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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75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.5'-Tetrachlorobiphenyl (PCB 49) 2.2-Dichloroethane (Ethylene dichloride) 1.4.2'.5'-Tetrachlorobiphenyl (PCB 44) 2.cdc.2'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2.4.6.1.4’.1-Dichloroethane 1.4'-Tetrabromodiphenyl ether (BDE 66) 2.3-Tetramethylbutyl] phenol) Triclosan (2.4'.4.5.4'-Pentabromodiphenyl ether (BDE 85) 2.1.5.3’.6-Pentabromodiphenyl ether (BDE 100) 2.4'-Tribromodiphenyl ether (BDE 28) 2.2'.4.2'3. The process for selection is described at http://www.2'.5'.3.1-Dichloroethene (Vinylidene chloride) cis-1.2'.4.4’.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.5.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2’. Table 1.2-Dichloroethene Dichloromethane (Methylene chloride) 1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2'. Paradichlorobenzene) 1.html.4'. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.2'.2-Dichlorobenzene (o-Dichlorobenzene) 1.2'4. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.5-Pentabromodiphenyl ether (BDE 99) 2.3.3-Dichlorobenzene (m-Dichlorobenzene) 1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4'.4'.2-Dichloropropane 2.3'.5.gov/exposurereport/chemical_selection.5'-Hexabromodiphenyl ether (BDE 153) 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4'-Tetrabromodiphenyl ether (BDE 47) 2.4'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4-Dichlorobenzene (p-Dichlorobenzene.6'-Hexabromodiphenyl ether (BDE 154) 2.4.5’.3.2'.4.1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4.4.What’s New in this Report What’s New in this Report In this Fourth Report.4-Tribromodiphenyl ether (BDE 17) 2.6-Heptabromodiphenyl ether (BDE 183) 2.4.4.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichloroethene trans-1.2'.4.1-Trichloroethane (Methyl chloroform) 1.1.3.

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

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

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

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

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

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

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

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

soil conditioners.2) 57.2-59. 2005). and is either metabolized to the reactive epoxide. 2005). and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.S. 2005). In 1997.7) 58.6) 90.0 (53. Recently. 2004. Elimination occurs mainly in the urine as mercapturic acid conjugates. ocular and dermal irritation from direct contact with acrylamide containing materials.3) 63.7) 75th 79. glycidamide.2 (58.S.9-61. gels.7 (63.7) 96.5) 66.9 (69.8 (57. in some sealing grouts. widely distributed in tissues.0) 57.S. 2005. are heated at temperatures used for frying and baking. Survey Geometric mean (95% conf. but are generally above the U. smoking.8 (91.7) 54.7) 73.3) 70. People may be exposed to acrylamide from foods.4-60.0) 85.1) 46. 2006).0-66.7 (58.6) 50. drinking water.2-70.2-67. such as potatoes and some grains.4 (54.4 (54. 2002).6-75.2 μg/kg/day (U.6 (56. EPA.9-52. Estimated intakes in children are about twice that of adults (DiNovi and Howard. 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.3-2. pulp and paper production.0-58.1-61.6-108) 61.4-76. Acrylamide is not thought to accumulate in the body at environmental doses. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. and binding agents.4) 100 (89.2) 57. In humans. and from dermal contact with products that contain residual acrylamide.0 (67. 1990.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.5 (79. EPA.3-71.1) 101 (95. or to glutathione conjugates (Calleman et al.3) 86.2-77. acrylamide has produced upper airway irritation following inhalation of high levels.1 (73. (NTP-CERHR..0 (69. 2006. population from the National Health and Nutrition Examination Survey.5) 58.9 (60. acrylamide is synthesized and used in the production of polyacrylamide polymer. 217 million pounds of acrylamide were produced commercially in the U.8-57. and in some cosmetics.9) 58..2-114) 163 (147-191) 96. Tareke et al.0.7-64. Polyacrylamides are useful water-compatible polymers used in water treatment.1) 53.2 (62.S. and an average daily intake is estimated as 0.6-65.5 (44.4-83.4) Selected percentiles ( 95% confidence interval) Sample 95th 192 (168-217) size 7101 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 54.7-64.1 (88.2-118) 98.0-108) 152 (139-175) 126 (111-142) 108 (86.6-61. 2005).7 (55. Natural substances in the food are converted to acrylamide.8 (52.4-60.9) 75.1 (47.4) 57. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.0-49.1-64. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. Fourth National Report on Human Exposure to Environmental Chemicals 11 . see Data Analysis section) for Survey year 03-04 is 3.Acrylamide Acrylamide CAS No.4) 57.7 (65. as an absorbent in disposable diapers. mineral processing..2-91.2-93.6) 73. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.3 (55.4 (53. These estimated intakes are hundreds of times lower than occupational exposures. and well below doses known to cause nerve damage or carcinogenicity in animals.9) 57.3 (53. 2004). but can covalently bind to form adducts with proteins. interval) 61.1) 62.5-80.1-57. FAO/WHO.2 (75.6 (81.5 (74.S.7-60. FDA.6-66.8-55.1 (52.0 (57.5-85. the main source of exposure is from the diet. in permanent press fabrics.8 (81.5 (52. Since acrylamide has limited volatility and high water solubility.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 61.0 μg/kg for adults (FAO/ WHO.6 (51.6) 71.9-105) 86.9) 63.4-89.4 (51. Fennell et al. and in the synthesis or compounding of dye materials. it was discovered that acrylamide is formed when starch-rich foods.9 (54. and cosmetics (NTP-CERHR.1-64.4 (59. Commercially. 2005).0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. EPA reference dose of 0.6-104) 82.1 (83. 1994). In the general population.1) 55. Animal studies indicate that acrylamide is well absorbed.

2005. interval) 59. 2005).0-62. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.4 (57. In addition.5-64.5 (42.8 (51. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 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.pdf. and other sites) (FAO/WHO.3) 59.9-64.4) 46.5) 75th 85.. 2006.. 2005.S.2) 65. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. 1997. glycidamide (NTP-CERHR.4 (90. Glycidamide has been shown to react with DNA (Doerge et al.1 (70.5) 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.S.3) 85. 2008). U. 2005).1-70.7-62..1) 60. Maniere et al.9 (57. although different analytic methods can affect results. NTP-CERHR. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.5 (83.0 (75. respectively) are markers of integrated acrylamide exposure over the preceding few months.4 (56. Axonal degeneration..5) 71. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. presynaptic nerve terminal binding (LoPachin. thyroid.3) 59. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. Schettgen et al.5) 87.7-86. 2005) and sperm DNA adducts (Xie et al.3-101) 95. see Data Analysis section) for Survey year 03-04 is 4.4 (81. 2004.3 (56.0. and cancer (mammary.1-62. and neuronal DNA reactivity (Doerge et al.1) 56..1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59. 2005.4-59.5-92.7 (61.4 (51.1-60.2-68.7 (87. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2002. adrenal. 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. Hagmar et al.7-64. 2006) have been demonstrated after acrylamide dosing.9-78.8 (44. Additional information is available from U.4) 53... 2005) have been demonstrated in animals.8-49. scrotal. Klaunig et al.7) 61.2 (56.1 (57.7) 90.epa.3-78.9) 59.0 (80. probably through its epoxide metabolite.7 (57. Acrylamide is clastogenic and can produce dominant lethal mutations.2) 55. 2009).9 (58. 12 Fourth National Report on Human Exposure to Environmental Chemicals . altered gene expression in testicular tissues (Yang et al. 2005. male germinal cell injury.1 (66. Rice.. 2005).. Schettgen et al. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2006).S. Puppel et al..9-138) 143 (130-159) 96.. 2005. Mucci et al. 2002.9-62. 2005..4) 83.4-98. Vesper 2005) and smoking (Bergmark..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. EPA at: http://www. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).2 (63.8-48.2 (72.5-66.2) 87...int/ ipcs/food/jecfa/summaries/summary_report_64_final.3) 59.7) 74..6-62.9) 87.4 (61. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.9) 65. Survey Geometric mean (95% conf.4-65.1 (56.5-94.9-76. Puppel et al. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.9 (81..7 (84. 2005.who. After exposure ceases.0) 94..8-61.0-93. reproductive effects (reduced litter size. dominant lethality). 2006).8) 60. 2004).4-103) 79. IARC classifies acrylamide as probably carcinogenic to humans.5 (56. Vesper et al. population from the National Health and Nutrition Examination Survey.9) 75. U.2-91. 2003. 2005).1-56.. 2005.7) 60.Acrylamide occupational exposures. 2001).6 (66. 2008).2-90. 1997.9-77.0 (70.5 (59.0) 118 (103-126) 121 (112-134) 113 (94.S.1 (82.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. fetal death. uterine. 2005. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. 2005..0 (52. EPA. 2005.6 (90. EPA.1) 62.6-64.6-90.8) 45.

DiNovi M and Howard D. Doerge DR. Human exposure and internal dose assessments of acrylamide in food. Spicer R. McDaniel LP. Bergmark E. Toxicol Sci 2005. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Uncertainties. Zhang S. Rosen I. 6013-6019. Adv Exp Med Biol 2005. J Agric Food Chem 2008. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose.. Bridson WE.580(1-2):131-141.120(1):45-54. Wilson KM. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide.561:49-62. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Mutat Res 2005.. Malmberg B. 64th Meeting: Summary and Conclusions (FAO/WHO). NIH Publication No.fda. Survey data on acrylamide in food: individual food products. Tornqvist M. Bergmark E.126(2):361-371. Toxicol Appl Pharmacol 1993.85:447-459. da Costa GG. Wu Y. Churchwell MI. Joint FAO/WHO Expert Committee on Food Additives. Axmon A. Nordander C. July. Illinois. 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. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Scand J Work Environ Health 2001. Granath F. 2001.56. Available at URL: http://cerhr. 2/3/09 Klaunig JE.27(4):219-226. In another study. Andersen M.pdf. Alexander J. He F. LoPachin RM. Kamendulis LM. Magnusson AL. AHA levels correlated with a neurologic symptom index and specific physiologic measures in an occupational setting and correlated better with clinical signs and symptoms than urinary excretion of the mercapturic acid metabolite (Calleman et al. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 2001). Mutat Res 2005. Yang JS. Metabolism and hemoglobin adduct formation of acrylamide in humans.cfsan. Paulsson B. Tornqvist M. Rome. and Research Strategies. Cheong HK. Haugen M. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. gov/~dms/acrydata. et al. 1999).3:406-412. Italy. Toxicol 2005. [Epub ahead of print] Dybing E. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Duale N. 2004. Maniere I.gov/chemicals/ acrylamide/Acrylamide_Monograph. Doerge DR. Chem Res Toxicol 1997 Jan. Acrylamide neurotoxicity: neurological. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.nih. Mutat Res 2005.pdf. Fennell TR.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Hagmar et al. April 13-15. smokers and nonsmokers. Tian G. 8-17 February 2005.. References Bergmark E. Farmer PB. Kautiainen A. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Chicago. Paulsen JE. morphological and molecular endpoints in animal models.10(1):78-84. Osterman-Golkar S. Calleman CJ. et al. Calleman CJ. 1993. Wirfalt E. Beland FA. 2/3/09 Perez HL. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Chem Res Toxicol 1990. February. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes.580(1-2):157-165. Available at URL: http://www. National Toxicology Program.43:365–410. Aprea P.niehs. 054472. Toxicol Sci. Food Chem. et al.561:21-37. Bruze M.. Costa LG.580(1-2):119-129. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Guffroy M.html#u1004. Burgess J. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Bjellaas T. et al. Acrylamide intake through diet and human cancer risk. Available at URL: http://www. Perez et al. Costa LG. Godard T. Fennell TR. Snyder RW. Food and Drug Administration (FDA). et al. Summer SCJ. Bergmark E. smoking habits and gender. 1994). 2005. Hagmar L. Mechanisms of acrylamide induced rodent carcinogenesis. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. 2006. Adv Exp Med Biol 2005. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.who. Calleman CJ. Becher G. Laurentie M. CFSAN/Office of Plant and Dairy Foods. 2/3/09 Hagmar L. The Updated Exposure Assessment for Acrylamide. 2004 Acrylamide in Food Workshop: Update Scientific Issues.Toxicol Appl Pharmacol 1994. 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. Churchwell MI. He F. 2009 Jan 8.Acrylamide In occupational settings. Mucci LA. Twaddle NC.

561:89-96. J Agric Food Chem 2002. Drexler H. Kutting B.gov/iris/subst/0286. Vesper HW. Hemoglobin adducts of ethylene oxide. Tjønneland A. Eriksson S. Anal Biochem 1999. Weiss T. Chemical Summary for Acrylamide. a carcinogen formed in heated foodstuffs. Analysis of acrylamide. Drexler H. September.epa. Available at URL: http://www. Xie Q. Licea-Perez H. The carcinogenicity of acrylamide. Schettgen T. Available at URL: http://www. EPA). Fueller F. Reprod Toxicol 2005. Washington (DC). Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Rice JM. Tareke E. Tjaden Z. Acrylamide. Chae C. Karlsson P. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Environmental Protection Agency (U. Toxicological effects of acrylamide on rat testicular gene expression profile. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Ding X. Rossbach B. Lee SH. Angerer J.134(1-3):65-70. Letzel S. Slimani N. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Mutat Res 2005 Feb 7. 2/3/09. Broding HC. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.gov/chemfact/s_acryla. Angerer J.S. Liu Y.56(15):6046-53. Marko D. Meyers T.19(4):527-34. Puppel N. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.580(1-2):71-80.207(6):531-9.epa. Han CH. 2/3/09 Vesper HW. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Yang HJ. Fu D. Adv Exp Med Biol 2005. Rapid Commun Mass Spectrom 2006. Ospina M. Hallmans G. Benetou V.S. Sun H. 1994. Int J Hyg Environ Health 2003. Choi JH.S. Liu K. Schettgen T. revised 1/3/06. J Agric Food Chem 2008.50(17):4998-5006. Integrated Risk Information System (IRIS). EPA). et al.htm.163(2):101-8.206(1):9-14. Angerer J. Myers GL. Ingham L. U. Han DU. Toxicol Lett 2006. Toxicol Lett 2002. Smith A. Office of Pollution Prevention and Toxics. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Meyers T. Rydberg P.S. Gray JG. Drexler H. Agudo A.Acrylamide glycidamide by gas chromatography-mass spectrometry. Mutat Res 2005.txt. Jin Y. Vesper HW. Environmental Protection Agency (U.580(1-2):3-20. Tornqvist M.274(1):59-68. Int J Hyg Environ Health 2004.20(6):959-64. propylene oxide. et al. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Lee MH. Ospina M. Schettgen T. U.

DHHS.770) .180) .02 (.28-1.312) .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.148-.5% nicotine by weight (Kozlowski et al. 2004).216 (.077) .05) 1.630 (.44) 2.506 (.040-.62) 2.050 (<LOD-.710 (.310) 90th 1.160 (.050) .96) 2. and exacerbated asthma (U.40) .540-. Survey Geometric mean (95% conf.188) .180 (.S.00) .44) 2. which may vary for some chemicals by year and by individual sample.080) < LOD .77 (2.302) .080 (.198) * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.060-.108) * .120 (.32-2.120-.26-1.65 (1.580-1.23 (2.15 (2.99) 2.57) 2.63 (2.110) .85 (1.00) 1.080) < LOD < LOD .45) 1.350 (.260) 1.075 (.100-.92 (1.17) .115-. and 17% had an LOD of 0.800 (.55 (1. DHHS.70-2.131 (.33-2.110 (.080-.01) 3.234) .997-3.180) .78) 2.18-3.19-2.47-3.50-1.110 (.163) .04 (1.42-4.44 (2.400-.23 (1.110 (.480-.047-.540 (.95) 1.770-1.110-. and various other disorders (U.040 (.23 (.110-.50) 3.140 (.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 .106-.180 (.180) .070-.308 (. 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.35 (2.860 (.043-. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.02) 1.60-2.220) .090-.084) .12 (1.040 (.50 (1.061) < LOD .124 (.14-1.570 (.187) .05.047-. stroke.120) .080-.690 (.360) .630 (. Fourth National Report on Human Exposure to Environmental Chemicals 15 .11) .030-.49) 1.12-4. 2004).087) < LOD < LOD .34 (1.79) 3.63-2.410) .20-2.110 (.015 ng/mL. acute respiratory illness.040-. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.080-.193) .280 (.840) 3.930 (.120 (.111-.53-4.62 (2.96-4.740-1.77 (1. 2006).32) 1.140-.670) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .200) 1.050 (.53 (1.740-1.12) 1.630 (.160) .076-.S.500 (.430-1.05 ng/mL.310-1.94) 1.660) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.600-1.96 (1.480-1. ear problems. acute respiratory infections. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.09-3.84-3. maternal exposure during pregnancy can result in lower birth weight.077) .428-.070 (<LOD-.015.43 (1.150) .310-1.350-.620-1.059-.089) Age group 3-11 years 99-00 01-02** 03-04 .48-2.070) 75th .052 (<LOD-.050-.16) . 1998).70) 2.910-1.140 (.Cotinine Cotinine CAS No.063) .20 (1.75) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.060 (.820) .12 (2. < LOD means less than the limit of detection.120 (.230) .310) .570-1.070) .066-.55-2.54 (1. ** In the 2001-2002 survey period.14) .88 (1.120 (.160 (.137-.68) .580 (.060) .160-.213) .080-.120-.104-.730 (.15) 2.190-.220-.087-.062 (.370-.09-3.126) .050 (<LOD-.050) .21-1.19) .54 (1.053 (<LOD-.42 (1. Cigarettes contain about 1.21 (.086 (.164 (.066) .17 (1.139) * .28) .088-.060-. emphysema.850 (.080 (.090-.350-.060 (<LOD-.180) .059-.09-2.39) 3.030-.050 (<LOD-. and 03-04 are 0..190-.140-.057-.38-2.89) 1. see Data Analysis section) for Survey years 99-00.990 (.130) .93) .17 (.49) 1.110) .39 (1.120 (.054 (.66 (1.175 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.190-.230 (.44 (1.920 (.060 (<LOD-.87-3.900-1.533-.240 (.145) .20) .220) .110-.040 (.167 (.450-.726) .81-2.S.110 (.030 (.625) .68 (1.66-3.154-.48-3.060-.160 (.058 (.050-.066 (.66) 1.23-2.68) 2. 83% of measurements had an LOD of 0.54) 1.087 (.030-.32-2.197) . 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.201) .070) .990) .160) .300) .76 (1. and 0.620 (.621-1.19) 1.164 (.83-2.01 (1. population from the National Health and Nutrition Examination Survey.130 (.068) .071 (.094) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.99) 2. respectively.052 (<LOD-.30) 2.068) .22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .77 (1.470-.153-.060 (.20) 1.071) .770) .790) .520 (.137 (.88 (.960-1.020-.142-.090-.320) .510 (.073) < LOD .505 (.260-1.180) .30) * .50-4.150) .20 (.950-1.21-1.050 (<LOD-.22) 2.144 (.30) 2.02) 1.163 (.210 (. cardiovascular disease.950 (.14) .580) .

and hair. salivation. The IARC and the NTP consider tobacco smoke to be a human carcinogen. 1991).. 2006). Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . Pirkle et al. The tobacco plant. seizures. 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. 2006). non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al. Children are primarily exposed to ETS by parents and caregivers who smoke. Cotinine can be measured in serum.. diaphoresis. variable changes in blood pressure and heart rate. chewing tobacco.3 to 30 µg/m3. and death. diarrhea. Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al. cognitive and sleep disturbances. 1998). mean air concentrations typically range from 2 to 14 µg/m3 (NTP. Perez-Stable et al.. Symptoms of 16 nicotine withdrawal include irritability. nasal sprays. Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff. tomatoes. Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. 2004).nih. or chewing gum. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. or skin patches that contain nicotine. a process involved in the development of addiction. Wilson et al. the adjusted geometric mean serum cotinine was higher in children (aged 4–11 years) than in adults among both non-Hispanic blacks and non-Hispanic whites (Pirkle et al. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans.. craving. 1999. Over the previous decade. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005. For an adult. and increased appetite. 2005. contains nicotine in larger amounts than other nicotine-containing plants. and peppers. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. 1996). In homes with one or more smokers. eggplants..nida. nicotine has a half-life in blood plasma of several hours (Benowitz. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. vomiting.. Hukkanen et al.. with heavy exposure to ETS producing levels in the 1–10 ng/mL range. More information about the effects of smoking and nicotine can be found at: http://www.. urine. Iwase et al. Soliman et al.. levels of exposure to ETS appeared to decrease since geometric mean cotinine serum concentrations in nonsmokers had fallen by approximately 70% and the rate of detectable cotinine in nonsmokers fell from 88% to 43% when NHANES 1988–1991 was compared to NHANES 1999–2002. 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. Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. Serum cotinine has been measured in many studies of nonsmoking populations. 1999. The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. 2005).. Acute tobacco or nicotine intoxication can produce dizziness. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation.gov/researchreports/nicotine/nicotine.. However. 1975. 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. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. Workers who harvest tobacco can be exposed to nicotine and become intoxicated as a result of the transdermal absorption of nicotine contained in the plant. Cotinine. 2004). 2005). NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration. 2006. nausea. Once absorbed. Hukkanen et al. the primary metabolite of nicotine. Nicotiana tabacum. 2005). 1998). Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system.. Differences in cotinine concentrations among race/ethnicity and age groups may be influenced by pharmacokinetic differences as well as by ETS exposure (Benowitz et al. NCI... 1994). Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al.Cotinine 1994. 1996).. html. (CDC. which include potatoes. 2005. saliva. 1999). Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. with higher levels measured in restaurants and bars. Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al. During each previous NHANES survey.

56:483-493. available at URL: http://mtn. Turner DM. Soliman S. Dollery CT. Coordinating Center for Health Promotion. 2004. Absorption and metabolism of nicotine from cigarettes. Benowitz NL.18:188-204. International Agency for Research on Cancer. Centers for Disease Control and Prevention. Brody DJ. Metabolism and disposition kinetics of nicotine.fr/ENG/Monographs/ allmonos90. Smoking and Tobacco Control Monograph 10 [online]. Jacob P III. Racial/ethnic differences in serum cotinine levels among adult U. U. Summary of Data Reported and Evaluation [online] 1986. Hukkanen J. Available at URL: http:// cancercontrol.php. IARC Monogr Eval Carcinog Risks Hum. Giovino G. Giovino GA. 1999. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Nicotine metabolism and intake in black and white smokers. 1991.iarc. Tob Control 1998. Herrera B.280:152-156. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. 4/13/09 International Agency for Research on Cancer.cancer. Benowitz NL. Warner K. National Center for Chronic Disease Prevention and Health Promotion. cigarette smokers: the Third National Health and Nutrition Examination Survey. Available at URL: http://monographs. Available at URL: http://www. Jacob P III. Department of Heath and Human Services. Clin Pharmacol Ther 1994. Vol 83.fr/ENG/Monographs/allmonos90. Int Arch Occup Environ Health 1991. Aiba M. and the United States.cdc. 1999-2002. Respiratory nicotine absorption in non-smoking females during passive smoking. Vol 38. In Report on Carcinogens. References Armitage AK. Metabolism of nicotine to cotinine studied by a dual stable isotope method. 4/13/09 Iwase A. Am J Public Health 2004. Lewis PJ. JAMA 1998. 4/13/09 Perez-Stable EJ.7:369-375.57(1):79115. Pirkle JL. Centers for Disease Control and Prevention. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.S. Pickett MA.275:1233-1240. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .S. DHHS). Vogler GP. Kira S. Brody DJ. Etzel RA. 4/13/09 Centers for Disease Control and Prevention (CDC). Exposure of the U.gov/ntp/roc/eleventh/profiles/ s176toba.niehs.php. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. et al.S Department of Health and Human Services (U. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Mowery PD. 1988-1991. Pharmacol Rev 2005. Sosnoff CS. et al. Houseman TH. June. Kozlowski LT. National Institute for Occupational Safety and Hygiene (NIOSH). Tobacco Smoke. JAMA 1996.gov/eid/rmca/critdocs/ criteriadoc/33. Caudill SP. Schwartz SS. Available at URL: http://monographs. the United Kingdom. Sweeney CT. Pollack HA. Department of Heath and Human Services.291(3):1196-1203. Strauss WJ.S. Environ Health Perspect 2006. Benowitz NL. Ethnic differences in N-glucuronidation of nicotine and cotinine. Modin G. 4/13/09 U. Bernert JT. iarc. Mehta NY.S.gov/library/ secondhandsmoke/. Centers for Disease Control. U. JAMA 1998. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.S Department of Health and Human Services (U.63:139-43. DHHS). U. Pechacek TF. National Toxicology Program (NTP). Tobacco related exposures. Pirkle JL. Richter PA. [online]. Office on Smoking and Health [online] 2006. Available at URL: http://ntp. Atlanta (GA): 2005. Epidemiol Rev 1996. Third National Report on Human Exposure to Environmental Chemicals.114(6):853-858. Tob Control 2006. Flegal KM. Maurer KR.pdf.nih.niosh. Herrera B. 1988-1991. Caraballo R. IARC Monogr Eval Carcinog Risks Hum. Benowitz NL. population to secondhand smoke: 1988-2002. Tobacco Smoke and Involuntary Smoking. Jacob P. Summary of Data Reported and Evaluation [online] 2004.15:302-307. Fong I. J Pharmacol Exp Ther 1999. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Jacob III P.94(2):314-320.surgeongeneral.4:313-316. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Perez-Stable EJ. BMJ 1975. Pechacek TF. Curtin LR. Bernert JT. Jarvis MJ.S. 11th ed. Schober SE.S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Benowitz NL.280:135-140. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Trends in the exposure of nonsmokers in the U. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.S. Coordinating Center for Health Promotion. George CF. Cotinine as a biomarker of environmental tobacco smoke exposure. 4/13/09 National Cancer Institute (NCI).pdf.gov/tcrb/monographs/10/.

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

220 (. DEET has low acute toxicity.130) < LOD .110 (<LOD-.140 (.epa.N.110 (. After absorption. have been reported as result of self-poisoning by ingestion or excessive dermal application. 1998).180) < LOD . Sudakin and Trevathan.110 (.100-. Neurological effects in humans.EPA.170 (. About 3-8% of dermally applied DEET is absorbed. DEET is also used in combination with dermal sun screens (U.110 (.140) < LOD .140-.130 (. DEET is not registered for use on agricultural commodities..1.S.S.190) < LOD .S.100-.150) < LOD . People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Survey Geometric mean (95% conf.140) < LOD .160) < 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 . and they range in concentration from 4% to 100%. including seizures and encephalopathy. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .449 and 0.130-.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130-. Urinary N. DEET is not genotoxic. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.180 (. 1998). Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.560) < LOD . One survey detected DEET in 74% of sampled streams in the U. There are over 225 insect repellents brands containing DEET. and it has not been rated by IARC or NTP with respect to human carcinogenicity.110-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 2003). 2002).120-.180 (.130 (.EPA. (U. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.N-Diethyl-meta-toluamide (DEET) CAS No.. DEET is not a developmental or reproductive toxicant in animals (U. 2005).100 (<LOD-.S.520) < LOD . Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. 134-62-3 General Information N.gov/pesticides/.140) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD.130) < LOD . < LOD means less than the limit of detection.210 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 .N-Diethyl-meta-toluamide (DEET) N.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 . 1995.130 (. Additional information is available from U.180 (. 2003).N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Its use is recommended for prevention of several vector-borne diseases.100-.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . DEET can be applied to clothing and the skin to repel biting insects.240) < LOD . DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. 2002).130-.110 (<LOD-.EPA at: http://www.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.110 (.130-.S.110-.170 (. (Kolpin et al. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.120-.250) < LOD .100-.100-.. population from the National Health and Nutrition Examination Survey.S. which may vary for some chemicals by year and by individual sample.100-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. EPA.

93) < LOD .170-.500 (.250-.140-.370) < LOD .270-. In this survey period. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.280 (.S.240-. 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.200 (.630) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.280-1.300 (. * 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.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.350-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.150) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.240) < LOD .270) < LOD . the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.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 .410 (.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary DEET levels as high as 5.350) < LOD .250 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.330 (.410-.300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .190 (<LOD-.490) < LOD .290-.390-.190 (.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250) < LOD .270 (.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.320 (.. 2007). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.370-.230-.S.350) < LOD . 2005).640 (. Urinary N.190-.440) < LOD .N. 20 Fourth National Report on Human Exposure to Environmental Chemicals .130 (<LOD-.410 (.320) < LOD .230-. representative subsamples from NHANES 2001-2002. 1992).150-.270 (<LOD-..230) < LOD .190 (.480 (.330 (.

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

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

Rubin C. and other organic wastewater contaminants in U. November 26. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. An evaluation of the possible carcinogenicity of bisphenol A to humans. Cohen JT. Koulova AI. with estrogen receptors alpha and beta. Hara K..S. Brussels. Howdeshell KL. hormones. Pharmaceuticals.nih. Toxicol Sci 2002.niehs. Leranth. Yang M. Twomey K. Doull J. Joint Research Centre Institute of Health and Consumer Protection. Haighton LA. 2/4/09 European Commission. et al. Kawamura N. Furukawa M.312(2):441-448. Harazono A.68(1):121-146. European Commission. Belgium. Richter CA. May 22. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. and Hardy MP. Reidy JA. Myers CB. Kiguchi M.137(3):353-362. Pyo MY. Klinefelter GR. Meyer MT. J Am Dent Assoc 2006. 4. Cunha G.59(4):403-408. Munro IC.. Joskow R. Arakawa C. Kim CS. DirectorateGeneral Health and Consumer Protection. 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. Zacharewski TR. 2/4/09 Ouchi K. Endocrinology 2008. Furlong ET. Hanaoka T. 5: 505-523. In vitro and in vivo interactions of bisphenol A and its metabolite. Serizawa S. Environ Health Perspect 2008. Reidy JA. Watanabe C. Shin HC. Needham LL.S. Barber LB. Ecotoxicity and the Environment (CSTEE). streams. Exposure of the U.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report.Environmental Phenols References Akingbemi BT.36(6):1202-1211. Thurman EM.145:592-603. Hum Ecol Risk Assess 2004.116(1):39-44. U. Regul Toxicol Pharmacol 2002. et al.. August 2001. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy.pdf.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325.nih.149:988-994.pdf . Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Reprod Toxicol 2001. Department of Health and Human Services.S. Hughes C. Needham LL. Barr DB. Biochem Biophys Res Commun 2003. 2008. Kim JC.113(4):391-395. National Institutes of Health. N. Proc Natl Acad Sci USA 2005.jrc. Needham LL. Kim YH. Keimowitz AR. Yoshinaga J. Timms BG. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). 2/4/09 Fujimaki K. Environ Sci Technol 2002. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Watanabe S. Calafat AM. Hlywka JJ.gov/chemicals/bisphenol/bisphenol. Ye X. Research Triangle Park. Han SS. Park S. Available at URL: http://cerhr. K. 2003.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Endocrinology 2004.35(2 Pt 1):238-254.69(22):2611-2625.gov/chemicals/bisphenol/BPAFinalEPVF112607. Gray GM.pdf. Occup Environ Med 2002. Sottas CM. J Chromatogr B Analyt Technol Biomed Life Sci 2002.europa. Ema M.10:875-921. Chung MK. Bisphenol A. Tyl RW. Barton L. vom Saal FS. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Available at URL: http://ec. MacLusky. Szigeti-Buck.eu/ health/ph_risk/committees/sct/documents/out156_en. National Institute of Environmental Health Sciences. Environ Health Perspect 2005. September. niehs. Life Sci 2001.102(19):7014-7019. McConnell EE. Kolpin DW. Tsugane S. bisphenol A glucuronide. Barr JR. Ispra. Rat two-generation reproductive toxicity study of bisphenol A. 2002. Rhomberg et al. niehs. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Available at URL: http://ntp. 1999-2000: a national reconnaissance. et al. NC. Human Health.780(2):365-370. Kroes R. Available at URL: http://cerhr. and Hajszan. Bradley S.J.pdf . Gender differences in the levels of bisphenol A metabolites in urine. Caudill SP. Marr MC. Imai H. Chem Res Toxicol 2001.pdf. 2007. Fujii S. Matthews JB. Koh WS. C. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Brine DR. Thomas BF. National Toxicology Program. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. T. Nippon Eiseigaku Zasshi 2004. Kuklenyik Z. Ekong J.Scientific Committee on Toxicity. Zaugg SD. Calafat AM. Wong LY. Cha SW. Han SY. Italy. Ikka T. Lynch BS. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Available at URL: http://ecb.59(9):625-628. Calafat AM.14(2):149-157.nih.

An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.113(8):926-33. Filser JG. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Jang JY. Chang SS. Csanady GA. Lee SM. Welshons WV. and nonylphenol at home and daycare. Sheldon LS. Wilson NK. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Hughes C. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Food Chem Toxicol 2002. Chuang JC. Environ Res 2007. Morgan MK. An observational study of the potential exposures of preschool children to pentachlorophenol. vom Saal FS. Large effects from small exposures.147(6 Suppl):S56-69. Dekant W. Yang M. III. Kawamoto T.103(1):9-20. Vom Saal FS. Chem Res Toxicol 2002.Environmental Phenols Volkel W. Kim SY. Lordo RA. bisphenol-A. Nagel SC.40(7):905-12. Biological monitoring of bisphenol a in a Korean population. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. et al. Endocrinology 2006. Witorsch RJ. Environ Health Perspect 2005.15:12811287.44(4):546-51. Colnot T. Arch Environ Contam Toxicol 2003.

80) 2.50-2.S. and some of their degradation products are toxic to aquatic life. The alkylphenols can bioaccumulate in some fish. which are anionic surfactants used in detergents. textiles. 4-octylphenol monoethoxylate was detected in 43. In 1999-2000.. to shorter chain alkylphenol ethoxylates.900 (.. Ying et al.90) 2.60-3.50) 1.50) .400 (.600-1. 2006. and the polyethoxy chain may consist of up to 50 ethoxy units. Blake and Boockfor..400 (. Laws et al.10-2.600) 1.500 (.60-3. 2000. and to alkylphenoxycarboxylates. and from contact with some personal care products and detergents.30 (1.600-1. 140-66-9 General Information 4-tert-Octyphenol.70 (1.500) . over 500.900 (.00 (1.900 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-2.60-3.30 (.600) . testicular atrophy. 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.369 (.g.30 (1. pesticides.500-1. During the 1980s and 1990s. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.00 (.20) 1. and was quickly eliminated from the blood (Certa et al.S. and emulsifiers.70 (1.20-2.500) .60) 1.2. 1995. In the 1990s. leading to inhalation as another potential exposure route (Rudel et al.300 (<LOD-.10) 2..90) 2. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).. Several alkylphenols.50 (1. including 4-tert-octylphenol. In rats.900 (.00 (.500-1.60-3.10 (1.10 (.60-3. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. < LOD means less than the limit of detection.40) 2.g. Bian et al. Disposition in humans has not been studied sufficiently.10) 1. altered estrus cycles and reproductive outcomes.600-1.20-2. fish) and drinking water.300 (<LOD-. Survey Geometric mean (95% conf.80 (1. Urinary 4-tert-Octylphenol (4-[1.30) 2.000 tons of alkylphenol ethoxylates were produced annually worldwide. population from the National Health and Nutrition Examination Survey. 34 Fourth National Report on Human Exposure to Environmental Chemicals .300-.70 (1.20) 2.3. and impaired spermatogenesis (e.40) * 03-04 03-04 03-04 . Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. Katsuda et al. Less frequently. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.40) 2.299-. altered neonatal sexual development.389 (. an alkylphenol.300 (<LOD-.20-2. the various alkylphenols have also been used as emulsifiers and modifiers in paints.60) .200-.300 (<LOD-. impaired steroidogenesis.5% of 139 U. which may vary for some chemicals by year and by individual sample.400) 1.600-1.60) 613 652 1092 Limit of detection (LOD.200-.60-3.40) 1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (1.30 (1..500) 75th .. Saito et al.400 (.900 (. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e..500) . and some personal care products.10 (. have demonstrated estrogenic effects particularly when injected at high doses in animals. 2000.274-.600) .800-1.50) 1. and through manufacturing waste streams (Warhurst.40) 1.30) 90th 1. The alkylphenol ethoxylates enter the environment through human use of products containing them.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 . Indoor and to a lesser extent. did not bioaccumulate. 2002).20 (1.20) 314 715 1488 03-04 03-04 * * . 2002). 2004).Environmental Phenols 4-tert-Octylphenol CAS No.700-1. streams in 30 states (Kolpin et al. 1996).497) * . industrial cleaners.20-2.300 (<LOD-..268-.70 (1. 1997.20-2. see Data Analysis section) for Survey year 03-04 is 0..80 (1.00) 1229 1288 03-04 03-04 03-04 * .50) 1.600-1. through sewage.40 (1. orally administered 4-tert-octylphenol was well absorbed.30 (1.50-3. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.30-2.477) .600) .507) * < LOD .357 (.30) 1.1. is used to manufacture alkylphenol ethoxylates.600-1. 2003. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.50) .300-.

25) 2.890-2.06 (2.62) .740 (. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.270 (. representative subsample of NHANES 2003-2004.03 (1.400) .59) 1. nonylphenol. at lower or environmentally relevant doses (Blake et al.20 (1. 2000.03-6..560) .850 (.630-1.420) . 2004.17 (.78) 1228 1286 03-04 03-04 03-04 * . Fourth National Report on Human Exposure to Environmental Chemicals 35 . Sweeney et al. 4-tert-Octylphenol is not considered directly genotoxic.1.54) * 03-04 03-04 03-04 .11-2.02-4.540-1. Survey Geometric mean (95% conf.S. Urinary 4-tert-Octylphenol (4-[1. 2001.. Nagao et al.640-1.450) 1.260 (<LOD-.S.730-1.05-2..570) .15) 1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. 2001).384) * .43) 1.00) 2.10-2.450) .269 (.11) 1.Environmental Phenols Myllymaki et al.85 (1. Yoshida et al.43-3. 1999).170-.62 (1.610) . 2004).31 (1.740 (.59 (1.00) 1.53-3.64 (.62 (1. Tyl et al.68-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.270 (.03 (1.500-1.280-.620) .11) 2.50 (2.470-1.460 (.65-3.22) .470-1.68) 2.300 (<LOD-.00 (.270-.71) 2.96-4.320 (<LOD-.00) 2.276 (.14) 314 713 1487 03-04 03-04 * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.435 (. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.43) 1. In a small number of adult Japanese volunteers. 2005. Calafat et al. Kawaguchi et al.18-4.73) 2.67-2.00 (. population from the National Health and Nutrition Examination Survey.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..29) 2.78) 3.620-1.160-.40-4. 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.770 (.860 (.550-1.910 (.36-3.470) 75th .33) 3.00) 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 . 2003.31-2.25-2.337-. or their corresponding ethoxylates with respect to human carcinogenicity.08) 1.380 (<LOD-.349) * < LOD .199-. IARC and NTP have not rated octylphenol.207-.530) .40 (1.60 (1.78 (1.41) . the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.76 (2.370 (<LOD-.410 (. It is unclear if estrogenic or other effects occur in animals through oral dosing.3. 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.81 (1.25) 90th 1.33 (2..

Takenaka A. Muller AM.799(1):119-125. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Ye X. Estrogenic activity of octylphenol. Wong LY. hormones. Barber LB.121(1):21-33. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Ono H. et al. Nair-Menon JU. polybrominated diphenyl ethers. Wang X.uk/resource/reports/ethoxylates_alkylphenols. Spengler JD. Nakagomi M. streams. Raychoudhury SS.207(1):59-68.pdf. Available at URL: http:// www. Onuki A. Saito I. Regul Toxicol Pharmacol 1999. and sertoli cell number. bisphenol A and methoxychlor in rats. nonylphenol. Qian J. Food Chem Toxicol 2006. et al. Watanabe G. Environ Sci Technol 2003. Yoshimura S. and other organic wastewater contaminants in U.37(20):4543-53. Fail PA. Furlong ET. Katsuda S. Nicol L. Makino T.36(6):1202-1211. Kawaguchi M. 1999-2000: a national reconnaissance. testis size. Kookana R. Maekawa A. Cooper RL. Paranko J. Yoshimura Y.S. and testosterone. Wiegand HJ. Laws SC. Blake CA. Two-generation reproduction study with para-tert-octylphenol in rats. Maekawa A. Yoshida M.folliclestimulating hormone. Brooks AN. Sakui N. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Roche JF. et al. Haavisto TE. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Rudel RA. Endocrinology 2000. Meyer MT.Environmental Phenols References Bian Q. prolactin. Katsuda S.165(3):217-226.co. Okada F. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion.71(1-2):112-122. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Chen J. Kawaguchi M. Anal Chim Acta 486:41-50. Biol Reprod 1997. Seto H. Nagao T.44(8):1355-1361. Tyl RW. Taya K. Millette CF. Inoue K. Usumi K. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Marr MC. et al. Calafat AM. Reprod Toxicol 2001. Environ Int 2002. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. McCoy GL. Horie M. Blake CA.15(6):683-692. Williams B. Fedtke N. Arch Toxicol 1996. Environ Sci Technol 2002. Zaugg SD. Certa H. Watanabe G. Inoue K. and other endocrine-disrupting compounds in indoor air and dust. 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. Taya K.57(2):255-266. Xu L. Phthalates. Reidy JA. Izumi S. Bolt HM. Carey SA. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Toxicol Sci 2000. Yoshida M. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. pesticides. Takai N. Camann DE. 2003.foe. Myers CB. Exposure of the U.18(1):43-51. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. 36 Fourth National Report on Human Exposure to Environmental Chemicals . 1995. Toxicol Appl Pharmacol 2000. Sweeney T. Indoor Air 2004.S. Korn LR. Ito R.28(3):215-226.30(2 Pt 1):81-95. Bodman GJ.14(5):325-332. Ferrell JM. Environ Health Perspect 2008. Boockfor FR. Thurman EM. Brody JG. Saito Y. Boockfor FR. Warhurst AM. Kolpin DW. Karjalainen M. Needham LL. Toxicol Appl Pharmacol 2005. Pharmaceuticals. Toppari J. alkylphenols.141(7):2667-2673. Toxicol Lett 2001. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Brine DR. 2/4/09 Ying GG. Reprod Toxicol 2004. Seely JC. Song L.54(1):154-167.116(1):39-44. Indoor air pollution by alkylphenols in Tokyo. Myllymaki SA.

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

7 (14.82 (8.55 (4.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.60 (8.0 (34.48 (8.5 (11.6-65.2-14.4 (38.22-10.0 (26.3 (11.6-15.9 (8.8) 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 9.6-14.43-13.2-58.4) 90th 249 (188-304) 03-04 03-04 03-04 8.94 (7.21 (6.8-112) 30.8-63.5-86. interval) 12.1) 14.4-18.20-13.45-10.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.89-11.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.3.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9-236) 193 (90.7 (28.5) 66.2 (37.Environmental Phenols Urinary Triclosan (2.0 (11.3-31.1 (45.2-58.0) 49.8-127) 37.00-8.70-16.6) 12.6) 90th 212 (172-241) 03-04 03-04 03-04 9.6 (12.8) 14.4.48-10.1) 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 (11. Urinary Triclosan (2.7 (11.9) 75th 47.8) 7.00 (4.72-13.30-14.7 (9.2) 9.54 (8.60 (6.4 (12.74 (5.40-11.16 (6.3-67.S.9) 32.1-39.3 (26.9 (50.4) 75th 43.6 (9.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8) 116 (39.3) 47.9) 7.4-19.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD. interval) 13.0 (8.4.0) 9.1) 9.2 (11.7) 10.20 (7.6-14.2 (27.80 (5.3) 10.6) 31.5) 13.50-10.50) 10. population from the National Health and Nutrition Examination Survey.9 (33.10) 84.32-14.92-12.4) 51.3-35. Survey Geometric mean (95% conf.4) 317 (231-433) 144 (96.7) 292 (151-432) 132 (78.86-12.93 (7.6-37.1) 9.2 (25.90-10.1) 7.1) 9.2 (13.0-213) 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 .6 (30.4) 25.5) 11.11-11.2) 12.6) 39.4 (11.6) 10.0 (36.8-60.S.29-12.7) 123 (36.5-14.0) 65. population from the National Health and Nutrition Examination Survey.0-73. Survey Geometric mean (95% conf.38-18.0-15.2-46.1 (15.1) 9.1) 50.3) 6.8 (21.3 (8.1) 13.9-61.9) 8.1) 11.2 (10.10-9.6-111) 33.4 (32.5) 20.6-20.1 (8.4) 73.20 (7.20-11.18 (5.3 (9.0-15.45 (5.2) 13.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.20-10.45-13.4) 7.3-15.6 (10.8-85.40-17.0-19.4) 357 (225-456) 203 (87.7 (39. see Data Analysis section) for Survey year 03-04 is 2.

Ekstrand J. streams. Readman JW. Chemosphere 2007. Benson WH.83(1):84.4. Aguera A. Aranami K. Teitelbaum SL. Williams PE. Reidy JA. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Adolfsson-Erici M. Clapson DJ. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Shiratsuchi H. Osachoff H. Br J Clin Pharmacol 1987. Kaneshima H. Veldhoen N.38(4):361370. Triclosan: applications and safety. Kolpin DW. IMS Ind Med Surg 1969. Ye X.24(3):209-218. Chelimo C. Gomez MJ. Wolff MS. Sandborgh-Englund G. Leonard PA. Environ Health Perspect 2007.7/2. Aquat Toxicol 2006. Percutaneous penetration and dermal metabolism of triclosan (2. Barber LB. 1999-2000: a national reconnaissance. Photolytic degradation of triclosan in freshwater and seawater. Wong LY.45 Suppl 2:S137-S147.. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.36(6):1202-1211. Skirrow RC. Ferrer I. Environ Sci Technol 2002. Lyman FL. Hernando MD. hormones. Ogawa H.17(5):637-644.S. The oral retention and antiplaque efficacy of triclosan in human volunteers. Windham G. Calafat AM. J Toxicol Environ Health A 2006. Environ Health Perspect 2008. et al.69(20):1861-1873. et al. Mar Environ Res 2000. Fernandez-Alba AR. Odham G. Furia T. and phenols in girls.524:241-247. Howes D. Am J Infect Control 1996. Bhargava HN.67(4):532-537. phthalates.S. Pilot study of urinary biomarkers of phytoestrogens. Nagao Y. Erratum in: Aquat Toxicol 2007. Hirano M. Kanetoshi A.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.80(3):217-227. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Gilbert RJ. Bodey GP. Biol Pharm Bull 2005. Furlong ET. Levy SB. et al. Toxicology of 2. J Invest Dermatol 1976. Pharmacokinetics of triclosan following oral ingestion in humans. Mezcua M. Food Chem Toxicol 2000.28(9):1748-1751. Evidence of 2.23(5):579-583.50(1-5):153-156. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.115:116-121. population: 2003-2004. Foran CM. Ishibashi H.66:1052-1056. Larson EL. Britton JA. Katsura E. Watanabe N. Pharmaceuticals. 4’-trichloro-2’-hydroxydiphenyl ether.4’-trichloro-2’hydroxydiphenyl ether). Matsumura N. Williams FM. Urinary concentrations of triclosan in the U. Wigmore H. Thurman EM. Zaugg SD. 4. Bennett ER.38(2):64-71. Hong HC. Ebersole R. Arch Environ Contam Toxicol 1988. Anal Chim Acta 1004. Meyer MT. and other organic wastewater contaminants in U.116(3):303-307. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Okui T. Moss T. Gunderson MP. Pinney SM.Environmental Phenols References Aiello AE. Needham LL. et al.

Effects including hyperthermia. air.350-.350) < LOD .350) < LOD .51) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .500-2.10) 1.350) < LOD .33-2.S. and dermal contact with PCP-treated products.350-1.890-1.5.90) 1.350) < LOD . and it is used primarily as a preservative for wood to be used outdoors (e.770 (.350-.58-2. with repeated or chronic exposure.350-.350) < LOD .00 (.660 (.350-.350-.350 (.47-5.350 (..30) 1.530) 1. < LOD means less than the limit of detection.73 (1.47-3.350) < LOD .350) < LOD .350 (. 1976.990-2.. The parent compound and conjugates.76) .75) 2.58-2.390 (.01 (<LOD-1.23 (.350) < LOD .48 (.350 (. population from the National Health and Nutrition Examination Survey.510-5. After a single dose. and possibly of lindane (IPCS.350-.80) . PCP is eliminated over a few days (Braun et al. bactericide.960) 1.350) < LOD . 40 Fourth National Report on Human Exposure to Environmental Chemicals .50) 1. Human exposure to PCP has become less common.30) .350-.350-2.350 (. Since 1984.350-.350-2. which may vary for some chemicals by year and by individual sample.350 (. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350) < LOD .90 (1.350-. 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.00) 1.350 (.70) 2. 1979).10) 1. 1986).350-.350 (. are eliminated in the urine.04) 1.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.510-3.30) 1. water and sediments because of the large amounts that were produced and used historically.83 (2.350-1.64) 1..350) < LOD .350) < LOD .25 and 0. PCP cannot be used on wood in residential or agricultural buildings. and animals.350 (.90) 2.650 (.990 (<LOD-2.590-1.350-.65 (.94 (1.00) 1. herbicide.10 (. General population exposure to PCP may occur by inhalation of contaminated air.350 (. other polychlorinated benzenes.350-.350 (. along with small amounts of tetrachlorohydroquinone and conjugates.350 (.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . PCP also may be eliminated in urine as a metabolite of hexachlorobenzene. After absorption.30 (.g.350) < LOD .76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350 (.350 (.32 (. and metabolic acidosis were observed in CAS No.60) 1.350-.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 .30 (.350-2.350 (.60) 1.54-2.350-2. 1997).350 (.650) 1.980 (.350-.S.350) < LOD < LOD 75th .350-.10 (<LOD-1.890 (.65 (.91 (1.70) .350 (.350-.350) 90th .480-2. PCP use in the U.680-1.94 (1.850-2.30 (1.67) 1.350-.350-1.350-.09) . utility poles and fence posts).40 (. mollusicide. PCP has been detected in soils.390 (.08-3.33) .350) .00) 2.37) . Acute.350 (.350 (. algaecide and insecticide. 2002.350 (.350 (.350-.350-1. ingestion of contaminated food or water. hypertension. PCP is distributed to most tissues and is not extensively metabolized.350-. has been restricted.350) < LOD .42) 696 680 521 696 603 951 Limit of detection (LOD.45-2. the elimination half-life may be a week or more (Uhl et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.860-2. plants. so it is relatively non-persistent.76) 1. PCP is degraded by sunlight and metabolized rapidly by microorganisms.350) < LOD .. PCP is absorbed rapidly and well by all exposure routes.62 (.37 (.18 (<LOD-1. To-Figueras et al. 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. In the environment. Kohli et al.78) 1.350-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0..48-2.10 (1.98 (1.630 (.350) < LOD . Survey Geometric mean (95% conf.350-. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-.

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.920 (.16-1.730) < LOD .780-1.330-.250 (. In NHANES 2001-2002 subsamples.0 mg/L.18) .73 (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.850 (. 2003).610 (.51) 1.25) 1. In a small sample of U. van Raaij et al. More information about external exposure (i. and the FDA has established a standard for bottled water.57 (. EPA has developed standards for PCP in drinking water and the environment.e.400 (. 1989).13 (.40) 1.29-3.560) < LOD ..56) 1..40) 1.510-.830) < LOD .94-3.570 (.310-.67-2.25 (1.220-.75 (<LOD-2. 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.370 (.800-1.48-2.35) 1.310) < LOD . chronically administered high doses of PCP were hepatotoxic.560-.220-.580-.18 (1.69 (1.94 (1.630 (.30) 1.gov/ pesticides/ and from ATSDR at: http://www.320) < LOD .21-2.440 (.30) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.09 (<LOD-2.82 (1.09-1.300 (.500-. Fourth National Report on Human Exposure to Environmental Chemicals 41 . The U.430-.55) 1. Pentachlorophenol is not mutagenic or teratogenic.260 (. OSHA has established an occupational standard.84) 1.52 (<LOD-1. children in the 1980’s.19) 2.79) 1..270-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10-2. 1991).19) 2.30-2. 2004.560) < LOD .36) . 1989).9 mg/L..25 (1. and adversely affected thyroid function (U.S.300 (.06 (. 2000).650 (.780) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08 and 5.590) < LOD .800) < LOD 1.10 (1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.710-1.760 (.40) 1.25-2. Death can result from seizures and cardiovascular collapse. 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.650 (.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .S.700-2.78) 1.290) < LOD .340-. respectively) (Becker et al.11) 2.19 (1.html.490) < LOD .. 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. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.270-.00-1.84-4.00-1.360-.350) < LOD .280) < LOD .atsdr.26 (1. inhalation.S.35) 1.590-1.09) 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 .950-1.290-.40) 1.250 (.90) 1. or skin absorption.500 (.990 (.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .84 (1.34 (.67-3. In animals.650) 90th 1.35-2.83 (1. environmental levels) and health effects is available from the U.26 (1..S.67 (1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.500-1.6 and 14.67 (1.52 (<LOD-1. 1995).240-.06-3.67 (1. population from the National Health and Nutrition Examination Survey.57 (1.40-2. Survey Geometric mean (95% conf.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .75) 1. EPA at: http://www.78) 1.92) 1.420) < LOD .510-.360 (..52 (1.67-3.40) 1.30 (.67 (1.52) 1.21 (..Fungicides adults and children severely exposed to PCP through ingestion.320) < LOD .00) 1.950-1.gov/ toxpro2.95) 3.320 (.19) 2.67 (1.290-.16 (.epa.94 (1.380-. respectively) (Seifert et al.910-1.82) 1.950-1.25-2.35-2. 2003).cdc.300 (.EPA.430) < LOD . Among adults in the NHANES 1999-2000 subsample.25-1.06) 1.470 (. carcinogenic.900-1.320) < LOD < LOD 75th .

Schmid P. Jones D. Otero R. Krause C. 11/30/2004. house dust. Int J Hyg Environ Health 2003. PCP: Human Risk Characterization [online]. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. et al. Chenoweth MB.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Braun WH. References Becker K. International Programme on Chemical Safety (IPCS). German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. et al. Safe A. Engel R. Can J Biochem 1976. Environ Health Perspect 1997. 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. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. J Expo Anal Environ Epidemiol 2000. Arch Environ Contam Toxicol 1989. r e g u l a t i o n s . hair. Environ Res 1995.71:99108. Gregg M. 42 Fourth National Report on Human Exposure to Environmental Chemicals . The metabolism of higher chlorinated benzene isomers. 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.58:182-186. EPA). Arch Environ Contam Toxicol 1989. Schulz C. Arch Toxicol 1986.org/documents/jmpr/jmpmono/2002pr08. 4/21/09 van Raaij JA. Rodamilans M. 206:15-24. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations.18:475-481. Barrot C. Hill RH Jr. van den Berg KJ. Shealy DB. Uhl S. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. To T. Hill RH Jr. Cline RE.18(4):469-474. Hill RH. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Sala M. Helm D. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. htm. Holler JS. Available at URL: h t t p : / / w w w.inchem.105(1):78-83. available at URL: http://www. Seiwert M.54(3):203-208. 4/21/09 Kohli J. Schulz C. Seifert B.S. Baker S. Phillips DL. Kaus S. Needham LL. urine. 2002. Blau GE. drinking water and indoor air. Fast DM. U. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Bragt PC.S. To-Figueras J. Pharmacokinetics of pentachlorophenol in man. Notten WR. Becker K. Seiwert M. Environmental Protection Agency (U. Toxicology 1991: 67(1):107-16. Seifert B.10:552-65. Head SL. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Dev Toxicol Environ Sci 1979. Santiago-Silva M. Schlatter C. Lindane. Smith SJ. Bailey SL.4:289296. Needham LL.

or 2-phenylphenol) and its water-soluble salt.610-1. are antimicrobial agents used as bacteriostats.696) * .50) < LOD .570-2.50) .10) 1. EPA.496 (.950) < LOD .600) < LOD 75th .30) < LOD 1.600-1.470 (<LOD-.560-8.500-2.92 (..389-.S. on ornamental plants and turfs.Fungicides ortho-Phenylphenol CAS No.370-. however.80) 1.480-1. and it has limited water solubility. Workers who manufacture.03) 1.90 (1.450 (<LOD-.890) 1.860 (. General population exposure can occur via dermal.07 (.402-.570-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.750-2.14 (<LOD-3.450 (<LOD-.20) < LOD 2.88) 1.50 (1.30 (1.386-.50) < LOD .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .890 (.90) .570-. Estimated human intakes have been below recommended intake limits (U.600-1.60 (1.640) < LOD .20 (1.820 (. 90-43-7 General Information Ortho-phenylphenol (OPP.600) < LOD . it was used in home sanitizers for surfaces.27 (.349-.600) < LOD 1.930 (.S.EPA.830 (.10-1.770 (.S.600) < LOD . and as a wood preservative.28 (.508 (.20) 2. Fourth National Report on Human Exposure to Environmental Chemicals 43 .22 (.09) 2.90) . such as fruits and vegetables.28-3.450 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (.638) * .570 (. Cnubben et al.00-2.490 (<LOD-. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.19 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.50 (1. OPP is still used as a disinfectant fungicide for industrial applications.800-3. formulate.10) 2.490 (<LOD-.00) . and sanitizers.22) 2.836) * .600-1.690) < LOD .540-2.433-.580-1. In the past.3 and 0.740 (.30) < LOD .10) .91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .60 (1. Both have been used in agriculture to control fungal and bacterial growth on stored crops.630) < LOD .60-3. 1998.20 (1.850 (. 1989).60-2. Timchalk et al.30) < LOD 90th 1.80) 1.645) * .350-1. 2006).420 (<LOD-.50-4. 2006).509 (.61) 2. leaving the chemical residue OPP.23) 695 680 520 695 603 953 Limit of detection (LOD.33 (.50) < LOD . or apply these chemicals may be more highly exposed than the general population. fungicides. Survey Geometric mean (95% conf.17 (.85) 2. which may vary for some chemicals by year and by individual sample.30-2. 2002.00) < LOD .S.490 (<LOD-.00 (1.550-1.40-2.76) 1.610 (..00 (1.493 (. 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.790) 2.50) 1.10 (1. Available evidence suggests that OPP does not accumulate in the body.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.20-2.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .567 (.390-.490 (<LOD-.00) .770 (.710-2.624) * . Both chemicals degrade within hours to weeks in the environment (U. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al. interval) . OPP is considered to be moderately toxic after acute oral doses in animal studies. 2006).498 (.00 (1.370-.970 (.10 (1.490 (<LOD-.60 (1. OPP is volatile.20 (. but OPP and SOPP are still used on pears and citrus (U.50 (1.621) * . population from the National Health and Nutrition Examination Survey. sodium ortho-phenylphenate (SOPP).20-3.40-5. Most agricultural food applications have been revoked.710) 3.40-7.90 (1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin..552 (.50-2.10) 1.34) 1. < LOD means less than the limit of detection.636) * . inhalational.90) 2. 2006).410-. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.10) .364-.742) * .3.30) 1. SOPP is applied topically to the crop and then rinsed off.00 (1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.840-1.370-.497 (. in paints.780) < LOD .670) 2.590-2.EPA.466 (.02) 1. 1998).40-5.90) 1. whereas SOPP is not volatile and is more water soluble.880-2.760-2.50-3.890 (.10) .80 (2.80-3.570 (.520 (.10-2.389-.690-1.30-7.20) < LOD 1.

Zhao et al.343 (.780-14.74 (1.770-2.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .91 (1.96-4.460-. 1992.32) 1.61 (2.EPA 2006).38) 1.0) 1.291-.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.17) 2.33-2.510 (<LOD-.382 (.610) < LOD 1.17 (. 1984.420 (<LOD-.484) * .64 (2.86 (1.13) 1.81) 1.88-4. Volunteers exposed to 0.S.690 (. 2002. Nakagawa et al. Biomonitoring Information Urinary OPP levels reflect recent exposure.08-2.00 (. 1998.810-1.S.900-1.11 (. 1997.28 (<LOD-4.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.93) 1.470 (<LOD-.33) .00 (1.gov/pesticides/.09-6.410 (<LOD-.18) 2.910-1. 2005).20) < LOD 3.508) * .75 (1.455-.4) 3. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. Brusick. Bomhard et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.51-3.05-2.590) * . Ito et al. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.550) < LOD .840 (.910 (<LOD-1.750-2.EPA at: http:// www.880-1.96) 1.29) 1.21 (.Fungicides anemia.329-. by possible genotoxic mechanisms (Hagiwara et al..750 (.04-4.11 (.S.670) < LOD . population from the National Health and Nutrition Examination Survey. U.24-2.570) < LOD 1.444 (.550-. Kwok et al.75 (1. 2005).93) . 44 Fourth National Report on Human Exposure to Environmental Chemicals . OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.270-.93 (1. 2002).666) * .510-. OPP was not found to be mutagenic.89 (1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.17 (.21-2.420 (<LOD-. and it has classified OPP as not classifiable with respect to human carcinogenicity.96 (1.670 (. 2002.650-1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .970) 1.46) < LOD 1.580) < LOD . reproductive. 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.656) * .32) 3. 1984.24-2.26) 1. interval) .640-1.360 (<LOD-.980 (.750 (.580-1. 1993.900) < LOD .28 (2.21) 1.940-2.11-1..06 (1.810) < LOD . ortho-phenylhydroquinone and ortho-phenylbenzoquinone. or. Additional information is available from U.EPA 2006)..470) < LOD .53) 1.385 (.52 (. 2005.09-3.. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. Murata et al.560-2.43-2. Smith et al.97 (2.07) 2.84 (1.500) < LOD .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1999.43) 3.560) < LOD 75th .29) 1.670 (.12) < LOD 1.93) . Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.480-.59) .353-.06-5.980 (<LOD-1.47) .epa.38-3.791) * .43 (1.860 (.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .568) * . Pathak and Roy.96 (1.453 (.403-.11) 4. Survey Geometric mean (95% conf.25-6.600-1.990) < LOD . or developmental toxicity was observed (Bomhard et al.58) 2.69 (1.440 (.59) 1.61 (.43-2.860 (.06-4. CDC.40-13.78 (2.248-.550 (.361-.800-1...11) < LOD 90th 1.514 (.08) 1.410 (<LOD-. leading to production of two metabolites.31) < LOD . 2000..496 (.380 (.320 (<LOD-.473) * .S. Detectable levels were seen in over half the U.950) < LOD . less likely.01) 1.09 (1.02 (. IARC has classified SOPP as a possible human carcinogen.44 (1.61 (1.780 (.12-2. U.38) 2.620-1.910 (.301-. 1986).311-.27) < LOD .558) Selected percentiles ( 95% confidence interval) Sample 95th 2.. In high dose animal studies.62) ..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 .620-1.. 1999.08-1. but no neurologic.

U. EPA)..EPA). Imaida K. Kwok ES. Timchalk C.159(1):18-24. Regul Toxicol Pharmacol 2002. Eastmond DA. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. St John MK. July 28.pdf. Nakagawa Y. Bromig KH. Smith RA. McNett DA. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. et al. Bartels MJ. Elliott GR. 2006. Ito N. J Chromatogr B Biomed Sci Appl 1997.pdf.150(2):402-413. Glas K. Shirai T. Moriya K. Toxicol Appl Pharmacol 1998. Cano M. Ito N. Arnold LL.17(8):411-417. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. 1989. 4/9/09.74(2):61-71. Christenson WR. Available at URL: http://www. Atlanta (GA). Cnubben NH. Fukushima S. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.22(10):809-814.niehs.epa.286(2):309-319. Sangha GK. IARC Sci Publ 1984. Roy D. Moldeus P.S. 2005.43(7):14311437. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Environmental Protection Agency (U. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Murata M. Timchalk C. Brusick D. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Meuling WJ. EPA-560/5-89-003. Comparative metabolism of orthophenylphenol in mouse. Available at URL: http://ntp. Mutat Res 1993. Selim S. rat and man.gov/oppsrrd1/REDs/ phenylphenol_red. Stanley JS. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Hakkert BC. 90-43-7) in Swiss CD-1 mice (dermal studies). food additives and natural products as promoters in rat urinary bladder carcinogenesis. U. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Vogel JS. Bomhard EM. van de Sandt JJ.Fungicides References Appel KE. Bartels MJ. Brendler-Schwaab SY. Freyberger A. Fukushima S.gov/ntp/htdocs/LT_ rpts/tr301. Hum Exp Toxicol 1998. Centers for Disease Control and Prevention (CDC). Drugs. Pathak DN. Zhao S. Turteltaub KW.(56):399-407. Mendrala AL. National Toxicology Program (NTP). J Agric Food Chem 2006.nih. Leser KH. Bartels MJ. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Richter M. Hagiwara A. J Agric Food Chem 2002.50(11):3351-3358. Kawanishi S. Hirose M. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Food Chem Toxicol 1984. Herbold BA. Toxicol Appl Pharmacol 1999.703(12):97-104.28(6):579594. 4/13/09 Onstot JD. Xenobiotica 1998. Buchholz BA. Moore GA.35(2 Pt 1):198-208. Third National Report on Human Exposure to Environmental Chemicals. March 1986. et al. Narang A. Biochem Pharmacol 1992. Gierthy J.45(5):460-481.S. Eadon G. Environ Mol Mutagen 2005. Shibata M. Bormett GA. Environmental Protection Agency (U. Christenson WR.54(16):5731-5735. O-phenylphenol and its sodium and potassium salts: a toxicological assessment.32(6):551-625. Identification of SARA compounds in adipose tissue. The carcinogenicity of the biocide ortho-phenylphenol. Bartels MJ. Inoue S.S. Crit Rev Toxicol 2002. Arch Toxicol 2000. Brzak KA. Roberts AL. EPA 739 R-06004. Sangha G. Tayama S. Carcinogenesis 1999.S. Hagiwara A. Coelhan M.20(5):851-857. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Office of Toxic Substances.

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

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

S.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2500 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 819 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1322 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 672 952 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * 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 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. < LOD means less than the limit of detection.1. 48 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 01-02 is 0.

Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Environ Health Perspect 2003. 2000. Dialkylquinonimines validated as in vivo metabolites of alachlor. Environmental Protection Agency (U. J Agri Food Chem 1989. Environ Sci Technol 2005. Feng PCC. Sanderson WT. Casida JE.cce.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Barr DB.111(5):749-756. Ward EM. et al. Barr DB. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. EPA). Jefferies PR. Centers for Disease Control and Prevention (CDC). Hladik ML.24(10):1003-1012. Wilson AG. acetochlor.15(6):500-508. Whyatt RM. EPA). J Expo Anal Environ Epidemiol 2005. Hodgson E. Lefevre PA.39(17):6561-6574. Rose RL. and metolachlor herbicides in rats. Tinwell H. EPA 738-R-00-009. Peter CJ.S. Volume 65. Roberts AL. 5/30/06 U. Chem Res Toxicol 1998. Sci Total Environ 2000. Green T. Environ Health Perspect 2000.cornell. pages 3682-3690. 1998. Available at URL: http://www. Third National Report on Human Exposure to Environmental Chemicals. J Expo Sci Environ Epidemiol 2007.S. Olsson AO. Striley CA. Hines CJ. Hsiao JJ. reservoirs and ground water in the Midwestern United States. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Available at URL(non U.37(4):10881093.11(4):353359. Deddens JA.html. Acetochlor (Harness) Pesticide Petition Filing 1/00. Davison KL. Reynolds SJ. Wratten SJ. Environmental Protection Agency (U. epa. Feil VJ. Kolpin DW. 2005. Linhart SM.EPA): http://pmep.S. sulfonamide.Herbicides References Ashby J. imidazolinone. Occurrence of sulfonylurea. Federal Register: January 24. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Kier L. Hein MJ. Furlong ET. Battaglin WA. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Comparative metabolism and elimination of acetanilide compounds by rat. Curwin BD. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Barr JR.248(2-3):115-122. Burkhardt MR. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Camann DE.S. and other herbicides in rivers. Coleman S. Linderman R. Thurman EM. U. Number 15.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Larsen GL. Kinney PL. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.15(9):702-735. March 2006. Heederik D. et al. Quistad GB.248(2-3):123-133.pdf. et al. Barr DB. Alavanja MC. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Andrews HF. Xenobiotica 1994. Sci Total Environ 2000. Bravo R.108(12):1151-1157. Atlanta (GA). Hum Exp Toxicol 1996.17(6):559-566.S. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. 5/30/06.

1998). U. 1996. 1994. U. Estimated human intakes have been below recommended limits (U... (2003) showed that 2. 1999 and 2007.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. Feng and Wratten. WHO.. 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. Because it can be absorbed through skin. 1997. 1998. and field workers.EPA. alachlor has demonstrated hepatotoxicity. 1989.S. Since the late 1980s alachlor use has been declining.EPA. 2003). WHO. It is absorbed by plants and inhibits plant protein synthesis. corn cropland was treated with alachlor. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates.S.S. IPCS. and on non-crop land for general weed control. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. as measured through conversion to deethylamine.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hines et al. including corn. 2005). stomach. 1995). Jefferies et al. Hladik et al. USGS. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates.S. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. 1998. 1995. whereas 60% of applicators had detectable amounts.. U. Kolpin et al. about 20-25% of the U. and uveal degeneration.S. 2003). alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. the latter may account for some observed effects (Davison et al. 1988. 2005. Alachlor has low potential for acute toxicity. In chronic animal testing. Hill et al. 2000. 1999. 2003).1 mg/L at various collection times (Sanderson et al. but another metabolic pathway can produce 2. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC.epa.EPA considers alachlor to be a probable human carcinogen at high doses. formulators. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. 1998). mercapturate conjugates were predominant metabolites.gov/pesticides/. In a study of applicators and workers exposed to alachlor. but not likely at low doses.. but has not shown developmental or reproductive toxicity in mammalian systems (U. WHO. 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. ranged from 0. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. WHO. hemosiderosis..S. 1998..1 to 1. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure.Herbicides Alachlor CAS No. In animal studies. In 1993-1995. 50 Fourth National Report on Human Exposure to Environmental Chemicals .. 2000. Biomonitoring studies on levels of alachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of alachlor than are found in the general population. EPA at: http://www. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. U. soybeans.EPA. NTP and IARC do not have ratings regarding human carcinogenicity. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. peanuts and other crops. Alachlor has a soil half-life of a few weeks. 1998). 2003). Additional information about is available from U.S.EPA. Tessier and Clark. 1996). mean values of urinary concentrations of alachlor metabolites.EPA. Alachlor itself is not considered mutagenic. 1996.6-diethylaniline and its reactive metabolite. but shows little bioaccumulation. the dermal exposure route is potentially significant for applicators. In animals.S.

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

Hines CJ. Andrews HF. World Health Organization. Larsen GL.11(4):353359.Herbicides References Battaglin WA. Available at URL: http://www.org/documents/pds/pds/pest86_e. Kimmel EC.44(18):1325. Circular 1291. Supplemental Technical Information (available on-line only). Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes.gov/oppsrrd1/ REDs/0063. Peter CJ. Sacramento.47(6):503-517. Geological Survey (USGS). Tolos W. Third National Report on Human Exposure to Environmental Chemicals. Casida JE. Casida JE. Henningsen G.56(9):883-889. March 2006.56(6):853-859. Thurman EM. J Ag Food Chem 1995. Comparative metabolism and elimination of acetanilide compounds by rat. 2005. Clark JM. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Jefferies PR. Xenobiotica 1994. Environ Health Perspect 2003. DNA adduct formation by alachlor metabolites. Sci Total Environ 2000. Reregistration Eligibility Decision (RED) Alachlor. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .htm. Lau H. Davison KL. Dialkylquinonimines validated as in vivo metabolites of alachlor. acetochlor. Roberts AL. Biagini RE. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Alachlor in Drinking-water. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Kolpin DW. 2007. Bull Environ Contam Toxicol 1996.18(6):363-391. Thake DC. Centers for Disease Control and Prevention (CDC). Background document for development of WHO Guidelines for Drinking-water Quality.php. Burkhardt MR.pdf.39(17):6561-6574. Environmental Protection Agency (U. WHO/ FAO Data Sheets on Pesticides. Shoemaker DA. Am Ind Hyg Assoc J 1995. et al. EPA).S. Occurrence of sulfonylurea. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. U. Heydens WF. revised February 15.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Whyatt RM. 2003.pdf. 2/27/09 Jefferies PR. Quistad GB. Tessier DM. Striley CA. Martens MA. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Deddens JA. 1998. 1997. 1992-2001.inchem. Kier LD. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. J Agri Food Chem 1989. Available at URL: http://www. 86.248(2-3):115-122. Quistad GB. Ann Occup Hyg 2003.37(4):10881093. Hines CJ. and other herbicides in rivers. Life Sci 1988. 98-4245 (by Barbash JE. Available at URL: http://water. Kolpin DW. EPA 738R-98-020. World Health Organization (WHO). imidazolinone. ALACHLOR. Wilson AG. Geological Survey (USGS). Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Environ Sci Technol 2005. 1999. Hull RD.43(9):2504-2512. International Programme on Chemical Safety (IPCS). Atlanta (GA). Feil VJ. Feng PCC.int/water_sanitation_health/dwq/chemicals/en/alachlor. et al. Hill AB. 1996. Erratum in: Life Sci 1989. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Brown MA. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Hill RH Jr. Brown KK. 2/27/09 U. sulfonamide. Kinney PL. who. Furlong ET.S. MacKenzie B.24(10):1003-1012. Sanderson WT. Geneva.248(2-3):123-133.43(25):2087-94.epa. and metolachlor herbicides in rats. 4/2/09 U. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Barr JR. Gilliom RJ). Chem Res Toxicol 1998. Wratten SJ.S. Available at URL: http:// www. reservoirs and ground water in the Midwestern United States. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Camann DE.usgs. Hsiao JJ. No. Sci Total Environ 2000. Barr DB.111(5):749-756. Hladik ML. December 1998.S. California. Biagini R. Linhart SM.395(2-3):159-171. 1999. Driskell WJ. Thelin GP. Mutat Res. Casida JE. Hum Exp Toxicol. Shealy DB.

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

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

et al. Moseman RF. Toxicol Sci 2000. diamino-S-chlorotriazine and hydroxyatrazine. Toxicol Sci 2003.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Eldridge JC. Fleenor-Heyser DG. 1993). Catenacci G. Grzywacz JG.. 2003. J Expo Anal Environ Epidemiol 2005.109(6):583-590. Hayes TB. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Stoker TE. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Biological monitoring of human exposure to atrazine. World Health Organization. 2001 [online]. J Toxicol Environ Health 1994. Barbieri F. References Adgate JL. 2001). A risk assessment of atrazine use in California: human health and ecological aspects. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Goodrow MH. Jones AD. Wetzel LT. Hermaphroditic. Ferrell JM. Quandt SA. Toxicol Lett 1993.org/documents/pds/pds/pest82_e.. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. 3/11/09 Laws SC.atsdr. Tyrey L. et al. Lee M. J Agric Food Chem 1982. Sanborn JR. Gillis JH.58(2):366-376. Goldman JM. et al.99(8):5476-5480. Bradway DE. Ann Occup Hyg 2003. Mendoza M. Perry et al. In a small number of field workers. Environ Health Perspect 2007. In the NHANES 2001-2002 subsample. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Hines CJ. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Barr DB. Gillis JH.. Toxicol Sci 2000.cdc. Available at URL: http:// www. No. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.inchem. Breckenridge CB. Hein MJ.53(2):297-307. Gammon DW. Barr DB. Cooper RL. Sanderson WT. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. WHO/ FAO Data Sheets on Pesticides. Vonk A. Noriega N.htm. Aldous CN.html. et al. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Striley CA. Shoemaker DA. Schmid J. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Reynolds SJ.76(1):190-200. Carr WC Jr. Clayton CA. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Curwin BD. Wetzel LT. Stoker TE. Agency for Toxic Substances and Disease Registry (ATSDR). ATRAZINE. Cooper RL. Laws SC. Pfeifer KF. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. 2005). 2007). Eberly LE. 1996. Simpkins JW. Collins A. Steroids 1999. Stevens JT. In a study of 60 farm worker children. Seiber JN. Freeman NC. Biagini RE.69(2):217-222. Extrom PC.115(8):1254-1260. et al... The geometric mean of urinary atrazine mercapturate was 1. Maroni M. Deddens JA. Lioy PJ. Centers for Disease Control and Prevention (CDC). Barr DB. Cooper RL. Lucas AD. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. 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.. et al. 3/11/09 Arcury TA.43(2):155-167. Pest Manag Sci 2005. In small studies of Maryland residents in 19951996 (MacIntosh et al.61(4):331-355. Stuart AA.gov/toxprofiles/tp153. J Toxicol Environ Health 1994. 82. levels of atrazine mercapturate were generally not detectable (CDC. Environ Health Perspect 2001. Brown KK. Atlanta (GA). Eldridge JC. Ferrell JM. Blewett C. Chen H. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.43(2):155-167. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Toxicological profile for atrazine. Tapia J. Geneva. Cottica D. 2005. Stoker TE. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. International Programme on Chemical Safety (IPCS).30(2):244-247.64(9):672-678. Third National Report on Human Exposure to Environmental Chemicals. 2000). Heederik D. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Proc Natl Acad Sci USA 2002. Ferioli A. atrazine was detected in only four children (Arcury et al.. McElroy WK. Bersani M.15(6):500-508.47(6):503-517. Saiz SG. Available at URL: http://www.

A longitudinal investigation of selected pesticide metabolites in urine. Sathiakumar N. Toxicol Sci 2000. Guidici DL.pdf.epa.pdf.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. 3/11/09 U. Dryzga MD. EPA). U. van den Berg M.182(1):44-54.6(1):107-116.195(1):23-34.S.56(2):69-109. Toxicology 1990. The Quality of Our Nation’s Waters. March 2006. Wood C. Pesticides in the Nation’s Streams and Ground Water. Circular 1291. Osborne DW. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Toxicol Sci 2002.S. Rayner JL. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Environmental Protection Agency (U.php.epa. Available at URL: http://www. Boerma J. Breckenridge CB.10(7):479.67(2):198-206. Laws SC. Christiani D. 6/1/09 U. Singzoni B. Available at URL: http://water. Geological Survey (USGS).gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Guidici DL.9(5):494-501.61(1):27-40. Sanderson JT. Office of Prevention. Chem Res Toxicol 1993. A risk characterization for atrazine: oncogenicity profile. Environmental Fate and Effects Division.S. J Toxicol Environ Health A 1999. Cooper RL. EPA Office of Pesticide Programs. Stevens JT. Stoker TE. J Expo Anal Environ Epidemiol 1999.usgs.58(1):50-59. May 2003a. 0062. Environmental Protection Agency (U.Herbicides development of a biomarker of exposure. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Timchalk C. Lansbergen GW. revised February 15.S. MacIntosh DL. Interim Reregistration Eligibility Decision For Atrazine. Case No. Toxicol Appl Pharmacol 2004. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat.gov/oppsrrd1/REDs/ atrazine_ired. Hammerstrom KA. Perry M. EPA). White paper on potential developmental effects of atrazine on amphibians. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Stoker TE. Cooper RL. 1992-2001. Langvardt PW. Tortorelli J. Laws SC. 2003b. Dagenhart D. Fenton SE. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .S. Kastl PE. Wetzel L. Toxicol Appl Pharmacol 2002. Supplemental Technical Information (available on-line only). 2007. Needham LL. Ryan PB. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Pesticides and Toxic Substances. Delzell E. A review of epidemiologic studies of triazine herbicides and cancer. Available at URL: http://www. Washington (DC). Ann Epidemiol 2000.27(6):599612. Crit Rev Toxicol 1997.

260 (<LOD-. 2.670-1.4-D is rapidly absorbed via oral and inhalation routes. hypotension.43) 1.60) 1.952 and 0.560-1.910) < LOD ..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 .4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.740 (. 4-D.810-1.490 (.. and delayed Urinary 2. and aquatic environments. by direct contact with agricultural and residential areas after applications. but at higher levels they are herbicidal.S.03) 695 659 520 668 589 892 Limit of detection (LOD. It is rarely detected in ground waters (USGS.930 (.540-.70) 1..48) < LOD 1.51 (1.320) 90th .22) < LOD . agricultural.2. 2.4-D) controls broadleaf weeds in residential.13) < LOD .4-D or exposed for prolonged periods.07 (. 2.S.690 (.610 (.330 (.30 (<LOD-2.690 (.4-D were used in the U.210 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms. 2004).4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. headache.80) 1.760 (.S. 2. population from the National Health and Nutrition Examination Survey.210-.55 (1.250 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 57 .40) 1.440-1.660) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.420-.27-2.4-D can be applied either as an aqueous salt or as oil-soluble esters.560-. Sauerhoff et al. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.16) < LOD . the chlorophenoxy herbicide 2. with a half-life of several days to several weeks.EPA.4-dichlorophenoxyacetic acid (2.Herbicides 2.10 (<LOD-1.310) < LOD . Human health effects from 2.350) < LOD < LOD < LOD . It is poorly bound in soils.27 (1.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .EPA.910) 1. 1989.690-1.EPA in 1948. these herbicides can enhance plant growth.4-Dichlorophenoxyacetic Acid CAS No. myotonia.24 (.05-2.690 (. nausea. it acts as a plant growth hormone. As much as 62 million pounds of 2.4-D may occur during residential applications. abdominal pain. dizziness.66) < LOD 1. It is not well absorbed through the skin. Survey Geometric mean (95% conf. renal and hepatic injury. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .610-.4-D have been below recommended intake limits (U.310 (.S. It was first registered with U.400) < LOD .32 (1. which may vary for some chemicals by year and by individual sample. At low levels.410) < LOD .21) 1.00-2.20 (<LOD-1.730 (.27 (. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.10 (<LOD-1.02-1.10) < LOD 1. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. 1977). < LOD means less than the limit of detection. General population exposure to 2.08) < LOD .230 (<LOD-. Once absorbed. MCPA. and mecoprop).370-.680-1.230-.930-1. and by consuming food or drinking water contaminated with 2. 94-75-7 General Information Widely used throughout the United States. 2005). Recent estimates of chronic intakes of 2. in 2001 (U.550-1.490) < LOD < LOD < LOD .4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al. Kohli et al. Similar to other chlorophenoxy herbicides.250 (<LOD-.890) < LOD .890 (.960-1.20 (.4-D has low acute toxicity.420) < LOD .S. 2007). 1974.

It is unclear whether these associations are related to the chlorophenoxy herbicides.410 (<LOD-.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.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. Average post-application urinary levels of 2. Frank et al. 2005).410) < LOD < LOD < LOD .32 (<LOD-2.780-1. in small samples of children (Hill et al. 2005.660 (. IPCS.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .S.440 (. or to contaminants in the herbicide formulations (specifically 2.17 (.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 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. 2005.820-1.EPA at: http://www.340-.41 (1. Knopp et al.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. 2005).08 (..4-D levels were detectable in less than a quarter of the individuals studied.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 .670 (<LOD-1.EPA. 2000).670 (.S..410) < LOD 1.35) < LOD .Herbicides neuropathy (Bradberry et al. eyes.24) 1.39) < LOD 1. developmental.3.. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.. population (Hill et al. 2005).270 (<LOD-..700 (. 1980.560-. 2005.780) .550-. Epidemiological studies have reported associations of several types of cancer. 2002. myotonia.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2003.05) . IOM.680) < LOD .S.EPA.13 (.850) < LOD .380) < LOD .. 1996.4-D production plant workers and a few forestry workers spraying 2.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1989). U.330-. Acute high doses administered to laboratory animals produced ataxia. 1994).520-.810-1. Hill et al.580-.390) < LOD < LOD < LOD . 2004). Biomonitoring Information Urinary levels of 2. or teratogenic effects in chronic rodent studies (Charles et al.920) < LOD 1. Kutz et al.620-..490 (.S.410) 90th . 1996.S.EPA 2005).4-D does not have significant reproductive. liver.740 (.19) . 2005.gov/pesticides/.790) 1. population from the National Health and Nutrition Examination Survey.380-.480 (.4-D reflect recent exposure.890-1. IPCS.980) < LOD 1.S.380 (<LOD-.EPA. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.990-1. 58 Fourth National Report on Human Exposure to Environmental Chemicals . Post-application levels in farmers and home gardeners were dependent on Urinary 2.340 (.790) < LOD .epa.4-D are eye irritants. Additional information is available from U. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. Pearce and McLean. 1996. thyroid.16) 1.660) < LOD .7. Kolmodin-Hedman and Erne.780 (. U.560-.640 (.S. In previous samples of the U. 2001. 1985. 2.810-1. The acid and salt forms of 2.890) < LOD 1.27-1..4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. U.590 (<LOD-1. CDC.. Survey Geometric mean (95% conf. 2.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.670 (.73) .350 (<LOD-.56) .380 (<LOD-. 2002. other exposures. 2. adrenals and gonads (NTP. 1992). and of adults and children (Baker et al. 1995). U. 1995.720 (. 2005).470) < LOD . urinary 2.270-.590 (<LOD-1.570) < LOD .930-1.08 (. and evidence of histological injury to the kidneys. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. IPCS.13 (.610-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.14 (. 2006.08 (.610-.

Finding a measurable amount of 2. Biomonitoring of herbicides in Ontario farm applicators.4-D were highest in the farmers who applied the 2. Kutz FW.18(4):469-474. Barr DB. Gupta BN. Available at URL: http://ntp. Honeycutt R. Pesticides residues in food: 1996 evaluations Part II Toxicology. Baker SE. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.4.32(4):233-257. Frank R. Shealy DB.4:427-435.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.4-dichlorophenoxyacetic acid and its forms. the amount of pesticide applied. Driskell WJ. 3/17/09 Institute of Medicine (IOM).gov/index. J Toxicol Environ Health 1992. Bus JS.71(2):99-108. Erne K.4-dichlorophenoxyacetic acid (2. the number of acres to which it was applied (Curwin et al.4:97-100. References Arbuckle TE. 2005). Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Fast DM. Needham LL. Philbert MA. Review of 2. Hein MJ. Barr DB. Arch Environ Contam Toxicol 1985. Alexander BH..31 Suppl 1:98-104. J Environ Sci Health B 1992. Estimation of occupational exposure to phenoxy acids (2.org/documents/jmpr/jmpmono/v96pr04.4:318-321. Biomonitoring for farm families in the farm family exposure study. Baker S. Environ Res 1995. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . geometric mean urinary levels of 2. Mandel JS. Sirons G J.4-D): exposure and urinary excretion. International Programme on Chemical Safety-INCHEM (IPCS). Smith SJ.31(2):121-125. 3/17/09 Knopp D.4-dichlorophenoxyacetic acid (2. Heederik D. To T. Centers for Disease Control and Prevention (CDC).51(3):152-159.60(1):121-131. Scand J Work Environ Health 2005. general population. Forestry workers involved in aerial application of 2. Crit Rev Toxicol 2002. Tandon JS. Toxicol Sci 2001. Tables. TOX-63: TOXICITY REPORT CURVES. Mandel et al. Selected pesticide residues and metabolites in urine from a survey of the U. Veterans and Agent Orange: update 2002. Stephenson GR.31 Suppl 1:90-97. J Expo Anal Environ Epidemiol 2005 Nov. Sanderson WT. Brody D. Xenobiotica 1974. Occup Environ Med 1994.4-D than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.5-T). 1992). Chapman P. TOX-63 Peroxisone Project (2.15(6):500-508. Hanley TR Jr. Cole DC. Hill RH Jr.4-D in urine does not mean that the level of the 2..4-D. 2006. Ritter L. In farm families. Arch Environ Contam Toxicol 1989. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.37(2):277-291. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.. Absorption and excretion of 2. 2005. Atlanta (GA). 914.htm.4-. Curwin BD.nap. Sircar KP.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. Wilson RD. Updated March 7. Gregg M. et al.27(1):23-38. 2.4-Dichlorophenoxyacetic Acid). Assessment of exposure to 2. Biomonitoring studies of 2. et al. Head SL. Arnold EK. Reynolds SJ. Kolmodin-Hedman B.4 dichlorophenoxyacetic acid (2. 2003. Bailey SL. Needham LL. Board on Health Promotion and Disease Prevention. Carter-Pokras OD. Cook BT. Harris SA. Washington (DC): National Academies Press. Garabrant DH. Khanna RN. Available at URL: http:// www. 2005).nih. Ripley BD. Developmental toxicity studies in rats and rabbits on 2.4-D). The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Vet Hum Toxicol 1989. Solomon KR. et al. 2005 Charles JM.edu/catalog.Herbicides the time since application. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. J Expo Anal Environ Epidemiol 2000. Holler JS.4-dichlorophenoxyacetic acid in man.10(6 Pt 2):789-798. Beeson MD.. Arch Toxicol Suppl 1980. Exposure of homeowners and bystanders to 2.4-D will result in an adverse health effect. National Toxicology Program (NTP). Campbell RA. Kohli JD. Pesticide residues in urine of adults living in the United States: reference range concentrations.php?record_id=10603. Baker BA.inchem. Available at URL: http:// www. Survival and Growth Curves from NTP Toxicity Studies.niehs. and the use of protective clothing or equipment (Arbuckle et al. Murphy RS. 2005. Harris et al. Acquavella JF. van Ravenzwaay B. Third National Report on Human Exposure to Environmental Chemicals. Hill RH Jr. Dichlorophenoxyacetic acid.4-D and 2. Beasley VR. Scand J Work Environ Health 2005.4-D) epidemiology and toxicology. Dhar MM.

June 2005.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Available at URL: http://water. 2004. Environmental Protection Agency (U. Available at URL: http://www. Geological Survey (USGS). EPA 738 F-05-002.EPA. The fate of 2. Blau GE. March 2006. Toxicology 1977.2000 and 2001 market estimates.pdf.Herbicides Sauerhoff MW. Gehring PJ. May.S.php. The Quality of Our Nation’s Waters.usgs.epa. Office of Prevention Pesticides and Toxic Substances. 60 Fourth National Report on Human Exposure to Environmental Chemicals . 3/17/09. 4/2/09 U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Environmental Protection Agency (U. Pesticide industry sales and usage . 3/17/09 U. 2.S.S.4-D) following oral administration to man.htm. revised February 15. Available at URL: http://www. Supplemental Technical Information (available on-line only).EPA). Washington (DC): U.gov/oppsrrd1/ REDs/factsheets/24d_fs.S. S. Pesticides in the Nation’s Streams and Ground Water. Braun WH. 1992-2001.4-dichlorophenoxyacetic acid (2. Circular 1291.S.8:3-1U.EPA).4-D RED Facts.epa. 2007.

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

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 .440 (<LOD-. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. see Data Analysis section) for Survey year 01-02 is 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240) 679 701 957 Limit of detection (LOD.S.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.200 (<LOD-. which may vary for some chemicals by year and by individual sample.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2.670 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. < LOD means less than the limit of detection.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 62 Fourth National Report on Human Exposure to Environmental Chemicals .200 (<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. Survey Geometric mean (95% conf.

Metolachlor in Drinkingwater.html. 3/26/09 U. Environ Sci Technol 2007. April 1995. Striley CA. Dialkylquinonimines validated as in vivo metabolites of alachlor. acetochlor.108(12):1151-1157. Comparative metabolism and elimination of acetanilide compounds by rat. Reynolds SJ. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Roberts AL.epa.37(4):10881093. Quistad GB. Available at URL: http://www. Centers for Disease Control and Prevention (CDC). Feil VJ. Sci Total Environ 2000. Atlanta (GA). streams and groundwater. Circular 1291. Barr JR. Kolpin DW. et al. Sacramento. imidazolinone. Kinney PL.pdf. Kolpin DW. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .S. 4/2/09 U. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.int/water_sanitation_health/dwq/chemicals/ metolachlor. Burkhardt MR. Peter CJ.47(6):503-517.S. EPA). Barr DB. Andrews HF. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Linhart SM. Larsen GL. and other herbicides in rivers.S. Environmental Protection Agency (U. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. J Expo Anal Environ Epidemiol 2005. Sanderson WT. Jefferies PR. R. Wratten SJ. Davison KL. Curwin BD.11(4):353359. Thurman EM. Available at URL: http://water.who. 1992-2001.ESTfeature_gilliom. Available at URL: http://water.24(10):1003-1012. and metolachlor herbicides in rats. Environ Health Perspect 2003. Ann Occup Hyg 2003. Deddens JA. Environ Sci Technol 2005. Thelin GP. Xenobiotica 1994. Camann DE. 2007. Biagini RE. Geological Survey (USGS).Herbicides References Battaglin WA. California. Hsiao JJ. March 2006. EPA 738R-95-006. Rose RL.gov/nawqa/ pnsp/pubs/wrir984245/text.248(2-3):115-122. sulfonamide. Barr DB. Environ Health Perspect 2000.39(17):6561-6574. 6/1/09 Whyatt RM. Hodgson E.S. Chem Res Toxicol 1998. Feng PCC. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Alavanja MC. Pesticides in U. Reregistration Eligibility Decision (RED) Metolachlor.php. Available at URL: http://water. Ward EM. Third National Report on Human Exposure to Environmental Chemicals. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. revised February 15. Shoemaker DA.pdf 3/30/09 Hines CJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.gov/nawqa/pnsp/pubs/files/051507. Coleman S. J Agri Food Chem 1989. Heederik D. 1998. et al. World Health Organization (WHO). Hein MJ.gov/oppsrrd1/ REDs/0001.usgs.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. usgs.pdf. Furlong ET. Background document for development of WHO Guidelines for Drinking-water Quality. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Available at URL: http://www. Casida JE. Gillion. Gilliom RJ). 2003. Occurrence of sulfonylurea. Sci Total Environ 2000. 1999. reservoirs and ground water in the Midwestern United States. Supplemental Technical Information (available on-line only). Geological Survey (USGS).S. Linderman R. 2005.15(6):500-508.248(2-3):123-133. U. Hladik ML. Brown KK.usgs.41:3409-3414. 98-4245 (by Barbash JE.111(5):749-756. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.

with an elimination half-life of approximately 19 hours (Arnold et al.5-T (Holson et al.5-T use as a herbicide in 1985. dizziness. headache. ranging from several weeks to many months. Nelson et al. Once absorbed into the body.4..5T is rapidly absorbed via oral and inhalation routes. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. hypotension.1.4. < LOD means less than the limit of detection.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.. 2. Agent Orange).5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.2 and 0. myotonia. 93-76-5 General Information 2. renal and hepatic injury.5-T was once applied as either an aqueous salt or as an oil-soluble ester.5-T is eliminated mostly unchanged in the urine.3.5-Trichlorophenoxyacetic Acid CAS No. Mohammad and St. 64 Fourth National Report on Human Exposure to Environmental Chemicals .7. it is not well absorbed through the skin. the general population is unlikely to be exposed to it. and delayed neuropathy (Bradberry et al.4.g. 2004). these herbicides can enhance plant growth.4.4. 2. 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. 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-T. and concern about contamination with 2.S. 2.. population from the National Health and Nutrition Examination Survey. Human health effects from 2. 1992). Survey Geometric mean (95% conf.4.4.4-D were used as defoliants in the Vietnam War (e. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.4. Epidemiological studies have reported associations of several types of cancer.5-T has been rarely detected in ground waters (USGS.Herbicides 2.. Kohli et al.4. nausea.. 1992.4..4. The half-life of 2. Omer. 1989.4.5-trichlorophenol and other degradates.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. 1974). see Data Analysis section) for Survey years 99-00 and 01-02 are 1. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.4. 1986.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. abdominal pain. Chlorophenoxy herbicides act as plant growth hormones.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4. Although 2.5-T in soil varies with conditions. Given the commercial unavailability of 2. which may vary for some chemicals by year and by individual sample. 2007). At low levels.5-Trichlorophenoxyacetic acid (2.5-T degrades to 2. Ester forms of 2.5-T and 2. but higher levels are herbicidal.4.

IOM.4.4. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of 2.4. similar to results of NHANES II (19761980).5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. IPCS..5-T does not mean that the level will result in an adverse health effect.5-T itself is not mutagenic.S. urinary levels of 2. 2003.4. 1980). Pearce and McLean. Biomonitoring Information Urinary levels of 2. Urinary 2. U.5-T also were below the limit of detection (Kutz et al. or to contaminants in the herbicide formulations (specifically 2.EPA at: http://www.gov/pesticides/.4. Mean urinary levels of 2. Biomonitoring studies on 2.epa. 2002. 1996.5-T were generally below the limit of detection. 2.5-T than levels found in the general population.7. 1992). other exposures.4.S. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. Survey Geometric mean (95% conf.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-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. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 2004).4.4. 2005. Additional information is available from U.Herbicides or contaminated herbicides.3.EPA.5-T reflect recent exposure.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. It is unclear whether these associations are related to the chlorophenoxy herbicides.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. in which urinary levels of 2.S.

Sheehan DM. Erne K.4. LaBorde JB. Available at URL: http:// www. Pesticides residues in food: 1996 evaluations Part II Toxicology. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Arch Int Pharmacodyn Ther 1974. Brody D.5-trichlorophenoxyacetic acid (2. Wolff GL. Review of 2. 2004.4. Gaines TB. Carter-Pokras OD.19(2):298-306.4. Agricultural exposures and non-Hodgkin’s lymphoma. Veterans and Agent Orange: update 2002. 914.31(2):121-125.4-. Centers for Disease Control and Prevention (CDC). Proudfoot AT. Toxicol Rev 2004. 210:250-255. S. Vale JA.2000 and 2001 market estimates. Washington (DC): National Academies Press. Multireplicated dose-response studies with technical and analytical grades of 2. McCallum WF.32(4):233-257. Sircar KP. Gaylor DW.4. Dichlorophenoxyacetic acid. International Programme on Chemical Safety-INCHEM (IPCS).org/documents/jmpr/jmpmono/v96pr04.S. et al. Kolmodin-Hedman B. Available at URL: http:// www. Bradberry SM. Vet Hum Toxicol 1989.Herbicides References Arnold EK. Washington (DC): U. Gaines TB. II.23(2):65-73. 2. Behavioral and developmental effects in rats following in utero exposure to 2.epa. Estimation of occupational exposure to phenoxy acids (2. Available at URL: http://www. Arch Toxicol Suppl 1980.31 Suppl 1:1825.5-trichlorophenoxy acetic acid in man. Office of Prevention Pesticides and Toxic Substances. Poisoning due to chlorophenoxy herbicides. Murphy RS. Garabrant DH.inchem.edu/catalog. J Toxicol Environ Health 1992. Kutz FW.5-T in four-way outcross mice. Tandon JS. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Philbert MA. Khanna RN.4-dichlorophenoxyacetic acid (2.5-T). Dhar MM.htm. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4-D/2. Environmental Protection Agency (U.37(2):277-91. U.EPA. McLean D. discussion 5-7. Nelson CJ. Holson JF. Scand J Work Environ Health 2005. 2003. Third National Report on Human Exposure to Environmental Chemicals. St Omer VE. general population. Fundam Appl Toxicol 1992. Developmental toxicity of 2. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Selected pesticide residues and metabolites in urine from a survey of the U. Developmental toxicity of 2.8(5):551-60.4-D and 2.19(2):286-297. I.4. Holson JF. Absorption and excretion of 2. Crit Rev Toxicol 2002.4. LaBorde JB. Board on Health Promotion and Disease Prevention. Fundam Appl Toxicol 1992.5-T).EPA).4:318-21. 3/17/09 Kohli JD.4-D) epidemiology and toxicology. 2005. Nelson CJ. Beasley VR. Pearce N.pdf.php?record_id=10603.S. et al. Cook BT.S. Gupta BN.4. 3/17/09 Institute of Medicine (IOM). Mohammad FK.nap.4.5-T). Neurobehav Toxicol Teratol 1986. Atlanta (GA).5-t mixture. Pesticide industry sales and usage .5-trichlorophenoxyacetic acid (2. May. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.

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

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

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

8 (9.124) .059 (.080-.9-38.110 (.5-15.8-25.2) 12.1) 14.3 (18.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.150 (.102 (.120 (.9 (14.5-17.1-24.180) .110) .070 (<LOD-.120-.0-25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.109 (.2) 14.7-19.0) 21.0 (11. see Data Analysis section) for survey years 01-02 and 03-04 are 10.130) .100 (.160 (.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.140) .147 (.138 (.1) 13.108-.090-.080) .055 (.6) 19.9-23.100-.6) 16.5 and 7.054-.090 (<LOD-.7 (<LOD-15.9 (12.110) .063-.064) 90th .070-.4) 19.110 (.90) 90th 15.077-.150 (.80-9. < LOD means less than the limit of detection.40-10.8.8) < LOD 8.4) 20.9 (13.062 (.062 (.086-.083-.1-18.088-.3 (19.109-. which may vary for some chemicals by year and by individual sample.056-.5-17.100-.0 (10.053 (<LOD-.070) .138) .30 (8.139 (.060) .2) 15.062-.112) 95th .242) .0 (15.075) < LOD .8-17.9 (12.4 (12.70 (7.090-.1) 15.110 (.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 .7-22.158) .8) 15.139 (.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .120 (.180) .170) .069) < LOD < LOD .9-22.30 (8.5) 21.117) < LOD .080 (.6 (14.096-.10 (<LOD-16.2) 11.8 (11. 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 .6-33.140-.7 (15.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.116) .1) 20.130-.113 (.6 (15.8-19.098 (.1) 10.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.073-.S.5 (16.130-.8 (18.1) 15.7 (14.6) 9.6 (15.120) .1-19.0 (10.4) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.3 (13.4-17.0) 19. 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.090-.084-.089 (.048 (<LOD-.0) < LOD 9.049-.00 (8.058) < LOD . Survey years 01-02 03-04 Geometric mean (95% conf.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .1-16.4) 95th 20.7) 15.103 (.4) 14.40-9.103 (.50 (8.130) .054-.054-.093) .1 (18.4) 539 456 484 487 980 885 Limits of detection (LOD.090 (.4 (12. which may vary for some chemicals by year and by individual sample.160 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .80 (<LOD-10.9 (13.130) .4) 21.S.2-15.60-10.5) 15.8-24.5 (<LOD-11.50) 15.109-.4-18. 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 9.110-.064 (.1) < LOD 9.140 (.120 (.101) .149) . population from the National Health and Nutrition Examination Survey.160) .3 (14.6-24.130-.100) .00-14.112-.80-10.3 (18.1 (13.077 (.0-21. Survey years 01-02 03-04 Geometric mean (95% conf.100-.130 (.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.190) .8) 14.190) .3-21.8-17.100) .5) 19.6-24.

Reprod Toxicol 2000. Edwards JW. either singly or in combination. Cancer Epidemiol Biomarkers Prev 2000. Grandjean P. 2 Classes of Pesticides.27:405-421. United States Geological Survey (USGS).gov/toxprofiles/ tp1. Chemosphere 2004. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.html.cdc. Shore RF. Organochlorine insecticides in substantia nigra in Parkinson’s disease.59:229-234.usgs. J Occup Environ Med 2005.fda. Finley B. 4/21/09 Hoyer AP. Teta MJ.html. PA. Environ Health Perspect 1995. Grajewski B. Psychopharmacology (Berl) 1987.inchem. Ellis H. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. International Programme on Chemical Safety (IPCS). References Agency for Toxic Substances and Disease Registry (ATSDR). Available at URL: http://www. David VL. Garrett N. Chlorinated Hydrocarbon Insecticides. 80 Fourth National Report on Human Exposure to Environmental Chemicals .103(Suppl 7):113-122. 2007 [online]. Sanchez-Ramos J. J Toxicol Environ Health 1989. Handbook of Pesticide Toxicology. Toxicological profile for aldrin/dieldrin [online]. No:429-436. Frey JM. Wienburg CL. 4/21/09 Jorgenson JL. Stehr-Green. Available at URL: http://pubs. Environmental Health Criteria 91.150:263-271. plasma dieldrin. Cox. and lymphocyte sister chromatid exchange. Demographic and seasonal influences on human serum pesticide residue levels. Available at URL: http://www.26:701-719. Part A 2000. Li AA. Olea N. Six high-priority organochlorine pesticides. Kitzazwa M. bioaccumulation. Needham LL. Schulte P. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. 1991. Chung KL. 15. Patterson DG Jr.org/documents/ehc/ ehc/ehc91.352:1816-1820. Aldrin and Dieldrin [online]. Finding a measurable amount of aldrin or dieldrin in serum does not mean that the level of aldrin or dieldrin causes an adverse health effect. 1992-2001. Academic Press. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Ginsburg KS. et al. Song S.64-65 Spec.atsdr.htm. Rosellini RA. Neurotoxicol 2005. Eds. In Hayes WJ. Daniel SE. Basit A. Food and Drug Administration (FDA). Inc.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). 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. Tully DB. Sonnenschein C.47:1059-1087.66(4):229-234.14:95-102. Environ Health Perspect 2001. Andersen A. Brock JW. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.cfsan. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Pesticides in the Nation’s Stream and Ground Water.gov/~dms/ pesrpts. Exp Neurol 1998. Mumtaz MM. VT.gov/ circ/2005/1291/. September 2002. Chapin RE. Toxicol Lett 1992. and epidemiology in the United States. McIntosh LJ. Soto AM. pp. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Patterson DG Jr. Int Arch Occup Environ Health 1994. Roy ML. Mann D. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Facca A. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Buckland SJ.9:1357-1367. Smith AG. 731-915. Fernandez MG. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. are nonestrogenic in transfected HeLa cells. Jr and Laws ER. Jr. Available at URL: http://www. 4/21/09 Bates MN. Organochlorine exposure and risk of breast cancer. Mink PJ. 6/1/09 Ward EM. Serrano FO. Revised Feb.91(1):122-126. Anantharam V. 1989. Lancet 1998.109(Supp1):113-139. August 2008. Jorgensen T. Vol. Kanthasamy AG. toxicology. New York.54:1431-1443. Priestly BG. Kanthasamy A. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Hartvig HB. J Toxicol Environ Health. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Turner W. Corrigan FM. Narahashi T. Carlson JN.

2 (39.9) 23.5-32.0-67. Fourth National Report on Human Exposure to Environmental Chemicals 81 .7 (32.7 (<LOD-32.3 (<LOD-19.9 (29. Technical grade chlordane had contained 7% trans-nonachlor.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.0) 27.9) 11.70 (<LOD-10. heptachlor use has been limited to treatment of fire ants near power transformers.3 (20. and 7.2) 37.1 (40.8) 27.4-40.8) 44.5 (<LOD-12.0) 41. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.5-47.3-45.7 (34. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.5 (41. Since 1992.S.7 (19.7 (34.1) 90th 34.8-33.3 (25.S.8 (17.5) 9.1-15.0-25.1 (15. the technical grade product of each chemical contains 10%-20% of the other chemical.2-21.8-31.2-26.6-53. Until 1988.7) 42.1) 30.7 (10.0 (37.2 (28.1) < LOD < LOD < LOD < LOD < LOD 8.9) 17.5-41.1 (<LOD-12.6 (16.0-12.8-32.0 (16.1) 22.6) < LOD 11.0-18.2-49.8) 52..6-12.10 (8.7) 9.1-25.6) 48.2-28. As a result of the manufacturing process.6-24.6-18. 1994.3-43.3 (26.30-11.9) 47.6) 36.8) 53.7) 31.0 (20.6) 49.7-56.7) 28.7 (17.6) 9.5 (33.2) < LOD 11.8-20.4-14. 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) 38.20 (<LOD-11.5-43. 10.9-21.5 (31. see Data Analysis section) for Survey years 99-00.8-33. Survey Geometric mean (95% conf.3-45.9 (36.9) 13.4 (<LOD-12. lawns. buildings.1-51.37 (8.6) 20. Chlordane is not currently produced or used in the U.1) 30. chlordane was used to kill termites and other insects on agricultural crops.5 (34.2) 46.S.8 (10. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.2) 33.2-49.6 (43. and 03-04 are 14.8-73.4-51.3 (27.9 (21.2 (21.1) 16.5) 44.5-44.5) 37.4) 18.1 (27.6) 39.9) 10.2) * 12.20-11.2 (41.2 (36.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.2-56. 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. Consequently.63 (8.3-32.9-21.9 (26.8 (10.6) 48.36-11.0-13.5.10-11.1) * 11.0) 37.9 (11. and dairy products are the usual sources of exposure to these chemicals in the general population.5.1-50. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.4) < LOD 11.6 (9.3) 18.5 (8.2) 22.3) 18.1 (44.4 (10.7) 19.Organochlorine Pesticides Chlordane CAS No.0) 21.3) 37. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.3) 10.5) 21.9) 23.7 (<LOD-13.7) 35. and in soil.5) 56. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.8 (42.6) 23.7-14.5) 10.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.4) 22.4) 37.3) 10.9 (15.3-49.9 (26.2) < LOD 11.5-40.5-42.4) 12.2) 34. from the early 1950’s until the mid-1980’s.4) 39.8) 52.0) 20.74 (<LOD-10.8 (18. population from the National Health and Nutrition Examination Survey.7-70.9-38.5) < LOD < LOD 9.1 (<LOD-12.4 (30.7) 19.0 (26.1 (20.8-23.1 (<LOD-12. 2007).1 (11. < LOD means less than the limit of detection.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.8) 18. in addition to trace amounts of numerous other related compounds (ATSDR.7-39.4-21.0 (32.5-13.2) 36.0) 75th 20.6) 8.20-10. 57-74-9 Heptachlor CAS No.4-45.2 (10.7-25.3-24. foods high in fat such as meat.89-10.1) * 11.0) 31.9) 11.1 (25.3 (11.1 (16.3) 41. 1994).7-12.4 (30.7 (42.9-42.8 (40.8-61.3 (9.9) 31.4) 29.9 (18.6) 11.4 (35.6-24.8 (17.9 (15.0 (<LOD-12.5-38.6-45.5-65.1-19.6 (25.1-65. 2007).2 (37.9) 37.0-61.9) 39.9 (17.9 (11.1 (17. 01-02.2 (9.90 (8.3 (28.69-10.6) 9.6 (9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-42.9-40.4 (22.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) < LOD < LOD < LOD 23.9) 36.10-18.8.1-25.3 (21.8-43. which may vary for some chemicals by year and by individual sample.4 (31.82-11.9 (31. fish.7 (43.0-33. respectively.5) < LOD < LOD < LOD < LOD 13.

200 (.220-. 2002.077) .136) .050 (<LOD-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.260 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.290-.130-.076) < LOD .340) . neonatal mortality.080) .320) .430) .058 (.070 (<LOD-.350 (. Takahashi et al.290-.189 (.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.068-.245-.069 (<LOD-.080) .189-.063) .056 (.270 (.064) < LOD . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.077) .063 (.250 (.320 (. The U.230-. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. and inhalation exposure.290) .310) .150 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. characterized by seizures and paralysis. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.115 (.190-.055-.053-.S. The major metabolite of heptachlor is heptachlor epoxide. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.126 (.110 (<LOD-.061-.300-..100 (<LOD-.350 (.360) .199-.180) .057 (.310) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.230-.073 (.290 (.079) < LOD < LOD < LOD .165-.090) .210-.066-.062) < LOD . 2007). Smith.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .108-.200-.130 (.071 (. IARC.070-. 2001.280-.140) .080) .300 (.065-.450) .100-.048-.050-.286 (.070) < LOD < LOD < LOD < LOD < LOD .510) .258-.270 (.092) . 2006).120-.280) . 1986).300) .112 (.240-.070 (.148) .070 (<LOD-.290-. Survey Geometric mean (95% conf.100-. Shindell and Ulrich.140-..070) .330 (. OSHA has established occupational exposure criteria.270 (.170) .170-.057) * .242-.170) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .070 (<LOD-.240) .287) . 1991). heptachlor.063) * .400) .230) .140-.300) .083 (.067 (.168-.160 (. Elimination of all these chemicals from the body occurs over months to years.063-.146) < LOD < LOD .320 (.207) .269 (. 1996.260-.104) . and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.140 (.130) .130-.400) .160) .090-.370 (.126) .100 (.410) .220 (. 2007.200-.280 (.150-.060 (<LOD-.320 (.091) .160) .130-. 1991.331) 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 * * * * .280-.290) . dermal. population from the National Health and Nutrition Examination Survey.130 (. and alterations in immune function of offspring.302) .560) . FDA established allowable residues of chlordane.220-.210 (.180-.063 (.315 (.146) .300) .S.120 (.077) .047 (<LOD-. Acute. chronic doses of heptachlor have produced liver enlargement and injury.150 (.231) .150) .058-.213) * .068) 75th . and the U.083) .130-.180-. EPA has established environmental criteria for chlordane and heptachlor.230 (. In laboratory animal studies.070-.087-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.057-.079) . which is also persistent in the body (ATSDR.150 (.230 (.073) < LOD < LOD < LOD < LOD .110-.450) .130) .170) . 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.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . 1977b.130 (.440) .070 (<LOD-.246-. to heptachlor.240 (..190-.260 (. 1977a. and breast milk is a major excretion route in lactating women.370 (.082 (..149 (.253-.216-.180) .119 (.160) . Rogan.058-.300) . which may vary for some chemicals by year and by individual sample.271 (.250-.066 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .225 (.320) .227) < LOD .115-.077) .106-.240-.260 (.140 (.080 (.280 (.049 (<LOD-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.066-.S.120-.068) .070-.280-.080 (.207 (.128 (.120-.170) .373) .203-.223) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .075 (.170) .Organochlorine Pesticides (Dallaire et al. Chlordane and heptachlor are absorbed after oral.380) . 1981).350) .074-.210 (.200-.133) 90th . 1986).310 (.286 (.258 (. Le Marchand et al.320 (.104-.063 (.230-. and heptachlor epoxide in foods and bottled water.340) .208 (.140 (.090) .130-.370 (.148-.310-.250 (.066 (<LOD-.053-.140 (.190-.204 (.063 (.348) .430) .310) .

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

5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Survey Geometric mean (95% conf.0 (15.7-25.2 (18.5 (<LOD-32.8) 14.5) 19.4 (11. 01-02.8) 21.8-46.9-29.2 (<LOD-62.9-25.3) 22. 10.8-24.8.3) 18.7 (16.6 (14.7-19.0) 13.8) 19.3 (<LOD-25.2 (<LOD-16.8) 13.9) 15.4 (15.3-18.4 (11.3) 23.2-16. see Data Analysis section) for Survey years 99-00.6.0-19.5.6 (12.7 (10.8 (13.8-24.2) 15.1 (16.6) 14.7 (13.6 (<LOD-27.1) 23.5 (11.0-54.2-17.8) 15. respectively.5 (<LOD-21.9 (12.7-18.3) 18.8) 16.2) 20.50) < LOD < LOD < LOD 17.6-21.9 (15.8 (18.6 (16.9-29.3) 18.5 (10.5 (18. and 7.2) 26.0-17.6) 13.0-17.6 (11.9-16.8 (<LOD-23.1 (19.8 (15. population from the National Health and Nutrition Examination Survey.4) 21.6-17.2-27.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6 (16.4 (<LOD-19.8-24.3) 10.5 (11.1) 20. 84 Fourth National Report on Human Exposure to Environmental Chemicals .0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.8 (18.8) 14.1-38.1-29.2 (<LOD-25. and 03-04 are 14.2-27.90 (<LOD-9.2) 13.9-23.3) 16.6) < LOD < LOD < LOD 27. which may vary for some chemicals by year and by individual sample.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.4) 18.8) 20.S.4 (<LOD-54.0 (11.1-15.20 (<LOD-9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 27.8-23.1) 13.6) 22.6 (13.0-16.5) < LOD 14.3 (13.5) 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 7.40) 15.6 (8.8) 13.1-16.9) * * * 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 8.8) 19.8 (13.10-13. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24. < LOD means less than the limit of detection.

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

5) 36. respectively.4) 19.5 (44.9-36.0) 13.3) 18.5) 20.3) 16.8 (17.3) 18.8 (26.9-20.5-17.7-20.7) 52.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.8-19.7) 35.2) 59.1-20.0 (13. and 03-04 are 14.5) 48.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.3 (49.7 (59.5) 14.0 (60.2 (26.6) 60.4) 55.2) 30.3) 15.9-69.8 (15.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.1 (22. see Data Analysis section) for Survey years 99-00.8 (42.0 (29.7) 73.0 (19.1-55.9-40.4 (30.2) 34.5-87.4) 16.0 (14.3) 19.2-21.8) 80.2 (14.9-22.6 (<LOD-14.1) 17.7-35.0 (42.5-95.6) 56.S.8 (28.6) 34.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.1 (65.4 (16.2-23.7) 59.1 (41. Survey Geometric mean (95% conf.5-19.3 (58.5) 14.6 (57.1 (17. and 7.1-22.7) 15.8 (13.6-82.4-62.0-24.5-69.9-65.9 (15.1) 17.8 (16.9 (29.2) < LOD 10.4-18.3) 32.0 (15.1-34.1) 17.2) 20.6) 54.8) 47.5) 26.9 (51.6-19.0-20.4) 48.7 (13.0 (16.1) 78.5) 22.2 (64.6-22.5) 9.0-22.5) 30.8 (45.0) 19.8 (13.3) 32.8-16.8 (12.70 (<LOD-12.2 (19.8 (71.4 (11. interval) 18.4 (67.9) 14.8 (26.7) 78.6 (52.1 (47.6-88.1-51.4) 20.9 (19.3-50.0-68.7-17.3) 30.1-34.9) 14.1) 17.7-32.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.2 (60.5) 78.1-28.3 (14.9-89.4-52.0-93.6) 10.8-21.0 (62.4-35.1) 30.8-90.8-16.8 (11.6 (15.0) 33.1) 62. 01-02.0) 18.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.6 (56.5-20.7) 28.0-93.9-58.7) 56.2-18.2-17.1 (10.7) 14.2-16.9-35.8-67.2 (14.1) 17.3 (45.8-110) 59.9 (<LOD-14.2-88.7 (18.0-59.6) 84.4-23.7-38.3) 25.5 (13.0 (42.5-36.0-123) 74.1 (48.8-19.1) 32.7) 17.8-90.2 (25.3 (17.4 (28.9 (15.0) 49. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (<LOD-11.7 (16.1) 17.9 (16.0) 75th 31.6) 13.2 (59.7-34.3-57.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.5-111) 68.7-18.1-18.5) 77.8 (<LOD-20. population from the National Health and Nutrition Examination Survey.3-39.5 (15.8) 51.2 (7.0) < LOD < LOD 8.6-66.7-23.1) 18.0 (16.9-65.1-16.9 (47.2-37.1) 14.3) 36.7 (11.0 (48.7 (35.7 (28.2 (36.1) 16.7 (30.4 (12.0-143) 112 (68.4 (45.9) 51.3 (16.9 (51.0) 40.5 (45.6 (50. which may vary for some chemicals by year and by individual sample.0-38.3) 30.8 (26.6 (16.6) 82.7-160) 86.5 (25.5) 35.5) 19.6 (32.6) 25.2 (15.86-13.8-79.1) 78.8 (28.1) 17.6) 56.3-58.9 (28.7-22.3 (56.5.7-29.8.7 (59.7-21.9-45.2-18.6 (12.6 (56.5) 90th 55.2) 17.3-21.0-23.8 (49.1-126) 67.2 (27.7-77.0-113) 68.5 (15.1) 18.8-77. < LOD means less than the limit of detection.2) 19.4-22.7 (74.8-41. 10.8 (28.8 (19.9 (66.8-129) 74.6-20.6-54.0-23.0 (13.3-86.7) 78.8 (30.4-36.8) 19.3-74.0-37.9 (36.3-30.3 (14.4) 59.7-113) 68.0 (15.1-16.9) < LOD < LOD < LOD 20.2) 39.4-67.4) 107 (84.9-64. 86 Fourth National Report on Human Exposure to Environmental Chemicals .3-32.9) 51.5.1) 31.

279-.640 (.630) .092 (.100 (.130 (.220 (.286-.093-.490) .089 (.054-.078 (.080-.684) .237) .288-.220 (.370 (.520 (.047-.094 (.210-.069-.120) .320-.060-.470-.210 (.173-.109 (.130) .120 (.580 (.079-.161) .210-.160-.210) .600) .400) .370 (.120) .371) .460-.340) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .232) .112 (.100-.071 (<LOD-.461 (.110 (.280) .520) .320-.290-.285-.128 (.090-.120 (.108) .090 (<LOD-.430-.106 (.250) .240 (.240) .080-.104-.130) .930) .420 (.310-.390) .690) .690) .250) .141) .090-.109 (.340-.220 (.400-.108 (.343 (.220 (.520 (.098 (.098) .450) .630) .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.110 (.380 (.100-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .580 (.085-.069) .106 (.110 (.430-.180-.405) .080 (.350-.630) .230 (.122) .090-.800) .158-.103 (.210) .090 (.190-.116 (.080-.960) .190-.130) .120-.096-.105 (.250) .680) .355 (. population from the National Health and Nutrition Examination Survey.301-.127) < LOD < LOD .440) .310-.081-.330-.260) .460) .410-1.210 (.360-.330 (.124) .420) .680 (.220 (.324 (.186 (.210) .090-.104 (.079-.106 (.120) .078-.237) .490 (.186-.130 (.150) .170 (.190-.131) .550 (.100-.119) Selected percentiles ( 95% confidence interval) Sample 95th .400 (.220 (. Survey Geometric mean (95% conf.110 (.409-.126) .060 (<LOD-.830) .190-.240-.108) 75th .177-.497-.097) .210 (.234) .120 (.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 . Fourth National Report on Human Exposure to Environmental Chemicals 87 .190-.20) .084-.500) .340-.651) .310-.099-.594) .360-.100-.098 (.300-.125) .600 (.090-.390 (.202 (.330-.114) .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.350 (.110 (.191 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .111 (.119) < LOD < LOD < LOD .470 (.055 (<LOD-.220 (.310 (.120-.414 (.395-.573 (.129) .367) .180-.091) .100 (.470 (.317 (.145-.093-.130) .205 (.480) .590) .110-.300) .565) .068-.559) . interval) .390 (.085-.310) .103 (.390 (.410-.160 (.183 (.440-.490-.242) .113) .080) .390 (.130) .116) .510-. which may vary for some chemicals by year and by individual sample.060) .430-.098-.288 (.395) .760 (.540) .090) .111-.110) .240) .400 (.327 (.190-.120-.470-.130) .310-.400-.117) .220) .096-.390-.110 (.082) .490 (.095-.260) .180-.510 (.112 (.590 (.061-.093) .417 (.171-.S.092 (.458 (.081 (.240) .150) .580 (.840) .120) .397-.130) .211) 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.134) .220 (.062 (.041 (<LOD-.096) .272-.085-.091-.080-.125 (.830) .113) < LOD .140) .090-.470 (.161-.116-.070 (.270-.087 (.093-.141) .390) .122) .460) .135 (.099-.590 (.

Chlordane and heptachlor [online].259(3):374-377. Odland JO. Keller JA. Head SL. et al. Laliberte C.28:497501.htm. 2006. Wohlleb JC. Voorspoels S. Smith AG. Toxicological profile for heptachlor and heptachlor epoxide [online].110:617-624.372:20-31. Canada).8:1-123. 1963-1967. Mortality of workers employed in the manufacture of chlordane: an update. KalubaSkotarczak A. JAMA 1988. Gilman A. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Glynn AW.htm. Bioassay of heptachlor for possible carcinogenicity.html. Shindell S and Ulrich S.cdc. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Sci Tot Environ 2006. Distribution of polychlorinated biphenyls. Kolonel LN.pdf.heptachlor. Van Oostdam JC. Vol. Takei G.atsdr. Aune M.330:55-70. 4/21/09 Baker DB.pdf. Wong L. Organochlorines in Swedish women: determinants of serum concentrations. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Poland. Hansen JC. Academic Press. International Agency for Research on Cancer (IARC) .50(3):108-118. Baker DB.84:151-161. Available at URL: http://www. Dendle WH. Lulek J.html. Organochlorine exposures and breast cancer risk in New York City women. Vol. 2 Classes of Pesticides. Inc. 1994-1997 organochlorine compounds. Available at URL: http://www. Barker J. Available at URL: http://ntp. Granath F.org/ documents/cicads/cicads/cicad70. Toxicological profile for chlordane [online]. 4/21/09 James RA. Senie R.cdc. gov/toxprofiles/tp12.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Siegel BZ.Summaries & Evaluations. LeMarchand L. National Toxicology Program (NTP). Pollutants in breast milk. Environ Health Perspect 2003. Bull Environ Contam Toxicol 1981:27:506-511. Atuma S. Jr and Laws ER.41:145–148. Bleiweiss IJ.niehs. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Organochloride pesticide residues in human milk in Hawaii. Dewailly E. Stehr-Green P. Loo S.gov/ntp/ htdocs/LT_rpts/tr008. Ayotte P.atsdr.nih. May 1994.nih. Drews K. 731-915. 6/1/09 National Toxicology Program (NTP). 1993. Handbook of Pesticide Toxicology. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. et al. Available at URL: http://www. maternal serum and milk from Wielkopolska region. 2001. Available at URL: http://www.inchem. et al. Environ Res 2000. New York. Brower S. J Occup Med 1986. Available at URL: http://ntp. Lawrence River (Quebec. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. 6/1/09 Rogan WJ. Charles MJ. Circumpolar maternal blood contaminant survey. et al. 88 Fourth National Report on Human Exposure to Environmental Chemicals . 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Muckle G.150:981-990. Takahashi W. Tartter P.niehs.inchem.html. Arch Pediatr Adolesc Med 1996. Sci Total Environ 2004. Environ Health Perspect 2002. Concise International Chemical Assessment Document 70 Heptachlor [online]. A Report to the Hawaii Heptachlor Research and Education Foundation. 4/21/09 Dallaire F. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Chashchin V. 1991 pp. Royce W.111:349355.gov/toxprofiles/tp31. Darnerud PO. Covaci A. 1986.org/site/foundation/ research/projects2. Dewailly E. International Agency for Research on Cancer (IARC). In Hayes WJ. Hawaii Med J 1991. Bjerselius R. August 2007.gov/ntp/ htdocs/LT_rpts/tr009.9:1-109. Saidein D. Jaraczewska K. Berkowitz GS. 1979-1980.org/documents/iarc/ vol79/79-12. Eds. Wolff MS. Environ Health Perspect 2002. 9/25/07 International Programme in Chemical Safety (IPCS). Available at URL: http://www. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Hertz-Picciotto I. Bioassay of chlordane for possible carcinogenicity. Chlorinated Hydrocarbon Insecticides.110(8):835-838. 79. Jr. Arch Environ Health. Willman E.

interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.6 (9. including 1. 2008.8) 15.8. air.0-35.1-27.7) 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. although DDT and DDE intakes have decreased over time (FDA.1’-(2. 1991).p’-DDT (65%-80%). The biodegradation half-life of DDT in soil varies from 2 to 15 years. DDT and DDE can cross the placenta. which is a mixture containing p. It was produced and used in the U.0) 26.6 (31.7 (19.1) 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 12.3-16.0 (18. Both Serum p.p’-DDD (4% or less).8) 30. 01-02.3) 21.5) 25. after World War II until 1972.8-39. 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. inhalation. Smith. DDT can be absorbed after ingestion.9) 29.2 (<LOD-40. and trace amounts of several related compounds.3) 22.9 (<LOD-20. DDT is converted to DDE and several other metabolites.3-236) 24.4) < LOD < LOD < LOD 61.4. It is still used in some countries.3-590) 293 (104-541) 48.4 (23.0) 19.5 (23.0 (18. and water. when virtually all use of it was banned.9 (10.2-bis(p-chlorophenyl) ethane (DDD).p’-DDT (15%-21%). population from the National Health and Nutrition Examination Survey.7.5-36. DDT usually refers to the technical product. Gunderson.3 (27. Food imported from countries that still use DDT may contain the chemical or its residues.2) < LOD < LOD 9.9 (10.7) 12. particularly for endemic vector and malaria control.9-34.1 (33.7 (15.0 (21.S.3 (<LOD-31. fish.50-11.6 (<LOD-25. o.7) < LOD 18. In the general U. and 7.0-15. as well as in plant and animal tissues.8-26.3 (<LOD-21.00 (<LOD-10.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. 1988). DDT was used at one time as a treatment for head and body lice. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.9) 17. respectively.2) 155 (59.0 (10.9) 14. Fourth National Report on Human Exposure to Environmental Chemicals 89 .5 (14. and dairy products.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70 (8.2) 30.6 (25.0-27. Survey Geometric mean (95% conf.10-13.2-95. or dermal exposure.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.9 (21.2-65.2 (11.0) 20. These chemicals are highly persistent in soil. p.90 (<LOD-12.3) 21. In the body.8-17.0) 40.1) 31. < LOD means less than the limit of detection.9) < LOD < LOD 9.5-54. particularly meat. population. DDT is converted in the environment to other more stable chemical forms.1’-dichloro-(2.S.9 (10.0-155) 83.1 (23.S. food. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 28.5 (23.9-28.6 (22. 17. 1991).0-53.1 (<LOD-39. resulting in fetal exposure. see Data Analysis section) for Survey years 99-00.5) < LOD < LOD 9. Only a small proportion of DDT is metabolized and excreted (Smith.5) 23.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.1-71.0-37.7-16. continues to be the primary source of DDT exposure. which may vary for some chemicals by year and by individual sample. sediments.6-33. and 03-04 are 20.8-23.5 (15. 2002.8) 36.8) 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. depending on conditions.10 (<LOD-12.4) < LOD 17.

061) < LOD < LOD < LOD .400 (.078 (.064 (.62 (.180) .075) 1. Calle et al.150-. Jusko et al.098-. 2004.220) .140) . 2006. Hayes et al.420) .240 (.170) .142 (.112 (.207) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .160-. overt signs of acute human toxicity include vomiting. A workplace standard for DDT has been established by Serum p.. and duration of lactation.00) .00 (. 2002.114-.095) < LOD . 2002. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 2006.069) .143) < LOD < LOD .570-4. Survey Geometric mean (95% conf. 1998). 2001). population from the National Health and Nutrition Examination Survey.128 (. reproductive organ abnormalities.087 (.150) .230) . In high dose. 1956).130 (<LOD-.01) .343) < LOD . Snedeker.200 (.150 (<LOD-. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th .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 . and seizures.146 (.054-.080-. dioxins and furans).130-.146 (....140-. premature delivery. 2002.059-.190-1. polychlorinated biphenyls.170 (.313 (.203) .. 2006. and leukemia have also been inconclusive (ADSDR.086 (.120 (<LOD-. Animal studies reported reduced fertility.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 .180 (. 2006). other organochlorines. Gray et al.250 (. In laboratory animals.290) . lung cancer.074-. 1995.078-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.084 (.170-.079) < LOD < LOD .. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. Studies of DDT exposure and pancreatic cancer.190 (.. Jusko et al..063 (<LOD-.530 (.627) .051 (<LOD-.240) .132-. 1997). tremor. 2006).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.Organochlorine Pesticides chemicals are excreted in breast milk. 2001). which may vary for some chemicals by year and by individual sample.130 (<LOD-.530) .120-.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .p’-DDE can produce anti-androgenic effects (Gray et al. 90 Fourth National Report on Human Exposure to Environmental Chemicals .130 (<LOD-.180 (..048 (<LOD-. Beard. 1996).180) . Gladen and Rogan.190 (.. have not been consistently demonstrated (Beard.180-.p’-DDD and p. accidental exposures.230) .150 (<LOD-.106) < LOD < LOD .260) . Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. resulting in exposure to nursing infants (Rogan. DDT may bind to estrogen receptors (Chen et al. and altered behavior after neonatal exposure (Eriksson and Talts.S. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.068-. Reproductive effects in humans affecting birth weight.150-.201 (.250-1.330-4.071-. 2001).220) .34) . 2001).108 (..106) .189-.400) .071 (. 2000. 2002.065-.106-. Mariussen and Fonnum. 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. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.g.26) 1.107) 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. 2006). Longnecker et al.105-. fertility. and o.

. Fourth National Report on Human Exposure to Environmental Chemicals 91 . 2002. environmental levels) and health effects is available from the U... EPA at: http://www. 2005).S.6. 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. population declined by about fivefold to tenfold.p’-DDT) as a possible human carcinogen. 2003).html. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.8. population from the National Health and Nutrition Examination Survey. IARC classifies DDT (p. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. see Data Analysis section) for Survey years 99-00. Stehr-Green. respectively.. 2002.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.. NTP considers DDT as being reasonably anticipated to be a human carcinogen.gov/ pestcides/ and from ATSDR at: http://www. Compared to females in the NHANES 1999-2000 subsample.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.3. 1998. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.epa. Biomonitoring Information DDE persists in the body longer than DDT. and 03-04 are 18. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. Smith. 1989). Link et al. 2004)..S.Organochlorine Pesticides OSHA and a guidance established by ACGIH. compared to levels observed in this Report (Anderson et al.0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD.6 (81. In general. 01-02. 1991). Declining DDE levels over time have also been observed in the German population. 8. Since the 1970’s. for males and females in the NHANES 19992000 subsample (Pavuk et al. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. In a population-based sample of men and women from eastern Slovakia. Heudorf et al.atsdr. 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. and 7. respectively.. More information about external exposure (i..gov/ toxpro2.e. 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. Survey Geometric mean (95% conf. mean serum levels of DDT and DDE in the U. 2003.7-119) 113 (100-140) 93. 2004).cdc.

04 (6.2-32.96) .00 (.4) 14.43 (5.69 (2.65 (1.30-1.07 (5.5) 5.02 (2.2 (9.10) 2.0) 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 .91-3.6 (17.557) 1.9-38.37 (1.7) 13.6) 9.25) 8.85-4.52-6.81-18.63 (6.92) 1.7) 16.54 (1.1) 40.31 (1.6) 9.90) 22.36-2. 2004).84-3. 2005).23 (7.9) 7.6) 13.17-3.40-4.419-.45 (1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.81) 11.456 (.796 (.41 (1.64-2.6 (9.22-1.55 (2.59) 6.58) 75th 3.54) 8.7 (8.2 (9.06) 1.49 (1.40-4.07) 1.49) 8.61 (1. considerably higher than levels in this Report (Smith.14) 2.57 (3.24 (1.11-1.25-14.623 (.63-15. 1989).32-1.4) 13.5) 22.430-.27-1.1) 12.56-2.11 (2. 309 versus 268 ng/g lipid.0 (9.27) 3.12-1.45 (1.9 (15.10-5.37-16.75 (8.01-15.40 (3.1) 7. or p.51 (1.07) 1.79) 4.6) 9.97-4.p’-DDT were below the limits of detection.19) 4.44) 1..69 (.71 (6.56-6.63 (1.49 (6. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.26 (1.48 (6.53-15.60-13.8 (13.36-1.22) .561 (.39) 1.85 (1.0 (12. 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.17 (3.32 (1.71 (5.516 (.16 (2.52 (1.25-16.82) 1.26-2.48-4.37-1.34-3.730) .51) 3.02) 1.860 ng/L) and DDE (about 14.84 (3.58) 1.32-1.5) 7.6 (8.p’-DDT (Stehr-Green.69 (1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.66) 3.646) .13) 4.83 (1.93 (7. In the NHANES 1999-2000.43-4.6) 12.40-8.6) 11. High mean levels of whole blood DDT (about 3. 2004).64) 3.37-4.47 (1.96) 1.520 (.4-19.18 (6.72) 1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.25 (.7-20.3) 13.53) 1.9-17.36 (3.41-12.534-.39 (3.68) 2.76) 1.34-11. 1971).56-3.5) 16.76-3.87 (5..71) 12.9 (26.4 (12.25) 1.80) 3.35) 1.14-9.21) 90th 7.09-1.Organochlorine Pesticides nearby agriculture (Botella et al.16-1.46-2.75) 6.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.3) 10.13 (1.00-1.8 (9.59) 3. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.59 (1.8) 15.72) 1.69) 4.90-8.24-17. 1991).66) 1.611-1.00 (6.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.3 (9.12 (.51-15.81 (1.66-4.7-19.18-4.99) 1.21) 3.8 (13. population from the National Health and Nutrition Examination Survey.32 (1. less than one percent had detectable serum levels of o.46 (1.53 (2.13-2.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.65) 1.68-4. 2001-2002 and 2003-2004 subsamples.57 (1.32-9.50-17.18-1.S.15-4.12 (6.91) 3.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.0) 2.57) 2.81-5.59 (1.2) 26.75) 1.965-1.66) 4.91-2.385-.76 (2.46 (1.92 (3.39-2. In a subsample of NHANES II (19761980) participants.590 (. Serum p.54-7.18-3.80) 1.92 (3.39-1.03-1.8 (14.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .14) 2.01-11.68 (2.30 (1.7) 9.3-43.38 (1.56) 2. Survey Geometric mean (95% conf.53) 7.26-10.57-13.1 (8.24) 1.75 (4.66-17.32) 1.28) 1.9) 5.26) 3.55-9.02-8.p’-DDT.6) 8.57-2.2) 19.75) 2.06) 3.76) 1.43-4.05) 1..85-10.01-5. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.36) 3.62-6.61-2.22 (7.82 (1.34) 6.71) 32.88-35.58) 1.01-11. interval) 1.4 (8.6) 9.31-2.01-1.91 (6.57 (1.3 (8.80) 1.70-3.51-49.30-1..1 (9.994-2. Finding a measurable amount of p.820-1.18) 1.18-1.34) 2.4) 9.03-4.5) 10.7-48.14 (1. serum levels of o.8-90.66) 1.870 (.66-2.680-1.59 (4.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.87-16.51) 1.2 (6.3) 16.890-1.2 (19.05 (3.01) 1.01) 1.38 (1.49 (1.30 (1.01-1.88 (2.80 (2.29 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.52 (3.31-12.10) .81 (7.78 (4.10-1.600) .14-1.37-10.00) 7.25 (1.635) 1.77 (1.97 (3.726) .69) 8.51-8.77 (1.33-1.20 (.34 (7.70) 1. o.63 (1.19-14.50 (2.36-11.04-1.47) 3.43-8.p’-DDT.6 (7.57-3.488-.500-.963-1.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 03-04 are 20.7. 01-02. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00.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. 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.4. 17. and 7. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 93 . < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.S.8. respectively.Organochlorine Pesticides Serum o.

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

Bloom MS. Klebanoff MA. Vorojeikina DP. Wolf CJ. and DDD [online]. J Assoc Off Anal Chem 1988. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Olea-Serrano MF. Beard J. Schulz C. Am J Epidemiol 2002. The Great Lakes Consortium.358:110-114. Environ Health Perspect 2003. et al. Needham LL. Falk C. Hayes WJ. Longnecker MP. India. Baker RJ. Hanrahan L. et al. Crespo J. Glynn AW. Piechotowski I.96:34-40. CA Cancer J Clin 2002. 4/21/09 Gladen BC. Becker K.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).205:297-308. Longnecker MP. Hediger ML. Seiwert M. Brock JW. Jusko TA. Rivas A. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Durham WF. Environ Res 2005. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Charles MJ.355:7889. Zaidi SS. Chen CW. HCH. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Cerrillo I.cfsan.21(1-2)37-48. Calle EE. Furr J. DDT and human health. Lepom P. Arnold SF.atsdr.112(17):1761-1767. Krause C. JAMA 1956. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Davis MD. Available at URL: http://www. Klebanoff MA.17(6):692-700..1-dichloro2. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.71(6):1200-1209.fda. Moysich KB.162:890-897. Swanson MK. Hum Reprod Updat 2001. Vena JE. Organochlorines in Swedish women: determinants of serum concentrations. Gabrio T. Olea N. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.53(8):1161-1172. Ostby J. DDE and shortened duration of lactation in a northern Mexican town. Zhou H. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Garrett N. lindane (g-HCH). Needham LL. April 1982 to 1984.html. Zhou H. et al. dietary intakes of pesticides. Effects of environmental antiandrogens on reproductive development in experimental animals. Heudorf U. Lambright C. Patterson DG Jr. hypospadias. Chemosphere 2004. Levels of DDT.cdc. and other chemicals. Needham LL.106(5):279-289. and HCB residues in human blood in Ahmedabad.155(4):313-322. Drexler H. Talts U. Rogan WJ. Bhatnagar VK. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Gray KA. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Paepke O. Angerer J. Cueto C.gov/ toxprofiles/tp35. Int J Hyg Environ Health 2003. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Notides AC. August 2008. Koepsell TD. Jr. Gray LE Jr.7(3):248-264. dichlorodiphenyldichloroethylene. Kulkarni PK. Profiles of ortho-polychlorinated biphenyl congeners. Brock JW. Klebanoff MA. Zoellner I. Lancet 2001. Hurd C.85:504508. Exposure of women to organochlorine pesticides in Southern Spain. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Gunderson EL. Eriksson P. Aune M. Jr. Available at URL: http://www. Burse VW. Neurotoxicol 2000. Organochlorines and breast cancer risk. Environ Health Perspect 1998. Maternal DDT exposures in relation to fetal and 5-year growth. September 2002. Darnerud PO. et al.111:349355. Olson JR. Chemosphere 2005. et al. Bull Environ Contam Toxicol 2004. Toxicological profile for DDT. Kashyap R. Biochem Pharmacol 1997. Link B. Thun MJ. DDE. Bates MN.58:1185-1201. Gladen BC.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Katz SH. Int J Hyg Environ Health 2002. Maternal serum level of 1. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Olson J. and polythelia among male offspring. Parks L. Sci Tot Environ 2006. Willman EJ.54:1431-1443. et al. hexachlorobenzene.html. Am J Public Health 1995. Saiyed HN. Food and Drug Administration (FDA).52:301-309. Biomonitoring of persistent organochlorine pesticides. Barr DB. Bjerselius R. Frumkin H. et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Botella B. Environ Res 2004. Herrman T. Kaus S.gov/~dms/ pesrpts. Granath F.206:485-491. Greenfield TA. Epidemiology 2006. Henley SJ.97(2):178192.72:261265. 4/21/09 Anderson HA. and dichloro(diphenyl)ethylene (DDE). et al. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Savitz DA. selected elements. FDA total diet study. Ellis H. Environ Health Perspect 2004. Buckland SJ. Atuma S.

Handbook of Pesticide Toxicology. Fonnum F. Astolfi E. Chemosphere 2004. DDE.27:405-421. PA. Jr and Laws ER. Pollutants in breast milk. Nims R. Chlorinated Hydrocarbon Insecticides.Organochlorine Pesticides Mariussen E. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Environ Health Perspect 2001. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Comparative pharmacodynamics of CYP2B induction by DDT. Demographic and seasonal influences on human serum pesticide residue levels. Petrik J. Lubet R. 2 Classes of Pesticides. 731-915. Eds. Lynch CF. Radomski JL. In Hayes WJ. children and newborn infants. Snedeker SM. Jones CR. Pesticides and breast cancer risk: a review of DDT. 96 Fourth National Report on Human Exposure to Environmental Chemicals . and DDD in male rat liver and cultured rat hepatocytes. Schecter A. Fox S. Academic Press. Vol.150:981-990. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Inc. and dieldrin. Jr. Arch Pediatr Adolesc Med 1996. Crit Rev Toxicol 2006.53:455-477.36:253-589. Reddy AB. Cerhan JR.20(2):186-193. Thomas PE.54:1509-520. Rey AA. New York. 1991 pp. Stehr-Green. Deichmann WB. et al. Smith AG. J Toxicol Environ Health 1989. J Toxicol Environ Health Part A 1998. Pavuk M. Chovancova J. et al. DDE.109:35-47. Toxicol Appl Pharmacol 1971. Rogan WJ.

endrin is converted rapidly to its major metabolite. 1992).Organochlorine Pesticides Endrin CAS No.09 and 7. unlike aldrin and dieldrin. At high doses. Kavlock et al. is no longer manufactured in the U. Fourth National Report on Human Exposure to Environmental Chemicals 97 . In the body. endrin usually is not detected in serum of exposed individuals. unless the dose is high and the exposure is very recent. manufactured. 1992). Depending on soil conditions. EPA.30 (<LOD-6. rodenticide and avicide. inhalation or dermal exposure routes.S.40-5. fatty infiltration. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.10 (<LOD-5. IPCS. 1981). High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Smith.. population from the National Health and Nutrition Examination Survey. and occasionally at low levels in sediment and surface waters. Endrin was used as an insecticide. 1987).10 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. have been cancelled by the U. which may vary for some chemicals by year and by individual sample. 1992. 2008). Ketoendrin is a major photodegradation product (IPCS. Because it is metabolized so rapidly. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. 1996.S.50) < LOD < LOD < LOD 5.S. Endrin is absorbed rapidly after ingestion.S.20 (<LOD-5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.40) < 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. An epidemic of acute endrin poisoning. endrin has been detected with declining frequency in U. 1992). Endrin has been detected in soils. a stereoisomer of dieldrin. endrin can persist for years.. < LOD means less than the limit of detection. Endrin does not accumulate in body tissues (IPCS. 72-20-8 General Information Endrin.30) < LOD 5.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.40 (<LOD-6.S. All uses of the pesticide in the U.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. 1991). Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or from contact with contaminated soils and sediments in areas where endrin was applied. 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 inflammation (Smith.20 (<LOD-5. Endrin was not widely used as a termiticide. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. Over time.. anti-12hydroxyendrin..50) < LOD 5. Survey Geometric mean (95% conf.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 5.60 (5. total diet surveys (FDA. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Hepatic effects of endrin exposure have included necrosis. 1979. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. 1991). or discarded.

interval) Selected percentiles ( 95% confidence interval) Sample 95th . IARC has determined that endrin is not classifiable with regard to human carcinogenicity.24 ng/g of serum) (Botella et al.. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. which may vary for some chemicals by year and by individual sample..020-.S. Survey Geometric mean (95% conf. with the highest value 6.24 ng/mL (about 6. population from the National Health and Nutrition Examination Survey.html.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020) < LOD .. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.020 (<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-.020) < LOD < LOD < LOD .020 (<LOD-. 2004.020 (<LOD-. Information about external exposure (i. serum levels of endrin were below the limit of detection. This finding is consistent with other general population studies (Bates et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2000). environmental levels) and health effects of endrin is available from ATSDR at: http://www. Ward et al.gov/toxpro2. and the FDA monitors foods for pesticide residues.020 (<LOD-.S.020) < LOD . Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. In a small study of Spanish women hospitalized for elective surgery.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 .020 (. EPA has established environmental standards for endrin.cdc.020) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. 2004). endrin was detected in 9% of serum samples.atsdr.020 (<LOD-.020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 98 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides The U. Workplace exposure standards for endrin have been established by OSHA.e.

54:1431-1443. Liddle J. Environ Res 2004. Olea-Serrano MF. Whitehouse DA. 731-915. Smith AG. Fourth National Report on Human Exposure to Environmental Chemicals 99 . 4/21/09 Bates MN. Ellis H. Patterson DG Jr. Available at URL: http://www. Sokal D. Cerrillo I. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Saleem M. Burse VW.21:141-150.htm. Exposure of women to organochlorine pesticides in Southern Spain.9:1357-136. Frey JM. Andersen A. Roy ML. Needham LL. Ward EM. et al. pp. Available at URL: http://www.html. Rowley DL. New York. Rivas A. 1992. Olea N. Jr and Laws ER. Grajewski B.gov/toxprofiles/tp89. Endrin [online]. Gray JA. Rab MA. Hanisch RC. Buckland SJ. 2 Classes of Pesticides. Chernoff H. Available at URL: http://www. Gray LE. Toxicology 1981.13:155-165. 1991. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Jr. 4/21/09 International Programme on Chemical Safety (IPCS).gov/~dms/ pesrpts. Pediatrics 1987. Inc. Toxicological profile for endrin [online]. August 1996.html. August 2008. Narahashi T. et al. Schulte P. Hardjotanojo W. Hanisch RC. Handbook of Pesticide Toxicology.fda.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).atsdr. Botella B.79(6):928-934. et al. Crespo J. Food and Drug Administration (FDA). 4/21/09 Kavlock RJ. Chemosphere 2004. Turner W. Chernoff N. Toxicol Lett 1992. In Hayes WJ. Gray LE.org/documents/ehc/ehc/ ehc130. Fetotoxic effects of prenatal exposure in hamsters. Rogers E. Perinatal toxicity of endrin in rodents. Environmental Health Criteria 130. Convulsions caused by endrin poisoning in Pakistan.inchem. Academic Press. Eds. No:429-436. Ginsburg KS. I. II. et al. Toxicology 1979. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Patterson DG Jr.96:34-40.64-65 Spec. Fetotoxic effects of prenatal exposure in rats and mice. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Chlorinated Hydrocarbon Insecticides. Kavlock RJ. Gray J. Vol. Cancer Epidemiol Biomarkers Prev 2000.cfsan. Garrett N. Perinatal toxicity of endrin in rodents.cdc.

4.6) < LOD < LOD 26. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.6) < LOD < LOD 25.5-14.0) < LOD < LOD 15..6 (24.9-15. water.3) < LOD < LOD 29.6-trichlorophenol (2. and sediment (Barber et al.9-24.0 (25.0) < LOD < LOD 15.2 (13.0-16.4) < LOD < LOD 23. 2008.3) * * 15. or game taken from areas with HCB contamination.6 (23.2-15.9-30.3 (22. 31.5-trichlorophenol (2. Therefore. and accumulates in fatty tissues where it persists for years.9 (23. and 03-04 are 118. respectively.0-19.8) < LOD < LOD 27. The general population may be exposed to HCB through diet. population from the National Health and Nutrition Examination Survey.S.5-15. see Data Analysis section) for Survey years 99-00.4.5 (14.. 100 Fourth National Report on Human Exposure to Environmental Chemicals . HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.7-26. and has been detected in soil.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. Although it is not manufactured as an end-product in the U. HCB is well absorbed after oral administration.6-26.3-26. and elimination occurs by renal and fecal routes. and 7. particularly by consuming fish. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (14.7-21.0 (18. Survey Geometric mean (95% conf.4.8-15.9) < LOD < LOD 28. 01-02.1-20.6) < LOD < LOD 24. which may vary for some chemicals by year and by individual sample.9-32.8 (15. < LOD means less than the limit of detection. and foods with a high fat content.9 (25.3) < LOD < LOD 20.7) * * 14.2 (14.2) < LOD < LOD 29. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.9-20. distributes widely throughout the body.9) < LOD < LOD 19.2-31. 1988). EPA cancelled its use in 1984.9) < LOD < LOD 15.3 (22.3 (20.7-16.5) < LOD < LOD 18.7-16. wildfowl.6-33.0-28.4) < LOD < LOD 18.9) < LOD < LOD 20.9 (14.9) < LOD < LOD 20.1 (17.6) < LOD < LOD 26.4) < LOD < LOD 14.7-15.4.2-15..5 (13. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. HCB is slowly metabolized.9 (25.7) < LOD < LOD 24.2 (17.3 (14.3) 24.6-TCP) (To-Figueras et al.6) < LOD < LOD 14.5-14.2 (14.1) * * 15.0) * * 15.0 (14. air.9-17.8 (22.Organochlorine Pesticides Hexachlorobenzene CAS No.7 (15.6-32.3-20.5-TCP) and 2.4 (11. The FDA dietary surveys have shown that over time.S.7-30.1-16.4 (18.3 (16.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.2) < LOD < LOD 13. Gunderson.3-22.S.1) < LOD < LOD 15.S. 1997).4) < LOD < LOD 33.4) < LOD < LOD 22.1 (13.4-15. Urinary metabolites include pentachlorophenol (PCP).4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.9) 19.5 (13. 2005).0) < LOD < LOD 24.5-33.4 (22.9) < LOD < LOD 16.6 (21.7 (27.3 (12.2 (24.8 (26. breast milk is an additional route of elimination in nursing women.7 (19.1 (14. 1976). primarily as a fungicide and seed treatment until the U.4-16.4. HCB has been detected in fewer foods since the 1980s (FDA.5-18.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. 2002). Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications..7-22.4) < LOD < LOD 19.0.0-25. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 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.7 (15.5-15.6-44. 2.7-29.4 (18.0 (18.8.6-19.7) 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.

094 (.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .092 (.085) * * . reproductive and developmental toxicities.123 (. 2002).163 (. HCB interferes with normal heme synthesis.091-.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . With chronic exposure.141) < LOD < LOD .092 (.099) < LOD < LOD .095 (.115 (.113-.109) * * .090 (. and many died before 2 years of age (Peters et al.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 * * .179 (.088-. anorexia. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.102) < LOD < LOD .095) * * .174-. and weakness.S.125 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .129) < LOD < LOD . as well as hypertrichosis. Schmid.073-.html. ACGIH has developed workplace exposure limits for HCB. very high.083) < LOD < LOD ..098 (.090-.118-. arthritis. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.118) < LOD < LOD .107-.095) < LOD < LOD 75th < LOD < LOD 90th * * .143-.203) < LOD < LOD . 1960).186 (.060-.173) < LOD < LOD .atsdr.135-.epa.123 (.079 (. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.114-.090 (. Survey Geometric mean (95% conf.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 * * .S.090 (.176-.121 (.099) < LOD < LOD . immunologic abnormalities. and liver and thyroid cancers (ATSDR.S.126) .176) < LOD < LOD .171 (.081 (.147-.258) < LOD < LOD .167 (.094) < LOD < LOD . Chronic feeding studies in animals have demonstrated kidney injury.225 (.152) < LOD < LOD .gov/pesticides/ and from ATSDR at: http://www.099) < LOD < LOD .132) < LOD < LOD .156 (.155) < LOD < LOD .123 (. environmental levels) and health effects is available from the U.064 (. which may vary for some chemicals by year and by individual sample. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.157-.086-.092-.097 (.gov/toxpro2.095-.Organochlorine Pesticides chemical.065 (. EPA at: http://www. In humans. thyromegaly.159-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.169-. 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.190 (. The U.130) < LOD < LOD . acute doses produce central nervous system depression and seizures.118-.100) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 101 .081-.082-.182 (. 1982.062-.089-.087 (.104 (.102 (. Biomonitoring Information Serum concentrations reflect the body burden of HCB.157 (.111) < LOD < LOD . Infants were exposed transplacentally and through breast milk. This condition.088-.127-.069) * * .078 (.085-.145-.203) < LOD < LOD .069) < LOD < LOD .089-.092 (.145-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.178-.107) < LOD < LOD . More information about external exposure (i.077-. and the FDA has established a bottled water standard for HCB.147 (.086) < LOD < LOD .196) < LOD < LOD . HCB levels were generally below the limits of detection Serum Hexachlorobenzene (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.cdc. population from the National Health and Nutrition Examination Survey.088-.072-.e.160 (.095 (.097) .120 (.111-.163) < LOD < LOD .114-.086-.148-.163-..122) < LOD < LOD .191 (.175) < LOD < LOD .140 (. EPA has established a drinking water standard.097) < LOD < LOD .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.

Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Zoellner I. Hexachlorobenzene in the global environment: emissions. J Assoc Off Anal Chem 1988. only 4. As a result of the lower limit of detection in NHANES 2003-2004. Lackman. 2002). Dogramaci I. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. April 1982 to 1984. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. 2005). Muller C... Jones KC. Bertram et al.135(4):400404. Peters HA. Aune M. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. IARC Sci Publ 1986... 2005). Available at URL: http://www. Dewailly E. Bertram HP. Gocmen A. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. respectively. Cripps DJ. FDA total diet study. et al. Bjerselius R. Atuma S. Sala M. Santiago-Silva M. Can J Biochem 1976. Arch Neurol 1982.. Lepom P.. Seiwert M. HCB detection in serum also was proportional to age. Environ Health Perspect 2003.. In the 1976-1980 NHANES subsample.349:144. Krause C. Sweetman AJ.gov/~dms/ pesrpts. Fenster L. Laliberte C. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.html. Link B.205:297-308. Gunderson EL. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. 4/21/09 Barber JL. 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.. August 2008. Gabrio T. however. 2005. Chemosphere 2005. 2006).17:388–399. 1989).77:173182.gov/ toxprofiles/tp90. et al. In Spain. Schulz C. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. and other chemicals.81(2):82-85. van Wijk D. Available at URL: http://www. Piechotowski I. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.. Food and Drug Administration (FDA). HCB levels were directly related to age. Sci Tot Environ 2005.54(3):203-208. Bradman A. 102 Fourth National Report on Human Exposure to Environmental Chemicals . 2002. Kohli J. levels. The metabolism of higher chlorinated benzene isomers. Schwartz JM. References Agency for Toxic Substances and Disease Registry (ATSDR). Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.9% of participants had quantifiable levels (Stehr-Green. Ozalla D. Link et al. trends and processes. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Lawrence River (Quebec. Barr DB.cfsan. Over the past two decades. more HCB levels were quantified. Arch Dermatol 1999. Herrero C. 1986. distribution. et al. Ayotte P. Int J Hyg Environ Health 2002. 2002) and among children (Link et al. Safe A. Darnerud PO.58:1185-1201. September 2002. Kemper FH. Muckle G. Eskenazi B.cdc.. and the geometric mean concentration of HCB in whole blood was 0.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples.111:349355. Kaus S. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Environ Health Perspect 2002.. Paepke O. Biomonitoring of persistent organochlorine pesticides. Herrman T. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Becker K. Granath F. Organochlorines in Swedish women: determinants of serum concentrations. Bryan GT.44 mg/L.71(6):1200-1209. dietary intakes of pesticides. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. 2003).html. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Bradman et al. et al. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. 2002. Lackmann. but overall. J Exp Sci Environ Epidemiol 2007. 1999).atsdr. Jones D. 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. Glynn et al. Canada). Reference values updated. 4/21/09 Glynn AW. In a representative sample of the 1998 German adult population. Biol Neonate 2002. Toxicological profile for hexachlorobenzene update [online].110(8):835-838. 2002.39(12):744-749.fda. Lecha M. Otero R. selected elements. Lackmann GM. 2002. Dallaire F. Holland NT.

Fourth National Report on Human Exposure to Environmental Chemicals 103 . Cutaneous porphyria in Turkey. Barrot C. J Toxicol Environ Health 1989. N Engl J Med 1960. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. PA. Rodamilans M. To-Figueras J. Sala M. Stehr-Green.27:405-421.263:397-398. Otero R. Environ Health Perspect 1997. Demographic and seasonal influences on human serum pesticide residue levels. et al.105(1):78-83.Organochlorine Pesticides Schmid R. Santiago-Silva M.

6) 16.8.2 (31.1 (30. 01-02.0-20.1-32.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.2 (9.7) 32.4 (8.4) 27.4) 901 1067 952 992 1224 1007 Females 11.04-10.9-178) 48.1-15. However.4 (16.80 (<LOD-14.8 (9.1-49.6-37.1 (16.6-135) 69.3) 51.5) 67. 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.1) 13. commonly known as lindane.7-166) 70. formerly referred to as benzene hexachloride.7) 10.9) 45.8) * * * * * * 15.0) 35.S.5-29.7 (25.3 (13.1 (12.5 (24.5-123) 49.6) 653 758 589 1240 1533 1370 20 years and older 10.46-11.4) < LOD 9.3 (42.4) 21.60-13. In 2006.9) 15.1) 31.4 (50. gamma.2-55.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. 2005). 2005).0-34. which may vary for some chemicals by year and by individual sample.6 (16.7) 56.80 (6.2) 142 (99.0-70.9-81.7-96.2-67.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.8 (64.0 (8.0) 8. and 03-04 are 9.2-52. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.6-62.66-12.90-8.8) 39. 104 Fourth National Report on Human Exposure to Environmental Chemicals .4-73.76. The gamma isomer.0) 7.30-11.6 (33.87 (9.7-96.3-85.4) 51.7) 18.9 (40. < LOD means less than the limit of detection.0 (33.1-27.8) 7.7) 97.6-89. See the section “What’s New” at the beginning of this Report for details.0 (<LOD-12.6) 47.7-20.8 (23.6 (10.8 (10.3 (62.90-8.S. As pesticide applications of HCH were increasingly restricted or eliminated.5 (11.7-69.7) 27.3 (26.5) 22. population from the National Health and Nutrition Examination Survey.90) 7. Technical grade HCH is a mixture of all four isomers.6) 18.8 (21.36.9-21.1 (9.5) 90th 42.7 (13.1 (27.2-42.0 (14. The other isomers can be formed during the synthesis of lindane.9 (26.0) 41. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1-32.5 (43.9-24.Organochlorine Pesticides Hexachlorocyclohexane CAS No.9 (32. EPA cancelled agricultural uses of lindane (ATSDR.1) 71. Lindane has a half-life of about two weeks in soils and water.3) 37. including alpha.0-21.3) 34. exists in several isomeric forms.7 (<LOD-16.5 (16.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.6) 35.70 (8.8-19.7 (30. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.3 (42.4) 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 21.7-26.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.70 (6.2 (50.9) 81.9 (11. particularly alpha and gamma have been detected widely in air.6-18.0-70.2 (29. HCH isomers are lipophilic. soil.9-51.9-56.2 (18.7-69.6-14. 58-89-9 General Information Hexachlorocyclohexane (HCH).4) 44.5) 16.8 (33.7) 10.0) 17.0) 71.2-22. beta.1 (21. **In survey period 2001-2002. 319-85-7 gamma-Hexachlorocyclohexane CAS No. interval) 9.2-20. containing about 64% alpha and 10%-15% gamma isomers.68 (<LOD-10.5) 14.5) 40. water.4 (12. and sediment as a result of historic production and use.89 (<LOD-9.8-16. and have been used either as fungicides or to synthesize other chemicals.0-23.43 (<LOD-9.8) 52. see Data Analysis section) for survey years 99-00.6-47.2) 13. environmental levels declined.4-45.5 (37.2-87.6) 36.5) 11. and 7.S.9-14.56-12.0-111) 70. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.8) 27.6 (40.3) 14.2-98.8 (32.1 (18.1) 12.0 (37.8-68.3) 25.61-12.0 (35.20-16.9 (50. the U.5 (14.9) 17. each result has been multiplied by 1.2) 36.4-111) 84.70-12.4) < LOD < LOD < LOD 46.1) 12.6) 50.8) < LOD 10. HCH isomers.8-199) 134 (85.4 (52.7 (53.70-19.9 (30.6-42.2) 62.1-36. so they can accumulate in fatty tissues of animals.6 (22.5528. 608-73-1 beta-Hexachlorocyclohexane CAS No.6-20.1 (9.2-17.7) 23. and delta. respectively.4-50.8-87.3-38.1-16.1-37.3-56.0 (19.2) 9.2-46.7 (35. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.1 (11.9 (9.7 (29.7) 73.5 (8.2 (48.4) 11.4) 10.2 (34.8-54.6 (17.8) 95th 68.4 (11.50) 8.8) 12.8 (17.5) 29.9 (62.7 (62. It is no longer produced or sold in the U. 6.

100 (.290) .680) .080-.200 (.270 (. 1983).240 (. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.100-.501) .300-.060) .290 (.814) ..103-.130 (.01 (.040-.120 (. probably by blocking inhibitory neurotransmitters in the central nervous system.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . 1981). The U.220-.090 (.070-.308-.092 (.167 (.125) < LOD < LOD < LOD .390 (.090 (.100) .120-. OSHA and ACGIH have established workplace standards and guidelines.390-.077) < LOD .910 (.470) .140) .360) .069) .073-.057 (<LOD-.056-.050-.140) .070-.100 (.210-.110) .310) .130-.100) .297-.072 (.103) 90th .580 (.150) . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.047-.174) .210 (. 2002).250 (.083) .050 (.280-.051 (<LOD-.580-1.234 (.070-.057-.119) .120-.062 (. each result has been multiplied by 1.050 (<LOD-.470 (.090 (.050-.370-.098 (.050) .057-.840) .Organochlorine Pesticides exposure to HCH is through the diet.460 (.214) . the serum half-life was about 20 hours among children (Ginsburg et al. IARC classifies Serum beta-Hexachlorocyclohexane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.240-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.600) . After dermal application of lindane 1% lotion. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.360-.160) . Rogan.056-.404) .250-.077) < LOD .175 (.144 (.083 (.710) .244-.124-.260-.521 (.058 (<LOD-.068-.070) .140 (.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 . **In survey period 2001-2002. The beta isomer accumulates in fatty tissues and is metabolized more slowly.220) .32) .103 (.180-.442 (.216 (. 1977). Fourth National Report on Human Exposure to Environmental Chemicals 105 .37) 1.690) . hepatic enzyme induction.110) .070 (..410 (.050 (.350) . 1971. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.200-.064 (.091) . EPA has established a drinking water standard. HCH isomers are absorbed after inhalation.131-.191-. 1986).450-.5528.221-..050-.340-.250) .480 (.380 (.340) .310 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane..170-.190) .460) .080 (.S.070 (..081-. ataxia.100-.048 (<LOD-. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.290 (.661) 901 1067 952 992 1224 1007 Females .139 (.290) .173-.250-.190-1.320 (.450) .089-.510) .560) . Workers who directly handled HCH have complained of headache. tremors. and seizures.372 (.410) .400) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al.067) .130) .080 (. enlarged livers.120 (.281 (.560 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .620-1.480) .146-.331 (. for lindane.287 (.062 (.078 (.150-.S.120) .420-.570 (.191-.260) . respectively.190) .412 (.160-. and nephropathy developed (IPCS. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or dermal exposure.350 (.170-.096) . U. ingestion. Distribution is mainly to fatty tissues.410-. See the section “What’s New” at the beginning of this Report for details.050-.118 (.067 (.065 (.382-.140) .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.051-.330 (.080) * * * * * * . and memory loss (Nigam et al.210) .410) .090-.059-. and FDA has established a bottled water standard and food residue tolerances for lindane. 1996.200-. Saxena et al.230-.065 (.110-.319) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .360 (. Gunderson 1988).294-.280-.220-.700) .089) . which may vary for some chemicals by year and by individual sample.190-.S.254) 95th .150 (.480 (.222 (.150) .400) . resulting in a half-life of about seven years.120) . paresthesias. 2008.620) .330-.450 (.310) .305) . When animals were chronically fed lindane at high doses.050 (<LOD-.100-.080-.587) 653 758 589 1240 1533 1370 20 years and older .250 (.080-.160 (.220 (.250 (.120 (.118-.290 (.120-.260) . population from the National Health and Nutrition Examination Survey.110) .080) . interval) .086) < LOD < LOD < LOD < LOD < LOD < LOD .064) .05) .210 (.

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

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

96:34-4Food and Drug Administration (FDA). Raju GS. Botella B. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. August 2008.54:1431-1443. Reisch JS. Lepom P. Toxicol Appl Pharmacol 1971. Needham LL.gov/~dms/pesrpts. Visweswariah K. Needham LL. Glynn AW. et al. Becker K.48:127-134. dietary intakes of pesticides. The Great Lakes Consortium.20(2):186-193. Exposure of women to organochlorine pesticides in Southern Spain. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Seiwert M. Potischman N. Gunderson EL. Kulkarni PK. Paepke O. and HCB residues in human blood in Ahmedabad. Sturgeon SR. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Organochlorines in Swedish women: determinants of serum concentrations. Crespo J. Granath F. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Bull Environ Contam Toxicol 2004.58:1185-1201. Zaidi SS. J Pediatr 1977. et al. J Assoc Off Anal Chem 1988. Bottimore DP. Darnerud PO. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). 2002.inchem. Environ Health Perspect 2003. Krause C. Demographic and seasonal influences on human serum pesticide residue levels. Cerrillo I. Occupational exposure to hexachlorocyclohexane. Zoellner I.150:981-990. Wood PH. et al.html.72:261265. org/documents/jmpr/jmpmono/2002pr08. gov/toxprofiles/tp43. Karnik AB.91:998-1000. Deichmann WB.htm. Gabrio T. Patterson DG Jr. Int Arch Occup Environ Health 1983. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Int J Hyg Environ Health 2002. VI. Placental transfer of pesticides in humans.fda. Absorption of lindane (g benzene hexachloride) in infants and children. Rogan WJ.111:349355.cfsan. Krishna Murti CR. et al. Siddiqui MKJ. Hanrahan L.71(6):1200-1209. Heinrich R. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Herrman T. Available at URL: http://www. et al. Bjerselius R. Environ Health Perspect 1998. 4/21/09 Anderson HA. Bhatnagar VK. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Rivas A. children and newborn infants. Aune M. Saiyed HN. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Cancer Causes and Control 1998. Kashyap R. Rey AA. 4/21/09 Kutz FW. Lowry W. Lindane.106(5):279-289. Olea-Serrano MF. Ellis H. Bai KM. Rothman N. Levels of DDT.52(1):59-67. August 2005.27:405-421. Atuma S. Arch Toxicol 1981. Nigam SK. Saxena MC. FDA total diet study.205:297-308. Bates MN. Garrett N. Astolfi E. India.cdc. et al. Available at URL: http://www.120:1-82.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Arch Pediatr Adolesc Med 1996.9(4):417-424. Needham LL. Bhargava AK. Chemosphere 2004. Link B. J Toxicol Environ Health 1989. Olea N. PA. Piechotowski I. Buckland SJ. Pollutants in breast milk. 4/21/09 Ginsburg CM. Maass R. April 1982 to 1984.html. and other chemicals. Int Arch Occup Environ Health 1986. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Radomski JL. Angerer J. Toxicological profile for hexachlorocyclohexanes update [online]. Kutty D. Olson J. Biomonitoring of persistent organochlorine pesticides. et al. Rev Environ Contam Toxicol 1991. International Programme on Chemical Safety (IPCS). Brock JW. available at URL: http://www.atsdr.57(4):315-320. Brinton LA. Chemosphere 2005. Schulz C. selected elements. Environ Res 2004. Metabolism of gammahexachlorocyclohexane in man. Stehr-Green. Burse VW. Falk C. Majumder SK. Kaus S. HCH.

or pesticide application. Mirex binds strongly to soil.S. Formerly. The most likely sources of human exposure to mirex are eating fish from contaminated water or living in areas with soil contaminated by historic mirex manufacturing. mirex was detected in human adipose samples.70-24.3) 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. after which it is widely distributed in the body and stored in fat. 1995). 2385-85-5 General Information Mirex has not been produced or used in the U. which may vary for some chemicals by year and by individual sample.0-374) 11. 01-02. < LOD means less than the limit of detection.5-291) 11. see Data Analysis section) for Survey years 99-00.1) 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 16.2) 51. Survey Geometric mean (95% conf. and 7.1 (<LOD-65.7) 8. disposal.2-230) 13.4) < LOD 15. 1991). Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (<LOD-108) 9. In studies conducted in the 1970’s and 1980’s. Mirex is not metabolized in the body.3-225) 15. and foods. water.6 (<LOD-31. 10. population from the National Health and Nutrition Examination Survey. animals.0 (12.7) < LOD 66. resulting in exposure to newborns and nursing infants.6) 9.10 (<LOD-15. and 03-04 are 14.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.0 (<LOD-108) < LOD < LOD 50.8.2 (7.S.4) < LOD 63.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.1 (13. where it was applied directly to soil and by aerial spraying.Organochlorine Pesticides Mirex CAS No.5-425) 40.8) < LOD 15. Mirex is absorbed through the skin and from the gastrointestinal tract.6-305) 15.90-29. it is a highly persistent chemical in the environment. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.0 (14.5 (<LOD-115) 153 (30.70 (<LOD-15. Mirex has been detected in air. sediments. where it has a half-life of 12 years. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.10-37.70-40. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. since 1977.5. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. especially those from persons living in the southeastern U. aquatic organisms.40 (<LOD-13.5 (<LOD-42. Fourth National Report on Human Exposure to Environmental Chemicals 109 .6) < LOD < LOD < LOD < LOD 71..3 (15.8 (<LOD-73.7 (12. Occupational exposure is limited to workers at sites where mirex contamination is present. respectively.3 (15.4-230) 18.S.8 (12.4 (8. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. (Kutz et al.6.S.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. Mirex can cross the placenta and be excreted in breast milk.5-82.7 (<LOD-47.S. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.6 (<LOD-23..1 (<LOD-104) < LOD < LOD < LOD < LOD 39. soil.5 (9. Some states and the U. 1985.1 (8.

Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.093 (.070-1.256 (. and 4.510) < LOD < LOD . 1995. 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.02) .470) . Smith. population from the National Health and Nutrition Examination Survey. environmental levels) and health effects is available from the ATSDR at: http://www. serum mirex levels were generally below the limits of detection (Stehr-Green.090-1. 7. EPA has established environmental standards for mirex. In samples obtained between 1994 and 1997.7 ng/g of lipid.470) .170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .062-.79) . The U.450 (. Biomonitoring Information In the NHANES 1999-2000..106) < LOD .106 (.108 (. 2004).470 (. Survey Geometric mean (95% conf.73) . and 2003-2004 subsamples.690) . 1991). and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.100 (<LOD-...090 (<LOD-.077 (<LOD-.635) < LOD .41) .220 (<LOD-.059 (<LOD-. More information about external exposure (i.310 (.S.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 .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 . 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.atsdr.090-1.089-. The geometric mean mirex levels of the Inuit mothers were 8.054 (<LOD-.37) .gov/toxpro2. which may vary for some chemicals by year and by individual sample.450) 1.08 (.92) . and NTP classifies mirex as reasonably anticipated to be a human carcinogen.100 (<LOD-.cdc. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. 110 Fourth National Report on Human Exposure to Environmental Chemicals .170-3.79) .112 (.053-. 2001-2002. as well as in a subsample of NHANES II (1976-1980) participants.080-1.430 (. reproductive toxicity included decreased fertility and testicular damage.410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110 (<LOD-.079 (<LOD-.e.170) < LOD .064 (<LOD-.102) < LOD < LOD < LOD < LOD .052-. 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.Organochlorine Pesticides exposures are unknown. In addition. IARC classifies mirex as possibly carcinogenic to humans. 2005).080-1.370 (.090-1.220) .090 (<LOD-.090 (<LOD-.8.140 (<LOD-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .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. 1989). Laboratory animals fed high doses developed liver enlargement and liver tumors.610) < LOD < LOD < LOD < LOD .055-.268) < LOD .html.

PA. 731-915. Chlorinated Hydrocarbon Insecticides. Inc. Demographic and seasonal influences on human serum pesticide residue levels. Chashchin V. In Hayes WJ.15:385-394.330:55-70.html. 4/21/09 Bloom MS. Stroup CR. Vena JE. Van Oostdam JC. Olson JR. Kutz FW. Dewailly E. 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. Profiles of ortho-polychlorinated biphenyl congeners. Jr and Laws ER.atsdr. et al. Jr. Academic Press. August 1995. 2 Classes of Pesticides. Handbook of Pesticide Toxicology. References Agency for Toxic Substances and Disease Registry (ATSDR).120:1-82. J Toxicol Environ Health 1989. The human body burden of mirex in the southeastern United States. Circumpolar maternal blood contaminant survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Stehr-Green. Moysich KB. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Watts DL. Strassman SC. Swanson MK. hexachlorobenzene.cdc. Available at URL: http://www.27:405-421. Eds. Leininger CC. Bottimore DP. Hansen JC. Sci Total Environ 2004. Gilman A. Carra JS. Wood PH.gov/toxprofiles/ tp66. Smith AG. et al. Kutz FW. 1991 pp. Environ Res 2005. Odland JO. Rev Environ Contam Toxicol 1991. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. 1994-1997 organochlorine compounds. New York. Toxicological profile for mirex and chlordecone [online]. dichlorodiphenyldichloroethylene. Vol.Organochlorine Pesticides effect. J Toxicol Environ Health 1985.97(2):178192.

interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.4.40 (1. Survey Geometric mean (95% conf.4.980-3.42 (<LOD-12.30 (. including hexachlorobenzene and hexachlorocyclohexanes. population from the National Health and Nutrition Examination Survey.0) 2. < LOD means less than the limit of detection.4.4. 2006).50 (.5-TCP) and 2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. 95-95-4 2.0) < LOD 5. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.6-TCP).10-3.0) 2. 112 Fourth National Report on Human Exposure to Environmental Chemicals .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. EPA.20 (4. Trichlorophenols are no longer manufactured commercially.00-8. may occur by inhalation or dermal routes. 1999).S.980-3.Organochlorine Pesticides 2.30-27.920-3. public drinking water systems did not detect 2.40) < LOD 4.4.30) < LOD < LOD < LOD < LOD < LOD 1.5-Trichlorophenol CAS No.4.80 (1.6-TCP in any of the samples (U. recent sampling of U.60-18.4.0 (5.30-27.40 (.90-33.S.50-25.40 (2. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.40 (2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.60 (4.0 (4.0) 2. Formation of 2.40 (2.03) 9.40-18. 2.31 (<LOD-9. surface water.0) < LOD 21.9.50-16.40) < LOD 1. Both chemicals have been detected in air.0) 2.0) 2. other organochlorines.4.5-trichlorophenol.50 (1.5TCP and 2.S.60 (2.4.00-3. and polychlorinated benzenes (Kohil et al.20) < LOD 1.0) < LOD 11.80 (2.0) < LOD 5.40 (1.30-11.4.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.42 (<LOD-8.5-trichlorophenol (2.7) 24.50) < LOD 1.19 (<LOD-6.60) < LOD 8. 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. are metabolites of several organochlorine chemicals.9 (<LOD-121) 9.0 (4.6-Trichlorophenol CAS No.950 (<LOD-1.80) < LOD 1.40 (2. 2.60 (..5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20) < LOD 5.0 (3.00-3.40) < LOD 6.40 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Historically.4.900-2.9 and 0.0 (8.20) < LOD 90th 5.8) 21. usually at herbicide production or waste incineration facilities.0) 14.30-27. soils. hexachlorobenzene.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 1976).0) < LOD 11.71 (<LOD-8.30-40. 1999).50-63.3.30-3.60-8.50 (2.0) 2.40-11. however.30-44.20-36.0) 5.6-trichlorophenol (2. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.940-3.6-TCP were used as intermediates in the production of certain pesticides.20-71.0 (4. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. Occupational exposures.27) 696 661 521 696 603 939 Limit of detection (LOD.30) < LOD 4.0 (3. 2. Such workers would probably Urinary 2.80-41. Exposure to trichlorophenols also may result from metabolism of lindane.7. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.00 (2.00 (3.4.0) < LOD 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .57 (<LOD-15.72) < LOD 1.71 (<LOD-8. which may vary for some chemicals by year and by individual sample.63) 18. and sediments.

82 (<LOD-32. animals showed hepatocellular abnormalities.6-TCP as reasonably anticipated to be a human carcinogen. 2003).9) 12. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. Radon et al.37) 696 661 521 695 603 939 < 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 113 .4.. as being possibly carcinogenic to humans.4.80 (1. NTP classifies 2. 1995) were similar.15) < LOD 2. Urinary 2.95 (3. furans..16) < LOD 90th 5.6-TCP.4. In the same 2-6 year old children.5-TCP nor 2. 1989).atsdr.93-11.2 (2.44 (1. Human health effects from 2. The 95th percentiles for 2. Laboratory animals chronically fed high doses of 2.24) < LOD 6.Organochlorine Pesticides be exposed to mixtures of chlorophenols.88-16.24 (3.4.920-2.4 (6.6-TCP had increased rates of hepatic tumors.19-12.3 (5.5) < LOD 12.4.1) 2.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 2003).3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .4.62-20.8) 4..53-3.9 (5.24) < LOD 5. which includes trichlorophenols.05-17.5-TCP.4.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. the 95th percentile urinary 2.16 (.57 (3.gov/toxpro2.13-13.8 (5.00) < LOD 4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).4.4) 5.31) < LOD 2.6) 4.64 (4.78 (3.5) 11.5-TCP or 2.74) 11.24-11. the 95th percentile urinary 2. At lower doses.73 (<LOD-8.75 (3.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. and lymphomas.5-TCP and limited for 2.69-18.78-19.49 (1.4) < LOD 3. Among 6-11 year old children in NHANES 1999-2000.e.0 mg/L.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 2.46 (1.4) < LOD 3.02) < LOD 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1989).36 (1.3 mg/L reported in German adults aged 18-69 years (Becker et al. population from the National Health and Nutrition Examination Survey..3 mg/L in a nonrandom subsample from NHANES III (Hill et al.8) < LOD 9. environmental levels) and health effects is available from ATSDR at: http://www.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.57 (<LOD-7.78) < LOD 1.19-4. leukemias. 1995) and up to 19 times higher than the 95th percentile value of 1.7 (4.44 (.29 (1.57 (<LOD-7.37) 16.68-4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.50) < LOD 2.32) < LOD 4..55 (4.6) 4.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. Neither 2.37-11.67 (1.27-17.02-3. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.1 (<LOD-58.47-8.68 (<LOD-8.05-8.43 (2.00-19.67 (1.6) 4.820-2.4.53-3. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. However.980 (<LOD-1.cdc.6-TCP levels at the 95th percentile were up to eight times higher than 3.81 (<LOD-9.60-3.75 (<LOD-6. Survey Geometric mean (95% conf.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and other chlorinated compounds.33) < LOD < LOD < LOD < LOD < LOD 2.79-4. urinary 2.4. More information about external exposure (i.43) < LOD 12. in addition to dioxins..90 (4..4. 2003.28-25.4.2) < LOD 5.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.S.0) 7.17) 9. 7.83-12. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.69 (2.00-29.24) < LOD 1.html.86 (3.. IARC classifies combined exposures to polychlorophenols..20-6. 2004).2) 2.

53) 4.7 (9.0 (14.32-4.48-26..9 (11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (4.5-TCP or 2.68 (<LOD-2.4 (10.4.23) 2.3.74-3.99) 6.0) 6.0) 11.4. 2004).75 (8.20-3.0 (6. 1998).5-46.84) 2. population from the National Health and Nutrition Examination Survey.7-16.95 (4.0) 15.18-3.53) 2.90 (4..0) 10.6-TCP in urine does not mean that the level of 2.52-3.04) 2.40) 4. Biomonitoring data will also help scientists plan and conduct research about 2.0-37.3) 20.89 (3.85 (2. In harbor workers exposed to chlorophenol-contaminated river silt.0-38.78 (2.30-11.0 (20.4.5-TCP or 2.0 (13.00-21.0) 19.80-25. 2003).45) < LOD 11.20) 4.0-43.70) 1.40-2.5-TCP and 2.40-32.4.98-7.0-41.6-22.69 (3.7) 33.10-3.57 (<LOD-2.0) 17.6 (11.4.4-17.46-3.40-14.0) 14.60-37.8-13.0-50.90) 2.0 (9.5 mg/g creatinine) were similar to the limit of detection for 2.0 (15.20 (3.06) * 2.31 (3.4 (8.0) 13.73-9.35-3. 1991). was about six times lower than the median urinary levels for males in this Report (Radon et al.87-14.6-19.7) 21. Mean values of 2.09-7.4.0 (16.5-TCP and 2.30-2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.09) 15.0) 13.0 (15.36 mg/g creatinine.70-6.00 (2.60-3.6TCP values.07 (<LOD-3.6-TCP exposure and health effects.6-TCP level.45 (5.60) < LOD 5. Urinary 2.40) 3.10 (5.74 (2.6) 21.0 (8.12) 2.44) 75th 4..60 (3.6) 26.1 (10..85) * 3.65 (5.0-44.0-54.32) * 3.80-7.70 (2.67) 4.80 (2.3) 37.7-3.90-8.45-9.0 (6.60 (2.58 (1.00 (4.4.63) 90th 15.45 (2.8-24.10) 2.50 (2.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al. interval) 2.6-17.0-18. < LOD means less than the limit of detection.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 2.7 (13.40) 2.3-26.00 (1.2-0.70-6.8) 32.3 (11.4. the median urinary 2.3) 23.0 (8.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.4.80 (2.3-17. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.51-12.10) 6.40 (2.4.70) 5.78 (2.0 (14.S.40) 2.4.0 (12.80) 1.5-TCP and to the median 2.8) 18.59-6.6TCP causes an adverse health effect.4.70) 5. 114 Fourth National Report on Human Exposure to Environmental Chemicals .0) 13.28) 24.72-10.30-33.6-TCP (0. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.2) 12. Survey Geometric mean (95% conf.52 (2.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.24 (2.9) 694 677 519 696 602 931 Limit of detection (LOD.30) 4.0) 9.0) 12.5-TCP (0.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.40 (2.80-6.56 (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 2.8-15.95) 3.4.25-11.0) 17.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.0 (11.40-4.5-TCP or 2.70-3.91-4.36 (1.7 mg/L.6 (12.0 (20.4.98-11.0-68. 0.55-3.0-38.30-2.47 (3.90 (3.4 (9.36-5.70 (2.32) 3.50-5.14 (2.2) 25.26 (2.0) 7. Urinary 2.95-6.4. similar to the limit of detection for this Report (Anderson et al.1) 16.59) 4.20-23.23) 3.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.70) 3.5-TCP or 2.10-2.4.0 and 1.31) * 2.20 (3.2 (14.79 (5.60-21.20-6. Biomonitoring studies on levels of 2.9) 13.5-TCP level of 0.1 (8.01-6.0 (14. Finding a measurable amount of 2.0 (7.9 (13.4.40-2.8 (9.0) 11.60 (3.66 (8.02) 2.89-6.3 (11.6-TCP than are found in the general population.65) 15. for males in NHANES 19992002 (Agramunt et al.23-2.28) * 2.00-4.0) 14.1-25. respectively.0) 10.80 (3.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.4 (17.6 mg/g creatinine) and 2.58-3.4. which may vary for some chemicals by year and by individual sample.4.76) 3.40-7.33-4.54) 6.0) 13.0) 19.0 (6.49 (6.0) 7.92 (2.60) 6.80-20.4.10-3.67-12.0) 9.08 (2.

53 (3.63-13.56-5.90 (1. population from the National Health and Nutrition Examination Survey.2) 19.14-2.0 (11.76) 1.88) * 2.88) 4.5) 9.04-16.35 (3.77) 2.43 (2.0) 10.38-5.09-3.29-4.42) 2.24 (1.8) 11.6) 13.50 (2.17-4.8 (7.33 (1.60 (4.9-32.01 (3.3-23.2 (7.0 (6.22-9.76) 4.38 (2.68) 2.78) 2.1 (8.88 (2.30-2.5) 8.08-2.52) 2.00) 4.9) 19.0 (9.5) 11.73-22.7) 25.70-9.5 (10.53) 4.76-8.87 (3.62-15.33-2.6 (12.6 (9.63-15.06) 4.18-4.72-16.81-9.14-13.2 (12.83-6.83-5.15 (1.2 (8.9-29.40 (7.46-14.75) 75th 4.43-7.8) 19.95-2.41-6. Fourth National Report on Human Exposure to Environmental Chemicals 115 .51-21.05 (6.32-19.56) < LOD 11.8) 21.59 (2.98) 10.82-2.63) * 4.65) 2.6 (10.91 (7.5) 12.44 (3.5) 11.17) 2.Organochlorine Pesticides Urinary 2.7) 6.17) 13.6 (9.71 (3.7-36.22 (<LOD-2.82 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.77-4.42 (2.87-6.13 (1.8 (8.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.88) 4.1-21.29 (6.00 (3.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.33 (7.82) 2.65) 18.00) 4.10 (6.19-5.83-6.89) 10.49-3.18-2.55-2.81) 2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.13-6.23 (1.78 (2.66-4.88) 1.5 (8.83 (3.1 (13.96) < LOD 4.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.38 (4.20-2.60-2.21-11.47-5.40 (2.16-10.32 (2.48-2.9 (9.11) 10.87) 2.52 (5.43 (<LOD-2.25 (3.22 (1. interval) 2.98 (1.26 (6.26-13.53) * 2.90) 2.10) 4.8) 12.25-17.3 (9.6) 8.52 (3.3) 8.79-17.51 (2.04-2.0) 8.91 (3.87) * 2.06) 11.2 (13.9) 8.9 (9.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.92) 4.6 (6.02) 3.4) 4.28-4.1) 14.S.06-2.65-21.63 (<LOD-2.4. Survey Geometric mean (95% conf.53-11.33) * 2.5 (7.10-9.4) 9.87-7.4) 8.15 (6.41 (3.63 (2.4 (12.00 (2.9-64.1-32.76) 2.29-4.27-9.6 (22.22-2.56 (7.5-28.25 (3.88-7.6-31.02 (1.67-17.4 (11.82 (3.49) 4.3-37.88) 5.1) 11.63) 4.94-13.72) 32.05 (3.25-15.89-2.78) 90th 12.52) 2.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.22 (3.9) 8.6 (5.25-2.65-2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.73) 5.91-2.9) 7.99-2.50-8.23) 4.68) 2.6) 12.9-34.54 (2.7 (14.38) 22.51) 18.58 (4.

Wegner R.cdc. Baur X.63:57-62. html. Fast DM. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Radon K.71:99108. Holler JS. et al. et al.18(4):469-474.45:440-445. 4/21/09 Agramunt MC. Environmental Protection Agency (U. Safe A. Jones D. Environ Health Perspect 1998. Head SL.atsdr.pdf. The metabolism of higher chlorinated benzene isomers. Anderson HA. The Great Lakes Consortium. Chlorophenol exposure in harbor workers exposed to river silt aerosols.gov/toxprofiles/tp107. Becker K.S. Can J Biochem 1976.106(5):279-289. Hill RH Jr. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Olson J. Poschadel B. Bailey SL. Hanrahan L.epa. U. Domingo JL. Domingo A. Seifert B. Am J Ind Med 2004. July 1999. S. Kohli J. December 2006 Draft. 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. Available at URL: http://www.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Burse VW. Baker S. Environ Res 1995.EPA). Int J Hyg Environ Health 2003.54(3):203-208. Schulz C. et al.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Corbella J. Needham LL. Lindroos L. Kaus S. Pesticide residues in urine of adults living in the United States: reference range concentrations. Szadkowski D. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Lett 2003. Seiwert M. Int Arch Occup Environ Health 1991. Luotamo M. Toxicological profile for chlorophenols [online]. Falk C. Urinary excretion of chlorinated phenols in saw-mill workers.146:83-91. 206:15-24. Heinrich-Ramm R. Smith SJ. Pekari K. Needham LL. Gregg M. Available at URL: http://www. Aitio A. Shealy DB. Arch Environ Contam Toxicol 1989. 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]. Jarvisalo J. Hill RH Jr. To T.

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

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

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

67) 3.79-7.32) 1.530 (<LOD-2.4) 17.98-12.29) * * 1.5 (11.0) 5.97) 8.52) 6.620-1.2 (9.8 (9.70-19.60 (5.2) 14.00-12.623-1.90) 3.9) 14.5-16.40-19.51) 2.40 (.54 (3.700-1.80) .85 (3.0) 6.890 (<LOD-2.56 (6.71-9.780) < LOD 3.0-27.4 (9.89) 9.90 (1.26-8.36-4.56 (4.0 (9.13 (2.01) * * 1.20 (.5 (8.10 (2.47) * * 1. which may vary for some chemicals by year and by individual sample.00-27.05-7. and 0.34-7.93-24.17-3.10) < LOD < LOD 4.0) 9.758-1.0) 7.46) 10.02-5.15) 14.2 (7.0) 10.08-15.40-14. < LOD means less than the limit of detection.16 (2.80) 2.20-7.2 (11.4) 20.954 (.72) 5.39 (3.21) 9.20 (.1) 95th 13.8) 7.95) 5.50 (4.20 (2.00-19.80) 4.94) 3.73) * * .4 (7.86 (1.0) 11.740-2.60-25.70) < LOD < LOD 75th 3.70-23.6) 7.50) 2.21 (.90-4.0) 10.71 (2.99 (5.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80) .1) 10.34-3.08-2.70) .0) 15.20-30.44-38.3) 16.860-2.63) 1.5-17.0 (7.599-1.83 (5.79 (5.0 (7.50-5.42-3.20 (.00-7.15-12.50 (.2 (14. population from the National Health and Nutrition Examination Survey.82-12.23-5.00 (5.86-15.0) 10.35-16.750-1.74 (8.60-11.14) * * .33-18.1) 13.7 (12.8-32.45 (2.58 (2.9-18.81) 1.0) 5.0 (8.61) 4.0) 6.44-3. respectively.16) 4. see Data Analysis section) for Survey years 99-00.70-11.2.22 (.58 (3.2) 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 1.81) 11.0) 6.32 (.91) 4.2) 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 1.955 (.11 (.50-36.58 (5.00) 3.47) 5.55-6.7) 11.8) 11.60 (1.19) 9.7 (14.94) * * .00 (1.52-11.2 (7.2. 01-02.44 (2.S.3-15. 120 Fourth National Report on Human Exposure to Environmental Chemicals .2) 16.670-1.30 (4.6) 18.0) 10.0 (9.90) 2.20 (.8 (14.80-24.80 (2. 0.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.70 (2.490-2.290 (<LOD-.0-28.30 (2.0 (6.12) 4.39 (8.30-6.74 (8.40-11.56 (1.66) * * 1.717-1.290 (<LOD-1.40-1.1-17.48-7.97) 90th 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40-5.70-14.80) 11.8 (12. interval) 1.60) .2 (14.04) < LOD 1.2 (7.810-1.35-11.12-19.8) 19.10 (.93 (4.3) 14.35-12.0 (8.10-7.0) 5.70) < LOD < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 11.30 (2.02) 4.8 (8.52) * * 1.00-12.70 (4.07-10.80) 3.9 (8.76 (2. and 03-04 are 0.96-3.2-20.4) 18.82) 10.4 (9.0 (5.13-2.03 (.00 (4.43-12.0 (7.2) 16.9) 8.27-15.80-4.28) 1.00-27.757-2.840-1.9) 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 1.26 (5.56-13.0 (7.55-8.00) 3.970-2.60-18.0 (6.80-22.80 (4.0 (12.0 (8.13 (2.1.600 (<LOD-1.8) 7.5) 20.98-5.579-1.2 (9.33 (5.10 (.26-6.80) 2.80) 2.0) 11.37 (3.30-4.0) 10.27-3.53) 4.20-4.0) 11.57-7.38-5.10 (2.68-7.0 (4.830 (<LOD-3.40-16.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.81) 11.0) 12.0) 20.981 (.10) < LOD .3) 17.1 (9.60) < LOD < LOD 4.61 (3.42) .90-5.50 (2.08 (<LOD-2.1 (10.5) 15.4 (7.1-23.

84) 7.574-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.40-3.42) 12.15-10.11-6.924 (.650-1.73 (1.50) 7.2) 5.03 (2.31 (3.9) 16.18 (.1 (7.28) 10.2) 7.960 (<LOD-2.54-11.890 (<LOD-1.34) < LOD < LOD .81 (1.80 (6.39 (2.53) 9.14 (3.932 (.95 (3.5) 11.66 (5.9 (5.00 (4.80) 9.77 (6.09 (.608-1.30) 2.83) 8.79-9.51-5.9) 11.02-2.07 (.7 (10.05 (.37-5.35 (1.36) * * 1.3) 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 1.10-13.90-5.7) 18.66 (2.05 (1.549-1.4) 4.53-11.74) 90th 7.2 (10.4 (9.40) 4.3) 16.620-1.00 (4.03) 2.82-26.2 (6.830-1.69) 2.93-9.56) 7.0 (8.34) * * .80 (7.55-20.8) 12.68) < LOD < LOD 3.8) 6.69-10.72) 11.S.61-29.60) 2.25) < LOD .47 (3.87 (1.41) Selected percentiles ( 95% confidence interval) Total * * 50th .29 (2.6 (9.45-5.56) 4.40-12.5) 12.05) .570-1.6) 9.88 (5.1) 4.03) 2.75) 14.46-5.98 (3.45-5.31-14.71-2.633-1.84 (5.83 (7.34 (6.0) 6.87 (3.1 (9.28 (5.37 (4.37-3.54-2.35) < LOD < LOD 3.98) 9.21-23.00) 8.27) < LOD 2.01-2.8 (10.57 (4.29) * * .82-6.3) 12.24-3.996 (.93-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.85 (6.00-19.68-4.78 (2.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.66 (1.1) 4.28 (2.23 (4.04-6.67) 1.57-10.8) 16.40-28.03 (7.75-7.85) 2.47) 2.66-15.0) 7.09-11.566-1.92-2.1 (6.7) 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 .58) * * 1.93) 9.19 (4.94-23.42 (3.28-9.67) 4.5) 8.34 (6.6) 11.23) 4.500-1.61-13.790 (.7 (8.5-13.540-1.57 (6.53 (6.61 (1.89) * * 1.45-11. Fourth National Report on Human Exposure to Environmental Chemicals 121 .1-15.13) 4.5-32.94-22.855 (.87-5.43) 2.6 (10.75 (3.03-6.62-5.1) 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 1.94-9.46) 2.870-2.82-14. interval) .32-12.26) * * .7 (9.9 (9.61 (1.54-15.5 (4.69 (4.76) < LOD .88) 2.82-14.02 (2.67-19.52) 4.71) 10.3) 5.37) 9.54-4.533-1.98) .56) .54) .66-34.8) 8.4 (4.89-3.900 (.98) .00-13.9 (9.2) 5.75) 2.04 (1.38) .98-22.25) 6.30 (1.4) 4.80 (2.7) 12.06-2.1 (10.95) 2.890 (<LOD-1.818 (.440 (<LOD-2.2) 9.98-5.9-28. population from the National Health and Nutrition Examination Survey.5) 7.75 (7.37 (5.883 (.920 (.860 (.00-17.2) 95th 12.1 (11.88-15.2 (8.92-5.9) 12.820 (.41-12.40) < LOD < LOD 75th 2.60-9.47) * * .40 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.74) 4.7) 5.5) 7.1 (8.94 (2.47 (1.76-4.960 (.79-3.40-5.81-5.40-14.60) * * .90-8.94-10.560-1.430-1.8) 7.88-10.750 (<LOD-1.57) 4.710 (<LOD-1.02 (7.43 (.510-1.47 (3.43 (3.10 (3.56-13.38 (1.6) 8.3) 15.62) .5-16.94 (4.6) 13.4) 13.5-20.20-8.2) 8.44 (2.09) 2.41) .64-5.780 (<LOD-1.773-1.28 (4.2) 13.02-14.69) 4.

33-11.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.35-3.40 (2.7-19.0) 12.01 (2.62-17.0) 14.9) 16.97-4.8-21.92) 9. < LOD means less than the limit of detection.28 (7.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.89) 2.88) 10.670 (<LOD-1.22 (6.90 (2.34 (6.24-5.5 (8.31) 1.0) 11.3) 14.670 (<LOD-1.90 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.740 (<LOD-1. and 03-04 are 0.39-13.670 (<LOD-1.790 (<LOD-1.20-8.15-6.41) 3.27) 4.7) 16.6-41.40 (2.6 (10.910 (<LOD-2.8) 8.3) 10. which may vary for some chemicals by year and by individual sample.4-17.14 (6.9 (7.9-17.8) 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. respectively.95 (2.1-23.00) 7.00) < LOD .82) 8.37 (3.70-8.0) 23.90 (1.3 (12.5-26.1 (10.31-12.0) 18.5.80-3.74) * * * * * 1.86-10.34-5.46-28.70-9. 0.680 (<LOD-1.18) * * * * * * * * 1.61 (3. 01-02.0) 12.0 (15.75 (2.67-10.60 (5.7) 15.00-9.51) < LOD 1.0-29.11-6. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .20-18.15-2.8) 9.80) .580-2.10 (.0) 9.78) 5.0) 6.50) 5.00-18.0) 11.89 (2.49-4.80-14.84-4.0-19.0 (5.88) 3. see Data Analysis section) for Survey years 99-00.0 (13.3 (9.30) 8. and 0.9) 9.34-3.53 (3.20) 3.90 (2.90-9.67) 4.00) 3.5 (8.96) 3.18 (3.8-17.0) 13.24 (2.61-32.3 (6.60) < LOD < LOD 2.73) 7.17 (7.72) 2.98-9.40) < LOD < LOD 75th 2.29-4.0 (9.90 (2.96) 90th 7.0-33.70 (8.31-7.52 (6.10-4.4) 11.34-10.30) 3.90-15.8 (12.7-21.80) .60 (6.0 (10.0) 12.46-4.00-16.30) < LOD < LOD .90-15. 122 Fourth National Report on Human Exposure to Environmental Chemicals .0 (8.12 (4.58.80 (2.00-4.0) 13.00) 3.20 (<LOD-2.00-4.7 (10.10-10.90 (5.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .8-20.S.7) 10.6) 14.0-24.50-5.3 (9.70) 2.90) 4.9-15.42 (1.2) 14.80-8.58 (1.90 (6.8-20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) 8.3) 8.80-6.04 (3.7 (11.50-4.45 (3.90 (6.66) 4.60 (2.80 (5.6) 14.0) 14.80 (2.30) 3.81-6.77-3.9) 95th 14.5 (9.3) 22.95 (5.20-4.4 (10.0 (14.37) 2.67) 3.77-14.2 (7.650-1.00) 8.3) 20.1 (10.59-3.80-21.35 (6.80-4.6-19.00 (.90 (6.1) 11.35) 4.29) < LOD < LOD < LOD < LOD 3.47-6.27 (7.0 (10.30) < LOD < LOD 4.70-5.6) 18.50) .80-12.22-12.9) 10.970 (<LOD-2.16-1.10 (<LOD-1.3 (7.0 (9.0-24.9-14.64) 10.92-17.50) 3.8 (12.27) 9.3 (11.5.63-14.39 (5.27 (3.0) 7.670 (<LOD-1.0 (7.75 (3.10) 6.6) 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 * * * 1.0) 9.22) 8. population from the National Health and Nutrition Examination Survey.7) 14.9 (12.4 (14.99 (3.80) 5.27) .4 (10.6) 11.90-31.06 (2.0) 19.95-9.20) .70-9.70 (1.5) 21.22 (6.6 (10.66-13.00-18.4) 7.25 (2.10-15.20) 3.7) 22.41-5.2 (9.

5-17.29 (2.2-15.78 (4.64-11.9 (9.3-34.6) 95th 16.15 (1.6) 13.00 (7.890-2.4-15.97) < LOD .9 (9.38 (2.11 (5.38-13.03 (2.86) 9.28 (1.5) 8.55) 16.4 (11.3) 6.87 (3.63 (6.9) 16.38 (.940) < LOD < LOD 1.67 (7.93 (6.1) 20.3-21.973 (.4) 7.91-9.780-1.4) 16.30) 7.50 (6.06) .61 (2.3) 9.0 (10.88-7.39-17.3-17.89-3.27) 1.7 (10.9-25.590 (<LOD-.12) < LOD < LOD 4.00) 8.93 (<LOD-2.99) 2.6 (10.21-21. population from the National Health and Nutrition Examination Survey.5 (15.4) 6.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.78) 4.00) 2.27) 5.54 (7.23-3.68) .8 (8.79-6.09-11.8 (10.96-11.07) 2.48 (2.6 (12.920 (<LOD-1.74-4.88 (1.03 (6.99 (4.7-19.95) 90th 8.8) 16.4-18.6) 7.0-21.78-10.0-19.89-3.15) < LOD < LOD 75th 2.530-1.12 (7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 14.30-5.2-30.02-4.3) 8.690 (.2) 12.09-11.00 (<LOD-1.77 (2.6) 12.95 (2.38) 1.20-3.1 (13.0 (11.70-35.950) .72-4.5) 13.3 (7.3-17.6) 6.6-19.67 (1.91) 3.16 (3.45) 6.73 (5.7 (11.83 (6.93-10.45) 3.41 (7.11-3.4-16.07-3.79-9.7 (8.21) * * * * * 1.6 (11.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .9-17.54) 9.80) 3.94-14.5 (9.4) 7.19) 3.37) 3.14 (2.03) 3.89 (2.4) 9.33-10.75-3.7-23.50-17.81 (7.5) 10.7) 9.S. Fourth National Report on Human Exposure to Environmental Chemicals 123 .7) 14.5 (11.43 (2.07) 2.52-3.68-19.85-8.63 (2.3-15.6 (11.96-10.4-16.86-3.38 (1.82-8.7 (10.34) < LOD < LOD < LOD < LOD 3.00 (2.34-18.42) 7.29 (5.1 (19.2) 16.07 (5.25-9.1) 13.2) 12.5 (8.6 (13.93 (2.55) .28-12.55 (2.77) 3.6) 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 * * * * * * .27) < LOD .77 (2.32) 2.32-8.25 (4.92) 3.71) < LOD < LOD 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .58 (4.7) 14.30) 2.89-13.68-4.85-17.47-9.760 (<LOD-1.0 (8.9) 19.5 (10.2) 8.9 (9.51-7.18) 2.6) 14.6) 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 1.2) 12.44-6.89 (3.7) 15.89) 5.4) 15.620 (<LOD-.00 (5.6 (13.75-3.37-5.06 (<LOD-1.59-3.910 (<LOD-1.68-10.8) 11.69-11.27-13.82-11.86 (3.28) 6.5) 22.2) 15.27) * * * * * * * * 1.92 (5.95) 3.00 (3.0) 14.53-8.4) 7.3) 12.78 (6.2) 19.2 (9.36 (2.42-19.0 (13.83 (7.29) 3.810 (<LOD-1.29-2.00 (<LOD-1.2 (9.71 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.51-10.850 (<LOD-1.74-19.54-5.30) 8.97-4.2) 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.05-3.70-2.89-10.16-14.1 (8.7) 12.33) 3.01-5.2) 10.04) 9.1) 10.42) 8.72) 4.94 (5.

36-4.700) .83) .550 (.850) < LOD .710) .780 (.20) 3.90) 2. respectively.20 (1.760 (.949) .680-1.45 (1.459 (.570 (<LOD-.39) 2.49) .390-.25-1.70-7.90) 3.590-.960) 1.64 (1.98 (2.83) 2.690-.70 (1.790 (.98) .70 (1.45 (1.570 (<LOD-.17) 1.800 (.95-5.35) 1.59-2.750-1.46 (2.34) 2.74-5.83) 1.22-8.50-2.00-4.90) 2. and 03-04 are 0.425 (.97 (2.720-1. population from the National Health and Nutrition Examination Survey.505 (.30) 4.388-.88) 1.05-2.41 (2.20-2.759) * .94 (2. 01-02.77-2.455 (.600-1.20-3.30 (.26) .13) .22 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 3.570-1.80) 2.05-3.560-.94 (3.584) .730) .30-1.930) < LOD .58 (1.860) < LOD < LOD .80 (2.398-.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 * .453 (.37-2.91) 2.20 (1. 0.592) * 50th .670) .600-.90-4.690 (. which may vary for some chemicals by year and by individual sample.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.65 (2.76-6.29-2.89-6.95) 2. < LOD means less than the limit of detection.740-.20) 1.50 (1.00) 1.59-6.380) .457 (.990-1.57 (2.70-2.467 (.350-.03) 1.61 (1.80) 5.510 (<LOD-.46 (1.587) * * .960) .510 (.46-3.95 (2.90 (1.680-1.201-.710 (.20 (1.26 (2.570) * .20) 1.960) .14 (1.940) < LOD .68-5.2.21) 3.592) * .700) .597) * .80) 3.22-2.34) 2.10) 1.240 (<LOD-.79) .490 (<LOD-.31-3.75-2.50-2.750) 1.500 (<LOD-.40 (1.350-.13) 2.600 (<LOD-.210 (<LOD-.50 (1.970) 1.30 (.83 (2.30-3.38) 1.32-1.30-3.73 (1. and 0.98-3.31) 95th 2.980) 1.910-1.440-.780 (.580-.17) 1.30) 1.30) 2.690-1.380-.78) .89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.31-3.390-.780) .1.340-.592-.50 (1.27 (2.19-1.40 (1.22-3.96-3.47 (1.32 (1.20) 2.60 (2.54) .930) 1.83 (2.22-3.00 (1.570 (.30) 4.657) * * .880) < LOD .80) 3.10-1.16) 2.343 (.11-3.910) 1. interval) Selected percentiles ( 95% confidence interval) Total * .94) .400) .930-1.740 (.23-3.20 (2.09 (.17-4.710 (.820 (.549 (.08 (2.80) 2.30 (1.75 (2.86 (1.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .960 (.41-5. see Data Analysis section) for Survey years 99-00.359-.54 (2.74) 3.11-3.720 (.01-3.70 (1.880 (.20) 3.580-1.08 (2.15) 2.01-1.55 (3.10) 1.16) 1.960-1.57 (1.18 (.303-.449 (.73-5.60-4.50) 1.20-1.45-4.950) 90th 1.50 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.460-.73 (2.89) 1.10) 1.353-.54-2.20) 2.45 (2.810) .970) .650-.618) * .550 (.79) .86) 3.77 (1.60) 2.89) .18 (1.930 (.04) 1.80) 3.09.382-.740-1.04) .80 (1.48 (1.50 (1.46) 1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .720-1.49) 2.87-3.33-2.160 (<LOD-.96-5.00) 2.20-2.260 (<LOD-.15) 2.69-4.47) 2.S.820 (.31) 2.32) 3.749 (.585) * * .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 * .690) .63 (1.27 (3.48 (2.450 (<LOD-.00-2.14-1.16-3.76 (1.540 (.380-.880) < LOD 75th .620-1.830 (.840 (.740 (.570 (.910 (.29) 1.30 (.280-.42-2.10) 3.10-1.336-.01) .

580-.71 (1.76) 1.00-3.60 (1.52 (1.60) .760) .318-.820) 1.66 (2.62 (1.720 (.560 (.520-.97) 2.66) .20-7.50 (1.08-2.57-4.64 (2.94) .02-3.65) 2.740) .20) 1.880) 1.44) 2.900) 1.71) .39 (1.22-2.64 (2.23) 3.377-.07 (.510 (.710 (.22) .43) 2.42) .67) 1.32) 5.00 (3.552 (.47-4.78) 3.509 (.69 (3.55-3.38 (2.50) 1.393 (.447 (.910) < LOD .95) 1.84 (2.372 (.305 (.06-2.700 (.81) 2.57-2.310 (<LOD-.72-4.07-3.22) 4.61) 2.740) < LOD 1.88) .510-.645) .53) .05) 1.820) .49-4.400-1.04-1.89 (1.320-.22-3.89-3.88 (1.61-3.69 (1.17-2.550-1.00-1.380-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.720-1.640 (.60 (2.580) .760) < LOD 75th .79 (1.33) .23) 2.05-4.471-.58 (1.530 (. Fourth National Report on Human Exposure to Environmental Chemicals 125 .42 (.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 * .73-3.47 (1.41 (.17) 2.300 (<LOD-.23) 1.34 (1.72) 1.590) * 50th .950-2.136-.480) .300-.07) 5.82) 2.280 (<LOD-.75) 6.44-2.08) 2.750 (.07) 1.70 (2.460) .790 (.800-1.57 (3.270 (<LOD-.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .840) 1.380-.460 (.390-1.750 (.370-.62 (2.92-8.470 (<LOD-.739) * .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.87 (2.67) .485) * * .28 (1.84-6.57 (1.43 (1.830 (.510 (.07) 1.18-2.32) 1.710 (.73 (2.82 (2.550) . interval) Selected percentiles ( 95% confidence interval) Total * .444-.08 (.47 (1.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.92 (1.368) * .36) 3.29-4.08-3.25-3.07) 1.500-.800) < LOD .688) * .730) .453 (.285-.43) 2.440-1.43) 1.250 (<LOD-.940-1.250 (<LOD-.270-.310 (<LOD-.58-6.20-2.31-1.14 (2.42-8.06) 4.640 (.330-.42-6.03-2.630) * .335-.180 (<LOD-.75-3.17) 2.08 (2.470) .22-3.597) * .11 (.07-2.32 (.710 (.270-.67-3.97 (1.S.550-.77-3.990-1.67 (1.05 (1.19 (1.400) .98) 1.690) < LOD < LOD .77-4.52) 3.591 (.870 (.515) * * .930-1.850) 1.16-1.830) 90th 1.61 (3.45 (1.448 (.08) 1.33 (1.80) 2.38 (1.32-1.03-1.72 (1.590-1.230 (<LOD-.550-.840) .330 (<LOD-.920) .08-2.02-6.540-.560-.22 (2.61-3.30) 3.700 (.253-.23 (.08-2.24) 4.02-3.390) .680 (.55 (1.72 (2.350) .05-2.980-1.45 (2.640 (.870) .63 (1.520 (.10) 2.22) 1.09) .320-.490 (.08-3.77 (3.90) 2.75 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75 (1.234 (.670 (.13 (1.72) 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 * .60) 1.71) 2.04-5.99) 1. population from the National Health and Nutrition Examination Survey.310-.99) 2.91 (1.742) * * .16-2.05) < LOD .535 (.660-.590 (.11) 1.412-.92) 3.49 (1.403) .11-2.460-1.348-.840) 1.30-2.79) 1.790) .700 (.560-.08-3.32) 2.58) 3.23) 2.16) 1.70 (3.08-3.39) 2.580 (.380) .97) 1.480-1.97 (1.38-3.67 (1.04) 95th 2.

5) 30.44) 2.1) 38.96) 5.42) 1.58) 16.94 (1.13) 12.05) 1.46 (.64-8.0) 13.0) 30.0 (6.53 (1.0) 3.0 (37.9) 17.74-2.1) 140 (46.7) 47.0-29.6-45.04) 3.76 (2.3 (12.11 (4.1 (25.80-2.0) 45.3) 33.81-3.6-54.70-17.5-27. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-40.0 (20.10-13. see Data Analysis section) for Survey years 99-00.0-92.0 (19.18) 6.0) 28.20-4.0 (38.25-3.0-53.60 (2.0) 6.0-39.6-22.40) < LOD 1.0-43.5-20.1-46.90) 11.83-2.4-22. population from the National Health and Nutrition Examination Survey.4-76.2) 31.23-2.3) 38.10) .9 (10.92-5.20) 1.5) 69.0-50.8) 41.8 (26.S.70 (.0-110) 42.41) 5.0-31.0) 15.81-2.1 (25.50-20. interval) 1.3 (14.45) 2.70 (7.60) < LOD 1.0 (38.0) 42.30) 4.59 (1.7 (12.05-3.50-17.0-230) 35.2 (12.70) 1.57-2.49-2.8-24.32 (2.1 (22.0-41.0) 20.7-22.5.50-7.0) 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. < LOD means less than the limit of detection.3) 26.0) 19.0 (11. 126 Fourth National Report on Human Exposure to Environmental Chemicals .470 (<LOD-1.5-40.23) 9.8) 32.0) 16.52 (4.0) 33.0) 18.35-6.3 (10.71) 5.0) 20.02 (2.1-19.0 (8.29-9.12) 1.87-7.20 (2.36-2.00-24.4) 38.59 (1.9) 18.9 (19.1-20.70) 1.50 (2.3 (24.9) 38.11) 2.64-3.5-74.1-47.830-3.2-62.0) 3.95 (5.0-260) 34.0) 17.44) Selected percentiles ( 95% confidence interval) Total * 2.92) * 2.5 (24.14) 5.40) < LOD 2.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.0 (40.1 (11.0-110) 34.00 (.0 (38.10-4.8 (12.30 (.48-2.30) 11.0) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (8.54 (3.6 (11.41) 1.18) 14.90 (1.04 (<LOD-2.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.69) 2.50-2.77 (1.16) * 1.4 (10.40-4.46-6.26 (.2-80.06 (1.71-2.1-25.19-2.45) 2.83 (3.53) * 2.82 (1.78) 9.2-27.610 (<LOD-1.7-41.2 (19.80) < LOD 1.97) 6.80) 1.21 (4.0-62.0-47.33 (5.0 (7.04-8.07-5.48) 5.65 (4.85 (1.98 (1.41-4.13 (1.0 (38.67 (1.10 (1.0 (8.29) 2.80) 90th 38.27-6.99 (2.0) 3.8) 39.4 (19.0 (24.5-45.0 (20.10 (1.88) 1.3) 28.00 (.44) 3.88) 3.48-2.9-21.6) 52.90 (1.0 (25.41) 1.83 (1.7 (12.1 (26.8 (12.10 (7.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.16) 2.61 (1.77) 38.44-7.83-2.6 (9.18) 20.19) 2.93-3.0 (13.0) 3.2-27. and 0.6-27.26) 75th 11.0) 28.1) 95th 48.66-5.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.72 (1.9 (27.0-58.1) 18.70 (1.57-2.98) * 2.30-14.71 (4.0-53.13 (1.600-2.2-33.86-3.70-6.690-3.10 (1.9 (19.17-2.0) 4.8 (22.3 (23.10 (1.830-4.0-69.0-58.6 (15.79 (2. which may vary for some chemicals by year and by individual sample.0 (26.76 (2.21 (1.78 (1.43-7.4. 01-02.0) 4.2) 16.40-16.79-2.70 (1.0-39.0) 16.54 (1.0) 4.50-5.0 (38.41 (1.8) 62.06) * 2.6 (26.0) 15.70) 5.3 (12.0 (38. 0.9) 48.0-41.91 (4.40) 50th 2.0) 32.53) 40.0-62.4) 19.29-4.90-8.09 (4.79 (1.9 (23.0) 31.05) * 2.0 (21.61-2.53) 1.0 (33. respectively.10) 39.0 (38.0-41.0 (32.7) 20.80-18.63-6. and 03-04 are 0.21 (3.530-4.86 (1.3) 31.0-49.8-21.46-2.2-39.12 (3.0) 17.4 (15.85) * 2.9-51.18.1) 38.7 (28.23-2.660-2.0) 8.31-6.75-14.0 (17.2-26.80) .1 (10.0-52.58-2.2-47.

0) 25.06) 1.5) 27.19-14.2) 33.890-4.7) 61. population from the National Health and Nutrition Examination Survey.4 (11.07-2.71) 8.12) 3.59-2.1) 27.6) 19.1-60.40-4.83 (.45-1.6 (11.7 (18.9) 3.03) 1.9-52. interval) 1.2 (22.12 (1.6) 3.0 (19.30) 28.9-37.95-16.2) 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 2.0) 48.870-3.25-3.2) 4.9 (13.35) .06) 1.46) 1.9) 12.82) 1.36-13.7 (18.95 (2.19-6.1) 52.9-18.20) Selected percentiles ( 95% confidence interval) Total * 1.00 (4.1-63.32 (3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.14-8.43-2.2-70.46-22.0 (6.3-22.4-21.94) 1.75) * 1.680-4.40-7.67 (1.11-2.0 (23.86) * 3.91 (6.3 (10.27 (6.4 (9.27) 50th 2.1) 13.69-18.02) 1.58-17.6 (7.17-3.51) < LOD 1.5-43.9-36.28) 1.22 (2.66 (1.75 (1.2 (8.4 (25.46-6.03-2.1 (50.18-1.8-26.3 (10.9) 24.2-34.7-47.2-47.27) 10.00) 1.97 (1.6-38.95-16.72) 2.8-37.66) 8.51) .58-2.82 (2.24 (1.07) 9.0 (17.9 (26.0) 10.08 (1.7) 15.80 (1.55 (2.6-49.15 (.66 (1.61 (1.5 (41.38 (3.1) 36.88 (1.53) 1.4-71.37 (1.23-1.3 (20.22 (.7 (24.19 (1.40 (2.90 (.33) < LOD 1.4 (5.0-70.9) 24.43-12.6) 3.2 (16.2) 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 1.6) 112 (40.26-4.9 (10.14 (.4-39.88 (1.27-3.9-95.3-27.54-2.6 (27.0) 13.1) 25.670-1.5 (15.3-19.18) 3.4) 3.2 (9.7-38.9) 54.4) 12.0-40.22-3.888-1.46-5.95) 90th 32.4 (19.94) 19.99-4.5-36.7) 66.64 (1.8) 15.0) 47.0) 30.02 (.5 (17.5 (13.8) 3.1) 27.34) * 1.16 (1.6) 7.7-43.96-16.7-37.2-38.7-20.62 (2.91-2.50 (2.00) 6.6) 23.5 (34.0 (39.3 (9.6-51.33) 1.60 (.70-4.0-118) 29.67-3.6) 11.75-6.8) 11.5) 70.2 (15.38-5.06-1.0 (25.7) 23.39 (1.7) 95th 51.23) 37.36) 10.7-19.01 (.1 (39.56 (2.7-109) 22.5-97.5 (6.7) 26.2) 13.4-67.69-5.08) 1.61-22.21 (4.33) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09 (5.67-16.33-5.19) 5.8) 32.7 (10.59-15.8-43.3) 13.3 (8.5 (15.47 (3.83) .71 (1.93) 5.48 (4.9 (19.37-2.0 (23.63-5.29-5.70 (1.0 (32.52-4.75 (1.80-8.1 (33.35) 1.16-2.8-34. Fourth National Report on Human Exposure to Environmental Chemicals 127 .2) 41.2) 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.79 (2.28 (1.0) 3.57) 4.1 (25.31) 2.1) 13.2 (21.96) 2.750 (<LOD-1.S.870-3.36 (4.1) 17.00-16.20-5.4 (21.930 (<LOD-1.8-45.3) 28.16 (1.71-2.1) 15.4 (25.3-42.8) 23.6-32.18) * 2.61-2.11) < LOD 1.5-190) 30.4-34.9 (39.16 (1.68) 47.76-2.1) 25.1-22.0) 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 (12.22-2.19) 5.4) 14.2-28.0 (14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06) 75th 9.43) * 2.23) < LOD 2.59-2.50-5.68 (1.60) 4.7 (11.8 (7.2) 36.45 (1.88 (4.9 (7.4) 12.860 (<LOD-1.4 (12.07-2.7) 30.47 (1.26-2.0-71.56) 1.67 (1.41 (2.84-13.2) 13.9) 3.9-41.6 (24.79-17.17) 2.8) 31.47-17.1 (34.5 (8.57 (6.38) 5.35 (2.02) * 1.899-2.94-20.54-15.7) 34.40 (5.870-3.62) 4.32-3.44) 9.86) * 2.88 (4.48) 1.52 (1.38-1.

560 (.130) .450 (.840) .540) .700-1.550) .380-.130-. respectively.840) .090 (<LOD-.380-.600 (.630 (.640) .610-.940 (.58) .10) .700-1.720-1.620 (.099-.640-1.410) < LOD < LOD < LOD < LOD .410-1.680-1.160) .410-.130 (.171) * * .10) .320-.610-1.580) 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 * * * * * * .090 (<LOD-.830 (.160-. see Data Analysis section) for Survey years 99-00.640 (.990) .870 (.230-.830 (.690-1.680-1.050-.680 (.05.10 (.200) < LOD < LOD .270 (.30) .640) .330-.300-1.560 (.460-.190 (.430-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .300-.700-1.400-.860) .850 (.870) < LOD .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.390 (.117 (.190 (.380-. which may vary for some chemicals by year and by individual sample.360-.130-.720) .30) .230) .40) .140) . 0.20) .080 (<LOD-.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.290) < LOD < LOD < LOD < LOD 90th .36) .450 (.350) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170-.1.13) .090 (<LOD-.440-1.130) .650) .770 (.410-.290 (<LOD-.540 (<LOD-.830) .30) . and 0.900 (.220 (.42) .820 (.850 (.490 (.180) .610 (.870 (.730) .140-.650-1.830) < LOD . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .770) < LOD 95th .450 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700-1.240 (<LOD-.820 (.460 (.680) . 01-02.310 (.160) .110-.870 (.650) .650 (.32) .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 * * * * * * * * * .210 (.120 (<LOD-.162) * * * * * .090 (<LOD-.930 (.420-.350) < LOD < LOD < LOD < LOD .090 (<LOD-.610 (.370-.720 (.730-.120-.470-1.360-.S.15) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .140-.310) < LOD < LOD < LOD < LOD .660 (.130-.080 (<LOD-.1.290) < LOD < LOD < LOD < LOD .310) < LOD < LOD < LOD < LOD .60) 1.540) .260 (.630 (.470 (.990 (.120-.210 (.12 (.190 (.10) .650-1.140-.100 (.530-.760) < LOD .390) < LOD < LOD .084-.740) < LOD .780) < LOD 1.150 (<LOD-.860-1.370-.320 (.850) < LOD . < LOD means less than the limit of detection.00) .03) .510-1.280) < LOD < LOD < LOD < LOD .310 (.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 .310-.090 (<LOD-. and 03-04 are 0.870 (.42) . population from the National Health and Nutrition Examination Survey.990) .870 (.570) .220 (<LOD-.430 (.150) .

410 (.260-.780 (.220) < LOD < LOD < LOD < LOD .390-.070 (<LOD-.02-1.880 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .100 (<LOD-.080 (.740) < LOD 1.110) .110) .290) < LOD < LOD < LOD < LOD 90th .170) < LOD < LOD .140) .270 (.24 (.700-1.540 (.03 (.860 (.510-.740 (.400 (<LOD-.570-1.140-.610-1.510) 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 * * * * * * * * * .330-.520-.057-.890 (.19 (.67) .140-.580) .880-1.00) < LOD .410) .570-.730 (.270) < LOD < LOD < LOD < LOD .360-.380-.02) .460 (.070 (<LOD-.660-1.140-.670 (.280) < LOD < LOD < LOD < LOD .S.380-1.24) .14) 1.170 (.490-1.670 (.580-1.100-.470 (<LOD-.070 (<LOD-.730) .380-.860 (.120) .66) 1.080) .800-1.960) .600-1.090 (.440 (.810 (.970) .700) .500-1.670-1.116 (.370 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.410-.340-.300 (.330-.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 .360-.090 (<LOD-.01 (.43) .700 (.500 (<LOD-.050 (<LOD-.190 (.190 (.110) .36 (1.410 (.560 (.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 * * * * * * .330 (.140-.540 (.450 (.230 (<LOD-.700 (.760) .240-.230-.250-.86) .03 (. population from the National Health and Nutrition Examination Survey.580) < LOD .320 (<LOD-.360 (.260) .870) .450) .990) .570 (.300-.730) .220 (.940) .550 (.400) .20) 1.78) .62) 1.720 (.440-1.210 (.03 (.330-.540) .110) .230) < LOD < LOD < LOD < LOD .111) * * * * * .300-.640-1.161) * * .410) < LOD < LOD .09) .12) < LOD .200 (.550 (.650-1.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.780) < LOD 1.110-.730) .170 (.860-2.060-.29 (.330 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.380-.120) .200 (.940) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .60) .03) .390-.86) .580 (.084-.720 (.750) < LOD 95th .500) .580 (.850 (.140-.360) < LOD < LOD < LOD < LOD .710-1.310) < LOD < LOD < LOD < LOD .080 (<LOD-.600) .190-.38) 1.650) < LOD .180-.58) 1.990) .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .070 (<LOD-.380 (.150-.410-.

population from the National Health and Nutrition Examination Survey.70-30.30) 95th 19.07) 1.0-38.29-10.640 (.0 (17.50) .20 (1. which may vary for some chemicals by year and by individual sample.48 (2.0) 4.360-1.770) 2.0) 5.730 (. respectively.40 (1.0) 5.88-3.16) 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 .210-1.840 (.23-6.691 (. and 0.83-3.83) 2.880) 5.53 (2.0) 2.0) 4.28-9.05 (3.380-.0 (17.60) 1.0) 2.07 (3.0-40.840-3.21-3.90 (1.70) 2.46 (1.580 (.00) .800) 90th 13.20-4.30 (1.0 (5.0) 2.21) 3.39 (2.68) 2.20) < LOD < LOD < LOD < LOD < LOD 1.0) 3.63 (3.190-1.830 (.53-7.50) 2.0-38.10 (3.24-7.40) 1.49 (1.480-.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.690 (.890 (.94 (1.10 (.30 (.83-3.400-1.13 (3.86) 4.250 (<LOD-.08.07 (1.0) 4.960 (.0 (17.40) 2.840 (<LOD-1.40 (1.61 (1.40-7.90 (2. see Data Analysis section) for Survey years 99-00.640 (. 130 Fourth National Report on Human Exposure to Environmental Chemicals .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 * * * * * * .99) 19.330 (<LOD-1.12) * * * * * * * * .0) 5.590 (.52 (1.425-1.90-37.97) 20.60) .47 (3.43-4.15) 14.0 (17.07-3.90) .90-28. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0 (17.76 (1.0 (5.74 (3.70-7.90) . and 03-04 are 0.96 (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.12-1.31) .S.610 (.70-50.67 (1.07-3.0) 2.30-6.51 (2.1.99) 11.90-9.6) 5.33 (4.03 (.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.39) .37) .32 (1.90-20.05 (2.800-4.55-4.900 (.07 (3.26 (2.38-3.30 (1. 0.740 (.170-1.31-10.42) 2.750-1.28) 1.0 (4.960 (<LOD-1.28) .0 (13.620-1.00 (1.35-10.800) 17.35) 5.0 (6.14) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 01-02.0 (3.36-3.11) 13.74) 5.600 (.66) 4.36-3.0) 2.110 (<LOD-.80 (4.49 (1.32-9.00) 1.370-.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 * * * * * * * * * .750-2.14) .080-1. < LOD means less than the limit of detection.0 (4.85-3.610) < LOD < LOD < LOD < LOD < LOD 2.15) 19.20-17.70-3.0-40.42) .0 (7.510-.67 (2.01) 5.05-3.48) 13.62-8.20 (1.97) 20.49) 17.30 (1.90) .82-4.40-8.14-5.99 (1.770 (<LOD-1.10 (3.70-17.35) 11.00 (.51-8.00) .30-7.20-4.00-17.63) 32.67) .350-.52) 5.350-.0) 7.11) .870) < LOD < LOD .0) 2.65) 1.0) 4.45 (2.0 (5.94-3.0-44.52 (1.18) 1.53) 20.30 (2.0) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (16.94-8.11 (1.55-8.30-3.0) 2.0 (5.10-3.0 (5.00-17.1.260-.10-3.0-39.40-20.40-4.720) 2.0-38.87) 12.850) 16.87) 5.10-9.910) 2.59-5.30) .

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.5) 2.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.02) .700) 6.1 (7.56) 2.40 (.04-16.830-3.43) .05) .15) 9.55 (3.67) 1.91-4.00-19.748 (.97) .7) 5.85 (1. population from the National Health and Nutrition Examination Survey.370-1.84) 9.670 (.30 (4.7) 3.65 (2.4-34.08) .44) .39) 20.820 (.630-1.31) .51-4.340-.86 (3.580) 16. 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 * * * * * * * * * .340 (.18) * * * * * * * * .85-3.27 (2.66-47.7) 6.320-1.44-11.83-11.22-27.474-1.370) < LOD < LOD < LOD < LOD < LOD 1.89 (2.600 (<LOD-1.62 (1.560 (.50 (2.88 (.790 (.580-1.710 (<LOD-1.9 (11.0 (4.860-2.49-2.S.96-8.310-.340-.40) 1.74 (2.14-6.00) .80) 3.33 (3.8 (20.960 (.21-3.07 (2.580 (.41 (4.450 (.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 .330-1.67 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.64-4.14 (1.80 (.56) .1) 2.740-1.12-4.92 (2.620-3.55) 21.83 (4.430) 1.370 (.38 (2.36 (.3) 3.45 (1.04 (1.730-3.88) 17.540 (.150 (<LOD-.28-6.25 (1.73 (4.340-.40-12.2-38.29 (4.700) < LOD < LOD < LOD < LOD < LOD 1.5 (8.10-3.01 (1.250 (<LOD-.71 (2.1 (5.88 (2.69) 2.53) 27.79 (.3) 2.57-40.8) 7.29-4.57 (.62-17.71 (.31) .580) 1.270 (<LOD-.13 (2.360 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.51-44.5) 2.4 (4.970-3.50) 11.470 (.47) .90-6.9) 5.11) .32) 9.50 (4.77 (.11-5.09-3.57) 8.270-.32-6.82-11.1) 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 * * * * * * .2 (8.8-33.69-7.650) 90th 10.88-3.40-2.850-3.260-.33-4.5 (11.7 (12.56 (1.59 (1.830 (.64) 30.03) 2.75) 5.52 (.690-5.12 (4.07-21.260-.96-25.31-7.53) .03) 16.190-1.98 (4.8) 1.91) 2.790) 11.1) 672 678 497 509 694 551 595 947 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.22) 2.33 (1.02 (1.9) 6.17) 5.820) .390-.48 (4.770) .67-6.24) 3.10) 2.48-7.02 (.18) 95th 21.500 (.5) 7.660) < LOD < LOD .81-17.7) 4.33-5.06 (.96) 2.57) 1.17 (1.0) 4.50) .840-3.8) 7.890 (.8) 2.930) .25-38.7 (6.25-9.33-3.10 (2.0 (9.23-7.780-4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.37) 4.5-40.8) 2.67) 2.55) 21.02-4.60 (1.590) 2.31-18.5 (9.47-10.86) .41) 18.940-4.47) 5.35 (.800-2.540-1.18) 1.240-.8) 4.4) 2.650 (.48-42.430 (<LOD-.47-10.

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The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. et al. Muniz J. Schenker M.S. Stephens R. Lasarev M. McConnell R. Terry AV Jr. et al. Environmental Protection Agency (U. Rothlein J.332(1-3):71-80. Washington (DC). Chrislip D. Scherer J. Dinoff TM.12(2):153-172.44(4):352-357. Pesticides in the Diets of Infants and Children. Stark A. Stokes L. J Occup Environ Med 2002. A behavioral evaluation of pest control workers with short-term. Rothlein J. McCauley L. Takamiya K. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Buccafusco JJ.43(1):38-45.338(8761):223-227. Jamal GA.pdf. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. J Toxicol Environ Health A 2005. Bradman A. Berry H. Am J Public Health 1994. Saieva C.12(2):134-141. vibration sense and tremor among South African farm workers.24(1):18-29. Washington (DC): U. Available at URL: http://books. Lewis JA.38(4):546-563. Int J Occup Environ Health 2006. Savage EP. Keefe TJ. 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. National Research Council (NRC). Claypoole K. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Petchuay C.113(4):504-508. Occupational exposure to organophosphate pesticides: a neurobehavioral study. O’Malley M. Robson MG. Muniz J. Lu C. Hore P. Am J Ind Med 1987. EPA). discrimination. Ames RG. Office of Prevention Pesticides and Toxic Substances. 2004. Steenland K. Seiber J.68(3):209-227 Maizlish N. U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. The Pesticide Health Effects Study Group. Irish RM.epa. Environ Health Perspect 2006. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Spurgeon A. metabolite clearance. Neurotoxicology 2005. Ruberu DK. 1991. Johnson C. and cholinesterase status of date dusters and harvesters in California. Hansen S. Rohlman D. Wickremasinghe AR. Arch Environ Contam Toxicol 2000. Sci Total Environ 2004. Visuthismajarn P. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Marshall E.S. Malathion deposition. Phillips J. National Academy of Sciences.114(5):691-696. Scand J Work Environ Health 1998. et al.58(11):702710. Eskenazi B. Lambert WE. Burcar PJ. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Myers JE. low-level organophosphate exposure on delayed recall.php?record_id=2126&page=1. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function.30(2):98-103. 1993 [online]. Bravo R. Arch Environ Health 1988. Effects of long-term organophosphate exposures on neurological symptoms.nap. Lancet. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Barr DB. Gladstone EA. Thompson ML.2000 and 2001 market estimates. Buchanan D. Weerasekera G. Smit LA. Mounce LM. Arch Environ Health 1975. Occup Environ Med 2001. Lancet 1995. EPA. Rosenstock L. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Neurotoxicol Teratol 1998. Daniell WE.52(10):648-653. Chronic neurological sequelae to organophosphate pesticide poisoning. and spatial learning in monkeys and rats. Prendergast MA.26(2):199-209. Pesticide industry sales and usage . Occup Environ Med 1995. Tumino R. 4/7/09 Young JG. Environ Health Perspect 2005. Gillham R. Vitayavirasak B. London L. Nell V.52(2):190-195. Levy LS. Russo J. Keifer M. Salvini S. Beach J. May. Effects of chronic. Masala G. S.20(2):115-22. Samuels S. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Santana J. Weisskopf C. 1/12/09 Peiris-John RJ. Pedersen L. et al. Rodnitzky RL. Heaton RK. Neurotoxicity among pesticide applicators exposed to organophosphates. Aprea C.345(8958):11351139. Calvert IA. Frasca G. Lasarev M.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Jenkins B. van der Hoek W. Narang A. Kidd M. et al. Caltabiano LM. Bull Environ Contam Toxicol 1994.84(5):731-736.edu/ openbook. low-level exposure to the organophosphate diazinon. Pilkington A. Available at URL: http://www.

In addition to reflecting exposure to the parent insecticide. For example. For general information about the organophosphorus class of insecticides. the level may reflect exposure to the environmental degradation products of these pesticides.” 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) 3.5. parathion and methyl parathion are metabolized to para-nitrophenol. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report.Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies.6-Trichloro-2-pyridinol (6515-38-4) 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol 2-Isopropyl-4-methyl-6-hydroxypyrimidine (2814-20-2) Malathion dicarboxylic acid (1190-28-9) para-Nitrophenol (100-02-7) 2-(Diethylamino)-6-methylpyrimidin-4-ol/one 134 Fourth National Report on Human Exposure to Environmental Chemicals . malathion is metabolized to malathion dicarboxylic acid.

S.40) 9.10 (5.0 (13.50 (2.47-13.90) 3.95) 7.15 (1.30 (2.10-17.70-11.0 (7. 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.79-2. It also has been applied directly on animals to kill mites.68 (7.86) 4.43-2.10) 6.28-3.3) 8.67 (2.63 (8.9 (9.20) 10.94 (4.80) 2.0 (7.EPA.S. 2007).60) 5.S. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.44-2.80) 4.7) 9.30-1.30-11.37) 5.47-11.51 (1.2 (10.70 (1.66-4.70 (1.0) 7.97) 4.90-4.20-14. chlorpyrifos was no longer registered for indoor residential uses in the United States.0) 8.44 (3.4 (8.20) 2.000 pounds are used per year.52-2.10 (3. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.7) 8.9) 697 660 521 701 602 947 Limit of detection (LOD.51) 1. applied to structures to kill termites.76 (1. The general population may be exposed to chlorpyrifos via oral.13 (1.72-4.92 (1.30-5.90 (1.90 (1.20 (4.20-3.47 (4. and sprayed to kill mosquitoes.40 (5.28) 2.30-12.0) 12.29-1. Survey Geometric mean (95% conf.5-24. 1999.30) 4.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.35) 1.0 (7.0) 10.24-1.0) 12.0 (10. and is infrequently detected in ground water (IPCS.0) 15.22) 2.90 (2.84) 1.1) 5.71 (6. For instance.32) 2. Exposure can also result from contact with contaminated surfaces.83) 1.20-2.50-4.00) 2.53 (1.61) 75th 3.24-3.63 (1.32-1.59-2.20) 4.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.90 (3.00) 3.77-15.63 (2.16) 2.02 (1.47-9.34) 1. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.17 (1. Chlorpyrifos is Urinary 3.70-17.30) 4.50-5.5) 7.50-4.20 (2.29) 90th 7.90 (6.0-28.40 (5.13-3.19 (1.60-4.37 (1.74-9.60 (2.21) 3.76 (1.50 (2. dermal.97) 7.30-9.19-3.46-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10. USGS.0 (7.66-15.68-2.39-2.and post-construction structural applications for termite control were to be phased out by 2005 (U.0) 9.64) 3.40-2.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.4.50-14.09 (2.90-8.03) 1.80-8.62-2.67 (2. and dust.5 (8. staying bound to soil particles.80) 1.27 (7.87-6.20-16.80 (7.0) 14. 2921-88-2 Chlorpyrifos-methyl CAS No.31-2.0) 12.97-7.80-10.4 (10.60 (4.8) 9.0) 6.67 (1.61-7.52-12.3 (8.47) 1. but can be detected in streams receiving runoff from application sites.50 (2.40-13.70-5. Approximately 80. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.80 (1.60 (5.09 (3. It has low leachability. interval) 1.60-3.44-5. 5598-13-0 General Information The chemical 3.04-10.6) 7.30-2.20-11.59) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.35) 2. 2002).3 (10.10) 2.90-2.20-4. 2005).30 (2.40-10.89-2.0) 18.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.02 (7.0) 11.96) 3.5.0) 8.50-2.88 (1.50-2.97) 2.50 (1.45 (1.10 (4.57 (2.80) 12.95 (4..9 (10.25) 1.01) 1.31-2.22 (1.99-4.4 (9.77) 1.61 (1.91 (1.4-15.89 (2.0 (7.9) 11.02) 1.36 (4.60-2.05-5.90-7.9-18.51-2.10 (1.1-16.55-5. After 2001.74 (1.43-2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.37 (4.50-8.5.60-3. Fourth National Report on Human Exposure to Environmental Chemicals 135 .90) 7.00-24.72) 2.81-2.4 and 0.70-16.98-15. and inhalation routes.8) 10.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.30 (4.04-10.40 (6.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3 (11.38 (3.97) 2.77 (1.77-6.26) 7. population from the National Health and Nutrition Examination Survey.71 (1. pre.9 (7.91) 16.7-23. Approximately 21-24 million pounds per year were used domestically from 1987-1998.0) 10.00-8.00) 1.05) 1.71 (2.20) 2. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 12.0) 12.40-26.40) 2.0) 10.30) 5.70-15.78 (7. in 142 urban homes and preschools in North Carolina.25) 3. and on plants for days to several weeks.8-15.0 (9. Estimated intakes from diet and water have not exceeded recommended intake limits. 2002).70) 1.50 (1. air.39) 4.EPA.7) 13.

12-1.11) 7.24 (1.81) 2.12-3.09-1.94-14.85 (3.00-8.35) 1.82-4.80-4.38) 3.75 (1. TCPy is more persistent in the environment than chlorpyrifos itself (U.91) 2. cholinergic effects.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.82 (3.54 (2.EPA.21-1.85) 1.51 (1. and other metabolites.24-4.47 (1.17-4.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.21-6.85-4.05) 3.16) 6.1 (10.26-14.75) 6.70-4.01) 3.47-2.6-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..62) 90th 5.3) 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 1.44 (5.39 (4.14) 1. 2005.91-4.62-7.80) 3.24-5.93 (1.27-1. 2002).93 (4.09-3.72) 2..72) 1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.27-7.23-1.29 (3.41 (1.85) 4.98 (6.20-1.33 (5.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.00) 1.16 (4.89) 4.03) 1.0) 6.53-5.76 (3.57) 9.45-1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.00 (7.88-8.30-1.44 (5.43-10.06-4.71 (1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.8) 9.83) 1.49 (1. Ricceri et al.48 (2.47 (1.69 (1.81 (3.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .37 (1.58 (4.02 (5. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.48 (1..79-13.74) 1.88-9.24-24.64-2. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.82) 8.02) 7.97 (3.11 (2.55 (4.25-1.24) 75th 2. 2006b).68) 1. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.92) 3. resulting in excess acetylcholine at nerve terminals.06 (5.S.3) 8.64 (1.33 (1.47 (5.49-2.28) 2.07) 1. Metabolic hydrolysis leads to the formation of TCPy.93) 2..62) 1.95 (3.44 (1.58) 5.91) 1.73 (1.63 (4.68) 6.35) 2.49-2. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.35-1.05-4. neurotransmission.20 (2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.6) 10. 2006.28) 2.33 (.05-1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.53 (2.88-8.7) 7.32) 1.86 (3. 2006.43 (4.45 (1.2 (7. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”)..19) 6.11 (2.50 (4.33) 2.65-11. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.39) 6.63 (5.91-13.60 (1.2) 6.3) 8. Howard et al.22 (4. Survey Geometric mean (95% conf.52 (5.09-2..0) 12.91 (3.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.82 (2.98 (7.40) 1.99) 1.56-2.85 (2.33-7.08) 6.09 (1.3 (7.31-4.84-6. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.83-11. 2005.30-4.99-8.66) 1.65-15.940-1.39 (2.96) 3.88 (1.05-8.88) 6.56 (1..55) 1.60-3. and seizures.63-2.78 (1.77) 1.49-2.56) 2.17-4.97) 3.59) 3.6) 9.25-11.86 (1. and producing acute symptoms such as nausea.88-10.55 (1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.1 (7. TCPy can also occur in the environment from the breakdown of the parent compounds.01) 1.92 (1.07) 5.44 (6.46 (2.36) 1. population from the National Health and Nutrition Examination Survey.54) 5.42 (6.90-9. 2006a.87-3.57-2.24) 5.12) 1.42 (5.66-11.05-3.22 (6.76 (2. Once absorbed.57-2. Betancourt et al.95 (1. 2005.46 (1.57) 2.1-21.58 (1.15 (4. Slotkin et al.19-1.93) 5.31-1..71) 3.58 (1.5.83-2. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.91 (4.64-7.58-5.14-8.93 (2.44-6. paralysis.24-1.91) 10.3) 9. Urinary 3.91) 1.34-1.23) 14.80-6.00-13.0) 16.97) 3.0) 10.06 (1. interval) 1.94-12..11-9. vomiting. Based on animal data and human cholinesterase monitoring during occupational exposure. In pesticide applicators. 1984).59-2.42-2.56) 5.19) 3.25-12.80-11.9 (12.19-2.66 (1.5 (6.72-2.44 (1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.86 (1.56 (4.22) 1.58) 1.5) 5. weakness.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.31) 1.4) 4.92-2.01) 3.97 (2. Roy et al. Thus.S.88 (1.22-6.97-3. 2000).39-1.1-38.

et al.epa. Koch et al. Whyatt et al. et al. Of 482 pregnant women living in an agricultural community. Perera et al. Chlorpyrifos exposure and biological monitoring among manufacturing workers. urinary TCPy levels in children were reported not to have increased (Hore et al. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.EPA. Carr RL.. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Lioy PJ. 2006). Aldridge JE. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. representative subsample of NHANES 19992000 (CDC. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Betancourt AM. 2005).109(6):583-590.gov/toxpro2. Betta A. Meyer A. Clayton CA. Fourth National Report on Human Exposure to Environmental Chemicals 137 . J AOAC Int 1999. Barr DB. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. In a probability-based sample of 102 Minnesota children aged 3-13 years.. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. 2001). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.atsdr. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Giordani B. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al.html and from U. Lotti A. Freeman NC. Garabrant D. EPA at: http://www. Curwin et al. 2005).gov/pesticides/... 2001) and Italy (Aprea et al.. Barisano A.S. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al.S. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.S. Occup Environ Med 2006. In Minnesota and South Carolina farmers who used chlorpyrifos.. Following crack-and-crevice application of chlorpyrifos in their homes. 2005).5.. 2005)...Reference values of urinary 3. Eberly LE. Levels of TCPy in the U. Environ Health Perspect 2001. 2007). In Iowa farm families using several different pesticides.S.113(8):1027-1031.63(3):218220. 2005). Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. References Adgate JL. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.82(2):305-312. 2005. Toxicol Sci 2006. Albers JW. Seidler FJ. Slotkin TA. 2005). U.. population (CDC. 2005. Burgess SC. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. MacIntosh et al.e. Haidar S. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Berent S. 1992.. 2005. 1999). 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. the geometric mean urinary TCPy levels were similar in parents and children. CDC. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 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. Additional information about external exposure (i. but not chlorpyrifos. Aprea C. but levels were roughly four to six times higher than the geometric means in the U. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al.. Magnaghi S. 2004).. 2000).. Catenacci G. 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. 2003.Organophosphorus Insecticides: Specific Metabolites 2004.92(2):500-506. environmental levels) and health effects is available from ATSDR at: http://www. 2002).6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Burns CJ. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al..cdc. 2004). Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity.S. Environ Health Perspect 2005.

Jett DA. gov/ntpweb/index. mothers and fathers living in farm and non-farm households in Iowa. Rauh V. Brain Res Dev Brain Res 2005. Head SL. Environ Health Perspect 2006a. Wartenberg D. Available at URL: http://ntp. Hines CJ. Available at URL: http://www.114(5):746-751. Toxicol Appl Pharmacol 1984. Weltzien E. Seidler FJ.108(4):293-300. Pesticide residues in urine of adults living in the United States: reference range concentrations. et al. Roy TS. Cometa MF. Environ Health Perspect 2005.S. Bennett DH. Adgate JL. J Expo Anal Environ Epidemiol 2005. Bucelli R. Hardt J.9(5):494-501. Lein PJ.111(2):201-205. Bailey SL. Chlorpyrifos: pharmacokinetics in human volunteers. Lu C. 4/7/09 Perera FP.113(2):211-219. Lioy PJ. Fortuna S. Lorenzini P.31 Suppl 1:98-104. 1999. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Howard AS. Herrick RF. Meeker JD. 2005. Int J Hyg Environ Health 2001. 1992. Saunders JH. Harley K. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.112(10):1116-1124. EPA). Freshour NL. Yang D. Environ Res 1995. Environ Health Perspect 2006b. Chlorpyrifos. et al.93(1):105-113.5. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.155(1):71-80. Environ Health Perspect 2006. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. Rick DL. Barr DB. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Tate CA. Levin ED. Baker BA. Gregg M. Jewell NP.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC).73:8-15. Hill RH Jr. Gurunathan S. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. et al.org/documents/jmpr/jmpmono/ v99pr03.71:99108. et al. Seidler FJ.6-trichloro-2-pyridinol. A longitudinal investigation of selected pesticide metabolites in urine. Chapman P. Tsai WY. 4/7/09 Koch HM. Toepel K. Jones PA.114(2):260-263.niehs. Slotkin TA. Environmental Health Criteria 198. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Sheldon LS. Hore P.204(2-3):175-180. Toxicol Appl Pharmacol 2005.nih. et al. Fenske RA. Needham LL. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Pellizzari E. Ryan PB. Shealy DB. Eskenazi B. Sharma V. 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Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 2921-882. Steenland K. Robson M.htm. Venerosi A. Barr DB. Reid TM. chlorpyrifos. Neurologic function among termiticide applicators exposed to chlorpyrifos. et al. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Bravo R. Irish R. Capone F. et al. Chrislip DW. Scand J Work Environ Health 2005. U. Angerer J.6-trichloro 2-pyridinol in their everyday environments. Barr DB. Ozkaynak H. Baker S. Striley C. Morgan MK. Zhang J. Curwin BD. Ricceri L. Urinary pesticide concentrations among children. Edwards RD.114(10):1542-1546. International Programme on Chemical Safety-INCHEM (IPCS).15(3):271-281. Atlanta (GA). J Expo Anal Environ Epidemiol 1999. Bradman A. Sanderson WT. Ryan L. Chuang JC. Environ Health Perspect 2000. Ryde IT. Biomonitoring for farm families in the farm family exposure study. Dick RB. Howell RJ. Freeman N. Environ Health Perspect 2003.S. Barr D. et al. Hammerstrom KA. Hein MJ. Heederik D. Environmental Protection Agency (U. Exposures of preschool children to chlorpyrifos and its degradation product 3. National Toxicology Program (NTP). Slotkin TA. Robertson GL. Mandel JS. Environ Health Perspect 2004. Third National Report on Human Exposure to Environmental Chemicals.

Barr JR. Camann DE. 6/1/09 Whyatt RM. Geological Survey (USGS). Available at URL: http://pubs.pdf. Barr DB. February 2002. 2007 [online].usgs.Organophosphorus Insecticides: Specific Metabolites 01-007.gov/circ/2005/1291/. Environ Health Perspect 2003. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. et al. The Quality of Our Nation’s Waters. Available at URL: http://www. 1992-2001.111(5):749-56. 1/14/09 U.epa. Pesticides in the Nation’s Streams and Ground Water.S. revised February 15. March 2006.gov/ oppsrrd1/REDs/chlorpyrifos_ired. Andrews HF. Fourth National Report on Human Exposure to Environmental Chemicals 139 . Kinney PL.

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

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 . 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 .670 (<LOD-1. population from the National Health and Nutrition Examination Survey.270) < LOD 659 701 920 Limit of detection (LOD. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 141 . population from the National Health and Nutrition Examination Survey.S. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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 .200 (<LOD-. < LOD means less than the limit of detection.S. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380 (<LOD-.200 (<LOD-.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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.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 . see Data Analysis section) for Survey year 01-02 is 0.2.

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

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

EPA at: http://www. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. Seifert and Pewnim.atsdr. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. resulting in excess acetylcholine at nerve terminals. 1998). diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 144 Fourth National Report on Human Exposure to Environmental Chemicals . 1998). although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.epa. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. In animals.cdc. Diazinon is not considered to be a mutagen. Additional information about external exposure (i. subsamples of NHANES 1999-2000 and 20012002.S. 2002).76 (<LOD-3. paralysis. respectively (Baker et al. and indoor applications have been documented. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection.45 and 1. vomiting.S. or reproductive toxicant (IPCS..e. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. animal carcinogen.S. The U. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. Diazinon has moderate acute toxicity in animal studies. respectively.html and from U.S.gov/toxpro2. environmental levels) and health effects is available from ATSDR at: http://www. 2003). diazinon does not accumulate in tissues (IPCS. weakness.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. and producing acute symptoms such as nausea. 2000. Survey Geometric mean (95% conf. 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.EPA considers diazinon unlikely to be carcinogenic in humans. In the U.gov/pesticides/. At high doses. 1986. population from the National Health and Nutrition Examination Survey... Thus. In two nonrandom samples of United States adults and children. 1986 Rajendra et al.45) < LOD < LOD < LOD < LOD 454 580 632 828 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. in the 2001-2002 subsample (CDC.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.49 μg/L. 1992).72 (<LOD-4. Intoxications in humans from intentional overdose. 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. teratogen. and seizures. cholinergic effects.... In addition to being a human metabolite of diazinon. agricultural. Olsson et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

revised February 15. Beeson MD. Barr DB.gov/ oppsrrd1/REDs/diazinon_ired.org/documents/ehc/ehc/ehc198. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. References Anthony J.htm. Barr DB. Atlanta (GA). Interim reregistration eligibility decision (IRED. Bull Environ Contam Toxicol 1986. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Carrier G.9(2):117-131. Ann Occup Hyg 2006. Sadowski MA. J Expo Anal Environ Epidemiol 2000. Environmental Health Criteria 198. Toepel K.114(2):260-263.inchem. May 2004.44(11):2243-2250. Irish R. Swan et al. Study for Future Families Research Group. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Environmental Protection Agency (U. 1998. Available at URL: http://www.10(6 Pt 2):789-798.epa. Environ Health Perspect 2006.S. Mason HJ.Organophosphorus Insecticides: Specific Metabolites 2005). Kruse RL. Banister E.134(1-3):105-113. 1/14/09 U. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. In 54 Canadian greenhouse workers. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. In a small number of men visiting fertility clinics in Missouri and Minnesota. Brunet RC. EPA 738-R-04-006. Oloffs PC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Geological Survey (USGS).50(5):505-515. Nguyen JV.S. Garfitt SJ.. Banister EW. Diazinon. Pewnim T. Noisel N. In 23 children. Drug Chem Toxicol 1986. Baker SE. Diazinon. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Effect of sublethal levels of diazinon: histopathology of liver. Pesticides in the Nation’s Streams and Ground Water. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. 2006). 2005. March 2006.37(4):501-507. 1992-2001. Biomonitoring studies of 2-isopropyl-4-methyl-6-hydroxypyrimidine provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of diazinon than are found in the general population. Dumas P.usgs. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Biochem Pharmacol 1992. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Rajendra W. et al. Cocker J. Fenske RA.pdf. Toxicol Lett 2002. EPA). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Barr DB. Swan SH. Seifert J. Available at URL: http://www. Jones K. Environ Health Perspect 2003. U.376(6):808-815. 2007 [online]. 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. Bouchard M.111(12):1478-1484. 4/7/09 Lu C. Bravo R.. Semen quality in relation to biomarkers of pesticide exposure. Redmon JB. Liu F. Needham LL. Olsson AO. Centers for Disease Control and Prevention (CDC).S. Anal Bioanal Chem 2003. Drobnis EZ. 2006).gov/circ/2005/1291/. Available at URL: http://pubs. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. The Quality of Our Nation’s Waters. Driskell WJ. Oloffs PC. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. International Programme on Chemical Safety-INCHEM (IPCS).

usually only a small fraction of the crop is treated. vomiting. 2000). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.64. and in government programs such as the USDA’s Boll Weevil Eradication Program. Estimated intakes for the general population have not exceeded recommended intake limits. 2007). Most of the estimated 15 million pounds used annually are applied to cotton (U. It has a short halflife in soils and water and is not considered persistent in the environment. in fruit fly control. 2006). inhalational. 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. but is more rapidly and efficiently absorbed via ingestion. In addition to being a metabolite of malathion. population from the National Health and Nutrition Examination Survey. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff. Survey Geometric mean (95% conf. malathion dicarboxylic acid. and plants.80 (<LOD-5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). weakness. 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. which is an organophosphorus insecticide that is used on a wide variety of agricultural crops.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. or oral routes (U. Limited general population exposure occurs through the diet. 2006). Pesticide applicators and agricultural workers can have higher exposures via dermal. Metabolism of malathion leads to the formation of malathion monocarboxylic acid. see Data Analysis section) for Survey year 99-00 is 2. and other metabolites. cholinergic effects. malathion has low acute toxicity. 146 Fourth National Report on Human Exposure to Environmental Chemicals . Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Malathion is also used medically in lotion form (0. < LOD means less than the limit of detection.S.EPA. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. paralysis. Malathion is slowly absorbed through the skin. 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion. 2003). phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide. Compared with other organophosphorus insecticides. Malathion is infrequently detected in groundwater sampling (USGS. Once they are absorbed. gardens. It is moderately to highly toxic to fish. At high doses. shrubs.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No.. depending on the species. Thus.EPA. and seizures. It is registered for use in public health mosquito control. When malathion is used on food or feed crops.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 2.5%) to kill body lice. and producing acute symptoms such as nausea. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. resulting in excess acetylcholine at nerve terminals. as well as lawns. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al. the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate. ornamental trees. which may vary for some chemicals by year and by individual sample.S.

.e. Giri et al.. 1987... 2005. environmental levels) and health effects is available from ATSDR at: http://www.EPA. Pluth et al. A study of agricultural workers reported preshift urinary levels of malathion dicarboxylic acid that were twofold to eightfold higher than detection limits in the NHANES 1999-2000 subsample (Krieger and Dinoff.S. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. Lu et al. but cholinesterase activity was not affected. EPA at: http://www.EPA. 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. 2006). Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al.50) < LOD < LOD 453 660 807 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 937 983 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 680 498 580 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey. but isomalathion. 1990). 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. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. CDC.5 and 5. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. 2005). representative subsample from NHANES 19992000 (Adgate..S. 1993. Of 382 pregnant women living in an agricultural community. 1996. Thomas et al. 2001. Flessel et al. Additional information about external exposure (i.html and from U.. 2000). 2002. and it is not considered an animal teratogen or a reproductive toxicant.S. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 2004). Malathion itself has not been considered genotoxic (U. IARC considers malathion not classifiable as a human carcinogen. 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.gov/toxpro2. Toxicity from unprotected bystander exposure during applications is rare (U. 2003).. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fourth National Report on Human Exposure to Environmental Chemicals 147 .cdc. 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..S.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. 2005).epa. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.atsdr. 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..74 (<LOD-5.. Human studies of single oral doses between 0. Survey Geometric mean (95% conf. 1999. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. 1999). some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.gov/pesticides/.

74(2):following table of contents. Bouchard M. Eberly LE. EPA). International Programme on Chemical Safety-INCHEM (IPCS). Hooper K. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Am J Epidemiol 1990. Eskenazi B. Barr DB. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Environ Health Perspect 2006. Giri A. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.gov/oppsrrd1/REDs/ malathion_red. July 2006. Swan SH. Jaloszynski P.38(4):546-553. Kedan G. Genetic toxicity of malathion: a review. et al. 2005. U. Rappaport E. Barr DB. Irish R. Environ Mol Mutagen 1993.514(1-2):223231.pdf.9(5):494-501. et al. Lu C. Szyfter K. Third National Report on Human Exposure to Environmental Chemicals. Giri S. Albertini RJ. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. MacIntosh DL.112(10):1116-1124. Arch Environ Contam Toxicol 2000. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 4/7/09 Kissel JC. Krieger RI. Dumoulin MJ.22(1):7-17. Clayton CA. Gosselin NH. Trzeciak A. Barr DB. Griffith W. Malathion deposition. Pesticides in the Nation’s Streams and Ground Water. Erratum in: Toxicol Sci 2003 Aug. J Expo Anal Environ Epidemiol 2005. Atlanta (GA). Quintana PJ. Ryan PB. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Bradman A. Goldhaber M. Centers for Disease Control and Prevention (CDC). Available at URL: http://www. Toxicol Sci 2003 May.77:1009-1010. Bravo R. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure.usgs. Lioy PJ. Fenske RA. Toepel K. Mutat Res 2002. March 2006.109(6):583-590.132(4):794-795. EPA 738-R06-030. The Quality of Our Nation’s Waters. Environ Health Perspect 2004. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. revised February 15. Harley K. Environ Health Perspect 2001. Reregistration eligibility decision (RED) Malathion.73(1):182-94. Neutra R. Needham LL. Dinoff TM. O’Neill JP. J Expo Anal Environ Epidemiol 1999. Prasad SB.S. Am J Public Health 1987. and cholinesterase status of date dusters and harvesters in California. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .org/documents/jmpr/jmpmono/v2003pr06. Sharma GD. Brunet RC. Samuel O. Reproductive outcome in women exposed to malathion. 1992-2001.114(2):260-263.gov/circ/2005/1291/.epa. Curl CL. Mutat Res 1999.inchem. Environmental Protection Agency (U. Malathion (addendum).S.56(10):2393-2399. Hammerstrom KA. Lu C. Geological Survey (USGS). Cancer Res 1996. Flessel P. A longitudinal investigation of selected pesticide metabolites in urine.15(2):164-171. Grether JK. Nicklas JA. Blasiak J. Petitti D. et al.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. htm. Hertz-Picciotto I.S. 2007 [online]. Pluth JM. Carrier G. metabolite clearance. Thomas D. Freeman NC.445(2):275-283. Jewell NP. Available at URL: http://www. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Available at URL: http://pubs. Harris JA. Barr DB. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Weltzien E. 6/1/09 U.

32-1.30-3.10 (3.00 (2.0) 2.80 (2.40-4. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.730 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 149 .0) 3.21 (2.50) 3.S.10 (3. was once a restricted-use insecticide with limited applications on certain agricultural crops.50) 3.700 (<LOD-. In animal studies. Once absorbed.70-3. more slowly absorbed through the skin.90 (1. Many previous registered agricultural uses of methyl parathion have been cancelled (U.10-1. on cereal grains.300-. 2002. Methyl parathion is not registered for residential use in the United States..45) 5.48) 90th 2. fish.860 (<LOD-1.57-4.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .09-1.67 (1.12) < LOD < LOD 1.10-11.11) 2.22-3. Methyl Parathion.13-1.89 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.85 (2.20-5.15-3. peak domestic use was as high as 5-6 million pounds per year.EPA. and of the chemical nitrobenzene.18-3. 2007).40-3.28 (1.47) 2.00 (2.40) 4. methyl parathion was rapidly absorbed after ingestion.01) 4. and has a short half-life in soils and on plants.30-5.71 (3.57) 1.27) 2.50 (2. ethyl parathion. Estimated intakes from diet and drinking water have been below recommended limits. but by 2003.50-14.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. and to a lesser extent.36-1.20 (<LOD-2.50 (1.70 (2.80 (2. 2003). 2000).50) 1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.37-2. Ethyl parathion.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .28-4.0 (3.91-3.69) 4.50 (2.10) 22. binds tightly to soils resulting in low leachability.33 (1.70 (2.910) < LOD < LOD .8 and 0.60-36. < LOD means less than the limit of detection.298-00-0 Ethyl Parathion CAS No.60-19.90-11.60 (4. 2006).72 (3.49 (1.30-16.0) 4. Given its limited use.50) 2.79) 4. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.770 (.70-6.62 (1.10 (<LOD-6. with limited applications in agriculture.02-6.67) < LOD 1.16) < LOD 1.S.790 (<LOD-.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .S. It had been applied to cotton.21-1.40) 1.46 (3.30 (1. Increased risk of exposure via dermal.32-3.34 (3. and aquatic invertebrates.20 (2.. first registered in 1948.70-6. population from the National Health and Nutrition Examination Survey.61) < LOD 1.92-2.45 (1. Methyl parathion use is highly restricted.32 (1.11-4.66 (2.50 (1.69 (2.33) 2.37-4.01) 695 660 518 679 603 941 Limit of detection (LOD.40 (1.850) < LOD .EPA.70) 2. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.50-9.61) < LOD 1.40) 2.70 (<LOD-3.70-3.50 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1977). all registered uses were voluntarily cancelled (U.60) 1. Morgan et al. and oral routes can occur in pesticide and agricultural workers (Muttray et al.10) 4.60-5.71 (2. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 1.70 (2.01-4..0) 3. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.70 (3. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.37-4.0) 3.26 (1.80 (1.32-1.28 (1.70) 2.74) 5.90-9.20) 5.19 (.1. pulmonary.910) < LOD .30 (2. In the 1990s.80) 2.0) 3.910) < LOD < LOD < LOD 1.940 (<LOD-2.58) 3. Both are toxic to birds.40-4.70) 2.37) 2.70-6. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.0) 3.60-24.41-4.44) 2.05) 4. Methyl parathion has low water solubility. and eliminated rapidly from the body after absorption (Kramer et al.00) 3.50 (1. which may vary for some chemicals by year and by individual sample.92) 5.990-1.

41-2.400 (<LOD-.790-. Methyl Parathion.04 (2..940 (<LOD-1..84) 3.44-3.11-4. ethyl parathion.78-2.720 (<LOD-.370 (<LOD-.20 (3.70) 3.83 (1. methyl parathion.23) 1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.500) < LOD < LOD .90 (1.17) .13) 4. Slotkin et al.29 (2.07) 2.93 (2.21-21.. In large doses.830-1.S. 1978. paranitrophenol. Additional information about external exposure (i.78 (2.82 (2.01 (. The metabolite.60) 2. Orsorio et al.16-4.92 (2.60-2.79) 1. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. Survey Geometric mean (95% conf.1) 2.01 (2.87 (1. Lores et al.33-3.79 (1.48-4.S. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.97 (2. Methyl parathion is not considered genotoxic.430 (. does not inhibit acetylcholinesterase enzymes.04) 1.840 (.89 (2.61) 4.82) < LOD . 150 Fourth National Report on Human Exposure to Environmental Chemicals . 2006. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.33-6.30-1.67 (3. and other metabolites.97-10.57-7.10 (1.26) 17.4 (3. In addition to being a metabolite of methyl and ethyl parathion.43) 4.15-10.EPA considers methyl parathion unlikely to be carcinogenic to humans.730-1.09) 2.720-1. 1990. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.80 (1.71 (1.17-4.37-1. gov/pesticides/.950) < LOD . and producing acute symptoms such as nausea. U. 1991).680 (<LOD-1. gov/toxpro2. 2005. 2004).800-1.25 (2.25) 1.55 (<LOD-3. and seizures.01-3.91) 1. Thus.Organophosphorus Insecticides: Specific Metabolites Metabolites”).11) 1.. At high animal doses of methyl parathion.20) .9) 1. and unintentional acute or chronic high-level occupational exposure (Hill et al.640) < LOD < LOD 1.91 (1.e.78-2.530) < LOD < LOD < LOD .39 (1.71) 1.2) 2.440 (<LOD-. environmental levels) and health effects is available from ATSDR at: http://www.7) 3.00 (1.80 (1.970 (.930 (. EPA at: http://www.78) 2.77-7.870) < LOD .. weakness. accidental exposure.56-2..96 (1. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.3) 2.73 (1.33-3. teratogenic.26 (1. resulting in excess acetylcholine at nerve terminals. WHO.38-3. 2003.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.39) 1.930 (.08 (1.88) 1.2) 2.980 (.10) 90th 2. 2004). the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.35-3.94-4.14-3..96 (1.76-14. paralysis. cholinergic effects.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .29) 1. Jaga and Dharmani.89 (2.21) 1.44-3.690-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.20) 3.72-2.86 (2.00) 2. Karanth and Pope et al.30) 3.970 (. but lists ethyl parathion as a possible human carcinogen. 1995).00 (1.08) < LOD .98-7. population from the National Health and Nutrition Examination Survey.13-12.57-2.60 (1.cdc. Parathion and methyl parathion have high acute toxicity in animal testing.57) 6.97 (<LOD-4.15) 3.html and from U. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.S.540) < LOD .05) 4. vomiting. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.08-3.59 (1.310-.94-47.07 (1.29) 2.95) 1. 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..epa.880 (. Zurich et al.67-2.31-3.790-1.atsdr.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .88 (1.55) 2.31) < 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 . 2006.850-1.35-3. 1995.

Barr DB. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. McCann et al. Pesticide workers may have much higher levels following pesticide applications. Jewell NP.htm. Rev Environ Health 2006. Hill RH Jr.110 Suppl 6:1085-1091. 2002. 2005). Toxicology 2005. Parathion-Methyl (addendum). Clark JM. et al. Barr DB. 4/7/09 Jaga K.33(5):270-276. 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. Weltzien E. Wellman SE. Head SL.15(2):164-171. Arch Environ Health 1978. Occup Environ Med 1999. Turner WE. et al. Environ Res 1995.. Role of individual susceptibility in risk assessment of pesticides. Pharmacokinetics of methyl parathion: a comparison following single intravenous.. 2005. Hryhorczuk DO. In a study of workers who handle parathion. Head SL. Griffith W. Neurotoxicol Teratol 2003. Kramer RE. Lores EM. Baker S.215(3):182-190. Kedan G.56(7):449553. 2004). Giordano G. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 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.S. and many residents were symptomatic (Barr et al..org/documents/jmpr/jmpmono/v95pr14. et al. Morgan DP. McCann KG. Environ Health Perspect 2004. Dharmani C.inchem.S. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. J Biomed Sci 2002. Bradman A. Runkle KD. Gregg M. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. McClure PC.. Moomey CM. Baker RC.25(5):599-606. Baker SE. Chicago area methyl parathion response. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Karanth S. Curl CL. References Barr DB. Ashley DL. Slach EF. Pesticide residues in urine of adults living in the United States: reference range concentrations. Available at URL: http:// www. Needham LL.14(4):213-216. 2005. Shealy DB. 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. Lu C. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Costa LG. Alley CC.71:99108. a range of values several hundred times higher than levels found in the U. 2002). Kissel JC. 2005.. Hill RH Jr.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Lewalter J. Eskenazi B. J Expo Anal Environ Epidemiol 2005. and levels were similar or slightly lower that those in a small convenience sample of the U. J Anal Toxicol 1990. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Environ Health Perspect 2002.. ACGIH recommends a BEI of 0. Rubin et al. et al. 1995. Arch Environ Contam Toxicol 1977. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. population (Olsson et al. International Programme on Chemical Safety-INCHEM (IPCS). Bailey SL. Laboratory investigation of a poisoning epidemic in Sierra Leone. Methyl parathion: an organophosphate insecticide not quite forgotten. CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. DiPietro E. Harley K. Bradway DE. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2002.110 Suppl 6:1075-1078. Pope C. oral or dermal administration.112(10):1116-1124. Moseman RF. Barr JR. Centers for Disease Control and Prevention (CDC). general population (CDC. 2002. Atlanta (GA). Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. 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.. 1995). Pathak S. Guizzetti M.5 mg (500 µg)/g creatinine for workers at the end of shift. Cline RE. et al.21(1):5767.6(2-3):159-173. 2005). Hetzler HL. Leng G.9:311-320. Lin LI. 1999). Barr DB. Rockhold RW. Hill et al.

Dunlop B. Geological Survey (USGS). Available at URL: http://www. Anal Bioanal Chem 2003. R. March 2006. 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. Ames RG. Environ Health Perspect 2006. gov/oppsrrd1/REDs/methylparathion_ired. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. U. 1992-2001. Mengle DC.376(6):808-815. Tate CA. pdf. EPA). 1/12/07 U. 2007 [online].110 Suppl 6:1047-1051.162(2-3):219-224. Yacovac R.E. Olsson AO. Barr DB. Environmental Protection Agency (U. Ohio. Environmental Protection Agency (U. September 2000. Seidler FJ.usgs. Available at URL: http://www. 1995-1996. Levin ED. Rosenberg J. 2004.S. Backer G. Hill G.gov/oppsrrd1/REDs/factsheets/0155fct. Toxicol Lett 2006. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.04/106. The Quality of Our Nation’s Waters. EPA). Interim reregistration eligibility decision (IRED) for Methyl Parathion. Hill RH Jr. Monnet-Tschudi F. Nguyen JV. Methyl parathion in drinking water.D. Costa LG. Letzel S. Case No. 1/14/09 U.20(4):533-546. Available at URL: http://www. Pesticides in the Nation’s Streams and Ground Water. Honegger P.Organophosphorus Insecticides: Specific Metabolites Muttray A. revised February 15. Toxicol Appl Pharmacol 2004. EPA-738-FOO-009. Ethyl parathion.S. External and internal exposure of wine growers spraying methyl parathion.epa. Available at URL: http://pubs. Ryde IT. Rubin C. et al. Environ Health Perspect 2002.201(2):97-104.S. Sadowski MA.S. Facts.pdf.S. Investigation of a fatality among parathion applicators in California.pdf. WHO/SDE/WSH/03. Osorio AM. Am J Ind Med 1991.114(10):1542-1546. 0153.int/water_sanitation_health/dwq/chemicals/ methylparathion. Schilter B.who. 152 Fourth National Report on Human Exposure to Environmental Chemicals . May 2003. 6/1/09 World Health Organization (WHO). Slotkin TA. Esteban E. 5/19/09 Zurich MG. Kieszak S.gov/circ/2005/1291/. Jung D.epa. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.

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

31) .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 .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .850 (.610 (<LOD-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. Survey Geometric mean (95% conf.840) 669 687 929 Limit of detection (LOD.580-1.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.780 (. < LOD means less than the limit of detection.950) < LOD < LOD 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .21) < LOD .S. 154 Fourth National Report on Human Exposure to Environmental Chemicals .680 (<LOD-.64) .210-1.820) < LOD < LOD .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .17 (.07) .780 (.840 (.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.15) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470 (.700-.740-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .500 (.250 (<LOD-. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.55) .S. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.760 (<LOD-.210-.27) .300-1.780 (<LOD-1.670 (<LOD-1.200-. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .700-1.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .210 (<LOD-.740 (.430 (<LOD-.94) .2.410 (<LOD-1.780 (<LOD-1.

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

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

Hu et al. neurochemical changes in cholinergic.23(6):665-673. 2004. Florio JC. Lemonica IP. Garey J. 1998. hypersensitivity. 2005). Estrogenicity of pyrethroid insecticide metabolites. 2002).1/15/09 Aziz MH. Ranft U. 2000. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Leng G. Lazarini CA. motor activity. Agrawal AK.S. Moniz AC. September 2003. 1999. References Agency for Toxic Substances and Disease Registry (ATSDR).gov/toxpro2. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Idel H. Bernardi MM. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Go V. Idel H.205(6):459-472. Lee SJ. 2006. Richardson JR. Pogo BG.cdc. Generally. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Leng G. McCarthy et al. Leng A. J Reprod Dev 2004.251(3):855-859. 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. Eriksson P. salivation. Toxicol Appl Pharmacol 2006. Varoli FM. Elwan MA. Shaw IC. In developing rodents. tremor. and permethrin) in the Hershberger and uterotrophic assays. Toxicol Appl Pharmacol 1991. 2001.. 2006. In California. 2003.300(3):161-165. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Song L. Garey and Wolff. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Kuhn K. Miller GW.. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. McCarthy AR. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Lazarini et al. 2001. Kamita Y. Leng G. Thomson BM. 2005). 2002. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation...107(3):173-177. Additional information about pesticides is available from U..Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Levsen K.gov/toxprofiles/ tp155.atsdr. WHO. et al. Moniz et al. 2003. Guillot TS. Environ Health Perspect 1999. Shukla Y. Abell AD. Ray et al. et al. Fredriksson A. Hu JY. Xenobiotica 1997. Neurosci Lett 2001. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Spinosa HS. Go et al. 2002). Soderlund et al. 1991.. Yang J. epa. Wang SL..8(1):197-202. Chen JH. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Yamada T. Kunimatsu et al. Kim HS. Sunami O. Neurotoxicol Teratol 2005. 2003. Wolff MS. 2005).html. Biochem Biophys Res Commun 1998. Seth PK.gov/pesticides/ and from ATSDR at: http://www. Okuno Y. and seizures (ATSDR. Available from URL: http://www. Bull Environ Contam Toxicol 1999.35(2 Pt 1):227-237. Cruz-Casallas PE. Toxicological profile for pyrethrins and pyrethroids. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.62:101-108. Sugiri D. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid..atsdr. Garey J. Effects of prenatal exposure to deltamethrin on forced swimming behavior. 2006). cdc. dopaminergic. Regul Toxicol Pharmacol 2002. and striatal dopamine levels in male and female rats. et al. 2005). Int J Hyg Environ Health 2002. Berger-Preiss E. Lewalter J. Kunimatsu T. J Environ Monit 2006. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Kim IY... Eriksson and Fredriksson. 2003. Elwan et al. Kang IH. Indoor pyrethroid exposure in homes with woollen textile floor coverings.. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Kuhn KH. EPA at: http://www. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.108(1):78-85.html.50(2):245-255. Shin JH. Ose K. Adhami VM. Pyrethroid pesticide-induced alterations in dopamine transporter function. Neurotoxicol Teratol 2001.27(12):1273-1283.27(4):609-614. Kim TS. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Pauluhn J. Shafer. bioallethrin and deltamethrin. choreoathetosis. Neurotoxic effects of two different pyrethroids. Bernardi MM.. Wieseler B. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Kim et al. Wolff MS. Salzgeber SA. fenvalerate.8(1):18-21. et al. Zhao RC..211(3):188-197. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Caudle WM. Fourth National Report on Human Exposure to Environmental Chemicals 157 .

Safety of pyrethroids for public health use. and therapy. Environ Health Perspect 2005. EPA). U.htm. Pyrethroid illnesses in California.who. 2005. resmethrin. pdf. Sheets LP. Spencer J.usgs. Available at URL: http://pubs. Pyrethroid insecticides: poisoning syndromes. O’Malley M. Environmental Protection Agency (U. Available at URL: http://whqlibdoc. synergies.epa. 5/26/09 Woollen BH. EPA). Rev Environ Contam Toxicol 2006.38:95-101. 5/26/09 U. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .htm. sumithrin synthetic pyrethroids for mosquito control. J Toxicol Clin Toxicol 2000.S. Available at URL: http://www.S. Lesser JE. 1992–2001. Laird WJ. March 2006. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).22(8):983-991. Meyer DA.pdf. Shafer TJ. Crofton KM.186:57-72. Reregistration Eligibility Decision for Cypermethrin. Available at URL: http://www. Available at URL: http://www. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Clark JM.S. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. June 2006a.171:3-59. Revised February 25. 2007.gov/oppsrrd1/REDs/cypermethrin_red. 19962002. 5/26/09 U. Pesticides in the Nation’s Streams and Ground Water. Pesticide and Evaluation Scheme. 5/26/09 U. Marsh JR.S.gov/ circ/2005/1291/. Toxicology 2002. Soderlund DM. Environmental Protection Agency (U.S. Piccirillo VJ.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Sargent D.S.S.113(2):123-136.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. World Health Organization (WHO).int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Mullin LS. Environmental Protection Agency (U. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Xenobiotica 1992. EPA). Geological Survey (USGS).10. Forshaw PJ.Pyrethroid Pesticides Ray DE. et al. June 2006b. Permethrin.epa.epa. April 2002.

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

2.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 831 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 701 594 957 Limit of detection (LOD.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection.2 and 0. 160 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. * 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. Fourth National Report on Human Exposure to Environmental Chemicals 161 .S. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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. population from the National Health and Nutrition Examination Survey.

Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. 19962002. Idel H. Williams RL. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Seiwert M. Drexler H. Schulz C.77(1):67-72. Angerer J.209(3):293-299. 2005. O’Malley M. Olsson AO.13(2):112-119.186:57-72. Krieger RI. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Angerer J. Bernard CE. Environ Health Perspect 2001. Heudorf U. J Expo Anal Environ Epidemiol 2003. Int Arch Occup Environ Health 2004. Rev Environ Contam Toxicol 2006. Ball M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.109(3):213-217. Pyrethroid illnesses in California. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2003.206(2):85-92. Int J Hyg Environ Health 2006. Arch Environ Contam Toxicol 2004. Berger-Preiss E. Barr DB. Sugiri D.Pyrethroid Pesticides References Baker SE. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Angerer J. Atlanta (GA). Int J Hyg Environ Health 2006. Angerer J. Heudorf U. Ranft U. Hoppe HW. Leng G. Spencer J. Centers for Disease Control and Prevention (CDC).209(3):221-233. et al. Hadnagy W. Butte W. Heudorf U.46(3):281-288. Becker K. Kolossa-Gehring M.

250-.180) .2-dichlorovinyl)2.460 (.2dichlorovinyl)-2.870) 1.770-1.200-.490-1.220-.08) .410) .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 .680-3.21) .270 (.2-dichlorovinyl)-2.630) .260 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .470-1.200) .300 (.210-.300-.12 (.730 (. The presence of cis-3-(2.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.47 (.460-1.and trans-isomers.280-.880 (.350) .680 (. Kuhn et al.630) .68359-37-5 Cypermethrin Permethrin CAS No. population from the National Health and Nutrition Examination Survey.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. the presence of trans-3-(2.300-. 52315-07-8 CAS No.13 (.520) .790-1. which may vary for some chemicals by year and by individual sample. Kuhn et al.570 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin. The chemical trans-3(2.500 (..740-1.430-. cis-permethrin.490-.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.710) .110 (<LOD-.420-.900 (.550) .07 (. but it can also reflect exposure to cis-3-(2.1.32) .710-1.220) .200) .280 (.68) .700) .2-dichlorovinyl)-2.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.910-5.28) 671 680 518 701 591 957 Limit of detection (LOD. In the body. Similarly. Biomonitoring Information Urinary levels of cis.160 (<LOD-.460-.53) .262) * * * < LOD < LOD .140 (.890 (.380-. cis-cypermethrin.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .S.80) .43) .960 (.77 (.670-1.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.690) .670-2.200-. Fourth National Report on Human Exposure to Environmental Chemicals 163 . 1999).1 and 0.510 (.580) 1.or trans-3-(2.380-.740 (.530 (.630-.730 (.220-.400-.110-.380) .180 (.670-1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.11) .270 (.600 (.340) .44 (.950-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. < LOD means less than the limit of detection.640 (.370-.790) .35) .140 (<LOD-.790 (. cis-3-(2.300 (.15) .670 (.240) .270-. 1985.2dichlorovinyl)-2. and ciscyfluthrin.68) .890 (.500 (.24) 1.250 (. but can also reflect exposure to trans-3(2.340-.270 (.790-1.120-.2-dichlorovinyl)-2. ciscypermethrin and cis-cyfluthrin.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .600) .240) .110-. more of the trans-metabolite than Urinary cis-3-(2.570-.160 (.600-1.920) 1.35) 1.410) .330 (.440 (.230) .120-.2-dichlorovinyl)- CAS No.730 (.630 (.650-1.155-.490-. 1999).160 (.50) .740-2. trans-permethrin.210) .610) .340) . trans-cypermethrin.120-.200) < LOD < LOD < LOD .770) .120-.110-.210) 90th .170 (. and trans-cyfluthrin.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.780) .330) ..2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.220-.370 (. 1985. transcypermethrin and trans-cyfluthrin. Cyfluthrin.580-1.380 (.220-.510 (.200 (.470 (.202 (.820 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.850 (. Generally.310) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.54) .380-.740) 1.610) .510 (.490-1.68 (.2-Dichlorovinyl)-2.150 (.

Schettgen et al.300 (.2-dichlorovinyl)-2. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. In a study of urban residents in Germany (Berger-Preiss et al.510-1.270 (..440-.180 (.690-1.21) . 2002).640-. In these volunteers. 2005) In a small group of indoor pest-control operators.2dichlorovinyl)-2.390 (. urinary trans-3-(2. 2002).230-.250) .150-.530 (. 2003).540 (.300) .450 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2-dichlorovinyl)-2. 2006. 2006).270) .190 (.210-.250-.S.2-Dichlorovinyl)-2.350) .290) . Other studies have provided evidence that urinary levels of cis. 2004).410) .. 2005).59) .260 (.440-. median urinary levels of trans-3-(2.550-1.260 (.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 .320) .640) 1.182) * * * < LOD < LOD . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.11) .250) .49) .680-1.160 (<LOD-.500 (.530 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.780 (.750-1.190) .250-.138 (.200-.580) ..240 (<LOD-.130-.29 (.800 (.810 (.260) . Lu et al.700-2. 164 Fourth National Report on Human Exposure to Environmental Chemicals .360-1.120 (.300) .550-1.080-.430-.320-. 2001) showed urinary levels of cis.590) .700) . Cyfluthrin. 2006).11 (. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.300-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.250-.380) .180-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .640-1.11) .37) . urinary levels of cis-3-(2.104-.31) .260 (.59 (1.340-.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC. 2006) and 1177 urban adults and children (Heudorf et al.600 (.370-.380 (. Studies in Germany of 396 children and adolescents (Becker et al.580-1.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .750 (..190) .390-.2-dichlorovinyl)-2.2-dichlorovinyl)-2.230-. 2001.340) .200-.280 (.430-1.400 (. representative NHANES 2001-2002 subsample (CDC.140-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.450-..12-2.33) .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.640-1.. 2005). 2003).640 (.67 (. the median and 95th percentile of urinary levels of cis-3-(2.380-. 2005).24) . population from the National Health and Nutrition Examination Survey.780) 1. In a study of volunteers.700) .390-.450-1.290) . post- Urinary cis-3-(2. 2006.370-.. Survey Geometric mean (95% conf.590 (.250) 90th .680-1.440 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.400-1.170) < LOD < LOD < LOD .2dichlorovinyl)-2..840 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.170 (.03) 1.150-.230-.230 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Pyrethroid Pesticides 2..540 (. 2005).680 (.150-.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.560) .550) .550) .59) .and trans-3-(2.2-dimethylcyclopropane carboxylic acid did not increase.840 (.11) 1. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.220) .350 (.67) .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.and trans-3(2.12 (.300 (.470-1.260-.290-.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .890 (. In the same residents.550 (.830) .880) .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.S.280-.220 (..440 (.540) .370-.200) .220 (.710 (.170 (.200 (.250 (<LOD-.33 (.920 (..270) .900 (.270-.290 (.80) .340) . 2004.710-3.430 (.560) 1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.420 (.570) .890) .

97-11.2-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.920-1.63) 1.68-2.40 (1.56 (1.840-1.85) 4.700) .55-5.Pyrethroid Pesticides application median urinary levels of summed cis.19) 1.14) 1.820) .500) .780 (.54) 4.07 (1.94 (1.77 (1.5) 2.830-1.11-2.70) 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 .2-dichlorovinyl)-2.95) 2.460-.26 (. population from the National Health and Nutrition Examination Survey. 2005). 2005). and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.500 (.480-. Finding a measurable amount of cis.910-1.17 (. Survey Geometric mean (95% conf.410-.700-1.11-1.27 (1.19 (2.and trans-3-(2.35) 1.64-4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.55-3.66) 691 680 518 690 595 954 Limit of detection (LOD. Biomonitoring studies on urinary levels of cisor trans-3-(2.520-. Fourth National Report on Human Exposure to Environmental Chemicals 165 .620) < LOD 2.60-4.43) 2.20 (.22 (1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .660) 1.17-1.87 (1.56 (1.01) 4.63) 1.42) 1.410 (<LOD-.56) 2.940 (.50 (1.860) .560 (. however.2-Dichlorovinyl)-2.03-1.23 (.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .41 (1.49-3.09 (.60) .68) 1.81) 2.2dichlorovinyl)-2.670) .560 (.460-.760) .08-4.4 and 0.14-2.41-14.20 (.490-1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .440 (<LOD-.2-dichlorovinyl)-2.810-1.68) 2.39 (1.01 (1.710 (.49-3.28 (1. trans-Cypermethrin.91 (1.10) 2.20 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.970 (.or trans-3-(2.580 (. Urinary trans-3-(2.69) 1.59 (1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.670) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.49-5.420 (<LOD-. The maximum post-application urinary levels.S.560 (.95) 3.470 (<LOD-.17 (.730) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08-6.520) .68) 1.07-3.850-1.55-4.680-1.76-4.03-1.14-6.76-3.89 (2.400 (<LOD-.28 (2.56) 2.60) 1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.68-3. which may vary for some chemicals by year and by individual sample.19 (3.84 (1.7) 2.910-1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.800-1.400-.39-5.470 (.610) 1.42 (2.66) .16) 1.23) 2.48) 4.410-.550 (.12-6.90) 1.54 (1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.77) 2.4.08) 1.25-3.570) 90th 1.410 (<LOD-.25 (1.530) .2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.500-. < LOD means less than the limit of detection.13) .69 (1.750) .77) 1.62 (1.37 (1.490 (<LOD-.

2-Dichlorovinyl)-2.880-1.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th . trans-Cypermethrin.970 (.440-.20 (1.55 (2.880 (.570-.65) 1.13) 1.15) 3.47-2.91-11.74) .35) 1.39 (1.770) < LOD 2. Survey Geometric mean (95% conf.70 (.56-5.98 (1.900 (<LOD-1.700 (.08 (.670) .11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .560 (.20-2.700 (.470-.640) .48 (1.64 (1.19 (1.13) .30-6.55 (2.610-.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .Pyrethroid Pesticides Urinary trans-3-(2.87) 1.08 (.15 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.07) 2.61) 1.81 (2.470 (.39) 1.40-2.850) .780 (<LOD-.720-1. population from the National Health and Nutrition Examination Survey.15-3.530 (.410-.65 (2. * 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 2.22) 1.570 (.47 (1.48-2.45-2.15) 2.12 (.570 (<LOD-.87-8.580) .850-3.44) 2.87-3.750) .720 (<LOD-.87) 1.68) 3.780) .31 (.45 (1.07) 2.41) 1.00-5.47-2.480-.07-1.07-2.36) 2.800-1.720-1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .780) 90th 1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.36 (1.28) 2.35 (1.37 (1.500-.930-1.33 (1.33-2.19) .57) 3.760 (.33-1.12-1.22-2.42) 1.74) 2.16 (1.91 (1.30-3.850) 1.29) 1.880 (<LOD-1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.700-.56 (1.02-1.15-3.60 (1.580 (.S.31 (2.00) 1.56-2.31) 1.34-4.60) 2.800-1.22-1.42 (.660) .27-2.55 (2.27-2.26 (1.11) .34-3.75 (1.00 (1.60) 2.87 (1.00) 1.3) 2.89) 2.80) 1.520 (<LOD-.00) 5.15-3.91) 1.57 (1.540) .86 (2.730) .820-2.07-3.530 (<LOD-.67 (2.740) .

Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). Permethrin and its two metabolite residues in seven agricultural crops. Int J Hyg Environ Health 2006. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Ranft U. Angerer J. Pearson M. Environ Health Perspect 2001. Ball M.134(1-3):141-145. Angerer J. Leng G. Environ Health Perspect 2006.209(3):221-233. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Hadnagy W. Angerer J. Bull Environ Contam Toxicol 1999. Berger-Preiss E. Angerer J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int J Hyg Environ Health 2003. Kuhn K. Fourth National Report on Human Exposure to Environmental Chemicals 167 .114(9):14191423.77(1):67-72. Int Arch Occup Environ Health 2003. Drexler H. Butte W. et al. Int J Hyg Environ Health 2006. Bravo R.68(6):1160-1163. Lu C. Drexler H.76(7):492-498. George DA. Indoor pyrethroid exposure in homes with woollen textile floor coverings.205(6):459-472. Levsen K. Angerer J. Seiwert M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Berger-Preiss E. Kolossa-Gehring M. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Leng G. Int J Hyg Environ Health 2002. Hoppe HW. 2005. J AOAC 1985. Wieseler B. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Hardt J. Idel H. Bartell S. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Int Arch Occup Environ Health 2004.62:101-108. Ranft U.206(2):85-92. Centers for Disease Control and Prevention (CDC). Heudorf U. Leng G. Heudorf U. Angerer J. Sugiri D. Idel H.Pyrethroid Pesticides References Becker K. Biological monitoring of workers after the application of insecticidal pyrethroids. Schettgen T. Schulz C. Heudorf U. Barr DB.209(3):293-299. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Heudorf U.109(3):213-217. Idel H. Sugiri D.

2006) and 1177 urban adults and children (Heudorf et al. Urinary levels for adults and children in these studies were similar (Heudorf et al. Deltamethrin can degrade to cis-3(2.2-dibromovinyl)-2.39 µg/L.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dibromovinyl)-2. in some situations replacing the use of DDT.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. 1990). mean peak urinary levels of cis-3-(2. 2005). The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 52918-63-5 General Information Cis-3-(2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.5 μg/L) than the detection limit (0.Pyrethroid Pesticides Deltamethrin CAS No. deltamethrin has been used against mosquitoes that carry malaria. Following residential spraying with deltamethrin for malaria protection in Mexico. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. 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.. 2004).2-dimethylcyclopropane carboxylic acid of 0. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2.2-dibromovinyl)-2. in detection of cis-3-(2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.. 2005). 2001.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dibromovinyl)-2.2-dibromovinyl)2. 2005).. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Biomonitoring Information Urinary levels of cis-3-(2. Thus.2-dibromovinyl)-2. (2004) reported a geometric mean concentration of cis-3(2. Outside the U. 2001) showed that urinary levels of cis-3-(2.2-dibromovinyl)-2.3-0.. Baker et al.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. urinary levels of cis-3-(2. Finding a measurable amount of cis-3-(2. In the NHANES 2001-2002 subsample.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. Studies in Germany of 396 children and adolescents (Becker et al.2dimethylcyclopropane carboxylic acid formed in the environment.2-dibromovinyl)-2..S.

which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 169 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD.Pyrethroid Pesticides Urinary cis-3-(2. < LOD means less than the limit of detection.S.1 and 0. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.1. * 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.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-Dibromovinyl)-2.

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

Centers for Disease Control and Prevention (CDC). Butte W. Torres-Dosal A. Deltamethrin. Int J Hyg Environ Health 2006. et al. Lopez-Guzman OD. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.inchem. Int J Hyg Environ Health 2006. Angerer J. et al. Heudorf U.Pyrethroid Pesticides References Becker K. Heudorf U. Heudorf U. Batres LE.209(3):221-233. and genotoxicity in exposed children. International Programme On Chemical Safety (IPCS). Carranza C. Kolossa-Gehring M. Available at URL: http://www. Int Arch Occup Environ Health 2004.77(1):67-72. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 171 . toxicokinetics. [online] 1990. 5/26/09 Ortiz-Perez MD. Atlanta (GA). Angerer J. Environ Health Perspect 2005.113(6):782-786.209(3):293-299.109(3):213-217. Drexler H. 2005. Seiwert M. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2001. Ball M. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Grimaldo M.org/documents/ehc/ehc/ ehc97. Schulz C. Hoppe HW. Environmental Health Criteria 97. Angerer J.htm. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.

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

595) .260 (.69) 3.33 (2.93 (1.427) .1) 3.374) 99-00 01-02 99-00 01-02 99-00 01-02 .510-.490) .41-2.34) 8.53-3.450 (.355) .34-6. Fourth National Report on Human Exposure to Environmental Chemicals 173 .25-7.321 (.1 and 0.8) 3.700 (. interval) .210-.49 (1.990) .32 (1.36) 1.850) . Survey Geometric mean (95% conf.13 (.640 (.21 (2.610) .56-5.28) 1.370) .71 (1.01 (1.940) 1.360) .63-3.417 (.315 (.25 (2.276-.800 (.280 (.428-.50 (2.265-.32-21.271-.30 (.600 (.190-.230-.78) 1.43) 3.390) .510-.90) 1.630) .14-6.800) 1.750) .18 (2.340) 75th .78) 6.190-.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.73) 1.230 (.92-3.246-.49-2.190-.373) .387) .406) .650 (.260 (.35) 2.27-2.340) 1.25 (2.325 (.362) .52-4.490-.320) .250 (.570-1.590-.230-.364) .292-.30 (1.270) .200-.49 (1.267 (.250-.45 (2.35) 2.63 (3.352-.336 (.870 (.26) 2.670 (.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 .27-2.86 (1.550-.29-1.160-.78 (1.295) .300 (.04-5.740 (.75 (1.23 (2.560-.330) .33) .430-.51-3.54) 1.560-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .320 (.290 (.64) 697 680 524 701 603 957 Limit of detection (LOD.02-6.160-.16) 1.260 (.840-1.530-.434) .300 (.730 (.454 (.288-.273 (.48-2.680 (.750) .12) 4.30) 3.247-.330) .311 (.320) .328 (.12 (.292 (.230-.35) 1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.18 (1.89-71.507 (.250 (.190-.83-11.62-8.320) .1) 3.238-.760 (.440) .520 (.41) 3.314) .78) 1.710 (.570-.820) .05) .210-.320) .240 (.46) 2.27-11.49-2.41 (1.180-.39) 2.72 (1.830) 90th 1.353 (.253-.601) .13) .420) .48-2.69 (1.240 (.850) .560-1.26) 2.51-6.25-1.260-.52-5.76 (1.41-3.62) 5.32 (2.53) 1.26-2.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .340) . population from the National Health and Nutrition Examination Survey.620-1.314 (.1) 3.42-2.38 (2.700-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.960 (.820) .250 (.1.38 (2.79) 3.33 (1.740 (.60) .710 (.233-.62-6.46) .270 (.369) .35 (1.05) 1.230 (.350-.34 (2.55 (1.81 (1.277-.430-.586) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.470-. Deltamethrin.384) .590 (.220-.200-.810) 1.03 (3.44) 5.12) .300 (.45-5.750-1.298 (.227-.530-.04) .830-2.300) .16-1.65 (1.226-.297 (.S.288 (.35 (2.266-.25-4.65-2.780) 4.200-.

860-1.410-.330) 1.670) 3.720 (.357) .320) .200-.550 (. population from the National Health and Nutrition Examination Survey.84 (1. interval) .400) .630) .09 (.13 (.21 (1.730) .43 (1.13-1.35) .40 (1.0) 3.200-.240 (.73) 1.440-.280 (.450 (.330 (.225-.72 (1.540 (.88-5.238-.220-.51-7.37) 1.378 (.316 (.41) 1.43-64.330) 75th .590-1.290) .264 (.150-.03-1.16-4.270 (.760) .210-.270) .63) 1.00) 1.960-1.311 (.36-6.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .740) .590) . Survey Geometric mean (95% conf.490 (.53 (1.290-.25-2.274-.43 (2.19-6.240-.09-2.63-3.60) 1.11 (.310) .365) 99-00 01-02 99-00 01-02 99-00 01-02 .43) 1.930) .67 (1.73-4.37 (1.227 (.02-1.460-.261 (.300-.55 (1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .62) 1.230-.07) 2.61-2.44 (1.270 (.202-.280-.216-.271-.440-.440-.590) .160-.13-1.350) .55) 3.03 (.730-1.550 (.309) .94 (1.329) .350 (.400-.490 (.534) .04 (3.280 (.83) 1.95) 1.25-5.200-.36 (1.510 (.330) .230-.240 (.250 (.240-.17 (.700-1.240-.224-.372) .272 (.321-. Deltamethrin.650) .280 (.510 (.67 (1.49) 3.510 (.860 (.580 (.11 (.730) .328) .500) .380-.560 (.272) .10 (2.250 (.09-2.480-.52 (1.190-.246 (.22 (1.54 (1.91) 9.32 (2.178-.96 (1.49) 1.323 (.423 (.530-.380 (.48 (1.35 (1.362 (.234 (.67) 1.173-.06-3.275 (.610 (.04 (.330) .250) .62) .370 (.270-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .80) 4.226-.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.200-.446) .261-.280) .300-.25) 2.530-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.220 (.410) .299-.270) .91-4.550 (.278) .860-1.810) 1.60-4.387) .21-4.90) 3.210 (.64-5.35-3.640 (.05-3.437) .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 .00) 1.190 (.19 (2.580) .840-1.91 (2.210 (.670) .400-.17-1.74) 3.27) 1.420-.52) 2.240 (.329) .49-2.15-2.590) .44) 2.75-8.02 (2.570) .190-.280) .S.460-.229-.390-.07-5.335-.41-4.309 (.91) .240-.253) .274 (.81 (1.49 (1.40) 2.35) 1.83 (1.930) 1.39) 1.240 (.490-.230) .401) .480 (.312 (.750-1.677) .19) 2.370-.09) 3.290) .86 (1.640 (.00) 5.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.720) 90th 1.

Indoor pyrethroid exposure in homes with woollen textile floor coverings. urban cohort. Godbold J. Pearson M. Batres LE. 2005. Third National Report on Human Exposure to Environmental Chemicals. Hoppe HW. Environ Health Perspect 2006.113(6):782-786. Environ Health Perspect 2005.Pyrethroid Pesticides References Baker SE. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Fourth National Report on Human Exposure to Environmental Chemicals 175 . GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Exposure to indoor pesticides during pregnancy in a multiethnic. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int Arch Occup Environ Health 2003. Carranza C. Berkowitz GS.111(1):79-84. Deych E. Bravo R. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Barr DB. Atlanta (GA). Leng G.76(7):492-498.114(9):14191423. Grimaldo M.46(3):281-288. Environ Health Perspect 2003. et al. Idel H. Arch Environ Contam Toxicol 2004. Barr DB.205(6):459-472. Ranft U. Lopez-Guzman OD. Angerer J. Sugiri D. Kolossa-Gehring M. Int J Hyg Environ Health 2002. Seiwert M. Torres-Dosal A. Olsson AO. Leng G. et al. Idel H. Biological monitoring of workers after the application of insecticidal pyrethroids. Ranft U. Berger-Preiss E. Bartell S. Int J Hyg Environ Health 2006.206(2):85-92. Ball M. Int J Hyg Environ Health 2003. and genotoxicity in exposed children. Hadnagy W. Obel J. Angerer J. Levsen K.209(3):221-233. Ortiz-Perez MD. Liu Z. Becker K. toxicokinetics. Lapinski R. Hardt J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Sugiri D. Berger-Preiss E. Centers for Disease Control and Prevention (CDC). Lu C. et al.

133) * .170-.320) .170 (.350) .180 (.S.300) .144) .220-.115-. People are exposed to antimony primarily through food and.115) .350 (.370-.154) .180-.200 (.150-.410-.169 (.130-.190 (.130 (.200 (.230) . and 0.410) .400) .260 (.470 (.160-.160) .180 (.120) .390) .130 (.420) .390-.07.210) .190-.400) .300 (.132 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.120 (.320 (.280-.320-.160) .130 (. 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.170-.220) .090-.135) * . ceramics.350 (.390) .184) .150 (.350) .090) 75th . and pewter. 01-02.140) . +3.130 (.130 (.330-.140 (.140-.440) .110-. Antimony enters the environment from natural sources and from its use in industry. water.119-.570) . The absorption.134 (.145) Selected percentiles ( 95% confidence interval) 50th .130-.148-.178) .114) .190 (.210 (.164-. respectively.190-.141-.330) .230-. and as a fire-retardant in textiles and plastics.360 (.087-.360) .190) .280-.310 (. storage batteries.510) .240 (.240 (.120-.330-.150) 90th .350) .430 (.140) .230 (.220) .120 (.110-.160) .180 (.090 (<LOD-.600) .500) .210 (.Metals Antimony CAS No.090 (.170-.175 (.04.112-.230-.330) 1132 1335 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .154) .126-.120 (.080-.460 (. 0.220 (.140) .110 (.200 (.200-.220 (.070 (<LOD-.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 .330) .250-.080) .230 (.120-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.310-. and +5.160-.330 (.470) .280) .190-. or other substances containing antimony is another means of exposure.100) .330 (. and 03-04 are 0.130) .140) .156-.123 (.210) .150-.160-.110) .080) .200) .250-.140 (.160-.310 (.126 (.137) .120) .280) .140) .400) . Workplace exposures can occur at smelters.207) .108-.095 (.200) . and glass. metal bearings.100-. 7440-36-0 General Information Antimony is found in ores or other minerals.490 (.190-.180) . and excretion of antimony vary depending on its oxidation state.200) .180 (.146 (.500) .400 (. see Data Analysis section) for Survey years 99-00.120 (.390-.400 (.190) . fireworks.170-.530) .130-.270) .330) .190) .270-.230) .120-.270) .280-.120) .110-.120-.170-.300-.350 (.200) . which may vary for some chemicals by year and by individual sample.160 (. enamels.250 (. solder.120-.093 (.270 (.137) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410) .130 (.240) .220) 95th .210) .240 (.128 (.350-.079-.310) .125 (.260) .100-.132 (.108 (.330 (.095-.130-.128 (.330) . and refuse incinerators that process or release antimony.160) .200 (.350-.180-.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 .230-.300) .440) .240 (.320-.350) .240-.130 (.280) .160) .390-.142 (.200-.176 (.260) .310 (.290 (.210-.440 (.260 (.190) .340 (. Dermal contact with soil.220-.145 (.157) .280-.170 (.150-.300) .490) .190 (.260-.122 (.280-.160 (.390) . Stibine is a metal hydride form of antimony used in the semiconductor industry.370) .220) .220-.190 (.710) .120) .320 (.280 (.210) .100 (.360) .143 (.140 (.200 (.120 (.200-.230-.110-.117-.140) .290-.119) .120-.160) .320) Total .130-.210-.230-.140 (.390) .190-.560) .200 (.280) .320-.130 (.150 (.320-.197) .350-. population from the National Health and Nutrition Examination Survey.250-. Antimony can exist in one of four valences in its various chemical and physical forms: -3.300-.310 (.180 (.300-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.190 (. 0.220-. It is used in metal alloys.190) .136-.158 (.430 (.134-.260 (.350 (.280 (.200-. interval) . It is also used in paints.154-.109-.150-.360-. < LOD means less than the limit of detection. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.300 (.340 (.460 (.250-.120-. from air and drinking water.240-.250 (.180-.180 (.130-.260-.220-.390 (.400-.430 (.088-.250 (.098-.150-.130) .230 (.131-.099 (.150) . to a lesser extent.240 (. sheet and pipe metal.460) .210) .130) .150) .136) * .070 (<LOD-.460 (.170) . distribution.230) .470) .117-. coal-fired plants.310-.340) .080 (<LOD-.360 (.160 (.250) .180) .270 (.120-.400 (.150 (.310) .120-. castings.270 (. ammunition.070-.290-.350 (.220-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .180-.150) .100 (.103) .130-.180-.270 (.130) < LOD .04.161) .105 (.260) .090-.

.082 (<LOD-.421) .061-.124) . myocardium.173-.115 (.143) 90th .255) .187) .267) .333 (.109 (.114 (.126) .148) * .108 (.120 (.400 (.126-.263-.102-.146-.130 (.068-.209) .208 (.138-.352 (.159-.343 (.112 (.143) .272) .188-.230) 95th .114 (.250-.208-.364 (.098) .321) .167-.127) .121 (.250-.163 (.209 (.137 (.115) .133) .255-. Histopathologic inflammatory and degenerative changes in the lung.444) .143) Selected percentiles ( 95% confidence interval) 50th .113) .391) .265-.135) .127) .181) .096-.116 (.320) .185-.118 (.115-.150-.140) < LOD . Workplace standards and recommendations for air exposure Urinary Antimony (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.131-.171) .248) .119 (.300 (.228 (.245) .104-.224 (.186) .189 (.115 (.318-.075 (.405) .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 .170 (.167 (.173 (.107-.135 (.129 (.146-.153 (.333-1.069-.276 (.188) .417) .107-.200-.338 (.087) .085) .333) .164) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.127 (.233-.391) .310) .116-.181) .111-.191 (.333-.126 (.308) . Acute antimony poisoning may cause a metallic taste.146) . population from the National Health and Nutrition Examination Survey.172-.100 (.156-.727) .108-.214) .162-.084) .192 (.194-.371 (.112 (.148-..081 (<LOD-.225) .183) .173 (.228-.438) .195 (. skin.200-.123 (.147-.741 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.261) .135) .071-.131 (.145) .079 (<LOD-.271-. 1962).281-.105-. and gastrointestinal symptoms such as vomiting. and route of exposure (Elinder and Friberg.128-.159-.124 (.269 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.117-.132 (.068 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.239-.086 (.152) .300) .235-.161) .266 (.300) .143 (.447 (.147) .182 (.152) ..138 (.089) .429 (.338) .098-. 1988.080 (.125 (.099-.199-.149) .253-.222 (.320-.164-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .103-.139 (.200-.268) .143) . and kidney have been demonstrated in high dose animal studies depending on the dose.109 (.138) * .111 (.086) 75th .122 (.117-.196 (.265 (.278 (.122 (.310 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.121) .120 (.153-.244-.204-.077) .164 (.129) * .107-.114 (.250) .333-.156 (.078 (.178 (. species.095-.138-.211) .256 (.203) .163 (.485) .317) .139 (.228 (.277 (.080 (<LOD-.124-.115-.320 (.185 (.250 (.136) .092) .129) .103-.130) .338 (.209-.176 (.320-.241-.278) .207) .076-.108-.149-.127) .095-. 1953).352) .129 (. Ming-Hsin et al.106-.134) .173) .Metals than for trivalent compounds (Elinder and Friberg.185 (.115 (.429) ..280-.317) . 1944).130) . Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.192-.176-.119-.233) . and eyes.417) .373) .193) .075 (.131) .135) .298 (.148-.230-.181) .286 (.203) .225 (.161) .229-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.238) .425) .238 (.238) .198) .118 (. Inorganic antimony salts irritate the mucous membranes.144-.242-.200) .120 (.106-.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 .414) .108-.081) . liver.082) .125-.076-.195-.267-.213 (.130) .099-.098-.209) .102-.119-.205-.192) .364 (.430) .357) .385 (.167 (.113-.179-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.104-. 1986).082) . and ulcers (Werrin.295 (.471 (.263 (.178-.280 (.241-.124-.500) .315) ..259 (.247) .471) .233 (.154-.206-.310) .317) .074 (.069-.741) . 1973).195-.480) . interval) .123) . abdominal pain. diarrhea.333 (.248-.313-.333 (.117-.113-.120 (.151) .135 (.112-.176 (.150-.132) .250 (.193 (.294) Total .226 (.217 (.220) .318-.127) .320 (.250-.288 (.S.308-.357-. 1995).267 (.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 . resulting in hemolysis with abdominal and back pain (Dernehl et al.30) .333-.160 (.175 (.257) .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.140) . 1958) and occupational exposures (Briegner et al.250-.227-.236 (. 1986).121 (.146-.109-.092-.253 (.167 (.444) . 1954).159-.380 (.097-.

Pilgrim L.)1954. Element reference values in tissues from inhabitants of the European community. Konings J. population. Suchenwirth R. Chin Med J 1958.. Kuo-Juie Y. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Stocks J. Hamilton EI. Stone FD. 2nd ed. Dezateux et al. Cheng-Wei L.. Friberg L. gov/toxpro2. Mahieu P.51:238-240. Dunkelberg.76(2):103-115. Weltle D. and 2003-2004. indium. Int Arch Occup Environ Health 1987. Dernehl CU. Industrial antimony poisoning. 20012002. EPA. Roland H. Chia-Yu H. Pozzoli L. Trace element reference values in tissues from inhabitants of the European community I. Urinary antimony in infancy. Minoia C. Matthews T. Iavicoli I. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. clinical efficacy. Arsine. 2004. Kentner M. 1995. Semisch CW. Piatnek DA.48:93-97. 1998). Stead FM. Petrucci F.S. Apostoli P. VI. and hydrogen sulfide. and a drinking water standard has been established by the U. Handbook on the toxicology of metals. Biological assessment of exposure to antimony and lead in the glass-producing industry. gallium. 1991. 1994) have reported values slightly higher than those in this Report. Industrial Medicine 1944.. even when exposure levels were below workplace air standards (Bailly et al. arsenic. 1998) or compiled reference ranges (Hamilton et al. Antimony. J Trace Elem Med Biol 2002. Chen J-R. et al.. Chest 1973.e. environmental levels) and health effects is available from ATSDR at: http://www. References Berman JD.cdc. et al. 26-42. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Schaller KH. Costeloe K. Lauwerys R. Sabbioni E. and antimony in optoelectronic industry workers.106:33-39.. Buchet JP. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Skulsukai G. Van der Venne MT. Review of elements in blood. Nordberg GF.158:165-190. Ho C-K. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. pp. Paschal et al. respectively. J Clin Pathol 1998. Rev Infect Dis 1988. stibine. Delves HT. Carelli G.Metals to antimony have been established by OSHA and ACGIH.59:469-474. 1990.. Lenert G. Sabbioni E. Sci Total Environ 1994. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Schacke G.46:931-936. Third National Report on Human Exposure to Environmental Chemicals. and future strategies.67:119-123. Ju-Sun P. Leinemann M. Biological monitoring of exposures to aluminum. Gallorini M. Biomonitoring of a worker population exposed to low antimony trioxide levels. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Antimony trioxide is rated by IARC as a possible human carcinogen. Yang C-Y. et al. Pietra R. Luedersdorf R. Stasney J. Atlanta (GA). 1998. J Occup Environ Med 2004. or exposure differences. Wade A. In: Friberg L. Caroli S. Fuchs A.521-523. Yu H-S. Earlier measurements in general populations (Minoia et al. Wu M-T. Gebel TW. O’Regan M. Chemotherapy for leishmaniasis: Biochemical mechanisms. External and internal antimony exposure in starter battery production. Delves HT. Vouk VB. Cordasco EM. 2002. Environ Health Perspect 1998. 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. Cullen A. Iavicoli et al.atsdr. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . 1997). Dezateux C. Shao-Chi C. Int Arch Occup Environ Health 1995. Elinder CG..76:432436. plasma and urine and a critical evaluation of reference values for the United Kingdom population.10(3):560-586.. Liao Y-H et al.. Mayer P. Bolten C. Centers for Disease Control and Prevention (CDC). Briegner H. HH.13:361-362.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kiberd B. 1987). Mayne P.html. Industrial Medicine and Surgery (Dec.16: 33-39. Ludersdorf et al. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Nau CA. which may be due to methodologic. Alimonti A. 1986. Bailly R. Information about external exposure (i. New York: Elsevier. Br J Ind Med 1991. Ming-Hsin H. eds.64(2):182-185. 2005. Arch Dis Child 1997. Pulmonary edema of environmental origin. Liao Y-H. Antimony in blood and urine of infants... Kentner et al.

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

5) 41.8) 17.30 (7. as alloy in metal bearings.55 (7.8-61.8) 30.4) 40.2 (12.00-9.30 (6.7) 24. copper arsenates.4 (26.80) 6. Survey years 03-04 Geometric mean (95% conf. Water sources contain mostly inorganic arsenate.5 (36.0-19.10 (6.8-77. Arsenic and its compounds have had many uses in the past and present as medicines. arsenocholine.9-62.2 (51. arsenic as elemental metalloids may be used in some ammunition. Although it is still widely used in the United States. 180 Fourth National Report on Human Exposure to Environmental Chemicals .1) 15. pesticides.40) 7. arsenic compounds.9 (8.0 (43. alloys.02-8. Arsenic trioxide (As2O3.2-20. ocean and fresh waters.5) 95th 65.08 (5.6) 11. 2001).4-65.70) 8.8 (48.57) Selected percentiles ( 95% confidence interval) 50th 7.0 (15.2) 15.1) 1281 1276 03-04 03-04 03-04 9.6-35. to a lesser extent. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. were used as treatments for syphilis.S.7) 65. and arsenates (oxidation states of -3.8) 33. +3 and +5). 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. to a lesser extent.5 (23. black.8) 7. gaseous hydride manufactured in small quantities for use in the semiconductor industry.6 (32. The United States no longer produces arsenic from mining but imports about 22.7 (11.4 (24. particularly arsenic trioxide.1 (38.2) 46. and indium arsenides are used in the semiconductor industry.9 (17.0 (11. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.9-46.5) 43. cacodylic acid.6) 618 722 1074 Limit of detection (LOD. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.90-7.13-8. Since the 1940s.7) 90th 37.84) 8.1) 290 725 1542 03-04 03-04 9.41 (7.4 (31. such as arsenopyrite (FeAsS) and realgar (As4S4). from coal burning.7-95.74. 2005). retaining walls.80 (5.0-60. and other metals. Gallium. trimethylarsine oxide. semiconductors.80-9.4) 13.97) 8.70-9. Also.90-8.5-178) 46.10-7. aluminum.90) 75th 16. and. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.7-83.5 (14.90 (7. General population exposure to inorganic arsenic can occur through consumption of drinking water and.10) 10. lead hydrogen arsenate.2 (41.3-111) 78. and as homicidal poisons.8) 34. In nature.8) 7. population from the National Health and Nutrition Examination Survey. and gray forms). and arsenosugars.12-10. lead.00 (6. and produce.3) 10.8) 29. mental disorders.90 (7.6 (15. arsenites.90 (5.5-41.27) 9.4) 60. sodium arsenite.1) 7.19-9. interval) 8. and foods. cancers.0 (14.3) 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 7.9) 68. it is found in over 200 crystalline or mineral forms.5 (40.30) 17. Arsine (AsH3) is a reactive.90-8.66-8.3-15. referred to as inorganic arsenic compounds.1-40. the smelting of copper. and play sets. psoriasis. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. grain.2-61.20 (8.2-17. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.Metals Arsenic CAS No.6-43. Arsenic trioxide is approved to treat acute promyelocytic leukemia.0 (22.6 (13. mostly for use in wood preservation (ATSDR.1-18. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. In the last century.3-19.50 (8.34-9.9) 21. solders.2 (13.6 (9. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.5 (34. Before the 20th century. Various arsenic compounds were used in paint pigments and for tanning animal hides. though in some locations arsenite may be prevalent (WHO.9-34. Arsenic is measurable in most soils.5) 66. and in lead-acid storage battery grids. and as a cosmetic to lighten complexion.90) 16.90-11.10-10.77) 6.4 (48. see Data Analysis section) for Survey year 03-04 is 0.5-19.90-14.6-141) 53.50-14.25-9.1 (32.70 (6. or rarely as elemental metalloids (yellow.84) 8. meats.12 (6.000 metric tons annually.29 (8.5-52.34-10.4 (7.2-93.

88) 7. 2001).. dose level.06 (4.S. Though modest bioconcentration occurs in some aquatic life.0-38.7-188) 27.7) 28.0) 14.8 (21.0-69.2) 90th 30.3 (24.96) 12. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.1 (11.3 (27.47 (7.0-26. trimethylarsine oxide (TMAO). 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.04) 7. shellfish.64 (7. gallium arsenide and indium arsenide.7) 95th 50. Chowdhury et al.8 (11.0 (31. Gamble et al.3) 9.88 (5. 2001).5) 290 725 1542 03-04 03-04 8.1 (14.. 2007.81-9. 2001).66 (7. Steinmaus et al.4 (42. 2001).44-11. interval) 8. Arsenate is reduced in the body to arsenite (oxidation state +3). 2007. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. but is poorly absorbed dermally (WHO. 2001).00 (6.. though some reduction may occur in the gut prior to absorption.66-8.20-9. are used in enclosed ultraclean operations within the semiconductor industry. Tseng. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.04 (5.93-9.4 (24.1) 24.28-7. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO..51) 75th 14.4 (12.33-10. organic arsenic can be converted back to methylated and inorganic arsenic. After absorption.4 (26.5-17.0-18.75 (5.50 (6.2-15.13) 8.8) 27. EPA’s maximum contaminant level (Hughes. EPA. and some other seafood can contain organic forms of arsenic including arsenobetaine.23-7. 2001. so exposure to the general population is extremely limited. Extremely high groundwater arsenic levels.7-18.6) 45.5) 17.g.3-62.47 (6.0) 26. kelp.7 (9.0) 1281 1276 03-04 03-04 03-04 8.1) 7.31 (6.S.8-32. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.1-36.2) 40. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. WHO.11 (5.93-8. In aquatic organisms.66-8.1) 8.25-9.4) 54. U.7-35.0 (17. cacodylic acid and monosodium methyl arsenate.8 (12.8) 22. mine tailings).3) 6.45) 5.75) 13.99-9.9-56.. WHO.3-64.35) 7. In aquatic sediments. arsenocholine. age. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.86-17. and folate status (Chen et al.44) 6.24 (7. Survey years 03-04 Geometric mean (95% conf.41) 6.40) 8.4 (11.18 (5. Inorganic forms of arsenic demonstrate high acute toxicity. as observed in Bangladesh where millions of people have been exposed. 2006.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.32 (5.6 (35.2-46. arsenic does not show biomagnification in the food chain (WHO.0) 42.7-34.1) 6.4-64.33 (6.7-17.01) 7.10-16. Direct exposure to DMA and MMA may result from use of the two pesticides. 2007.61 (7. 2001).1) 58.3-53.6 (17.S.7 (25.4 (40.8 (27.58-10. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.59) Selected percentiles ( 95% confidence interval) 50th 7.9) 53.01) 11.6 (10.7 (11.10-8.3-41. 1988). Fish. dust. 2003.76 (6.12-10. and contact with CCA-preserved wood structures. have caused clinical arsenic poisoning. and arsenosugars.5-120) 40.0) 33. selenium.47-6. NRC.9 (45. 2001.8-62.. 2001).6-17. 2001).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 8.9) 13. inorganic arsenic is widely distributed within the body. The semiconductor dopants.8-75.2 (12. Smoking tobacco is also a source of inorganic arsenic. 2006. population from the National Health and Nutrition Examination Survey.5 (9.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . 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.2) 15. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.0) 12.8 (20.30-9.07-9.4) 32.25 (6. Children may have additional exposures from ingestion of contaminated soils (e.38-10.

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. and it also will inhibit succinate dehydrogenase. Chronic arsenic exposure in humans is considered to be a cause of skin.20 (<LOD-1.10 (<LOD-1. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 2001). and by uncoupling oxidative phosphorylation (NRC. 2001.S.. population from the National Health and Nutrition Examination Survey. renal failure. increased oxidative stress. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.10 (<LOD-1. and bladder cancer (IARC. including drinking water sources with elevated arsenic levels (e. arsenic trioxide) includes hemorrhagic gastritis with nausea. NRC. 2004. leading to a decrease in adenosine triphosphate energy production.60) 1.80) 1. 2006. 1998. and endothelial injury (Kumagai and Sumi. 2004). 2000.EPA. Chronic elevated arsenic intakes have been associated with diabetes. 2001. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. WHO.20 (<LOD-1. Bredfeldt et al. but additional or confirmatory research is needed (Kapaj et al. drinking water have not been associated with increased cancer rates (Schoen et al. apoptosis. Studies of arsenic at levels typical of U. and hyperpigmentation of the skin (NRC. U.. interference in signal transduction pathways. gluconeogenesis.10 (<LOD-1..60) 1.. which can lead to dehydration and shock.. 2001). hyperkeratosis. and childhood neurodevelopmental effects in observational human studies. Bangladesh. see Data Analysis section) for Survey year 03-04 is 1. food residue. fatty acid oxidation.g..g. WHO. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. cytotoxicity. 2001).30) 1. noncirrhotic portal hypertension. Chile). Acutely. hematocytopenias.20 (<LOD-1. 2001). and DNA repair inhibition (Cohen et al. Although arsenate is reduced in the body to arsenite. Chronic human intake of arsenic at less than acutely toxic doses. Raml et al.20 (<LOD-1.10 (<LOD-1.EPA has established drinking water. 2006) or when exposure occurs in smokers (Chen et al. can cause peripheral sensorimotor neuropathies. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. and altered gene expression. WHO. Taiwan. Such actions may lead to decreased energy production. 2001). 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. respectively.S. The organic forms of arsenic occurring in seafood have little known toxicity.10 (<LOD-1. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. 2004). 2007. 2001). Arsenic has many actions demonstrated in cellular studies... * Not calculated: proportion of results below limit of detection was too high to provide a valid result. lung.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.S. Cohen et al. cell transformations. 2006.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf. Cellular glucose uptake..50) 1. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. NRC.50) 621 725 1078 Limit of detection (LOD. WHO. With chronic exposure. hepatotoxicity. 2007). peripheral vascular disease.0.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1..30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. some of these effects may take years to develop. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.S. vomiting. and diarrhea. 2006. The U.. Cardiac arrhythmias. 2007. and production of glutathione may be affected as well. substitution in phosphate metabolism. 182 Fourth National Report on Human Exposure to Environmental Chemicals . including inhibition of numerous enzymes. hypertension. which may vary for some chemicals by year and by individual sample.. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. < LOD means less than the limit of detection.

although urinary arsenic levels were not associated with CCA contact (Shalat et al. Consequently.S. 1986).75 (<LOD-2. 1998...69 (<LOD-3.. Additional information about external exposure (i..75 (<LOD-2. 2008). Calderon et al. Levels of total urinary arsenic in the U.S.e. 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. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. and were about two-fold lower than those for the U. 1999). higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. Caldwell et al. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U....19) 3. 2001). 2001). environmental levels) and health effects is available from ATSDR at: http://www..33 (<LOD-3. 2008). arsenic has been fetotoxic and teratogenic..html.. 2006). Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2006. population from the National Health and Nutrition Examination Survey. 2007. had decreased since the prior 1990– 1992 survey. DMA produced bladder cancer in some chronic rat studies (Cohen et al.50) 1. 2006.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.. In the German Environmental Survey III of 1998. and the FDA has established a bottled drinking water standard. In a Nevada town where groundwater levels were naturally elevated.80 (<LOD-4. 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.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Shalat et al. Meza et al..33 (<LOD-3. 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. WHO. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.. population (Rubin et al. 1999. population in NHANES 2003–2004 (Schulz 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.. gov/toxpro2. 2000). 2006). In animal studies.. 2004. 2006.18 (<LOD-3. Compared with this Report..cdc. 2006).89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2..Metals compounds. 2006).. median urinary total arsenic levels in 4052 adults varied with seafood intake.S.18) 3. Caldwell et al.. Vahter et al. 1992. 1999. Josyula et al. 2008.00) 1. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 2004.41) 3. Though CCA-treated wood contains several thousand times more arsenic than untreated wood... Valenzuela et al.S. 2007. 2001). Pellizzari and Clayton. Pellizzari and Clayton 2006). 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.atsdr. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Pellizzari and Clayton.. but generally only at maternally toxic doses (WHO. 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. Offergelt et al.04 (<LOD-3. Shalat et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.61 (<LOD-3. 2003. Survey years 03-04 Geometric mean (95% conf.. 2000.

and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.. Some noncancer effects of arsenic (e..80 (3.20 (.20 (1.500-1.45 (1.80 (.8-50. population showed a higher contribution of arsenobetaine (Caldwell et al. 2008).50) .6..3% of a representative sample of the U. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.55 (1.S. and TMAO. In most human studies.19 (.10) 8.g. 2000.50) 90th 16.93) 1. Valenzuela et al.9 (7. see Data Analysis section) for Survey year 03-04 is 0.80 (4.11-1. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90-7.60-3. Chowdhury et al.7) 13. Pellizzari and Clayton. After recent seafood ingestion.68) . Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic..400-.4.20-25. geometric mean levels were about 70-fold higher than for the U.. population (Ahsan et al.800-4. 4...20-190) 31.50-6.00-6. population (Sun et al.10) 4.00-4. 2008.31-1.2 (6.8) 35. Sun et al.37 (1.0) 29.4 (16.80-5..74 (1.66 (1.8 (12.83) Selected percentiles ( 95% confidence interval) 50th 1.800 (.20) 7.28) 1.70-21.0-23.3) 35. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.900-1.1) 18.e.10 (4. Caldwell et al.80) 1. Tseng et al.40-6.62) 2.3) 95th 35. arsenite. 2005.800) 1. and duration of exposure are also considered important.871-1. 1996. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. 2000.7 (13. arsenobetaine. < LOD means less than the limit of detection. Arsenate. 2008)..2-38.S.00 (. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. Individually measurable species resulting from inorganic arsenic exposure are arsenate. methylation capacity.17-1.00-1.3 (21.70 (5.700-1.800 (.1) 45.S.. 2000. DMA and MMA. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.20-3. 2001.6 (13.05) < LOD ..4) 23.30) 10. Caldwell et al.50) ...5) 32. with DMA.7) 15. Caldwell et al..4) 31. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. Blom et al. which may vary for some chemicals by year and by individual sample.70) 6. 2008.. 2007). 2001).8-40.900 (.6 (11.5) 29. in NHEXAS 1995–1996. Aposhian et al.40) 5. 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.30 (2.9) 13.20) 18.2-35.30) 2.Metals other areas of the world (Ahsan et al.8. and 0. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.S. China.0) 4. population from the National Health and Nutrition Examination Survey. 2005. When seafood intake is avoided. 2008).7 (21.90-29.3) 1284 1284 03-04 03-04 03-04 1. arsenite. 2003). 1.S. 1985. 184 Fourth National Report on Human Exposure to Environmental Chemicals .20) 3.30 (1. vasospasm.0 (26. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.00) 3. In the late 1980s.70-21.700-1. dermal keratosis. MMA.800-1. 2007) with higher levels of arsenic in the drinking water.4-35.5 (14.1-94. For residents of Inner Mongolia.0 (27.20 (2. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. and other factors such as nutrition.9 (6. Caceres et al.. Measurable organic arsenic species in this Report are three biologically generated environmental forms. arsenocholine.6-44.1-25. arsenocholine.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. In the residents of a Chilean town who consumed water with high levels of arsenic. The higher percentiles of total urinary arsenic levels in the U. when seafood organic arsenic is subtracted).6..5 (26.00-12.7-22.1-51.40) 75th 5. Survey years 03-04 Geometric mean (95% conf. 2008)..40-7.48-2..9-23. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.43-1.600 (.5) 292 728 1548 03-04 03-04 1.3 (9. 1990.29 (1. population in the NHANES 2003–2004 subsample.8 (17.60) 1. and two methylated metabolic products. respectively. interval) 1.20 (4.70 (3. 2006). WHO.3-39. Also. and TMAO were detected in only 7.6 (25. These associations are stronger at higher urinary levels.00 (1. 2005.5) 621 725 1078 Limit of detection (LOD.

78 (3..901-2.53 (.51) 5..4) 32. interval) 1.47 (1.64-29.6) 19.40) 1.9 μg/L. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..4-21. Fourth National Report on Human Exposure to Environmental Chemicals 185 .36) 2.9) 32. population for the sum of inorganic related species was 18.9 (25. Caldwell et al.25-7. The 95th percentile of the U.938-1.. 1992.83) 8.2 (12.612-1.21) 5. not to imply a safety level for general population exposure.9 (13.61-6.1-18.18-1.1-36.4) 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 * * 1.531 (.91) 90th 16. 1986. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. WHO.5 (18. 2001).400-.15-4.28) 1.4) 292 728 1548 03-04 03-04 1.7) 9.2 (13..29-14.3) 95th 29.44 (1.2 (4.30-1.50-15.S. 2006.S.83) 2.11 (. 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.00 (1.16 (.833-1.80-153) 17.05) 1.6-46.638) 1.58 (3.72) 12.7) 17.15-1. Sun et al.70) 5. Vahter et al.6-29. Survey years 03-04 Geometric mean (95% conf.43) 14.6 (9.43) 75th 5.50-7.68 (1.10 (.40 (1. 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.13-39.32-7. Offergelt et al.88 (5.9-18.909-1.959-1. 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.4 (11.37-2.78-5.00 (3.19-2..4-28.3 (10.67) 1.4-82.65 (1.0-36.5) 17.05 (.29 (4. population from the National Health and Nutrition Examination Survey. 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.25 (. 2001).1 (26.47 (2.82) 4.3 (10. 2007).62-6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.80) .88) 2.4 (24.76-27.45) 1.15-1.8) 29.81 (4.3-24.67) 4.12) < LOD . these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.9) 14.877 (.3) 1284 1284 03-04 03-04 03-04 1. In recent years. which is below the ACGIH BEI (Caldwell et al.5 (18..4) 13.1) 26.73-6.6 (6.39-3. 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. 1998.91 (4.14 (1.7) 30.. 2003.55) 1. 2008).5-20.79 (1. 2008).5) 26.82) Selected percentiles ( 95% confidence interval) 50th 1.6-32. Information about the biological exposure indices is provided here for comparison.Metals as with DMA.30) 1.0 (9.51-2.786-1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.54 (1.93 (1.2 (12.

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

00 (<LOD-2. population from the National Health and Nutrition Examination Survey.40 (<LOD-1.00 (<LOD-3.S.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. see Data Analysis section) for Survey year 03-04 is 1.44) 2.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 1.95 (<LOD-2.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.S.08 (<LOD-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 03-04 Geometric mean (95% conf. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.20 (<LOD-1. Fourth National Report on Human Exposure to Environmental Chemicals 187 .80) < LOD 621 725 1078 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.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. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.

69-6. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.32-10.34-4.00-12.70-4.62) 4.15) 4.50-5.60-6.0) 17.34) 3.18 (6. population from the National Health and Nutrition Examination Survey.06) 5.00-3.9) 13.20-12.42) 3.0) 13.03 (3.28) 2.48 (3. Survey years 03-04 Geometric mean (95% conf.60-4.81 (5.95 (4.0) 9.44 (2.70 (3.71-4.60-7.12-4.0) 12.34 (3.5) 12.03-6.34-4.46 (4.65-6.77 (3.00) 12.52) 3.69 (3.24) 3.0) 11.50-15.39-3.27 (3.71 (4.55 (2.86-7.00-7.00-4.50 (4.00) 3.00-11.2) 10.78) 4.94) 3.0 (12.9) 5.61-11.27-2.0 (9.4 (7.0 (8.0 (13.0) 10.0) 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 4.48 (2.73 (3.00-22.0-25.0) 292 728 1548 03-04 03-04 4.16 (4.00 (5.00-4.80) 2.5 (11.00-12.17 (2.95-6.11) 4.82-9.7) 12.8) 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 3.0 (13.31) 4.00) 75th 6.00 (7.0-19.25 (4.00) 7.94-3.00-11.61-16.0) 621 725 1078 Limit of detection (LOD.05) 10.69-3.32 (8.31-4.70) 5.00 (3.10) 6.65-8.7) 1284 1284 03-04 03-04 03-04 4.0) 16.69 (3.00 (3.45) 8.00 (3.95-4.86 (2.00-4.80-3.3 (8.22) 4.84-8.0-16.00-7.80-6.70-3.73) 6.82) 3.0) 14.34 (3.00-15.30) 3.49) 10.0-16.0 (10.20) 11.16-11.00-4.80 (4.00) 9.97-3.00) 4.14) Selected percentiles ( 95% confidence interval) 50th 3.80) 7.00) 6.8) 7.11 (3.00-15.00 (3.78 (4.0) 9.91) 75th 5.00-9.45) 3.0-17.79 (3.33-4.14) 3.85 (3.32 (4.9) 12.00 (6.08 (2.27 (2.S.00) 3.82-5.00-13.0) 9.0 (8.0 (9.59 (6.7.8) 7.37 (3. interval) 3. population from the National Health and Nutrition Examination Survey.00-4.17-6.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .1-15.6-18.49-4.S.90) 5.0-17. Survey years 03-04 Geometric mean (95% conf.1-18.00 (7.90 (3.00 (3.00-10.9 (7.45 (8.00 (5.57 (3.00-5.0 (9.60-3.89 (3.0) 13.95-3.00) 5.05) 3.00 (5.0-18.3 (8.00 (5.74 (2.7) 13.00-7.24-4.6) 1284 1284 03-04 03-04 03-04 4.84-18.19) Selected percentiles ( 95% confidence interval) 50th 3.16 (2.0 (14.27-5.0 (10.00-11.74) 90th 9.20-4.0 (11.9 (11.7-16.09 (7.00 (3.00-15.00 (5.00-8.0 (10.6) 292 728 1548 03-04 03-04 3.57-5.00) 6.1 (8.05) 5.0 (12. see Data Analysis section) for Survey year 03-04 is 1.00-3.44) 5.0) 11.90) 2.00-4.13-4.10) 3.71) 3.17-4.92) 3.0 (10.7 (10.33) 3.92-12.38 (3.98) 4.12 (3.29-4.67) 9.30 (7.00) 6.00-7.1-22.3 (7.72 (4.71 (3.0) 95th 16.88 (4.00) 4.00) 6.5) 95th 13.00 (6.9) 11.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0-12.00 (4.0) 17.0) 16. interval) 3.80-5.6 (9.37 (2.70-12.67) 8.00 (6.00) 90th 11.86-21.

90) 2.54) 90th 2.40) 1.05-1.14-1.62) 2.00) 2.86 (2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10-1.10 (<LOD-1.50 (2.53-2.33 (1.30) 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.85) 1.50) 1.77) 1. Survey years 03-04 Geometric mean (95% conf.80) 1. see Data Analysis section) for Survey year 03-04 is 0.71-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33 (1.00 (<LOD-1.36 (1.S.40-3.30) 2.40 (1.22) 3.90) 2.00 (2.36) 1.00 (<LOD-1.88 (1.40) 2.50-2.10) 95th 2. < LOD means less than the limit of detection.985) 1.70-2.60 (2.30-2.70-2.07) 2.S.70-2.28 (1.9.18-1.80 (1.40-3.00) 1. which may vary for some chemicals by year and by individual sample.00-2.10 (. Fourth National Report on Human Exposure to Environmental Chemicals 189 .900-1.50 (<LOD-1.18-1.10 (.80-2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.30 (1.30-1.90 (2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-4.40) 1.20) 2.34) 2.853-1.52 (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 1.07-3.86) 3.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.80-2.07 (1.30) 1.73-2.50 (1.35-3. population from the National Health and Nutrition Examination Survey.60 (1.00 (1.00-1.90) 1.20 (1.17) 2.60-2.20 (1.15-1.70-3.84-3.20-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.46-2.20 (1.22 (1.31-3.20-1.11-1.88-2.61) 2.10-1.30 (1.46 (1.80 (1.30-1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.93) .30 (2.10-3.43-3.60) 2.20 (1.31 (1.53 (1.85) 2.60) 2.28 (1.00-1.16 (2.40-2.90 (1.70) 2.82-2.50) 621 725 1077 Limit of detection (LOD.20 (1.00 (2.10 (1.79) 2.20 (1.10 (1.88 (1.30 (1.40 (2.00) 1.816 (<LOD-.37 (1.40-2.80 (1.00-2.10) 2.70-2.80) 1.00) 2.23) 1. Survey years 03-04 Geometric mean (95% conf.45) 3.57) 95th 2.80 (2.81) 1.86 (2.96-2.63 (<LOD-1.80 (1.50 (1.00) 1.86) 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.61-3.82-2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.60) 1.58) 2. population from the National Health and Nutrition Examination Survey.30) 90th 1.

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

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24-1.20-8.70) 5.65) 3..30) 3.52 (4.29-1. 7440-39-3 Medically.02 (7.90) 2.00) 1.S.70 (1.86-4.30) 4.24-1.16 (1.94-6.71) 95th 6.36-1.30 (2.12-1.90 (4.36 (1.78) 1.8 (6.19) 2.70-8.36) 5.26) 2.35) 5.86 (4.15 (6.90 (1.40 (5.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80) 6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (2.51) 7.39) 4.49) 8.96-2.66 (4.88) 4.20 (3.52 (1.57) 3.67) 6.90-2.92) 2.78-3.40 (1.95-6.35 (3.30) 2. Some barium salts are freely soluble in water.15-11.20-1.60 (2.56 (1. fireworks.87-14.30 (5.20-1.15 (1. 0.01 (4.21-8.21-2.60) 4.64 (1. In single dose animal studies.76-3. and 03-04 are 0. 2001).90-9.4) 6.49-9.30) 5.76-2.50-6.43) 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. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Workers employed by industries that make or use barium compounds can be exposed to barium dust.34 (2.30 (3.11 (3.20-8.40 (5.43) 2.30-3.82) 1.80) 7.20-1.20-1. such as brazil nuts.37) 1.29-5.05-2.74-3.25 (1.59-11.31-2.04-2.72) 4.06-1.54-1.50-1.30-2.54 (2.18 (6.78-2.87 (6.48-4.40 (1.40-13.35-4.80-5.70) 1.59) 3.50) 4.70-3.30-5.4) 7.80 (5.88) 1.44-5.46-1.20) 2.4) 9.51) 2.45 (1.15-1.82) 2.76 (3.36-1.70) 4.50 (1.87-7.51) 1.25-11. soluble forms of barium.80 (1.49) 4.27 (1.87-3.71-9.90) 4.53) 2.49) 11.63 (2.90) 1.80 (2.10-5.08-8.90-13.22) 6. see Data Analysis section) for Survey years 99-00. interval) 1.35-1.74-2.90 (6.48) 1. bricks.66) Selected percentiles ( 95% confidence interval) 50th 1.93 (4.60) 1.00 (1. Certain foods.62) 1.30-1.12 (2. water.40 (5.64-3.25-1.55-3.45) 7.34) 2.37-8.47) 4.01-7.30) 8.56) 4.40) 7.35-1.54 (6.65) 1.05% of the earth’s crust.18) 3.00-8. population from the National Health and Nutrition Examination Survey.99-5. respectively.12 (2.00) 1.90) 2.63 (8.04-6.20 (1.87 (5.30) 5.34 (1.32-7.50) 2.91) 6.53) 1.73 (5.56) 1.22-1.73) 3.00 (2.50 (2. The general population can be exposed to low amounts of barium in air.41-1.65) 1.77-3.38) 8.50 (1.40) 7.70-5.48-4.38 (1.41-3.31 (2.40) 3.72) 75th 3.70) 7.63) 1.53-5.85 (2.12.50 (3.71) 2.39-1.60) 3.07 (2. Small amounts of barium can be released into the air during mining and other industrial processes.20-6.97 (1.60-2.73 (6.56 (6.91 (2.50-1.78) 1.60 (1.61 (5. depilatories.37-1.21 (1.56 (1.32-1.80 (1.46) 1.26-7.81-3.38 (1.12.60-6.54-8. Barium compounds are used by the oil and gas industries to make drilling muds.75-3.03 (1.76-7. and 0.35 (1.Metals Barium CAS No.69 (1.87) 7. 01-02.12) 7.30-2.56 (2.71) 1.57-7.91) 2.28) 90th 5.55-7.43 (5.11-1.50 (4.47-1. it combines with other chemicals such as sulfur or carbon and oxygen.71 (2.14 (6.82-6.10 (4.77) 1.57 (5.62 (1.70-2.50 (6.73) 1.10) 5.24 (4.9) 5.80-2.14-1.99 (4.44-2.18-1.61 (2.47-1.39 (1.50 (4. Barium salts have also been available as rodenticides.15 (2.10) 3.g.09 (2.43) 6.86-5.20-8.84) 5.2) 6.61 (3.80 (2.86 (4.86) 6.49-1.60-6.17-1.61-8.26-1.73-5.88 (5.60-3. such as barium chloride.37 (4.74) 3.48) 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 1.65-8.28-1.27 (1.51 (1. and food.54) 1.21 (1.72) 1.14-6.64) 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 2.62) 1.50 (1.63) Total 1.11 (2.20 (4.00-76.50 (1.39 (1.34 (1.30-1.00) 4. are high in barium (Genter.63) 1.63 (1. glass.36 (4.22-1.54) 2.50 (4.81-2.30 (5.63 (5.61 (1. barium sulfate and barium carbonate).43 (1.62 (1.80-7.19-1.50 (1.98) 1.37) 5. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose). In nature.70-2.76) 1.39) 1.95 (4.70 (5.49 (1.75) 2.20-5.00) 6.30) 5.06-2.81-2.8) 5.33 (1.15-1.09 (1.77 (3.70) 3.10 (3.46) 1. rubber.38) 2.80 (1.65-1.30 (1.93-8.65-5.1) 9.43 (1.70-6.87-9.50) 2.54) 1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0. tiles. whereas others are practically insoluble (e.44 (1.15) 5.88) 7.12) 6. Fourth National Report on Human Exposure to Environmental Chemicals 193 .50-6.00-3.31.8) 9.70) 1.32) 8. and ceramics.27) 2.29) 5.50 (5.60-10.80) 1.85) 1.40 (1.42 (1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.48 (6.16) 5.60) 1.54-1.26) 5.41) 1.11 (3.40 (4. Barium compounds are also used commercially in paint.35 (2.80-3.10-4.65 (5.61 (1.08 (6.85) 1.50) 1.93-2.68 (1.49) 2.

45-6.64 (1.48-1.62 (4.01) 1.51 (1.55 (1. and route of exposure. The health effects of exposure to barium compounds depend on the dose.921 (.81-6.91-2.92) 2.10-1.04 (2.28 (1.83) 3.31) 5.26-1.47-8. weakness.20-1.61 (4.80) 3.52-10.16-1.39 (2.76 (3.70) 1.27-1.36-1..13-3.59) 1.00 (2.0) 5.96) 4.24-1.72) 4.56) 4.55 (4.68-3.37 (1.54) 1. vomiting.881 (.57 (6.49-1.24 (3.29-4. diarrhea.03-1.20 (1.38) 1.45 (3. NTP.20-8. Toxicity from soluble barium salts is rare.34 (1.69 (5.88 (6.97-4.24-1. Symptoms following acute high dose include perioral paresthesias.880-1.48 (1.37) 2.24-3.60 (1.48-5.76-3.57-5. hypertension.68 (3.33-4.03-1.02) .38 (1.96-6.55 (5.75) 1.24-6.84-2.34-3.97-3.38 (4.710-1.41 (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 2.91) 2.31 (4.88 (2. paralysis.00) 1.47 (2.83) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.35-1.80-6. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.49 (1.49 (1. water solubility.45-1.42) 1.30 (1.29-1.52) 2.22-1.40-1.29 (3.64) 7.59 (1.25-11.77) 5.73-4.74) 1.11) .67-6.48-3.34) 1.75-22.32 (1. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.62 (2.37-1.96) 7.41) 5.36 (1.23-2.45-1.04) 5.58) 1.19-1.64 (1.8) 4.60 (2.39-1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.52) 1.77) 1.57-7.99 (4. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.46 (2.77-5.02) 4.70) 10.32) 2.34-5.91 (3.39 (2.39 (2.53) .76) 2.78 (2. Insoluble barium salts.81-6.43) 1.25 (1.39-5.57) 2.S. 1994.73-2.01 (5.28-7.79) 1.0) 6.74) 1.49-1.72) 6.62) 2.55) .84-5.754-1.11-2.39-1.02-5.42) 1.60 (1.36-1.96 (4.3) 6.10) 6.64 (1.29-4.00 (3.29-7. Following intravenous injection in animals.75) 2.26-4.75) 2.74 (5.26-1.12) 2.45) 95th 6.38) 4.50) 1.05-1.39 (3.20) 4.22-2.42 (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 1.32) 2.58-6.68) 1.24 (5.32 (1.61) 2.35-3.81-7.63) 1.44-2.52 (3. a benign condition that may occur among barite ore miners. Perry et al.65 (5.56-3.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .64) 7.51 (1.36 (5.2) 6.28-6.26-1.33 (1.97 (4.43-6. 2001).60 (2. Barium is not rated for human carcinogenicity. 1985.87) 1.29) 1.59) 1.2) 5.47) 1.39-10.00-1.82) 1.96) 4.59 (1.89) 90th 4.915 (.3 (6.52) 7.34-1.75-3. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.24-6.40 (1.56 (1.46) 2.27-3.27) 7.50 (4. 1990).60 (5.44-2.45 (1.10-2. chemical form.38-7.56 (1.36 (3.51) 4. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.19-1.29 (1.38-5.45) 1.41) 4.33) 6.16) 11.02 (3.86 (2.96 (4.48) 2.09) 6.16 (1.32 (2. in urine. and cardiac dysrhythmias.891 (.62 (1.58) 4.68) 3.70) 4. 1986).39) 4.44 (1.38) 1. interval) 1.28-1.58 (2.31 (1.47) 4.0) 7.48 (1.90-2. 1989).80) 4. such as those used in medical radiographic procedures.72 (2. 1984.97) 1.36 (3.56) Selected percentiles ( 95% confidence interval) 50th 1.38 (1.45-8.51-3.703-1.86) 5. Chronic high doses in animals resulted in kidney damage (McCauley et al. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.06) 2.36-2.58) 75th 2.69-9.30) 2.10 (6.75) 1.46-22.63-4.53-21.55-6.11) .03) 3.30 (1.51) 4.76 (4.04) 1.13-2.21 (1.58 (4.31-1.963 (.40 (1.52-4.00) 4.777-1.76) 1.73) 2.22-1.51 (3.55 (1.66 (1.54 (1.18 (1.50) 2.89 (2.29-3.2 (3.00 (5.99) 1.33 (5.00 (3.27 (2.Metals was eliminated primarily in feces and to a lesser extent.4 (5.59) 2.00-7.00) 4.10) 3.37 (1.38 (4.31-1.28-11..68 (3.47) 10.77) Total 1.20-2.37-2.19-2.64 (1.33-1.06) .31-1.55-5.25) 4.08-2.59-7.24-11.18 (1.92 (4..46) 1.98 (2.23-1.832-1.76 (2. population from the National Health and Nutrition Examination Survey.33 (1. are not absorbed when administered.96) 4.54 (2.15-4.68 (2.48 (1.77) 1.46) 3.50) 1.23-5.38-1.97 (5.35-1.01 (4.79-5.76) 2.36 (1.47) 1.14-2.57-10.85-5.51) 6.84 (3.82) 1.54) 2.26) 4.68-3.4) 5.41 (1.91 (3.86-7.53 (2.65 (2.77) 1.22-4.49-1.40 (1.28) 5.03) 2.24) 3.03) 1.08-1.00) 6.19-1.47 (5.26-1.905 (.71 (5. Wones et al.41 (2.99 (2.33) 1.84) 2.

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

near some hazardous waste sites. computer. which may vary for some chemicals by year and by individual sample. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.13. and 0.150) < 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 .13.140 (<LOD-. and machine-parts industries. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Exposure to beryllium occurs mostly in the workplace. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.S. nuclear. aircraft. electrical. eating food. soil.130 (<LOD-. are mined for commercial recovery of beryllium. Two types of minerals. and refined beryllium is used in mirrors and special metal alloys for the automobile. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. beryllium is used in instruments. Beryllium compounds are commercially mined. Low-level beryllium exposure in the general population can occur through breathing air.Metals Beryllium CAS No.130 (<LOD-.160) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . In studies of laboratory animals. respectively. and can be found in mineral rocks. and from breathing tobacco smoke. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. and dental bridges.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 . 7440-41-7 General Information Pure beryllium is a hard gray metal. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. the lightest of all metals. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. and volcanic dust. or drinking water containing the metal. bertrandite and beryl. 196 Fourth National Report on Human Exposure to Environmental Chemicals .13. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. 0. In medicine. and 03-04 are 0. see Data Analysis section) for Survey years 99-00. coal. x-ray machines. 01-02.

2002). Fourth National Report on Human Exposure to Environmental Chemicals 197 . or berylliosis. 2003.333) < 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 .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 .281 (<LOD-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and drinking water and environmental standards have been established by U. NTP considers beryllium to be a known human carcinogen. Skin exposure can result in delayed hypersensitivity reactions. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. Maier. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. respectively. More information about external exposure Urinary Beryllium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Chronic beryllium disease.. based upon excess lung and central nervous system cancers in studies of workers.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. 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 .346 (<LOD-. population from the National Health and Nutrition Examination Survey. EPA.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. S. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. including contact dermatitis and subcutaneous nodules. 1990).231 (<LOD-. IARC has classified beryllium as a human carcinogen. which produces pneumonitis. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.

Pozzoli L. population were generally undetectable in NHANES 1999-2000. Pirkle JL. Genetic and exposure risks for chronic beryllium disease. 1990. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000.cdc. Ting BG. VI. and serum of Italian subjects. 2001). Maier L. Hamilton et al. Paschal DC. and 2003-2004. Ash KO. patient population and literature reference intervals for urinary trace elements.. Sampson EJ.95:89-105. Levels of beryllium in urine for the U. environmental levels) and health effects is available from ATSDR at: http://www.. et al.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.e. Clin Chest Med 2002. HLA-DPB1 and chronic beryllium disease: a HuGE review.157:388-398.76(1):53-59. et al.gov/toxpro2.S.S. which approximate this Report’s limit of detection.74:162-166. References Apostoli P. Review of elements in blood. 1990. Jackson RJ. Schaller KH.. Comparison of representative ranges based on U. Sabbioni E. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. blood. Pietra R. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Weston A.e. 1998). Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Trace metals in urine of United States residents: reference range concentrations. A study of 46 elements in urine.1 μg/L). Am J Epidemiol 2003. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. They reported urinary beryllium levels ranging from 0.org/documents/ehc/ehc/ ehc106. Van der Venne MT. it is likely that urinary beryllium levels in the U. Sabbioni E.S. Third National Report on Human Exposure to Environmental Chemicals. and the fact that most NHANES participant levels were undetectable. 0. less than 0. Morrow JC. McCanlies EC. Howerton K. Minoia et al.html. and the 95th percentile for males in NHANES 2001-2002. Costa R. Andrew M.296(1-2):71-90. Hamilton EI. Int Arch Occup Environ Health 2001. Sci Total Environ 1994. 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. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Minoia C. 20012002.12 to 0. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Environ Res 1998.23:827-839. 3/27/08 Komaromy-Hiller G. Sci Total Environ 1990.158:165-190. Available at URL: http://www.atsdr. population are lower than levels in workers. Kriess K. International Programme on Chemical Safety (IPCS).. Paschal et al.inchem. Clin Chim Acta 2000.13 μg/L.. Element reference values in tissues from inhabitants of the European community. Centers for Disease Control and Prevention (CDC).Metals (i. Trace element reference values in tissues from inhabitants of the European community I. Gallorini M. 106. In other studies. Given these results. Atlanta (GA) 2005. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental Health Criteria. Beryllium [online]. Apostoli P.htm.

00 (.800-1.30) 1.600) .300-.700 (.393 (.420 (.50 (1. 01-02.20) 95th 1.425 (.395 (.300-.00 (.20 (1.600) .313 (. < LOD means less than the limit of detection.60 (1.500 (.600) .400-.20-1.700-1.200-.300 (<LOD-.00-1.300) .500-.00 (1. Since 2001.275-.600) .400) .usgs.80 (1.400) < LOD .300 (.400-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.500-.400 (.800) .300 (.10 (.304 (.426-.30-1.50) 1.10) 1.70) 1.00) .70) 1.421 (.900-1.304-.400) .300 (<LOD-.900-1.300) .20) .60-1.289-.400 (.400-.500-.800 (.600 (.400 (.300 (.359-.00-1.20-1.700) 1.30-1. population from the National Health and Nutrition Examination Survey.500) .400 (.20) 1.500 (.300-.400) .266-.900-1.500 (.500-. and 0.00-1.00 (.300) .400-.300) .600 (.500-.00) .500) .500-.10 (1.40-1. EPA.216-.50-1.400) .368-.367-.600-.900-1.300-.500-.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 . Other uses include pigment production.400) .40) 1.400) .00-1.600 (. and 03-04 are 0. malleable.10) 1. and nonferrous alloys.20-1.800-1.00 (.300) .10 (1.412 (.300-.400) .300) .500 (.700) .400) < LOD .10) 1.700) .400 (. interval) .S. during refining of lead and copper from sulfide ore.300 (.300-.400-.300) .400) < LOD < LOD < LOD .400 (.500-.900-1.300-.600) 1.300-.309-.200) .500 (.235 (.700) .300-.900 (.361-.400) .400) . U.400-.10) 1.40 (1.300 (.500) .400 (.400 (.700-1.300-. Cadmium also may be emitted into the air from zinc. 0.00-1.200 (<LOD-.378 (.400) .400) .800) .40 (1.00 (.337) .600 (.500) .331) .600) .200 (.500 (.378-.300 (.30) 1.30) 1.300) .700) .00-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.20-1.300) 1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .10) 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 .300) .700) .50) 1.300-.600 (.200-.400 (.200 (. or copper smelters (U.00-1.326 (.20) .382 (.600) .50 (1.500) .300-.600-1.500-. coatings and plating. respectively.20) 1.513) .50-1.600-.300-.10) 1.600) .500-.200 (<LOD-.460) .300 (.400-.900-1.50-1.600 (. see Data Analysis section) for Survey years 99-00.80) 1.300-.500-.20) 1.10 (1.200) .50 (1.400 (.50 (1.300 (.60) 1.400) .424) * .255) .500-.300-. The predominant commercial use of cadmium is in battery manufacturing.20) 1.500 (.200 (.30 (1.60) 1.300 (.400 (.500-.600 (.300 (.300) 75th .700) .3.60) 1.20) 1.60 (1.600 (.300) .900-1.30-1.900-1.200-.600 (.600) .300-.300-.70) 1.366) * * .300 (.400 (.600 (.296-.00 (1. and incineration of municipal waste materials.400) .500-.427) * .441) * .300 (<LOD-.344) .500-.400-.304 (.400 (.376-.300) .300 (.40 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.449) Selected percentiles ( 95% confidence interval) 50th .700-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (.300-.300) .20-1.400-.10 (1.80) 1.40 (1.600) .300-.403) .40 (1.20) 1.S.400) . which may vary for some chemicals by year and by individual sample.S.20-1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.20) 1.400-.40 (1.470) * .20) 1.386-.300) . as zinc sulfide) and to a lesser extent.900-1. cadmium use has declined in response to environmental concerns (http:// minerals.40 (1.398) < LOD < LOD < LOD < LOD < LOD < LOD .400) < LOD .452) .400-.10 (1.300 (<LOD-. lead.283 (.gov/minerals/pubs/commodity/cadmium).500) .50) 1.40-1.900 (.600) 90th 1.600-.00-1.10 (1.60 (1.600 (.00 (.500 (.500-.14.90) 1. Fourth National Report on Human Exposure to Environmental Chemicals 199 .70) 1.10) 1.Metals Cadmium CAS No.700) . 7440-43-9 General Information Cadmium is a soft.468 (.00 (.333 (.500 (.600 (.40) 1.600 (.30-1.60 (1. plastic stabilizers.300 (.500) .900-1.400 (.300-.3.30) .300 (.00 (.800 (.400 (.00 (.300-.500-.600 (.00-1.20-1.362-.60) Total * .60 (1.200-.30-1.400 (.50-1.10 (1.10) 1.400 (.300-.700) .00 (.500-.403 (.800) 1.

141 (.336) . 2003.160 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.813 (.47) 1.400-.114-.48 (1.06.855-1.279 (.210 (.820) 1.302 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (1.270 (.500) 90th . however.196-.390-.892-1.550 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.351-.763-.04 (.061 (<LOD-.362) .090) .316 (..589 (.41 (.843-1.559 (.447 (.203 (.817 (.061-.82) 1.20-1.700-.171-.220-.189-.110-.257) .211 (.450 (.193 (.980) .886-1. respectively.121 (. 2003).440 (.189) .067-.238) .482) .310 (.191-.329 (.211-.839 (.190-.157) .490) 1.38) 1.445 (.13 (.381-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .313) . drinking water is a source for cadmium intake.820 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.13) .134) .580) .22 (1.240) .57) 1. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.231) .455 (.265 (. copper) and protein. 2003).09-1.972 (.263) .748-1.233) . Cadmium is absorbed via inhalation and ingestion.733) .201 (.229) .480) .202 (.01) . Cadmium in soil is absorbed by plants.25) 1.366) .686-.01 (.249) . 2003).284) .280 (.412) .222) .730-.077 (.470-.596) .200-.235) . Cadmium absorption may be increased with iron deficiency (Berglund et al.322 (. wheat.15 (.445 (.36) 1.261-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .170-.120 (. calcium.06.107-.06) .890-1.195-.806) .135-.170 (.607) .04 (.977) .175 (. and various seeds.858 (.38) 1.270 (.440-.875 (.178-.078 (.22 (.980) .299) .200-.880) .200 (.456-.165-.181 (.490) .918-1. whose body burdens of cadmium can be approximately twice that of nonsmokers.237-.239 (.372) .38) .886) .170-.339) .475 (.28) 1..83) 1.065-. 2004a.173) .360) .960) 1.800 (.092 (.20 (1.206 (.220-.257-.733-.265) .227 (. 1999.198) .208-.175 (.210) .191-.30-1.15) 1.308) .140 (.680 (.136) .24) 1.423-.189-. 1994).220 (.230) 75th .249-.860) 1.810-1.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.481) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .220) .700-.493-.204 (. ingestion through food is the largest source of exposure. and 03-04 are 0.28 (1.223 (.366-.10 (1.12 (.476-.092) .479) .390 (.128 (.03) .295) .281 (.12-1.077 (. Diamond et al.210 (.388-.32 (1.820-1.226) .260 (.623) .817 (.260-.19) 1.210 (.240-.190-.72) 1. an inducible metal binding protein.232) .892 (.192-. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.551 (. zinc.180 (..327 (.277 (.519) .080 (.741-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.430-.530 (.230 (.115-.200 (.510-.790 (.251) .326) .366-.15) .191 (.963-1.633 (.272-.394-.238-.160-.705-.440 (.210 (.202-.790 (.330-. potatoes.206) .255) . To a lesser extent. **All results are corrected for molybdenum oxide interference in the ICP-MS method.203) .219 (.633-1.151-.167-.519) .17 (.848 (. For nonsmokers who are not exposed to cadmium in the workplace.700-.234 (.890 (.260-.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 .960 (.101) .210) .875) .135 (.246) .169-.262) .545 (. Kikuchi et al.193-.130 (.067-.753-.20 (1.221) .717-.289-.51 (1.187 (.06-1.153-.194-.090) .310) .184-.919) .290-.390-.261-.466 (.300 (.400-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.273 (.38) .306 (.. cadmium accumulates in the liver and kidneys where it is bound to metallothionein..148) .714-1. 01-02. including many food crops such as cereal grains. population from the National Health and Nutrition Examination Survey.452 (.247) . 0.150) .510) .157-.498-.177-.520-. With chronic exposure.989-1.232 (.229) .540) . 2001).539) .350 (.940-1.214-.060-.179-.551) .450 (.713) .492 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.07-1.640) .087-.100-.190-.255) .13-1.393-.219 (.06.870) .34) 1.S.458 (.199 (.766 (. rice.25 (1. and 0.433-.980-1.507) .243-.52 (1.17 (.980-1.285-.160) .800-.221 (.06-1.02-1. Renal tubular and glomerular damage.183-.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.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 .109-.300) .283 (.530) . see Data Analysis section) for Survey years 99-00.192-.980 (.209 (.** Survey Geometric mean (95% conf.387) . Horiguchi et al.148-.282 (.610) .150-.74) 1.28-1. interval) .01-1.500) .255) .836-1.207-.233) .43) 1..210 (.109 (.081) .430) .253-.160) .320) .216 (.436-.17 (.354) .Metals 2000).462 (.20) 1.112-.426 (.17) .990) .241) .126) .230) .229-.818 (.219 (.

789 (.183 (.226) 75th .663 (.783 (.591 (.223) .722-.084-.622 (.850) .418-. 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.650-.107) .123-.185) .168 (.. most often a result of occupational exposure (Roels et al.308 (.263 (.182) .154 (.293-.131-.647-.111-.242) .700 (. Noonan et al.316) .094) .071 (.175-.783) .224 (.479 (.614) .084 (.718 (.288-.137-.212 (.917) .340) .078-.274) 1.388-.181-.38) .175 (.283 (.247-.240) .201-.185 (.184-.940-1. 2002.329 (.236-.784) .500-.143-.873 (.247-.075 (<LOD-. 1999).962) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * ...472) .159 (.143-.941 (.631) ..16) 1.678 (.190 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .208-.865 (.140-.147 (.321) .434 (.813-1.122 (.292) .106) .906) .856) .182) .350) .171-. 2003..826-1.491-.288 (.148 (.884) .140-.13) .250) .239-.562-.382) .202 (.083-.266) .00 (.245 (.187-.219 (.143) .645-.112) .876-1.813-.263-..228-.536 (.617 (.421 (.075-. Jarup et al..740 (.929) .06 (.240) .288) .414 (.444-.481 (.343-.157-.074-.170-.538) .190 (.261) .433-.091 (.674-1.135) .630-.418) .156 (.826-1. Olsson et al.725-1.473 (.16) .668-.412 (.166 (.235) .423-.917 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.163) .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.423 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.325 (.233 (.769 (.173 (.234 (.207-..07 (.531 (.931 (.449) .476) .144-. 2002.078 (.194-.985 (.818) .696-.830) . 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. 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.130-.196 (.979 (.09 (.767) .227-.827) .280 (.470) .210) .607) .270 (.364) .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 .267 (.181 (.232) .168-. 2004).909-1.256-.559-.176 (. 1999).093 (.146-.404) .304-.303) .545) .391-.446) .178) .220 (.261 (.693 (.729 (.156-.10) 1.211 (.187) .261-.440) .136-.667) .123-.207) .161-.700) .289) .255-.438-.178-.441-..308) .387 (.086 (.335 (.170 (.156) .398-.919 (.415) .184-. 1996.757 (.802 (. Horiguchi et al.137 (.516-.159 (.282 (.104) .02 (.426-.678-.154-.181 (.184) .158-.551) .311) .830-1.273 (.690-.560-. 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.336-.779 (.173-.414-.063-.238) .387-.719 (.221 (.828) .232) .267 (.300-.833-1. 2000..05) 1.08) .198) . Staessen et al.253 (.792 (.157-.438) 90th .338 (.927-1.297) .216-.077-.168-.189-.712 (.085 (.241) .206-.191) .818) .175 (.174-.S.147-.653) .225) .289) .162 (.316 (.518) .150-.304) .176 (.199-.234) .096) . 2004b). 1999).209) Selected percentiles ( 95% confidence interval) Sample 95th . can result from high dose chronic exposure.197-.296 (.209) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.098) .795) 1.377-.767 (.104) .281) .204-.183) . 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.507-.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 .101) .950) .210 (.** Survey Geometric mean (95% conf.686 (.221-.856 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.757) .205 (.091) .754) .222-.874-1.090 (.181) .238-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .091 (.247-.177) .281) .126 (.218) .940 (.051-.163 (.210 (.318 (.067-.085-.07) .716) . At lower environmental exposures.541) .490 (.839) .690 (. population from the National Health and Nutrition Examination Survey.199 (.537-. 2002.688-.690-.268 (.12) 1.431) .219 (.382-.687-.17) .352) .253) .691-.191-.484 (.432 (. However.687 (.998) .229) .331 (.113-.234-.225) .252 (.147-.727-.136-.100 (.00 (.470) .278) .501 (.182) .666-.191 (.266-.533) .806-1.097) .215 (.192) . During the 1950’s and 1960’s.850) .440) .208 (.381-.200 (.708-1.487 (.404 (.716-. interval) .

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

Nermell B. Berglund M. Friedman LS.354:1508– 1513. Savage-Brown A. Vahter M. Sanz P. Akesson A. Seifert B. et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. patient population and literature reference intervals for urinary trace elements.66(Pt A):2141-2164. et al. Persson B. Lison D. Environ Res 2006. Fukui Y. Bo M. Serra J. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure.45:43-52. Schulz C. Greves HM.cdc. 196:114-123. Zhu G. Occup Med 1996. Bernard A. Neurotoxicology 2003. Stock AL. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Ikeda Y. Howerton K. Atlanta (GA). Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. iron deficiency.html. 1999 [online]. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Mannino DM. Dekio F. et al. Komaromy-Hiller G. et al. Ezaki T. Kumagai N. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. et al. Oguma E. Comparison of representative ranges based on U. Occup Environ Med 2000. Anthropometric.76:186-196.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. Cadmium fume inhalation and emphysema. et al.148(1-2):11-20. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Alfven T. 2005. Nordberg G. Oguma E. Ukai H. Lukyanova EM. Nomiyama T. Choudhury H. Environ Health Perspect 2002. Fukui Y. Lidfeldt J. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Machida M. Fernandez MA. Becker K. Kundiev YT. et al. Third National Report on Human Exposure to Environmental Chemicals. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Fatal chemical pneumonitis due to cadmium fumes. Toxicol Appl Pharmacol 2004a. Darbyshire J.000 women in the Japanese general population: a nationwide large-scale survey. Vahter M.1(8587):663-667.95:20–31.96:353-359. Int J Hyg Environ Health 2003. Miyamoto K. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. diabetes mellitus. Furuki K. Sasaki S. Seiwert M. Available at URL: http://www. possibly better than b2microglobulin. Environ Res 2004. 206:15-24. Thorax 2004. Consonni D. Diamond GL. Elinder CG. Carlsson MD. population. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Holguin F. Kaus S. Lundh T. Int Arch Occup Environ Health 2003. Int J Hyg Environ Health 2002. Krause C. Clin Chim Acta 2000.59:194-8. Tsukahara T. Hellstrom L. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Ash KO. Horiguchi H. Chiappino G. Toxicol Lett 2004. Pickering CA. Costa R. Becker K. Ikeda Y. Venables KM. Jarup L. Fayers PM. Mucha A. Lauwerys R. Seiwert M. Furuki K. Schulz C. 102:10581066.24:717-724. Bellerup P. Hotz P.110:699-702. Jones RL. environmental.59:497]. Palomar M. Horiguchi H. Comprehensive study of the effects of age. Miyamoto K.atsdr. et al. Nerbrand C. Grubb A. Taylor AJ. References Akesson A. Olfactory function in workers exposed to moderate airborne cadmium levels. et al. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Toffoletto F. Gadea E. J Occup Health 2003. Chislovska NV. Kaus S. ShkiryakNizhnyk AZ. Takebayashi T. Centers for Disease Control and Prevention (CDC).102:83-89.S. Uemura T. Kikuchi Y. Jin T. Environ Res 2004b. Jarup L. Okamoto S. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study.13(11):1627-1631. Machida M. J Toxicol Environ Health 2003. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Lancet 1988.57:668-672. Lepom P. Buchet JP.205:297-308. Mascagni P.gov/toxprofiles/tp5. Tsukahara T. Thayer WC. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Moriguchi J. 4/8/09 Alfven T. Bregante G.296(1-2):71-90. Davison AG. Sasaki S. et al. Ezaki T. Wang H. Ye T. Agency for Toxic Substances and Disease Registry (ATSDR).46:372-374. Environ Health Perspect 1994. Environ Health Perspect 2005. Toxicological profile for cadmium update. et al.S. Lancet 1999. Moriguchi J.

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01-6. However.0) 12.25 (3.71-8.7 (9.0) 12.12-11. and clay.2-13.70 (8.2 (9.02 (4.53-11.0) 12. 0.4 (10.90-12.54-11.27 (7.0 (9.37) 5.80 (8.99) 7.08-5.5-14.80-10.2) 12.92-13.40-5.49 (5. scintillation counters.30-5.80-13.2-13.08 (6.14.36) 3.35-5.40-5.50) 5.12) 5. and high-power gas-ion devices.32) 4. Fourth National Report on Human Exposure to Environmental Chemicals 205 .01) 7.74) Selected percentiles ( 95% confidence interval) 50th 4.81) 9.9 (11. nausea.9 (10.20) 5.90-12.6 (11.55-11.6 (9.74-5.30 (6.64) 5.5) 12. infrared lamps.6) 11.13 (5.20 (4.95) 5.59 (5.15-8.60 (8.99-6.83) 6.60) 7.7 (11.29 (4.00 (7. Whether cesium compounds are carcinogenic is unknown.8) 12.26 (3.36 (3.76-6.87 (4.34) 9.71 (8.21 (4.45-5.6 (11.1 (10.8) 12. 01-02.81 (4.22 (4.70 (6.36 (6.40) 5.34 (4. Little is known about the health effects of this metal.12 (4. Radioactive 137Cs has been used medically to treat cancer.5 (8.05) 5.14 (4.95-4.97 (7.8 (10.9) 12.80 (8.70 (6.26) 4.10-9.0) 10.40-11.1-12.10 (8.95 (3.59-5.4) 95th 11.99) 9.80 (4.52-9.91-8.09) 5.96 (6.52) 7.56-11.60-7.49) 4.10 (8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.70 (4.23-4.83-4.00) 7.66 (7.10 (6.90) 5.4) 11.98 (7.5) 10.7) 10. the body half-life is estimated to be 70-109 days based on 137Cs exposures.86-11.8) 11.17-6.87 (4.9) 8.4) 10.13 (7.50 (4.90-8.61-6.33-5.7) 10.80-6.90-10.84) 8.46) 7.1 (11.79 (4.3) 9.90 (4.S. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.60 (7.54) 4.9 (11.74 (4.16-6.77 (9.64 (4.13 (8.40-5.5-13.7 (10.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.0) 9.72-7.91 (7.05-5.Metals Cesium CAS No.42) 6.40-5.84) 5.5-14.7 (9.1-13.0) 11.60-5.42) 7.64-10.81-14. interval) 4. and 03-04 are 0.50-7.05-5.97) 4.5) 9.39) 7.62) 4.09-5.67 (4.00-10.05) 5.88 (8.77 (9.30-10.1) 11.00-8.16-6.80 (4.80) 7.60-6.00-8.20-8.00-4.80 (4.00) 4.6 (9.77 (4.23) 9.25-5.3-13.3-15. respectively.03 (4.47-8.08 (7.60-7.53 (6.2 (9.50 (4.1) 10.82-4.3) 12.68) 9.71-9. see Data Analysis section) for Survey years 99-00.07-11.1) 11.17) 4.33 (6.90) 9.89-5.00-9.47-4.56) 5.43-8.13-8.1) 9. Most human exposure to cesium occurs through the diet.42-7.97-7.32-5.21) 90th 9.56 (4.59-5.86 (7.35 (4.50 (4.9) 11. For absorbed cesium salts.84-9.2.9) Total 4.8) 11.80-11.3) 10.55 (7.20) 7. cesium hydroxide is corrosive and irritating at high concentrations.7) 11.35 (4.03 (4.6 (9.00) 6. photographic emulsions.60-6.24) 4.70-8.64) 5.94 (4.60) 7. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.80 (8.20-5.70) 5.04) 7.40-7.87-7. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.94-4.38) 5.40) 7.8 (10.50 (6.90 (6.04 (4.97) 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. population from the National Health and Nutrition Examination Survey.93 (4.60) 5.56 (4.59) 7.8) 12.72) 4.62 (5.4-13.9 (11.64-5.20) 4.59-5.44 (8.90) 5.4) 12. although cesium was generally of low toxicity when given to animals.40-11.8) 9.94) 4.10-8. soil.32 (3.5 (10.7-14.50) 9.14.40) 5.71 (4.82) 5.20) 8.4) 9.80-10.30 (6. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and cardiac arrhythmia (ATSDR.62 (5.86-12.5-16.03-4.37) 7.31-8.2) 11.1 (9.64) 4.84-5.45-8.40 (4.10-5.90) 4.30) 7.26) 7.70) 7.3) 10.55 (4.77-8.87) 5.6) 10.7 (10.4) 12.98 (7.9 (10.3 (8.89) 5.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 0.39-4. semiconductors.27) 4.70-5.3-13.20-7.0 (10.68 (7.70 (9.0) 11.49) 75th 7. and as polymerization catalysts.81) 4.2-14.57-5.7 (10.10 (6.29) 4.60-12.25) 4.69-6.87 (4.2-12.73-11.49 (4.90-10.2-13.10-7.70 (5.6 (9.70) 5.20 (6.90-10.84 (4. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.8 (11.81) 4.8-13.01-8.33 (5.7 (8.1) 9.17 (6.12-5.30) 5.3) 10.26-11.7 (9.8) 9.7) 11.63 (4.63-4.94 (4.9 (11.80-10.3) 10.08-5.71) 4.50 (7.0-15.73-5.0-13.70 (8.22-4.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.89) 4.27-5.4 (9. 2004).07) 4.99-11.61) 7.20-4.99-11.71-5.63) 6. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.90) 7.43 (5. diarrhea.4) 10.1-12.4 (9.08) 7.3 (8.

9) 10.50-5.04-5.54 (5.88-4.75 (6.07) 8.08 (3.31-4.12) 3.30) 10.08-7.90-8.84-11.00-8.04) 6.94) 7.76-6.75-11.26 (4.50) 8.50) 4.81 (4.45-6.13) 7.24-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.55) 4.5) 7.92) 3.S.91-7. 1990).03) 5.99-9.98 (6.27 (8.60-10.27 (6.30 (7.27-6.29) 4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31-6.41) 4. population.8 (9.98) 5. Using clinically submitted specimens.44 (4.26-6.93-9.08) 4.16) 5.72 (4.6) 6.79-5.91 (5.37-3.3 (8.64 (4.30-4..43-6.70 (7.67 (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 3.56-10.68) 3.98 (7.00 (8.96-4.47 (7.44-9.39 (5.04) 5.38-12.78) 4.44) 3.88-10.02-4.90-8.64) 5.05-3.30) 10.42-4.84-7.64) 4.86 (4.99-4.96 (4.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .91-6.21 (2.95-6.59-8.28) 7.57) 3.27 (6.58 (6.38) 10.43 (4.97-5.78) 4.50 (5.18-6.62) 5.05-3.49) 3.08-3.18 (7.05 (4.09) 4.46-4.20-4.96) 4.79) 6.36-6.14-7.43-11.20-4.6 (9.41-4.80) 6.95) 10.33 (5.50) 4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.93-7.00-5.3 (10.43 (3.10 (5.60-20.95) 4.3-15.18-7.41) 9.38 (3.52-5.58) 8.06 (5.71 (7.50 (6.44-5.05) 6.99) 4.91 (5.3) 11.58) 3.62-8.40) 7.8) 5.09 (4.99 (3.85) 4.47 (4.S.39) 8.72-5.35-11.73 (3.41-7.48) 90th 7.6 (9.15-4.43 (4.67) 5.72) 4.06) 5.96) 4.66 (5.66-6. 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.3 (9.36-10.74 (4.07 (5.42 (4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.77 (4.14) 4.60) 3.09) 8.13-9.03) 6.27) 4.05) 3.50) 4.35-7.12 (3.54 (3.64 (8.17-4.25) 4.9 (10.00) 6.79) 9.20-4. population results shown in this Report (Alimonti et al.43 (8. interval) 4.97) 8.97-4.47) 4.00-4.00-5.41 (4. Minoia et al.08) 3.55 (3.14-4.13 (3.71) 6.11 (5.14 (6.06) 4..63) 6.84-7.46) 6.30 (3.17) 4.53) 3.61-3.39) 5.46-8.11 (5.83) 8.15 (7.25) Selected percentiles ( 95% confidence interval) 50th 4.10 (3.43) 8.24-10.68) 4.61 (7.35 (4.21-3.29) 5.0) 7.02 (5.63 (6.2 (8.29-3.30 (4.19-3.40) 6.20) 5.08 (5.35 (3.40-5.46 (8.73-4.84-9. (2000) found urinary cesium levels that were slightly lower than those reported for the U.83-6.0 (7.74) 75th 5.29-3.2 (8.60 (5.30-4.70) 6.16-8. 2004).79 (5. and were also roughly similar to those in this Report.2) 11.85-4.21-5.47) 6.68) 6.06 (3.26 (3.33-8.47) 6.74) 3.54 (4.16-8.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.4) 10. Two small studies of European populations reported urinary cesium levels similar to U.16-5.82) 7.87-4.56) 4.65-3.14) 4.20-8.48-6.44 (8.77-5.74 (5.56 (4.00-9.03-6.65 (6.07) 8.68-11.91-9.50 (7.28 (4.04-11.53 (4.08) 4.63-6.96-4.8) 6.81 (4.41 (8.33-3.90 (7.90-3.91) 4.76-9.13-9.24 (3.48) 7. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.51) 4.87) 5.64) 9.27-4.63 (4.77 (6.22 (3.58 (4.38 (3.77) 4.98) 5.10 (3.33 (5.05-4.51 (7.0) Total 4.S.54 (4.01-8.65-4. Komaromy-Hiller et al.31 (4.51 (3.5 (9.00-10.1) 11.60 (3.34 (5.99-9.83-7.8) 10.10) 7. 2005.51 (4.82-4.51 (4.79) 4. population from the National Health and Nutrition Examination Survey.74-11.89-4.63-6.42-4.95) 8.12-6.70) 7.68 (4.55-5.91) 5.47) 7.42 (5.17) 9.87 (5.59) 4.63 (7.14-6.42-6.7-12.36-3..78 (3.37) 4.66 (5.75 (7.29) 4.66 (6.64-6.31 (4.53) 6.77 (7.18) 8.92 (5.95-12.19-6.3) 9. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.08 (6.07-4.22-11.95 (5.7) 10.23 (7.46 (7.7) 10.15) 95th 8.9 (9.03-5.67 (5.51 (3.28) 8.21-4.56) 3.5) 9.91) 5.15-11.17 (6.95 (3.84-9.85) 5.22) 6.45 (4.41 (5.10-4.56) 4.28 (5.58-5.38-7.78 (3.94 (5.53 (6.35) 3.5) 9.2) 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.

et al. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Apostoli P. Rapid Commun Mass Spectrom 2005. Gallorini M.95:89-105. Available at URL: http://www. Assessment of urinary metals following exposure to a large vegetative fire. Forte G.cdc. Comparison of representative ranges based on U.gov/toxprofiles/tp157. Ash KO. Sewell CM. Minoia C. Mincione G. 4/8/09 Alimonti A.S. Voorhees RE. Atlanta (GA) 2005. Centers for Disease Control and Prevention (CDC). Sabbioni E. 2000.2004 [online].19:3131-3138. Ronchi P. Sci Total Environ 1990. Komaromy-Hiller G. patient population and literature reference intervals for urinary trace elements. Howerton K. Mott JA. Wood CM. antimony and tungsten. Spezia S.html. Paschal D. A study of 46 elements in urine. cesium.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).14:120-128. Clin Chim Acta 2000. et al. and serum of Italian subjects. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Toxicological profile for cesium. J Expo Anal Environ Epidemiol 2004. Trace element reference values in tissues from inhabitants of the European community I. et al. blood.296(1-2):71-90. Third National Report on Human Exposure to Environmental Chemicals. New Mexico. Costa R. Pietra R. Wolfe MI. Pozzoli L.atsdr. Gatti A.

shiny. 01-02.410 (.S.900-1.790-.24 (1.650 (.520) .410) .980-1.37-1.26) 1.47 (1.760 (.410-.380-.350) 75th .630 (.15 (1. diamond-polishing wheels.540) 1. industry is imported or obtained by recycling scrap metal that contains cobalt.05 (.373) .520 (.370-.800-.520 (.430 (.16 (1.380 (. Cobalt compounds are also used in manufacturing battery electrodes.810) .890) .417) .370-.670 (.660) .523) .515 (.285 (.379 (. steel-belted radial tires.690-.65) 1.880 (.418 (.01 (.394) .590 (.670-.09 (.750-.22-1.01 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.400-.06-1.610-.374 (.461 (.22 (1.348-.390 (.620-.650-.427-.68 (1.570-. blue-colored pigments.580 (.570) .520-.327-.410) .81) 1.355-.460 (.550-. 0.336-.460) .860 (.680) .600) .03-1.64) 1.520) .454 (.680) .07-1. and inks.810-.583) .373-.360-. automobile airbags.339 (.300 (.75 (1.32 (1.398) .670 (.352 (.372) . respectively.490-.399) .470) .20 (1.92) 1.920-1.313) .710) 1.360-.870-1.99) 1.452 (.03) 1.280-.730) 1.56) 1.435 (.740-. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.15-1.388-.17 (1.380 (.800) .310-.940 (.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 .380-.550 (.560 (.410 (.343 (.570-.00) .32) 1. large appliances.03 (.520 (.450) .496) .750 (. 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.450) .36) 1.340 (.410 (.53) 1.430) .850) .630-.450) .28-2.640) .386) .570 (.29 (1.04 (.16-1.530 (.404) .340-.367 (.16) 1.44) 1.02-1.294 (.48) 1.770) .680 (.900) .800-.550) 90th .370) .850-1.710) .790 (. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.28 (1. population from the National Health and Nutrition Examination Survey.319) . seawater.350-. It is emitted into the environment from burning coal and oil and car and truck exhaust. interval) .850) 1.431) .07.890-1.840) .820 (.50 (1.340) .26-1.430-.450) .290-. varnishes.540-. and soil.50) 1. Cobalt occurs naturally in airborne dust.460 (. Cobalt is used as a drying agent in paints.543) .620-.670 (.S.410 (.487) .430 (.14) .460-.08) .520-. and 03-04 are 0.47) 1.330) .17 (1.910-1.04-1.259-.502) .04) 1.480 (.330 (.270-.23-2.09 (.590-.870 (. and fertilizers.01-2.316-.710 (.900) . Usual human exposure is from food sources. and in synthesizing polyester and other materials.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 .480-.580 (.820 (.300-.950-1.890-1.950 (.670-.424) .340) .350-.450-.398 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.06 (.700) .950 (.420 (.32 (1.26-2.330-.740-.46 (1.32) 1.17-1.33-1. and magnetic recording media. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.370 (.320 (.900-1.520 (.04-1.620-.540-.301 (.520-.430) .700) .490-.740 (.370-.680 (.47 (1.14-1.416) .348-.28 (1. hard metal or in combination with other elements. Cobalt compounds are used as catalysts in producing oil and gas.350 (.04-1.470 (. see Data Analysis section) for Survey years 99-00.12) 1.920) 1.01-1.600 (.13) 1.390-.750 (.16) 1.81) 1.428-.Metals Cobalt CAS No. and kitchenware.410-.580 (.369 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.47) 1.375 (.410-.420) .07-1.405-.530) .390 (.950-1.690-.06 (.940-1.630 (.67) 1. hard metal (alloys of cobalt and tungsten carbide).500 (.270-.390 (.23) .610) .310 (.377-.480 (.60 (1.390) .21) 1.371 (.900) .350-.333-.12) 1.33 (1.360-.07 (.950) .930 (.308-.333-.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 .28 (1.52 (1.890) 95th 1.940-1.660-.419) Selected percentiles ( 95% confidence interval) 50th .460) .17 (.340-.305-.830-1.08-1.22) 1.291-.45 (1.07.465) .610) .564) .469-.59 (1.414) .380 (.16 (.03) 1.03 (.590-.750 (.19) .980) .930) .790) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .760) .48) 1.09) .440-.520-.880-1.581) .25-1.690 (.05 (. The cobalt used in U.16 (1.620) .810) .850-1.590) .26) Total .434 (.39) 1.570) .334) . and 0.32-2.359 (.460) .499 (.960-1.463-.600-.03) .338-.610 (.640) .660) .08.530-.540-.430 (.431) .870 (.519 (.640) .450-.540-.270-.393-.500) .24 (.650 (.331-.510) 1.420) .42) 1.890-1.16-1.379 (.73) 1.410 (.820 (.316 (.930-1.05) 1.364-.

35) 1.298 (.821 (.10-1.339-.534-.600-.851 (.634-.348) .471-.60) 1.638-1.938-1. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.727 (.781-1.533 (.343-.407) .29) 1.380-.452-.425) .777-.523 (.368) .19) .917) .475 (.879-1.487-.542 (.402 (.30 (1.327-.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 .29 (1.847) .550-.14 (.372) .595) .290 (.317 (.343 (.297-.239-.426 (.363) .368 (.313-.419) .844 (.12 (..537 (.608 (.434-.16 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).03-1.257-.503-.615) .278-.574-.829-1.27) 1.898 (.609) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.335 (.396) .29 (1.289) .963-1.513 (.468) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.382-.508-.301) .10) .785) .362) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.376 (.408 (.33) .355) .562) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.313 (.635 (.303-.581) .329 (.275-.362 (.929) .495 (.429) 1.334) .36) 1.301-.630-.00 (.250) .06 (.505) .662) .983-1.15) 1.272-.365-.310) .361 (.861 (.328 (.983) .279 (.513) .861-1.352 (.455 (.911-1.611) .29) .329-.872 (.753-.392 (.955) .296) .457 (.237-.60) 1.10 (.259) .561) .44 (.324) . A portion of cobalt retained for long periods is concentrated in the liver.04 (.257 (.50) 1.248-.781) 95th 1.964 (.582-.333-.738 (.358 (..534 (.10) Total . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week...439) .306) 75th .297) .417 (.640) .444 (.337) ..290 (.543) .728) .24) .274-.362-.700 (.407 (.905) .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 .963-1. in the feces.593) .932-1.554 (.16) .00 (.738 (.522) .952 (.404-.830 (.728 (.700 (.279) .548 (.25 (.33) 1.50 (1.476-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.15 (.703-. population from the National Health and Nutrition Examination Survey. with pulmonary clearance half-lives of from one to two years (Hedge et al.667-1.435 (.467-.323) .353-.804) 1.707) .16 (.529 (.838 (.378-.309) .691 (.353 (.55) .259-.234 (.463-.554 (.28) 1.273 (.83) 1.361-.275-.361-.328) .369 (.673-.344-.563-.585) .857-1.792 (.737 (.259 (. or using diamond-polishing wheels that contain cobalt metal.73) 1.326-.733-1.378 (.750-. 1979).12-1.704-.850 (.417) .306 (.333 (.378-.488) .442-.756 (.271 (.433) .57) 1.598 (.960 (.644 (.457-.313-. 1972).552 (.36) 1. and to a lesser extent.00 (.591 (.300) .500-.487-.848 (.660-.247 (.290 (.824 (.316 (.708) .821-3.736-.955) .342-.990) .740-1.757-1. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.562) .328 (.409) .547 (.963) .500 (.679-.428-.449) .00) .396) .384) .630-.304-.976 (. using hard metal cutting tools.215-.606 (. Exposure in the workplace may come from electroplating.938) .616-.400 (.35) .286) .513-.669) .753) 1.479-.895-1.694) .281) .293 (.388 (.280-.611) .268 (.462) .365) .23 (1.27) 1.282-.500-.256-.333-.391 (.949) .50) 1.. refining or processing alloys.352) .750) .393-.523 (.00-1.479) .963) .352 (.829) .626-. an essential human nutrient.296-.S.248-.744) 1.327 (.361 (.599) .461) .11-1.632-. interval) .667-1.990-1.360) .723 (.282 (.469-.394) .324-.29 (1.438) .792-1.560-.381) .302-.243-.314 (.03 (.391) Selected percentiles ( 95% confidence interval) 50th . Once absorbed and distributed in the body.251-.515 (.842) .337 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged. 1972).09) 1. 1994).00 (. cobalt is excreted predominantly in the urine.786-.04-1. Smith et al.471-.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 .17) .457) .277-.387) .760-1.346 (. respectively.774 (.49) 1.291 (.647) .900-1.333-.02 (.421) .294-.471 (.11-1.319-.331-.16 (1. 2003).425-.313-.975 (.25 (.850-1.368) .386 (.826-1.435-.388 (.689 (.278 (. 1994.313-.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 .313-.378-.Metals fabricated from cobalt alloys (Lhotka et al.449-.54) 1.683-.833-1.895-1.349) .00) . Cobalt is absorbed by oral and pulmonary routes.481) 90th .304) .937 (.594) .393 (.

1994). Shirakawa et al.. Information about external exposure (i. Arch Environ Health 1988. Lison et al. Lauwerys and Hoet. 1988). environmental levels) and health effects is available from ATSDR at: http://www. not to imply that the BEI is a safe level for general population exposure.e.cdc. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. Iavicoli et al. 1997. Grumbein SL.html. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. 1993). References Alexander CS. Blood and urinary concentrations as estimators of cobalt exposure. usually in combination with tungsten carbide (Cugell et al.. 1999). Atlanta (GA). a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen.Metals Toxic effects of cobalt have been encountered in workplace settings. Morgan WKC. Haseman JK. Perkins DG. 1988). 1994. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al.. Swennen et al. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (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.. with mean levels that were about 15-20 times higher than in the general U. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans.. although substantial occupational exposures have produced elevated urinary levels for many weeks. Cugell DW. Available at URL: http://www.. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring studies on levels of cobalt provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cobalt than are found in the general population. 1994. Toxicol Sci 1999. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. 2001. Roycroft JR. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Information about the BEI is provided here for comparison. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes.. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. 2005 [online]. Dunstan et al. 2003). The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. 2001. 2001). Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al.S. 2003. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U.49:56-67. Cobalt-beer cardiomyopathy.43(4):299-303. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda..S. 1993). Daniel et al. Alexandersson R. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. 1955). Hailey JR. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al.. 1990). 210 2006. et al. For workers exposed to cobalt in the air...atsdr.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1992)... 2005.cdc. Inhalation toxicity and carcinogenicity studies of cobalt sulfate.. “Hard metal” disease. has been associated with exposure to dusts that contain cobalt.. Lisi. White and Sabbioni. MacDonald et al.gov/toxpro2. Krause et al. Thomassen et al. 2003. 4/3/08 Christensen JM. Cobalt was once added as a foaming agent to beer. Linnainmaa and Kiilunen.53:395417. 2001. 2006. 1989). 1972). Rubin A. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. Urinary measurements mainly reflect recent exposure. 1998). Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. population results in this Report (Kristiansen et al. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Centers for Disease Control and Prevention (CDC). Poulsen OM...gov/ exposurereport/. A 1982-1992 surveillance programme on Danish pottery painters. Third National Report on Human Exposure to Environmental Chemicals. Bucher JR. Sills RC.. 1997).. population (CDC. Sci Total Environ 1994.... 1985. 1998). 2005... Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. Am J Med 1972.50(13):95-104. A clinical and pathological study of twenty-eight cases.

Tilley S. Respiratory health of cobalt production workers. Shirakawa T. Unwin P. et al. Clin Orthop Relat Res 2003. Sci Total Environ 1998. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Int Arch Occup Environ Health 1997. Lung cancer risk in hard-metal workers. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group.88(4):443448. Vitali MT. Kriss JP. Am J Epidemiol 1998. Cobalt cardiomyopathy. Health Phys 1972. Salama A. Chest 1989. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Lauwerys RB. Fujimura N.36:732-734. Salvatori S. Br J Ind Med 1993. Buchet JP. Angerer J. 3rd ed. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Trace element reference values in tissues from inhabitants of the European Union. Smith T. Christensen JM. et al.204:147-160. Bourne RB. Lasfargues G. J Trace Elem Med Biol 2006.21(2):189-195.51(7):447450. Weber A. Lhotka C. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Lisi P. Stanescu D.34:620-626. Roto P. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. 2001. Co-sensitivity between cobalt and other transition metals. Occup Environ Med 1994. Hoher T. Laippala P. Thabe H. Romazini S. Goto S.44:124-132. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Occup Environ Med 2001. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Bozec C. Ziaee H. Lison D. J Bone Joint Surg Br 2006. Chess DG. McCalden RW. Kuska Y.157:117121. MacDonald SJ. Szekeres T. Schaller KH. Zedda S. Hammon E.45:246-247.55(4):269-276. Heki S. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Sci Total Environ 1994.533:135-152. The release of metals from metal-onmetal surface arthroplasty of the hip. Diepgen TL. Kusaka Y. Long-term clearance of inhaled 60Co. Daniel J. Jarvis JQ. Cannon SR. Molders J. Wild P. et al. Kirsch-Volders M. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Am J Ind Med 2003. HoffmannB. Kato M. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. oxides. Edmonds CJ. Sabbioni E. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds.95:29-37. De Boeck M. Mosconi G. Hedge AG. Swennen B. Meyer zum Buschenfelde K-H. Thakker DM. Bunn HF. Weyher I. J Occup Med 1992.69(3):193-200.50(9):835-842. Gross RT. Linnainmaa M. Biological monitoring of workers exposed to cobalt metal. Leghissa P. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Outcome of occupational asthma due to cobalt hypersensitivity.406:282-296. salt. Pradhan C. Lauwerys R. Sci Total Environ 1994. Goto S. and cobalt metals. et al. et al. J Bone Joint Surg Br 2005. Blunn G. Cobalt and antimony: genotoxicity and carcinogenicity. Hoet P. Radulescu M. Int Arch Occup Environ Health. Health Phys 1979. Rorabeck CH. Carnes WH. Dickel H. Arch Intern Med 1990. Cleland D. McMinn DJ.87(5):628-631. Dunning SP. Sci Total Environ 1997. Zhuber K. Kiilunen M. cobalt salts. Occupationallyinduced “isolated cobalt sensitization. Peltier A. Iavicoli I. X. Falcone G. Uitti J.Metals effects of cobalt. Absorption and retention of cobalt in man by whole-body counting.216:253-270. Contact Dermatitis 2003. and hard metal dust. Lauwerys R.” Contact Dermatitis 2001. Oksa P. Palmroos P. Ichikawa Y. Sabbioni E. Kristiansen J.150:177-183. Zweymuller K. Moulin JJ.(1-3):133-139. Dunstan E. Buchet JP. Zobelein P. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Bacis M.22:359367. Mutat Res 2003. Sanghrajka AP.28(5):1121-1128. Robinson C. Swennen B. Lison D. et al. Boca Raton (FL): Lewis Publishers.242:1412-1415.150(1-3):167-171.20(1):25-31. Schramel P. Barnaby CF.150. Schank M. Iversen BS. a study of 13 elements in blood and urine of a United Kingdom population. Alessandrelli M. Cresti R. A report of two cases from mineral assay laboratories and a review of the literature. Steffan I. Thomassen H. Meier R.58(10):631-634. 1985. Kraus T. Ghat IS. DeSantis V. J Orthop Res 2003. Goldberg MA. Pisati G. Lison D. Epidemiological survey of workers exposed to cobalt oxides. White MA.148:241-248.48:172-173. Linna A. Sabbioni E. Science 1988. J Rheumatol 2001.

00) 5.g.60 (3.90-2.10 (1.70) 4.50) 4.10) 1. such as lead phosphate and tetraethyl lead.04-1.00) 4.00) 6.25 (1.00 (1.00) 2.00-4.50-2.30 (1.60) 2.60 (2.10-2.80 (2.51 (1.50-2.80 (5.80 (1.81) 1.00-4.68-1.90) 5.90-4.30-2.30 (2.70 (5.19 (1.40-5. solders.50) 1.899-.50-1.56 (1. respectively.80 (4.60-1.70-1.900 (.69 (1.10-2.60) 1.60) 5.40-1.20) 3.10 (1. bronze).80) 3.60 (3.14-1.80-4.37-1.90) 1.37 (1.60) 2. Elemental lead can be combined with other elements to form inorganic and organic compounds.80) 2.20) 3.40) Total 1.50) 5.10-2.22 (1.23 (1. and 03-04 are 0.55-1.66 (1.10 (2.40) 5.80-3.60 (2.00) 1.800-1.40-3. ceramic glazes.65 (1.70-6.70-1.90) 2.90-4.30-2.52-1.60) 1.40 (1.20) 1.30) 2.00-5. blue-gray metal that occurs naturally in soils and rocks.70) 3.62) 1.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20 (1.20-1.32-1.60 (1.90 (1.90 (3.10) 2.90 (1.50-2.60-1.90 (2.60 (4.43 (1.50) 1.60) 4.50 (3.30-5.10 (2.40-1. population from the National Health and Nutrition Examination Survey. leaded glass.70 (1.20 (3.50 (2.80 (1.20-3.30-2.40-3.50) 1.80) 1. and 0.66) 1.40 (5.30 (2.80 (3.70-2.37 (1.30-1.69) 1.20 (2.10-1.00) 2.40) 1.70-1. brass.20 (3.80-2.70) 4.72) Selected percentiles ( 95% confidence interval) 50th 1.40-1.50-6.00) 1.90 (3.40) 2.3.20-3.60) 4.20-2.00) 1.50 (3. metal alloys (e.20 (3.70) 1.70 (2.40-3.10) 2.00-1.39-1.80-4.80 (1.60 (1.70 (1.10) 1.878-1.62-1.80 (1.90-2. In the past.70-5.50-3.40-6.70) 2.80-4.90 (4.51) 1.70-4.00 (4.71-1.90-4.50 (2.90) 3.02) 1.10-2.40-2.50 (4.30 (1.50) 7.20) 4.80 (1.50-5.30) 95th 5.50-1.90 (3.36-1.70 (1.10-4.52 (1.96-2.60 (2.80) 1.10) 4.10-6.53) 1.87) 1.91) 1.60) 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 2.70) 1.10-3.80) 2.60-4. the main source of lead exposure for the general U. 0.S.89) 1.60) 2.80) 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 1.40-1.80) 2.90-4.60) 4.10) 1.30-2.90-2. interval) 1.39) 1.20-2.10-6.10-2.36-1.60-4.20 (3.75-1.80 (4.10) 3.60) 2. 01-02.90) 1.30-1.36) 1.70) 3. 212 Fourth National Report on Human Exposure to Environmental Chemicals .50-1.20-3.32-1.30-1.3.30-1.00) 2.30) 2.50 (1.95) 1.28.20-6.60-2.00) 3.10-2.87 (1.46 (1.20) 4.75) 1.50 (1.60 (2.10 (1.20 (3. Before the 1980’s.14-1.43-1.78 (1.00 (2.70 (3.90) 2.00-2.20) 5.60 (3.50-4.50 (1.17) .30 (2.20-1.10-4.40) 2.10-3.40 (2.50) 1.43) 1.50 (2.70 (2. antique-molded or cast ornaments.80) 1.40) 1.80 (5.30 (4. Since lead has been eliminated from gasoline.70) 1.34-1.30 (3.Metals Lead CAS No.90-2. ammunition.10) 5.60) 3.30 (4.60 (3.00-4.00 (4.50-2.93-2.60 (1. 7439-92-1 General Information Elemental lead is a soft.20) 2.49-1.60-2.20 (1.31) 1.90-3.62 (1.80-3.00 (5.60) 5.70 (1.90 (3.43 (1.50-1.900 (.10-8.70-2.00) 4.10-1.75-2.86) 1.20) 90th 3.40 (1.80-3.10) 3. see Data Analysis section) for Survey years 99-00.43) 1.00) 1.60-3.50-5. and for radiation shielding.70) 1.30-1.50 (2.40 (4.40) 2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.90) 3. Lead was used in plumbing for centuries and may still be present.60 (1.60) 3.40 (1.30 (2.30 (1.50-3.40-2.69 (1.60) 1.50 (4.30 (2.48) 1.00) 1.40 (2.60) 1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10 (3.30) 1.40-2.60-1.09) 1.30-1.20) . Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.60 (1.60-1.77 (1.50 (2.70) 4.40) 4.20 (1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.25) 1.30 (2.80 (2.30-6.60) 4.60 (2.83 (1.80) 1.40-4.69) 1.80-3.50-4.40) 2.60 (1.50) 3.30-4.90 (2.60 (1. malleable.10-1.10-3.52-1.50) 5.50-1. dense.01 (1.30) 5.946 (.70-3.80 (2.50) 2.00) .70) 1.00) 3.90-6.70 (2.55-1.00-1.90) 2.30 (1.S.80) 2.40 (3.70) 4.50) 4.00) 2.55 (1.30) 2.20) 3. Lead is most often mined from ores or recycled from scrap metal or batteries.80) 1.00 (6.20 (3.20 (4.30 (4.20 (2. Lead has a variety of uses in manufacturing: storage batteries.20-3.40 (1.20 (1.90) 2.50 (1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.45-1.60) 2.90) 1.10 (4.25 (1.12-1.70 (3.900-1.20 (1.40) 1.80-5.986) .30 (2.10) 3.60) 1.40-1.60 (2.60) 3.50) 2.00 (3.10-3.14-1.40) 3.80 (1.50) 75th 2.70) 3.942 (.60-6.75 (1.20 (3.40-6.10 (2.00 (1.20-4.90 (3.40-1.00-6.20) 3.70-2.60) 3.90) 2.45 (1. plastics.

80-2.580-.700 (.40 (1.815 (.540-.90-2.00 (1.70-3.Metals occupational (e.11 (1.60 (2.595-.52-1.620) 1.710-1.600-. 01-02.810-1.940 (.10-3.40 (2.731 (.90) 2.80 (2.900 (.30) .90 (2.600-.60) 2.700 (.590 (.600 (.10) 2.00) 2.700-.50-1.535-.1. CDC.04-2.60-3. 2007.560-.07-1.70 (2.10 (.900) .862) .50 (2.30 (1.82 (1.11) 2.30-1.700-.10 (1.18-1.00 (.50-2.80 (1.20 (1.62) Total .610 (.90 (1.90-4.10 (1.27) 1.40 (1. imported children’s trinkets and toys.35 (.795 (.78-2.00-1.40 (2.10-5.80) 2.700) .625-.60-2.00) 2.80) 3. lead-based painted surfaces undergoing renovation or demolition. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.591 (.00) .60-2.700 (.90) 1.S.30-3.10-1.920 (.573 (.20) .10-1.00-2.941) . 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.59-2.833 (.671-.70) 3.808 (.80) 2.49 (1.78-2.40) 3.00-1. dust.10) 1.72) 1.848 (.661-.03-2.00-1.02 (.745-.540 (.10) .690) 75th 1.40-1.990) 1.701) .616) .900) .900 (.86-2.09) 1.90-2.710-.00 (1.50-2. battery and radiator manufacturing) and recreational sources.70) 3.02) 1.41) 2.23) .757-.10 (.40) 1.60 (1.910-.960-1.30) 1.50) 2.10-3.33. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.70 (2. population from the National Health and Nutrition Examination Survey.24-1.70) 1.80) 2.915-1.931) .91) 2.40-1.600) . However.674) 1.20 (1.90 (1.97) 4.86) 1.900-1.52-1.700-.700 (.20 (1.10-1.800) .818) .10 (1.20-1.07 (.1.20) .14-1.30-1.630 (.680-.80) 1.30) 1.73 (1.90-3.80 (1. and 03-04 are 0.89) 2.822-1.640 (.64) 2.20) . and contact with soil.749) .691-.20 (2. older plumbing systems with leaded pipes or lead soldered connections.700-1.40-2.90 (1.700 (.10-1.60 (1.40) 2.32 (1.50) 1.695 (.766 (.80) 3.900) .20) 1.04 (.680) .10) 2.800) .31-3.90 (2.50 (1.14 (1.30-1.700-.800 (.20) 1.60 (1.680-.955-1.10 (1.23-4. 0.651) . lead-contaminated dust in indoor firing ranges.800) .44-2.688 (. see Data Analysis section) for Survey years 99-00.30 (2.33 (2.70 (2. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.50-3.12) 90th 2. and 0. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.00-2.90-2.00) .506-.21 (2.840 (.752 (.33-2. interval) .90-3.75) 3.90) 2.960 (.20 (1. 2000).820-1.10-1.990) 2.800) .70 (1.50 (2.800) .900-1. Approximately half of the absorbed lead may be incorporated into bone.637-.553-.753 (.828) Selected percentiles ( 95% confidence interval) 50th .20 (1.40) 2. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.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 1.00 (2. pewter utensils and drinking vessels.700) 1.70) 1.773) .50) 1.80-3.04) 2.50) 1.66 (2.80) 1.708-.20) .27 (1.480-.86 (1.636 (.40) 1.30-5..738) .500-.22) 1.10 (.900 (.50) 2.800 (.13) .40 (1. or after soluble lead compounds are ingested.50) 3.589-.40) 1.718) .700-.935) 1.20 (3.29 (2.06) .03 (1.40 (1.50 (1.50-2.00 (1.31 (1.50 (2.730 (.40) 1.556-.677 (.579-.90 (2.600-.40) 1.30) 1.659 (.40 (2.30) 1.60-3.70) 1.850 (.80) 2.30-1.20 (2.800 (.625 (.30-2.20 (2..650) 1.g.30) 1.20 (1.600-. respectively.13-3.600) .600-.579-.900) .40-3.80-2. stained glass framing.00-2.00) .17 (1.613) .30 (3.729-. bullet fragments retained in human tissue.620 (.59) 1.700 (.800-1.40 (1.785) .640-.20-2.970-1.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.90) 2.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.800 (.920 (. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.900-1.570-. In the blood.40-1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .900) .14 (1.70) 2. lead-containing folk remedies and cosmetics.558 (.82 (2.30) 2.20) 1.790 (.66 (2.20-1.80) 1.642 (.800-.78-2.900-1.40) 2.833-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10-3.857) .30) 2.60 (1.923 (.52 (1.572-.00 (1.40-1.80) 2.62-4.90-2.30) 2.49) 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 .605) .86) 95th 2.526-.641-.70 (2.04) .29) 2.19 (1. 1991).800-1.20-2.20-1.564 (.604 (.600 (.04 (.75) 4.00) 1.00) .960-1.660) .70-2. or water contaminated by mining or smelting operations.628) 1.800-.986) .900) .40-5.60-1.10) .40) 2.40 (2.

11-1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.61) 1.94 (1.51) 1.673) .78-4.529-.11 (.33 (1.44) 1.09-1.94-2.11 (1.63) 1.681-. 1996). abdominal pain. 1995.47) 1.721 (. and nails (Leggett.03) 1. 1995).375 (.86 (1.657) 1. 1993.50 (1.85-2.10) 1.641 (.47 (2.10) 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 .571-.43) 1.758) .938-1.85-2.683-.638 (.838) .594-. and iron.31) 1.648 (.72-2.551-.Metals 90% of the body lead burden in most adults.82) 1.62-2.720 (.603-.50-2.12-1.23 (1.914-1.621 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.61) 1.20) .753) .29 (1.56) 3.75-2.918-1.997-1.633 (.03) 1.990 (.957-1.18) 1.36-2. zinc.75 (2.992-1.38 (2.37-1.898) .38 (2.88) 1.56-3.56 (1.04-3.710) .607-.742) Selected percentiles ( 95% confidence interval) 50th . The toxic effects of lead result from its interference with the physiologic actions of calcium.08) .571-.77) 2. encephalopathy.870 (.975-1. population from the National Health and Nutrition Examination Survey.43 (2.652 (.69 (1.17-1.508) .914 (.739) .48 (1.933-1.40-1. kidney injury.702) .41-1.09-1.98-2.15-2.460-.71-2.11) 1.588-. Large amounts of lead in the body can cause anemia.730) 1.492-.971 (.02) 1. scant amounts are lost through sweat.31 (1. with a half-life of years to decades.18 (1.89-2.588-.61) 1.992-1.88 (1.625 (. Staessen et al.68 (1.62) 2.793-1.31 (2.62-3. The skeleton acts as a storage depot.47 (1.561-.763) .50-1.46 (1.605-.34-1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.05 (.622 (.696 (.71 (1. Approximately 70% of lead excretion occurs via the urine.38 (2.746) .667-.15-2.85) 1.851) .14) 1.35) 2. Schwartz.400) .18) .408-.44 (1.06 (.73) 2.586-.645-.688) .98) 2.876-1. O’Flaherty.18) 1.722 (.679-.639 (.07 (..755 (.14 (1.22) .645-.59-3.608 (. 1991.01) .639) .609 (.33-1.612-.917-1.04) 2.774 (.73-2.64-2.810 (.09-1.800-.00 (1.19-5.615 (.988-1.05 (1. In 1991.594-.98 (1.606-. and paralysis.03) .62-1.79 (1.342-.765) . hair.55 (1.97-18.662) 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. 2004.64) 2.33) 1.08) .66) 2.781-1.635 (.03 (.24 (1.496 (.25-1.00) .383-.72) .88) 2.686) .979 (.43-1.469 (.658 (.718) 1.46 (2.11) .963-1.708 (.938 (.45 (1. with lesser amounts eliminated via the feces.677 (.78 (2. 1993). Lead can cross the placenta and enter the developing fetal brain.812-1.10 (.02-1.933) .583-.87) 1.701 (.682) .03) 2.615 (.52) 1.28-1.07-1.914 (.70 (1.25-1.841-1.900 (.603-.17 (.404-.698) .01 (.603 (.58) 1.0) 3.623 (.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 .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 .63) 4.601-.83 (2. CDC.66 (1.26) 2.702-.31 (1.828) .89-5.S.667-.718) .593 (.22-2.51 (1.654) .702) .50) 1.649 (.828-1.604-.11 (1. 2003.97) 1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.66 (1.88) 2.404 (.988 (.03) .15) 1.946-1.41) .03 (.15) 1.893) .707 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.06) 1.22) 1.55 (1.962 (.15-3.10 (1.712 (.20-3.671 (.380-.639 (.541-.50-2.20) .49 (1.535) .31) 1.701) .52 (1.734) .41 (1.03) 90th 1.05-1.977) 1.08-2.579-.11 (.79) 1.53-1.918 (.65 (1.639 (. BLLs and associated toxic effects differ in children and adults.720 (.85 (1.882-1.67-4.920-1. and through binding to ion channels and regulatory proteins.461) .853-1. through the inhibition of certain enzymes.569 (.03 (.404 (.681-.709 (.43) 2.670) 1.618 (.677-.03 (1.623 (.06) .632 (. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.742) .27 (1.33) 2.61) 1.510-.655-.796-1..50-2.65-2..676) .26) Total .39-1.19) 1. seizures.05-1.64 (1.644 (.693 (.06 (1.677) .926 (.64) 95th 2.668-.44 (1.436) .07) .655) .432 (.37-1.698) .617-.53) 1.83) 1.28) .428) .56-2.88-2.887 (.00 (.92) 2.722 (.61) 3.96 (1.559-.03-2.592-.655) 75th 1.667) .03) 2.09) 1.644) . 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.679) 1.659-.97 (1.43 (1.981-1.703) .18) 2.587-.28) 2.74 (1.72-2.700-.79) 2.97) 1.725) .940 (.00 (1.22) 1. 2007). based on prospective population studies.862-.731-.725) .22-1. Nash et al. For instance. interval) .00 (1.608-.790) .

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

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Acquisition and retention of lead by young children. Lanphear BP. References Agency for Toxic Substances and Disease Registry (ATSDR). Meyer PA. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.cdc. 4/14/09 Centers for Disease Control and Prevention (CDC). Caldwell KL. 4/14/09 Centers for Disease Control and Prevention (CDC). Inorganic and Organic Lead Compounds.115:521-529. Vupputyuri S. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Neurodevelopmental effects of postnatal lead exposure at very low levels. Ga. Homa DM.cdc. 4/14/09 Centers for Disease Control and Prevention (CDC). Atlanta (GA). Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Lead and hypertension in a sample of middle-aged women. Environ Health Perspect 1993. Hunter DJ. 1999-2002. Cory-Slechta DA. Lepom P.287:1-11. Rios C. Korrick SA. Batuman V. JAMA 1996. Environ Res 2000. Wigg NR. Stanek KL. Bellinger D. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Am J Epidemiol 1999. Kaufman JD. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention.cdc. Am J Public Health 1999.26:359-371. Hu H. 2003-2004.87:1-471.123:e376-e385.73:409-420. Speizer FE. Vimpani FB. Neurotoxicol Teratol 2004. Jusko TA. Pirkle JL. Aro A. Brody DJ. Kaus S. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Scand J Work Environ Health 1984. Korrick S. Hernberg S. Muller CH. Available at URL: http://www. Teratogen update: lead and pregnancy.82:60-80. Blood lead levels—United States. Jones RL. Sparrow D. MMWR Morb Mortal Wkly Rep 2006. Cox C. Available from URL: http://www. Bavazzano P. Neri A. Available at URL: http://www. IARC Monogr Eval Carcinog Risks Hum 2006. Kuehnemann TJ. Payton M. Luukkonen R. Hu H.53:411-416. Reese YR. 2002 [online]. Managing Elevated Blood Lead Levels Among Young Children. Preventing Lead Poisoning in Young Children. Adult blood lead epidemiology and surveillance—United States.54(20):513-516. Rotnitzky A. Birth Defects Research (Part A). Sparrow D. Int J Hyg Environ Health 2002. Jacobson JL. Becker K. Krause C. McMichael AJ.8(3):395-401. van Netten C. Dietrich K. Apostoli P. Public Health Rep 2000. Aug 2007 [online].113(4):1016-1022. Toxicological profile for lead. Roberts RR. N Engl J Med 2003. Jacobson SW.gov/nceh/lead/publications/ books/plpyc/contents. JAMA 1996. Auinger P. Checkoway H. Bellinger D. Chiodo LM. Canfield RL. Borja-Aburto VH. Occup Environ Med 1996. CDC. Muntner P. The relationship of bone and blood lead to hypertension. Angle CR. Semen quality of men employed at a lead smelter.gov/nceh/lead/ CaseManagement/caseManage_main. 1988-2004. Rotnitzky A.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. 2005. Cox C.htm.55(32):876-879. Age-specific kinetic model of lead metal in humans. et al. Atlanta (GA). Leggett RW. Manton WI. Kim R. Hu H. 2005b.gov/mmwr/preview/mmwrhtml/ mm5532a2. et al.cdc. Ewers TG. Hertz-Picciotto I.89:330-335. Neurotoxicol 1987.htm. et al.atsdr. Seiwert M. Blood lead levels measured prospectively and risk of spontaneous abortion. Baghurst PA. Coresh J. Baj A. Robertson EF. Hänninen H. Schulz C. 4/14/09 Alexander BH.1542/peds:2007-3608.htm.205:297-308. Pediatrics 2004. Pediatrics 2009. Centers for Disease Control and Prevention (CDC). gov/mmwr/preview/mmwrhtml/mm5420a5.275(15):1171-1176.html. et al. doi:10.10:43-50. 1991 [online]. 4/14/09 Centers for Disease Control and Prevention (CDC). Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Mantere P. Wager C. Rojas LM. Available at URL: http://www. Weiss ST.gov/toxprofiles/tp13.101(7):598-616.cdc. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Weiss ST. Lanphear BP. MMWR Morb Mortal Wkly Rep 2005a. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.275:1177-1181. Available at URL: http://www. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study.htm. Ronchi L.348:15171526. Atlanta. Ganzi A. Sci Total Environ 2002. Lead. Farias P. et al. Henderson CR.150(6):590-597. Blood lead reference values: the results of an Italian polycentric study. Third National Report on Human Exposure to Environmental Chemicals. Blanco J.

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600) 1.30) 3.400-. In addition.40-2. 2002).50-2..285-. sulfur. and organic forms. thimerosal.563 (. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.797 (.30-5. 1998. elemental mercury is absorbed mainly by inhaling volatilized vapor.g. which can bioaccumulate in aquatic and terrestrial food chains. 1993). mercuric chloride).g.90 (4. have often required public health intervention (Zeitz et al.574) .10-3..40) 1.300) .800-1.70) 911 856 2081 4525 03-04 03-04 . synthetic organomercury compounds were once used in pharmaceutical applications. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).60-6.800 (.80) 4.80 (1. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.80 (3.90-3.979 (.00-1.927) .00) .900) .80) 3.50) 4.372) . Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.60 (1.800 (.886) .877 (.60 (2.40-2.50) 5.900) 1. IARC.90) 95th 4. which create an episodic potential for volatization and inhalation of mercury vapor. predominantly from fish and other seafood.10) .40 (3.30-6.919) .30 (2.753-1.00 (2.00 (. electrical lamps.800 (.. to form inorganic mercury compounds or salts.40 (4. Also.419 (.800-1.472-.700-. Apart from methyl mercury.90 (1.70 (1. interval) ..700-. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges. Woods et al.903) Selected percentiles ( 95% confidence interval) 50th .714-.70 (1. The kinetics of the different forms of mercury vary considerably..00-5.00) 3. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.900) 75th 1. The ingestion of methyl mercury. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. 2007).50) 2.900) 1.00 (.20-4. thermostats and switches).490 (.00 (. Kingman et al.40 (4.300 (.20) 2.30-2. Other major uses include electrical equipment (e. merbromin).S.02) .40-3. and is distributed to most tissues. 1994. After elemental mercury is absorbed.700-.90) 3. constitutes the main source of dietary mercury exposure in the general population. and mining and smelting.70-2.363-.00 (1.60-3..326 (. 1980. Poorly absorbed from the gastrointestinal tract.700-. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.600 (.20 (2.00) 4. and mercury compounds are still used as preservatives (e. Atmospheric elemental mercury can be deposited on land and water. 218 Fourth National Report on Human Exposure to Environmental Chemicals .. such as chlorine (e. sphygmomanometers and barometers. Survey years 03-04 Geometric mean (95% conf. an organic form of mercury.700 (.12) .30-4.900) 1.90) 90th 3.60) 1.70 (4.00) 1.60) 1.700-.2.60) 2085 2293 3478 Limit of detection (LOD.781 (.Metals Mercury CAS No.400-.814 (. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.860-1.800-1.60 (1.30) 5. phenylmercuric acetate) or topical antiseptics (e.689-.50-3. with the highest concentrations occurring in the kidneys (Barregard et al.400 (.300-. solid-waste incineration.900 (.g.80 (1.30) 1.500 (.672) .g.40 (3.60-2.70 (3.418-.. may contain inorganic mercury.60-6.00 (2.50) 1. or oxygen.30) 3.00) 1.00 (.80 (1.30) 4132 4241 03-04 03-04 03-04 .30 (1.703-.484) .700) .800-1. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. Accidental spills of elemental mercury.40) 3. Elemental mercury is a shiny.60-5.800 (.500-. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach..500 (. 1999 .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 . inorganic.500-.655-. and dental amalgam.00 (2.40-1.20-3.S. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). thermometers.800-1.30) 1.776 (.90 (1.700) . Hursh et al.20-4.40-1.500) . Some cosmetic skin creams from countries other than the U.80) 1. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.50-1.

90 (1. for both acute and chronic exposures.30 (1.700-1.30-11. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.820 (.833 (.500-.90) 2.667 (. Methyl mercury enters the brain and other tissues (Vahter et al.14 and 0.06-1.70-5.500-1.14. 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.10 (1. Geometric mean Survey years (95% conf.900 (. 1994). population.10 (. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.00) . Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.20) .. interval) Selected percentiles (95% confidence interval) 50th .10 (5.00-2.80 (3.60) 3. National Health and Nutrition Examination Survey.. Vimy et al.700-1.800) 1.80) 579 527 370 436 588 806 Limit of detection (LOD.. Miettinen et al..40 (1.800-1.70-5. 1996).824) 1. 1993).800-1..700 (.500-.268-.10 (3.871-1.50-3..00-3.50 (2. 1992).300) .00-2.200-. a measure of accumulated dose (Cernichiari et al.40-1.10) ..90 (4. 1991.60 (1.300) .400-.300 (.27) .10 (.00 (1.726-1.90) 90th 1.06 (.300) . McDowell et al.200 (.00-2.919) . 1971).90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .70 (1..70) 4.10) ..50) 1. 1995. 1975.70-3. 1998).7) 4. 1996. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.800) 75th .377 (. 1994.50-2.3) 4.269-.369) 1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.00 (3. 1999-2002..30-4.. Excretion occurs by renal and fecal routes.80 (1.318 (.900-1.700-.30-4.200 (.407) .00-6.800 (.70 (1.500 (.500 (.297-..30-6.300) . Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.35 (1.90 (4.374) . Vahter et al.40-2.10) 1. thereafter.307 (.900 (.60 (1.600) . 1994) and then undergoes slow dealkylation to inorganic mercury. 1999).00) 1.00 (2. 2003).40) 2.541-.30-6. 1973). The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.70 (1.20 (2.40) 5.50) 95th 2.900 (.00) 4.50) 3.60 (2.300 (.. with most elimination occurring through in the feces (Sherlock et al.. 1969.70-3.60) 1.00) 2.700 (. Myers et al.30-2.60) 2.50) 2.00) 6.Metals the tissues to mercurous and mercuric inorganic forms. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.30-5.300) ..700 (. 2003). 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .395) .20-2.265-.20 (.00 (2.800) 1.825-1.00-1.20) . 2005).70-6.50) 1.200-. 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..697-.20-3.500-.40-2.00 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10-1.80) 1.20-3.800 (.940) Race/ethnicity (females.73) 1.200-. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al..30) 1.10 (1. 1993).600 (.90 (1.500-.256-.80-3.800) .40 (1.317 (.10-3. Smith et al.20) 1.30-3. and a useful marker of exposure in epidemiologic studies (Grandjean et al.S.944 (. 1984.664-1.10 (1.377) .600) .20-3.30) 1. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.70) 4.01) .40) 1. Fourth National Report on Human Exposure to Environmental Chemicals 219 .0) 4. Methyl mercury is incorporated into growing hair.200-. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.. 2004. Smith and Farris.300) . 1992 and 1999.700) 2.90) 5. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.30) 3.800-1. 1998).800) .30-6.299-.300 (.90) 2.70) 1.90 (3.329 (.90) 3.30 (1.700 (.900-1. Sandborgh-Englund et al.60 (1.50 (1.23) .300 (.200-. 1990)..700-. After exposure to elemental mercury.738-.343 (.200-.00) 7.. 1992. Jonsson et al.20-11.800 (.29) ..60 (3.30 (1.475) .02 (.60 (3.30 (. Suzuki et al.500-.50-12.60) 1.00) 1.

.600-. Bellinger et al.. 2006. typically after a latent period of weeks to months.600-. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.600) .. 2004. In recent epidemiologic studies.600) . hearing impairment..700 (.600 (. pain in the extremities.600) .600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700) . Rissanen et al. 2002.. Acute.500 (<LOD-. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. DeRouen et al. limb deformities. 2000. dysarthria.500-. 1983). At levels below those that cause acute lung injury.500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600) . and neurocognitive and behavioral disturbances. altered physical growth.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 . Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. 2000).700-.700 (.600 (. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury... 1998.. Stern 2005. overt signs and symptoms of chronic inhalation may include tremor.42. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. cerebellar ataxia. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. Oskarsson et al.700 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. Overt poisoning from methyl mercury primarily affects the central nervous system.600 (. anorexia..600-. sensory impairments. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.500-. Sakamoto et al. 220 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection. 2004). population from the National Health and Nutrition Examination Survey.. 1995. particularly irritability.600) . 1963). Survey Geometric mean (95% conf.500-. 2006.500-. fatigue.600-. 1970. 2005.700-.500-. short-term memory loss. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. depression.. Salonen et al. 1995. Once absorbed. see Data Analysis section) for Survey year 03-04 is 0. gingivitis. and cerebral palsy (NRC.600 (.. Rice. 1987). 2005)..600 (. 1951. causing parasthesias. Sakamoto et al.800) . and sleep disturbance (Bidstrup et al.500-.600) .700 (.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . dysarthria..500-. Vupputuri et al. irritability. 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. Inorganic mercury exposure usually occurs by ingestion.500) ..600) . and pinkish discoloration of the hands and feet (Tunnessen et al. which may vary for some chemicals by year and by individual sample. 2003). Drexler and Schaller. hypertension.600) . 1996).500 (.700 (. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.. 2004. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (. the existence of a causal relation is unresolved (Chan and Egeland.600 (.Metals may be more efficient for inorganic mercury (Grandjean et al.500 (.800) .700) 2007 2240 3406 Limit of detection (LOD. ataxia.500-... insomnia. 2000. 1993).600) . Factor-Litvak et al.S. and progressive constriction of the visual fields. 2004).600 (.600 (. The constellation of findings may include anorexia. Smith et al.700-. Smith et al.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .500 (<LOD-. maculopapular rash. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.

14) 90th 2. total blood mercury increased with age.05) 1.54 (2.940 (. 2002). From 1996 through 1998..549) . the total blood mercury concentration is due mostly to the dietary intake of organic forms.08 (1.555) .460 (.46) 3. 1997.24) 1.18) 2..447 (.Metals standard for inorganic mercury has been established by U.07 (.46 µg/L for children.840-1.9 years). Total blood mercury levels increase with greater fish consumption (Dewailly et al.382-.05) 3.570) .534) . 2001.460) . 2009).250) .cdc.430 (.67-2.870-1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.8 years. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.77-2.31) 2.360-..88) 287 722 1529 03-04 03-04 . Urinary mercury consists mostly of inorganic mercury (Cianciola et al.24 (2. Survey years 03-04 Geometric mean (95% conf.97) 2.09 (2. 2009). Grandjean et al.55 µg/L.304) . 1998). IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. and the age-related changes differed across the groups (Caldwell et al. Mahaffey et al.408) .S.61) 1.890 (. average age 33 years.60 (1.520) .16 (.610-1.00 (.396-.93 (1.430) .78-2. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.14. EPA. and increased slightly in non-Hispanic white children (Caldwell.78 µg/L for adults and 0.370) .28) 1. In NHANES 19992002.406-.340-. EPA at: http://www.413-.39-3.68 (2.76-3.epa.e.441 (.480) 75th 1.23) .509) . Sanzo et al.213-. interval) .405-.31) 1266 1272 03-04 03-04 03-04 .19 (2.88-3. Schober et al.52) 2.76-4.930-1.atsdr.530) . 2004.463) .30) 3.96 (1.65) 1.442-. Benes et al. 2003). Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. range 40 years to 78 years) had an average total blood mercury concentration of 2.26 (1.60-2.330-.358 (.420 (.700 (. In Germany the geometric mean for blood mercury was 0.12 (. 758 children.66) 3.580) .13-2. 1995. Information about external exposure (i.770-1. aged 18 to 69 years.254 (. Fourth National Report on Human Exposure to Environmental Chemicals 221 .400 (.S.360-.433 (.. slightly higher total blood mercury levels were found in U. 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.700-1.19 (1.gov/mercury and from ATSDR at: http:// www...96 (1.416 (.00) 1.330-.840) 1.S. Kingman et al.67-3..530) . the median concentration of blood mercury was 0.330 (. Among the three racial/ethnic groups..476 (.58 µg/L for 4645 adults..08 (1.63-2. A cohort of 1127 U.200 (.360 (..290-. environmental levels) and health effects is available from the U.S. 2006). total blood mercury geometric mean levels in females aged 16-49 years did not change.60) 619 713 1066 Limit of detection (LOD.480 (. Over the NHANES 1999-2006 survey periods.160-. et al. Biomonitoring Information In the general population.870-1. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.42) 95th 3. adult women in several ethnic subgroups (Hightower et al.492) Selected percentiles ( 95% confidence interval) 50th .88 (1.14-2.280-.34-3.33 (2.350-. see Data Analysis section) for Survey year 03-04 is 0. During the same survey periods.420 (.509) .S.530-.960 (.410-.29) 1.03-4. 2000).90) 2.01 (.16 (1. who participated in a 1998 representative population survey (Becker et al..430 (.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 . However.20 (1.23) 2. average age 9. population from the National Health and Nutrition Examination Survey. particularly methyl mercury.840-1..495 (.89) 3.85-2. military veterans (mean age 52. These distinctions can help interpret mercury blood levels in people. 2003).330-.313-.76-3.gov/toxprofiles. 1998). 2001.. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.440 (.99-6.

875-1.990) .455-.280-.522-.376-. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.616) .391) .03) 2..333-.31 (1.246-.368) .255 (. and on average.S. et al.696 (.714-1.297 (.447 (. a biomarker of perturbation in renal tubular function.443 (. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.51-2. 2006.1 µg/L for each surface with a dental amalgam (Kingman et al.306 (.392-. Urinary mercury levels in recent German (Becker et al.67 (1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell..79 (1.532 (.88 (1.964-1.225-.208-.630) .04-3.40 (1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.970 (.566) .476 (.455) .498) 75th .65 (1. 1992). 2009). ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.301-.196-.464 (. Urine mercury and the number of dental amalgams were correlated.07) 1.587 (. 1998).400) .309-.289) .768 (.525 (. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.217 (. population from the National Health and Nutrition Examination Survey.62 (1.23-2.347) .343 (.63) 1. 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. Survey years 03-04 Geometric mean (95% conf.46-2.85) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2537 03-04 03-04 03-04 .11) 2.362 (.652) .79) 1.28 (.06 (..11-2.32 (1.S.472-. Information about the biological exposure indices is provided here for comparison.417) .S.275) .S.54 (2. 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. An expert-panel report recently prepared for the U.485 (.. reversible increase in urinary N-acetyl-glucosaminidase.508 (.76 (1.06 (. et al.88-2.667-1. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.404-.11) 1.40-1.384 (. DeRouen et al.39) 1.620-.30) 1.00) 90th 1.12-3.365 (. Department of Health and Human Services noted that several studies have observed a modest.16) 1. 2009)..S.30) 2.61) 1.391-.358) .785-1.784) 1. 2002)... mean urinary mercury was 3.. and Italian (Apostoli 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.87) 2. women of childbearing age have generally been much lower than these levels (CDC.265-. not to imply a safety level for general population exposure.365 (. military veterans with dental amalgams.00) 286 722 1529 03-04 03-04 .56) 1266 1271 03-04 03-04 03-04 .307-.44) 1.21) 1.67 (1. 2005). In the study of U. Langworth et al.969-1. 1988.01) 2.09) 1.486) Selected percentiles ( 95% confidence interval) 50th .86) 95th 2. Levels in U.535) 1.88-2.32-2.35 (1.78-4..537) . interval) .619-.800-1. 2003).77 (2.00 (.385-.588) .1 µg/L..909 (.599) .13-2.13 (1.447-. the urine mercury increased by approximately 0.463 (. Czech (Benes et al.687) .90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .41-2.Metals 2000). 2006).276 (.455-. 2002) adult population surveys were similar to those in a U.87 (1.64-2.400-.480) .25 (.18-1.545 (.

04-1.57-4.450-.41 (2.91 (2.650 (.22 (.85) 4.84 (2.55) 90th 3.07-2.710 (.09-1.723 (.636-.81 (3.61-6.87-4.508-.47) 1. National Health and Nutrition Examination Survey.540 (.79) 3.45) 2.44) 3.30-2.55-3.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .799) .84 (2.410-. Geometric mean Survey years (95% conf.41 (1.68) 3.15 (2.07-5.22-3.30 (1.00 (3.580 (.41 (1.97) 2.501-.13-4.592 (. Geometric mean (95% conf.17) 95th 5.24) 6.03) 1.665) .721 (.89 (2. population.95 (2.94) 1.15-1.14 and 0.892) .833) .65-4.526-.560 (.43-1.420-.14-1.31 (1.831) .832-1.50 (1.475-.522 (.710 (.631-.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .656-.53-3.83-3.23-1.56 (1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for females aged 16 to 49 years in the U.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.45-3.710) 1.21 (1.52) 3.790) .610-.27 (1.24-1.99-2.51) .59-5.553-.07) 1.909-1.18) 3.56) 4.624-.56) 3.45 (1.45-2.809) .14) 3.41-6.615 (.97 (1.686) .14.98 (5.582-.69 (1.06 (.62 (4.930) .Metals Urinary Mercury−Females Aged 16-49 Years Old.502-.03 (.516 (.760 (.77) 2.622-.32) 2.14-2. 16-49 years) 99-00 01-02 .92) 3.565 (.540-.699) 1.99) 1.42) 90th 2.30 (2.69-3.00) 2.616-.846) .387-.45) 2.810) .42-3.605-.740 (.664) .85-3.45) 95th 3.910) .772 (.3) 5.578-.04-10.824) .42) 2.596 (.850-1.870) .97) 2.658 (.31-1.639 (.S.76) 2.28 (1.25) 2.77) 1.744) 1.54) 595 531 381 442 594 826 Limit of detection (LOD.79) 1.35) .724 (. 1999-2002.606 (.62 (3.05 (3.806) .37 (1.62 (1.37) 1.10-2.35 (1.00 (2.51 (3.16) 5.92) 2.13 (2. interval) Selected percentiles (95% confidence interval) Survey years 50th .65) 1.10-4.620 (.61) 1.38) 4.47) 1.50 (2. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.05 (2.426-.03 (.774) .706 (.670) 75th 1.657 (.03-2.68-3.48 (2.500-.966) . 1999-2002.S. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U. National Health and Nutrition Examination Survey.520-.691) .18 (3.21-3.27 (2.46 (1.632 (.580-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .70 (2.520-.72) 1.709) .76 (1.46-4.600 (.39-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.650) 1.99 (3.16-5.81-6.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.50-4.742-1.99 (2.655 (. interval) Selected percentiles (95% confidence interval) 50th .569-.557-.719 (.32 (1.831) . 16-49 years) 99-00 01-02 .23-1.650 (.560-.27-1.21 (2.579-.76-5.97) 2.92) 4.32-3.68 (3. population.09-1.46) 3.709) 75th 1.30 (2.685 (.637) .91-7.

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5-66.8) 40.2-53.0 (42.9 (33.8 (42.3) 37. Excretion occurs predominantly via the kidneys.6-82.1-55.4 (48.6-58.7-41.9 (32.5 (41.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.6) Selected percentiles ( 95% confidence interval) 50th 50.7 (37.2 (56.7 (44. 2001). and 03-04 are 0.8. lubricants.2-79.6) 71.3) 83.2) 40.1-44.3 (71.9 (73.6 (43.0-77.7-51.9 (40. hydrogenation catalysts. 1997).7-96. More recently.7-91.0 (46.0) 45. population from the National Health and Nutrition Examination survey.4) 76.7-50.0) 55.3 (46.5 (49.1) 82.6) 51.3 (53.7) 75th 84. and xanthine oxidase (Kisker et al. 1996).9-82.6-62.1) 126 (106-147) 109 (94.5) 44.5-46.4) 45.8) 39. 7439-98-7 General Information Elemental molybdenum is a silver-white.0-71.4) 42.0-100) 63.0 (48.5-52.2) 41.7-39.0) 39.9-56.8) 48. inks.2-91.0-38.7 (73. urinary excretion over six days CAS No.2 (49.6-46. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.Metals Molybdenum or ore deposits.5-41.4-52. At a daily oral molybdenum dose of 24 µg.7 (50.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.8-94.0) 97.6) 53.7-68.5) 85.4) 49. aldehyde dehydrogenase. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (74.1-52. see Data Analysis section) for survey years 99-00.2 (69.2-59.7 (36.0 (42.5) 60.0 (43.0-85.5) 47.5-52.4) 52.7) 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 78.3 (47.4-75.9 (78.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.2 (63.1-88.5.8 (85.7) 45.3 (84.2) 79. 2001.1) 35.5 (67.5) 80.7-60. 01-02.1 (34.3 (55.5-68.3 (64.1) 60.3-91.0) 60.7-47.2-70.3-44.3) 54.7-122) 93.3) 65.3-75.9) 67.8) 75.6-72.2) 37.2 (55.9 (34.8) 44. WHO.7 (45. In humans.9) 34.0 (76.9 (52.6 (55.1-51.4-61.6-42.7) 86.7) 77.9-55.3) 41.6-96.5 (43.1 (38.3) 85.9-83. 0.6 (55.7-105) 69.5 (37..1-48.3-108) 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. Fourth National Report on Human Exposure to Environmental Chemicals 227 .2 (61.3 (38.7) 46.6) 93.9) 62. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.8. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.3 (55.3 (37.9 (44.9-109) 97.6-111) 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. and in pigments for ceramics. and paints. Compounds of molybdenum are also used as corrosion inhibitors.4 (72.2) 53.2 (38.8-46.4 (48.6) 71.7-92. 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. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.1-52. which exert homeostatic regulation over molybdenum balance.2-59.0) 84.7 (58.2-42.4 (80.3 (79. chemical reagents in hospital laboratories.0-53. and 1.2 (49.0 (81.8 (67.4-82.7) 51.5-91.9 (37.4) 41.4 (79.7-84.7-73.5 (41.0) 54.8-108) 87.3 (73.5-124) 108 (92.7) 78.S.0-56.1) 59.8-49.3-115) 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.3) 47.6 (73.2) 48.8-90.0 (41.5) 80.2-37.0-65.0-110) 90.7) 78.8-106) 88.5-65. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.6-55.7 (71.2 (40. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.0) 62.9-55. respectively.9-85. semiconductor and battery industries have begun to use molybdenum.1-63.7 (51.1) 46.1) 57.0-101) 82.6 (40.2) 52.8 (82.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.2 (83.1 (71.1-59.5 (81.4) 56.6 (40. interval) 45.0-62.3-47.7) 57.4 (34.5 (48.6 (52.1 (91.8) 46.

2) 43.1) 56.5 (35.2-121) 107 (92. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6-45.7-137) 129 (109-155) 112 (97.9) 40.8) 38.7) 53.8 (90.7-38.7-62.2) 37. respectively.1 (82.9) 92.2-46.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.9 (49.3-44.4-107) 85.5 (65.2-80.9-41.9) 79.0) 39.1) 65.9 (79.8 (56.2) 38.4) 58.1-34.8 (36.4-120) 101 (84.1 (54.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.4 (53.0) 36.5) 71. U.5-92.4 (67.1-127) 90.0-46.3-52.5 (35.9-117) 57.5-48.7-100) 77.0-41.4-118) 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) 39.2 (33.9 (35.3) 44.1 (33.9-42.2-49.1-45.1-100) 86.5 (80.3 (36.8 (75.5) 63.3) 41. 2001).6) 48.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.5 (41.9 (40.2-65.0-46. 1999).8-47.7) 112 (95.7-93.8 (37.6 (57.3 (37.9 (64.3-43.03 mg/kg/day in humans (IOM.4 (59.5-45.1 (44.0) 62.4 (40.6-41. 1993).4 (44..4 (55.3 (71.4 (78.0 (80.6) 39.2 (69.5-97.9-45.1-81.8) 45.7) 57. 1995).5 (50.9-87.3-141) 109 (81.6 (38..5-69.4-39.4) 44.4-66.3 (51.6 (36.9) 44.4) 48.2) 42.6 (42.8-118) 81.6) 43.0-56. Molybdenum is generally considered to be of low human toxicity.2 (37. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown..5-62.1) 101 (83.S.8-46.1) 37.5 (37.3-56.5 (79.5-119) 90.S.4-41.0-120) 85.5-46.9-96.6 (71.2 (40.7) 75th 63.3 (37.5 (34.2-96.2) 37.1-109) 89.3 (36.1) 43.9 (39. and clinical or epidemiologic evidence of adverse effects is limited.7-40.1 (30. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.8) 37.8-84.1-79.3-115) 98.5 (39.6-61.2) 58.4-106) 85.7 (30.8) 39.5 (39.0) 72.9-45.0-133) 119 (88.7) 62.8-67.7) 41.5-60.1-39.1-43.Metals was 18% of the ingested dose.8) 62. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (37.4 (56.9 (36.3 (58.3) 37. and urinary levels reflect intake from all sources.5-44.6-63. population from the National Health and Nutrition Examination survey. urinary excretion over six days rose to 50% and 67%.6) Selected percentiles ( 95% confidence interval) 50th 41.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.9 (39.1-41.6) 36.4-42.7 (75.9) 41.9-118) 91.7) 42.3) 64.1-39.2) 55. In industry. but available epidemiologic data are scant.7 (66.3) 61.1 (39.2-96.2 (40.5) 72.9-71.3 (53.5 (38.8-65.9 mg/kg/day and established a tolerable upper intake level of 0.7-43.4-76. 1997).5 (78.1 (49.6-88.6-63.0 (35.1-67.6 (59.4) 89.2 (36. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.3) 57.4) 40.0) 33.2-41.9) 31.9-61.0 (74.7) 115 (93.5 (37.8) 38.2-40.3-45.5) 73.2 (73.8-52.2) 42.9 (73.2 (43.6-78. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.6-76. Biomonitoring Information Molybdenum is an essential element for health.3 (55.3 (83. of the ingested dose (Turnlund et al.7-120) 87.2) 39.3-46.5-50.0-103) 103 (90.4) 77.3) 40. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5 (40.5 (36.8) 61.8-66.6-61.1-43.5) 60.4) 60.6) 39.5 (40.7-52.3) 56.2 (57.5 (59.5 (83. interval) 43. Based on studies finding adverse reproductive effects in rats and mice.2 (40.1 (38.3 (71.3-59.0) 44.8-47.1-38.3-68.4) 47.4 (37.4) 122 (107-133) 109 (99. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.9-68.1-40.7) 45.2 (50.1-112) 78.3) 43.5-99.0) 53.5 (54.2 (52. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.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) 37.8 (57.0 (58.7 (77. EPA.1) 40.1 (42.2) 39.5 (41.4) 116 (101-126) 104 (88.1 (38.2-47.7-44.4) 61. at daily oral doses of 95 µg and 428 µg. 1961.8) 71.8) 79.5-70.4-185) 106 (94.9-40.1 (40.6 (36.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.9 (64.0-38.0) 38.8-42.5-35.5) 90th 108 (97.5 (65.0) 88.

66:233-267. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.22(3):179-191. EPA).S. manganese.S. World Health Organization (WHO). Available at URL: http://books. U. Kisker C. 1998. TR-462. 2002. pp.epa. Molybdenum in infancy: methodical investigation of urinary excretion. et al.62(4):790-796. 4/14/09 Iversen BS. 2005). Schleyerbach U. Minoia et al. In: Trace elements in human nutrition and health. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Aprea C. Dietary reference intakes for vitamin A. 4/14/09 White MA. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Koval’skiy GA. chromium. References Centers for Disease Control and Prevention (CDC). A study of 13 elements in blood and urine of a United Kingdom population. Peiffer GL. vitamin K. Zhurnal Obshchey Biologii 1961. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Occupational risk factors of lung cancer: a hospital based case-control study. Environmental Protection Agency (U. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Sabbioni E.123(1):81-85. 2001). Available at URL: http://www.Metals in urine for the U.. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Trace element reference values in tissues from inhabitants of the European Union. nickel. 56:322-327.nih. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Van Meerbeeck JP. and zinc: a report of the Panel on Micronutrients. 420-441. (DC): National Academy Press. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No.nap. 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. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8.niehs.php?record_id=10026&page=420. J Trace Elem Med Biol 2001. copper. Schaub J. Third National Report on Human Exposure to Environmental Chemicals. Droste JHJ. iron. boron. 144-154. excretion. 1996. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Institute of Medicine (IOM).gov/iris/ subst/0425.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sciarra G.gov/index. Sabbioni E. van Sprundel MP.216:253-270. 2005. Shmavonyan DM. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Yarovaya GA. Keyes WR. Molybdenum 1993 [online]. Christensen JM. 2001. Am J Clin Nutr 1995. Gatti A. Turnlund JR. X. Kristiansen J. Weyler JJ. silicon.. 4/14/09 Sievers E. Rapid Comm Mass Spectrom 2002. Ronchi A. Ann Rev Biochem 1997. Sci Total Environ 1998. Washington. White and Sabbioni.htm. Occup Environ Med 1999. 16:1313-1319.. pp. Minoia C. National Toxicology Program (NTP). Food and Nutrition Board. Rees DC. Vermeire PA. vanadium. Geneva: WHO. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. edu/openbook. Menne C. Available at URL: http://ntp. Atlanta (GA). molybdenum. Schindelin H. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Analyst 1998. arsenic. Turci R. Molybdenum absorption. White MA. 1998).15(2-3):149-154. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Molybdenum. iodine.

Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. strength at high temperatures. Important properties of platinum are resistance to corrosion. thick-film circuits printed on ceramic substrates. as oxidation catalysts in chemical manufacturing. and 0. however. 7440-06-4 General Information Platinum is a silver-gray. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 03-04 are 0.04. respectively. 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. which may vary for some chemicals by year and by individual sample. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. population from the National Health and Nutrition Examination Survey. copper. see Data Analysis section) for Survey years 99-00.04. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. carboplatin) in the treatment of cancer. 230 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection.. cisplatin. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.07. 1998). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. jewelry. and high catalytic activity. the ambient air concentrations of platinum associated with its use in automotive engine catalytic converters are estimated to be thousands of times lower than occupational exposure limits.. 01-02. and as drugs (e. 0. and iron.g. Platinum compounds are used in electrodes.S. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. dental alloys.Metals Platinum CAS No.

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

Ruff F: Histamine release by sodium cholorplatinate...10:63-71. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.13(1):24-30. et al. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Iavicoli I. Nowak D. 1998). and in blood and urine in the United Kingdom. Kulka U. Saindelle A. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 2004. Environ Health Perspect 1975b. Jankofsky M. Seiwert M. Turfeld M. ruthenium. which elevate urinary platinum by five to twelve-fold (Begerow et al. Br J Pharmacol 1969.htm. Duneman L:Long-term urinary platinum.207(1):69-73. Analyst 1998.. Uptake of antineoplastic agents in pharmacy and hospital personnel. Saindelle A. 3/31/08 Moore W Jr. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.org/documents/ehc/ehc/ ehc125. 289-380.61(7):636-9. 206:15-24. Hauff K. 1999. Angerer J.55(2):138-140. Part 1: monitoring of urinary concentrations. Schulz C. Schierl R. 2001). et al. Several studies have shown that background concentrations in general populations were usually less than 0. Czerczak S. J Expo Anal Environ Epidemiol 2003. Allergy and histamine release due to some platinum salts.19:685-691. Boos KS.. Powell CH. Ewers U. Begerow J.76(1):5-10. 2003. Biomonitoring Information Urinary platinum levels reflect recent exposure. Int Arch Occup Environ Health 2003. Platinum concentrations in urban road dust and soil. Pethran et al. Available at URL: http://www. Urinary excretion of platinum from platinum-industry workers. Ensslin AS... Ruff F: Platinum and platinosis. New York: John Wiley & Sons. Int J Hyg Environ Health 2004.. population were below the limit of detection (0. pp. Environ Res 1975a. 2003. Wilhelm et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations.70(3):205-208.123(3):451-454. Environmental Health Criteria 125. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Patty’s Toxicology. 1998). Kazantzis G. Huber R. Modest (ten-fold or less) elevations in urinary platinum concentrations were associated with handling of cisplatin and carboplatin by pharmacy and other hospital personnel (Ensslin et al. Bocca B. palladium. palladium. Moore W Jr. Wilhelm M.htm. Parrot JL. Schierl R. Seifert B. International Programme on Chemical Safety (IPCS). 2000. Schulz C. eds.9:152-158. Schierl et al. 5th ed. 1991 [online]. Grimm CH. 2004) or less than 0. Influences on human internal exposure to environmental platinum. Gieler U. Kavanagh P. Hysell D.56(3):283-286. Carelli G. Kuster W. Biomarkers 1999. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Fries HG. Arch Environ Health 2001. Petrucci F. International Journal of Hygiene and Environmental Health 2003. Occup Environ Med 1998. 2004).01 µg/L (Becker et al. Alimonti A. van de Weyer C. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Crocker W.4(1):27-36.. 2003). 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. Herr et al. Pethran A.04 µg/L) in this Report. Kaus S. 1997.. Hebert R. Pethran A.org/documents/ehc/ehc/ehc125. Int Arch Occup Environ Health 1997. Stilianakis NI. Herr et al. et al.005 µg/L (Iavicoli et al. Biomonitoring of traffic police officers exposed to airborne platinum. Campbell K. Herr CE. Rommelt H. Nickel. Fruhmann G. Blanks R. Schierl. In: Bingham E. Senofonte O. Schierl R. Hysell D. Platinum. Schierl R. Cohrssen B. References Becker K. Urinary platinum levels associated with dental gold alloys. Thornton I. Neuendorf J. and platinum. Gromiec JP. osmium.S. 2003.. rhodium.Metals the International Programme on Chemical Safety at http:// www.. Levels of platinum in urine for the U. Hall L. Arch Environ Health:1969.inchem. Occup Environ Med 2004. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Farago ME. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Kelly J. and gold excretion of patients after insertion of noble-metal dental alloys. et al.inchem. Raab W.35:313-321.

400 (.360-.400) .270-.159 (.180-.330) .163) .217) .520 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.172 (.159 (.165 (.270-. In the United States.220) .290) .260 (.156-.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 .310 (.160 (.220 (.250-. respectively.470 (.390-.290) .300 (.450 (.440 (.370 (.162-.290) .220 (.480) .390) .300) . see Data Analysis section) for Survey years 99-00.330) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.310-.178) .240-.340-.220) .470 (.171 (.160-.196) .350-.280 (.320-.430-. In the past.480) .500 (.450 (.320 (.330) . population from the National Health and Nutrition Examination Survey.290 (.380 (.240-.240) .176 (.200 (.190 (.450 (.192) Selected percentiles ( 95% confidence interval) 50th .250-.260 (.360 (. 2005).350) .410 (.250-.430) .500) .400-.280 (.145 (.170-.440 (.148-. representing distribution into other tissues.290) 90th . thallium was obtained as a by-product of smelting other metals.360) .560) .135-.200 (.440-.145-.340-.180 (.350-.430) .180) .270-.520) .300 (.390-.400-.480) .370-.180 (.310 (.230 (. 01-02. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.220 (.500) .167 (.400 (.390 (.230) .250 (.149 (.150-.360 (.290 (.218) .380-.260 (.590) .220) .340-.S.137-.300) .218) .190 (.185-.02.400 (.430 (.196) .150-.183) .320) .280 (.410-. the latter being the current major industrial consumer of thallium in this country.410-.230-.290-.167-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.217 (.134-.250-.440) .270 (..330) .280) .470) .260-. thallium readily crosses the placenta and also distributes into breast milk.440) .177) .400-.170) .350-.350) . however.270) .420 (.200) .350-.250) .330-.240) .420) .206) .400 (.420-.160-.470) .420) .590) .230-.450 (.180) 75th .159 (.215) .440) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .410-.390) .270 (.420) .460-.157-.155 (.390) .430 (.370) .230-. it has not been specifically mined or refined in the United States since 1984.480) .220-.490) .190 (.290 (.156) . 0.220 (.230) .520) .290-.440 (.210) .310 (.370-.190 (.380-.360-.300) .184 (.260-.420) .370 (.430-.160 (.270) .380) .172) .410) .133-.270 (.320) .520) .150-.156) .360 (.200 (.180-.330-.340 (.240-.158) .350 (.190-.510) .370 (.290 (.202) .280-.250-.173) .460 (.170-.450 (.420-.191 (.410 (.200-.420) .450 (.360-.240) .410-.360-.480) .239) .430-.500) .170-.02.370-.290 (.200 (.400) .320) .180-.490) .280) .390-.310) .490) Total .420-.400-.450 (.420) . and 0.150-.173) .630) .167-.225) .220) .410 (.420) .350-. and 03-04 are 0.300 (.170 (.280-.250 (.160 (.202 (.260-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.170-.340) .400-.290) .450 (.290 (.200) .190 (.202 (.390 (.201 (.170-.350-. In addition.160-.170 (.147-.330-.200) .410 (.220 (.470) .300-.147-.243) .153-.390-.280) .430 (.380 (.170) .182-.170-.173-.370 (.150-.179-. Human health effects from thallium at low environmental CAS No.370 (.175) .200-.160 (.220) .190 (.410 (.510 (.170-.220) .147-. From these and other sources.270 (.390) .187-.370-.400) .172 (.400 (.490 (.330-.188) .250-.270 (.260-.200 (.370) .250-.170) .410-.Metals Thallium depilatory cosmetics.360-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.260-.144 (.690) .230) .150-.460) .440 (.430 (.200) .260) .250-.450) .210 (.200) .400) .330-.197-.360 (.160-.410 (.370 (.180-.154-.370 (.146 (.340-.170 (.550 (.350 (.510) 1200 1313 1281 1213 1340 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .200) .640) .400) 95th . Thallium disappears from the blood with a half-life of several days.197 (.180 (.210-.185 (.300) .183) .490) .200-.201 (. 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.140-.181-.410-.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 .230) .200-.200 (.210 (.340) .02.450 (.160-.330-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.420-.145-.330-. interval) .160 (.

321 (.162 (.164) .370 (.207-.337-.292 (.157-.286-.128 (.273-.156) .138 (. Information about external exposure (i.143 (.191-.179) .176) .153-.208-.125-.233 (.412 (.281-.158-.237-.214-.456) .238) .143-.178 (.263-.238-.235 (. Thallium produces toxicity by replacing intracellular potassium in the body.256 (.241) .184-.129-.458) .307 (.273-.366 (.330-.216 (.153 (.176) .317 (. (ATSDR.333 (.212) .234-.222 (.271-.258-.377) .300) .274-.148-.326-.162-.365) .170-.343 (.198-.145 (.244 (.156 (.184-..170) .181) .188 (.286 (.402) .148 (.219) . Severe accidental thallium poisonings from ingesting of rat poisons that contained water-soluble thallium salt have occurred.162) .317) .214) .206 (.356) .317 (.144-.153 (.184-.142 (.375 (.135-. population from the National Health and Nutrition Examination Survey. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.133-.229) .208) .180) .297 (.154 (.293 (.271-.235-.278 (.350 (.348) .278) . neurologic injury.173) .133 (. interval) .304) .189) .221 (.304) .269) .380 (.350) .338-.278 (.154 (.200) .204) .150) .280) .272 (.364 (.148-.286) .342) .182 (.324) .383 (.151) .424) .173 (.217-.155) .147-.377) .313 (.250-.200-.160 (.153) .214 (.148-.146) .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 .149) . environmental levels) and health effects is available from ATSDR at: http://www.148-.147-.157 (.176) .283 (.162-.297) .167 (.293) .250-.145-.137-.146 (.215-.300 (.200-. and death.304) 95th .378 (.260 (.146 (.167 (.203-.166 (.146-.S.349 (.532) . Peripheral neuropathy and alopecia are well-documented effects of acute and chronic exposures.304 (.134-.131-.170) .153-.196-.369 (.226) .346) . arthralgias.313 (. and a drinking water standard has been established by U. Biomonitoring Information Urinary thallium levels reflect recent exposure.194 (.213 (.369) Total .325-. respectively.364 (.171) .321) .149 (.389) .144-.141-.211 (.412 (.222) .198) .422) .158 (.135-.161 (.153) .211 (.229-.154 (.140 (. Levels of thallium in urine for the U.363) 861 674 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites 234 Fourth National Report on Human Exposure to Environmental Chemicals .333) .166 (.187-.327) .196 (. Chronic high-level exposures have been associated with weight loss.226-.383) . and polyneuropathy.333-.223 (.176) .300-.364) .236) .167-.S.231) .155 (.271-.164) .286-.179-.469) .278-.271-.140 (.151-.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 .333-.278) .152) .167) .185 (.356-.306-.215) .202 (.286 (.224 (.340-.215 (.198-.248) .244-.205 (.254 (.240) .282-.161 (. 1992) Workplace air standards and guidelines for external exposure are established by OSHA and ACGIH.343 (.171-.149-.html.155-.atsdr.e.282 (.153-.222 (.267-.269 (.119-.146-.233) .306-.169-.146-.319) .156 (.156 (.142 (.312 (.155-.333-.135-.152) .169 (.318-.368 (.458 (.207 (.299-. IARC and NTP consider the evidence for the carcinogenicity of thallium as inadequate or unclassifiable.214 (.280-.289) .198-.172) .191-.192-.297 (.167-.230) . EPA. 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.462) .243) .169) .S.304) .157) .272-.192 (.266-.204 (.197) .387) .255 (.364) .210 (.333 (.167 (.153 (.161) .462) .gov/toxpro2.145) .177) .313-.307) .156 (.366) .160) 75th .160) .301-.348-.154 (.286 (.600) .278-. although additional mechanisms of action are possible.362) .328 (.250) .153 (.143) .171) .346-.153 (.200 (.254-.338 (.361 (.286 (.159 (.167 (.246-.152) .148 (.136 (.287 (.222-.194 (.223) .cdc.180-.323 (.Metals doses or at biomonitored levels from low environmental exposures are unknown.162) .328-.146) .287-.264 (.289) .192-.313-.389) .227 (.159-.237) .160) .300) .128-.221) .402) .149-.348 (.142-.424 (.217) .306 (.291-.273 (.231-.161) .218 (.197-.140-.333) .207) .278) .173) Selected percentiles ( 95% confidence interval) 50th .143 (.168 (.167) .265-.400-. Relatively high-dose intentional or accidental ingestion can result in gastrointestinal symptoms followed by multiorgan failure.260-.387) .147-.329) .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 .162) .143-.389-.214) .150) .221) .145-.160-.200-.259) .122-.208-.159) .258 (.222) 90th .217-.

Pietra R. Manke G. 1981. Schaller et al.76(1):53-59. Martin J-C. Jackson RJ. Environ Res 1998. Pirkle JL. Toxicological profile for thallium. References Agency for Toxic Substances and Disease Registry (ATSDR). 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. Apostoli P. 7/15/09 Blanchardon E. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Challeton-de Vathaire C. Gallorini M. Investigations of thallium-exposed workers in cement factories.html. Ting BG. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust.cdc. Paschal et al. Valentin H. Raithel HJ. Trace element reference values in tissues from inhabitants of the European community I. et al. Fourth National Report on Human Exposure to Environmental Chemicals 235 . A study of 13 elements in blood and urine of a United Kingdom population. 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. Boisson P. Radiat Prot Dosim. 1990. with concentrations ranging up to 76. Buhlmeyer G. Sabbioni E.5 μg/L. 2005. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. White MA.113(1):47-53. Centers for Disease Control and Prevention. Sci Total Environ 1990. Sabbioni E. Celier D. Dolger R. Schmidt M. et al. 1992 [online]...95:89-105. Cassot G. White and Sabbioni. Marcus RL. Sci Total Environ 1998. Ewers U.35(1):4-9. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Pozzoli L. Brockhaus A.atsdr. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Trace metals in urine of United States residents: reference range concentrations. Morrow JC. and serum of Italian subjects.47(3):223-231. Kramer U. Schaller KH. Sampson EJ. J Soc Occup Med 1985. Trace element reference values in tissues from inhabitants of the European Union. Brockhaus et al. 1998). Available at URL: http://www.Metals (CDC. Wiegand H. A study of 46 elements in urine. 2005.265 people living near a thallium-emitting cement plant in Germany. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. 1985). Atlanta (GA).gov/toxprofiles/tp54. Investigation of a working population exposed to thallium. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Int Arch Occup Environ Health 1981. X.48(4):375-389. et al. (1981) studied 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1 mg/m3 (Marcus..S. Paschal DC. Int Arch Occup Environ Health 1980. 1998. Minoia C. blood.. Third National Report on Human Exposure to Environmental Chemicals.216:253-270. 1980. 2005) and are shown with results from NHANES 2003-2004 in this Report. Minoia et al. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Soddemann H.

340-.370 (.090) .160-.065 (.640 (.073-.240 (.270 (.210 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .073) . and for producing ferrotungsten.070-. Evidence is lacking for the carcinogenicity of tungsten.130 (.090-.400-.060-.084) .00) .250) .090) .160) .120) .460) .080) .180-.070 (.510 (.060-.260) .370-.800) .360 (.310-.110 (.400) .082-.250) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.150 (.130) . mainly as scheelite (CaWO4).240-.340-.090-.190-.130-.690) .060-.330) .084-.560) .460 (.190-.080-.380 (.180-.064-.290-.150-.130-.310-.470 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.160 (.090-.160) . and as catalysts in the petroleum industry.350) .113 (.100-.109) .060 (. Tungsten compounds are used as lubricating agents.430 (.076 (.120) .074-.110 (.310) .160-.065-.101-.062 (.078-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.120-.130) .100-.300-.100 (. 0.550) .160 (.330 (.53) .090 (.100) .380-. which is used in the steel industry.105 (.096-.086 (.270-.080 (.270 (.560) .087-.400 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.082 (.470) .080 (.510-1.204) .250-.090) .113 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).420-.380-.190 (.790) .320) .380-.101 (.360 (.060-.080-.110 (.390 (.270-.180-.069) .120-.300 (.130) .100) .310-.122) .470-.290) .050-.080 (.095-.090-.120) .460) .550) .560) .210-.350 (.080) .050-.190 (. and 03-04 are 0.570 (.490) .068) .132) .270-.250-.810) .090 (.440) .310 (.450 (.081 (.Metals Tungsten CAS No.380-.082 (.071-.091) .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 .390) .430-.066-.120-.290-.058-.070-.320 (.370-.170 (. which are used in rock drills and metal-cutting tools.210 (.170) .230-.500) .450-.470 (.190) .360-.060 (.073-.170-.140 (.230) .260-.135) .092 (.076 (.050-.290 (.550 (.060 (.110) .160-.120 (.070 (.420-.260 (.300) 95th .093 (.050-. interval) .620) .430) .430-.580) .130 (.093-.140) 90th .290-.140-.140 (.140 (.105) .060 (.180) .270 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.280 (.500 (.080) .092) .830) .190-.084 (.056-.250) .082) .210 (.110) .093) . Occupational exposure is from dusts released during grinding or drilling of hard metals.120-.080 (.130) .069-.330-.530 (.250) .150 (.150) .097-.137 (.110 (.770 (.071 (.120) . bronzes in pigments.430 (.230-.170) .350) . Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.060 (.070 (.111-.180) .073 (.140-.160 (.200-.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 .280-.410-.360) .500 (.070-.070) .110 (.090-.220 (.480) Total .060-.570 (.530 (.151) .520) .100 (.370 (.590) .300 (.410 (.360 (.400 (.090) .096 (. filaments for incandescent lamps. Little information is available on the toxicity of tungsten.04.360-.100 (.062 (.620 (.060 (.140 (.116) .160 (.460 (.180) .130-.080-.110-.220-.330-.088 (.620) .100) .04.550) .230 (.077-.220) .04.650) .260-.070-.180) .080 (.150 (.104) . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.113 (.950) .520) .130-.092 (.160 (.230-.340) .123-.370 (.070-. population from the National Health and Nutrition Examination Survey.670) .310-.120) .080) 75th . 01-02.560) .200) .490 (.300 (.170) .088) .113 (.530 (.300) . Tungsten is used mainly for producing hard metals.133) .100) .460 (.370) .090 (.120-.100-.230-.170 (.180 (.220) .340-.120) .330) .250) .158 (.220) . see Data Analysis section) for Survey years 99-00.060-.200 (.090-.250) .560 (.120-.070) .070) .260 (.110-.320-.170) .190-.510-.090-.350) .100) Selected percentiles ( 95% confidence interval) 50th .090-.180 (.320-.520) .310-.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 . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.100) .400 (.070) .430 (.160-.056-.110-.S.270-.280 (.087) .210) .210 (. respectively.630) .107 (. and 0.800) .320 (.470) .180-.126) .210 (.260-.230) .380) .095-.380 (.100 (.400 (.350-1.130) .290) .

188-.167) .074 (.081 (. 2001-2002.265 (.326) .073 (.133) .667 (.077) .063 (.358) .109-.063-.300) .053-.146 (.071 (.122-.497 (.216-.167-..554) .333) .354) .066 (.293 (.088) .072-.145 (.439 (.253-.201) .105 (. 2003.197) . and 2003-2004 (Paschal et al.136-.157) .161) .143 (.383 (.S.216 (.066 (.214-.083 (.098) .206-.270 (.082) . population.084) .065-.106 (.245-.287) .075-.133) 90th .089) .294 (. 2005).084 (.168 (.267-.070 (.150-.130-.215) .060-.082 (.091) .086) .062 (.075) .150-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.231 (.164 (.209-.084) .064-.148 (.094) .279 (.170-.080-.155-. measure urinary tungsten.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 .333 (.069-.179-.426) .078) ..308) .131-.133) .431) . Using neutron activation analysis to 2000.130 (. interval) .094-.089 (.079) .065 (.059-.329 (.065 (.124 (.104-.148) .068 (.116) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.267) .119 (.073 (.057-.823) .116-.231-.667) .353 (.111 (.179-.086) .086) .108) .065) .538) .049-.059-.174 (.154) .250-.237-.087) .414) .054-.063 (.333-.136 (.354-.431) .071-.059-.075 (.222-.078) .217-.067-.302-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.385 (.199 (.331-.091) .158) .412 (.364 (.125) .095) Selected percentiles ( 95% confidence interval) 50th .211 (.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 .098-.079) .203-.176-.237) . Patients with medically-inserted tungsten found at increased levels in drinking water.078 (.315-.197-.103-.090-.255 (.056-.079 (.078-.386) .060-.139-.392) .302-.169) .222) .087 (.091) .198) .075 (.083) .071 (.169 (.482 (.739) .063-.119-.146 (.285) .187) .283) .S.344-.138) .279 (.250 (.070 (.077-.261-.484 (.452-.055-.075) .074-.317 (. 2001).215 (.153-.150 (.080-.077) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.082) . 1998).122-.136-.067 (.465) .253) 95th .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 .108-.088) .153) .100 (.072-.068-.079) .074-. population (CDC.090-.085) .158 (.341 (.069 (.431) .317) .117) .100) .096) .176-.078 (.727) .093) .073 (.117 (.139 (.063-.094) .634 (.359 (.061-.180-.121 (.138 (.151 (. similar to those in this Report (Schramel et al.100) .28) .300-.120) . or exposure that a control group of non-metal workers had mean levels differences.099-.125 (.439 (.216-.286-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.136-.216 (.083-.500) .436-1. Nicolaou et al.300-.085-.074) 75th .121-.091 (.218 (.255-.339 (.126-.081-.216-.278-.061-.079 (.098 (.190) .181 (.081 (.120) .138 (.300 (.375) .122 (.279 (.439) Total .301) .797) .214) .258-.333) .109 (.200-.453) .143-.085 (.095-.198-.184 (.301) .272-.255 (.060 (.061-.197 (.379 (.880) .071) .065-.462) .075-.091 (.065-.081) .284) .069 (.258 (.317-.167) .083 (.240-.086-.233-.098-.098-.186 (.144-.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 .136-.174) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.360 (.582) .308) .426) .250 (.275 (.105 (.. (1987) found possibly due to methodologic.077-.555 (.436) .058-.080 (.605) .217-.158) .(Kraus et al.339 (.063-.092) .201 (.073 (.144 (.340 (.084 (.079) . 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.197) .381) .199 (.237) .465) .347 (.152-.167-.333-.333 (.080 (.056-.333 (.353 (.064-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.071 (.333 (.359 (.107-.091) .410-. population from the National Health and Nutrition Examination Survey.329-.116 (.067 (.057-.071) .072 (.484) .299 (.054-.154) .200-.124-.074) .301) .208-.083) .224) .205-.071) .158) .146) .059 (.139) .165) .306) .253 (.S.459) . 1997). Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.093-.

Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Paschal DC. Int Arch Occup Environ Health 1997. Occup Environ Med 2001. References Bachthaler M. Morrow JC. tellurium.Metals blood. Link J. urine. Angerer J. lead. [online] 2003. 238 Fourth National Report on Human Exposure to Environmental Chemicals .htm.58(10):631-634. National Center for Environmental Health. Lenhart M. Paetzel C. Third National Report on Human Exposure to Environmental Chemicals.62:380-384. Schaller KH. Pietra R. Manke C. Seghizzi P. Weber A. Atlanta (GA). Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Nicolaou G. Schramel P. 2005.69(3):219-223. 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. Kraus T. J Trace Elem Electrolytes Health Dis 1987. Sabioni E. Nevada Exposure Asssessment. Jackson RJ. Zobelein P. Ting BG. et al.. 4/15/09 Centers for Disease Control and Prevention. Centers for Disease Control and Prevention. bismuth. Sampson EJ. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Cancer Clusters.cdc. Churchill County (Fallon). 2004). palladium.(2):73-77. platinum. Trace metals in urine of United States residents: reference range concentrations.76(1):53-59. Environ Res 1998. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. cadmium. Schramel P. Cassina G. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Angerer J. mercury. Wendler I. and hair (Bachthaler et al. Catheter Cardiovasc Interv 2004. The determination of metals (antimony. Feuerbach S. Mosconi G. thallium. Pirkle JL. Available at URL: http://www.gov/nceh/clusters/Fallon/study.

009 (.014 (.020-.036 (.009) .020-.006 (.010) .011) .009) .008 (.013 (.010) .027 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.034-.007-.009) .021-.029-.017 (.008-.037) .007-.006-.072) .009 (.007) .039) .017-.006-.005-.035-.011) .020) . and 03-04 are 0.027) .013 (.008-.006 (.022-.047 (.012 (.051) .010) .008 (.010) .018) .011-.023-. and 234U.040-.007) .013) 90th .008-.009 (.050) .054) .055 (.017-. human exposure occurs primarily by inhaling dust and other small particles.009) .114 (.016) .012 (.011-.009-.038) .S.021) . 0.009-.018) .007) . Uranium has many commercial uses.024-.007-.037) .023-.022-.012-.006-.008) .024 (.011-. interval) .033-.069) .007-.009) .021-.031 (.017 (.010 (.039-.008 (.008 (.035) .046 (.016-.046 (.011 (.023-.052 (.008-.028 (.026 (.031 (.045) .72%).019-.158) .021 (. or processing.Metals Uranium CAS No.008-.011-.011) .037) .008) .008 (.018) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.009) .016) .015 (.050) .012) .009-.019-.017) .007-.127) .012-.046 (.036) .009 (.027 (.016-.010-.016-.062) .017) .025-.010) .015 (. milling.009-.024-.007-.033 (.023) .008 (.027 (.009-.010-.033) .014 (.008 (.027) .010 (.046) .019-.010) .014 (.007 (.007 (. see Data Analysis section) for Survey years 99-00.036-.008 (.020-. in some ceramics.007 (.020) .006-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.026-.066) .019 (.008 (.007 (.007-.006-. Variable concentrations of uranium occur naturally in drinking water sources.008 (.034-.012-.037-.004.015) .008 (.033 (.011-.018 (.007 (.028-.005-.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 .009) .008-.026 (. including nuclear weapons.043 (.012) .009 (.041 (.017-. 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.023) .015) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.005-.016) .007 (.031 (.022-.027-.020-.008 (.067) .009 (.010 (.036 (.026) .008-.013 (.049) .010 (.088) .017) .005-.019-.010) .023) .009) .044 (.011-.007 (.032 (.011) .023-.007) .064 (.006-.009) .018) .015 (.006-.007) 75th .012-.010) * .279) .015 (.005-.006 (.007-.039) .042) .026) 95th .017-.009-. respectively.026 (.011) .030-.009) Selected percentiles ( 95% confidence interval) 50th .006-.006-.008 (. In workplaces that involve uranium mining.011) .007-.007-.045) .007-.009) .006-.007-.013 (.007-.040) .021 (.031 (.013) .016) .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 .053) .040 (.022) .035) .008 (.020 (.009) .017) .016 (.009-.041 (. 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. and 0.048 (.027-.010) . and as an aid in electron microscopy and photography. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).020-.008 (.054-.067) . nuclear fuel. Thus.007-.031 (.027-.013 (. Since the 1990’s.014 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .027 (.018-.065) . 235U (about 0.010-.017-. 01-02.056) .030 (.012 (.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 .006-.007 (.046 (.007-.009) * .009 (. population from the National Health and Nutrition Examination Survey.009 (.009-.013-.040) .026) .007 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.015-.008) .010) * .049) .021) .014 (.007 (.038 (.073) .029-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.006-.046-.013 (.037 (.030 (.027) .010 (.040 (.006 (.021) .036-.040-.037) Total .065) .021 (.013-.008) .010-.016) .005.026-.023 (.009-.030) .028 (.008) .012-.012 (.010-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.024-.023 (.028-.014 (.012) .013-.007 (.030 (.017-.042 (.036) .011 (.007-.016) .007-.053 (.009) .012-.012) .011) .054) .007) .008 (.012 (.004.029 (.048) .056) .043) .007-.027) .063) .031-.018 (.009) .009 (.009-.028 (.009 (.008-.011-.006-.022 (.010-.008 (.017) .013 (.060 (.012 (.023 (.034) .

about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.010) * .012 (.019) .008-.029) .028) .008-.007 (.007 (.007 (.013 (.034 (.051 (.025-.010 (.005-.034-.019 (. Depending upon the specific compound and solubility.033 (.074) .024) .056) .009) .025 (.012) .020-.009) .270) .008 (.010-.026 (.006-.012 (.028 (.007 (. population from the National Health and Nutrition Examination Survey. interval) .015 (.018-.010-.050) .005 (.024-.014-.006) . 240 Fourth National Report on Human Exposure to Environmental Chemicals . where limited absorption occurs (less than 5%).009) .018-.010-.039) .006 (.013 (.030 (.017-.039) .017) .025 (..010-. 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.021) .028 (.008 (.006 (.011) * .030-. Uranium is eliminated in feces and urine.009) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.006-.013 (.006) . 2005). After exposure to soluble uranium salts.014-.007-.006) .024-.008) .020) .027-.010) .051) .007 (.022 (.146) .017-.011) .011-.027) .005-.017-.009) . Health effects from uranium exposure result from chemical toxicity to the kidney.012 (.015) .007 (.050) .007 (.020-.026-.015-.034) .015) .024) .009) . the shrapnel acts as a source of chronic.007 (.063) .024) .006) .007-.042) .028-.012-.019 (.006-.007 (.1%-6% of an ingested dose may be absorbed.031-.029 (.048) . 1992).043 (.019) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.027 (.005-.006 (.006) .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 .007 (.006 (.013 (.006-.011-.058) .016-.030 (.Metals impact.006-. which represents distribution and excretion.019 (.010-.030 (.005-.015) .008 (.008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .021 (.040 (. with much slower elimination from bone.006 (.039) .051) .010-.009-.032) .013 (.008 (.014-.018-.011-.006-.010) .013-.007 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.020 (.011) .034-.007 (.018-.026 (.021-.010-.014) .021 (. 0.030-.019-.029) .006-.008-.008 (.012 (.020 (.006-.008-.009-.018) .006-.010 (.014 (.023-.010) .054) .033) .018 (.006-.009) .035 (.005 (.007) .009 (.017 (.016-.011 (.012 (. After long term or repeated exposure.008) .025) 95th .006-.006-.025-.029 (.029) . After inhalation. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.009-.042-.026) .006-.010) .019-.027 (.022 (.008 (.009) .007-.018-.016) .019-.033 (. kidneys.013) .013 (.100 (.027) .009) .008) .006-. liver.045 (.016 (.016) .077) .051) .005-.005-. Radiation risks from exposure to natural uranium are very low.033 (.013) .028) .007-.041) .024 (.024 (. Inhaled uranium-containing particles are retained in the lungs.011-.067) .009) .007-.006-.029) .009-. which can occur occasionally from high occupational exposure.034 (.010 (.022 (.009) .031 (.010-.015-.013 (.019-.009 (.037 (.011-. 2003).008 (.016) . low level exposure.007 (.008) .015) .006-.010 (.007 (.035 (.006-.007-.015 (.006-.015-.013 (.015 (.042) .017-.004-.008 (.007 (.008-.010) .006-.025-.011) .011-.048) .053) .010-.013 (.010-.024) .008) .005 (.009) Selected percentiles ( 95% confidence interval) 50th .039) Total .009-.007) .034 (.030) .011-.008) .S.009 (.028) .007-.029 (.024 (.012) .006-.027-.007 (.015 (.009 (.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.011-.006-.008-.014) 90th .008) .080) .020-.022-..032) .012-.044) .020-.015-.050 (.010-.007 (.027 (.026 (.053) .004-.014 (.017) .024-.007-.007 (.008 (.016) .013 (.017 (.010) .005-.012) .008) .009) * .007 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.008 (.033 (.008) .016-.016-.010 (.007 (.011-.027-.008) .007 (.020 (.012 (.007-..017) .059 (.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 .007) .058) .021 (.022) .014) .016) .047) .008) 75th .016) .011 (.019-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006 (.006-.012 (.022-.006-.034 (.034 (.016) .027-.013) .009-.009 (.024) .028) .005 (.006-. In cases of retained DU shrapnel.007-.014) .061) .022-.021 (.030) .016) .025-.015-.008) .

. Pillai KC.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.S. Fourth National Report on Human Exposure to Environmental Chemicals 241 . the median urinary concentration was 0. eds. 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. 2000). Dietz LA. pp. Zimmerman I. Hamilton MM. environmental levels) and health effects is available from ATSDR at: http://www. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 41 (1). EPA. Ejnik JW. McDiarmid M. (May et al.65 μg/L). 2006.. Atlanta (GA). Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Breitenstein BD. population.1992. Pullat VR. Centers for Disease Control and Prevention (CDC). 1994. In 17 U.. during.S. 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. The U. ingestion. Kent (England): Nuclear Technology Publishing. Sci Total Environ 1991.107:143-157. Komaromy-Hiller et al.. Horan P..S. 2006)..S. but in whom no shrapnel was embedded.1996. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Muggenburg BA. Tolmachev et al. Metivier H. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. in that the levels were below their respective detection limits (Byrne et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. urinary levels of uranium were as high as 9.cdc.. the median urinary uranium concentration was 2. the geometric mean urinary uranium concentration was 0. and no consistent effects on multiple endpoints of kidney function were found. Karpas et al. 1978). Volf V. 2005. 2002. McDiarmid et al. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Radiation protection dosimetry.. Boyd P. 2004). and 2003-2004 (Dang et al. Mil Med 2003.61 μg/g creatinine. Durakovic A.011 μg/L (McDiarmid et al.gov/ toxpro2. Hamilton et al..55 μg/L (median 0. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Vol. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Squibb K. Benedik L. Six workers in a depleted uranium program showed concentrations of 0. had a mean urinary uranium concentration of 0. Galletti... A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. IARC and NTP have no ratings for uranium human carcinogenicity.168(8):600-605. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.. 28 soldiers who may have been exposed to DU by inhalation. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.. 2004). 2006). 2003.. 2006). A cohort of 46 U. NRC. Drinking water and other environmental standards have been established by U.S. 1991. et al. In the same study.078 μg/L (ranging up to 5.62:562-566.78:143-146. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. 2001-2002. Third National Report on Human Exposure to Environmental Chemicals. Health Phys 1992. In a study of 105 persons exposed to natural uranium in well water.066 μg/g creatinine (Gwiazda et al.html. Carmichael AJ. 1-49. Health Phys 2000. In: Gerber GB.S.e. 1992. with emphasis on quality control. 2000). Byrne AR... 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. Information about external exposure (i. respectively. although slightly increased during and after deployment. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 2002).. Stradling GN. 2006). Dang HS.110 to 45 μg/L (Ejnik et al. or wound contamination. 2004).atsdr. References Bhattacharyya MH. Uranium content of blood. (Kurttio et al. 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. Thomas RG.162 μg/L) (Orloff et al. 2004). soldiers evaluated before..

Hamilton EI. Human exposure to uranium in groundwater. Scott K. Salonen L. U. Costa R. Int Arch Occup Environ Health 2006. Health Phys 2003. Auvinen A. Health Phys 1996. Kuwabara J. Comparison of representative ranges based on U. McDiarmid MA. et al. Environ Health Perspect 2002. Komulainen H. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Ejnik J. Cordero S. Biokinetic modeling of uranium in man after injection and ingestion. Oliver M.158:165-190.67(8-10):697-714. Hollriegl V. Review of elements in blood. Military deployment human exposure assessment: urine total and isotopic uranium sampling results.86:12-18. et al.81:45-51. D’Annibale L. Sampson EJ. Jackson RJ. Oberbroekling KJ. Van der Venne MT. Howerton K. Jarrett JM.87:51-56. Am J Kidney Dis 2006. Radiat Environ Biophys 2005. Squibb K.Metals Galletti M. Inductively coupled plasma mass spectrometry as a simple. Kalinsky V.47(6):972-982. et al. Auvinen A. Paretzke HG. VI. Uranium and thorium in urine of United States residents: reference range concentrations. Charp P. Kidney toxicity of ingested uranium from drinking water. et al. Komaromy-Hiller G. McDiarmid MA. Biologic monitoring for urinary uranium in Gulf War I veterans. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Tolmachev S. Li WB. Makelainen I. Ash KO. Heller J. Pekkanen J. Roiz J. Karpas Z.296(1-2):71-90. Paschal DC. U. Noguchi H. Environ Res 1999. Renal effects of uranium in drinking water.S. Ough EA. Kane R. Karpas Z.85:228-235. Hancock RG. McDiarmid M. Wilson PD.91(2):144-153. Sci Total Environ 1994.22–Bioassay at uranium mills. Health Phys 2006. Health Phys 2004. Harmionen A. Squibb K. Smith D. July 1978. Ting BG. Oeh U. Kurttio P. Bennett LG. 242 Fourth National Report on Human Exposure to Environmental Chemicals .S. Andrews WS.S.71(6):879-85. Wahl W. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Orloff KG. et al. Health Phys 2004. Sabbioni E. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.44:29-40. Nuclear Regulatory Commission (NRC) Guide 8. Saha H. May LM. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Shelly T. Kurttio P. Lorber A. Marino R. rapid. Gwiazda RH. patient population and literature reference intervals for urinary trace elements. Environ Res 2004. Katorza E. Uranium daily intake and urinary excretion: a preliminary study in Italy. Gucer P. Mistry K. Marko R. Salonen L. Cremisini C. Halicz L. et al. Element reference values in tissues from inhabitants of the European community. Roth P.110(4):337-342.94:319-326.79(1):11-21.82(4): 527-532. Lewis BM.S. NRC). Engelhardt SM. Washington (DC): NRC. J Toxicol Environ Health A 2004. Pirkle JL. Pinto V. Health Phys 2002. Nuclear Regulatory Commission (U. Clin Chim Acta 2000. concentration and daily excretion of uranium in urine of Japanese. Englehardt SA. Metcalf S. Saha H.

90 (5. and electroplating.16) 3.89-3.20 (6.45-4.11) 4.60-7.0 (8.80 (6.10-4.22-5.40 (4.18-3.90-11.29-3.0 (9.40) 6.90-3.40-7.00-6.66) 3.0) 11.0) 10. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0 (9.90 (4.50-4.0) 13.81-16.g.90-11. 2002).30 (2.70 (3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.80-4.40-5.22 (2. fabric dyeing.0 (8.70-9.49-3.20 (2.0) 13.90-9. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.88) 3.00-5.40) 3.0) 8.0) 11.00) 3.10) 5. 2005).51 (3. It is normally found and produced as the anion of a sodium.51 (3.20) 3.0-17.0) 14. Drinking water.65) 3.80) 75th 6.40 (5.0 (9.0 (8.70-3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0 (12.10-12.20-12.0) 13.10 (6.05. lettuce) can be the main sources of intake for humans (FDA.0 (10.20 (5.20-4.0 (11.60) 5.10-11.0) 13.50-3.10 (7.S. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.70 (3.80 (3.0) 9.30-17.70) 3.50) 5.40-6.0 (11.26 (2.70-6.40) 3.10-7. Survey years 01-02 03-04 Geometric mean (95% conf. 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.46) 3.30 (5.81) Selected percentiles ( 95% confidence interval) 50th 3.0 (8.60 (7.0-23.31) 2.80-6.20-4.S.0-18.10) 12.0) 95th 14. milk.0) 11.35 (3.0) 10.30-6.11) 3.76 (3. In addition.00-6.75-3. and reducing agents.0) 9.0) 15.60 (4.19-4.05 (2. Other manufactured uses include fireworks.0-17.50-11.0 (12.60) 8.0 (11.40 (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 3.20-11.80 (7.44-4. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0-15.80 (3.30) 6.50) 5.03) 3.40) 4.87-3. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (11.80) 3.68) 4. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.76) 4.00) 7.0) 15.5 hours and has a small estimated volume of distribution (Crump and Gibbs.30 (2.30-7.60-6.90 (2.0-19.70 (3.80-15.0) 14.0-14.0-17.75 (3.50) 3. 2005).56) 3.20 (4.0 (11.20 (4.93-3.0-15.90) 5.0) 8.0) 13.20-3.EPA.0-17.50-4.20 (8.20 (7.80-8. potassium.10) 3.0-18..90) 6.0) 9.40 (3.50 (8.0) 9.0 (11.0 (12.0 (11.S.0 (9.80-12.54 (3.90-10.40 (3.50-7.74-3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.67-5.01 (2.10 (6.30-7.30) 6. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al. 2007).50 (5.0 (9.93 (4. leather tanning.00) 4.0-17.40) 3.90 (5.10) 3.0-17. matches.05 and 0.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.00) 3.50) 6.50 (3.70-12.90 (3.60) 3.07-4. and limited applications in pharmaceutics.0 (12.70-3. but has strong oxidant properties in the presence of concentrated acids. Perchlorate was added to the U.0 (11. or ammonium salt.96 (3.0-20. interval) 3.21 (2.40-11.10) 5.0-18. laboratory analysis.0) 12.62 (3.80-4.0) 10.0) 9.12) 3.19 (3.0 (8.30 (5.10 (5.0 (11.40) 2.0 (9.90-12.40-13.47-4.90 (5.32 (3.60 (4.20) 4.90-6.0) 14.30-19. Perchlorate is stable under most environmental and physiological conditions.80) 12.93-4. 1998).0) 708 617 681 652 1228 1092 Limit of detection (LOD.20) 7. population from the National Health and Nutrition Examination Survey.40) 90th 10.39-4.90-9.0) 13..40-4.Perchlorate Perchlorate (Urbansky.0) 13.0) 13.90-3.02 (3.0) 19.84) 14.40 (5.0) 16.0 (11.00) 5. certain catalytic metals.0 (13.70-5.0-29.0) 9.40-4.08-3.09) 3. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.10-11.40 (4.79 (2.80) 7. and certain plants with high water content (e.70-7.38) 5.50) 11.40 (8.70-11.20 (2.10 (2. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0 (9.

4) 8..37 (4. population from the National Health and Nutrition Examination Survey.20 (7.40) 3.60) 3.61 (5.83 (5.20-9.60-3.04-3.14 (2.93-5.. Lamm and Doemland.86) 4.60-5.10 (4.59) 3.64-3.30 (5.22 (2. 2002.S.26 (3.30) 75th 5. 2007).87 (5.0-19.60-8.20-3. However.90 (4. Many factors may be important in consideration of perchlorate action on the thyroid: dose.4) 13.10 (6.0 (8.07 (2.87-3.S.87 (7.09) 3.33-12.72 (3.90-9.80 (4. thiocyanate.09 (7.1 (11.00 (6.00-11.51-4.0) 12.02-4.30-5.0) 13.30) 90th 9. chronicity of exposure.82 (5.35 (4.0) 10.40 (4.60) 10.10) 13.30) 3.05 (4.1-13.0-14. 2006.75) 3.S..1-14.99 (5.00 (2. in a representative sample of U.56-3.10 (2.0 (9.96) 2.00-2. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al. 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.10 (1.S.80-3.56 (3. nitrate.39 (3. 2003.25) 5.61-10.67) 5.50 (3.80) Selected percentiles ( 95% confidence interval) 50th 3.90-20.99-3.90-3.4 (11.6-17.0 (11.0-44. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures.76-3. 2005.0) 9. U.60 (3.39-4. dietary iodine intake.8 (11. 2005.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.25) 5.33-6.0) 4. levels.20) 3.10) 3.84) 2.50 (6.61-5.70 (2.54 (2.10-3.1-16.3) 8.g.40 (7.30-5.02) 3.0) 7.70-3.95 (2. 2005).. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.40) 5.. Greer et al.98) 3.30 (6. Li et al.0-14.46-13.1 (8. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.90-2.3) 11. 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.19-6.0) 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 3.60-6.0) 11. interval) 3.40-10.80-3.34-3.58) 2.EPA.81-3. NAS.12 (6.30) 5.20 (2.S.36 (8.52-9.24-2.20-10.64) 5..20 (3.93-7.10 (4.24 (4. although iodine intake was higher than U.87) 2.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.20) 8.50) 9.2) 8.12-2.4 (8.22-4.60-11.0 (10.60-5.5 (13.21 (2..4 (11.20-4.51 (3.0 (9. 2005).16-3.00) 3.0 (11.40 (3.45-2.7 (11. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.70-4.50) 2.50) 2.70) 10.90 (7.0 (9.18-3.2) 8.3 (10. 2000).0 (11.10) 6.90 (2.66) 3.89 (2. menopausal status. 2002.43) 6. 2002).Perchlorate inhibition (RUI).0) 12.60-15.08) 3.44) 3.93-8.45) 3.22-6.00 (4.20-3.0-17.00-3. Steinmaus et al.70) 2. levels and sufficient in most participants (Tellez et al.76 (3.80 (7.0) 9. age.26) 4.3-14.50) 95th 12.40) 17.0) 12.08 (3.70 (2.0) 13.50-9.10) 4.46 (3..87) 7.33 (7.1) 8.90 (2.44-6.35) 3.47) 2. medications).S.50-3.37-13.0) 14.60-8.19-10.77 (3. perchlorate is negative in most genotoxic assays (U.54 (3.35 (2.91) 4. gender.0) 6.29-6.80 (7.03 (2.50-5.74) 7.. 2005). 2001.29) 2. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.70-15.S.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3. Also.70 (4.93-5. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.90-11.00) 9. 1999.60-11.15-12.53 (2. and the presence of other substances known to affect thyroid function (e.20 (4.25) 5.04-3.41-9. up to 68% RUI has been demonstrated.22-4.60) 8.71 (5.0) 12.30-10.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .10-7.73) 3.4-16.42 (3.20 (6.5) 8.25 (3. Survey years 01-02 03-04 Geometric mean (95% conf.90-15. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.0 (8. During gestation and infancy. Lawrence et al.93) 3.32) 5.1-22.30 (3.50) 6. women with urinary levels of iodine less than 100 micrograms per day.90) 5.6) 20..89-3.40 (3.00) 4.39) 2. In the U.70-5.52 (8.6) 12. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.4 (10.97-5.50) 5.46-4.3) 12.EPA.

Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Erratum in: J Occup Environ Med 2004. Lawrence J. Lamm SH. Analysis of relative source contributions to the food chain. Goodman G. National Research Council of the National Academies. most of the population is considered to be below the U. Also. Lamm SH. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Lamm SH. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. thiocyanate.114(12):1865-1871. Valentin-Blasini L. Mauldin JP. Greer SE. et al. 2005.17(4):400-407. Blount BC. Food and Drug Administration (FDA). Deyhle GM. et al. Erratum in: Environ Health Perspect 2005. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Braverman LE. Crump KS. et al. The effect of perchlorate. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.S. Perchlorate Exposure of the US Population. Thyroid 2001. Osterloh JD.113(8):10011008. J Occup Environ Med 2000.42(2):200-205. et al. and nitrate on thyroid function in workers exposed to perchlorate long-term. Neonatal thyroxine level and perchlorate in drinking water. Li FX. May 2007. Health Implications of Perchlorate Ingestion. Jackson WA. Caldwell KL. 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. Lamm S. References Blount BC. CFSAN/Office of Plant & Dairy Foods. Osterloh JD. Braverman LE. Thyroid 2000. Pirkle JL. 2005). Byrd D. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.. 2005).10(8):659-663. Lau EC. population. Skeels MR. Li Z. J Expo Sci Environ Epidemiol 2007. Pino S. (2007) analyzed a subsample of NHANES 2001-2002 which demonstrated detectable perchlorate in all urinary samples and showed slightly higher levels in children as compared to adults. Daaboul JJ. J Occup Environ Med 2003.41(5):409-411.EPA at: http://www. Cross M. Magnani B. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. He X.html and from ATSDR at: http://www. Perchlorate in the United States.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. epa. Sesser DE.htm. 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. Braverman LE. Dyke JV. Primary congenital hypothyroidism. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.115(9):1333-1338. Pino S. Chacon PM.gov/toxpro2.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Steinmaus C. Landingham CB. Rutherford GW. Miller MD. 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. Environ Health Perspect 2002. 2007). 2001-2002.40(21):6608-6614. Page Last Updated: 05/28/2009.. The effect of short-term low-dose perchlorate on various aspects of thyroid function. 6/2/09 Greer MA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Clin Endocrinol Metab 2005. National Academy of Sciences (NAS).S.fda.11(3):295. Kelsh MA. Environ Health Perspect 2005.110(9):927-937. Howd R. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Pirkle JL.atsdr. Benchmark calculations for perchlorate from three human cohorts. Pleus RC. Tellez RT.113(11):A732.45(10):1116-1127. Environ Sci Technol 2006.S. Available at URL: http://www. and environmental perchlorate exposure among residents of a Southern California community. newborn thyroid function. Richman K. Kirk AB.46(5):509. Doemland M. Blount et al. Abarca CR. Environ Health Perspect 2006.90(2):700-706. EPA reference dose (Blount et al. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Lawrence JE. Additional information about exposure and health effects is available from the U.gov/safewater/ccl/perchlorate/perchlorate. Barnard JC. Gibbs JP. Environ Health Perspect 2007. Washington (DC): National Academy Press.html. Dasgupta PK.. Buffler PA. Valentin-Blasini L.cdc. Blount BC. Crump KS. Low dose perchlorate (3 mg daily) and thyroid function.

gov/iris/quickview.Perchlorate pregnancy and the neonatal period.S. Environmental Protection Agency (U.9(3):187-192. Thyroid 2005.S. Doc. Environmental Protection Agency (U.epa. Perchlorate as an environmental contaminant. No. Integrated Risk Information System (IRIS). Perchlorate. cfm?substance_nmbr=1007. 1988.S. Revised 2/11/05. EPA). EPA).S. U. Drinking Water Contaminant Candidate List. Environ Sci Pollut Res Int 2002.15(9):963-975. Urbansky TF. 246 Fourth National Report on Human Exposure to Environmental Chemicals . EPA/600/F-98/002 Washington (DC).1/15/06 U. Available from URL: http://cfpub.

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

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

50) .900 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. However. 2001..600 (. Fei et al.400-1.. 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 (.500 (. Olsen et al. At high but non-toxic maternal doses of PFOS. Fourth National Report on Human Exposure to Environmental Chemicals 249 .400-1.400) .500-1. 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. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. 2004. 2003a.10) . Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.800 (. and perfluorononanoic acid (PFNA) are detectable in a high percentage of the participants and PFOS levels are generally 3-10 times higher than PFOA levels (Calafat et al.400 (<LOD-. monkeys. 2004). PFOS. 2007b. 2007. 2007).80) 640 1454 03-04 03-04 * * < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0. 2005).700 (. 2004). Thibodeaux et al. reproductive. thyroidal). Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. the median PFCs values tend to be roughly similar in these age categories (Olsen et al..900 (. PFOA. 2003.500 (. Cook et al. 2003).3. Lau et al.108 times higher than background serum levels in humans (Butenoff et al. At doses causing maternal toxicity.500) .00) . Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U..00) .500-1. 2004b)..500-1. In comparing three separate reports on adults..800) 1. 2003a. U. 2007a. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.800 (.300 (<LOD-. 2003a. and changes in thyroid hormone concentrations (Grasty et al. elderly and children.. < LOD means less than the limit of detection.40) ..S.. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. hepatotoxicity.S. In such studies. development in offspring was stunted and hypothyroxinemia was observed.400-1.20) . EPA. and humans.800) 1. perfluorohexanesulfonate (PFHxS). Harada et al..600 (.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al..400-1...500) 90th . interval) Selected percentiles ( 95% confidence interval) Sample 95th .400-. 2005).500) . 2004a.300 (<LOD-. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.500 (<LOD-1..500-1. 2007a..00) . 2004. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. and there was no clear evidence of excess all-cause or diseasespecific mortality. 2003). Olsen et al. EPA. Survey Geometric mean (95% conf.600-2.00 (.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 . PFOA. 2003).300 (<LOD-. 2003a).500-.600 (.400 (<LOD-.. 2007b).500) .400 (<LOD-..300-1. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. the potential to estimate risks to humans from animal doses is uncertain.10) * 03-04 03-04 * * < LOD < LOD < LOD . Animal studies of PFOS have demonstrated weight loss. PFOS. possibly related to lung immaturity (Lau et al.. 2003..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 1992. 2003. which may vary for some chemicals by year and by individual sample.10 (. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. population. population from the National Health and Nutrition Examination Survey.80) 485 538 962 Limit of detection (LOD.900 (.S..400-. 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.400-1.800 (. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. Kennedy et al.500) .500-3. 1999.S.700) . Olsen et al. U. developmental and teratogenic effects were demonstrated in offspring. 2003a).10) .

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

S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) 485 538 962 Limit of detection (LOD.0.300 (<LOD-. < LOD means less than the limit of detection.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .500 (<LOD-.S.3.600) < LOD . which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 251 . population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 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.500-.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (<LOD-.400 (.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 . Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900) < LOD .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.300-.400 (<LOD-.600 (. see Data Analysis section) for Survey year 03-04 is 1. < LOD means less than the limit of detection.400) . see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.

14 (.26) 2.51) 1.80) 5.30) 3.50-10.70-6.30) .03) 1.50 (4.92 (1.30 (1.20-1.10 (1.700-1.966 (.0) 8.42 (1.40) 640 1454 03-04 03-04 1. population from the National Health and Nutrition Examination Survey.05-2.S.10) 4.60 (1.70-2.27) 1.90) 1.80-7.50 (1.50 (2.40) 640 1454 03-04 03-04 2.80) 3.10) 5.30-6.60-8.60) 1.900-1.20 (6.30) 03-04 03-04 .6) 7.800-1.900-1.04) .80-6.44 (2.40 (1.10) 6.10 (.70) 2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.60-2.10) 1.08) 2.86 (1.80) 90th 2.54) .20) 03-04 03-04 2.73-2.70-2. population from the National Health and Nutrition Examination Survey.900) 1.30 (6.40) 1.90) 3.93 (1. interval) 1.00 (1.10-9.30 (7.40) 2.91) 2.3.00-1.80-12.70) 2.10) 1.834-1.60-4.90) 8.20-1.816-1.90) 90th 5.20 (1.00) 1.00-6.20-3.30 (1.00 (2.50 (4.60) 2.00-7.40) 1.689 (.80-2.70) 3.900 (.50 (1.80-3.67-2.30) 3.10-9.00 (5.30-9.50-6.16) .90-2.40 (1.835-1.00 (.20) .90-19.10) 75th 1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) 485 538 962 Limit of detection (LOD.17-1.50 (1.60-2. see Data Analysis section) for Survey year 03-04 is 0.600-.20 (1.10) 1053 1041 03-04 03-04 03-04 .12) .900-1. Survey Geometric mean (95% conf.5) 5.10 (4.S.60) 3.80-7.56-1.80) 4.30 (2.50) 2.800 (.30 (2.60 (6.60-3.1.60) 9.20 (1.20 (6.90 (4.00) 3.00) 2.721-1.40-3.809) 1.30 (1.984 (.77-2.90 (2.20-1.700 (.10 (.50 (1.60-4.10 (.00 (.70) 13.861 (.60-2. 252 Fourth National Report on Human Exposure to Environmental Chemicals .00 (1.90 (1.70 (1.10 (4.70-7.90 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.20) 2.90) 1.80 (4.50) 6.01 (1.60-7.50 (6.826-1.00-8.60 (1.80-4.0) 1053 1041 03-04 03-04 03-04 1.09 (.80-3.90) 1.3 (9.40-1.62-2.1) 485 538 962 Limit of detection (LOD.40-1.90 (1.00) 1. see Data Analysis section) for Survey year 03-04 is 0.20) 1.80-4.912-1.80-8.80) 1.00-1.852 (.40) 4.50-6. interval) .900-1.30 (1.72 (1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.20 (1.40 (1.900-1.70-5.70 (2.40 (1.20) 1.30-2.20-1.30 (3.00 (1.5) 8.40 (2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.10) 75th 3.697-1.10) 6.80 (1.40) .60 (1.10) 8.10-5.70) 1.70-10.30) 3.10) 4.900-1.586-.80 (1.50 (6.963 (.30-12.60-3.50-3.900 (.00 (1.90 (1.80-8.50) 2.90 (4.17 (1.20-2.72) 1.90-10.87-2.70) 1.80-4.70) 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.

70-10.4) 20.21-3.20) 7.8) 32.5 (28.10) 5.40) 3.8-35.30-11.2 (21.10 (3.50-13.7-53.0) 43.6 (44.6) 18.8-78.47-4.20-5.0) 90th 41.70 (3.30) 6.4-17. population from the National Health and Nutrition Examination Survey.5) 1053 1041 03-04 03-04 03-04 14.84-3.20) 4.1-24.6) 21.9-19.7 (43.20 (4.7) 39.9 (17.10-3.6) 7.3-22.90 (7.35) 3.5) 32.65-4.50 (3. interval) 3.1 (19.80 (7.7 (7.79) 4.9-38.50) 4. Survey Geometric mean (95% conf.60) 03-04 03-04 3.20) 5.4 (23.82) 4.0-66.2 (18.6 (35.6-50.99-3.2-57.8 (37.70-7.3 (28.6) 42.9) 9.60 (6.1.6-45.1-35.70) 3.30-6.0) 03-04 03-04 19.S.4 (28.60 (3.7 (35.4 (17.40-6.2 (27. see Data Analysis section) for Survey year 03-04 is 0.2) 45.1-33.7 (13.18 (3.11 (2.00 (5.6-24.30) 7.80) 8.40-10.70 (5.80 (6.0-16.60 (5.7-23.5-33.4-25.5) 9.40) 75th 5.1-36.53) 3.9) 22.60-6.70-5.1) 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 4.40-14.00 (5.9) 22.90-12.67-4.9 (22.7-69.40-6.8-81.0) 21.6 (19.2) 30.9) 27.20-4.3-61.00 (3.40 (4.50-4.89 (3.50 (4.30-5.5) 7.8-30.10 (6. Survey Geometric mean (95% conf.3) 28.0) 21.60-13.60 (6.70-9.90-4. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60) 8.37 (2.20) 7.70 (5.70) 6.20-9.4-42.80 (5.9 (19.0) 485 538 962 Limit of detection (LOD.80 (6.1 (24. interval) 20.1) 57.96 (3.4) 21.7-49.2) 30.9-23.8-22.6) 1053 1041 03-04 03-04 03-04 3.1-52.0-20.3 (44.70-7.3) 485 538 962 Limit of detection (LOD.30-3.30 (5. population from the National Health and Nutrition Examination Survey.07-4.3 (35.27) 4.30 (3.20) 10.4) 640 1454 03-04 03-04 23.0) 23.90) 6.95 (3.0-70.40 (6.30 (3.7-33.60 (7.1) 15.8) 46.70) 4.8 (45.9 (13.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50) 7.5-23.91) 3.2) 640 1454 03-04 03-04 4.60-14.5-62.00) 3.4) 56.60-9.5) 8.6) 62.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.8-22.20 (4.40) 5.50-6.1 (23.90 (7.7-30.4 (19.10 (3.40) 90th 7.5) 57.8 (34.3 (17. see Data Analysis section) for Survey year 03-04 is 0.4) 75th 30.90-4.40-17.20) 5.30-8.4.2 (19.3) 41.5) 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. Fourth National Report on Human Exposure to Environmental Chemicals 253 .7 (43.6 (42.0 (20.4 (19.7 (35.85-4.80-4.0 (27.5 (28.6) 9.2-22.60 (4.90 (7.3 (35.1-25.2 (28.80-9.80-12.8-22.5-21.47 (4.8) 27.90 (5.6) 35.7 (19.5) 19.S.5) 18.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.2 (16.0) 36.3) 42.

500) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .300-. Survey Geometric mean (95% conf.300) . 254 Fourth National Report on Human Exposure to Environmental Chemicals .300) .S.500) 485 538 962 Limit of detection (LOD.300 (.300) .200 (<LOD-.500) < LOD 485 538 962 Limit of detection (LOD.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample. which may vary for some chemicals by year and by individual sample.200-.200-.300 (.200-.300-.300 (.300 (.200-.4.2.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (. < LOD means less than the limit of detection.300-.200-.300) .200-.300 (. population from the National Health and Nutrition Examination Survey.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 .400 (<LOD-.300 (.300 (.200-. see Data Analysis section) for Survey year 03-04 is 0. Survey Geometric mean (95% conf.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. population from the National Health and Nutrition Examination Survey.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.300 (.300) .S.300 (. see Data Analysis section) for Survey year 03-04 is 0.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.200-.500) .300) .300 (.200-.300) .300 (.300 (. < LOD means less than the limit of detection. 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 .500) .

00 (.300-2. Fourth National Report on Human Exposure to Environmental Chemicals 255 .500 (<LOD-.S.40) < LOD < LOD .80) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1. see Data Analysis section) for Survey year 03-04 is 0.20 (1.3.900-1.400 (<LOD-1.40) 1. see Data Analysis section) for Survey year 03-04 is 0.30 (1.10-1. < LOD means less than the limit of detection.700 (<LOD-.700) 90th 1.300 (<LOD-1.10 (.10-1.700 (<LOD-.800) .30 (1.10 (1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .30) .900-1.700 (<LOD-. which may vary for some chemicals by year and by individual sample.10 (.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .800) .10) .400 (<LOD-. < LOD means less than the limit of detection.900) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-1.900-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .600) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10) 1.90) .700 (<LOD-.70) 1.700) 1.10) * 03-04 03-04 * * < LOD < LOD .900-1.10-1.10) . population from the National Health and Nutrition Examination Survey.900 (<LOD-1.00-1.700 (<LOD-2.30) 1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .300 (<LOD-.900 (.600 (<LOD-1.60) 485 538 962 Limit of detection (LOD.600 (<LOD-.900-1.600 (<LOD-1.00 (.80) 1.30) 1.800 (<LOD-.6.900-1. which may vary for some chemicals by year and by individual sample.00 (.50 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900) 485 538 962 Limit of detection (LOD.50 (1.700 (<LOD-.900-1.700) 1.900) 1.20) 1.30 (1. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.700) .S.10 (.00) < LOD .700 (<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.600 (<LOD-1.00 (.10) 1. Survey Geometric mean (95% conf.

Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Holmstrom KE. et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Witter FR. Watanabe T.40:21282134. Toxicol Sci 2001. Toxicol Appl Pharmacol 1990. 2007b. Jarnberg U. et al. Needham LL. Occup Environ Med 2003. Peterson RE.68(6):465-471. Morikawa A. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Liu RC. Calafat AM. Kawashima Y.38(10):2857-2864. Grasty RC. Burris JM. Needham LL. Birth Defects Res B Dev Reprod Toxicol 2003. Moore RW. Evans TJ. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. O’Connor JC. Ye Y. Olsen J. Seacat AM.115(11):1670-1676. Koizumi A. Kannan K. Reidy JA. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Loganathan BG. Halden RU.41:2237-2242. Toxicol Appl Pharmacol 1995. Hekster FM. Frame SR. Dinglasan MJ. Gaylor DW. Corsolini S. Rodricks J. Kannan K. Keller JM. Cook JC. Chem Biol Interact 2000. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Kumar KS. Kuklenyik Z. Reidy JA. Aguilar-Villalobos M. Needham LL. O’Connor JC. Tully JS. Calafat AM. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Kuklenyik Z. Harada K. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000.60(10):722729. The toxicology of perfluorooctanoate. Olsen GW.Koizumi A.39(23):9057-9063.39(23):9101-9108. Needham LL. Biegel LB. Kamiyama S. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Inoue K. Mandel JS. Moore JA. Seneviratne HR. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. et al. Yun SH. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Saito N. Kannan K. Fei C. de Voogt P. Herbstman JB. Environ Sci Technol 2007a.104(2):322-333. Tully JS. Reidy JA. Cook JC. Caudill SP. Rogers JM. Tarone RE. Grey BE. Biegel LB. Bandai N. Rev Environ Contam Toxicol 2003. Butenhoff JL. Characterization of risk for general population exposure to perfluorooctanoate. and perfluorinated contaminants in livers of polar bears from Alaska. Kudo N. Wong LY. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth.113(2):209-217.39(3):363-380. and ex vivo studies. Cook JC. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. et al. Suzuki E.S.34(4):351-384.134(1):18-25. Environ Res 2005. Olsen GW. brominated. Saito N. Calafat AM. Taniyasu S. Hurtt ME. Kennedy GL Jr.38(17):4489-4495. Frame SR. Environ Sci Technol 2004. Laane RW. Hurtt ME.60(1):44-55. in vivo. Butenhoff JL.63:490496. Regul Toxicol Pharmacol 2004. Calafat AM.99(2):253-261. Environ Sci Technol 2005. Environ Health Perspect 2007. Environ Sci Technol 2005. Environ Sci Technol 2006a. Environ Health Perspect. Chlorinated. Olsen GW.115(11):1596-1602. Mandel JH. Hurtt ME. Wijeratna S. et al. Edwards EA. Guruge KS.Perfluorochemicals References Alexander BH.46(2):141-147. Arendt MD. Yoshinaga T. Chemosphere 2006b. Environ Sci Technol 2005. Environ Sci Technol 2004. Taniyasu S. Mandel JH. et al. The influence of time. Perkins RG. Day RD. Katakura M. Serum concentrations of 11 polyfluoroalkyl compounds in the U. McLaughlin JK. Reidy JA. Calafat AM. Yamashita N. Toxicol Appl Pharmacol 1992.7(4):371-377. et al.115(11):1677-1682. Crit Rev Toxicol 2004. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Fluorotelomer alcohol biodegradation yields poly. Yamashita N. Ingall GB.and perfluorinated acids. Perfluorinated chemicals in selected residents of the American continent. Bignert A. Mabury SA.1968--2003. Harada K. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Environ Health Perspect 2007. Apelberg BJ. Environmental and toxicity effects of perfluoroalkylated substances. Lau CS. Mohotti KM. J Environ Monit 2005. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Falandysz J.179:99-121. Inoue K. Bookstaff RC. Caudill SP.S. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Yoshinaga T.39(1):80-84. Kuklenyik Z. Polyfluoroalkyl chemicals in the U. Murray SM. Kuklenyik Z. J Occup Health 2004.124(2):119-132. Sasaki S. Fillmann G.

Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. van Belle G. Hansen KJ. Seacat AM. (Erratum in: Environ Health Perspect. Seymour C.111(16):1892-1901. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. et al. Petrick G. Kannan K. et al. Burris JM. Hansen KJ. Half-life of serum elimination of perfluoroo ctanesulfonate. et al. Buck RC. et al.epa. Washington. Butenhoff JL.. fish. et al.45(3):260-270. perfluorooctanoate andother fluorochemicals in human blood. Yamashita N. Olsen GW.) Tittlemier SA. fate and transport of perfluorocarboxylates. Olsen GW.74(2):369-381. (Erratum in: Toxicol Sci 2004. Burris JM. Ehresman DJ.68(1):249-264. et al. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Olsen GW. I: maternal and prenatal evaluations. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle.1177(2):183-190. Rogers JM. Butenhoff JL. 2007a. Environ Health Perspect 2003a. Helzlsouer KJ. Chemosphere 2007b. Lundberg JK. Lau C. J Occup Environ Med 2003b. fish. Olsen GW. Zobel LR. Grey BE.S. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Larson EB.26(1):47-51. Nesbit DJ. Chemosphere 2004a. Korzeniowski SH. Yamashita N. The developmental toxicity of perfluoroalkyl acids and their derivatives.51(8-12):658-668. Miller JP.perfluorohexanesulfonate. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts.Perfluorochemicals Kudo N.113(5):539-545. Peterson RE.gov/opptintr/pfoa/pfoara. Kannan K. Toxicol Sci 2003.111(16):1900) Olsen GW. Stanton ME. Gamo T. Horii Y. Rogers JM. Environ Sci Technol 2003. Environmental Protection Agency (U. and perfluorooctanoate in retired fluorochemical production workers. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Huang HY. A global survey of perfluorinated acids in oceans. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Butenhoff JL. Burris JM. Biochim Biophys Acta 1993. Butenhoff JL. Grey BE. Toxicol Appl Pharmacol 2004. Olsen GW. Thibodeaux JR. Rogers JM. Coordinate induction of acyl-CoA binding protein. Sources. and food items prepared in their packaging. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.40(1):32-44. U. Butenhoff JL. J Ag Food Chem 2007. Mandel JH.2(1):53-76. htm. Horii Y. Reagen WK. Church TR. Moisey J. 1/15/06 Vanden Heuvel JP. Taniyasu S. Environ Sci Technol 2006. Richards JH. Ellefson ME. Environ Health Perspect. Biol Pharm Bull 2003. Church TR. Toxicol Sci 2002. Kawashima Y.82(1):359. 2003. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. J Children’s Health 2004b. Bronson R.37(12):2634-2639. Butenhoff JL. Burris JM. Mar Pollut Bull 2005. Olsen GW. Froehlich JW. Prevedouros K. Environ Health Perspect 2005. Barbee BD.198(2):231-241. Burlew MM. Hanari N. Olsen GW.55:3203-3210.S. Thomford PJ. and humans from Japan. Hanson RG. II: postnatal evaluation. Hansen KJ. Seacat AM. Mair DC. Hansen KJ.41(9):799-806. J Occup Environ Med 1999.74(2):382-392. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. fast foods. Church TR. Hansen KJ. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Mandel JH. Thibodeaux JR.54(11):1599-1611. Available from URL: http://www. Historical comparison of perfluorooctanesulfonate. Lundberg JK. Hanson RG. Cousins IT.115(9):1298-1305. Pepper K. Cao XL et al. Case MT. Fourth National Report on Human Exposure to Environmental Chemicals 257 . birds. Taniyasu S. Lau C. Mandel JH.68:105–111. EPA). Mandel JH. Burris JM. Toxicol Sci 2003. Olsen GW. Ehresman DJ. 2003a. Sterchele PF.

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

18(12):10681074. 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. testicular atrophy. Environ Health Perspect 1997.. gender. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 .gov/toxpro2. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. 2006). In Staples CA (ed). Silva MJ.. Matthews HB.. Hoppin et al.. Herbert AR. Schroeder JL.gov/ toxprofiles/tp9. Drug Metab Rev 1989. 2000b. However. efficiency of intestinal absorption. variation also occurs in the same person during repetitive monitoring (Fromme et al. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. 2003.html. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. phthalates produced anti-androgenic effects by reducing testosterone production and. Scotter MJ. Albro PW and Lavenhar SR. Toxicological profile for di-n-butyl phthalate update [online]. van der Broek PH. dibutyl phthalate (DBP). 2002. 227-262.html. 2004). and race/ethnicity (Silva et al. Also.. Massey RC.. Hauser et al.html). pp.html. 2001. reducing estrogen production. Clark K.. Evaluation of a recombinant yeast cell estrogen screening assay.nih. 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. phthalates have been shown to induce peroxisomal proliferation in rodents. 105:734-742. interactions with macromolecules and species differences in metabolism of DEHP..Phthalates and metabolites have been tested.. Population estimates of concentrations of specific phthalate metabolites may differ by age. McDonnell DP. 1982). Springer. 2004.805:49-56.21:13-34. Jongeneelen FJ.. Environ Health Perspect 1982. atsdr. 2000c. NTP-CERHR. Part Q: Phthalate Esters. 2004. ovarian abnormalities in the female animals (Jarfelt et al. Calafat AM. Kessler et al. 2002). The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. but there are known species-related differences in the hydrolysis of diester phthalates. These differences may contribute to species-specific differences in toxicity (ATSDR. 1982. Silvapathasundaram S. Mackay D. 2001. 2001). 2005.e. and extent of metabolite conjugation to glucuronide (Albro et al. 2003.gov/ reports/index. and Sertoli cell abnormalities in the male animals and. Dave M. 2007. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 2005). Lovekamp-Swan and Davis. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Springall C.New York.. Toxicological profile for di(2-ethylhexyl)phthalate update [online].niehs. which may be a pathway to the development of liver toxicity and cancers in these animals. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Jordan S. 1986). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006). In animals. Food Addit Contam 2001. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al.. 2004. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Hauser et al. Vol. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. 2004. Cousins IT. Available at URL: http://www.45:19-25.atsdr. Dirven HA. 2007). Metabolism of di(2-ethylhexyl) phthalate.gov/toxprofiles/ tp135. Available at URL: http://www. at very high levels.cdc. McKee et al. Peck and Albro. Rhodes et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Pharmacokinetics. Information about external exposure (i.. Sauer MJ. 4/20/09 Albro PW.cdc.3.atsdr. The Handbook of Environmental Chemistry. 2002). 2000a. 1985. High doses of di2-ethylhexyl phthalate (DEHP). Corbett JT. 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. Castle L. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Anderson WA. J Chromatogr B 2004. Coldham NG. Connor C. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al... Assessment of critical exposure pathways.. at higher doses. Needham LL.cdc. Slakman AR.

niehs. Nielsen J.html. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Park S. Yoshimura M. Research Triangle Park (NC). Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals .25(2):293-302. 2000c [online]. Hagmar L. Lovekamp-Swan T.110(5):515-518. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hartle RW.niehs. Giwercman A. Am Ind Hyg Assoc J 1985. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Pan G. Hass U. et al. Mechanisms of phthalate ester toxicity in the female reproductive system. Research Triangle Park (NC). Research Triangle Park (NC).18(1):122. Available at URL: http://cerhr. Toxicol Appl Pharmacol 2004. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.112(17):1740]. Epidemiol 2005. Anal Bioanal Chem 2005. Silva MJ.nih. Leffers H. Yokoyama Y. Liss GM.nih. Environ Health Perspect 2004. Meeker JD. Koch HM. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Phthalate ester exposure—air levels and health of workers processing polyvinylchloride.Phthalates in human urine samples. Zhang S. gov/chemicals/dehp/dehp-eval. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro.195:142-153. 6/2/09 Okubo T. Brock JW. Research Triangle Park (NC). Wang P. Tsukino H. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Reynolds T. Kalita JC.nih. Jacobsen H. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Available at URL: http://cerhr. Duty SM.210:21-33. Calafat AM.111(2):139-145.html. Baird DD.46(11):643-647. Silva MJ.gov/chemicals/dehp/dehp-eval. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Parker MG. Albro PW. et al. Biol Pharm Bull 2003. Hoppin JA. Mortensen GK. 6/2/09 NTP-CERHR.11(5):381-387.nih. Bolte G. Brock JW.105:802-811. Jarfelt K. Reprod Toxicol 2004. Singh NP. Hauser R. Calafat AM. Environ Health Perspect 2003. Chen Z. Davis BJ. Duty S. Hanaoka T.gov/chemicals/ phthalates/dbp/dbp-eval. Ryan L. consumer milk. Silva MJ. Hauser R. Environ Health Perspect 1995. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate.106(1):23-26. Scand J Work Environ Health 1985. Skerfving S. Butala JH. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.19(4):505-515.niehs. The estrogenic activity of phthalate esters in vitro.382:10841092. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Park MG. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Kano K. 2000a [online]. Determination of phthalate monoesters in human milk. Csanády G. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. et al. Henttu P. Environ Health Perspect 2002. Ladefoged O.22(3):688-695. Akesson B. Andersson A-M. Stringer WT. White R. Reprod Toxicol 2005.64(8):555-560. Balasubramanian AV. Meeker JD. Rylander L. Filser J.html. 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Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Jackson SJ. et al.46:282-293. Toxicol Sci 1998.58:339349. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Klinefelter GR. Environ Health Perspect 1982. Pratt IA.36:459-479. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Wu ZF. Clemons JH.Phthalates phthalate (DEHP): a cross-sectional study in China. Reidy JA.65:299-308. Peck CC. Environ Health Perspect 2006. Barr DB. Malek NA.45:11-17.112(3):331-338. Toxicol Sci 2000. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Albro PW. 112(5):A270]. Environ Health Perspect 2004. et al. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Caudill SP. Crit Rev Toxicol 2006. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Parks LG. Environ Health Perspect 1986. Ostby JS. Zacharewski TR. Batten PL. Cunningham ML. Bratt H. Silva MJ. Lambright CR. Orton TC. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Matthews JB. Urinary levels of seven phthalate metabolites in the U. Peters JM. Rhodes C.114(11):1643-1648. Meek MD.S. Hodge CC. Rusyn I. et al. Fielden MR. Barlow NJ. Abbott BD.

262 Fourth National Report on Human Exposure to Environmental Chemicals .8) 63.9) 14.8-14.3) 13.9) 11.8 (28. IARC considers BzBP not classifiable with respect to human carcinogenicity.9-30.9 (39.7 (70.9 (16.7-14.0 (43.4 (13.7-17.7) 38.3-21.6) 37.2-183) 101 (78.4) 12.4) 98.5-94. and 0.5-14. population from the National Health and Nutrition Examination Survey.2 (10.1-43.0) 90th 67.6-92.9 (28.3-91.3) 94.5 (67.4) 35.3 (12.6-92.5-18.1) 29.9 (21.1 (20.4) 33. 2000).5-33.2-20.2) 33.4 (32.1-39.5) 30.8-133) 89. it can be released into the ambient air during use or disposal of the products.5 (47.1) 32.3) 54.4) 14.0 (26. 2000).2-17.3-27. and diet is the major source for general population exposure.6) 13.4-92.9) 13.1) 67.9 (11.0 (55.3-88.8) 33.2-33.4 (27.7 (53. interval) 15.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.7-58.4) 80.1 (13.0) 32.2) 15.6 (13.S. vinyl tile.7) 23.1-120) 52.8-16.8-35.3.8-13.1-116) 122 (93.8-76.0 (12.4) 81.3-18.2-39. particularly male animals (McKee et al.8-17.4) 49.2-16.5 (76.2) 17.7-16.3-161) 99.2) 13.6-43.4) 71. sealants.6) 14.1) 68. can produce developmental and reproductive toxicity in rodents.1) 12.0 (23.0 (20.0 (11.7-25.5) 15.0 (14.5) 65.6 (12.8 (53.2 (47.3 (29.5) 82.2) 22.6-132) 103 (84.2) 78.4 (68.0) 16.5) 23.5-41.6) 29.9) 12.7 (51.8 (50.1) Selected percentiles ( 95% confidence interval) 50th 17.8 (21.6-17.5 (55.1-16.1 (13.5 (57.7 (12.6 (13. Food crops take up BzBP.6-29. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.4-62.S.8) 24.8-64.4 (29.9) 14.7 (15.7 (82.0) 33. residents (Blount et al.6) 63.2-116) 122 (102-143) 101 (84.6) 24.3) 13.0-55.1 (58.9-27.8-48.7 (80.4 (53.0 (30.5 (13.8 (71.2 (25.5-35.3-82. respectively.6 (13.8.2) 14.6) 16.8-17. 0.3 (12.4-16.2 (43.6-18.7-16. BzBP can be released into the environment during its production and.6) 35.3-43.8-72.3 (54.2 (19. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.9) 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 39.7-16.9-190) 86.7-13.1) 14.9 (70. and 2003-2004 were generally similar those reported in U.8-98.2-155) 91.4) 51.8 (10.6) 95th 103 (94.4) 129 (98.6) 15.4) 35. High dose BzBP and its monoester metabolites.5 (66.4 (32.8-14.3-18.1) 13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-214) 166 (116-191) 145 (110-213) 88.2) 12.4 (53.3) 37. 2004.3-75.5-36.9-87.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6-38.8) 28.6 (66.1 (10.1-35. including MBzP.8-121) 79.2) 32.8 (80.3 (22.0 (15.5-62.0-26.6 (53.0 (33.1) 76.7-172) 103 (74.9) 18.4-25.7-170) 169 (134-198) 152 (99.4) 108 (96.2 (11.6-79.1) 31.8 (12.6 (32.5) 27.6) 13.0) 70.8-18.3-12.7-35.2 (14.0-85.3 (12.5 (27.9-49.6-116) 122 (102-142) 101 (85. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.4 (48.Phthalates Benzylbutyl Phthalate CAS No.9) 49.9-28.9-16.0 (27.2-40.6-150) 94.8 (86..0 (15.5-36.1-18.3 (30.0 (34. 01-02.5 (61.2) 69.4-120) 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 13.1 (14.1 (55.2) 14.3-34.9 (12.6) 50.1-61.5-40.5-145) 138 (106-241) 143 (127-179) 120 (99.7-15.3 (33.8 (14. NTPCERHR.5) 55.6) 25.4) 65.9 (12.4 (10.0-130) 101 (86. car care products.9) 43.2) 66.6 (13.6-39.9-14.1-16.3-125) Total 15.5) 15..8 (71.2-16.2-115) 113 (91.5 (26.9 (13.1-15.2-38.6 (21.8-41.5) 16.3 (13.6-72.7-119) 99.4 (31. 2001-2002.8-16.6 (41.6) 14.4 (63.1-15. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2 (19.2-31. see Data Analysis section) for Survey years 99-00. and 03-04 are 0.7-82.4-24.1 (32.9 (22.4) 75th 35. some personal care products.9) 15.2-19.3) 23.0) 20.3 (44.1-90.0-106) 58.9-62.4 (59.4-15.6) 35.1.7 (13.7) 40.9-47.3) 63.5-25.1 (19. because it is not bound to products in which it is incorporated.5-84. and to a lesser extent.0) 24.5-97.8) 14.1-38.6) 67.4) 38.4-127) 80.0 (30.1 (14.3) 15.3 (29.3-130) 122 (88.8 (30.3-74.4 (10.7 (11.8 (38.0) 23.0) 34.

6-40. in men attending a Boston infertility clinic (Duty et al.7 (13.6) 25.2-57.1) 80.4-99.4 (63.6) 73..5) 13.3) 12.7-90..7-123) 77.3) 55.7-397) 70.4 (33.1) 23.6-47.4 (21.8 (57.7-12.4-27.1-27.6) 58.1 (46.7-15.5) 46.9) 42.7) 25.3) 13.9-14.4) 51.0 (13.7-29. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.5) 78.5-58. In NHANES 1999-2000.1 (21.9) 100 (80.1 (21.2-21.5 (10.8) 53.9 (15.2-51.4-19.7 (11.5-38.5-26.5-76.1 (21.8) 16.2-15.9) 11.1 (41.8-80.0-26.8-13.1 (11.4-116) 73.0 (33.4-14. 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) 27.0 (41.1) 39.1) 24.4-79.4 (11.1 (23.4) 90th 50.3-11.1 (25.5 (48.8-48.4) 104 (89.3-38.4 (26.1-35.8) 13.5-23. 2003).8 (10.2-49.5) 14.7 (11.1-12.7 (23.9 (22.0 (11.6 (19.9-13.0-90.6-13.8-15. interval) 14.8) 26.0-51.7) 38. and in a small sample of German residents (Koch et al.7-14.4) 28.5) 17.6-81.2 (69.1-125) 86.0) 15.7) 46.4) 25.8) 33.9-23.8 (64.1 (18.4 (25.4-17.7 (55.8) 68.1) 35.0 (62.9) 12.8-15.9 (24.9 (54.3) 36. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 12.6-20. population from the National Health and Nutrition Examination Survey.8-64.4 (34. 2003).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) 14.9) 12.5) 41.8-27.4) 60.7 (12.7) 11.0) 24.9 (10.5 (35.4-14.9 (51.6) 13.2) 26.3 (15.6 (30.8) 56.7-19.7 (11.9-115) 57.6 (15.4-42.7 (54.3-16. 2005.0) Selected percentiles ( 95% confidence interval) 50th 13.8-14.9) Total 14.8 (69.3) 13.0 (38.2-15.1 (13.3 (13.4 (11.5 (9. 2002).4 (10..6) 30.5-13.9 (24.4) 15.6 (30.8-69.6) 12. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.2) 11.4-102) 70.5-58.9) 12.5-57.7 (19. in young Swedish men (Jonsson et al.5) 16.7) 56.2) 15.0-27.8) 53.2-78.9-28..5-29.5-79. 2007).1 (53.8-13.1-79.3 (12.6 (11.2) 32.6 (51.7 (18.8) 11.3) 67.Phthalates York City (Adibi et al.1 (15.4) 21.3) 18.9 (39.3) 29..1-120) 77.8) 33.69-11.8) 34.8-42.2-13.3-73.0 (41.1 (13.73-12.3 (35.1-58.9 (15.6) 53.0-15.95-14.8) 54.6-15.0-53.9 (10. adolescents compared with adults.2-12.0 (10.6 (57.3) 16.9 (9.3 (39.8 (49.3-34.6) 38..0 (67.9) 52.9-16.2) 11.2) 67. 2004).1 (34.8-39.1-29.3-64.0) 12.3) 37.8-14.8-16. 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.3) 90.6 (11.8) 46.8 (11.7-20.2 (56.4) 12. 2006).4) 13.7 (38.6) 75th 25.7) 19.3 (24. 2004. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.9-104) 62.4 (69.1) 17.1) 12.4-15.2) 12.8-13.4 (11.5 (11.5 (12.4) 44.2 (41.2 (40.6-116) 74.5-26.2) 11.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .9 (43.5-42.9) 24.0 (12.0) 60.5 (10.9-69.7-19.1 (43.9 (29.6-12.2-117) 95.0-48.7 (59.7 (21.9-40.5-16.7-14.9-13.3) 21.1 (14. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In an annual sample of German university students.2-13.4 (60.4 (46. A small study of African-American women in Washington.0) 24.7-69..2-17.7-15.8 (30.2-26.3) 73.8 (50.4) 13.5 (56.6 (11.3) 14.6-99.4 (13.0 (12.9-62.4) 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 12.6 (24.1-14.1) 24. Hoppin et al.5) 10.4) 17.1-12.4 (74.8) 80.0 (49.6 (34.6 (22.5-31.6 (36..5) 95th 77. 2007)..6 (14.4-18.5) 23.7-31.5-61. Weuve et al.8-173) 195 (121-305) 229 (99.9) 64.1 (21. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.3) 13.. Hauser et al.4) 50.5) 20.7-61.3 (23.S.4 (12.0) 13.9) 11.8-85.4-93.2 (27.0) 11.8) 108 (75.8-34.4-142) 134 (116-176) 136 (85. 2002.0) 49.3 (38.1) 142 (99.7-56. 2005).9 (12.8 (12.5-213) 49.9-83.7 (13.4-90.8-60.5 (42.3) 89.6) 12.7-20.4-60.0-109) 65.8 (46.9 (55.6-26.7 (14.8 (13.1 (9.3 (60. and females compared to males (Silva et al.8) 24.5-99. 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.5 (49.9 (12.8) 71.3) 14.8) 15.4-23.1 (19.6-86.

The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.111(14):1719-1722. Brock JW. David RM. Dobler L. Chen Z. Needham LL. 2005. et al. Brock JW. Butala JH. Pirkle JL.nih.S. Blount BC. Levels of seven urinary phthalate metabolites in a human reference population. Koch HM. Gans G. et al. Schettler T. Giwercman A. et al.16(4):487-493. Environ Health Perspect 2006. Int J Hyg Environ Health 2007. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.25(2):293-302. Silva MJ. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Angerer J. Environ Health Perspect 2000. Hilborn ED.114(9):1424-1431. Silva MJ. Calafat AM.112(3):331-338. Jedrychowski W. Available at URL: http://cerhr. Caudill SP. J Androl 2004. Barr D. Camann DE. Hagmar L. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).93:177-185. McKee RH. Sanchez GN. Caudill SP. et al. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Third National Report on Human Exposure to Environmental Chemicals. Meeker JD. Rylander L.18(1):122. Bull Environ Contam Toxicol 2002. Barr DB. Silva MJ. Jacek R. Reprod Toxicol 2004. Ryan L. Malek NA.108(10):979-982. Duty S. Needham LL. Hodge CC. Eckard R.22(3):688-695. Weuve J. Atlanta (GA). Davis BJ. et al.68:309-314. 112(5):A270].Phthalates References Adibi JJ. Duty SM. Environ Res 2003. Drexler H. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. NTP-CERHR. Richthoff J. Jonsson BAG. Environ Health Perspect 2002. Koch HM. Hu H. Green RA. 4/20/09 Silva MJ. Caudill SP. Reidy JA. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Sampson EJ. Centers for Disease Control and Prevention (CDC). Singh NP. et al. Epidemiol 2005. Poland. Hoppin JA. Hum Reprod 2007. Perera FP. Reproducibility of urinary phthalate metabolites in first morning urine samples.110(5):515-518. Helm D. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Urinary levels of seven phthalate metabolites in the U. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Rossbach B. Hauser R.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. 2000 [online]. Wiesmuller GA. Phthalate monoesters levels in the urine of young children. Brock JW.210(3-4):319-333. Environ Health Perspect 2003. Ryan L. et al.niehs. Wittassek M. Calafat AM. Baird DD. Silva MJ. Prenatal exposures to phthalates among women in New York City and Krakow. Research Triangle Park (NC). Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.html. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Environ Health Perspect 2004.

60 (5.28-5.40-12.6-20.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.20-2. NTP-CERHR.3 (16.10) 8.8 (9.50) 90th 12.1) 22.30) 10.5) 12.90 (4.3) 33.00) 6.20-6.40-5.1 (13.90 (6. 2003).30-6.10) 2.7 (9.20) 4.96) 3.10-9.30-11.0-18.0 (11. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.72-3..50 (6. 2004. population from the National Health and Nutrition Examination Survey.5) 18. OSHA has established a workplace air standard for external exposure to DBP.63) 3.6 (13.1-25. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.9 (16.1-12.6-14.46 (3. 2005).30-3.5) 18.80 (3.80) 75th 5. DBP can produce reproductive toxicity in male rodents (McKee et al.20 (6.56 (3.20-12.5) 19.4-12.1-17.00-9.30) 2. they have been referred to as monobutyl phthalate (MBP).6 (10.50-4.70-4.00 (7.S.40-4.70 (5.46 (2.6) 17.9-23.44-2..7-18.3-20.50-2.2 (11.6 (13.73-5.3.5 (17.0) 24.4-27.20) 7. and insecticides.5-16.3-24.2) 5.30-6. 84-74-2 Di-isobutyl Phthalate CAS No.90 (4. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.0 (13. Fourth National Report on Human Exposure to Environmental Chemicals 265 .6-34.3 (11.20 (3.50-10.73 (2.7) 14. 2004.40-17. Biomonitoring Information Median concentrations reported in the NHANES 19992000.07 (3.26 (2.68 (2. 2000.0) 20.6 (14.50-6.85-6.80 (2.70) 5.4) 22.0) 12.70-4. 2001).8) 40.55 (3.56) 3.10-9. 2005.10-2. 2000).20-9.10 (4.90-4.2 (12.5 (20.5 (11.5) 14.19-3.7) 18. mostly as MnBP (Anderson et al.30-7. in men attending a Boston infertility clinic (Duty et al.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.50) 8..5-29.6) 17. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.46) 2.60 (2.0-14. and in a small sample of Japanese adults (Itoh et al.67 (5.81 (3.30-2.7) 15.0) 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 2.0-38.46-5.6 (11.0) 9.6 (10.10) 9.30 (1.9-14.24-8.00) 7.30) 6.10) 3. Following oral administration of DBP to humans.70 (2.70) 3.97-7. Survey Geometric mean (95% conf.0-25.7-31.56 (5.7-20. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.6) 16.60 (4.00-11. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.22) 3.60-6. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.97) 4. In addition.2-33.80-5.6) 26.91) 4.5) 22.90-7.3-18.0 (13.5-16.80 (5.1) 25.00) 4.10) 11. Koch et al.00-6.37) 6.66) 2.3 (13.8) 677 652 703 699 1216 1088 Limit of detection (LOD.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.30 (3..1 (8.00) 10.1-20.6 (14.02) 4.60) 3..2-14. and also in some printing inks.4) 12.90-2.8) 21.40-3.7 (17.6 (29.5) 23.50) 2.4) 5. 2003).17) 4.0 and 0.50 (3.50) 5. CDC.4 (20.5-24.Phthalates Di-n-butyl Phthalate CAS No. 2005).30 (4.3 (19.7 (18. 2005).7-31.80 (2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.50) 7.17 (2.80 (5.71 (2.3-48.10 (3.9) 10.40 (7.40 (2.6) 12.97) 2.6) 16. about 65% to 80% of a dose is eliminated in urine within 24 hours. 2007).20 (7.6-18.1) 16.22 (3...70-8.90-4.40 (6.50) 18. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics. pharmaceutical coatings.90) 12. When total DBP metabolites have been measured. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.00-4.40) 5.3) 3.0) 13.7) 7. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.40 (2.10 (4.30-13.20-12.3 (16.00) 4.11-3.2 (8.00 (5.80-5.30) 10.00-6.7 (7.40 (3.33 (2.48 (2. Hauser et al.0 (19.3 (18..5) 25.4 (14.3-19. interval) 2.6-26.40-4.3-30.9) 15..60 (8. in a small sample of pregnant women in New York City (Adibi et al. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.40-9.3 (13. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.2-22.6) 10.55) 2.9 (16. Studies of children found age-related differences in urine MBP levels.7) 4.7 (17.56-4.S.40-3.7 (16. residents (Blount et al.82-3.30) 5.49-2.5 (27.59) 3.3-43.5 (10.90 (3.84) 4.43) 6.6 (9.3) 18.

04) 7. 2004).3) 13.43) 3.1) 4.32 (7.74-3.7 (21.5) 15.5 (11.18 (4.46-11.51) 5.38 (6. In an analysis of NHANES 1999-2000.1-12.11) 5.11-2.30 (6.38-10. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.20-4.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .59 (4. 2005).82) 4. 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.25) 5.72) 5.13-6.2-15.8-13.66) 4.57-4.0 (10.04) 3.18) 3.03-11.00-3.1-15.76 (3.53-4.81 (3.99-4.7 (9.64-10.54 (4. Weuve et al.98 (2.20-3.32) 7.62-12.44 (3.51) 2. 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.2 (11.6) 11.56-4.6) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2. up to four and 13 fold.47 (3.33 (3.00 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.30) 2.1 (11.0-18.7 (11.68) 3..8 (9.00-3..39-3.9-40.88 (2.79-8.3) 28.9 (15.6 (9.9-26. samples from German university students had consistently higher median urine levels of MnBP and MiBP..1) 13.92 (7.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.5-19.56-15.1) 10.3 (13.69) 6.97-2.8 (8.31) 2.52) 3.81) 4.37) 3.0 (12.9) 12.94) 6.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.66) 2.6-19.43) 3.9 (11.S.66) 10.7) 19.57 (3.82 (4. 2007).20 (2.29-8.28-13.24) 3.00-7.2 (10.02 (7.8 (10.89) 6.18 (1.9-16.80-3.and gender.11 (5.26-2.34 (3.75 (6.46) 3.5) 13.27-12.78) 9.0) 3.5 (9.76-15.08-2.8-36.86-4.1-25.56) 5.64-7.66 (8.76-3.81 (6.64-7.17-12.17 (2.4) 7.52-3.0) 7. Survey Geometric mean (95% conf.21 (5.18) 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.6 (8.74 (4.13 (2.28 (4.69 (2. interval) 2.7) 10.18-4.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.22 (2.54 (2.. 2007).18-10.6-19.68 (2.2-13.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.7-28.78-8.1) 15.36-2.35) 3..19 (2.81) 9.53-3. 2005).08) 75th 4.73 (5.52-20.15-4.79 (4.58-4.4 (12. respectively.61-3.6 (15.31 (2.1 (10. population from the National Health and Nutrition Examination Survey.01-2.14 (4.69-7.83 (2.0) 15.8-18.8) 10.84 (8.20-2.76-3. 2002.72-7. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.79-6.80 (3.6 (8.78) 8.31 (7.6) 13.36-7.21) 10. 2004).69) 4.3) 18.85 (2.1-24.96 (3.42) 2.15) 3. An analysis of NHANES 2001-2002 showed similar age.4) 15.7) 3. while MnBP declined (Wittassek et al.45) 3.32 (3.2) 9..07-5.7 (13.94 (5.10-5.3) 13.20 (7. 2006).3) 16.86) 6.1) 11.2) 24.4) 23.1) 7.09-2. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.52 (2.33-9.31) 2.47-5.2) 8.03 (5. Over this time.3 (17.41 (2.68) 5.33 (2.4-16.8-18.26 (2.99) 7..65-4.84 (4.29-3.89-5.07 (2.51) 15.62 (6.47-12.67-5.58-3.33) 3.17) 90th 8.7) 11. Between 1998 and 2003.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. to about two to fourfold higher (Fromme et al.94-12.03-7.65-11. than adults in NHANES subsamples during the same time period.20 (2.57 (3.65 (4.43) 3.95-3.56) 2.80) 7. the students’ median values for MiBP levels remained relatively unchanged.53-5.0) 11.95) 10.9 (9.6 (10.46 (2.05) 2.55-6.91-6.89 (3.75 (4.54) 2.04-5.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.6 (12.02-10.39) 5.95) 2. ranging from more than one-tenth the NHANES median (Itoh et al.0 (8.93-6.

2-24.0-32.7 (51.S.1) 30.0 (17.5) 24.6-29.7) 52.7 (16.9 (17.9 (17.7 (22.6) 17.2-87.1 (51.1-24.0 (45.3) 19.0) 120 (98.3) 36.6-69.1 (19.0-24.1 (36.1 (34.6-48.6-113) 108 (90.5) 40.5 (74.1-92.7) 124 (98.8) 58.8-119) 90.4) 64.7-106) 69.6-20.4-26.9 (79.2-22.5-44.0) 20.1-80.5) 36.4 (84.7-116) 95.2 (25.4.5) 85.4 (35. interval) 24.9) 26.0-58.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.5) 17.7) 92.5-47.2 (21.6-36. 1.2) 42.8) 19.4-44.2 (21.1 (17.6) 46.6 (22.2) 26.1) 25.1) 36.0 (72.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.6-44.2 (19.7 (38.7 (18.2-32.0-51.7) 42.0) 30. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7 (64.5 (59.4 (72.7-124) 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.7-24.2 (59.2 (58.4 (21.0 (15.4 (19.1) 46.7-92.1 (54.4-25.6 (44.9 (79.4-60.2 (78.8) 75th 51.3 (56.4 (35.7 (24.7-111) 64.9.2) 32.9-22.6 (90.8-123) 101 (90.6 (19.2) 20.4-31.5-47.8-42.6 (16.4 (35.3) 23.7-34.6 (32.4) 22.0) 31.6) 80.7 (70.1) 23.0 (18.7 (19.2 (75. Survey Geometric mean (95% conf.1) 20.9) 46.7-53.1) 19.2-33.7-20.6-40.3 (36.8-29.5-117) 95.2-93.6) 71.7-42.5 (28.2 (18.5 (30.5-60.2 (20.3-145) 85.3-79.2-56.9-87.0-26.1-75.9-92.2-159) 92.4-18.5) 65.5-27.5) 31.8 (19.6-31.7) 28.6-29.5 (59.7-117) 118 (108-143) 93.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.6-143) 127 (99.5) 20.4 (35.0) 117 (104-131) 112 (84.1-51.1-29.0 (78.3-136) 137 (107-162) 119 (90.5 (29.4 (38.1 (26.2 (74.5) 95.0-73.9) 36.1 (19.1 (28.4 (36. 01-02.0 (36.2) 90th 98.7 (43.1-20.9 (20.2) 68.0-19.4 (25.8 (57.4-159) 107 (84.0-19.3-85.0 (31.3-24. Fourth National Report on Human Exposure to Environmental Chemicals 267 .3 (23.0-21.2-23.5) 21.7-26.4) 52.7 (28.5) 47.9) 29.6) 21.2 (17.4 (23.6 (48.1 (16.1-82.1-22.7-121) 97.7 (18.9) 18.9-114) 116 (97.5) 36.2-63. referred to as monobutyl phthalate (MBP).3) 26.0) 84.5) 19.9-28.8) 23.0) 38.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1) 23.3 (60.7-42.9-53.9-42.7) 74.6-24.1 (58.4) 20.3-76.5) 78.1 (18. population from the National Health and Nutrition Examination Survey.6) 20. and 0.1) 23.5-43.6 (26.6) 38.3 (42.8-22.6) 35.3) 21.2) 62.0 (23.1 (41.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.8) 48.0 (25.3-96.7-34.4) 59.6 (55.1 (31. *In the 1999-2000 survey period.0) 21.5-53.7 (33.8) 62.6 (65.3 (30.5) 37.9-79.9) 71.0-24. and 03-04 are 0.6-49.6-37.1 (21.3 (30.8) 43.1) 17.2) 38.8-25.1 (19.6-33.3-40.5-42.3 (51.3 (37.5) 34.5) 26.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.3-67.6) 39.2 (79.1.3) 24.1-27.1 (19.5-121) 106 (94.6 (61.7-91.9) 21.1) 31.0 (20.4 (71. respectively.0) 27.2-21.3 (23.1) 47.9-22.3 (17.3) 40. see Data Analysis section) for survey years 99-00.3-21.2-49.3) 18.9-33.8-132) 95.9) 75.1 (62.3-60.4-20.7-127) 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 22.9-101) 77.0 (30.2-114) 73.4-42.

4) 51.3 (19.8) 75th 38.5) 91.5) 39.7-23.7-28.4) 21.6-53.4 (50.9-38.3-78.7) 20.0 (69.4 (16.0) 25.3-40.3-71.5 (81.1 (29.1) 17.2-85.0) 53.8) 13.4 (18.6) 23.2) 21.8) 20.8 (65.9 (20.6) 64.2-16.8) 30.6) 31.4) 53.4 (45.1) 22.9-26. 268 Fourth National Report on Human Exposure to Environmental Chemicals .1 (15.0 (43.3 (17.0-75.1) 53.9 (16.3) 59.0 (18.0) 28.8 (18.4-47.2) 159 (102-263) 147 (93.6 (41.2) 74.1 (56.0 (61.6-74.4-131) 81.9) 62.6) 39.7 (14.4 (33.7 (12.6) 24.1) 21.3 (69.6 (25.2-179) 84.6 (25.4) 15. Survey Geometric mean (95% conf.7-19.6) 34.7-51.4 (23.4 (50.9-68.2-106) 64.8) 34.0) 35.8-23.9 (30.8-32.7) 42.3 (17.4 (19.7 (16.0) 55.4 (13.3 (24.5-142) 89.9 (21.5) 134 (93.4 (47.6) 25.6-19.9-14.1-62.6) 18.6-28.8) 35.1 (46.0 (50.9 (39.5 (14.0 (71.1) 20.6-43.0 (27.0-41.9-34.5 (18.1-32.4 (16.2-21.7-20.1) 50.9) 52.5 (64.2) 31.3) 19.5-41.4) 62.9 (58.1 (61.5) 84.3) 35.5-18.1-83.2-22.3-39.8) 28.3) 20.4-34. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1 (32.1-23.6-42.7-26.2 (19.3-20.3) 17.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.4-135) 71.5 (30.2-28.4) 19.7 (60.5-22.8) 19.6 (61.8) 17.4-76.9-36.7 (73.6-155) 91.9 (35.8) 23.6-22.3 (28.6 (19.9-84.0 (52.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2-22.6) 65.1 (21.3 (17.5-76.3-18.3 (21.0-90.9) 30.2-61.6 (31.9 (56.7-21.0-60.7-78.6) 38.7 (43.3-23.8 (18.1-21.2) 65.2 (19.7 (20.0 (15.4 (56. interval) 22.8 (25.0) 59.0) 26.2-73.6-119) 63.0 (18.3-106) 74.0) 29.6) 37.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.0-92.3-21.1 (34.7 (27.1) 37.6) 24.8-24.9) 14.6-23.0-19.5 (18.4) 16.4 (53.7 (28.4-72.5-142) 81.3) 67.4) 15.0 (70.9-68.9) 49.9) 28.3 (52.5) 82.3 (60.9) 19.7-19.7 (60.1-128) 97.S.9) 24.0-38.4 (17.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.6-128) 96.2-27.0) 75.8 (33.0 (19.8 (13.2-22.9) 20.4 (31.5-23.2-48.3-21.9 (19.8 (17.8) 17.4-61.1-18.9 (64.8-235) 137 (108-198) 88.0-113) 104 (83.6-24.3-81.3) 33.6) 14.5) 60.5-30.0) 41.3-32.2-18.6-27.4) 20.2 (38.3 (76.3 (52.0-17.6-50.8) 40.6-16.2) 59.3 (71.5-16.9-49.0 (20.8 (22.3-17.7) 36.4 (20.1) 44.3 (46.5-21.5) 17.6-23.8) 34.5-64.3-38.3 (42.2) 16.3) 52.7-37.2-86.0 (34.7) 19.6 (74.4-65.6-44.1-99.5-37.6-92.3-114) 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 17.6-32.5-15.4 (31.3 (16.4 (31.0-47.9) 39.8 (16.0 (26.6-24.4 (37.3) 33.4 (68.8) 22.5) 21.3) 21.5 (15.6 (29.3) 18.4-24.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9) 91.9-100) 86.7-80.2 (16.9-56.6) 83.3 (55.3-49.9-105) 85.8 (50.1) 42.9-70.6 (27.3 (48. population from the National Health and Nutrition Examination Survey.4-103) 117 (83.5-70.0) 94.8-24.8-43.9 (30.8) 20.9 (35.6 (72.6-44.7-42.0 (16.0) 19.7 (19.8) 17.1) 61.3) 19.5) 90th 68.6 (57.0) 70.1) 35.7 (54.4 (17.9 (73.0) 81.1-99.3-26.6-26.8 (18.8) 63.9 (37.4-164) 96.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.2 (83.7-39.1) 20.2 (35.6 (17.7 (81.0) 108 (71.9 (30.7 (57.

Fourth National Report on Human Exposure to Environmental Chemicals 269 . Hauser R.93:177-185. Koch HM. David RM. Available at URL: http://cerhr. Castle L. et al. Drexler H. Poland. Hum Reprod 2007. Third National Report on Human Exposure to Environmental Chemicals. Jacek R. Camann DE. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Caudill SP.112(3):331-338. Needham LL.210:21-33. Scotter MJ.16(4):487-493. Calafat AM. Caudill SP. et al. Ryan L. et al. Massey RC. Reidy JA. Boehmer S. 2005. Blount BC.210(3-4):319-33. Phthalate monoesters levels in the urine of young children. et al. Richthoff J. Silva MJ. Int J Hyg Environ Health 2007. Yoshida K. Masunaga S. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Ryan L. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Rossbach B. Dobler L. Environ Res 2003. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Jonsson BAG. Brock JW. Koch HM.108(10)979-982. Rylander L. J Androl 2004. Duty SM. Malek NA. Springall C. Environ Health Perspect 2000. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. et al. et al. Sampson EJ. Hagmar L. Meeker JD.18(12):10681074. Environ Health Perspect 2003. Barr D. Int J Hyg Environ Health 2005. Giwercman A. Reprod Toxicol 2004.111(14):1719-1722. Helm D.S. Weuve J. McKee RH. Food Addit Contam 2001. Epidemiol 2005. Caudill SP. Research Triangle Park (NC). NTP-CERHR. Needham LL. Int J Hyg Environ Health 2007. Hodge CC. Perera FP. Duty S. Environ Health Perspect 2004.114(9):1424-1431. Hu H. Chen Z. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.html. Hilborn ED. Koch HM. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Silva MJ. 2000 [online].niehs. Gans G. Singh NP. Calafat AM. Itoh H. Schettler T. Angerer J. Urinary levels of seven phthalate metabolites in the U. Sanchez GN. Prenatal exposures to phthalates among women in New York City and Krakow. Wiesmuller GA. Brock JW. Anderson WA. Eckard R. Silva MJ.Phthalates References Adibi JJ. Levels of seven urinary phthalate metabolites in a human reference population. Wittassek M. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Centers for Disease Control and Prevention (CDC). Pirkle JL.68:309-314. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach.gov/chemicals/ phthalates/dbp/dbp-eval. Barr DB. Bull Environ Contam Toxicol 2002.18(1):122. Silva MJ. Environ Health Perspect 2006. Jedrychowski W. 112(5):A270]. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. et al. Bolte G. Atlanta (GA). Butala JH. Green RA. Fromme H.25(2):293-302. et al. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.nih. Angerer J. Drexler H. 4/20/09 Silva MJ.22(3):688-695. Urinary phthalate metabolites and biomarkers of reproductive function in young men.208:237-245.

600) .300-.500) < LOD 1.300) < LOD .90) .300-.300-. Survey Geometric mean (95% conf.300 (<LOD-.200-.500) . Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.700) .Phthalates Dicyclohexyl Phthalate CAS No.500) . and polymers.400 (<LOD-.500) 1.300 (.400 (.300 (.500 (.400-. and polyvinyl chloride.200-.00-2. only levels at or above the 90th percentile could be characterized.400 (.3.700) . 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.400 (. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400-.00 (<LOD-1. 270 Fourth National Report on Human Exposure to Environmental Chemicals .500-. polyvinyl acetate.50) .300-.300 (.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 . 0.20) . In this Report.10 (<LOD-1.400-.200-.70) .500) .500 (.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 1.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.600) .700) .200-.500 (. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.300 (.00 (<LOD-1. 01-02.400 (<LOD-.500 (. and 0.400 (.600) .00) .2. and 03-04 are 0.300-.300) < LOD .300-. see Data Analysis section) for Survey years 99-00.900-1.500 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. respectively.70) .80) .400 (.500 (.600) < LOD . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.50) .200 (<LOD-.500 (. < LOD means less than the limit of detection.500) 1.300 (.9.400-.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .70 (1. population from the National Health and Nutrition Examination Survey.400) < LOD < LOD .10 (<LOD-1.500 (.200-.400 (.00 (<LOD-1.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . which may vary for some chemicals by year and by individual sample.500) 1. resins. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.500) .400) < LOD 1.600) .400-.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300-.500) < LOD < LOD .400-.400 (<LOD-.500) < LOD < LOD .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400-.400) 1.70 (1.400) 1.10) . including nitrocellulose.300 (.10 (<LOD-2.600 (.00-3.600) .S.300-.10 (.200-.400 (<LOD-.500 (.300-.400 (. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

33 (<LOD-3.34) .770-1.17) .82 (1.670-1.54) .310-.910 (.260-.510 (.910 (.370 (<LOD-.310) < LOD .530) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf.06) .530-.690) < LOD 2.590 (<LOD-.36-1.500 (.420-.330 (.400-.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 .450 (.16) .410 (.290-.53) .500-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .420-.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. Fourth National Report on Human Exposure to Environmental Chemicals 271 .710) .05) .880 (.480 (.360-.470 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.590 (.740) < LOD < LOD .270) < LOD .690-1.530) 1.690) < LOD < LOD .12-1.74) .54-6.82) .250 (.500) 3.830) 1.10) .510-.14 (<LOD-3.53) .800-1.44) .790-1.43 (1.16 (<LOD-3.560) 1.350-.620) < LOD .770) < LOD 2.630 (<LOD-.220 (<LOD-.670 (<LOD-.11) .330 (.67 (1.590) 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 .06) .530-1.690) < 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 1.170-.33) .00 (<LOD-3.910 (. population from the National Health and Nutrition Examination Survey.950 (.380-.770-1.470) 3.380 (.740) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.660) .390 (.54 (<LOD-2.690 (.940 (.450 (.610 (.910 (.530 (.630 (<LOD-.240-.770 (.S.18) .420-.660) < LOD < LOD .22 (<LOD-1.490) .770-1.400-.00) .

Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.2-102) 95.3-103) 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf..8-111) 85.1-93. Biomonitoring Information MEP levels in the NHANES 1999-2000.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.4. 272 Fourth National Report on Human Exposure to Environmental Chemicals .7) 71.7 (70. population from the National Health and Nutrition Examination Survey. and hand lotions.9-92.Phthalates Diethyl Phthalate CAS No.1 (71. 2007). a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.. 2002). 2001-2002. interval) 179 (156-204) Selected percentiles ( 95% confidence interval) 50th 164 (136-201) 169 (141-194) 174 (151-208) 75th 454 (370-538) 465 (415-527) 502 (457-555) 90th 1260 (1010-1480) 1230 (1040-1440) 1380 (1170-1750) Total 178 (159-199) 193 (169-220) Sample size 2840 (2150-3770) 2536 2500 (1860-3220) 2782 2700 (2160-3310) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 91.3 (74.9. 0. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. Products that may contain DEP include perfumes. see Data Analysis section) for Survey years 99-00. and 03-04 are 1. 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. respectively.. deodorants. 2003) and African-American women in Washington. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.9 (61. and also in men attending a Boston infertility clinic (Hauser et al. DC (Hoppin et al. and 0. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.5) 81.2. shampoos.S. In contrast. particularly those containing fragrances. soaps.3 (82.4 (62. 01-02. 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. colognes.

. 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. Analysis of NHANES 2001-2002 showed similar findings.2 (66. 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. In an analysis of NHANES 1999-2000.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 . 2005).0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-110) 96. 2003) were slightly lower than levels found in NHANES 2001-2002.5-114) 101 (87.5-113) 122 (93..9 (82. population from the National Health and Nutrition Examination Survey.3-105) 87. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.0 (66.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. 2004). Biomonitoring studies on levels of MEP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEP than are found in the general population. This age-related trend is opposite the direction seen for other phthalates. 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. Other population estimates also differed by sex and race ethnicity (Silva et al.7-110) 81.6 (77.6 (65.. 2002). Median MEP levels found in a small sample of German residents (Koch et al.

Duty S. Hoppin JA. Brock JW. Poland. Perera FP. Phthalate monoesters levels in the urine of young children. Brock JW. Environ Health Perspect 2004.68:309-314. Hodge CC. Camann DE. Reproducibility of urinary phthalate metabolites in first morning urine samples. Koch HM. Silva MJ. Bull Environ Contam Toxicol 2002. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Malek NA. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Meeker JD. Baird DD.110(5):515-518. Barr DB. Caudill SP.Phthalates References Adibi JJ.S. Reidy JA. et al. Third National Report on Human Exposure to Environmental Chemicals. Needham LL. Hauser R. Jedrychowski W. Environ Health Perspect 2003. Centers for Disease Control and Prevention (CDC). Barr D.111(14):1719-1722. et al. Drexler H. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.112(3):331-338. 2005. Hilborn ED. Environ Res 2003. Angerer J. Silva MJ.22(3):688-695. Caudill SP. Singh NP. 112(5):A270]. Urinary levels of seven phthalate metabolites in the U. Jacek R. Hum Reprod 2007.93:177-185. Prenatal exposures to phthalates among women in New York City and Krakow. Atlanta (GA). Ryan L. et al. Davis BJ. Environ Health Perspect 2002. Silva MJ. Rossbach B.

7-58.0 (17.40-12.5-41.96) 4.23 (3.4) 13.57-7.80-4.10 (3.82) 3.5 (12.40) 4.10 (3.0 (19.90-5.50 (3.80 (8.1-27.90 (1.40) 75th 7.56 (2.00) 11.40) 8.91-3.40 (6.89-3.40-8.4-27.4-40.1) 22.10) 8.23) 3.10-5.6-130) 31.93) 6.5) 43.2-28.5-17.14 (1.30 (3.12 (4.50) 9.40 (4.40-8.50-8.16-3.24-4.41 (3.00) 1.7) 6.54) 4.26-2.5-28. interval) 3.50-2.0-84.00 (7.5) 37.0 (14.5 (11.00-3.5 (18.0) 11.6) 9.2-39.0-19.42) 3.2 (11.7) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.00-3.6) 39.63-4.8) 17.1-17.60) 7.50-11.2-17.9 (15.9) 27.9 (17.30-8. population from the National Health and Nutrition Examination Survey.10-11.10) 3.10) 3.0) 35.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.0 (18.9) 18.50 (7.50 (8.00-4.80-4.9) 13..4) 6.5) 40.50-3. toys.1-48. see Data Analysis section) for Survey years 99-00.50-6.40 (2.70 (3.68 (3.2-35.70 (1.10-3. Albro and Lavenhar.1-17.5-36.60) 90th 14.6 (41.90-8.8-50.9-55.50 (7.1) 29.85 (3.10-5.60) 3.80 (4.0) 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 3.5-40.30 (6.70-4.9-26.4 (16.0-29.5) 23.90) 4.3 (11.1-29.67-4. 1.90 (3.10) 3. After parenteral administration.6 (12.9 (17.5 (31.10) 2.27 (3.80 (1.80-9.00-5.7) 35.7) 37.1) 19.40) 1.1 (11.00 (5.10-5. Concentrations in plastic materials may reach 40% by weight. which is used for many consumer products.80-8. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).70 (8.83) 2.50 (3.10 (4.9) 5.80-5.30-13.3 (24.31-4.60) 4.6 (9.2) 42.42-5.0 (19.34 (2.1) 25.40) 9.40-11.6-23. Peck and Albro.0) Total 4.9 (26.5 (25.3 (19.60) 8.0 (9.5) 31.4) 5.0 (13.7) 19.19-3.37-4.8) 15. mainly polyvinyl chloride.3 (10.21 (2.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 01-02. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).86) 2.4 (13.1 (8.4-20.87-2.49 (3.0) 23.4-53.70 (1.35 (1.1982).50-20.21 (2.5 (12. and 0.3-25.50-5.0 (21.3) 28.92-2.2) 29.60) 9.2 (29.2) 6.6 (10.16 (2.10 (6. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.9) 13.70-5. 1982.8-36.5-28.3) 52.4) 7.90) 1.70-2.60-11.6-28.70) 16.4) 33.6) 15.20 (1.30) 2.90-3.8 (17.60-7. Following ingestion.0 (16.31 (3.2) 23. 1989.60 (5.00) 3.0) 23.8-47.50 (3.S.92-2.