmacol 1994. gov/~dms/acrydata. Mucci LA.. Available at URL: http://cerhr. Chicago. CFSAN/Office of Plant and Dairy Foods. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Calleman CJ. Adv Exp Med Biol 2005. Mechanisms of acrylamide induced rodent carcinogenesis. 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.html#u1004. Toxicol Sci.gov/chemicals/ acrylamide/Acrylamide_Monograph.3:406-412.pdf.561:21-37. Fennell TR. Nordander C. 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. References Bergmark E. Spicer R.580(1-2):119-129.10(1):78-84. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Hagmar L. et al. 64th Meeting: Summary and Conclusions (FAO/WHO). et al. 2004. Fennell TR. 2/3/09 Perez HL. 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.126(2):361-371. Joint FAO/WHO Expert Committee on Food Additives. Bruze M.

Schettgen T. Lee MH.S. U. Kutting B. Rapid Commun Mass Spectrom 2006. Fueller F. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Myers GL.epa. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Jin Y. Han DU. Int J Hyg Environ Health 2004. Environmental Protection Agency (U. Environmental Protection Agency (U. Ospina M.19(4):527-34. Mutat Res 2005. September. Agudo A. Licea-Perez H. et al.207(6):531-9. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Xie Q. Ingham L. Meyers T. Analysis of acrylamide. Angerer J.S.gov/iris/subst/0286. Toxicol Lett 2002. Angerer J. J Agric Food Chem 2002. The carcinogenicity of acrylamide. 2/3/09.134(1-3):65-70. Office of Pollution Prevention and Toxics.gov/chemfact/s_acryla.56(15):6046-53. Smith A. Hallmans G. Tjønneland A.274(1):59-68. Lee SH. J Agric Food Chem 2008. Mutat Res 2005 Feb 7. Fu D. Benetou V. propylene oxide. Available at URL: http://www. Integrated Risk Information System (IRIS). et al. Toxicological effects of acrylamide on rat testicular gene expression profile. a carcinogen formed in heated foodstuffs. Drexler H. Broding HC.50(17):4998-5006.163(2):101-8. EPA). Meyers T. Vesper HW. Hemoglobin adducts of ethylene oxide. U. Angerer J. Ospina M. Ding X. EPA). Schettgen T. Rydberg P. Toxicol Lett 2006.S. Washington (DC). Choi JH. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Tareke E. Liu Y. Chae C.S.epa. Tornqvist M. Liu K. Drexler H. Slimani N. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.206(1):9-14.Acrylamide glycidamide by gas chromatography-mass spectrometry.561:89-96. Acrylamide. Anal Biochem 1999. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Gray JG. Tjaden Z.20(6):959-64. Available at URL: http://www. Adv Exp Med Biol 2005. Letzel S. Yang HJ. Schettgen T.htm.txt. Chemical Summary for Acrylamide. 2/3/09 Vesper HW.580(1-2):71-80. revised 1/3/06. Vesper HW.580(1-2):3-20. Weiss T. Sun H. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Rice JM. Marko D. Drexler H. Puppel N. Rossbach B. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. 1994. Int J Hyg Environ Health 2003. Reprod Toxicol 2005. Eriksson S. Han CH. Karlsson P. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells.

052 (<LOD-.68 (1.163 (.110-.39 (1.180) .23-2.790) .09-2.02) 1.260-1. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.533-.180 (.040 (.800 (.20 (.280 (.110-.120 (.87-3.050 (. which may vary for some chemicals by year and by individual sample.45) 1.310-1.21-1.950-1.910-1.19-2.620-1.160-.080 (.080-.050-.197) .080) < LOD .990 (.140 (. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.115-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .410) .120-.145) .09-3.12) 1.160) .770) .62) 2.44) 2.53-4.30) 2.015.770-1. Survey Geometric mean (95% conf.02 (.48-3.600-1.48-2.63-2.087-.580) . and exacerbated asthma (U.190-.66-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.062 (.140 (.120 (.96) 2.15) 2.96-4. emphysema.302) .84-3.740-1.075 (.110 (.55 (1. 2006).180) .070) .040 (.054 (.200) 1.470-.216 (.110-.26-1.164 (.05 ng/mL. 1998).480-1. and 0.16) .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.220) .057-.090-.058 (.131 (.370-.120 (.030-.428-.167 (.997-3.01) 3.81-2.360) .920 (. and 17% had an LOD of 0.050-.070) .93) . 2004).060-.213) . producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.66) 1.79) 3.052 (<LOD-.42-4.726) . DHHS.32) 1.104-.78) 2.17) .S.066 (.060 (.42 (1.120 (.44) 2.01 (1.04 (1.506 (.110 (.068) .83-2.030-.54 (1.310) 90th 1.88 (1.88 (.164 (.68) 2.047-. maternal exposure during pregnancy can result in lower birth weight.160 (.350-.234) .99) 2.09-3.33-2. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.188) .050) .106-.153-. 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.89) 1.312) .060-.35 (2.080-.22) 2.088-.071 (.94) 1.850 (.660) .063) .090-.300) .77 (1.02) 1.510 (.625) .120 (.70-2.066-.060 (.220-.54) 1.20) .70) 2.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .060) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.20) 1.230) . population from the National Health and Nutrition Examination Survey.015 ng/mL. respectively.124 (.050 (<LOD-.180 (. acute respiratory illness.480-.00) .050 (<LOD-.20 (1.190-.570-1.130 (.43 (1.17 (1.730 (.060 (<LOD-.060 (<LOD-.05.084) . Cigarettes contain about 1.50-4.087 (.17 (.076-.60-2.23 (2.63 (2.094) .070) 75th .240 (.080-.55-2.080 (.580-1.087) < LOD < LOD .030-.620 (.150) .32-2.49) 1.21-1. 2004).30) * .Cotinine Cotinine CAS No.23 (1.180) .175 (.040 (.28) .621-1. Children exposed to ETS are at increased risk for sudden infant death syndrome.050 (<LOD-.140-.75) 1.860 (.080) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 83% of measurements had an LOD of 0.230 (.110) . Fourth National Report on Human Exposure to Environmental Chemicals 15 .140-.142-.190-.430-1.5% nicotine by weight (Kozlowski et al.110 (.53 (1.50 (1.49) 1.15 (2.92 (1.840) 3.40) .137 (.040-.990) .32-2.100-.160 (.160 (.44 (1.080-.154-.66 (1..47-3.77 (1.086 (.900-1.180) .068) .580 (.201) .077) .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 .11) .400-.148-. acute respiratory infections. stroke.108) * .350 (.320) .077) .187) .030 (. DHHS.05) 1.111-.137-.050) .20-2.34 (1.930 (. and various other disorders (U.310) .38-2.21 (. and 03-04 are 0.220) .073) < LOD .130) .630 (.710 (.30) 2.110) .210 (.066) .150) .198) * . ear problems.690 (.540-.193) .500 (. ** In the 2001-2002 survey period.960-1.740-1.820) .308 (.163) .44 (2.059-.54 (1.090-.570 (.070-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.260) 1.043-.99) 2.950 (.39) 3.S.061) < LOD .060-.160) .00) 1.020-.139) * .96 (1.12 (2.505 (.630 (.23 (.126) .059-.310-1.053 (<LOD-.520 (.350-.144 (.19) 1.68) .50-1.180) .110 (.28-1.57) 2.14-1.14) .120) .540 (. cardiovascular disease.65 (1.62 (2.770) .S.85 (1.110 (.120-.95) 1.12 (1.070 (<LOD-.040-.50) 3.450-.19) .071) .77 (2.14) .76 (1.050 (<LOD-. 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.670) .12-4.089) Age group 3-11 years 99-00 01-02** 03-04 .18-3.630 (.047-.

1996).. nausea. and hair. 1998). Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff. non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al.. and death. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. However. 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. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005. cognitive and sleep disturbances. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al..gov/researchreports/nicotine/nicotine. with heavy exposure to ETS producing levels in the 1–10 ng/mL range. nasal sprays. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. 1994).. variable changes in blood pressure and heart rate.. 1999). or chewing gum. chewing tobacco. Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . contains nicotine in larger amounts than other nicotine-containing plants. html. Cotinine can be measured in serum. tomatoes. The tobacco plant.nih... 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. diaphoresis. Cotinine. Wilson et al. The IARC and the NTP consider tobacco smoke to be a human carcinogen. mean air concentrations typically range from 2 to 14 µg/m3 (NTP. Perez-Stable et al. 2006. vomiting. with higher levels measured in restaurants and bars. 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. Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. 2006).3 to 30 µg/m3. 1998). 1999. 2005). The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0.. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration. seizures. NCI. Soliman et al. 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. urine. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. The serum cotinine levels seen in the NHANES 20032004 appear approximately similar to levels seen in the previous survey period (NHANES 2001-2002) for the total population estimates. 2004). Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans. Nicotiana tabacum. Iwase et al. 1999. In homes with one or more smokers. 2005. 2004). 2006). Pirkle et al. Serum cotinine has been measured in many studies of nonsmoking populations.. Symptoms of 16 nicotine withdrawal include irritability.. Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al. 1975.. or skin patches that contain nicotine. Hukkanen et al. which include potatoes. Acute tobacco or nicotine intoxication can produce dizziness. 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. craving. More information about the effects of smoking and nicotine can be found at: http://www. nicotine has a half-life in blood plasma of several hours (Benowitz. (CDC.. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. and increased appetite. 1991). 2005).. Once absorbed. and peppers.nida. salivation. Hukkanen et al. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al.. Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. 2005). 1996). a process involved in the development of addiction. For an adult.. eggplants. Over the previous decade. diarrhea. the adjusted geometric mean serum cotinine was higher in children (aged 4–11 years) than in adults among both non-Hispanic blacks and non-Hispanic whites (Pirkle et al. saliva. 2005.Cotinine 1994. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. Children are primarily exposed to ETS by parents and caregivers who smoke. the primary metabolite of nicotine. During each previous NHANES survey.

Maurer KR. Benowitz NL. 4/13/09 Iwase A. the United Kingdom.S Department of Health and Human Services (U. et al. available at URL: http://mtn.280:135-140. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Pechacek TF. BMJ 1975. Available at URL: http://www. Centers for Disease Control. 4/13/09 Centers for Disease Control and Prevention (CDC). 2004. 4/13/09 U.fr/ENG/Monographs/allmonos90. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Racial/ethnic differences in serum cotinine levels among adult U.S.cdc. Available at URL: http://monographs. Clin Pharmacol Ther 1994. Schwartz SS. Mehta NY.18:188-204. Caraballo R. Bernert JT. Department of Heath and Human Services. Fong I. Centers for Disease Control and Prevention. Strauss WJ. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.iarc. National Center for Chronic Disease Prevention and Health Promotion. Available at URL: http://monographs. [online]. Houseman TH. In Report on Carcinogens. Kira S.S Department of Health and Human Services (U. 1991. Summary of Data Reported and Evaluation [online] 1986. Curtin LR. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.94(2):314-320. Vol 83. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Soliman S. Jarvis MJ. Coordinating Center for Health Promotion. JAMA 1998. Aiba M. Pollack HA. Metabolism and disposition kinetics of nicotine.63:139-43. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. DHHS). IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Epidemiol Rev 1996. Herrera B.S. DHHS). Tobacco Smoke. Jacob P. Modin G. 1999-2002. U.S. Etzel RA. 4/13/09 National Cancer Institute (NCI). Turner DM. Vogler GP.4:313-316. Pirkle JL. Richter PA. Mowery PD. Trends in the exposure of nonsmokers in the U. Pickett MA.S. International Agency for Research on Cancer. Nicotine metabolism and intake in black and white smokers. iarc. Dollery CT. Absorption and metabolism of nicotine from cigarettes. Pharmacol Rev 2005. George CF. IARC Monogr Eval Carcinog Risks Hum. Pechacek TF. National Institute for Occupational Safety and Hygiene (NIOSH).15:302-307. 4/13/09 Perez-Stable EJ. 4/13/09 International Agency for Research on Cancer. Environ Health Perspect 2006.57(1):79115. Pirkle JL. Perez-Stable EJ. J Pharmacol Exp Ther 1999.php. Int Arch Occup Environ Health 1991. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. 1999.S. U. Tobacco related exposures. Herrera B. June.pdf. Sweeney CT.php. Jacob P III. Available at URL: http://ntp.pdf.275:1233-1240.surgeongeneral. JAMA 1996. Cotinine as a biomarker of environmental tobacco smoke exposure.7:369-375. Schober SE.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. JAMA 1998. Tob Control 2006. Sosnoff CS. Kozlowski LT. Office on Smoking and Health [online] 2006. Respiratory nicotine absorption in non-smoking females during passive smoking. U.fr/ENG/Monographs/ allmonos90. Giovino GA. Jacob P III. Benowitz NL. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. 11th ed. Summary of Data Reported and Evaluation [online] 2004. population to secondhand smoke: 1988-2002. Hukkanen J.291(3):1196-1203.gov/tcrb/monographs/10/. Benowitz NL. Jacob III P.cancer. Available at URL: http:// cancercontrol. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Department of Heath and Human Services. IARC Monogr Eval Carcinog Risks Hum. Lewis PJ. Tobacco Smoke and Involuntary Smoking. 1988-1991. Ethnic differences in N-glucuronidation of nicotine and cotinine. Warner K.114(6):853-858. Bernert JT. et al.280:152-156.gov/library/ secondhandsmoke/.56:483-493. 1988-1991. cigarette smokers: the Third National Health and Nutrition Examination Survey.gov/eid/rmca/critdocs/ criteriadoc/33.S. Caudill SP. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Brody DJ.gov/ntp/roc/eleventh/profiles/ s176toba. Vol 38. National Toxicology Program (NTP). Benowitz NL.S. Atlanta (GA): 2005. Exposure of the U. Brody DJ. Coordinating Center for Health Promotion. Centers for Disease Control and Prevention.niehs.nih. Benowitz NL. Flegal KM. and the United States. Giovino G. References Armitage AK. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Tob Control 1998. Am J Public Health 2004.niosh. Third National Report on Human Exposure to Environmental Chemicals. Smoking and Tobacco Control Monograph 10 [online]. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.

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

130) < LOD .N-Diethyl-meta-toluamide (DEET) CAS No.S.. 1998).100-.560) < LOD . Sudakin and Trevathan.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. EPA.130-.140-. About 3-8% of dermally applied DEET is absorbed. Survey Geometric mean (95% conf.120-.160) < LOD .220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .250) < LOD . 2003). and it has not been rated by IARC or NTP with respect to human carcinogenicity. Additional information is available from U. 2003).130 (.130-. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.130 (. Urinary N.180) < LOD . (Kolpin et al.110 (.110 (<LOD-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Fourth National Report on Human Exposure to Environmental Chemicals 19 .270) 688 678 518 700 598 956 Limit of detection (LOD.210 (.130 (.120-.100-. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. One survey detected DEET in 74% of sampled streams in the U.100-.110 (<LOD-.N.170 (.190) < LOD .140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130-.S.EPA.epa. have been reported as result of self-poisoning by ingestion or excessive dermal application.110 (.100-. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.S.gov/pesticides/.140) < LOD .140 (. including seizures and encephalopathy. 1998).EPA at: http://www.180 (. which may vary for some chemicals by year and by individual sample.140) < LOD .150) < LOD .170 (. Neurological effects in humans. (U.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 . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 134-62-3 General Information N.130-. 2005). 1995. After absorption.110-.S. DEET is not genotoxic.240) < LOD .210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and they range in concentration from 4% to 100%.EPA.100-.110-. DEET has low acute toxicity.. 2002). Its use is recommended for prevention of several vector-borne diseases..130) < LOD . There are over 225 insect repellents brands containing DEET.N-Diethyl-meta-toluamide (DEET) N. DEET is also used in combination with dermal sun screens (U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.110 (.S.180 (. population from the National Health and Nutrition Examination Survey.100-.110 (. 2002).140) < LOD .520) < LOD .S. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. DEET is not a developmental or reproductive toxicant in animals (U.449 and 0.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.220 (. DEET can be applied to clothing and the skin to repel biting insects.1. DEET is not registered for use on agricultural commodities. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.100 (<LOD-.180 (.

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 (. 2007).N.150) < LOD .190 (.140-.370-.230) < LOD .350) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.93) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals .250 (.290-.250-.270 (<LOD-.130 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.390-..410-.410 (.280-1.190 (<LOD-.500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .S.250) < LOD .240-.S.370) < LOD .230-.350-.190-.320) < LOD .630) < LOD . Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population. 2005).240) < LOD . representative subsamples from NHANES 2001-2002.. Survey Geometric mean (95% conf.300 (.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. Urinary N.480 (.170-.200 (.150-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .500 (.350) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Urinary DEET levels as high as 5.270-. In this survey period. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1992).280 (.330 (.440) < LOD .320 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.270 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.190 (.300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .330 (.490) < LOD .640 (.230-.270) < LOD . population from the National Health and Nutrition Examination Survey.

Available at URL: http://www. U. Bell JW. Third National Report on Human Exposure to Environmental Chemicals. DeBord KE.S.S. 1993-1997. metabolism. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Veltri JC.S. September 1998.S. Smallwood AW. Available at URL: http://www. and excretion of N.36(6):1202-1211. Gabriel KL.N. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Int J Toxicol 2002. Osimitz TG. Washington (DC): U. hormones.S. Quandt SA. 4/9/09 U. 2005.EPA). Pharmaceuticals.115(8):1254-1260. pp. Human exposures to N. Schoenig GP.N-diethyl-mtoluamide following dermal application to human volunteers. U. Thurman EM.EPA. Meyer MT. and other organic wastewater contaminants in U. Lowry LK. 2005 Kolpin DW. Barr DB. Chemical Summary. Grzywacz JG.EPA). J Toxicol Clin Toxicol 2003. pdf. Environ Sci Technol 2002. 1-118.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Environmental Protection Agency (U. Reregistration Eligibility Decision (RED): DEET. Selim S.2:341352. Page BC. Barber LB. Toxicity and Exposure Assessment in Children’s Health. Fundam Appl Toxicol 1995. Diethyltoluamide (DEET). Zaugg SD. N.S. 1999-2000: a national reconnaissance. Chen H.S.epa. Sudakin DL. Hartnagel RE Jr. streams. EPA 738-R98-010. Absorption. Environmental Protection Agency (U.gov/teach/chem_summ/ DEET_summary. J Anal Toxicol 1992.16(1):10-13. et al. Trevathan WR. Atlanta (GA). Tapia J.N-Diethyl-meta-toluamide (DEET) References Arcury TA.gov/oppsrrd1/REDs/0002red.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Environ Health Perspect 2007. DEET: a review and update of safety and risk in the general population.25:95-100.epa. Centers for Disease Control and Prevention (CDC). Furlong ET.41(6):831-839.pdf. EPA.

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

Yoshinaga J. Zaugg SD.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Bisphenol A. Chem Res Toxicol 2001. 2007.35(2 Pt 1):238-254. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Department of Health and Human Services. Rubin C. Belgium. Shin HC.eu/ health/ph_risk/committees/sct/documents/out156_en. niehs. Gender differences in the levels of bisphenol A metabolites in urine. Imai H. Pharmaceuticals. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. niehs. Regul Toxicol Pharmacol 2002.Scientific Committee on Toxicity. Furukawa M. September. Ecotoxicity and the Environment (CSTEE). 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Ema M.. Szigeti-Buck. Reprod Toxicol 2001. 1999-2000: a national reconnaissance. Brine DR. with estrogen receptors alpha and beta. Exposure of the U. Leranth. Life Sci 2001.J. Han SS. Joint Research Centre Institute of Health and Consumer Protection. Zacharewski TR. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Needham LL. Thomas BF. Lynch BS. Available at URL: http://ntp. DirectorateGeneral Health and Consumer Protection.. Myers CB. Yang M. Koulova AI. et al. hormones. and other organic wastewater contaminants in U.niehs. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.59(9):625-628. Barr DB. Kim CS. Occup Environ Med 2002. Klinefelter GR. Munro IC. K. Serizawa S. Tyl RW.68(1):121-146. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats.gov/chemicals/bisphenol/bisphenol.137(3):353-362. Meyer MT. Ispra. Kolpin DW.nih. Kim JC. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Kroes R. Research Triangle Park. Hum Ecol Risk Assess 2004. Chung MK. Pyo MY. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Reidy JA. and Hardy MP. Hughes C. Matthews JB. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Fujii S. U. Environ Health Perspect 2005. Sottas CM.Environmental Phenols References Akingbemi BT. Caudill SP.gov/chemicals/bisphenol/BPAFinalEPVF112607.nih. 2/4/09 European Commission.pdf. Calafat AM.312(2):441-448. European Commission. National Toxicology Program. Endocrinology 2004. Hlywka JJ. Watanabe C..S. Kawamura N. National Institutes of Health. Nippon Eiseigaku Zasshi 2004. Needham LL. 2/4/09 Ouchi K. Bradley S. MacLusky. Timms BG. 5: 505-523.145:592-603. Proc Natl Acad Sci USA 2005. Ye X. Available at URL: http://ec.pdf. Watanabe S. Wong LY. Arakawa C. Needham LL.nih. Toxicol Sci 2002. N. Cohen JT. 2008. Park S. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Rhomberg et al. May 22. et al. Richter CA. November 26. Marr MC.pdf.europa. Available at URL: http://cerhr. McConnell EE.jrc. Reidy JA. Tsugane S. Barr JR.10:875-921. Howdeshell KL. Italy. Ekong J. Doull J. NC. Hanaoka T. streams.36(6):1202-1211. Biochem Biophys Res Commun 2003. J Chromatogr B Analyt Technol Biomed Life Sci 2002. vom Saal FS.59(4):403-408.780(2):365-370. 2003.149:988-994. August 2001.pdf . Endocrinology 2008. Joskow R. Human Health.pdf . Koh WS.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Twomey K. Brussels. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Haighton LA. Cunha G. Environ Sci Technol 2002. Cha SW.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. T. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. J Am Dent Assoc 2006. Environ Health Perspect 2008.116(1):39-44. Barber LB. and Hajszan.14(2):149-157. 4.102(19):7014-7019. C. Hara K. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Harazono A. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Barton L. An evaluation of the possible carcinogenicity of bisphenol A to humans. Calafat AM. 2/4/09 Fujimaki K. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. In vitro and in vivo interactions of bisphenol A and its metabolite. Kuklenyik Z.113(4):391-395. Kim YH. Han SY. 32 Fourth National Report on Human Exposure to Environmental Chemicals . 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. Kiguchi M. 2002. Thurman EM. Gray GM. Keimowitz AR. National Institute of Environmental Health Sciences. et al.S. Ikka T. bisphenol A glucuronide. Furlong ET. Available at URL: http://cerhr. Available at URL: http://ecb.S. Calafat AM.69(22):2611-2625. Rat two-generation reproductive toxicity study of bisphenol A.

Wilson NK.40(7):905-12. Environ Health Perspect 2005. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Endocrinology 2006. Welshons WV. Biological monitoring of bisphenol a in a Korean population. Arch Environ Contam Toxicol 2003.Environmental Phenols Volkel W. Colnot T. Large effects from small exposures. Kawamoto T. Chang SS. Lee SM.103(1):9-20. Environ Res 2007. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Filser JG. Kim SY. Jang JY. vom Saal FS. Food Chem Toxicol 2002. and nonylphenol at home and daycare. An observational study of the potential exposures of preschool children to pentachlorophenol. Dekant W.15:12811287. Csanady GA. Lordo RA. Yang M. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Nagel SC.44(4):546-51.113(8):926-33. Hughes C.147(6 Suppl):S56-69. et al. III. Chuang JC. Sheldon LS. Witorsch RJ. Fourth National Report on Human Exposure to Environmental Chemicals 33 . bisphenol-A. Vom Saal FS. Morgan MK. Chem Res Toxicol 2002.

600) . 2002).30) 2.500-1. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.80 (1.60-3. textiles.369 (.300 (<LOD-. Bian et al.g. is used to manufacture alkylphenol ethoxylates.600) .00 (1.. and the polyethoxy chain may consist of up to 50 ethoxy units.60-3. and impaired spermatogenesis (e.90) 2.900 (.500) .. and from contact with some personal care products and detergents..3. Blake and Boockfor.00) 1229 1288 03-04 03-04 03-04 * .30 (1. industrial cleaners. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.70 (1. 2000.600) 1. through sewage.60) .30 (. Urinary 4-tert-Octylphenol (4-[1. and was quickly eliminated from the blood (Certa et al.20-2.50) 1.40) 1.300 (<LOD-.80 (1.10) 2.20-2.600-1.700-1. Ying et al.50 (1.10) 1.50-2.299-. Katsuda et al.20) 2.60) 1.. 2006.60) 613 652 1092 Limit of detection (LOD. In the 1990s. and through manufacturing waste streams (Warhurst.600-1.50-3.30 (1.000 tons of alkylphenol ethoxylates were produced annually worldwide.800-1.900 (. and emulsifiers.00 (.70 (1.500) .10-2.507) * < LOD .400 (.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 .40 (1. 2003. In rats. 2004).00 (. including 4-tert-octylphenol.40) 1.477) . Less frequently. 34 Fourth National Report on Human Exposure to Environmental Chemicals .300 (<LOD-.20) 1. The alkylphenols can bioaccumulate in some fish. 140-66-9 General Information 4-tert-Octyphenol.500) 75th .40) 2.600) .20-2.400 (. which are anionic surfactants used in detergents.274-.500 (. In 1999-2000.30 (1.10 (1.300 (<LOD-. have demonstrated estrogenic effects particularly when injected at high doses in animals.300-.600-1.400 (.60-3. Several alkylphenols. an alkylphenol. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. 2002). Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates. and some personal care products.40) 2. which may vary for some chemicals by year and by individual sample. testicular atrophy. streams in 30 states (Kolpin et al..50) 1. leading to inhalation as another potential exposure route (Rudel et al.357 (.400) 1.10 (. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. to shorter chain alkylphenol ethoxylates.900 (.268-. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.60-3.600-1.30) 1.60-3...40) * 03-04 03-04 03-04 .. and some of their degradation products are toxic to aquatic life.30-2.1.80 (1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70 (1. Indoor and to a lesser extent..300 (<LOD-.300-.2.60-3. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown. did not bioaccumulate.50) 1.500-1.S.600-1. impaired steroidogenesis.900 (. 1996). Saito et al.500) . These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.20-2. orally administered 4-tert-octylphenol was well absorbed.20 (1.600-1.497) * .389 (. altered estrus cycles and reproductive outcomes..S. the various alkylphenols have also been used as emulsifiers and modifiers in paints. and to alkylphenoxycarboxylates. Laws et al. 2000.Environmental Phenols 4-tert-Octylphenol CAS No.50) .90) 2.20-2. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.70 (1.10 (.5% of 139 U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.30 (1. pesticides. over 500.80) 2. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). 1995. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. altered neonatal sexual development.200-. During the 1980s and 1990s. The alkylphenol ethoxylates enter the environment through human use of products containing them. 1997.20-2. see Data Analysis section) for Survey year 03-04 is 0.200-.900 (.50) . < LOD means less than the limit of detection. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. 4-octylphenol monoethoxylate was detected in 43.g.20) 314 715 1488 03-04 03-04 * * . fish) and drinking water. Disposition in humans has not been studied sufficiently.30) 90th 1.

00) 1.S. 2004.54) * 03-04 03-04 03-04 .199-.770 (.03 (1.50 (2.. 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.380 (<LOD-.384) * .96-4.300 (<LOD-.08) 1.62 (1.470) 75th .435 (. Kawaguchi et al. 4-tert-Octylphenol is not considered directly genotoxic.320 (<LOD-.53-3.40 (1. Survey Geometric mean (95% conf.11-2. at lower or environmentally relevant doses (Blake et al.280-.00 (. 2004)..31 (1.530) .3. It is unclear if estrogenic or other effects occur in animals through oral dosing.14) 314 713 1487 03-04 03-04 * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.20 (1.02-4.10-2. 2000.76 (2.25) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25) 90th 1.78) 3.29) 2..470-1.730-1.560) .620-1.22) . Sweeney et al.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 .450) 1.850 (.S.78) 1228 1286 03-04 03-04 03-04 * .43-3.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.640-1.00) 2.270 (.160-.740 (. Tyl et al.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.740 (.860 (.40-4. 1999). Nagao et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.11) 2.68) 2.59) 1.33 (2.269 (.17 (.270-.62 (1.03-6. or their corresponding ethoxylates with respect to human carcinogenicity.11) 1..570) .71) 2..260 (<LOD-. representative subsample of NHANES 2003-2004.67-2.18-4. Yoshida et al. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U. 2005.03 (1. nonylphenol.910 (.207-.62) .450) .06 (2.890-2.1.540-1. In a small number of adult Japanese volunteers.78 (1.500-1.550-1.170-.43) 1.36-3. 2001).05-2.73) 2.400) . Urinary 4-tert-Octylphenol (4-[1.610) .460 (. Calafat et al.81 (1.370 (<LOD-.64 (.68-2.60 (1.349) * < LOD .33) 3.43) 1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.270 (.59 (1.85 (1. 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. 2001.41) . IARC and NTP have not rated octylphenol.337-.620) .31-2. Fourth National Report on Human Exposure to Environmental Chemicals 35 .Environmental Phenols Myllymaki et al.420) .65-3.00 (..25-2. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.00) 2.276 (. 2003.410 (.470-1. population from the National Health and Nutrition Examination Survey.630-1.15) 1.

Kookana R. Katsuda S. Xu L. Cooper RL. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Brooks AN. Saito Y. Environ Health Perspect 2008. Meyer MT. Horie M. Anal Chim Acta 486:41-50.207(1):59-68. Chen J. Yoshida M. Pharmaceuticals. Available at URL: http:// www. Reidy JA. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Carey SA.165(3):217-226.S. Regul Toxicol Pharmacol 1999. nonylphenol. Reprod Toxicol 2001. Endocrinology 2000. Wiegand HJ. Izumi S.foe. Usumi K. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Boockfor FR. Muller AM. Two-generation reproduction study with para-tert-octylphenol in rats. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Environ Sci Technol 2003. Nair-Menon JU. Reprod Toxicol 2004. and other endocrine-disrupting compounds in indoor air and dust. Indoor air pollution by alkylphenols in Tokyo. Karjalainen M. alkylphenols. Camann DE. Song L. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Phthalates. et al. Blake CA. Onuki A. Katsuda S. Toxicol Sci 2000. Brody JG. 2/4/09 Ying GG. Ye X. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Furlong ET. Yoshimura Y. Myllymaki SA. Nicol L. and testosterone. Rudel RA. Millette CF.116(1):39-44. pesticides.folliclestimulating hormone. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Brine DR. Tyl RW. 1995. Seely JC. Needham LL. Taya K. Toxicol Lett 2001. polybrominated diphenyl ethers. Certa H. Seto H. Biol Reprod 1997. Toxicol Appl Pharmacol 2005. Indoor Air 2004. bisphenol A and methoxychlor in rats. streams. Zaugg SD. Paranko J.54(1):154-167. 1999-2000: a national reconnaissance. Calafat AM. Sweeney T.pdf. Food Chem Toxicol 2006. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Bolt HM. Ito R. Kawaguchi M. J Chromatogr B Analyt Technol Biomed Life Sci 2004.71(1-2):112-122. Spengler JD. Fail PA. prolactin. Nagao T. Yoshimura S.14(5):325-332.141(7):2667-2673. Makino T. Estrogenic activity of octylphenol.44(8):1355-1361. hormones. Watanabe G.18(1):43-51. Haavisto TE. Nakagomi M. Inoue K. Warhurst AM.S. and sertoli cell number. Barber LB. Ono H. and other organic wastewater contaminants in U. Maekawa A.30(2 Pt 1):81-95. et al. Roche JF. Qian J. 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.799(1):119-125. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Korn LR. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Saito I. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. et al. Exposure of the U. Thurman EM. Takai N. et al. Kawaguchi M. Arch Toxicol 1996. Fedtke N.15(6):683-692. Watanabe G. Inoue K. Toxicol Appl Pharmacol 2000. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Sakui N. McCoy GL. Taya K. Wang X. Raychoudhury SS. Williams B. Environ Int 2002. testis size.28(3):215-226. Toppari J. Laws SC. 2003. Takenaka A. Ferrell JM.uk/resource/reports/ethoxylates_alkylphenols. Boockfor FR.37(20):4543-53. Wong LY.co. Marr MC. Myers CB.121(1):21-33. Bodman GJ.57(2):255-266. Okada F. Environ Sci Technol 2002. Yoshida M. Maekawa A.Environmental Phenols References Bian Q. Blake CA.36(6):1202-1211. Kolpin DW.

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

5-14.4) 51.5-86.20 (7.80 (5.7 (14.8-60.7) 123 (36.4 (32.0-15.48-10.2 (11.7 (11.72-13.90-10.4) 73.20-13.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-46.4) 90th 249 (188-304) 03-04 03-04 03-04 8.4 (38.94 (7.8-85.60 (8. Urinary Triclosan (2.6) 31.3-67.2) 9.6) 10.2) 13.8-63.2-14.8-127) 37.7 (39.6-14.1) 9.1) 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 9.9) 32.9 (8.9 (33.6) 39.1) 50.9 (50.9) 7.70-16.2 (13. interval) 12.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.3-31.8) 14.6-37.50-10.1) 13.0-15.0-73.0-19.20-10.1 (45.1) 9.2-58.3) 6.6) 12.32-14.Environmental Phenols Urinary Triclosan (2.11-11.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9 (11.5 (11.18 (5.74 (5.40-17.7) 292 (151-432) 132 (78.50) 10.00 (4.6) 90th 212 (172-241) 03-04 03-04 03-04 9.0-213) 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 .0 (8.9-236) 193 (90.48 (8.92-12.86-12.9) 8.6 (30.22-10.4-18.1) 9.5) 66.20 (7.8) 7.S.4 (12.3-15.7 (28.8 (21.1) 11. Survey Geometric mean (95% conf.5) 13.3.40-11.1 (8.45-10.45-13.6-14.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.82 (8.1) 14. interval) 13.4) 317 (231-433) 144 (96.4) 25.1-39.54 (8.3) 10.6 (10.8) 116 (39.30-14.0) 65.0 (26.93 (7.S.2 (27. Survey Geometric mean (95% conf.8) 9.10-9.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.6-65.7) 10.4 (11.2 (25.60 (6.2 (37.55 (4.4) 357 (225-456) 203 (87. see Data Analysis section) for Survey year 03-04 is 2.7 (9.8-112) 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 16.43-13.3 (8.6 (12.1 (15.4) 7.0 (34.0) 9.16 (6.3) 47.0 (11.0 (36.9) 75th 47.3 (11.4.6-20.21 (6.4-19.38-18.1) 9.00-8.0) 49.89-11.20-11.2) 12.6-15.4) 75th 43.4.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.45 (5.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.1) 7. population from the National Health and Nutrition Examination Survey.5) 11.2 (10.3-35.29-12.2-58.10) 84.3 (26.3 (9.9-61.6-111) 33.5) 20.6 (9.

Kanetoshi A. Ishibashi H.7/2.S. Moss T. Bodey GP. Zaugg SD. IMS Ind Med Surg 1969.4. phthalates. Mar Environ Res 2000. Food Chem Toxicol 2000. Evidence of 2. Okui T. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Br J Clin Pharmacol 1987. Larson EL. Anal Chim Acta 1004.S.524:241-247. Benson WH. Mezcua M. Wigmore H. Fernandez-Alba AR. Kaneshima H. Teitelbaum SL. Foran CM. Aranami K. Meyer MT. Bhargava HN. et al. streams. Barber LB. Erratum in: Aquat Toxicol 2007. and phenols in girls.4’-trichloro-2’hydroxydiphenyl ether). Pinney SM. Readman JW. Furlong ET.50(1-5):153-156. 4’-trichloro-2’-hydroxydiphenyl ether. Am J Infect Control 1996. Triclosan: applications and safety. Katsura E. J Invest Dermatol 1976. Pharmaceuticals. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Reidy JA.36(6):1202-1211. Britton JA. Nagao Y.. Leonard PA. Pharmacokinetics of triclosan following oral ingestion in humans. Bennett ER. Kolpin DW. Urinary concentrations of triclosan in the U. Chemosphere 2007. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Percutaneous penetration and dermal metabolism of triclosan (2. Environ Health Perspect 2007.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Hong HC.17(5):637-644. Shiratsuchi H. Chelimo C. Arch Environ Contam Toxicol 1988. 4. J Toxicol Environ Health A 2006.83(1):84.28(9):1748-1751. Environ Health Perspect 2008.Environmental Phenols References Aiello AE. Howes D. Needham LL. Watanabe N. Pilot study of urinary biomarkers of phytoestrogens. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Furia T. Lyman FL. Wolff MS. Osachoff H. Ferrer I. Clapson DJ. Windham G. Ye X. et al.116(3):303-307. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Adolfsson-Erici M. et al. Environ Sci Technol 2002. Odham G. Aguera A.80(3):217-227.45 Suppl 2:S137-S147.38(4):361370. Photolytic degradation of triclosan in freshwater and seawater. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Williams FM. population: 2003-2004. hormones.67(4):532-537. Biol Pharm Bull 2005. Skirrow RC. Calafat AM. Thurman EM. Levy SB. Gilbert RJ. Wong LY.24(3):209-218. Ebersole R. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. and other organic wastewater contaminants in U. 1999-2000: a national reconnaissance. Aquat Toxicol 2006.66:1052-1056.38(2):64-71. The oral retention and antiplaque efficacy of triclosan in human volunteers.23(5):579-583. et al. Hernando MD.69(20):1861-1873. Hirano M. Sandborgh-Englund G. Toxicology of 2.115:116-121. Veldhoen N. Gomez MJ. Ogawa H. Williams PE. Matsumura N. Ekstrand J. Gunderson MP.

40 Fourth National Report on Human Exposure to Environmental Chemicals .10 (1. bactericide. PCP is eliminated over a few days (Braun et al.350-.770 (. other polychlorinated benzenes.350-.480-2.350-. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.890 (.350-.70) .990 (<LOD-2.350 (.350 (.73 (1.37 (. Kohli et al. water and sediments because of the large amounts that were produced and used historically.510-3.350-.S. so it is relatively non-persistent.350-.350-.350-.350 (. and it is used primarily as a preservative for wood to be used outdoors (e. population from the National Health and Nutrition Examination Survey.350-.390 (.350 (.350-.75) 2.78) 1.01 (<LOD-1. Since 1984.350 (. General population exposure to PCP may occur by inhalation of contaminated air. Human exposure to PCP has become less common.350-2. PCP is absorbed rapidly and well by all exposure routes.g. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350-. < LOD means less than the limit of detection.350 (.890-1.30) 1.350) < LOD .10) 1.45-2.90 (1.350-..5.350-2.350) < LOD .350 (.25 and 0.350-.650 (. PCP is distributed to most tissues and is not extensively metabolized.350-1.50) 1. plants. and metabolic acidosis were observed in CAS No.990-2.10 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350-2.350 (.660 (. After absorption.350 (..350-.650) 1. The parent compound and conjugates. has been restricted. In the environment.350-1. along with small amounts of tetrachlorohydroquinone and conjugates.51) 1.00 (.60) 1.350) < LOD .350) .30 (1.350-2.350) < LOD .18 (<LOD-1.94 (1.350) < LOD < LOD 75th .94 (1.48-2.47-3. 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.00) 1.32 (.860-2.350) < LOD .64) 1.76) 1.350 (.350 (. PCP cannot be used on wood in residential or agricultural buildings.65 (.83 (2. Survey Geometric mean (95% conf.91 (1. and animals. hypertension. utility poles and fence posts). PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.90) 2.30 (.350-.510-5.590-1.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . and possibly of lindane (IPCS.30 (.530) 1. 1986). 1997).350-1. To-Figueras et al.30) .30) 1.00) 2.67) 1.350) < LOD . PCP has been detected in soils.350) < LOD .980 (. algaecide and insecticide.350 (. Acute.350 (.850-2..08-3. After a single dose. air.350) < LOD .350-.98 (1.350) 90th ..58-2. PCP use in the U.47-5.54-2.62 (.350 (.350-.350 (. 2002.48 (.33-2. are eliminated in the urine.33) . 1979).350-.58-2.09) . the elimination half-life may be a week or more (Uhl et al.350-. and dermal contact with PCP-treated products.350 (.40 (.960) 1.37) .350) < LOD .04) 1.10) 1.S.350) < LOD .350-2.350 (.500-2.350) < LOD .90) 1. * 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. mollusicide.65 (.630 (.390 (.350-.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .70) 2.350 (.350-1.76) .350) < LOD .350) < LOD .10 (<LOD-1.350) < LOD . high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. Effects including hyperthermia. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.680-1.42) 696 680 521 696 603 951 Limit of detection (LOD. herbicide.00) 1.. PCP is degraded by sunlight and metabolized rapidly by microorganisms.80) .350 (.350 (.350 (.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 .42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350-.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.23 (. 1976.350) < LOD .350-. ingestion of contaminated food or water. with repeated or chronic exposure.350) < LOD .60) 1.

In NHANES 2001-2002 subsamples.780-1.35-2. Among adults in the NHANES 1999-2000 subsample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.6 and 14.610 (.S.35-2.16 (.06-3.360-. EPA at: http://www.40-2.67 (1.590) < LOD .18) .16-1.10 (1.25-1.950-1.780) < LOD .40) 1.300 (.500-1.800) < LOD 1.06) 1.320) < LOD .580-.35) 1.08 and 5. 2003). EPA has developed standards for PCP in drinking water and the environment.. The U. chronically administered high doses of PCP were hepatotoxic.650) 90th 1.470 (.78) 1.19) 2. inhalation. respectively) (Becker et al.cdc.370 (.400 (.260 (. 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 (4.630 (.700-2. Fourth National Report on Human Exposure to Environmental Chemicals 41 .S.. 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.gov/ pesticides/ and from ATSDR at: http://www.09-1.280) < LOD .300 (.52 (<LOD-1.Fungicides adults and children severely exposed to PCP through ingestion.570 (. population from the National Health and Nutrition Examination Survey.25 (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 .320 (.67-2.67 (1.650 (.950-1.82) 1.25-2.220-. 2004.730) < LOD .11) 2.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * . or skin absorption.19 (1.94 (1. and adversely affected thyroid function (U.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.21 (.52 (1.30) 1.34 (.850 (.73 (1.510-. 2003).310) < LOD .00-1. 1995).00) 1.560) < LOD .56) 1.75) 1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al. respectively) (Seifert et al.650 (.36) .67 (1. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.84-4.270-.320) < LOD . 1989)..S.290-.800-1.250 (.67 (1.290-.40) 1.25 (1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.490) < LOD .270-.92) 1.240-.EPA.57 (.560-.25-2.35) 1.500-. More information about external exposure (i.21-2.430) < LOD .900-1.95) 3. Death can result from seizures and cardiovascular collapse.26 (1.25) 1.67-3..830) < LOD .55) 1.epa.360 (.320) < LOD < LOD 75th .310-.500 (.40) 1.84 (1.75 (<LOD-2. and the FDA has established a standard for bottled water.40) 1.990 (.06 (.560) < LOD .300 (.52 (<LOD-1. carcinogenic. children in the 1980’s...84) 1.09 (<LOD-2.340-.48-2. Survey Geometric mean (95% conf. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.94-3. In a small sample of U.19) 2.0 mg/L.67 (1.290) < LOD .710-1.30 (.40) 1.57 (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.83 (1.69 (1.330-.350) < LOD . environmental levels) and health effects is available from the U.920 (. 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.13 (..19) 2.9 mg/L.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1991).atsdr.00-1.94 (1.510-.440 (.52) 1.250 (.18 (1.760 (.590-1.gov/ toxpro2. Pentachlorophenol is not mutagenic or teratogenic.29-3.430-.910-1. In animals.79) 1. 2000).82 (1. OSHA has established an occupational standard.S. 1989)..78) 1.10-2.67-3.90) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.26 (1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .420) < LOD .950-1.220-.30-2.380-. van Raaij et al.html.e.51) 1.30) 1.

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. Gregg M. hair. Smith SJ. 2002. Sala M. Hill RH Jr. Otero R. Hill RH Jr. Phillips DL. Seiwert M. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Holler JS. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. 206:15-24. Needham LL. Safe A. Schulz C. Int J Hyg Environ Health 2003. U. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. et al.S. Cline RE. 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. Rodamilans M. Barrot C. van den Berg KJ. The metabolism of higher chlorinated benzene isomers.18:475-481. 4/21/09 Kohli J. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.54(3):203-208. house dust. Arch Toxicol 1986. Krause C. Notten WR. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. drinking water and indoor air.inchem. Baker S. Can J Biochem 1976. Braun WH. Engel R. Environ Res 1995. Pesticide residues in urine of adults living in the United States: reference range concentrations. et al. Shealy DB.S. r e g u l a t i o n s . Dev Toxicol Environ Sci 1979. Bragt PC. Bailey SL. 11/30/2004. Arch Environ Contam Toxicol 1989. 42 Fourth National Report on Human Exposure to Environmental Chemicals . PCP: Human Risk Characterization [online].58:182-186. Environ Health Perspect 1997. International Programme on Chemical Safety (IPCS). Head SL. Becker K. Hill RH. Needham LL. Pentachlorophenol measurements in body fluids of people in log homes and workplaces.10:552-65. Seifert B. Santiago-Silva M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. To-Figueras J. Jones D. Toxicology 1991: 67(1):107-16. Kaus S. Helm D. htm.4:289296. Uhl S. urine. To T. available at URL: http://www. Seiwert M. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood.105(1):78-83. 4/21/09 van Raaij JA. Fast DM. J Expo Anal Environ Epidemiol 2000. Available at URL: h t t p : / / w w w. Environmental Protection Agency (U. Pharmacokinetics of pentachlorophenol in man. EPA). et al. Schlatter C.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Lindane. References Becker K.org/documents/jmpr/jmpmono/2002pr08.18(4):469-474. Chenoweth MB. Schulz C. Arch Environ Contam Toxicol 1989.71:99108. Schmid P. Blau GE. Seifert B.

60-2.28-3. Fourth National Report on Human Exposure to Environmental Chemicals 43 .490 (<LOD-. < LOD means less than the limit of detection.40 (.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .770 (.349-.820 (. Estimated human intakes have been below recommended intake limits (U.S. on ornamental plants and turfs.386-.30) 1. or 2-phenylphenol) and its water-soluble salt..10-1. and it has limited water solubility.740 (.600) < LOD 75th .600) < LOD .370-.497 (.350-1.508 (.61) 2.710-2.50 (1.370-. 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. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.17 (. leaving the chemical residue OPP.20 (1.00 (1. OPP is considered to be moderately toxic after acute oral doses in animal studies.30) < LOD 90th 1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.10 (1. however.60-3. General population exposure can occur via dermal. Most agricultural food applications have been revoked. population from the National Health and Nutrition Examination Survey.930 (.S.490 (<LOD-.670) 2.600-1.410-.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .80) 1.389-.90 (1.570 (.370-.S.33 (.10) .890 (.00) .60 (1.567 (.30) < LOD 1. 2002.624) * .402-.466 (.570-.23) 695 680 520 695 603 953 Limit of detection (LOD.30 (1.640) < LOD .770 (.690-1.27 (. Timchalk et al.40-5.10) ..20-2. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley..850 (.520 (.80) 1.570 (.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 .830 (.90) 2.50) 1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.00 (1. which may vary for some chemicals by year and by individual sample. but OPP and SOPP are still used on pears and citrus (U.590-2.490 (<LOD-. EPA. such as fruits and vegetables.02) 1. and sanitizers.40-5.20) < LOD 1. it was used in home sanitizers for surfaces. OPP is still used as a disinfectant fungicide for industrial applications.450 (<LOD-.90) .00) .10-2.420 (<LOD-.780) < LOD .85) 2. and as a wood preservative.493 (.690) < LOD .696) * .22 (.710) 3.19 (. 1998). in paints.00 (1.600) < LOD . 90-43-7 General Information Ortho-phenylphenol (OPP.600) < LOD 1.20 (.88) 1.760-2.00-2.50-2. 2006).EPA.92 (.22) 2.550-1.10 (1.860 (.30-2.50 (1.638) * .Fungicides ortho-Phenylphenol CAS No.890 (.90 (1.880-2.50-3.10) .890) 1.390-.20) < LOD 2. OPP is volatile. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Both have been used in agriculture to control fungal and bacterial growth on stored crops. Survey Geometric mean (95% conf. sodium ortho-phenylphenate (SOPP).3.600-1.570-1.433-.490 (<LOD-.636) * .364-.560-8.90) 1.80-3.450 (<LOD-. SOPP is applied topically to the crop and then rinsed off.50 (1.509 (.20 (1. formulate.496 (.800-3. 2006).28 (.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .645) * . In the past. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. or apply these chemicals may be more highly exposed than the general population.80 (2.14 (<LOD-3.90) .742) * .570-2.600-1.50-4.EPA.40-2. whereas SOPP is not volatile and is more water soluble.498 (. 1998.50) < LOD .50) < LOD .10) 2.840-1. 1989).552 (. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.610-1.490 (<LOD-. are antimicrobial agents used as bacteriostats. 2006).30) < LOD .790) 2. Workers who manufacture.389-.60 (1.580-1.621) * . fungicides.00) < LOD .3 and 0.10) 1.20-3.470 (<LOD-.07 (.50) < LOD .970 (.76) 1.60 (1.09) 2.34) 1.610 (.450 (<LOD-. inhalational. Cnubben et al.500-2.540-2. 2006).00 (1.30-7. interval) . OPP is efficiently absorbed from the gastrointestinal tract and through the skin.10) 1.S.630) < LOD . Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Available evidence suggests that OPP does not accumulate in the body.480-1.950) < LOD .750-2.03) 1.40-7. Both chemicals degrade within hours to weeks in the environment (U.836) * .20) 2.50) .

500) < LOD .13) 1.670 (.17 (.08-2.656) * .29) 1. U.301-.78 (2.800-1.02 (.91 (1.46) < LOD 1.610) < LOD 1.380 (.453 (.650-1.780 (. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.00 (1.361-.410 (<LOD-.860 (.550-.89 (1.EPA at: http:// www.59) . Additional information is available from U.43-2..S..455-. Smith et al. IARC has classified SOPP as a possible human carcinogen.4) 3. CDC. or. 1999.510-.470 (<LOD-.910 (<LOD-1.900) < LOD .910 (.47) .08-1.20) < LOD 3.81) 1.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .06-5.44 (1.28 (2.11 (.550 (.590) * .950) < LOD .410 (<LOD-.311-. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.epa.04-4.690 (. Volunteers exposed to 0.970) 1.06-4.670 (. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.12) < LOD 1. less likely.444 (.21-2.93 (1.580) < LOD . Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.33-2.64 (2.353-.61 (.270-. reproductive.11) 4.385 (.880-1. Biomonitoring Information Urinary OPP levels reflect recent exposure. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.0) 1.38-3.69 (1. OPP was not found to be mutagenic.32) 3.900-1.29) 1.440 (.25-6.75 (1.33) .780-14.43-2. Detectable levels were seen in over half the U.403-. Nakagawa et al.21 (. 2005.24-2. Ito et al.810-1.S..291-.560) < LOD 75th .18) 2.382 (.12-2.620-1.59) 1.27) < LOD . 1997. 2000. 1992.910-1.51-3.gov/pesticides/.96 (1. and it has classified OPP as not classifiable with respect to human carcinogenicity.480-. In high dose animal studies.38) 1. 2002..38) 2.84 (1.560-2. Pathak and Roy.558) Selected percentiles ( 95% confidence interval) Sample 95th 2. 2005). 1993.640-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.510 (<LOD-. Zhao et al.17 (. 2002).43) 3.24-2.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .S. Murata et al.93) ..320 (<LOD-. interval) .666) * .06 (1.11-1.248-.670) < LOD .750-2.61 (2.EPA 2006).26) 1.21) 1.620-1.43 (1..S.07) 2.96-4.01) 1.EPA 2006).17) * 99-00 01-02 99-00 01-02 99-00 01-02 .420 (<LOD-.860 (. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.343 (.93) 1.329-.11) < LOD 90th 1.S.484) * . These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.580-1.508) * .96) 1. U.11 (.74 (1.. but no neurologic.05-2. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. 1999.96 (1. 1998. Kwok et al.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.52 (.980 (<LOD-1.17) 2.420 (<LOD-.31) < LOD .09-3.570) < LOD 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.08) 1. 44 Fourth National Report on Human Exposure to Environmental Chemicals .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 .09 (1. 1984.473) * . or developmental toxicity was observed (Bomhard et al.360 (<LOD-.990) < LOD .568) * . 2005). 1984.61 (1.93) .810) < LOD .940-2.550) < LOD .750 (. by possible genotoxic mechanisms (Hagiwara et al..750 (.58) 2.53) 1. 1986).980 (.791) * .470) < LOD .62) .Fungicides anemia. leading to production of two metabolites.97 (2. 2002.09-6.32) 1.840 (.75 (1.28 (<LOD-4.600-1.770-2.460-. Bomhard et al. Survey Geometric mean (95% conf.496 (.88-4.514 (.86 (1. Brusick.40-13.00 (..

et al.gov/oppsrrd1/REDs/ phenylphenol_red. Shirai T.pdf. IARC Sci Publ 1984. St John MK. Toxicol Appl Pharmacol 1999. Kwok ES. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Moore GA. Zhao S. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Environmental Protection Agency (U.45(5):460-481.22(10):809-814. Herbold BA. Christenson WR.74(2):61-71. Food Chem Toxicol 1984. Bomhard EM. Timchalk C. 2005. U.32(6):551-625. Comparative metabolism of orthophenylphenol in mouse. EPA 739 R-06004.pdf. rat and man. Richter M.703(12):97-104. Meuling WJ.S. Bormett GA. Regul Toxicol Pharmacol 2002. 90-43-7) in Swiss CD-1 mice (dermal studies). Hirose M. 4/13/09 Onstot JD.(56):399-407. Biochem Pharmacol 1992. Toxicol Appl Pharmacol 1998.50(11):3351-3358. July 28. Bartels MJ. Hagiwara A. Elliott GR. food additives and natural products as promoters in rat urinary bladder carcinogenesis.S.159(1):18-24.S. Hakkert BC. Ito N. Bartels MJ. et al. Brusick D. EPA-560/5-89-003.S. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Buchholz BA.17(8):411-417.niehs. Vogel JS. Smith RA. The carcinogenicity of the biocide ortho-phenylphenol. Centers for Disease Control and Prevention (CDC). Eastmond DA. Available at URL: http://www. Imaida K. Kawanishi S. Bartels MJ. 2006. National Toxicology Program (NTP). Environ Mol Mutagen 2005. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice.gov/ntp/htdocs/LT_ rpts/tr301. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Crit Rev Toxicol 2002. Freyberger A. Coelhan M. Inoue S.54(16):5731-5735. Mutat Res 1993. Mendrala AL. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Fukushima S. Moldeus P. Office of Toxic Substances. Narang A. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol.epa.nih.35(2 Pt 1):198-208. Arnold LL.EPA). Roberts AL.286(2):309-319. Carcinogenesis 1999. Cano M. March 1986. Fukushima S. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. McNett DA. Tayama S. J Agric Food Chem 2006. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Selim S. Eadon G. Nakagawa Y. 1989. Brzak KA. J Agric Food Chem 2002. Drugs. Arch Toxicol 2000.150(2):402-413. Atlanta (GA). Pathak DN. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Christenson WR. U. Sangha GK. Turteltaub KW. 4/9/09. Murata M. Leser KH. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. EPA). Bartels MJ. Stanley JS. Environmental Protection Agency (U. J Chromatogr B Biomed Sci Appl 1997. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Brendler-Schwaab SY. van de Sandt JJ.43(7):14311437. Shibata M. Roy D.20(5):851-857. Available at URL: http://ntp.28(6):579594. Identification of SARA compounds in adipose tissue. Cnubben NH. Hum Exp Toxicol 1998. Xenobiotica 1998.. Moriya K.Fungicides References Appel KE. Bromig KH. Sangha G. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Gierthy J. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Third National Report on Human Exposure to Environmental Chemicals. Ito N. Hagiwara A. Glas K. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Timchalk C.

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

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

* 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. population from the National Health and Nutrition Examination Survey. 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. 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. which may vary for some chemicals by year and by individual sample. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1. Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.S. see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey. 48 Fourth National Report on Human Exposure to Environmental Chemicals .Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection.S.

Quistad GB. Striley CA. Hodgson E. 5/30/06. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.html. et al. acetochlor. EPA). Wilson AG. Burkhardt MR. Centers for Disease Control and Prevention (CDC). Comparative metabolism and elimination of acetanilide compounds by rat. Larsen GL. Barr JR. Volume 65. Hines CJ. Olsson AO. Hladik ML. 1998. Kolpin DW.39(17):6561-6574. Sci Total Environ 2000. Linderman R. reservoirs and ground water in the Midwestern United States. Furlong ET. sulfonamide. Casida JE. Environmental Protection Agency (U.11(4):353359. Green T. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Third National Report on Human Exposure to Environmental Chemicals. Sci Total Environ 2000.cornell. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Feng PCC. Barr DB. Acetochlor (Harness) Pesticide Petition Filing 1/00. 5/30/06 U.248(2-3):123-133. Kier L. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Rose RL. Deddens JA. EPA 738-R-00-009. March 2006.Herbicides References Ashby J. Camann DE. Atlanta (GA). Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Available at URL: http://www. Barr DB. 2000. Barr DB.111(5):749-756. Environmental Protection Agency (U. Thurman EM. U.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Roberts AL. Andrews HF. EPA). and metolachlor herbicides in rats. Peter CJ. J Expo Anal Environ Epidemiol 2005. Kinney PL.17(6):559-566. Ward EM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.15(6):500-508.15(9):702-735. Feil VJ. Number 15.108(12):1151-1157. Alavanja MC. Dialkylquinonimines validated as in vivo metabolites of alachlor. pages 3682-3690. 2005.EPA): http://pmep. J Agri Food Chem 1989. and other herbicides in rivers.S. Heederik D. Whyatt RM. Hsiao JJ. Davison KL. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Environ Sci Technol 2005. Sanderson WT. Chem Res Toxicol 1998. Lefevre PA. Hum Exp Toxicol 1996. Battaglin WA. epa.S. J Expo Sci Environ Epidemiol 2007.cce. Coleman S. Jefferies PR. et al.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.S. Wratten SJ. imidazolinone. Available at URL(non U.24(10):1003-1012. Environ Health Perspect 2000. et al. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Hein MJ.S.S.pdf.248(2-3):115-122. Linhart SM. Xenobiotica 1994. Bravo R. Federal Register: January 24. Occurrence of sulfonylurea.37(4):10881093. Curwin BD. Reynolds SJ. Tinwell H. Environ Health Perspect 2003.

S. 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.gov/pesticides/. Alachlor has a soil half-life of a few weeks.. stomach. IPCS. mean values of urinary concentrations of alachlor metabolites. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. Jefferies et al. 1988.S.EPA. WHO. including corn. about 20-25% of the U..epa. 1998. but not likely at low doses. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.EPA. whereas 60% of applicators had detectable amounts. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. Feng and Wratten.EPA considers alachlor to be a probable human carcinogen at high doses.. 2003). Hines et al. and on non-crop land for general weed control.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. 50 Fourth National Report on Human Exposure to Environmental Chemicals .EPA. Hladik et al. 1994. 1989. but has not shown developmental or reproductive toxicity in mammalian systems (U. hemosiderosis. Kolpin et al. 2005.S. corn cropland was treated with alachlor. 1999. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. In chronic animal testing. 1998.S. but another metabolic pathway can produce 2. 2003).. (2003) showed that 2. Additional information about is available from U. 2003). In a study of applicators and workers exposed to alachlor. U.1 to 1. 1995. Because it can be absorbed through skin. as measured through conversion to deethylamine. 1997. WHO.Herbicides Alachlor CAS No. formulators. Alachlor has low potential for acute toxicity. 1998). 2003). 1996. Tessier and Clark. U. In animal studies..S. In animals. 1996. U. 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. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure... ranged from 0.1 mg/L at various collection times (Sanderson et al. 2000.S.S. Hill et al. It is absorbed by plants and inhibits plant protein synthesis. USGS. 1998. 2000. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. but shows little bioaccumulation. 1995). WHO. 1999 and 2007. WHO. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC.S. Since the late 1980s alachlor use has been declining. NTP and IARC do not have ratings regarding human carcinogenicity. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment.EPA. the latter may account for some observed effects (Davison et al. Alachlor itself is not considered mutagenic. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. Biomonitoring studies on levels of alachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of alachlor than are found in the general population.. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. the dermal exposure route is potentially significant for applicators. mercapturate conjugates were predominant metabolites. and uveal degeneration. peanuts and other crops. 1996).6-diethylaniline and its reactive metabolite.. 1998).EPA. alachlor has demonstrated hepatotoxicity. and field workers. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. soybeans. Estimated human intakes have been below recommended limits (U. In 1993-1995. 2005). EPA at: http://www. 1998). U.

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. 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. Fourth National Report on Human Exposure to Environmental Chemicals 51 .S. Survey Geometric mean (95% conf.S. Survey Geometric mean (95% conf.18. * 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 99-00 is 1.Herbicides Urinary Alachlor mercapturate Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

S. Geological Survey (USGS). California. Wilson AG. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Shoemaker DA.11(4):353359. Kolpin DW. Available at URL: http:// www. Furlong ET. 4/2/09 U. Tolos W.43(25):2087-94. J Agri Food Chem 1989. Kolpin DW. Andrews HF. Heydens WF. December 1998. Circular 1291. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Wratten SJ. World Health Organization (WHO). Ann Occup Hyg 2003. reservoirs and ground water in the Midwestern United States. Quistad GB. Centers for Disease Control and Prevention (CDC). et al.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Environ Sci Technol 2005. Biagini R.pdf. Comparative metabolism and elimination of acetanilide compounds by rat. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Brown KK. and metolachlor herbicides in rats. Driskell WJ. Camann DE.56(6):853-859. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Am Ind Hyg Assoc J 1995.pdf. Sanderson WT.epa.44(18):1325. Environ Health Perspect 2003. Larsen GL. Lau H. 1992-2001. Erratum in: Life Sci 1989. Hines CJ. DNA adduct formation by alachlor metabolites. Alachlor in Drinking-water. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Xenobiotica 1994. Roberts AL. Hsiao JJ. Henningsen G. revised February 15. 2007.S. Biagini RE. Available at URL: http://water. Kinney PL. Geological Survey (USGS). Linhart SM. Thurman EM. and other herbicides in rivers. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. J Ag Food Chem 1995. Kier LD. Sci Total Environ 2000. Martens MA. Available at URL: http://www. Jefferies PR. Sci Total Environ 2000. Dialkylquinonimines validated as in vivo metabolites of alachlor. Clark JM. Occurrence of sulfonylurea. Bull Environ Contam Toxicol 1996.43(9):2504-2512. EPA). March 2006.24(10):1003-1012. Barr JR. Available at URL: http://www.inchem. sulfonamide. Hill RH Jr. Atlanta (GA). 1997. Feil VJ. imidazolinone. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes.gov/oppsrrd1/ REDs/0063. who. et al. U. Hill AB. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Striley CA. Whyatt RM. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. World Health Organization. Thelin GP.18(6):363-391. Casida JE. Casida JE. Peter CJ. Sacramento. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Hum Exp Toxicol. ALACHLOR. Feng PCC.47(6):503-517. Third National Report on Human Exposure to Environmental Chemicals. Mutat Res. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor.395(2-3):159-171. International Programme on Chemical Safety (IPCS). Environmental Protection Agency (U. Brown MA. Supplemental Technical Information (available on-line only). Hladik ML. 2/27/09 U. 1999. MacKenzie B. Hines CJ. Tessier DM. 1999.S. Quistad GB. WHO/ FAO Data Sheets on Pesticides. Life Sci 1988. An evaluation of the carcinogenic potential of the herbicide alachlor to man.248(2-3):115-122.Herbicides References Battaglin WA.htm. Chem Res Toxicol 1998. Thake DC. 1998. Gilliom RJ). Barr DB.39(17):6561-6574. Background document for development of WHO Guidelines for Drinking-water Quality. Deddens JA. 1996. 2003. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. No.248(2-3):123-133.56(9):883-889.int/water_sanitation_health/dwq/chemicals/en/alachlor.org/documents/pds/pds/pest86_e. acetochlor.37(4):10881093. Hull RD. Reregistration Eligibility Decision (RED) Alachlor. Geneva. Kimmel EC. Davison KL.S.usgs. Casida JE. 86.php. EPA 738R-98-020. Shealy DB. 2/27/09 Jefferies PR. Burkhardt MR.111(5):749-756. 98-4245 (by Barbash JE.

For the general population. Timchalk et al. 2003b). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 809 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1315 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 684 550 918 Limit of detection (LOD. with about 75% of corn cropland receiving treatment. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination. Bacteria and plants can metabolize atrazine to hydroxyatrazine. it is one of the more commonly detected pesticides in surface and ground waters (USGS. Atrazine is applied pre. As a result.791 and 0.S... Atrazine is well absorbed orally. and cyanazine. all of which act by inhibiting plant photosynthesis. 1996. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. propazine. In regions where atrazine is used. metabolized. Atrazine was first registered as an herbicide in 1958.. but it is leachable into ground and surface waters. 2002. 2003a). U. More than 70 million pounds have been applied annually in recent years. Applicators of atrazine may be exposed dermally and by inhalation. which may vary for some chemicals by year and by individual sample. Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which have half-lives of several months. 1982. and then eliminated in the urine over a few days (Bradway et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Atrazine has limited water solubility and is not tightly bound to soil. but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. 1993). population from the National Health and Nutrition Examination Survey. Related chlorotriazine herbicides include simazine. < LOD means less than the limit of detection. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al.3. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. It is also used as a non-selective herbicide.S.EPA. Hayes et al. drinking water is an infrequent source of atrazine exposure. In animals and humans. The dealkylated chloroatrazine metabolites.EPA. U. 2005. atrazine is slowly degraded to dealkylated products.. Survey Geometric mean (95% conf.. 2007). Atrazine does not bioaccumulate.EPA.Herbicides Atrazine CAS No. 2003b). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. glutathione conjugation appeared to be the major route of biotransformation.S. Catenacci et al. Fourth National Report on Human Exposure to Environmental Chemicals 53 . In soils. 1993.and post-emergence to agricultural land for crops such as corn and sorghum. resulting in atrazine mercapturate and N-dealkylation products (IPCS.S. 1990).

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

Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Simpkins JW. Atlanta (GA).cdc. Stevens JT. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. WHO/ FAO Data Sheets on Pesticides. Cooper RL. Hermaphroditic. Cooper RL. Chen H. Pfeifer KF. et al. Ferrell JM. Stoker TE. Gillis JH. Steroids 1999.. Tyrey L.. Stoker TE. 1996. Toxicol Sci 2000. Maroni M. 2005). Eldridge JC. Goodrow MH.76(1):190-200.61(4):331-355. urinary concentrations ranged from 5-1756 μg/L (Lucas et al.15(6):500-508. J Agric Food Chem 1982. Reynolds SJ.inchem. Gammon DW. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . J Toxicol Environ Health 1994. Mendoza M.html. Ferrell JM. 3/11/09 Arcury TA. Barr DB. Biagini RE. diamino-S-chlorotriazine and hydroxyatrazine. Cooper RL. 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. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. et al. Collins A. Ann Occup Hyg 2003. et al. The geometric mean of urinary atrazine mercapturate was 1. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.58(2):366-376. Carr WC Jr. Extrom PC. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.org/documents/pds/pds/pest82_e. A risk assessment of atrazine use in California: human health and ecological aspects. J Expo Anal Environ Epidemiol 2005. Lioy PJ. Vonk A. Catenacci G. et al. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Geneva. Deddens JA. 1993). Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Third National Report on Human Exposure to Environmental Chemicals. Clayton CA. In a study of 60 farm worker children.43(2):155-167. 2005. Brown KK. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. International Programme on Chemical Safety (IPCS). 2000). Proc Natl Acad Sci USA 2002. Environ Health Perspect 2007. Toxicol Sci 2000. Goldman JM. Fleenor-Heyser DG. 82. World Health Organization.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Grzywacz JG..53(2):297-307. Biological monitoring of human exposure to atrazine. Centers for Disease Control and Prevention (CDC). Aldous CN.99(8):5476-5480. levels of atrazine mercapturate were generally not detectable (CDC. Barr DB. Jones AD. Bersani M. Perry et al.atsdr. 2007). Toxicol Lett 1993. Breckenridge CB. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Eberly LE. Freeman NC. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. 2001). et al. Cottica D. Sanderson WT. 2005). Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. et al. Environ Health Perspect 2001. Lucas AD. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Hines CJ..30(2):244-247. atrazine was detected in only four children (Arcury et al.115(8):1254-1260. Eldridge JC. Heederik D. Lee M. J Toxicol Environ Health 1994. Wetzel LT. Tapia J.gov/toxprofiles/tp153. Saiz SG.47(6):503-517.43(2):155-167. Barbieri F. Available at URL: http://www. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.64(9):672-678. 3/11/09 Laws SC. Noriega N. Toxicological profile for atrazine. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate).. Moseman RF. Sanborn JR. No. Gillis JH.109(6):583-590. Blewett C. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.. Bradway DE. Hein MJ. Hayes TB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Striley CA. Toxicol Sci 2003. Schmid J. In a small number of field workers. Laws SC. Seiber JN. Ferioli A. Pest Manag Sci 2005. Quandt SA. In the NHANES 2001-2002 subsample. Wetzel LT. McElroy WK. References Adgate JL. ATRAZINE. 2001 [online]. Curwin BD. Agency for Toxic Substances and Disease Registry (ATSDR). Barr DB.. 2003. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. In small studies of Maryland residents in 19951996 (MacIntosh et al. Stoker TE.htm.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Available at URL: http:// www. Stuart AA. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.69(2):217-222. Shoemaker DA.

Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Cooper RL.56(2):69-109. van den Berg M. Christiani D. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. White paper on potential developmental effects of atrazine on amphibians. 1992-2001. Boerma J. Available at URL: http://www.10(7):479. Laws SC.S. Osborne DW. Rayner JL. 2003b. March 2006. Environmental Protection Agency (U. Fenton SE. 0062. Pesticides and Toxic Substances. Toxicology 1990. Perry M. revised February 15. Hammerstrom KA. J Toxicol Environ Health A 1999. Dryzga MD. Ann Epidemiol 2000. A review of epidemiologic studies of triazine herbicides and cancer. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Washington (DC).Herbicides development of a biomarker of exposure. Needham LL. Guidici DL. Geological Survey (USGS).58(1):50-59. A longitudinal investigation of selected pesticide metabolites in urine. Circular 1291.epa. A risk characterization for atrazine: oncogenicity profile. Toxicol Appl Pharmacol 2004. Stoker TE.S.pdf. Toxicol Appl Pharmacol 2002. The Quality of Our Nation’s Waters. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Tortorelli J. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .S. Environmental Protection Agency (U. Kastl PE.gov/oppsrrd1/REDs/ atrazine_ired. Available at URL: http://water.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Environmental Fate and Effects Division. Wetzel L.182(1):44-54. Case No. Stoker TE. J Expo Anal Environ Epidemiol 1999. May 2003a. Crit Rev Toxicol 1997.9(5):494-501.S. U. Cooper RL.27(6):599612. Sathiakumar N. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Delzell E. Supplemental Technical Information (available on-line only). Available at URL: http://www.S. Sanderson JT. Toxicol Sci 2000. MacIntosh DL. Chem Res Toxicol 1993.61(1):27-40. Singzoni B. Ryan PB. Dagenhart D. Langvardt PW. Office of Prevention. Breckenridge CB.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.195(1):23-34. EPA).php. Wood C.epa. Stevens JT.67(2):198-206.pdf. Guidici DL. 3/11/09 U. 2007. EPA).6(1):107-116. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Pesticides in the Nation’s Streams and Ground Water.usgs. Toxicol Sci 2002. Interim Reregistration Eligibility Decision For Atrazine. Laws SC. EPA Office of Pesticide Programs. 6/1/09 U. Lansbergen GW. Timchalk C.

13) < LOD .420) < LOD .21) 1.320) 90th .690 (.910) 1. and aquatic environments.730 (. Kohli et al.4-D can be applied either as an aqueous salt or as oil-soluble esters.910) < LOD .48) < LOD 1.960-1.350) < LOD < LOD < LOD ..27 (.4-D or exposed for prolonged periods.27-2.02-1.4-D have been below recommended intake limits (U.4-D is rapidly absorbed via oral and inhalation routes.250 (<LOD-.32 (1. in 2001 (U. and mecoprop).420-. 2.4-D) controls broadleaf weeds in residential.890 (. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.00-2.490) < LOD < LOD < LOD .EPA.4-dichlorophenoxyacetic acid (2.S. these herbicides can enhance plant growth. Human health effects from 2. It is poorly bound in soils.20 (<LOD-1.24 (. and delayed Urinary 2.410) < LOD .4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al. General population exposure to 2.540-.210 (<LOD-. Once absorbed.670-1. It is rarely detected in ground waters (USGS.230 (<LOD-. 2007).4-Dichlorophenoxyacetic Acid CAS No. dizziness. with a half-life of several days to several weeks. but at higher levels they are herbicidal.930 (. MCPA. 1974.20 (.260 (<LOD-. abdominal pain. 1989..10 (<LOD-1.30 (<LOD-2.4-D may occur during residential applications. As much as 62 million pounds of 2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.08) < LOD . agricultural.60) 1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .760 (. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.EPA.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .310 (. Fourth National Report on Human Exposure to Environmental Chemicals 57 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.680-1. the chlorophenoxy herbicide 2.27 (1.560-1.22) < LOD .EPA in 1948.890) < LOD . At low levels.4-D has low acute toxicity. and by consuming food or drinking water contaminated with 2. 2004). 2005). 2.10) < LOD 1. 2.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .660) 1. nausea.S. headache.43) 1.690 (.03) 695 659 520 668 589 892 Limit of detection (LOD.40) 1.330 (.70) 1. Similar to other chlorophenoxy herbicides. 2.370-.690-1.440-1. Sauerhoff et al.2.230-. 1977).550-1..490 (.610 (. by direct contact with agricultural and residential areas after applications. < LOD means less than the limit of detection. 94-75-7 General Information Widely used throughout the United States. Survey Geometric mean (95% conf. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.250 (<LOD-. which may vary for some chemicals by year and by individual sample. It was first registered with U.952 and 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.66) < LOD 1.4-D were used in the U.310) < LOD .S.55 (1. it acts as a plant growth hormone.05-2.07 (. myotonia.S.10 (<LOD-1.51 (1. renal and hepatic injury. population from the National Health and Nutrition Examination Survey. 4-D. It is not well absorbed through the skin. hypotension. Recent estimates of chronic intakes of 2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Herbicides 2.210-.810-1.690 (.80) 1.560-.610-.740 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.400) < LOD .930-1.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD .S.16) < LOD .

S.350 (<LOD-.19) .4-D reflect recent exposure.S..13 (. 2. Hill et al. Pearce and McLean.. 2005). and of adults and children (Baker et al.S.4-D does not have significant reproductive.590 (<LOD-1.4-D levels were detectable in less than a quarter of the individuals studied.520-.4-D production plant workers and a few forestry workers spraying 2.41 (1.05) . 2005.610-.980) < LOD 1.560-. 2000).EPA.. CDC. and evidence of histological injury to the kidneys.480 (. The acid and salt forms of 2.. 1996.4-D are eye irritants. 1989).560-.820-1.Herbicides neuropathy (Bradberry et al.epa.620-.780-1..890-1. 1996.440 (. 2006.EPA at: http://www.. IPCS..570) < LOD . 1995. Kutz et al.270 (<LOD-.550-. liver.08 (.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.580-.08 (.340 (. 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.3. Frank et al.340-.35) < LOD . 2005.380 (<LOD-.700 (. 2. Knopp et al. 2005). 2.S.670 (.EPA.610-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. or teratogenic effects in chronic rodent studies (Charles et al.16) 1.14 (.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.660) < LOD .08 (. Biomonitoring Information Urinary levels of 2. 1996. Epidemiological studies have reported associations of several types of cancer.27-1.810-1.410) 90th .720 (.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .410) < LOD 1.26) 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 .40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . urinary 2.780) . 58 Fourth National Report on Human Exposure to Environmental Chemicals .EPA 2005).73) . such as soft tissue sarcoma and non-Hodgkin’s lymphoma. other exposures.680) < LOD .410) < LOD < LOD < LOD ..990-1. 1980.330-.56) . 2003. in small samples of children (Hill et al. U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660 (.790) < LOD .390) < LOD < LOD < LOD . 1995).39) < LOD 1. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.380) < LOD . or to contaminants in the herbicide formulations (specifically 2.13 (.740 (.24) 1. In previous samples of the U.gov/pesticides/.470) < LOD .7. population from the National Health and Nutrition Examination Survey.S.EPA. IPCS.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Kolmodin-Hedman and Erne.670 (<LOD-1. IPCS. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. adrenals and gonads (NTP. 1985. 2002. It is unclear whether these associations are related to the chlorophenoxy herbicides.640 (. population (Hill et al. developmental. 2001. Acute high doses administered to laboratory animals produced ataxia. 2005.810-1. Additional information is available from U. Average post-application urinary levels of 2.17 (. eyes.590 (<LOD-1.380-.. 2005). myotonia. 2005.270-.850) < LOD .. U.410 (<LOD-. thyroid.890) < LOD 1.790) 1.930-1. Post-application levels in farmers and home gardeners were dependent on Urinary 2. 2004).920) < LOD 1. 2005). U. 1994). 1992).4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. Survey Geometric mean (95% conf.32 (<LOD-2.4-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. 2002.780 (.380 (<LOD-. IOM.S.490 (.670 (. U.

Beeson MD. Selected pesticide residues and metabolites in urine from a survey of the U. TOX-63: TOXICITY REPORT CURVES. Gregg M. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.51(3):152-159.4-D were highest in the farmers who applied the 2. Hanley TR Jr. Hill RH Jr. Beasley VR. Kutz FW. Kohli JD.37(2):277-291. Biomonitoring for farm families in the farm family exposure study.4-D. Bus JS. Centers for Disease Control and Prevention (CDC). Curwin BD.4-dichlorophenoxyacetic acid (2.31(2):121-125.4-.nap. Kolmodin-Hedman B. Baker BA.4-dichlorophenoxyacetic acid in man. Holler JS. Exposure of homeowners and bystanders to 2. Estimation of occupational exposure to phenoxy acids (2.S. Arnold EK. Dichlorophenoxyacetic acid. Environ Res 1995. Available at URL: http://ntp.4-D) epidemiology and toxicology. 3/17/09 Knopp D. Scand J Work Environ Health 2005. the amount of pesticide applied. Developmental toxicity studies in rats and rabbits on 2.32(4):233-257. Smith SJ. Alexander BH. Philbert MA. Ripley BD. Biomonitoring studies of 2. the number of acres to which it was applied (Curwin et al. Driskell WJ. Tandon JS. Cole DC.31 Suppl 1:98-104. Sanderson WT. J Environ Sci Health B 1992. Washington (DC): National Academies Press. Updated March 7.Herbicides the time since application. Forestry workers involved in aerial application of 2. Needham LL. et al.htm. and the use of protective clothing or equipment (Arbuckle et al.php?record_id=10603. Xenobiotica 1974. Ritter L. Crit Rev Toxicol 2002. Biomonitoring of herbicides in Ontario farm applicators. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .inchem. Khanna RN.edu/catalog. Hill RH Jr. Survival and Growth Curves from NTP Toxicity Studies. J Toxicol Environ Health 1992. Harris et al. 2005.4-D in urine does not mean that the level of the 2. et al. Reynolds SJ. Veterans and Agent Orange: update 2002. Fast DM. 2005).4-dichlorophenoxyacetic acid (2.org/documents/jmpr/jmpmono/v96pr04. Barr DB.. 2003. Sirons G J. 914. Board on Health Promotion and Disease Prevention. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 2005. general population.10(6 Pt 2):789-798.4-Dichlorophenoxyacetic Acid). Campbell RA. Wilson RD. Occup Environ Med 1994. Heederik D. Available at URL: http:// www. Sircar KP. Hein MJ.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. Barr DB. Acquavella JF.4-D than levels found in the general population. Brody D. Chapman P.60(1):121-131.. J Expo Anal Environ Epidemiol 2000.4:427-435. Stephenson GR. Pesticides residues in food: 1996 evaluations Part II Toxicology. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.18(4):469-474. Harris SA. Baker SE.4-D and 2. Erne K. Mandel et al. Assessment of exposure to 2.71(2):99-108. To T. Arch Environ Contam Toxicol 1989. Tables. Murphy RS. References Arbuckle TE. Scand J Work Environ Health 2005. Arch Toxicol Suppl 1980.5-T). Vet Hum Toxicol 1989. Frank R.31 Suppl 1:90-97.27(1):23-38.4:318-321. J Expo Anal Environ Epidemiol 2005 Nov.4. Carter-Pokras OD. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.. 1992). van Ravenzwaay B..4-D): exposure and urinary excretion.4-D).nih. geometric mean urinary levels of 2. TOX-63 Peroxisone Project (2. Gupta BN.4-D will result in an adverse health effect. Atlanta (GA).4 dichlorophenoxyacetic acid (2. Baker S. Head SL. Needham LL. Finding a measurable amount of 2. 3/17/09 Institute of Medicine (IOM). Mandel JS. Shealy DB. 2006. Dhar MM. Review of 2. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Toxicol Sci 2001. Solomon KR. Pesticide residues in urine of adults living in the United States: reference range concentrations. 2005 Charles JM. Arch Environ Contam Toxicol 1985. Cook BT.gov/index. Absorption and excretion of 2. 2005). Bailey SL. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. In farm families.4-dichlorophenoxyacetic acid and its forms. Third National Report on Human Exposure to Environmental Chemicals.4:97-100. Honeycutt R. Available at URL: http:// www.15(6):500-508. 2. Garabrant DH.niehs. National Toxicology Program (NTP). International Programme on Chemical Safety-INCHEM (IPCS). et al.

Toxicology 1977.Herbicides Sauerhoff MW. Office of Prevention Pesticides and Toxic Substances. 2. Supplemental Technical Information (available on-line only).EPA). gov/oppbead1/pestsales/01pestsales/market_estimates2001.S. Pesticides in the Nation’s Streams and Ground Water. Environmental Protection Agency (U.epa.gov/oppsrrd1/ REDs/factsheets/24d_fs.pdf.4-D) following oral administration to man. 2007. 3/17/09. revised February 15.EPA. Available at URL: http://water.S.4-D RED Facts. 2004.4-dichlorophenoxyacetic acid (2.S. Environmental Protection Agency (U.php.S. Washington (DC): U. The Quality of Our Nation’s Waters. 3/17/09 U. Gehring PJ. 4/2/09 U.2000 and 2001 market estimates.8:3-1U. The fate of 2. March 2006. Pesticide industry sales and usage . May. EPA 738 F-05-002. S. Circular 1291.htm. Blau GE. Geological Survey (USGS). Available at URL: http://www. 1992-2001.S. Braun WH. Available at URL: http://www.usgs. 60 Fourth National Report on Human Exposure to Environmental Chemicals .EPA).gov/nawqa/pnsp/pubs/ circ1291/supporting_info. June 2005.epa.

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

Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.440 (<LOD-.240) 679 701 957 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 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 .220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. see Data Analysis section) for Survey year 01-02 is 0.S. 62 Fourth National Report on Human Exposure to Environmental Chemicals . 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.200 (<LOD-.S.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2. population from the National Health and Nutrition Examination Survey.200 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . * 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 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.670 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

Finding minimal herbicide concentrations in ground water? Try looking for their degradates.15(6):500-508.11(4):353359.usgs. Thelin GP. Kinney PL. California.37(4):10881093. Background document for development of WHO Guidelines for Drinking-water Quality. R. March 2006.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. et al.Herbicides References Battaglin WA. Environ Sci Technol 2007. Geological Survey (USGS).gov/nawqa/ pnsp/pubs/wrir984245/text. Thurman EM. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Striley CA. Sacramento. Hein MJ. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .S.who. streams and groundwater. Environ Health Perspect 2000.248(2-3):123-133. Pesticides in U. Reregistration Eligibility Decision (RED) Metolachlor.S. 4/2/09 U. acetochlor. Kolpin DW. April 1995. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Davison KL. Barr JR.24(10):1003-1012. Heederik D. 1999. Hladik ML. Metolachlor in Drinkingwater. Linhart SM.pdf. Roberts AL. Chem Res Toxicol 1998. Available at URL: http://www.html.S. Environ Sci Technol 2005. 2007.gov/nawqa/pnsp/pubs/files/051507. 98-4245 (by Barbash JE. Xenobiotica 1994. Quistad GB.47(6):503-517.111(5):749-756. Gillion.pdf 3/30/09 Hines CJ. J Expo Anal Environ Epidemiol 2005. Third National Report on Human Exposure to Environmental Chemicals. U.epa.php. Gilliom RJ).int/water_sanitation_health/dwq/chemicals/ metolachlor. Biagini RE. Available at URL: http://water. Feil VJ. revised February 15. Camann DE. and metolachlor herbicides in rats. Sci Total Environ 2000. Jefferies PR. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Larsen GL. Curwin BD.S. Shoemaker DA. Coleman S. 1992-2001. Available at URL: http://www. sulfonamide.usgs. Available at URL: http://water. Alavanja MC. Dialkylquinonimines validated as in vivo metabolites of alachlor. Burkhardt MR.pdf. Atlanta (GA). et al. EPA 738R-95-006. Ward EM. 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. Centers for Disease Control and Prevention (CDC). EPA). J Agri Food Chem 1989. Occurrence of sulfonylurea. 2005. Rose RL. World Health Organization (WHO). 2003. Ann Occup Hyg 2003. Hsiao JJ.41:3409-3414. Hodgson E. 1998.39(17):6561-6574. Comparative metabolism and elimination of acetanilide compounds by rat. Barr DB. Environmental Protection Agency (U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Andrews HF. Kolpin DW. reservoirs and ground water in the Midwestern United States.248(2-3):115-122. Casida JE.gov/oppsrrd1/ REDs/0001.108(12):1151-1157.ESTfeature_gilliom. Supplemental Technical Information (available on-line only). Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. 3/26/09 U. and other herbicides in rivers. Circular 1291. Feng PCC. 6/1/09 Whyatt RM. Wratten SJ. Brown KK. Furlong ET. Sci Total Environ 2000. Geological Survey (USGS). Linderman R. usgs. Deddens JA. Peter CJ.S. Barr DB. Sanderson WT. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Environ Health Perspect 2003. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Reynolds SJ. imidazolinone.

renal and hepatic injury. and concern about contamination with 2.4.4.5-T use as a herbicide in 1985. Once absorbed into the body.1. headache.5-T has been rarely detected in ground waters (USGS.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD. the general population is unlikely to be exposed to it. Kohli et al.Herbicides 2.2 and 0.5-T (Holson et al. Agent Orange). hypotension.3. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. nausea.5-T degrades to 2.4.g. Epidemiological studies have reported associations of several types of cancer. myotonia. 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.4.5-T and 2. 1992). Mohammad and St. Omer. Nelson et al.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.. 2. < LOD means less than the limit of detection.4.. and delayed neuropathy (Bradberry et al. 1986. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. dizziness. 93-76-5 General Information 2.4..5-T in soil varies with conditions. Although 2.4.4. 64 Fourth National Report on Human Exposure to Environmental Chemicals . Chlorophenoxy herbicides act as plant growth hormones.. it is not well absorbed through the skin.. 2. ranging from several weeks to many months. abdominal pain.4. which may vary for some chemicals by year and by individual sample.S.4.5T is rapidly absorbed via oral and inhalation routes. 2. 2. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1974).5-Trichlorophenoxyacetic Acid CAS No. Given the commercial unavailability of 2. 2007). but higher levels are herbicidal.4.5-T was once applied as either an aqueous salt or as an oil-soluble ester.4-D were used as defoliants in the Vietnam War (e.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.5-T is eliminated mostly unchanged in the urine. The half-life of 2. 1989. these herbicides can enhance plant growth. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4.4. At low levels. Human health effects from 2.5-trichlorophenol and other degradates. Ester forms of 2. 2004).4.. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.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.5-T.7. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. 1992.5-Trichlorophenoxyacetic acid (2.4.

Fourth National Report on Human Exposure to Environmental Chemicals 65 . 2005). 2003. other exposures. IOM. Additional information is available from U.3. Finding a measurable amount of 2. population from the National Health and Nutrition Examination Survey.5-T were generally below the limit of detection. Survey Geometric mean (95% conf. 2004).8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-T reflect recent exposure. Biomonitoring studies on 2.Herbicides or contaminated herbicides. It is unclear whether these associations are related to the chlorophenoxy herbicides. 2005.5-T itself is not mutagenic.4.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.4. IPCS.4.epa. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.7.4. Biomonitoring Information Urinary levels of 2.S. 2.4.5-T than levels found in the general population. U.S.4. similar to results of NHANES II (19761980). Pearce and McLean. 2002.EPA at: http://www.S.4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary 2. 1980).4.gov/pesticides/.5-T does not mean that the level will result in an adverse health effect. 1992). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. in which urinary levels of 2. or to contaminants in the herbicide formulations (specifically 2. 1996. 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.. Mean urinary levels of 2.5-T also were below the limit of detection (Kutz et al.EPA. urinary levels of 2.

Review of 2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. McCallum WF. Dhar MM. general population. Available at URL: http://www.4. Centers for Disease Control and Prevention (CDC). Khanna RN. St Omer VE. Gaines TB. Gupta BN. Arch Toxicol Suppl 1980.org/documents/jmpr/jmpmono/v96pr04. Philbert MA. Fundam Appl Toxicol 1992. Washington (DC): National Academies Press. Erne K. Environmental Protection Agency (U. Board on Health Promotion and Disease Prevention. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .5-T in four-way outcross mice.S. Sheehan DM.4-dichlorophenoxyacetic acid (2.S. Multireplicated dose-response studies with technical and analytical grades of 2. Third National Report on Human Exposure to Environmental Chemicals.4. International Programme on Chemical Safety-INCHEM (IPCS). Pesticide industry sales and usage .5-T).4. Bradberry SM. Carter-Pokras OD. Absorption and excretion of 2. discussion 5-7. I. Available at URL: http:// www. Sircar KP. LaBorde JB. Nelson CJ. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.Herbicides References Arnold EK.EPA). Arch Int Pharmacodyn Ther 1974. Kolmodin-Hedman B.4:318-21. Pesticides residues in food: 1996 evaluations Part II Toxicology.19(2):298-306. Mohammad FK.23(2):65-73. Selected pesticide residues and metabolites in urine from a survey of the U. U. Behavioral and developmental effects in rats following in utero exposure to 2.4.5-trichlorophenoxy acetic acid in man. Dichlorophenoxyacetic acid.8(5):551-60. Crit Rev Toxicol 2002. Gaines TB. Veterans and Agent Orange: update 2002. Vale JA. Murphy RS. McLean D.37(2):277-91.S. Beasley VR. May. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. 3/17/09 Institute of Medicine (IOM). 210:250-255. Proudfoot AT. 2.31 Suppl 1:1825.4-D) epidemiology and toxicology. Pearce N.4. II.pdf. Gaylor DW. gov/oppbead1/pestsales/01pestsales/market_estimates2001.2000 and 2001 market estimates. et al.4.epa.5-trichlorophenoxyacetic acid (2. Holson JF. Office of Prevention Pesticides and Toxic Substances.nap. Agricultural exposures and non-Hodgkin’s lymphoma.4. Tandon JS.32(4):233-257. Washington (DC): U. Neurobehav Toxicol Teratol 1986.4-D and 2.edu/catalog.inchem. Cook BT. Garabrant DH.5-T).19(2):286-297. Fundam Appl Toxicol 1992. 2004.5-trichlorophenoxyacetic acid (2. Holson JF. Brody D.php?record_id=10603. Estimation of occupational exposure to phenoxy acids (2. Vet Hum Toxicol 1989.htm. Available at URL: http:// www. 2005.5-T). 914.31(2):121-125. Scand J Work Environ Health 2005. Poisoning due to chlorophenoxy herbicides.EPA. Kutz FW. LaBorde JB. 2003.4. 3/17/09 Kohli JD.4-. Nelson CJ. et al. Toxicol Rev 2004. Developmental toxicity of 2. Developmental toxicity of 2. J Toxicol Environ Health 1992.5-t mixture.4-D/2. Atlanta (GA). S. Wolff GL.

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

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

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

138) .9 (14.059 (.088-.077 (.8-19.8-24.6) 16.9-38.1-19.180) .40-9.120 (.50 (8.158) .1 (18.242) .4) 20.7) 15.090-.8 (11.120 (.6 (15.5 and 7.130-.5-17.1-16.60-10.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .4) 14.149) .140-.5 (<LOD-11.0 (10.069) < LOD < LOD .202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.110 (.130) .147 (. population from the National Health and Nutrition Examination Survey.8) < LOD 8.2) 14.117) < LOD .00 (8.6) 19.3 (19.120 (.101) .8-17.098 (.6 (14.6-33.30 (8.130-.3 (18.110-.80-9. Survey years 01-02 03-04 Geometric mean (95% conf.170) .160 (.3 (13.089 (.070-.2) 12.100) .5 (16.058) < LOD .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.112-.0 (15.100) .1) < LOD 9.1) 20.5-17.147) 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.80 (<LOD-10.086-.1 (13.50) 15.056-.2) 11.100 (.120) .109 (.6) 9. which may vary for some chemicals by year and by individual sample.160) .8 (18.130 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .40-10.083-. Survey years 01-02 03-04 Geometric mean (95% conf.109-.9 (13.7 (14.110) .100-.90) 90th 15.8-17.00-14.0 (11.S.4 (12.180) .30 (8.1) 14.70 (7.0) 19.062 (.109-.100-.1-24.150 (.8) 14.9 (13.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.103 (.8-25.139 (.090 (<LOD-.075) < LOD .0 (10.102 (.4-17.140) .1) 15.108-.8.062-.7-19.7-22.080 (.1) 10.4) 19.110) .5) 19.2) 15.2-15.4 (12.3 (18.8 (9. < LOD means less than the limit of detection. 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 .0-25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5) 21.070) .055 (.113 (.3-21.048 (<LOD-.1) 15.6-24.054-.S. population from the National Health and Nutrition Examination Survey.4) 21.139 (.3 (14.7 (<LOD-15.150 (.9-23.6 (15.110 (.5) 15.049-.054-.073-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .063-. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD 9.103 (.060) .080) .4) 539 456 484 487 980 885 Limits of detection (LOD.6-24.080-.160 (.1) 13.5-15.090 (.138 (.093) .130) .120-.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 8.116) .0) 21.7 (15.Organochlorine Pesticides Serum Dieldrin (lipid adjusted) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.130-.090-.190) .110 (.112) 95th .4) < LOD < LOD 16. 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.064 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.053 (<LOD-.8) 15.9 (12.190) .130) .1-18.084-.090-.054-.9-22.0) < LOD 9.070 (<LOD-.096-.9 (12.100-.124) .140 (.80-10.0-21.077-.10 (<LOD-16.062 (.064) 90th .4) 95th 20.4-18.

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

6) 9. Until 1988.2) 34.5-42. Survey Geometric mean (95% conf.7 (32.1 (25.7) 9.3 (20.0 (26.10-18.4 (31.2) 36.9) 23.8-23.9) 31.5 (41.7) 31.70 (<LOD-10.6) 36.0-25.5) 10.3) 18.9) 36.8-73.8) 18.5) 38.8) 27.1) 90th 34.7 (10.1 (16.2 (21. see Data Analysis section) for Survey years 99-00. Fourth National Report on Human Exposure to Environmental Chemicals 81 .1) 22.4-40.2 (28.6) 49.4) < LOD 11.82-11.0 (20. and in soil.5) < LOD < LOD 9.3-45.2 (9.69-10.8-43.6) 39.9 (21.2 (37.6) 48.4 (22. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988. 10. respectively.3) 37.2 (36.8 (17.2) * 12.0 (16. fish.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 * * * * 11.9) 23.1 (15.89-10.9-42.7) 35.7 (<LOD-13.4 (30.9) 10.20 (<LOD-11.7 (43.3 (<LOD-19.5) 44. heptachlor use has been limited to treatment of fire ants near power transformers.9-38.4) 39.3 (27.5) < LOD < LOD < LOD < LOD 13.9 (26.S.6-24.5.9 (11.0-13.5-47.8) 53.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. and 7.6 (9.5 (<LOD-12.7-25. population from the National Health and Nutrition Examination Survey.1 (44.5 (34. 1994).8) 44.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. chlordane was used to kill termites and other insects on agricultural crops.8-33.20-11.2) 37.1) 16.7 (42.3) 18.8) 52. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.30-11.2-49.7-39.1 (11.9 (15.8-20.1) * 11.3) 10.2-21.8-31.9-21.10-11.3-49.36-11. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.3 (21.3 (26. 2007). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.3-43. 01-02.7) 28.2) < LOD 11. in addition to trace amounts of numerous other related compounds (ATSDR.8-42.5-38.4) < LOD < LOD < LOD 23.9-21.3-45.7-70.7 (19.9 (36. and dairy products are the usual sources of exposure to these chemicals in the general population.4) 37.9) 17.9-40. and 03-04 are 14. 1994.0-12.2-56.4-51.2) 33. 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.5.5) 21.0) 37.S.2-28.. As a result of the manufacturing process.9 (11.8 (18. the technical grade product of each chemical contains 10%-20% of the other chemical.8 (17.5) 56. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.6) 8.5-13.4 (35.0-33.6 (43.3) 10.9 (18. from the early 1950’s until the mid-1980’s.1) < LOD < LOD < LOD < LOD < LOD 8.5-44.0) 75th 20.0-67. < LOD means less than the limit of detection.7-56.4) 12.2-49.4) 22.0-61.90 (8.7-14.5-41. 57-74-9 Heptachlor CAS No.Organochlorine Pesticides Chlordane CAS No.0) 21.8.5-43.6 (25.74 (<LOD-10.2 (41.8 (10.4 (10.10 (8.6) 48.6) 23.5 (8.4-21.8 (40.S.5) 9.0) 41.0 (<LOD-12.8 (10.6 (16. 2007).4-45.9) 13.2) < LOD 11. buildings.3 (11.3 (9.1-65.5 (31.3-24.1) 30.6) 11.4 (30.8 (42.6) 20.0 (37.0 (32.9 (26.9) 37.3 (28.7-12.1 (<LOD-12.7 (34.2 (10. lawns.1 (<LOD-12.3 (25.7 (34.4) 18.2) 46.9 (31.9 (17.9 (15.6 (9.1 (20. Since 1992.1-50.7) 19.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.5 (33.6) 9. Consequently.9) 11. foods high in fat such as meat.3-32.6-45. which may vary for some chemicals by year and by individual sample.7 (<LOD-32.3) 41.0) 31.1-19.5) 37.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.7 (17.4) 29.4-14.8-61.5-65.9) 11.9 (29. Chlordane is not currently produced or used in the U.1 (40.0-18.6-18.1) 30.5-40.20-10.2 (39. 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. 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) 52.5-32.1 (17.37 (8.6) < LOD 11.2) 22.7) 19. Technical grade chlordane had contained 7% trans-nonachlor.6-53.1-15.1-51.63 (8.8-32.1-25.4 (<LOD-12.9) 47.1 (<LOD-12.1-25.6-12.8-33.0) 27.2-26.9) 39.0) 20.6-24.1) * 11.7) 42.

258 (.130-.068-.130-.076) < LOD .290-.108-.115-. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.253-.S.133) 90th . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.150-.083) .220-.110-.070) < LOD < LOD < LOD < LOD < LOD .066-.180-.130) .190-.450) . Chlordane and heptachlor are absorbed after oral.069 (<LOD-.223) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.208 (.210 (.210-.350) .061-. 2001.070) . Survey Geometric mean (95% conf.280 (. 1996.260 (.200-. to heptachlor. and inhalation exposure. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.067 (.083 (. The U. 2006).126 (. 2002.286 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.258-.090) .070-.250 (.130-.373) .370 (.148) .216-.269 (.203-. and alterations in immune function of offspring.199-.310) .140) .080) .400) . IARC.210 (.062) < LOD .300) .150 (.286 (.110 (<LOD-.242-.056 (. OSHA has established occupational exposure criteria. EPA has established environmental criteria for chlordane and heptachlor.070-.080) .090-.126) .300) .090) .066-. The major metabolite of heptachlor is heptachlor epoxide.280-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .200 (.057-.440) . 1986).063 (.170) .170) .180) .245-.063 (.077) .180) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .077) . dermal.300 (.190-.120 (.400) .230-. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.120-..053-. Rogan.331) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .070-.140 (.220-. and breast milk is a major excretion route in lactating women.068) 75th .055-.082 (. 1991).058-.057) * .225 (.270 (. Takahashi et al.104-. and the U.350 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1986).062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .170) .080 (.070 (<LOD-.063 (.146) < LOD < LOD .240) .130 (.160) .250 (.057 (.430) .270 (.240 (.290-.207) .370 (.320 (.510) . and heptachlor epoxide in foods and bottled water.168-.130-.260 (.120-.230-.140 (.060 (<LOD-.S.231) .140-.410) .200-.230 (.207 (. chronic doses of heptachlor have produced liver enlargement and injury. 2007.280 (.320 (.227) < LOD .302) .280-.320 (.200-.290) . 1991.079) .075 (..073 (.136) .230-.140 (.204 (.560) .165-.148-.079) < LOD < LOD < LOD . 1977a.063-.119 (.068) .130-.092) .140-.087-.115 (.246-.213) * .280-.100-.050-.290 (.071 (.120-.230 (.Organochlorine Pesticides (Dallaire et al.070 (. Shindell and Ulrich.050 (<LOD-. 1977b.140 (.310 (. heptachlor.290-.315 (.189-.370 (.271 (.070 (<LOD-.260 (.130 (.048-. 2007).290) . Le Marchand et al. characterized by seizures and paralysis.053-.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.270 (.065-.260-.170) .310) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.240-. which is also persistent in the body (ATSDR.300) .280) .100-.350 (.360) .150 (.063) .080) ..077) .100 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. Elimination of all these chemicals from the body occurs over months to years.160) .073) < LOD < LOD < LOD < LOD .300-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.348) .340) .180-.310-.049 (<LOD-.380) .063) * .160 (. Smith. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.106-.190-.080 (.287) .340) .130) .189 (.130 (.220 (.058 (.250-.149 (.047 (<LOD-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.240-.066 (<LOD-..058-.320) .320) .104) .430) .170) .320 (.S. 82 Fourth National Report on Human Exposure to Environmental Chemicals .100 (<LOD-.330 (.070 (<LOD-.160) .300) .070 (<LOD-. In laboratory animal studies.310) .112 (.128 (.150) .450) .066 (. neonatal mortality.170-.063 (.091) . Acute.064) < LOD .150 (.077) . FDA established allowable residues of chlordane. 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. 1981).074-.230) .146) .

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

8) 21.4 (11.1) 20.7 (16.0-19. population from the National Health and Nutrition Examination Survey.2) 20.5) 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. and 03-04 are 14.2-17.4) 18.6.1 (16.3-18.8-24.3) 16.3 (13.2-27. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-23.6 (12.6) < LOD < LOD < LOD 27. respectively.6) 14.3) 10.3) 18.8) 16.5 (11.9-29. 01-02.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5) 19. see Data Analysis section) for Survey years 99-00.0-17.5 (11.8) 19.1) 23.8) 14.6) 22.2 (18.6 (14. 10.2-27. and 7.0) 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 13.4 (<LOD-19.1-38.4 (11.20 (<LOD-9.9-25.6 (<LOD-27.0-17.1-15.5 (10.7 (13.8-46.6-17.8 (13.2) 26.3) 18.4) 21.6 (16.5) < LOD 14.7-25.8 (13. which may vary for some chemicals by year and by individual sample.8) 19.8) 14.4 (15.6-21.8-24.0 (15.8 (18.0) 13.9 (15.8) 15.8.S.7 (10.2) 15.2 (<LOD-62.9-23.4 (<LOD-54.9-29.2) 13.6 (8.7-19.3) 18.1) 13.5 (<LOD-32.3) 23.2 (<LOD-25.3) 27.8 (18.3) 22. 84 Fourth National Report on Human Exposure to Environmental Chemicals .8) 13.6) 13.6 (11. < LOD means less than the limit of detection.1-29.8 (<LOD-23.7-18.9-16.2-16.6 (16.10-13.8) 20.5 (<LOD-21.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) 13.5.6 (13.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.9 (12.8 (15.0-54.9) 15. Survey Geometric mean (95% conf.8-24.50) < LOD < LOD < LOD 17.1-16.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.0-16.0 (11.40) 15.2 (<LOD-16.90 (<LOD-9.5 (18.3 (<LOD-25.1 (19.

173) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130-.120-.150 (.120 (.104) .170) .053-.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.135 (.076-.096 (.157) .190) .100-.128 (.140-.200) .074-.063) < LOD < LOD < LOD .097) < LOD .170 (<LOD-.113-.190 (.140) .135 (.130 (.087 (.150 (<LOD-.240) .057 (<LOD-.180 (.126 (.067-. which may vary for some chemicals by year and by individual sample.106-.170) .098 (.108) .170 (. Survey Geometric mean (95% conf.090-.190) .180) .310) .090 (<LOD-.310) .170 (.090 (.082-.094 (.220) .111) .270) .S.180) .120) .130) .130-.110-.170) .111-.090-. population from the National Health and Nutrition Examination Survey.094 (.120) .100 (.063) .116) < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .101 (.108-.110 (<LOD-.069 (.130-.120 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 85 .077-.071-.090-.113) .090-.120 (<LOD-.110 (.130-.110 (<LOD-.133 (.200) .090-.110) .100 (<LOD-.173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110-.110 (.150 (.130) .100 (.Organochlorine Pesticides Serum Heptachlor epoxide (whole weight) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.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 .149) .100 (.100-.077-.130 (<LOD-.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .170 (.100 (.107-.117) .180 (<LOD-.070-.380) .110) .180) .180) .190) .055 (<LOD-.101 (.140) .200 (.090-.

9 (16.3-39.9 (36.5) 14.8 (17.1) 32.3) 18.7) 28.3-50.0 (42.2) < LOD 10.5-36.6 (56.8-19.3 (49. and 7.1 (41.9-35.2-18.0) 40.7-34.0) 19.6 (52.6-20.6-19.3) 19.7 (35.8-110) 59.3-86.3) 16.1-34.2-23.2 (14.9 (15.8 (42.0 (29.9 (28.8) 47.7-20.5) 90th 55.5.0-20.9-65.6) 56.8) 80.0) < LOD < LOD 8.1) 14.4 (16.0-24.3) 32.2 (15.8 (30. 10.2) 19.8-67.5 (44.3) 25.4) 59.3) 30.7-35.2-16.4-23.5) 19.8-16.5) 9.8 (16.1-28.1 (22.2 (64.8 (13.7 (59.4-67.8.2 (14.3) 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.3-21.9 (19. and 03-04 are 14.4 (67.4 (28.9 (<LOD-14.2 (60.7 (74.4-18.7) 17.2-17.4-36. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 54.2) 59.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.8-129) 74.7 (13.4) 19.7 (30.70 (<LOD-12.6) 10.7-77.0 (48.7 (18.8 (45.6 (12.4) 20.3-74.5 (45.1-18.4-62.0-113) 68.1-20.9) 51.0) 18.0-23.3-58.1 (65.7-22.3) 36.5) 26.0 (62.7-113) 68.6 (32.5 (15. 01-02.2-37.1) 17.4 (45.5) 30.9 (29.8 (15.0-37.5) 77.2-88.6) 56.8-79.0-23.3-30.6-88.9) 51.9-89.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.9-40.7) 73.4 (11.9-65.8-90.8 (<LOD-20.1 (10.2) 30.6 (<LOD-14.1) 17. < LOD means less than the limit of detection.2) 39.2-18.7) 52.5) 20.8 (49.5) 36.7) 78.8 (28.3 (45.5-19.0 (19.7-38.9 (51.3-32.6) 34.0 (60.4) 107 (84.8 (13.5-111) 68.0-93.1) 17.3 (17.9-45.6 (15.2-21.4) 48.7) 35.3 (56. which may vary for some chemicals by year and by individual sample.9-64.0 (16.0 (15.1) 18.7) 59.1-34.6) 60.0) 13.6) 82.1) 30.1) 78.6) 25.5-20. Survey Geometric mean (95% conf.0-93.5 (25.4 (30.9) 14.8) 19.3) 15.2 (25.2 (36.9 (15.8 (26.1) 17. respectively.0 (15.6 (16.6) 84.1-51.1 (17.8 (28.9) < LOD < LOD < LOD 20.3) 30.2) 20.S.0-68.0 (13.3) 32.5) 35.7) 56.6) 13.3 (16.5-17.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.2 (7.3-57.0) 33.8 (71.1-126) 67.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.9 (47.6-82.2 (26. 86 Fourth National Report on Human Exposure to Environmental Chemicals .0-38.6 (50.5 (13.0-59.5-87.3) 18.1-55.7-23.7-18.9-58.4-52.2 (59.8 (26.7-32.4-22.1 (47.9 (51.5) 22.8-77.7 (16.1) 78.0) 75th 31.7) 78.8-21.0) 49.7-160) 86.7-17.8 (19.0 (42.5) 14.5-69.4) 55.1 (48.8-41.1) 17.1) 16.0-143) 112 (68.6 (57.9 (66.1) 18.5 (15.6-22.7 (59.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.3 (14.0 (14.9-69.9-20.1) 17. see Data Analysis section) for Survey years 99-00.2 (27.5) 78.1) 17.1-16.1-22.1-16.7-21.8-90.2 (19. interval) 18.9-36.1) 31.86-13.7-29.3 (58.2) 34.8-19.0 (13.7) 14.6 (56.5) 48.0-22. population from the National Health and Nutrition Examination Survey.0 (16.10 (<LOD-11.9) 14.0-123) 74.8 (28.2) 17.8) 51.6-66.3 (14.4 (12.5.7) 15.4) 16.5-95.4-35.1) 62.8 (26.8-16.8 (11.6-54.7 (11.9-22.7 (28.8 (12.

410-1.191 (.094 (.108) 75th .430-.141) .630) .590) .600) .330-.125 (.250) .405) .520) .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.540) .500) .234) .130) .120) .100 (.490) .120 (.830) .109 (.079-.190-.343 (.130) .180-.120) .100-.060-.099-.220 (.594) .078 (.106 (.091) .260) .470-.100-.400 (.300) .340) .237) .099-.288 (.390-.120-.092 (.110 (.220) .470 (.120-.103 (.630) .417 (.116 (.320-.288-.440) .090 (<LOD-.360-.220 (.122) .085-.130) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .110 (.580 (.082) .170 (.470-.237) .090) .310-.095-.430-.060 (<LOD-.104-.113) .183 (.960) .119) Selected percentiles ( 95% confidence interval) Sample 95th .079-.180-.550 (.250) .760 (.098 (.250) .190-.242) .390 (.120-.371) .126) .128 (.089 (.129) .096-.109 (.180-.110) .161) .240) .160-.130) .093) .190-.071 (<LOD-.301-.390 (.210-.069-.134) .105 (.112 (.041 (<LOD-.520 (.520 (.360-.098 (.055 (<LOD-.684) .140) .100 (.370 (.490 (.470 (.047-.327 (.690) .220 (.410-.470 (.070 (.090-.330 (.400-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .840) .145-.110-.460) .390) .090-.173-.124) .651) .177-.090-.272-.104 (.420 (. Survey Geometric mean (95% conf.096-.108) .111 (.060) .310) .190-.093-.110 (.310 (.310-.440-.310-.260) .116-.114) .390 (.270-.286-.093-.085-.240 (.081-.320-.160 (.310-. population from the National Health and Nutrition Examination Survey.211) 90th .558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .232) .171-.120) .S.125) .400 (.127) < LOD < LOD .120 (.186 (.600 (.640 (.130) . which may vary for some chemicals by year and by individual sample.091-.106 (.380 (.279-.690) .110 (.130) .430-.081 (.580 (.340-.061-.116) .220 (.559) .390) .062 (.210 (.080 (.355 (.087 (.092 (.150) .370 (.290-.161-.20) .240) .080-.085-.460-.080-.317 (. interval) .630) .510 (.400) .800) .324 (.220 (.117) .458 (.450) .510-.093-.497-.230 (.240-.090-.210 (.103 (.097) .098) .120 (.090-.130) .930) .590 (.080-.130 (.080-.680) .350 (.202 (.141) .461 (.120) .122) .108 (.580 (.054-.090 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .400-.135 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.096) .210-.300-.113) < LOD .100-.490-.190-.367) .240) .111-.078-.460) .100-.397-.131) .110 (.573 (.090-.480) .220 (.110 (.130 (.680 (.190-.210) .210) .330-.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 .395) .210) .565) .080) .210 (.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.590 (.350-.205 (.830) .220 (.420) .119) < LOD < LOD < LOD .395-.340-.084-.068-.490 (.158-.112 (.414 (.069) .186-.220 (.390 (.106 (.285-.409-.280) .098-.150) .

Brower S. Atuma S. Available at URL: http://ntp. 88 Fourth National Report on Human Exposure to Environmental Chemicals . New York. International Agency for Research on Cancer (IARC). 4/21/09 Dallaire F.heptachlor.111:349355. Glynn AW. Concise International Chemical Assessment Document 70 Heptachlor [online]. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. maternal serum and milk from Wielkopolska region. Takei G.nih.org/ documents/cicads/cicads/cicad70. 79. Tartter P.htm. Organochlorine exposures and breast cancer risk in New York City women. Handbook of Pesticide Toxicology.110(8):835-838. Baker DB. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. 1994-1997 organochlorine compounds.atsdr. 2 Classes of Pesticides. Dewailly E. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Inc. Environ Res 2000.inchem. et al. Van Oostdam JC. 1991 pp. Loo S. 9/25/07 International Programme in Chemical Safety (IPCS). Bull Environ Contam Toxicol 1981:27:506-511.330:55-70. Organochloride pesticide residues in human milk in Hawaii. Smith AG. Wong L. Lulek J.259(3):374-377. Wolff MS. Available at URL: http://ntp. A Report to the Hawaii Heptachlor Research and Education Foundation. 731-915.inchem. Arch Pediatr Adolesc Med 1996.atsdr. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Berkowitz GS. Odland JO. Shindell S and Ulrich S. Available at URL: http://www.84:151-161. Bjerselius R. Pollutants in breast milk. KalubaSkotarczak A. et al. National Toxicology Program (NTP). 1986.nih. International Agency for Research on Cancer (IARC) . Available at URL: http://www. Environ Health Perspect 2002.cdc.gov/toxprofiles/tp31. Royce W. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. 4/21/09 Baker DB. Jr. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. et al. Dendle WH. 6/1/09 Rogan WJ.htm. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Wohlleb JC.html. et al.372:20-31. J Occup Med 1986.9:1-109.html. Poland. Hawaii Med J 1991.50(3):108-118. Toxicological profile for chlordane [online]. May 1994.Summaries & Evaluations.niehs. Keller JA.110:617-624. Bleiweiss IJ. Gilman A.cdc.pdf. Environ Health Perspect 2003.org/documents/iarc/ vol79/79-12.150:981-990. Covaci A. Saidein D. gov/toxprofiles/tp12. Head SL. Vol. Distribution of polychlorinated biphenyls. JAMA 1988. Hansen JC. 1993. Senie R.html. Toxicological profile for heptachlor and heptachlor epoxide [online]. Available at URL: http://www. Dewailly E. Vol. 4/21/09 James RA. Environ Health Perspect 2002. Jr and Laws ER. Bioassay of heptachlor for possible carcinogenicity. Stehr-Green P. Charles MJ. Sci Tot Environ 2006. Organochlorines in Swedish women: determinants of serum concentrations. 1979-1980. Barker J.org/site/foundation/ research/projects2. Canada). Willman E. Muckle G. Siegel BZ. Eds. Bioassay of chlordane for possible carcinogenicity. Circumpolar maternal blood contaminant survey. 6/1/09 National Toxicology Program (NTP). Granath F.niehs.41:145–148. Drews K.28:497501. Chlorinated Hydrocarbon Insecticides. In Hayes WJ. Arch Environ Health. Darnerud PO.pdf.gov/ntp/ htdocs/LT_rpts/tr008. Aune M. Jaraczewska K.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 1963-1967. August 2007.8:1-123. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Sci Total Environ 2004.gov/ntp/ htdocs/LT_rpts/tr009. Kolonel LN. Lawrence River (Quebec. Ayotte P. Academic Press. LeMarchand L. Available at URL: http://www. 2001. Laliberte C. Chlordane and heptachlor [online]. Chashchin V. Takahashi W. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Available at URL: http://www. Hertz-Picciotto I. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Voorspoels S. 2006. Mortality of workers employed in the manufacture of chlordane: an update.

6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 19.5) 23.0-53. and trace amounts of several related compounds. 2002.8. and dairy products.1-27.8) 15. fish. and 03-04 are 20.0 (10.3 (<LOD-21.6 (25.9) < LOD < LOD 9.7) 12. Smith.90 (<LOD-12.0-35.9 (21.2-95.2) < LOD < LOD 9.8-39.0 (21. 1988). food.5 (15. population from the National Health and Nutrition Examination Survey.4.2) 30.9) 14. The biodegradation half-life of DDT in soil varies from 2 to 15 years. after World War II until 1972.7 (19.5 (23.7 (15.9-34. 17.3-236) 24.9) 17. It is still used in some countries.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6 (9.0-37.3) 21.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.0-155) 83. DDT and DDE can cross the placenta.0-27. 1991).1’-(2.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. particularly for endemic vector and malaria control. p.1 (<LOD-39. resulting in fetal exposure.00 (<LOD-10. including 1. Food imported from countries that still use DDT may contain the chemical or its residues.7) < LOD 18.1) 31.1’-dichloro-(2.5) < LOD < LOD 9.6 (31.0) 26. < LOD means less than the limit of detection. o.2 (<LOD-40. see Data Analysis section) for Survey years 99-00.p’-DDT (15%-21%). inhalation. or dermal exposure.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. These chemicals are highly persistent in soil.0 (18.9 (10. as well as in plant and animal tissues.4) < LOD < LOD < LOD 61.8-23.3) 22.2-bis(p-chlorophenyl) ethane (DDD).1 (23. It was produced and used in the U.3 (27. 2008.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.3-590) 293 (104-541) 48.8-17. Only a small proportion of DDT is metabolized and excreted (Smith. population. depending on conditions. DDT is converted in the environment to other more stable chemical forms. respectively.1 (33.70 (8.10-13.7-16.8) 36. Survey Geometric mean (95% conf. DDT usually refers to the technical product.0 (18.2-65. DDT was used at one time as a treatment for head and body lice.p’-DDD (4% or less).50-11.9-28. and 7. which is a mixture containing p. and water.5 (23.4) < LOD 17.5) 25.9) 29. which may vary for some chemicals by year and by individual sample.5 (14.3 (<LOD-31.0) 40.1-71.6 (<LOD-25.8) 30.2) 155 (59. continues to be the primary source of DDT exposure.S. when virtually all use of it was banned.8-26.S. Fourth National Report on Human Exposure to Environmental Chemicals 89 .p’-DDT (65%-80%). 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.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. 01-02.7.6-33. In the body. sediments.0) 20. Gunderson. particularly meat.9 (<LOD-20.6 (22. DDT can be absorbed after ingestion. 1991). although DDT and DDE intakes have decreased over time (FDA.S.3-16.7) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 10.4 (23. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. DDT is converted to DDE and several other metabolites. In the general U.9 (10.5-36.3) 21. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-15.10 (<LOD-12.9 (10.2 (11. air.5-54. Both Serum p.3) 28.

resulting in exposure to nursing infants (Rogan.00) .240) .146 (. have not been consistently demonstrated (Beard.059-.220) .075) 1. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.130 (<LOD-.086 (.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. 1998).240 (.p’-DDD and p. Jusko et al. accidental exposures.084 (. 2004.190 (. and seizures.143) < LOD < LOD .112 (.627) . 1995.420) .313 (.190 (. dioxins and furans).071 (. Survey Geometric mean (95% conf. 2006). fertility.260) .064 (. 90 Fourth National Report on Human Exposure to Environmental Chemicals .170 (.250-1.108 (.180-.105-.150-. tremor.150 (<LOD-. lung cancer. 1996). reproductive organ abnormalities. Gray et al.114-. Animal studies reported reduced fertility.00 (.095) < LOD .. premature delivery.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 ..074-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .078-.. 2006).180) .200 (.098-.180 (.220) . 2001).S.343) < LOD .530 (.150-.180) . 2002.62 (.570-4.120 (<LOD-. Mariussen and Fonnum. 2002.128 (.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 ..170) .150) .190-1.g.079) < LOD < LOD . 2001).068-.01) . and altered behavior after neonatal exposure (Eriksson and Talts...530) .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 .071-.203) .132-.063 (<LOD-... Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2001). 2002.130-.106) < LOD < LOD .150 (<LOD-.140) .065-. Snedeker. 2001). although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. In laboratory animals.201 (.230) . polychlorinated biphenyls. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and o. Longnecker et al. Beard. DDT may bind to estrogen receptors (Chen et al.250 (.180 (.p’-DDE can produce anti-androgenic effects (Gray et al. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. 2002..061) < LOD < LOD < LOD . In high dose.. population from the National Health and Nutrition Examination Survey.069) . Jusko et al.170-.230) . Studies of DDT exposure and pancreatic cancer. Hayes et al.26) 1.400 (.048 (<LOD-.080-. which may vary for some chemicals by year and by individual sample. A workplace standard for DDT has been established by Serum p. 2006. other organochlorines.130 (<LOD-.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.142 (. Reproductive effects in humans affecting birth weight. and duration of lactation. overt signs of acute human toxicity include vomiting. Calle et al.106-.290) .140-.106) .167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .120-.400) .087 (.330-4. 2006. 2000. 1997).189-. 2006). 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. and leukemia have also been inconclusive (ADSDR. Gladen and Rogan. 2006..34) .Organochlorine Pesticides chemicals are excreted in breast milk.160-.078 (.130 (<LOD-.054-.146 (. 1956).051 (<LOD-.

2004). 8. respectively.atsdr.6 (81. mean serum levels of DDT and DDE in the U. More information about external exposure (i...gov/ pestcides/ and from ATSDR at: http://www. 2003). and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. compared to levels observed in this Report (Anderson et al.S. Biomonitoring Information DDE persists in the body longer than DDT..e. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person..gov/ toxpro2.S.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. see Data Analysis section) for Survey years 99-00. Stehr-Green. respectively..html. Heudorf et al.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD. 2003.p’-DDT) as a possible human carcinogen.S. Smith. 2005). for males and females in the NHANES 19992000 subsample (Pavuk et al. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. Link et al.. 2002.. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. EPA at: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 91 . In a population-based sample of men and women from eastern Slovakia. Since the 1970’s. In general. Survey Geometric mean (95% conf. and 7. 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.epa. 1989). 1991). population declined by about fivefold to tenfold. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. Compared to females in the NHANES 1999-2000 subsample. and 03-04 are 18..7-119) 113 (100-140) 93.6. population from the National Health and Nutrition Examination Survey. 2004). NTP considers DDT as being reasonably anticipated to be a human carcinogen.cdc. Declining DDE levels over time have also been observed in the German population. 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. 01-02.8.3. IARC classifies DDT (p. 1998.Organochlorine Pesticides OSHA and a guidance established by ACGIH. environmental levels) and health effects is available from the U. 2002.

43-4.01-5.5) 5.8-90.38 (1.39-1.18-4.07 (5.47) 3.82 (1.96) .91-3.0 (12.87 (5.30 (1.69) 4.37-10.85-10.6) 12.p’-DDT were below the limits of detection.18-3.385-.49) 8.18-1.38 (1.16 (2.10-1.88 (2.77 (1.p’-DDT (Stehr-Green.43-8.15-4.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.p’-DDT.00-1.40-4.47 (1.71 (6.57 (3.0 (9.6 (17.04-1.8 (13.25 (1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.25) 1.03-4.65 (1.22) .3) 13.611-1.8 (13.03-1.00 (6.51-15.730) .8 (14.32 (1.Organochlorine Pesticides nearby agriculture (Botella et al.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.30-1.68) 2.81 (1.70-3.90-8.80) 3.75) 6.36-11.70) 1.51) 3.34 (7.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.81 (7.2 (9.59) 3.57-2.31-12.40 (3.04 (6.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.32-9.27) 3.7-19.37-4.12 (.2) 19.26) 3..79) Selected percentiles ( 95% confidence interval) Sample 95th 11.7) 13.7 (8. Serum p.14) 2. population from the National Health and Nutrition Examination Survey.9 (15.50 (2.25-16.69 (.3) 10.85 (1.46 (1.76-3.45 (1.57 (1.59 (4.9) 5. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.6) 9.57) 2.81-18. Survey Geometric mean (95% conf. 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.36 (3.4) 13.01-11.30 (1. considerably higher than levels in this Report (Smith.01) 1.32) 1.71 (5.62-6.25) 8.57-3.69 (2.456 (.22-1.66) 1.88-35.6) 9.50-17. 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.81-5.00 (.76) 1.49 (6.83 (1.92) 1.02) 1.8 (9. 309 versus 268 ng/g lipid.557) 1.10-5.8) 15.85-4.92 (3.31 (1.99) 1.81) 11.4) 9.0) 2.91-2.58) 1.p’-DDT.01-11.20 (.25 (.30-1.2 (6..44) 1..9-38.68 (2.600) .24 (1.82) 1.63 (1.39 (3.4 (8.14-9. or p.24-17.55 (2.34) 6.4-19.520 (.80 (2.419-.24) 1.S.57-13.41 (1.1 (8.963-1.60-13.18-1.4) 14.17-3.796 (.32 (1.0) 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 .28) 1.43 (5.26-10.1) 7.75 (8.54 (1.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.59) 6.870 (.97-4.54) 8.01-15.05 (3. 2004). interval) 1.71) 32.37 (1.71) 12. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.40-8. 1991).51-8.6) 9.22 (7.3-43.11 (2.72) 1.45 (1.6) 9.01) 1.66-2. 2005).500-.93 (7.00) 7.820-1.64) 3.77 (1.66) 4.69 (1.90) 22. serum levels of o.40-4.59 (1.84 (3.2) 26.18) 1.39-2.59 (1.35) 1.51 (1.69) 8.36-1.5) 7.6 (9.92 (3.56-2.49 (1.5) 16.41-12.96) 1.52 (1.2 (19.12 (6.17 (3.13 (1. High mean levels of whole blood DDT (about 3.21) 3.21) 90th 7.49 (1.11-1.84-3.65) 1.2-32.52-6.66-17.55-9.14) 2.635) 1.43-4.3 (8.488-.64-2.7-48.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .37-1.9-17.13-2.561 (.34-3.72) 1.63 (6. 1971).9 (26.46-2.80) 1.9) 7.06) 1.1) 40.534-.26 (1.37-16.57 (1.46 (1.07) 1.75) 1.53) 7.726) .58) 75th 3. o.76) 1.14-1.01-1.29 (1.6) 8.68-4.18 (6.5) 22.48-4. 2004).66-4.13) 4.34) 2.31-2.54-7.680-1.78 (4. In the NHANES 1999-2000.53) 1.6 (7.6) 13.02 (2.56-3.66) 3. less than one percent had detectable serum levels of o. In a subsample of NHANES II (19761980) participants.79) 4.7-20.53-15.10) .430-.09-1.66) 1.75 (4.53 (2.58) 1.76 (2.16-1. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.27-1. 2001-2002 and 2003-2004 subsamples.61-2.5) 10.63-15.19) 4.87-16.965-1.61 (1.07) 1.56-6.25-14.3) 16.516 (.2 (9.590 (.860 ng/L) and DDE (about 14.63 (1.1 (9.890-1.36) 3.23 (7.91) 3.52 (3.36-2.75) 2.19-14.4 (12.994-2.7) 9.01-1.80) 1.32-1.7) 16.32-1.6 (8.1) 12.6) 11.97 (3. Finding a measurable amount of p.3 (9..39) 1.05) 1. 1989).10) 2.51-49.48 (6.33-1.623 (.56) 2.12-1.06) 3.646) .51) 1.14 (1.91 (6.26-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.34-11.02-8.

and 7.Organochlorine Pesticides Serum o. 01-02. 17. < 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.S. population from the National Health and Nutrition Examination Survey.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. respectively.8. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 03-04 are 20. which may vary for some chemicals by year and by individual sample.7.4. see Data Analysis section) for Survey years 99-00. Fourth National Report on Human Exposure to Environmental Chemicals 93 .

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

Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Profiles of ortho-polychlorinated biphenyl congeners. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. and dichloro(diphenyl)ethylene (DDE). India. Notides AC.atsdr. Biomonitoring of persistent organochlorine pesticides. Paepke O. Rivas A. et al. Food and Drug Administration (FDA). Davis MD. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Int J Hyg Environ Health 2002. Barr DB. et al.html. Am J Public Health 1995. Schulz C. Zaidi SS.106(5):279-289. et al. Environ Health Perspect 1998.52:301-309. Baker RJ. lindane (g-HCH).58:1185-1201. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Atuma S. Gunderson EL. Gray LE Jr. Beard J. Zhou H. Needham LL. The Great Lakes Consortium. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Frumkin H.17(6):692-700. Bloom MS. Rogan WJ. and HCB residues in human blood in Ahmedabad. Gray KA. Vena JE. and other chemicals. hexachlorobenzene. 4/21/09 Anderson HA. Aune M. Organochlorines and breast cancer risk.97(2):178192. Henley SJ. J Assoc Off Anal Chem 1988. Durham WF. Toxicological profile for DDT.7(3):248-264. Biochem Pharmacol 1997. dietary intakes of pesticides. Klebanoff MA. Becker K. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Greenfield TA. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP).gov/~dms/ pesrpts. Burse VW. DDE. Hum Reprod Updat 2001. Epidemiology 2006. Available at URL: http://www. Saiyed HN. Needham LL. dichlorodiphenyldichloroethylene. Olea-Serrano MF. August 2008. hypospadias. Olson JR. Glynn AW. Bates MN. Longnecker MP. Environ Health Perspect 2003.gov/ toxprofiles/tp35. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Granath F. Darnerud PO. Moysich KB.96:34-40. et al.1-dichloro2. Garrett N. Heudorf U. Am J Epidemiol 2002. Bjerselius R. Lancet 2001. Chemosphere 2005. Lambright C. Koepsell TD. Seiwert M. Bull Environ Contam Toxicol 2004. CA Cancer J Clin 2002. Hayes WJ.cdc. Chen CW. et al. Levels of DDT. Wolf CJ.html. Chemosphere 2004. Zoellner I. Crespo J. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. selected elements. Zhou H. Savitz DA. Buckland SJ. et al.fda. FDA total diet study. Parks L. JAMA 1956.355:7889.162:890-897. Bhatnagar VK. HCH. Angerer J. Effects of environmental antiandrogens on reproductive development in experimental animals. Brock JW. Cerrillo I. Maternal DDT exposures in relation to fetal and 5-year growth. Exposure of women to organochlorine pesticides in Southern Spain. Jusko TA.85:504508. Willman EJ. Jr.71(6):1200-1209.. and polythelia among male offspring. Olea N. Calle EE. and DDD [online]. Kulkarni PK.206:485-491. Kashyap R.21(1-2)37-48. Olson J.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Piechotowski I. Klebanoff MA. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.54:1431-1443. Herrman T.155(4):313-322. Sci Tot Environ 2006. Patterson DG Jr. Arnold SF. Ostby J. Cueto C. Talts U. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Falk C.111:349355. Krause C. Neurotoxicol 2000. Vorojeikina DP. Klebanoff MA. Botella B. Longnecker MP. Gladen BC. Environ Health Perspect 2004. April 1982 to 1984. Lepom P. Needham LL. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Swanson MK. Thun MJ. Maternal serum level of 1. Brock JW. Eriksson P. Hediger ML. Organochlorines in Swedish women: determinants of serum concentrations.53(8):1161-1172. Katz SH.cfsan. et al. Furr J.358:110-114. September 2002.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Hurd C. 4/21/09 Gladen BC. Environ Res 2004. Jr. et al. Available at URL: http://www. Environ Res 2005. Charles MJ. DDE and shortened duration of lactation in a northern Mexican town. Int J Hyg Environ Health 2003. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Kaus S. Ellis H. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Gabrio T. Drexler H.112(17):1761-1767. Link B.72:261265. DDT and human health. et al. Hanrahan L.205:297-308.

Chemosphere 2004. and dieldrin. Smith AG. Nims R. Toxicol Appl Pharmacol 1971. New York.20(2):186-193.54:1509-520. Environ Health Perspect 2001. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. et al. Eds. Pollutants in breast milk. children and newborn infants. Inc. Crit Rev Toxicol 2006. 96 Fourth National Report on Human Exposure to Environmental Chemicals . J Toxicol Environ Health Part A 1998. DDE. et al. 2 Classes of Pesticides. Arch Pediatr Adolesc Med 1996. J Toxicol Environ Health 1989.150:981-990. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Demographic and seasonal influences on human serum pesticide residue levels. Academic Press. Pavuk M. Reddy AB. Stehr-Green. Snedeker SM. Rogan WJ. Astolfi E. PA. Rey AA. 731-915. Fox S. Radomski JL. In Hayes WJ. Cerhan JR. Schecter A. Jr. Chlorinated Hydrocarbon Insecticides. 1991 pp.36:253-589. Jones CR. Handbook of Pesticide Toxicology. Fonnum F. Chovancova J. Petrik J. Jr and Laws ER.27:405-421.Organochlorine Pesticides Mariussen E. Lubet R. Lynch CF.109:35-47. and DDD in male rat liver and cultured rat hepatocytes. Vol. Thomas PE. Deichmann WB. Neurochemical targets and behavioral effects of organohalogen compounds: an update.53:455-477. DDE. Comparative pharmacodynamics of CYP2B induction by DDT. Pesticides and breast cancer risk: a review of DDT.

Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. total diet surveys (FDA. All uses of the pesticide in the U.20 (<LOD-5. < LOD means less than the limit of detection. 1992). unlike aldrin and dieldrin. fatty infiltration.. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. 1992). 1992. unless the dose is high and the exposure is very recent. Endrin has been detected in soils. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Ketoendrin is a major photodegradation product (IPCS. An epidemic of acute endrin poisoning. IPCS. Endrin was used as an insecticide. Survey Geometric mean (95% conf. 1996.. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.30 (<LOD-6. In the body. At high doses. 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.10 (<LOD-5. Because it is metabolized so rapidly. Smith. inhalation or dermal exposure routes. manufactured.30) < LOD 5. 72-20-8 General Information Endrin. Hepatic effects of endrin exposure have included necrosis.40-5. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. endrin has been detected with declining frequency in U. 1981). 1991). Endrin is absorbed rapidly after ingestion.S.40 (<LOD-6. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Depending on soil conditions. Endrin was not widely used as a termiticide. 1979.10 (<LOD-5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. a stereoisomer of dieldrin. or discarded. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Endrin does not accumulate in body tissues (IPCS. endrin is converted rapidly to its major metabolite. 1992). endrin can persist for years.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. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al...09 and 7. population from the National Health and Nutrition Examination Survey. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.8. and occasionally at low levels in sediment and surface waters. Over time. anti-12hydroxyendrin.50) < LOD < LOD < LOD 5.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.S.70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. rodenticide and avicide.60 (5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) < LOD 5. Kavlock et al. 2008). is no longer manufactured in the U. EPA.S.Organochlorine Pesticides Endrin CAS No. endrin usually is not detected in serum of exposed individuals. and inflammation (Smith. have been cancelled by the U.S. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 1987). which may vary for some chemicals by year and by individual sample.20 (<LOD-5. or from contact with contaminated soils and sediments in areas where endrin was applied.S.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. 1991).

020 (<LOD-. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. 2004. IARC has determined that endrin is not classifiable with regard to human carcinogenicity..020 (<LOD-. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020 (<LOD-.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. EPA has established environmental standards for endrin.020 (<LOD-.020) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th . Workplace exposure standards for endrin have been established by OSHA. Information about external exposure (i.html. which may vary for some chemicals by year and by individual sample. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. population from the National Health and Nutrition Examination Survey..S.. and the FDA monitors foods for pesticide residues. 98 Fourth National Report on Human Exposure to Environmental Chemicals . Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.cdc.24 ng/mL (about 6.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. serum levels of endrin were below the limit of detection. In a small study of Spanish women hospitalized for elective surgery.gov/toxpro2.Organochlorine Pesticides The U. Ward et al. Survey Geometric mean (95% conf.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 .atsdr.24 ng/g of serum) (Botella et al.020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . with the highest value 6.020) < 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 studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population.020) < LOD < LOD < LOD .020 (<LOD-.020-.020) < LOD . 2004). 2000).e. This finding is consistent with other general population studies (Bates et al.020 (<LOD-. endrin was detected in 9% of serum samples.S. environmental levels) and health effects of endrin is available from ATSDR at: http://www.020 (.

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

Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.4. 1997).9) < LOD < LOD 15.9-24. 2005).0) < LOD < LOD 15.3 (16.9-32.7-16.3) 24.6-44.2-31.S. respectively.4) < LOD < LOD 22. 2002).3 (20.0-19. Therefore. particularly by consuming fish.6-32.6) < LOD < LOD 25.7-16.5) < LOD < LOD 18. Gunderson.5-15. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.6-TCP) (To-Figueras et al. and sediment (Barber et al.9) < LOD < LOD 16. water.0) < LOD < LOD 15. and accumulates in fatty tissues where it persists for years.0-28.2 (14. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. and elimination occurs by renal and fecal routes. 31.Organochlorine Pesticides Hexachlorobenzene CAS No.6 (23.7) < LOD < LOD 24.7-21. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.9) < LOD < LOD 28.5 (13.6) < LOD < LOD 14.0-25.0-16.5-14. 1988).0) < LOD < LOD 24. 1976). which may vary for some chemicals by year and by individual sample. 2008.7-26. 100 Fourth National Report on Human Exposure to Environmental Chemicals .9) < LOD < LOD 20.1-20..4 (22.5 (13.3) < LOD < LOD 29..6 (21. HCB has been detected in fewer foods since the 1980s (FDA.4) < LOD < LOD 14.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.7 (15.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.0.3-22.4) < LOD < LOD 33.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.9-15.9-17.8 (15. see Data Analysis section) for Survey years 99-00. and has been detected in soil.5 (14.1 (14.3 (22. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.7) * * 14. The general population may be exposed to HCB through diet.9) < LOD < LOD 19. 2.9 (25.9) 19.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.9 (14.5-18.5-33.4 (18.S.4.1) < LOD < LOD 15.7 (15.3) * * 15.7-15.2-15. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. HCB is well absorbed after oral administration.3-20.1) * * 15. primarily as a fungicide and seed treatment until the U.1 (14. and foods with a high fat content.6-33.9 (25.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4 (18.6-26.0 (18.7 (19.3) < LOD < LOD 20.4.7-30.4.6) < LOD < LOD 26.0 (14.6) < LOD < LOD 26.4) < LOD < LOD 23. population from the National Health and Nutrition Examination Survey.9) < LOD < LOD 20. wildfowl.2) < LOD < LOD 29.2 (17.S.6) < LOD < LOD 24.4 (11.2-15.6-trichlorophenol (2.7-22. HCB is slowly metabolized.6 (24. or game taken from areas with HCB contamination.1 (13. Survey Geometric mean (95% conf.0) * * 15.8.4-16.9 (23.9-30. The FDA dietary surveys have shown that over time. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.0 (18.5-TCP) and 2.3-26. air.3 (12..2 (13.5-14. and 7.5-trichlorophenol (2.S.2 (14. Although it is not manufactured as an end-product in the U.1 (17.7-29.3 (14.9-20. EPA cancelled its use in 1984..4) < LOD < LOD 18.8 (22.1-16.8-15.5-15.4-15.3 (22.4) < LOD < LOD 19. Urinary metabolites include pentachlorophenol (PCP).8 (26. 01-02.4.2 (24.8) < LOD < LOD 27. 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. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. < LOD means less than the limit of detection.7 (27. distributes widely throughout the body.2) < LOD < LOD 13. and 03-04 are 118.6-19. breast milk is an additional route of elimination in nursing women.0 (25.

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

more HCB levels were quantified. The metabolism of higher chlorinated benzene isomers. and the geometric mean concentration of HCB in whole blood was 0. 2003)... Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Darnerud PO.. J Exp Sci Environ Epidemiol 2007. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.html. Can J Biochem 1976. Otero R. Lawrence River (Quebec. In Spain. Jones D. 2005). Herrero C.9% of participants had quantifiable levels (Stehr-Green. et al. Bradman et al. however. Over the past two decades. Lepom P. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. 2002. Chemosphere 2005.77:173182. Dallaire F. April 1982 to 1984. Paepke O.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Available at URL: http://www. Safe A.gov/ toxprofiles/tp90. Toxicological profile for hexachlorobenzene update [online]. August 2008. HCB detection in serum also was proportional to age. distribution. Fenster L. Lecha M.135(4):400404.atsdr. In the 1976-1980 NHANES subsample. Link B.. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.. Glynn et al. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. In a representative sample of the 1998 German adult population. 1986. Bertram HP. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al.111:349355. Lackman. 2002. selected elements. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.. Ayotte P. trends and processes. Environ Health Perspect 2003. et al. Eskenazi B. Seiwert M.. As a result of the lower limit of detection in NHANES 2003-2004. Laliberte C. Gocmen A. 1989). Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Bjerselius R. Schulz C. J Assoc Off Anal Chem 1988. 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. Peters HA.. September 2002. 2002) and among children (Link et al. Lackmann. Arch Neurol 1982. Bertram et al..gov/~dms/ pesrpts.205:297-308. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Lackmann GM. Atuma S. Sci Tot Environ 2005. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.cfsan. 2002. Santiago-Silva M. respectively. Granath F. 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. Kaus S. only 4. Sweetman AJ. 2005. Gunderson EL. Dewailly E. Schwartz JM. Canada). Muckle G.58:1185-1201. Krause C. 2005). Jones KC. Food and Drug Administration (FDA). 4/21/09 Barber JL. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Biomonitoring of persistent organochlorine pesticides. FDA total diet study. Bradman A. Zoellner I. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Gabrio T. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 1999). levels. Dogramaci I. van Wijk D. Available at URL: http://www. Biol Neonate 2002. Barr DB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.349:144. Arch Dermatol 1999.. Becker K.39(12):744-749. HCB levels were directly related to age. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. References Agency for Toxic Substances and Disease Registry (ATSDR). dietary intakes of pesticides. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Organochlorines in Swedish women: determinants of serum concentrations.110(8):835-838. Piechotowski I. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. et al. 2006).54(3):203-208. Reference values updated. 2002. et al. Kemper FH.17:388–399. 102 Fourth National Report on Human Exposure to Environmental Chemicals . but overall. Muller C. Hexachlorobenzene in the global environment: emissions. Holland NT. Sala M. Kohli J. Aune M.44 mg/L. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene.71(6):1200-1209. Link et al. Int J Hyg Environ Health 2002. Bryan GT. IARC Sci Publ 1986.81(2):82-85.html. Cripps DJ. Environ Health Perspect 2002. Herrman T..cdc.fda. 4/21/09 Glynn AW. 2002). and other chemicals. Ozalla D.

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

46-11. 608-73-1 beta-Hexachlorocyclohexane CAS No.5528.8) 12.0) 8.1-37.8) 39.0 (<LOD-12.4-50.2-46.1 (30.6) 47.4) < LOD 9.1-32. 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.6 (10.9 (11.7 (35.0) 17. 58-89-9 General Information Hexachlorocyclohexane (HCH).9-24.4) 901 1067 952 992 1224 1007 Females 11.3 (62. commonly known as lindane.1-32.2-42.7 (30.20-16.8) 52.4) 11.6 (40.9 (9. beta.5) 29.8 (10.8) * * * * * * 15. see Data Analysis section) for survey years 99-00.80 (<LOD-14. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.7-20.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.1 (12. particularly alpha and gamma have been detected widely in air. containing about 64% alpha and 10%-15% gamma isomers. respectively.2-52.7-69.9 (50.S. each result has been multiplied by 1.7-166) 70.5 (37.50) 8.4) 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 21.4) < LOD < LOD < LOD 46.43 (<LOD-9.7-69. 104 Fourth National Report on Human Exposure to Environmental Chemicals .80 (6.6 (17.9 (32.1-27.3 (42.0 (14. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.2) 142 (99.90) 7.0) 41.4-45.7) 10.0) 7.4) 10.7) 23.7) 10.8) < LOD 10.3) 14.9) 15.6-42.4 (50.8-16. which may vary for some chemicals by year and by individual sample.04-10.70-12. gamma.9-21. and 03-04 are 9.0 (8.6-37.2 (31.5) 16.0-111) 70.4) 27. formerly referred to as benzene hexachloride.8 (64.0-34. However.6) 653 758 589 1240 1533 1370 20 years and older 10.8 (33.2-17.61-12.6-14.2-98.2 (48. soil.4) 44.9 (26.Organochlorine Pesticides Hexachlorocyclohexane CAS No.2) 62.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.2-67.4 (11. exists in several isomeric forms.0 (19.5) 67.8-68.3-85.2) 9.5 (8.6-62.4 (16. 2005).6) 50.5 (24.2-20. interval) 9.0-21.8 (23.9 (40. population from the National Health and Nutrition Examination Survey.4 (12.1) 71.9) 81. EPA cancelled agricultural uses of lindane (ATSDR.0-20.1 (11. It is no longer produced or sold in the U.3) 37.2-22.66-12.5-29.3 (42.6-18.0-70.70 (6.8-199) 134 (85.7 (13.5) 11.7) 32.2-55.0 (33.3) 34.70 (8.4 (52.3-38. 2005). < LOD means less than the limit of detection.3) 25.5) 40. **In survey period 2001-2002. and delta.36.1) 31.1 (21.90-8.5 (43.1 (9.0 (37.7 (<LOD-16. 01-02. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 (50.3-56.5 (14. 6.7) 97.6-89.8) 7.9) 17.8) 27.6-47.6 (16. the U.1 (16.2) 13.1) 13.8) 95th 68.1-49.9-178) 48.6) 18.0-23.1 (9.6) 35.5-123) 49.9 (30.4) 21.0) 35.9-14.8 (17.60-13.0) 71. and sediment as a result of historic production and use.89 (<LOD-9. Lindane has a half-life of about two weeks in soils and water.4 (8.7) 56.6-20.1-15.68 (<LOD-10.30-11.1-36.5) 22.2) 36.6 (22. HCH isomers.3 (13.7 (53.1) 12.76.4) 51.7-96.6-135) 69.8 (21.7 (29.2 (29.S.1) 12. water. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.2 (9.8-87.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.9 (62. Technical grade HCH is a mixture of all four isomers.4-73.56-12.5 (11.1 (18.7) 73. The gamma isomer.5) 90th 42.7) 18.8-19.5) 14.0 (35.6) 36.9) 45.7) 27.8 (32.7 (62.7 (25.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.7-96.9-51. environmental levels declined.8. and have been used either as fungicides or to synthesize other chemicals.6 (33.1-16. so they can accumulate in fatty tissues of animals.9-81.70-19.2 (18. See the section “What’s New” at the beginning of this Report for details.3 (26.4-111) 84. 319-85-7 gamma-Hexachlorocyclohexane CAS No.9-56. HCH isomers are lipophilic. As pesticide applications of HCH were increasingly restricted or eliminated.90-8.87 (9. including alpha.6) 16. The other isomers can be formed during the synthesis of lindane. In 2006.1 (27.2 (34. and 7.5 (16.3) 51.8 (9.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.7-26.S.0-70. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.2-87.8-54.

150) .140) .350 (.120 (.37) 1.501) .124-.150-.190) . tremors. 2008.270 (.250-.080) .160-.220) . the serum half-life was about 20 hours among children (Ginsburg et al.340-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .103) 90th .118 (.390 (.210 (.040-. 2002).120-. OSHA and ACGIH have established workplace standards and guidelines.120-. and memory loss (Nigam et al.090 (. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.175 (.050) . or dermal exposure.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .220-.098 (..057-.150 (. each result has been multiplied by 1.360 (. and nephropathy developed (IPCS.331 (.910 (.103-.146-.086) < LOD < LOD < LOD < LOD < LOD < LOD .410-.240 (.078 (.214) . Rogan.100-.05) .281 (.070-.110) .051 (<LOD-.120-.047-.222 (.064 (. ingestion.139 (.370-.120) .050-.120 (.310 (.710) .521 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.051-. 1981).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 .230-.240-.600) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .587) 653 758 589 1240 1533 1370 20 years and older . Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.380 (. 1977).290) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .083) . FDA pesticide monitoring program has shown a temporal decline in the detection of lindane. When animals were chronically fed lindane at high doses.140) .089-.400) .110) .100 (. See the section “What’s New” at the beginning of this Report for details.130) ..310) .060) .080 (.382-.234 (.200 (.210 (.460) .057-.5528.050 (.460 (.221-.390-. for lindane..Organochlorine Pesticides exposure to HCH is through the diet.480 (.070-.700) .420-.065 (.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.. Gunderson 1988). Saxena et al.S.220 (.410 (.070) .01 (.080-.119) .294-.068-.260) .065 (.170-.056-. U.050 (<LOD-.450) .072 (.048 (<LOD-.058 (<LOD-.067) .050-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.050-.050 (. enlarged livers.360-.056-. 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.330-.310) .620) .305) .067 (. The U.057 (<LOD-.110-. which may vary for some chemicals by year and by individual sample.062 (.150) .190-1.160) .073-.319) .410) .144 (.290) .470) .450 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al. EPA has established a drinking water standard.059-.570 (.560) .350) .174) .110) .250 (.100-.297-. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.120 (.191-.250-.32) .070 (.170-.210) .191-.320 (.092 (.300-.080-.100) .680) .254) 95th .180-.287 (.580-1. interval) .250 (.250 (.480) .080 (.080) * * * * * * .050 (<LOD-. After dermal application of lindane 1% lotion.661) 901 1067 952 992 1224 1007 Females .100 (.062 (.814) .330 (.160 (.070 (.450-.118-..400) .069) .125) < LOD < LOD < LOD . 1996.308-. resulting in a half-life of about seven years.280-.S.580 (.131-. 1986). population from the National Health and Nutrition Examination Survey.280-. HCH isomers are absorbed after inhalation.077) < LOD .200-.140) .190-. 1983).050-.220-.442 (.620-1.404) .190) . Workers who directly handled HCH have complained of headache. Distribution is mainly to fatty tissues.083 (. 1971.216 (.470 (.290 (.560 (.290 (.100) .089) .080-.173-.070-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.260) .840) .077) < LOD .340) .360) .090 (.130-.167 (. paresthesias.S.130 (.290 (.140 (.690) . hepatic enzyme induction. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.410) .260-. and seizures.412 (.510) . The beta isomer accumulates in fatty tissues and is metabolized more slowly. **In survey period 2001-2002.096) .103 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.372 (. probably by blocking inhibitory neurotransmitters in the central nervous system.091) . ataxia. respectively.090-.210-.100-.244-.120) .081-.090 (.480 (.064) .200-.250) . and FDA has established a bottled water standard and food residue tolerances for lindane.

5. In populationbased studies of New Zealand adults and German adults and children. 1971. 106 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00. the maximum and 95th percentile beta-HCH values.8.. EPA at: http://www. Sturgeon et al. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens.S..S. serum levels of lindane were generally below the limits of detection. were similar to the 95th percentiles in this Report.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. More information about external exposure (i.gov/toxpro2. Biomonitoring Information Because of its longer half-life.. 2002. 1991. 2004. 01-02.atsdr. 2005.. < LOD means less than the limit of detection..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 1998. Stehr-Green. and 7. 10. male sex. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004) and India (Bhatnagar et al.html. In recent years. which may vary for some chemicals by year and by individual sample. respectively. respectively. Kutz et al.e. Survey Geometric mean (95% conf. aged 9-11 years. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. 2004). studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. 1998).epa.. older age. 2001-2002. 1989. Link et al. 2005. 1989).. 1991. 2002). In an earlier (1996-1997) sample of German children.. population from the National Health and Nutrition Examination Survey. In NHANES 1999-2000. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. 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. Becker et al.. Bates et al.5. environmental levels) and health effects is available from the U. 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.cdc.. Additional factors associated with higher beta-HCH levels include rural residence.. Stehr-Green. and 03-04 are 14.. and 2003-2004. Kutz et al. and a diet that includes meat (Becker et al. Radomski et al.

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

html. Gabrio T. and HCB residues in human blood in Ahmedabad.150:981-990. Needham LL. available at URL: http://www. VI. Buckland SJ.57(4):315-320. Aune M. Lowry W. Rey AA. Exposure of women to organochlorine pesticides in Southern Spain. Paepke O. Krause C. FDA total diet study. Cancer Causes and Control 1998. Granath F. Rogan WJ.gov/~dms/pesrpts. Needham LL. Wood PH. et al. children and newborn infants. Zoellner I. Patterson DG Jr. Bai KM. Kaus S. Crespo J. Organochlorines in Swedish women: determinants of serum concentrations. Arch Toxicol 1981. Lepom P. Bhatnagar VK. Angerer J. org/documents/jmpr/jmpmono/2002pr08. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Stehr-Green. Botella B. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Int J Hyg Environ Health 2002. Kashyap R.27:405-421. Majumder SK. J Pediatr 1977. et al. Hanrahan L. Occupational exposure to hexachlorocyclohexane.48:127-134. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Arch Pediatr Adolesc Med 1996. Kulkarni PK. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.96:34-4Food and Drug Administration (FDA). Seiwert M. Metabolism of gammahexachlorocyclohexane in man. Cerrillo I. Link B. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Astolfi E.72:261265.html. Environ Health Perspect 2003. Olea-Serrano MF. Demographic and seasonal influences on human serum pesticide residue levels. Zaidi SS. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Rev Environ Contam Toxicol 1991. Krishna Murti CR. et al. J Assoc Off Anal Chem 1988. PA. Becker K. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Bates MN. dietary intakes of pesticides. Available at URL: http://www. Ellis H. Reisch JS. India. Deichmann WB. 4/21/09 Anderson HA. Karnik AB. Herrman T.111:349355. Schulz C. The Great Lakes Consortium. Chemosphere 2004. Olson J. et al.9(4):417-424.htm.205:297-308. Darnerud PO. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Maass R. Bull Environ Contam Toxicol 2004. et al. Falk C. Nigam SK. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Brinton LA. 2002.fda. Bottimore DP. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.atsdr. Sturgeon SR. Piechotowski I. Gunderson EL. April 1982 to 1984. August 2005. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Toxicological profile for hexachlorocyclohexanes update [online]. Placental transfer of pesticides in humans.52(1):59-67.54:1431-1443.91:998-1000.106(5):279-289. Rothman N. International Programme on Chemical Safety (IPCS). Siddiqui MKJ. Potischman N. Brock JW. Rivas A. Biomonitoring of persistent organochlorine pesticides. Levels of DDT. Raju GS. Radomski JL. Garrett N. Absorption of lindane (g benzene hexachloride) in infants and children. 4/21/09 Kutz FW. August 2008. Needham LL.20(2):186-193.inchem. Olea N. Int Arch Occup Environ Health 1986. gov/toxprofiles/tp43. Heinrich R. Glynn AW. Bjerselius R. Burse VW. Kutty D. Saiyed HN. Chemosphere 2005. Available at URL: http://www. selected elements. Saxena MC. et al.120:1-82.71(6):1200-1209. Lindane. et al. Environ Res 2004. Int Arch Occup Environ Health 1983. Bhargava AK.cdc.cfsan. Atuma S. Environ Health Perspect 1998. and other chemicals. Toxicol Appl Pharmacol 1971. Visweswariah K.58:1185-1201. 4/21/09 Ginsburg CM. HCH. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Pollutants in breast milk. J Toxicol Environ Health 1989.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. Fourth National Report on Human Exposure to Environmental Chemicals 109 . respectively. Mirex is absorbed through the skin and from the gastrointestinal tract.5-291) 11.S.40 (<LOD-13.5-425) 40.10 (<LOD-15. soil. disposal..6) 9.0) * * * 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 19.70 (<LOD-15. see Data Analysis section) for Survey years 99-00. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) < LOD 15.2-230) 13.6) < LOD < LOD < LOD < LOD 71.5-82. Some states and the U.6. which may vary for some chemicals by year and by individual sample. Occupational exposure is limited to workers at sites where mirex contamination is present. population from the National Health and Nutrition Examination Survey. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. and 03-04 are 14. mirex was detected in human adipose samples. Mirex has been detected in air. aquatic organisms. where it was applied directly to soil and by aerial spraying.6 (<LOD-108) 9.90-29.S.3 (15.7) < LOD 66.S. Mirex is not metabolized in the body. since 1977.0-374) 11.8.0 (14.3-225) 15.4) < LOD 63.6 (<LOD-31.5 (<LOD-115) 153 (30.3) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.5 (<LOD-42. (Kutz et al. and 7.6-305) 15.2) 51.Organochlorine Pesticides Mirex CAS No. where it has a half-life of 12 years.10-37.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. or pesticide application. Mirex can cross the placenta and be excreted in breast milk. 01-02.7 (12. Formerly. it is a highly persistent chemical in the environment. 1995). Mirex binds strongly to soil. 2385-85-5 General Information Mirex has not been produced or used in the U.7) 8.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.4-230) 18. Survey Geometric mean (95% conf.70-24.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. 10.8 (<LOD-73.S.. < LOD means less than the limit of detection. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. after which it is widely distributed in the body and stored in fat.8) < LOD 15.5.4 (8.70-40.S.3 (15.2 (7. In studies conducted in the 1970’s and 1980’s. animals. 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.1 (8.1) 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 16.5 (9.1 (<LOD-65. 1985. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.8 (12.6 (<LOD-23. water.1 (13. 1991). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. sediments.7 (<LOD-47. and foods. especially those from persons living in the southeastern U.0 (12. resulting in exposure to newborns and nursing infants.0 (<LOD-108) < LOD < LOD 50.

92) .170) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.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 .cdc.410 (. and NTP classifies mirex as reasonably anticipated to be a human carcinogen. and 4..064 (<LOD-. More information about external exposure (i. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al. In addition. EPA has established environmental standards for mirex.054 (<LOD-.S. serum mirex levels were generally below the limits of detection (Stehr-Green. population from the National Health and Nutrition Examination Survey. environmental levels) and health effects is available from the ATSDR at: http://www.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .e.079 (<LOD-.110 (<LOD-.170-3. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.055-.Organochlorine Pesticides exposures are unknown. Survey Geometric mean (95% conf.059 (<LOD-. and 2003-2004 subsamples.470) . Biomonitoring Information In the NHANES 1999-2000.100 (<LOD-.02) .7 ng/g of lipid. 110 Fourth National Report on Human Exposure to Environmental Chemicals .090-1. as well as in a subsample of NHANES II (1976-1980) participants. In samples obtained between 1994 and 1997.090-1.112 (. The U.470) .080-1. 1995. 7.430 (. 2005).310 (. reproductive toxicity included decreased fertility and testicular damage.gov/toxpro2.S.077 (<LOD-. Smith.atsdr.73) .79) .102) < LOD < LOD < LOD < LOD .html.41) .690) . 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.370 (.070-1.100 (<LOD-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .090-1.256 (.8. Laboratory animals fed high doses developed liver enlargement and liver tumors.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample..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 .090 (<LOD-. Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.510) < LOD < LOD .220 (<LOD-.635) < LOD .450) 1.090 (<LOD-.062-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .450 (.268) < LOD .052-. 2004). 1991). 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.089-.470 (.37) .08 (.79) . 1989). The geometric mean mirex levels of the Inuit mothers were 8. 2001-2002.106 (.093 (.610) < LOD < LOD < LOD < LOD .106) < LOD .108 (.053-.080-1.140 (<LOD-. IARC classifies mirex as possibly carcinogenic to humans..220) .090 (<LOD-.

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

20) < LOD 90th 5.40) < LOD 4.0 (4.40 (.60 (4.0) 2. 2006). Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.0) 2.0) 2. Such workers would probably Urinary 2.30-27.4.5-trichlorophenol (2.30-27.40 (2. 2.30 (.S.4. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.31 (<LOD-9.9 and 0.50) < LOD 1.5-trichlorophenol.5TCP and 2. 2.0 (4. may occur by inhalation or dermal routes.5-TCP) and 2.4.0) < LOD 5.00 (3.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.19 (<LOD-6.0) < LOD 5.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Both chemicals have been detected in air.50-63.Organochlorine Pesticides 2.20) < LOD 5.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.0 (4.9 (<LOD-121) 9.30) < LOD < LOD < LOD < LOD < LOD 1.950 (<LOD-1.20-71.50-16. surface water.80) < LOD 1. public drinking water systems did not detect 2.80 (1.0) < LOD 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.71 (<LOD-8.30) < LOD 4.90-33.0) 2.0) 2.30-11. however.10-3.0) 5. 1999). Occupational exposures.60) < LOD 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) < LOD 1.63) 18. 1976).5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.980-3. 2. and polychlorinated benzenes (Kohil et al.40 (. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.6-Trichlorophenol CAS No.4.4.00-3.0 (3.4.00-8.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.4. hexachlorobenzene.920-3. Exposure to trichlorophenols also may result from metabolism of lindane.30-27.30-3.5-Trichlorophenol CAS No.42 (<LOD-12.0) 14.6-trichlorophenol (2.7. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40 (1.4. Trichlorophenols are no longer manufactured commercially.50 (2.00-3. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.40 (1.6-TCP). < LOD means less than the limit of detection.8) 21.6-TCP were used as intermediates in the production of certain pesticides.40) < LOD 1. and sediments. usually at herbicide production or waste incineration facilities.6-TCP in any of the samples (U.30-44.S.3.60-18.7) 24.71 (<LOD-8.00 (2. including hexachlorobenzene and hexachlorocyclohexanes.940-3.50-25. 95-95-4 2.50 (1.4. Formation of 2.40 (2. other organochlorines.60-8.4.40) < LOD 6.72) < LOD 1.9.80 (2.980-3. Survey Geometric mean (95% conf.30-40. 1999). are metabolites of several organochlorine chemicals.20 (4.60 (.57 (<LOD-15. recent sampling of U.03) 9.20-36.0) < LOD 21.4..4.S. EPA.0 (5. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.900-2.40 (2.40-18.42 (<LOD-8.40 (2.27) 696 661 521 696 603 939 Limit of detection (LOD. Historically.0) < LOD 11. 112 Fourth National Report on Human Exposure to Environmental Chemicals .0) 2.80-41.50 (.40-11. soils. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.0) < LOD 11.0 (8.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .60 (2.0 (3.

Organochlorine Pesticides be exposed to mixtures of chlorophenols.820-2.4.78 (3.1 (<LOD-58.4.9 (5.73 (<LOD-8.46 (1. 2003). leukemias. Radon et al. which includes trichlorophenols. and lymphomas.37-11. furans.4) 5.5-TCP nor 2.57 (<LOD-7.19-12.4. IARC classifies combined exposures to polychlorophenols..4. the 95th percentile urinary 2. 1989).4.00) < LOD 4. Fourth National Report on Human Exposure to Environmental Chemicals 113 . NTP classifies 2. environmental levels) and health effects is available from ATSDR at: http://www.6) 4.5) 11.atsdr.8 (5.4 (6.36 (1.3 mg/L reported in German adults aged 18-69 years (Becker et al. 2003).33) < LOD < LOD < LOD < LOD < LOD 2.S. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.9) 12.31) < LOD 2.75 (3. Neither 2.6) 4..57 (<LOD-7.4.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2.53-3..43) < LOD 12.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0) 7.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).20-6.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . At lower doses.4.8) < LOD 9. 1995) and up to 19 times higher than the 95th percentile value of 1.44 (1.53-3..6) 4.0 mg/L.24) < LOD 5.4. Survey Geometric mean (95% conf.83-12.4.68-4.86 (3.75 (<LOD-6.4) < LOD 3. as being possibly carcinogenic to humans.6-TCP levels at the 95th percentile were up to eight times higher than 3.81 (<LOD-9. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. urinary 2.4.24) < LOD 1. and other chlorinated compounds.37) 696 661 521 695 603 939 < 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.17) 9.6-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.69 (2.37) 16. Among 6-11 year old children in NHANES 1999-2000.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.82 (<LOD-32.90 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 2.95 (3.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4) < LOD 3.67 (1.78) < LOD 1.980 (<LOD-1. the 95th percentile urinary 2.3 (5.02) < LOD 7. 2004).00-29.69-18.16) < LOD 90th 5..6-TCP as reasonably anticipated to be a human carcinogen. The 95th percentiles for 2.00-19. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.7 (4. However. Human health effects from 2.02-3.html.49 (1.1) 2.79-4. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.gov/toxpro2. More information about external exposure (i.15) < LOD 2..32) < LOD 4.55 (4.24-11.13-13.5-TCP or 2.2) < LOD 5.50) < LOD 2. 2003.24 (3.2 (2. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.8) 4..4.. 1989). 1995) were similar.cdc.74) 11.5-TCP and limited for 2.62-20.44 (.64 (4.4.78-19.80 (1.19-4.5-TCP.47-8.24) < LOD 6.68 (<LOD-8. animals showed hepatocellular abnormalities.05-8.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.e.920-2.88-16.6-TCP had increased rates of hepatic tumors.43 (2.4.6-TCP.5) < LOD 12. Urinary 2.28-25. Laboratory animals chronically fed high doses of 2.93-11.67 (1.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 7..05-17. In the same 2-6 year old children.29 (1.57 (3.27-17. in addition to dioxins.16 (. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.60-3.

04) 2.23-2.30) 4.60-37.0 (6.0) 19.40-14..6-TCP level.32-4.4.0 (11.47 (3.60-3. was about six times lower than the median urinary levels for males in this Report (Radon et al. interval) 2.5-TCP and to the median 2.0 (20.59-6.98-11.40-4.40) 3.9) 694 677 519 696 602 931 Limit of detection (LOD.40-7.5-TCP and 2.24 (2.67) 4.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.80 (2.0 (20.6-TCP exposure and health effects. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.70) 1.31) * 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-8. Urinary 2.35-3.9) 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 2.80 (3.40-32.0) 11.44) 75th 4.1 (8.70 (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.0 (13.10) 6.6-TCP in urine does not mean that the level of 2. 114 Fourth National Report on Human Exposure to Environmental Chemicals .65) 15.20) 4.02) 2.0) 19.55-3. Biomonitoring data will also help scientists plan and conduct research about 2. Urinary 2.8-15.07 (<LOD-3.20 (3.40) 2.75 (8.9 (13.10-3.98-7.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.0) 17.8-13.36 (1.74 (2. 0.4.0 (15.79 (5.0) 7.60 (2.4 (8.3) 20.95-6.60) 6.0-50.00-4.5-TCP or 2.30-33.6TCP values.28) 24.76) 3.90 (4.06) * 2.40 (2.30-2. Mean values of 2.4.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.4.70 (2.0) 13.5-TCP and 2.S.5-TCP or 2.7 (13.7) 21.4.23) 2.0 (14.2) 12.57 (<LOD-2.52-3.48-26.80-25. similar to the limit of detection for this Report (Anderson et al.5 mg/g creatinine) were similar to the limit of detection for 2.0 (6.32) 3.0 (14.9 (11.0) 12.40-2.70-6.0) 9.0 (8.6) 26.68 (<LOD-2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.95) 3.7 mg/L.69 (3.00 (2.67-12. the median urinary 2.60-21.60) < LOD 5.0 (8.74-3.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.70-6.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.95 (4.0-37.53) 4.36 mg/g creatinine.7-3.0) 15.53) 2.51-12. 2004).3.0 (7.4 (17.0-41.6-19.10) 2.20-6.89 (3. 1998).4.6 (12.0 (15.36-5.6) 21.0 (6.0-54. which may vary for some chemicals by year and by individual sample.18-3.50-5.90) 2.0 (14.0 (16.45) < LOD 11.7) 33.63) 90th 15.80-7. Survey Geometric mean (95% conf. for males in NHANES 19992002 (Agramunt et al.78 (2.45 (5.73-9. 1991).6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.90 (3.4-17.14 (2.4.0-38.0-68. In harbor workers exposed to chlorophenol-contaminated river silt.80 (2.80-20.28) * 2.58 (1.0 (9.1) 16.65 (5. respectively.70) 5.50 (2.12) 2.0 (12.4 (10.10-3.6TCP causes an adverse health effect.80-6. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.4.6-TCP (0.0) 9.00 (4.31 (3.84) 2.9) 13.7 (9.40 (2.1-25.32) * 3.4.0) 6.2 (14.10 (5.91-4.3) 23.0-38.30-11.3 (11.89-6.0 (4.6 (11.2-0.40) 2.4.4.4.00-21.5-46.5-TCP or 2.0) 14. 2003).10-2.92 (2.2) 25.40) 4.20 (3.3) 37.30-2.0-44.09) 15.80) 1.46-3.. Biomonitoring studies on levels of 2.0-43.08 (2.3 (11.40-2.5-TCP (0.6-22.3-26.56 (3.01-6.0) 10.60 (3.66 (8.4.0) 17.0) 13.4 (9.0-18.0 and 1.78 (2.09-7.20-23.0) 10.4..8) 18.20-3.6-17.85) * 3.4.26 (2.5-TCP or 2.70) 3.23) 3.00 (1.59) 4.45-9.0) 7.45 (2.6 mg/g creatinine) and 2. < LOD means less than the limit of detection.52 (2.4.0) 14.7-16.3-17.4..4.33-4.0) 13.60 (3.6-TCP than are found in the general population.5-TCP level of 0.0) 11.4. population from the National Health and Nutrition Examination Survey.72-10.8-24.87-14.4.0) 13. Finding a measurable amount of 2.70) 5.99) 6.25-11.49 (6.58-3.85 (2.8) 32.70-3.1 (10.8 (9.54) 6.

53-11.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.56-5.87) 2.19-5.6) 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 2.82-2.5) 12.32-19.96) < LOD 4.56) < LOD 11.72-16.1-32.5) 8.50-8.88 (2.89) 10.99-2.98 (1.25 (3.33 (7.68) 2.6 (22.63) 4.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.25-17.26-13.02 (1.83-6.23 (1.88-7.17-4.8) 19.01 (3.18-2.62-15.51) 18.0 (6.5 (8.6) 13.73) 5.4.46-14.68) 2.76) 2.3 (9.73-22.2 (12.9-29.83-5.30-2.4) 9.16-10.2 (13.82 (8.58 (4.06) 11.38 (4.9-64.00) 4.52) 2.42 (2.09-3.25-2.04-2.S.65) 18.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.83 (3.33-2.0) 10.04-16.65-2. Survey Geometric mean (95% conf.47-5.40 (7.22 (1.18-4.53) * 2.63-13.5) 11.7 (14.49) 4.43-7.00 (2.59 (2.10 (6.60 (4.10-9.3-23.71 (3.02) 3.14-2.33) * 2.88) * 2.83-6.1 (13.10) 4.00 (3.33 (1.15 (1.15 (6.90) 2.8) 11.6-31.1) 14.3) 8.88) 1.22 (3.Organochlorine Pesticides Urinary 2.1-21.52 (3.5) 11.51 (2.1) 11.13 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.63 (2.43 (<LOD-2.2 (8.79-17.7-36.41 (3.87) * 2.70-9.9) 7.38) 22.72) 32.52 (5.17) 13.4 (11.22-9.92) 4.28-4.17) 2.6 (12.78) 90th 12.49-3.29-4.42) 2.21-11.6 (5.6) 12.53 (3.88) 5.08-2.53) 4.4) 4.3-37.25-15.67-17.54 (2.81-9.52) 2.6) 8.98) 10.00) 4.0) 8.22 (<LOD-2.87-6.9-34.41-6.7) 25.1 (8.38 (2.88) 4.55-2.94-13.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.4 (12.9 (9.24 (1.4) 8.29-4.9) 8.63) * 4.51-21.91 (3.6 (9.8) 21.7) 6.9-32.88) 4.0 (9.6 (10.5 (10.44 (3.77) 2.65) 2.6 (6.87-7. population from the National Health and Nutrition Examination Survey.5 (7.60-2.8 (7.76) 4.2) 19.35 (3.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.05 (6.77-4.91 (7.29 (6.8 (8.9 (9.27-9.0 (11.75) 75th 4.56 (7.81) 2.23) 4.76-8.05 (3.43 (2.48-2.5-28.5) 9.9) 8.11) 10.78 (2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.2 (7.25 (3.14-13.90 (1.32 (2.6 (9.20-2.06-2.26 (6.9) 19.8) 12.78) 2.40 (2.13-6.76) 1.22-2.91-2.82 (3.63-15. interval) 2.06) 4.65-21. Fourth National Report on Human Exposure to Environmental Chemicals 115 .89-2.87 (3.50 (2.38-5.63 (<LOD-2.82) 2.66-4.95-2.

Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Lindroos L. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Kaus S. Toxicological profile for chlorophenols [online]. et al. Gregg M. July 1999.pdf. Wegner R.54(3):203-208.S. Burse VW. Falk C. Jarvisalo J. Toxicol Lett 2003. Baur X. Hanrahan L. et al. Aitio A. Hill RH Jr. Smith SJ. Szadkowski D. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .146:83-91. Int J Hyg Environ Health 2003. Available at URL: http://www. html. Int Arch Occup Environ Health 1991. Holler JS. Baker S. Anderson HA. S.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Pesticide residues in urine of adults living in the United States: reference range concentrations. Kohli J. Schulz C. Bailey SL. Seifert B. Environ Health Perspect 1998. Seiwert M. Luotamo M.gov/toxprofiles/tp107. December 2006 Draft. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Needham LL.18(4):469-474. Olson J. Fast DM.atsdr.71:99108. Domingo JL. Environmental Protection Agency (U. Jones D. Arch Environ Contam Toxicol 1989. 4/21/09 Agramunt MC. Poschadel B. Am J Ind Med 2004.EPA). Can J Biochem 1976. Safe A.63:57-62. Shealy DB. To T. Hill RH Jr. Environ Res 1995. Chlorophenol exposure in harbor workers exposed to river silt aerosols. The Great Lakes Consortium. 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]. Urinary excretion of chlorinated phenols in saw-mill workers. Needham LL. The metabolism of higher chlorinated benzene isomers. Domingo A. Available at URL: http://www.cdc. U.45:440-445.106(5):279-289.epa. Radon K. et al. Corbella J. Pekari K. Heinrich-Ramm R. Head SL. 206:15-24. Becker K.

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

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

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

37 (3.3) 17.290 (<LOD-.0) 10.40-16.0) 5.0 (5.4) 20.14) * * .03 (.860-2.74 (8.34-7.8-32.47) * * 1.981 (.13 (2.60) < LOD < LOD 4.530 (<LOD-2.1) 10.0) 6.0) 7.39 (8.07-10.20 (.620-1. and 0.80) 2.30-6.99 (5.50) 2.56 (6.81) 11.60) .750-1.2) 14.9) 8.810-1.8) 11.19) 9.5) 15.80) .58 (2.70) .89) 9.2) 16.20-30.70 (4.39 (3.9-18.71 (2.54 (3.71-9.33-18.20 (2. < LOD means less than the limit of detection.20-7.79 (5.70) < LOD < LOD 75th 3.0) 11.56 (1.954 (. and 03-04 are 0.4 (9.50 (4.10) < LOD < LOD 4.00) 3.29) * * 1.40-11.6) 18.70 (2.00-19.82-12.8 (14.890 (<LOD-2.0 (6.50-5.35-11. 01-02.0 (8.80) .290 (<LOD-1.0-27.02-5.4 (7.2.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.16) 4.60 (5.00-27.10 (.28) 1.93 (4.840-1.94) 3. which may vary for some chemicals by year and by individual sample. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (1.53) 4.15) 14.8) 19.40-14.33 (5.0) 10.74 (8.0 (8.2 (7.90) 3.7 (14.47) 5.0 (12.40-5.50 (2.60 (1.60-18.2) 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 1.85 (3.0) 9.2 (7.2 (11.27-3.80-22.600 (<LOD-1.91) 4.16 (2.56 (4.50 (.55-8.90-5.73) * * .90 (1.700-1.10 (2.20 (.35-16.80) 11.2 (7.60-25.12) 4.68-7.44 (2. see Data Analysis section) for Survey years 99-00.670-1.599-1.2 (9.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.04) < LOD 1.0 (6.8 (9.1) 13.42-3.00-7.02) 4.5-16.30 (2.63) 1.35-12.2 (9.97) 8.20 (.00 (5.5 (11.01) * * 1. 120 Fourth National Report on Human Exposure to Environmental Chemicals .623-1.98-5.21 (.50-36.0) 6.52-11.90-4.4 (9.79-7.61 (3.757-2.2 (14.67) 3.0 (9. interval) 1.56-13.10 (2.70) < LOD < LOD 1.26-6.0) 10.5-17.4 (7.0) 15.1-23.80-24.26-8.95) 5.0) 20.3) 16.70-14.6) 7.4) 17.86 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.5) 20.0) 10.00-12.76 (2.86-15.32) 1.82) 10.8) 7.36-4.758-1.22 (.48-7.05-7.1-17.2.9 (8.13 (2.34-3.80 (2.26 (5.70-23.8) 7.7) 11.72) 5.0) 6.0) 5.830 (<LOD-3.70-19.9) 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 1.00-12.5 (8.80 (4.45 (2.93-24.2 (14.2) 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) 12.90) 2.80) 2.23-5.0) 10.0) 5.0-28.3-15.7 (12.0 (7.10-7.40 (.30 (2.0 (7.52) * * 1.00-27.51) 2.97) 90th 7.43-12.0 (9.740-2.00) 3.80) 3.17-3.0) 11.780) < LOD 3.10) < LOD .490-2.44-38.12-19.2) 16.1) 95th 13.8 (12.80) 4. 0.83 (5.1.11 (.98-12.S.80-4.13-2.60-11.27-15.30-4.9) 14.57-7.81) 11.94) * * .32 (.80) 2.0) 11.30 (4.0 (8.579-1.717-1.0 (4.40-19.2-20.20 (.42) .08-15.61) 4.70-11. population from the National Health and Nutrition Examination Survey.55-6.46) 10.3) 14.38-5.0 (7.8 (8.52) 6.44-3.08-2.1 (9.00 (4.0) 11.955 (.15-12.20-4.1 (10.21) 9.0 (7.66) * * 1.58 (5.81) 1.10 (.4) 18.40-1.970-2.96-3.08 (<LOD-2.58 (3. respectively.

47 (1.25) < LOD .94-10.1) 4.549-1.1) 4.88) 2. interval) .996 (.85) 2.05 (.28-9.9 (5.2 (10.00-19.50) 7.64-5.34 (6.3) 12.574-1.45-5.34 (6.43) 2.1 (6.37 (4.47 (3.93-9.09-11.94-23.818 (.0) 6.4 (4.47) * * .27) < LOD 2.8) 6.79-9.87-5.79-3.03-6.89) * * 1.81 (1.860 (.500-1.80 (6.95 (3.87 (3.18 (.2) 9.960 (.00-17.74) 90th 7.94 (2.53 (6.10 (3.60) 2.06-2.93-5.S.88-10.9-28.83 (7.6 (9.3) 5.43 (3.75) 14.76-4.87 (1.94 (4.26) * * .37-5.2) 8.37 (5.440 (<LOD-2.09) 2.5) 8.77 (6.890 (<LOD-1.40-5.69) 4.8) 8.75) 2.68-4.780 (<LOD-1.10-13.00-13.4 (9.620-1.39 (2.41) .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.633-1.47) 2.95) 2.19 (4.47 (3. population from the National Health and Nutrition Examination Survey.84 (5.6) 11.62-5.6) 9.00) 8.84) 7.8) 12.3) 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 1.2) 13.830-1.04-6.58) * * 1.66 (5.9 (9.82-6.05) .67) 4.7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .46-5.1) 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 1.7) 18.29 (2.29) * * .98-22.5) 11.56) 4.40-14.2) 95th 12.98) 9.9 (9.920 (.54-2.41-12.3) 16.34) * * .5-16.07 (.31-14.40-12.0 (8.03) 2.5-32.9) 12.37) 9.8 (10.82-26.72) 11.54-15.88-15.820 (.66-15.69-10.55-20.7) 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.76) < LOD .5-20.66 (2.75 (7.7 (8.5) 12.60) * * .28 (5.98) .83) 8.05 (1.8) 16.02 (2.85 (6.2) 5.2 (8.1 (11.42) 12.44 (2.82-14.870-2.43 (.54-11.40-3.98) .69 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.81-5.32-12.98 (3.73 (1.54-4.98-5.74) 4.61 (1.773-1.37-3.7) 5.8) 7.53-11.40-28.790 (.21-23.23 (4.15-10.1 (8.56) .6) 8.28) 10.54) .03 (7.5 (4.93) 9.608-1.710 (<LOD-1.14 (3.34) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 121 .36) * * 1.04 (1.38 (1.92-2.7 (9.1-15.0) 7.560-1.00 (4.57) 4.890 (<LOD-1.540-1.40) < LOD < LOD 75th 2.71-2.5) 7.67-19.4) 4.9) 16.41) Selected percentiles ( 95% confidence interval) Total * * 50th .40) 4.45-5.69) 2.35 (1.89-3.66-34.924 (.9) 11.66 (1.5-13.75-7.7) 12.855 (.31 (3.932 (.61-13.62) .60-9.42 (3.35) < LOD < LOD 3.92-5.57 (6.71) 10.02-14.56-13.650-1.00 (4.1 (9.883 (.75 (3.38) .09 (.82-14.68) < LOD < LOD 3.61-29.45-11.6 (10.78 (2.02-2.40 (3.533-1.52) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (7.1 (10.25) 6.28 (4.570-1.6) 13.67) 1.20-8.2) 7.430-1.80 (2.80 (7.94-9.03 (2.80) 9.5) 7.57-10.51-5.566-1.4) 13.3) 15.88 (5.28 (2.02 (7.57 (4.900 (.750 (<LOD-1.510-1.23) 4.56) 7.13) 4.03) 2.4) 4.90-5.2 (6.7 (10.53) 9.01-2.94-22.960 (<LOD-2.90-8.30) 2.46) 2.30 (1.61 (1.2) 5.24-3.11-6.

90 (6.9) 16.S.12 (4.2) 14.3) 8.3 (11.67-10.16-1.7) 14.70-9.70 (8.80-3.01 (2.10 (<LOD-1. < LOD means less than the limit of detection.90) 4.75 (3.80) 5.0 (15.6 (10.31) 1.50-4.99 (3.52 (6.27) 9.80-14.790 (<LOD-1.8-20. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .15-6.670 (<LOD-1.3) 10.0-19.0) 18.20-4.8-17.0) 11.5 (9.9-15. population from the National Health and Nutrition Examination Survey.64) 10.70-9.80-4.5.24-5.40 (2.74) * * * * * 1.34-5.35 (6.95 (2.90-15.92-17.50) .34-3.80 (2.20-18.40) < LOD < LOD 75th 2.9 (12.0) 7.7-19.00-4.70 (1.45 (3.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .00-4.78) 5.3) 20.30) 3.86-10.80 (2.8) 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 1.81-6.63-14.06 (2.18 (3.0) 12.8) 8.80-6. respectively.70) 2.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.10) 6.0) 9.5) 21.4-17.18) * * * * * * * * 1.1 (10.90 (1.3) 14.8-20.4 (10.35-3.88) 10.41) 3.0) 12.3) 22.37) 2.11-6.95 (5.0-33.77-3.10 (.3 (9.47-6.90 (2.6-41.30) < LOD < LOD .00) 8.0 (13.92) 9.5 (8.61-32.90 (5.95-9.7) 22.70-8.0) 14.10-10.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) 7.9-14.90-9.20) 3.22-12.0 (7.80-8.1-23.00) 7.70-5.90-31.53 (3.3 (9.00-16.25 (2.80-21.5.7) 16.31-7.39 (5.61 (3.27 (3.1) 11.7) 15.6-19.6) 14.0 (9.3 (7.4 (10.90-15.0 (14.8 (12.00) 3.90 (6.680 (<LOD-1.98-9.80 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.84-4.90 (6.82) 8.27 (7.9) 9.49-4.0 (9.50-5.6 (10.7) 10.0) 19.90) 8.60) < LOD < LOD 2.40 (2.3 (6.58.9-17.20) .2 (7.80) .90 (2.00) 3.0) 13.2 (9.0) 11.970 (<LOD-2.5-26.00-9.33-11.90 (6.29) < LOD < LOD < LOD < LOD 3.5 (8.670 (<LOD-1.59-3.22 (6.77-14.73) 7.8 (12.20-8.60 (5.60 (6.27) 4. and 03-04 are 0.30) 3.670 (<LOD-1. and 0.14 (6.29-4.1 (10.0 (10.4) 11.0) 9.30) 8.10-4.58 (1.97-4.34 (6.8) 9.9 (7.50) 3.75 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0-24.00-18.9) 95th 14.51) < LOD 1.41-5.27) .4 (14.66) 4.80-12.42 (1.650-1.46-28.66-13.04 (3.00 (. which may vary for some chemicals by year and by individual sample.22 (6.0 (8.24 (2.35) 4.62-17.580-2.0-29.670 (<LOD-1.46-4.9) 10.3 (12.0) 6.7 (10.88) 3.39-13.22) 8.96) 90th 7.00-18.0 (10.80) .31-12.0) 12.15-2.7-21.10-15.0) 14.90 (2.0-24.740 (<LOD-1. 01-02.17 (7.00) < LOD .7 (11.67) 3.8-21. 0.89 (2. 122 Fourth National Report on Human Exposure to Environmental Chemicals .0) 13.50) 5.6) 11.0 (5.37 (3.0) 23. see Data Analysis section) for Survey years 99-00.96) 3.6) 18.6) 14.28 (7.34-10.910 (<LOD-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67) 4.30) < LOD < LOD 4.20 (<LOD-2.89) 2.72) 2.60 (2.20) 3.

940) < LOD < LOD 1.93 (6.2) 12.910 (<LOD-1.7 (11.93-10. Fourth National Report on Human Exposure to Environmental Chemicals 123 .44-6.950) .3) 8.68-19.99 (4.2) 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.12 (7.5 (10.32-8.68-4.7-23.45) 6.99) 2.1 (19.S.52-3.6 (10.78-10.29-2.4) 7.4) 7.03) 3.45) 3.6) 95th 16.9) 16.3-17.2-30.7) 14.3-15.89-10.78 (4.3) 9.2-15.28-12.54-5.4-16.2) 10.00 (7.21-21.68-10.94 (5.1 (8.6 (11.21) * * * * * 1.5-17.09-11.89 (3.69-11.7 (10.7-19.03 (2.00 (3.07) 2.72) 4.51-10.63 (2.50-17.29) 3.27-13.11-3.6) 6.6) 7.6-19.4) 9.30) 8.77 (2.42) 8.2 (9.27) < LOD .95) 90th 8. population from the National Health and Nutrition Examination Survey.25-9.38 (1.3-21.74-19.11 (5.3 (7.2) 15.6) 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 1.6 (13.0 (11.920 (<LOD-1.47-9.0-21.18) 2.58 (4.68) .2) 19. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .92) 3.04) 9.8 (10.34) < LOD < LOD < LOD < LOD 3.3-17.54) 9.12) < LOD < LOD 4.06) .42) 7.77) 3.6) 12.6) 14.54 (7.55) .34-18.67 (1.91) 3.6 (12.38 (.16 (3.00 (<LOD-1.67 (7.15) < LOD < LOD 75th 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.33-10.72-4.29 (5.28) 6.7 (8.38) 1.1) 10.83 (7.23-3.88-7.4) 6.2) 12.850 (<LOD-1.9 (9.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.5 (15.4) 7.590 (<LOD-.48 (2.8) 11.29 (2.7) 15.620 (<LOD-.2) 12.86-3.01-5.7) 9.8) 14.07-3.89-3.2) 16.0 (13.973 (.00 (<LOD-1.89) 5.0 (8.2 (9.530-1.71 (1.07 (5.3) 12.28 (1.78 (6.0) 14.63 (6.30) 7.94-14.37-5.6 (11.5) 8.00 (5.38-13.5) 22.96-10.78) 4.5 (8.88 (1.16-14.9 (9.5) 13.4-16.760 (<LOD-1.89-13.00) 8.74-4.8 (8.75-3.9) 19.27) * * * * * * * * 1.43 (2.0 (10.87 (3.06 (<LOD-1.41 (7.7) 14.97) < LOD .25 (4.75-3.85-8.27) 1.15 (1.53-8.4 (11.86) 9.32) 2.79-9.61 (2.96-11.05-3.2) 8.19) 3.00) 2.6) 13.73 (5.91-9.4) 15.7 (10.1) 13.33) 3.8) 16.02-4.0-19.70-2.14 (2.42-19.36 (2.97-4.71) < LOD < LOD 2.09-11.82-11.4-15.89 (2.03 (6.93 (<LOD-2.9-17.70-35.5 (9.690 (.00 (2.80) 3.79-6.7) 12.6 (13.5) 10.4-18.92 (5.30) 2.86 (3.81 (7.1 (13.39-17.1) 20.82-8.780-1.64-11.95 (2.3-34.55) 16.810 (<LOD-1.85-17.89-3.6) 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 * * * .37) 3.3) 6.95) 3.55 (2.38 (2.9-25.83 (6.9 (9.77 (2.30-5.20-3.51-7.27) 5.07) 2.50 (6.59-3.890-2.93 (2.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .5 (11.4) 16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

80) 3.780 (.550 (.10) 1.70 (1.22-2.89) 1.710 (.730) .83) 1.20-2.97 (2.30-3.570 (<LOD-.382-.50-2.353-.S.18 (.690 (.457 (.390-.592) * 50th .570 (.42-2.70 (1.840 (.14 (1.90) 2.30 (.00-4.830 (.970) 1.860) < LOD < LOD .77-2.45 (1. respectively.01-3.31) 95th 2.78) .54) .30) 1.95-5.380) .20) 3.34) 2.59-2.80) 5.810) .05-3.83 (2.88) 1.33-2.98) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 0.50 (1.30) 4.740-1.459 (.587) * * .930 (.15) 2.98-3.20) 3.336-.650-.16-3.76-6.570-1.35) 1.90) 2.94) .13) .30) 2.30 (.04) .89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.41 (2.600-1.260 (<LOD-.690-1.69-4.425 (.350-.09 (.30 (1.590-.820 (.87-3.455 (.80) 2.710) .73 (1.49) .14-1.440-.740-.720 (.58 (1.960 (.30 (.20-3.73-5.760 (.380-.19-1.94 (2.592-. interval) Selected percentiles ( 95% confidence interval) Total * .26 (2.16) 1.600-.90-4.70-2.37-2.20) 1.73 (2.80 (2.60) 3.950) 90th 1.11-3.09.61 (1.11-3.30-3.25-1.570 (.89) .95 (2.47) 2.30-1.570 (<LOD-.505 (.30) 4.780 (.39) 2.31-3.20 (1.680-1.960) 1.86 (1.29-2.86) 3.960) .720-1.10-1.960) .759) * .22 (1. and 03-04 are 0.1.27 (2.749 (.240 (<LOD-.80) 3.23-3.60) 2.490 (<LOD-.90 (1.13) 2.46-3.90) 3.210 (<LOD-.29) 1.49) 2. see Data Analysis section) for Survey years 99-00.690) .2.01) .450 (<LOD-.580-.64 (1.17) 1. and 0.47 (1.910) 1.20) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.96-3.910 (.79) .398-.510 (.680-1.930) 1.50) 1.16) 2.820 (.83) 2.46) 1.800 (.949) .22-8.04) 1.41-5.27 (3.549 (.657) * * .600 (<LOD-.343 (.00) 1.63 (1.17) 1.780) .359-.95) 2.03) 1.960-1. < LOD means less than the limit of detection.00 (1.350-.880) < LOD 75th .340-.740 (.08 (2.75-2.550 (.790 (.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 * .10) 1.400) .48 (1.720-1.50 (1.78) 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 * .970) .70-7.990-1.74-5.70 (1.710 (.940) < LOD .930-1.80) 3.380-.750) 1.57 (1.453 (.500 (<LOD-.388-.54-2.54 (2.930) < LOD .201-.700) .48 (2.750-1.80) 2.50 (1.510 (<LOD-.20 (1.21) 3.880) < LOD .17-4.32) 3.55 (3.40 (1.620-1.00) 2.585) * * .20-1.60-4.05-2. population from the National Health and Nutrition Examination Survey.40 (1.45 (2.18 (1.65 (2.910-1.76 (1.584) .22-3.59-6.580-1.20 (2.98 (2.303-.38) 1.15) 2.94 (3.670) .700) .77 (1.31) 2.83 (2.36-4.618) * .50-2.390-.68-5.50 (1.80 (1.540 (.83) .850) < LOD .10) 1.32 (1.740 (.10-1.08 (2.46 (2. 01-02.01-1.60 (2.57 (2.570) * .75 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.96-5. which may vary for some chemicals by year and by individual sample.10) 3.32-1.592) * .00-2.34) 2.690-.74) 3.91) 2.280-.20 (1.45-4.980) 1.50 (1.20-2.597) * .89-6.20) 2.160 (<LOD-.22-3.26) .449 (.880 (.460-.560-.20) 1.467 (.79) .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 * .45 (1.46 (1.31-3. 124 Fourth National Report on Human Exposure to Environmental Chemicals .

60) .370-.70 (2.71 (1.590 (.88) .510 (.444-.630) * .318-.02-3.92 (1.485) * * .69 (1.285-.480-1.25-3.180 (<LOD-.560-.680 (.760) < LOD 75th .700 (.07) 1.00-1.17) 2.08-3.730) .23) 1.73 (2.64 (2.60 (1.500-.980-1.710 (.02-6.645) .690) < LOD < LOD .49 (1.61 (3.88 (1.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .447 (.66 (2.32) 1.07) 1.32 (.98) 1.920) .720 (.72 (1.335-.368) * .840) 1.270-.67-3.372 (.412-.305 (.580) .310 (<LOD-.250 (<LOD-.800-1.08-3.790) .84-6.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.550) .950-2.42-8.710 (.739) * .380-. Fourth National Report on Human Exposure to Environmental Chemicals 125 .24) 4.07-2.43 (1.640 (.23) 2.17) 2.530 (.310 (<LOD-.47-4.710 (.62 (1.75 (1.38-3.320-.75) 6.597) * .270-.73-3.75-3.39) 2.590) * 50th .38 (2.270 (<LOD-.00 (3.300-.22-3.14 (2.380-1.61-3.89-3.760) .57-4.58 (1.18-2.32-1.740) < LOD 1.591 (.510 (.688) * .840) .36) 3.990-1.22) 4.910) < LOD .670 (.520 (.310-.57 (1.22) .61) 2.62 (2.89 (1.22) 1.16) 1.08 (2.60 (2.87 (2.750 (.11) 1.75 (2.08) 1.330 (<LOD-.64 (2.04-1.30-2.17-2.23) 2.S.22 (2.82 (2.870) .640 (.34 (1.65) 2.10) 2.08-2.72-4.550-1.22-3.77-3.16-1.70 (3.448 (.870 (.700 (.552 (.92-8.50) 1.32) 5.740) .393 (.30) 3.580 (.403) .850) 1.320-.63 (1.590-1.66) .97) 1.750 (.471-.72) 1.44) 2.470 (<LOD-.330-.07-3.77-4.880) 1.97 (1.55-3.300 (<LOD-.08-2.790 (.560 (.460 (.43) 1.940-1.76) 1.550-.28 (1.540-.61-3.348-.800) < LOD .23 (.136-.38 (1.50 (1.72 (2.53) .16-2.67) 1.930-1.350) .03-1.99) 1.390-1.80) 2. population from the National Health and Nutrition Examination Survey.07 (.47 (1.234 (.09) .19 (1.13 (1.560-.52 (1.29-4.460) .57-2.08-3.72) 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 * .06) 4.44-2.92) 3.41 (.79 (1.84 (2.33 (1.509 (.33) .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.57 (3.67 (1.830) 90th 1.453 (.00-3.78) 3.460-1.720-1.08-3.390) .840) 1.510-.535 (.05) < LOD .39 (1.03-2.400-1.06-2.830 (.742) * * .580-.515) * * .58) 3.97) 2.69 (3.04-5.250 (<LOD-.42 (.47 (1.470) . interval) Selected percentiles ( 95% confidence interval) Total * .700 (.02-3.05 (1.95) 1.20-2.91 (1.79) 1.42) .55 (1.07) 1.08 (.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 * .05-2.20) 1.04) 95th 2.97 (1.45 (1.58-6.280 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20-7.71) .11 (.377-.480) .42-6.640 (.660-.05) 1.05-4.253-.67) .77 (3.380) .49-4.82) 2.99) 2.71) 2.400) .820) 1.43) 2.22-2.820) .43) 2.94) .230 (<LOD-.11-2.31-1.23) 3.67 (1.490 (.32) 2.520-.81) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08) 2.60) 1.90) 2.900) 1.550-.07) 5.45 (2.08-2.52) 3.440-1.

80-2.4 (19.21 (3.1) 38.10 (1.65 (4.0-58.12 (3.54 (1.3) 28.83 (3.92) * 2.6 (11. and 03-04 are 0.13 (1.41) 1.04-8.40-16.7-41.49-2.0) 3.35-6.3) 31.600-2.90) 11. see Data Analysis section) for Survey years 99-00.0-41.9 (10.74-2.26) 75th 11.9 (23.830-3.80) < LOD 1.0) 8.0) 33.9-21.0 (26.10-13.2) 31.0 (32.0) 28.0-62.0-62.0) 30.32 (2.71-2.0) 6.06 (1.71) 5.0-31.59 (1.81-2.0) 31.18) 6.830-4.30 (.3) 26.9) 17.0-52.33 (5.2-27.02 (2.98) * 2.1 (26. respectively. which may vary for some chemicals by year and by individual sample.5 (24.0-53.0) 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 2.70 (.0) 15.41) 1.12) 1.50 (2.0) 20.10) .48) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.46-2.45) 2.20-4.70 (1.40) < LOD 1.0 (20.9) 38.0 (38.3 (12.26 (.9) 18.67 (1.30-14.70-17.81-3.40) 50th 2.1 (25.7) 20. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.88) 1.76 (2.20 (2.0 (25.80) 90th 38.41 (1.3 (14.0) 16.1-20.0) 28.61 (1.82 (1.8-24.8) 62.92-5.9) 48.41-4.13 (1.0) 45.70) 1.70) 1.530-4. and 0.7) 47.5) 69.0) 4.0-53.0) 5.6-54.0 (17.53) 40.1 (25.1) 140 (46.0) 32.30) 11.8) 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. 01-02.2 (12.00-24.30) 4.95 (5.90-8.97) 6.1-40.0 (20.80) 1.2-62.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.1-25.46 (.10 (7.69) 2.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-110) 34.0 (6.06) * 2.1-19.0 (38.0 (37.1) 95th 48.91 (4.10 (1.70-6.0) 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 2.25-3.10) 39.11 (4.44) 3.9-51.0-29.50-17.0-39.2 (19.0) 4.18.0 (8.0-41.23-2.14) 5.4-76.71 (4.54 (3.2-26.43-7.77 (1.63-6.60 (2.52 (4.77) 38.0-230) 35.05) * 2.0-50.4.04 (<LOD-2.79 (2.99 (2.1) 38.93-3.42) 1.50-7.0-47.40) < LOD 2.09 (4.2-27.0 (38.00 (.36-2.83 (1.3) 38.8 (12.44) Selected percentiles ( 95% confidence interval) Total * 2.87-7.44) 2.85) * 2.610 (<LOD-1.0) 18.45) 2.5-74.0-49.11) 2.0) 16.90 (1.4) 38.8) 32.1-47.0) 20.6) 52.0-43.88) 3.2-47.2-80.0) 15.4-22.0 (11. interval) 1.6-22.0) 42.20) 1.58-2.50-5.18) 14.6 (26.21 (4.3 (24.0 (21.98 (1.9 (19.0 (38.29-9.0 (24.660-2.64-3.0 (38.58) 16.5-45.59 (1.1) 18.50-20.70) 5.85 (1.70 (7.0) 3.0-58.31-6.90 (1.29-4.72 (1.9 (27.0) 17.57-2.8) 39.70 (1.0 (19.0 (13.78) 9.0-39.05) 1.6 (15.0 (38.27-6.5-20.7-22.86 (1.18) 20.0 (7.8-21.690-3.07-5.5-27.7 (12.10 (1.19) 2.6-45.5-40.23-2.86-3.470 (<LOD-1.4) 19.0 (8.1 (10.53) 1. < LOD means less than the limit of detection.80) .60) < LOD 1.9 (19.0-110) 42.23) 9.6-27.83-2.8) 41.5.0-260) 34.16) 2.3) 33.4 (10.13) 12.96) 5.2-33.2) 16.1 (22.3 (12.6 (9.48-2.10-4.0) 3.16) * 1.79-2.83-2.8 (12.10 (1.46-6.0) 17.48-2. population from the National Health and Nutrition Examination Survey.0) 4.41) 5.75-14.0-41.2-39.8 (22.3 (10. 0.94 (1.19-2.64-8.05-3.5) 30.53 (1.S.79 (1.76 (2. 126 Fourth National Report on Human Exposure to Environmental Chemicals .21 (1.1 (11.0 (8.0) 3.17-2.57-2.1-46.80-18.00 (.40-4.8 (26.0) 19.7 (12.0 (40.0) 13.7 (28.53) * 2.04) 3.0-69.4 (15.44-7.29) 2.0 (33.78 (1.0 (38.3 (23.50-2.66-5.0-92.61-2.

6) 19.88 (4.0 (23.670-1.2) 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 1.52-4.2) 4.0) 13.62) 4.07-2.2 (9.23-1.95-16.5 (34.6-51.45 (1.28) 1.40-7.2) 41.12) 3.67-16.76-2.7) 61.8) 31.95) 90th 32.5) 27.52 (1.96) 2.4) 12.3-27.3-42.33) 1.870-3.7-43.1) 25.40-4.83 (.6) 3.39 (1.8-43.5-36.8-26.S.1 (34.38-1.1) 27.27) 10.14 (.7-37.2 (22.2-70.19 (1.4-39.2 (16.71 (1.9 (26.860 (<LOD-1.0 (6.02) 1.870-3.37 (1.5 (17.75-6.9 (10.82) 1.4) 3.7 (24.19) 5.930 (<LOD-1.6-32.5 (41.7-38.14-8.7) 30.5-97.6 (24.36) 10.6 (7.1-63.07) 9.00 (4.4) 12.86) * 3.8) 23.0-70.22-2.1 (33.4-34.68) 47.23) 37.18-1.43-2.17) 2.9) 24.67 (1. Fourth National Report on Human Exposure to Environmental Chemicals 127 .3) 28.86) * 2.0 (25.0) 3.16 (1.2-47.4-71.0) 48. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.888-1.16 (1.32 (3.7-20.9) 24.58-17.9-18.6) 11.79-17.11) < LOD 1.9-37.46-22.8) 3.48) 1.66 (1.38-5.91 (6.22 (2.22-3.54-15.75 (1.27 (6.2 (21.20-5.71-2.1 (12.4 (11.0 (19.26-4.19) 5.18) 3.3 (8.06-1.6) 3.0-118) 29.9) 3.70 (1.2 (8.46-5.35 (2.61 (1.0 (17.46-6.02) * 1.58-2.9) 54.51) < LOD 1.1 (39.1) 13.7 (10.68 (1.3 (10.02 (.6) 23.1) 52.35) 1.56) 1.2) 13.9 (7.67-3.26-2.1) 15.1 (25.08) 1.63-5.7-19.8) 11.4-21.33) 2.67 (1.0-40.4 (21.38 (3.00) 1.1) 25.3) 13.8-37.9 (13.00) 6.93) 5.1) 17.5-43.35) .28 (1.2-34.7 (18.5-190) 30.88 (1.4 (19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 66.0 (39.43) * 2.7) 23.1 (50.3-22.0) 47.84-13.71) 8.95-16.53) 1.8-45.47-17.7 (18.20) Selected percentiles ( 95% confidence interval) Total * 1.50-5.4) 14.4 (5.870-3.57) 4.9-52.33) < LOD 1.5 (6.51) .7) 26.03-2.4 (9.08 (1.9) 3.94-20.61-22.25-3.2) 13. interval) 1.3 (20.80 (1.30) 28.680-4.16-2.0 (14.06) 1.54-2.7) 15.36 (4.70-4.6) 7.2 (15.59-2.3 (9.01 (.95 (2.7-47.0) 30.90 (.23) < LOD 2.2) 36.5 (15.33-5.91-2.8) 32.6-38.69-18.6 (11.4 (12.75 (1.9) 12.9-41.4 (25.24 (1.6 (27.66 (1.96-16.1) 27.19-6.88 (1.97 (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.60 (.19-14.5 (8.9-36.9 (39.8) 15.0 (23.750 (<LOD-1.31) 2.99-4.4-67.2-28.43-12.27-3.7 (11.7-109) 22.41 (2.64 (1.2) 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 2.57 (6.47 (1.21 (4.6-49.16 (1.2) 33.03) 1.29-5.6) 112 (40.22 (.3-19.82 (2.40 (5.8 (7.4 (25.17-3.27) 50th 2.37-2.18) * 2.83) .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 1.1-60.1-22.3 (10.899-2.45-1.06) 75th 9.69-5.94) 19.55 (2.2-38.9-95.62 (2.5 (13.0-71.0) 25.46) 1.7) 95th 51.00-16.59-15.47 (3.72) 2.8-34.48 (4.12 (1.94) 1.38) 5.60) 4.59-2.09 (5.56 (2.15 (.75) * 1.11-2.1) 13.32-3.61-2.07-2.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.50 (2.9 (19.34) * 1.88 (4.40 (2.80-8.5 (15.06) 1.0) 10.0 (32.79 (2.5) 70.7) 34.1) 36.44) 9. population from the National Health and Nutrition Examination Survey.66) 8.36-13.890-4.

770) < LOD 95th .171) * * .084-.190 (.120 (<LOD-.420-.720 (.090 (<LOD-.300-.140-.32) .15) .130-.310 (.430 (.240 (<LOD-.850) < LOD .58) .700-1. see Data Analysis section) for Survey years 99-00. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140-.280) < LOD < LOD < LOD < LOD .13) .700-1.870 (.42) .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 * * * * * * .160-.740) < LOD .640-1.090 (<LOD-.S.600 (.30) .330-.120-.690-1.090 (<LOD-.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 .560 (.610 (.40) .450 (.840) .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 * * * * * * * * * .30) .620 (.290 (<LOD-.360-.310) < LOD < LOD < LOD < LOD .080 (<LOD-.1.12 (.770 (.410-1.1.540 (<LOD-.870 (.820 (.630 (.390 (.310) < LOD < LOD < LOD < LOD .640) .570) .470 (.230) .190 (.440-1.20) .050-.410) < LOD < LOD < LOD < LOD .990 (.60) 1.990) .210 (.310-.410-.450 (.130-.860) .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .42) .170-.430-.090 (<LOD-.10) .380-.30) .090 (<LOD-.990) .720-1.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.320-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .090 (<LOD-.120-.180) .640 (.780) < LOD 1.850 (.260 (.03) .162) * * * * * .360-.760) < LOD .560 (.840) .130 (.650-1.200) < LOD < LOD .140-.610 (. respectively.610-1.150 (<LOD-. 01-02.700-1.190 (.540) .300-1.650) .450 (.290) < LOD < LOD < LOD < LOD 90th .110-.870 (.370-.130-. population from the National Health and Nutrition Examination Survey.490 (.830) .470-1.400-.680) .080 (<LOD-.130) .650 (.530-.900 (.870 (.00) .610-.220 (.730-.680 (.460-.270 (.230-.460 (. 0.380-.370-.410-.730) .720) .860-1.100 (.140) . which may vary for some chemicals by year and by individual sample.540) .870 (.10) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660 (.10) .940 (.350) .850 (. and 0.680-1.630 (.700-1.350) < LOD < LOD < LOD < LOD .550) .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.640) .117 (.830 (.05.160) .650-1.380-.150) .160) .390) < LOD < LOD .310 (.680-1.830) < LOD .820 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .290) < LOD < LOD < LOD < LOD .130) .930 (.36) .830 (.650) .099-.510-1.320 (. < LOD means less than the limit of detection.220 (<LOD-. and 03-04 are 0.10 (.870) < LOD .210 (.

410-.220) < LOD < LOD < LOD < LOD .780) < LOD 1.720 (.14) 1.080 (<LOD-.730) .360) < LOD < LOD < LOD < LOD .260) .330-.330-.380-.570 (.230) < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .940) .700-1.330 (.140-.070 (<LOD-.490-1.380-.890 (.01 (.02-1.03 (.650) < LOD .78) .730 (.300-.550 (.410 (.00) < LOD .730) .760) .740 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.580 (.330-.100 (<LOD-.140) .66) 1.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .450 (.540 (.280) < LOD < LOD < LOD < LOD .540 (.161) * * .880-1.60) .S.080 (.03 (.24 (.100-.090 (.62) 1.116 (.24) .440-1.500 (<LOD-.230-.110) .410) < LOD < LOD .550 (.580 (.111) * * * * * .800-1.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.170 (.450) .270 (.110) .440 (.170) < LOD < LOD .58) 1.410 (.400) .250-.67) .220 (.670 (.400 (<LOD-.260-.080) .860-2.050 (<LOD-.03 (.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 * * * * * * .390-.38) 1.810 (.43) .86) .270) < LOD < LOD < LOD < LOD .190-.750) < LOD 95th .084-.300 (.36 (1.640) 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 .120) .960) .190 (.060-.660-1.740) < LOD 1.990) .03) .110) .140-.320 (<LOD-.340-.940) .057-.170 (.780 (.540) .200 (.300-.850 (.410) .610-1.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.120) .700) .580) .180-.460 (.390-.230 (<LOD-.070 (<LOD-.110-.700 (.330 (.360 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .380-1.580) < LOD .310) < LOD < LOD < LOD < LOD .730) .500) .090 (<LOD-.110) .880 (.150-.990) .380 (.09) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600-1.070 (<LOD-.710-1.860 (.190 (.210 (.380-.410-.370 (<LOD-.860 (.510-.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 * * * * * * * * * .02) .570-.240-.360-.290) < LOD < LOD < LOD < LOD 90th .870) .670 (.360-.140-.560 (.640-1.470 (<LOD-.670-1.700 (.19 (. population from the National Health and Nutrition Examination Survey.12) < LOD .140-.200 (.970) .570-1.20) 1.500-1.140-.070 (<LOD-.600) .520-.580-1.86) .29 (.650-1.720 (.

00) 1.0 (4.18) 1.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .30) .30-3.00-17.3) 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 * * * * * * * * * .35) 11.0 (5.870) < LOD < LOD .590 (.67) .67 (2.770 (<LOD-1.36-3.51 (2.55-8.53 (2. < LOD means less than the limit of detection.46 (1.03 (.85-3.30-6.0) 2.0) 4.90) .11) .70-17.40 (1.960 (.840 (<LOD-1.910) 2.800-4.90-37.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0) 3.60) 1.580 (.730 (.250 (<LOD-.0 (7.11 (1.48 (2.6) 5.425-1.330 (<LOD-1.840 (.0 (17.86) 4.350-.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.40-4.01) 5.S.28) 1.49 (1.0) 5.770) 2.05 (2.70-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-30.80 (4.0 (5.720) 2.14) .24-7.20 (1.0-40.0) 7.43-4.691 (.0-38.260-.90-28.14) 2.30-7.52 (1.63 (3. 01-02.35-10.31) .12-1.49 (1.170-1.0 (17.360-1.99) 11.370-.90-20.350-.10 (3.55-4.07-3.30 (1.15) 19.0 (5.59-5.65) 1. 0.83-3.20-4.66) 4.40 (1.39) .82-4.10 (3.0) 4.00 (1.07 (3.42) 2.640 (.610 (.0-44.00) .32 (1.850) 16.28-9.07-3.52 (1.00) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (5.12) * * * * * * * * .0) 4.0 (17.94-3.52) 5.47 (3.0 (13.890 (.0) 5.800) 17.74) 5.48) 13.190-1.1.61 (1.40-7.0-39.400-1.30 (.10-3.40) 1.480-.750-2.70-7.960 (<LOD-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.900 (.14-5.0 (16.36-3.45 (2.0) 2.0) 5.0) 2.83-3.0) 2.0 (4.880) 5.080-1.51-8.97) 20.42) .0) 2.20 (1.0 (17.76 (1.10-3.20-17.99 (1.0) 5. and 0.74 (3.60) .15) 14.13 (3.11) 13.640 (.30 (2.83) 2.94-8.23-6.35) 5.07 (1.210-1.29-10.05 (3.30 (1.0) 4.49) 17.90 (1.40) 2.31-10.88-3. population from the National Health and Nutrition Examination Survey.28) .62-8. 130 Fourth National Report on Human Exposure to Environmental Chemicals .39 (2.1.53-7.07) 1.20) < LOD < LOD < LOD < LOD < LOD 1.70-50.00 (.87) 12.38-3.0 (5.07 (3.00-17.0 (3.620-1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.08.20-4.50) 2.40-20.32-9.510-.90 (2.90-9. which may vary for some chemicals by year and by individual sample.53) 20.94 (1.690 (.33 (4.0-40.90) .40-8.10 (.600 (.380-.840-3.96 (1.30) 95th 19.0-38.800) 90th 13.68) 2.97) 20.99) 19.830 (.0 (17.0-38.87) 5.50) .0) 2.10-9.750-1.0) 2. respectively.30 (1.90) .610) < LOD < LOD < LOD < LOD < LOD 2.0 (6.740 (.21-3. and 03-04 are 0.26 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.70) 2.67 (1.37) .05-3. see Data Analysis section) for Survey years 99-00.21) 3.63) 32.110 (<LOD-.

47) 5.47-10.840-3.96-8.74 (2.55) 21.02) .18) * * * * * * * * .40) 1.96) 2.48-7.940-4.86 (3.5) 2.33-3.84) 9.33 (3.7) 5.57 (.66-47.88) 17.98 (4.670 (.320-1.64-4.53) .700) 6.80) 3.8) 2.32-6.64) 30.11-5.88 (2.260-.700) < LOD < LOD < LOD < LOD < LOD 1.960 (.03) 2.4-34.340-.0) 4.90-6.67-6.540 (.33-5.830-3.01 (1.00-19.580 (.57-40.32) 9.67) 1.15) 9.13 (2.31-7.65 (2.1) 2.370-1.970-3.14 (1.03) 16.780-4.40 (.48-42.62 (1.474-1.27 (2.60 (1.50) 11. Fourth National Report on Human Exposure to Environmental Chemicals 131 .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 * * * * * * * * * .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.29-4.1) 672 678 497 509 694 551 595 947 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.9) 5.1 (7.71 (.92 (2.3) 3.11) .340-.96-25.56) .67) 2.69) 2.77 (.730-3.5) 7.10 (2.51-4.56) 2.5) 2.770) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.820) .620-3.85-3.37) 4.5 (11.24) 3.82-11.8) 4.09-3.56 (1.28-6.260-. population from the National Health and Nutrition Examination Survey.22) 2.12 (4.660) < LOD < LOD .67 (2.23-7. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.540-1.25-9.04-16.560 (.40-12.748 (.600 (<LOD-1.8 (20.07-21.18) 1.97) .190-1.710 (<LOD-1.44-11.48 (4.5 (8.88 (.50) .500 (.29 (4.08) .83 (4.2 (8.83-11.790 (.360 (.830 (.7 (12.57) 1.5-40.02 (1.580-1.800-2.S.4) 2.650) 90th 10.50 (2.690-5.8) 2.40-2.39) 20.38 (2.18) 95th 21.7) 3.47) .69-7.270-.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 * * * * * * .630-1.91-4.04 (1.55) 21.14-6.33-4.73 (4.50 (4.340 (.8-33.9) 6.370 (.240-.21-3.590) 2.75) 5.55 (3.470 (.5 (9.80 (.05) .53) 27.330-1.41 (4.59 (1.4 (4.88-3.10) 2.81-17.1 (5.150 (<LOD-.41) 18.35 (.79 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06 (.31) .370) < LOD < LOD < LOD < LOD < LOD 1.850-3.12-4.52 (.340-.89 (2.790) 11.3) 2.10-3.0 (4.44) .47-10.31-18.930) .8) 7.31) .22-27.30 (4.740-1.890 (.0 (9.02-4.820 (.2-38.17) 5.86) .860-2.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.390-.00) .7) 4.02 (.430 (<LOD-.8) 7.85 (1.580) 1.430) 1.62-17.450 (.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 .7 (6.25-38.250 (<LOD-.33 (1.57) 8.07 (2.580) 16.43) .25 (1.8) 1.7) 6.45 (1.310-.17 (1.49-2.9 (11.51-44.71 (2.36 (.270 (<LOD-.650 (.91) 2.

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Stokes L.338(8761):223-227. Wickremasinghe AR. Salvini S. Tumino R.2000 and 2001 market estimates.332(1-3):71-80. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Weerasekera G. Hansen S. Neurotoxicology 2005. Aprea C. Johnson C. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Washington (DC). Arch Environ Contam Toxicol 2000. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Keifer M. Petchuay C.43(1):38-45.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Occup Environ Med 2001. Dinoff TM. metabolite clearance. Bull Environ Contam Toxicol 1994. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Buccafusco JJ. Robson MG. Jamal GA. U. 1991. May. EPA). Kidd M. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. National Research Council (NRC). 2004.44(4):352-357. Chrislip D. Scherer J. Hore P. Available at URL: http://books. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. A behavioral evaluation of pest control workers with short-term.114(5):691-696. Pilkington A.52(2):190-195.113(4):504-508. Weisskopf C.epa. low-level exposure to the organophosphate diazinon. Neurotoxicol Teratol 1998.52(10):648-653. Keefe TJ. Takamiya K. McConnell R. Environ Health Perspect 2005. Masala G. S. Claypoole K. Rosenstock L. Levy LS. Rohlman D. J Toxicol Environ Health A 2005. Prendergast MA.nap.30(2):98-103. Stephens R. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Seiber J. Phillips J. J Occup Environ Med 2002. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Muniz J. The Pesticide Health Effects Study Group. Frasca G. Arch Environ Health 1988.php?record_id=2126&page=1. discrimination. Beach J.12(2):134-141. O’Malley M. Saieva C. Schenker M. et al. Berry H. Sci Total Environ 2004. Russo J.345(8958):11351139. Occup Environ Med 1995. Chronic neurological sequelae to organophosphate pesticide poisoning. Rothlein J. Caltabiano LM. Effects of long-term organophosphate exposures on neurological symptoms. Gladstone EA. McCauley L. Ruberu DK. Scand J Work Environ Health 1998. Lu C.24(1):18-29.pdf.26(2):199-209. Pesticide industry sales and usage . and spatial learning in monkeys and rats. Occupational exposure to organophosphate pesticides: a neurobehavioral study.12(2):153-172. Irish RM. London L. low-level organophosphate exposure on delayed recall. Environ Health Perspect 2006. Pesticides in the Diets of Infants and Children. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Calvert IA. Office of Prevention Pesticides and Toxic Substances. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Lambert WE.84(5):731-736. Stark A. Bravo R. Thompson ML. Daniell WE. Ames RG. Barr DB. Int J Occup Environ Health 2006. Rothlein J. 4/7/09 Young JG. Lancet. Lancet 1995. 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. Spurgeon A. Myers JE. Effects of chronic. and cholinesterase status of date dusters and harvesters in California. Santana J. Am J Ind Med 1987. Washington (DC): U. Buchanan D. EPA. Pedersen L. van der Hoek W. Samuels S.S. Lewis JA. Bradman A. National Academy of Sciences. Marshall E. Available at URL: http://www. Malathion deposition.68(3):209-227 Maizlish N. Gillham R. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Vitayavirasak B. Eskenazi B. et al. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Nell V. Lasarev M. Lasarev M.edu/ openbook.20(2):115-22. Arch Environ Health 1975. 1993 [online]. Muniz J.58(11):702710. Am J Public Health 1994. et al. Steenland K. Jenkins B. Environmental Protection Agency (U. Visuthismajarn P. Savage EP. et al.38(4):546-563. vibration sense and tremor among South African farm workers. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Burcar PJ. Narang A. Mounce LM. 1/12/09 Peiris-John RJ. Rodnitzky RL. Heaton RK. Neurotoxicity among pesticide applicators exposed to organophosphates. Smit LA. Terry AV Jr.S. et al.

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. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.5. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. parathion and methyl parathion are metabolized to para-nitrophenol. For general information about the organophosphorus class of insecticides. For example.6-Trichloro-2-pyridinol (6515-38-4) 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol 2-Isopropyl-4-methyl-6-hydroxypyrimidine (2814-20-2) Malathion dicarboxylic acid (1190-28-9) para-Nitrophenol (100-02-7) 2-(Diethylamino)-6-methylpyrimidin-4-ol/one 134 Fourth National Report on Human Exposure to Environmental Chemicals . In addition to reflecting exposure to the parent insecticide. malathion is metabolized to malathion dicarboxylic acid.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3. the level may reflect exposure to the environmental degradation products of these pesticides.

0) 14.20 (2. staying bound to soil particles.70 (1.0 (13.40 (5.62-2.40-13. For instance.9) 697 660 521 701 602 947 Limit of detection (LOD.40 (5.0) 12.55-5. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.1) 5.97) 4.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.97) 7.95) 7.50 (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 1.60 (2.9 (9.40) 9.20-2.1-16.9) 11.95 (4.7) 9.0) 10.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.79-2.90 (1.90-2.47-11.70-5.0) 7. It also has been applied directly on animals to kill mites.72-4.91 (1.47-13.00-24.53 (1. chlorpyrifos was no longer registered for indoor residential uses in the United States.30-5.68 (7.44 (3.97) 2.22 (1.000 pounds are used per year.90-7.00) 1.30-12. and sprayed to kill mosquitoes. Estimated intakes from diet and water have not exceeded recommended intake limits.51 (1.80-10.9-18.0 (7.28) 2.86) 4.09 (2.74 (1.00) 2.77) 1.36 (4.7-23.77-6.0) 9.37 (1.40-2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.0) 10.80) 2.S. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 12.51) 1.4 (9.8-15. in 142 urban homes and preschools in North Carolina.09 (3..4-15.70-15.02 (7.10 (1.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.21) 3.20-16. Chlorpyrifos is Urinary 3.20) 2.25) 3.0) 10.71 (2.4 (8.77 (1.30 (4.70-17.9 (7.0 (7. applied to structures to kill termites. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60-2.13-3.59-2.10 (5.05) 1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.29-1.80) 12.66-4.16) 2.38 (3.37 (4.76 (1.02) 1.8) 9.15 (1.87-6. Approximately 21-24 million pounds per year were used domestically from 1987-1998.71 (6.0 (7.90) 7.3 (10.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.02 (1. After 2001.EPA.39-2.8) 10.40-26.26) 7. 2007).32) 2. pre.EPA.4 and 0.17 (1. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.03) 1.39) 4.4.70-11.50-2. and dust.5.50 (1.20-3.30-9.0 (9.92 (1.50 (2.05-5.70) 1.30-1.88 (1.72) 2.67 (1. and is infrequently detected in ground water (IPCS.7) 8.3 (8.64) 3. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.S.60-3.67 (2.70-16.61) 75th 3.96) 3.20) 10.90 (3.97) 2.90 (6.S. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 135 .04-10. 1999.5 (8.35) 2.5.30) 5. dermal.47-9.20) 2.0 (7.0) 12.20 (4.0) 12.40) 2.83) 1.0) 18.50-14.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.32-1.0) 8.00-8.89-2. The general population may be exposed to chlorpyrifos via oral.80 (7.10) 2.43-2.0) 11.80) 4.90 (1.40-10.30) 4.0) 12. Approximately 80.94 (4.43-2.77-15.50-4.19-3.68-2.10 (4.59) 2.89 (2.67 (2.50-2.50-8.24-3.60) 5.0 (7. 2921-88-2 Chlorpyrifos-methyl CAS No.47 (4.61 (1.57 (2. It has low leachability.40 (6.60 (5.44-5.30-2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.66-15.80-8.10 (3.91) 16.50 (2.35) 1.29) 90th 7. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators. USGS.71 (1. and inhalation routes.0) 6.50 (2.99-4.81-2.4 (10.10-17. Exposure can also result from contact with contaminated surfaces.76 (1.5-24.04-10.45 (1.0 (10.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.22) 2.80 (1.7) 13.10) 6. but can be detected in streams receiving runoff from application sites.13 (1.30 (2.25) 1.24-1.90) 3. air. 5598-13-0 General Information The chemical 3.90-4.60 (4. Survey Geometric mean (95% conf.63 (8.30 (2.84) 1.5) 7.61-7.6) 7.3 (11.60-4. 2005).27 (7.19 (1. 2002).28-3.2 (10.0) 8.60-3.52-12.30) 4.78 (7.74-9.44-2.51-2.20-4.46-2.47) 1.80) 1.52-2.20-11.and post-construction structural applications for termite control were to be phased out by 2005 (U.63 (2. and on plants for days to several weeks.20) 4.20-14.00) 3. interval) 1.90-8.0) 15.01) 1.31-2.70 (1.3) 8.50-4.63 (1.50-5.90 (2. 2002).98-15.9 (10.37) 5.34) 1.0-28.31-2. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.30-11.97-7.

86 (1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.14-8.89) 4.90-9.19) 6.S.93) 2. 2006.51 (1.85) 4..49-2.93) 5.42-2.20-1.43 (4.23) 14.30-4. neurotransmission.09-3. Howard et al.97) 3.88 (1.01) 3.24-24. 1984).24-4. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.81 (3.39) 6.5) 5..82) 8.82 (3.91 (3. and other metabolites.47 (1.49-2.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.2) 6.0) 12.66-11.56 (1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.99) 1.12) 1.92 (1.1-21.21-6.59-2.34-1.58) 1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.31-1.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.24 (1.35) 1.97 (3.3) 9. vomiting.42 (5. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.940-1. Survey Geometric mean (95% conf.24-1.0) 10.12-1.45-1.00 (7.76 (3. Betancourt et al.30-1.0) 16.07) 1.00) 1. Metabolic hydrolysis leads to the formation of TCPy.39 (2.45 (1.22) 1.66 (1. weakness.11) 7. cholinergic effects.05-1.88) 6.47 (1.91) 1.44 (5.72-2.71 (1.91) 10.01) 3.95 (1. interval) 1.44 (1.64-7.93 (2.37 (1.22 (4.79-13.S.33 (5. TCPy can also occur in the environment from the breakdown of the parent compounds.66) 1.63 (4. Slotkin et al. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.80-6.88-8.85) 1.24) 75th 2.7) 7.57) 2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.8) 9.31) 1.65-15.06 (1.75 (1.11 (2.21-1. 2005.28) 2.02) 7.19) 3. Roy et al.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.97 (2.35-1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).85 (2.92-2.91-13.09-2.64 (1.25-11.15 (4. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.03) 1.54 (2.75) 6.86 (1.76 (2.3 (7.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.00-13. and producing acute symptoms such as nausea.82 (2.85 (3.57-2.19-1.83-11.71) 3.87-3.27-7.26-14.09 (1.39-1. Based on animal data and human cholinesterase monitoring during occupational exposure.91 (4.49-2.6-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 addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.80-11..33 (1.55 (4. 2000).56 (4.55) 1.47-2.22 (6.43-10.80) 3.49 (1. 2006a.27-1. Ricceri et al.11-9.5.25-12.17-4.EPA.59) 3.70-4.56) 5.91) 1. Thus.46 (1..42 (6..62) 1.05) 3.0) 6. Once absorbed. paralysis.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.09-1.82-4.07) 5...24-5. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.88-9.3) 8.73 (1.28) 2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.1-38.40) 1.94-14.05-3.39 (4. population from the National Health and Nutrition Examination Survey.9 (12.57-2.05-4.17-4. In pesticide applicators.38) 3.6) 10.16 (4.22-6.63-2.29 (3.33-7. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. 2006b). and seizures.85-4.88-8.6) 9.41 (1.88 (1.47 (5.12-3. resulting in excess acetylcholine at nerve terminals.35) 2.93 (4.92) 3.52 (5.74) 1.99-8.80-4.3) 8.33 (. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.78 (1.24) 5. Urinary 3.50 (4.58-5.11 (2.96) 3.91-4.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.5 (6.62-7. 2005.56-2.63 (5.1 (7.57) 9.05-8.68) 1.56) 2.68) 6. TCPy is more persistent in the environment than chlorpyrifos itself (U.64-2. 2005..06-4.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .20 (2.72) 1.60-3.54) 5.32) 1.48 (2. 2002).44 (6.33) 2.44 (5.06 (5.4) 4.83-2.97) 3.58 (1.84-6.00-8.77) 1.62) 90th 5.08) 6.53-5.86 (3.60 (1.97-3.94-12.46 (2..58 (4.36) 1.65-11.53 (2.98 (7.16) 6.19-2. 2006.55 (1.1 (10.58 (1.95 (3.48 (1.81) 2.44 (1.44-6.25-1.69 (1.93 (1.14) 1.58) 5.72) 2.31-4.98 (6.88-10.83) 1.91) 2.2 (7.02 (5.23-1.01) 1.

2005). Berent S. Freeman NC.. et al. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al.S. 2004). Toxicol Sci 2006. Garabrant D.epa.109(6):583-590. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.63(3):218220. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. In Minnesota and South Carolina farmers who used chlorpyrifos.. Carr RL. Curwin et al. 2006). Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Additional information about external exposure (i. J AOAC Int 1999. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.. Biomonitoring studies of TCPy provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of chlorpyrifos or chlorpyrifos-methyl than are found in the general population. Catenacci G. Burgess SC.S. Eberly LE.Organophosphorus Insecticides: Specific Metabolites 2004. In a probability-based sample of 102 Minnesota children aged 3-13 years.113(8):1027-1031. 2002).. but levels were roughly four to six times higher than the geometric means in the U. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Magnaghi S. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Haidar S. 2005.. Slotkin TA. 2001).gov/toxpro2. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Burns CJ.. Aldridge JE. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Meyer A. 2001) and Italy (Aprea et al.. 2005). Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al.Reference values of urinary 3. environmental levels) and health effects is available from ATSDR at: http://www.. but not chlorpyrifos. Albers JW. Occup Environ Med 2006. Levels of TCPy in the U. 2005).S. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. et al. urinary TCPy levels in children were reported not to have increased (Hore et al. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. Whyatt et al. Koch et al. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Environ Health Perspect 2005.html and from U.e... 2005).S. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity.S. CDC.EPA.. 1999). Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al.92(2):500-506. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.atsdr. EPA at: http://www. Of 482 pregnant women living in an agricultural community. et al.. MacIntosh et al. Betta A.. 2005. In Iowa farm families using several different pesticides. 1992. Fourth National Report on Human Exposure to Environmental Chemicals 137 . 2005). 2004).. 2007).82(2):305-312. Giordani B. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. the geometric mean urinary TCPy levels were similar in parents and children. Biomonitoring Information Urinary TCPy levels reflect recent exposure. U. References Adgate JL. Environ Health Perspect 2001.5.. Aprea C. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. representative subsample of NHANES 19992000 (CDC. Barisano A. Seidler FJ. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Following crack-and-crevice application of chlorpyrifos in their homes.gov/pesticides/.cdc. Perera et al. 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. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Clayton CA. 2000). Barr DB. Lioy PJ. 2003.. Betancourt AM. Chlorpyrifos exposure and biological monitoring among manufacturing workers. Lotti A. 2005).

Hines CJ. gov/ntpweb/index. Chlorpyrifos. Croghan CW.155(1):71-80.93(1):105-113.114(10):1542-1546. Weltzien E. Biomonitoring for farm families in the farm family exposure study. et al. 4/7/09 Koch HM. Available at URL: http://ntp. Third National Report on Human Exposure to Environmental Chemicals. Seidler FJ. Levin ED. Tsai WY. Howell RJ.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Gregg M. EPA). et al. Environ Res 1995. Lein PJ. Robson M. Saunders JH. Gurunathan S. 4/7/09 Perera FP. Hore P. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Levin ED. Robertson GL. Adgate JL.114(2):260-263. Harley K. Sanderson WT. Environ Health Perspect 2004.S. Lorenzini P. Chrislip DW. 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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.5. Ozkaynak H. Ricceri L. Herrick RF. Venerosi A.S. Edwards RD. Tate CA. Neurologic function among termiticide applicators exposed to chlorpyrifos. Barr DB. Chlorpyrifos: pharmacokinetics in human volunteers. Bradman A. Toepel K. Hill RH Jr. J Expo Anal Environ Epidemiol 2005. Baker S. Alexander BH. Environmental Health Criteria 198. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.9(5):494-501. Curwin BD.108(4):293-300. Eskenazi B. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Pellizzari E.31 Suppl 1:98-104. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Sheldon LS.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Freeman N. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Jett DA. Morgan MK. Striley C. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice.114(5):746-751.6-trichloro 2-pyridinol in their everyday environments.15(4):297-309.15(3):271-281.org/documents/jmpr/jmpmono/ v99pr03. Camann D. Brain Res Dev Brain Res 2005. Bennett DH. Toxicol Appl Pharmacol 2005. Meeker JD. Lu C.6-trichloro-2-pyridinol. Bruun D. J Expo Anal Environ Epidemiol 2000.5. Fortuna S. 2005.111(2):201-205. Environmental Protection Agency (U. Bailey SL.73:8-15. Temporal variability of urinary levels of nonpersistent insecticides in adult men. et al. Dick RB.51(1):53-65. Yang D. Rick DL.113(2):211-219. Lioy PJ. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. mothers and fathers living in farm and non-farm households in Iowa. Baker BA. Barr D. Seidler FJ. National Toxicology Program (NTP). et al. 1992. Scand J Work Environ Health 2005.inchem. Available at URL: http://www. Sharma V. Shealy DB. February 5. Mandel JS.204(2-3):175-180.nih. Exposures of preschool children to chlorpyrifos and its degradation product 3. et al. Freeman N. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Wartenberg D. Nolan RJ. Slotkin TA. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Roy TS. et al. Atlanta (GA). Toxicol Sci 2006. A longitudinal investigation of selected pesticide metabolites in urine. Fenske RA.10(4):327-340.htm. Hardt J. Irish R. Executive summary of safety and toxicity information. Seidler FJ. Int J Hyg Environ Health 2001. 1999. Barr DB. Environ Health Perspect 2006b. Ann Occup Hyg 2007. et al. Cometa MF. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. J Expo Anal Environ Epidemiol 1999. Slotkin TA. Environ Health Perspect 2003. et al. Chuang JC. Bravo R.71:99108. Environ Health Perspect 2006a. Reid TM. Bucelli R. Urinary pesticide concentrations among children. U.207(2):112-124. Honeycutt R. International Programme on Chemical Safety-INCHEM (IPCS).

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

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

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 . 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 0.200 (<LOD-. population from the National Health and Nutrition Examination Survey.200 (<LOD-.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * 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. Survey Geometric mean (95% conf.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. Fourth National Report on Human Exposure to Environmental Chemicals 141 .380 (<LOD-.S.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.670 (<LOD-1.27) < 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 . Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2.270) < LOD 659 701 920 Limit of detection (LOD. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.

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

Diazinon is not well-absorbed through the skin. population from the National Health and Nutrition Examination Survey.S. aerial.49 (<LOD-2. 2004). Most granular formulations.2 and 0.7. in the past. 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. Once absorbed. Prior to 2000. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. 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. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. It is also used for cattle ear tag applications to control flies and ticks and. Estimated intakes from diet and water do not exceed recommended intake limits (U. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity.S. It is toxic to birds. and forage crops. 2004). 1998. vegetable. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. 2007). 1998). since 2004.45 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. Before these restrictions. which may vary for some chemicals by year and by individual sample.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. < LOD means less than the limit of detection.S.EPA. and particularly when it was ingested in granular form.EPA. but these uses have been phased out. seed and foliar applications are planned to be phased out (U. in some pest strips. diazinon produced wild bird kills before use restrictions were in place. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. and other metabolites. diazinon cannot be sold for residential use.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. but is rapidly absorbed orally (IPCS. fruits. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Inhalational and dermal routes of exposure can be significant for pesticide applicators. an organophosphorus insecticide that is used to control insects on nuts. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 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.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. diazinon was widely used in residential and garden application. Fourth National Report on Human Exposure to Environmental Chemicals 143 . USGS.

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

htm. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Third National Report on Human Exposure to Environmental Chemicals. In 23 children. Bravo R.gov/circ/2005/1291/.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Baker SE. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Nguyen JV. Kruse RL. Liu F. Study for Future Families Research Group. Atlanta (GA). 4/7/09 Lu C. Anal Bioanal Chem 2003.. Swan SH. Cocker J. Jones K. Available at URL: http://www. Carrier G. revised February 15.usgs.S.S. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Toepel K. Available at URL: http://www. Barr DB. 1/14/09 U. Toxicol Lett 2002. Driskell WJ. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Diazinon. Mason HJ. Fenske RA. Noisel N.9(2):117-131. J Expo Anal Environ Epidemiol 2000. Barr DB. et al.inchem. Ann Occup Hyg 2006. The Quality of Our Nation’s Waters.10(6 Pt 2):789-798.org/documents/ehc/ehc/ehc198. Drug Chem Toxicol 1986. Semen quality in relation to biomarkers of pesticide exposure. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers.pdf. Drobnis EZ. Sadowski MA. EPA).37(4):501-507.epa. Bull Environ Contam Toxicol 1986. References Anthony J. Brunet RC.376(6):808-815. Olsson AO. Effect of sublethal levels of diazinon: histopathology of liver. Environ Health Perspect 2003. Biochem Pharmacol 1992. Oloffs PC. 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. EPA 738-R-04-006. Swan et al. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Redmon JB.111(12):1478-1484. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Oloffs PC.44(11):2243-2250. Environmental Health Criteria 198. May 2004.134(1-3):105-113. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Beeson MD. Centers for Disease Control and Prevention (CDC). 2006). 2006). Irish R. Barr DB.50(5):505-515. 1992-2001. Geological Survey (USGS).gov/ oppsrrd1/REDs/diazinon_ired. 2005. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 1998. Seifert J. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Barr DB. In 54 Canadian greenhouse workers. In a small number of men visiting fertility clinics in Missouri and Minnesota. March 2006. Bouchard M. Dumas P. 2007 [online]. Banister EW.S.Organophosphorus Insecticides: Specific Metabolites 2005). Environ Health Perspect 2006. Garfitt SJ. Environmental Protection Agency (U. Available at URL: http://pubs. Pewnim T. U. International Programme on Chemical Safety-INCHEM (IPCS). Diazinon.114(2):260-263. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Interim reregistration eligibility decision (IRED. Pesticides in the Nation’s Streams and Ground Water. 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. Rajendra W. Needham LL. Banister E.

or oral routes (U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. 2000). phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide. Compared with other organophosphorus insecticides. and in government programs such as the USDA’s Boll Weevil Eradication Program. It is moderately to highly toxic to fish. Metabolism of malathion leads to the formation of malathion monocarboxylic acid. usually only a small fraction of the crop is treated. population from the National Health and Nutrition Examination Survey.64. in fruit fly control. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 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. cholinergic effects. ornamental trees. When malathion is used on food or feed crops. 2007).. Thus. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 2003). which may vary for some chemicals by year and by individual sample. gardens.S. Malathion is infrequently detected in groundwater sampling (USGS. shrubs.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. Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. vomiting. resulting in excess acetylcholine at nerve terminals. paralysis. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al. Limited general population exposure occurs through the diet. but is more rapidly and efficiently absorbed via ingestion. and other metabolites. depending on the species. 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. malathion has low acute toxicity. which is an organophosphorus insecticide that is used on a wide variety of agricultural crops. 2006). as well as lawns.S. < LOD means less than the limit of detection. Once they are absorbed. and plants. Survey Geometric mean (95% conf. 2006). Malathion is slowly absorbed through the skin.EPA. In addition to being a metabolite of malathion.80 (<LOD-5.5%) to kill body lice. 146 Fourth National Report on Human Exposure to Environmental Chemicals . and seizures. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff.S. malathion dicarboxylic acid. It is highly toxic to aquatic invertebrates and rare fish kills have been reported from wide area applications onto surface waters and runoff into waters. Estimated intakes for the general population have not exceeded recommended intake limits. 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion. the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate. Most of the estimated 15 million pounds used annually are applied to cotton (U. see Data Analysis section) for Survey year 99-00 is 2. At high doses.EPA. Pesticide applicators and agricultural workers can have higher exposures via dermal. and producing acute symptoms such as nausea. It is registered for use in public health mosquito control. inhalational. weakness. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. It has a short halflife in soils and water and is not considered persistent in the environment. Malathion is also used medically in lotion form (0.

CDC.5 and 5. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al.html and from U. 1990).. 1996. 2001.EPA. 1993. environmental levels) and health effects is available from ATSDR at: http://www. 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.74 (<LOD-5.S. Thomas et al. 2005). Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al.cdc. Survey Geometric mean (95% conf.epa. 2006). A study of 13 children from an agricultural region of Washington State reported median levels that were below the detection limit in the NHANES 1999-2000 subsample (Kissel et al. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 2006). 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.EPA.. 1987. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. Urinary Malathion dicarboxylic acid (creatinine corrected) Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2000). population from the National Health and Nutrition Examination Survey.. 2003).. Lu et al. IARC considers malathion not classifiable as a human carcinogen. 2005. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak 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. 2002. but cholinesterase activity was not affected. Human studies of single oral doses between 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. A study of agricultural workers reported preshift urinary levels of malathion dicarboxylic acid that were twofold to eightfold higher than detection limits in the NHANES 1999-2000 subsample (Krieger and Dinoff. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.S..Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 1999). Flessel et al. Fourth National Report on Human Exposure to Environmental Chemicals 147 . and it is not considered an animal teratogen or a reproductive toxicant. EPA at: http://www. 2006).e.S. Malathion itself has not been considered genotoxic (U. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. 2005)...0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Pluth et al. Additional information about external exposure (i. Of 382 pregnant women living in an agricultural community. Giri et al. Toxicity from unprotected bystander exposure during applications is rare (U.gov/pesticides/.. 2004). representative subsample from NHANES 19992000 (Adgate.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. 1999.gov/toxpro2..atsdr..S. but isomalathion.

Geological Survey (USGS).9(5):494-501. J Expo Anal Environ Epidemiol 1999. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Bradman A.38(4):546-553. Pesticides in the Nation’s Streams and Ground Water.S. J Expo Anal Environ Epidemiol 2005. Curl CL. Kedan G. Lu C. Grether JK.132(4):794-795. Barr DB. Environ Health Perspect 2006. Hertz-Picciotto I. Cancer Res 1996. Erratum in: Toxicol Sci 2003 Aug.514(1-2):223231.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.73(1):182-94. Sharma GD. EPA). Fenske RA.22(1):7-17. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Genetic toxicity of malathion: a review. and cholinesterase status of date dusters and harvesters in California.56(10):2393-2399. Mutat Res 2002. Freeman NC. et al.445(2):275-283. 4/7/09 Kissel JC. Petitti D. Clayton CA. htm.114(2):260-263.15(2):164-171. Brunet RC. Needham LL. Trzeciak A. Carrier G. Hammerstrom KA. Goldhaber M. Reproductive outcome in women exposed to malathion. A longitudinal investigation of selected pesticide metabolites in urine. Krieger RI. Thomas D. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Available at URL: http://www. MacIntosh DL. Rappaport E. Samuel O.gov/circ/2005/1291/. Ryan PB. Dinoff TM. Jewell NP.inchem. Harris JA. Harley K. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. 1992-2001. Third National Report on Human Exposure to Environmental Chemicals. metabolite clearance. Mutat Res 1999. Albertini RJ. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Bouchard M. Malathion (addendum). Griffith W. Weltzien E. Centers for Disease Control and Prevention (CDC). Am J Epidemiol 1990.usgs. Environ Mol Mutagen 1993. Barr DB. EPA 738-R06-030. Environ Health Perspect 2001.77:1009-1010. Lu C. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Reregistration eligibility decision (RED) Malathion. Available at URL: http://pubs. O’Neill JP. Am J Public Health 1987. Neutra R. Barr DB. Eskenazi B. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Environmental Protection Agency (U. Eberly LE. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.109(6):583-590. Flessel P. Blasiak J.S. Swan SH. 2005. Nicklas JA. Barr DB. Lioy PJ. Malathion deposition.112(10):1116-1124. 6/1/09 U. Environ Health Perspect 2004. Bravo R. revised February 15. Gosselin NH.S. Giri A. et al.epa. Quintana PJ. Pluth JM. Dumoulin MJ. 2007 [online]. Toxicol Sci 2003 May.org/documents/jmpr/jmpmono/v2003pr06. Arch Environ Contam Toxicol 2000. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. U. Giri S.pdf. The Quality of Our Nation’s Waters. Available at URL: http://www. Atlanta (GA). Hooper K. International Programme on Chemical Safety-INCHEM (IPCS). Toepel K.74(2):following table of contents.gov/oppsrrd1/REDs/ malathion_red. et al. Szyfter K. July 2006. Jaloszynski P. Prasad SB. Irish R. March 2006.

00) size 1989 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.50-14. Both are toxic to birds.21 (2.30 (1.67 (1. which may vary for some chemicals by year and by individual sample.34 (3.50) 2.910) < LOD .60-5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.80 (2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.910) < LOD < LOD .70) 2.30-3.90-9.70) 2.70-6.30 (2..69 (2.0) 3.36-1.60) 1. and to a lesser extent.41-4.33) 2.02-6.1.730 (<LOD-. methyl parathion was rapidly absorbed after ingestion. and eliminated rapidly from the body after absorption (Kramer et al.49 (1. 2003).11-4. 2000). first registered in 1948.80) 2.27) 2.67) < LOD 1.860 (<LOD-1.10 (3.70-3.30-16.18-3.40) 1.50 (1.70 (2.910) < LOD < LOD < LOD 1.10-11.91-3.71 (3. Methyl parathion is not registered for residential use in the United States.71 (2.33 (1.26 (1.45 (1. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.92-2.80 (1.32-3.66 (2. Increased risk of exposure via dermal.20 (<LOD-2. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. Survey Geometric mean (95% conf.70-6. Morgan et al. Given its limited use.16) < LOD 1. and of the chemical nitrobenzene.70 (2. Many previous registered agricultural uses of methyl parathion have been cancelled (U.13-1.50) 3.940 (<LOD-2.. Estimated intakes from diet and drinking water have been below recommended limits.10 (<LOD-6. binds tightly to soils resulting in low leachability. In animal studies.28-4. Ethyl parathion.50-9. Methyl parathion use is highly restricted.50 (1.62 (1.70) 2.10 (3.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . < LOD means less than the limit of detection.298-00-0 Ethyl Parathion CAS No. all registered uses were voluntarily cancelled (U.32-1.10-1.79) 4. fish.8 and 0. 1977).44) 2.11) 2.850) < LOD .92) 5. population from the National Health and Nutrition Examination Survey.46 (3.0) 3.40) 4.40 (1. and aquatic invertebrates.50 (1. 2007).50 (2.70 (<LOD-3.50) 1.01) 695 660 518 679 603 941 Limit of detection (LOD.90 (1.15-3.09-1. with limited applications in agriculture.990-1.40-3. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.89 (2.40-4.60 (4..60-24.00 (2.21-1.70-3.70-6.0) 4.60-36.69) 4. 2002.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .20) 5.05) 4.61) < LOD 1.40) 2.700 (<LOD-.70 (3.0 (3.770 (. and has a short half-life in soils and on plants.37) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.32 (1.30-5. peak domestic use was as high as 5-6 million pounds per year.58) 3.90-11.72 (3.EPA.45) 5.50) 3.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.790 (<LOD-.0) 3. and oral routes can occur in pesticide and agricultural workers (Muttray et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 149 .S. ethyl parathion.22-3.70 (2.85 (2.32-1. pulmonary. more slowly absorbed through the skin.S.00 (2.50 (1.0) 3.20-5.300-.60-19.74) 5.40-4.00) 3. on cereal grains.01) 4.0) 2.48) 90th 2. It had been applied to cotton.50 (2.28 (1.47) 2. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.10) 4. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. Methyl Parathion.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Once absorbed.EPA.12) < LOD < LOD 1.28 (1. was once a restricted-use insecticide with limited applications on certain agricultural crops.57) 1.S.0) 3. 2006).20 (2.37-4.37-2.61) < LOD 1.80 (2.10) 22. In the 1990s.37-4.01-4. Methyl parathion has low water solubility. but by 2003.57-4.19 (. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

and producing acute symptoms such as nausea.680 (<LOD-1.33-3.29) 1. accidental exposure. 2003.97 (2.17-4.72-2.S.2) 2.20 (3.S.60) 2. At high animal doses of methyl parathion. 1995).. and seizures. weakness. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.790-1.92 (2.79) 1. U. and unintentional acute or chronic high-level occupational exposure (Hill et al.59 (1.e.00 (1.. 2006.01 (.57-2.37-1.76-14.21-21.55 (<LOD-3. methyl parathion. Additional information about external exposure (i. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.980 (.S.88) 1.970 (.96 (1.00 (1. Jaga and Dharmani.atsdr.epa.17) .29 (2. paralysis.640) < LOD < LOD 1.91 (1.82 (2.08) < LOD .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 .1) 2.26 (1.23) 1.82) < LOD .03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 1991).71 (1. does not inhibit acetylcholinesterase enzymes.14-3.3) 2.720-1.04 (2.540) < LOD .7) 3.940 (<LOD-1.950) < LOD . In addition to being a metabolite of methyl and ethyl parathion.80 (1.56-2. paranitrophenol. EPA at: http://www.440 (<LOD-.61) 4. Survey Geometric mean (95% conf.80 (1. 2004).38-3.78 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. Methyl parathion is not considered genotoxic. 2004).html and from U.07 (1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Parathion and methyl parathion have high acute toxicity in animal testing.930 (.31-3.25 (2.67 (3. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.11) 1. gov/pesticides/.73 (1. teratogenic. cholinergic effects. Slotkin et al.39) 1.60 (1.97 (<LOD-4.310-..840 (.35-3.00) 2..20) .71) 1.430 (.500) < LOD < LOD .30) 3.91) 1.44-3.800-1.84) 3.96 (1.78-2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.89 (2.2) 2.88 (1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . but lists ethyl parathion as a possible human carcinogen. Methyl Parathion. 1990. 150 Fourth National Report on Human Exposure to Environmental Chemicals . and other metabolites.880 (.4 (3.720 (<LOD-.08 (1.31) < LOD .530) < LOD < LOD < LOD .01-3.87 (1. 2006.930 (.77-7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.35-3.78-2.93 (2.9) 1.EPA considers methyl parathion unlikely to be carcinogenic to humans.11-4.57-7. Lores et al. vomiting. 1978. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.78) 2.30-1. 2005.10 (1. 1995.95) 1.29) 2.400 (<LOD-. ethyl parathion. Karanth and Pope et al.26) 17.09) 2. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.86 (2.41-2. population from the National Health and Nutrition Examination Survey.39 (1.79 (1.94-4.370 (<LOD-. The metabolite.94-47.05) 4.13) 4.13-12.01 (2.. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.07) 2.44-3.830-1.790-.70) 3. Orsorio et al. In large doses.16-4.850-1.33-6.55) 2.67-2.89 (2. WHO.83 (1. environmental levels) and health effects is available from ATSDR at: http://www.25) 1.04) 1.cdc.970 (.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.870) < LOD .730-1.21) 1. gov/toxpro2.57) 6.60-2. Zurich et al.43) 4.Organophosphorus Insecticides: Specific Metabolites Metabolites”).. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.98-7.15-10..33-3.15) 3. Thus.690-1.08-3.97-10.48-4.90 (1. resulting in excess acetylcholine at nerve terminals.20) 3..10) 90th 2. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .

Barr DB. DiPietro E. Environ Health Perspect 2002. Pharmacokinetics of methyl parathion: a comparison following single intravenous.htm. Morgan DP. 2002. Gregg M. 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.71:99108. Chicago area methyl parathion response. Lin LI. Bradman A.25(5):599-606. Rubin et al.inchem.33(5):270-276. Rev Environ Health 2006. Moseman RF.9:311-320.5 mg (500 µg)/g creatinine for workers at the end of shift. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Harley K. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Pesticide workers may have much higher levels following pesticide applications. References Barr DB. Dharmani C. A study of 13 children from an agricultural region of Washington State reported median levels that were more than threefold higher than median levels in the NHANES 1999-2000 subsample (Kissel et al. Environ Health Perspect 2002. 1995). Neurotoxicol Teratol 2003. McCann et al.. Environ Health Perspect 2004. 4/7/09 Jaga K. 2005.. Lores EM. Environ Res 1995. Parathion-Methyl (addendum).110 Suppl 6:1085-1091. Baker RC. Hill RH Jr. Slach EF. Kedan G. J Expo Anal Environ Epidemiol 2005. 1999). Pathak S. Head SL. Eskenazi B.org/documents/jmpr/jmpmono/v95pr14. Lewalter J. Kissel JC. 2005.112(10):1116-1124. et al. Rockhold RW. oral or dermal administration.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Giordano G. Fourth National Report on Human Exposure to Environmental Chemicals 151 . 2005). Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. a range of values several hundred times higher than levels found in the U. and many residents were symptomatic (Barr et al. Costa LG. Curl CL. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Arch Environ Health 1978. Third National Report on Human Exposure to Environmental Chemicals. Clark JM.. ACGIH recommends a BEI of 0. Available at URL: http:// www. Barr DB. Hill RH Jr. CDC. Hryhorczuk DO. International Programme on Chemical Safety-INCHEM (IPCS).14(4):213-216. Guizzetti M. Wellman SE. Leng G.. 2004). population (Olsson et al. Alley CC.. Hetzler HL. Kramer RE.6(2-3):159-173. et al. Ashley DL. Karanth S. and levels were similar or slightly lower that those in a small convenience sample of the U. Weltzien E. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.21(1):5767. Moomey CM. Laboratory investigation of a poisoning epidemic in Sierra Leone. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.56(7):449553. Centers for Disease Control and Prevention (CDC). Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State..S. Turner WE. et al.15(2):164-171. Pesticide residues in urine of adults living in the United States: reference range concentrations. Head SL. Pope C. Baker S. Occup Environ Med 1999. 2002. et al. Hill et al. Bailey SL. Shealy DB. McClure PC.. et al. 2002). Arch Environ Contam Toxicol 1977.S. Methyl parathion: an organophosphate insecticide not quite forgotten. McCann KG. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Lu C. 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. 2005). Barr DB. Barr JR. Role of individual susceptibility in risk assessment of pesticides. J Anal Toxicol 1990. Needham LL. Runkle KD. 2005. Atlanta (GA). In a study of workers who handle parathion. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Jewell NP. 1995. Toxicology 2005. general population (CDC. 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. Baker SE.215(3):182-190.110 Suppl 6:1075-1078. Griffith W. J Biomed Sci 2002. Cline RE. Bradway DE.

Schilter B. 5/19/09 Zurich MG. Ryde IT.epa. Ohio. Hill G.04/106. Yacovac R. Osorio AM. 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.D. U.201(2):97-104.pdf.who. Available at URL: http://www.Organophosphorus Insecticides: Specific Metabolites Muttray A.S. Backer G. Methyl parathion in drinking water. March 2006. EPA).gov/circ/2005/1291/. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. revised February 15. Mengle DC.114(10):1542-1546. Costa LG. Tate CA. Investigation of a fatality among parathion applicators in California. 1/14/09 U. Rubin C. Dunlop B. Available at URL: http://pubs. Olsson AO. Sadowski MA. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Hill RH Jr. 1992-2001. EPA-738-FOO-009. Kieszak S. Barr DB. Environmental Protection Agency (U. Geological Survey (USGS). May 2003. Am J Ind Med 1991. Slotkin TA. 1/12/07 U. Pesticides in the Nation’s Streams and Ground Water. Anal Bioanal Chem 2003. 2004. Ethyl parathion.S.20(4):533-546. Honegger P. Seidler FJ.E. Facts. September 2000. Ames RG. Nguyen JV.S. Environ Health Perspect 2006. 0153. pdf.int/water_sanitation_health/dwq/chemicals/ methylparathion. Levin ED.162(2-3):219-224. WHO/SDE/WSH/03. 152 Fourth National Report on Human Exposure to Environmental Chemicals . A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.S.pdf.110 Suppl 6:1047-1051. External and internal exposure of wine growers spraying methyl parathion. 2007 [online]. et al.376(6):808-815. Environ Health Perspect 2002. Toxicol Appl Pharmacol 2004. Esteban E. Jung D. EPA). gov/oppsrrd1/REDs/methylparathion_ired.epa. 6/1/09 World Health Organization (WHO).usgs. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Letzel S. Available at URL: http://www.gov/oppsrrd1/REDs/factsheets/0155fct. 1995-1996. Rosenberg J. Environmental Protection Agency (U. Available at URL: http://www. The Quality of Our Nation’s Waters. Case No.S. Monnet-Tschudi F. Toxicol Lett 2006. R.

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

670 (<LOD-1.780 (.07) .780 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.55) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.950) < LOD < LOD 1.500 (.740 (. Survey Geometric mean (95% conf. 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.580-1.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.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250 (<LOD-.780 (<LOD-1.300-1. population from the National Health and Nutrition Examination Survey.64) .470 (.410 (<LOD-1.780 (.850 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .680 (<LOD-.770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .31) .840 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .740-1.S.27) . 154 Fourth National Report on Human Exposure to Environmental Chemicals .700-.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .840) 669 687 929 Limit of detection (LOD.21) < LOD .2.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.430 (<LOD-. < LOD means less than the limit of detection.94) .210-1.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .S.200-. Survey Geometric mean (95% conf.210-.760 (<LOD-.210 (<LOD-.820) < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .610 (<LOD-1. population from the National Health and Nutrition Examination Survey.17 (.15) < LOD . which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 01-02 is 0.700-1.

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

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

2005). Environ Health Perspect 1999. 2003. Thomson BM. Biochem Biophys Res Commun 1998. choreoathetosis. Idel H. Regul Toxicol Pharmacol 2002. Neurosci Lett 2001. Ose K. 2006. Bull Environ Contam Toxicol 1999. Pyrethroid pesticide-induced alterations in dopamine transporter function. Chen JH.atsdr. Kuhn KH. Wolff MS. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. 2002). et al. Go V. 2004. Additional information about pesticides is available from U. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. motor activity. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.. Moniz et al. epa. Kamita Y.. tremor. 1998.. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. 2001. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. salivation.108(1):78-85. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Wolff MS.. Toxicol Appl Pharmacol 2006. Neurotoxicol Teratol 2005. Spinosa HS. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. 2005). Yamada T.atsdr.251(3):855-859.. and striatal dopamine levels in male and female rats. Garey and Wolff. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. et al.html. Miller GW. Neurotoxic effects of two different pyrethroids.. Estrogenicity of pyrethroid insecticide metabolites. hypersensitivity. Caudle WM. McCarthy AR.35(2 Pt 1):227-237.27(12):1273-1283. Pogo BG..50(2):245-255. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley.62:101-108. Garey J. Lazarini CA. 2005). Idel H. cdc. WHO. Kim HS. Go et al.gov/pesticides/ and from ATSDR at: http://www. Leng G. Seth PK. Shaw IC. Florio JC. Song L. et al. Toxicological profile for pyrethrins and pyrethroids. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Bernardi MM. Int J Hyg Environ Health 2002. Kim et al. Wang SL.S. Salzgeber SA.205(6):459-472.8(1):197-202. Okuno Y.cdc. 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. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. J Environ Monit 2006. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Levsen K. Lee SJ.8(1):18-21. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid.. Hu JY. Berger-Preiss E. Fourth National Report on Human Exposure to Environmental Chemicals 157 .300(3):161-165.. Garey J. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. In California. Shin JH. Moniz AC. Lemonica IP.. Neurotoxicol Teratol 2001. Elwan et al. Kim TS. In developing rodents.27(4):609-614. Wieseler B. Xenobiotica 1997. Sunami O. Agrawal AK. Abell AD.1/15/09 Aziz MH. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Leng G. and seizures (ATSDR. Varoli FM.html. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Shafer.gov/toxprofiles/ tp155. Kunimatsu T. fenvalerate. Yang J. 2002). Leng G. Pauluhn J. Cruz-Casallas PE. Ray et al. Kim IY. and permethrin) in the Hershberger and uterotrophic assays. Toxicol Appl Pharmacol 1991. bioallethrin and deltamethrin. 2006. 2003. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. 2006). Richardson JR. 1999. et al. 2002.23(6):665-673.211(3):188-197. on immature and adult mice: changes in behavioral and muscarinic receptor variables.gov/toxpro2. Hu et al. McCarthy et al. Kuhn K. Soderlund et al. Shukla Y. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Guillot TS. Leng A. Generally. 1991. Elwan MA. dopaminergic. Fredriksson A. Lazarini et al. J Reprod Dev 2004. Eriksson P. Adhami VM. 2005). 2000. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. September 2003.. Sugiri D..Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Kang IH. Kunimatsu et al. EPA at: http://www. References Agency for Toxic Substances and Disease Registry (ATSDR). Eriksson and Fredriksson. Zhao RC. Lewalter J. Available from URL: http://www. Ranft U. 2003.107(3):173-177. neurochemical changes in cholinergic.. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. 2001. 2003. Bernardi MM. Effects of prenatal exposure to deltamethrin on forced swimming behavior.

Revised February 25.Pyrethroid Pesticides Ray DE. Meyer DA.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Available at URL: http://whqlibdoc. Spencer J. Pesticides in the Nation’s Streams and Ground Water. Piccirillo VJ.S.htm. June 2006a. 2007.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.epa. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. 5/26/09 U. EPA). Environmental Protection Agency (U.38:95-101. Environmental Protection Agency (U. Sheets LP. Soderlund DM. J Toxicol Clin Toxicol 2000. O’Malley M. Mullin LS. U.22(8):983-991. Shafer TJ.gov/oppsrrd1/REDs/cypermethrin_red. 5/26/09 U. synergies.S. Rev Environ Contam Toxicol 2006. April 2002.10. et al. Pesticide and Evaluation Scheme. 2005. Reregistration Eligibility Decision for Cypermethrin.who. Clark JM. June 2006b. Environ Health Perspect 2005.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.pdf. pdf.S. Marsh JR.113(2):123-136. World Health Organization (WHO).S. EPA).S.171:3-59. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).gov/ circ/2005/1291/. 19962002.epa. Environmental Protection Agency (U. EPA). Pyrethroid insecticides: poisoning syndromes. Crofton KM. 5/26/09 U. Laird WJ. and therapy. Permethrin. 5/26/09 Woollen BH. sumithrin synthetic pyrethroids for mosquito control. Available at URL: http://www. March 2006. Safety of pyrethroids for public health use. 1992–2001.epa. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .usgs. Pyrethroid illnesses in California. Toxicology 2002.S.186:57-72. Available at URL: http://pubs.htm. resmethrin. Lesser JE. Available at URL: http://www. Geological Survey (USGS).S. Forshaw PJ. Xenobiotica 1992. Available at URL: http://www. Sargent D.

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

see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2. 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. 160 Fourth National Report on Human Exposure to Environmental Chemicals .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. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.S. < LOD means less than the limit of detection.2 and 0. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

Berger-Preiss E. Arch Environ Contam Toxicol 2004. Rev Environ Contam Toxicol 2006. Drexler H. Barr DB. Angerer J. Angerer J. Human exposure to indoor residential cyfluthrin residues during a structured activity program. J Expo Anal Environ Epidemiol 2003. Butte W. Third National Report on Human Exposure to Environmental Chemicals. Idel H. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.209(3):221-233. Kolossa-Gehring M. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Olsson AO.209(3):293-299. Heudorf U. Bernard CE. Hadnagy W. Int Arch Occup Environ Health 2004. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Krieger RI. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Pyrethroid illnesses in California. Angerer J. Heudorf U. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.46(3):281-288. Ranft U. Sugiri D. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.77(1):67-72. Spencer J.Pyrethroid Pesticides References Baker SE. et al. Atlanta (GA). Leng G.13(2):112-119. Int J Hyg Environ Health 2006. 19962002. O’Malley M. Angerer J. Ball M. 2005. Environ Health Perspect 2001. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.206(2):85-92. Hoppe HW. Heudorf U. Williams RL. Seiwert M. Centers for Disease Control and Prevention (CDC).109(3):213-217. Int J Hyg Environ Health 2003. Schulz C.186:57-72. Becker K. Int J Hyg Environ Health 2006.

1.490-.180) .790) .270 (.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin. Generally.21) . trans-cypermethrin.or trans-3-(2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.550) . more of the trans-metabolite than Urinary cis-3-(2. 1999).740-2. transcypermethrin and trans-cyfluthrin.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .780) .210-.880 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.210) .740-1. Fourth National Report on Human Exposure to Environmental Chemicals 163 .50) .460-1..690) .and trans-isomers.08) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.28) 671 680 518 701 591 957 Limit of detection (LOD.300-.120-. Kuhn et al. The presence of cis-3-(2.610) .1 and 0.630) .370-.740) 1.110-.47 (.580-1.300 (.370 (. The chemical trans-3(2.68) .610) .380-.600-1. In the body.680-3.700) .155-.270 (.2-Dichlorovinyl)-2. Kuhn et al.280 (.340) .35) .250 (.220-.54) .210) 90th .200-.510 (.670-2.2dichlorovinyl)-2.490-.2-dichlorovinyl)-2.200-.430-.110-. < LOD means less than the limit of detection.12 (.160 (<LOD-.. Similarly.200) < LOD < LOD < LOD . The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin. cis-permethrin.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.530 (.11) .380-.790-1. the presence of trans-3-(2.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-dichlorovinyl)- CAS No.202 (.630 (.10) size 1951 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .440 (.770-1.230) .S.870) 1.670-1.410) .670 (.340) .380-.890 (.490-1.330 (.200 (.43) .570-.460 (.490-1.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .580) 1.44 (. cis-3-(2.710) . which may vary for some chemicals by year and by individual sample.24) 1.13 (.280-.380) .260 (.350) .630-.2-dichlorovinyl)-2. Biomonitoring Information Urinary levels of cis.890 (.35) 1.53) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.600) .730 (.2-dichlorovinyl)2.220-.410) . Survey Geometric mean (95% conf.500 (.520) .960 (.140 (.730 (.300-.460-. 1999).510 (.120-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.730 (.170 (. 1985.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.920) 1.160 (.710-1.330) .2dichlorovinyl)-2.262) * * * < LOD < LOD .180 (.120-.200) .650-1.160 (.300 (.15) .600 (.240) .68 (. but it can also reflect exposure to cis-3-(2.80) . 52315-07-8 CAS No.510 (. 1985. ciscypermethrin and cis-cyfluthrin.470 (.2-dichlorovinyl)-2.340-. but can also reflect exposure to trans-3(2.640 (.740 (.950-2. and trans-cyfluthrin.570 (.250-.07 (.220-.820 (.110-.220-.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George. cis-cypermethrin. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.850 (.420-.790-1.500 (.68359-37-5 Cypermethrin Permethrin CAS No.140 (<LOD-. trans-permethrin.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.900 (.770) .630) .910-5.670-1.400-. population from the National Health and Nutrition Examination Survey.790 (.32) .77 (.270 (.150 (.220) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. and ciscyfluthrin.470-1.680 (.380 (.310) .110 (<LOD-.200-.200) .240) . Cyfluthrin.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.270-.68) .120-.

140-.600 (.11) .24) .290 (.880) .300 (.290-. 2006).2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.150-. 2005).920 (.190) . 2001) showed urinary levels of cis.200-. Schettgen et al.420 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.67 (.590) . Cyfluthrin.890 (.550-1..and trans-3-(2.390 (.230-. 2006).580) . 2003).340) .250-.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.690-1.640-1.450-.80) .430-.300) .170 (.550) . 2006) and 1177 urban adults and children (Heudorf et al.240 (<LOD-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.270 (. In the same residents.2-dimethylcyclopropane carboxylic acid did not increase.590 (..390-.340) .170) < LOD < LOD < LOD .11) .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC. urinary trans-3-(2.12-2.380) .560) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.410) . In these volunteers.430-1.540 (.370-. 2005) In a small group of indoor pest-control operators.840 (.250 (<LOD-.550) .Pyrethroid Pesticides 2.260 (.470-1.. 2004).640) 1.33) .320-.29 (. 2005).250) .700) .570) .230 (. In a study of urban residents in Germany (Berger-Preiss et al.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.190 (.250) .440 (.and trans-3(2.700) .210-.260 (.12 (.440 (.900 (.700-2.280 (.21) .380-. median urinary levels of trans-3-(2.260-.560) .290) .170 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.550 (. Lu et al.440-..200) .250-.500 (.680 (.800 (.450 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.680-1.180-.2dichlorovinyl)-2.150-.2dichlorovinyl)-2. Other studies have provided evidence that urinary levels of cis.220 (.540 (. Survey Geometric mean (95% conf. post- Urinary cis-3-(2.11) 1.380 (.2-dichlorovinyl)-2.450-1.290) .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 . 2001.890) .190) .. 2005).830) . 2002).370-. In a study of volunteers.33 (.360-1.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.270-.31) .430 (.300) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.780 (. representative NHANES 2001-2002 subsample (CDC.2-Dichlorovinyl)-2.130-.710-3.530 (.340-. 2006.104-.250) 90th .180 (.138 (. 2004.540) .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.59) .230-. population from the National Health and Nutrition Examination Survey.2-dichlorovinyl)-2.67) . 2002). urinary levels of cis-3-(2.300 (.510-1.270) .300-.200-.. 2006. 2003).2-dichlorovinyl)-2..710 (.270) . the median and 95th percentile of urinary levels of cis-3-(2.37) . 164 Fourth National Report on Human Exposure to Environmental Chemicals .S.182) * * * < LOD < LOD .59) .350 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220) .530 (..680-1.640 (.59 (1.750 (.280-. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * ..200 (.11 (.150-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.440-. 2005).120 (.2-dichlorovinyl)-2.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.080-.810 (.49) .250-.840 (.320) .750-1.640-1. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.400-1.550-1.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .640-.400 (.160 (<LOD-.. Studies in Germany of 396 children and adolescents (Becker et al.370-..260 (.580-1.230-.03) 1.260) .780) 1.220 (.350) .390-.

480-.01 (1.17 (.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.55-3.750) .60-4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.620) < LOD 2.410 (<LOD-.700-1.08-6.23) 2.59 (1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .27 (1.460-.580 (.64-4.520-.28 (1.820) . Urinary trans-3-(2.62 (1.56 (1.2-dichlorovinyl)-2.12-6.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer. 2005).910-1.49-3.470 (<LOD-.780 (.14-6.37 (1.14) 1.490-1.68-3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.11-1.89 (2.19) 1.940 (.840-1.14-2.84 (1.560 (.470 (.50 (1.28 (2.440 (<LOD-.20 (.4 and 0.800-1.08-4.S.90) 1.26 (.2-dichlorovinyl)-2.860) .85) 4.500-.77) 2.55-4.49-3.66) 691 680 518 690 595 954 Limit of detection (LOD.4.400 (<LOD-. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.11-2.670) .400-.68) 1.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.16) 1. trans-Cypermethrin.670) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (. < LOD means less than the limit of detection.10) 2.2dichlorovinyl)-2.550 (.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.97-11.13) .69) 1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.970 (.530) .570) 90th 1.42 (2. population from the National Health and Nutrition Examination Survey.68-2.03-1.54) 4.43) 2.17-1.420 (<LOD-.41 (1.41-14.25-3.56) 2.710 (.19 (3.22 (1.56 (1.460-.19 (2.25 (1.76-3.40 (1.17 (.410-.2-Dichlorovinyl)-2.70) 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 .08) 1. which may vary for some chemicals by year and by individual sample.77) 1. The maximum post-application urinary levels.410-.03-1.68) 1.20 (.and trans-3-(2.7) 2.81) 2.60) . Fourth National Report on Human Exposure to Environmental Chemicals 165 .910-1.60) 1.76-4.660) 1.760) .850-1.700) .77 (1. Biomonitoring studies on urinary levels of cisor trans-3-(2.68) 2.63) 1.87 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.560 (.810-1.5) 2.55-5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.56) 2.09 (.66) .35) 1.94 (1.07 (1.500) .680-1.410 (<LOD-.23 (. however.42) 1.69 (1. 2005).920-1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . Finding a measurable amount of cis.Pyrethroid Pesticides application median urinary levels of summed cis.95) 2.or trans-3-(2.01) 4. Survey Geometric mean (95% conf.730) .77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .830-1.07-3.560 (.490 (<LOD-.54 (1.95) 3.39-5.39 (1.49-5.91 (1.520) .48) 4.20 (.63) 1.610) 1.

12 (.S.700-.00 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.86 (2.15-3.900 (<LOD-1.930-1.98 (1.65) 1.580) .02-1.580 (.19 (1.74) 2.89) 2.56 (1.880 (<LOD-1.55 (2.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .74) .61) 1.60) 2.36) 2.33-1.87 (1.34-4.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.22-2.55 (2.970 (.30-3.08 (.570-.33-2.640) .56-5.47-2.42 (.720-1.500-.40-2.70 (.880-1.07) 2.520 (<LOD-.55 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.47 (1.67 (2.00) 1.800-1.56-2.60) 2.42) 1.36 (1.470-.87-3.35) 1.27-2.760 (. trans-Cypermethrin.07-1.570 (<LOD-.29) 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.81 (2.33 (1.780 (<LOD-.22) 1.00) 5.670) .440-.13) .91-11.44) 2.37 (1.15) 3.880 (.15-3.480-.850) .11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.20 (1.68) 3.87-8.3) 2.48 (1.750) .35 (1.540) .660) .15) 2.560 (.07) 2.57 (1.780) 90th 1.530 (.75 (1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .770) < LOD 2.47-2.820-2.08 (.19) .530 (<LOD-.610-.740) .27-2.57) 3.30-6.80) 1.780) .700 (.22-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-5.07-2.11) . population from the National Health and Nutrition Examination Survey.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .31) 1.12-1.07-3.850) 1.15-3.48-2.87) 1.87) 1.570 (.850-3.470 (.28) 2.39 (1.410-.39) 1.800-1.91 (1.34-3.65 (2.45 (1.16 (1.60 (1. Survey Geometric mean (95% conf.13) 1.41) 1.720 (<LOD-.31 (.730) .31 (2.700 (.26 (1.15 (1.720-1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .2-Dichlorovinyl)-2.00) 1.91) 1.64 (1.45-2.20-2.Pyrethroid Pesticides Urinary trans-3-(2.

J AOAC 1985. Hoppe HW. Permethrin and its two metabolite residues in seven agricultural crops. Biological monitoring of workers after the application of insecticidal pyrethroids. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Leng G. 2005. Hadnagy W. Idel H. Third National Report on Human Exposure to Environmental Chemicals. Heudorf U. Int Arch Occup Environ Health 2004. Lu C. Leng G.68(6):1160-1163.62:101-108. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Angerer J. Angerer J. Angerer J. Angerer J. Berger-Preiss E. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Schettgen T. Environ Health Perspect 2006. Int J Hyg Environ Health 2003. Barr DB. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Idel H.209(3):293-299.109(3):213-217. Bull Environ Contam Toxicol 1999. Leng G. Schulz C.77(1):67-72.209(3):221-233. Sugiri D. et al. Levsen K. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Bartell S. Butte W. Kolossa-Gehring M.114(9):14191423. Idel H. Int J Hyg Environ Health 2002. Environ Health Perspect 2001. Heudorf U. Bravo R. Kuhn K. Berger-Preiss E.Pyrethroid Pesticides References Becker K. George DA. Ranft U. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Drexler H. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Wieseler B. Ranft U. Sugiri D. Hardt J. Atlanta (GA).134(1-3):141-145. Int J Hyg Environ Health 2006. Drexler H. Pearson M. Ball M. Angerer J.76(7):492-498.205(6):459-472. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int J Hyg Environ Health 2006. Heudorf U. Int Arch Occup Environ Health 2003. Centers for Disease Control and Prevention (CDC).206(2):85-92.

.2dimethylcyclopropane carboxylic acid formed in the environment. 2005).2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. deltamethrin has been used against mosquitoes that carry malaria. Studies in Germany of 396 children and adolescents (Becker et al.1 μg/L) for the NHANES 2001-2002 subsample (CDC. Deltamethrin can degrade to cis-3(2. in detection of cis-3-(2. 2001) showed that urinary levels of cis-3-(2. urinary levels of cis-3-(2.2-dibromovinyl)2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population. 2005). In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2001.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. (2004) reported a geometric mean concentration of cis-3(2. Outside the U. 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.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dibromovinyl)-2. 2005). 52918-63-5 General Information Cis-3-(2. mean peak urinary levels of cis-3-(2.2-dibromovinyl)-2. Thus. Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2.3-0.2-dimethylcyclopropane carboxylic acid of 0.S..2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.39 µg/L...2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.Pyrethroid Pesticides Deltamethrin CAS No. Baker et al.2-dibromovinyl)-2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)-2.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample.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. Urinary levels for adults and children in these studies were similar (Heudorf et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of cis-3-(2. in some situations replacing the use of DDT.. 2004). 168 Fourth National Report on Human Exposure to Environmental Chemicals .5 μg/L) than the detection limit (0. 1990). 2006) and 1177 urban adults and children (Heudorf et al..

1.Pyrethroid Pesticides Urinary cis-3-(2.1 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.2-Dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 169 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

et al. Ball M. Int J Hyg Environ Health 2006. International Programme On Chemical Safety (IPCS). Seiwert M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. [online] 1990.113(6):782-786. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Heudorf U. Third National Report on Human Exposure to Environmental Chemicals. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.Pyrethroid Pesticides References Becker K. Atlanta (GA).htm. Environmental Health Criteria 97.109(3):213-217. Heudorf U. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Hoppe HW. and genotoxicity in exposed children. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Available at URL: http://www. Lopez-Guzman OD. Angerer J. Environ Health Perspect 2001. Int Arch Occup Environ Health 2004. Deltamethrin. Carranza C. Angerer J. Schulz C. Grimaldo M.inchem. Heudorf U.org/documents/ehc/ehc/ ehc97. Angerer J. Drexler H. Environ Health Perspect 2005.77(1):67-72. Int J Hyg Environ Health 2006. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Batres LE. Angerer J. Kolossa-Gehring M. 2005.209(3):221-233.209(3):293-299. Torres-Dosal A. et al. toxicokinetics. Butte W. Centers for Disease Control and Prevention (CDC). 5/26/09 Ortiz-Perez MD.

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

Fourth National Report on Human Exposure to Environmental Chemicals 173 .90) 1.260-.72 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.33) .65 (1.406) .18 (1.210-.71 (1.300 (.507 (.470-.610) .510-.78) 1.454 (.321 (.49-2.570-.89-71.21 (2.265-.352-. Survey Geometric mean (95% conf.940) 1.300 (.12) 4.260 (.277-.53-3.05) 1.1) 3.340) .740 (.820) .23 (2.35) 2.38 (2.42-2.79) 3.267 (.53) 1.04-5.190-.560-1.230-.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.45 (2.560-.12) .247-.490) .320) .295) .530-.373) .830) 90th 1.590 (.550-.86 (1. Deltamethrin.220-.41-3.46) 2.27-2.16) 1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.45-5.240 (.25 (2.650 (.29-1. population from the National Health and Nutrition Examination Survey.253-.233-.340) 1.270) .350-.35 (2.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .230-.51-6.32 (2.190-.46) .48-2.S.750) .390) .32 (1.311 (.63 (3.210-.570-1.320) .26) 2.374) 99-00 01-02 99-00 01-02 99-00 01-02 .83-11.364) .710 (.33 (1.440) .780) 4.384) .800 (.355) .34) 8.27-11.600 (.434) .990) .530-.65-2.41 (1.92-3.75 (1.78) 1.320) .230 (.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 .38 (2.39) 2.740 (.586) .27-2.297 (.490-.750-1.160-.41) 3.13) .250 (.12 (.05) .298 (.35) 2.43) 3.266-.03 (3.25-4.52-4.280 (.54) 1.601) .69 (1.710 (.320) .25-7.246-.250 (.560-.315 (.850) .292 (.300 (.240 (.62) 5. interval) .330) .30) 3.34 (2.417 (.370) .180-.1) 3.227-.02-6.288 (.430-.200-.49 (1.420) .870 (.238-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.428-.360) .8) 3.30 (1.52-5.250-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .290 (.340) 75th .78 (1.620-1.520 (.190-.226-.288-.271-.450 (.69) 3.260 (.76 (1.1.800) 1.30 (.700-1.25 (2.387) .01 (1.510-.33 (2.18 (2.850) .26-2.700 (.35) 1.62-6.78) 6.336 (.51-3.314) .353 (.640 (.270 (.427) .760 (.300) .64) 697 680 524 701 603 957 Limit of detection (LOD.56-5.200-.160-.369) .590-.1) 3.60) .320 (.840-1.32-21.48-2.595) .55 (1.276-.16-1.260 (.430-.230-.730 (.93 (1.750) .04) .34-6.14-6.314 (.28) 1.62-8.49-2.670 (.630) .960 (.190-.328 (.820) .810) 1.81 (1.250 (.830-2.273 (.292-.1 and 0.200-.35 (1.63-3.73) 1.362) .26) 2.36) 1.230 (.330) .49 (1.41-2.25-1.680 (.50 (2.13 (.325 (.44) 5.

00) 1.580) .590) .19) 2.11 (. Survey Geometric mean (95% conf.220 (.280) .740) .229-.224-.74) 3.437) .55) 3.15-2.930) 1.272) .41) 1.16-4.261 (.362 (.330) .94 (1.860-1.280 (.440-.670) 3.49) 1.290) .53 (1.88) 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 .200-.226-.240 (.400-.210-.274-.390-.03 (.13 (.480-.80) 4.610 (.510 (.323 (.246 (.36-6.61-2.860-1.95) 1.550 (.22 (1.190-.750-1.220-.550 (.350 (.490-.216-.0) 3.43) 1.178-.52) 2.677) .62) 1.81 (1.280-.930) .25-5.75-8.43 (2.590) .270) .278) .91-4.52 (1.510 (.43-64.190 (.44) 2.440-.02-1.446) .370 (.250 (.41-4.17-1.19 (2.299-.64-5.261-.630) .387) .36 (1.490 (.309) .960-1.372) .330) 1.06-3.00) 5.330 (.312 (.00) 1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .200-.49-2.530-.274 (.39) 1.240-.380-.73-4.07) 2.640 (.540 (.230-.275 (.290) .730) .02 (2.37) 1.500) .35) 1.840-1.67 (1.05-3.480 (.72 (1.91 (2.03-1.420-.91) .43 (1.90) 3.330) .280 (.410-.329) .270) .309 (.321-.17 (.460-.13-1.329) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.91) 9.173-.250 (.32 (2.63-3.590-1.730-1.378 (.51-7.21-4.73) 1.670) .400-.11 (.200-.67) 1.440-.450 (.234 (.380 (.83) 1.400) .250) .07-5.310) .04 (3.300-.530-.37 (1.534) .510 (.550 (.225-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .62) .640 (.311 (.264 (.370-. population from the National Health and Nutrition Examination Survey.240 (.270-.423 (.60) 1.272 (.650) .40) 2.270 (.19-6.320) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.210 (.720) 90th 1.35) .48 (1.10 (2.730) .330) 75th .227 (.860 (.240-.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .490 (.35-3.63) 1.49 (1.316 (.160-.240 (.40 (1.270 (.S.88-5.60-4.21 (1.580 (.410) .290-.27) 1.09-2.280 (.253) .25-2.04 (.86 (1.720 (.401) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.240-.570) .35 (1.590) .328) .230-. Deltamethrin.460-.210 (.55 (1.350) .240-.700-1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .238-.560 (.190-.271-.13-1.202-.09 (.280) .83 (1.09-2.230) .49) 3.44 (1.96 (1.54 (1.25) 2.300-. interval) .760) .200-.84 (1.240 (.335-.67 (1.150-.357) .09) 3.810) 1.

Lopez-Guzman OD. Angerer J. Torres-Dosal A. Environ Health Perspect 2003. Grimaldo M. Environ Health Perspect 2006.114(9):14191423. Seiwert M. Carranza C. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.205(6):459-472. Berger-Preiss E.76(7):492-498. et al. Hadnagy W. Hoppe HW. Ranft U. Leng G. Lu C. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Olsson AO. Ortiz-Perez MD. Liu Z. Environ Health Perspect 2005. Obel J. Ball M. Sugiri D. Barr DB. urban cohort. Int Arch Occup Environ Health 2003. Levsen K. Leng G. Becker K. Bartell S. Third National Report on Human Exposure to Environmental Chemicals.113(6):782-786. Kolossa-Gehring M.111(1):79-84. Arch Environ Contam Toxicol 2004. Batres LE. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Barr DB. Idel H. Exposure to indoor pesticides during pregnancy in a multiethnic. Deych E. 2005. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Berger-Preiss E.46(3):281-288. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.206(2):85-92. Godbold J. Int J Hyg Environ Health 2003. et al. Berkowitz GS. Lapinski R. Bravo R. Sugiri D. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2002. et al.Pyrethroid Pesticides References Baker SE. Hardt J. Atlanta (GA). and genotoxicity in exposed children. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Pearson M.209(3):221-233. Idel H. Biological monitoring of workers after the application of insecticidal pyrethroids. Ranft U. Centers for Disease Control and Prevention (CDC). toxicokinetics. Angerer J.

The absorption.350 (.220 (.170-.280) .430 (.125 (.130) < LOD .200 (.080 (<LOD-. 7440-36-0 General Information Antimony is found in ores or other minerals.260 (.390 (.220) .110-. and refuse incinerators that process or release antimony.150-.154) .190 (.130 (.098-.120-.07.130 (.390-.130-.150) . and 03-04 are 0.04. 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.430 (.119) .330) .133) * .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.260) .250-.250 (. metal bearings.470) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.350) .310) .160-.114) .117-.230-.140 (.128 (. It is also used in paints. 176 Fourth National Report on Human Exposure to Environmental Chemicals .400) .207) .095 (. respectively.310) .184) .370) .430 (.130 (.130-.470) .140 (.100 (.130 (.190) .190-.220-.270 (.110-.350-.560) .190) . < LOD means less than the limit of detection. Dermal contact with soil.158 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.460 (.144) .157) .140) .230-.330-.460) .120-.310 (.400) .140 (.280-.135) * .210 (.360) .200 (.160-.136-.120-.130-.115) .280-.170 (.090) 75th .280 (.200-.110-. or other substances containing antimony is another means of exposure.100 (.04.350-.160-.200) .220) .230) .460 (.130) .140 (. see Data Analysis section) for Survey years 99-00.570) .230-.137) .200 (.120 (.400 (.320-.210) .320-.250-.120) .131-.140) .130 (. solder.240 (.270) .150-.100) .090 (<LOD-.070-.320) Total .160) .126 (.109-.180-.160) .290-.220-.130-. enamels.350) . and as a fire-retardant in textiles and plastics.160) .176 (.110) .120-. 0.210) .141-.280-.340 (.300-.080-.230) .470 (.400 (.200) .270-. and pewter.350 (.200 (.260) .120 (.500) .600) . ceramics.180 (.360) .120 (.210-. 01-02. 0.290 (.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 .260-.190 (.190-.105 (.280 (.120) .390) .136) * .164-.300 (.210-. and 0.130-.190 (.250) . population from the National Health and Nutrition Examination Survey.079-.240) .150-.088-.100-.330-.154) .170 (.180-.087-.200) .120-.330 (.220 (.250 (.110 (.240 (.130) .120-.145) Selected percentiles ( 95% confidence interval) 50th .150 (.230) .140) .320-.340 (.190) .180 (.160) .115-.170) .530) .160 (.103) .070 (<LOD-.360-.320 (.440) .340) .190 (.178) .132 (.140) . Antimony enters the environment from natural sources and from its use in industry.130 (. sheet and pipe metal.270 (.150 (.310 (.390) .510) .390-.080) .160) . interval) .120) .180 (.160 (.170-. storage batteries.330) .150-. from air and drinking water. coal-fired plants.220-.160) .080) .150) 90th .360 (.370-. castings.230-. ammunition.090 (.320) .490) .210) .460 (.120-.200 (.280-.110-.250 (.170-.120 (.175 (.250-.190-.126-.180-.210 (.099 (.440 (.240-.350 (.350) .128 (.240 (.310-.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 .250-.090-.143 (.108-.170-.220-. and +5. fireworks.300-.260-.210) .146 (.500) .220-. water.120 (.400) .190-.350-.270 (.300 (.220) 95th .070 (<LOD-. which may vary for some chemicals by year and by individual sample.180 (.390-.260) .108 (.280) .119-.134-.240 (.710) .400 (.169 (.122 (.180-.150 (.220) .310 (.156-.390) .140) . to a lesser extent.130-.142 (.270 (.210) .S.310-.220-.230 (.123 (.150-.130) .140) .280) .310 (.160 (.197) .240 (.410) .180) .280) .190 (.440) .350 (.230-.420) .230 (.120) .130 (.161) .090-.330 (.320-.300) .320 (. and excretion of antimony vary depending on its oxidation state.130 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.093 (. People are exposed to antimony primarily through food and.190) . distribution. Stibine is a metal hydride form of antimony used in the semiconductor industry. It is used in metal alloys.120-.200 (.Metals Antimony CAS No.130-.137) .180 (.280-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.140-.100-. Workplace exposures can occur at smelters.360 (. and glass.200) .120-.270) .190-.170-.350 (.330) .400-.410) .145 (.112-.330) .200-.200-.190) .300-.330 (.150) .148-.390) .117-.134 (.410-.300) .260 (.490 (.154-.160-.290-.095-.180-.230 (.180) .240-.132 (.150) .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 .260 (.200-.180 (.350) .300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. +3.

081 (<LOD-.203) .127) .205-. and route of exposure (Elinder and Friberg. 1944).228-.248) .280-.741) .104-.097-.113-.137 (.198) .126) .120 (. skin.085) . diarrhea.130) .269 (.333) . abdominal pain.357-.107-.400 (.294) 316 368 290 663 762 725 1297 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .161) .191 (.123) .241-.151) .267-.109 (.250) .257) . 1995).119 (.352 (.333-.333 (.176 (.167-.208 (.082) .156-.278 (.294) Total .140) < LOD .220) .153 (.113) .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.135 (.195-.391) .248-.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 .247) .225 (.185-.117-.086 (.471) .149) .263 (.156 (.159-.300) .167 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.096-.150-.144-..30) .164 (.082 (<LOD-.111-. 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.163 (.373) .193 (.089) .136) .164-.209 (.173 (.162-.429 (.320-.272) .081) .250-.143) .152) .233 (.214) .343 (.120 (.135) .154-.176 (.129 (. 1958) and occupational exposures (Briegner et al.087) .102-.126-. Inorganic antimony salts irritate the mucous membranes.380 (.114 (.295 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.176-..200-.267 (.100 (.208-.320 (.153-.080 (.124 (. 1988.114 (.112 (.119-.204-.131-.310) . and eyes.159-.170 (. 1986).333 (.131) .145) . Ming-Hsin et al.417) .315) .308-.225) .124-.277 (.194-.186) .143) Selected percentiles ( 95% confidence interval) 50th .207) .135) .195 (.121) .118 (.357) . Acute antimony poisoning may cause a metallic taste. population from the National Health and Nutrition Examination Survey.242-.300) .138) * .098) .092) .178 (..129) * .317) .106-.321) .076-.115) .125 (.438) .148-.147) .338 (.444) .281-.727) .288 (.068 (.127) .077) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.124-.320-.125-.171) .. 1973).Metals than for trivalent compounds (Elinder and Friberg.266 (.173-.152) .268) .213 (.391) .146) .175 (.271-.172-.139 (.317) .430) .253 (..238) .116-.103-.099-.122 (.092-.255) .233-.471 (.095-.333-.138-.179-.102-.138 (.075 (.131 (.095-.261) .130 (.250 (.333-.086) 75th .129) .310 (.333-1.189 (.193) .352) .122 (.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 .333 (.139 (.124) .068-.173 (.250-. 1986).265 (.135 (.256 (.187) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.192 (.182 (.206-.111 (.108-.108-.741 (.118 (.129 (.250-.298 (.196 (.146-. and gastrointestinal symptoms such as vomiting.371 (.192) .480) . species.120 (.417) .098-.161) .300 (.318-.222 (.265-.115 (.074 (.181) . Histopathologic inflammatory and degenerative changes in the lung.228 (.132 (.236 (.263-. and ulcers (Werrin.112 (.178-.133) .127 (.250 (.132) .109 (.107-.143) 90th .188) .S.146-.080 (<LOD-.078 (.120 (.278) .364 (.317) . 1953).414) .444) .313-.425) . myocardium.126 (.079 (<LOD-.148-.084) .405) .235-.239-.364 (.500) . interval) . 1954).140) .209) .280 (.209) .241-.320) .115 (.318-.061-.115-.173) .106-.183) .135) .238 (.200-.429) .276 (.167 (.230) 95th .233) . 1962).164) .250-.310) .112-.185 (.224 (.238) .114 (.209-.076-.117-.385 (.267) .108-.143) .146-.230-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.195-.147-.075 (.217 (.200-.109-.185 (.200) .127) .108 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.069-.160 (.338) .121 (.259 (.115 (.119-.082) .107-.116 (.121 (.098-.117-.115-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.286 (. and kidney have been demonstrated in high dose animal studies depending on the dose.113-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .134) .149-.255-.192-.150-.447 (.227-.130) .138-. liver.104-.253-.123 (.211) .130) .181) .199-.069-.338 (.143 (.188-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.244-.163 (.228 (.485) .103-.099-.203) .308) .127) .159-.421) .229-.245) .071-.105-.320 (.167 (.148) * .128-.181) .226 (.

and a drinking water standard has been established by the U.158:165-190. Br J Ind Med 1991. Rev Infect Dis 1988. HH. Trace element reference values in tissues from inhabitants of the European community I. New York: Elsevier. 1995... which may be due to methodologic.cdc. Chen J-R. Biological monitoring of exposures to aluminum.html. Cheng-Wei L. Piatnek DA. Industrial antimony poisoning. Liao Y-H.. respectively. Schacke G. Iavicoli I.. Ju-Sun P. Yang C-Y. Stone FD. eds.Metals to antimony have been established by OSHA and ACGIH.521-523. et al.10(3):560-586. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Friberg L. Caroli S. Antimony trioxide is rated by IARC as a possible human carcinogen. Petrucci F. Nau CA. Mayne P. Industrial Medicine 1944. Sabbioni E. arsenic. Element reference values in tissues from inhabitants of the European community. Luedersdorf R. Briegner H. Stead FM. Kiberd B. J Clin Pathol 1998. Kentner et al. 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. stibine. Alimonti A. 2nd ed. Fuchs A. Wu M-T. Roland H. VI. EPA. or exposure differences. Minoia C. Semisch CW. Delves HT. J Trace Elem Med Biol 2002. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Hamilton EI. Dunkelberg. 2005. Cordasco EM. Third National Report on Human Exposure to Environmental Chemicals. Apostoli P. Chemotherapy for leishmaniasis: Biochemical mechanisms. Centers for Disease Control and Prevention (CDC). Pulmonary edema of environmental origin.13:361-362. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.. Kuo-Juie Y.64(2):182-185. et al. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect.. Shao-Chi C.. Lenert G. Vouk VB. Dernehl CU. Pietra R. Suchenwirth R. 1994) have reported values slightly higher than those in this Report. 20012002. 1998) or compiled reference ranges (Hamilton et al... Paschal et al.106:33-39.)1954. environmental levels) and health effects is available from ATSDR at: http://www. Environ Health Perspect 1998. and hydrogen sulfide. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Antimony in blood and urine of infants. Review of elements in blood. population. Konings J. Int Arch Occup Environ Health 1987. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. gov/toxpro2. Cullen A.48:93-97. 1990. Iavicoli et al. Carelli G. 1986. Mahieu P. Int Arch Occup Environ Health 1995. Costeloe K. 1998). Atlanta (GA). Van der Venne MT. External and internal antimony exposure in starter battery production. 2004. indium. Bolten C. Kentner M. Lauwerys R.46:931-936. Handbook on the toxicology of metals. and 2003-2004. and future strategies. Weltle D. Yu H-S. Pilgrim L. Matthews T.76(2):103-115. 2002. Pozzoli L. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. clinical efficacy. Mayer P. Liao Y-H et al. Urinary antimony in infancy. even when exposure levels were below workplace air standards (Bailly et al. Leinemann M. gallium. Chia-Yu H. and antimony in optoelectronic industry workers. Industrial Medicine and Surgery (Dec. 1998. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Biomonitoring of a worker population exposed to low antimony trioxide levels. O’Regan M. Arsine. Ho C-K. Buchet JP. Ming-Hsin H. Dezateux C. Elinder CG. Sci Total Environ 1994. Wade A. Gebel TW. Schaller KH. Earlier measurements in general populations (Minoia et al. pp.. Arch Dis Child 1997.S. Sabbioni E. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Delves HT. Chin Med J 1958.51:238-240. Nordberg GF.. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Biological assessment of exposure to antimony and lead in the glass-producing industry.67:119-123. Skulsukai G.16: 33-39.59:469-474. 1991. Stasney J..e. 1997). Gallorini M. Bailly R. Antimony. Ludersdorf et al. In: Friberg L. Information about external exposure (i. References Berman JD. plasma and urine and a critical evaluation of reference values for the United Kingdom population. et al. J Occup Environ Med 2004. 26-42. Stocks J. Dezateux et al. Chest 1973. 1987).76:432436.atsdr.

Paschal DC. Quarterly Bulletin of the Association of Food and Drug Officials 1962. et al. Sampson EJ. Renes LE.76(1):53-59. Chemical food poisoning. Antimony poisoning in industry. Pirkle JL. Fourth National Report on Human Exposure to Environmental Chemicals 179 .Metals in urine. 27:38-45. Ting BG. Trace metals in urine of United States residents: reference range concentrations. Environ Res 1998. and serum of Italian subjects. Morrow JC. Werrin M. Industrial Hygiene and Occupational Medicine 1953. Jackson RJ.99-108. blood. Sci Total Environ 1990.95:89-105.

were used as treatments for syphilis.1 (32. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. In the last century. referred to as inorganic arsenic compounds. to a lesser extent.1-40.90 (7.5) 95th 65.2) 15.5) 41. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. Arsine (AsH3) is a reactive.6 (9. gaseous hydride manufactured in small quantities for use in the semiconductor industry. cancers.90 (5.5 (14.55 (7.8) 33.5) 66.00 (6. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.90 (7. cacodylic acid.5) 43.20 (8.S.90-8.50 (8.19-9.9 (8.77) 6. lead hydrogen arsenate.1) 7.1) 15.2) 46. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1) 1281 1276 03-04 03-04 03-04 9.8-61.3-15.10-7.84) 8.50-14.90-11. and arsenosugars.6-43. though in some locations arsenite may be prevalent (WHO. and. and play sets.4-65. Survey years 03-04 Geometric mean (95% conf. Arsenic is measurable in most soils. psoriasis. General population exposure to inorganic arsenic can occur through consumption of drinking water and. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. mental disorders.7-83.2 (41.4) 40. Gallium. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.2-61.3-111) 78. Arsenic trioxide is approved to treat acute promyelocytic leukemia. and foods.1 (38.8-77.70) 8.3) 10.3-19. The United States no longer produces arsenic from mining but imports about 22. Arsenic trioxide (As2O3. grain.5 (23.25-9.9-62.Metals Arsenic CAS No.8) 30. arsenic as elemental metalloids may be used in some ammunition.5-41.5-19.9) 21.30) 17.12 (6.1) 290 725 1542 03-04 03-04 9.4 (24.2-20.2 (13.5 (34.5 (40. such as arsenopyrite (FeAsS) and realgar (As4S4).2-93.30 (6. pesticides.0-19.00-9.8) 7. copper arsenates.9-46. Arsenic and its compounds have had many uses in the past and present as medicines.9 (17. and other metals. as alloy in metal bearings.8) 17.7) 90th 37.4 (26. In nature. and produce. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.6) 618 722 1074 Limit of detection (LOD.0 (14. or rarely as elemental metalloids (yellow. meats.9-34.2-17.70 (6.66-8.80-9. it is found in over 200 crystalline or mineral forms.6-35. Various arsenic compounds were used in paint pigments and for tanning animal hides.27) 9.10 (6. Although it is still widely used in the United States. arsenic compounds.12-10. ocean and fresh waters. population from the National Health and Nutrition Examination Survey. to a lesser extent. and arsenates (oxidation states of -3. and gray forms). Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. 2005). alloys. black. and as a cosmetic to lighten complexion.8) 34.90-14.10) 10.0-60. the smelting of copper.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. +3 and +5).7 (11.000 metric tons annually. Since the 1940s.90-8.30 (7.0 (43.1-18.4) 13. sodium arsenite. arsenocholine.70-9. arsenites.90) 75th 16. from coal burning.5 (36. Water sources contain mostly inorganic arsenate. aluminum. solders. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.4 (7.9) 68.4 (48. particularly arsenic trioxide.6) 11.10-10. 2001).0 (11.5-178) 46.8) 29. lead.90) 16.34-9.4) 60. semiconductors.6 (15. mostly for use in wood preservation (ATSDR.84) 8.4 (31.90-7.80) 6.0 (22.57) Selected percentiles ( 95% confidence interval) 50th 7.41 (7.6 (13.13-8.6 (32.80 (5.02-8.6-141) 53. and in lead-acid storage battery grids. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.8 (48.97) 8. see Data Analysis section) for Survey year 03-04 is 0.0 (15.7) 65.7-95. interval) 8. Also.08 (5.5-52.29 (8. and as homicidal poisons.74. retaining walls. Before the 20th century.8) 7. and indium arsenides are used in the semiconductor industry.34-10.2 (12.2 (51.40) 7. trimethylarsine oxide.7) 24. 180 Fourth National Report on Human Exposure to Environmental Chemicals .

4-64. gallium arsenide and indium arsenide. U.5) 290 725 1542 03-04 03-04 8.38-10..88 (5.g. 2007. age. The semiconductor dopants. as observed in Bangladesh where millions of people have been exposed.66-8. organic arsenic can be converted back to methylated and inorganic arsenic.8 (12. shellfish. Fish.4) 54.7-35. EPA.7-34. 2001).6 (10.8-62.76 (6.96) 12. inorganic arsenic is widely distributed within the body.3-41.06 (4. 2001). population from the National Health and Nutrition Examination Survey. have caused clinical arsenic poisoning. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.4 (11. Direct exposure to DMA and MMA may result from use of the two pesticides.0 (17.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .66-8.0 (31.33 (6.0) 12.1) 7.4) 32.41) 6.5-17.0) 42.88) 7.28-7. Extremely high groundwater arsenic levels.2) 15.44) 6.01) 7. kelp.86-17.47 (7. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. dose level.1) 8..0) 1281 1276 03-04 03-04 03-04 8.0-69.S. trimethylarsine oxide (TMAO).4 (40.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.18 (5. Though modest bioconcentration occurs in some aquatic life.7 (25..20-9.10-8.07-9.8-32.3 (27. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.32 (5. 2001.0) 33.01) 11.7-188) 27. but is poorly absorbed dermally (WHO. WHO. selenium. and arsenosugars.9-56. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.45) 5. arsenic does not show biomagnification in the food chain (WHO. In aquatic sediments.7) 95th 50. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.2-46.0) 14.7 (9.2) 90th 30.5 (9.44-11.66 (7..7-17.9) 53.4 (12.8 (27. 2001). 2007.33-10.30-9.5-120) 40.0-26.6) 45.25-9. Smoking tobacco is also a source of inorganic arsenic.8) 22.3-62.3-53.2 (12.1 (11.61 (7. are used in enclosed ultraclean operations within the semiconductor industry.99-9.2) 40.7 (11.6 (35. Children may have additional exposures from ingestion of contaminated soils (e.04) 7.6 (17. mine tailings).S. dust.24 (7. Inorganic forms of arsenic demonstrate high acute toxicity.3) 9.75 (5.59) Selected percentiles ( 95% confidence interval) 50th 7.93-8.51) 75th 14.4 (42.31 (6. 1988). Arsenate is reduced in the body to arsenite (oxidation state +3). EPA’s maximum contaminant level (Hughes.47-6.8) 27. 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. 2001). arsenocholine. 2001).1) 6.8 (21.0) 26.0-38. 2001). 2001). Some studies suggest that variation in the degree of methylation among persons is related to the susceptibility of arsenicinduced disease and may involve consideration of genetic polymorphisms. and folate status (Chen et al.8 (20.40) 8.4 (26.9 (45.64 (7. 2006.5) 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 8.3) 6. 2007.1-36.93-9.75) 13.7) 28. 2003.7-18. WHO.81-9. cacodylic acid and monosodium methyl arsenate.00 (6.6-17.5) 17. Gamble et al. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.4 (24.3-64. interval) 8.50 (6.S. 2001.0-18.47 (6.8 (11. NRC.1) 24.04 (5.11 (5. After absorption.8-75.. Steinmaus et al. so exposure to the general population is extremely limited. In aquatic organisms.3 (24.23-7.25 (6.13) 8.9) 13. 2006. Survey years 03-04 Geometric mean (95% conf. and some other seafood can contain organic forms of arsenic including arsenobetaine. Chowdhury et al.1 (14. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.58-10. and contact with CCA-preserved wood structures. though some reduction may occur in the gut prior to absorption.12-10. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.10-16. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. 2001). Tseng..2-15.35) 7.1) 58.

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

In the German Environmental Survey III of 1998.. 2001).. and were about two-fold lower than those for the U.75 (<LOD-2. 2000).80 (<LOD-4. WHO. Compared with this Report. Valenzuela et al. Caldwell et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 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. Levels of total urinary arsenic in the U. 2008). Pellizzari and Clayton. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 2000.Metals compounds. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. median urinary total arsenic levels in 4052 adults varied with seafood intake.69 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.html. arsenic has been fetotoxic and teratogenic. DMA produced bladder cancer in some chronic rat studies (Cohen et al. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3.. Josyula et al.50) 1..50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2... Pellizzari and Clayton.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. gov/toxpro2. 1986). 1992. In a Nevada town where groundwater levels were naturally elevated.. Shalat et al. 2008).e. In animal studies. 2008. 1999.. 1999). Meza et al. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. and the FDA has established a bottled drinking water standard. environmental levels) and health effects is available from ATSDR at: http://www. 2001). 2006.. Consequently. 2001).00) 1.33 (<LOD-3. Offergelt 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..18) 3.. population from the National Health and Nutrition Examination Survey. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.S.. Caldwell et al..70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Calderon et al.33 (<LOD-3. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.. 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... 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.atsdr. 2006. 1998. 2004. but generally only at maternally toxic doses (WHO. 2006). Shalat et al. 2007. 2003.18 (<LOD-3. Survey years 03-04 Geometric mean (95% conf. 2006). IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Pellizzari and Clayton 2006). population (Rubin et al. 1999..S.41) 3. although urinary arsenic levels were not associated with CCA contact (Shalat et al. had decreased since the prior 1990– 1992 survey. 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.. 2006).19) 3.S...S. population in NHANES 2003–2004 (Schulz et al.75 (<LOD-2. 2004. Vahter et al. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.04 (<LOD-3.. 2006). 2006. 2007..cdc. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.. Additional information about external exposure (i.61 (<LOD-3.

3 (21. 1. arsenocholine. and duration of exposure are also considered important.8 (12.20) 18. 2001. After recent seafood ingestion.3) 35.3% of a representative sample of the U. 2008). DMA and MMA.70-21.30 (2. In the late 1980s.19 (. WHO.1-94. arsenocholine.6.1) 18.37 (1.S.. Individually measurable species resulting from inorganic arsenic exposure are arsenate. In the residents of a Chilean town who consumed water with high levels of arsenic. 1990.20 (2.20-3.8-50.29 (1..30 (1. Survey years 03-04 Geometric mean (95% conf.4) 23. Also.40-7.90-7.8) 35.5 (14.8. 2007). DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. Blom et al.30) 10..800-4. For residents of Inner Mongolia.9 (7.4 (16.1-25.80) 1. dermal keratosis.48-2. Caldwell et al.00 (1.7) 15. see Data Analysis section) for Survey year 03-04 is 0.2-38. population (Sun et al. When seafood intake is avoided.50) 90th 16.600 (.66 (1.900 (.1) 45.50-6. These associations are stronger at higher urinary levels. and TMAO..3) 1284 1284 03-04 03-04 03-04 1.50) .17-1. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. in NHEXAS 1995–1996. 2000.5 (26.3 (9. arsenobetaine. with DMA.62) 2.8-40. Caceres et al.43-1. methylation capacity.20-190) 31.e. population showed a higher contribution of arsenobetaine (Caldwell et al.6 (11.4) 31.. which may vary for some chemicals by year and by individual sample. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.10) 8.40) 75th 5.93) 1.800-1.2-35. Pellizzari and Clayton. geometric mean levels were about 70-fold higher than for the U.Metals other areas of the world (Ahsan et al..45 (1.700-1.5) 29.05) < LOD .20 (.7 (13.40) 5.70 (5.5) 292 728 1548 03-04 03-04 1. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8 (17.0 (26..9-23. 1985.. Tseng et al.20) 7.30) 2.. 2005. Valenzuela et al. 2008).11-1.800 (. and 0. 2001).0) 29.. Aposhian et al. 2006). population (Ahsan et al.6-44..80-5. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. In most human studies.6. China. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.4.20) 3.7 (21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 184 Fourth National Report on Human Exposure to Environmental Chemicals .0 (27.70 (3. vasospasm.80 (3. 4. respectively.50) .00-6.S. 2008).871-1.00-1.3) 95th 35. The higher percentiles of total urinary arsenic levels in the U.9) 13.31-1.83) Selected percentiles ( 95% confidence interval) 50th 1.20-25. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. 2000.7) 13. Chowdhury et al..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. 2008. Caldwell et al.5) 32. population from the National Health and Nutrition Examination Survey.2 (6.3-39.00 (. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.. when seafood organic arsenic is subtracted). and other factors such as nutrition. Arsenate. 1996.. 2007) with higher levels of arsenic in the drinking water.28) 1. and two methylated metabolic products.10) 4.20 (4.S.80 (. 2005.7-22. Measurable organic arsenic species in this Report are three biologically generated environmental forms.700-1.00) 3.9 (6. arsenite..900-1. MMA. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. 2003).20 (1.00-12. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.5) 621 725 1078 Limit of detection (LOD.74 (1. < LOD means less than the limit of detection.. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.800 (. interval) 1...80 (4.40-6.0) 4.60-3.4-35.68) . Some noncancer effects of arsenic (e. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.g..70-21. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.6 (13. 2008. 2008).400-.S. and TMAO were detected in only 7. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. Sun et al. 2005.90-29. 2000.1-51. arsenite.S.70) 6.500-1.800) 1. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.00-4.10 (4.. population in the NHANES 2003–2004 subsample.55 (1. Caldwell et al.0-23.60) 1.6 (25.

51) 5. 1992.37-2.13-39..55) 1.4 (11.4-21.2 (12. Fourth National Report on Human Exposure to Environmental Chemicals 185 .9 (13.Metals as with DMA.21) 5.51-2.14 (1. 2008).72) 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Information about the biological exposure indices is provided here for comparison.30-1.0 (9.91 (4. The 95th percentile of the U. 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) 13. 2007).4) 292 728 1548 03-04 03-04 1.5) 26. interval) 1.2 (12. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3) 95th 29.3-24.00 (1.4-82.18-1.6-46.531 (. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.5) 17.7) 30..47 (2.6 (9.S.15-1.2 (13.938-1.15-4.36) 2.7) 9.9 μg/L.8) 29.29 (4.65 (1.2 (4.88) 2.16 (.12) < LOD . Vahter et al.6-32.612-1.58 (3.7) 17. 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.25 (. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.64-29. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.43) 14.43) 75th 5..909-1. 2001).4-28.61-6.3) 1284 1284 03-04 03-04 03-04 1.81 (4. 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.67) 4.50-7... 2001)..638) 1. which is below the ACGIH BEI (Caldwell et al.83) 8.82) Selected percentiles ( 95% confidence interval) 50th 1.50-15. 1986.3 (10.28) 1.786-1.6) 19.6-29.82) 4.73-6.68 (1.80-153) 17. In recent years.88 (5. Sun et al.32-7.4) 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 * * 1.29-14.76-27.80) .54 (1..53 (.10 (. not to imply a safety level for general population exposure. WHO. population from the National Health and Nutrition Examination Survey.40) 1.39-3. population for the sum of inorganic related species was 18.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..05) 1.30) 1.40 (1.83) 2.400-.93 (1. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.78-5.25-7.877 (.5-20.9) 14.79 (1.3 (10.9-18.19-2. Survey years 03-04 Geometric mean (95% conf.833-1.78 (3.1 (26.47 (1.5 (18.6 (6.62-6.45) 1.901-2.15-1.5 (18.67) 1.11 (.4 (24. Offergelt et al. 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. 2008).959-1. 1998.00 (3.0-36. 2006.91) 90th 16. 2003.S.44 (1.05 (.1-36. Caldwell et al.1) 26.9) 32.1-18.70) 5.4) 32.9 (25.

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

29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 187 . interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Urinary Arsenous (III) Acid (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. see Data Analysis section) for Survey year 03-04 is 1.76) < 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.44) 2.40 (<LOD-1.20 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < 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. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.80) < LOD 621 725 1078 Limit of detection (LOD.2.00 (<LOD-3.00 (<LOD-2.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95 (<LOD-2.08 (<LOD-4.70) < 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 2.00) 1. Survey years 03-04 Geometric mean (95% conf. Survey years 03-04 Geometric mean (95% conf.

00-4.0-16.73 (3.0-17.81 (5.11 (3.60-6.3 (8.67) 9.00-4.0) 11.17-4.95-6.6) 292 728 1548 03-04 03-04 3.69 (3.10) 3.3 (8.70-12.00-7.59 (6.03 (3.92-12.49-4.00-7.0 (13.00) 6.34 (3.0) 13.00-5.0 (10.5 (11.0 (11.57-5. interval) 3.0) 292 728 1548 03-04 03-04 4.00 (7.00 (4.15) 4.27 (3.45 (8.32 (4.0-17.0-18.24) 3.S.00-12.0) 95th 16.94) 3.00-9.05) 10.0) 17.60-7.16-11.89 (3.0-19.73) 6.0 (14.34-4.71 (3. Survey years 03-04 Geometric mean (95% conf.31) 4.98) 4.00 (7.20) 11.0 (10.00-7.78) 4.70-3.00-11.25 (4.0) 11.0 (9.00 (5.00-15.49) 10. 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 1.95 (4.00 (3.00-13.70) 5.57 (3.32-10.0 (12.00 (5.0) 621 725 1078 Limit of detection (LOD.4 (7.0) 9.91) 75th 5.13-4.34-4.95-4.0 (10.94-3.80-3.69-3.7) 1284 1284 03-04 03-04 03-04 4.0) 16.00-10.9) 13.61-11.19) Selected percentiles ( 95% confidence interval) 50th 3.62) 4.06) 5.16 (2.0) 9.9) 12.14) Selected percentiles ( 95% confidence interval) 50th 3.6-18.00 (6.00-11.95-3.33-4.45) 8.00) 9.77 (3.00-11.00) 6.48 (3.00) 5.8) 7.0) 9.33) 3.45) 3.28) 2.37 (2.97-3.5) 95th 13.7) 12.92) 3.69 (3.00) 4.12 (3.34) 3.90) 5.65-8.0) 17.00-3.79 (3.80) 7.39-3.3 (7.00) 90th 11.09 (7.0-16.61-16.1-15.71-4.00) 3.00) 75th 6.00) 6.70-4.00 (5.03-6.00 (3.7-16. Survey years 03-04 Geometric mean (95% conf.05) 3.00 (3.74 (2.90) 2.0 (9.0) 12.72 (4. population from the National Health and Nutrition Examination Survey.48 (2.00-15.44) 5.38 (3. population from the National Health and Nutrition Examination Survey.86 (2.8) 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 3.6 (9.84-18.84-8.6) 1284 1284 03-04 03-04 03-04 4.16 (4.0) 14.82-9.52) 3.30 (7.74) 90th 9.00 (6.00-3.11) 4.00-4.18 (6.80-5.0) 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 4.00-4.90 (3.0 (12.34 (3.86-7.2) 10.32 (8.00 (5.20-12.70 (3.60-3.5) 12.0) 16.0-25.55 (2.7) 13.7.00 (3.67) 8.00 (3.50-15.50 (4.9) 11.00-4.46 (4.08 (2.0) 10.00 (3.0 (13.0 (8.00-15.00-8.00 (5.00) 6.27 (2.00-7.00-4.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .69-6.S.00) 3. interval) 3.14) 3.80 (4.88 (4.0 (9.60-4.78 (4.1-22.00) 12.29-4.17-6.65-6.00) 7.9 (7.37 (3.22) 4.27-5.85 (3.0 (10.71) 3.30) 3.80-6.80) 2.44 (2.27-2.86-21.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7 (10.31-4.20-4.00 (6.00) 4.1-18.24-4.05) 5.17 (2.12-4.00-22.42) 3.00-12.0) 13.9 (11.10) 6.82-5.82) 3.8) 7.0-12.50-5.9) 5.0 (8.71 (4.1 (8.

70-3.71-2.00-2.70-2.80) 1.16 (2.20 (1.23) 1.00-4.07) 2.20-1. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.81) 1.11-1.10 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.S.57) 95th 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .90) 1.30-2.17) 2.82-2.40 (2.00 (2.985) 1.30 (1.50 (<LOD-1.60) 2.96-2.10-3.60 (2.79) 2.40-3.50 (2.53 (1.00 (1.14-1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80-2.73-2.07-3.00-1.900-1.52 (2.10 (.34) 2.40-2.77) 1.30 (1.30 (2.31 (1. 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.33 (1.00 (<LOD-1.28 (1.40-2.00) 1.33 (1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.20 (1.S.53-2. see Data Analysis section) for Survey year 03-04 is 0.00) 2.63 (<LOD-1.85) 2.60) 2.18-1.61) 2.30 (1. < LOD means less than the limit of detection.46-2.22) 3.82-2.93) .30-1.40) 2.31-3.20) 2.00-2.00) 1.36 (1.90 (1.40) 1.90) 2.30) 2.35-3.80-2.60) 1.00) 2.20 (1.10) 2.00 (2.40-3.10-1.80 (1.15-1.30-1.90) 2.36) 1.20-3.70-2.60-2.40 (1.10) 95th 2.60 (1.10-1.50 (1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.61-3.70-2.86 (2.28 (1.20 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10 (<LOD-1. Survey years 03-04 Geometric mean (95% conf.86 (2.18-1.43-3.84-3.22 (1.90 (2.40) 1.07 (1.50-2.86) 2.80 (2.54) 90th 2.10 (1.00-1.58) 2. population from the National Health and Nutrition Examination Survey.85) 1.80) 1.88 (1.10 (.50 (1.05-1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30) 90th 1.80 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) 621 725 1077 Limit of detection (LOD.70-2.45) 3.20 (1.80 (1.20 (1.00 (<LOD-1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30) 1.50) 1.62) 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 1.80 (1.37 (1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.70) 2.816 (<LOD-.853-1.86) 3.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.46 (1.88 (1.9.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.30) 1.88-2.00) 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. see Data Analysis section) for Survey year 03-04 is 1. 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.S. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 190 Fourth National Report on Human Exposure to Environmental Chemicals .0. < LOD means less than the limit of detection. 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. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.

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Garcia-Montalvo EA. Buchet JP.57(2):79-91. 2001. Investigating childhood leukemia in Churchill County. Arsenic in drinking water-2001 update. Sun G. Calderon-Aranda ES. Wang Z. 2001. Yuan Y.S.49(6):387-393. et al. J Anal Toxicol 2006. Buckley BT. Shipp M. Ferreccio C. Kieszak SM.367(1):80-88. CruzGonzalez MB. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. Pellizzari ED. Erratum in: Toxicol Appl Pharmacol 2006. Chen CJ. et al. Toxicol Appl Pharmacol 2005. Environmental Protection Agency (U.222(3):374-380. Tseng CH. Rubin CS. Valenzuela OL. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells. Holmes AK. Tseng CH. Arsenic. 1998 [online]. 2nd ed. urinary arsenic metabolites and human diseases: current perspective. Gandolfi AJ. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS). et al. Sci Total Environ 2006. Toxicol Appl Pharmacol 2007.inchem. Washington (DC) National Academy Press.115(4):648-652. Environ Res 2004. Moore LE. EPA 815-F-00-015. Rumpler A. Solo-Gabriele HM. Xu Y. Li B. Garcia-Vargas GG. Lauwerys RR.S. html. A pilot study of children’s exposure to CCAtreated wood from playground equipment. Int J Hyg Environ Health 2007. EPA). using a routine LC-ICP-MS method. Nevada. Jhangri GS. Huang YK. pp. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. In:Industrial Chemical Exposure. Schulz C. Zhang H. U. Chem Res Toxicol 2007. Borja-Aburto VH. Kalman D. Jones RL. Offergelt JA.S. Environ Health Perspect 2006. Sonora.20(8):1120-1125.epa. Flanders WD.htm. Becker K. Huang YL. Francesconi KA. Jin Y.113(3):250-254. inorganic. Nygren A. Environ Health Perspect 2005. Clayton CA. 8/7/07 U. Int Arch Occup Environ Health 1986.210(3-4):271-297. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Environ Health Perspect 2006. Ochi T. Kopplin MJ.25(1):1-22. Lauwerys R. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals .36-37. et al.114(2):220-227. Available at URL: http://www. Roels H. Lu X. Arsenic methylation. Burgess JL.211(2):175.Metals Kwon E. Arsenic exposure. Li L. Rahnster B. Liaw J.206(3):299-308. Environ Health Perspect 2007. Morton J. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Smith AH. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Boca Raton (FL). Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. Arsenic on the hands of children after playing in playgrounds. Chung CJ. Naranmandura H. Marshall G. Yang MH. Arsenic. Lewis Publishers. Fleming LE. Available at URL: http://www. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Mexico. Available at URL: http://www. National Research Council (NRC). 8/7/07. 3rd Ed. Guidelines for Biological Monitoring. Suzuki KT.30(5):293-301. Li X. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. Kolossa-Gehring M.K.70(2):159-170. Vahter M. Ibata K. Environmental Health Criteria 224. urinary arsenic speciation. January 2001 [online]. Biggs ML. Belson MG.gov/safewater/arsenic/regulations_factsheet. Friberg L. China. Goessler W. et al.115(1):151-157.htm. Black K. J Toxicol Environ Health A 2007. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U.S. Fok N. Genetic polymorphisms in MTHFR 677 and 1298. Mason H. Meza MM. Raml R. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Integrated Risk Information System.epa. Conrad A. Environ Health Perspect 2004. Sun X. Rey OA. Arsenic in Drinking Water. Boeckx M.org/documents/ehc/ ehc/ehc224. Br J Ind Med 1992. Vahter M. Environmental Protection Agency (U. Geneva 2001.gov/iris/subst/0278.114(8):1293-1296. Hoet P. Environ Health Perspect 2007. von Ehrenstein O. World Health Organization (WHO). Nolinder P.112(14):1375-1380. et al. Shalat SL. Seifert B. GSTM1 and T1. Seiwert M. Fact Sheet: Drinking Water Standard for Arsenic. Steinmaus C.96(2):119126. et al. EPA). and metabolism of arsenic. Arsenic and Arsenic Compounds. Jimenez M.

63 (8.4) 6.1) 9.90) 2. tiles.66 (4.49) 4.87-9.72) 4.65-1.06-1.11-1.73) 3.62 (1.21 (1.57-7.87 (5. Barium salts have also been available as rodenticides.80-5.71) 1.80) 1.54-1.51) 1.31.80 (2.37-1.10) 3.73 (6. water.30 (5.46) 1.39) 1.40) 3.59) 3.15-1.70) 3.22-1.70 (5.35 (2.60-2.60) 3. and ceramics. such as barium chloride.02 (7.18-1.27 (1.87-14.48) 1.63) 1.30-2.35 (1. respectively.65) 1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.62) 1.53) 2.80 (1.77-3.70-2.20-8.90 (4.86-5.30) 5.14 (6.76-7.39 (1.12 (2.28-1.65-8.74-2.50) 4.40 (5.50) 2. barium sulfate and barium carbonate).01-7.34) 2.70) 1. 01-02.10-4.53-5.50 (1.63 (1.73 (5.43 (1.90-9.52 (1.40 (1.60-6.61-8.93-8.43 (1.29-5.60) 1.40 (1.88) 1.20-5.54-1.95-6.30 (5.60) 1.14-1. 0.S.63) Total 1. it combines with other chemicals such as sulfur or carbon and oxygen.70-6.75) 2.50 (6.12) 7.00-76.50 (2.56) 4.29) 5. rubber.30 (2.60) 4.50 (3.80 (1.53) 1.43) 6.65) 3.51 (1.47) 4.49-9.60-10.56 (6.16 (1.86-4.26-1.74) 3.88) 7.70-8.12. depilatories.21-2.00) 1.50) 1.73) 1.30) 5.8) 9.19-1.78) 1.20 (3. Certain foods.54 (6.85) 1.87) 7.55-7.10 (3.06-2.04-2. Fourth National Report on Human Exposure to Environmental Chemicals 193 .65 (5.38) 2.54) 2.36 (1.40 (5.41) 1.50-6.90) 2.15) 5.11 (3.90 (1. and food.56 (2.40-13.77) 1.04-6.41-1.20-8.51) 7.37) 1. whereas others are practically insoluble (e.71) 95th 6.00) 1.61 (2.40) 7.90 (6.36-1.08 (6.50-6.56 (1.50 (4.18) 3.00-3.50 (1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.57 (5.01 (4.62 (1.44 (1.35-1.50) 2.48 (6.93 (4.18 (6.99-5.50-1.74-3.37 (4.30-1.49) 8.85 (2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.75-3.46-1.54 (2.35-1.30-2.80-7.11 (2.66) Selected percentiles ( 95% confidence interval) 50th 1.80 (1. Small amounts of barium can be released into the air during mining and other industrial processes.71) 2.99 (4.51) 2.90-2.50-1.40 (4.82) 1.80-2.10-5.05-2.39) 4.72) 1.25 (1.63 (5.48-4.90) 4.55-3. are high in barium (Genter.59-11.82-6.32-1.37-8.22) 6.20 (4.24-1.52 (4.87 (6.61 (1.27) 2.98) 1.65-5.g.43) 2.15-11.30 (3.12) 6.70) 7.70) 5. 7440-39-3 Medically.20-8.15 (2.67) 6.27 (1. and 0.69 (1.54) 1. The general population can be exposed to low amounts of barium in air.20) 2.35) 5.95 (4.85) 1.48) 1. see Data Analysis section) for Survey years 99-00.25-1.15-1.91 (2.82) 2.77 (3.00 (2.60-6.30-1.47-1.43) 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. Barium compounds are also used commercially in paint.71-9.8 (6.50 (1.10 (4.81-2.88) 4.81-3.30) 2.63 (2.84) 5.19) 2.94-6.09 (1.24 (4.26) 5.38 (1.61 (5.91) 6. Some barium salts are freely soluble in water.78-3.11 (3.12-1.07 (2.50 (5.38) 8.56) 1.12.97 (1.87-7.34 (1.22-1.15 (1.78-2.30 (1. soluble forms of barium.20-1. interval) 1.80 (5.00-8.00) 6.40 (5.00) 4.38 (1.86 (4.70) 1.8) 5.40 (1.70 (1.12 (2.10 (2.76-3.09 (2.70) 4.4) 9.20-1.86) 6.76-2.05% of the earth’s crust.56 (1. In single dose animal studies.48-4.37) 5.34 (1.35-4.00 (1.2) 6.71 (2.78) 1.24-1.20-1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.70-2.36-1.25-11.64) 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 2.30-3.9) 5.Metals Barium CAS No.62) 1. such as brazil nuts.36) 5.34 (2.4) 7.49) 11.80) 7. 2001).80-3.49-1.92) 2.93-2.41-3.88 (5.70-5.60 (1.28) 90th 5.63) 1.57) 3.21-8.33 (1. and 03-04 are 0.61 (1.14-6.20 (1.54) 1. fireworks.60 (2.50 (1. glass.15 (6.49) 2.73-5.10) 5.26-7.90-13.21 (1.42 (1.36 (4.20-6. Workers employed by industries that make or use barium compounds can be exposed to barium dust.29-1.68 (1.44-5. bricks. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (4.87-3.31 (2.43 (5.64 (1.44-2.30-5. Barium compounds are used by the oil and gas industries to make drilling muds. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).86 (4. population from the National Health and Nutrition Examination Survey.32-7. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.30) 5.80) 6.26) 2.90) 1.76) 1.20-1.32) 8. In nature.39-1.40) 7.17-1.70-3.03 (1.31-2.30) 4.16) 5.96-2.39 (1.76 (3.30) 8.80 (2.72) 75th 3.45) 7..47-1.08-8.50 (4.35 (3.91) 2.54-8.61 (3.65) 1.50 (1.64-3.49 (1.81-2.30) 3.60-3.45 (1.46) 1.

29-7.96 (4.66 (1.47-8.76) 1.31 (4. and route of exposure.22-4.29-3.33 (1.16) 11.85-5.96 (4.96) 7.37 (1.22-1.37-1.42) 1.36 (3.60 (2.39 (3.01 (4.2) 6.881 (.86) 5.19-1.19-2.00) 4.35-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.81-6.02) .25) 4.16-1.8) 4.40 (1.56 (1.96) 4.31-1.29-4.63) 1.38 (4.4) 5.777-1.60 (5.30 (1.64 (1.32 (1.88 (2.33 (5.64 (1.55 (1.38-5.11-2.38) 4.47 (5.73-2.32) 2.51-3.00-1.27-1.65 (5.76 (3.02) 4.34 (1.79) 1.77) 1.00) 1. NTP.76 (2.04 (2.81-6.10-1.33 (1.01 (5. chemical form.58-6.52) 1.96-6.36 (1.32) 2.42 (4.38-7.52) 2.84-5.0) 6.38 (1.76) 2.06) .68 (2.03-1.53-21.63-4.45 (3.88 (6.74 (5.880-1.00-7. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.96) 4.60 (1.97 (4.10) 3.76-3.23-5.35-1.46) 1.0) 7.44-2.91 (3. Chronic high doses in animals resulted in kidney damage (McCauley et al. weakness.00 (3.40 (1.62 (4.47) 1.34) 1.30) 2.75-3.10) 6.24-1.79-5.83) 2.891 (.59 (1.64 (1.25-11.57) 2.56) 4. a benign condition that may occur among barite ore miners.91) 2.28-1.S.18 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.48-1.82) 1.41 (2.20) 4.78 (2.23-1.41 (1.41 (1.81-7.28-7.40 (1.00) 4.754-1.29 (1.10-2.28) 5.43) 1.57 (6.58) 1.36-1.26-4.45-8.25 (1.55 (5.70) 10.50) 1.68) 3.89) 90th 4.55) .86-7.77) Total 1.62) 2.48-3.703-1.2 (3.36 (1.96) 4.33) 6.54) 1.90-2.37 (1. paralysis.03-1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.38 (1.33-1.58) 75th 2.710-1.02-5. The health effects of exposure to barium compounds depend on the dose. 1985.12) 2. Insoluble barium salts.49-1.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .0) 5.31 (1.48 (1.00 (3. vomiting.47) 1.03) 2.29-1.38 (4.34-5.62 (2.31) 5.46 (2.47) 10.14-2.06) 2.28-11.55-6.51) 6.4 (5.11) .03) 1.48 (1.39-5.24 (5.60 (2. 2001).13-2.74) 1.58 (2.73) 2.27) 7. 1994..26-1.51 (1.58 (4.04) 1.48) 2.42) 1.41) 5.49-1.05-1.20 (1.45 (1.52-10.16 (1.27-3.00) 6.68 (3. diarrhea.32 (2.21 (1.37-2.51 (1.08-2.75-22.97-3.38-1.32 (1.83) 3.39-10.77-5.38) 1..34-3.72) 6.27 (2.26-1.39) 4. 1984.87) 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 2.24-6.56-3.963 (.54) 2.41) 4.48-5. in urine. hypertension.915 (.55 (4..50 (4.46) 3.52 (3.45) 1.68-3.65 (2.19-1.35-1.59 (1.50) 2.75) 1.10 (6.39 (2.54 (1.98 (2.70) 4.39-1.08-1.99 (2.00 (5. and cardiac dysrhythmias.24 (3.61 (4.45) 95th 6.45-1.22-1. Toxicity from soluble barium salts is rare.89 (2. 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.49 (1.36 (5.52) 7.74) 1.55 (1.67-6.01) 1.19-1.39 (2. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.69 (5.59) 2.97 (5.24-3.24-1.921 (.84) 2.36-2.44 (1.61) 2.2) 5. such as those used in medical radiographic procedures.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.23-2.99) 1.56 (1. 1989). Barium is not rated for human carcinogenicity.76 (4.03) 3.38) 1.48 (1.02 (3.20-1.73-4.80) 4.51) 4.69-9.51 (3.26) 4.59) 1.22-2.64 (1.53 (2. interval) 1.11) .55-5. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.18 (1.00 (2.72 (2.64) 7.3) 6.832-1. water solubility.Metals was eliminated primarily in feces and to a lesser extent.76) 2.3 (6.62 (1.09) 6.64) 7.24-11.54 (2.68-3.72) 4.49 (1.31-1.71 (5.33) 1.52-4.45-1.29) 1.82) 1.53) .29 (3.97-4. Symptoms following acute high dose include perioral paresthesias. are not absorbed when administered. population from the National Health and Nutrition Examination Survey.91-2.20-2.45-6.80-6.92 (4.33-4.60 (1.15-4.97) 1.56) Selected percentiles ( 95% confidence interval) 50th 1.50) 1.26-1.77) 1. 1986).86 (2.36 (3.46) 2. Perry et al.99 (4.92) 2. Wones et al.57-7.29-4.39-1.49-1.34-1.40-1.47) 4.57-10.44-2.905 (.59) 1.77) 5.91 (3.26-1.46-22.84-2.75) 2.30 (1.24) 3.68) 1.24-6.37) 2.04) 5.59-7.75) 2.51) 4. Following intravenous injection in animals.80) 3.57-5.20-8.36-1.68 (3.84 (3.58) 4.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.70) 1.28 (1.31-1.43-6.77) 1. 1990).75) 1.28-6.47 (2. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13-3.39 (2.

1986. 84-94. eds. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Advances in modern toxicology. 1989. 1990. Magnesium. Levy. New York: Elsevier.e. A study of 46 elements in urine. Minoia C.cdc. and serum of Italian subjects. Zschiesche W.nih. Princeton (NJ): Princeton Scientific Publications.64(1):13-23.niehs. Kopp SJ. Jr.. et al. 2005. p. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. the welders had no obvious adverse clinical effects (Zschiesche et al. Inc. Patty’s toxicology. 4/8/09 Paschal DC. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).gov/toxpro2. Vol 2: Specific Metals. 1992). environmental levels) and health effects is available from ATSDR at: http://www.. Clin Chim Acta 2000. p. Environ Health Perspect 1990. Sabbioni E. Weltle D.S.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Epidemiological study of barium in Illinois drinking water supplies. In: Inorganics in drinking water and cardiovascular disease. Paschal et al. Calabrese EJ. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Investigations into the effect of drinking water barium on rats.95:89-105. Int Arch Occup Environ Health 1992. Perry HM. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Sci Total Environ 1990. 221-252 Komaromy-Hiller G. Stadler BL. 1984. Pietra R. Sampson EJ. 1985. Ting BG. LA. 1998). et al. EPA.. eds. Nordberg GF. Lack of effect of drinking water barium on cardiovascular risk factor. Exposure to soluble barium compounds: an interventional study in arc welders. Costa R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005.. Available at URL: http://ntp. Perry EF. New York: John Wiley & Sons. Vouk VB. Reeves AL.S. Cohressen B. barium.gov:8080/cs. J Toxicol Environ Health. Apostoli P. Pozzoli L. PS.niehs. 231-249. strontium.85:355-359. 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. Comparison of representative ranges based on U. et al. Gallorini M. National Toxicology Program (NTP). p.html?charset=iso-88591&url=http%3A//ntp. et al. Handbook on the Toxicology of Metals.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. 2001.gov/ntp/htdocs/LT_rpts/tr432. and radium In: Bingham A.. Trace metals in urine of United States residents: reference range concentrations. pp. Minoia et al. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Genter MB.. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. and 2003-2004 (CDC.. Howerton K. Barium. patient population and literature reference intervals for urinary trace elements. 2001-2002. Information about external exposure (i. and a drinking water standard has been established by U. Laurie RD.28(3):373-388.. Centers for Disease Control and Prevention (CDC). Jackson RJ. Ash KO. References Brenniman GR. NTP. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals.76(1):53-59. Biomonitoring Information Levels of urinary barium reflect recent exposure..296(1-2):71-90. McCauley PT. Princeton NJ: Princeton Scientific Publications. 1994. [online]. Morrow JC. 5th ed. 2nd Ed. In Friberg L. blood. Schaller KH. Trace element reference values in tissues from inhabitants of the European community I. 2000) to levels in NHANES 1999-2000 and 2001-2002.nih. Wones RG. Powell C. In: Calabrese EJ.atsdr. ed.html. Frohman. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. ed. Douglas BH. Pirkle JL. Environ Res 1998.197210. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. calcium.

the lightest of all metals. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. and machine-parts industries. Low-level beryllium exposure in the general population can occur through breathing air.Metals Beryllium CAS No. coal. 0. or drinking water containing the metal. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.130 (<LOD-. electrical. < LOD means less than the limit of detection.13. which may vary for some chemicals by year and by individual sample. In studies of laboratory animals.13. near some hazardous waste sites. and 03-04 are 0. population from the National Health and Nutrition Examination Survey. Two types of minerals. 7440-41-7 General Information Pure beryllium is a hard gray metal. respectively. 01-02.130 (<LOD-. soil. beryllium is used in instruments. aircraft. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. and dental bridges.S.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 . eating food. and from breathing tobacco smoke. Beryllium compounds are commercially mined.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. see Data Analysis section) for Survey years 99-00.150) < 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 . Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. In medicine. are mined for commercial recovery of beryllium. and volcanic dust. bertrandite and beryl. computer. 196 Fourth National Report on Human Exposure to Environmental Chemicals . nuclear. and refined beryllium is used in mirrors and special metal alloys for the automobile. Exposure to beryllium occurs mostly in the workplace. and can be found in mineral rocks. 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. x-ray machines. and 0.13. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.140 (<LOD-. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

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

Costa R.. Clin Chim Acta 2000. Van der Venne MT. 198 Fourth National Report on Human Exposure to Environmental Chemicals .e.74:162-166. Pozzoli L. Beryllium [online]. Maier L. it is likely that urinary beryllium levels in the U. Clin Chest Med 2002. and the fact that most NHANES participant levels were undetectable. Review of elements in blood.23:827-839.gov/toxpro2. Howerton K. Sabbioni E. Morrow JC. 20012002. International Programme on Chemical Safety (IPCS).S. patient population and literature reference intervals for urinary trace elements.. Andrew M. Given these results.95:89-105.cdc. Trace element reference values in tissues from inhabitants of the European community I. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. and serum of Italian subjects. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Metals (i. Jackson RJ. Genetic and exposure risks for chronic beryllium disease. environmental levels) and health effects is available from ATSDR at: http://www. They reported urinary beryllium levels ranging from 0. 1990. et al.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Apostoli P.157:388-398.. 1990.12 to 0. In other studies.htm. Pirkle JL. Third National Report on Human Exposure to Environmental Chemicals.296(1-2):71-90. A study of 46 elements in urine. 1998). 106. Sci Total Environ 1990. Weston A. 3/27/08 Komaromy-Hiller G. Ash KO. Environmental Health Criteria.. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Paschal et al.. Levels of beryllium in urine for the U. Sabbioni E.atsdr.158:165-190. and the 95th percentile for males in NHANES 2001-2002. Minoia et al. less than 0. References Apostoli P. population are lower than levels in workers. Available at URL: http://www. Schaller KH. Hamilton et al.13 μg/L. HLA-DPB1 and chronic beryllium disease: a HuGE review.S. Sampson EJ.html. VI. population were generally undetectable in NHANES 1999-2000. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Environ Res 1998. 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. which approximate this Report’s limit of detection. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Comparison of representative ranges based on U.1 μg/L). Trace metals in urine of United States residents: reference range concentrations. Atlanta (GA) 2005.S.org/documents/ehc/ehc/ ehc106. Centers for Disease Control and Prevention (CDC). Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. 2000. et al.e. Int Arch Occup Environ Health 2001. Kriess K. and 2003-2004.76(1):53-59. 2001). McCanlies EC. Hamilton EI. Minoia C. Pietra R. Am J Epidemiol 2003. blood. 0. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Paschal DC. Ting BG. Gallorini M. Sci Total Environ 1994. Element reference values in tissues from inhabitants of the European community. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.inchem.

20) 1.10) 1.usgs.200 (.30-1.289-.300) .40 (1.378-.400) < LOD < LOD < LOD .30 (1.366) * * .500) .20-1.600 (.400) .400 (.400) .20-1.300-.400 (.400-.300 (.441) * .50) 1.00 (.500-.10) 1.00 (.500-.393 (.600 (.296-.700) .500 (.300-.70) 1.00-1.S.304 (.313 (. 0.368-.600-.400-.30-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.255) .427) * .449) Selected percentiles ( 95% confidence interval) 50th . Cadmium also may be emitted into the air from zinc.50 (1.900-1.50-1.900-1.10) 1.326 (.20 (.80) 1.412 (.400-.216-.700-1.200-.500 (.20-1.400-.400 (.300) .30-1.900-1.400) .gov/minerals/pubs/commodity/cadmium).00 (.50-1.800) 1.400 (.300) .304-.200 (<LOD-.40) 1.600 (.283 (.60-1.400) .300) .400) .600 (.300) .30) 1.600 (.70) 1.400 (.600) .600 (.00-1.20-1.600) .500 (.700) .300) 1.300-. and incineration of municipal waste materials. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400) .400-.300) .400-.50 (1.60) 1.900-1.10 (1.10 (1.300-.600) .400 (.200 (.800 (.300-.500 (.300 (.900-1.300 (<LOD-.468 (.300-.60 (1.800) .900-1.382 (.300-.10 (1.500-.200) .400 (.300-.395 (.700) 1.600) .S.600) .30) 1.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .00 (.800) .600) .40 (1.337) .500) .60) 1. as zinc sulfide) and to a lesser extent.400 (.14.500 (.10) 1.500-.10 (1.500-.20) 1.400-.300 (.400 (.00-1.300 (.50 (1.300 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite. and 0.00 (1.00 (.359-. coatings and plating.400 (.40-1.426-.900 (.376-.331) .367-.470) * .400) .20) 1.800-1.400) .20-1.70) 1.235 (.600-.300-.500-.20-1.20 (1.300) .600-1.300 (.700 (. Other uses include pigment production.300 (.700) .300) . and nonferrous alloys.344) .60 (1.20) 95th 1.300-.800-1.400) .400) < LOD .500-.20) 1.3.452) .50-1.400 (.300-.S.400) < LOD .40 (1.20) 1.00 (.40 (1.300 (<LOD-.300-.400) .500-. plastic stabilizers.600) .90) 1.30) 1. which may vary for some chemicals by year and by individual sample.403 (.20) 1.50-1.60 (1.403) .300) .400 (.400 (.424) * .275-.362-.600) 1.200) . Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.700) . or copper smelters (U.700) .00-1.60 (1.421 (.420 (.40 (1.300-. respectively.3.500-.700-1.50) 1.60) 1. and 03-04 are 0.386-.500-. The predominant commercial use of cadmium is in battery manufacturing.200-.900-1.300-.10) 1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00 (.600) 90th 1.00 (.300 (.600) .500-.500-.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * . cadmium use has declined in response to environmental concerns (http:// minerals.00 (. EPA.304 (.400 (.300-.400-. population from the National Health and Nutrition Examination Survey.300 (.10 (1.398) < LOD < LOD < LOD < LOD < LOD < LOD .700) .600 (.400) . < LOD means less than the limit of detection.300) .60) Total * .300) .00-1.500 (.500-.60 (1.200 (.500 (.400) . during refining of lead and copper from sulfide ore.500 (.30-1.333 (. malleable.600 (.40 (1.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .Metals Cadmium CAS No.40 (1.500-.40) 1.10) 1.500 (.300-.00 (1.00-1.300 (.300) 75th .300-.500) .500-. interval) .500) .300 (<LOD-.700-1.600 (.10 (1.80 (1.300-.900-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.20) 1. see Data Analysis section) for Survey years 99-00.900-1.400-.00) .600 (.700) .500) .200 (<LOD-.500-.00 (.800 (.70) 1. 7440-43-9 General Information Cadmium is a soft.400 (.500-.00) .30-1.400-.10 (.20) .00-1.300 (. U. Since 2001.10) 1.378 (.400) .300 (<LOD-.500) .20) . 01-02.513) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .200-.300-.300 (.266-.50) 1.400) .20-1.00-1.400 (.900-1.600) .600 (.50 (1.300 (.400-.200-.40-1.10) 1.400 (.200-.300-.700) .00-1.400) < LOD .500) .900 (.460) .30) .361-.300) .309-.300 (.600-.425 (.600 (.300) .500-. lead.10 (1.600 (.300-.20) 1.600 (.80) 1.

270 (.290-.300 (.476-.284) .240) .183-.238) .239 (.800-.219 (.204 (.210) .38) .202-. 1994). zinc. population from the National Health and Nutrition Examination Survey.04 (.329 (.169-.196-.559 (. interval) .433-.078 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.813 (. 2003).540) .190-.184-.03) .806) .220-.423-.255) .190-.48 (1.190-.15) .17) .157-.74) 1.065-. **All results are corrected for molybdenum oxide interference in the ICP-MS method. Cadmium absorption may be increased with iron deficiency (Berglund et al.458 (. With chronic exposure.330-.980-1.13-1.430-.220-.466 (.295) .160-.141 (.263) .51 (1.680 (. drinking water is a source for cadmium intake.12 (.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 .060-.238-.366-. For nonsmokers who are not exposed to cadmium in the workplace. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.165-.390 (.440-.279 (.623) .855-1.177-..800 (.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 .400-.260-.160) .843-1.150-.198) . and 03-04 are 0. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.06-1.550 (.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.134) .38) 1.400-.36) 1.336) .753-. Inhalation of cigarette smoke is a predominant source of exposure in smokers.199 (.390-.640) .633-1.500) 90th .170-.28) 1.310 (.530 (.436-.232 (.109-.265) .160 (.282 (.270 (.940-1.989-1. 1999.539) .227 (.482) .980 (.211-.192-..918-1.120 (.249-. 01-02.272-.Metals 2000).980) .790 (.820-1.206) .858 (.06.160) .450 (.081) .110-.440 (.300) .15 (.498-.262) .193-.818 (.960) 1.200-.202 (.219 (.977) .350 (.545 (.810-1.510-. Diamond et al.700-.890-1.223 (..919) .261-.234 (.229) .237-.82) 1.17 (. 0.339) .114-.170 (.500) .193 (.214-.717-.067-.251) .493-. To a lesser extent. ingestion through food is the largest source of exposure.201 (.351-.200-.101) .121 (.445 (.520-.S. Kikuchi et al.452 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.15) 1.43) 1.462 (.06.135 (.870) .180 (.210 (.206 (. Renal tubular and glomerular damage. an inducible metal binding protein.283 (.157) .892 (.080 (.20 (1.210 (.306 (.848 (.820) 1.83) 1.210 (.257-.221) .136) .189) . rice.817 (.447 (.580) . calcium.226) .148-.327 (.273 (.249) .181 (.733) .713) .880) .07-1.207-.222) .360) .393-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.313) .233) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .440 (.187 (.126) .980-1.790 (. potatoes.551) . Cadmium in soil is absorbed by plants.633 (.061 (<LOD-.115-.211 (.30-1.261-.22 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * . however.210 (.366-.748-1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.481) . and various seeds.390-. copper) and protein. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Cadmium is absorbed via inhalation and ingestion.128 (.507) .972 (.705-.235) .366) .57) 1.02-1.886-1.475 (.241) .445 (.01) .216 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals . 2003.38) .135-.17 (.219 (.277 (.230) 75th .426 (.210) .151-.381-.189-.13) .28-1.208-.886) .260 (.28 (1.551 (.766 (.210 (.24) 1.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.890 (.839 (.372) .289-.232) .191-.47) 1.700-. 2001).455 (.178-.596) .302 (.192-.06.519) .** Survey Geometric mean (95% conf.700-.148) . wheat.280 (.253-.175 (.38) 1.479) .960 (.326) .150) .247) . Horiguchi et al. see Data Analysis section) for Survey years 99-00.01-1.817 (.255) .077 (.763-.490) 1.12-1.191 (.510) .456-.153-.265 (.130 (.246) .140 (.240-.01 (..875) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.310) .470-.530) .322 (.09-1.230 (.72) 1.112-.200 (..260-.06-1.308) .963-1. respectively.229-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.100-.167-.22 (1.220 (.430) .255) .06) ..170-.229) .209 (.220) .741-1.860) 1.320) .233) . 2003). including many food crops such as cereal grains.41 (.980) . and 0.10 (1.200 (.281 (.686-.20) 1.19) 1.17 (.077 (.362) .25 (1.990) .299) .175 (. 2003).836-1.354) .221 (.061-.892-1.875 (.171-.230) .04 (.34) 1.173) .090) .285-.820 (.13 (.20 (1.20-1. 2004a.607) .203) .714-1.257) .490) .090) .231) .610) .092 (.087-.179-.450 (.109 (.730-.067-.243-.191-.733-.092) .195-. The kidney is a critical target and shows the earliest sign of cadmium toxicity.107-.52 (1.388-.519) .492 (.194-.387) .189-.394-.25) 1.32 (1.20 (1.316 (.203 (.412) .589 (.480) .

156-.234) .426-.112) .168 (.828) .250) .423 (.288-.283 (.175-.792 (.491-.162 (.541) .224 (.097) .190 (.191) .150-.159 (.940-1.181) .329 (.531 (.232) .147-.197-.210) .377-.229) .234-.559-.931 (..166 (.175 (.630-.421 (.136-.178-.223) .182) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .432 (.381-.267 (.719 (.091) .484 (.434 (.725-1.917 (.202 (.500-.663 (.267 (. However.136-.210 (.472) .238-.247-.784) .438) 90th .143) .218) .063-.318 (.253 (.106) .209) .826-1.159 (.144-.235) .686 (..209) Selected percentiles ( 95% confidence interval) Sample 95th .560-.387 (.104) .181-.261) .754) .757 (.398-. Jarup et al.212 (.350) .839) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.137-.783 (.174-.221-.962) .591 (.07 (.653) .470) .404 (.336-.078-.607) .431) .813-. Horiguchi et al. 2004b).516-.163) .551) .874-1.261-.833-1.696-. 2004).441-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.071 (.123-.533) . 1999).331 (.304-.085-.220 (.826-1.941 (.687-.182) .16) 1.176 (.086 (.280 (.316 (.225) .316) .181 (.205 (.273 (.631) .767) .154-.919 (.05) 1.256-.126 (.388-.173 (.233 (.094) .156) .690 (.300-.185) .211 (.101) .147-.818) . 2002.077-. interval) .104) .196 (.240) .075-.289) .13) .473 (..170 (.148 (.830) .123-.708-1.783) .10) 1.700) .146-.850) .168-.335 (.00 (.813-1.476) .418-.143-.199-.470) .00 (.173-.740 (.187-.232) .423-.199 (. 1999).802 (.221 (.292) .757) .157-.158-.325 (.S. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.667) .856) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .311) .122 (.156 (.856 (.184) .207-.207) .274) 1.490 (.198) ...909-1. 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.147 (.247-.622 (.240) .226) 75th . 2003.208-.288) .181 (.111-.789 (.481 (.308 (.449) .876-1.236-.140-.691-. population from the National Health and Nutrition Examination Survey.176 (.227-.242) .238) .343-.163 (.282 (.268 (.404) .391-.382) .418) .865 (.252 (.085 (.727-.518) . Olsson et al..210 (.562-.364) . 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.338 (.873 (.537-.183) .278) .191 (.074-.075 (<LOD-.614) . can result from high dose chronic exposure.206-.228-.239-..204-.261 (.266) .382-.303) .647-.927-1. 2002. During the 1950’s and 1960’s.208 (.090 (.270 (.507-.387-.690-.700 (.906) .263-.216-.154 (.501 (. Staessen et al.940 (.107) . 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.096) .979 (.687 (. 1996.219 (.440) .098) .189-.412 (.113-. At lower environmental exposures.917) .414-.168-.827) .051-.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 .091 (.321) .225) .769 (.091 (.187) .446) .850) .293-.17) .281) .190 (.487 (.137 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.716-.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 . 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.767 (.712 (.440) .16) ..04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .929) .06 (.192) .185 (.674-1.415) .178) .688-.200 (.084-.479 (.08) .** Survey Geometric mean (95% conf.222-.130-.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.12) 1.140-.678 (. 1999).830-1.067-.201-.219 (.352) .668-.433-.716) .234 (.288 (.078 (.722-.183 (. 2002.718 (.545) .693 (.135) .184-.806-1.536 (.171-.175 (.247-..617 (.07) .729 (.795) 1.414 (.184-.645-.241) .09 (.191-.297) . most often a result of occupational exposure (Roels et al..253) .255-.263 (.194-.678-.985 (. 2000.084 (.143-.281) .950) .177) .690-.093 (.100 (.666-.02 (. Noonan et al.538) .289) .998) .083-.266-.818) .38) .182) . 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.304) .779 (.650-.157-.245 (.215 (.170-.131-.340) .308) .161-.438-.444-.296 (.884) .

has resulted in severe.. Staessen et al.. 2003..S. Staessen et al. not to imply a safety level for general population exposure. Olsson et al. Occupational standards are provided here for comparison only. 2006. Olsson et al. Cadmium can produce lung. respectively....S. 1999).....cdc. Friedman et al. 2002..html. Noonan et al. 1988). Information about external exposure (i. 2004. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. Suwazono et al.. Jin et al.gov/ toxpro2. 2003. 2003. Acute and heavy exposure to airborne dusts and fumes. environmental levels) and health effects is available from ATSDR at: http://www. 2006).... 2004b). potentially fatal pneumonitis (Fernandez et al. Becker et al. Staessen et al. In the typical environmental exposure... Wilhelm et al.. 2002). Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Komaromy-Hiller et al. 1996. Jarup et al. 2002). two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1. Creatinine-corrected urine cadmium values in U.. 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. 2002).Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1..atsdr.. Women had higher blood and urine cadmium levels compared to men of similar ages. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. maternal blood or maternal urine and birth weight (Nishijo et al. 2002. 2004. 1999. Becker et al.. 2004. 2000. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . Wennberg 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.. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. 2003). Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al.. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. Ezaki et al. Becker et al. 2006).. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2004). and drinking water and environmental standards have been established by U.. In postmenopausal women. 1996). 2002.. Blood and urine cadmium levels are typically higher 202 in cigarette smokers.46 mg/gram of creatinine) (Ezaki et al. Moriguchi et al. Olsson et al. For NHANES 19992000.. 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. 2002. 2003. 2005. 2002). 2003. Jarup et al....26 and 3. Animal studies have demonstrated reproductive and teratogenic effects. data (CDC. CDC. Further research is needed to address the public health consequences of such exposure in the United States. 2000). intermediate in former smokers and lower in never-smokers (Becker et al. Mannino et al.. 2006. Horiguchi et al.e.. 2002) and length at birth (Nishijo et al. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. However.. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. 2005. 2002.. with peak values observed in the fifth to sixth decades (CDC. 2004. 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). Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. 2002. EPA. 2002).S. Zhang et al. Both IARC and NTP consider cadmium a human carcinogen. In adults aged 60 years and older.. respectively. Ezaki et al. 2000.. as may occur from welding cadmium-alloyed metals. Salpietro et al. 2000. Wennberg et al. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. Horiguchi et al.. 2005).. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. 1999). 2005.. approached these values associated with subclinical changes in renal function and bone mineral density. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. 2005.1 mg/L (Alfven et al... 2003. 2004b. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.

Nomiyama T. Tsukahara T. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Mannino DM. possibly better than b2microglobulin. Neurotoxicology 2003. Jarup L. Serra J. Savage-Brown A. Olfactory function in workers exposed to moderate airborne cadmium levels. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U.102:83-89.296(1-2):71-90. Holguin F. Int J Hyg Environ Health 2003. Moriguchi J.000 women in the Japanese general population: a nationwide large-scale survey. Carlsson MD. Bernard A. diabetes mellitus. Seiwert M. Ezaki T. Miyamoto K. Lauwerys R.76:186-196. Costa R. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Schulz C. Environ Health Perspect 1994. et al.gov/toxprofiles/tp5. Gadea E. Venables KM. 196:114-123. Lison D. Toxicol Lett 2004. Ezaki T. Kumagai N.atsdr. Toxicological profile for cadmium update. Palomar M. Miyamoto K. Vahter M. Sasaki S. iron deficiency. Horiguchi H. Jones RL.html.66(Pt A):2141-2164. Machida M. Atlanta (GA). Schulz C. Howerton K. Davison AG.96:353-359. Agency for Toxic Substances and Disease Registry (ATSDR). Fukui Y. Environ Health Perspect 2002. et al. 102:10581066. Komaromy-Hiller G. Nordberg G. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Environ Res 2006. Available at URL: http://www. Tsukahara T. Toffoletto F. Lundh T. Lepom P. Comprehensive study of the effects of age.205:297-308. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Furuki K. et al. Clin Chim Acta 2000. patient population and literature reference intervals for urinary trace elements. Furuki K. Chiappino G. Hellstrom L.59:497]. et al. Int Arch Occup Environ Health 2003. population.46:372-374. References Akesson A. et al. Lukyanova EM. Okamoto S. Kaus S.S. Comparison of representative ranges based on U. 1999 [online]. Nerbrand C. Mucha A. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Oguma E. Lidfeldt J. Fatal chemical pneumonitis due to cadmium fumes. Stock AL. Sasaki S. Akesson A. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction.95:20–31. Taylor AJ. Fayers PM. 206:15-24. Darbyshire J. Choudhury H. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Buchet JP. Oguma E. Grubb A. Hotz P. Bo M. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Ikeda Y. Pickering CA. Krause C. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Ukai H. et al. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Diamond GL. Seiwert M. environmental. Lancet 1988. Ash KO. Nermell B. 4/8/09 Alfven T. Fukui Y.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. Lancet 1999.354:1508– 1513. Occup Med 1996. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Takebayashi T. Thayer WC. Moriguchi J. Kikuchi Y. Cadmium fume inhalation and emphysema. 2005. et al. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Persson B. Mascagni P. Becker K. Centers for Disease Control and Prevention (CDC). J Toxicol Environ Health 2003. Zhu G. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Third National Report on Human Exposure to Environmental Chemicals.45:43-52.110:699-702. Vahter M. Alfven T. Greves HM. Becker K. Seifert B. Horiguchi H. Int J Hyg Environ Health 2002. Consonni D.1(8587):663-667. Bregante G. Chislovska NV. Elinder CG. Environ Health Perspect 2005. Anthropometric. Toxicol Appl Pharmacol 2004a. Fernandez MA. et al.148(1-2):11-20. J Occup Health 2003. Machida M. Kaus S. Uemura T.59:194-8. Bellerup P.24:717-724. Berglund M. et al. Environ Res 2004b.57:668-672.cdc. Occup Environ Med 2000. Ikeda Y. Jarup L.13(11):1627-1631.S. Thorax 2004. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Dekio F. Ye T. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Sanz P. Jin T. et al. Environ Res 2004. Wang H. ShkiryakNizhnyk AZ. Friedman LS. Kundiev YT.

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86 (7.01-8.0) 11.07-11.30 (6.70 (6.13 (8.90) 5.7 (9.7 (11. although cesium was generally of low toxicity when given to animals.60-6.71-9.3-13.0) 12.7 (10.81) 4.04) 7.Metals Cesium CAS No. and 0.13-8.21 (4.2 (9. and 03-04 are 0.00-4. infrared lamps.35 (4.9 (11. see Data Analysis section) for Survey years 99-00.26) 7.71-8.82) 5.40-7.2) 12.90 (6.70 (8. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.09-5.10-7.47-4. Most human exposure to cesium occurs through the diet.2) 11.5-14.92-13.50-7.87-7.3 (8. and as polymerization catalysts.83) 6.63) 6.60-7.8) 12. population from the National Health and Nutrition Examination Survey.1) 9.84 (4.70) 7. 0.59-5.60-7.71) 4.33 (6.71 (4.27-5.20) 8.9) 8.90) 7.80 (8.6 (11. However.10-8.88 (8.20-4.8) 12.40-5.4) 10.03 (4.71 (8.84-9.8-13.00 (7.60-6.01) 7.7 (8.70 (5.3-15.6 (9.69-6.35 (4.9 (11.74 (4.7) 11.7 (9.5 (8.90) 4.6 (9.6) 11.95 (3.74) Selected percentiles ( 95% confidence interval) 50th 4.0 (10.90) 5.08-5.90-12.80-10.14.9) 11.89) 4. Little is known about the health effects of this metal.1-13.56) 5.3) 10.90-8.84) 8.40-11.17-6.25) 4.17) 4.60 (7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.4 (10.53 (6.33-5.56-11.30-10.80-11.99) 9.04 (4.46) 7.87 (4.37) 5.32) 4.40-5.52) 7.4) 95th 11.6 (9.90 (4.08) 7.4 (9.12-5.10 (6.20-7.77-8.54) 4.00-8.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10 (6.60-12.1) 11.80-6.4) 10.21) 90th 9.80-10.05) 5.6 (11.6) 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 4.10-5.60 (8.87) 5.77 (4.38) 5.66 (7.26-11.07) 4.90-10.4) 12.8) 12.86-11.22-4.7 (9.8 (10.91 (7.80 (4.08 (6.83-4.00-9.39-4.50) 5.08-5.64 (4. Whether cesium compounds are carcinogenic is unknown.39) 7.54-11.8 (11.03-4.95) 5.5) 12.70 (6.70 (8.71-5.80 (8.0) 10.00) 6.09) 5.42) 7.0-15.5-14.59-5.50 (6.05) 5.30 (6.99-6.81-14.40) 5.4 (9.1-12.68) 9.70) 5.80 (4.56 (4.79 (4.20 (6.05-5.40-11.00-8. and clay.1 (9.0) 11.60) 7.12-11.10 (8.5-16.50 (4.64) 4.2-14.2-13.5) 9.2 (9.9) 12.8) 9.84-5.26) 4.4) 12.63-4.64-10.86-12.9 (10. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.80 (4.49 (4.50) 9.49) 4.64-5. For absorbed cesium salts.17 (6.90-12.40) 7. 01-02.96 (6.36 (3.6) 10.3) 12.35-5.00) 7.94 (4.1-12.9) 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 4.59) 7.80-10.70 (9.9 (11.40-5. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.62) 4.30-5. and cardiac arrhythmia (ATSDR.99-11.94) 4.84) 5.55 (4.36 (6.40-5. interval) 4.8) 11.20 (4.30) 7.62 (5. 2004).97) 4.7-14.30) 5.4-13.94-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 11.31-8.3 (8.87 (4.36) 3.00-10.3) 10.2-13.90) 9.43 (5.7) 11.62 (5. Radioactive 137Cs has been used medically to treat cancer.14 (4.89-5.44 (8.0 (9.0-13.52-9.8) 9.13 (5.81) 9.1) 9.01-6.02 (4.1) 10.55 (7.12) 5.33 (5.59-5.64) 5.23-4.56 (4.93 (4.47-8.3-13.91-8.20) 7.20) 4.72-7.45-5.34) 9.73-11.43-8.73-5.8) 11.5) 10.32-5.3) 10.27 (7.45-8.97) 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 4.9) Total 4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.76-6.15-8.7 (10.60-5.12 (4. and high-power gas-ion devices.22 (4.8 (10.13 (7.99-11.40) 5.37) 7.98 (7.3) 9.42-7. respectively.50 (4.24) 4.10-9.34 (4.70 (4.0) 12.9 (10. diarrhea.61-6.60) 7. photographic emulsions.80) 7.97-7. scintillation counters.55-11. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 5.9 (11.20) 5.90-10.87 (4.7 (10.0) 12.81 (4.40 (4.50 (4.72) 4.89) 5.4) 9.20-8.77 (9.14.42) 6.82-4.61) 7.25 (3.68 (7.53-11.7) 10.0) 9.5-13.20-5.16-6.25-5.2-13.05-5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .94 (4.3) 10.23) 9.29) 4.26 (3.70) 5.1 (10.1) 11.70-8.80 (8.00) 4.57-5.2. cesium hydroxide is corrosive and irritating at high concentrations.77 (9.S.90-10.49 (5.1 (11.63 (4.03 (4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.74-5.32 (3.95-4.10 (8.99) 7. soil.27) 4.81) 4.64) 5.6 (9.2-12.16-6.67 (4.7) 10.98 (7.29 (4. nausea.59 (5.50 (7. semiconductors.80-13.97 (7.49) 75th 7.5 (10.08 (7.70-5.

and were also roughly similar to those in this Report.14 (6.0) Total 4.06) 5.66-6.00-9.50) 8.00) 6.30 (4.40) 7.27) 4.99-4.36-10.19-6.46 (7.40) 6.95-12.10 (3.56) 3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.77 (6.00-4.07 (5.22-11.12-6.09) 8.08) 4.73 (3.44) 3.2) 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 3.50) 4.64 (4.43 (8.39) 8.57) 3.41-4.77 (4.75 (7.29-3.08 (5.58-5.74 (4.6 (9.1) 11.55 (3. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.24-4.68) 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.99-9.44 (8.92) 3.81 (4.31 (4.36-3.17) 4.44 (4.44-9.56-10.79) 6.92 (5.7) 10.52-5.05-3.25) Selected percentiles ( 95% confidence interval) 50th 4.60-20.43 (3.47) 6.14-6.97) 8.78) 4.47) 4.08-7.26-6.99) 4.3 (9.50 (7.04-11.26 (3.89-4.S.10) 7.59-8.58) 3.95) 8.37-3.63 (4.84-9.00-10.88-4.60-10.75-11.98) 5.67 (6.74-11.35) 3.72 (4.20) 5.0) 7.29) 5.33 (5.90-8.14) 4.28 (4.2) 11.00-8. Using clinically submitted specimens.42-4.70) 7.91-9.43 (4.64) 9.28) 7.83-6.. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.81 (4.24-10.7) 10.98 (7.97-4.51 (7.58 (6.05-4.43) 8.33 (5.21-4.91 (5.64 (8.71 (7.05 (4.43-11.95 (5.85) 4.00-5. interval) 4.14) 4.45 (4.13 (3.23 (7.79-5. Two small studies of European populations reported urinary cesium levels similar to U.20-8.17-4.96-4.86 (4.20-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.84-11.91-7.63 (6.53) 6.73-4.12) 3.20-4.14-7.8) 5.13-9.95) 10.77) 4.90-8.47) 7.35 (3.83-7.13) 7.31-4.48) 90th 7.14-4.42-6.10 (3.47) 6.38-12.35-11.82-4.51 (3. population.63) 6.55-5.93-7.58 (4.54 (5.41) 9.63-6.96) 4.66 (5.90 (7.08-3.50) 4.27-6.46-4.96-4.44-5.33-3.50-5.87) 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 5.53 (4.64) 5.74) 75th 5.72-5. 1990).85) 5. population from the National Health and Nutrition Examination Survey.64) 4.6) 6.61-3.0 (7.38 (3. 2005.65-3.3) 9. Komaromy-Hiller et al.79 (5.9) 10.11 (5.66 (5.87) 5.43-6.5) 9.56) 4.9 (10.27 (8.07) 8.27-4.98) 5.22 (3.51 (4.09 (4.64-6.39) 5.05) 3.13-9.29-3.48) 7.04) 6.60) 3.38 (3.33-8.07) 8.46-8.8) 6.2 (8.77-5.67 (5.46 (8.51 (3.70 (7.04) 5.79) 4.19-3.27 (6.21 (2.53 (6.87 (5.95-6.06) 4.54 (4.02 (5.94) 7.74) 3.51) 4.56 (4.08 (3.60 (5.83) 8.40-5.29) 4.41 (4.6 (9.10-4.41 (8.02-4.06 (3.98 (6.05-3.61 (7.20-4.36-6.76-9.12 (3.08 (6.15 (7.71) 6.99-9.38) 10.10 (5.8 (9.04-5.03) 5. population results shown in this Report (Alimonti et al.05) 6.47 (4.30-4.49) 3.30) 10.51 (4.01-8.95) 4.55) 4.96 (4.07-4.79) 9.39 (5.96) 4.43 (4.16-8.91) 5.18-7.62-8.50) 4.06 (5. 2004).17 (6.59) 4.18-6.30 (7.9 (9. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.78) 4.47 (7.42 (5.50 (5.27 (6.16-8.95 (3.08) 4.29) 4.21-5.93-9.35-7. (2000) found urinary cesium levels that were slightly lower than those reported for the U.82) 7.09) 4.50 (6.42 (4.91-6.75 (6.3 (8.84-7.41-7.58) 8.18 (7.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.54 (4.15-11.54 (3.97-5.03) 6.8) 10.11 (5.70) 6.80) 6.91 (5.26 (4.00-5.5) 9.21-3.90-3.03-5.87-4.48-6.65-4.15) 95th 8.28) 8.76-6.66 (6.30 (3.68-11.31-6.16-5.67) 5.2 (8.00 (8.31 (4.91) 5.84-7.68) 4.62) 5.85-4..S.65 (6.42-4.63-6.3) 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 3.15-4.63 (7.56) 4.88-10.S.08) 3.3) 11.77 (7.22) 6.34 (5.46) 6.45-6.3 (10.60 (3.41 (5.78 (3.78 (3.7-12.74 (5.84-9.4) 10.72) 4.37) 4.5) 7.17) 9.5 (9.30-4.99 (3.68 (4.16) 5.30) 10.24 (3.91) 4.41) 4.28 (5.38-7.3-15..18) 8.03-6.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .35 (4.68) 6.53) 3.94 (5.25) 4. Minoia et al.

Comparison of representative ranges based on U.14:120-128. 4/8/09 Alimonti A. Wood CM. et al.2004 [online].19:3131-3138. Pietra R. Howerton K.S. J Expo Anal Environ Epidemiol 2004. Atlanta (GA) 2005. Ash KO. Forte G. 2000. A study of 46 elements in urine. et al. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium.atsdr.gov/toxprofiles/tp157. antimony and tungsten. Third National Report on Human Exposure to Environmental Chemicals.296(1-2):71-90. Costa R. Trace element reference values in tissues from inhabitants of the European community I. Komaromy-Hiller G. et al. patient population and literature reference intervals for urinary trace elements.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Voorhees RE. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Sabbioni E. Wolfe MI. Mott JA. Rapid Commun Mass Spectrom 2005. Centers for Disease Control and Prevention (CDC). Assessment of urinary metals following exposure to a large vegetative fire.html. blood. Available at URL: http://www. Ronchi P. Minoia C. Paschal D. Apostoli P. Pozzoli L.cdc. Spezia S. Sci Total Environ 1990. Gatti A. Clin Chim Acta 2000.95:89-105. cesium. Sewell CM. Gallorini M. New Mexico. Mincione G. Toxicological profile for cesium. and serum of Italian subjects.

750 (.416) .940 (.510) 1.67) 1.06 (.04-1.850-1.590 (.350-.319) .520-.430-.04 (.47) 1. steel-belted radial tires. and 0.92) 1.59 (1.690 (.290-.24 (1.16-1.19) .500 (.26-1.660-.45 (1.890) 95th 1.740-. interval) .520 (.33-1.820 (.490-.890-1.540-.440-.410) .333-.470) .330 (.830-1.21) 1.452 (.50 (1.420) .16-1.590-.480 (.26-2.580 (.300-.372) .940-1.750 (. and in synthesizing polyester and other materials.500) .23) .430) .630 (.20 (1.418 (.22-1.32) 1.564) .47 (1.650 (.570 (.65) 1.680 (.16 (1.32) 1.800-.56) 1.417) .435 (.01-1.515 (.550-.37-1.930 (.32-2.590-.360-.469-.930-1.420) .360-.350) 75th .460) .270-.340) .05 (.338-.890-1.359 (.15 (1.340-.352 (.377-.496) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.900-1.28 (1.393-.29 (1.44) 1.520-.487) .502) .463-.770) .75 (1.47 (1.390 (.S.305-. and kitchenware.570-.336-.431) .380 (.12) 1. It is also a component of porcelain enamel applied to steel bathroom fixtures.460) .427-.680) . diamond-polishing wheels.348-.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 208 Fourth National Report on Human Exposure to Environmental Chemicals .670 (.520 (.670 (.460) .740 (.800-.870-1.52 (1.730) 1. Cobalt is used as a drying agent in paints.880 (.680 (.523) .327-.379 (.01-2.760 (.36) 1.68 (1.520) .285 (.48) 1.880-1.450) .460 (.810) .364-.580 (.650 (.660) .460-.17 (1.810-.570) .950-1.350-.620-.490-. blue-colored pigments.800) .310-.790 (.750 (.790-.388-.850) . and fertilizers.259-.630-.73) 1.316-.520 (.375 (.399) .410 (.S.26) Total . see Data Analysis section) for Survey years 99-00. industry is imported or obtained by recycling scrap metal that contains cobalt.670 (.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 .410-.580 (. Usual human exposure is from food sources. large appliances.09 (.980) .930) .380-.454 (.424) .540-.32 (1.99) 1.430 (.23-2.333-.370-.270-.950 (.940-1.07 (.331-.390-. population from the National Health and Nutrition Examination Survey.340) .28 (1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.340 (.410 (.16) 1.28-2.16 (.900) .640) .540) 1.04) 1.04-1.22 (1.07-1. and inks.431) .405-.294 (.60 (1.670-.620-.39) 1.410 (.620-.42) 1.900-1.450-.25-1.17-1.14) .530-.350-.410-.750-.50) 1.630 (.291-.540-.461 (.14-1.910-1.369 (.570) .810) .270-.05) 1.465) .740-.870 (.32 (1.Metals Cobalt CAS No.450) .81) 1.480 (.386) . 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. The cobalt used in U.520-.650-.520-.950 (.03-1.419) Selected percentiles ( 95% confidence interval) 50th .355-.690-.313) .540-.670-.499 (. hard metal (alloys of cobalt and tungsten carbide). respectively.320 (.08-1.581) .420 (.339 (.430 (.950-1.374 (.450) .590) .450-.900) .04-1.33 (1. 01-02.09) . automobile airbags.570-.330) .850-1.280-.24 (.394) .530) .367 (.583) .400-.64) 1.710) .81) 1.343) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .316 (.600) . Cobalt compounds are also used in manufacturing battery electrodes.920) 1. It is emitted into the environment from burning coal and oil and car and truck exhaust.890-1. seawater. 0.640) .790) .428-.700) .610) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.06 (.450) . and magnetic recording media. and 03-04 are 0.330-.640) .17 (1.850) 1.301 (. Cobalt occurs naturally in airborne dust.434 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.610) .15-1.680) .410-. shiny.16 (1.960-1.380 (.340-.06-1.600 (.820 (.430) .03) 1.28 (1.300 (.47) 1.350 (.03 (.370-.690-.01 (.334) .410 (.343 (.410 (.16) 1.398) .371 (.890) .660) .09 (.22) 1.870 (.950) .02-1.310 (.430 (.610 (.470 (.53) 1. and soil.08) .03) .710 (.398 (.920-1.520 (.390 (.600-.308-.980-1.900) .390) .379 (.380 (.710) 1.820 (.760) .07.03 (.48) 1.840) .07.03) 1.370 (.348-.373) .404) .520) .860 (.560 (.530 (.26) 1.13) 1.410) .08.380-.370) .620) .12) 1.01 (.370-.07-1.610-.460 (.360-.46 (1. Cobalt compounds are used as catalysts in producing oil and gas.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 .543) .373-.17 (.480-.550 (.700) .519 (.00) . varnishes. hard metal or in combination with other elements.390 (.550) 90th .05 (.414) .

Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.439) .708) .534-.343 (.753) 1.700 (.36) 1.275-.15) 1.740-1. cobalt is excreted predominantly in the urine.469-.306) 75th .513) .529 (.523 (.700 (.777-. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).382-.365-.543) .324) .36) 1.879-1.606 (.756 (.455 (.471-.949) .09) 1.738 (.434-.259) .786-.435-.428-.279) .857-1.376 (.829) .753-.274-.294-.475 (.598 (.248-.280-.433) .257-.333-.419) .309) .290 (.850 (.300) .851 (.11-1.83) 1.19) .638-1.513 (.792 (.247 (.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 .963) .268 (.54) 1.349) .848 (.369 (.344-..387) .872 (.368) .334) .361 (.306 (.57) 1.435 (.463-.384) .381) .847) .585) .286) .689 (.297-.442-.368) .599) .S.297) .895-1.388 (.905) .611) .29 (1.425) .391) Selected percentiles ( 95% confidence interval) 50th .396) .444 (.660-.626-.781) 95th 1.301-.983) .10) Total .647) .505) .393-.462) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.595) .04-1.343-.421) .679-. in the feces. Exposure in the workplace may come from electroplating.73) 1.50 (1.452-.282 (.16 (.990-1.361-.35) 1.703-.296-.44 (. A portion of cobalt retained for long periods is concentrated in the liver.964 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.522) .16) .55) .781-1.313-.00) .983-1.630-.29 (1.495 (.281) .361-.24) ..487-.378-.298 (.348) .895-1.723 (.17) .352) .290 (.955) .481) 90th .667-1.429) 1. 1994).333-. using hard metal cutting tools.963-1.824 (. interval) .503-.358 (.409) .673-.929) .774 (.342-.243-.353-.00) .533 (.917) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.319-.27) 1.325) 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 .733-1.313-.277-.324-.407 (.296) .12-1.250) .317 (.328 (.513-.561) .704-.842) .28) 1.00-1.323) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.278-.15 (.449) .337) .02 (.550-.600-. population from the National Health and Nutrition Examination Survey.06 (.271 (.757-1.272-.830 (.900-1.346 (.301) .50) 1.407) .488) .955) .00 (.932-1.00 (.635 (.560-.937 (.826-1.554 (.378 (.314 (.396) .630-.691 (.35) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.313-.352 (.329-. 1979).736-.339-.215-.990) ..03-1.694) .313-.508-.850-1.333 (.335 (.362) .378-.562) .542 (.611) .313 (.259-. 2003).449-.29) .500-.368 (.30 (1.471 (.326-.10) .360) .404-.256-.33) 1.804) 1.333-.327-.400 (.476-.609) .792-1.728 (.304-.457 (.402 (.683-. and to a lesser extent.562) .251-.534 (.293 (.291 (. Smith et al.563-.468) .426 (.50) 1.844 (.461) .581) .248-.785) .471-.259 (.582-.457) .. Cobalt is absorbed by oral and pulmonary routes.386 (.00 (.615) ..378-.737 (.417) .33) .362 (.608 (.963-1.750) .963) .29 (1.552 (.239-.16 (.04 (.574-.00 (.14 (.60) 1.362-.523 (.898 (.457-.11-1.728) .554 (.380-.744) 1.547 (.976 (.838 (.938) .23 (1.938-1.500-.275-.500 (.327 (.632-.417 (.616-.302-.25 (.290 (.591 (.425-.821 (.392 (.548 (.29) 1.33) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .25 (.821-3.975 (.667-1.394) . 1972).10-1.365) .515 (.303-.594) .282-.952 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.278 (.363) .960 (.03 (.304) .372) .310) .273 (.829-1.257 (.487-.438) .408 (.634-.353 (.352 (.Metals fabricated from cobalt alloys (Lhotka et al. an essential human nutrient.279 (.27) 1.234 (. 1994. Once absorbed and distributed in the body.391 (.861-1.313-.537 (.467-.593) .911-1.393 (.337 (.328) .361 (.10 (.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 .316 (.479) . refining or processing alloys.738 (.289) .727 (.331-.329 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.49) 1..669) .16 (1.707) .237-.833-1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.12 (. 1972).861 (.388 (.662) . respectively.760-1.750-.479-. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al. or using diamond-polishing wheels that contain cobalt metal.640) .328 (.355) .60) 1.644 (.

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

Chess DG. Lung cancer risk in hard-metal workers.55(4):269-276. MacDonald SJ. Bozec C. Zobelein P. Bunn HF. A report of two cases from mineral assay laboratories and a review of the literature. Lauwerys R. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Gross RT. DeSantis V.51(7):447450. Sabbioni E. Lauwerys R. Arch Intern Med 1990.148:241-248. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Roto P. Health Phys 1972. Health Phys 1979. Kraus T. Moulin JJ. Occup Environ Med 1994. J Rheumatol 2001. Sabbioni E.Metals effects of cobalt. Science 1988. Lauwerys RB. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors.216:253-270. Lasfargues G. Edmonds CJ. Absorption and retention of cobalt in man by whole-body counting. Peltier A. Int Arch Occup Environ Health 1997. Sci Total Environ 1994. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Kiilunen M. Goldberg MA.150. cobalt salts. Weber A. Zhuber K. Radulescu M. Sci Total Environ 1997. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Cresti R. McMinn DJ. J Orthop Res 2003. Zweymuller K. Dunstan E. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Biological monitoring of workers exposed to cobalt metal. Occupationallyinduced “isolated cobalt sensitization. Linna A. Schaller KH.204:147-160. Blunn G.(1-3):133-139. Salama A. Uitti J. Rorabeck CH. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Sabbioni E. Jarvis JQ. Hoet P. Lhotka C. Clin Orthop Relat Res 2003. Cobalt and antimony: genotoxicity and carcinogenicity.88(4):443448. White MA. Kusaka Y. Goto S.21(2):189-195. McCalden RW. Cannon SR. et al. Dunning SP. 3rd ed. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Falcone G. Palmroos P. Am J Ind Med 2003. Dickel H. et al. Pisati G. a study of 13 elements in blood and urine of a United Kingdom population. Long-term clearance of inhaled 60Co. Boca Raton (FL): Lewis Publishers. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.28(5):1121-1128.150(1-3):167-171.157:117121. Trace element reference values in tissues from inhabitants of the European Union. Smith T. Carnes WH. Molders J. Am J Epidemiol 1998. HoffmannB. Kristiansen J. Weyher I. Bourne RB. 1985. J Bone Joint Surg Br 2005. et al. Kato M. Laippala P. Cobalt cardiomyopathy. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Kirsch-Volders M. Iavicoli I. Co-sensitivity between cobalt and other transition metals. Pradhan C. Thakker DM.150:177-183. Buchet JP. Cleland D. Wild P. Mosconi G. Lisi P. salt. J Trace Elem Med Biol 2006. Leghissa P.45:246-247. Buchet JP. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds.533:135-152. Romazini S. Lison D.58(10):631-634. Alessandrelli M. Christensen JM. Unwin P. Kriss JP. et al. Hoher T. Sci Total Environ 1998.242:1412-1415. Steffan I. Ghat IS. Iversen BS. Outcome of occupational asthma due to cobalt hypersensitivity. et al.69(3):193-200. Chest 1989.” Contact Dermatitis 2001. et al.44:124-132. Thabe H.22:359367.48:172-173. Int Arch Occup Environ Health. Goto S. Kuska Y. Fujimura N.406:282-296. oxides. J Occup Med 1992. Swennen B. Barnaby CF. Robinson C. Ziaee H. Lison D. Thomassen H. Schramel P. Hammon E.34:620-626.36:732-734. Occup Environ Med 2001. The release of metals from metal-onmetal surface arthroplasty of the hip. Vitali MT. Swennen B. J Bone Joint Surg Br 2006. Diepgen TL. Br J Ind Med 1993. Salvatori S. Daniel J. Szekeres T. Lison D. Angerer J.87(5):628-631. and hard metal dust. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. X. and cobalt metals. Bacis M. Schank M. Linnainmaa M. Sci Total Environ 1994. Sanghrajka AP. Mutat Res 2003. Shirakawa T. Contact Dermatitis 2003. Epidemiological survey of workers exposed to cobalt oxides. Ichikawa Y. Meyer zum Buschenfelde K-H.50(9):835-842. Zedda S. Respiratory health of cobalt production workers. Stanescu D. Meier R.20(1):25-31.95:29-37. Heki S. 2001. Oksa P. Hedge AG. Tilley S. De Boeck M.

90) 2.60) 3.00-4.00) 2.942 (.60) 3.50) 5.95) 1.20-2.50) 2.80-4.90 (4.90) 1. interval) 1.50 (2.04-1.20) 3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.10-1.50-3.80) 2.60) 3.10) 2.50-4. bronze).Metals Lead CAS No.60 (2.60 (1.60) 1.25) 1.20 (3.56 (1.45 (1.90 (2.20 (4.70 (3.60) 2.90 (3.70 (1.66 (1.40 (3.90) 2. plastics.91) 1.10) 1.80) 1.50-2.50) 1.40 (1.20 (2.60) 5.20-2.40-1.00-1.878-1.80 (1.10 (1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .50-5. leaded glass.30-1.14-1.10-2.93-2.23 (1.70-2.00) 1.60 (1. see Data Analysis section) for Survey years 99-00.40-3.37-1.90-4.90-6.00 (3.60) 1.40 (1.50-1.60) 1.50 (4.60 (3.10-3.50 (1.20-3.66) 1.39) 1.70 (5.80 (3.43-1.40-3.40) 2.40) 3.g.80) 1.90-4.946 (.43 (1.20) 4.40 (1.46 (1.30 (1.62 (1.39-1.10-2.60 (3.28.00 (1.80 (5.90) 3.51 (1. solders. respectively.60 (2.00) 6.30) 95th 5.80) 3.10 (2.50 (1.00) 3.80 (4.87 (1. 0.62) 1.43 (1.90 (3.80 (2.50 (2.40 (2. and 03-04 are 0.90) 2.68-1.10 (1.80) 2.60-1.80) 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 1.78 (1.70-1.40) Total 1. blue-gray metal that occurs naturally in soils and rocks.30 (1.60) 5.70) 4.20 (3.90-3.86) 1.30-1.60-3.80-3.986) .50) 1.70 (2.71-1.20 (3.40-1. Since lead has been eliminated from gasoline.30) 2.75-1.30-2.90-2.40) 4.10) 2.00) 2.90) 3.S.20 (1.40-3.51) 1.50) 1.60) 4.01 (1.90) 1.89) 1.00) 4.70-2.55 (1. Lead has a variety of uses in manufacturing: storage batteries.50-1.32-1.20 (3. 01-02.20-1.25 (1.60 (1.20-6.60-1.40) 2.14-1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50) 1. brass.70 (1.49-1.60) 1.20-1.60 (4.43) 1.50) 2.00-4.10-8.20 (1.00-4.70-2.52-1.60 (2.00) 4.10) 1.36-1.30-2.20) 4.10 (2.90-4.90 (3.40-2.90-2.70-6. Lead was used in plumbing for centuries and may still be present.800-1.80 (1.40 (5.32-1.60-6.20-3.30) 2. In the past. such as lead phosphate and tetraethyl lead.00) 5.40-1.40 (4.70-4.40) 5.40-2.50-3.00-2.40-1.55-1.36) 1.52 (1.70) 3.90) 1.70) 4.00) 1.60-4.40) 1.20) 1.81) 1. Before the 1980’s.12-1.20-4.40-2.30-1.30 (2.02) 1.83 (1.10 (2.80 (1.70-1.30 (2.10-4.10-2.60) 1.37 (1.10 (1.80 (2.90 (3.70) 4. ammunition.48) 1.20-3.50) 7.10-6.40-5.69) 1.40-6.80) 1.20 (3.60) 2.30) 1.10 (3.40-1.70) 4.60) 3. metal alloys (e.75-2.40-1.31) 1.69 (1.20) 2.50) 4.20) 3.40 (1.80-3.50-1.10-1.50 (2.70) 1.90 (2.60 (2.70) 3.62-1.10-3.50-2.17) . population was aerosolized lead emitted from combustion engines that used leaded gasoline.60) 2.70 (3.30-1.10) 1.00) 1.30 (1.30-2.60-2.10-2.90) 2.50) 5.70) 1.90-2.900-1.50) 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 2.00-5.10-4.80 (1.09) 1.53) 1.90) 2.20 (1.90 (3.30 (2.60) 4.80-3.30 (4.45-1.34-1.40 (2.900 (.20) 90th 3.30) 2.60) 2.50-1. Elemental lead can be combined with other elements to form inorganic and organic compounds.60 (1.60 (1.10-2.43) 1.20 (3. ceramic glazes.75 (1.40) 2.75) 1.00-1.50-6.80-5.22 (1.50 (2.70) 1.40-6.70 (2.00 (5.10) 3.50 (1.20) .25 (1.10-2.00) 2.00) .40) 1. and for radiation shielding.80-4.70) 1.70 (1.10-3.00) 1.30 (4.3.00) 2.10) 3.60-4.90) 5.30-6.19 (1.50 (3. malleable.30-2.72) Selected percentiles ( 95% confidence interval) 50th 1.40) 1.40) 2.60 (1.80-3.10-6.00 (1.20) 5.50-4.30-1.80) 1.00) 3. dense. population from the National Health and Nutrition Examination Survey.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.80) 2.70) 3.50 (3.96-2.00 (6.20) 3.60 (3.10-1. and 0. 7439-92-1 General Information Elemental lead is a soft.60-1.20 (2.80 (2.87) 1.3.80) 2.20 (3.70-5.40-4.10) 5.60 (2.60) 4.50-2.70 (1.37 (1.30) 5.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60-1.30 (4.10 (4.30 (1.20-3.90 (1.80) 1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.69) 1.30 (3.80 (4.80 (5.60 (3.50-2.90-2.60 (2.50-1.00 (4.55-1.60-2.10) 4.60) 2.80 (1.50 (1.50-5.60) 4.77 (1.30 (2.30-5.70) 1.00 (4.20 (1.20) 3.S.50) 75th 2.80 (1.50 (2.30-4.30 (2.10) 3.70-1.900 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00) 1.52-1.70 (2.50 (4.30-1.90-4.90 (1.00-6. Lead is most often mined from ores or recycled from scrap metal or batteries.60 (1.70-3.65 (1.00 (2.80-2.30 (2.30 (2.80-4.36-1.899-.20 (1.14-1.69 (1.50) 4. antique-molded or cast ornaments. the main source of lead exposure for the general U.70) 2.50) 3.10-3.

50-2.20 (1.60 (1.70) 2.40-1.70-2.04 (.710-1.80) 3. 1991).10-1.700) 1.00) .30 (1.828) Selected percentiles ( 95% confidence interval) 50th . Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.70) 3.80 (1.540 (.688 (.753 (.40) 1.900 (.30) 2.815 (.40-3. However.718) .00-2.02) 1.12) 90th 2.60-1.07 (.30) .572-.90 (2.20) 1.90-2.86) 95th 2.900-1.40 (1.33 (2.900 (.990) 2.00 (. Approximately half of the absorbed lead may be incorporated into bone.30-1.13-3.915-1.610 (.591 (.600 (.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 1.20) .10) 1.50-2.72) 1.30-2.680) 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 1.29 (2. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.33.616) .30-1.90 (1.960-1.661-.506-. 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.800) .27 (1.90) 2.14-1.620) 1.59-2.745-.680) .700-.30 (2. lead-based painted surfaces undergoing renovation or demolition.52-1. dust.810-1.19 (1. bullet fragments retained in human tissue.700 (. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.03-2.31-3.640 (.90 (2.650) 1.40) 2.00 (1.90) 2.20-1.89) 2.30) 1.700-.60 (2.695 (.20-2.900-1.50) 2. CDC. 0.10 (.00-1.10-3.570-.70 (2.30) 1.11 (1. respectively.09) 1.20) 1.40-1.955-1.75) 4.18-1.50 (1.785) .20 (2.671-.S.50-2.640-. see Data Analysis section) for Survey years 99-00.17 (1.833 (.579-.20 (2.80) 1.10) 2.50-1.24-1.90-2.78-2.800 (.10) .90 (1.60 (1.00-1.32 (1.690) 75th 1.641-.535-.64) 2.800) .10-1.900) .730 (.73 (1.600) .75) 3. 2000).90) 2.86-2.659 (..40 (2.600-.800) .10-3.70 (1.50-3.60-3.23-4. older plumbing systems with leaded pipes or lead soldered connections.480-.20) 1.04 (. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.680-. In the blood.20 (2.600-.848 (.20 (3.700 (.49 (1.40) 3.30-1.80) 2.60 (1.20-1.40 (1.931) .40-5.857) .701) . pewter utensils and drinking vessels. Fourth National Report on Human Exposure to Environmental Chemicals 213 .757-.10 (1.20 (1.680-.00) .91) 2.10-1. stained glass framing.790 (. or water contaminated by mining or smelting operations.729-.80-2.Metals occupational (e.60-2.90-3.80) 2. and 03-04 are 0.00 (2. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR. battery and radiator manufacturing) and recreational sources.20) .800) .90 (1.600 (.10) 2.52 (1.738) .800-.29) 2.50 (2.749) .40) 2.40 (2.35 (.00) .10 (.660) .21 (2.800 (.30) 1.80) 1.50) 3.10-1.10 (1.70-3.03 (1.04-2.900) .31 (1.70 (2.630 (.800 (.00 (1.90) 1.808 (.556-.40-2.40 (1.625 (.620 (.90-2. interval) .700-.80) 2.822-1.66 (2.752 (.00 (1.20 (1.50 (2.62) Total .604 (.920 (.700 (.10-5.50) 2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.27) 1.80) 1.605) .40 (1.80) 2.66 (2. and 0.70 (2.800-.600) .637-.70 (2.900) .700-1.40) 1.731 (.00) 1.30 (3.10) .500-.40 (2.30) 1.82 (1.540-.86) 1.795 (.00-2.700) .970-1.06) .80-3. population from the National Health and Nutrition Examination Survey.833-1.80 (1.573 (.90-3.70) 1.40 (1.00) .900) . or after soluble lead compounds are ingested.82 (2.20 (1.580-.90 (2.00) 2.820-1.900 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al. and contact with soil.920 (.773) .14 (1.691-.00-1.00 (1.80) 2.30-1.595-.50) 1.40-1.800) .579-.800-1.40-1.766 (.674) 1.33-2.526-.70) 1.40) 2.960 (.900-1.600-.708-.07-1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .20-2.30) 2. lead-contaminated dust in indoor firing ranges.10 (1.60-3.50) 1.60) 2.62-4.986) .600-.941) .10-3.13) .00-2.560-.80 (2.80-2.613) .20) .700-.60-2.78-2.00) 2.700-.558 (.60 (1..900) .78-2.90-4.04) .840 (.625-.80) 3.44-2. 01-02.700 (.10 (1.910-.20-1.651) .02 (.50 (1.940 (.600-.40) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (1.30-5.10-1.04) 2.70) 1.900-1. imported children’s trinkets and toys. 2007.990) 1.11) 2.700 (.20) .97) 4.40) 2.22) 1.23) .800-1.1.30-3.50) 1.90-2.935) 1.70) 3.20 (1.636 (.677 (.1.52-1.30) 1. lead-containing folk remedies and cosmetics.40) 1.642 (.41) 2.553-.50 (2.923 (.710-.960-1.862) .30) 2.818) .59) 1.86 (1.700 (.564 (.850 (.14 (1.800 (.590 (.900) .628) 1.40 (2.g.10 (.589-.

52 (1.20) .72) .19-5.607-.404-.47 (1.586-.725) .742) Selected percentiles ( 95% confidence interval) 50th .27 (1.992-1.10 (.594-.649 (.61) 1.37-1.615 (.Metals 90% of the body lead burden in most adults.592-.755 (.18 (1.571-. through the inhibition of certain enzymes. hair.606-.41) .621 (.720 (.469 (. encephalopathy.862-.15-2. For instance.17-1..51 (1.838) .742) .75-2.39-1.83) 1.41 (1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.796-1.66 (1. Schwartz. BLLs and associated toxic effects differ in children and adults.89-2.644) . based on prospective population studies.718) .25-1.933-1.00) .876-1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.608 (.61) 1.933) .97 (1.790) .635 (. Large amounts of lead in the body can cause anemia.639) .22) . O’Flaherty.529-.75 (2.679) 1.604-.731-.734) .696 (.86 (1.940 (.404 (.09-1.893) .841-1.992-1.380-.50-2.36-2.926 (.10 (1.667) .40-1.655) 75th 1.72-2.11 (.56-2.63) 4. 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.85-2.938 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09) 1.655-.0) 3.18) 1. CDC.56) 3.918-1.33) 2.654) .61) 1.08-2.898) .673) .00 (1.03 (.460-.18) 2.730) 1.85) 1.03) 1.78 (2.587-.18) 1.971 (.26) Total .03) .51) 1.71-2. 2004.561-.66 (1.05-1.938-1.648 (.65 (1.89-5.01) .43-1.920-1.06) 1.20) .44 (1.88) 1.655) .55 (1.988-1.53) 1.812-1.58) 1.946-1.87) 1.94-2.682) .50) 1.708 (.917-1.623 (.667-.41-1.17 (.632 (.00 (1.722 (.05-1.618 (.29 (1.56 (1.03-2.702) .44) 1.64) 95th 2.03) 2.638 (. population from the National Health and Nutrition Examination Survey.31 (1.S.73-2.15-3. and iron.65-2.49 (1.31) 1.08) .644 (.10) 1.00 (1.33 (1. and through binding to ion channels and regulatory proteins. with lesser amounts eliminated via the feces.603 (.55 (1. 1995).828) .00 (. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.50-1.914 (.496 (.461) .679-.48 (1.641 (.08) .639 (.667-. with a half-life of years to decades.02-1.668-.04) 2.342-.28-1.701 (.579-.72-2.43) 1. 1991.14 (1. interval) .588-.50-2.686) .50 (1.97-18.62-2.33) 1.853-1.38 (2.61) 3.85-2.88) 2.98) 2.53-1.92) 2.78-4.45 (1.639 (.676) .645-.569 (.765) .38 (2.22) 1.98 (1.753) .763) .918 (.508) .71 (1.851) .659-.707 (.52) 1.88-2.28) 2.67-4.639 (.96 (1.658 (.702-.593 (.981-1.64) 2.22) 1.571-.88) 2.603-.50-2.68 (1.62-1.710) .677 (.23 (1.975-1.03) 2.535) . and paralysis.22-1.09-1. scant amounts are lost through sweat.05 (.781-1. Approximately 70% of lead excretion occurs via the urine.43 (1.608-. Nash et al.47 (2.62) 2.828-1.11-1.44 (1.810 (..609 (.98-2.07) . 1995. and nails (Leggett.20-3.720 (.700-. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.06) .64 (1. 2003.15) 1.701) .623 (.11) 1.79) 2.900 (.09-1.625 (.79 (1.. Lead can cross the placenta and enter the developing fetal brain.721 (.957-1.11 (.38 (2.88 (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 .03 (.03 (1.33-1.22-2.979 (.722 (.31 (2.14) 1.551-.698) .688) .61) 1.46 (2.79) 1.404 (.28) .64-2.383-.914 (. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton. In 1991.510-.712 (.615 (.622 (.436) .73) 2.94 (1.709 (.887 (.35) 2.66) 2.26) 2. seizures. 1993).601-.19) 1.693 (.25-1.408-.18) .24 (1. 1996).83 (2.74 (1.683-.725) .677) .670) 1.559-.541-.657) 1.97) 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 .870 (.988 (.758) .56-3.962 (.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 . 1993.12-1.594-.914-1.02) 1.718) 1.612-.37-1.617-.34-1.11) .05 (1.31) 1.681-.11 (1.588-.698) . abdominal pain.07 (.375 (.59-3.03) 1.85 (1.46 (1.800-. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.15) 1.62-3.01 (.400) .671 (. The toxic effects of lead result from its interference with the physiologic actions of calcium.43 (2.11 (1.583-.03 (.97) 1.70 (1.06 (1.977) 1.492-.793-1. kidney injury.990 (.69 (1.681-. The skeleton acts as a storage depot.43) 2.07-1.82) 1.963-1.428) .882-1. Staessen et al.677-.739) .15-2.774 (.702) .63) 1.03) .603-.645-.633 (.746) .703) .77) 2.605-.04-3.03) 90th 1. zinc.06 (. 2007).652 (.31 (1.432 (.47) 1.997-1.

1999). 1991. At low environmental exposures. Lanphear et al. almost double the geometric mean of 1. Overall. the prevalence rate has declined annually since 1994 (CDC. 2003. and spontaneous abortion (Baghurst et al. Borja-Aburto et al. 2006). 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.S. 2003. Korrick et al.3 million children tested had BLLs of 10 mg/dL or higher (http://www. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. higher than 100-200 µg/dL).html. adults in the 19992000 NHANES sample (Apostoli et al.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.6% in NHANES 1988-1991 to 1. 2002a). the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.21% of approximately 3. Bellinger 2005. adults in the 1999-2000 NHANES sample.000 adults.S. Both drinking water and ambient air standards for lead have been established by the U. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. particularly in the skeleton.cdc. including minority race or ethnicity. reduce sperm count. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. and decrease fertility (Alexander et al. High dose occupational lead exposure.. 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. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.. 1996. 1984.S. Staessen et al.S.e. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. In NHANES 1999-2002 in children 1-5 years old. and low family income (CDC. Data submitted through state public health programs from 2006 showed that 1. 2009). CDC. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.g. with overt encephalopathy. IARC considers inorganic lead compounds probable human carcinogens. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 2005b).. 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... Telisman et al.. More recently. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 2002. the geometric mean BLL was 3.5 per 100.gov/toxpro2. Schwartz et al. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.07 µg/dL (Becker et al. 1994).. Information about external exposure (i.. 1987. BLLs reflect both recent intake and equilibration with stored lead in other tissues. residing in housing built before the 1950’s. when the geometric mean BLL was 2. 2003.. 1996. and peripheral neuropathy generally occurring at much higher levels (e.Metals µg/dL or higher as the level of concern in children.cdc. The U. 2001)..0 µg/dL in females (Soldin et al. usually with BLLs greater than 40 mg/dL. 1995.75 µg/dL in U. adult residents. In occupationally exposed adults. which is an 84% decline. Urine levels may reflect recently absorbed lead. respectively.. urban residence.. 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... 2007). 2006).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. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. seizures.2 µg/dL in males and 3. Jones et al.. 2003). Schwartz. Pirkle et al. 1996.atsdr. For example. Payton et al. lead in women may be associated with hypertension during pregnancy.7 µg/dL and 4. premature delivery.. 1998). Surveillance data reported by U. 2000). approximately 11.. and organic lead compounds not classifiable with respect to human carcinogenicity. 2000). environmental levels) and health effects is available from ATSDR at: http://www. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. 2002). may alter sperm morphology.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 1999). 2005b.. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.. 2005a).4% in NHANES 1999-2004. Fourth National Report on Human Exposure to Environmental Chemicals 215 .S.S. EPA. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.4% of children had BLLs of 10µg/dL or higher (CDC... Muntner et al. both the geometric mean (1... adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. However.xls).6%) were lower than those from NHANES 1991-1994.

Atlanta (GA). Weiss ST. van Netten C. Apostoli P. 4/14/09 Alexander BH.htm. Ganzi A. MMWR Morb Mortal Wkly Rep 2006.275(15):1171-1176. Seiwert M. Age-specific kinetic model of lead metal in humans.8(3):395-401.cdc.gov/nceh/lead/ CaseManagement/caseManage_main. Kim R. Luukkonen R. 2002 [online]. 4/14/09 Centers for Disease Control and Prevention (CDC). Becker K. Stanek KL. MMWR Morb Mortal Wkly Rep 2005a. et al.cdc. Manton WI. Angle CR. Vupputyuri S. Jones RL. Canfield RL. Aro A. Available at URL: http://www. Pediatrics 2009. Preventing Lead Poisoning in Young Children. Atlanta (GA).1542/peds:2007-3608. Cox C. Neurotoxicol Teratol 2004.htm.115:521-529. Occup Environ Med 1996. Sparrow D. Blanco J. Wager C. Chiodo LM. Korrick SA. Environ Res 2000. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Blood lead levels measured prospectively and risk of spontaneous abortion.53:411-416. Toxicological profile for lead. Neri A. Lead and hypertension in a sample of middle-aged women.gov/toxprofiles/tp13.348:15171526.gov/nceh/lead/publications/ books/plpyc/contents. Managing Elevated Blood Lead Levels Among Young Children.html.10:43-50. 1991 [online]. Robertson EF. Sci Total Environ 2002. Semen quality of men employed at a lead smelter. Dietrich K. Available from URL: http://www. 1988-2004.205:297-308. Public Health Rep 2000. Kuehnemann TJ. Caldwell KL. Rios C. Auinger P. Blood lead levels—United States. Centers for Disease Control and Prevention (CDC). Lanphear BP. Jusko TA. Hernberg S. Lepom P. Am J Epidemiol 1999. Hänninen H. Ronchi L. Ewers TG. 4/14/09 Centers for Disease Control and Prevention (CDC).54(20):513-516. Bavazzano P. 2003-2004. Rotnitzky A. et al. Kaufman JD. Krause C. gov/mmwr/preview/mmwrhtml/mm5420a5.htm. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 2005b.55(32):876-879. Homa DM. Batuman V. 4/14/09 Centers for Disease Control and Prevention (CDC). References Agency for Toxic Substances and Disease Registry (ATSDR). Cory-Slechta DA. Hertz-Picciotto I. Lanphear BP. Baj A. 1999-2002. Korrick S. Environ Health Perspect 1993.287:1-11. Hu H. Leggett RW. N Engl J Med 2003. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Int J Hyg Environ Health 2002. Bellinger D. Henderson CR. Wigg NR. et al. Farias P. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.cdc. Vimpani FB. Aug 2007 [online]. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 2005.89:330-335. Muntner P. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Hunter DJ. Adult blood lead epidemiology and surveillance—United States. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. IARC Monogr Eval Carcinog Risks Hum 2006. Available at URL: http://www. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.atsdr. Jacobson SW. Muller CH. Sparrow D. Reese YR. Available at URL: http://www. Neurotoxicol 1987. doi:10. Mantere P. Am J Public Health 1999. Teratogen update: lead and pregnancy. Meyer PA. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Cox C. et al.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.cdc. Rotnitzky A. Kaus S.26:359-371. Weiss ST.123:e376-e385. Payton M. Birth Defects Research (Part A). Coresh J. Pediatrics 2004. Available at URL: http://www. JAMA 1996. Hu H.113(4):1016-1022. Jacobson JL.275:1177-1181.gov/mmwr/preview/mmwrhtml/ mm5532a2. Ga. Borja-Aburto VH.cdc. Acquisition and retention of lead by young children. Checkoway H.101(7):598-616.150(6):590-597. JAMA 1996. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Speizer FE. Inorganic and Organic Lead Compounds. Roberts RR. Pirkle JL. Baghurst PA. Neurodevelopmental effects of postnatal lead exposure at very low levels.82:60-80.htm.87:1-471. Schulz C. McMichael AJ. Rojas LM. et al. Atlanta. Scand J Work Environ Health 1984.73:409-420. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 4/14/09 Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. The relationship of bone and blood lead to hypertension. Blood lead reference values: the results of an Italian polycentric study. Bellinger D. Brody DJ. Lead. Hu H. CDC.

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70 (1. such as chlorine (e.30) 5. Accidental spills of elemental mercury. thermometers. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).700-.800 (. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. sulfur.70 (1. electrical lamps. an organic form of mercury. and organic forms. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.30-5.20) 2.20-4. Poorly absorbed from the gastrointestinal tract.30) 1.30) 3. predominantly from fish and other seafood. with the highest concentrations occurring in the kidneys (Barregard et al. Survey years 03-04 Geometric mean (95% conf. Kingman et al.700) . silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.70-2.00 (1. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. mercuric chloride).40) 3.40 (3.60 (2.50-1.2.40-2. Apart from methyl mercury.500) .30-2.919) .50) 4.753-1. Woods et al.S.70 (3.714-.30) 1.700-.g.00 (. thimerosal. synthetic organomercury compounds were once used in pharmaceutical applications. and mining and smelting.00) 1.90 (1. population from the National Health and Nutrition Examination Survey.60) 1.90) 90th 3.00) .600 (. 1998.400-.797 (. 2002).80 (1.877 (.00 (.00) 3. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.900) .30) 3.400 (.886) .g.363-.00-1.g.419 (.40 (4. merbromin).30-6..60-5.484) ..800-1.12) .30-4. 1999 . water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.Metals Mercury CAS No...90 (1.490 (.20 (2.903) Selected percentiles ( 95% confidence interval) 50th . 1994.80) 1.30) 4132 4241 03-04 03-04 03-04 .800 (.900) 75th 1. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).00) 1.20-4. sphygmomanometers and barometers.40-3.60-6.672) . 2007).60 (1.40-1.600) 1.979 (.30 (1. see Data Analysis section) for Survey year 03-04 is 0.372) . 218 Fourth National Report on Human Exposure to Environmental Chemicals .00 (2.00 (.700-.563 (. which can bioaccumulate in aquatic and terrestrial food chains.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 .10) . which create an episodic potential for volatization and inhalation of mercury vapor.781 (.800 (.20-3. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. Elemental mercury is a shiny.60-2. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.574) .10-3.60-6. constitutes the main source of dietary mercury exposure in the general population.40 (4.g.900) 1.80) 4.00) 4.400-. Other major uses include electrical equipment (e.90 (4. and dental amalgam. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.90) 95th 4.80) 3.40) 1.. Some cosmetic skin creams from countries other than the U.00 (.50) 5.50-3.285-.60) 2085 2293 3478 Limit of detection (LOD.472-. Also. to form inorganic mercury compounds or salts.655-. 1980.860-1.700) .30 (2. solid-waste incineration.500 (.300 (. The ingestion of methyl mercury. or oxygen.927) .326 (. 1993).40-1.418-.S.800-1.60-3.80 (1.900) 1. and mercury compounds are still used as preservatives (e.814 (. In addition. may contain inorganic mercury.689-.00 (2. interval) .700-..80 (3.70 (4.00 (2. IARC.. thermostats and switches).500-.00-5.900 (.50) 2. have often required public health intervention (Zeitz et al.60 (1.500 (.300) ..40-2.40 (3. The kinetics of the different forms of mercury vary considerably. inorganic.500-.60) 1.50-2.700 (.02) . and is distributed to most tissues.50) 1.700-.800 (. elemental mercury is absorbed mainly by inhaling volatilized vapor.900) 1. phenylmercuric acetate) or topical antiseptics (e. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.90-3. After elemental mercury is absorbed.800-1.776 (.90) 3. Atmospheric elemental mercury can be deposited on land and water.80 (1.800-1.703-.300-.800-1.70) 911 856 2081 4525 03-04 03-04 . Hursh et al..

.369) 1. McDowell et al.60 (1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.14 and 0. Fourth National Report on Human Exposure to Environmental Chemicals 219 .268-.7) 4.200-.400-.70-5.30) 3.00-2.300) . The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.317 (. Jonsson et al.824) 1.00-2. 1992.. 2005).30) 1..200-.70-3.23) .Metals the tissues to mercurous and mercuric inorganic forms.300) .29) .00) 6.900 (. Methyl mercury enters the brain and other tissues (Vahter et al.800 (.90 (3.700-1.0) 4.700-.900 (.40) 2.80 (1..20-3.700 (.40-2. with most elimination occurring through in the feces (Sherlock et al. 1994)..833 (..300 (.800) .395) . 1998).60 (2..50) 1.407) . 1993).900 (.70) 4.60) 1.50) 3.90) 3.200-.200-. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.. 1994.20-3. 1992 and 1999.297-.90 (4.30 (1.40-2.20 (.10 (3.60 (1.900-1. 2004. 1996.800-1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.800 (.. Geometric mean Survey years (95% conf.20-3.329 (. 1996)...50-12. a measure of accumulated dose (Cernichiari et al.01) .73) 1. and a useful marker of exposure in epidemiologic studies (Grandjean et al.90) 2.00-3.10-1.50) 1. 1984. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .800-1.300) .10 (. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.30-4.500-.60 (1.800) 1.27) .70 (1.90) 2.00-2.70) 4.300) . 1969. 1975.300 (.200-.30-3. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.697-.30-6. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.60) 1.00 (2.318 (.30) 1.00) 1.299-. 1973).80) 1.14.20-2.20 (2.30 (1.374) .00) .10 (1.50) 2.60) 3.00) 4..70-6. 1998)..00) 1. 1992).944 (.800-1. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.70-3.90) 5. Suzuki et al.40 (1. Myers et al.S.700-. 1995.200 (.10 (5.00 (2.800) .00) 2.500-.700 (. 1990). for both acute and chronic exposures.300 (.. Vahter et al.30-5. 1999-2002..00-6..90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .40-1.738-.377) .10 (1.600) . 1994) and then undergoes slow dealkylation to inorganic mercury. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20) .900-1.40) 5.. Smith et al.00 (2.269-.500-. population.10-3. Sandborgh-Englund et al..600) .500-1.10) .50-3.700-1. 1993).30-6.80) 579 527 370 436 588 806 Limit of detection (LOD.307 (. 2003). 1999).600 (.300) .541-.70 (1. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.20-11..820 (.700 (.200-.06 (. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.200 (.00 (1.377 (.500-. Smith and Farris.726-1.30 (1.300) .300 (.343 (. Miettinen et al.00 (3.10 (1.256-.919) .500 (.50 (1.70) 1. National Health and Nutrition Examination Survey..800) 1.50-2..02 (.30-4..800) 75th .20) 1. Vimy et al.60 (3. Methyl mercury is incorporated into growing hair.700) 2. After exposure to elemental mercury. Excretion occurs by renal and fecal routes.3) 4. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.50) 95th 2.30-11.10) 1. 1991.500-.40) 1.30 (.70 (1.940) Race/ethnicity (females.667 (. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.10 (.60 (3.06-1.10) .00) 7.70-5.30-2.90 (1.40 (1.20) .500 (.35 (1. 1971).60) 2.475) .90 (1.664-1.80 (3. 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. thereafter. 2003).700 (.800 (.00-1.90 (4.265-.50 (2.90) 90th 1.825-1.80-3.871-1. interval) Selected percentiles (95% confidence interval) 50th .30-6. 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.

600 (. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.600 (. sensory impairments..500-. irritability. Rice.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 . short-term memory loss. and cerebral palsy (NRC. typically after a latent period of weeks to months.. Factor-Litvak et al. population from the National Health and Nutrition Examination Survey. Oskarsson et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . overt signs and symptoms of chronic inhalation may include tremor. 1963).600) . which may vary for some chemicals by year and by individual sample. Sakamoto et al. limb deformities..700 (. Smith et al. particularly irritability. In recent epidemiologic studies. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.500-.500 (.600) ..600 (. ataxia. dysarthria.. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.500 (<LOD-. Overt poisoning from methyl mercury primarily affects the central nervous system. 2005). depression.600 (. 1996). Vupputuri et al.600-.600) .. lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC.700 (.600 (. gingivitis. 1987). DeRouen et al.500-.600 (..Metals may be more efficient for inorganic mercury (Grandjean et al.. 2004). maculopapular rash. 2004.700-. 2005. Once absorbed.600 (. Smith et al. 220 Fourth National Report on Human Exposure to Environmental Chemicals .600) . and sleep disturbance (Bidstrup et al. anorexia. 1995.500-. fatigue.600-.700 (.500) ... Salonen et al. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. Rissanen et al.700 (.. 2000. Bellinger et al.500 (<LOD-. 2006.800) .600) .500-. Sakamoto et al. dysarthria.. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. 2002. causing parasthesias. and pinkish discoloration of the hands and feet (Tunnessen et al.700 (. insomnia.600 (. 2000).500 (. cerebellar ataxia.42. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 2003).600-. 2006.700-.800) . and progressive constriction of the visual fields.500-..800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .. < LOD means less than the limit of detection. 2004).600-. At levels below those that cause acute lung injury.500-.. 1995.600) . Acute. 2004. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.500-. and neurocognitive and behavioral disturbances. 2000.S.. Inorganic mercury exposure usually occurs by ingestion. pain in the extremities. 1993). hypertension.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .700) 2007 2240 3406 Limit of detection (LOD. 1951. the existence of a causal relation is unresolved (Chan and Egeland. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.700 (. see Data Analysis section) for Survey year 03-04 is 0. Stern 2005. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. Survey Geometric mean (95% conf.700-. 1970. The constellation of findings may include anorexia. altered physical growth. 1983)..600) . hearing impairment.700) .600) .500-.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Drexler and Schaller. 1998.

These distinctions can help interpret mercury blood levels in people..480) 75th 1. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. In Germany the geometric mean for blood mercury was 0. Sanzo et al.304) .30) 3.42) 95th 3.463) .e.840-1.213-.. total blood mercury increased with age.440 (.78-2.400 (.S.23) 2.61) 1. 2000).93 (1. interval) . 2003).433 (.54 (2.447 (.509) . and the age-related changes differed across the groups (Caldwell et al.gov/toxprofiles.160-.14.89) 3.05) 1. 1998).420 (.55 µg/L. average age 9. 1997.Metals standard for inorganic mercury has been established by U.52) 2.254 (.350-.60 (1.08 (1. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.. environmental levels) and health effects is available from the U.. and increased slightly in non-Hispanic white children (Caldwell.405-. During the same survey periods.330 (. A cohort of 1127 U.330-.33 (2.12 (.07 (.360 (. who participated in a 1998 representative population survey (Becker et al.313-.382-.420 (.01 (. average age 33 years. military veterans (mean age 52.31) 1266 1272 03-04 03-04 03-04 .530-.406-. 1998). 2002).13-2.. adult women in several ethnic subgroups (Hightower et al.90) 2. 2006).940 (.250) .S.495 (.77-2. EPA at: http://www.890 (. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. Benes et al.700 (..430 (.60) 619 713 1066 Limit of detection (LOD.39-3. Fourth National Report on Human Exposure to Environmental Chemicals 221 .67-3.09 (2.534) ..16 (.cdc.46) 3.S.gov/mercury and from ATSDR at: http:// www.416 (.330-. 2001. see Data Analysis section) for Survey year 03-04 is 0.24 (2.epa. Survey years 03-04 Geometric mean (95% conf.430 (. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. Among the three racial/ethnic groups. From 1996 through 1998.96 (1..76-3.430) .330-. Kingman et al. 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. 1995.700-1.68 (2.58 µg/L for 4645 adults.00 (.76-4.840-1.14-2. range 40 years to 78 years) had an average total blood mercury concentration of 2.930-1. the median concentration of blood mercury was 0. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.530) .408) .85-2.442-.19 (2.65) 1.441 (.24) 1.03-4.360-.460) .78 µg/L for adults and 0. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.413-.340-.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 .360-. Over the NHANES 1999-2006 survey periods. 2009).23) .88-3.99-6.46 µg/L for children.410-.S.200 (.34-3. 758 children. 2009).67-2.549) .370) .26 (1.88) 287 722 1529 03-04 03-04 .08 (1. Schober et al.60-2.. 2004.610-1.. 2003).S.580) . slightly higher total blood mercury levels were found in U. aged 18 to 69 years.480 (. Mahaffey et al.555) .. total blood mercury geometric mean levels in females aged 16-49 years did not change. In NHANES 19992002.31) 2.88 (1.29) 1. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.840) 1.76-3.96 (1.570) .530) .460 (..492) Selected percentiles ( 95% confidence interval) 50th . Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U..16 (1. Total blood mercury levels increase with greater fish consumption (Dewailly et al.28) 1.atsdr.396-.14) 90th 2.960 (.770-1.97) 2. Biomonitoring Information In the general population. 2001.66) 3. et al. EPA.476 (.280-.509) .8 years. particularly methyl mercury.520) . However.290-.00) 1.05) 3. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.18) 2. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.9 years).63-2.870-1. Grandjean et al. the total blood mercury concentration is due mostly to the dietary intake of organic forms. population from the National Health and Nutrition Examination Survey.20 (1.870-1.. Information about external exposure (i.358 (.19 (1.

Metals 2000). In the study of U.307-..404-..217 (.400-. 2005).61) 1.76 (1.358) .620-.343 (.385-.362 (.909 (.11) 1.04-3.30) 2.498) 75th .476 (. Department of Health and Human Services noted that several studies have observed a modest.875-1.537) .21) 1. mean urinary mercury was 3.88 (1.970 (.28 (. Urine mercury and the number of dental amalgams were correlated.800-1.964-1. et al.40 (1..365 (. 1992).297 (.13-2.41-2. the urine mercury increased by approximately 0.522-. DeRouen et al. not to imply a safety level for general population exposure.88-2.67 (1.347) . 2002).64-2..01) 2. reversible increase in urinary N-acetyl-glucosaminidase.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 . 1998).00) 286 722 1529 03-04 03-04 .51-2.32 (1..485 (. population from the National Health and Nutrition Examination Survey.306 (.09) 1..S.00 (.196-.07) 1. Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al.32-2.508 (.67 (1.368) . 2009). Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. 1988.208-.54 (2.969-1.696 (.289) .376-.S. Levels in U.630) .455-.46-2.78-4.566) .06 (.88-2.785-1.588) .06 (.1 µg/L for each surface with a dental amalgam (Kingman et al. et al.44) 1.S.391) .525 (.384 (.472-. military veterans with dental amalgams.464 (.391-. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.486) Selected percentiles ( 95% confidence interval) 50th .1 µg/L.86) 95th 2. 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.455) . The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al. 2006). ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.784) 1.652) .62 (1.587 (.39) 1.365 (. Czech (Benes et al. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.79 (1.40-1. interval) ..246-.455-. Information about the biological exposure indices is provided here for comparison.00) 90th 1.768 (.265-.333-.447-.714-1.392-.. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.535) 1.S.276 (.255 (.12-3.11-2.417) .599) .90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .31 (1.532 (.11) 2.65 (1.. women of childbearing age have generally been much lower than these levels (CDC. Urinary mercury levels in recent German (Becker et al.23-2. 2009).63) 1.275) . Langworth et al.443 (.545 (.87) 2.79) 1. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. a biomarker of perturbation in renal tubular function.480) .687) .667-1.619-.13 (1.87 (1. 2002) adult population surveys were similar to those in a U. 2006. and on average.S.25 (.16) 1.30) 1.03) 2. and Italian (Apostoli et al.990) .301-.77 (2.225-. 2003). Survey years 03-04 Geometric mean (95% conf.447 (.309-.616) .18-1.280-.35 (1.463 (.400) .56) 1266 1271 03-04 03-04 03-04 . An expert-panel report recently prepared for the U.

70 (2.14.57-4.831) .35 (1.30 (1.04-10.450-.23-1.69 (1.23-1.05 (2.31 (1.42) 2.87-4.25) 2.46-4.27-1.50 (1.39-3.99 (3.77) 2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.68 (3.624-.68-3. National Health and Nutrition Examination Survey.84 (2.00 (3.540 (.72) 1.578-.97) 2.426-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .35) .516 (.721 (.520-.79) 3. interval) Selected percentiles (95% confidence interval) Survey years 50th .710) 1.32-3.53-3.665) .709) 75th 1.32 (1.553-.31-1.565 (.56) 3.790) .22-3.582-.724 (.10-4.24-1.13-4.22 (.740 (.85-3.580 (.77) 1.14-1.772 (. 16-49 years) 99-00 01-02 .526-.846) .03) 1.560-.38) 4.03 (.760 (.81-6.657 (.09-1.44) 3.650 (.806) .55) 90th 3.97 (1.18 (3.579-.09-1. population.61) 1.670) 75th 1. 1999-2002.632 (.592 (.658 (. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.16-5. 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.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.37) 1. population.47) 1.892) .557-.810) .65-4.95 (2.45) 95th 3.21 (1.Metals Urinary Mercury−Females Aged 16-49 Years Old.774) .710 (.508-.17) 95th 5.37 (1.14 and 0.69-3.56) 4.636-.85) 4.51 (3.04-1.655 (.387-.98 (5.569-.59-5.520-.501-.21-3.91-7.94) 1.52) 3.14-2.54) 595 531 381 442 594 826 Limit of detection (LOD. 16-49 years) 99-00 01-02 .28 (1.83-3.46 (1.664) .27 (1.809) .92) 4.03-2.596 (.84 (2.580-.56 (1.32) 2.47) 1.41 (1.27 (2.S.709) .99-2.41-6.18) 3.650) 1.966) .650 (.91 (2.631-.00) 2.616-.639 (.606 (.62 (3.45-2.76-5.719 (.744) 1.13 (2.76) 2.14) 3.42-3.21 (2. Geometric mean (95% conf.742-1.699) 1.51) .50-4.909-1.07) 1.930) .420-. interval) Selected percentiles (95% confidence interval) 50th .710 (.30 (2.831) .97) 2.622-.07-2.06 (.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .43-1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.97) 2.410-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.15 (2. 1999-2002.99 (2.79) 1.48 (2.89 (2.65) 1.62 (4.686) .07-5.560 (.615 (.870) .910) .832-1.45) 2.68) 3.500-.24) 6.92) 3.55-3.42) 90th 2.799) .45 (1.81 (3.41 (2.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .00 (2.605-.850-1.46) 3.S.610-.61-6.685 (.691) .30 (2.706 (.656-.05 (3.03 (.540-.45) 2.62 (1.76 (1.600 (.92) 2.10-2.824) .16) 5. Geometric mean Survey years (95% conf.15-1.637) .45-3. National Health and Nutrition Examination Survey.50 (2.723 (.475-.99) 1.3) 5.522 (.502-.30-2.41 (1.833) .620 (.

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7-39.9-82.9-55.3 (53. 01-02.2 (38.8 (82. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.1-48.7-51.1-59.9-85.2) 53.8-108) 87. urinary excretion over six days CAS No.5) 80.1 (71.0-62.2) 48. WHO.6-58.4) 42.6-111) 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 52.0 (42.3 (37.6 (52.6-96.1 (91. which exert homeostatic regulation over molybdenum balance.2-70. aldehyde dehydrogenase.4) 56.9 (44.0 (42.3) 41. 7439-98-7 General Information Elemental molybdenum is a silver-white.7) 78.1) 57. At a daily oral molybdenum dose of 24 µg.8) 39.7-105) 69. Fourth National Report on Human Exposure to Environmental Chemicals 227 .3) 37.0-56.4 (79.6-72.2-53.5 (74.4-52.7) 77.0-85.7-122) 93.2) 40.3 (55.4 (48.0 (48. Excretion occurs predominantly via the kidneys.5-65.6-42.5) 47.3 (71.6-46. 2001.7-41. Survey years 99-00 01-02 03-04 Geometric mean (95% conf..5) 85.7) 45.1) 82.8 (85.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.5-52.6 (40.5 (43. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2 (49.4-61. population from the National Health and Nutrition Examination survey.3) 54. 0.7) 78. semiconductor and battery industries have begun to use molybdenum.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 (98.2) 37.7 (58.9 (32.8) 44.7-84.3-115) 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.7 (71.9-56.8) 48. 1996).4 (48.1 (34.3 (79.7 (50.1) 46.3 (73.3-108) 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 47.1-44. 2001).4) 49.0) 60.3) 85.4) 76.2 (61.0) 45.8) 75.7 (36.3 (46.3 (84.3-47.3 (64.5-68.7-91.7 (45.7-50.6-55.5 (49.9 (40.4 (72. 1997).0 (76.7-92. and xanthine oxidase (Kisker et al.4) 41.7-73.7-68.8 (42.6) 93.0) 55. see Data Analysis section) for survey years 99-00.5 (81.1-52.9 (33.8) 40.5 (41.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.5 (67.5.0-71.1) 60.0) 62.5-66.4 (34.9 (34.3-75.7-47.5-52.0) 97.2-59.5-91.9) 62.8-94.7) 46.1-55.4-75.7 (73.6) 51.9-55. Compounds of molybdenum are also used as corrosion inhibitors.3) 83.2-59.6-62.1) 35.7 (37.2 (63.5) 44.6-82.0) 84.9 (52.5 (48.0 (46. inks.7-60.0-38.2-37. and 1.2-42.2) 52.8) 46.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78. and in pigments for ceramics.3 (47. In humans.2 (83.1-52.8.5 (41.1-51.6 (43.1-88.8-49.8-106) 88.0-100) 63.1) 126 (106-147) 109 (94.4 (80.1 (38.0-110) 90.9 (73.9 (78.9-109) 97.6) 53.2 (40.5-124) 108 (92.3 (55.9) 34.3) 65.3 (38.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM. respectively.0-53.5-46.0-101) 82.0 (41. More recently.6 (73.3-91.5) 60.2-79.0-77.4) 52.6 (55.2 (55.0 (81. and 03-04 are 0.4) 45. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.6 (40.S. hard metal widely used to add strength and hardness and retard corrosion in metal alloys. interval) 45.3) 47.0 (43.7-96.8 (67.2 (69.5-41.8-90.1-63.9) 67.1) 59. chemical reagents in hospital laboratories.0) 54. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-91. and paints. hydrogenation catalysts.4-82.7 (44.0) 39.5) 80.6) 71.2) 41. lubricants.6) Selected percentiles ( 95% confidence interval) 50th 50.8-46.3-44.2) 79.Metals Molybdenum or ore deposits.7) 57.0-65.6 (55.7) 51. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.2 (56.9-83.5 (37.2 (49.7) 86.9 (37.8.7 (51.7) 75th 84.6) 71.

1 (37.2-40.1 (54.6-41.4) 116 (101-126) 104 (88.5) 90th 108 (97.4-185) 106 (94.8 (56.1-41.8 (37.3) 37.5-99.0-38.0-56.7 (77.4 (78.5 (83.6-61.8-47.9-42.4 (40.2-80.2) 42.1-34.2-103) 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 42.8 (36. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. In industry.0) 39.8-67.5 (79. 1995).8) 71.0-120) 85.5-70.9) 40. 1993).6-76.6 (71.1 (33.0) 33.1 (49.8-84. at daily oral doses of 95 µg and 428 µg.3-45.8-118) 81.3-102) 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 40.1) 43. 1997).7) 45.4 (59.4 (37.4) 77. population from the National Health and Nutrition Examination survey.5-62.8 (57.8-52.1-67.9-68.3 (37.4-106) 85.5 (37.3 (53.2 (40.9 (40.4) 58.0) 38.6-78.3 (83.2 (52.2) 58.9 (73.4) 122 (107-133) 109 (99.1 (44.2 (33.6-88.4-39.1-100) 86.6) 39.7-40.3 (36.3 (71.9-118) 91.0) 72.7) 112 (95.5 (65.6 (36.2-121) 107 (92.5-119) 90.3-59.4 (55.9-40.6) 36.8) 62. 1961.7-38. and urinary levels reflect intake from all sources.3) 64.0) 88.7-93. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.4) 61.5 (38.9) 92.2) 39.5-46.5) 73.4 (67.5-69. U.6 (38. respectively.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0) 53.5-97.5 (41.7-120) 87.1-127) 90.7-43.2) 37. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.7 (30.8-65.9 (79.1) 40.9 (39.5 (39.6-45.6) 48.7-137) 129 (109-155) 112 (97.9) 79.0) 39.2-65. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.2) 39.4 (56.5-50.0) 36.1-81.1) 101 (83.7 (75.2) 38.1 (30.8-42.4) 40.1-38.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.3) 57.4) 60.2-49.3-43.9-87.8) 45.9-117) 57.5 (36.6-61.5 (65.3 (51.3-46.4-41.2) 37.03 mg/kg/day in humans (IOM.6 (36.9) 44.5) 63. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 44. interval) 43.0 (35.1 (38.9) 31.5) 72.9-61.8) 79.8) 38.1-79.9 (64.9-96.0) 62.6 (59.1 (82.8 (90.9 (49.2 (37.0 (58.0-103) 103 (90.9-45.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.3) 56.6-63.4) 89.1-39.1 (39.7) 62.1-40. EPA.1-112) 78.1-43.1 (42.2) 55.5 (40.4 (53.7-44.8-66.2 (69.7) 75th 63.9-45.6 (42.3-52.5 (40.2 (43.2-96.6) 43..2 (57.S.2 (36.7) 57.3-56.7) 42.4-42.0-46.5-35.2-46.5-45.1) 56.7-52.0 (80.3-141) 109 (81.4-107) 85.7-62.4 (44.4) 47.7) 41.2-41.3) 44.5) 71. of the ingested dose (Turnlund et al. Based on studies finding adverse reproductive effects in rats and mice.8-47.3) 43.8) 38.3 (71. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.8) 61.3) 41.6) Selected percentiles ( 95% confidence interval) 50th 41.2-47.0 (74.1) 37.9-41. Molybdenum is generally considered to be of low human toxicity.1-109) 89.7) 53.0) 44.5 (37.5 (80.5-92.0-41.0-46.S.3 (37.3 (58.8) 37..1 (38.6) 39.1-43.5-44.2) 43.4-76.2) 42.9 mg/kg/day and established a tolerable upper intake level of 0.6 (57.Metals was 18% of the ingested dose.3-68.9 (64.2-96.0-133) 119 (88.1-39.4-120) 101 (84. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5 (59.1 (40.3) 40.5 (35.8 (75.5-48.7-100) 77.4-66.1-45.3-44..9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5-60.5) 60.9 (35.5 (34.7 (66.6-63.8-46.3) 61. Biomonitoring Information Molybdenum is an essential element for health.3 (36.2 (73.2 (40.5 (78.9 (36.5 (35.5 (50.8) 39.5 (41.2 (50.5 (54.5 (39.3-115) 98.9-71.4) 48.2 (40. 1999).7) 115 (93.9) 41.1) 37. but available epidemiologic data are scant.1) 65.9 (39. 2001). and clinical or epidemiologic evidence of adverse effects is limited. urinary excretion over six days rose to 50% and 67%. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.3 (55.

Menne C. Institute of Medicine (IOM). Sabbioni E. Koval’skiy GA. Third National Report on Human Exposure to Environmental Chemicals.S. Food and Nutrition Board. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8.66:233-267. Sciarra G. Vermeire PA. vitamin K. edu/openbook. Ronchi A. U. Zhurnal Obshchey Biologii 1961. References Centers for Disease Control and Prevention (CDC).22(3):179-191. Van Meerbeeck JP. Gatti A. van Sprundel MP. Peiffer GL. 1996. 1998). 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. et al. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Minoia C. Geneva: WHO.216:253-270. National Toxicology Program (NTP). World Health Organization (WHO). molybdenum. Turci R. (DC): National Academy Press.123(1):81-85. Occupational risk factors of lung cancer: a hospital based case-control study. copper.gov/iris/ subst/0425. Schindelin H. nickel. 16:1313-1319. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. 2005. 4/14/09 Iversen BS.nap. iron. Analyst 1998. iodine. silicon. pp. arsenic. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Sci Total Environ 1998.gov/index. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect.nih.niehs. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. 2001.. A study of 13 elements in blood and urine of a United Kingdom population. White and Sabbioni. Available at URL: http://www. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Kisker C. 1998. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. 420-441.epa. Trace element reference values in tissues from inhabitants of the European Union. Molybdenum absorption. Available at URL: http://ntp. 144-154. Schleyerbach U. 2001). 56:322-327. Turnlund JR. 4/14/09 White MA. and zinc: a report of the Panel on Micronutrients. Molybdenum 1993 [online]. In: Trace elements in human nutrition and health. 2005). Droste JHJ. EPA). boron.htm. Weyler JJ. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. X. Rees DC. Kristiansen J. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum.S. Molybdenum. Minoia et al. Yarovaya GA. chromium. Am J Clin Nutr 1995.62(4):790-796.php?record_id=10026&page=420. excretion. Keyes WR. Atlanta (GA). Ann Rev Biochem 1997. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al.15(2-3):149-154.Metals in urine for the U. Environmental Protection Agency (U. Washington. Dietary reference intakes for vitamin A. Schaub J. Molybdenum in infancy: methodical investigation of urinary excretion. 2002. TR-462. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. pp. Rapid Comm Mass Spectrom 2002. Shmavonyan DM. Aprea C. Sabbioni E.. J Trace Elem Med Biol 2001. vanadium.. Occup Environ Med 1999. Christensen JM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. manganese. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Available at URL: http://books. 4/14/09 Sievers E. White MA.S.

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

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

Alimonti A. Senofonte O. palladium. Iavicoli I. Occup Environ Med 1998. Int J Hyg Environ Health 2004. Petrucci F. 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. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. rhodium.76(1):5-10. Kaus S. Neuendorf J. Seifert B. Schierl R. Platinum concentrations in urban road dust and soil. Huber R. Carelli G. 2004. Kulka U. Fruhmann G. 1998). 1991 [online]. 289-380. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Schulz C. Nowak D. Hall L.70(3):205-208. Hebert R. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Int Arch Occup Environ Health 1997. Environmental Health Criteria 125. Kavanagh P. Schierl et al.. Hysell D. 1997. and platinum.13(1):24-30.S. Farago ME.01 µg/L (Becker et al. Fries HG. Wilhelm et al. Biomarkers 1999.inchem. Urinary excretion of platinum from platinum-industry workers. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.org/documents/ehc/ehc/ehc125. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Influences on human internal exposure to environmental platinum. 2004). Several studies have shown that background concentrations in general populations were usually less than 0. Parrot JL. Herr et al. Begerow J.htm. Duneman L:Long-term urinary platinum. Patty’s Toxicology. Levels of platinum in urine for the U.56(3):283-286. population were below the limit of detection (0. Angerer J.. 2001). Campbell K. Occup Environ Med 2004. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. ruthenium. 3/31/08 Moore W Jr.35:313-321. Hauff K. Platinum. Ruff F: Histamine release by sodium cholorplatinate. Urinary platinum levels associated with dental gold alloys. Boos KS. osmium. 1998). and in blood and urine in the United Kingdom.9:152-158. References Becker K.04 µg/L) in this Report. pp. Moore W Jr. Ewers U.. International Journal of Hygiene and Environmental Health 2003. Arch Environ Health:1969. Analyst 1998.123(3):451-454. eds. Turfeld M. Herr CE. Crocker W. Part 1: monitoring of urinary concentrations.10:63-71. Ensslin AS. et al. Raab W.. Biomonitoring Information Urinary platinum levels reflect recent exposure. Schierl R..org/documents/ehc/ehc/ ehc125.. Grimm CH. Cohrssen B. Thornton I. 206:15-24. Br J Pharmacol 1969. Rommelt H. Blanks R. 1999. J Expo Anal Environ Epidemiol 2003. Kazantzis G. Saindelle A. et al. Environ Res 1975a. Kuster W.inchem. Powell CH. 2003. Schulz C. 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.. Schierl. 2000. palladium. Environ Health Perspect 1975b. Allergy and histamine release due to some platinum salts. Schierl R. Kelly J.. Nickel. Gromiec JP. Stilianakis NI. Arch Environ Health 2001. et al. Herr et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Ruff F: Platinum and platinosis.61(7):636-9. Int Arch Occup Environ Health 2003.htm. 2004) or less than 0. 2003. Saindelle A. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Pethran A. New York: John Wiley & Sons. Jankofsky M.19:685-691.. et al. In: Bingham E.4(1):27-36. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Czerczak S. Schierl R.005 µg/L (Iavicoli et al. 2003. Uptake of antineoplastic agents in pharmacy and hospital personnel. van de Weyer C.207(1):69-73.55(2):138-140. Biomonitoring of traffic police officers exposed to airborne platinum..Metals the International Programme on Chemical Safety at http:// www. 5th ed. Gieler U. and gold excretion of patients after insertion of noble-metal dental alloys. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. 2003). Available at URL: http://www. Pethran et al. Wilhelm M. Pethran A.. Hysell D. International Programme on Chemical Safety (IPCS). 232 Fourth National Report on Human Exposure to Environmental Chemicals . Bocca B. which elevate urinary platinum by five to twelve-fold (Begerow et al. Seiwert M.

440 (.290) .290) .240-.400-.173) .310-.400) 95th .250) .260 (.172 (. see Data Analysis section) for Survey years 99-00.360-.270 (.370 (. thallium readily crosses the placenta and also distributes into breast milk.250 (.134-.220-.480) .410-.340-.180-.330) .300 (.400-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.360-.200) .210-.280 (.172) . 01-02.147-.192) Selected percentiles ( 95% confidence interval) 50th .270-.380-.590) . however.370-.470) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.510 (.420) .410-.200-.145-.250-.173-.146 (.220 (.330-.202 (.280) .173) .360-.250-.220) .218) . respectively.340-.520) .202) .210) .190 (.178) .200) .170 (.370-.430-.640) .240) .590) .370 (. Human health effects from thallium at low environmental CAS No.200 (.300) .520 (.450) .160-.220 (.420-.410-.490) .180) .330-.380) .200) .390 (.460-.510) 1200 1313 1281 1213 1340 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .410 (.182-.370-.150-.440) . In the United States.330-.171 (.350-.200 (.250-.290 (.360 (.300) .160-.150-.162-.400) .370 (. In addition.260 (.190 (.160 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.420-.490) .290) 90th .187-.196) .220 (.410-.490) .180 (.183) .165 (.410 (.350-.300 (.360) .220 (.370) .400 (.370-.176 (.310 (.450 (.180 (.360-.300-.380 (.400 (.260-.480) .280) . In the past.300) .390-.230 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .390) .340 (.370) .167-.159 (.260-.270) .191 (.210 (.390) .500) .270-.330) .170-.197-.280) .201 (.290-.330) .320-.390-.Metals Thallium depilatory cosmetics.410 (.190 (.220) .410 (.185 (.270 (.145-.320) .200 (.450 (.170) .420-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.170 (.470 (.420) .202 (.188) .217 (.170-.200-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.630) .02.160-.420-.430 (.450 (.330-.140-.260) .290 (.290 (.160 (.440) .158) .340) .350-.02.520) .390) .260-.156) .150-.133-.260-.350-.220 (.160 (.330-.190 (.180-.360 (.430-.360 (. From these and other sources.350-.470) .280-.200-.163) . 2005).510) .370 (.177) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.550 (.350-.340-.400-.170) .240) .159 (.350 (.155 (.310 (.230) .350 (.149 (.400) .400-.167 (.410) .230) .147-.370 (.280 (.250-. interval) .560) .170 (.02.170-.250 (.420 (.230-.500) .320) .172 (.420) .370 (.154-.137-.150-.200-.520) .250-.420) .156) .290) .220) .400) .144 (.470 (.330-.290 (.250-.250-.220) .440 (.400 (.270 (.147-.410 (.420) .243) .170-.215) .340) .300) .148-.190 (. 0.310) .230-.390-.160 (.410-.690) .225) .480) .350) .390) .210 (.420) .400 (.175) . and 03-04 are 0.270-.218) .200) .340-.440 (.450 (.190-.280 (.500 (.240-.156-.280-.450 (. thallium was obtained as a by-product of smelting other metals.185-.400) .250-.157-.440) .230) .179-.190 (.180-.159 (.170) .490) Total .167-.180-.183) .200 (.184 (.270) .320 (.239) .460) . the latter being the current major industrial consumer of thallium in this country.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 .420) .430) .430 (.480) .217) .380 (.196) .440 (.180) 75th .390 (.390-.201 (.360 (.200 (.220) .300 (.430 (.160-.200) .145 (.360-.170-..S. population from the National Health and Nutrition Examination Survey.240) .450 (. representing distribution into other tissues.180 (.170-.350) .440-.450 (.135-.470) .450 (. and 0.400 (.430) .150-.450 (.460 (.260 (.430-.160 (.330) .490 (.370 (.197 (.260-.200 (.290 (.220) .480) .320) .270 (.310 (.153-.200) .206) . it has not been specifically mined or refined in the United States since 1984.500) .290) .270 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.230) .230-.290 (.380-.430 (.240-.150-.330-.400-. 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.170-.290-.410-.410 (.181-. Thallium disappears from the blood with a half-life of several days.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 .160-.

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

Ting BG. Challeton-de Vathaire C. (1981) studied 1. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Wiegand H. References Agency for Toxic Substances and Disease Registry (ATSDR). 1992 [online]. Valentin H. Schaller et al. Trace element reference values in tissues from inhabitants of the European Union.35(1):4-9. Pirkle JL. Buhlmeyer G. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Kramer U. Sabbioni E.cdc. 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. A study of 13 elements in blood and urine of a United Kingdom population.265 people living near a thallium-emitting cement plant in Germany.html. Cassot G. White and Sabbioni.113(1):47-53. Raithel HJ. et al. Apostoli P. Pozzoli L. Toxicological profile for thallium. Ewers U. Brockhaus A.47(3):223-231.. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Atlanta (GA). Sampson EJ. Schaller KH. 2005. Investigation of a working population exposed to thallium. et al. Sabbioni E. Marcus RL.gov/toxprofiles/tp54. 1981. Soddemann H.atsdr. Gallorini M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Metals (CDC. Investigations of thallium-exposed workers in cement factories. Minoia C.5 μg/L. 2005. Paschal DC.. Schmidt M. 1980. Third National Report on Human Exposure to Environmental Chemicals. Minoia et al.S.216:253-270. Trace element reference values in tissues from inhabitants of the European community I. Biomonitoring studies on levels of thallium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of thallium than are found in the general population. Sci Total Environ 1990. Celier D. Environ Res 1998. with concentrations ranging up to 76. White MA. 1985). Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Centers for Disease Control and Prevention. et al.76(1):53-59. X.. 2005) and are shown with results from NHANES 2003-2004 in this Report. Paschal et al. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Dolger R. Available at URL: http://www.95:89-105. Int Arch Occup Environ Health 1981.1 mg/m3 (Marcus. 1990. A study of 46 elements in urine. 7/15/09 Blanchardon E. Int Arch Occup Environ Health 1980. Radiat Prot Dosim. Jackson RJ. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. 1998). Boisson P. Trace metals in urine of United States residents: reference range concentrations. Pietra R. 1998.. population) are thought to correspond to workplace exposures at the threshold limit value of 0. blood. Manke G. Morrow JC.48(4):375-389. Martin J-C. Fourth National Report on Human Exposure to Environmental Chemicals 235 . and serum of Italian subjects. Sci Total Environ 1998. J Soc Occup Med 1985. Brockhaus et al.

065-.130-.250) .070-.560 (.670) . Evidence is lacking for the carcinogenicity of tungsten.550) .250) .310-.280 (.270-.093) .800) . and 03-04 are 0.056-.620 (.066-.076 (.350 (.076 (.080-.084-.100-.490) .071 (.190-.370 (.070-.370) .00) .440) .081 (.180-.430) .280-.160 (.310-.110) .270-.160 (.088 (.111-.090) .090 (.090-. and for producing ferrotungsten.078-.088) .150 (.470 (.190 (.080) .060 (.150 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.560) .210 (.100-.180-.120) .095-.130-.380) .320 (.082) .070) .170 (.100 (.110 (.270-.340-.04. filaments for incandescent lamps.380 (.250) . and 0.093-.300-.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 .071-.410 (.090-.340) .170) .082 (.380 (.190-.092 (.113 (.120) .270 (.065 (.350) .070-.140 (.210-.530 (.460) .220) .110-.180) .100) .150-.300) .210 (.060 (.130) .090) .250) .087) .060-.460) .230) . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.220 (.810) .160 (.062 (.510 (.580) .120-.290 (.060 (.130 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.360 (.500) .150) .320-.690) . Little information is available on the toxicity of tungsten.04. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 236 Fourth National Report on Human Exposure to Environmental Chemicals .190) .400-.370-.520) .530 (.170 (.082 (.097-.101 (.113 (.100 (.180) .630) .084 (.070 (.270 (.050-.520) .120 (.360) .160 (.220) .100) .620) .310-.160-.290-.230) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).260 (.070 (.370 (.060 (.460 (.380-.190 (.210 (.095-. mainly as scheelite (CaWO4).790) .S.290-.120) .133) .260-.140-.330-.420-. Tungsten is used mainly for producing hard metals.430-.090-.470 (. Tungsten compounds are used as lubricating agents.062 (.830) .120-.137 (.340-.330) .122) .390) .087-.090 (.280 (.620) .070 (.170) .080) .240-.090-.077-.190-.380-.080) 75th .230-.120-.250-.360 (.330-.230-.360 (.650) .160-.090-.170-. bronzes in pigments.130) .460 (.410-.360-.140 (.073 (.310) .096 (.090-.300 (.074-.123-.120-.070) . which is used in the steel industry.260 (.290-.570 (. which are used in rock drills and metal-cutting tools.Metals Tungsten CAS No.101-.080 (.170) .230-.310-.140 (.090-.320) .260) .158 (.060-.060-.53) .560) .190-.110 (.092 (.180-.380-.500 (.210) .120) .160-. Occupational exposure is from dusts released during grinding or drilling of hard metals.073) .140-.058-.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 .330 (.104) .091) .120-.250) .400 (.150 (.130) .270-.070) .350-1.060-.100) .510-1.300) 95th .105) .082-.240 (.060-.080-.135) .450-. respectively.050-.320 (.096-.204) .430 (.550) .590) .130) .550 (.230 (.086 (. population from the National Health and Nutrition Examination Survey.080) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.210 (.126) . and as catalysts in the petroleum industry.180) .160) .110-.070-.110-.640 (.430) 320 363 290 679 744 725 1339 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .100) .360-.220) .132) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.064-.100 (.250) .500 (.490 (.100 (.110 (. see Data Analysis section) for Survey years 99-00. interval) .110 (.470) .170) .120) .120) .770 (.400 (.210 (.430 (.290) .130) .160) .430 (.200-.330) .180) .080 (.120-.430-.060 (.200) .092) .130-.050-.570 (.180 (.270 (.110) .380-. 01-02.151) .140) 90th .350) .420-.450 (.400 (.107 (.320-.200 (.250-.080 (.100-.370 (.070-.113 (.560) .080 (.370-.100) .070) .160-.105 (.073-.130-.470-.113 (.520) .460 (.470) .400 (.550) .060-.390 (.300 (.180-.290) .480) Total .260-.073-.400) .180 (.050-.510-.116) .310-.560) .130 (.068) .260-.230-.04.084) .080 (.340-.090) .220-. 0.080-.060 (.140 (.090) .950) .530 (.090-.160 (.350) .800) . Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.310 (.100) Selected percentiles ( 95% confidence interval) 50th .069-.056-.090 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.109) .110 (.093 (.300 (.069) .

176-.072-.412 (..085) .300) .245-. population (CDC.080 (.075 (.414) .287) .326) .063-.300 (.158) .331-.197-.253) 95th .214) .064-. Nicolaou et al.083) .109 (.086-.070 (.084 (.071) .138 (.333) . 2005).224) .089) . interval) .153-.215) .073 (.333 (.072-.333) ..216 (.080-.067 (.071 (.215 (.214-.S.091) .250 (.161) .067 (.065-.354-.167) .079) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.218 (.267-. (1987) found possibly due to methodologic.069 (.151 (.077-.258 (.065) .179-.197) .278-.180-.080 (.061-.208-.124-.216-.082) .317 (.059 (.155-.364 (.169 (.797) .148 (.065-.329 (.120) .094) .339 (.116-.100) .209-.119 (.431) .333 (.117) .078 (.074 (.078) .436-1.121-.105 (.431) .079 (.138 (.381) .077) .347 (.231 (.081 (.823) .079) .143-.240-.555 (.170-.080-.426) .300-.079 (.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 .071) .073 (.333 (.082) .105 (.056-.093-.065 (.154) .074) .392) .056-.086) .055-.133) 90th .484 (.104-.078 (.087 (.136-.060 (.143 (.078-.065 (.139 (.057-.300-.049-.301) .436) .084 (.098-.386) .582) .139) .079) .203-.091) . population from the National Health and Nutrition Examination Survey.086) .150-.293 (.272-. Using neutron activation analysis to 2000.333 (.301) .174) .126-.116) .061-.148) .083 (.066 (.165) .237) .091) .359 (.383 (.152-.462) .066 (.880) .081-.074-.145 (.153) .136-.439 (. and 2003-2004 (Paschal et al.083) .057-.200-.167-.068 (.205-.094-.085-.333-.255-. 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.064-.285) .302-.206-.538) .410-.116 (.136 (.302-.084) .150 (.465) .250-.124 (.231-.070 (.201) .255 (.200-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.067-.054-. Patients with medically-inserted tungsten found at increased levels in drinking water.059-.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 .093) .121 (.086) .279 (.154) .250 (.098-.315-. 1998).120) .130 (.130-.139-.329-.088) .739) .108) .073 (.075) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.341 (.075-.197) .146 (.059-.063 (.125 (.308) .216 (.340 (.255 (.222-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.279 (.088) .253 (.179-.308) .091 (.146) .090-.176-.S.077-.237-.360 (.353 (.275 (.286-.199 (.199 (.077) .063 (.081) .091) .164 (.431) .426) .068-.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 .184 (.058-.157) .258-.092) .103-.168 (.060-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.075 (.28) .375) .075-.344-.150-.379 (.211 (.089 (.136-.(Kraus et al.216-.122 (.074) 75th .605) .358) .284) .265 (.131-.100) .667 (. measure urinary tungsten. population.144 (.167) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.098 (.439 (.727) .198) .069-.122-.188-.063-.108-.294 (.133) .181 (.261-.500) .125) .095) Selected percentiles ( 95% confidence interval) 50th .091 (.060-.081 (.087) .119-.667) .083-.634 (.090-.216-.353 (.138) .078) .359 (.071) .237) .054-.085 (.109-.063-.217-.062 (.453) .146 (.075) .484) .107-.354) .158 (.187) .106 (.158) .299 (.144-.071-.099-.122-.073 (.339 (. 1997).096) .082 (.100 (.061-.465) .317) .197 (.333-.098-.279 (.283) .059-.083 (.217-.385 (.554) .. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.136-. 2001). 2001-2002.301) .233-.222) .074-.072 (.198-.079) . similar to those in this Report (Schramel et al.270 (.167-.065-.063-.201 (.169) .094) .452-.117 (.095-.317-.459) .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 .S.186 (.306) .069 (.253-.071 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.133) .267) .158) . or exposure that a control group of non-metal workers had mean levels differences.497 (.098) .111 (.053-.071 (.190) .439) Total .482 (.084) .174 (. 2003.

Paetzel C.cdc.(2):73-77. lead. Seghizzi P. Ting BG. Link J. Lenhart M. Available at URL: http://www. Jackson RJ.gov/nceh/clusters/Fallon/study. Catheter Cardiovasc Interv 2004. Kraus T. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. mercury. 238 Fourth National Report on Human Exposure to Environmental Chemicals . The determination of metals (antimony. Third National Report on Human Exposure to Environmental Chemicals. [online] 2003.62:380-384. Nevada Exposure Asssessment. palladium. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry.Metals blood. urine. Manke C. Sabioni E. Cancer Clusters. Trace metals in urine of United States residents: reference range concentrations. References Bachthaler M. National Center for Environmental Health. Sampson EJ. Schramel P. and hair (Bachthaler et al. Feuerbach S. Cassina G. 2004). Occup Environ Med 2001. thallium.58(10):631-634. Atlanta (GA). 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. J Trace Elem Electrolytes Health Dis 1987. Morrow JC. Wendler I. Pirkle JL. Centers for Disease Control and Prevention. 2005. bismuth. Mosconi G. cadmium. platinum. Schaller KH. Schramel P. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Angerer J.76(1):53-59. Zobelein P. Int Arch Occup Environ Health 1997. 4/15/09 Centers for Disease Control and Prevention. Nicolaou G. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. tellurium.htm. et al..69(3):219-223. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Pietra R. Paschal DC. Environ Res 1998. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Angerer J. Churchill County (Fallon). Weber A.

008 (.014 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.027-.024-.009 (. 235U (about 0.018 (.012-.008 (.030) .014 (.023 (.008-.064 (.053) .012) .010-.008) .012 (.050) .007 (.009) .007-.050) .040-.010 (.016) . and 03-04 are 0.010-.012 (.006-.008) .007) .010-.008-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).038 (.017) .006-.011) .022-.009) .013 (.030 (.039) .012 (.007-.008-.006-.053 (.014 (.014 (.026 (.016) .007-.015) . Variable concentrations of uranium occur naturally in drinking water sources.013 (.005-.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 .023) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.020) .036 (.047 (.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 .031 (.037) .031 (.011-.008 (.010-.009) . in some ceramics.014 (.016) .010-.S.028 (.021 (.012) . Thus.010) * .005-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks. respectively.040 (.006-.048) .007 (.045) .016-.067) .012-.008-.009) .023 (.008 (.014 (.026-.036-. In workplaces that involve uranium mining.046) .038) .024 (. or processing.006-.009 (.017-.036 (. 0.034-.008 (.008 (.013 (.027) .015 (.026) 95th .023-.018 (.007-.018-.049) .009) .023 (. and 0.006 (.060 (.020-.006 (.021-.011-.017 (.010 (.006-.042) .018) .017-.010) .021) .006-.72%).Metals Uranium CAS No.127) .013 (.037) Total .011) .018) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .011) .007 (.027 (.010) .010) .030 (.012-.008-.013-.020) .009) .011) .028 (.008 (.007-.007 (.027-.008 (.037) .088) .007-.043 (.008-.023-.039) .018) .005-.011-.010) * .021 (.031 (. population from the National Health and Nutrition Examination Survey.007) 75th .007-.019-.046 (.054) .031-.044 (.008 (.017) .010 (.009) .067) .008 (.052 (.007-.009 (.007) .008 (.011 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.073) .009) .012 (. Since the 1990’s.066) .009-.022) .009) * .011-.019-.006-.069) .023) .028 (.015 (.013-.016) .010) .012-.016 (.029-.031 (.041 (.009-.046-.023) .009-.013 (.008 (.010 (.005-.012-.026 (.007-.036) .023-.012 (.007-.054) .006-.017-.027 (.007-.011) .022 (.011-.009 (.011) .037) .026) .024-.013) 90th .007 (.040) .008-.008 (.008) .009-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.027 (.009) .033 (.008 (.007) .036) .009 (.051) . and as an aid in electron microscopy and photography.010) .005.026 (.054-.029-.033 (. including nuclear weapons.062) .037 (. milling. see Data Analysis section) for Survey years 99-00.009 (.011-.025-.007-.007 (. and 234U.114 (.009) .013 (. Uranium has many commercial uses.030 (.030-.027 (.005-.041 (.007-.008-.034-.019-.035) .008 (.037-.007) .009-.035) .055 (.036-.010) .010) .019-.012) .009-.007-.022-.158) . human exposure occurs primarily by inhaling dust and other small particles.028-.027) .046 (. 01-02.011) .007 (.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .072) .007-.009 (.009-.018) .056) .017) .009 (.040-.017-.009) .056) .007 (.024-.020-.279) .012) .009) .042 (.006 (.009-.013-.017 (.033) .006 (. nuclear fuel. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.065) .007-.065) .063) .008 (.007-.015) .004.009 (.006-.007-.028-.016) .043) .013) .007) .010) .035-.027-.040 (.033-.015 (.016) .017) .008) .019 (.049) .006-.015 (.039-.027) . interval) .017) .026-.013 (.020-.016-.032 (.017-.046 (.021) .010 (.034) . 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.045) .027) . Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.046 (.009-.009 (.011 (.021 (.007 (.008 (.007 (.031 (.009) Selected percentiles ( 95% confidence interval) 50th .011-.020-.021) .007 (.008) .021-.015-.029 (.022-.016-.006-.017-.020 (.040) .020-.023-.012 (.026) .009) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.048 (.012-.009-.006-.010-.004.

029) .009) .024-.005-.019 (.037 (.021-.030-.024) .006-.019) .013 (.024) .014-.008 (.005 (.021 (.007 (.006-.008 (.006-.033) .042-.028 (.005 (.008) .009-.034 (.007 (.010-.020 (.011) * .012-.008-.021) .025) 95th .007 (.011 (.006-.013 (.022-.016) .013 (.013) .050) .009) .025-.050) .007 (.S.033 (.011-.025 (. interval) .034 (.014) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.029) .007 (.016-. Radiation risks from exposure to natural uranium are very low.010-.010-.005-.039) Total .008 (. In cases of retained DU shrapnel.029 (. Depending upon the specific compound and solubility.016) .008-..007 (.007 (.008-.015-.008) .013-.012 (.011-.025-.032) .044) .007-.014) 90th .008) .021 (.011 (.011-.025-.007 (.030 (.032) .010-.006-.006) .009-.013 (.017-.022 (.028) .016) .009-.005-.014 (.006) .010) .010 (.012-.016 (.026-.010 (.043 (.006-.011) .007-. Uranium is eliminated in feces and urine.056) .017-.007 (.009) .006-.027) .008 (. where limited absorption occurs (less than 5%).009) .016-.024) .012 (.008 (.013 (.011) .008 (.010) .006-.006-.034-.007 (.018) .028 (.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 .047) .015 (.034 (.012) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .010 (.009) Selected percentiles ( 95% confidence interval) 50th .008) .004-.033 (.005-.024 (.006-.006-.051 (.005-.023-.017-.005 (.019 (.028) .017-.017 (.009) .025 (.015 (.005-.010) * .010) . After inhalation.146) .014-.017) .030-.005-.007-. Inhaled uranium-containing particles are retained in the lungs.024 (.014) .006-.019-.006-.024) .034 (.063) .010-.006 (.020) .050 (.007 (. 1992).012 (.031 (.006) .011-.005 (.1%-6% of an ingested dose may be absorbed.015) . kidneys. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.007) .018-.015-.006-.030) .013 (.009 (.008) .024-.017) .007 (. low level exposure.006-.020 (.016) .034) .027-.018-.010 (.027) .011-.015) .027 (.074) .054) .008-.008 (.018-.028) .013 (.004-.006 (.029) .006-.030 (.020-.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 .006-.026 (.008 (.007) .012) .010) .033 (.020-.010) .007-.013 (.006-.006-.024) .011-.042) . population from the National Health and Nutrition Examination Survey.007-.017 (.026 (.027-.010) .013 (.010-.058) .009) .022-. 0.010-.022-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.009 (.009) .026 (.015-.020 (.024-.061) .006 (.029) .007-. the initial half-life of uranium is about 15 days (Bhattacharyya et al. which represents distribution and excretion.009-.008 (.016) .018-. 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.016) .270) .007-.010-.028-.006 (.080) .009) .006-..007 (.007 (.009-.007 (.020-.014 (.008) .006) .016) .008) .008) 75th .021 (.018 (.025-.008 (.Metals impact.051) .041) .007 (.031-.027-.011-. liver.039) . 2003).015-.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.015) .039) .033 (.008-.015) .027 (.019-.042) .011-.015-.058) .007-.028) .008) .012) .019 (.029 (.059 (.012 (.006-.027-.022 (.030) .010 (.006 (.012 (.009 (.030 (.014) . After exposure to soluble uranium salts. the shrapnel acts as a source of chronic. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.009) * .016-.007) .011) .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 .013 (.006) .018-.019) .009) .010-.034-.013) . Health effects from uranium exposure result from chemical toxicity to the kidney.008) .009) .012 (.006-.008) .019-.015 (.035 (.045 (.007 (.017) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.020-.010-.022 (.026) .100 (.. with much slower elimination from bone.022) .013) . 2005).007-.011-. After long term or repeated exposure.006 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.053) .051) .029 (.027 (.048) .012 (.007 (.009 (.048) .034 (.007 (.035 (.024 (.008-.016-.008) .014-.019-.019-.006-. which can occur occasionally from high occupational exposure.016) .010-.009) .006-.009-.009 (.007-.040 (.007 (.077) .053) .007 (.051) .039) .067) .015 (.021 (.

IARC and NTP have no ratings for uranium human carcinogenicity. with emphasis on quality control...066 μg/g creatinine (Gwiazda et al. In two studies of a Finnish population with high natural uranium concentrations in their drinking water... Hamilton et al. and 2003-2004 (Dang et al.. McDiarmid M. Radiation protection dosimetry. had a mean urinary uranium concentration of 0. 2006.62:562-566. Kent (England): Nuclear Technology Publishing. Breitenstein BD. 2004).. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Vol. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Drinking water and other environmental standards have been established by U. Karpas et al. eds. the geometric mean urinary uranium concentration was 0.078 μg/L (ranging up to 5. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. 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.162 μg/L) (Orloff et al. 2003. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.. Pullat VR. Stradling GN. 1978). 2004). 1994. in that the levels were below their respective detection limits (Byrne et al... Durakovic A. A cohort of 46 U. Health Phys 1992.65 μg/L).e. Third National Report on Human Exposure to Environmental Chemicals. Health Phys 2000. 1-49.cdc.. ingestion. References Bhattacharyya MH. Pillai KC. (May et al.S. 2004).. soldiers evaluated before. but in whom no shrapnel was embedded.S. The U. Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals 241 . 2000). In 17 U. In the same study. 2004). urinary levels of uranium were as high as 9. 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.. 1991. 1992. In a study of 105 persons exposed to natural uranium in well water. 2000).. 41 (1).gov/ toxpro2.. or wound contamination. Six workers in a depleted uranium program showed concentrations of 0. 2006).. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Galletti.. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure... Volf V. Komaromy-Hiller et al. Uranium content of blood. (Kurttio et al. Muggenburg BA. 2006). Tolmachev et al. although slightly increased during and after deployment. respectively.1996. 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. Carmichael AJ. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.55 μg/L (median 0. Horan P.78:143-146. Metivier H. Dietz LA. et al. Mil Med 2003. Hamilton MM.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Information about external exposure (i. Sci Total Environ 1991.1992. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 28 soldiers who may have been exposed to DU by inhalation. 2006). the median urinary concentration was 0. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.html. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. EPA.atsdr. during. Thomas RG.S. pp. NRC. 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.168(8):600-605. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. population. Squibb K.61 μg/g creatinine. Ejnik JW. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 2002. Atlanta (GA).011 μg/L (McDiarmid et al. 2001-2002. 2002).110 to 45 μg/L (Ejnik et al. Benedik L.107:143-157. environmental levels) and health effects is available from ATSDR at: http://www. Zimmerman I. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.S. 2005. Byrne AR. Boyd P. Dang HS.S. the median urinary uranium concentration was 2. McDiarmid et al. 2006).S. In: Gerber GB. and no consistent effects on multiple endpoints of kidney function were found.

Uranium and thorium in urine of United States residents: reference range concentrations. et al. Human exposure to uranium in groundwater. Ting BG. Saha H.85:228-235. Kane R. Am J Kidney Dis 2006.S. Auvinen A. U. Jackson RJ.91(2):144-153. Noguchi H. D’Annibale L. Metcalf S. Makelainen I. Marino R. Element reference values in tissues from inhabitants of the European community. McDiarmid MA. Hamilton EI. et al. Health Phys 2004.71(6):879-85. Van der Venne MT. Kidney toxicity of ingested uranium from drinking water. Englehardt SA. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. McDiarmid MA.22–Bioassay at uranium mills. U. Roth P. Oeh U. Scott K. Roiz J. et al. Marko R. Pirkle JL.44:29-40. Jarrett JM. Oberbroekling KJ. Kurttio P. Comparison of representative ranges based on U. Sampson EJ. Hollriegl V. Halicz L. Karpas Z. Environ Health Perspect 2002. Biokinetic modeling of uranium in man after injection and ingestion. NRC). Smith D. July 1978. Nuclear Regulatory Commission (NRC) Guide 8.S. Squibb K. Auvinen A. Paretzke HG.158:165-190. concentration and daily excretion of uranium in urine of Japanese. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Komulainen H. Health Phys 2002.67(8-10):697-714. Li WB. Kuwabara J. Heller J. Int Arch Occup Environ Health 2006. VI.47(6):972-982. Hancock RG. Harmionen A. et al. Wilson PD.81:45-51.82(4): 527-532. Lorber A. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Sci Total Environ 1994. Wahl W. Gucer P. McDiarmid M. Katorza E. Health Phys 2004. Ough EA. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium.110(4):337-342. Cremisini C. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Review of elements in blood. Squibb K. Clin Chim Acta 2000. Costa R.87:51-56. Gwiazda RH.79(1):11-21. Health Phys 2003. Mistry K. May LM. Saha H. Lewis BM. Andrews WS. et al. et al. Health Phys 2006. Washington (DC): NRC. Cordero S. Pekkanen J.94:319-326. Uranium daily intake and urinary excretion: a preliminary study in Italy. Renal effects of uranium in drinking water. Nuclear Regulatory Commission (U.S. Kalinsky V. Ash KO.Metals Galletti M. Charp P. Tolmachev S. Karpas Z.86:12-18. Shelly T. Orloff KG. Engelhardt SM. Inductively coupled plasma mass spectrometry as a simple. Salonen L. Ejnik J. Environ Res 1999. Oliver M. rapid. J Toxicol Environ Health A 2004. Bennett LG. Radiat Environ Biophys 2005. Pinto V.S. Komaromy-Hiller G. Environ Res 2004. Biologic monitoring for urinary uranium in Gulf War I veterans. Paschal DC. Health Phys 1996. Howerton K. Sabbioni E.296(1-2):71-90. patient population and literature reference intervals for urinary trace elements. Kurttio P. Salonen L. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Military deployment human exposure assessment: urine total and isotopic uranium sampling results.

0 (12.50-4..20-4.0 (8.0) 9.Perchlorate Perchlorate (Urbansky.30-17.0 (9.76) 4.0) 9.80-6.49-3.30 (2.22-5. 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.40-7.30-7.10-12.0) 15.00-5.0) 8.31) 2.10-11. 1998).80-8.20 (2. 2007).67-5.0) 13.0) 13.90-9.0 (11.70 (3.40 (5.60-7.20) 7.75 (3.50) 5.0-19.20-4.07-4.30 (5.30-7.0 (9.0) 10.10 (2.30 (5.40) 2.39-4.80 (3.10-7.0-17. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS. leather tanning.90) 6.0) 12.0 (8. certain catalytic metals.60-6.21 (2.0 (11.50-11.40-5. and reducing agents..93 (4.29-3.90 (5.05 and 0.56) 3.70-6.0) 13.90 (4.40 (8.20-12.50-4.90-6.80) 7.0 (8.54 (3.70 (3.80-4.0) 9.40 (5.70-3.0-14. population from the National Health and Nutrition Examination Survey. Survey years 01-02 03-04 Geometric mean (95% conf. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.03) 3. 2005).89-3.80-12.30-19.0 (8.0 (11.00) 3.60 (7.70) 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 3.10) 5.5 hours and has a small estimated volume of distribution (Crump and Gibbs. interval) 3.0 (10.0 (12.90-10.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.68) 4.0 (12.20 (5.10) 5.20-3.93-4. laboratory analysis.0) 14. Other manufactured uses include fireworks.10 (7.18-3.51 (3.0 (11.79 (2.0) 16.02 (3.20 (2.81-16.05 (2.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0) 10.70-12.0 (11.40-13.0) 13.10 (6.00-6.0-17.40 (4. 2005).50-7.19-4.60 (4.0) 13.70-3. In addition.0 (9.30-6.20 (6.75-3.93-3.50 (3.0 (8.40) 3.10 (5.12) 3.0-20.0 (9.50) 6.50 (5.EPA.81) Selected percentiles ( 95% confidence interval) 50th 3.40-6.90 (5.0-18.10) 12.76 (3.80 (7.0) 9.01 (2.0-17.50) 3.00) 4.S.0) 14. or ammonium salt.0 (12.0 (13.11) 3.40) 3.70-11.70-9. and certain plants with high water content (e.46) 3.45-4.0) 19. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.50) 11.90 (3.66) 3.90-11.80) 3.0) 15. Perchlorate is stable under most environmental and physiological conditions.00) 7.0) 13. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.60) 5. Drinking water.0-18.16) 3.11) 4.S.96 (3.0-18. 2002).10-11. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.30) 6.00) 5.0-23.20) 4.50-3.87-3.51 (3.08-3.80) 75th 6.74-3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0 (11.65) 3. 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.0) 10.10) 3.30 (2.0) 8.70-5. but has strong oxidant properties in the presence of concentrated acids.0-17.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0) 11.0-15.0) 11.20 (4.g.44-4.70-7. and electroplating.20 (4.30) 6.40) 4.00) 3.0) 13.S. Perchlorate was added to the U.20) 3.0 (11.90-12. milk.40-4.35 (3.60 (4.0) 11.05.0-17.40) 90th 10.40-11.50 (8.40 (5.26 (2. 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.0-17.90 (5.40) 3.0-15.0 (11.80) 12.20-11.84) 14.60) 3.00-6.80-15. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 95th 14.0) 9. fabric dyeing.10-4.09) 3.0 (9.90-3.90-9.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.40-4.38) 5.20 (8.62 (3.90 (2.10 (6.80-4.40 (4.60) 8.20 (7.22 (2.32 (3.70 (3. It is normally found and produced as the anion of a sodium.0-29. and limited applications in pharmaceutics.0) 14.40 (3.90) 5.90-3.80 (3.40) 6.40 (3. lettuce) can be the main sources of intake for humans (FDA.47-4.50) 5.90-11.0) 9.0) 13. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0 (11.10) 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.80 (6. matches.0 (9.0 (11. potassium.88) 3.0 (9.19 (3.

60) 8. levels and sufficient in most participants (Tellez et al.0) 10.0 (10. 2005.90 (7.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.87-3.S.0-19.10) 6.60 (3.0-14.70) 2.20) 3.52-9.1-13. perchlorate is negative in most genotoxic assays (U.51-4.74) 7.0 (9. age.33-12.20 (7.3 (10.4-16.80 (7.32) 5.4 (11. However. Li et al.0) 12.81-3.30) 5.41-9.10 (4.08 (3.0 (9.00-2.30-5.50) 9.Perchlorate inhibition (RUI).0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.00) 3.40) 5. Lawrence et al.. 2003.10) 4.6-17.50) 2. 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.03 (2.0) 9. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.02-4. up to 68% RUI has been demonstrated..10) 13.. In the U.0) 12.5) 8. During gestation and infancy.60-5.43) 6.3-14.00 (2.50) 2.60-8.75) 3.0 (8.6) 20. Survey years 01-02 03-04 Geometric mean (95% conf.37 (4.7 (11.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .40) 3.0 (8.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.4) 8.1-22.60-6.S. 2005.3) 11.90 (4. 2005).90-2.51 (3.97-5.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3. 2002).07 (2.30 (6.61-10.89 (2.60) 10.25) 5.96) 2.56 (3.61 (5.0 (11.0) 13.22 (2. Also.50-3.40 (3. gender.09 (7.2) 8.90-3.80 (4.25) 5.99-3.EPA.71 (5.S. Greer et al. in a representative sample of U. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.4 (11.80) Selected percentiles ( 95% confidence interval) 50th 3.05 (4.22-6. 2002.56-3.50) 5.64) 5.1) 8.12-2.93-5.42 (3.20-4.90-9.25 (3.91) 4..3) 12.52 (8.10 (6. 2007).2) 8.10-3.0) 6. thiocyanate.95 (2.19-6.S.g..0-14.30-5.36 (8.30 (5.87) 7. 2002.29-6.39) 2.60-11. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.80-3.50) 6.1-16.70-5.40 (4.22-4.00-11.S.40-10.66) 3.70-3.86) 4.10 (1.S..87 (7.1-14.35) 3.20-3.60-5.0) 12. menopausal status.45) 3.0 (9. Many factors may be important in consideration of perchlorate action on the thyroid: dose.70-15.8 (11.25) 5.4 (10.04-3.35 (2.61-5.90 (2.10 (2.67) 5.90-11.20) 8.76 (3.00) 4. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.4) 13. levels.70 (2.0) 4.80-3. interval) 3.46-13.72 (3.24-2.89-3.90 (2.00 (6.98) 3.14 (2.44-6.29) 2.53 (2. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.58) 2.40 (3.93-7.39 (3. and the presence of other substances known to affect thyroid function (e. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.60) 3.93) 3.00 (4. U..EPA.00) 9.93-5. 2005).4 (8.1 (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.0) 14.70 (4. medications).50 (6.44) 3.30 (3.33-6.60-11.20 (6.0-17.30) 90th 9.50-5.10 (4. Steinmaus et al. 1999.30) 3.24 (4.40 (7.64-3.18-3.70-4.00-3.0) 11.50 (3.5 (13.45-2.60-8.46-4.30-10.34-3.6) 12.1 (8.59) 3.10-7.15-12. Lamm and Doemland.0 (11.20-9..80 (7.47) 2.26) 4.46 (3.12 (6.08) 3.50) 95th 12.73) 3.82 (5.04-3.90) 5.37-13.60-15.19-10. 2005).20-3. although iodine intake was higher than U.83 (5.87) 2.S.10) 3.90-20.50-9.0) 12.21 (2.0) 7.99 (5.16-3.02) 3.60-3. chronicity of exposure.0) 9. 2006..30) 75th 5.54 (3.70) 10.76-3.20 (4. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.90-15. 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.0) 13. dietary iodine intake.54 (2.93-8. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al. population from the National Health and Nutrition Examination Survey.22-4.09) 3. NAS. 2000).70 (2.77 (3. 2001.20-10.33 (7.26 (3.20 (3. women with urinary levels of iodine less than 100 micrograms per day.35 (4.0 (11.3) 8.0-44..40) 17.84) 2.20 (2.87 (5. nitrate.39-4.

Daaboul JJ. Lamm SH. Gibbs JP.. 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. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States.46(5):509. Blount BC. Additional information about exposure and health effects is available from the U. Neonatal thyroxine level and perchlorate in drinking water. Dyke JV. Skeels MR. Abarca CR. Goodman G. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Thyroid 2001. Byrd D.114(12):1865-1871. 2005).11(3):295. Lamm S.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . J Occup Environ Med 2000.cdc.atsdr. He X. Dasgupta PK. Environ Health Perspect 2006. May 2007. 2001-2002. Erratum in: J Occup Environ Med 2004.fda. et al. Landingham CB. Miller MD. References Blount BC. Environ Health Perspect 2007. Blount BC. National Research Council of the National Academies. Thyroid 2000. Doemland M. Benchmark calculations for perchlorate from three human cohorts. Valentin-Blasini L. Mauldin JP.gov/safewater/ccl/perchlorate/perchlorate. epa.17(4):400-407.htm. Deyhle GM. Perchlorate in the United States.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis.115(9):1333-1338. Available at URL: http://www. Osterloh JD. 2005. Pino S. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. 2007).40(21):6608-6614. Valentin-Blasini L. Rutherford GW. Environ Sci Technol 2006. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Richman K. Tellez RT. CFSAN/Office of Plant & Dairy Foods.42(2):200-205.41(5):409-411.113(8):10011008.. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Pirkle JL. Analysis of relative source contributions to the food chain. Osterloh JD. (2007) analyzed a subsample of NHANES 2001-2002 which demonstrated detectable perchlorate in all urinary samples and showed slightly higher levels in children as compared to adults. Washington (DC): National Academy Press.html.S. Pleus RC. Primary congenital hypothyroidism. National Academy of Sciences (NAS). population. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. J Expo Sci Environ Epidemiol 2007. Pirkle JL. J Clin Endocrinol Metab 2005. Also. most of the population is considered to be below the U. 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. newborn thyroid function. Food and Drug Administration (FDA). Page Last Updated: 05/28/2009. Kelsh MA. Crump KS. 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. Li FX. Li Z. Health Implications of Perchlorate Ingestion. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. The effect of perchlorate.110(9):927-937. Braverman LE. Jackson WA. J Occup Environ Med 2003.90(2):700-706.45(10):1116-1127. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. and environmental perchlorate exposure among residents of a Southern California community. Cross M. Caldwell KL. Lamm SH. Steinmaus C.gov/toxpro2. Braverman LE. Pino S. and nitrate on thyroid function in workers exposed to perchlorate long-term. Magnani B. Erratum in: Environ Health Perspect 2005.10(8):659-663. Barnard JC. Sesser DE. Environ Health Perspect 2002. thiocyanate. Buffler PA. et al. Perchlorate Exposure of the US Population. Lawrence J.html and from ATSDR at: http://www. Howd R.. 6/2/09 Greer MA.EPA at: http://www. Braverman LE. et al. Lamm SH. Environ Health Perspect 2005. Chacon PM.S. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.113(11):A732. Blount et al. Greer SE. Low dose perchlorate (3 mg daily) and thyroid function. Lau EC. Lawrence JE. Kirk AB. EPA reference dose (Blount et al. 2005). Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Crump KS.

Perchlorate pregnancy and the neonatal period.S. U.S. Integrated Risk Information System (IRIS). Environ Sci Pollut Res Int 2002.9(3):187-192. EPA/600/F-98/002 Washington (DC).1/15/06 U.gov/iris/quickview. Perchlorate as an environmental contaminant.epa. 1988.S. Urbansky TF. EPA). 246 Fourth National Report on Human Exposure to Environmental Chemicals . Drinking Water Contaminant Candidate List. No. Doc. Thyroid 2005.15(9):963-975. Perchlorate. Revised 2/11/05. Environmental Protection Agency (U.S. Environmental Protection Agency (U. Available from URL: http://cfpub. cfm?substance_nmbr=1007. EPA).

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

may metabolize or degrade to PFOA (Dinglasan et al. which may vary for some chemicals by year and by individual sample. 2005. and in offspring. Some of the effects in animals may be mediated through peroxisomal proliferation. 2007). PFOA is mostly excreted in the urine in animal studies.e.S. 2005. 2004. U. 1990). 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins... but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. 2005)... Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and β-oxidation of lipids (Kudo et al.. 2002.. Guruge et al. 2005). 2005.. Survey Geometric mean (95% conf. 2006a.. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. environmental fate. human toxicokinetics.. endocrine and immune effects... Tittlemier et al. 1995.. 2003). environmental breakdown products of the telomers used to make fluoropolymers or the metabolic products of fluorochemicals in the body can produce PFCs that are measured human blood. Olsen et al... All sources of human exposure are uncertain. kidney. the 8-2 telomer. hepatotoxicity. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. Vanden Heuvel et al. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. 2006.. Lau et al. Lau et al. by high protein binding in plasma and other proteins. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. Unlike many organohalogen contaminant chemicals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. in a wide variety of marine and land animals (Kannan et al.. growth retardation and delayed sexual maturation (Kennedy et al. including immunologic effects and tumor induction. For instance.. 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. pancreas. population from the National Health and Nutrition Examination Survey. 2004. The PFCs often measured in human serum are listed in the table. Prevedouros et al.. peroxisomal proliferation.. there is limited information on the sources.. Bookstaff et al. 2004. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. 2004). 1993). C5. or effects of other PFCs. < LOD means less than the limit of detection. C7). Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. Keller et al.5 years and for PFOS. 2003). 2004). and in human blood and semen (Calafat et al. 2003.8 years (Olsen et al.. Kannan et al. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. PFOA has been reported to cause liver. Taniyasu et al. Excepting PFOS and PFOA.. In some cases. EPA. in part. 2000.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). but probably include dietary sources (Kannan et al. C6. 2005). approximately 4. heptadecafluoro-1-decanol. see Data Analysis section) for Survey year 03-04 is 0. 2007a). but still can have long residence times in the body.. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al.4.. The elimination half-life of PFOA in humans is roughly estimated to be 3. 248 Fourth National Report on Human Exposure to Environmental Chemicals . It is unclear if environmentally degraded telomer products are a major source of other PFCs. thymus and spleen.S. 2003a and 2004a). 2004.

900 (.. In comparing three separate reports on adults. U.. 1999.. hepatotoxicity. 2003). interval) Selected percentiles ( 95% confidence interval) Sample 95th .500) . and no substantial age trends were seen within adults ages 20-69 (Olsen et al. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.400-. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. developmental and teratogenic effects were demonstrated in offspring.10) . Olsen et al.. 2003. PFOA.400 (<LOD-.S..500-1. PFOA. development in offspring was stunted and hypothyroxinemia was observed. 2004.400-1..S.. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. Lau et al.. or increased cancer rates (Alexander et al.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.800 (. 2003a).800) 1.. 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.20) . Cook et al.800 (.3.500) 90th . 2003).S. However. 2007).500) . possibly related to lung immaturity (Lau et al. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.500-1. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years..10 (. 1992. At doses causing maternal toxicity.500-3.80) 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 . 2003a.500 (. EPA. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) * 03-04 03-04 * * < LOD < LOD < LOD ..400-1.. see Data Analysis section) for Survey year 03-04 is 0. 2007. 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.. 2005).400-1.300 (<LOD-. 2004. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.50) . PFOS. Olsen et al.500-. < LOD means less than the limit of detection. Harada et al.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 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..300-1.80) 640 1454 03-04 03-04 * * < LOD < LOD .40) . 2004b). thyroidal). perfluorohexanesulfonate (PFHxS). the median PFCs values tend to be roughly similar in these age categories (Olsen et al. Survey Geometric mean (95% conf.400 (<LOD-.400 (<LOD-.00) . 2004).900 (. and changes in thyroid hormone concentrations (Grasty et al. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.800) 1. the potential to estimate risks to humans from animal doses is uncertain.80) 485 538 962 Limit of detection (LOD. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al..700) . 2007a.600-2. Olsen et al. 2001.900 (..400-1.800 (. Thibodeaux et al. population from the National Health and Nutrition Examination Survey. 2003a). 2007a. 2003. which may vary for some chemicals by year and by individual sample. At high but non-toxic maternal doses of PFOS.400-.500-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. 2003).00) . Kennedy et al. 2007b). Fourth National Report on Human Exposure to Environmental Chemicals 249 .500 (<LOD-1.300 (<LOD-.500) ..600 (. Fei et al. 2003.. and there was no clear evidence of excess all-cause or diseasespecific mortality.108 times higher than background serum levels in humans (Butenoff et al.500-1.S...20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .00 (. EPA.400) . 2003a. elderly and children. U.400-1.600 (. 2005).700 (.00) .800 (.300 (<LOD-.10) . 2004).500) . reproductive. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. In such studies. and humans.500 (. population. Animal studies of PFOS have demonstrated weight loss.600 (. monkeys. PFOS. 2007b. 2004a. 2003a.

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

Fourth National Report on Human Exposure to Environmental Chemicals 251 . which may vary for some chemicals by year and by individual sample.400 (<LOD-.500 (<LOD-.900) < LOD .600 (.300 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 0.S.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. < LOD means less than the limit of detection.500) 485 538 962 Limit of detection (LOD.300 (<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. interval) Selected percentiles ( 95% confidence interval) Sample 95th .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .3. see Data Analysis section) for Survey year 03-04 is 1.400 (<LOD-.300-. which may vary for some chemicals by year and by individual sample.0. Survey Geometric mean (95% conf.S. < LOD means less than the limit of detection. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (.500-. population from the National Health and Nutrition Examination Survey.400) .600) < LOD . * 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.

16) Selected percentiles ( 95% confidence interval) Sample 95th 8.80) 5.689 (.60 (1.700-1.30) 3.10) 6.70-10.50 (1.900-1. interval) 1.10 (.10) 1.10 (.90 (4.90) 8.40 (1.40 (2. population from the National Health and Nutrition Examination Survey.00 (.50 (1.10-9.10 (.80-7.30) 3.900 (.42 (1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .80 (1.861 (.900-1.70-6.60-2.60) 3.10) 1053 1041 03-04 03-04 03-04 .70-2.10-9.90 (1. Survey Geometric mean (95% conf.3 (9.05-2.30 (7. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20 (1.70) 1.20) 2.700 (.40) 640 1454 03-04 03-04 1.10) 75th 1.60-4.00 (1.80-4.50 (4.60 (1. see Data Analysis section) for Survey year 03-04 is 0.10 (4.40) 4.40) 2.44 (2.70) 13.30) 03-04 03-04 .40) .30 (1.60-7.20) 1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.60-3.90 (1.50-6.60-3.10) 5.20 (1.70 (1.816-1.86 (1.586-.60-2.80-8.0) 8.80) 1.90) 1.835-1.30) .697-1.900 (.00-7.04) .60) 1.00) 2.50 (4.40) 1.01 (1.54) .20 (6.72 (1. population from the National Health and Nutrition Examination Survey.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50-3.10) 75th 3.00-1.30 (3.00 (1.900-1.900-1.80-7.12) .826-1.50 (6.77-2.963 (.93 (1.20 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.00) 1.72) 1.5) 5.80-4.62-2.3.800-1.00) 3.20-1.51) 1.67-2.90) 90th 5.80-2.30-6.16) .00-1.60 (1.80-4.14 (.1.00 (1.0) 1053 1041 03-04 03-04 03-04 1.73-2.90-10.20-3.20 (6.50-6.30 (1.70-2.900-1.60 (6.90) 1.00) 1.80 (4.90) 1.70) 3.10) 6.40-1.87-2.60-2.00-8.20-1.30 (6.90-2. see Data Analysis section) for Survey year 03-04 is 0.90 (2.10) 4.60) 9.50 (1.834-1.80) 90th 2.1) 485 538 962 Limit of detection (LOD.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 1.721-1.70-5.00 (.91) 2.40 (1.600-.80-3.17-1. Survey Geometric mean (95% conf.852 (.20-1.966 (.40-3.30-12.50) 6.80-3.90-19.80-12.00 (1.20) 485 538 962 Limit of detection (LOD.00 (2.30-2.20-1.10) 8.30 (1.92 (1.20-2.09 (.03) 1.50) 2.20) .912-1.900-1.10) 4.50 (6.10-5.984 (.10) 1.50-10.80 (1.70 (2. interval) .30 (2.90 (4.30 (2.70) 2.40) 640 1454 03-04 03-04 2.26) 2.30 (1.40) 1.60-8.08) 2.20 (1.60-4.20) 1.10 (1.80-8.90) 3.30) 3.50 (2.00 (5.80-6.00-6.50 (1.10 (4.S.70-7.56-1.5) 8.90 (1.60) 2.809) 1.27) 1.800 (.50) 2.17 (1.40 (1.900) 1.70) 1.40 (1.70) 2.80) 4.30-9.80) 3.20) 03-04 03-04 2.6) 7.90 (1.S.40-1.

5-62.9 (13. see Data Analysis section) for Survey year 03-04 is 0.30 (3.50-13. population from the National Health and Nutrition Examination Survey.60) 03-04 03-04 3.30-8.80) 8.4 (17.70-5.40 (4.7-23.4) 640 1454 03-04 03-04 23.4) 75th 30.4 (19.40-14. Fourth National Report on Human Exposure to Environmental Chemicals 253 .0) 36.47-4.90-4.80-12.0) 21.8-78.8-22.6) 7.4-17.1-36.2 (16.6 (19.9 (19.8-81.7 (35.9 (22.S.8) 27.5) 32.8 (34.4 (23.90 (5.5) 9.30) 6.3) 28.2 (19.21-3.6) 9.90 (7.11 (2.20) 7.20 (4.0) 03-04 03-04 19.1-25.4) 56.7 (43.37 (2.60) 8.20 (4.6 (42.50 (3.90-4.3 (44.60 (6.00 (5.4 (28.0) 485 538 962 Limit of detection (LOD.60 (5.35) 3.70) 4.8-35.20) 7.40) 3.70) 6.07-4.60-9.1-52.85-4.30-11.89 (3.7 (19.80 (6.7 (7.00 (3.67-4.80-9.9-23.6-24.9-19.30-6.9-38.50) 4.5) 57.2) 640 1454 03-04 03-04 4.10 (3. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.8-22.30-5.3-22.96 (3.90) 6.3) 41.6) 21.1-24.40-10.3 (35.6) 1053 1041 03-04 03-04 03-04 3.5) 18.0) 23.80 (5.00 (5.70 (5.4-25.70 (3.6) 35.7-69.95 (3.2) 30.50 (4.91) 3.30 (5.6-45.1 (19.18 (3.6 (44. interval) 3.1) 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 4.4) 21.30-3.9 (17.2 (21.30) 7.2 (18.70-10.7 (35.0-16.8) 46.5) 8.90 (7.0) 21.3) 485 538 962 Limit of detection (LOD.60-14.6) 18.2) 30.1-33.40-17.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.8 (37.50-4.7-33.4.0-70.5-23.6 (35.2-57.5) 1053 1041 03-04 03-04 03-04 14.3 (28.0 (27.1.7 (13.70-7.60-13.50) 7.3 (35.0) 43.5 (28.3-61.1) 57. Survey Geometric mean (95% conf.7) 39.30 (3.7 (43.80-4.4-42. population from the National Health and Nutrition Examination Survey.90 (7.40 (6.60 (6.70-9.9) 22.10) 5.84-3.2 (28.6) 42.20) 4.9) 22.8) 32.80 (6.90-12.40-6.8 (45.4 (19.70 (5.1 (24.5-21.S. interval) 20.9) 9.53) 3.47 (4.1) 15.7-30.70) 3.0-66.60 (3.2-22.1-35.7-49.20-5.6-50. see Data Analysis section) for Survey year 03-04 is 0.5) 7.82) 4.5) 19.50-6.20-4.2 (27.20) 5.40) 90th 7.60 (4.40-6.10 (6.9) 27.20) 10.27) 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 21.20) 5.5-33.99-3.79) 4.6) 62.0 (20.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.0) 90th 41.5 (28.60 (7.3 (17.70-7. Survey Geometric mean (95% conf.2) 45.10 (3.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.0-20.1 (23.10-3.65-4.40) 75th 5.40) 5.60-6.80 (7.8-30.7-53.3) 42.20-9.4) 20.00) 3.8-22.

Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.200-.500) .300 (.4.300 (.300) .300 (.300 (.200-.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .500) .300 (. which may vary for some chemicals by year and by individual sample.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD . Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300-.300 (.500) < LOD 485 538 962 Limit of detection (LOD.300 (. population from the National Health and Nutrition Examination Survey.300) . see Data Analysis section) for Survey year 03-04 is 0.2.S.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-.300 (.300 (.500) .200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (. population from the National Health and Nutrition Examination Survey.300 (.300 (.300-.300) .300-.S.200-.300 (.200-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) . which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.200-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-.200-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .200-.200-.300 (.300-.500) 485 538 962 Limit of detection (LOD.300) .300) .400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.300) .

30) 1.30) .50 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (.800) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .700 (<LOD-.10) .900 (.500 (<LOD-.30 (1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.400 (<LOD-.700 (<LOD-.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .900-1.40) < LOD < LOD .00 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-1.900-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .40) 1.6.10) 1. Survey Geometric mean (95% conf.600) .900) .00 (.900-1. population from the National Health and Nutrition Examination Survey.10 (1.3.400 (<LOD-1. Survey Geometric mean (95% conf.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. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.700 (<LOD-.80) 1.900-1. < LOD means less than the limit of detection.700) 1.10-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.900-1.800 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.10 (.S.70) 1.30 (1.20 (1.900) 485 538 962 Limit of detection (LOD.60) 485 538 962 Limit of detection (LOD.30 (1.900) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD .300-2.600 (<LOD-.600 (<LOD-1.900-1.600 (<LOD-1.700 (<LOD-.30) 1.10) . population from the National Health and Nutrition Examination Survey.90) .10 (.10-1.300 (<LOD-.700 (<LOD-2.700 (<LOD-.10-1.20-1.S.00) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 255 .00-1.10-1.50 (1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .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.700) . see Data Analysis section) for Survey year 03-04 is 0.700 (<LOD-.700) 1.900 (<LOD-1.00 (.10) * 03-04 03-04 * * < LOD < LOD .10) 1.800) .00 (.600 (<LOD-1.300 (<LOD-1.700) 90th 1.20) 1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80) 1.

Inoue K. et al. Environ Sci Technol 2006a. and perfluorinated contaminants in livers of polar bears from Alaska. Reidy JA. Calafat AM.38(10):2857-2864. Evans TJ. Olsen GW. Calafat AM. Tarone RE. Taniyasu S. 2007b. Morikawa A. Edwards EA.S. Olsen GW. Rogers JM. Lau CS. Murray SM. Environ Health Perspect. Kawashima Y. Olsen J.34(4):351-384. Toxicol Appl Pharmacol 1992. Wijeratna S. Jarnberg U. Saito N. brominated. Watanabe T. Wong LY. Calafat AM. Calafat AM. Chem Biol Interact 2000. Corsolini S. Kuklenyik Z. Ingall GB. Mohotti KM. Bandai N.60(10):722729. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Environ Sci Technol 2004.39(3):363-380. Cook JC. Ye Y. Environ Res 2005. Aguilar-Villalobos M. Taniyasu S. et al. Yoshinaga T. et al. Kennedy GL Jr. Kuklenyik Z. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Appl Pharmacol 1990. Birth Defects Res B Dev Reprod Toxicol 2003. Halden RU. Grey BE. J Environ Monit 2005. Apelberg BJ. Laane RW. Hekster FM. et al. Mandel JS. Butenhoff JL.115(11):1596-1602. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Witter FR. Environ Sci Technol 2005. Sasaki S.38(17):4489-4495. Environ Sci Technol 2007a. Frame SR. The influence of time.99(2):253-261. Kannan K.and perfluorinated acids. Fei C. Harada K. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Cook JC. Kannan K. Cook JC. Day RD. Harada K. Rodricks J. Dinglasan MJ. The toxicology of perfluorooctanoate. Gaylor DW. Katakura M. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Characterization of risk for general population exposure to perfluorooctanoate.7(4):371-377.134(1):18-25.60(1):44-55. Hurtt ME. Moore JA.Perfluorochemicals References Alexander BH.104(2):322-333.68(6):465-471. Kamiyama S.46(2):141-147. Fillmann G. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Environmental and toxicity effects of perfluoroalkylated substances. de Voogt P.S. Rev Environ Contam Toxicol 2003. Falandysz J. in vivo. et al. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Biegel LB.115(11):1670-1676. Regul Toxicol Pharmacol 2004. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Mabury SA. Inoue K. Hurtt ME. Koizumi A. Polyfluoroalkyl chemicals in the U. Loganathan BG. McLaughlin JK. Chlorinated.39(1):80-84.113(2):209-217. Moore RW. Yun SH. Suzuki E. Kuklenyik Z. Environ Health Perspect 2007. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Yamashita N.39(23):9101-9108. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Seacat AM. Reidy JA. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Grasty RC. Peterson RE. Seneviratne HR. Calafat AM. Keller JM. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Tully JS.Koizumi A. O’Connor JC. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Toxicol Appl Pharmacol 1995. Arendt MD. Crit Rev Toxicol 2004. et al. Fluorotelomer alcohol biodegradation yields poly. Burris JM. Environ Sci Technol 2005. O’Connor JC. Bookstaff RC. Herbstman JB. Holmstrom KE. Liu RC.115(11):1677-1682. Environ Health Perspect 2007.1968--2003. Environ Sci Technol 2004.179:99-121.41:2237-2242. Chemosphere 2006b. Kumar KS. Frame SR. J Occup Health 2004. Caudill SP. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Olsen GW. Kannan K. Perfluorinated chemicals in selected residents of the American continent. Needham LL. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Saito N. and ex vivo studies. Biegel LB. Reidy JA. Mandel JH. Needham LL. Kudo N. Occup Environ Med 2003. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries.63:490496.124(2):119-132. Tully JS. Reidy JA. Yamashita N. Caudill SP. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. et al. Guruge KS. Kuklenyik Z. Mandel JH. Needham LL. Toxicol Sci 2001. Needham LL.40:21282134. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Butenhoff JL.39(23):9057-9063. Yoshinaga T. Environ Sci Technol 2005. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Bignert A. Perkins RG. Hurtt ME.

perfluorohexanesulfonate. Lundberg JK. Toxicol Appl Pharmacol 2004. J Occup Environ Med 2003b. Mandel JH.26(1):47-51.S. The developmental toxicity of perfluoroalkyl acids and their derivatives. I: maternal and prenatal evaluations. Toxicol Sci 2003. Buck RC. Peterson RE. A global survey of perfluorinated acids in oceans. Prevedouros K.2(1):53-76. Historical comparison of perfluorooctanesulfonate. and food items prepared in their packaging. fate and transport of perfluorocarboxylates. Gamo T. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. U. Burris JM. Butenhoff JL. Butenhoff JL. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. birds. Sources. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Thomford PJ.113(5):539-545. et al. Ehresman DJ. Butenhoff JL. Biochim Biophys Acta 1993. Lau C. Toxicol Sci 2003. perfluorooctanoate andother fluorochemicals in human blood. et al. Burris JM. Seymour C. Rogers JM. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Case MT. Hansen KJ. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. fish. J Ag Food Chem 2007. Butenhoff JL. II: postnatal evaluation. Church TR. et al. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors.51(8-12):658-668.68:105–111. Grey BE.40(1):32-44. Olsen GW. (Erratum in: Environ Health Perspect.37(12):2634-2639. Richards JH. Seacat AM.. Biol Pharm Bull 2003.198(2):231-241. Church TR. Moisey J. Korzeniowski SH. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Froehlich JW.115(9):1298-1305. Cao XL et al. Olsen GW. Lau C. Toxicol Sci 2002. Rogers JM. Ellefson ME. Coordinate induction of acyl-CoA binding protein. Olsen GW.45(3):260-270. Bronson R. Ehresman DJ. Thibodeaux JR. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Burlew MM. Half-life of serum elimination of perfluoroo ctanesulfonate. Olsen GW. Petrick G. Taniyasu S. (Erratum in: Toxicol Sci 2004. van Belle G. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. et al. Chemosphere 2004a.111(16):1900) Olsen GW. Larson EB. Stanton ME. Olsen GW. Environmental Protection Agency (U.74(2):369-381. Huang HY. Available from URL: http://www. Church TR. Burris JM. 2003a. Washington. Pepper K. Grey BE. Cousins IT. Hanson RG. Zobel LR. Olsen GW. Taniyasu S. Lundberg JK. 2003.74(2):382-392. Yamashita N.Perfluorochemicals Kudo N. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Hansen KJ. Reagen WK. Nesbit DJ. Helzlsouer KJ. Horii Y.111(16):1892-1901. 2007a. Seacat AM. Environ Sci Technol 2003. Environ Health Perspect 2003a. Barbee BD. Hansen KJ. Hansen KJ. Mandel JH. Mar Pollut Bull 2005. Olsen GW.54(11):1599-1611. Butenhoff JL. Hanson RG. htm. Hansen KJ. Burris JM. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations.55:3203-3210. Butenhoff JL. Miller JP. fish. Kannan K. Environ Sci Technol 2006. Rogers JM. et al. Kawashima Y. Sterchele PF. Mandel JH. J Children’s Health 2004b.68(1):249-264. EPA). Horii Y. Thibodeaux JR. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. and perfluorooctanoate in retired fluorochemical production workers. Olsen GW. Burris JM.epa. et al. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Chemosphere 2007b.gov/opptintr/pfoa/pfoara. Mair DC. Environ Health Perspect.41(9):799-806. 1/15/06 Vanden Heuvel JP. fast foods. Hanari N. and humans from Japan. Mandel JH. J Occup Environ Med 1999. Environ Health Perspect 2005. Yamashita N. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Kannan K.1177(2):183-190.S.82(1):359.) Tittlemier SA.

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

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

2000b [online]. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Chahoud I. 6/2/09 Okubo T. Reproducibility of urinary phthalate metabolites in first morning urine samples. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int J Hyg Environ Health 2007. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Reynolds T. et al. Environ Health Perspect 2004. Angerer J. Borch J. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Davis BJ.22(3):688-695. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Butala JH. Available at URL: http://cerhr. Jonsson BAG. Research Triangle Park (NC). Kessler W. Hauser R. Leffers H. gov/chemicals/dehp/dehp-eval. Epidemiol 2005. Akesson B. 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DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Albro PW. Dalgaard M. Hanaoka T. Brock JW.niehs. Anal Bioanal Chem 2005.niehs.html. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic.nih. Boehmer S. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Main KM. Int Arch Occup Environ Health 1993.nih.105:802-811. Csanády G. Chen Z. Hass U. White R. Hartle RW. Rylander L. Biol Pharm Bull 2003. Park MG.382:10841092. Duty SM. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Jobling S. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Milligan SR. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Reprod Toxicol 2005.16(4):487-493. Environ Health Perspect 2003. Ladefoged O. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. 2000c [online]. Kano K. Kano I. et al. The estrogenic activity of phthalate esters in vitro. Giwercman A. Am Ind Hyg Assoc J 1985. Mortensen GK. Ryan L. Grote K. Skakkebaek NE. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Yokoyama Y. et al. Environ Health Perspect 1997.112(17):1734-1740. Urinary phthalate metabolites and biomarkers of reproductive function in young men.46(11):643-647. and infant formula by tandem mass spectrometry (LC-MS-MS). 6/2/09 NTP-CERHR. Lovekamp-Swan T. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro.64(8):555-560. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride.niehs. Meeker JD. Duty S. Meeker JD. 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Barr DB. Clemons JH. et al. Orton TC.114(11):1643-1648. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Peters JM. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Rhodes C.45:11-17. Wu ZF. Parks LG. Zacharewski TR.Phthalates phthalate (DEHP): a cross-sectional study in China. Fielden MR. Klinefelter GR. Crit Rev Toxicol 2006. Jackson SJ. Toxicol Sci 1998. Environ Health Perspect 1982. Peck CC.S. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Hodge CC. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Reidy JA. 112(5):A270]. Albro PW. Barlow NJ.58:339349. Toxicol Sci 2000. Urinary levels of seven phthalate metabolites in the U. Malek NA. Cunningham ML.46:282-293. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Environ Health Perspect 2006. Silva MJ. et al. Meek MD. Environ Health Perspect 1986. Lambright CR. et al. Batten PL. Rusyn I. Bratt H. Pratt IA. Environ Health Perspect 2004. Caudill SP. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Abbott BD. Matthews JB. Ostby JS. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat.112(3):331-338.65:299-308.36:459-479.

8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.8 (71.1-43. interval) 15.1-38.9-47.1 (20.6 (12.9 (39. BzBP can be released into the environment during its production and. some personal care products.8-18.1) 14.3-161) 99.6) 13.6-72.2 (19.5) 65.9 (12.0 (33.6) 13.4) 12.2) 14.7-25.0 (27.4) 129 (98.6-92.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.3-74.6) 25. respectively.9 (13.5-25.2) 78.3 (29.8-48. population from the National Health and Nutrition Examination Survey. and 2003-2004 were generally similar those reported in U.7-13.4 (68.5 (27.2) 12. 0.2 (14.8 (21.4 (53. 2000).2-40.4-92.5 (26.5 (67.4) 81. and 0.1-35.6) 37.8 (80.0 (11.1-16.6) 95th 103 (94.3) 37.8-72.4-25.0) 32.6) 35.5-35.7-119) 99.6 (13.1 (14.0-85.9-27.3 (12.5) 55.7-172) 103 (74. 2001-2002.6) 50.1-16.2) 13. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1 (55.4-127) 80.8-13.2-19.2) 15.5) 23.6-116) 122 (102-142) 101 (85.7-17.2-33.3 (12.8-16.3-43.1-39.8 (10.0 (30.3) 13.1) 31.5 (47.2) 33.3 (13.2) 69.3-130) 122 (88.8.0) 33.8) 33.6-150) 94.8-64.5) 15.9 (21.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. see Data Analysis section) for Survey years 99-00.5-62.2) 32.4) 75th 35.7-58.3) 94.4) 49.6) 29.4) 80.6) 14.8 (14.1) 67. IARC considers BzBP not classifiable with respect to human carcinogenicity.0 (26.5-41.4-16.5) 15.0) 23. and 03-04 are 0.6-18.4 (27.0-26.2) 14.4-62.1-15.2-155) 91.1) 13.7-15.4-24.4) 35.9) 14.5) 30.8 (12.1) Selected percentiles ( 95% confidence interval) 50th 17.4) 51.2-38.5 (13.5 (76.3.5-97.1-18.8-16.7-16.9) 12.7 (13.9) 14.9-28.5-33.2-115) 113 (91.5-40.3 (44.3 (33. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-130) 101 (86.4 (10.5-84.1) 12.2) 66.4 (63.4 (10.2-20.8) 14.8 (30.0 (20.6 (13.9 (22.1-116) 122 (93.S.6-38.6) 16.6-132) 103 (84.3-88.4 (48.9 (11.9-62.0 (30.8-17.5 (55.2) 17.0) 90th 67.7-16.1) 29.7 (80.8-121) 79.2-16.9) 15.7-35.6 (53.0 (14.1.3-12. because it is not bound to products in which it is incorporated.2 (43.9 (70.3) 23. NTPCERHR.0) 16.7 (51.4 (31.Phthalates Benzylbutyl Phthalate CAS No.9) 11.6) 35.3-21.0 (15. and diet is the major source for general population exposure.9) 49.0) 70.9-14.5) 27.8 (50.3 (30.9) 18.7 (53.6 (13.1 (14.4 (53. 2000). residents (Blount et al.4) 33.2 (19.1 (58.8-41.9 (12.6-43.6 (66.5-36.4) 35.1) 32. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.4) 108 (96.1 (13.6 (13.8-17.5-14.6-92.9-190) 86.1-61.6) 14.0-55.8) 24. particularly male animals (McKee et al.4-15. car care products.9 (28.8-76.1-15.5-94.1-120) 52. can produce developmental and reproductive toxicity in rodents.1 (13.3-34.5-36.4) 38.3-75.2 (11.9-30.6-17.3-125) Total 15.8-35.6) 67.5 (66.5 (61.2-16.S.3 (22.3 (12.1 (32.4 (32.8 (28. 01-02.8) 28.9-16.8-98.0 (23.4 (59.2-17. sealants.9-87.7-16.0) 24.3-27.7 (11.4) 14.3) 54.3-91.6-39.7) 40.6-29.3-18.4) 98.8) 63.8 (86.4 (29.9 (16.8-14.4 (13.4) 71. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.6 (21..2-116) 122 (102-143) 101 (84. including MBzP.9) 13.8-14.5 (57.8 (38.5) 16.3) 15.0) 20. vinyl tile. High dose BzBP and its monoester metabolites.3 (54.0 (12.4 (32.8 (71.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.2 (47.2-31.7 (12..7) 38.1 (10.9-49.3) 63.2) 22.0) 34.0 (15.2-183) 101 (78.1-90.4-120) 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 13.7-14. Food crops take up BzBP.1) 68.2 (10.3) 13.8-133) 89.6 (41.7 (70.8 (53. 2004.5-18.6) 24.2-39.7 (15.6) 15.1-214) 166 (116-191) 145 (110-213) 88.1 (19.6 (32.7-82.0 (55.7) 23.3 (29.7 (82.0-106) 58.7-170) 169 (134-198) 152 (99.3-82.5-145) 138 (106-241) 143 (127-179) 120 (99.0 (43.3-18.0 (34. 262 Fourth National Report on Human Exposure to Environmental Chemicals .9) 43.4) 65.6) 63.1) 76. and to a lesser extent.5) 82.6-79. it can be released into the ambient air during use or disposal of the products.2 (25.

2002). 2002.5) 23.5) 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 .8) 56.8-69.9-115) 57.2 (69.4-42.6-47.4 (21.7-14.7 (19.6 (22.5-13.6 (14.3) 16.0 (12..2) 11.0-48.6-86.7) 56.6 (34.6 (30.9-83.8 (50.7-31.2-49.1-14.7) 19. in young Swedish men (Jonsson et al.95-14.7 (12.0 (41.5 (9.6-40.5 (56.4) 13.4) 90th 50.2 (41.2) 12.4) 21. Hauser et al.1) 35.6 (11.0) 12.0) 24.3-73.7 (23.1) 24. 2007).0 (10.1) 12.7 (59..9-14. 2006).0) 24. 2005).9) 64.0) Selected percentiles ( 95% confidence interval) 50th 13.8) 53.6-12.0-15.9 (9.8) 68.9 (12.4-19.9) 52.0) 49.8) 54.6) 73.4 (60.5) 95th 77.7-15.8) 53.8) 15.1) 27.9) 12.8-39.6-13.7-12.3) 36.3 (39.3) 13.3-64.6) 38.5-61.6-15.3) 90.8-27.5-31.4-18.3 (13.3-34.8) 108 (75.3 (23.6) 58.6 (11.7 (55.5-38.2) 11.3) 18.8 (12. 2003).3-16.4-116) 73.9 (12. 2007).1 (19.9-40.5) 46.3) 12.2-12.0) 11.1 (23.4 (26.8 (13.5-29.8) 33.6 (51.6-99.8 (64.9-13.1 (14.4-90.2) 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 12.3) 29. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 26.4 (69. In an annual sample of German university students.2-21.7-69.9 (43.5) 14.0 (12.0 (11.7-90.6 (36.1-120) 77. and females compared to males (Silva et al. and in a small sample of German residents (Koch et al. In NHANES 1999-2000.2-26.6 (15.1 (11.1) 80.6) 25.4) 12.8-64.3) 73.1 (21.. 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) 17. 2004.6) 53.5-58.1 (13.5 (12.S.1) 23.4 (34. interval) 14.8-48.5-213) 49.0 (62.5 (35.Phthalates York City (Adibi et al. A small study of African-American women in Washington.9-62.5) 78.9 (10.3-11.1-12. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.3 (24.6) 75th 25.7 (21.8 (46.8-14.0 (41.4 (11. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.9 (24.7) 46.7 (13.8 (69.6-116) 74.1-29.4-60.1 (21.7 (13.7 (38.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.4 (11.5-23.1 (34.4 (13.9) 11.8-42.3) 89.0) 15.1 (43.4) 17.8-14.4) 15.7 (14.2-78.2-13.8) 80.0 (13.3-38.2 (56.2 (27.4-93.7 (54.2-117) 95.4) 28.7-20.4 (33.9-104) 62.6 (19.4) 104 (89.5) 17.0-53..3) 13.7 (11.4 (10.1 (9.4-99.5) 41.4-27.4-15..3) 37..0-27.8-80.9-13.8) 24.9 (24. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.6 (11.2-15.8) 46.4-142) 134 (116-176) 136 (85. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.1) 142 (99.7-397) 70.7) 38.0-51.7 (11.1 (53.1) 39.8 (57.9 (10.8) 11.9 (29.1-12.7-56.8-60.3 (60.8) 71.2) 67.5-26.7) 11.4-14.0) 13.6) 12.8-15.5) 10.7-61.1 (21.5-26.9) 12.1 (15.3 (38.2) 15.0 (38.9) 100 (80.5 (11.6-26.9) Total 14.4) 13.4) 14.9-23.1 (25.2-13.8 (49.9 (15.5 (49.5 (48. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al. in men attending a Boston infertility clinic (Duty et al.4 (46.3) 14.6 (57.3) 13.1-27.4) 25.73-12..4-79. 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.6 (30.4 (11.8-85. 2004).8) 13.9 (39.0 (33.5-99.4 (63.3) 14.4) 51.9) 24.5) 16.1 (41.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.7-19.9 (51.6-20.9-16.5-16.8-34.4-14.5 (10.5-79.5 (42.1 (13.8-13.3) 67.6) 13. Hoppin et al.1-35.8) 16.6-81.6 (24.2-57.0 (49.4) 44.5-76.0-109) 65..9-28.1) 24.2-51.9) 12.8) 33.8 (10.5 (10..3 (35.9 (22.5) 13.7 (11. population from the National Health and Nutrition Examination Survey.2) 32.9 (54.1-58.8 (30.8) 34.5-42.8-16.5-58. 2005.4 (74.7-19.0-90.2-15.1 (18.2) 11. Weuve et al.4 (25.2 (40.4) 50.1-125) 86.5) 20..4-102) 70.3) 55.6) 12.8-13.8-173) 195 (121-305) 229 (99.8-13.1 (46. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9 (55.8-15.7) 25.9) 11.1-79.69-11.1 (21.7-20.6) 30.3 (12.2-17. 2003).7-15.4-23. adolescents compared with adults.4) 60.0-26.7-29.7-123) 77.7 (18.9) 42.9-69.7-14.9 (15.4-17.4 (12.0 (67.3 (15.2) 26.5-57.8 (11.0) 60.3) 21.

gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Brock JW.93:177-185. Duty SM. Barr DB. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Koch HM. Brock JW. Barr D. Blount BC. Butala JH. Environ Health Perspect 2006.nih.25(2):293-302.111(14):1719-1722. Weuve J. Hu H. Environ Health Perspect 2002. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Baird DD. Calafat AM. Perera FP. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Ryan L. Environ Health Perspect 2004. 2005. Sanchez GN. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Malek NA. Helm D. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2000. Needham LL.22(3):688-695. Hoppin JA. Meeker JD. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Caudill SP. Angerer J. Green RA. J Androl 2004. Environ Health Perspect 2003. Dobler L. Int J Hyg Environ Health 2007. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Ryan L. Urinary levels of seven phthalate metabolites in the U. David RM. Atlanta (GA). Epidemiol 2005. Needham LL. 112(5):A270]. Caudill SP. Environ Res 2003. et al. Levels of seven urinary phthalate metabolites in a human reference population. Duty S. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.niehs. Reidy JA. Reproducibility of urinary phthalate metabolites in first morning urine samples. NTP-CERHR. Phthalate monoesters levels in the urine of young children. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.68:309-314. et al. Bull Environ Contam Toxicol 2002. Brock JW. Calafat AM. et al. Third National Report on Human Exposure to Environmental Chemicals. Sampson EJ. Silva MJ. Hilborn ED.112(3):331-338.110(5):515-518. Silva MJ.114(9):1424-1431. et al. Schettler T. et al. Gans G. Reprod Toxicol 2004. et al. Davis BJ.18(1):122. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Jedrychowski W. Silva MJ. Hodge CC. Singh NP. Pirkle JL. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.210(3-4):319-333. Hauser R.Phthalates References Adibi JJ. Caudill SP. Wittassek M. Prenatal exposures to phthalates among women in New York City and Krakow. 2000 [online]. Hum Reprod 2007. Giwercman A. Available at URL: http://cerhr. Eckard R. Chen Z. Research Triangle Park (NC).16(4):487-493. Jonsson BAG. Centers for Disease Control and Prevention (CDC). et al. Drexler H. Hagmar L. Richthoff J. Silva MJ.html.108(10):979-982. Rossbach B.S. Koch HM. Rylander L. Jacek R. Camann DE. McKee RH. Wiesmuller GA. Poland. 4/20/09 Silva MJ.

50 (6.4 (20. OSHA has established a workplace air standard for external exposure to DBP.3 (11. in men attending a Boston infertility clinic (Duty et al.1 (13.90 (4. 2005).6 (14.46-5.0 (13.68 (2.8) 40.3) 18. interval) 2.6) 17.26 (2. 84-74-2 Di-isobutyl Phthalate CAS No.48 (2.40 (7.2 (11.40-4.2-33. pharmaceutical coatings.10-2.5) 14.0) 24. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.43) 6.10) 8.20-12.1) 16.7 (17.00) 4.0 (11.6 (10.80-5.80 (5.7) 15.63) 3.3-19.5) 18.70 (5.20) 4.70-4.70 (2.6-20.00) 4.9) 15.17) 4.46 (2.4-12..9-14.22) 3.00-6.50-2.40 (2.50) 7.0-25.90 (3.1-20.20-12.50) 18.2-22. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC. and in a small sample of Japanese adults (Itoh et al.56) 3.00 (7.7-31. Fourth National Report on Human Exposure to Environmental Chemicals 265 .1 (8.40 (6.70-8.. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.0-38.6) 16.11-3.20-2.90 (6.6-18.50) 90th 12.40 (3.9 (16.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.46 (3.5-29.10 (4. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.56 (5.1-12..17 (2.40-3.33 (2.66) 2.6-34.2 (8.3-20.8) 21.50 (3.6) 17. Hauser et al.6 (11.10 (4.82-3.3 (13.0 and 0.7 (9.6 (13.96) 3..6) 26.10-9.80 (5.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.30-6.5-24.4 (14.30 (1. 2005).3.60 (4.59) 3.0 (13. Koch et al.7-20.20-9.7 (7.02) 4. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.90 (4. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. Studies of children found age-related differences in urine MBP levels.00-11.44-2.70-4.24-8.40) 5.00 (5.5) 18. they have been referred to as monobutyl phthalate (MBP).5) 12.60) 3.00-4.60 (8.00) 7.7) 4.5-16.6 (9.4-27. Survey Geometric mean (95% conf.6 (14.2-14. 2003). Following oral administration of DBP to humans.4) 22.56 (3.40-17.60-6.7 (16.5) 19.10) 11.07 (3. 2005).30-13.40-9.10 (3.50-10.6) 12.73 (2.30-7. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.7-18.30-2. 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.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.5) 23.40-3. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.3 (18. in a small sample of pregnant women in New York City (Adibi et al.70) 3.50-6.0-18.20 (6.3-48..30) 5.2 (12.0 (19.70) 5.40 (2.5 (17.6 (29.60 (2..30 (4.0-14.7-31.73-5.5 (10.40-5. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.00-6. residents (Blount et al.3) 3.50) 8. and insecticides.0) 12.S.3-43.85-6.30 (3.30) 10.10) 3.3 (16.0) 20.1-25.5 (27.9-23.90-7.7 (18.80 (2.1) 22.80-5.28-5.81 (3.72-3.90-2.3 (13. 2003). NTP-CERHR.5) 25.20-6.6 (13.2) 5.S.00-9.20 (3.8) 677 652 703 699 1216 1088 Limit of detection (LOD.3) 33.55) 2.71 (2.90-4. 2007).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 2.60 (5.6 (10.49-2.80 (3. Biomonitoring Information Median concentrations reported in the NHANES 19992000.50-4.55 (3.10) 9. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.3 (19.00) 6.91) 4. CDC.97-7. 2005.30) 2.30-6.30) 10.5-16.30-11.5 (11.0) 9.3 (16. and also in some printing inks.3-30. 2001).3-18.7) 7.7 (17.6) 10.50) 5.84) 4.37) 6.10-9. population from the National Health and Nutrition Examination Survey. 2000.20 (7. mostly as MnBP (Anderson et al.8 (9.6) 16. 2000).97) 4.30) 6.40-4.3-24.19-3.Phthalates Di-n-butyl Phthalate CAS No.10) 2.4) 5....0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.80 (2.67 (5.5 (20.22 (3.50) 2. In addition. When total DBP metabolites have been measured. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.1-17.1) 25. DBP can produce reproductive toxicity in male rodents (McKee et al.9) 10.80) 75th 5.40-12.56-4.46) 2.4) 12.90) 12.7) 14.20) 7.6-26. 2004.00) 10. 2004.5) 22.9 (16.30-3.6-14. about 65% to 80% of a dose is eliminated in urine within 24 hours.7) 18.97) 2.90-4.0) 13.

26 (2.53-3.5 (11.8-13.69) 6.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.46) 3.1 (10.81) 9.2-15. to about two to fourfold higher (Fromme et al. respectively.1) 4.68) 3.30 (6.8 (10.4) 15.95-3.8 (8.82) 4. 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.5) 15.52-3.58-3.62-12.72-7.1-15.91-6.78) 9.32) 7.86-4.21) 10.64-10.64-7.9 (11.0) 15.4-16.74-3.79 (4.67-5.2) 24.13-6. samples from German university students had consistently higher median urine levels of MnBP and MiBP.02-10.08) 75th 4.74 (4.3) 18.81 (6.11-2.6) 13. 2006).53-4. 2007). 2005).related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.69-7.94-12.09-2.47-12.96 (3.0) 7.43) 3.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.72) 5.24) 3.7) 3.9 (15. Over this time.10-5.20-4.98 (2. the students’ median values for MiBP levels remained relatively unchanged.38-10.04) 7.26-2. 2004).52 (2.20-3.80) 7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.36-2.9-26.6) 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 2.51) 5.0 (8.0) 3.55-6.08-2.20 (7.33 (3.33-9.03-11.27-12.92 (7.86) 6.22 (2.61-3.54 (4.S.47 (3.66) 4. population from the National Health and Nutrition Examination Survey.1) 11.99) 7.54 (2.1) 13.94) 6.2) 8.18 (4.57 (3..29-8.6 (8.3) 13.59 (4.3) 16.31) 2..75 (6.and gender. In an analysis of NHANES 1999-2000.28-13.07-5.80-3.56) 2.21 (5.56) 5.73 (5.32 (3.1-25.14 (4. interval) 2.64-7.46 (2.88 (2.18-10.6-19.89-5..66 (8.18-4.31) 2.39) 5.4) 7.53-5. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.81 (3.6 (12.81) 4.80 (3.65 (4.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .15) 3.03-7.46-11.00 (3.2 (11.1-24.33 (2.39-3.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.28 (4.94 (5.36-7.07 (2.7 (21.2 (10.57-4.03 (5.99-4.1) 15.00-3.02 (7.0) 11.75 (4.05) 2.3) 13.3 (13.65-11.62 (6.85 (2.30) 2. Weuve et al.11) 5.04-5.41 (2.34 (3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. 2004).97-2.79-6. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.44 (3.6 (15. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.9 (9. ranging from more than one-tenth the NHANES median (Itoh et al.3 (17.6) 11.8-36.76-3. 2005).17) 90th 8.8 (9.78-8.5-19.93-6.6 (10.76-3.79-8.9-16.2-13.3) 28.0 (10.00-3.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.17 (2.7) 19.01-2.0 (12.8-18.66) 10..1-12.89) 6. up to four and 13 fold.38 (6.18) 3.2) 9.6 (9.29-3. Finding a measurable amount of MnBP or MiBP in urine does not mean that these levels or the parent compound cause an adverse health effect.8-18.66) 2.20 (2.78) 8.13 (2. An analysis of NHANES 2001-2002 showed similar age.7) 11.42) 2.7-28.5 (9.76 (3.7 (13.58-4.33) 3.6 (8.7) 10.15-4.1) 10.7 (11.57 (3.89 (3.5) 13. while MnBP declined (Wittassek et al..95) 2. 2002.37) 3.32 (7.1) 7.31 (2.20 (2. 2007).1 (11.17-12.52) 3.00-7.83 (2.25) 5.6-19.65-4.82 (4.20-2.0-18.9-40.84 (8.4 (12.68 (2.8) 10.54) 2.35) 3. Between 1998 and 2003.7 (9.52-20.9) 12.51) 2.4) 23.45) 3.76-15. 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.69 (2.31 (7.56-4..56-15.51) 15.47-5.19 (2.43) 3. than adults in NHANES subsamples during the same time period.18 (1. Survey Geometric mean (95% conf.95) 10.84 (4.69) 4..43) 3.11 (5.68) 5.04) 3.18) 4.

2 (19.5) 26.2-114) 73.9 (79.1 (34.2-24.5) 40.5) 47.2-87. 01-02. 1.9) 75.1-20.3-40.2 (75.9-101) 77.8) 58.7-124) 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.8-29.7-42.1) 23.9.7) 124 (98.2) 90th 98.8) 48.3 (36.6) 21.7-24.1) 47.2-93.5) 36.9-87.1 (19.8) 43.3 (17.1 (41.6 (22.7-92.6) 17.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.6 (65.7 (70.3 (23.5-47.9-22.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.7-34.9-114) 116 (97.4-159) 107 (84.8) 23.6-33.1-92.5) 21.9) 46.7 (43.6 (61.0) 84.7 (18.8-123) 101 (90.7) 28.5 (59.4 (71.0-26.7 (64.3-145) 85.3 (56.2 (18.3) 36.0) 31.0-58.1) 25.5-121) 106 (94.7) 92.7-127) 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 22.9-42.4) 52.2-63.1) 20.6-48.3 (60.2) 42.3 (30.5) 85.4 (84.9) 29.4) 22.1 (28.3-79.0 (31.8-22.5 (30.6) 80.2-22.0-21.1) 46.0 (23.9) 36.3 (42. referred to as monobutyl phthalate (MBP).3 (30.1 (16.4 (35.5) 95.8) 62.5-44.5) 34.1 (31.1 (18.6-31.4-42.5-117) 95.7-121) 97.5) 78.7) 42.6-37.8 (19.6-29.4-18.3-76.2-49.4 (72.4) 20.7-34.6) 38.8 (57.7 (51.0 (18.1) 17.6-40. respectively.7 (18.3) 40.9) 18.2) 26.6 (90.4) 59.6 (48.4-31.9 (17.6-113) 108 (90.5-43.0) 27.3-24.9 (17. Fourth National Report on Human Exposure to Environmental Chemicals 267 .5 (28.9-22.7 (38.2) 38. population from the National Health and Nutrition Examination Survey.6-20.5) 20.3-21.7-111) 64.S.2 (25.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.3) 23.4 (19.4 (35.0 (72.4 (21.7-20.2-21.1) 19.2 (20.7 (19.4.3-85.6) 71.1-27.7 (28.0) 38.7 (24.1 (58.9 (20.1 (19.6-29.3-60.1 (51.1 (19.5-53.6) 20. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.9) 21.2 (21.3 (51.0 (36.5-47.2) 68.1.1) 36.6-24.4-20.0-51.5) 24.6 (55. Survey Geometric mean (95% conf.3) 24.1) 23.1 (26.1-51.6 (19.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1-80.2) 32.2 (17.5 (59.3-67.9-92.7-117) 118 (108-143) 93.7) 74.1-75.7-106) 69.9) 71.5-27.0) 30.4 (23.1-22.4 (25.6-44.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. and 0.0-19.0-73.1 (19.2-23.2 (74.1 (36.5-42.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7 (22.3) 26.5) 65.5) 36.5-60.6-143) 127 (99.4) 64.1 (21.7-116) 95.6 (44.7 (33.2) 62.2-33.1-24.9-28.8) 19.9-33. see Data Analysis section) for survey years 99-00.6-69.4-44.1) 30.3) 21.0 (45.0-24.9) 26.0) 20.2 (79. interval) 24.8-42.6-49.4-26.5) 31.6-36.0 (25.2-56.8-25.0) 21.5) 17.2 (78.6 (26.4-60.7-26.6) 46.7-91.4 (35.0-19.6) 35.5) 19.8) 75th 51.7-53.0-24.3) 19.1 (54. and 03-04 are 0.0 (20.4 (35.1 (62.6) 39.9-79.4 (38.7) 52.0 (15.3-136) 137 (107-162) 119 (90.1) 23. *In the 1999-2000 survey period.8-132) 95.1-29.1) 31.1 (17.2 (59.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2 (58.3) 18.0) 117 (104-131) 112 (84.0 (17.4-25.9 (79.6 (32.5 (74.5) 37.5 (29.0-32.7 (16.9-53.1-82.4 (36.2-159) 92.3-96.2-32.0 (30.2) 20.3 (37.8-119) 90.7-42.3 (23.2 (21.6 (16.0) 120 (98.0 (78.

8 (65.9-100) 86.9) 52.9 (20.2-22.1) 53. interval) 22.1 (46.4) 19.1) 44.0) 75.1) 17.5) 134 (93.2-18.4 (31.3-20.5) 39.3 (48.5-76.6-23.4-103) 117 (83.7) 42.0) 53.4) 53.6) 31.5 (30.6) 39.9 (73.2-85.5-37.8) 19.3 (17.3-32.9-14.3) 33.8 (18.2) 74.6-43.1) 20.6-92.0) 41.8-23.2-22.0 (43.3-21.6-155) 91.6) 23.3-49.1) 35.6 (74.1) 50.3-38.9 (19.6 (57.9) 20.6-50.9-70.9 (30. Survey Geometric mean (95% conf.7 (28.2-22.2 (19.0) 81.4-65.6) 38.4 (31.4 (16.6 (41.2-16.1-18.0-47.6) 24.0-41.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9-26.3 (17.4 (13.9 (16.4 (37.9) 30.1) 22.1-128) 97.0) 25.4) 51.1) 20.3) 19.7 (57.7 (12.6 (72.3-40.7-20.7) 20.9 (30.6-19.3-17.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.3-81.8-24.5-18.2-108) 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.7 (20.3) 18.9) 14.6) 64.4) 15.8 (18.3 (17.7 (54.8) 63.4 (50.9) 39.3 (60.5-21.7) 19.5) 91.3 (52.1-23.3 (52.0 (69.2-48.0-38.8) 30.5 (15.6 (25.3) 59.0 (15.5-15.4 (33.4 (16.0) 26.8) 75th 38.3 (19.3-18.5-30.8) 13.4-34.2) 21.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.3-39.5) 60.0-75.1-99.4) 16.7-19.0) 19.6-27.4 (18.4-135) 71.7-78.2 (83.0 (16.2-28.6-42.9 (21.5) 17.5-142) 89.6) 65.9) 49.7-21.9) 91.3-23.8 (13.8) 34.3 (76.3 (71.9 (64.3 (55. population from the National Health and Nutrition Examination Survey.6 (27.3 (46.7-28.3 (69.6-44.4 (50.4) 21.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.3) 33.8 (33.4 (31.8) 22.2-179) 84.5-22.7 (73.9 (37.3 (24.7-42.7-19.8) 17.0) 94.1-32.7) 36.6-22.5) 21.5 (14.8) 35.8 (50.6) 83.8) 17.6 (31.4-47.7-37.0 (18.3) 20.7-39.4-24.8) 40.0) 108 (71.9-36.4) 20.2-86.3) 67.6-24.6) 18.0 (19.4 (56.3-71.5) 82.5-41.9-56.3) 17.4-61.7 (14.3) 52.2) 65.8-32.8) 23.4-76.8-43.2) 16.6-23.1-83.0) 28.3-78.0 (70.1 (15.0) 29.6) 25.2 (16.8 (25.0 (50.5) 90th 68.9) 19.0) 70.3-26.0-90.4 (45.5 (18.3 (16.9 (56.9) 62.0) 55.S.4 (20.3) 19.9 (58.9-84.8 (17.1-62.5-70.6-44.0-17.0-113) 104 (83.0 (71.1-21.7 (16. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2-73.1 (29.6-16.0 (18.9 (39.3-106) 74.5-142) 81.0 (27.8) 17.2 (38.5) 84.1) 61.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.7 (81.0-92.7-80.1 (56.9-34.9 (35.3 (21.9) 24.3) 35.6-28.4 (19.0-19.4 (17.0 (61.2-106) 64.4) 15.1 (32.1 (61.4 (47.2 (35.1 (34. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0-60.8-24.2-27.4-164) 96.0 (20.2-21.1-99.6-32.8 (16.4 (23.6) 34.0 (26.8 (18.8) 28.0 (52.6-24.7-26.3 (28.6-128) 96.5-64.9 (35.7 (60.9-68.6) 37.9) 28.7 (43.7 (27.6 (19.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.3-21.0) 59.9-49.0 (34.1) 21.5-23.7-23.8) 20.2) 59.1) 42.0) 35.5 (81.6 (25.1) 37.6-53.8) 20.6) 14.6-26.4-131) 81.8 (22.5-16.2-61.7 (19.7 (60.7-51.4 (68.3) 21.1 (21.2) 159 (102-263) 147 (93.6 (29.9 (30.6) 24.6 (61.9-38.4 (53.9-105) 85.4-72.3 (42.4) 62.6-119) 63.5 (64.8) 34.2 (19.8-235) 137 (108-198) 88.5 (18.4 (17.9-68.6-74.2) 31.6 (17.

Jacek R. 2000 [online].nih. Koch HM. Springall C.gov/chemicals/ phthalates/dbp/dbp-eval. et al. Hum Reprod 2007. Green RA.108(10)979-982.niehs. Rylander L. Caudill SP. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP).22(3):688-695. Fromme H. Needham LL. Perera FP. Anderson WA. Jedrychowski W. Meeker JD. Silva MJ. Hagmar L. Koch HM. Ryan L. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Angerer J. Phthalate monoesters levels in the urine of young children. Int J Hyg Environ Health 2007. Brock JW. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.25(2):293-302. Richthoff J. Helm D. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Hauser R. Urinary levels of seven phthalate metabolites in the U. Eckard R.112(3):331-338. Drexler H. Third National Report on Human Exposure to Environmental Chemicals. Duty S. Reidy JA. Environ Health Perspect 2000. et al. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Masunaga S. Barr DB. Giwercman A. et al.18(12):10681074. Koch HM. McKee RH. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.18(1):122.16(4):487-493. Environ Health Perspect 2003. Environ Health Perspect 2004. et al.68:309-314. Int J Hyg Environ Health 2005. Atlanta (GA). Calafat AM. Environ Health Perspect 2006. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Sampson EJ.111(14):1719-1722. Reprod Toxicol 2004. Malek NA. et al. Weuve J. Brock JW. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.210(3-4):319-33. Bolte G.S. Hilborn ED. J Androl 2004. Hodge CC. Chen Z. Silva MJ. 4/20/09 Silva MJ. 2005. Silva MJ. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Boehmer S.208:237-245.210:21-33. 112(5):A270].114(9):1424-1431. Jonsson BAG. Caudill SP. Centers for Disease Control and Prevention (CDC). Available at URL: http://cerhr. Yoshida K. Camann DE. Bull Environ Contam Toxicol 2002. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Calafat AM. Blount BC.93:177-185. Food Addit Contam 2001. et al. et al. Int J Hyg Environ Health 2007. Itoh H. Duty SM.html. Epidemiol 2005. et al. Silva MJ. David RM. Drexler H. Schettler T. Needham LL. Pirkle JL. Angerer J. Research Triangle Park (NC). Barr D. Levels of seven urinary phthalate metabolites in a human reference population. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Butala JH. Scotter MJ. Massey RC. Rossbach B. Prenatal exposures to phthalates among women in New York City and Krakow. Gans G. Hu H.Phthalates References Adibi JJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Sanchez GN. Environ Res 2003. Dobler L. Wittassek M. NTP-CERHR. Poland. Singh NP. Wiesmuller GA. Castle L. Ryan L. Caudill SP.

500 (. only levels at or above the 90th percentile could be characterized.500) < LOD < LOD .500) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300-.200-. including nitrocellulose.10 (<LOD-1. < LOD means less than the limit of detection. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.400) < LOD 1.300 (<LOD-.10 (<LOD-2. and polyvinyl chloride.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300) < LOD . 01-02.500 (.600) .400 (.700) .500 (.500) < LOD < LOD .Phthalates Dicyclohexyl Phthalate CAS No.300 (.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) < LOD .400 (<LOD-.300-.300-.400 (.400 (.500) .200-.500) < LOD 1. see Data Analysis section) for Survey years 99-00. and polymers.400-.00-3.500) 1.70 (1.300 (. which may vary for some chemicals by year and by individual sample.S.3.500) .300-.300 (.00 (<LOD-1.400 (.400 (.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.200-.400-.300 (.200 (<LOD-.80) .500 (.400 (.400-.90) . 270 Fourth National Report on Human Exposure to Environmental Chemicals . respectively.500-.2.500 (.400 (.9.300 (.70) .70 (1.600) .600) .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 .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500 (. and 0.500) 1.50) .600 (. 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) 1. 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) 1.400) < LOD < LOD .500 (. resins.300-.500 (.400 (<LOD-.10 (.00 (<LOD-1.700) .10 (<LOD-1.70) .500) .300-.300 (.300 (. and 03-04 are 0.400-.700) .400-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400 (<LOD-.00) .200-.20) . Survey Geometric mean (95% conf.200-.10) . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.00 (<LOD-1.400 (<LOD-.500 (.300-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.400) 1. population from the National Health and Nutrition Examination Survey. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.900-1.200-.00-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. polyvinyl acetate.400-.600) .400-.300-. 0.600) .300) < LOD . In this Report.300-.50) .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 .

560) 1.690) < LOD < LOD .11) .410 (.880 (.360-.530-.12-1.380 (.470) 3.690) < LOD 2.420-.770-1.690 (.620) < LOD .10) .350-.660) .170-.33 (<LOD-3.370 (<LOD-.67 (1.17) .790-1.630 (<LOD-.54-6.610 (.00) .910 (.480 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .800-1.05) . population from the National Health and Nutrition Examination Survey.290-.770 (.670 (<LOD-.500) 3. Fourth National Report on Human Exposure to Environmental Chemicals 271 .16) .690-1.590 (.770-1.34) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 (.910 (.53) .950 (.54 (<LOD-2.660) < LOD < LOD .670-1.530-1.510-.470 (.54) .06) .740) .530 (.400-.630 (<LOD-.330 (.710) .22 (<LOD-1.82 (1.830) 1. Survey Geometric mean (95% conf.250 (.33) .44) .18) .510 (.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 .220 (<LOD-.74) .00 (<LOD-3.420-.270) < LOD .53) .530) 1.490) .770) < LOD 2.390 (.43 (1.500 (.500-.420-.770-1.450 (.380-.400-.310) < LOD .940 (.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 .240-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.590 (<LOD-.450 (.36-1.910 (.S.14 (<LOD-3.310-.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 1.740) < LOD < LOD .260-.16 (<LOD-3.330 (.82) .06) .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.

2. 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 91.7 (70. 0. 272 Fourth National Report on Human Exposure to Environmental Chemicals .S. and also in men attending a Boston infertility clinic (Hauser et al. 2003) and African-American women in Washington.4.2-102) 95. and 03-04 are 1. deodorants.9 (61. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. respectively. shampoos.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. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 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.1 (71.9-92. particularly those containing fragrances.7) 71.. 2007).9. and hand lotions.4 (62. 01-02.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. Biomonitoring Information MEP levels in the NHANES 1999-2000.5) 81. see Data Analysis section) for Survey years 99-00.1-93.. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. Products that may contain DEP include perfumes. 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. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.3 (82. DC (Hoppin et al. soaps. 2002).3 (74. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. colognes. In contrast.8-111) 85. and 0. 2001-2002. population from the National Health and Nutrition Examination Survey.

5-113) 122 (93.Phthalates 2002 (Brock et al. 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. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups..9 (82. 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. 2004). Other population estimates also differed by sex and race ethnicity (Silva et al. 2002).6 (77.2 (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. 2005). This age-related trend is opposite the direction seen for other phthalates. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.3-105) 87. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. In an analysis of NHANES 1999-2000.7-110) 81. Median MEP levels found in a small sample of German residents (Koch et al.0 (66. 2003) were slightly lower than levels found in NHANES 2001-2002. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Analysis of NHANES 2001-2002 showed similar findings..9-110) 96.5-114) 101 (87.0-156) 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 .S.6 (65.

Meeker JD. Rossbach B. et al. Duty S. Brock JW. Hilborn ED. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Caudill SP. Davis BJ. Drexler H.111(14):1719-1722. Brock JW. Reproducibility of urinary phthalate metabolites in first morning urine samples. Malek NA. Jedrychowski W. Hauser R.S. Silva MJ. Barr D. Needham LL. Environ Health Perspect 2002. Silva MJ.68:309-314. Singh NP. Barr DB.Phthalates References Adibi JJ. 2005. Silva MJ. Camann DE. Prenatal exposures to phthalates among women in New York City and Krakow. Third National Report on Human Exposure to Environmental Chemicals. Reidy JA.110(5):515-518. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.22(3):688-695. Hum Reprod 2007. Baird DD. Centers for Disease Control and Prevention (CDC). Phthalate monoesters levels in the urine of young children. et al. Hodge CC. Poland. Angerer J. Environ Health Perspect 2004. Ryan L. Bull Environ Contam Toxicol 2002. 112(5):A270]. et al. Caudill SP. Environ Health Perspect 2003. Atlanta (GA). Koch HM. Jacek R.93:177-185. Perera FP. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.112(3):331-338. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Hoppin JA. Urinary levels of seven phthalate metabolites in the U. Environ Res 2003.

50-14.9) 18.3) 28.1-17.5 (18.57-7.00) 2.14 (1. packaging film.0 (14. see Data Analysis section) for Survey years 99-00.3-64.3) 52.S.7 (17.67-4.9 (17.60) 10.96-5.26-2.Phthalates Di-2-ethylhexyl Phthalate CAS No.9-55.60) 8.50-5.4) 20.50-3.9) 13.2 (29. 1989.0) 31.6-23.9) 27.80-8.00) 1.10 (4.34 (2.93) 6.86) 2.60-7.5-27.50-11.1 (10.5 (24.37-4.41) 3.77 (2.9 (13.92-2.79) 2.70 (8.6) 9.7-18.4) 22.6-60.03-2.75 (3. toys.70-2.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.80-3.2-28.8 (19.40-8.50 (3.92) 4.50-2. population from the National Health and Nutrition Examination Survey.70) 2.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.96) 4.1 (8.0) 11.9-29.0 (19.90-8. Peck and Albro.9 (17. After parenteral administration. 1.6-28.5-28.42-5.50) 4.40-8.60 (5.4) 15. 01-02.40) 4.3 (24.9-57. and in humans.10-11.7) 19.0) 39.91-3.2) 6.5) 40.7) 6.6 (20.62) 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 5.50-16.51) 4.5-41.6) 39.70 (5.27) 2.70) 7.50-6.70-5.0 (21.25-3.0-18.40 (4. as glucuronide conjugates (Albro et al.32 (3.60) 7.70-3.30-13.80-9.8) 17.6-38.6-25.90-11.5-28. 2002.80 (2.9) 13.70 (7.90-3.5) 37.5-40.9 (16.0) 23.00) 1.10-4.82 (3.49 (3.40 (2.90-5.23 (3.5 (12.90) 4.40) 75th 7. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9) 15.6 (16.46) 3.84 (2.2) 42.40-9.07-4. interval) 3.20 (3.4 (13.5) 21.43 (3.60) 90th 14.2) 23.10) 3.50-3.60-11.90-4.16-3.4 (16.0) 23.5) 23. 1982.00-4.5 (12.8 (19.70-4.4-42.89-3.5 (25.9 (29.20 (3.3 (11.10) 3. DEHP has been removed from or replaced in most toys and food packaging in the United States.9. and blood product storage and intravenous delivery systems. ATSDR.00-3.50 (3.9-26.00) 5.92-2. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).83) 2.00-5.27 (3.31 (3.12 (4.0 (9.2 (7.40 (6.1) 29.7) 27.80) 9.9 (26.00 (7.10) 3.94-3.70 (1.5 (18. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.7) 18.30-11. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.10) 2.4) 22. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce